30 May 2012

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.

27 May 2012

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.

26 May 2012

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:

20 May 2012

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:

18 May 2012

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.

13 May 2012

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.

11 May 2012

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.

05 May 2012

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.