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.

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 Catherine Carpenter, an associate professor from University of California, Los Angeles.

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.

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.

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).

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.

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 sugar) for prevention of obesity and chronic disease.

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.

sciseekclaimtoken-4fabbdce94baf

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.

The typical recommendations for adults as they lose muscle and gain weight by nutritionists is to simply exercise at least 30 minutes three times a week, eat fewer calories, and get the recommended daily intakes of protein (0.8 g per kg). But this advice has had little to offer for guarding against the heavy toll that time has on muscle. However, in the last few hours of Experimental Biology 2012 on April 25, I was fortunate enough to meet a scientist who gave a lecture on a different approach to overcoming anabolic resistance in aging.

 Kinesiologist Stuart Phillips, a professor McMaster University, is a lifelong athlete who has participated in several sports enjoying everything from hockey, football, rugby to swimming and triathlons. "Muscle has always been near and dear to my heart (no pun) and my passion," he told me via email after the event. "I don’t compete in sports much anymore except with my wife and my three boys (13, 10, and 7), who are my stiffest competition yet! So now it's about staying healthy, active, and maintaining my muscle mass, strength, and health and high-quality protein is a big part of that."

Anabolic resistance, as Phillips defines it, "is the inability of skeletal muscle in aged persons to mount a full protein synthetic response similar to that seen in the young. In other words, older people just don’t put the protein they eat into their muscles as efficiently as young people. That means as we age that our muscles gradually begin to make less protein and so out muscle mass declines otherwise called sarcopenia." But according to Phillips, the quality of protein and how much can make all the difference for holding on to muscle with age. Specifically proteins with a higher concentration of branched-chain amino acids including leucine are key to repairing and gaining muscle with age. That means a greater reliance on animal-sourced proteins like whey protein. Plant-based sources just don't cut it because of the difference in amino acid profile. Now, there's something to think about before ever considering a completely plant-based diet.

Phillips explains, for example, that soy is an excellent high quality protein as its PDCAAS (protein-digestibility corrected amino acid score) would suggest. But whey is superior for repairing and gaining muscle, as shown in several studies (1-4). Even milk protein (containing a combination of whey and casein) is better than soy for promoting lean mass gain (2; 3).

 "Our work, and that of other research groups also, suggests that it's the high leucine content of whey protein, which is an amino acid that is highly stimulatory for muscle protein synthesis and muscle growth," Phillips told me, "that along with all of the other ‘essential' (i.e., we need to eat them because we cannot make them ourselves) amino acids are present in just the right quantities to support an optimal rate of protein accretion."

Adults at an age past 60 will also need dietary protein in amounts that exceed RDIs, Phillips adds. Consuming greater quantities of proteins high in leucine such as whey can help aging adults "'overcome' (or at least minimize)" the anabolic resistance of aging and slow sarcopenia. "I'd never say you could reverse sarcopenia, but good food choices and good high-quality proteins, along with physical activity, are a big part of slowing it down!"

Exactly how much protein per day and when to get it? According to two dose-response studies by Phillips and his colleagues (5;6) young men required 20g of quality protein to maximally stimulate muscle synthesis after exercise; older men needed approximately double the dose, 40g, to gain the same maximal stimulation. That, Phillips thinks, suggests that the young should eat at least 20g per meal and older people 40g per meal.

 This is a far cry from the typical American diet of which usually consists of about 5-6g of protein at breakfast, 10-12g at lunch, and upwards of 60g at dinner. "That’s not the best way to hang onto your muscle mass," Phillips said.

 Exercise certainly is an important factor, too. Because it increases the sensitivity to leucine in muscles, Phillips suggests that it be physical activity needs to happen every day in aging adults. "In a sense, exercise, for a short-time, 'reverses' aging! In fact, what it really does is reverses the effects of inactivity, but oftentimes aging and inactivity are one and the same! So even aged muscle, when exercised, becomes sensitive to leucine and amino acids again." 

Summing up his advice, Phillips offers four steps to keep muscle (again, a critical metabolically active tissue), important to guard against sarcopenic obesity and chronic disease:

1. "Exercise and get some form of physical activity every day"
2. "Consume protein at levels higher than the current RDA" 
3. "Consume three equal protein-containing meals throughout the day containing at least 20g to 40g of high-quality protein" -- high quality meaning proteins high in BCAAS like whey, fish, or other animal-sourced proteins; simply put, most plant-based proteins have poor concentrations of BCAAs 
4. Lastly, "it should maybe go without saying, but fruits, vegetables, and dietary fiber are also important – I like the DASH [eating plan], for example, but with more protein." -- a DASH (Dietary Approaches to Stop Hypertension" eating plan is a diet rich in low-fat, low-sodium dairy products, fish, chicken, lean meats along with a large amount of whole grains, fruits, and vegetables. 

Ultimately, the research of Phillips and his colleagues could have large implications considering that the world's population of people ages 60 and older will reach an estimated two billion people by 2050 -- all who could benefit from holding on to muscle as long as possible.  

References provided by Dr. Phillips 


1. Burd NA, Yang Y, Moore DR, Tang JE, Tarnopolsky MA and Phillips SM. Greater stimulation of myofibrillar protein synthesis with ingestion of whey protein isolate v. micellar casein at rest and after resistance exercise in elderly men. Br J Nutr 1-5, 2012. 
2. Hartman JW, Tang JE, Wilkinson SB, Tarnopolsky MA, Lawrence RL, Fullerton AV and Phillips SM. Consumption of fat-free fluid milk after resistance exercise promotes greater lean mass accretion than does consumption of soy or carbohydrate in young, novice, male weightlifters. Am J Clin Nutr 86: 373-381, 2007. 
3. Josse AR, Tang JE, Tarnopolsky MA and Phillips SM. Body composition and strength changes in women with milk and resistance exercise. Med Sci Sports Exerc 42: 1122-1130, 2010. 
4. Tang JE, Moore DR, Kujbida GW, Tarnopolsky MA and Phillips SM. Ingestion of whey hydrolysate, casein, or soy protein isolate: effects on mixed muscle protein synthesis at rest and following resistance exercise in young men. J Appl Physiol 107: 987-992, 2009. 
5. Moore DR, Robinson MJ, Fry JL, Tang JE, Glover EI, Wilkinson SB, Prior T, Tarnopolsky MA and Phillips SM. Ingested protein dose response of muscle and albumin protein synthesis after resistance exercise in young men. Am J Clin Nutr 89: 161-168, 2009.

6. Yang Y, Breen L, Burd NA, Hector AJ, Churchward-Venne TA, Josse AR, Tarnopolsky MA and Phillips SM. Resistance exercise enhances myofibrillar protein synthesis with graded intakes of whey protein in older men. Br J Nutr 1-9, 2012.

Holding on to brain function through nutrition

By the year 2050, the number of people in the world over 80 years old will reach 370 million. About 50 percent of adults currently 85 and older have Alzheimer’s disease. The statistics are sobering and warn of a growing and serious epidemic. A high prevalence of Alzheimer’s disease, which is a debilitating and costly disease, can severely impact the population.

With this perspective, the American Society for Nutrition hosted a symposium on the nutritional prevention of cognitive decline on Wednesday at Experimental Biology in San Diego. At the event, speakers presented a comprehensive overview of epidemiological, animal, and clinical trials regarding the role of B vitamins, omega-3s, vitamin D, and caffeinated beverages such as coffee and tea in the prevention and treatment of cognitive impairment.

Martha Morris, Ph.D., an epidemiologist at Tufts University, discussed the relationship of folic acid, B12, and homocysteine to age-related cognitive decline, dementia, and Alzheimer’s disease. In summary, she said, the evidence suggests that sufficient B12 intake could protect against cognitive decline related to elevated levels of homocysteine. However, once B12 status was replete, there was no further protection.

The next speaker to follow was Lenore Arab, Ph.D., nutritional epidemiologist at University of California, Los Angeles, who presented on the effects of caffeinated beverages coffee and tea. The popular drinks, of which many in attendance wished for during the early morning talk, showed promise in helping to slow cognitive decline according to evidence from observational, animal, and clinical data.

Tommy Cederholm, M.D., Ph.D., of Uppsala Universitet, Sweden, discussed the large amount of epidemiological studies and human clinical trials exploring the role of omega-3s. The data suggest plenty of biological mechanisms such as reducing inflammation and protection against amyloid-beta protein deposits.

"Fish is good for your brain," Dr. Cederholm said, noting that intake may assist in early stages of cognitive impairment. However, he added, intake did not appear to assist in patients who already had Alzheimer's disease.

Lastly, Joshua Miller, Ph.D., a professor of pathology of University of California, Davis, discussed new research findings that vitamin D played a major role in the brain development and function. The epidemiological and animal studies suggest a positive effect in the prevention or treatment of cognitive impairment, he said, but randomized controlled trials in humans were lacking. Unlike other micronutrients, he added, vitamin D has a complexity because of seasonal variation, which suggests it's important to measure both in summer and in winter when performing studies.

How to fight "job-esity"

Workplace programs are an effective and worthwhile way for employers to help improve the health of their employees and reduce medical costs, scientists said Tuesday at Experimental Biology 2012 in San Diego at a session organized by the American Society for Nutrition. 

The medical expenses for employees who are obese are estimated at about 42 percent higher than for those with a healthy weight, according to the Centers for Disease Control and Prevention. Yet for the approximately 60 percent of Americans who are employed, it may be the workplace itself that is at the root of weight gain in the first place.

Shirley Beresford, Ph.D., professor of epidemiology of University of Washington, expressed optimism that workplace obesity programs could help reduce obesity based on a history of research. She explained that programs offered a way for employers to partner in intervention; however, she noted that the enthusiasm of employees for behavioral change may fall short.

The trouble with the workplace of Americans is that too often the mix of job insecurity, stress, sedentary behavior, and social eating present an "obesogenic environment," said Sai Krupa Das, Ph.D., assistant professor at the Friedman School of Nutrition Science and Policy, Tufts University.

Preliminary findings of the Tufts Healthy Weight Study offered a more promising picture for workplace intervention, Das said. The study resulted in substantial weight loss at six months that was sustained for at least a year.

Among the reasons why the intervention worked, Das said, are multiple components: encouraging physical activity combined with diet instead of either alone, behavioral counseling versus educational approaches, a high intensity versus a moderate intensity support group, and a structured maintenance protocol versus an unstructured self-directed program.

"These promising practices provide a broad framework for going forward," Das said. "We had a very robust intervention."

A workplace intervention program is likely to be cost effective for companies, according to economist Chad Meyerhoefer, Ph.D., an assistant professor of Lehigh University. In his presentation on cost-benefit projections for healthcare savings for employers, he gave the estimate that for every 5 pounds of weight loss the savings could range from $30 to $80 per person annually.  

William Dietz, Ph.D., director of the division of nutrition, physical, and obesity at the CDC, discussed a toolkit named LEAN Works! that was developed to promote worksite interventions. To set the example "at home," Dietz said, The toolkit was adopted on CDC campus. 

"We focused on changes on the environment," he said. For example, the campus featured music in stairwells to encourage their use, conducted a walkability audit, redesigned the campus to be more walkable, and installed lactation rooms. In addition, the CDC introduced fruit-and-vegetable vendors on campus so that employees could buy fresh produce once a week, made campuses smoke-free, and installed "lifestyle centers" (gyms).

The future of nutrition research

There is little question that nutrition provides the foundation of health and wellbeing and that research into better nutrition is central to enabling a population live healthier, more productive, and longer lives.

With this perspective in mind, the American Society for Nutrition assembled a working group of leading nutrition thought leaders to identify a list of nutritional research areas that required greater or further analysis and prioritization.

In a symposium entitled "The Future of Nutrition Research" on Tuesday at Experimental Biology 2012 (#EB2012), these thought leaders outlined what was generally agreed as the six areas of nutrition research that deserved attention.
The areas of the research comprised of the following:

1. Understand variability in responses to diet and food—a broad area that includes research in epigenetics, proteomics, and metabolomics.
2. Understand the nutritional impact on healthy growth, development, and reproduction
3. The role of nutrition in health maintenance—with emphasis in determining how nutrition and fitness play into optimal health of the body (immune, cognitive, skeletal, and muscular function) over a lifespan.
4. The role of nutrition in medical management—how nutritional factors influence disease and response to therapy.
5. Nutrition-related behaviors—identifying how food choices can affect or become imprinted on the brain.
6. Understanding the food supply environment—investigating the “farm to fork” influence on diet and physical activity and how biotech and nanotech can play a role.

The group also identified five tools in need of further development of which would be required to overcome barriers of nutrition research. The following tools, they said, would enhance the efficiency of research in each of the six areas listed above.

1. Databases—for collection and assessment of food intake data.
2. Biomarkers—needed to improve tracking and monitoring of food intake and response to treatments.
3. Omics—biomarkers that provide data on how genes interact with nutrients, their metabolites, and proteins.
4. Bioinformatics—application of computer science in biology and medicine.
5. Cost-benefit analysis—tools to calculate and compare costs of interventions.

The multi-disciplinary working group included John Milner, of the National Cancer Institute, Dennis Bier of Children’s Nutrition Research Center, Houston, Catherine Ross of Penn State University, Z. Li of University of California, Los Angeles, David Klurfeld, of USDA, J Mein of Monsanto, and Pat Stover of Cornell University. Each of the individuals of the group presented about their respective areas.

A way forward: Meeting vitamin and mineral needs globally

Lindsay Allen

Efforts to curb or eliminate vitamin and mineral deficiencies globally have existed for almost a century, although there are now still as many questions if not more than ever before about what the next steps should be. There are seldom solutions that are simple to guide public policy internationally and there remain large challenges when it comes to making informed recommendations. 

Lindsay Allen, Ph.D., R.D, who is the 2012-2013 recipient of the E. V. McCollum International Lectureship in Nutrition, discussed a new way forward to improve the health of infants, children, and pregnant women internationally on April 22 at the McCollum Lecture organized by the American Society for Nutrition at Experimental Biology 2012 in San Diego. She currently serves as the Center Director of the USDA, ARS Western Human Nutrition Research Center. 

She discussed the challenges faced in global research and policy on micronutrient deficiencies as well as new methodologies on the horizon to improve research. She also called for the bringing together of more nutritional biology expertise—such that was present at the meeting—to assist in overcoming the difficulties in nutritional research such as ethical considerations when performing intervention studies in pregnant women and children.

In her presentation, Allen pointed out that modern technologies could assist in surmounting the unreasoned differences in recommendations of micronutrient intake such as that of iron or folic acid from one age to another either upwards or downwards. For example, there are measurements now available that can make use of samples of saliva, hair, or urine.

"I think that the methods we have been using like growth of babies, biochemical markers in blood are just not picking up changes in metabolism and immune function," she said. "You have these special tools to do genomics, metabolomics, and looking at gut microbiota. If we can draw in the expertise and ideas as well of people in the society and put all those different things in context of the studies we have ongoing, then we can really understand what’s happening when we give micronutrients to people."

She added, "The way forward is to bring that kind of expertise into the kind of rigorous field work that people are doing in developing countries.”

Another next step proposed by Allen is to encourage more basic nutritional science to be done in the United States of which could have an impact on health across the globe. For example, she said, there is more research needed in how micronutrients are absorbed in the diet and how micronutrients interact with each other. 

Moreover, Allen noted, there exists a greater need for research in methods development. For example, the development isotope analysis could bring new tools for use in international micronutrient deficiency research.

Former E.V. McCollum lecturer Andrew Prentice, Ph.D., who introduced and closed the lecture, called Allen’s presentation a "comprehensive tour de force" of micronutrient research and policy. He said Allen proposals presented a more agnostic approach to micronutrient research versus having various camps, such as the zinc promotional camp or iron or vitamin A. The key is to ask questions more intelligently.

"It would be so lovely if we could come up with very simple solutions and say we know that this is the policy process that we should undertake. It’s just a matter of implementing it," Prentice said. "In one or two cases that is true. Vitamin A supplementation of children has very clear-cut benefits. But with most of the other micronutrients we really don't know what to do, in whom to do it, at what levels to do it, and what would be the benefits."

Read more about Allen's talk in Nutrition Notes Daily, a publication circulated by the American Society for Nutrition.

Sugar Showdown: Science Responds to "Fructophobia"

The scientific community lashed out against "sugar is toxic" sensationalism on Sunday, April 22, identifying it as a distraction from more meaningful areas of research and debate on the causes of obesity and disease.

In a highly attended debate at Experimental Biology 2012 in San Diego sponsored by the Corn Refiners Association, scientists expressed clear frustration about the repeated assaults on sugar both in recentnews reports and in the scientific literature.

"You don't often see this at a meeting," said John White, Ph.D., of White Technical Research, to me after the event, referring to what he said was "the groundswell of researchers pushing back" against inflammatory remarks and overstatements.

The symposium organized by the American Society for Nutrition showcased both sides of the controversy surrounding the metabolic effects and health implications of sugar—fructose, sucrose, and high-fructose corn syrup—using latest available and emerging scientific findings.

As the first presenter, White presented data from the National Health and Nutrition Examination Surveys showing that no correlation existed between total fructose and the prevalence of obesity and that total added sugars and intake of sugar-sweetened beverages have declined for more than a decade.

"The support for fructose as a metabolic threat at current levels of intake is weak," White affirmed.

White also made the point that high-fructose corn syrup and sucrose are not different, suggesting the former might've been more appropriately called "medium-fructose corn syrup" because of its similarity to table sugar and other sugars.

Presenting a contrasting view, George Bray, M.D., chief division of clinical obesity and metabolism, showed data that soft drink consumption had increased from 1950 to 2000. Sugar-sweetened beverages, he argued, provide add-on calories that lead to weight gain, particularly from intra-abdominal fat.

In what promised to be a highly charged attack on sugar, characteristic of his appearance in media reports, Robert Lustig, M.D., began with a title slide displaying: "Fructose: alcohol without the 'buzz'". He argued that fructose metabolism was similar to that of ethanol's and that a "beer belly" was not far off from a "soda belly."

In his limited time, fast-talking Dr. Lustig quickly explained metabolic pathways and repeated remarks that fructose may be addicting to the brain like ethanol, based on animal research, and that fructose may be several times more likely than glucose to form advanced-glycation end products (a hallmark feature of uncontrolled diabetes).

Next to speak was cardiologist James Rippe, M.D., who presented a convincing argument that while fructose alone may have "qualitative differences," they were not "quantitative differences." He argued that research comparing pure fructose to pure glucose was not relevant to human nutrition. 

Sharing White's viewpoint, Dr. Rippe added that there were no metabolic differences between the sugars or fructose by itself—that is, there are no clinically meaningful effects on blood lipids at levels consumed by people normally, and no effects on uric acid or blood pressure.

He said the hot topic was an emotional issue creating a "perfect storm" for mistaken identity.

Dr. Rippe said afterward that Dr. Lustig's logic about fructose being uniquely responsible for disease was like going into "an alternate universe" that just did not stand up to scientific scrutiny. Yet it garners attention because of the public's habit of playing "the blame game" mixed with misconceptions about high-fructose corn syrup.

"People called him on it today," Rippe told me. By going to the media directly, he said, Dr. Lustig didn't have to have the same standards of proof that scientists usually must have. 

The last presenter was David Klurfeld, Ph.D., of the United States Department of Agriculture, who rounded out the debate again affirming that there was no evidence suggesting that sugar presented a unique metabolic danger.

"Is there a metabolic difference between sugars? Of course," Klurfeld said, "Is it biologically meaningful?" The answer was that it wasn't, according to the available evidence.

"The dose makes the poison," Klurfeld added. Should there be sugar regulation or taxation? There is insufficient data to justify any decision, Klurfeld said, quipping that whole milk would be next.

A question-and-answer period followed the debate giving a voice to disgruntled attendees who called Dr. Lustig out for suggesting that sugar was a metabolic danger. Dr. Lustig agreed that "everything can be toxic" at a dose, but sugar is abused and addictive.

One commenter (later identified as Richard Black, Ph.D., of Kraft Foods) responded saying that media should stop comparing sugar to cocaine by showing images where the brain lights up in the same areas. "The brain is supposed to light up in response to food," he said.

In an amusing but perhaps humbling moment for Dr. Lustig, he singled out the commenter asking if he had children. The commenter responded that he did. Dr. Lustig then asked him if as infants his children more easily liked sweet foods. The commenter said that, yes, of course they did because breast milk was sweet. Dr. Lustig replied that it was not. His reply caused an immediate reaction (notably, from mostly women) in the room who voiced in unison, "Yes, it is!"

John Sievenpiper, M.D., of St. Michael's Hospital told me after the event he was pleased that the speakers framed their arguments in a way that put the controversy in perspective. As shown in recent meta-analyses of which he co-authored, fructose demonstrated no significant effect on body weight or blood pressure in calorie-controlled trials. Fructose also demonstrated improvement of glycemic control at levels comparable to that obtained in fruit.

"It's hard to change people's minds," Dr. Sievenpiper said, stating concern that people would reduce intake of fruit in response to fears about the metabolic effects of fructose.

Don't miss this Storify story from folks on Twitter using the #sugarshowdown hashtag during the debate. Also, check out video blogger Emily Tomayko's recap on the ASN blog here.

Update 24-May-12: As a follow-up to this report, I've posted an interview with Dr. Sievenpiper here. Hopefully, it will help bring more clarity to the issues and answer several questions people have. If you wish to comment, please do so after reading that post. I've now closed comments on this blog post. 

Update 8-June-12: Check out videos (just published) of each of the talks. Here they are: White, Lustig, Bray, Rippe, and Klurfeld. Oh, and there is a video of the Q&A too. 

Beyond calories in, calories out -- look to the Amish

What is wrong with "eat less, move more"? Most of us are familiar with this mantra as weight-loss advice. However, a new consensus statement from the American Society for Nutrition (ASN) and the International Life Sciences Institute (ILSI) contends that this energy-in-energy-out framework isn't really so simple.

The problem lies in that consuming fewer calories and burning more through physical activity doesn’t always translate well to weight management. That is not to say that the framework of energy balance—negative energy balance for weight loss; positive energy balance for weight—is wrong. At some level, it’s right; however, several factors come into the equation.

During a Saturday morning session of Experimental Biology (#EB2012) in San Diego, Calif., researchers discussed the topic of this complexity and promoting a new paradigm on energy balance.

Energy balance is not just about addition of diet and exercise; each affects the other, so that changing one changes the others, explained Jim Hill, professor of pediatrics and medicine at the University of Colorado School of Medicine, Denver, and new recipient of the W.O. Atwater Lectureship awarded by the American Society for Nutrition.

What must be appreciated is the body's system of active regulation, he said.

"It's not just a little man in your head that," he said, adding that the body may rely on a 'set point' or 'settling point' type of system that attempts to balance energy, energy stores, glucose, glycogen, fat stores, and temperature.

"You might argue that up to the 1970s, the system worked pretty well," Hill said. "This whole system is based on inherited factors. If you look at what’s really changed since the 70s, it's really the environmental factors. We don't have to hunt and kill our food anymore. We go to the supermarket and fill our carts. We also sit in some form of fashion every day."

Obesity, a problem of overwhelmed "active regulation"

Most of these environmental influences are designed to increase energy intake. It becomes more difficult to avoid overeating and underactivity. These influences, summed up, overwhelm active regulation and the body’s energy balance system. Then the body's physiology adjusts.

Are there things in the food supply that cause to eat more? Are they influences that affect our brains and nervous system? Hill said that however they may affect us, it is still through energy balance. He said he "laughs every time" he sees studies questioning whether the rise of obesity epidemic is related to energy intake or expenditure.

"Diet and physical activity interact," he said. "Please don't ask if it's diet or physical activity. The answer is 'yes'."

What wrong with diets? No matter which diet, Hill said, the results are always the same: Body weight may increase, may not change, or may decrease. The inconsistent outcomes may be because of poor compliance, physical activity, metabolic rate differences, or food intake adjustments. Eventually, what goes wrong is that environment affects behavior so strongly that over time that people are gaining a little weight. They don’t gain a lot, but they gain about a pound or two a year with some push back from their active regulation systems.

One way to combat the obesity epidemic is by encouraging an environment more like that of a half a century ago, Hill said. How the old order Amish live today is a good example.

"The Amish walk 18 thousand steps a day. They don’t have spandex or a gym membership. That explains about 400 to 600 calories a day. A typical person in the U.S. walks only five to six thousand steps a day," Hill said.

Hill suggests preventing weight gain with small steps—or, more specifically, 2 thousand steps daily.

"We have a poor ability to maintain weight loss, but we have a better ability to prevent weight loss,” he said. “This is why we started a movement to move. Two-thousand steps a day is not going to create weight loss, but might prevent weight gain."

What role can small changes play in an environment where we need bigger systemic changes? Hill argues that it will "set the table" for bigger change. Another factor may be that it may help to improve performance or "reset" active regulation.

"Our biology works best at high levels of physical activity. Obesity is in the 'unregulated zone.' When physical activity increases, you enter 'regulated zone'. Physical activity may help the 'regulatory system' work better."

Stealth health

Until bigger changes can be created in the environment, Hill is a fan of "stealth health" strategies for reducing obesity. That is, finding ways of encouraging better energy in, energy out balance without the public noticing.

For example, Hill explains, at Disney parks and at Starbucks, drinks are now made with low-fat milk. Does anyone notice the difference? What about portion sizes? Would anyone notice a 5 percent reduction at restaurants?

Another idea Hill proposed was that of regulation of school drop offs—so that they would be 500 steps away from the school. Would it be so far that the children would notice a difference?

The implementation of these "stealth health" strategies would increase physical activity and reduce overeating. Combined with teaching children energy balance skills, it could reduce childhood and overall obesity.

What also may be important is to combine both diet and physical activity guidelines for society? But how can this be achieved when studies show that energy balance is such a dynamic versus static process?

Learn more about the questions raised about energy balance at Experimental Biology from the American Society for Nutrition’s cover page story in Nutrition Notes Daily. 

Can carotenoids in the brain protect against Alzheimer’s?

Carotenoids are thought to protect against Alzheimer's disease because of their antioxidant properties and their accumulation in the brain. However, a new study from Tufts University is putting the theory into question.

More than a century has passed since the German physician Dr. Alois Alzheimer first presented evidence on the case of Auguste Deter, who at only 51 suffered from severe memory loss and other psychological changes. At autopsy, Dr. Alzheimer found his patient had severe shrinkage and abnormal deposits of the nerve cells.

"That was in 1906," said nutritionist Annie Roe, a USDA researcher at Tufts University, who presented her laboratory's findings on April 21 at Experimental Biology 2012 in San Diego. "There's still disparity among scientists as to the etiology of this rapidly growing disease as we now know as Alzheimer's disease."

Currently, in the United States there are 5.3 million people with Alzheimer's disease. Unless new methods of intervention are available, however, the number is expected to reach 16 million by 2050. While the cause of the disease is not known, the deposits that Dr. Alzheimer first noted are now known to be amyloid-beta peptide deposits.

These deposits, or plaques, are a "hallmark diagnostic feature" of Alzheimer’s disease. Within the same region amyloid-beta plaques are found, increased concentrations of oxidized proteins, lipids DNA are also observed. It’s not yet clear whether or not that these products of oxidative stress caused the amyloid-beta plaque build-up or vice versa.

However, Roe said, it is clear that oxidative damage promotes neurotoxicity and is involved in cognitive impairment. Epidemiological studies have found that a higher dietary intake of carotenoids from fruits and vegetables are associated with reduced risk of age-related chronic diseases including Alzheimer’s disease. Other studies measuring the concentration of carotenoids in plasma have found an inverse relationship with chronic diseases.

Fruits and vegetables are the major sources of carotenoids in the diet, the most common of which are beta-carotene and beta-cryptoxanthin—two provitamin-A carotenoids. There is also lycopene, lutein, and zeaxanthin, which have no vitamin A activity. There are several biological mechanisms being explored for carotenoids' potential protection to the brain.

However, Roe explained that her laboratory research focuses on the role of antioxidants and their relationship to Alzheimer's disease, clinically determined by increased cognitive impairment. Since Alzheimer's affects brain tissue, the researchers' study purpose was to determine the concentration and magnitude of lipid peroxidation in brains diagnosed with Alzheimer’s disease compared with age-matched controls.

The Tufts laboratory received brain tissue samples from the National Institute for Child Health and Human Development (NICHD) Brain and Tissue Bank for Developmental Disorders. The samples were obtained from 15 individuals with Alzheimer’s disease and half with no known dementia. The samples were from subjects in their late 70s or early 80s, most of whom were Caucasians. The samples were of four different brain regions: occipital cortex, frontal cortex, hippocampus, and auditory cortex. To assess lipid peroxidation, the researchers extracted malondialdehyde (MDA)—a marker of oxidative damage—through HPLC.

When looking at relative distribution of major carotenoids between Alzheimer’s disease and controls, the study found the provitamin A carotenoids contributed to a significantly higher percentage of total carotenoids in the Alzheimer’s brains compared to the controls. Non-provitamin-A carotenoids contributed to higher concentration in control brains compared to Alzheimer’s disease brains, but there was no statistically significant difference.

In addition, Roe said, the absolute concentrations of provitamin-A carotenoids were higher in Alzheimer’s diseased samples versus control samples. There was no difference in absolute concentrations of lutein, zeaxanthin, or lycopene. There was also no significant difference between malondialdehyde concentrations and carotenoid concentrations.

Consistent with findings of increased pro-vitamin A carotenoids, retinol (vitamin A) concentration was significantly greater in the Alzheimer’s disease brains. However, when the study looked at malondialdehyde concentrations, there was not a significant difference between the two groups.

The findings "were interesting but unexpected," Roe said, adding that when she looked at each region separately, she saw the same pattern in the hippocampus, a region that is highly vulnerable to the disease.

Since prior research has shown both in cell culture and in clinical studies that vitamin A can have a positive effect on beta-amyloid aggregation, it is possible that caregivers or physicians confounded results. For example, they may have encouraged their patients after diagnosis to consume more fruits and vegetables. It may be that carotenoids are beneficial to the brain, but simply not after the disease has set in. Roe suggests future studies should include dietary intake assessments and target people with earlier stages of dementia.

"This is just a snapshot view of a small group of people at the end of life, so we can't infer any type of causation and certainly should not interpret the results to mean that vitamin A is bad for the brain," Roe said.

The study's results contradicted that of previous research, also presented at the conference by Neal Craft of Craft Technologies, which found an age-related decline of carotenoids in elderly brains that suggested that diminishing levels may be associated with Alzheimer's disease.

New and old tools of science communications

Sci-comm thrives on social media. 

"Writing is thinking on paper" is one of the many beautiful phrases by William Zinsser, author of On Writing Well. Only, if Zinsser had put those words down more than three decades later, he might have added that writing is also thinking on blogs, Twitter, Facebook, and Google+.

As I prepare to head off to San Diego for Experimental Biology (#EB2012)—where I’ll be blogging about The American Society for Nutrition's meeting—I’ve been thinking a good deal about Zinsser’s phrase and about Mary Canady's (@comprendia) call for those attending #EB2012Tweetup to share their new media science communications success stories. My own story begins with me simply blogging and tweeting as a way to think and as a way to remember what it was that I thought. 

I learned early on that I was never very good at thinking about new information clearly or remembering my thoughts later—unless I wrote my thoughts down. So, I originally began to write (as I'm sure many writers do) as simply a way to make sense of the world around me. Writing then became part of my education and eventually led to a profession in science writing (see "About David").

Why do I now blog and tweet about health? At first, I simply found blogging was a good way to take notes on new tidbits I was learning about as part of my master’s degree in human nutrition. Later, when I started attending science conferences, I discovered tweeting combined with blogging became a way to engage and network with the smart, like-minded people around me. I found that these new social media tools represented excellent ways to encourage discussion and debate about science. And, especially as it comes to health-related science, healthy skepticism is key.

 For these reasons, I often encourage others to blog and tweet—scientists and non-scientists alike—about topics such as food, nutrition, and medicine. Social media tools are the perfect avenues by which science can thrive. After all, science itself is all about collecting data, sharing information, and establishing consensus.

 It's also the engagement with science-minded people, the discussion, and, sometimes, the argument that encourages me to continue to blog. Most of all, it's the collective thinking. Thinking, after all, will always be a part of writing however or wherever it is done.

As Zinsser himself points out in the introduction of his 30-year anniversary edition of his classic, "I don't know what still newer marvels will make writing twice as easy in the next 30 years. But I do know they won’t make writing twice as good. That will still require plain old hard thinking… and the plain old tools of the English language."

Blogging the ASN Meeting at EB 2012

Welcome new followers!

I'm excited to report that I've been selected as official blogger for The American Society for Nutrition (ASN) 76th Scientific Sessions and Annual Meeting in conjunction with Experimental Biology 2012 (EB 2012) on April 21 through 25 in San Diego, Calif.

Click here for a peek at the preliminary program.

What exactly is EB 2012? The conference is a highly anticipated annual event where six scientific societies hold their joint scientific sessions and annual meetings. Besides ASN, other societies represented are: the American Association of Anatomists (AAA), the American Physiological Society (APS), the American Society for Biochemistry and Molecular Biology(ASBMB), the American Society for Investigative Pathology (ASIP), and the American Society for Pharmacology and Experimental Therapeutics (ASPET).

The conference attracts leading researchers from several different life-science disciplines. There will be new findings presented and it is sure to be interesting!

So, for EB 2012 updates, be sure to stop by this blog during the conference April 21 through 25. You can also follow my tweets at @daviddespain. I will be covering the ASN portion of the meeting, which will be about all the latest developments in nutrition science. Nutrition science -- that's my thing. You can also follow ASN official updates on Twitter at both @nutritionorg and @BioactivesRIS (the Dietary Bioactive Components Research Interest Section). UPDATE 3-28-12: Another Twitter account to follow is @NutImmRIS (Nutritional Immunology Research Interest Section.

If you're interested in more, be sure to follow the updates of other meeting bloggers/writers including these fine people:

• Donna Krupa, @phyziochick: Communications Director, American Physiological Society 
• Cara Santa Maria, @carasantamaria: Huffington Post science correspondent 
• Heather Doran, @hapsci: the official meeting blogger for ASBMB 
• Scicurious, @scicurious: the official meeting blogger for The American Society for Pharmacology and Experimental Therapeutics 
• Kelly Warren: science writer 
• Geoff Hunt, @GoodbyeShoe: outreach coordinator for ASBMB 
• Angela Hopp, @angelahopp: editor for ASBMB Today 

Lastly, if you're a meeting attendee or someone who simply wants to stay on top of all EB 2012 news, don't forget to use the Twitter hashtag #EB2012 during the meeting.