What journalists should know before writing about fructophobia

"Pick your poison" Sugars by vavroom, on Flickr

In his new book, Fat Chance, 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.

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 article 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?

Why you can all stop saying meat eating fueled evolution of larger brains right now

Hadza returning from hunt in Tanzania. Credit Andy Lederer.

In William Shakespeare's comedy Twelfth Night, 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.

On November 15th's episode of The Colbert Report, Stephen Colbert interviewed one of the world's foremost paleoanthropologists, Chris Stringer of the Natural History Museum, about his newly published book. During their conversation, Stringer sums up nicely why meat eating may have been the primary force that drove evolution of a brain-gut tradeoff, where a shrinking gut allowed for more energy input into the brain. Here is Stringer's explanation at about minute 18:30 in the episode:

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."

Stephen Colbert: "That's why vegetarianism seems so stupid to me."

Human vs. chimps: What the "regulome" tells us about meat eating & bigger brains

Source: Greg Wray

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.

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.

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" annual conference in Durham, North Carolina, Wray said that the Encyclopedia of DNA Elements (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.

Food is "star stuff"

Champagne supernova. Credit: Space Daily

"If you want to make an apple pie from scratch, you must first invent the universe."

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 Cosmos: A Personal Voyage.

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 chemistry of life, our own evolution, and to that of our close cousins, then on to our current situation, and the future, this blog has explored all sorts of topics relating to diet and health in the past and forthcoming.

Why lemurs get sick: A lesson for humans, too

Female blue-eyed lemur

What lessons can humans learn from our far distant prosimian primate cousins about living well and eating a healthy diet?

This was the question on my mind as I toured the Duke Lemur Center in Durham, North Carolina with colleagues attending Science Writers 2012. (Read Christie Wilcox’s full report about our tour over at Science Sushi on Scientific American.)

When I learned on the tour that lemurs were getting sick, I inquired further from our tour guides, education associate Chris Smith 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.

Of bunnies and bacteria

I remember when I first learned that a rabbit ate its food twice.

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.

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.

Why aren't we talking about organic GMOs? And, why can't we all get along?

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 divisive talk, the reasoned talk, and the rat-shi# crazy talk.

What I want to ask is this: Why aren't there more people, beyond scientists and academics, talking about organically grown GMOs? 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.

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 phosphorus 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.

Making lazy, stupid plants work harder

Plants with larger root systems take up minerals more easily.

Plants these days. They're coddled, entitled, fed with a silver spoon.

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.

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.

"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.

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.

When I won't accept a guest post

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.

Sievenpiper: Fructose should not "worry" in diabetes

As 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.

Even health professionals and organizations like the American Diabetes Association have taken a cautious approach 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.

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.)

Changes in genetic expression during weight loss and weight maintenance

by Amanda Jensen* 

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?

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.

Videos from the EB2012 Sugar Showdown and a Few Comments from Dr. Lustig

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 Storify story in case you missed it). The event was sponsored by the Corn Refiners Association.  

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.

One of those scientists was Dr. John Sievenpiper, of St. Michael's Hospital, University of Toronto, who told me in an interview 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."

Why a fat brain made us more vulnerable to heart disease

Natural 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.

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 de novo, 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.

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.

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.

Good insulin, bad insulin: Its role in obesity?

Gary Taubes makes insulin out to be a bad guy. In his latest article in Newsweek Magazine commenting on HBO's Weight of the Nation documentary, he once again challenges energy balance (energy intake versus energy expended) as a paradigm for understanding obesity. The author of Good Calories, Bad Calories 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."

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.

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 or 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.

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.

Fate of fructose: Interview with Dr. John Sievenpiper

Fructose metabolism. Ref: Tappy & Ka 2010.

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 rant post about media reporting unfairly that hummingbird fuel 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.

As a follow-up to my report 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.

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.

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:

Have a cuppa pesticide and #dontdestroyresearch

Earlier today, biologist Mary Mangan (@mem_somerville) 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 here).

Mangan wrote on her Google+ page:

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.

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:

Confusing messages about sugar are stupid

I'm a bit late in weighing into the "Sugar Makes You Stupid" mess of poor health reporting on a rat study. At the Embargo Watch blog, Ivan Oransky already covered the mishandling of the study's embargo and ripped into the press release for misleading readers into believing that the study had any meaningful conclusions for college students. Then, Deborah Blum at Knight Science Journalism Tracker went further, bringing more reason and logic, by clarifying what the rat study was really about -- the neuroprotective role of omega-3 fatty acids!

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 hummingbird fuel, aka sugar, will make people walk around aimlessly as brainless as zombies. It's nonsense, of course, that sugar makes you stupid. 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.

What environmental groups don't understand about biotech

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.

- Charles Darwin

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 website, 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.

In an interview 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.

BMI 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.

In my last post, I discussed the scary, growing problem of sarcopenic obesity (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.

Nevermind body fat; put focus on muscle with age

With all the attention given to body fat, a result of the high prevalence of obesity and type 2 diabetes, skeletal muscle is often given the back seat. Yet holding on to lean muscle mass alone, in itself, may be the most important factor in avoiding health problems above. What's often forgotten is that skeletal muscle is a metabolically active tissue that plays a critical role in consuming energy and determining metabolic rate, it's the large site for fat burning, and it's a primary site for blood glucose disposal. It's time to give muscle its due.

When you reach age 60 or older, it gets harder to keep, let alone build, muscle. The reasons are a combination of lack of energy, exercise, dietary protein, and hormones. One more is a blunted protein synthesis response that is described as anabolic resistance in aging. Left to run their course, these factors eventually bring on a decrease of muscle mass over time, or sarcopenia. The loss is also often accompanied with an increase in fat mass, or sarcopenic obesity. Sarcopenic obesity brings along with it the lack of both mobility and physical function, with compounding effects, that eventually lead to increased risk of chronic disease.