Category Archives: Diet and Nutrition

The Delectable Myths of Healthy and Healthier Obesity.

by Kenneth W. Krause.

Kenneth W. Krause is a contributing editor and “Science Watch” columnist for the Skeptical Inquirer.  Formerly a contributing editor and books columnist for the Humanist, Kenneth contributes frequently to Skeptic as well. He can be contracted at


Why, sometimes I’ve believed as many as six impossible things before breakfast.–The Queen, to Alice in Through the Looking Glass.

Wouldn’t it be splendid to have our cakes and eat them too? Arguably, both ideology and popular culture allow their followers to do just that.  Until they don’t, of course.  At that point, when facts and logic can no longer be denied, the rudely awakened find themselves confronted with difficult choices.

The concept of healthy obesity, for example, has gained much traction during the last fifteen years. At one end of the continuum, members of the popular but clearly flawed “Healthy at Every Size (HAES)” movement profess the nonexistence of excess adiposity and suggest that even the most obese people can lead perfectly healthy lives (“Every size”—really?).  On the other end, and somewhat more credibly, others allege the existence of an “obesity paradox” and a “metabolically healthy obesity.”  Such are the tantalizing subjects of this column.

Cardiologist and obesity researcher, Carl J. Lavie, has described the paradox as follows: “Overweight and moderately obese patients with certain chronic diseases … often live longer and fare better than normal-weight patients with the same ailments” (Lavie 2014). In addition to his own research, Lavie’s conclusions are based on a revolutionary and, in some circles, much-celebrated JAMA study led by Katherine Flegal at the US Centers for Disease Control and Prevention, who reviewed 97 studies of more than 2.88 million individuals to calculate all-cause mortality hazard ratios for standard body mass index (BMI) classifications (Flegal et al. 2013).

Katherine Flegal

Katherine Flegal

Flegal’s team reported as follows: Relative to normal weight, all combined grades of obesity were associated with an 18 percent higher incidence of all-cause mortality. In cases of more extreme of obesity, the association rose to 29 percent.  By itself, however, the mildest grade of obesity was not correlated with a significantly elevated risk, and the overweight but not obese category was actually associated with a 6 percent lower incidence of all-cause mortality.  Predictably, the popular media quickly seized on the overweight population’s presumed appetite for these tempting results.


Metabolically healthy, or “benign,” obesity, on the other hand—which Lavie dubs the “ultimate paradox”—appears to have no standard definition or list of qualifying criteria, but is often characterized generally as “obesity without the presence of metabolic diseases such as type 2 diabetes, dyslipidemia or hypertension” (Munoz-Garach et al. 2016). Retained insulin sensitivity, however, is the hallmark trait of this subpopulation.  Researchers have assigned up to 32 percent of the obese population to this phenotype.  It applies more prevalently to women than men, but is thought to decrease with age among both sexes.  Researchers have yet to determine whether these obese are genetically predisposed to decreased risks of disease or mortality.  But their existence, along with that of the metabolically unhealthy normal-weight population, suggests that factors other than excess adiposity are at play.

All of which might sound at least somewhat comforting to the now 600 million obese worldwide (and still growing) who have been told for decades that obesity per se will significantly increase one’s susceptibility to heart disease, stroke, cancer, diabetes, and arthritis, for example. Preferences and popular reports aside, however, it appears we may yet be forced to choose between possessing our cakes and consuming them, because an impressive body of new and well-conceived research has called both the paradox and healthy obesity into serious question.

Consider, for example, a truly enormous international meta-analysis published last July in The Lancet by the Global BMI Mortality Collaboration (GBMC 2016).  Led by Harvard professor of nutrition and epidemiology, Frank Hu, this study poured over data from more than 10.6 million participants who were followed for up to 14 years.  239 large studies conducted in 32 countries were included.  Importantly, the Collaboration attempted to control for a “reverse causation bias,” in which low BMI was the result, rather than the cause, of an underlying or preclinical illness by excluding current or former smokers, those who suffered from chronic disease at the study’s inception, and those who died during the initial five years of follow-up.  In other words, Hu’s team addressed the potential for potent confounders that Flegal’s team, for lack of data, was forced to ignore.

The Collaboration’s results were startling. Interestingly, Hu “was able to reproduce [Flegal’s results] when conducting crude analyses with inadequate control of reverse causality, but not when [he] conducted appropriately strict analyses.”  In the end, then, the Collaboration found that, worldwide, participants with a normal BMI in the 22.5 to 25 range enjoyed the lowest risk of mortality and that such risk increased significantly throughout the overweight and obese ranges.  In fact, every five units of BMI in excess of 25 was associated generally with a 31 percent greater risk of premature death—specifically, 49 percent for cardiovascular-related, 38 percent for respiratory-related, and 19 percent for cancer-related mortality.  According to Hu, his team had succeeded in “challeng[ing] previous suggestions that overweight and grade 1 obesity are not associated with higher mortality, bypassing speculations about hypothetical protective metabolic effects of increased body fat in apparently healthy individuals.”

Frank Hu

Frank Hu

Consider too, a large prospective cohort study published last October in the BMJ in which about 115,000 participants—free of cardiovascular disease and cancer at baseline—were followed for up to 32 years (Veronese et al. 2016).  Evaluating the combined associations of diet, exercise, alcohol consumption, and smoking with BMI on the risk of all-cause and cause-specific mortality, this study was also designed to address Flegal’s peculiar 2013 results.  A lead author here as well, Frank Hu first noted, once again, that previous examinations suggesting an obesity paradox, including Flegal’s, had allowed for potentially confounding bias by failing to distinguish between healthy normal-weight individuals and a “substantial proportion of the US population” in which “leanness is driven by other factors that can increase risk of mortality,” including existing or preclinical chronic diseases and smoking.

Contrary to the alleged paradox, Hu discovered that when lifestyle factors were taken into serious consideration, the lowest risk of all-cause and cardiovascular mortality was enjoyed by participants in the slightly low-to-normal, 18.5 to 22.4 BMI range—that is, when those subjects also displayed at least three out of four healthy lifestyle factors, including healthy eating, adequate exercise, moderate alcohol intake, and no smoking. In the end, according to Hu’s team, “the U-shaped relation between BMI and mortality observed in many epidemiological studies is driven by an over-representation in our societies of individuals who are lean because of chronic metabolic and pathological conditions caused by exposure to smoking, a sedentary lifestyle, and/or unhealthy diets.”  The optimal human condition, in other words, is not overweight of any kind or to any degree, but rather “leanness induced by healthy lifestyles.”

So much for the obesity paradox, at least for now. But what of its somewhat less voracious cousin, the notion of metabolically healthy obesity?

Recognizing prior support for so-called “benign obesity,” a trio of Canadian diabetes researchers led by Caroline Kramer conducted a systematic review and meta-analysis of eight studies evaluating over 61,000 subjects—many of whom were classified as metabolically healthy obese—for all-cause mortality and cardiovascular events (Kramer et al. 2013). When all studies were considered, regardless of follow-up duration, the healthy obese subjects displayed risks similar to those of healthy normal-weight participants.  However, when considering only those studies that followed-up for at least ten years, Kramer and colleagues discovered that the purportedly healthy obese were significantly more likely than their normal counterparts to perish or suffer serious cardiovascular trouble.

Caroline Kramer

Caroline Kramer

Should we infer, then, that the healthy obese are, in fact, healthy until circumstances render them otherwise a decade later? Not according to Kramer.  Regardless of metabolic status, she warned, even in the short term, obesity is associated with subclinical vascular disease, left-ventricular abnormalities, chronic inflammation, and increased carotid artery intima-media thickness and coronary calcification.  In the end, the Canadians found no support for the “benign obesity” phenotype and declared with no uncertainty that “there is no ‘healthy’ pattern of obesity.”

Most recently, however, a diverse and impressively creative group of Swedish scientists used transcriptomic profiling in white adipose tissue to contrast responses to insulin stimulation between never-obese, unhealthy obese, and, again, supposedly healthy obese subjects. (Ryden et al. 2016). Led by Mikael Ryden at the Karolinska Institutet, this group revealed, first, clear distinctions between the never-obese and both groups of obese participants, and, second, nearly identical and abnormal patterns of gene expression among both insulin-resistant and insulin-sensitive obese subjects, independent of other cardiovascular or metabolic risk factors.

Said Ryden during a post-publication interview: “Insulin-sensitive obese individuals may not be as metabolically healthy as previously believed.” (ScienceDaily 2016). His team’s findings, he continued, “suggest that vigorous interventions may be necessary for all obese individuals, even those previously considered … healthy.”

To Lavie’s credit, he generally acknowledges obesity’s proven hazards. He also recognizes serious and consistent exercise as the most reliable strategy for attaining and maintaining good health.  Far less defensible, however, is Lavie’s insistence that exercise can render obesity a benign condition.  First, as much of the research presented here demonstrates, the chronic diseases strongly associated with obesity are, by definition, progressive and apt to cause damage down the road.  Second, in the real world, excess adiposity always leaves meaningful exercise a far more difficult and, thus, far less likely prospect.


Obese or not, our health continues to be undermined by the popular, ever-emotion-manipulating media, the misguided and oppressive forces of political correctness, and, most crucially, our own subjective prejudices and appetites. But as their numbers continue to swell, the overweight and obese grow increasingly vulnerable to seductive messages inviting self-deception and failure.  As in all other contexts, their liberation from these influences derives only from an unflinching appreciation for the methods of science—that is, empiricism, rationality, candor, and the assumption of responsibility for individual experimentation.  In a word, skepticism.


Flegal, K.M., B.K. Kit, H. Orpana, et al. 2013. Association of all-cause mortality with overweight and obesity using standard body mass index categories. Journal of the American Medical Association 309(1): 71-82.

Global BMI Mortality Collaboration. 2016. Body-mass index and all-cause mortality: individual-participant-data meta-analysis of 239 prospective studies in four continents. The Lancet 388: 776-786.

Kramer, C.K., B. Zinman, and R. Retnakaran. 2013. Are metabolically healthy overweight and obesity benign conditions? Annals of Internal Medicine 159(11): 758-769.

Lavie, Carl J. 2014. The Obesity Paradox: When Thinner Means Sicker and Heavier Means Healthier. NY: Plume.

Munoz-Garach, A., I. Cornejo-Pareja, and F.J. Tinahones. 2016. Does metabolically healthy obesity exist? Nutrients 8: 320.

Ryden, M., O. Hrydziuszko, E. Mileti, et al. 2016. The adipose transcriptional response to insulin is determined by obesity, not insulin sensitivity. Cell Reports 16: 2317-2326.

ScienceDaily. 2016. More evidence that “healthy obesity” may be a myth.” 18 August 2016.>.

Veronese, N., L. Yanping, J.E. Manson, et al. 2016. Combined associations of body weight and lifestyle factors with all cause and cause specific mortality in men and women: prospective cohort study. BMJ. DOI:10.1136/bmj.i5855.


Obesity: “Fat Chance” or Failure of Sincerity?

by Kenneth W. Krause.

Kenneth W. Krause is a contributing editor and “Science Watch” columnist for the Skeptical Inquirer.  Formerly a contributing editor and books columnist for the Humanist, Kenneth contributes frequently to Skeptic as well. He can be contracted at

popular culture3

Man is condemned to be free.—Jean-Paul Sartre.

Beginning about five years ago, the chronically overweight and obese were offered a new paradigm, one more consistent with their majority’s shared experiences in the twenty-first century. Emerging science from diverse fields, certain experts argued, complicated—perhaps even contradicted—the established view that weight maintenance was a straightforward, if not simple, matter of volitional control and balancing energy intake against energy expenditure.

As a host of potential complexities materialized, the frustrated members of this still expanding demographic were notified that, contrary to conventional wisdom, they had little or no control over their conditions. The popular literature especially began to hammer two captivating messages deeply into the public consciousness.  First, from within, the overweight and obese have been overwhelmed by their genomes, epigenomes, hormones, brains, and gut microbiomes, to name just a few.  Second, from without, their otherwise well-calculated and ample efforts have been undermined, for example, by the popular media, big food, government subsidies, poverty, and the relentless and unhealthy demands of contemporary life.

In a 2012 Nature opinion piece, Robert Lustig, Laura Schmidt, and Claire Brindis—three public health experts from the University of California, San Francisco, compared the “deadly effect” of added sugars (high-fructose corn syrup and sucrose) to that of alcohol(1).  Far from mere “empty calories,” they added, sugar is potentially “toxic” and addictive.  It alters metabolisms, raises blood pressures, causes hormonal chaos, and damages our livers.  Like both tobacco and alcohol (a distillation of sugar), it affects our brains as well, encouraging us to increase consumption.

Apparently unimpressed with Americans’ abilities to control themselves, Lustig et al. urged us to back restrictions on our own choices in the form of government regulation of sugar. In support of their appeal, the trio relied on four criteria—“now largely accepted by the public health community,”—originally offered by social psychologist Thomas Babor in 2003 to justify the regulation of alcohol: The target substance must be toxic, unavoidable (or pervasive), produce a negative impact on society, and present potential for abuse.  Perhaps unsurprisingly, they discovered that sugar satisfied each criterion with ease.

Robert Lustig.

Lustig, a pediatric endocrinologist and, now, television infomercial star, contends that obesity results primarily from an intractable hormonal predicament. In his wildly popular 2012 book, Fat Chance, Lustig indicted simple, super-sweet sugars as chief culprits, claiming that sucrose and high-fructose corn syrup corrupt our biochemistry to render us hungry and lethargic in ways fat and protein do not(2).  In other words, he insisted that sugar-induced hormonal imbalances cause self-destructive behaviors, not the other way around.

Lustig’s argument proceeds essentially as follows: In the body, insulin causes energy to be stored as fat.  In the hypothalamus, it can cause “brain starvation,” or resistance to leptin, the satiety hormone released from adipose tissue.  Excess insulin, or hyperinsulinemia, thus causes our hypothalami to increase energy storage (gluttony) and decrease energy consumption (sloth).  To complete the process, add an increasingly insulin-resistant liver (which drives blood insulin levels even higher), a little cortisol (the adrenal stress hormone), and of course sugar addiction.  In the end, Lustig concludes, dieters hardly stand a chance.

Journalist Gary Taubes, author of the similarly successful Why We Get Fat, was in full agreement(3).  Picking up the theoretical mantle where Lustig dropped it, Taubes expanded the list of nutritional villains considerably to include all the refined carbohydrates that quickly boost consumers’ glycemic indices. In a second Nature opinion piece, he then blamed the obesity problem on both the research community, for failure to fully comprehend the condition, and the food industry, for exploiting that failure(4).

Gary Taubes with Dr. Oz.

Gary Taubes with Dr. Oz.

To their credit, Lustig and Taubes provided us with some very sound and useful advice.  Credible nutrition researchers agree, for example, that Americans in particular should drastically reduce their intakes of added sugars and refined carbohydrates.  Indeed, most would be well-advised to eliminate them completely.  The authors’ claims denying self-determination might seem reasonable as well, given that, as much research has shown, most obese who have tried to lose weight and to keep it off, have failed.

On the other hand, failure is common in the context of any difficult task, and evidence of “don’t” does not amount to evidence of “can’t.” One might wonder as well whether obesity is a condition easily amenable to controlled scientific study given that every solution—and of course many, in fact, do succeed(5)—is both multifactorial and as unique as every obese person’s biology.  So can we sincerely conclude, as so many commentators apparently have, that the overweight and obese are essentially powerless to help themselves?  Or could it be that the vast majority of popular authors and health officials have largely—perhaps even intentionally—ignored the true root cause of obesity, if for no other reasons, simply because they lack confidence in the obese population’s willingness to confront it?

Though far less popular, a more recently published text appears to suggest just that.  In The Psychology of Overeating, clinical psychologist Kima Cargill attempts to “better contextualize” overeating habits “within the cultural and economic framework of consumerism”(6).  What current research fails to provide, she argues, is a unified construct identifying overeating (and sedentism, one might quickly add) as “not just a dietary [or exercise] issue,” but rather as a problem implicating “the consumption of material goods, luxury experiences, … evolutionary behaviors, and all forms of acquisition.”

Kima Cargill.

Kima Cargill.

To personalize her analysis, Cargill introduces us to a case study named “Allison.”  Once an athlete, Allison gained fifty pounds after marriage.  Now divorced and depressed, she regularly eats fast food or in expensive restaurants and rarely exercises.  Rather than learn about food and physical performance, Allison attempts to solve her weight problem by throwing money at it.  “When she first decided to lose weight,” Cargill recalls, “which fundamentally should involve reducing one’s consumption, Allison went out and purchased thousands of dollars of branded foods, goods, and services.” She hired a nutritionist and a trainer.  She bought a Jack Lalanne juicer, a Vitamix blender, a Nike Feulband, Lululemon workout clothing, an exclusive gym membership, diet and exercise DVDs and iPhone apps, and heaping bags full of special “diet foods.”

None of it worked, according to the author, because Allison’s “underlying belief is that consumption solves rather than creates problems.”  In other words, like so many others, Allison mistook “the disease for its cure.”  The special foods and products she purchased were not only unnecessary, but ultimately harmful.  The advice she received from her nutritionist and trainer was based on fads, ideologies, and alleged “quick-fixes” and “secrets,” but not on actual science.  Yet, despite her failure, Allison refused to “give up or simplify a life based on shopping, luxury, and materialism” because any other existence appeared empty to her.  In fact, she was unable to even imagine a more productive and enjoyable lifestyle “rich with experiences,” rather than goods and services.

Television celebritism: also mistaking the disease for its cure.

Television celebritism: also mistaking the disease for its cure.

Like Lustig, Taubes, and their philosophical progeny, Cargill recognizes the many potential biological factors capable of rendering weight loss and maintenance an especially challenging task.  But what she does not see in Allison, or in so many others like her, is a helpless victim of either her body or her culture.  Judging it unethical for psychologists to help their patients accept overeating behaviors and their inevitably destructive consequences, Cargill appears to favor an approach that treats the chronically overweight and obese like any other presumably capable, and thus responsible, adult population.

Compassion, in other words, must begin with uncommon candor.  As Cargill acknowledges, for example, only a “very scant few” get fat without overeating because of their genes.  After all, recently skyrocketing obesity rates cannot be explained by the evolution of new genes during the last thirty to forty years.  And while the food industry (along with the popular media that promote it) surely employs every deceit at its disposal to encourage overconsumption and the rejection of normal—that is, species appropriate—eating habits, assigning the blame to big food only “obscures our collusion.”  Worse yet, positioning the obese as “hapless victims of industry,” Cargill observes, “is dehumanizing and ultimately undermines [their] sense of agency.”

Education is always an issue, of course. And, generally speaking, higher levels of education are inversely associated with the least healthy eating behaviors.  But the obese are not stupid, and shouldn’t be treated as such.  “None of us is forced to eat junk food,” the author notes, “and it doesn’t take a college degree or even a high school diploma to know that an apple is healthier than a donut.”  Nor is it true, as many have claimed, that the poor live in “food deserts” wholly lacking in cheap, nutritious cuisine(7).  Indeed, low-income citizens tend to reject such food, Cargill suggests, because it “fails to meet cultural requirements,” or because of a perceived “right to eat away from home,” consistent with societal trends.

Certain foods, especially those loaded with ridiculous amounts of added sugars, do in fact trigger both hormonal turmoil and addiction-like symptoms (though one might reasonably question whether any substance we evolved to crave should be characterized as “addictive”).  And as the overweight continue to grow and habituate to reckless consumption behaviors, their tasks only grow more challenging.  I know this from personal experience, in addition to the science.  Nevertheless, Cargill maintains, “we ultimately degrade ourselves by discounting free will.”

popular culture4

Despite the now-fashionable and, for many, lucrative “Fat Chance” paradigm, the chronically overweight and obese are as capable as anyone else of making rational and intelligent decisions at their groceries, restaurants, and dinner tables. And surely overweight children deserve far more inspiring counsel.  But as both Lustig and Taubes, on the one hand, and Cargill, on the other, have demonstrated in different ways, the solution lies not in mere diet and exercise, per se.  The roots of obesity run far deeper.

Changes to basic life priorities are key. To accomplish a more healthful, independent, and balanced existence, the chronically overweight and obese in particular must first scrutinize their cultural environments, and then discriminate between those aspects that truly benefit them and those that were designed primarily to take advantage of their vulnerabilities, both intrinsic and acquired.  Certain cultural elements can stimulate the intellect, inspire remarkable achievement, and improve the body and its systems.  But most if not all of its popular component exists only to manipulate its consumers into further passive, mindless, and frequently destructive consumption.  The power to choose is ours, at least for now.


(1)Lustig, R.H., L.A. Schmidt, and C.D. Brindis. 2012. Public health: the toxic truth about sugar. Nature 482: 27-29.

(2)Lustig, R. 2012. Fat Chance: Beating the Odds Against Sugar, Processed Food, Obesity, and Disease. NY: Hudson Street Press.

(3)Taubes, G. 2012. Treat obesity as physiology, not physics. Nature 492: 155.

(4)Taubes, G. 2011. Why We Get Fat: And What to Do About It. NY: Knopf.

(5)See, e.g., The National Weight Loss Control Registry.

(6)Cargill, K. 2015. The Psychology of Overeating: Food and the Culture of Consumerism. NY: Bloomsbury Academic.

(7)Maillot, M., N. Darmon, A. Drewnowski. 2010. Are the lowest-cost healthful food plans culturally and socially acceptable? Public Health Nutrition 13(8): 1178-1185.

The Underappreciated Role of Physical Activity in the Battle Against Obesity—Part 3: Adults and the Relationship Between Physical Activity and Adiposity.

by Kenneth W. Krause.

[Notable New Media]

Kenneth W. Krause is a contributing editor and “Science Watch” columnist for the Skeptical Inquirer. Formerly a contributing editor and books columnist for the Humanist, Kenneth contributes frequently to Skeptic as well. He can be contracted at

Exercise adult 4

Is physical activity, including structured exercise, an effective strategy in the battle against overweight and obesity? Some have recently suggested that successful weight loss and weight maintenance are the results of improved diet alone.

In part one of this article, I reviewed evidence suggesting that, despite popular media misinformation, most people who maintain weight loss do so through a combination of diet and physical activity. Nor does it appear true, as many have reported, that exercisers completely compensate for energy expenditure through increased sedentary time or energy intake.  In part two, I examined evidence showing that both moderate-to-vigorous physical activity and television viewing time significantly affect adiposity in children.

The National Academies’ Institute of Medicine recently gathered preeminent experts in several relevant fields to summarize the current science exploring “the impact of physical activity in the prevention and treatment of overweight and obesity” (IOM 2015). Here, I discuss the panel’s conclusions relating specifically to adults.

Robert Ross, professor in the School of Kinesiology and Health Studies at Queen’s University, Kingston, Ontario, Canada, presented the most credible evidence on the subject from randomized controlled trials. Before doing so, however, he distinguished between efficacy trials, which ask what happens physiologically when adults actually do exercise, and effectiveness trials, which investigate instead what occurs in terms of behavior change when adults are in one way or another encouraged to exercise.

In terms of efficacy trials, Ross described the results of his own extensive work. First, he found that when previously active male and female participants increased their exercise time and caloric intake, they either did not gain weight or found it challenging to avoid weight loss (Ross et al. 2000, 2004).  As such, exercise appears at the very least to prevent weight gain, even when accompanied by an increase in consumption.

Second, in a study of 300 mostly inactive obese adults who were asked to maintain caloric intake but to add five days of supervised exercise per week for six months, Ross’s team observed an impressive loss of body weight along with decreased waist circumference among all treatment groups (which varied in terms of exercise amount and intensity) (Ross et al 2015). Importantly, they revealed as well that participants did not compensate for elevated energy expenditure through increased sedentary time.

Such results appear to bode very well for those committed to an intelligent and consistent exercise program. “I just don’t think there is any ambiguity here,” Ross commented.  Even for the obese, unless one eats more, an increase in exercise will translate to lost weight.

Exercise adult 8

But what happens in terms of behavior change when people are simply asked to lose weight? The results of effectiveness trials are encouraging, but, sadly, less than spectacular.  For example, in a systematic review of nine diet and exercise trials including 1595 women and 375 men and involving a variety of behavior change strategies, investigators found a significant but modest difference in weight gain in only five trials, largely due to gain among control group members (Lombard et al. 2009).

In another diet and exercise trial incorporating three distinct interventions—one clinic-based, one correspondence-based, and one informational only (the control group)—researchers discovered trends among women toward weight gain in the informational and correspondence groups, and toward gain prevention only in the clinic group (Levine et al. 2007).  According to Ross, most prevention effectiveness trials have demonstrated success in achieving a similarly modest yet significant goal, but of course have been unable to distinguish between the effects of improved diet and increased exercise.  Higher quality trials have yet to be conducted.

From these results, researchers including Ross have concluded that prevention of weight gain, rather than substantial weight loss, appears to be the most achievable goal. Which might seem intuitive, given that overweight and obesity renders effective exercise a much more difficult, though certainly not impossible, prospect.  On the other hand, a commitment to weight gain prevention requires considerable foresight and, at least during the earliest stages, an apparently rare ability to decline immediate gratification in exchange for future health and performance benefits.

But the evidence is clear: exercise works.  Less plain is why that message has failed to fully penetrate developed societies, certain regions of the United States in particular.  Perhaps the answer should be obvious.  The goal of the popular media is seldom to enlighten, after all, and much less to encourage discipline.  Their primary aim, rather, is almost always to manipulate and indulge consumer emotions.  Arguably, it’s a wonder anyone ever succeeds in his or her battle against an unhealthy bulge.

In any case, evidence of “don’t” is not evidence of “can’t,” and the fact that some do succeed tends to show that many more can. Consistent with the evidence presented here, and as I have frequently argued in the past, true success for the obese and overweight is entirely attainable.  But it surely requires extraordinary candor, personal growth beyond the typical, and, in most if not all instances, substantial modifications to life priorities.


IOM (Institute of Medicine). 2015. Physical activity: moving toward obesity solutions: workshop summary. Washington, D.C.: The National Academies Press.

Levine, M.D., M.L. Klem, M.A. Kalarchian, et al. 2007. Weight gain prevention among women. Obesity 15(5):1267-1277.

Lombard, C.B., A.A. Deeks, and H.J. Teede. 2009. A systematic review of interventions aimed at the prevention of weight gain in adults. Public Health Nutrition 12(11):2236-2246.

Ross, R., D. Dagnone, P.J. Jones, et al. 2000. Reduction in obesity and related comorbidity conditions after diet-induced weight loss or exercise-induced weight loss in men: A randomized controlled trial. Annals of Internal Medicine 133(2):92-103.

Ross, R., I. Janssen, J. Dawson, et al. 2004. Exercise-induced reduction in obesity and insulin resistance in women: A randomized controlled trial. Obesity Research 12(5):7898798.

Ross, R., R. Hudson, P.J. Stotz, et al. 2015. Effects of exercise amount and intensity on abdominal obesity and glucose tolerance in obese adults: A randomized controlled trial. Annals of Internal Medicine 162(5):325-334.


The Underappreciated Role of Physical Activity in the Battle Against Obesity—Part 2: Children and the (Bidirectional?) Relationship Between Physical Activity and Adiposity.

by Kenneth W. Krause.

[Notable New Media]

Kenneth W. Krause is a contributing editor and “Science Watch” columnist for the Skeptical Inquirer.  Formerly a contributing editor and books columnist for the Humanist, Kenneth contributes frequently to Skeptic as well.  He can be contracted at

Exercising Children 3

Is physical activity, including structured exercise, an effective strategy in the battle against overweight and obesity?  In part one of this article, I reviewed evidence suggesting that, despite popular media misinformation, most people who maintain weight loss do so through a combination of diet and physical activity.  Nor is it true, as many have reported, that exercisers completely compensate for energy expenditure through increased sedentary time or energy intake.

The National Academies’ Institute of Medicine recently gathered preeminent experts in several relevant fields to summarize the current science exploring “the impact of physical activity in the prevention and treatment of overweight and obesity” (IOM 2015).  Here, I discuss the panel’s conclusions relating to children specifically.

The two most common study designs used to examine children’s health are the cross-sectional and prospective longitudinal models.  While the former measures the explanatory variable (physical activity, in this case) and the outcome (adiposity) at the same time, the latter measures those variables on multiple occasions.  While neither “proves” cause and effect, the longitudinal design is especially capable of supporting inferences that compliment randomized controlled trials by providing important information about real-world patterns.

Panelist Kathleen Janz, professor of health and human physiology and associate director of the University of Iowa Obesity Research and Education Initiative, focused initially on the Iowa Bone Development Study (IBDS), a sixteen-year longitudinal program with which she has been intimately involved since its inception (Kwon et al. 2013, 2015).  The IBDS was one of the first to use an accelerometer to more accurately measure physical activity.  Janz’s team also used dual-energy X-ray absorptiometry (DXA) to sort body composition into lean, fat, and bone tissues, and to distinguish between visceral and subcutaneous fat.

In the IBDS, Janz and her team followed 500 children from the age of five and, to date, have conducted at least eight clinical exams of each child.  Defining obesity as 32 percent body fat in girls and 25 percent in boys, twelve percent of study participants were obese from the beginning.  Unfortunately, another ten percent had joined them by the age of nineteen.

Exercising Children 1

So which variables were found to be potentially explanatory?  Total sedentary time did not matter, according to Janz.  But television viewing time (a subset of total sedentary time) and moderate-to-vigorous physical activity (MVPA) did.  Janz explained her findings in the context of a typical eleven-year-old study participant.  Averaging every variable other than MVPA, her group discovered a 7.5 difference in adiposity between females with high and low levels of MVPA, and a five percent distinction in males.  Averaging every variable except TV time, they revealed a five percent difference in adiposity between girls who watched a great deal of TV and very little TV, and a 9.3 percent difference in boys.  When averaging all variables except both MVPA and TV, Janz’s team found an 11.8 percent difference in female adiposity and a whopping 21.3 percent difference in males.

In a recent cross-sectional study of more than 6000 children aged nine to eleven residing at twelve different locations across the world, another group of researchers came to a similar conclusion (Katzmarzyk et al. 2015).  The best predictor of reduced obesity, they found, was MVPA, rather than either sedentary time or vigorous-intensity physical activity.  More specifically, 55 minutes of daily MVPA was the most reliable predictor of lower obesity rates.

But might inferred causality run in the opposite direction as well?  In other words, does higher adiposity predict less physical activity?  If so, one would be forced to question the logic underlying the Health at Every Size (HAES) movement, as well as the increasingly popular claim that physical fitness, but not excess adiposity, is the more accurate predictor of superior health outcomes.

Indeed, one accelerometer study showed that, while MVPA at age seven did not predict decreased body fat between the ages of seven and ten, body fat percentage at age seven did in fact predict decreased MVPA between ages seven and ten (Metcalf et al. 2011).  More specifically, a ten percent increase in adiposity at age seven was associated with four fewer minutes per day of MVPA at age ten.  According to Janz, a “bidirectional relationship” between physical activity and adiposity might signal the existence of a “positive feedback loop.”

Summarizing the data from the IBDS, Janz instructed that children who consistently engaged in at least 45 minutes of MVPA every day “were 60 percent less likely to end up obese at the age of nineteen than children whose level of MVPA decreased as they aged.”  This evidence, she concluded, supports the current national guidelines emphasizing at least 60 minutes of MVPA per day and two hours or less of television.

Exercising Children 2



IOM (Institute of Medicine). 2015. Physical activity: moving toward obesity solutions: workshop summary. Washington, D.C.: The National Academies Press.

Katzmarzyk, P.T., T.V. Barreira, S.T., S.T. Broyles, et al. 2015. Physical activity, sedentary time, and obesity in an international sample of children. Medicine & Science in Sports & Exercise 47(10):2062-2069.

Kwon, S., K.F. Janz, T.L. Burns, et al. 2011. Effects of adiposity on physical activity in childhood: Iowa Bone Development Study. Medicine & Science in Sports & Exercise 43(3):443-448.

Kwon, S., K.F. Janz, E.M. Letuchy, et al. 2015. Developmental trajectories of physical activity, sport, and television viewing during childhood to young adulthood: Iowa Bone Development Study. JAMA: Pediatrics 169(7):666-672.

Metcalf, B.S., J. Hosking, A.N. Jeffery, et al. 2011. Fatness leads to inactivity, but inactivity does not lead to fatness: a longitudinal study in children (EarlyBird 45). Archives of Disease in Childhood 96(10):942-947.

The Underappreciated Role of Physical Activity in the Battle Against Obesity (Part 1).

by Kenneth W. Krause.

[Notable New Media]

Kenneth W. Krause is a contributing editor and “Science Watch” columnist for the Skeptical Inquirer.  Formerly a contributing editor and books columnist for the Humanist, Kenneth contributes regularly to Skeptic as well.  He may be contacted at

Could it be that Time magazine’s August 17, 2009 cover story announcing “The Myth About Exercise” misled millions of potential exercisers about the true relationship between physical activity (PA) and weight loss and maintenance?  James Hill, professor of pediatrics and medicine at the University of Colorado Denver, and co-founder of the National Weight Control Registry and the America on the Move initiative, seems to think so.


In the spring of 2015, the National Academies’ Institute of Medicine convened a two-day workshop titled, “Physical Activity: Moving Toward Obesity Solutions.”  Gathering preeminent experts in several relevant fields, the panel’s expressed purpose was to summarize the current science exploring “the impact of physical activity in the prevention and treatment of overweight and obesity and to highlight innovative strategies” for physical fitness.  Their results were recently published by the National Academy of Sciences (IOM 2015).

We all understand that, in the limited context of weight loss and maintenance, those predisposed to excess adiposity cannot outrun, or out-exercise, a poor diet.  And while it might take three minutes to consume a 560-calorie hamburger, for example, one would have to exercise forty-five to sixty minutes, depending on intensity, among other things, to burn it off.  But does that necessarily mean, as the 2009 Time article implied, that PA is a trivial strategy in the difficult battle against an unhealthy bulge?

Not according to Hill, and not according to the science.  Consider first the issue of “compensation.”  Through many popular sources, including Time, we have been led to believe that those who increase their level of PA tend to compensate by either consuming more calories or increasing sedentary behavior.

But, as Hill reveals, a recent systematic review of 30 studies shows that, in most cases, exercisers did in fact not compensate with reductions in non-exercise PA (Washburn et al. 2014).  Another study demonstrated that people who increased their PA tended not to completely compensate with increased caloric intake (Schubert et al. 2013).  In summary, according to Hill, “the scientific literature indicates that when physical activity is added to a weight loss program, the majority of people do not compensate, at least not completely.”  The “net result” of PA, in other words, is “a negative energy balance.”

Between 1960 and 2010, daily occupational (including housework) energy expenditure decreased by 120 calories per day, and more recent statistics suggest a further and continuing decline.  “That is enough,” Hill argues, “to explain most of obesity.”  Every study conducted on highly palatable, energy-dense diets, he continues, has demonstrated less weight gain when PA is added to improved nutrition—“even among people genetically susceptible to weight gain.”

Physical Activity

Here, Doctor Hill draws our attentions to two important concepts.  First, “metabolic flexibility” determines how efficiently our bodies can switch fuels.  During a relative fasting state, a flexible metabolism can quickly suppress glucose oxidation and enhance fat oxidation, whereas an inflexible metabolism maintains “a blunted preference for fat oxidation” and remains unable to suppress the use of glucose.  During an insulin-stimulated state, by contrast, the flexible person can suppress fat oxidation and increase her use of glucose, while the inflexible person is less capable of suppressing fat use and stimulating glucose oxidation.

Metabolic flexibility, Hill contends, is directly related to PA.  While weight loss alone does not necessarily improve the situation, “[w]hen people stop moving, their metabolism loses its flexibility.”  The resulting inflexibility, he reasons, renders people, including calorie-restricting dieters, “more susceptible to storing rather than burning fat.”

Second, some researchers believe that one can control personal energy balance far more efficiently by crossing a “threshold of PA.”  Above that threshold is the “regulated zone,” and below it is the “unregulated zone.”  In the former zone, we would expect to observe “a total compensation of energy intake with increased physical activity” and no weight change.  In such cases, physical activity is “driving the bus” and “food is just along for the ride.”  In the latter, unregulated zone, however, “as physical activity decreases, food intake actually increases.”  Here, a tight coupling between PA and caloric intake collapses, and food is now “driving the bus.”

Physical activity threshold

Hill suspects that decreasing PA “is the reason why most people today occupy the unregulated zone.”  When people do lose weight, of course, their energy needs decrease.  If a 220-pound person, for example, were to lose ten percent of his body weight, his energy demands would also plummet by roughly 170 to 250 calories per day.  What’s the best solution?  Fill that “energy gap,” Hill prescribes, with an increase in PA—which of course is far more sustainable than a decrease in energy intake.

Based on data from Hill’s National Weight Loss Registry, a paltry eight percent of the population will maintain a reduction in weight achieved by improved diet alone.  Despite popular media manipulation and misinformation, most people who maintain weight loss do so through a combination of physical activity and diet.  It is therefore extremely unlikely, Hill stresses, that any individual case of obesity can be resolved with improved nutrition alone, or that the obesity epidemic can be reversed without increasing PA in the broader population.



IOM (Institute of Medicine). 2015. Physical activity: moving toward obesity solutions: workshop summary. Washington, D.C.: The National Academies Press.

Schubert, M.M., B. Dresbow, S. Sabapathy, and M. Leveritt. 2013. Acute exercise and subsequent energy intake: a meta-analysis. Appetite 63:92-104.

Washburn, R.A., K. Lambourne, A.N. Szabo, et al. 2014. Does increased prescribed exercise alter non-exercise physical activity/energy expenditure in healthy adults? A systematic review. Clinical Obesity 4(1):1-20.

Mom, Dad, and the Epigenetics of Childhood Obesity.

[Notable New Media]

by Kenneth W. Krause.

Kenneth W. Krause is a contributing editor and “Science Watch” columnist for the Skeptical Inquirer.  Formerly a contributing editor and books columnist for the Humanist, Kenneth contributes regularly to Skeptic as well.  He may be contacted at

A relatively new field of inquiry, epigenetics (literally, “above the genes”) contemplate how heritable and stable changes in gene expression can occur without altering underlying DNA sequences.  It’s also one form of “developmental programming,” where, during critical periods of child development, environmental stimuli can have persistent, even lifelong, impacts on gene expression, metabolism, and disease risk.  As such, parents’ pre-pregnancy and, in the mother’s case, prenatal and postnatal lifestyle choices and environments can affect their children’s risk of subsequent obesity and associated chronic diseases, for example.

Perhaps the clearest instance of epigenetic dysregulation was discovered in an animal study.  Genetically identical agouti mice developed into either the lean brown or obese yellow phenotype depending on the degree of DNA “methylation” (one epigenetic mechanism) at the Avy gene locus.  In humans, however, the classic example occurred during the Dutch Hunger Winter of 1944-1945 when food shortages resulted in dramatic decreases in daily energy intakes.  Here, it was shown that children born to mothers exposed to famine during pregnancy suffered an increased risk of obesity, heart disease, and diabetes later in life–indeed, 60 years after the famine.

To explain this strange effect, the “mismatch hypothesis” is frequently invoked.  Poor maternal nutrition, some researchers argue, might signal to the fetus that food is scarce and cause the fetus to adapt its metabolism epigenetically by reducing energy demands and increasing its propensity to store fat.  It has been further suggested that such a mechanism might also account for the rapid rise in obesity rates in still-developing nations where populations continue to migrate from rural to urban areas and begin to experience a novel abundance of energy-rich foods.

But what about parental over-nutrition–can moms and dads unwittingly predispose their developing fetuses to obesity and its related diseases because of their excessive eating (and inadequate exercise) habits?  In Examining a Developmental Approach to Childhood Obesity: the Fetal and Early Childhood Years, the Institute of Medicine gathered a diverse group of scientists to explore how the risk of childhood obesity can be affected by (1) maternal and paternal nutrition prior to conception, (2) maternal and placental nutrition during pregnancy, and (3) maternal and infant nutrition following delivery.

Epigenetics of Childhood Obesity

Although the precise means of such changes remain obscure, much evidence now suggests that parental over-consumption behaviors do indeed affect their unborn and newborn children’s risks of overweight and its associated complications.  According to Jacob Friedman, professor of pediatrics at the University of Colorado, Denver, “obesity begets obesity.”  Both animal and human studies, he reports, demonstrate that prenatal and postnatal exposures to maternal obesity predispose infants to early-onset metabolic disease and childhood obesity.

For example, Friedman continued, the pre-pregnancy BMI of mothers can predict higher newborn liver fat at two weeks of age, which continues to increase during lactation.  During breastfeeding, maternal diet and obesity can also affect the child’s immune system along with infant behavior, weight gain, and risk of obesity.  Epidemiological evidence also suggests that, independent of lifestyle factors, the effect of maternal obesity can haunt children over their entire life spans.

So understood, the fact that overweight and obesity rates among women of childbearing age have “increased fairly dramatically” in recent years–with the largest increases found in the Americas, Oceania, and the Caribbean–seems to demand our immediate attention.  Sixty percent of all women aged 20 to 39, and nearly 80 percent of black and Hispanic women in the same age range, are now overweight or obese.  Predictably, the fastest-growing rates of childhood obesity are found among low-income populations.

Although mothers certainly possess a greater capacity to shape their children’s phenotypes, fathers are not necessarily off the hook.  Their sperm can also be exposed to harmful (as well as beneficial) behaviors and other environmental influences, and some researchers believe that epigenetic mechanisms may affect certain RNA molecules–previously implicated as having an early developmental role in obesity–delivered to the oocyte via the male gamete.

The authors are careful, of course, to caution us that epigenetic causation has yet to be firmly established.  Nevertheless, they argue, “Increasing evidence suggests that a number of environmental factors, including nutrition, can affect the epigenome and that the epigenome seems most susceptible to those environmental factors during the prenatal, neonatal, and pubertal periods.”

Why would nature provide such a mechanism?  The epigenome, unlike its “host” genome, can respond to rapidly changing environments that are likely to change again.  Its effects are not necessarily permanent.  So the good news is that parents might save their children a great deal of trouble and suffering simply by substituting good nutritional behaviors and environments for bad.



Institute of Medicine. 2015. Examining a developmental approach to childhood obesity: The fetal and early childhood years: Workshop summary. Washington D.C.: The National Academies Press. 159 pp.

Time to Rethink Omega-3s?

[Notable New Media]

by Kenneth W. Krause.

Kenneth W. Krause is a contributing editor and “Science Watch” columnist for the Skeptical Inquirer.  Formerly a contributing editor and books columnist for the Humanist, Kenneth contributes regularly to Skeptic as well.  He may be contacted at

Nutrition researchers have long touted the heart-health benefits of Omega-3 polyunsaturated fatty acids, typically found in wild oily fish and flaxseed, for example.  General recommendations to consume foods rich in Omega-3s and even to supplement with fish oil derived in part from evidence showing that the cold-climate Inuit, for example, have persisted quite healthfully–that is, with a low incidence of cardiovascular disease–on traditional marine diets rich in fat, especially Omega-3s.  The inference was that the Omega-3 fatty acids were protective against heart disease, perhaps because they lowered LDL and raised HDL cholesterol levels in the blood.

But do such benefits accrue to all human populations more or less equally?  Perhaps not.  In a study recently published in Science, researchers scanned the genomes of 191 Greenland Inuit (formerly known as Eskimos, whose ancestors had lived in the Arctic for thousands of years) and compared them to the genomes of 60 Europeans and 44 Han Chinese.  What did they find?  The native Greenlanders had developed special mutations to genes involved in fat metabolism (fatty acid desaturases) that likely evolved through natural selection to help counteract the effects of a diet high in fat, mostly from seals and whales that consume oily fish.

According to these researchers, that 100 percent of the Inuit, but only 2 percent of the Europeans and 15 percent of the Chinese, possessed these adaptations implies that, on average, members of each population might synthesize Omega-3s very differently from members of the other populations.  In other words, one group’s unique evolutionary adaptations–in this case, to cold weather and a traditional, high-fat diet–might render them an inappropriate population upon which to base nutrition advice to the general public.

But those who take personal health seriously already knew better than to receive generalized nutrition advice as gospel.  First, as I’ve argued more than once before, nutrition science is inherently volatile.  Myriad confounding factors, difficult to isolate and measure, often make it nearly impossible for researchers in this field to offer concrete advice.  Second, for many reasons, every individual requires a personalized diet and exercise plan that also evolves as the individual grows older and as continuing and disciplined personal experimentation (that is, science) reveals his or her special health and performance needs.