tag:blogger.com,1999:blog-59957547779069783142024-02-19T02:36:10.637-08:00Evolving HealthEyeing the world of food, nutrition, and medicine through the lens of evidence and evolution.daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.comBlogger457125tag:blogger.com,1999:blog-5995754777906978314.post-91957009746615902372013-04-14T15:21:00.003-07:002013-04-14T15:21:56.218-07:00The Evolving Health blog is moving to evolvinghealth.wordpress.comAlthough I've enjoyed posting from Blogger for five years now, I've found that Wordpress offers me a lot more of the functionality that I need.<br />
<br />
So, I hope you'll join me for more posts about evidence-based food, nutrition and medicine updates over at <a href="http://www.evolvinghealth.wordpress.com/">http://www.evolvinghealth.wordpress.com</a>.<br />
<br />
Also, don't miss my coverage of <a href="http://evolvinghealth.wordpress.com/2013/04/13/preview-of-american-society-for-nutrition-meeting-at-eb-2013/">Experimental Biology 2013</a> from April 19-24!<br />
<br />
Sincerely,<br />
David daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com0tag:blogger.com,1999:blog-5995754777906978314.post-55954249067273871372013-04-09T00:54:00.002-07:002013-04-09T12:54:51.274-07:00Why we should adopt a "zoobiquitous" approach to health<div style="text-align: center;">
<a href="http://evolvinghealth.files.wordpress.com/2013/04/800px-grizzlybear55.jpg"><img alt="Image" class=" wp-image aligncenter" height="345" id="i-636" src="http://evolvinghealth.files.wordpress.com/2013/04/800px-grizzlybear55.jpg?w=650" width="520" /></a></div>
We are all animals. It's a fact that may be unsettling for some, but for others it is a fountain of understanding and of inspiration. Since 1859, thanks to Charles Darwin, our place in the animal world has been firmly established. Yet, to this day, it is all too common within medicine (and nutrition) to have the tendency to develop a narrow-mindedness about ourselves that disconnects us from the natural world. Rarely do medical doctors ever look beyond, to other animals, for a broader perspective about their fields. As the veterinarian insider joke goes, <em>"What do you call a physician? A veterinarian who can only treat one species." </em><br />
<br />
This is where <em>zoobiquity</em> (a different, <em>zoobiquitous</em> approach to medicine)<em> </em>comes in.<br />
<br />
What is <em>zoobiquity</em>? When a story of how two obese Alaskan grizzlies lost hundreds of pounds helps inform nutritionists about how they might advise their human patients on weight management, you could say that is an example of <i>zoobiquity</i>. When a psychiatrist finds she is able to kindly comfort a patient diagnosed with anorexia by pointing out that an eating disorder is nothing ashamed of and that, in fact, it is quite common across several species, that's <em>zoobiquity</em>. And, when a veterinarian oncologist and human oncologist come together to discuss the similarities of their animal and human patients and share data in an effort to improve medical outcomes of their patients, that's <em>zoobiquity</em>.<br />
<a name='more'></a><br />
<br />
<div>
The term, a merge of the words "zoo" and "ubiquity," was coined by UCLA cardiology professor Barbara Natterson-Horowitz, M.D., and science journalist Kathryn Bowers as a way to describe their call for a coming together of three scientific fields: human medicine, veterinary medicine, and evolutionary biology. The duo also used the word as the title of their book, <em>Zoobiquity: The Astonishing Connection Between Human and Animal Health,</em> the <a href="http://www.amazon.com/Zoobiquity-Astonishing-Connection-Between-Vintage/dp/0307477436/ref=sr_1_1?ie=UTF8&qid=1365486660&sr=8-1&keywords=zoobiquity">paperback version</a> of which has just gone on sale today. I highly recommend you purchase a copy to read even if you are not necessarily interested in medicine; the book is still worth the read because of what Bowers calls "cocktail party fodder."<br />
<br /></div>
<div>
</div>
<div>
In the book, for example, you'll learn all sorts of interesting facts: that dinosaurs also suffered from cancer, that fish faint, that horses suffer from sexual dysfunction, that all sorts of wild animals can at times develop eating disorders or overeat and become obese, that koalas suffer from chlamydia, that birds self-injure, and that wallabies get stoned. A passage that best sums up the message of the book is this one about breast cancer resulting from a genetic mutation of the BRCA1 genes that is shared among different species: "When it comes to breast cancer, a jaguar originating in South America and an English springer spaniel in Sweden might be medically more relevant to an Ashkenazi Jewish woman than her next-door neighbor is."<br />
<br /></div>
What led me to read the book was a long-held fascination with the topic of how health in the animal world relates to the human world. Because of my interest, I sought out a conversation with the co-authors and, now, I'm delighted to offer you this interview from last Sunday: <em></em><br />
<strong><br /></strong>
<strong>Edited interview with <i>Zoobiquity </i>authors</strong><br />
<br />
<strong>DESPAIN</strong>: How did you come up with the term, <em>zoobiquity</em>?<br />
<br />
<strong>DR. NATTERSON-HOROWITZ</strong>: We had been thinking a lot about all these overlaps from everything from cancer and heart disease to obesity to eating disorders in adolescence. We were looking for clinically relevant points of intersection that brought together human medicine, veterinary medicine, and evolutionary biology. And we found ourselves really struggling to describe it not only other people, but for our own purposes. There wasn't really a word that would describe bringing these three fields together. So we decided to coin our own word. We tried to find a word that brought together elements we wanted. So, "zoo" and "ubiquity" became "zoobiquity."<br />
<br />
<a href="http://evolvinghealth.files.wordpress.com/2013/04/wallaby.jpg" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img alt="wallaby" class="size-medium wp-image-643 alignright" height="199" src="http://evolvinghealth.files.wordpress.com/2013/04/wallaby.jpg?w=300" width="300" /></a><strong>DESPAIN:</strong> What's your favorite example of <em>zoobiquity</em>?<br />
<br />
<strong>BOWERS:</strong> I'm really interested in the shared physiology that we have across species. That seems in some ways the lowest-hanging fruit, that we share blood and bones and other physiologic systems with other animals. I've been really interested in the crossovers in the psychiatric realm, how animal behavior and human psychiatry have more in common than we thought. What in humans we might call a mental illness, or eating disorders, or anxiety, or obsessive-compulsive disorder. In our book, we have examples of self-injury. If a human was exhibiting this, they would be taken to a psychiatrist. We think of them as maybe being part of our human cultures, but they're actually shared with other animals because the roots may be even deeper in mechanistic or physiologic areas that create behaviors seen across species.<br />
<br />
<strong>DR. NATTERSON-HOROWITZ:</strong> When psychiatrists typically think about problems like cutting, or anorexia, or bulimia, there's a tendency to think about those problems in a pre-frontal cortex capacity. Psychotherapists use language to access those symptoms and to treat them with talking therapy. The idea that animals would share these in the first place required us to take a little bit of a step that's longer than what we typically do when we think about animals.<br />
<br />
<b>D</b><strong>ESPAIN:</strong> One of the chapters in your book is about the "Fear of Feeding". This is related to what you're talking about.<br />
<br />
<strong>DR. NATTERSON-HOROWITZ:</strong> If you look at the fear of feeding or of eating disorders, you find that psychiatrists will tell us that, in human beings, most patients diagnosed with an eating disorder will also have an anxiety disorder. It's common to have a comorbic psychiatric condition if you have an eating disorder. So if an anxiety disorder is extremely associated to eating disorders, what does that tell us? Well, it suggests that there's something about eating that connects to fear. And, you start looking at connections between fear and eating in the animal kingdom and it becomes very clear that an unsafe environment absolutely affects animal eating behavior. We have examples of that: an environment that has a high density of predators where there's a lot of risk, prey animals may restrict the amount they eat, the time they eat, perhaps the range of where it eats. When the predatory threat is reduced, the animal is more relaxed and the animal gets fatter, because the animal eats over a greater period of time. When you look at a human patient with anorexia, when they're in the throes of the disease, when they are extremely anxious, you see their eating is highly restricted. As the treatment continues and is hopefully successful, and as anxiety is reduced, there's this loosening up, a relaxation of eating. We think that parallel speaks to this highly conserved neurophysiologic system, whether it is the autonomic nervous system, or whether its mammalian or even pre-mammalian, it really suggests these are highly conserved systems. This is a new way for psychotherapists and psychiatrists to think about these eating disorders in human patients.<br />
<br />
<strong>BOWERS</strong>: Barbara has mentioned predatory stress, but there's even the idea of social stress. Social stress can affect animals and their eating either by where they are in their social hierarchy or almost by the way they need to behave. We were just talking with <a href="http://www.nationalgeographic.com/explorers/bios/lain-couzin/">Iain Couzin</a> who was giving a lecture at UCLA and he was describing locusts swarms and how big a deal cannibalism is in the way that those animals organize their group behavior, so even just putting something like eating and social movement in the same arena, I think, really opens up what a human nutritionist might be able to think about when counseling a single human being.<br />
<strong><br /></strong>
<strong>DESPAIN</strong>: Being a nutritionist, one of my favorite chapters in your book was <i>Fat Planet</i> where you tell the story of two obese Alaskan grizzlies Jim and Axhi who were treated at Chicago's Brookfield Zoo by nutritionist Jennifer Watts. Watts changed their diet and lifestyle in ways that was informed by knowledge of their natural ecology. It wasn't a "perfect wild diet" -- as that's fantasy -- but there were changes like considering the environment's cyclical periods of abundance and scarcity as well as season's effect on their intestinal microbiomes. Previously, I've written about nutritionists doing similar things both with lemurs and Komodo dragons that suffer from obesity and diabetes. What would you say are the key takeaways in dietary advice that humans can learn from your examples?<br />
<strong><br /></strong>
<strong>DR. NATTERSON-HOROWITZ:</strong> There were so many surprises that we encountered in researching the book. One early misconception that we bumped up against was this idea that only human beings overeat. There seems to be this fantasy that animals in their natural setting have internal regulatory systems that would result in eating only to satiety and that would be it. This idea was so wrong. We now understand that, actually from an evolutionary perspective, animals are likely to encounter periods of scarcity. And, when they encounter periods of abundance, they are going to absolutely overconsume and sometimes spectacularly overconsume. That was already the beginning of a set of really surprising findings. If there's abundance and there's no predatory threat, they'll just consume and consume.
The other real biggie was that (and I went to medical school and, for 20 or 25 years, have been practicing medicine), I've seen a lot of overweight and obese patients; it's pretty much been assumed until very recently that it was all about calories in, calories out. I think most physicians have had patients that say they are not losing weight, and they swear to you that they're eating 900 calories a day -- do you really think that that's true? I think most physicians would be skeptical and think that their patients are probably not telling the truth or not aware of how much they're eating. So one of the exciting and surprising aspects of researching this chapter was to learn about all of these other factors that go beyond calories in and calories out. These could very well be influencing metabolism in both individual human patients and other species as well -- things like the seasonal microbiome, and circadian variation, even climate change, endocrine-modifying chemicals, and perhaps antibiotics in the environment. These are really interesting ideas to think about even in [the context of] the obesity epidemic as not being isolated to human beings, but perhaps being more species-spanning.<br />
<strong><br /></strong>
<strong>BOWERS:</strong> Even the approach that a physician or nutritionist might take with a human being, we think might be expanded and informed by the way veterinarians treat their animal patients. Because a veterinarian is not usually going to treat their patient as an individual, but really going to look at them as part of a group in an environment -- that's the social environment built around the animal. In human medicine, we put a lot of it on the patient -- you're eating too much and you need to exercise more. A veterinarian would really think about what's going on around the animal that makes them overconsume.
<br />
<strong><br /></strong>
<strong>DESPAIN: </strong>Gut length variability throughout the season was something I'd never heard of until I read your book. I found that fascinating.<br />
<strong><br /></strong>
<strong>BOWERS:</strong> We were pretty intrigued by that also. We were really interested in the idea that gut length could vary seasonally in the same animal. It can lengthen and expand.<br />
<br />
<strong>DR. NATTERSON-HOROWITZ:</strong> Kathryn and I had a lot of these fun moments. If you take a look at the human small intestine, and even if you look at the colon, you see this ribbon of smooth muscle. What is that smooth muscle for? Yes, it's involved in peristalsis [intestinal movement], but perhaps there are factors involved in lengthening and shortening the gut. Even if it was only 5 to 10 percent that would be quite significant over a long period time. Then again, the overarching point of the book is to look at a human patient as a human-animal patient and think of them comparatively, which is not something that we learn about in medical school these days.<br />
<br />
<strong>DESPAIN:</strong> You say that working with veterinarians changed how you practiced human medicine. What do you think medical doctors can gain from this perspective?<br />
<br />
<strong>DR. NATTERSON-HOROWITZ:</strong> You know, it's funny, people have asked the question in a different kind of way. Why is there resistance? What are the barriers? What is the benefit? Is there a benefit? Is there a way to teach medical students in a better way and will they be better doctors? Will this result in the creation of new hypotheses that will lead to new knowledge The answer is that we believe that they will. These are early days so there are only a couple of areas where we've seen leaps from this approach and we expect there will be more. There really have been two areas where there has been quite a lot of work done. The first is in the area of cancer research. The National Cancer Institute, about 10 years ago, started the comparative oncology program. And that program is looking at cancers that occur spontaneously in humans and mostly dogs and cats (companion animals). We're talking about osteosarcoma, which is a very serious bone cancer that affects adolescents and large-breed dogs. The biology of the cancer is very similar between the two species. There's a lot that can be done to understand tumor biology and clinical course by looking at dogs. If you just look at oncology, there's been real advances through a comparative approach. The other area where human medicine can absolutely benefit, through the lens of evolutionary biology, is the issue of antimicrobial resistance. There are some excellent and fascinating models that look at the emergence of resistance in an evolutionary context. At UCLA, we, as well as a chairman of evolutionary biology, started a program in evolutionary medicine and we had a wonderful speaker, Andrew Reid, that is talking about trying to evolution-proof antibiotics. So, there's many areas around this issue of infection and antibiotics where we can gain from working collaboratively with the veterinary world.<br />
<br />
<strong>DESPAIN:</strong> What do you think is a benefit from a patient's perspective? For example, I have joked in the past that the real reason why I decided to become a nutritionist and never pursue medicine is because I faint at the sight of blood or even when someone draws blood from me -- I've found this incredibly annoying. Now, from your book, I've learned that I share that phenomenon with several animals including fish and perhaps it may even have a protective effect in survival terms -- beyond the fight or flight response. Do you find that your patients find comfort or understanding in knowing they share their circumstances, say like cardiovascular disease, obesity, or cancer, with animals?<br />
<br />
<strong>DR. NATTERSON-HOROWITZ:</strong> It really varies. This message really resonated with us. The fact that animals can self-injure, get addicted, get obese, get anorexia nervosa, or have self-induced vomiting -- I think for some patients it can be profoundly de-stigmatizing. There's this kind of human grandiosity that our disorders are human disorders and that we are so uniquely disordered. That we have this spectrum with other animals is very humbling, very connecting, very destigmatizing, very deshaming. For some patients, it might not have that affect, but for some I think it has.<br />
<br />
<strong>DESPAIN:</strong> Your book has been out a year now. How do you think your approach has been received? I see there's now an annual conference. What kinds of people turn up at this event?<br />
<br />
<strong>BOWERS:</strong> We're having our third conference this fall. It's a place where we are really trying to make this happen. We're putting out a rallying cry. The conference is for working physicians and working veterinarians and we're really excited about the next one. It's going to be in New York City with faculty from Cornell, and NYU, and the Bronx Zoo. There's one group that has understood it from the very beginning: that's the veterinarians. But we're starting to get the message out to physicians as well and even general patients. We also get letters from general readers, and teachers, and its bolstering their interest in biology and evolution.<br />
<br />
<strong>DR. NATTERSON-HOROWITZ:</strong> It's fun because we have an auditorium full of half Ddms and half MDs, all very prominent academics. On stage, we've had a veterinarian oncologist and then we've had a human oncologist. And the veterinarian comments on the human case, and the human oncologist comments on the animal case. We also did that for heart disease. Then, everyone grabbed boxed lunches and we went on "walk arounds" (like in a teaching hospital) at the zoo. We had the veterinarians there and we were trying to make the point that we're all doctors. So we wanted to start the conversation.<br />
<br />
<strong>DESPAIN:</strong> Barbara and Kathryn, thank you for your time.<br />
<br />
<strong>DESPAIN</strong>: I found <i>Zoobiquity</i> a lot of fun to read, extremely entertaining, and also offered plenty of useful facts I can use to entertain with at a party.<br />
<br />
<strong>BOWERS</strong>: Cocktail party fodder!<br />
<br />
<em>Photo credits: Wikipedia.</em>daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com1tag:blogger.com,1999:blog-5995754777906978314.post-62994471132877216422013-02-19T17:23:00.000-08:002013-03-01T20:48:39.589-08:00Calories aren't right on labels and maybe that’s OK<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgcob28TRhGXneZ8BM6I1fAU5LDFhIn18U3CPzOGUvjHL-o3W7Zpykhj5MYwhs40ZAAnomLimG4hYIgAF9QHiCSm_DiIux2WZm0SWx-r7_hsV5bOBwaivB38vyk1hVEu9d57qJEIq1cDzA/s1600/apple_vs_donut.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="212" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgcob28TRhGXneZ8BM6I1fAU5LDFhIn18U3CPzOGUvjHL-o3W7Zpykhj5MYwhs40ZAAnomLimG4hYIgAF9QHiCSm_DiIux2WZm0SWx-r7_hsV5bOBwaivB38vyk1hVEu9d57qJEIq1cDzA/s320/apple_vs_donut.jpg" width="320" /></a></div>
Has it ever crossed your mind that the number of listed Calories (Kcals) of, say, a large, raw, whole apple at 116 Kcals and that of a glazed doughnut at 125 Kcals might not be an accurate comparison*? Surely, you might think, isn’t the doughnut more likely to add inches to your waistline?<br />
<br />
You'd be right. The difference that you might have understood intuitively is that, although the number of listed Kcals are similar, your body is likely to extract more of them from the doughnut than the apple. Why the disparity then on the Kcals listing? You can lay blame on the shortcomings of the Atwater Specific-factor System.<br />
<br />
Here's a little nutrition science history lesson: In the early 20th century, American chemist William Olin Atwater pioneered calculation of energy values from measures of heat combustion of proteins, fats and carbs. This is how we arrived to the familiar protein at 4 Kcals per gram, lipids at 9 Kcals per gram, and carbs 4 Kcals per gram. It would come to be known as the Atwater General Factor System. At the time, Atwater couldn’t account for fiber, so, in 1955, Bernice Watt and Annabel Merrill refined the system with specific Calorie conversion factors of foods, which has led to what the system is now.<br />
<a name='more'></a><br />
But the Atwater Specific-factor System still doesn't take a lot of other variables into account. For example, it doesn’t consider digestion energy costs of one food versus another, such as those from chewing, secretion of gastric acid and digestive enzymes, intestinal movement (peristalsis) and production of heat after eating (diet-induced thermogenesis). It also doesn't account for losses to your friendly gut microbes, which can devour up to half of calories from any digestion-resistant starches (as found in a raw apple) that arrive in the large intestine after escaping breakdown by gastric acid and pancreatic enzymes in the stomach and small intestine.<br />
<br />
Now, in the wake of news that McDonald's and other restaurants will start listing the numbers of calories next to menu items—a requirement under a new regulation included under the Affordable Care Act—comes a fresh challenge on the Atwater Specific-factor System and those Kcals listings for being inaccurate. That challenge is from an unlikely group of experts from diverse fields that include evolutionary biology and comparative physiology on mice and pythons. (Yes, pythons! I should spare you the yucky details, but I won't.)<br />
<br />
On Monday, February 18, at the American Association for the Advancement of Science <a href="http://aaas.confex.com/aaas/2013/webprogram/Session5859.html">annual meeting</a> (Twitter hashtag: #AAASmtg) in Boston, the group convened to summarize their findings. In addition, the group announced, they hope to write a position paper on the topic within the next few months. In some cases, the group reports, Kcal counts on food labels could be off as much as 15 percent or more.<br />
<br />
<b>Evolution and pythons</b><br />
<br />
Richard Wrangham and Rachel Carmody of Harvard are not part of the so-called "nutrition establishment"; they are a pair of biological anthropologists who study primates and human evolution. Over the last decade and a half, Wrangham has studied the role of fire in the evolution of humans (as regular readers of my blog surely are aware). Carmody's research is in evaluating what effect basic food processing (e.g. pounding) and cooking (as adopted by our ancestors probably beginning with Homo erectus) had on freeing up available Kcals from raw foods so as to drive increase in survival and human adaptations including larger brain size.<br />
<br />
Carmody detailed what was the first Harvard lab experiment on effects on energy gain that mice experienced when they ate foods—sweet potatoes and lean beef—that were either raw and whole, raw and pounded, cooked, or pounded and cooked. She found that pounding increased energy gain of the meat by 8 percent, cooking by 15 percent. Pounding increased energy gain from the tuber by 3 percent, cooking by 39 percent, the combination by 40 percent. The mice also showed greater preference for foods that were pounded and cooked after the trial.<br />
<br />
In addition, Carmody presented preliminary data that cooked versus raw food made an impact on gut microbial communities and genetic expression related to nutrient metabolism and immunity—the raw beef induced the most expression from immunity-related genes (possibly in response to pathogen load), which costs more energy. As hypothesized by Carmody, the pounding and cooking reduced diet-induced thermogenesis in the mice and, thus, reduced energy expenditure.<br />
<br />
Diet-induced thermogenesis, aka specific dynamic action (SDA) as it's referred to often by comparative physiologists, is the subject of research by biologist Stephen Secor of University of Alabama. "There's no such thing as a free meal," Secor likes to remind. "Every time you consume a meal, there's a metabolic expense." Again, that is not accounted for in the Atwater system.<br />
<br />
Secor, whose research is in reptiles, explains that contributions to SDA involve pre-absorptive (chewing, swallowing, bile and pantreatic secretions, peristalsis) and post-absorptive (nutrient breakdown and transport) phases. The gastric acid production, however, can heavily influence digestion costs—up to 25 percent for some foods—and varies greatly depending on the animal. "There are more mitochondria in cells responsible for acid production than anywhere else," Secor said.<br />
<br />
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; margin-left: 1em; text-align: right;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgan_d6I-2Wtx3i0cmQqpfUFDJuofhI0-Zt6b4lNOMDrrp3YTTOSxdvD7IQrFg-MTVTOtehmrBGZZj5cOuVrGx3yor8utbppwLSlecRl0JxNQYKZuxEsw3OEM3U_ITen6FfJWE1hhlN_6g/s1600/python_stomach.gif" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="80" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgan_d6I-2Wtx3i0cmQqpfUFDJuofhI0-Zt6b4lNOMDrrp3YTTOSxdvD7IQrFg-MTVTOtehmrBGZZj5cOuVrGx3yor8utbppwLSlecRl0JxNQYKZuxEsw3OEM3U_ITen6FfJWE1hhlN_6g/s320/python_stomach.gif" width="320" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">X-ray image of a Burmese python while digesting its meal.</td></tr>
</tbody></table>
OK, about the pythons: when pythons eat a rat whole, Secor says, they have a huge gastric acid and SDA response (they get so hot, it's like "they're on fire"). That makes them a <a href="http://jeb.biologists.org/content/206/10/1600">perfect model</a> to study the effects of processing and cooking as it relates to reduction in SDA. To study these effects, Secor's lab wrapped a steak around a rat and fed it to the snake (apparently, "you can feed anything to a python as long as you put a rat's head on it"). The research group also blended up a rat smoothie and delivered it via tube down a snake's throat and deposited it directly into the snake's stomach (bypassing the swallowing phase). From these experiments, Secor estimates that cooking and grinding reduces SDA by a whopping 25 percent.<br />
<br />
Knowing what we do about how the size of meals increasing gastric secretion, especially those containing protein, Secor's findings suggest there are greater digestion costs on a less processed or raw diet, particularly if consisting of large meals with protein. <br />
<br />
<b>The fate of carbs</b><br />
<br />
Cooking and processing also strongly affects the gastrointestinal fate of carbohydrate in meals and their energy contributions. When starch is provided as intact granules, it can be resistant to hydrolysis from enzymes during digestion, explains Klaus Englyst of Englyst Carbohydrates Ltd, Southampton, UK. Once heated, especially if moisture is involved, the starch gelatinizes allowing amylase (starch enzyme) to more easily break it down for rapid digestion and absorption. The resistant starches, on the other hand, might end up in the intestine where microbes will ferment it using some of its energy up and producing short-chain fatty acids (which we absorb).<br />
<br />
Englyst hints that resistant starches and fibers (cellulose, beta-glucan, etc.) deserve more attention for their possible role in providing the protective effects as seen in studies on low-glycemic diets. In fact, he said he's concerned that the term <i>low glycemic</i> in itself is an inconsistent message. <i>Low glycemic </i>refers to a diet based on the glycemic index (as developed by David Jenkins of University of Toronto) that quantifies blood glucose level rises after eating specific foods. One could argue that a hamburger is low glycemic, since it may not spike blood sugar, yet it contains very little resistant starch or fiber.<br />
<br />
Despite shortcomings of <i>low glycemic</i> as a term overall, Dr. David Ludwig, a physician at Boston Children's Hospital (who filled in on behalf of Peter Turnbaugh at the conference), says it's useful for discussing the different kinds of carbohydrates. Unprocessed grains have fiber and intact grain structures causing pancreatic enzymes to really have to work at breaking them down, whereas today’s highly processed grains have their kernels milled to fine particulate and fiber stripped away. That’s how they become high glycemic (able to spike blood sugar). "You're left with Wonder Bread and there are thousands of iterations of this product," he said.<br />
<br />
He also shares the view that the USDA's "low-fat" message and the Food Pyramid (with grains as its base) has been harmful over the last few decades. "You can take fat out, replace it with highly processed starch molecules that are immediately susceptible to attack from amylase," Dr. Ludwig said. Last June, Dr. Ludwig and his colleagues published a study in <i><a href="http://www.ncbi.nlm.nih.gov/pubmed/22735432">JAMA</a> </i>that found that a low glycemic diet made it easier for subjects to maintain weight loss over time as compared to a low-fat or low-carb diet.<br />
<br />
Dr. Ludwig also hinted that there may be more to the low-glycemic story in ways beyond greater digestion costs of resistant starches and fibers and into the bloodstream. Interesting new findings, he told me after his talk at the conference, suggest high-glycemic meals could have an impact on hormones in terms of how they influence appetite, metabolic rate, and energy storage (I wonder what he thinks of "<a href="http://evolvinghealthscience.blogspot.com/2012/05/good-insulin-bad-insulin-its-role-in.html">insulin hypothesis</a>").<br />
<br />
Nutritional biochemist Geoff Livesey, of Independent Nutrition Logic Ltd., is the lead author of a meta-analysis of prospective cohort studies that Dr. Ludwig told me was the most well-designed study available on low-glycemic diets to date. The study, just published in <i><a href="http://ajcn.nutrition.org/content/early/2013/01/30/ajcn.112.041467.abstract">American Journal of Clinical Nutrition</a></i>, indicated a "strong and significantly lower type-2 diabetes risk" in those consuming low-glycemic diets. Livesey added that it’s unclear whether or not it’s the lack of highly processed carbs and fats that make the low-glycemic diet protective, or the inclusion of more protein and fiber that produce the protection; protein and fiber, for example, have a greater satiety effect than do carbs and fats that could contribute to an easier time eating reduced calories.<br />
<br />
Livesey agreed with the panel that the Atwater Specific-factor System had failures and could be improved to be more accurate, but he cautions that the group had an uphill battle if they were going to change it. It would take changing the position of the Food and Agriculture Organization of the United Nations (FAO). Also, many in the "nutrition establishment" (Ludwig's choice of words) are likely to disagree that the Atwater system needs to change at all.<br />
<br />
<b>Does it matter if food labeling is inaccurate?</b><br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEijSkpd5SobQRJQNWcMYGEMMpYFi4r-6Fxe8txkxaQ2V2xpdevY4ZqCgiylHRvCaiFtg-bz2zDdIn5HwmD59m2wsff31WxpXEqogHmV-ce1j4ZKpRhaecjUtEW9oNfuP41pFW_gJJvy_Bc/s1600/food_label.jpg" imageanchor="1" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><img border="0" height="178" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEijSkpd5SobQRJQNWcMYGEMMpYFi4r-6Fxe8txkxaQ2V2xpdevY4ZqCgiylHRvCaiFtg-bz2zDdIn5HwmD59m2wsff31WxpXEqogHmV-ce1j4ZKpRhaecjUtEW9oNfuP41pFW_gJJvy_Bc/s200/food_label.jpg" width="200" /></a></div>
The FAO, in fact, brought together an expert committee to write a <a href="http://www.fao.org/docrep/006/Y5022E/Y5022E00.HTM">report</a> after a technical workshop in Rome that evaluated the topic of food energy and the Atwater Specific-factor System in 2002. In the report, the committee concluded that, yes, it was true that foods can differ substantially in terms of their "net metabolizable energy." But more data need to be collected before determining any major changes and, in the context of the total diet for most countries, the Atwater Specific-factor System isn't likely to introduce a lot of error—they estimated less than 5 percent, except on a few subsistence diets, which rely on a lot of native foods, where errors may increase to up to 18.5 percent.<br />
<br />
I asked John Peters, Chief Strategy Officer of the New Health and Wellness Center at the University of Colorado Anschutz Medical Campus, to comment further on the topic. He told me, "Every step of the digestion and metabolism process introduces multiple variables that will be unique to the individual." For example, he told me, the "digestible energy of lard (made of palmitic, stearic and oleic acids) will depend on the calcium level in the diet of the organism consuming the lard because calcium will bind to stearic acid in the gut and reduce its absorption."<br />
<br />
Individual variability adds complexity that is compounded by the metabolic energy costs that are heavily determined by protein content of meals because of the need to remove amino acid waste, along with fermentable fiber content, rate of absorption of foods into the body, and other elements of nutritional status. "As you can imagine," he told me, "these are variable from meal to meal and from individual to individual. Because of this complicated mix of effectors, the current labeling system was an attempt to blend simplicity with the 80:20 rule… it's about right for most things found in most diets.” <br />
<br />
Mark Haub, a professor of human nutrition at Kansas State (aka the <a href="http://www.cnn.com/2010/HEALTH/11/08/twinkie.diet.professor/index.html">Twinkie diet professor</a>), explains that his belief is that people misunderstand or simply fail to remember the components of thermodynamics. "One factor is that food contains a constant amount of energy, and then the potentiallly incongruent piece is that the energy in the food may or may not be bioavailable" (as metabolizable energy). So, a processed food would, indeed, tend to have energy that is more bioavailable than raw food because the energy is more difficult to extract because it's more difficult to digest.<br />
<br />
Yet he agrees that when it comes to changing food labeling, "that becomes tricky." The absorption of energy from oranges, for example, can change simply depending on how much is eaten. When large amounts are eaten, more will likely "get dumped" into the large intestine. In addition, Haub told me, the rate of digestion can change depending on accompanying foods like those containing fiber or protein. "Do we digest an apple the same every time we eat it? I have a hard time thinking that is the case."<br />
<br />
He's right about the differences in apple absorption considering that people are likely to eat them raw sometimes, processed (as in apple sauce), and cooked (as in apple pie on Thanksgiving). When eaten raw, according to Carmody's findings, it would yield fewer Kcals. But since the Atwater Specific-factor System basically assumes all foods are processed or cooked, at least consumers can safely predict that the apple would not yield more than the listed 116 Kcals.<br />
<br />
So, perhaps that's a better way to look at the problem: labels wouldn't be so misleading if we thought of their Kcal listings not as<i> total Kcals</i>, but as <i>max Kcals</i> you could get from any given food. And, if one is to determine some kind of main takeaway dietary message from all this discussion, it may be simply this: that by eating more whole, raw foods (like other animals and like our pre-human ancestors did), you can count on fewer Kcals (thank your microbes for halving the amounts of Kcals you absorb once food reaches your intestine); and you can count on greater digestive and metabolic costs by eating well-balanced meals containing plenty of fiber and protein per meal (think "python diet").<br />
<br />
*Kcals from USDA's nutrient database.<br />
<br />
Photo credits: iStockphoto and <i><a href="http://jeb.biologists.org/content/206/10/1600.full">Inside JEB</a></i>.<br />
<div>
<br /></div>
daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com9tag:blogger.com,1999:blog-5995754777906978314.post-8129633310604548622013-02-11T23:57:00.002-08:002013-02-12T21:02:34.031-08:00Experts on the evolution of human nutrition<div class="separator" style="clear: both; text-align: center;">
<a href="http://www.uctv.tv/images/series/widescreen/717.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="225" src="http://www.uctv.tv/images/series/widescreen/717.jpg" width="400" /></a></div>
Want to eat a diet that mimics that of our Paleolithic ancestors? It might be a little more complicated than what the popular books say.<br />
<br />
The fact is, there was never one Paleo Diet; it's more likely there were hundreds of them and that they were continually changing and broadening over evolutionary time.<br />
<br />
That was the overarching message of an impressive lineup of experts on ancient human diets at a symposium entitled "<a href="http://carta.anthropogeny.org/events/the-evolution-of-human-nutrition">The Evolution of Human Nutrition</a>" organized by the Center of Academic Research and Training in Anthropogeny (CARTA) at UC San Diego on December 7, 2012.<br />
<br />
Now, I'm happy to report, the videos of a few of the talks have been made available (embedded in this post below). You can also read what other folks on Twitter had to say about the event using the #CARTAsymp hashtag in my <a href="http://storify.com/daviddespain/cartasymp-evolution-of-human-nutrition">Storify story</a>.<br />
<a name='more'></a><br />
President of the Wenner-Gren Foundation for Anthropological Research Leslie Aiello, who chaired the symposium, expressed some amusement over folks who aspire to the great lengths of trying to live like <a href="http://www.nytimes.com/2010/01/10/fashion/10caveman.html?pagewanted=all">cavemen in the big city</a>.<br />
<br />
However flawed their premise, she noted, the gaining interest into the diet of our ancestors was one to be welcomed. After all, it could lend clues into current causes of epidemics of obesity, type-2 diabetes, and cardiovascular disease.<br />
<br />
<b>What we still don't know</b><br />
<br />
Aiello gave a refreshing perspective on the history and complexity of studying ancient human diets. Back in 1995, she and Peter Wheeler were the first to <a href="http://www.jstor.org/discover/10.2307/2744104?uid=3739552&uid=2&uid=4&uid=3739256&sid=21101787827327">propose</a> the "expensive tissue hypothesis" -- one that proposed that we gained our energy-hungry brains by sacrificing our large guts.<br />
<br />
Yet as early 2011, Aiello explains, even the well-founded theory she and Wheeler had proposed was challenged. Ana Navarrete, Carel P. van Schaik, and Karin Isler of the University of Zurich found <a href="http://www.nature.com/nature/journal/v480/n7375/full/nature10629.html">no evidence</a> of a brain-gut tradeoff among any other mammals.<br />
<br />
Navarrete and her colleagues now have a competing theory: that larger brains came as a result of our abilities to store body fat. Among mammals, they suggest, those with larger brains acquire them by sacrificing adipose tissue for energy storage. But humans "buck the trend," Aiello said.<br />
<br />
But there are so many other variables that could have also played important roles -- perhaps even billions of them.<br />
<br />
The relationships that hominins had with microbes at the time might have contributed to adaptations, according to biological anthropologist Steven Leigh of University of Illinois, Urbana-Champaign. Microbes in the intestine continue to contribute for up to 7 percent of our daily energy supply in form of short-chain fatty acids and they also supply valuable B vitamins and hormones.<br />
<br />
Leigh's preliminary findings are that microbial communities can change drastically depending on where primates live. Rainforest monkeys, for example, harbor more species of microbes in comparison to those living in semi-deciduous forests or in captivity. Changes affecting early humans may have factored into adaptations over evolutionary time.<br />
<br />
<b>What we may know </b><br />
<br />
Current hunter-gatherers offer a "window" into how early humans lived and ate, according to Alyssa Crittendon. But the nutritional anthropologist and behavioral ecologist of University of Nevada, Las Vegas, adds, "Hunter-gatherers are not living fossils. They are contemporary modern populations just like you and I."<br />
<br />
Based on her research analyzing energy values of foods eaten by the Hadza of Tanzania, Crittendon said hunter-gather diets can vary widely depending on plants and animals of the season. During the dry season, for example, Hadza get most of their energy from meat. In the wet season, the energy contribution shifts dramatically to plant foods, especially berries.<br />
<br />
Honey is Hadza's most preferred food being made up of 80 to 95 percent sugar and they have learned to obtain it more regularly through unusual means. A bird aptly named the greater honeyguide has learned to lead Hadza men to beehives in exchange for a share of the honeycomb. It is an extraordinary partnership of food sharing.<br />
<br />
A look into the past is also provided through the diets of other primates such as chimpanzees, according to Peter Ungar of University of Arkansas. For example, judging from the jaw structure of chimpanzees one can find similarities with that of <i>Ardipithecus ramidus</i>.<br />
<br />
This direct ancestor was likely to have eaten fruit, soft leaves, and soft legumes as chimpanzees are fond of doing today (depending on their region).<br />
<br />
But the best evidence available on ancient human diets is from fossil teeth, Ungar adds. Clues from tooth size, shape, and structure can be combined with dental microwear and enamel chemistry.<br />
<br />
Summarizing evidence from teeth "food prints," Ungar shares:<br />
<br />
<ul>
<li><i>Australopithecus </i>likely ate mostly soft or tough foods like fruits, and leaves in a mixed setting 4 to 2 million years ago, but could handle a fairly broad diet. Around 2.5 may, there was a fork in the evolutionary road.</li>
<li>Our <i>Paranthropus</i> cousins had more specialized teeth and likely had different diets in different places. Some ate tough savanna foods like grasses and sedges; others had harder items such as nuts and seeds in a mixed setting. </li>
<li>Our early <i>Homo</i> ancestors had less specialized teeth and likely had a broader or more variable diet including both savanna and forest resources, along with some meat. </li>
</ul>
<br />
Alison Brooks of George Washington University adds that Neandertal teeth, as well as their large caloric needs, indicate that they too must have eaten plant foods.<br />
<br />
The microfossil evidence reveals starchy grains that also suggest Neandertals cooked and boiled their food. Now it's up to archaeologists to find pots, Brooks said.<br />
<br />
That Neandertals ate plants is despite what the nitrogen isotope data show, anthropologist and research archaeologist Margaret Schoeninger of UCSD said.<br />
<br />
It's necessary to rethink the nitrogen isotope data, Schoeninger said, because all humans -- whether subsisting on plants or animals -- and some plant themselves return a signal as a "top predator."<br />
<br />
Cooking may also play in as a factor, she suggested.<br />
<br />
<b>What we know were crucial for modernity and leaving Africa: Cooking, food sharing, division of labor</b><br />
<br />
Understanding that the introduction of fire was a major precursor to modern humans has long been argued by Primatologist Richard Wrangham of Harvard to be an essential part of better studying early human diets.<br />
<br />
He presented new data showing that cooked carbohydrates and proteins also contribute more calories than when raw. The data support that cooking could have helped lead to expansion of large brains while at the same time reducing gut size.<br />
<br />
Clues into what early humans ate in a setting can also be gathered through study of decisions that might our ancestors may have made based on "return on investment" scenarios, anthropologist Mary Stiner of University of Arizona said.<br />
<br />
For example, hunting a large or small animal each can take a lot of effort, yet the larger one yields a higher return and is preferable. Comparatively, some plant foods represent greater or lower effort with higher or lower yields compared to others depending on investment into obtaining them, processing them, and/or cooking them.<br />
<br />
It would make sense, she reasons, that cooking, food sharing and division of labor were crucial for humans to insulate infants and children (which need a great deal more attention, compared to those of other primates) from variations in food supply.<br />
<br />
The likelihood is that each of these human characteristics -- cooking, food sharing, and division of labor -- were apparent at the time of our direct ancestor <i>Homo erectus</i> around 1.89 million and 143,000 years ago.<br />
<br />
<i>Homo</i> had evolved to be "eating machines," Schoeninger said in an earlier discussion on the topic at Eleanor Roosevelt College (video embedded below).<br />
<br />
Schoeninger noted that it was <i>H. erectus</i> that first left Africa and needed fire to stay warm. On their journey, Schoeninger suggests, it was likely that they subsisted on animal foods during the winter and on seed heads from grasses (cereal grains) as familiar food when traveling into Asia and Europe (because of unfamiliarity with fruits and vegetables of other regions).<br />
<br />
<b>Agriculture and population health decline</b><br />
<br />
By 15 to 10,000 years ago, modern humans had taken over the landscape and were already shifting from foraging to farming, which represented a major transition in the human diet, Schoeninger said.<br />
<br />
The shift was was one from a varied, broad diet that changed with seasons to be replaced with one that included specific plant foods such as cereal grains as a dietary staple, according to anthropologist Clark Spencer Larsen.<br />
<br />
This reliance on single foods such as grains as staples with characteristically low nutritional quality, along with more availability of food and more sedentary lifestyle, he said, was the start of health decline as evidenced by study of bones and teeth of the era.<br />
<br />
Barry Bogin, a biological anthropologist of Loughborough University, UK, has witnessed this sort of population health decline first-hand while studying the Maya who in recent years have made the switch from their traditional varied diets to ones that are more modern and containing a great deal more animal products, cereal grains, and added sugars. <br />
<br />
Unfortunately, Maya children will ultimately suffer the most from the dietary transition with higher risk of obesity and chronic diseases such as type 2 diabetes.<br />
<br />
Judging from the history, isn't it understandable that folks would be compelled to change their diets (and propose that others change theirs) to one that is relatively more similar to that of our hunter-gatherer ancestors?<br />
<br />
But when asked about dietary advice (including what food groups to be consumed and to not be consumed) that can be gathered from an extensive knowledge of evolution of the human diet, Ungar simply shrugs and responds, "I tell people to go see a nutritionist."<br />
<br />
<b>Videos from CARTA</b><br />
<br />
Steven Leigh, Peter Ungar, Alison Brooks, and Margaret Schoeninger:<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<iframe allowfullscreen='allowfullscreen' webkitallowfullscreen='webkitallowfullscreen' mozallowfullscreen='mozallowfullscreen' width='320' height='266' src='https://www.youtube.com/embed/Y92iIeN46GM?feature=player_embedded' frameborder='0'></iframe></div>
<br />
Mary Stiner, Alyssa Crittenden, and Steven Leigh:<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<iframe allowfullscreen='allowfullscreen' webkitallowfullscreen='webkitallowfullscreen' mozallowfullscreen='mozallowfullscreen' width='320' height='266' src='https://www.youtube.com/embed/Cuyp1bvuaxA?feature=player_embedded' frameborder='0'></iframe></div>
<br />
"Eating Machines" - Margaret Schoeninger from Feb 20, 2012 at Eleanor Roosevelt College:<br />
<br />
<div class="separator" style="clear: both; text-align: center;">
<object class="BLOGGER-youtube-video" classid="clsid:D27CDB6E-AE6D-11cf-96B8-444553540000" codebase="http://download.macromedia.com/pub/shockwave/cabs/flash/swflash.cab#version=6,0,40,0" data-thumbnail-src="http://2.gvt0.com/vi/RSh8v_2Mzj4/0.jpg" height="266" width="320"><param name="movie" value="http://www.youtube.com/v/RSh8v_2Mzj4&fs=1&source=uds" /><param name="bgcolor" value="#FFFFFF" /><param name="allowFullScreen" value="true" /><embed width="320" height="266" src="http://www.youtube.com/v/RSh8v_2Mzj4&fs=1&source=uds" type="application/x-shockwave-flash" allowfullscreen="true"></embed></object></div>
<br />
<br />daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com8tag:blogger.com,1999:blog-5995754777906978314.post-38926266409893490152013-01-20T22:26:00.002-08:002013-02-23T18:46:04.468-08:00The nutritional biology of human skin color <div class="separator" style="clear: both; text-align: center;">
<iframe allowfullscreen='allowfullscreen' webkitallowfullscreen='webkitallowfullscreen' mozallowfullscreen='mozallowfullscreen' width='320' height='266' src='https://www.youtube.com/embed/tLsFl6QiFh4?feature=player_embedded' frameborder='0'></iframe></div>
<br />
The amount of melanin found within our skin has long been a source of division for humans culturally, but anthropologist Nina Jablonski of Penn State tells the story of how human skin color unites us all biologically.<br />
<br />
It's become one of my favorite stories to share as it relates to nutritional biology: More pigment was naturally selected because it acted as a sunscreen needed to protect against DNA damage and destruction of folate, needed for reproduction. Depigmentation was selected for when humans dispersed from Africa and into the Northern Hemisphere where they needed skin light enough to absorb sufficient UVB rays to produce vitamin D.<br />
<br />
I first heard Jablonski discuss the nature of human skin pigmentation almost two years ago at the <a href="http://evolvinghealthscience.blogspot.com/2011/02/nature-of-human-skin-pigmentation.html">AAAS conference</a> in Washington DC. Later, I discovered her TED talk, which I've posted above. It's older, but worth watching over and over again. Jablonski has a simple message: instead of using skin color to discriminate, use skin color to teach people about evolution and health.<br />
<a name='more'></a><br />
Now Jablonski has a new, richly illustrated book out called <i>Living Color. </i>It serves to complement to her previous book, <i>Skin Color: A Natural History. </i>You can read an excerpt from her book <a href="http://www.utne.com/mind-body/the-meaning-of-skin-color-ze0z1211zsau.aspx">here</a>, which includes this paragraph:<br />
<i><br /></i>
<i>The properties of our skin — including color — affect our health. Most of us think that humans have used our collective intelligence to overcome biological limitations in a way that cultureless species cannot do. But at least with respect to our skin, this hubris is unwarranted. Many common health problems like skin cancer and vitamin D deficiency are caused by a mismatch between our habits and our heritage. The amount of pigment that our skin contains, which determines how our bodies deal with sunshine, evolved in our ancestors. Today, many of us live under very different conditions from those experienced by our predecessors and pursue dramatically different lifestyles. People living thousands of years ago did not have indoor jobs and go on vacation; they lived outside most of the time and generally didn’t travel much or very far. Because of these factors, many of us have an inherited skin tone that is not adapted to our current circumstances, and that mismatch places us at risk for specific health problems. Knowing our own particular risk factors can be a matter of life or death.</i><br />
<br />daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com3tag:blogger.com,1999:blog-5995754777906978314.post-41377710165604917742013-01-20T17:28:00.002-08:002013-01-20T17:33:04.015-08:00What a Komodo dragon can teach us about energy balance<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="http://www.sandiegozoo.org/images/uploads/lizard_hero.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" src="http://www.sandiegozoo.org/images/uploads/lizard_hero.png" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Credit: San Diego Zoo</td></tr>
</tbody></table>
Try telling a Komodo dragon that physical activity doesn't matter and that all one needs to do to lose weight is eat a diet lower in carbohydrates.<br />
<br />
Meet Sunny, the obese Komodo dragon. Her San Diego Zoo keepers have put her on a strict diet based on her animal energy and metabolic requirements. She eats only mice, rats, and ground turkey mixed with vitamins and calcium. Yet, it's not enough to keep Sunny from steadily gaining weight. When in captivity, dragons are prone to obesity because of their mainly sedentary lifestyle. They do little else than sleep, bask in the sun or shade, and eat breakfast or supper.<br />
<br />
In their native habitat of Indonesian islands, Komodo dragons are extremely active. They travel up to 10 kilometers a day, run up to 13 miles per hour, swim several kilometers from island to island, then dig or climb as they hunt. Once they capture their prey, they can eat as much as 80 percent of their body weight in a single meal. That energy they will serve to store for often days or weeks.<br />
<br />
When I asked senior zookeeper Ken Morgan what he was doing to help get Sunny moving and losing weight, he replied that they were trying a series of enrichment programs. But getting a 200-pound dragon to do any activity at all is no easy task, he said. It takes some creativity. One enrichment program Morgan has used involves burying a ball with a dead mouse inside. Sunny picks up the scent, spends some time searching for it, then digs around before finally discovering the treasure. It's activity accomplished. These games can help Sunny burn more calories to keep weight off.<br />
<a name='more'></a><br />
<br />
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEix44u4-hN_XRRwdxd90439kzMBHZGnbFU3Lo6Lw7GBsXK0N3ovAoIXM3GhYElNB2Fnwavj7UsoClV6_LZXaT-LIqmorkt6D42tBwRq45nT9MvkLrxc3XESM4Y0JYNyD_G-km5vPQ8Lv4Q/s1600/Screen+shot+2013-01-20+at+1.21.08+PM.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="159" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEix44u4-hN_XRRwdxd90439kzMBHZGnbFU3Lo6Lw7GBsXK0N3ovAoIXM3GhYElNB2Fnwavj7UsoClV6_LZXaT-LIqmorkt6D42tBwRq45nT9MvkLrxc3XESM4Y0JYNyD_G-km5vPQ8Lv4Q/s320/Screen+shot+2013-01-20+at+1.21.08+PM.png" width="320" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Credit: Jordan A. Veasley and Giorgio Guerra</td></tr>
</tbody></table>
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
Similar efforts are going on at other zoos. At Woodland Park Zoo, Jordan Veasley and Giorgio Guerra of the University of Washington decided to <a href="http://www.cfr.washington.edu/academicPrograms/undergrad/esrm/Komodo.pdf">compare</a> the amount of activity produced by some of the most popular enrichment programs on two Komodo dragons -- Loki and Selat. They found that the most successful program was the "scent trail." This treasure hunt of sorts involves using meat juice to create a simple, yet intricate path around a dragon's enclosure that would lead to a dead mouse. When the dragons performed the activity, the researchers found that it displaced a lot of the time that would normally be used for simply resting. Instead, the dragons swam, dug, climbed and honed the skills of these endangered animals for greater possibility of successful release into the wild. The researchers also noted that the Komodo dragons performing the activities had greater levels of "excitement and joy."</div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjWZ5Qsl0LLumLNMUNkbArKe2CeSR_LBanHDxNwwwDUKAtChs3ZqHWO37EvctE6MrH9Kadz-Z7OfagyYenhO2XMX-9iHc9dvI6DQCLxiGgsmMtPvHoDEOw1Vjn8nvaqYclbEDgSZPKpDPE/s1600/Screen+shot+2013-01-20+at+1.22.18+PM.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="192" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjWZ5Qsl0LLumLNMUNkbArKe2CeSR_LBanHDxNwwwDUKAtChs3ZqHWO37EvctE6MrH9Kadz-Z7OfagyYenhO2XMX-9iHc9dvI6DQCLxiGgsmMtPvHoDEOw1Vjn8nvaqYclbEDgSZPKpDPE/s400/Screen+shot+2013-01-20+at+1.22.18+PM.png" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Credit: Jordan A Veasley and Giorgio Guerra. </td></tr>
</tbody></table>
Komodo dragons, of course, aren't the only animals in the zoo that are prone to obesity. Proper diet and environment play important roles, to be sure. But most zoos recognize the critical role of enrichment activities as part of an overall approach to help their animals keep weight off. I mainly focus on the example of Sunny, because it so nicely serves as a model to illustrate the why the energy balance paradigm isn't going to go away anytime soon. As a way to battle obesity, we humans might also <a href="http://evolvinghealthscience.blogspot.com/2012/04/beyond-calories-in-calories-out-look-to.html">learn</a> a thing or two from the zookeepers.</div>
<br />
<br />
<br />daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com5tag:blogger.com,1999:blog-5995754777906978314.post-29565829589160120312013-01-20T10:14:00.004-08:002013-03-02T15:04:37.739-08:00What journalists should know before writing about fructophobia<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="http://www.flickr.com/photos/vavroom/4461870826/" style="margin-left: auto; margin-right: auto;" title="Sugars by vavroom, on Flickr"><img alt="Sugars" height="332" src="http://farm3.staticflickr.com/2781/4461870826_72fb3a3b18.jpg" width="500" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">"Pick your poison" Sugars by vavroom, on Flickr</td></tr>
</tbody></table>
<br />
In his new book, <i>Fat Chance, </i>Dr. Robert Lustig argues that "sugar is more toxin than it ever was nutrient." He writes that sugar is as addictive as cocaine, that it should be regulated like tobacco, and that children should be carded before having a soda. He compares the fructose component of sugar to ethanol. "Pick your poison," he writes, arguing that fructose will "fry your liver and cause all the same diseases as does alcohol." He also challenges energy balance (calories-in-calories-out) as the dominant paradigm of understanding obesity and and argues that sugar is harmful in ways beyond the calories it provides.<br />
<br />
With statements as controversial as these, it's no wonder that the media, who tend to crave sensationalism to obtain readers or viewers, eat them up like candy. And Dr. Lustig knows what he's doing and just what to say to elicit attention. He's no stranger to the spotlight, as Elizabeth Weil writes in her <a href="http://www.psmag.com/health/robert-lustig-sugar-obesity-diet-50948/#.UN3llNERlRE.twitter">article</a> featuring the pediatric endocrinologist. The showman-doctor also knows just how to tell a classic falling-prey-to-cruelty story. He'd have his readers believe just what they want to hear: that their weight gain is not their fault, that the great evil monster of the food industry is putting addictive "poison" in their food in the form of sugar, and that the government is standing "idly by" letting it all happen. After reading Dr. Lustig's book, it's easy to understand why readers are entertained and maybe even enraged enough to give up on sugary sodas, cheese cake, and apple pie. But are the arguments Dr. Lustig makes in the book right or wrong?<br />
<a name='more'></a><br />
Sparked by my <a href="http://evolvinghealthscience.blogspot.com/2012/04/no-dr-gupta-hummingbird-fuel-is-not.html">ire</a> of journalists buying into the sensationalism without so much as offering a contrasting view, I previously wrote about how Dr. Lustig's eyebrow-raising claims didn't appear to hold water. For example, one need only check the evidence from systematic reviews of human intervention trials (not rodents) to find that: 1) fructose has no significant effects on body weight, blood pressure, or uric acid when compared to other carbohydrates contributing the same amount of calories in the diet; 2) fructose in high doses providing excess calories increases body weight as expected from its contribution of excess calories and not because of any unique property of fructose; 3) and fructose at the levels normally found in fruit, which equals to around 10 grams per meal, is shown to improve glycemic control long-term. Does that sound like an ingredient that is "toxic"? I didn't think so and neither do most nutrition scientists who've reviewed the evidence. For these reasons, scientists lashed out against Dr. Lustig's inflammatory rhetoric and overstatements in a symposium sponsored by the Corn Refiner's Association at Experimental Biology last April. I wrote about the debate, which I dubbed the "<a href="http://evolvinghealthscience.blogspot.com/2012/04/sugar-showdown-science-responds-to.html">Sugar Showdown</a>", and then followed up with an <a href="http://evolvinghealthscience.blogspot.com/2012/05/fate-of-fructose-interview-with-dr-john.html">interview</a> with Dr. John Sievenpiper, a lead author of several systematic reviews and meta-analyses evaluating fructose's effects on health of the body, to bring more clarity to the subject.<br />
<br />
Despite the push-back from his scientist-peers, however, it's evident that Dr. Lustig is pressing on with his mission to demonize sugar and his published book has gained him plenty of new attention in articles and interviews. I've found it difficult to keep up with it all and have lagged behind, having been busy with other projects (like moving to a new house). Fortunately, exercise physiologist and sports dietitian <a href="https://twitter.com/davidmdriscoll">David Driscoll</a> took up the charge to set the record straight on fructose around the World Wide Web. I'm indebted to Driscoll for nicely summarizing my own thoughts, pushing my blog article, and bringing my attention to other articles. And I would encourage any journalist or blogger who is writing about sugar, fructose, or Dr. Lustig's book first read Driscoll's comment and follow each of the links. He told me over Twitter that he posted the following comment, or ones like it, on at least 50 different sites over five days:<br />
<blockquote class="tr_bq">
<div style="background-color: white; color: #424243; font-family: helvetica, arial, sans-serif; font-size: 12px; line-height: 15.421875px; margin-bottom: 1em; margin-top: 1em;">
While Dr Lustig's theories and evidence may seem convincing to the general public and reporters, the real test is how well he performs with his fellow scientists!</div>
<div style="background-color: white; color: #424243; font-family: helvetica, arial, sans-serif; font-size: 12px; line-height: 15.421875px; margin-bottom: 1em; margin-top: 1em;">
He was certainly called out for overstating the evidence and poorly extrapolating rat research at a conference he spoke at earlier in the year - check out the Q and A video in the attached article by David Despain (as well as the other lectures)!</div>
<div style="background-color: white; color: #424243; font-family: helvetica, arial, sans-serif; font-size: 12px; line-height: 15.421875px; margin-bottom: 1em; margin-top: 1em;">
<a href="http://evolvinghealthscience.blogspot.com.au/2012/04/sugar-showdown-science-responds-to.html" rel="nofollow" style="color: #9a2d92; outline: 0px; text-decoration: initial;" title="http://evolvinghealthscience.blogspot.com.au/2012/04/sugar-showdown-science-responds-to.html">http://evolvinghealthscience.blogspot.com.au/2012/04/sugar-showdown-scie...</a> for a full review and links to all lectures - if not just watch the Q and A at <a href="http://www.youtube.com/watch?v=ypWe6npULUQ" rel="nofollow" style="color: #9a2d92; outline: 0px; text-decoration: initial;" title="http://www.youtube.com/watch?v=ypWe6npULUQ">http://www.youtube.com/watch?v=ypWe6npULUQ</a> and <a href="http://www.youtube.com/watch?v=cnGhfX2yaU4" rel="nofollow" style="color: #9a2d92; outline: 0px; text-decoration: initial;" title="http://www.youtube.com/watch?v=cnGhfX2yaU4">http://www.youtube.com/watch?v=cnGhfX2yaU4</a></div>
<div style="background-color: white; color: #424243; font-family: helvetica, arial, sans-serif; font-size: 12px; line-height: 15.421875px; margin-bottom: 1em; margin-top: 1em;">
What research shows that it is fructose that causes addiction? At the Q and A at the Sugar Symposium, Dr Lustig was called out on this and one researcher showed that rats liked glucose based carbohydrates over sucrose, and another questioned the applicability of rat research to be extrapolated to humans!</div>
<div style="background-color: white; color: #424243; font-family: helvetica, arial, sans-serif; font-size: 12px; line-height: 15.421875px; margin-bottom: 1em; margin-top: 1em;">
Also a recent rat studied suggests that it might be the sweet taste and NOT the fructose (as they used an artificial sweetener) although the article title gets it wrong also!<br />
<a href="http://www.health.msn.co.nz/healthnews/8582942/sugar-as-addictive-as-cocaine-nicotine" rel="nofollow" style="color: #9a2d92; outline: 0px; text-decoration: initial;" title="http://www.health.msn.co.nz/healthnews/8582942/sugar-as-addictive-as-cocaine-nicotine">http://www.health.msn.co.nz/healthnews/8582942/sugar-as-addictive-as-coc...</a></div>
<div style="background-color: white; color: #424243; font-family: helvetica, arial, sans-serif; font-size: 12px; line-height: 15.421875px; margin-bottom: 1em; margin-top: 1em;">
The major issue with Dr Lustig's theory is looking at US Sugar intake over history - levels were still high in the early 20th century - so saying it is sugar is either an oversimplification or there is a threshold value that we have recently crossed. Methinks that it is a perfect storm of more sugar and less burning it up with physical activity!</div>
<div style="background-color: white; color: #424243; font-family: helvetica, arial, sans-serif; font-size: 12px; line-height: 15.421875px; margin-bottom: 1em; margin-top: 1em;">
<a href="http://davidgillespiesbigfatlies.com/wp-content/uploads/2012/09/sugar-intake-20th-century.jpg" rel="nofollow" style="color: #9a2d92; outline: 0px; text-decoration: initial;" title="http://davidgillespiesbigfatlies.com/wp-content/uploads/2012/09/sugar-intake-20th-century.jpg">http://davidgillespiesbigfatlies.com/wp-content/uploads/2012/09/sugar-in...</a></div>
<div style="background-color: white; color: #424243; font-family: helvetica, arial, sans-serif; font-size: 12px; line-height: 15.421875px; margin-bottom: 1em; margin-top: 1em;">
I hope you get a chance to review these before the interview - especially the video lectures linked to within the article by David Despain</div>
</blockquote>
In my own reading of Dr. Lustig's book over the last few days, I've found that apart from the claims about sugar, the rest of the book is relatively tame. In fact, it reminds me of why I tend to hate popular diet books and find them boring. There is one chapter where Dr. Lustig calls out out insulin as "the bad guy," as Gary Taubes does, and I've discussed why this is shortsighted in my post "<a href="http://evolvinghealthscience.blogspot.com/2012/05/good-insulin-bad-insulin-its-role-in.html">Good insulin, bad insulin: Its role in obesity</a>". He also dismisses physical activity as having a participating role in weight management (although he does say it's good for you for other reasons); as I've <a href="http://evolvinghealthscience.blogspot.com/2012/05/nevermind-body-fat-put-focus-on-muscle.html">written</a> before, exercise is critical because of the role of skeletal muscle in consuming energy and determining metabolic rate. Mainly, however, the book regurgitates a lot of the same arguments are about what's wrong with the food system, some controversial and some not. Overall, many nutritionists would probably agree that Dr. Lustig is non-controversial. His recommendations for weight management are sound. He summarizes them by shortening Michael Pollan's <i>"Eat food. Not too much. Mostly plants."</i> to just simply <i>"Eat food."</i> He argues that if you cut out all processed foods and sugar, people are bound to lose weight. He calls for completely cutting out anything with a Nutrition Facts label, which denotes that it is a "processed food". It's a no-brainer that people who go to this extreme would likely lose weight from lack of contributing calories from those foods. But it's not the only approach one can take to lose weight.<br />
<br />
One might ask, why all the fuss about scientific accuracy? What's the problem with the cause of getting people to limit intake of sugar if it leads to a common good of reducing obesity? My answer to people who ask me this is the same that other scientists have voiced, which is that singling out of any ingredient and to make it the scapegoat for the obesity epidemic is just distracting. It's<i> </i>not helpful to call sugar "toxic" and ultimately does nothing to change people's habits, except maybe causing them to forgo buying any food with high-fructose corn syrup for a while. In the end, people will still continue to eat too much, exercise too little, and gain weight.daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com9tag:blogger.com,1999:blog-5995754777906978314.post-16255433246765483732012-12-02T14:38:00.004-08:002013-01-20T11:07:26.362-08:00Why you can all stop saying meat eating fueled evolution of larger brains right now<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="http://www.flickr.com/photos/ledr/3672595111/" style="margin-left: auto; margin-right: auto;" title="Returning from hunt by Andy Lederer, on Flickr"><img alt="Returning from hunt" height="334" src="http://farm3.staticflickr.com/2447/3672595111_63374930f7.jpg" width="500" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Hadza returning from hunt in Tanzania. Credit Andy Lederer.</td></tr>
</tbody></table>
In William Shakespeare's comedy <i>Twelfth Night, </i>Sir Andrew, who was worried that a joke may have been made at his expense, reasons out loud that maybe his diet had something to do with his lack of intelligence, saying, "But I am a great eater of beef, and I believe that does harm to my wit" (Act I, Scene III). Dialogue like that was how Shakespeare famously poked fun at what he considered "foolery" in his time; it was a common belief of the Elizabethan Age that eating too much meat made you a meat-head. Now, it appears the tables have turned. Vegetarians are getting a taste of similar medicine from comedians of our time.<br />
<br />
On November 15th's episode of <i>The Colbert Report, </i>Stephen Colbert interviewed one of the world's foremost paleoanthropologists, Chris Stringer of the Natural History Museum, about his newly published <a href="http://www.amazon.com/Lone-Survivors-Came-Humans-Earth/dp/0805088911">book</a>. During their conversation, Stringer sums up nicely why meat eating may have been the primary force that drove evolution of a <i>brain-gut tradeoff</i>, where a shrinking gut allowed for more energy input into the brain. Here is Stringer's explanation at about minute 18:30 in the <a href="http://www.colbertnation.com/full-episodes/thu-november-15-2012-chris-stringer">episode</a>:<br />
<blockquote class="tr_bq">
Chris Stringer: "There's a thing called 'expensive tissue hypothesis'. And this says we evolved our large brains by changing our diets. Our ancestors had great big guts because they were vegetarian. They never had enough spare energy because their guts were using 20 percent of their energy; they never had enough spare energy to evolve a large brain. When we started eating meat, a much more concentrated sort of food, it freed up energy and we could start to run a bigger brain."</blockquote>
<blockquote class="tr_bq">
Stephen Colbert: "That's why vegetarianism seems so stupid to me."<br />
<a name='more'></a></blockquote>
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
There's little use challenging the evidence that meat, whether eaten raw or cooked, was "brain food" for our ancestors. The fossil record shows a clear correlation between the appearance of hominin meat eating some two million years ago -- as evidenced by stone tools, cutmarked bones, and changes in hominin teeth structure -- and the drastic increase in cranial size that continued until the agricultural revolution. Studies in genetics and in <a href="http://evolvinghealthscience.blogspot.com/2011/09/what-chimpanzee-predatory-behavior-can.html">primatology</a> add more support that meat helped enable our ancestors to attain the nutrients required for the development of all our extra neurons. In my last <a href="http://evolvinghealthscience.blogspot.com/2012/11/human-vs-chimps-what-regulome-tells-us.html">post</a>, for example, I discuss Greg Wray's research on how changes in differences of fat metabolism and neuronal signaling that may have developed as a result of more meat in the diet and probably helped produce our fatter brains.<br />
<br />
However, while meat eating may have played a role, the arguments espoused often by writers, "paleo" and Atkins enthusiasts, and meat-lovers of all kinds are often flawed from a nutritional standpoint. The problem is, it just doesn't make a lot of sense that meat eating could have fueled evolution of our larger brains. It's more likely that carbs did.<br />
<br />
<b>Neurons run on glucose, not meat</b><br />
<br />
Neurons, which use twice the energy as any other cell type in the body, run almost exclusively on glucose. They don't run on protein and fat.* Moreover, because neurons aren't able to store glucose as glycogen as other cells in the body do, they must receive glucose in constant supply. That's glucose that must be received from the bloodstream 24 hours a day, seven days a week, even while you're asleep. That's glucose for some 86 billion neurons, more than any other primate; by comparison, gorillas contain about 33 billion and chimpanzees only 28 billion neurons. That's glucose in amounts that could not possibly be supplied by any abundance of meat eating.
<br />
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="http://upload.wikimedia.org/wikipedia/commons/4/4e/Human_and_chimp_brain.png" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="320" src="http://upload.wikimedia.org/wikipedia/commons/4/4e/Human_and_chimp_brain.png" width="240" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">A human brain is ~3x larger than a chimp's.</td></tr>
</tbody></table>
<br />
To get an expert's standpoint on the topic, I wrote to Peter Ungar, distinguished professor and chair of anthropology at University of Arkansas, who was recently <a href="http://newswire.uark.edu/article.aspx?id=19791">named</a> a fellow of the American Association for the Advancement of Science, what his take was on the role of meat eating versus carbs in human brain evolution. He wrote back,<br />
<blockquote class="tr_bq">
Even the staunchest meat advocates recognize that protein and fat cannot power the brain – and we lose much of our gluconeogenesis capabilities at weaning. The argument is that meat eating provided the calories needed to power other parts of the body, freeing available carbohydrates to focus on the brain… Even in that case, it’s carbs, not meat that powers the brain (even though meat facilitates the process).</blockquote>
So, let me repeat in my own way: Why was meat important for evolution of larger brains? Although meat does provide some valuable micronutrients and essential fats, there may not be anything incredibly special about meat nutritionally except that it freed up carbohydrate calories for feeding brains that were roughly three times larger than chimps without the use of gluconeogenesis (synthesis of glucose). <br />
<br />
According to Wray's evidence from regulatory genes, humans also developed double the glucose transporters in the brain in comparison to chimps. Chimps, on the other hand, have double the glucose transporters in their muscles. That translates to about four times more glucose going to our brains versus our muscles in comparison to chimps. When I asked Ungar what he thought regarding the role of other types foods (e.g. tubers), as well as preparation techniques (e.g. cooking) in also freeing carbs for the brain, he responded,<br />
<blockquote class="tr_bq">
I believe the hominin lifestyle is more about a broadened niche than meat per se… Lots of people live in lots of places because they can find something to nourish themselves in whatever environment they find themselves in. Western Australian aboriginals did quite well without lots of meat. </blockquote>
On Wray's research, Ungar also added,<br />
<blockquote class="tr_bq">
I’m not an expert on fueling the brain, but it makes sense to me that we’re more efficient at getting glucose across (we need it). One could argue that this allows LESS carb intake for a given brain size… Since our brains are roughly 4x the size of Chimps, does that mean we need about the same number of carbs to power them? </blockquote>
<blockquote class="tr_bq">
As for evidence of increased starchy food intake – I think the amylase gene copies didn’t take off until relatively recently. Still, evidence of a broadened subsistence base in Homo could certainly have included starchy foods, meat, or anything else they could get their hands on. </blockquote>
<blockquote class="tr_bq">
I’m pretty conservative in terms of single-cause, magic bullet explanations without solid evidence from the fossils themselves… Maybe it’s my time chasing broad-diet primates in the rainforest, but I’m hesitant to invoke one food type to explain brain expansion.</blockquote>
Lastly, he wrote,<br />
<blockquote class="tr_bq">
...the problem now is coming up with ways of testing those hypotheses (meat, cooking, flexibility, fish, etc). In the end, I woudn’t be surprised if there were no magic bullet… but after all the new and exciting findings coming from isotopes, microwear, etc. not much would surprise me re: the evolution of human diet.</blockquote>
So there you have it -- it's more appropriate to say that a "broadened niche" is what helped fuel evolution of larger brains. Meat provided micronutrients, but more of it more often probably did nothing more than provide more calories so that we could use carbs to fuel our brains. It's certainly possible that other foods like cooking, shore-based foods, and other foods could've played the same role, too. <br />
<b><br /></b>
<b>Cooking Was More Important Than Meat for Brains</b><br />
<br />
In a recent live chat with science writer Ann Gibbons over at <a href="http://news.sciencemag.org/sciencenow/2012/11/live-chat-did-cooking-lead-to-b.html">ScienceLive</a>, biological anthropologist Richard Wrangham at Harvard and comparative neuroanatomist Suzana Herculano-Houzel had a few interesting things to say on this topic while discussing their recent study published in <i>Proceedings of the National Academy of Sciences. </i>Their study showed that humans would have to spend more than nine hours a day eating raw foods to feed hungry brains (at 2,000 kcal a day) despite whether raw meat was included or not. <br />
<br />
In the chat, Wrangham said, as he's argued in his <a href="http://www.amazon.com/Catching-Fire-Cooking-Made-Human/dp/0465020410">book</a>,<br />
<blockquote class="tr_bq">
Cooking increases the net energy gained from food from 2 main routes. (1) It increases digestibility (the proportion of food that gets digested and absorbed). For instance cooking is estimated to increase the digestibility of starch in grains by around 30%. It also increases the digestibility of meat, by denaturing the protein. (2) It reduces the physiological costs of digesting our food - because cooking softens food, so it is easier to digest.</blockquote>
A commenter, Fred, questioned the role of meat eating versus cooking in leading to larger brains, to which Wrangham responded,<br />
<blockquote class="tr_bq">
The meat vs. veg question is totally unresolved! Recent hunter-gatherers ate least meat near the equator, about 35% of diet, rising to ~100% near the poles. But recent hunter-gatherers are not necessarily good models for our ancestors. They have technology (bows and arrows, and poisons) that made hunting easier; but there again, there may have been more animals in the past. Also, the truly great places for hunter-gatherers to live in may have been those where farmers took over in masses, such as the Nile delta, with terrific plant supplies. So the 'paleo-diet' idea that our ancestors were all heavy meat-eaters doesn't acknowledge the likely large variation in % meat / % plant. Anyway, nowadays vegetarians have about the same body mass index as meat-eaters. So meat doesn't seem to do much to affect energy gain. (But raw-dieters, whether vegetarian or meat-eaters, are much thinner on average than cookivores, whether vegetarian or meat-eaters.) Bottom line: meat is less important than cooking when it comes to energy gain.</blockquote>
Is Wrangham suggesting redemption for raw dieting and vegetarianism as a healthy dietary approach in a modern world? Some people might think so. Although, as a nutritionist, I wouldn't recommend them a raw or vegetarian diet. After all, animal protein is valuable for maintaining or building muscle because of its higher quality <a href="http://evolvinghealthscience.blogspot.com/2012/05/nevermind-body-fat-put-focus-on-muscle.html">amino acid profile</a>; specific animal fats (DHA and EPA) are <a href="http://evolvinghealthscience.blogspot.com/2012/05/why-fat-brain-made-us-more-vulnerable.html">valuable</a> for cardiovascular and brain health; and animal foods generally do provide necessary micronutrients such as zinc that are important for brain health.<br />
<br />
Yet, the point here is there was probably "no magic bullet" that led to evolution of human brains and that meat is not necessarily a brain food. Whatever the combination of factors -- cooking, broadened niche, even <a href="http://evolvinghealthscience.blogspot.com/2010/11/food-sharing-role-in-human-evolution.html">food sharing</a> -- that led to larger brains, carbs are what really fuel your neurons, and that's not to say you should overconsume carbs either; most of us already do too much of that. So, there's no sense in using evolution of larger brains as an argument for gorging on steak. Too much beef (and too little glucose), as The Bard would've believed, really might do "harm to your wit."<br />
<br />
Update: I'm thrilled to share that this blog post was blogged about by Barbara J. King of NPR over at 13.7 -- check it out <a href="http://www.npr.org/blogs/13.7/2012/12/02/166360654/carbs-not-meat-fueled-evolution-of-the-enlarged-human-brain?guid=1354552380257">here</a>. Enjoy!<br />
<br />
<i>*12-7 note: Many of you have pointed out my statement "They don't run on protein and fat" is not entirely accurate. Amino acids can be used to synthesize glucose, although this is a metabolically costly process in terms of ATP. As Ungar said, gluconeogenesis is limited in humans. Also, it is possible for the brain to use products of fat catabolism called ketones as fuel (to spare muscle amino acids; in fact, muscle will use ketones first); however, ketones are only use in the brain in periods of prolonged starvation (or on a diet extremely low in calories with little to no carbohydrates) and may lead to adverse health consequences. </i></div>
daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com23tag:blogger.com,1999:blog-5995754777906978314.post-57774300803792214702012-11-11T23:19:00.000-08:002013-02-16T11:53:44.801-08:00Human vs. chimps: What the "regulome" tells us about meat eating & bigger brains <table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjObmc5576QkCMQY2MYNX3dhMbkpfcrVkWisv_hH5M-8Eaalh6GQomu3kTvpwD8M-7sqW8T4NTrXj7q2qNs8sJSQVl7hHIEQYMkVBgEdZ4LCdd4OM-3KTq6iK1Bj3w76C_JY2vq-UVHJD0/s1600/Evolution+of+the+Brain.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="291" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjObmc5576QkCMQY2MYNX3dhMbkpfcrVkWisv_hH5M-8Eaalh6GQomu3kTvpwD8M-7sqW8T4NTrXj7q2qNs8sJSQVl7hHIEQYMkVBgEdZ4LCdd4OM-3KTq6iK1Bj3w76C_JY2vq-UVHJD0/s400/Evolution+of+the+Brain.png" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Source: Greg Wray</td></tr>
</tbody></table>
The story about how humans evolved bigger brains begins some seven million years ago in central Africa. There, in a dense rainforest, there lived the last ancestor that we share with our closest living relatives. Our evolutionary paths diverged when the global climate changed and a new habitat took shape. While ancestors of chimpanzees retreated deeper into the rainforest to subsist on a diet mainly of fruits, our ancestors found themselves in on strange, new, dry grassland.<br />
<br />
The savanna would mean a new way of life for our ancestors. They'd learn to use tools, communicate with each other using language, and work together to hunt animals for food. Based on fossil evidence and stable isotope data, our hominin ancestors shifted to a diet where meat was a principal energy source about two million years ago. It would be a major shift in diet that coincided with an increase in cranial capacity.<br />
<br />
Now, scientists like Greg Wray, a professor of biology at Duke University, are beginning to better understand the genetic basis for the adaptation to eating meat and how it guided the development of our larger brains. During his plenary talk at the Council for the Advancement of Science Writing's (CASW) "New Horizons in Science 2012" <a href="http://today.duke.edu/2012/10/sciconference">annual conference</a> in Durham, North Carolina, Wray said that the <a href="http://www.nature.com/encode/#/threads"><span style="color: #2000ee; text-decoration: underline;">Encyclopedia of DNA Elements</span></a> (ENCODE) project gave scientists like himself a "detailed street map" for seeking out the genetic changes that took place since the divergence of humans and chimpanzees over evolutionary time.<br />
<br />
<a name='more'></a>Wray said that the major diet shift to meat eating is written right into the "software" that runs our genes: the <i>regulome. </i>Previous to ENCODE, these non-coding regulatory regions were thought of only as "junk" DNA. In this new post-ENCODE, however, scientists are finding that these regions have central regulatory roles in the genome and may play a central role in adaptation and divergence of species.<br />
<br />
In the regulome, Wray said, his lab found that evidence of genetic changes resulting from our ancestors' change in diet that would mean stark differences in how we metabolize fats and sugars in comparison to chimpanzees. The genetic changes could also explain how we're able to feed our energy-hungry brains and why we are more susceptible to specific diseases such as diabetes.<br />
<br />
<b>Mini-ENCODE for humans and chimps</b><br />
<br />
The lab focused their research on five tissue samples because of their importance in understanding dietary adaptations—cerebral cortex, cerebellum, liver, adipose tissue, and skeletal muscle. The research would be like a "mini-ENCODE" comparing evolutionary changes between humans and chimpanzees since their divergence from a last common ancestor.
<br />
<br />
According to Wray, his lab found a "huge signal" of changes in cell signaling genes that meant a lot of coordination going on between metabolism, development, and neural functions. For example, of the 61 genes that are known participants in insulin signaling, 31, almost half, were different. The differences in insulin signaling genes may explain why humans are so much more susceptible to diet-related diseases such as type 1 and 2 diabetes than are chimpanzees. "That's what's changed between humans and chimps," he said.<br />
<br />
What's not changed are more general functions involved in DNA transcription, replication, and repair; RNA processing and translation; and protein translation and localization.<br />
<br />
Looking at general patterns, Wray also found a lot of signals for metabolism and neural function changes. When humans are compared to rhesus macaques, the changes are still clear along the longer evolutionary span. However, comparing chimps to rhesus macaques finds that the neural signaling is gone while the metabolism signal is still there.
<br />
<br />
"If you do this kind of analysis for these functional categories, you can start to parse out what's different about human evolution versus other aspects of primate evolution," Wray said.<br />
<br />
<b>Fat cells behave differently in humans versus chimps</b><br />
<br />
In humans versus chimps, Wray said, there are also stark differences in how we store fat, produce fat, (de novo synthesis of fatty acids) and how we burn fat for energy (beta-oxidation) because of differently regulated genes. "Pretty much every aspect of fat cell function has been altered between humans and chimps," Wray said.<br />
<br />
Investigating further, Wray's lab used adipose tissue stem cells from humans and from chimps and performed a series of petri dish experiments. The cells were grown "under different diets"—that is to say that they grew in the presence of either more carbohydrate, oleic acid (which is the dominant fatty acid found in meat), or linoleic acid (the dominant fatty acid found in grains).<br />
<br />
A clear signal was returned: each of the enzymes for fatty acid synthesis was higher among the human adipose tissue cells. In a habitat where the principal energy source would switch from simple sugars from fruit to fatty acids from meat, it'd make sense to have these enzymes upregulated. The findings could explain how humans were able to grow brains thrice the size.<br />
<br />
"If you're going to make a bigger brain, a brain that's about three times larger than the chimp-human ancestor, you need to make a whole lot more building material," he said. "You don't need to just make these membrane materials you need to constantly turn them over. So the flux through this pathway is probably pretty important to building a bigger brain."<br />
<br />
Although with the reward of a bigger brain through an adaptation to push more fatty acids through pathways came an unintended side effect, Wray said. Another major shift in diet at the agricultural revolution would introduce a large amount of omega-6 fatty acids. A high influx of omega-6 fatty acids would produce higher levels of arachidonic acid, involved in production of pro-inflammatory eicosanoids implicated in insulin resistance and atherosclerosis.<br />
<br />
<b>Expensive-tissue hypothesis at the metabolic level</b><br />
<br />
Making larger brains came with other costs, as well, and it had to do with a tradeoff of energy allocation. The brain is an exceptionally energy-hungry tissue consuming almost 10-fold higher than the rest of the body even while asleep. "What that means is that if you triple the size of the brain, you’re not making one organ a little bigger, you're essentially raising the energy budget of the body by a lot," Wray said.<br />
<br />
As anthropologists and physiologists have long argued, a larger brain meant taking energy away from somewhere else, preferably another energy-hungry tissue. "Expensive-tissue hypothesis" may be partly explained by the fact that our human guts are a little shorter and our muscles are smaller than that of chimpanzees. But it's "not enough," Wray said. His lab suggests that the regulome could explain the tradeoff from a metabolic and molecular level, not at the level of gross organ size.<br />
<br />
Sugar transporters show signals of positive selection in the regulatory region, Wray said. A couple of genes called SLC2a1 and SLC2a4 (SLC – transport protein; 2 – sugar transport; a1 and a4 and so forth are different members of those families) are uniquely positioned to mediate the tradeoff. SLC2a1 is expressed predominantly in the brain and SLC2a4 is expressed predominantly in the skeletal muscle.<br />
<br />
"We hypothesized that if you increase the expression of the brain transporter and decrease the expression of the muscle transporter, the common point of energy metabolism (glucose)—is going to be allocated differently, just by mass action" Wray said.<br />
<br />
What Wray's lab found was that when they compared brain specific expression of the sugar transporter, it was much higher in humans than it was in chimps and rhesus macaques. In muscle, conversely, it's higher in chimpanzees than it is in humans. Double the glucose transporters in the brain and half in the muscle would mean a four-fold difference in glucose getting across the membrane into the brain. As a way of maximizing energy supply to the brain "that's pretty large change," Wray said.<br />
<br />
Comparatively, it is well known in the medical field that children with deficiencies in glucose transporters (Glut1 deficiency syndrome) have cognitive deficits. "The brain literally starves," Wray said. "We had to have that increase [in glucose transporters] in the metabolic scope of the brain to allow it to get bigger."<br />
<br />
<b>Of mice and bigger brains</b><br />
<br />
During the last few minutes of his talk, Wray shared with his audience one other project his lab was working on, shared as a teaser: It was to clone out pieces of the regulome thought to be responsible for changes in human and chimp brains and testing them in mice embryos.<br />
<br />
Wray's lab found that mice embryos with either the "chimp enhancers" or the "human enhancers" had strong signals of neural stem cells production and greater neuron production. In particular, the embryos with the human enhancers came on stronger and lasted longer.<br />
<br />
"What we haven't done yet is see what happens if these mice grow up and see if they have cognitive changes, behavioral changes, or detail changes in the structure of their brains," Wray said. <i>Those big-brained mice are going to grow up?</i><br />
<br />
<b>Questions and FADS</b><br />
<b><br /></b>
After Wray's talk, there were plenty of questions asked by his audience, who were mainly science writers attending Science Writers 2012 (see Keith Eric Grant's #sciwri12 <a href="http://storify.com/ramblemuse/science-writers-2012-wray">Storify story</a>). These included ones about his own diet -- less starch, some animal products, mostly fruits and vegetables, a higher omega-3 to omega-6 ratio -- and how Richard Wrangham hypothesis that cooking could explain energy tradeoff might've figured into the equation -- yes, Wray agreed, cooked food is easier to digest and absorb.<br />
<br />
There was also a question about whether or not Wray's lab would be looking at comparing the human regulomes with that of other hominin species such as Denisovan and Neandertal. It was something, Wray said, that he was definitely looking into doing in the future.<br />
<br />
One of the questions I asked Wray was about genetic variation between different human populations, specifically with regards to the <a href="http://evolvinghealthscience.blogspot.com/2012/05/why-fat-brain-made-us-more-vulnerable.html">FADS region</a> of the genome. The region has been subject of special interest and speculation among researchers because variations of rate-limiting enzymes encoded by FADS1 and FADS2 for biosynthesizing long-chaing fatty acids may also help explain larger brains.<br />
<br />
"I think it's a layered processing," he said. "Originally, there was probably upregulation of the FADS genes simply because we had so much more fatty acids in our diet. That probably coincided with the shift to a more animal-rich diet."<br />
<br />
Wray added that because both the omega-6s and omega-3s flow through enzymes encoded by the FADS region, it also may explain why a post-agricultural revolution diet higher in grains puts us at higher risk of chronic disease. The high omega-6 to omega-3 ratio of our modern diets puts us "way out of balance," he said, with more omega-6s moving through pathways to produce pro-inflammatory compounds.<br />
<br />daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com2tag:blogger.com,1999:blog-5995754777906978314.post-23382273579976241432012-11-09T05:52:00.003-08:002012-12-28T12:17:05.601-08:00Food is "star stuff"<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhkjV0QOkVUyQtXnPZ9YxMGL54wms8acLXtERCZDF0dybrJ3qfcL2XLkOoQV9HLQ7an8acUP5jaYD400OAe_WwYe1bPYR0oCe9aBNnhhcf5iYaIjOnu-vxL60skGRuQs980Fc_oEWpgYMU/s1600/champagne.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="240" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhkjV0QOkVUyQtXnPZ9YxMGL54wms8acLXtERCZDF0dybrJ3qfcL2XLkOoQV9HLQ7an8acUP5jaYD400OAe_WwYe1bPYR0oCe9aBNnhhcf5iYaIjOnu-vxL60skGRuQs980Fc_oEWpgYMU/s400/champagne.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Champagne supernova. Credit: Space Daily</td></tr>
</tbody></table>
"If you want to make an apple pie from scratch, you must first invent the universe."
<br />
<br />
When you eat a slice of apple pie, or any pie, or any food at all today, on Carl Sagan Day, it may be worthwhile to reflect on this quote, one of the beloved television series host's most famous from <i>Cosmos: A Personal Voyage.</i><br />
<i><br /></i>
A look back at our origins is a good way to gain some perspective, amidst the accumulating scientific evidence, on how to understand our own biology and predicting ways in which we can keep our own healthy.
Or, at least, that has been my conclusion.
Starting at the beginning with the <a href="http://evolvinghealthscience.blogspot.com/2011/02/pornography-in-primordial-soup.html">chemistry of life</a>, our own <a href="http://evolvinghealthscience.blogspot.com/2010/12/how-diet-shaped-human-evolution.html">evolution</a>, and to that of our <a href="http://evolvinghealthscience.blogspot.com/2011/09/what-chimpanzee-predatory-behavior-can.html">close cousins</a>, then on to our <a href="http://evolvinghealthscience.blogspot.com/2012/05/why-fat-brain-made-us-more-vulnerable.html">current situation</a>, and the <a href="http://evolvinghealthscience.blogspot.com/2012/04/future-of-nutrition-research.html#more">future</a>, this blog has explored all sorts of topics relating to diet and health in the past and forthcoming.<br />
<a name='more'></a><br />
<br />
Over the years, what's evident is that there exist numerous ongoing debates in the world of food, nutrition, and medicine. Some are scientific and some are not so. Frustrations arise. Tension happens. People disagree. That is the nature of progress albeit it can be slow going at times much like evolution.
<br />
<br />
Sometimes, setting aside any so-called <i>dietary dogmas</i>, one can find some simple peace in the knowledge that all life and our foods are based on basic chemistry. After all, as the father of nutrition Antoine Lavoisier once said, "Life is a chemical process."<br />
<br />
In addition, nutritional biochemist Michael Crawford and David Marsh once wrote, that "every particle of matter in the delicate tissues which build our bodies is made of elements that were transmuted into their present form in an unimaginable heat and pressure" (1).<br />
<br />
<a href="https://twitter.com/d_a_howell">Andy Howell</a> a staff scientist at Las Cumbres Observatory Global Telescope Network and an adjunct professor of physics at University of California, Santa Barbara is someone who might just have a grasp on the temperature and pressure that furnished our basic elements.
<br />
<br />
In his entertaining talk, given on dark matter, zombie stars and supernovae at the Science Writers 2012 meeting in Raleigh, North Carolina, Howell gave an overview of the history of physics, the known universe, and then showed models of stellar thermonuclear explosions.
<br />
<br />
He described how the temperature and pressure in supernovae, such as the Type 1a supernova he and fellow astronomers including Ben Dilday discovered (2), are capable of producing the very iron in our blood and the calcium in our bones is created.<br />
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; margin-left: 1em; text-align: right;"><tbody>
<tr><td style="text-align: center;"><a href="http://farm1.staticflickr.com/19/107224599_0eaae1c008_z.jpg" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="240" src="http://farm1.staticflickr.com/19/107224599_0eaae1c008_z.jpg" width="320" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Credit: Neven Mrgan</td></tr>
</tbody></table>
<br />
While the astronomer discussed the nature of "alchemy," or the fusing of matter into atoms and elements, and how each of these elements (e.g. calcium) shoot out from exploding stars, I could only fixate my attention on the sobering fact that every particle of matter in me and an apple pie (carbon, hydrogen, oxygen, nitrogen, calcium, iron) was produced in a supernova in the same way.
<br />
<br />
And, the eloquence of that celebrated man came to mind, because of one other wonderful thing he famously said. This quote should be cherished by all scientists -- chemists, astronomists, biologists, and food scientists alike:
<br />
<br />
"The nitrogen in our DNA, the calcium in our teeth, the iron in our blood, the carbon in our apple pies were made in the interiors of collapsing stars. We are made of star stuff."<br />
<br />
<b>References</b><br />
<br />
<ol>
<li>Crawford M and Marsh D. <i>Nutrition and Evolution</i>. New Canaan, Ct: Keats Publishing; 1995.</li>
<li>Dilday B, Howell DA, Cenko SB, et al. PTF 11kx: A Type Ia Supernova with Symbiotic Nova Progenitor. <i>Science </i>24 August 2012: 337(6097);942-945. DOI: <a href="http://www.sciencemag.org/content/337/6097/942">10.1126/science.1219164</a></li>
</ol>
daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com0tag:blogger.com,1999:blog-5995754777906978314.post-37941960164021687992012-11-07T17:15:00.000-08:002012-12-01T22:43:35.834-08:00Why lemurs get sick: A lesson for humans, too<div class="separator" style="clear: both; text-align: center;">
</div>
<div>
<!--[if gte mso 9]><xml>
<o:DocumentProperties>
<o:Revision>0</o:Revision>
<o:TotalTime>0</o:TotalTime>
<o:Pages>1</o:Pages>
<o:Words>1296</o:Words>
<o:Characters>7393</o:Characters>
<o:Company>Isagenix</o:Company>
<o:Lines>61</o:Lines>
<o:Paragraphs>17</o:Paragraphs>
<o:CharactersWithSpaces>8672</o:CharactersWithSpaces>
<o:Version>14.0</o:Version>
</o:DocumentProperties>
<o:OfficeDocumentSettings>
<o:AllowPNG/>
</o:OfficeDocumentSettings>
</xml><![endif]-->
<!--[if gte mso 9]><xml>
<w:WordDocument>
<w:View>Normal</w:View>
<w:Zoom>0</w:Zoom>
<w:TrackMoves/>
<w:TrackFormatting/>
<w:PunctuationKerning/>
<w:ValidateAgainstSchemas/>
<w:SaveIfXMLInvalid>false</w:SaveIfXMLInvalid>
<w:IgnoreMixedContent>false</w:IgnoreMixedContent>
<w:AlwaysShowPlaceholderText>false</w:AlwaysShowPlaceholderText>
<w:DoNotPromoteQF/>
<w:LidThemeOther>EN-US</w:LidThemeOther>
<w:LidThemeAsian>JA</w:LidThemeAsian>
<w:LidThemeComplexScript>X-NONE</w:LidThemeComplexScript>
<w:Compatibility>
<w:BreakWrappedTables/>
<w:SnapToGridInCell/>
<w:WrapTextWithPunct/>
<w:UseAsianBreakRules/>
<w:DontGrowAutofit/>
<w:SplitPgBreakAndParaMark/>
<w:EnableOpenTypeKerning/>
<w:DontFlipMirrorIndents/>
<w:OverrideTableStyleHps/>
<w:UseFELayout/>
</w:Compatibility>
<m:mathPr>
<m:mathFont m:val="Cambria Math"/>
<m:brkBin m:val="before"/>
<m:brkBinSub m:val="--"/>
<m:smallFrac m:val="off"/>
<m:dispDef/>
<m:lMargin m:val="0"/>
<m:rMargin m:val="0"/>
<m:defJc m:val="centerGroup"/>
<m:wrapIndent m:val="1440"/>
<m:intLim m:val="subSup"/>
<m:naryLim m:val="undOvr"/>
</m:mathPr></w:WordDocument>
</xml><![endif]--><!--[if gte mso 9]><xml>
<w:LatentStyles DefLockedState="false" DefUnhideWhenUsed="true"
DefSemiHidden="true" DefQFormat="false" DefPriority="99"
LatentStyleCount="276">
<w:LsdException Locked="false" Priority="0" SemiHidden="false"
UnhideWhenUsed="false" QFormat="true" Name="Normal"/>
<w:LsdException Locked="false" Priority="9" SemiHidden="false"
UnhideWhenUsed="false" QFormat="true" Name="heading 1"/>
<w:LsdException Locked="false" Priority="9" QFormat="true" Name="heading 2"/>
<w:LsdException Locked="false" Priority="9" QFormat="true" Name="heading 3"/>
<w:LsdException Locked="false" Priority="9" QFormat="true" Name="heading 4"/>
<w:LsdException Locked="false" Priority="9" QFormat="true" Name="heading 5"/>
<w:LsdException Locked="false" Priority="9" QFormat="true" Name="heading 6"/>
<w:LsdException Locked="false" Priority="9" QFormat="true" Name="heading 7"/>
<w:LsdException Locked="false" Priority="9" QFormat="true" Name="heading 8"/>
<w:LsdException Locked="false" Priority="9" QFormat="true" Name="heading 9"/>
<w:LsdException Locked="false" Priority="39" Name="toc 1"/>
<w:LsdException Locked="false" Priority="39" Name="toc 2"/>
<w:LsdException Locked="false" Priority="39" Name="toc 3"/>
<w:LsdException Locked="false" Priority="39" Name="toc 4"/>
<w:LsdException Locked="false" Priority="39" Name="toc 5"/>
<w:LsdException Locked="false" Priority="39" Name="toc 6"/>
<w:LsdException Locked="false" Priority="39" Name="toc 7"/>
<w:LsdException Locked="false" Priority="39" Name="toc 8"/>
<w:LsdException Locked="false" Priority="39" Name="toc 9"/>
<w:LsdException Locked="false" Priority="35" QFormat="true" Name="caption"/>
<w:LsdException Locked="false" Priority="10" SemiHidden="false"
UnhideWhenUsed="false" QFormat="true" Name="Title"/>
<w:LsdException Locked="false" Priority="1" Name="Default Paragraph Font"/>
<w:LsdException Locked="false" Priority="11" SemiHidden="false"
UnhideWhenUsed="false" QFormat="true" Name="Subtitle"/>
<w:LsdException Locked="false" Priority="22" SemiHidden="false"
UnhideWhenUsed="false" QFormat="true" Name="Strong"/>
<w:LsdException Locked="false" Priority="20" SemiHidden="false"
UnhideWhenUsed="false" QFormat="true" Name="Emphasis"/>
<w:LsdException Locked="false" Priority="59" SemiHidden="false"
UnhideWhenUsed="false" Name="Table Grid"/>
<w:LsdException Locked="false" UnhideWhenUsed="false" Name="Placeholder Text"/>
<w:LsdException Locked="false" Priority="1" SemiHidden="false"
UnhideWhenUsed="false" QFormat="true" Name="No Spacing"/>
<w:LsdException Locked="false" Priority="60" SemiHidden="false"
UnhideWhenUsed="false" Name="Light Shading"/>
<w:LsdException Locked="false" Priority="61" SemiHidden="false"
UnhideWhenUsed="false" Name="Light List"/>
<w:LsdException Locked="false" Priority="62" SemiHidden="false"
UnhideWhenUsed="false" Name="Light Grid"/>
<w:LsdException Locked="false" Priority="63" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Shading 1"/>
<w:LsdException Locked="false" Priority="64" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Shading 2"/>
<w:LsdException Locked="false" Priority="65" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium List 1"/>
<w:LsdException Locked="false" Priority="66" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium List 2"/>
<w:LsdException Locked="false" Priority="67" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 1"/>
<w:LsdException Locked="false" Priority="68" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 2"/>
<w:LsdException Locked="false" Priority="69" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 3"/>
<w:LsdException Locked="false" Priority="70" SemiHidden="false"
UnhideWhenUsed="false" Name="Dark List"/>
<w:LsdException Locked="false" Priority="71" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful Shading"/>
<w:LsdException Locked="false" Priority="72" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful List"/>
<w:LsdException Locked="false" Priority="73" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful Grid"/>
<w:LsdException Locked="false" Priority="60" SemiHidden="false"
UnhideWhenUsed="false" Name="Light Shading Accent 1"/>
<w:LsdException Locked="false" Priority="61" SemiHidden="false"
UnhideWhenUsed="false" Name="Light List Accent 1"/>
<w:LsdException Locked="false" Priority="62" SemiHidden="false"
UnhideWhenUsed="false" Name="Light Grid Accent 1"/>
<w:LsdException Locked="false" Priority="63" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Shading 1 Accent 1"/>
<w:LsdException Locked="false" Priority="64" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Shading 2 Accent 1"/>
<w:LsdException Locked="false" Priority="65" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium List 1 Accent 1"/>
<w:LsdException Locked="false" UnhideWhenUsed="false" Name="Revision"/>
<w:LsdException Locked="false" Priority="34" SemiHidden="false"
UnhideWhenUsed="false" QFormat="true" Name="List Paragraph"/>
<w:LsdException Locked="false" Priority="29" SemiHidden="false"
UnhideWhenUsed="false" QFormat="true" Name="Quote"/>
<w:LsdException Locked="false" Priority="30" SemiHidden="false"
UnhideWhenUsed="false" QFormat="true" Name="Intense Quote"/>
<w:LsdException Locked="false" Priority="66" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium List 2 Accent 1"/>
<w:LsdException Locked="false" Priority="67" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 1 Accent 1"/>
<w:LsdException Locked="false" Priority="68" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 2 Accent 1"/>
<w:LsdException Locked="false" Priority="69" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 3 Accent 1"/>
<w:LsdException Locked="false" Priority="70" SemiHidden="false"
UnhideWhenUsed="false" Name="Dark List Accent 1"/>
<w:LsdException Locked="false" Priority="71" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful Shading Accent 1"/>
<w:LsdException Locked="false" Priority="72" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful List Accent 1"/>
<w:LsdException Locked="false" Priority="73" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful Grid Accent 1"/>
<w:LsdException Locked="false" Priority="60" SemiHidden="false"
UnhideWhenUsed="false" Name="Light Shading Accent 2"/>
<w:LsdException Locked="false" Priority="61" SemiHidden="false"
UnhideWhenUsed="false" Name="Light List Accent 2"/>
<w:LsdException Locked="false" Priority="62" SemiHidden="false"
UnhideWhenUsed="false" Name="Light Grid Accent 2"/>
<w:LsdException Locked="false" Priority="63" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Shading 1 Accent 2"/>
<w:LsdException Locked="false" Priority="64" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Shading 2 Accent 2"/>
<w:LsdException Locked="false" Priority="65" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium List 1 Accent 2"/>
<w:LsdException Locked="false" Priority="66" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium List 2 Accent 2"/>
<w:LsdException Locked="false" Priority="67" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 1 Accent 2"/>
<w:LsdException Locked="false" Priority="68" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 2 Accent 2"/>
<w:LsdException Locked="false" Priority="69" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 3 Accent 2"/>
<w:LsdException Locked="false" Priority="70" SemiHidden="false"
UnhideWhenUsed="false" Name="Dark List Accent 2"/>
<w:LsdException Locked="false" Priority="71" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful Shading Accent 2"/>
<w:LsdException Locked="false" Priority="72" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful List Accent 2"/>
<w:LsdException Locked="false" Priority="73" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful Grid Accent 2"/>
<w:LsdException Locked="false" Priority="60" SemiHidden="false"
UnhideWhenUsed="false" Name="Light Shading Accent 3"/>
<w:LsdException Locked="false" Priority="61" SemiHidden="false"
UnhideWhenUsed="false" Name="Light List Accent 3"/>
<w:LsdException Locked="false" Priority="62" SemiHidden="false"
UnhideWhenUsed="false" Name="Light Grid Accent 3"/>
<w:LsdException Locked="false" Priority="63" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Shading 1 Accent 3"/>
<w:LsdException Locked="false" Priority="64" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Shading 2 Accent 3"/>
<w:LsdException Locked="false" Priority="65" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium List 1 Accent 3"/>
<w:LsdException Locked="false" Priority="66" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium List 2 Accent 3"/>
<w:LsdException Locked="false" Priority="67" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 1 Accent 3"/>
<w:LsdException Locked="false" Priority="68" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 2 Accent 3"/>
<w:LsdException Locked="false" Priority="69" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 3 Accent 3"/>
<w:LsdException Locked="false" Priority="70" SemiHidden="false"
UnhideWhenUsed="false" Name="Dark List Accent 3"/>
<w:LsdException Locked="false" Priority="71" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful Shading Accent 3"/>
<w:LsdException Locked="false" Priority="72" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful List Accent 3"/>
<w:LsdException Locked="false" Priority="73" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful Grid Accent 3"/>
<w:LsdException Locked="false" Priority="60" SemiHidden="false"
UnhideWhenUsed="false" Name="Light Shading Accent 4"/>
<w:LsdException Locked="false" Priority="61" SemiHidden="false"
UnhideWhenUsed="false" Name="Light List Accent 4"/>
<w:LsdException Locked="false" Priority="62" SemiHidden="false"
UnhideWhenUsed="false" Name="Light Grid Accent 4"/>
<w:LsdException Locked="false" Priority="63" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Shading 1 Accent 4"/>
<w:LsdException Locked="false" Priority="64" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Shading 2 Accent 4"/>
<w:LsdException Locked="false" Priority="65" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium List 1 Accent 4"/>
<w:LsdException Locked="false" Priority="66" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium List 2 Accent 4"/>
<w:LsdException Locked="false" Priority="67" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 1 Accent 4"/>
<w:LsdException Locked="false" Priority="68" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 2 Accent 4"/>
<w:LsdException Locked="false" Priority="69" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 3 Accent 4"/>
<w:LsdException Locked="false" Priority="70" SemiHidden="false"
UnhideWhenUsed="false" Name="Dark List Accent 4"/>
<w:LsdException Locked="false" Priority="71" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful Shading Accent 4"/>
<w:LsdException Locked="false" Priority="72" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful List Accent 4"/>
<w:LsdException Locked="false" Priority="73" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful Grid Accent 4"/>
<w:LsdException Locked="false" Priority="60" SemiHidden="false"
UnhideWhenUsed="false" Name="Light Shading Accent 5"/>
<w:LsdException Locked="false" Priority="61" SemiHidden="false"
UnhideWhenUsed="false" Name="Light List Accent 5"/>
<w:LsdException Locked="false" Priority="62" SemiHidden="false"
UnhideWhenUsed="false" Name="Light Grid Accent 5"/>
<w:LsdException Locked="false" Priority="63" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Shading 1 Accent 5"/>
<w:LsdException Locked="false" Priority="64" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Shading 2 Accent 5"/>
<w:LsdException Locked="false" Priority="65" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium List 1 Accent 5"/>
<w:LsdException Locked="false" Priority="66" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium List 2 Accent 5"/>
<w:LsdException Locked="false" Priority="67" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 1 Accent 5"/>
<w:LsdException Locked="false" Priority="68" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 2 Accent 5"/>
<w:LsdException Locked="false" Priority="69" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 3 Accent 5"/>
<w:LsdException Locked="false" Priority="70" SemiHidden="false"
UnhideWhenUsed="false" Name="Dark List Accent 5"/>
<w:LsdException Locked="false" Priority="71" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful Shading Accent 5"/>
<w:LsdException Locked="false" Priority="72" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful List Accent 5"/>
<w:LsdException Locked="false" Priority="73" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful Grid Accent 5"/>
<w:LsdException Locked="false" Priority="60" SemiHidden="false"
UnhideWhenUsed="false" Name="Light Shading Accent 6"/>
<w:LsdException Locked="false" Priority="61" SemiHidden="false"
UnhideWhenUsed="false" Name="Light List Accent 6"/>
<w:LsdException Locked="false" Priority="62" SemiHidden="false"
UnhideWhenUsed="false" Name="Light Grid Accent 6"/>
<w:LsdException Locked="false" Priority="63" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Shading 1 Accent 6"/>
<w:LsdException Locked="false" Priority="64" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Shading 2 Accent 6"/>
<w:LsdException Locked="false" Priority="65" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium List 1 Accent 6"/>
<w:LsdException Locked="false" Priority="66" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium List 2 Accent 6"/>
<w:LsdException Locked="false" Priority="67" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 1 Accent 6"/>
<w:LsdException Locked="false" Priority="68" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 2 Accent 6"/>
<w:LsdException Locked="false" Priority="69" SemiHidden="false"
UnhideWhenUsed="false" Name="Medium Grid 3 Accent 6"/>
<w:LsdException Locked="false" Priority="70" SemiHidden="false"
UnhideWhenUsed="false" Name="Dark List Accent 6"/>
<w:LsdException Locked="false" Priority="71" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful Shading Accent 6"/>
<w:LsdException Locked="false" Priority="72" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful List Accent 6"/>
<w:LsdException Locked="false" Priority="73" SemiHidden="false"
UnhideWhenUsed="false" Name="Colorful Grid Accent 6"/>
<w:LsdException Locked="false" Priority="19" SemiHidden="false"
UnhideWhenUsed="false" QFormat="true" Name="Subtle Emphasis"/>
<w:LsdException Locked="false" Priority="21" SemiHidden="false"
UnhideWhenUsed="false" QFormat="true" Name="Intense Emphasis"/>
<w:LsdException Locked="false" Priority="31" SemiHidden="false"
UnhideWhenUsed="false" QFormat="true" Name="Subtle Reference"/>
<w:LsdException Locked="false" Priority="32" SemiHidden="false"
UnhideWhenUsed="false" QFormat="true" Name="Intense Reference"/>
<w:LsdException Locked="false" Priority="33" SemiHidden="false"
UnhideWhenUsed="false" QFormat="true" Name="Book Title"/>
<w:LsdException Locked="false" Priority="37" Name="Bibliography"/>
<w:LsdException Locked="false" Priority="39" QFormat="true" Name="TOC Heading"/>
</w:LatentStyles>
</xml><![endif]-->
<!--[if gte mso 10]>
<style>
/* Style Definitions */
table.MsoNormalTable
{mso-style-name:"Table Normal";
mso-tstyle-rowband-size:0;
mso-tstyle-colband-size:0;
mso-style-noshow:yes;
mso-style-priority:99;
mso-style-parent:"";
mso-padding-alt:0in 5.4pt 0in 5.4pt;
mso-para-margin:0in;
mso-para-margin-bottom:.0001pt;
mso-pagination:widow-orphan;
font-size:12.0pt;
font-family:Cambria;
mso-ascii-font-family:Cambria;
mso-ascii-theme-font:minor-latin;
mso-hansi-font-family:Cambria;
mso-hansi-theme-font:minor-latin;}
</style>
<![endif]-->
<!--StartFragment-->
<br />
<div class="MsoNormal" style="tab-stops: 80.2pt;">
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjmrG4RGghNrqdpZqhsgIhVrDGNS-iPdGoLlr7p65t0RFzDdFzKy4I8TdR-S0tOl6a5L_kfXNTqaY0e0iIkXgVfKwLyeWeq0-XYdPWoDyVyIjwT-myoiw_KWtqsJYWSqh-2mXEPN8o9bqo/s1600/Brown+lemur.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="296" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjmrG4RGghNrqdpZqhsgIhVrDGNS-iPdGoLlr7p65t0RFzDdFzKy4I8TdR-S0tOl6a5L_kfXNTqaY0e0iIkXgVfKwLyeWeq0-XYdPWoDyVyIjwT-myoiw_KWtqsJYWSqh-2mXEPN8o9bqo/s400/Brown+lemur.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Female blue-eyed lemur</td></tr>
</tbody></table>
What lessons can humans learn from our far distant prosimian primate cousins about living well and eating a healthy diet?<br />
<br />
This was the question on my mind as I toured the <a href="https://twitter.com/DukeLemurCenter">Duke Lemur Center</a> in Durham, North
Carolina with colleagues attending Science Writers 2012. (Read Christie Wilcox’s full report about our tour over at <a href="http://blogs.scientificamerican.com/science-sushi/2012/10/31/falling-in-love-with-the-worlds-most-endangered-primates/">Science Sushi</a> on <i>Scientific American.</i>)<br />
<o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 80.2pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 80.2pt;">
When I learned on the tour that lemurs were getting sick, I inquired further from our tour guides, education associate <a href="https://twitter.com/EnvEdChris">Chris Smith</a> and
education manager Niki Barnett. The thought of these adorable creatures—somehow related to me because of a common ancestor some 50 to 80 million years ago—suffering from the same types of chronic diseases as modern-day humans encouraged me to want to find out more about their care and treatment.<br />
<a name='more'></a><br />
Lucky for me, Chris, who might’ve tired from me
badgering with so many questions, helped me arrange an interview with the
center’s senior veterinarian. On my second visit to the center at a later date,
Dr. Cathy Williams described for me, and showed me, what it was like to work as a
clinician in the world of lemurs.<br />
<br />
<b>Lemurs and humans, not so different</b><br />
<br />
There are multiple parallels between why
humans get sick and why the lemurs do, Dr. Williams told me.</div>
<div class="MsoNormal" style="tab-stops: 80.2pt;">
<o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 80.2pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 80.2pt;">
"They mainly have to do with diet,"
she said. The diets for lemurs at the center are not necessarily ideal—even in
this magical place, home to the largest population of the world's most
endangered primates outside of Madagascar.<o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 80.2pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
Routine physical exams and
dental cleanings make up most of a day in the life of a senior veterinarian,
Dr. Williams told me. The veterinarians and keepers work hard to make life for
the lemurs as healthy and comfortable as possible.</div>
<br />
<o:p></o:p>
<br />
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; margin-left: 1em; text-align: right;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiwChCvoBLwr0AO2xR_WtmOEe3HGhCoTMojae-6ZjA4Y_X1jvApguNEvF3YkIko5Uhb54b8QMb9jQWL7jeErGA6nTiVmwvNz_kneDT0gZRJm-zw3a1k7PBr2UPsOPKjxRaojSlEvza-TJQ/s1600/Lemur_Sifaka.jpg" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="200" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiwChCvoBLwr0AO2xR_WtmOEe3HGhCoTMojae-6ZjA4Y_X1jvApguNEvF3YkIko5Uhb54b8QMb9jQWL7jeErGA6nTiVmwvNz_kneDT0gZRJm-zw3a1k7PBr2UPsOPKjxRaojSlEvza-TJQ/s200/Lemur_Sifaka.jpg" width="149" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Sifakas eat primarily leaves</td></tr>
</tbody></table>
I was interested to find
out that captive lemurs often get a lot of tartar build-up on their teeth while
wild lemurs do not. The reason is mainly because the diets of captive lemurs
are mainly composed foods that are often much higher in sugars and starches
than in Madagascar. <o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
"There is less fiber, the
fruits are softer, and there’s less chewing and pulling leaves from trees," Dr.
Williams said. Chewing and pulling in the wild act as nature’s way of brushing
and flossing, Dr. Williams said, "We see a lot of gum
diseases. I’ve never seen that in the wild at all." </div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
<o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
<br />
<b>Dental care</b><br />
<br /></div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
Lemurs in the center receive
dental cleanings every couple of years. If one of the animals has dental
problems, they get cleanings more often. Dr. Williams also encourages behavioral trainers
to regularly floss the teeth of the lemurs, time and human-power permitting. <span style="mso-spacerun: yes;"> </span><o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
Similar to lemurs, dental
caries are somewhat of a novelty among humans, according to Randolph Nesse
and George Williams. The authors of <i style="mso-bidi-font-style: normal;"><a href="http://www.amazon.com/Why-We-Get-Sick-Darwinian/dp/0679746749">Why We Get Sick: The New Science of Darwinian Medicine</a> </i>wrote that tooth decay and cavities only became
more common because of today’s frequent and prolonged exposure to starches and
sugars that feed the bacteria responsible for producing acid that causes
demineralization of teeth.</div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
<o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
Caries exist in alongside a long list of chronic health-related problems caused by "modern dietary inadequacies and
nutritional excess," Nesse and Williams write. Others we're all familiar
with are obesity and diabetes. <o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 180.45pt;">
<b style="mso-bidi-font-weight: normal;">Choosing appropriate foods <o:p></o:p></b></div>
<div class="MsoNormal" style="tab-stops: 180.45pt 282.55pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 180.45pt 282.55pt;">
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; margin-left: 1em; text-align: right;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjKNIQ0WosbZ7xrwTnyw8FViXZV3yD9PM-pR77PcRJ2jI6MyUs2eDm4W6fvKR9p4nMon42O8kmW9PdELm3SeT2YHUPXDmsLSNYZC9dHIY-dOHyWHpjaQSr9PT3FtmVU99nNyYZZl1647JQ/s1600/lemursintrees.jpg" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="298" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjKNIQ0WosbZ7xrwTnyw8FViXZV3yD9PM-pR77PcRJ2jI6MyUs2eDm4W6fvKR9p4nMon42O8kmW9PdELm3SeT2YHUPXDmsLSNYZC9dHIY-dOHyWHpjaQSr9PT3FtmVU99nNyYZZl1647JQ/s400/lemursintrees.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Blue-eyed lemurs and sifaka play together, but have different diets.</td></tr>
</tbody></table>
When I asked Dr.
Williams if obesity was a growing problem among captive lemurs,
she said that it was, although not so much at the center. <o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 180.45pt 282.55pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 180.45pt 282.55pt;">
Because the center is in
the habit of loaning animals out to other zoos around the country, they've seen obesity become a problem in part because of the difficulty in training zookeepers on how to
appropriately feed the lemurs appropriately. <o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 180.45pt 282.55pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 180.45pt 282.55pt;">
The major challenge, she
said, is in simply educating keepers to understand that feeding strategies are
different for different species of lemur. All lemurs are similar
in that they are herbivorous hindgut fermenters having simple stomachs and
large cecums (as opposed to foregut fermenters, which are generally ruminant
species like cows); however, intestinal transit times between lemurs vary greatly.</div>
<div class="MsoNormal" style="tab-stops: 180.45pt 282.55pt;">
<o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 180.45pt 282.55pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 180.45pt 282.55pt;">
On one end of the
spectrum, you have the red-ruffed lemur. In this species, the intestinal
transit time is short, so fermentation in the cecum is bypassed. Their feeding
strategy is to eat easily digestible foods, and a lot of them. They primarily
eat a lot of fruits, but don't absorb a lot when they do. "The joke goes: it goes
in a banana, it comes out a banana," Dr. Williams said.</div>
<div class="MsoNormal" style="tab-stops: 180.45pt 282.55pt;">
<o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 180.45pt 282.55pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 180.45pt 282.55pt;">
On the other side of the spectrum, there
are bamboo lemurs and sifakas with long intestinal transit times.<span style="mso-spacerun: yes;"> </span>These lemurs eat primarily leaves and rely on their fermentation for production of short-chain fatty acids to supply the majority of
their energy (similar to <a href="http://evolvinghealthscience.blogspot.com/2011/09/what-chimpanzee-predatory-behavior-can.html">gorillas versus chimps</a>). In comparison, the ring-tailed, brown and blue-eyed lemurs tend to be more generalist in eating a variety of leaves, fruits, and some insects. Ring-tailed lemurs may even make a meal out of a small bird on occasion.<br />
<br />
Many of the problems result from insufficient knowledge or
misunderstanding on the part of zookeepers. If a red-ruffed lemur is put on a
diet of leaves, the animal won't absorb enough nutrients to survive for very long.
Conversely, if a sifaka is fed a diet high in fruit, the diet will favor growth
of microflora that uses starch more efficiently and doesn't ferment fibers well;
the resulting changes in pH alone will give the animal diarrhea until its probable death.</div>
<div class="MsoNormal" style="tab-stops: 239.7pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 239.7pt;">
To prevent sickness and death of animals that
are on loan, Dr. Williams said zookeepers are now required to come to the
center to be trained, "They'll learn that, yes, sifakas like banana, but, no,
we can't feed it to them. Yes, they will eat it, but it's not good for them."<o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 239.7pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 239.7pt;">
<b style="mso-bidi-font-weight: normal;">Controlling portions and low-glycemic foods<o:p></o:p></b></div>
<div class="MsoNormal" style="tab-stops: 239.7pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 239.7pt;">
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; margin-right: 1em; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgdyvjDM3lo_cYeRyyCivO4v9zRqX5Xzo8wCTENj36GoBKNYdytorE79olqiYjCgPnX2qyYSecid4r9e84e7w9V9EPdehdVf4V3yAeA-DGvdPQq9EQ_LAAomt9p7W3DZDv4KjGdYuYVR78/s1600/ringtaileds.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="239" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgdyvjDM3lo_cYeRyyCivO4v9zRqX5Xzo8wCTENj36GoBKNYdytorE79olqiYjCgPnX2qyYSecid4r9e84e7w9V9EPdehdVf4V3yAeA-DGvdPQq9EQ_LAAomt9p7W3DZDv4KjGdYuYVR78/s320/ringtaileds.jpg" width="320" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Ringtailed eat a mix of fruits, leaves, insects, and even birds.</td></tr>
</tbody></table>
Earlier this year, it was at one of these Prosimian Husbandry Workshops where Dr. Williams shared new information with zookeepers on what feeding
strategies in the center have been used to help prevent or control obesity and diabetes.
<o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 80.2pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 80.2pt;">
One important bit of knowledge Dr.
Williams passes on is that "when we say 'frugivore,' we're talking about a
wild diet that is very high in fiber, low in starches. But when folks think
'frugivore' in captivity, they think apples, bananas, and grapes—these are not
at all like fruits in the wild."<o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
<br />
Lemurs at the center are never overfed, Dr. Williams told me, but diabetes is still a significant issue. "The diabetics in our colony were never obese, but we're still causing problems that lead to insulin resistance," she said. In addition, kidney failure and cancer are other main causes of death.<br />
<br /></div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
Much in the same way
humans might like "marshmallows and chocolate eclairs," as Nesse and Williams write in their book, the problem with lemurs is that they have "mismatch of tastes evolved for stone age conditions."<br />
<br />
All lemurs enjoy the
types of fruits and starchy vegetables we've cultivated for our taste buds, Dr.
Williams said, which can easily lead to overfeeding with these kinds of foods and that can lead to
obesity and diabetes.<br />
<br />
<b>Lemur care, age, and inflammation</b><br />
<br />
Once an animal has
diabetes, it must be controlled with a low-glycemic diet—consisting of leaves
and primate biscuits that are higher in fiber, lower in starch and sugar—alongside anti-diabetic medications such as metformin.</div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
<o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 358.2pt;">
<span style="mso-tab-count: 1;"> </span><o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 80.2pt 180.45pt;">
I asked Dr. Williams how the lemurs responded
to being put on their low-glycemic biscuits versus their normal, more palatable, sugary, cookie-like treats.
She said they responded in the same way as a human would after hearing, "OK, you're
not eating anything but bran and leafy greens for now on." Not very well at all.</div>
<div class="MsoNormal" style="tab-stops: 80.2pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 80.2pt;">
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; margin-right: 1em; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEitKwrMSbjq3AI0YY2B5bJTJ4L277uHnUqmmpKJ4cdmKRGuDoPYpAXUhrS7KQyarocnph00H14nIue5Ay-qp-bKe-2gIEuODmllOW66p4moYqBVsi5ODbe9xM0tCbSb-Hsrjie6blwEfZM/s1600/lemur+inside.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="200" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEitKwrMSbjq3AI0YY2B5bJTJ4L277uHnUqmmpKJ4cdmKRGuDoPYpAXUhrS7KQyarocnph00H14nIue5Ay-qp-bKe-2gIEuODmllOW66p4moYqBVsi5ODbe9xM0tCbSb-Hsrjie6blwEfZM/s200/lemur+inside.jpg" width="149" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Why can't I play outside?</td></tr>
</tbody></table>
<br /></div>
<div class="MsoNormal" style="tab-stops: 80.2pt;">
There are several contributing
factors to chronic disease in lemurs, Dr. Williams said. One may be simply be age, since the animals at the
center, depending on the species, can usually live well into their 20s and
30s, which is not normal in the wild. <o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 80.2pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 80.2pt;">
These older animals also have
limited mobility, resulting from age-related wear and tear, and are not able to enjoy some of the free-range enclosures the lemur center
provides. A more sedentary lifestyle indoors can lead to less insulin sensitivity and, while the center does offer enrichment programs to encourage activity, Dr. Williams notes, the rewards used in these programs is usually sweet treats. <br />
<br />
<b>Seeking the ideal lemur diet</b><br />
<o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 275.25pt;">
<b style="mso-bidi-font-weight: normal;"><span style="mso-tab-count: 1;"> </span></b><o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 275.25pt;">
How these aging lemurs are fed and what they're fed in their diets are still not what Dr. Williams would consider ideal. "It could be better," she said; for instance, the lemurs usually receive all their food in one or two feedings daily while, in the wild, they generally graze throughout the day. More feedings over the course of the day may help stabilize blood sugar.</div>
<div class="MsoNormal" style="tab-stops: 275.25pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 275.25pt;">
In addition, Dr. Williams has noted mild, low-grade inflammation is a factor. As part of her clinical duties, she performs autopsies whenever a lemur dies. Histopathological exams of tissues upon death often reveal a mild chronic colitis or hepatitis. "We don’t know what the cause
is," Dr. Williams told me.</div>
<div class="MsoNormal" style="tab-stops: 275.25pt;">
<o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 275.25pt;">
<span style="mso-spacerun: yes;">
</span><o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 275.25pt;">
One possible contributing factor,
Dr. Williams told me, may be in the type of ingredients used in the flavored
primate biscuits or other foodstuffs the lemurs eat. The biscuits are primarily grain-based, she said, containing corn,
soy, or wheat to provide one source of starch, soluble fiber, and insoluble
fiber, along with protein sources.<br />
<br />
Ideally, she said, a lemur's diet
should consist of diverse types of fiber found in the same types of wild fruits and vegetables found on Madagascar.
These could include several types of pectins, gums, and other fermentable
fibers. Another area of concern may be omega-6 to omega-3 ratio of the lemurs' chow.</div>
<div class="MsoNormal" style="tab-stops: 275.25pt;">
<o:p></o:p></div>
<div class="MsoNormal" style="tab-stops: 275.25pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 275.25pt;">
<b style="mso-bidi-font-weight: normal;">Education outreach and lemur nutrition research <o:p></o:p></b></div>
<div class="MsoNormal" style="tab-stops: 275.25pt;">
<br /></div>
<div class="MsoNormal" style="tab-stops: 275.25pt;">
<div style="text-align: left;">
</div>
<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: right; margin-left: 1em; text-align: right;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgKoOQcLdZustx79vUb9VXc0X-wqP3OKOCaHKcpUgTxweN38vmwvRSJ5Ysc1zt8GS6rDW_1wCliwYvNKMN4fua6Dbt1N598-KsWPQPOr3ljpfGWFXzW_r9gSU8U5c85wNQFMAq1vVw7v0s/s1600/CathyWilliams.jpg" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="149" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgKoOQcLdZustx79vUb9VXc0X-wqP3OKOCaHKcpUgTxweN38vmwvRSJ5Ysc1zt8GS6rDW_1wCliwYvNKMN4fua6Dbt1N598-KsWPQPOr3ljpfGWFXzW_r9gSU8U5c85wNQFMAq1vVw7v0s/s200/CathyWilliams.jpg" width="200" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Dr. Williams </td></tr>
</tbody></table>
A major challenge is in the need of further nutritional research in primates as a whole and, more specifically, with lemurs. Then, afterward, educational outreach.<br />
<br />
After my interview with Dr. Williams, I contacted Michael Schlegel, Ph.D., director of nutritional services for the Zoological Society of San Diego to discuss her recommendations. Dr. Schlegel's role is to formulate meals for all the animals in at the San Diego Zoo and supervise how they are fed.<br />
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
Dr. Schlegel found Dr. Williams's findings highly interesting, saying, "We're always looking for new research and we do balance diets so that fruit is only a component. They do get vegetables, but we know more is what's good for them."</div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
<br /></div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
Zoo keepers and zoo nutritionists like Dr. Schlegel rely on guidelines given by the National Research Council's <i><a href="http://www.nap.edu/openbook.php?record_id=9826&page=182">Nutrient Requirements of Nonhuman Primates</a>, </i>much as Americans rely on Institute of Medicine for dietary guidelines.</div>
<div>
<br />
"We look at publications, and adjust to individual needs. We try to base diets on animal energy and metabolic requirements," he said.</div>
<br />
Schlegel agreed that current dietary requirements for all primates are based on limited studies. Further research is needed in areas such as analysis of dietary composition of wild diets as well as controlled trials with lemurs as a species.</div>
<div class="MsoNormal" style="tab-stops: 275.25pt;">
<br />
As it stands, the science of nutrition and diet is still young for humans and lemurs alike, but so far the similarities on how the modern world affects human health and how captivity affects our far distant cousins are striking. </div>
<!--EndFragment--></div>
daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com2tag:blogger.com,1999:blog-5995754777906978314.post-46474079484311177372012-10-05T16:41:00.003-07:002012-10-05T21:08:36.005-07:00Of bunnies and bacteria<div class="separator" style="clear: both; text-align: center;">
<a href="http://www.flickr.com/photos/rmislevy/7789081464/" title="Rabbit by ramislevy, on Flickr"><img alt="Rabbit" height="333" src="http://farm9.staticflickr.com/8430/7789081464_a2867ed38d.jpg" width="500" /></a></div>
<br />
I remember when I first learned that a rabbit ate its food <a href="http://blog.coturnix.org/2010/08/19/food-goes-through-a-rabbit-twice-think-what-that-means/">twice</a>.<br />
<br />
This curious dietary practice, called coprophagy, is something I'd witnessed as a child raising my own rabbits and guinea pigs in the backyard. Disgusted by the sight of my pets eating their own feces, I recall trying to keep their cages as clean as possible. Had I known better, I would not have been so quick to remove droppings from their cage because I might've put these animals at risk for nutritional deficiency (1-2). Luckily, I wasn't ever very consistent at keeping their cages clean all the time.<br />
<br />
Rabbits and guinea pigs, as it turns out, need to eat their own droppings because they provide a valuable source of nutrients like vitamin B12. In the wild, they will normally leave soft droppings at the mouths of their burrows while they go off foraging at dawn or dusk. When they've had their fill of foliage, they return and -- far from being repulsed by having a stack of droppings at the foot of their doorstep -- they eat up these droppings, which are by this time a nutrient-rich fermented dessert. <br />
<a name='more'></a><br />
Being non-ruminant herbivores, rabbits and guinea pigs are adapted to half-digest their food to re-consume it later. Cows, on the other hand, have millions of microorganisms residing within their own multi-compartmental stomachs working to break down their food and producing nutrients. Other mammals, including sheep, apes, and humans have large intestines where microbes live and flourish. Predators don't have a need for such large guts, since they can obtain their nutritional requirements from prey.<br />
<br />
Interestingly, humans share a behavior with rabbits and guinea pigs: not that we eat our own feces, but that we allow food to ferment for full nourishment later. Although humans are unique in the sense that we've developed quite a taste for fermented foods. The sheer variety we eat is mesmerizing: yogurt, cheese, wine, beer, vinegar, pickles, kefir, olives, breads, miso and kimchi. All human cultures are dependent on fermented products of some kind as a food source leading to a large variety of human microbiotas across the world (3, 4). Fermented foods are deeply interwoven into the human tale of survival. They are a valuable source of nutrients as well as a valuable method of preservation of foods. There is also much written about how our "<a href="http://www.nytimes.com/2012/06/19/science/studies-of-human-microbiome-yield-new-insights.html?pagewanted=all">inner ecosystems</a>" are important for digestion and our health.<br />
<br />
With the development of the <a href="http://www.hmpdacc.org/">Human Microbiome Project</a> and other research projects by scientists related to microbes, I look forward to better understanding how fermented foods may have also helped shape human evolution. As researchers have <a href="http://www.scientificamerican.com/article.cfm?id=backseat-drivers">argued</a>, microbes may be just as important as genes in driving evolution, the human microbiome as important as the human genome. In addition, if we were to take a cue from those <a href="http://www.scientificamerican.com/article.cfm?id=evolving-bigger-brains-th">scientists</a> who believe that the use of fire and cooking helps explain how we were able to grow bigger brains while shrinking our guts, it's logical to believe that fermented foods may have had their place as well in the shaping of modern humans.<br />
<br />
One thing that's plainly clear is that dietary change (or change in nutrient availability) plays a heavy role in natural selection apart from climate and geographical change. Evolutionary biology is rich in examples of animals relying on bacteria to supply important nutrients in their diets. These are classic cases of higher organisms "delegating" responsibility of digestion or nutrient production to lower organisms. What I find intriguing is learning how much the interaction with bacteria may have guided natural selection in shaping morphological and physiological traits as well as behaviors of different animals including ourselves.<br />
<div>
<br /></div>
References<br />
<ol>
<li>Bellier R, Gidenne T, Vernay M, & Colin M. In vivo study of circadian variations of the cecal fermentation pattern in postweaned and adult rabbits. <a href="http://www.journalofanimalscience.org/content/73/1/128"><i>J Anim Sci</i></a> 73(1):128-35.</li>
<li>Hooper DC, Alpers DH, Burger RL, Mehlman CS, Allen RH. <i>J Clin Invest</i> 1973 December; 52(12): 3074–3083. doi: <a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC302582/">10.1172/JCI107506</a></li>
<li>Scott R, Sullivan WC. <a href="http://www.humanecologyreview.org/pastissues/her151/scottandsullivan.pdf">Ecology of Fermented Foods</a>. <i>Research in Human Ecology </i>2008;15(1):25-31.<i> </i></li>
<li>Yatsunenko T, Rey FE, Manary MJ, Trehan I, Human gut microbiome viewed across age and geography <i>Nature</i> 486, 222–227 (14 June 2012) doi:<a href="http://www.nature.com/nature/journal/v486/n7402/full/nature11053.html">10.1038/nature11053</a></li>
</ol>
daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com1tag:blogger.com,1999:blog-5995754777906978314.post-67300117443545058532012-09-25T14:44:00.000-07:002012-09-26T17:39:43.896-07:00Why aren't we talking about organic GMOs? And, why can't we all get along?<div style="text-align: right;">
</div>
You've heard the rants about Mitt Monsanto versus Organic Obama. You've read the arguments on both sides for "Yes" or "No" on labeling GMOs in California. You've read the research surrounding the wholesomeness of "organic" versus "conventional." There's the <a href="http://www.nytimes.com/roomfordebate/2012/09/10/is-organic-food-worth-the-expense">divisive talk</a>, the <a href="http://blogs.berkeley.edu/2012/06/06/why-labeling-of-gmos-is-actually-bad-for-people-and-the-environment/">reasoned talk</a>, and the <a href="http://articles.mercola.com/sites/articles/archive/2012/09/22/superbugs-destruct-food-supply.aspx">rat-shi# crazy</a> talk.<br />
<br />
What I want to ask is this: Why aren't there more people, beyond scientists and academics, talking about<i> organically grown GMOs?</i> These last few weeks have had me thinking a lot about how the terms used to describe our food -- "organic," "conventional," and genetically modified" -- which only serve to confuse and distract from greater issues at hand.<br />
<br />
The greater issues (in a nutshell): Agricultural and food scientists are given a heavy task of feeding nine billion people by 2050. Most will agree that it will come with substantial costs. Soil quality will suffer, excess pesticide and herbicide use will destroy biodiversity, nutrient runoff will keep fueling the algal booms, or "dead zones," that suffocate life in our lakes and oceans. The world's <a href="http://evolvinghealthscience.blogspot.com/2011/07/phosphorus-and-foods-future.html">phosphorus</a> reserves will be depleted. If you add in climate change to the mix, you can count on destroyed crops and suffering farmers, especially in the developing world. Food production will be more expensive. Food will be more expensive. Small farmers and the poorest among us will suffer.<br />
<a name='more'></a><br />
<b>Organic is not the answer, but</b> <b>offers lessons</b><br />
<br />
"Organic" farming defined as it is now is not the answer. <i>Scientific American</i> blogger Christie Wilcox (<a href="http://twitter.com/NerdyChristie">@nerdychristie</a>) deserves high praise for <a href="http://www.nytimes.com/roomfordebate/2012/09/10/is-organic-food-worth-the-expense/the-ecological-case-against-organic-farming">shattering</a> myths about organic foods and for <a href="http://www.nytimes.com/roomfordebate/2012/09/10/is-organic-food-worth-the-expense/the-ecological-case-against-organic-farming">challenging</a> their use as being better for the environment. She also rightly <a href="http://blogs.scientificamerican.com/science-sushi/2012/09/24/pesticides-food-fears/">challenges</a> the notion that organic pesticides are healthier or that fewer pesticides overall in food are healthier for you. (I'll add that some pesticides are <i>good for you</i> including my favorite: caffeine!).<br />
<br />
Huge limitations are that organic agriculture requires more land and more labor. Organic agriculture also excludes synthetic pesticides (natural ones are not as effective and not safer) and herbicides aren't permitted (despite that ones like glyphosate degrade rapidly in soil). Organic farming is, thus, more expensive and more devastating to the environment because of increased carbon emissions. And, although reports vary widely, yields of organic agriculture are also estimated to be only half in comparison to conventional agriculture.<br />
<br />
Yet the ideals of organic agriculture are still good -- less use of pesticides, herbicides, and fertilizers while protecting soil. There are also lessons to be learned from organic agriculture. For example, crop rotation can help prevent nutrient depletion in soil. And, the use of animal manure and decaying plants instead of commercial fertilizer helps improve water-holding capacity of soil. Better water-holding capacity diminishes runoff.<br />
<br />
<b>Bringing in biotech</b><br />
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
</div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
</div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
Now, allow me to get back to my argument and questions -- What if we added biotechnology to the picture? Why not organically grown GMOs, legislation to support expanding "Certified Organic" to include GMOs, and investment and research into more sustainable GMOs? </div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
<br /></div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
Finally, what if more of the public learned to appreciate the very scientists who are trying to make these developments possible? Too few people are familiar with (and too few companies have invested in) important research using recombinant DNA going on right now that could surely help reduce the impact of agriculture on the environment. For example, </div>
<ul>
<li>There are the scientists researching varieties of <a href="http://evolvinghealthscience.blogspot.com/2012/05/what-environmental-groups-dont.html">wheat</a> genetically engineered to emit a non-toxic pheromone, which could lead to less use of pesticide. </li>
<li>There are the scientists who've engineered <a href="http://evolvinghealthscience.blogspot.com/2012/09/making-lazy-stupid-plants-work-harder.html">rice</a> to have larger root systems that take up more nitrogen and phosphorus from the soil, which reduces nutrient runoff. </li>
<li>There are the scientists whose <a href="http://www.scientificamerican.com/article.cfm?id=farming-the-future-gm-crops">research</a> involves improving abilities of crops to capture more light (improving yields), withstand extreme weather changes, high salt concentrations, or have greater resistance to diseases. </li>
<li>There are also the scientists whose <a href="http://www.scientificamerican.com/article.cfm?id=algae-biofuel-of-future">research</a> is in genetically engineered algae that can help displace use of corn ethanol and petroleum while sucking carbon dioxide out of the atmosphere.</li>
<li>And, there are the scientists who actively promote this kind of research and thinking such as plant geneticists <a href="http://scienceblogs.com/tomorrowstable/">Pamela Ronald</a>, of UC Davis, and <a href="http://evolvinghealthscience.blogspot.com/2012/02/can-we-prevent-food-crisis-while.html">Nina Fedoroff</a>, of Penn State. </li>
</ul>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
<b></b></div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
Currently, public perception and debate hinders the discussion of organic GMOs. Most lay people that I talk to appear to be only familiar with stories of either poor behavior from GMO-corporations like Monsanto, or their Roundup Ready crops as a source of overuse of fertilizer and pesticide, the destruction of biodiversity through expanded use of monoculture crops, and the spread of pesticide-resistant weeds. (Unfortunately, they are also familiar with the bat-shit crazy <a href="http://academicsreview.org/2010/02/jeffrey-smith-false-claims-unsupported-by-science/">Jeffrey Smith</a>, <a href="http://www.thatsjustme.com/2012/08/what-quack-dr-mercola-donates-800000-to-benefit-prop-37-gmo-labeling/">Mercola</a>, and <a href="http://www.sciencebasedmedicine.org/index.php/mike-adams-on-dr-mehmet-ozs-colon-polyps-spontaneous-disease/">Mike Adams</a>). </div>
<div>
<b><br /></b></div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
<b>What about conventional ag and food technology?</b></div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
<br /></div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
Let's not leave out "conventional" agriculture. There are also solutions to gain from developments in conventional agriculture, too. Too few people know about the new developments because ideologies tend to trump the science and technology. Yet a couple of years ago, food scientists from a variety of disciplines produced a <a href="http://www.ift.org/knowledge-center/read-ift-publications/science-reports/ift-scientific-review-feeding-the-world-today-and-tomorrow.aspx">scientific review</a> on behalf of the Institute of Food Technologists that offered these solutions: </div>
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
</div>
<ul>
<li>"No-till" agriculture - retains organic matter and stops soil erosion</li>
<li>Integrated pest management - using pesticide only where it's needed, decreasing amount</li>
<li>Precision agriculture - targeting fertilizer to seed, pesticide to plant</li>
<li>Drip irrigation - controlling water</li>
<li>New technologies for recovering nitrogen and phosphorus from wastewater (like Bill Gates toilets) </li>
</ul>
I'll also add in food technology. Despite the massive criticism received by food technologists ("Big Food") for fueling the obesity epidemic, it will be their task for providing additional food processing solutions to feed the world's nine billion.<br />
<br />
For example, there are many improved technologies for preserving food and extending shelf life of these foods. The technologies we have now (besides cooking) are mechanical operations (extraction and separation of oils), thermal treatments (blanching, pasteurization, and canning), refrigeration, dehydration, fermentation, acidification, etc. New <a href="http://live.ift.org/2012/06/27/comparing-alternative-processing-methods-in-tomatoes/">technologies</a> like faster thermal methods (microwave and ohmic heating) and high-pressure processing could help feed people in the future. <br />
<br />
<a href="http://evolvinghealthscience.blogspot.com/2012/02/one-tomato-at-time-feeding-world-with.html">Controlled-environment agriculture</a> looks promising, too; that is, the designing of high-tech greenhouses that can be produced almost anywhere, including Antarctica, and can produce up to 10 times more produce than conventional farms with only a tenth or less of the resources. Cost is the prohibitive factor there. <br />
<b><br /></b>
<b>A Unified Approach</b><br />
<br />
So, why the dividing lines? Excluding GMOs from the label of "Certified Organic" is based in ideology and not in science. Too many people have it in their minds that GMOs are "anti-organic." It doesn't have to be that way. Food labeling of GMOs does little to solve this problem, but only discourages investment into biotechnology and its commercialization. The "Certified Organic" labeling also distracts from focusing on the progress that biotechnology and other technologies offer for more sustainable, environmentally friendly practices.<br />
<br />
Catastrophe has been avoided before. In the 1960s and '70s, population growth outpaced food production. Bringing science to agriculture turned the tables and improved plant breeding techniques, which increased yields of common crops like wheat. Thanks to scientists like <a href="http://www.scienceheroes.com/index.php?option=com_content&view=article&id=68&Itemid=116">Norman Borlaug</a> (and <a href="http://www.scienceheroes.com/index.php?option=com_content&view=article&id=441:haber-fertilizer&catid=195&Itemid=528">Fritz Haber</a>, for that matter), the Green Revolution saved millions, mainly in China and India.<br />
<br />
<div>
It can happen again. The goals shared should be improving crop yields in harsh environments, reducing nutrient runoff, reducing use of pesticides and herbicides, and reducing food waste and pollution through a combination of the best that organic, GMOs, and conventional techniques have to offer. There simply needs to be a more unified approach to improving food production and reducing its impact on the environment.<br />
<br />
Update 09-26-12: And, about that flawed rat study everyone's talking about, I believe plant scientist Peter Bickerton beautifully summarizes my own thoughts, over on the "Topical Poetry" blog, with this <a href="http://jugglingdoctor.blogspot.co.uk/2012/09/a-rebuke-to-false-french-gm-study-on.html">masterpiece</a>. Enjoy!</div>
daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com10tag:blogger.com,1999:blog-5995754777906978314.post-26362907852518422752012-09-07T21:43:00.001-07:002012-10-08T13:00:19.649-07:00Making lazy, stupid plants work harder<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="http://sols.asu.edu/people/images/lg_gaxiola_plant_roots.jpg" imageanchor="1" style="clear: right; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="215" src="http://sols.asu.edu/people/images/lg_gaxiola_plant_roots.jpg" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;"><i>Plants with larger root systems take up minerals more easily.</i></td></tr>
</tbody></table>
Plants these days. They're coddled, entitled, fed with a silver spoon.<br />
<br />
Use of man-made fertilizer and traditional breeding, over the years, has selected for traits that led to today's modern-variety plants that grow fat with yields.<br />
<br />
But the downside of easy access to nutrients is that it has allowed for the breeding out of desirable traits that has left plants, well, acting like enabled, spoiled children.<br />
<br />
"They're lazy," said plant biochemist Roberto Gaxiola, an assistant professor of cellular and molecular biosciences at Arizona State University. Because nutrients are plentiful, they don't bother with growing large root systems. Yet, he explained to me, larger root systems are needed for them to take up more phosphate and nitrogen from the soil.<br />
<br />
More now than ever, plants depend on these fertilizers for growth. Wild crop plant varieties, on the other hand, have had to evolve in an environment of everyday nutrient scarcity. It's these wild crop plant root systems that have been the focus of Gaxiola's research for more than a decade.<br />
<a name='more'></a><br />
<b>Root engineering </b><br />
<br />
Gaxiola told me that these wild varieties have learned to use more efficient pathways of transporting sugars from leaves to roots. They produce larger root systems that do a better job at acidifying soil and taking up minerals like nitrogen, phosphate, potassium.<br />
<br />
He's identified genes involved in overexpression of a type of kinase, an H+-PPase, that phosphorylates a process of loading sugar. The localization of this kinase is in cells that surround the vascular tissue, which is used to synthesize and transport sugar.<br />
<br />
"It’s the only way that roots can grow and be active," Gaxiola told me. "You cannot grow a root if you don't move sugar from the leaves. What does this kinase regulate? It could be one of the genes, but clearly it's multifactorial. It's upregulating sugar transport for a larger root system."<br />
<br />
Last May, Gaxiola and his colleagues published their latest of a series of papers detailing how his lab inserted genes from wild rice, tomatoes and arabidopsis into modern-yield, salt-tolerant varieties (1). These genes, as part of commercial varieties through root engineering, could lead to more efficient use of phosphorus and increase crop biomass and seed yields.<br />
<br />
Another paper, recently published in <a href="http://www.nature.com/nature/journal/v488/n7412/full/nature11346.html"><i>Nature</i></a> by scientists from the International Rice Research Institute, uses a similar approach (2). These scientists isolated and inserted a gene from a wild variety of rice into commercial strains to produce larger roots that better take up phosphorus, nitrogen, and potassium.<br />
<br />
Gaxiola said, "It's interesting work. We have similar results, but with a different gene." Again, a kinase is involved that regulates synthesis of sugar for transport to the roots to become more active, grow, and take up minerals.<br />
<br />
<b>Phosphorus and the future</b><br />
<br />
"It's a good example of how crop domestication made crop plants 'stupid' and dependent on heavy external fertilizer inputs. Their plants seem very promising indeed," said biologist James Elser, a subject of a previous <a href="http://evolvinghealthscience.blogspot.com/2011/07/phosphorus-and-foods-future.html">post</a>.<br />
<br />
Elser, also an ASU professor, is raising more awareness about the need for sustainable phosphorus. His wish, he'd said to me before, is to hear "President Obama say the word 'phosphorus',"as the problem deserves serious attention. <br />
<br />
According to Elser, plants that can more efficiently use phosphorus could end up being highly beneficial to poor people, such as in underdeveloped Asian countries. As phosphorus availability becomes depleted and costs for fertilizer rises, farmers in these countries can't afford fertilization of their rice plants. They're also hit with the fact that the roots won't take nutrients. Often the soils have the phosphates, but they're bound to the soil. The roots need to acidify the soil to release the phosphate that's bound.<br />
<br />
Plants that efficiently use phosphorus could also reduce eutrophication. The problem is caused when fertilizer run-off enters streams, rivers, lakes, and oceans. These extra nutrients cause algae to bloom and create "dead zones," Elser said, one of the most famous examples of which is the <a href="http://serc.carleton.edu/microbelife/topics/deadzone/index.html">Gulf of Mexico Dead Zone</a>.<br />
<b><br /></b>
<b>Hurdles of funding and anti-GM sentiment</b><br />
<br />
With so much to gain from plants that can grow in phosphorus-poor soil or with less fertilizers, I had to ask Gaxiola, <i>How close are we to seeing salt-tolerant, large-rooted plants being used commercially?</i> Gaxiola's plants, for example, as he described, are "one of the strongest phenotypes" ever produced for the market.<br />
<br />
"Oh, my friend," Gaxiola replied gently to my question, in a way I've found to be typical of his native Mexico City, "there are field trials, heavy investment, and then you have to pray that a company like Monsanto gets interested."<br />
<br />
Why Monsanto? Because there are few other large biotechnology companies who could jump through the hoops required to commercialize a genetically engineered crops. It's unfortunate, Gaxiola told me, because to reduce the impact of fertilizer overuse on the environment and biodiversity, what we really need is more investment into plant engineering and more commercialization of nutrient-efficient plants.<br />
<br />
One is led to wonder: <i>With all it's focus on growing crops organically, is anti-GM sentiment actually hindering development of plants that could help the environment? Also, who is anti-GM sentiment helping if not only Monsanto? If only Monsanto can invest in GM? Wouldn't less regulations on GM help other biotechnology companies get in the game?</i> These are questions worth more exploration.<br />
<br />
<b>References</b><br />
<br />
<ol>
<li>Gaxiola RA, Sanchez CA, Paez-Valencia J, Ayre BG, Elser JJ. Genetic Manipulation of a "Vacuolar" H+-PPase: From Salt Tolerance to Yield Enhancement under Phosphorus-Deficient Soils. <i>Plant Physiol</i> 159, 2012;3-11. doi: <a href="http://www.plantphysiol.org/content/159/1/3">10. 1104/ pp. 112. 195701</a></li>
<li>Gamuyao R, Chin JH, Pariasca-Tanaka J, Pesaresi P, Catausan S, Dalid C, Slamet-Loedin I, Tecson-Mendoza EM, Wissuwa M, Heuer S. The protein kinase Pstol1 from traditional rice confers tolerance of phosphorus deficiency. <i>Nature</i> 488, 535–539 (23 August 2012) doi: <a href="http://www.nature.com/nature/journal/v488/n7412/full/nature11346.html">10.1038/nature113466</a></li>
</ol>
<br />
<i>Photo credit:</i> ASU
daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com0tag:blogger.com,1999:blog-5995754777906978314.post-22908102040771520512012-08-23T20:39:00.002-07:002012-08-28T19:46:19.170-07:00When I won't accept a guest post<div class="separator" style="clear: both; text-align: center;">
<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiXo-4dxYnkVB2HJ68PwYkZSW1BmRL7EA0esElOdZ1rdJjRowchyphenhyphenyNi0ctSO4vDkcMUDGjC2a-N774JYKIapaXnPjHaadHnCeAk-XLJfXigARBmdtGCV10jdxVF2jTE1oGwe2LeYqHoyTw/s1600/Screen+shot+2012-08-22+at+9.18.34+PM.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="162" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEiXo-4dxYnkVB2HJ68PwYkZSW1BmRL7EA0esElOdZ1rdJjRowchyphenhyphenyNi0ctSO4vDkcMUDGjC2a-N774JYKIapaXnPjHaadHnCeAk-XLJfXigARBmdtGCV10jdxVF2jTE1oGwe2LeYqHoyTw/s400/Screen+shot+2012-08-22+at+9.18.34+PM.png" width="400" /></a></div>
<br />
I get regular requests from people who want to guest post on my blog. Then, I got this unbelievable one yesterday. More unbelievable was that I saw it almost directly after giving a lecture on evidence-based nutrition. Thought I'd share.daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com3tag:blogger.com,1999:blog-5995754777906978314.post-61214114116385518062012-07-07T18:26:00.002-07:002012-07-07T22:28:52.284-07:00Sievenpiper: Fructose should not "worry" in diabetesAs the fructose debate rages on, one serious concern has been what the message should be for people who have diabetes. There's no question that the alarming media headlines, articles, and YouTube videos have confused many with prediabetes and both type 1 and type 2 diabetes.<br />
<br />
Even health professionals and organizations like the American Diabetes Association have taken a cautious <a href="http://care.diabetesjournals.org/content/29/9/2140.full">approach</a> by recommending avoidance of fructose as a sweetening agent. That is, for fear it may raise plasma lipids. They stop short of recommending people avoid fructose from fruit.<br />
<br />
There is also the extreme arguments of Internet marketers like Joe Mercola blasting out articles about the supposed danger of fructose including that of which comes from fruit. (I've had more questions than I can count about Mercola's unreasonably scary headlines and viral copy. He makes baseless recommendations that those with diabetes should cut fructose from all sources to amounts of less than 15g per day.)<br />
<a name='more'></a><br />
In my prior <a href="http://evolvinghealthscience.blogspot.com/2012/05/fate-of-fructose-interview-with-dr-john.html">interview</a> with John Sievenpiper, M.D., of St. Michael's Hospital, University of Toronto, we talked of the controversies surrounding fructose, as well as rhetoric used by scientists like Dr. Robert Lustig and others, which he said could lead people to reduce intake of fruits. "That's the danger," Dr. Sievenpiper said, "that people will say that fruit is a source of fructose and won't consume fruit because it may induce obesity, metabolic syndrome, and so on. It's not just the lay public that may take this message to heart, but health professionals."<br />
<br />
As the lead author of three systematic reviews and meta-analyses evaluating fructose's effects in randomized controlled feeding trials, Dr. Sievenpiper offered some perspective to the metabolic fate of this simple sugar in humans (versus animals). In short, these analyses found fructose had no significant effect on body weight or blood pressure in humans (as it does in rats, for example). In fact, fructose in amounts similar to that found in fruit improved glycemic control in humans.<br />
<br />
Now, Dr. Sievenpiper and his colleagues -- including Dr. David Jenkins (who first introduced the concept of a low-glycemic index) -- has released yet another meta-analysis and systematic review to evaluate the effect on fructose on long-term glycemic control in diabetes.<br />
<br />
The new study, published in <i>Diabetes Care,</i> included 18 controlled feeding trials that included 209 individuals with type 1 and type 2 diabetes. The study's results: The isocaloric exchange of fructose improves long-term glycemic control as determined by significantly reduced glycated proteins, namely hemoglobin (HbA1c) and glycated albumin.<br />
<br />
Moreover, the isocaloric exchange of fructose reduced HbA1c by an average of 0.53 percent, which is the equivalent to taking a hypoglycemic or anti-hyperglycemic agent like glucophage (Metformin). The fructose also didn't significantly affect fasting glucose or insulin. <br />
<br />
When I asked Dr. Sievenpiper what people with diabetes should take away from the results of the study, what they should make of fructose's contribution to total carbohydrates, and its use as a substitute for other carbohydrates in the diet, he wrote:<br />
<blockquote class="tr_bq">
In the context of a healthy, nutritionally balanced, weight-maintaining diet, people with type 2 diabetes do not need to worry about avoiding sources of fructose. </blockquote>
<blockquote class="tr_bq">
Provided weight management goals are being met, no one dietary pattern has shown itself to be best for the nutritional management of diabetes. A number of dietary patterns have shown benefit in people with diabetes. These include a low-glycemic index, Mediterranean, or vegetarian dietary patterns, as well as those which emphasize specific foods such as dietary pulses or nuts or allow for a range of macronutrient distributions. The range of possibilities allows for the individualization of diets based on treatment goals and the values and preferences of the individual. </blockquote>
<blockquote class="tr_bq">
Within this context, using small to moderate amounts of fructose in place of other sugars and starch may offer added benefit. This would be expected to be especially true where the sources are low-glycemic index fruits and cereal grain products, both of which have shown metabolic benefit. </blockquote>
<blockquote class="tr_bq">
That being said, we need larger, longer, and higher quality trials to clarify the benefit of fructose in people with diabetes. We are currently planning such trials. </blockquote>
Fructose, far from being "toxic," may be a uniquely beneficial carbohydrate in diabetes when given in amounts equivalent to what's found in fruits, according to the evidence. Once again, the study drives home the point further that <i>dose matters</i>, as it does with most nutrients and bioactive compounds, and that fructose can be healthy when eating as part of a well-balanced diet.<br />
<br />
With the virtues of a low-glycemic diet extolled recently in the media for healthy weight loss (mainly after Dr. David Ludwig and colleagues published an impressive three-way crossover study in the <i><a href="http://jama.jamanetwork.com/article.aspx?articleid=1199154">Journal of American Medical Association</a> </i>evaluating low-fat, low-glycemic index, and very low-carb diets)<i> </i>it's odd that more attention hasn't been given to the value of fructose as a source of low-glycemic carbohydrate.<br />
<br />
The most likely reason, perhaps, as addressed in my previous posts, is the continuing fears people have about high-fructose corn syrup. Despite the fact that it's chemical makeup being almost identical to plain sucrose, the ingredient is still often singled out as somehow uniquely problematic. Greater intake of all foods, especially all carbohydrate sources, is what is most likely what has led us down the road of the obesity epidemic.<br />
<br />
Bottom line? Fruit is still healthy. Fructose is most likely good for folks in amounts equivalent to what's found in fruit. Moderation in the diet needs to be the key message as it comes to any nutrient. Plus, more focus could be put on the intake of low-glycemic carbohydrates along with balanced amounts of proteins and good fats as part of a reduced-calorie diet for weight management.<br />
<br />
<b>Reference</b><br />
<br />
<div class="MsoNormal">
<br /></div>
<div class="MsoNormal">
Cozma AI et al. Effect of Fructose on Glycemic Control in
Diabetes: A Systematic Review and Meta-analysis of Controlled Feeding Trials. <i style="mso-bidi-font-style: normal;">Diabetes Care</i> 2012;35:1-10.doi: <a href="http://care.diabetesjournals.org/content/35/7/1611">10.2337/dc12-0073</a></div>daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com8tag:blogger.com,1999:blog-5995754777906978314.post-28213075001498297672012-06-13T16:42:00.000-07:002012-09-08T13:20:22.328-07:00Changes in genetic expression during weight loss and weight maintenance<i>by Amanda Jensen* </i><br />
<br />
<span style="float: right; padding: 5px;"><a href="http://www.researchblogging.org/"><img alt="ResearchBlogging.org" src="http://www.researchblogging.org/public/citation_icons/rb2_large_gray.png" style="border: 0;" /></a></span>
Losing weight is an ambition with no end. To get fit, live longer, reduce injury, look better, feel better and sleep better will pave the road toward your skinny. Yes, losing weight is known to help the heart and boost insulin sensitivity, but the question still asked is: how?<br />
<br />
There are differences between losing weight and keeping it off. From the Department of Clinical Sciences Malmo in Sweden, researchers found seven key genes expressed in adipose tissue (fat tissue) that change with weight loss and weight maintenance—a finding that brings science one step closer to understanding how the body responds to and regulates fat loss.<br />
<a name='more'></a><br />
This randomized controlled trial shows that the genes expressed by adipose tissue change when an obese person trims down, and stays down. "For most people," the authors report, "maintaining a reduced weight is a difficult but important task to fully obtain the beneficial effects of weight loss."<br />
Researchers placed 12 obese adults on a low-calorie diet for three months. After subjects lost 10 percent of their body weight, they embarked on a weight-maintenance program for an additional six months. The researchers took biopsies of adipose and blood samples at baseline, immediately following weight loss, and after the period of weight maintenance.<br />
<br />
The participants had an average reduction of almost 19 percent of body weight, the researchers report. If trimming down wasn’t news enough, immediately following the weight-loss phase, insulin sensitivity and blood triglycerides improved. Improvements to HDL (the "good" cholesterol) were realized after weight loss had been sustained.<br />
<br />
<b>Gene Interactions</b><br />
<b><br /></b>
In total, the researchers reported 2,163 genes were affected during weight loss and 1,877 different genes were modified during weight maintenance. Two genes that were among the most strongly expressed, CETP and ABCG1, are likely responsible for the improvements to HDL observed after sustained weight loss. A high HDL gives the body has a greater capacity to clear cholesterol from the tissues and send it back to the liver to be recycled or excreted. Both genes code for enzymes that promote cholesterol transfer to HDL—lowering cholesterol is a way that weight loss may be effective for bolstering heart health.<br />
<br />
Most dieters have found that the body really resists weight change. Researchers found that expression of the weight-guarding gene CIDEA was higher when the subjects were working to maintain their weight loss. In mice, blocking expression of CIDEA prevents weight gain during over-feeding. The increased expression of CIDEA in individuals trying to maintain weight loss supports the notion that the body defies shedding pounds by dropping metabolic rate.<br />
<br />
A person carrying too much weight is also carrying too much stress for their body. Many of the problems linked with obesity occurs because the body to trying to cope. The researchers focused on two genes; MMP9 and TNMD, which were down-regulated as a result of weight loss and weight maintenance. MMP9 and TNMD are genes that may be responsible for adaptations in conditions like obesity and metabolic syndrome.<br />
<br />
MMP9 codes for a matrix metallopeptidase. The structure of a cell is often referred to as a matrix, think of the scaffolding in building that can be moved, modified, or degraded. These metallopeptidases are the contractors for cells. Fewer MMPs means that fewer cells are broken down and fewer are built up. The result is perhaps more, but smaller fat cells.<br />
<br />
TNMD codes for a protein tenomodulin: the contractor (or modulator) of the blood vessels. TNMD is higher in obese individuals and has been linked to fat mass as well as poor blood sugar control. The authors write that "taken together, low amounts of tenomodulin and matrix metallopeptidase 9 or related proteins may be important for the beneficial effects of weight loss."<br />
<br />
<b>Keeping the Weight Off</b><br />
<br />
Adipose tissue, once thought to be a dormant receptacle of energy stores and an extra layer of insulation, is a metabolically active organ. Yes, fat cells do function and perform work. According to these researchers, they contain genes that affect immune response, hormonal balance, and even metabolism—all involved in creating a "set point" for weight.<br />
<br />
Weight loss is no easy feat, especially when the body finds security in fat. Losing weight can feel like an uphill battle, the yo-yo dieting, and perpetual cycles of weight loss and weight gain do not do anyone any favors. With weight loss the body begins to fight for its fat stores; hormones change, satiety is impaired, and metabolic rate shifts. This resilience, according to researchers, is largely a product of the genes being expressed.<br />
<br />
"Future research on the beneficial effect of weight loss should focus on long-term effects assessed after a period of weight stability" recommend the researchers. These results provide exciting insights into the physiology of fat and its genetic adaptations. Anyone can lose weight but, according to the authors, sustaining it is the true battle with true benefit.<br />
<br />
<b>Reference</b><br />
<br />
<span class="Z3988" title="ctx_ver=Z39.88-2004&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.jtitle=American+Journal+of+Clinical+Nutrition&rft_id=info%3Adoi%2F10.3945%2Fajcn.111.020578&rfr_id=info%3Asid%2Fresearchblogging.org&rft.atitle=Differential+gene+expression+in+adipose+tissue+from+obese+human+subjects+during+weight+loss+and+weight+maintenance&rft.issn=0002-9165&rft.date=2012&rft.volume=&rft.issue=&rft.spage=&rft.epage=&rft.artnum=http%3A%2F%2Fwww.ajcn.org%2Fcgi%2Fdoi%2F10.3945%2Fajcn.111.020578&rft.au=Johansson%2C+L.&rft.au=Danielsson%2C+A.&rft.au=Parikh%2C+H.&rft.au=Klintenberg%2C+M.&rft.au=Norstrom%2C+F.&rft.au=Groop%2C+L.&rft.au=Ridderstrale%2C+M.&rfe_dat=bpr3.included=1;bpr3.tags=Health">Johansson, L., Danielsson, A., Parikh, H., Klintenberg, M., Norstrom, F., Groop, L., & Ridderstrale, M. (2012). Differential gene expression in adipose tissue from obese human subjects during weight loss and weight maintenance <span style="font-style: italic;">American Journal of Clinical Nutrition</span> DOI: <a href="http://dx.doi.org/10.3945/ajcn.111.020578" rev="review">10.3945/ajcn.111.020578</a></span>
<br />
<br />
<i>*Introducing the wicked-smart Amanda Jensen, in her first guest appearance on the Evolving Health blog. She enjoys science, writing, Indian food, traveling to all sorts of places, and playing tennis. She's also a good friend to have in case you're ever in need of in-depth conversation about lipid metabolism. She's also a recent graduate of Arizona State University's nutrition program. Congrats!</i><br />
<div>
<br /></div>
daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com6tag:blogger.com,1999:blog-5995754777906978314.post-44703943766991652282012-06-08T21:59:00.001-07:002012-06-08T23:01:43.662-07:00Videos from the EB2012 Sugar Showdown and a Few Comments from Dr. Lustig<span class="Apple-style-span">If you've been following this blog, then you're probably aware that back in April I blogged about a highly attended debate at Experimental Biology 2012 in San Diego (dubbed the #sugarshowdown in a hashtag on Twitter; here's the <a href="http://storify.com/daviddespain/sugarshowdown" style="color: #923e1a; text-decoration: none;">Storify story</a> in case you missed it). The event was</span><span class="Apple-style-span"> sponsored by the Corn Refiners Association. </span><br />
<br />
In that symposium, Dr. Robert Lustig, of University of California, San Francisco, who is famed for sensationalizing the position that sugar is "toxic" in media coverage and the scientific literature, was seriously challenged by not only speakers, but also by fellow scientists (from industry and non-industry alike) in the crowd during the question-and-answer period.<br />
<br />
One of those scientists was Dr. John Sievenpiper, of St. Michael's Hospital, University of Toronto, who told me in an <a href="http://evolvinghealthscience.blogspot.com/2012/05/fate-of-fructose-interview-with-dr-john.html">interview</a> after the event, "Having both sides better represented was far more balanced than what came out of his two-million hit sensation on YouTube and a lot of the media coverage."<br />
<a name='more'></a><br />
I wrote about one of the unbalanced media reports <a href="http://evolvinghealthscience.blogspot.com/2012/04/no-dr-gupta-hummingbird-fuel-is-not.html">here</a>.<br />
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
<span class="Apple-style-span">The Sugar Showdown videos are now published online. </span>Now, you can check out each of the talks for yourself and make your own judgment on the state of the research. Here are the talks in order of appearance:</div>
<ul>
<li><a href="http://www.visiond.com/ASN_2012/Sun_Sym_Fructose/White.html" style="color: #923e1a; text-decoration: none;">John White, Ph.D., of White Technical Research</a> </li>
<li><a href="http://www.visiond.com/ASN_2012/Sun_Sym_Fructose/Lustig.html" style="color: #923e1a; text-decoration: none;">Dr. Lustig</a> </li>
<li><a href="http://www.visiond.com/ASN_2012/Sun_Sym_Fructose/Bray.html" style="color: #923e1a; text-decoration: none;">Dennis Bray, M.D.</a> </li>
<li><a href="http://www.visiond.com/ASN_2012/Sun_Sym_Fructose/Rippe.html" style="color: #923e1a; text-decoration: none;">James Rippe, M.D. (cardiologist), of Rippe Health</a> </li>
<li><a href="http://www.visiond.com/ASN_2012/Sun_Sym_Fructose/Klurfeld.html" style="color: #923e1a; text-decoration: none;">David Klurfeld, Ph.D. of the USDA</a> </li>
<li>In addition, there is a video of the <a href="http://www.visiond.com/ASN_2012/Sun_Sym_Fructose/QandA.html" style="color: #923e1a; text-decoration: none;">Question-and-Answer Period</a> too (can't miss that!).</li>
</ul>
Perhaps you'll agree with Dr. Sievenpiper that the symposium presented a "far more balanced" view on the subjects of sugar, high-fructose corn syrup, and fructose than what has been seen lately in media coverage.<br />
<br />
One more thing I'll add is that last weekend I had a discussion with Dr. Lustig at the National Lipids Association <a href="http://www.lipid.org/meetings/2012/annual/index.php">annual meeting</a> held in Scottsdale. We discussed Dr. Sievenpiper's views on the debate on sugar and where they may differ in their views.<br />
<br />
After speaking with him, I gathered that Dr. Lustig and Dr. Sievenpieper actually do tend to agree more than disagree on the data. For example, Dr. Lustig told me that he understood full well that the animal data and ecological analyses shouldn't be used for arguing his position that fructose is a unique metabolic danger. He also agreed that answers needed to come from randomized controlled feeding trials in humans, which is really what Dr. Sievenpiper's research has been about.<br />
<br />
So far, the meta-analyses and systematic reviews on randomized, placebo-controlled feeding trials comparing fructose to other carbohydrates have not revealed to have any quantitatively meaningful metabolic effects. That is, fructose has demonstrated no significant effect on body weight, blood pressure, or uric acid in calorie-controlled trials. On the other hand, fructose demonstrated improvement of glycemic control at levels comparable to that obtained in fruit.<br />
<br />
What Dr. Lustig and Dr. Sievenpiper obviously do disagree on is in their choice of rhetoric. Dr. Lustig's uses with words like "toxic," "addictive," and purposely compares the fruit sugar's metabolism to that of alcohol. Dr. Sievenpiper is more reserved, suggesting that fructose (like anything else) can be beneficial at some levels, such as in amounts found in fruit, and harmful only at extremely high levels (even then, not any different than other sources of carbohydrate).<br />
<br />
In response, Dr. Lustig reported at the Scottsdale event that he would be following up with some more research. He mentioned, in fact, that he would be involved at UCSF in conducting controlled feeding trials of his own. Stay tuned!daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com6tag:blogger.com,1999:blog-5995754777906978314.post-13621663080003418692012-05-30T08:33:00.002-07:002012-05-31T12:36:55.273-07:00Why a fat brain made us more vulnerable to heart diseaseNatural selection granted us large brains. The evolutionary cost is having to feed them. The human brain's high-energy demands led to development of a strong preference for fat. We consume more fat than any other primate on average. We are also adapted to more easily digest and metabolize fats.<br />
<br />
There are two major kinds of fat that our brains depend on most for its development and regular maintenance. These are the long-chain polyunsaturated fatty acids (LC-PUFAs), omega-3 docosahexaenoic acid (DHA) and omega-6 arachidonic (AA). These two LC-PUFAs can't be made <i>de novo</i>, making them essential in the diet. DHA and AA are supplied by seafood, eggs, or animals. They can also be supplied as their 18-carbon precursors alpha-linolenic acid (ALA) and linoleic acid (LA), found mainly in plants and their seeds.<br />
<br />
ALA and LA precursors require conversion to become long-chained through a series of steps of desaturation and elongation. In particular, delta-5 and delta-6 fatty acid desaturases build onto the carboxyl end of the carbon chains of the ALA and LA by introducing double bonds. These converting enzymes are rate-limiting.<br />
<br />
The rate-limiting enzymes are encoded into the genome by FADS1 and FADS2. The FADS region has been of special interest to researchers because of variations in single-nucleotide polymorphisms (SNPs) that could lend clues about human evolution including our larger brains. Yet, to date, there have not existed any studies evaluating FADS mutations among humans and related species.<br />
<a name='more'></a><br />
Now, researchers from Uppsala University, in Sweden, along with scientists at MIT, Harvard, and major European Universities, have found genetic variation in the FADS region in present-day humans that made them uniquely adapted to biosynthesize DHA and AA. The same adaptations could also help explain why some ethnicities have a higher susceptibility to chronic disease today.<br />
<br />
The international team set out to investigate by using genomic data from contemporary human populations, archaic hominins, and more distant primates. They used SNP genotype data from more than 5,600 individuals across five European population cohorts. They evaluated mutations in the FADS region that are strongly associated with omega-3 and omega-6 fats.<br />
<br />
<b>Two common FADS haplotypes</b><br />
<br />
Among present-day humans, they report, exist two common FADS haplotypes, or groups of alleles defined across a set of 28 SNPs, that are "dramatically different in their efficiency" to biosynthesize DHA and AA from he shorter ALA and LA.<br />
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEisqqXyaEBB9-PYiRTlyLYoNCSCdtCZMxcNT8NQCin1F7k0qTkVsPPb4YMsZKdQd8xnAuxJODsWcujd98rlWcFM6nW2UoITmTYrKbA4WtHCylK2KxdfKa40ULFoTH23XM99p9Qi4QCjmzo/s1600/Screen+shot+2012-05-30+at+7.02.10+AM.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="203" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEisqqXyaEBB9-PYiRTlyLYoNCSCdtCZMxcNT8NQCin1F7k0qTkVsPPb4YMsZKdQd8xnAuxJODsWcujd98rlWcFM6nW2UoITmTYrKbA4WtHCylK2KxdfKa40ULFoTH23XM99p9Qi4QCjmzo/s400/Screen+shot+2012-05-30+at+7.02.10+AM.png" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">The 28 SNPs of two main haplotypes (A in red, D in blue) and nucleotides of species.</td></tr>
</tbody></table>
<br />
<br />
Haplotype A, limited in conversion efficiency, appeared nearly 606 thousand years ago. Rhesus monkeys, chimpanzees, gorillas, and Denisovans all bear haplotypes "very similar" to haplotype A. Neandertals too, although based on incomplete sequences, have similar haplotypes to haplotype A.<br />
<br />
Haplotype D, having greater conversion efficiency, appeared somewhere between the lineage split with Neandertals. That was around 500 thousand years ago and before the exodus from Africa some 50 to 100 thousand years ago. Both haplotypes must've been present during the exodus or else we wouldn't see the existence of them in modern humans today.<br />
<br />
The researchers speculate that "a very rapid increase in brain size of hominoids" probably involved selection and the increased frequency of haplotype D. That does not mean that haplotype D had any direct effect on brain size, but that it was highly advantageous in environments where there was limited access to AA and DHA to feed the brain.<br />
<br />
<b>Haplotypes A and D in Present-day Humans</b><br />
<br />
Nowadays, the researchers found, nearly all individuals of African descent had haplotype D. The high frequency indicates positive selection for the haplotype with more efficient conversion in the face of limited availability of LC-PUFAs in early Africa.<br />
<br />
On the other hand, nearly all Native Americans had haplotype A. The reason, the researchers propose, may be because of a "bottleneck effect in the colonization of the American continent, possibly in combination with relaxation of the selective pressure as a result of a diet higher in essential LC-PUFAs."<br />
<br />
The data are mixed in those descended from Europe, Oceania, East Asia, who are reported to have haplotype D at a greater frequency.<br />
<br />
<table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgMTjMEvNXckRxcV-3Af1GeoIzXIrnL1osz1hl7RJXA1c-2a2U5Uvra45SmhUxwXAW1brTvPrm7BUHTjg2eDQ0Hco4kWgW01Kkaktnf3uL_cAtveLtN89YbOp0f9sjxlEus_zz_vkVvQ5Y/s1600/Screen+shot+2012-05-30+at+6.57.28+AM.png" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="267" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgMTjMEvNXckRxcV-3Af1GeoIzXIrnL1osz1hl7RJXA1c-2a2U5Uvra45SmhUxwXAW1brTvPrm7BUHTjg2eDQ0Hco4kWgW01Kkaktnf3uL_cAtveLtN89YbOp0f9sjxlEus_zz_vkVvQ5Y/s400/Screen+shot+2012-05-30+at+6.57.28+AM.png" width="400" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">The frequencies of A (blue), D (red), and mixed (gray) haplotypes.</td></tr>
</tbody></table>
<b><br /></b><br />
<b><br /></b><br />
<b>Health Implications</b><br />
<b><br /></b><br />
How can the knowledge of these haplotypes inform guidance on diet? The differences in haplotypes may explain why individuals of specific ethnicities may be more susceptible to chronic disease compared to others. <br />
<br />
Individuals with haplotype D biosynthesize more AA and DHA than individuals with haplotype A. While this adaptation may have been useful on the African savannah, the researchers propose it has drawbacks as a "thrifty genotype" in our modern world. As plentiful as LA (from corn and soy) is in the Western diet, haplotype D may lead to higher levels of AA-derived pro-inflammatory eicosanoids, which raise the risk of atherosclerosis and coronary artery disease.<br />
<br />
A different set of problems are presented for individuals with haplotype A. These individuals may be protected against a high-LA diet to a degree because of limited conversion to AA. However, they are more dependent on animal foods for adequate amounts of DHA due to inability to convert sufficient ALA to the longer-chained counterpart on a more plant-based diet.<br />
<br />
The researchers propose, "FADS genotyping should be included as a diagnostic for dietary recommendations."<br />
<br />
As genetic testing is not yet widely available, here's a more viable solution for the sake of a large human brain and a genome not well adapted to a high-LA diet: eat less LA; and, eat more foods enriched in long-chained omega-3s such as eggs, grass-fed animals, and seafood.<br />
<br />
<b>Reference</b><br />
<br />
Ameur et. al. Genetic Adaptation of Fatty-Acid Metabolism: A Human-Specific Haplotype Increasing the Biosynthesis of Long-Chain Omega-3 and Omega-6 Fatty Acids. American Journal of Human Genetics, April 12, 2012 DOI: <a href="http://www.cell.com/AJHG/abstract/S0002-9297(12)00158-9">10.1016/j.ajhg.2012.03.014</a><br />
<br />
<b>Related Posts</b><br />
<br />
<ul>
<li><a href="http://evolvinghealthscience.blogspot.com/2010/01/book-review-queen-of-fats-by-susan.html">Omega-3 Overview and Book Review of "Queen of Fats" by Susan Allport</a></li>
<li><a href="http://evolvinghealthscience.blogspot.com/2011/04/boost-omega-3-by-reducing-omega-6.html">Boost omega-3 by reducing omega-6</a></li>
<li><a href="http://evolvinghealthscience.blogspot.com/2010/12/how-diet-shaped-human-evolution.html">How diet shaped human evolution</a></li>
</ul>daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com7tag:blogger.com,1999:blog-5995754777906978314.post-8177470021841589252012-05-27T18:32:00.001-07:002012-05-29T08:11:19.322-07:00Good insulin, bad insulin: Its role in obesity?<div class="separator" style="clear: both; text-align: center;">
</div>
Gary Taubes makes insulin out to be a bad guy. In his latest <a href="http://www.thedailybeast.com/newsweek/2012/05/06/why-the-campaign-to-stop-america-s-obesity-crisis-keeps-failing.html">article</a> in <i>Newsweek Magazine</i> commenting on HBO's <i><a href="http://theweightofthenation.hbo.com/">Weight of the Nation</a></i> documentary, he once again challenges <i>energy balance</i> (energy intake versus energy expended) as a paradigm for understanding obesity. The author of <i>Good Calories, Bad Calories </i>offers an alternative theory: refined sugars and grains trigger insulin, which leads to fat accumulation. He also doesn't think much of physical activity as playing a "meaningful role in keeping off the pounds."<br />
<br />
Is Taubes right? Not according to Jim Hill, Ph.D., a professor of pediatrics and medicine at the University of Colorado School of Medicine, Denver. Hill is the cofounder of the National Weight Control Registry, a registry of individuals who've succeeded in maintaining weight loss over time. He is also the co-founder of America on the Move, a national weight-gain prevention initiative.<br />
<br />
At a session at Experimental Biology, Hill said that the the "energy-in energy-out" framework continues to dominate as correct in current scientific literature on obesity. When asked whether or not the rise of obesity epidemic is related to diet <i>or</i> physical activity, Hill simply responds, "Yes." That is because studies have shown that either restriction of calories or greater physical activity can lead to weight loss.<br />
<br />
Then, what's wrong with Taubes's insulin hypothesis? First, it's important to point out that insulin is also a good guy. As kinesiologist John Ivy, Ph.D., of the University of Texas at Austin, pointed out to me a few years ago, insulin is too often misunderstood. The unfortunate consequence can be a detriment of muscle and strength. Ivy's own research is on muscle insulin resistance and how it is reduced with exercise.<br />
<br />
<a name='more'></a>Insulin's role is more clearly explained in Ivy's book <a href="http://www.amazon.com/Nutrient-Timing-Future-Sports-Nutrition/dp/1591201411"><i>The Future of Sports Nutrition: Nutrient Timing</i></a>. He writes that, yes, insulin is a promoter of fat synthesis. But it is also a crucial hormone for promoting protein synthesis, reducing protein degradation (including suppressing cortisol, which can be catabolic in nature), and promoting glucose uptake and glycogen storage in muscle. Insulin, notably, also suppresses appetite.<br />
<br />
According to Ivy, the most important factor involved in whether or not insulin promotes fat storage, carbohydrate storage, or protein synthesis is the "individual's body state." For example, under conditions where insulin sensitivity heightened in fat cells (a sedentary lifestyle), there will be more promotion of fat storage. On the other hand, after physical activity, when muscle cells are more insulin sensitive, insulin will promote glycogen and protein synthesis. <br />
<br />
Perhaps where Taubes goes wrong is in failing to realize the role of muscle in body metabolism. It wouldn't be the first time. As I've discussed before in a <a href="http://evolvinghealthscience.blogspot.com/2012/05/nevermind-body-fat-put-focus-on-muscle.html">post </a>about the work of another kinesiologist, Stuart Phillips, Ph.D., of McMaster University, skeletal muscle is often forgotten in discussions of obesity. However, as Phillips affirms, skeletal muscle is a highly metabolically active tissue, consuming a great deal of energy as a primary site for glycogen storage and the largest site for fat burning. Skeletal muscle mass also helps determine metabolic rate. <br />
<br />
Taubes, in this latest article, also fails to mention that carbohydrate is not the only macronutrient that stimulates insulin. Protein stimulates insulin too; in fact, it's the branched-chain amino acids (leucine, isoleucine, valine) that trigger the insulin release -- these same amino acids are also the key players in triggering protein synthesis, which is explained in part by their effects on insulin.<br />
<br />
Ivy explains that insulin has earned the title "anabolic regulator of muscle," meaning it's the most important hormone to increase muscle and strength. Yet, by Taubes's judgment, insulin release should be avoided as much as possible. Taken to its logical conclusion, Taubes's mindset means that one should eat less carbohydrate and protein per day, and eat plenty more fat -- <i>along with the dismissal of exercise as being important, that's the perfect recipe for gradual muscle degradation and (what?) insulin resistance, hyperglycemia, and hyperinsulinemia! </i><br />
<br />
Is there something really wrong with "eat less, move more"? After all, this "tired advice" as Taubes calls it has largely failed in producing results in the United States. There still exists an obesity epidemic and it's getting worse. Is there another alternative theory to energy balance? Hill says energy balance still stands, although he acknowledges "eat less, move more" is too simplistic as advice. He offers his own new paradigm, which largely represents what other nutrition scientists have concluded including the American Society for Nutrition (see my report <a href="http://evolvinghealthscience.blogspot.com/2012/04/beyond-calories-in-calories-out-look-to.html">here</a>). It's that "diet and physical activity interact." And how they interact may explain how the body regulates -- with a sort of "settling point," according to Hill -- balance of energy, energy stores, glucose, and temperature.<br />
<br />
Looking at the problem from historical standpoint, Hill reminds, we no longer have to hunt or travel long distances to gather food anymore. We no longer have to farm to produce our food. Now, it's all about heading to the supermarket, filling our carts, and sitting in some form or another for the rest of the day. Our environment has changed. What's the solution to an obesity epidemic? Hill suggests in taking "small steps" for changing our environment back; this means continuing with "eat less, move more," and finding any opportunity to bring reduced-calorie eating, walking, and other physical activities back into lifestyles.<br />
<br />
Another recommendation comes from Ivy and Phillips, which is to make greater use of the "anabolic regulator of muscle" and focus on muscle maintenance and growth through regular physical activity. They also encourage balanced eating with healthy portions of quality protein, carbohydrates, and fats. Yes, carbohydrate is important for endurance and maximal recovery of glycogen stores.<br />
<br />
Resistance training is primary for muscle building; aerobic exercise also helps in depletion of glycogen stores. Both forms of physical activity make muscles more insulin sensitive, cause greater uptake of glucose into muscles, and they also help keep extra calories from heading toward fat stores. Far from Taubes's advice that physical activity is meaningless, these kinesiologists suggest some form of exercise should happen every single day.<br />
<br />
To greater understand the role of "nutrient timing" and how carbohydrate and protein relate to exercise, read Ivy's book and see this 2008 <a href="http://www.ncbi.nlm.nih.gov/pubmed/18834505">position statement</a> from the International Society of Sports Nutrition where Ivy serves as part of the editorial board.<br />
<br />
Update: Those of you who've read <i>Good Calories, Bad Calories</i> or <i>Why We Get Fat </i>may also be interested in Yoni Freedhoff's review of the latter over on his "<a href="http://www.weightymatters.ca/2011/01/book-review-gary-taubes-why-we-get-fat.html">Weighty Matters</a>" blog. I have only read the first book<i>.</i>daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com16tag:blogger.com,1999:blog-5995754777906978314.post-77955865418428142682012-05-26T08:40:00.002-07:002012-06-03T08:24:24.389-07:00Fate of fructose: Interview with Dr. John Sievenpiper<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left; margin-right: 1em; text-align: left;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjg5CkvRbtiqQtYOOLlEJAeLc06BrNmvZzleLaUYHTHATzIk0wzdKIIZFD4h-n8Te1zT0SGh6DtWfDMOPLQkbAWE8dIamxjdOKe9A_HzZ2M1YpeFEmSxtHwyCeAB23z1lvkixRKPVd0YO8/s1600/Fructose_fate.png" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img border="0" height="186" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjg5CkvRbtiqQtYOOLlEJAeLc06BrNmvZzleLaUYHTHATzIk0wzdKIIZFD4h-n8Te1zT0SGh6DtWfDMOPLQkbAWE8dIamxjdOKe9A_HzZ2M1YpeFEmSxtHwyCeAB23z1lvkixRKPVd0YO8/s200/Fructose_fate.png" width="200" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Fructose metabolism. Ref: Tappy & Ka 2010.</td></tr>
</tbody></table>
Sugar is a hot topic these days. Evidently, it's also a touchy topic. I've been a little amazed at some of the responses (both positive and negative) received since my first <strike>rant</strike> post about media reporting unfairly that <a href="http://evolvinghealthscience.blogspot.com/2012/04/no-dr-gupta-hummingbird-fuel-is-not.html">hummingbird fuel</a> was "toxic". There clearly exists a continued need for education about the state of the evidence as it stands now surrounding sugar and its implications on health.<br />
<br />
As a follow-up to my <a href="http://evolvinghealthscience.blogspot.com/2012/04/sugar-showdown-science-responds-to.html">report</a> of the "Sugar Showdown" at Experimental Biology -- a debate where scientists voiced clear dissatisfaction with the sensationalism surrounding sugar both in news reports and in the scientific literature -- I decided to seek out greater insight by an expert who was at the event.<br />
<br />
John Sievenpiper, M.D., of St. Michael's Hospital, University of Toronto, brings a valuable perspective to our understanding of sugar. He is the lead author of three recent systematic reviews and meta-analyses evaluating fructose's effects on body weight, blood pressure, and glycemic control in humans from randomized controlled feeding trials.<br />
<br />
With only very light edits made (for clarity) to my transcribed interview with him by telephone, I give you the take of Dr. Sievenpiper on fructose in his own words:<br />
<a name='more'></a><br />
<i>DD: What did you think of the debate in San Diego? Do you think it helped clear up confusion among the scientists about the state of evidence on sugar and, particularly, fructose? </i><br />
<br />
JS: I absolutely did. It was a very useful debate just because I think the debate to this point has been dominated by people like Dr. Lustig. I have a lot of respect for and certainly am on friendly terms with Dr. Lustig. We have had very cordial and academic discussions in email and when I've spoken with him. We obviously disagree where the data lies. Unfortunately, I think he's done a better job at knowledge translation than the people on the other side of the argument. Certainly, I'd say I’m not on the other side of the argument. I'm in the middle of the argument trying to make sense of it. Having both sides better represented was far more balanced than what came out of his two-million hit sensation on YouTube and a lot of the media coverage that has resulted from that of Gary Taubes and some others as a result of that video.<br />
<br />
<i>DD: Where do you think there's still confusion? Where is the real scientific debate?</i><br />
<br />
JS: The confusion really lies in that a lot of this debate has been underpinned by the animal literature and ecological studies without recognizing the flaws and translating that information into real-world human scenarios. The problem has really been with someone like Lustig who can run through the pathways at very impressive clip and can convince someone that, OK, there's so much biological plausibility, so it must be true. People aren't asking the question, "Well is it? What happens when we do look at humans? Do we actually see this signal?"<br />
<br />
What we're finding with our meta-analyses is that, no, we don't see that signal. Or, we do where energy is part of the equation and seems to be dominant. I think that is the disconnect that has really come because of the use of the animal data and ecological analyses. It's very seductive. Because they do show reproducible, consistent effects of a harmful signal.<br />
<br />
<i>DD: You're saying that signal isn’t something that was found in humans per your meta-analyses on isocaloric trials in humans?</i><br />
<br />
JS: Correct. That was the reason we did the meta-analyses in the first place. We didn't set out an <i>a priori </i>hypothesis that fructose doesn't do these things. In fact, our hypothesis would've been "Well, everyone's talking about it. The animal data is suggestive of an adverse effect of fructose." If anything, our hypothesis was that there's going to be an adverse effect.<br />
<br />
We set out to do these meta-analyses to answer that question – whether that phenotype that we see in animals that can be so robustly reproduced, the signal we're seeing from ecological data (where we are looking at populations), and whether that actually translates into human models where we actually feed people and control for all extraneous variables.<br />
<br />
We decided to use the gold standard or highest level of evidence in nutrition or, really, in most fields -- which is controlled trials; and, in nutrition, is controlled dietary feeding trials. We wanted to apply the best tools we have, which was systematic review and meta-analyses tools to synthesize that knowledge and information to try to answer the question.<br />
<br />
Is it true? What we found was that it wasn't. We looked at bodyweight -- which is the <a href="http://www.annals.org/content/156/4/291.abstract">Annals [of Internal Medicine]</a> data that you're aware of -- in each case there was no effect of fructose when it was isocalorically exchanged. There was no adverse effect on bodyweight, <a href="http://www.ncbi.nlm.nih.gov/pubmed/22331380?dopt=Citation">blood pressure</a>, or <a href="http://www.ncbi.nlm.nih.gov/pubmed/22457397">uric acid</a>. We do see a very consistent and strong effect on bodyweight when fructose is providing excess energy.<br />
<br />
<i>DD: The strong effect on bodyweight was in comparison to other carbohydrates?</i><br />
<br />
JS: That's comparison to a control diet. The fructose is providing excess energy. Is it the fructose you're adding? Is it the energy from fructose? Those are actually difficult to interpret. What we found is that the energy is dominant when you look at neutral, positive, or negative energy balance studies. We found that as long as fructose was isocalorically exchanged, there was no effect. Fructose wasn't having an effect beyond energy. Our conclusions looking were that energy appears to be dominant in particular case to bodyweight. The bodyweight increase we saw was predicted by the energy was consumed. We would say the same thing, although we didn’t have as many studies, for uric acid. In our <a href="http://www.ncbi.nlm.nih.gov/pubmed/19592634">lipid analyses</a>, we find the same thing again. Energy is dominant.<br />
<br />
<i>DD: Let me ask a question about those hypercaloric trials in relation to animal studies and the flaws of which you speak. Recently, for example there was what I call the "sugar makes you stupid" study [covered <a href="http://evolvinghealthscience.blogspot.com/2012/05/confusing-messages-about-sugar-are.html">here</a>]. When I read it, I found it was simply a hypercaloric trial where rats were given fructose in addition to a control diet, which led to insulin resistance. </i><br />
<br />
JS: I think you hit the nail on the head. There is really the disconnect between animal carbohydrate metabolism and human carbohydrate (or fructose) metabolisms. One of my criticisms of using animal data is that they feed at superphysiological levels at 60 percent energy. No one is consuming that.<br />
<br />
The 50th percentile for intake in the United States is 49g per day, which is just a little less than 10 percent per day of energy from fructose. We're talking of a six-fold difference in what people are really consuming and what these models are feeding. If you look at even the 95th percentile for intake of fructose in US population from using NHANES data, the 95 percentile for intake for NHANES for fructose consumes 87g of sugar or little less than 20 percent energy. (NHANEs is intake data as opposed to disappearance data, what the USDA collects, which is just availability of sugars, but tends to overestimate because it doesn't account for waste; it looks at how much went onto the market; when you only fill your coffee half full with that sachet of sugar and throw away the rest, it doesn't count for how much was thrown away). So these models are feeding even three-fold, if we're generous, compared to the 95th percentile of the population are consuming, which is really super-physiologic. Just based on the feeding pattern and paradigm of those models, you can't equate them.<br />
<br />
On top of that, we know that if you look at comparative physiological studies, animals metabolize carbohydrates differently than do humans. In animals on a high-carbohydrate diet not providing excess energy, you find that <i>de novo lipogenesis</i> [conversion by the liver to fatty acids] is anywhere from 50 percent or higher. They basically make fatty acids for at least 50 percent of the carbohydrate [consumed]. De novo lipogenesis accounts for at least 50 percent carbohydrate. In humans, it is very, very hard under isocaloric (neutral energy) conditions, let alone in overfeeding conditions, to push that beyond 10 percent or even 20 percent.<br />
<br />
A lot of the outcomes that have been implicated, have really centered on this hypothesis of de novo lipogenesis. I have a really big problem when people want to extrapolate from an animal study where their feeding (1) superphysiological amounts of fructose and (2) in a model where the metabolism is not the same as in humans – it's very different. It's bad for rats or mice (you name your study and adverse effect of fructose), but it doesn't mean that's the case in humans. Again, that's the reason why I think we need good human data and that's why we wanted to synthesize the human data. We do have almost 50 controlled feeding studies on different questions related to cardiometabolic control.<br />
<br />
<i>DD: At Experimental Biology, Dr. Rippe argued that the amount of de novo lipogenesis in humans was pretty negligible in response to fructose eaten normally in the U.S. Can you comment on what he shared? </i><br />
<br />
JS: That is correct. If you actually look at the animal studies where you feed them high fructose, you make this beautiful metabolic syndrome phenotype (where they have very high TGs, low HDL, hypertension, obesity, and insulin resistance). We don't see that in humans. It doesn't hold true because when you actually look at carefully conducted studies.<br />
<br />
Dr. Rippe was actually quoting Luc Tappy's <a href="http://www.ncbi.nlm.nih.gov/pubmed/20086073">work</a>. He has put together a really excellent review of his own work and that of others who've done careful stable isotope tracer studies where you can label acetate, fructose, and different metabolites. You can see where fructose is going and where fructose is ending up. What he's found is that with a fructose load 50 percent goes to glucose, about 25 percent goes to lactate, greater than 15 percent and up goes to glycogen, the remainder would be oxidized directly [going to CO2 through the TCA cycle], and a small portion contributed to <i>de novo lipogenesis</i>. I can't remember what Dr. Rippe had on his diagram, but even as low as, let's say, 3 percent, it is really quantitatively non-significant. In animals, <i>de novo lipogenesis</i> is quantitatively significant. It doesn't appear in humans with high-carbohydrate feeding and the same is true even under high-fructose feeding. We see this very robust <i>de novo lipogenesis</i> in animals. We don't see it in humans.<br />
<br />
That I think is a problem because this is one of the underpinning mechanisms by which antagonists like Dr. Lustig and others are hanging their arguments in terms of why we're seeing an increase in overweight and obesity, metabolic syndrome, diabetes, and the metabolic syndrome phenotype in general that fructose is thought to elicit.<br />
<br />
<i>DD: Why do you think Lustig continues to argue that de novo lipogenesis makes fructose intake a metabolic danger?</i><br />
<br />
JS: When you look at someone like Rob Lustig, who, again, I actually I have a lot of respect for because I think he's well-intentioned and he's sincere about his belief. But I think his passion and enthusiasm in this area are clouding his judgment a bit. You could say the same for Gary Taubes or anyone who has kind of taken a very extreme position on the data.<br />
<br />
If you look at the data carefully, sort out the wheat from the chaff, and look for the well-controlled data to drill down on some of these mechanisms -- OK, let's look in humans and not animals; let's look under basic normal energy balance conditions, and let's use the best or most elegant tools we have, which are stable isotope tracers -- this is the answer you get: 50 percent glucose, 25 percent lactate, greater than 15 percent to glycogen. These may vary a bit just based on the rest of the background diet and activity level of the organism or human in this case. But in general, this is the fate of fructose.<br />
<br />
It's not what Dr. Lustig and others would have you believe -- massive influx into de novo lipogenesis to hugely raise triglycerides, overweight, obesity, metabolic syndrome. You don't see it through this mechanism. We just don’t see the signal of increase in bodyweight or even for triglycerides; only the very high doses.<br />
<br />
<i>DD: What about a possible benefit from fructose? For example, in one of your meta-analyses you found a benefit on glycemic control. </i><br />
<br />
JS: The <a href="http://www.ncbi.nlm.nih.gov/pubmed/22354959">study</a> you're quoting, or the meta-analysis we did, was looking at so-called small or catalytic doses of fructose at a level that would be obtainable from fruit (so, basically, less than 10g per meal). We took that to mean 36g per day (meaning 10g per meal and two snacks with 3g each; like 30 percent of a meal). That's how we came up with eligibility criteria for that meta-analysis. That was just a snapshot that looked at low doses of fructose.<br />
<br />
We saw this benefit for hemoglobin A1c (HbA(1c)) -- almost a 0.5 percent reduction. That's a 0.5 percent absolute reduction (not a proportion) similar to what you would see with antidiabetic agents at the lower range of efficacy. And, we saw that without adverse effects on triglycerides, body weight, insulin, and uric acid. So, we concluded that there was an overall a net metabolic benefit from these low doses of fructose at a level really that is obtainable from fruit.<br />
<br />
That correlated quite nicely with what we saw in a very large glycemic index trial we published in patients with type 2 diabetes. What was the most important low-glycemic index food item that best predicted reduction of HbA(1c)? It was low-glycemic index fruit. The level of fructose that you would've obtained with the most commonly consumed <a href="http://www.ncbi.nlm.nih.gov/pubmed/20978741">low-glycemic index fruit</a> (apples, it turns out) would be 10g per serving. So it fit nicely with this idea of this catalytic dose of about 10g per meal. And in that study we saw an identical 0.5 percent reduction of HbA(1c) units. So, further confirming that there may be something to fruit.<br />
<br />
<i>DD: How will a metabolic benefit from fructose change the debate?</i><br />
<br />
JS: Part of the issue is about balancing the argument. I think we can learn a lot from someone like Robert Lustig because he has done the knowledge translation piece so well. Whether he's done it intentionally or not, he has brought a lot of attention to his issues. On the other hand, we’ve done -- at least the people with a more balanced view -- a very poor job at trying to communicate that balanced view. Yes, there may be some signals [that fructose has an adverse effect] or, no, there aren't, or it may be conditional on energy. With all the nuances, we’ve done a pretty bad job at communicating it as opposed to the simple message of "Fructose at any level is poison." We're trying to say it depends on the dose, it depends on the energy, and that’s a hard message to communicate. We've been dwelling on harm. We’ve been saying "Well, it doesn’t support harm except where there is excess energy."<br />
<br />
The nice thing about the glycemic control outcome is that we can actually talk about benefits. We can switch that argument back on its heel in a way to say, "Yeah, there's issues around harm. We need to really find out where the dose response lies." Now, we can start talking about a benefit. We can start talking about a level of fructose at a dose and where do we see a benefit without adverse effects which we may see at very high doses. And we can go back to moderation and even moderation having a benefit. As Dr. Klerfeld put so nicely [quoting <a href="http://www.brainyquote.com/quotes/authors/p/paracelsus.html">Paracelsus</a>, "The dose makes the poison"], the toxin is determined by the dose. Even water is toxic if you drink too much of it.<br />
<br />
<i>DD: In response to Dr. Lustig in </i>Nature, <i>you <a href="http://www.nature.com/nature/journal/v482/n7386/full/482470e.html">commented</a> about fruit fructose. Similarly, you commented to me at the symposium in San Diego that you had a concern that unwarranted fears of fructose would lead to reduced intake of fruit.</i><br />
<br />
JS: Again, part of the reason Dr. Lustig and Gary Taubes are so good at getting this message out is that it's so one-sided, very easy, very palatable message. They've oversimplified it so much where there is no level of safe intake, that it is a poison, that it should be just like tobacco (to paraphrase what he says in his video), and that it should be regulated accordingly. He doesn't say it so much in his <i>Nature</i> piece.<br />
But he doesn't actually talk about dose, where the dose response lies, and he doesn't address fruit, which may be a healthy form (I think should be an uncontroversially healthy form) of fructose. The problem with these arguments and these very extreme positions is that we don't talk about dose and we don't talk about the form of fructose.<br />
<br />
That's the danger -- that people will say that fruit is a source of fructose and I won't consume fruit because it may induce obesity, metabolic syndrome, and so on. It's not just the lay public that may take this message to heart but professionals. We had an endocrinologist here at our hospital at University of Toronto who was telling patients not to consume fruit because of the fructose content precisely because of all the commentaries, editorials, and reviews that Rob Lustig had been publishing. The danger is that people will take the message to extreme. They'll start saying "I should cut these things out (apples, pears) to cut my fructose exposure." That is a really wrong-headed approach. When I talk to Dr. Lustig on the side, I do get a sense that he does think that there's a dose threshold, but it doesn't come out in the writing, or the YouTube piece.<br />
<br />
<i>DD: I've heard about similar situations happen where people are cutting out fruit and taking Lustig's message to the extreme. Dr. Sievenpiper, you've given me, us, people a lot to think about. I appreciate your time. </i><br />
<br />
<div style="font-style: normal; margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
<i><i></i></i></div>
<div style="display: inline !important; margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
<i><i>Note: When I reached out to Dr. Sievenpiper, he was gracious enough to point me to a just-published "lovely, balanced, well-written paper" by respected physiologist Luc Tappy of Université de Lausanne, in Switzerland. The paper, Dr. Sievenpiper said, summarized much of Dr. Tappy's own take after the event in San Diego and would help answer more questions. (The open-access paper can be found <a href="http://www.biomedcentral.com/1741-7007/10/42">here</a>.)</i></i></div>
<i>
</i><br />
<div style="font-style: normal; margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
</div>
<i>
</i><br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
</div>
<i>
</i><br />
<div>
</div>
<i>
<br />
</i>daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com21tag:blogger.com,1999:blog-5995754777906978314.post-30783675968444226082012-05-20T18:27:00.001-07:002012-05-21T08:09:31.824-07:00Have a cuppa pesticide and #dontdestroyresearchEarlier today, biologist Mary Mangan (<a href="http://twitter.com/#!/mem_somerville">@mem_somerville</a>) shared the bad news that anti-biotechnology activists had succeeded in breaking into and damaging a publicly funded research project at Rothamsted Research Station in Harpenden, England. The vandalism happened only a week ahead of a planned demonstration organized by the Take the Flour Back environmentalist group (which I wrote previously about <a href="http://evolvinghealthscience.blogspot.com/2012/05/what-environmental-groups-dont.html">here</a>).<br />
<br />
Mangan wrote on her <a href="https://plus.google.com/u/0/115686712405727979216/posts/6dLXmDarKHC">Google+</a> page:<br />
<blockquote class="tr_bq">
Sadly, the destruction has begun. Forces opposed to science have vandalized a research project in the UK that has been underway for many years. It is a publicly funded project, and it attempts to use a biological method of control of insects on wheat plants. It could someday help reduce the use of pesticides and improve food security.</blockquote>
This led to a series of comments from people who mostly expressed sadness and anger about the damage. But, then, there were both of these comments: <br />
<a name='more'></a><br />
<blockquote class="tr_bq">
Thank god for this!!! GMO anything is not healthful to the environment or to us as humans! You are altering the genetic chemistry of that plant and when it cross-breeds with another plant (yes I said when), that one now has insect resistance, and soon insects will develop a way to eat these plants and then we're back to square one, but worse for wear because now we have to come up with some new ingenious way to keep insects from eating our crops.</blockquote>
<blockquote class="tr_bq">
We may have been altering the genetic makeup of plants, but only through natural selection and never through any artificial genes that were never supposed to exist in a specific species. Insect resistance is not a gene normally found in any living plant species that I know of. There are poisonous plants which I suppose could provide insect resistance, but you don't see them cross-pollinating with any other species that we eat.</blockquote>
<div>
That's when Mangan, as she puts it, spit out her "carcinogen-laden coffee" and decided to "help this person understand the reality."<br />
<br />
Clearly, what the person above didn't understand while making these comments, is that plants have been in arms race with pests for millenia. Part of a plant's defense are often thousands of natural pesticides, insecticides, and herbicides. It's a common misconception that "all-natural" and "organic" means "free of pesticides." They may simply mean not grown with synthetic pesticides, although organic crops are often grown with plenty of organic pesticides, and are likely to contain more naturally produced pesticides than conventionally grown plants.<br />
<br />
I might've also made light of the situation with this person, as I have to others with similar arguments, that pesticides shouldn't always be thought of as a "bad thing." After all, humans have long enjoyed consuming pesticides with glee (healthy and nonhealthy). For example, Mangan alluded to the fact that caffeine and other bitter compounds in a cup o' joe are themselves, in fact, natural pesticides. The coffee plant produces them with intent of simply repelling, paralyzing, or killing insects. Resveratrol and piceid, the bitter stilbene compounds produced by grape skins in response to stress, are pesticides that end up contributing to the flavor of red wine (and they may account for some of its health benefits). There's also tetrahydrocannabinol (THC), the psychoactive compound of cannabis, a pesticide that some enjoy along with a load of carcinogenic compounds. Nicotine, too, is a natural pesticide from tobacco. <br />
<br />
In response to the uniformed comments, Mangan posted links and quotes about plants producing their own pesticides naturally. That's when I joined the conversation, via Twitter, because I thought it would be a good idea to house a few of the links relating to natural pesticides in one place. Graciously, Mangan put her bookmarks together and posted them all on the Biofortified forum entitled <a href="http://www.biofortified.org/community/forum/?vasthtmlaction=viewtopic&t=189.0">"Plants making pesticides"</a>. It will be useful for helping educate people about naturally produced plant pesticides. In the forum post, she includes references to work from biochemist <a href="http://www.pnas.org/content/87/19/7777.abstract">Bruce Ames</a>, who famously triggered controversy by writing:<br />
<blockquote class="tr_bq">
We calculate that 99.99% (by weight) of the pesticides in the American diet are chemicals that plants produce to defend themselves. </blockquote>
Getting back to the purpose of this post -- there needs to be more intelligent conversation about pesticides. Without doubt, there's a need to reduce use of pesticides on plants to protect biodiversity. The overuse of pesticides and herbicides, unfortunately, kills off both harmful and beneficial insects and plants and can lead to pest resistance.<br />
<br />
Overall pesticide reduction is what makes the Rothamsted research so important. The publicly funded project tests a variety of wheat genetically engineered with a mint compound that leads to emission of a pheromone that acts as a aphid repellent. As a crop, wheat is one of the world's most important crops and an aphid-repellent variety could significantly reduce pesticide use across the globe.<br />
<br />
These are the reasons why I signed the <a href="http://www.senseaboutscience.org/petition.php">Sense about Science petition</a> to support the appeal scientists at Rothamsted. </div>daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com4tag:blogger.com,1999:blog-5995754777906978314.post-25695912256492242292012-05-18T06:10:00.000-07:002012-05-29T08:10:51.326-07:00Confusing messages about sugar are stupidI'm a bit late in weighing into the "Sugar Makes You Stupid" mess of poor health reporting on a rat study. At the <a href="http://embargowatch.wordpress.com/2012/05/15/sugar-makes-embargoes-stupid-and-doesnt-do-wonders-for-a-press-release-either/">Embargo Watch</a> blog, Ivan Oransky already covered the mishandling of the study's embargo and ripped into the <a href="http://www.eurekalert.org/pub_releases/2012-05/uoc--smy051512.php">press release</a> for misleading readers into believing that the study had any meaningful conclusions for college students. Then, Deborah Blum at <a href="http://ksjtracker.mit.edu/2012/05/17/sugar-and-stupidity/">Knight Science Journalism Tracker</a> went further, bringing more reason and logic, by clarifying what the rat study was really about -- the <i>neuroprotective role of omega-3 fatty acids!</i><br />
<br />
Mainly, I hope to bring a little more overall perspective to a study that, while perhaps could be valuable, has brought along with it unnecessary fears that a little <i><a href="http://evolvinghealthscience.blogspot.com/2012/04/no-dr-gupta-hummingbird-fuel-is-not.html">hummingbird fuel</a></i>, aka sugar, will make people walk around aimlessly as brainless as zombies. It's nonsense, of course, that sugar <i>makes you stupid</i>. After all, neurons run on a constant supply of glucose delivered by the bloodstream (as they don't store glucose as glycogen like other cells), a fact that several media reports completely failed to mention.<br />
<a name='more'></a><br />
But my main grief with the press release and several subsequent reports, as well as quotes from the scientists themselves, is how they confuse readers by making a villain of high-fructose corn syrup (HFCS), especially its fructose moiety. (Ranging from the not-so-bad to horrible, there's <a href="http://www.forbes.com/sites/alicegwalton/2012/05/16/fructose-may-make-you-stupid-but-omega-3s-can-smarten-you-back-up/">this one</a> - not so bad, <a href="http://www.latimes.com/news/opinion/opinion-la/la-ol-sugar-may-make-you-stupid-20120516,0,1823439.story">this one</a>, <a href="http://www.motherjones.com/blue-marble/2012/05/sugar-corn-syrup-dumb">this one</a>, <a href="http://www.livescience.com/20329-sugar-stupid.html">this one</a>, and, <a href="http://weeklyworldnews.com/opinion/48170/study-sugar-makes-you-stupid/">this one</a> - horrible.) These articles simply play into the already common misconception that HFCS as a sweetener is somehow <i>uniquely </i>dangerous to health. The scare tactics may bring more hits and interest from readers, but it's poor health reporting.<br />
<br />
Let's just point out again that HFCS is metabolically the same as sucrose (plain table sugar) -- they each are made up of almost equal amounts of glucose and fructose. HFCS's content of fructose is hardly "high" in comparison to other sugars; it may have been more appropriately called <i>medium-fructose corn syrup</i>. The fructose content is relatively similar (or less) to what's found naturally in honey, agave, and other natural sugars.<br />
<br />
Now, a review of the study (1) from <i>Journal of Physiology</i>; if you read any of the articles linked to above, then you probably already know the story: UCLA researchers trained rats fed normal chow and drinking water on a maze twice daily for five days to establish a baseline. Then, they separated the rats into two groups and supplemented both groups' drinking water with fructose (15 percent) -- essentially, putting them all on a high-sugar diet that would, basically, lead to hyperglycemia and insulin resistance.<br />
<br />
On to the interesting part of the experiment: The first group of rats received a diet deprived of omega-3 fatty acids. The second group, however, also received a supplement of omega-3 fatty acids (0.5 percent flaxseed oil and 1.2 percent docosahexaenoic acid (DHA)). Strong evidence supports that omega-3s, specifically DHA, is neuroprotective through a variety of mechanisms (with positive effects on inflammation and insulin resistance).<br />
<br />
A quick note before we move on -- we already knew that giving mice a high-sugar diet leads to insulin resistance. Nothing new so far. We <i>also</i> knew that insulin resistance and hyperinsulinemia themselves can have large effects on the brain. What is well established is that metabolic syndrome, obesity, and diabetes all make animals and humans more vulnerable to mental illness. So, this study is not really about sugar. It's really about the possible role of omega-3s as a protective nutrient in a metabolic syndrome rat model.<br />
<br />
So, what of the findings? After six weeks on the high-sugar diet, the DHA-deprived rats were slow and didn't do so well in the maze suggesting declines in neuronal signaling while the DHA-supplemented rats zipped through the maze without any troubles. Conclusion? Basically, the study showed DHA protects against disrupted insulin signaling in rats' brains.<br />
<br />
What really bothers me: The headlines of media reports hardly touched the real news: "DHA protects brains of rats from effects of insulin resistance," which could eventually have implications in those with metabolic syndrome, diabetes, and obesity. Instead, the press release and articles mainly focused on the whole idea of winning readers by playing on already existing fears about HFCS and fructose. Moreover, fructose is made out to having a central role in causing "stupidity." Nevermind that other sources of carbs (e.g white flour) or calories (e.g. fat) eaten in excess would also lead to insulin resistance.<br />
<br />
The scientific literature suggests no unique metabolic danger of fructose in humans versus other carbs that is quantitative. Consider the findings of a series of recent meta-analyses that reviewed randomized controlled isocaloric trials in humans by Sievenpiper et al (2, 3): f<i>ructose did not have any significant effect on body weight compared to other carbohydrate sources. </i>In fact,<i> at levels normally found in fruit, fructose could even support blood sugar control. </i>That's quite the opposite of being unique in increasing risk of insulin resistance. The facts are that overconsumption in general of any carbohydrates or other sources of calories (mice fed a high-fat diet get insulin resistance, too) is the main problem when it comes to metabolic syndrome factors.<br />
<br />
As argued by scientists at <a href="http://evolvinghealthscience.blogspot.com/2012/04/sugar-showdown-science-responds-to.html">Experimental Biology 2012</a>, it's time to stop playing the "blame game" when it comes to obesity and metabolic syndrome factors. There's nothing good that comes of demonizing a single ingredient whether it be HFCS, fructose, table sugar, or fat. It only leads people to switch and eat/drink too much of something else. The end result is still the same: obesity, insulin resistance, metabolic syndrome, and diabetes. Then, insulin resistance still ends up harming the brain (I played with the idea of titling this post "It's insulin resistance, stupid").<br />
<br />
Don't get me wrong -- I cringe every time I see a child or adult ordering a large HFCS-sweetened soda from a restaurant or gas station. But, it's also frustrating to see the words "no high-fructose corn syrup" acting like a kind of "health halo" on high-calorie food products (like the marketing of a Starbucks Frappuccino containing nearly 25 teaspoons of table sugar). The majority of people do need to reduce consumption of sugar and overall calories, as well as exercise more, to help maintain a healthy weight, maintain or put on muscle, and improve their insulin sensitivity.<br />
<br />
The message of this study and reports finally should have been simply, <i>"Don't overeat because it leads to insulin resistance and brain trouble; and a new study in rats suggests DHA could offer protection if you do."</i><br />
<br />
References<br />
<ol>
<li>Agrawal R and Gomez-Pinilla F. ‘Metabolic syndrome’ in the brain: deficiency in omega-3 fatty acid exacerbates dysfunctions in insulin receptor signalling and cognition <i>J Physiol</i> 590.10 (2012) pp 2485–2499. doi: <a href="http://jp.physoc.org/content/590/10/2485.full.pdf+html?sid=827c0bba-c4ab-444e-a106-ede4bd3059c6">10.1113/jphysiol.2012.230078</a></li>
<li>Sievenpiper JL, de Souza RJ, Mirrahimi A et al. Effect of Fructose on Body Weight in Controlled Feeding Trials: A Systematic Review and Meta-analysis. <em><a href="http://www.ncbi.nlm.nih.gov/pubmed/22351714?dopt=Citation">Ann Intern Med</a></em> 2012;156:291-304.</li>
<li>Sievenpiper JL, Chiavaroli L, de Souza RJ et al. 'Catalytic' doses of fructose may benefit glycaemic control without harming cardiometabolic risk factors: a small meta-analysis of randomised controlled feeding trials. <em>Br J Nutr</em> 2012;1-6. doi: <a href="http://www.ncbi.nlm.nih.gov/pubmed/22354959">10.1017/S000711451200013X</a></li>
</ol>
Related Posts<br />
<ul>
<li><a href="http://evolvinghealthscience.blogspot.com/2012/04/sugar-showdown-science-responds-to.html">Sugar Showdown: Science Responds to "Fructophobia"</a></li>
<li><a href="http://evolvinghealthscience.blogspot.com/2012/04/no-dr-gupta-hummingbird-fuel-is-not.html">No, Dr. Gupta, Hummingbird Fuel is Not "Toxic"</a></li>
</ul>
<br />
<br />
<br />daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com11tag:blogger.com,1999:blog-5995754777906978314.post-21534190304549145192012-05-13T14:11:00.002-07:002012-10-03T12:26:11.657-07:00What environmental groups don't understand about biotech<blockquote class="tr_bq">
<blockquote class="tr_bq">
It is not the strongest of the species that survives, nor the most intelligent that survives. It is the one that is the most adaptable to change.</blockquote>
<blockquote class="tr_bq">
- Charles Darwin</blockquote>
</blockquote>
On May 27, the "Take the Flour Back" environmentalist group plans to take "mass action" in efforts to remove more than $1 million worth of research in biotechnology. Their purpose, according to their <a href="http://taketheflourback.org/launch-press-release/">website</a>, is one of "mass decontamination" of what they see is a threat to farmers, the food supply, health of consumers, and biodiversity. What this protest group doesn't understand is that it's exactly this kind of research that they, as environmentalists, should be placing on a pedestal.<br />
<br />
In an <a href="http://www.biofortified.org/2012/05/interview-with-dr-gia-aradottir/#comment-133815">interview</a> with Karl Haro von Mogel, Rothamsted's biologist Dr. Gia Aradottir explains the details of the experiments the protest group wants to uproot at Rothamsted Research Station in Harpenden, England: The research is on a variety of wheat that is genetically engineered to emit aphid alarm pheromone (E)-β-farnesene (EBF); in other words, the scientists are testing plants that can produce their own non-toxic aphid repellent, using pheromones. An aphid-resistant wheat variety could lead to less use of pesticides overall, less pesticide runoff, less effects on beneficial plants and insects in the surrounding environment, less possibility of pesticide resistance.<br />
<a name='more'></a><br />
This is precisely the kind of research that could help lead to the "marriage" of organic agriculture (the kind that is pesticide-free) and genetic engineering called for by plant geneticists such as Pamela Ronald (see her most recent blog post <a href="http://scienceblogs.com/tomorrowstable/2012/04/study_points_to_role_for_both.php">"Thinking Beyond Organic"</a>). It's also the kind of research that former AAAS president Nina Fedoroff has said (see my prior post <a href="http://evolvinghealthscience.blogspot.com/2012/02/can-we-prevent-food-crisis-while.html">here</a>) will help prevent an eventual Malthusian crisis in combination with severe loss of biodiversity.<br />
<br />
Contrary to the beliefs of the "Take the Flour Back" group, the research could mean a better crop for farmers, more dependable wheat production for the food supply, and an ultimately greater protection of biodiversity. EBF and similar pheromones are also already emitted by several other plant species, so there should be no indication of it being a potential health hazard.<br />
<br />
<div>
However, despite <a href="http://www.senseaboutscience.org/pages/rothamsted-appeal.html">pleas of reason</a> from Rothamsted for the group to not destroy years of expensive research, the anti-GM group insists that the aphid-resistant wheat is still a danger. They point to <a href="http://taketheflourback.org/open-letter-to-rothamsted/">findings</a> from another environmental group, Friends of Earth International, that GM crops have led to increased amounts of herbicides and pesticides, not less. They also harp on the idea that the synthesized gene bears more resemblance to one found in a "cow" versus a "plant" -- an obvious scare tactic -- and they question Rothamsted's assertion that their publicly funded results won't be sold off to a agrochemical companies.</div>
<br />
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
Without a doubt, in the last few weeks, biotechnology-proponents have been following this story (along with the Kashi "<a href="http://www.usatoday.com/money/industries/food/story/2012-04-29/kashi-natural-claims/54616576/1">controversy</a>") with disbelief. The distrust the general public has toward genetically engineered foods has reached new levels. That is unfortunate, because biotechnology is the most promising technology we have for protecting the environment in our ever-changing, ever-more-populated, world. With <i>real</i> threats of arable land and water scarcity, loss of biodiversity, disease-resistance, and global warming all looming over us, environmentalists should welcome biotechnology as one of our most important technologies for countering the forces of change. <br />
<br /></div>
</div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
Perhaps what these protesters and the general public need is a serious understanding of the history of agriculture and why biotechnology is critical for the future. For instance, genetic manipulation has gone on for thousands of years in plant breeding. And, in the last 50 years or so, mutations have been induced through technologies such as thermal neutron radiation. New methods of genetic modification and gene transfer should be considered simply as extensions of previous technologies.</div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
<br /></div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
Rothamsted has the right idea, calling for an open discussion, in hopes of educating the public about the potential benefits of biotechnology. Let's hope it's enough to save their research from destruction! Learn more at <a href="http://www.senseaboutscience.org/pages/about-us.html">Sense about Science</a>. <br />
<br />
<a href="" name="sense">Update Oct 3, 2012:</a> Good news - The GM wheat trial has been successfully harvested! That's despite the protest group and significant damage following a <a href="http://evolvinghealthscience.blogspot.com/2012/05/have-cuppa-pesticide-and.html">break-in</a>. I received the following message today via email because I signed the "don't destroy research" <a href="http://www.senseaboutscience.org/petition.php">petition</a> at Sense about Science:<br />
<blockquote style="font-family: Calibri;" type="cite">
<div>
Dear Petition Signatories </div>
</blockquote>
<blockquote style="font-family: Calibri;" type="cite">
<div>
The GM wheat trial crop at Rothamsted Research has been harvested. It is far too early to talk about results yet, but the team at Rothamsted wanted to let you know about the harvest and to pass on their thanks. The protest group who said they were going to destroy the crop earlier in the summer did not have enough support to carry out their threat; this was because of you. </div>
</blockquote>
<blockquote style="font-family: Calibri;" type="cite">
<div>
Professor John Pickett said<i>: "The team and I were overwhelmed by all the messages of support we received from the petition signatories. You all have a significant role to play in ensuring this important, independent scientific study continues to progress so we can better understand whether this technology could help us deliver more environmentally sustainable food production in the future. We are only half way through our experiment and to ensure we get robust scientific results we need to continue the experiment next year and then get the data thoroughly analysed and independently peer reviewed for all to see. After all the great work done by Sense about Science this year, we hope next year's phase will pass without the threat to damage it."</i> </div>
</blockquote>
<blockquote style="font-family: Calibri;" type="cite">
<div>
Síle Lane, Sense About Science said<i>: "We were thrilled by the support for the researchers. We are still reading through the comments 6060 people left on the petition. This is ongoing research so it's good for the scientists to know there's so much support for them from so many people. The questions you sent us have been a great way to clarify the research and Frances Downey is going to continue this. If you have further questions get in touch with her at <a href="mailto:fdowney@senseaboutscience.org">fdowney@senseaboutscience.org</a>.”</i> </div>
</blockquote>
<blockquote style="font-family: Calibri;" type="cite">
<div>
We have gathered some of the comments of support for the researchers from petition signatories, politicians and high profile supporters here (PDF)<a href="http://www.warpmailbox.com/li.aspx?cu=4904699&link=63965">http://www.senseaboutscience.org/data/files/Dont_destroy_research/Dont_destroy_research_public_support_June_2012.pdf</a> </div>
</blockquote>
<blockquote style="font-family: Calibri;" type="cite">
<div>
The questions researchers worked hard to answer are here<a href="http://www.warpmailbox.com/li.aspx?cu=4904699&link=63966">http://www.senseaboutscience.org/pages/plant-science-qa.html</a> </div>
</blockquote>
<blockquote style="font-family: Calibri;" type="cite">
<div>
There’s a time line of the summer's events, including Rothamsted's offer to debate with Take the Flour Back before the protest, here:<a href="http://www.warpmailbox.com/li.aspx?cu=4904699&link=63967" target="_blank">http://www.rothamsted.ac.uk/Content.php?Section=AphidWheat&Page=Protest</a> </div>
</blockquote>
<blockquote style="font-family: Calibri;" type="cite">
<div>
Protestor Hector Christie was ordered to pay £3,850 in compensation to Rothamsted Research in August after breaking onto the site and causing property damage. He failed to disrupt the experiment: <a href="http://www.warpmailbox.com/li.aspx?cu=4904699&link=63968" target="_blank">http://www.bbc.co.uk/news/uk-england-19373852</a> </div>
</blockquote>
<blockquote style="font-family: Calibri;" type="cite">
<div>
If you would like to get general news from Sense About Science you can sign up for our newsletter here <a href="http://www.warpmailbox.com/li.aspx?cu=4904699&link=63969" moz-do-not-send="true">http://www.senseaboutscience.org/pages/support-us.html</a> and keep up to date with the fantastic work of the researchers at Rothamsted on their website<a href="http://www.warpmailbox.com/li.aspx?cu=4904699&link=63970" moz-do-not-send="true">http://www.rothamsted.ac.uk/</a></div>
</blockquote>
<blockquote class="tr_bq">
Thank you again for your support. </blockquote>
</div>
<div style="margin-bottom: 0px; margin-left: 0px; margin-right: 0px; margin-top: 0px;">
<br /></div>
daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com4tag:blogger.com,1999:blog-5995754777906978314.post-1313361155720885432012-05-11T21:54:00.001-07:002012-05-12T06:56:07.135-07:00BMI puts young Asian-American women at risk of being "skinny fat"As if we needed any more reason to pick on Body Mass Index (BMI): new research finds that this most accepted approach for assessing overweight and obesity based on height and weight could lead to misclassification of young Asian-American women as healthy when they're really "skinny fat," which could put them at greater risk for type 2 diabetes and cardiovascular disease.<br />
<br />
In my last <a href="http://evolvinghealthscience.blogspot.com/2012/05/nevermind-body-fat-put-focus-on-muscle.html">post</a>, I discussed the scary, growing problem of <i>sarcopenic obesity</i> (aka "skinny fat") in older adults, described as age-related muscle loss in combination with the accumulation of body fat. One common result of sarcopenic obesity is a misclassification using BMI as "normal-weight" in these aged individuals. Misclassification in older adults with sarcopenic obesity is just one reason why BMI is loathed by those interested in public health.<br />
<a name='more'></a><br />
Sadly, I learned at Experimental Biology, misclassification also occurs frequently across all ages depending on ethnicity. Asian Americans with normal weight sarcopenic obesity, for example, are often misclassified even in a college-aged population, according to nutritional epidemiologist <a href="http://nursing.ucla.edu/body.cfm?id=113&ref=179">Catherine Carpenter</a>, an associate professor from University of California, Los Angeles.<br />
<br />
In a symposium organized by the American Society for Nutrition to discuss the topic of obesity and BMI classification, Carpenter presented findings of a yet-to-be-published cross-sectional study that evaluated BMI and percent body fat measured by biolectrical impedance analysis among on the multi-ethnic college students on campus. The study's findings were that college-aged Asian American women were most likely to be misclassified by BMI.<br />
<br />
Kindly, Carpenter provided me with further details about the study after the event. The study included 940 college students recruited over four consecutive years. The average participant was 21.4 years old with an average normal weight BMI of 22.9 kilogram over meter squared (kg/m2). The average percent body fat was 24.8 percent. The ethnic samples consisted of four ethnic groups: 49 percent Asian, 23 percent Caucasian, 7 percent Hispanic, and 21 percent as Other.<br />
<br />
Among the college-age students, Asian-American women had the lowest BMI (21.5 kg/m2), but the second highest percent body fat (27.8 percent). In comparison, Hispanic women had the highest percent body fat (29.9 percent) and the highest BMI (23.5 kg/m2).<br />
<br />
These findings suggest Asian-American women are most likely to be misclassified by BMI, which could mean greater likelihood risk of normal-weight obesity gone unnoticed. Ultimately, greater risk of obesity-related chronic disease such as type 2 diabetes and cardiovascular disease is the result. <br />
<br />
No question, studies like these will continue to reveal the limitations of BMI. Once again, I'll repeat that it may be better to focus physical activity and amount of skeletal muscle mass (along with or maybe more than dietary calories or macronutrients like <a href="http://evolvinghealthscience.blogspot.com/2012/04/sugar-showdown-science-responds-to.html">sugar</a>) for prevention of obesity and chronic disease.<br />
<br />
Skeletal muscle is critical as a large site for fat burning, glucose disposal, and metabolic rate. Sarcopenia in college-age adults should be most disturbing! It's much easier to hold on to muscle than it is to gain it back. Prevention, as usual, is key; and, prevention can be achieved with daily physical activity and a balanced diet -- with sufficient daily intake of quality protein, especially after exercise and throughout the day.<br />
<br />
<span style="display: none;">sciseekclaimtoken-4fabbdce94baf</span>daviddespain.secrethttp://www.blogger.com/profile/13271527839470084409noreply@blogger.com1