Tag Archives: obesity

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 krausekc@msn.com.

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.

References:

(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. http://www.nwcr.ws/Research/default.htm

(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.

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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 krausekc@msn.com.

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.

References:

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.

dog-situps

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 krausekc@msn.com.

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

 

References:

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.

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 krausekc@msn.com.

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.

 

Reference:

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.

Obesity: What Does the Science Say (Or Not Say)?

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 krausekc@msn.com.

Since the 1940s, the concept of “energy balance” (EB) has governed obesity research worldwide.  Springing intuitively from the laws of thermodynamics, this model proposes that excess adiposity results whenever energy intake overtakes energy expenditure.  Thus, the behaviors of overeating and failure to exercise, i.e., “gluttony” and “sloth,” have been emphasized over complex metabolic processes and the unique effects certain foods might have on those processes.

The conventional wisdom of EB continues to dominate public policy today.  According to the U.S. Centers for Disease Control, “Weight management is all about balance—balancing the number of calories you consume with the number of calories your body uses,” and the World Health Organization, “The fundamental cause of obesity … is an energy imbalance between calories consumed on one hand, and calories expended on the other.”

So instead of testing more sophisticated strategies, dieters are encouraged to count their calories—whether derived from steak, spinach, potatoes, Wonder bread, or Mountain Dew—as if they were all created equal.  Unsurprisingly, the relevant popular science literature also tends to reflect this paradigm.  As American nutrition scientists Marion Nestle and Malden Nesheim reiterate in their new book, Why Calories Count, the ingestion of too much energy is “arguably the most important cause of public health nutrition problems in the world today.”

Nevertheless, some scientists, physicians, and science journalists have recently challenged the EB equation.  In its place, they propose models highlighting the roles of hormones like insulin, leptin, cortisol, and estrogen—even to the absolute exclusion of personal control and responsibility.  Here, assorted nutrients—or foods that should be distinguished for their lack of nutrients—are treated very differently because of the chains of metabolic events they are thought to initiate.

For example, Jonathan Wells and Mario Siervo—nutrition researchers from the UK and Italy, respectively—contend that EB fails to explain, among other things, why people continue to gain weight, rather than plateau, after the point when their gains reestablish energy equilibrium (Wells and Siervo 2011).  They also remind us that, despite the theoretical logic of EB, neither behavioral prevention nor behavioral treatment has generally proven successful.

“The relationship between energy balance and weight gain,” the Europeans argue, “is a truism, not an explanation, hence no direction of causation can be inferred”.  Indeed, the conventional wisdom of EB might have the “logic” entirely backwards.  Reversing the direction of causation, Wells and Siervo propose, does not contradict the laws of thermodynamics, or even the EB equation per se.  But it does permit us to reconsider the associations between behavior, metabolism, and weight change.

We’ve long understood that hormones regulate weight gain—in growing children and pregnant women, for example.  And since the 1930s, European clinicians have used insulin—a hormone released from the pancreas in response to elevated blood glucose levels—to fatten underweight patients.  Is it just a coincidence that both obesity rates and the consumption of sweeteners and refined carbohydrates have skyrocketed in recent decades?

The obesity problem is surely a complex and multifaceted one.  But testing multiple hypotheses of potential merit is better than testing only one, or none at all.  By any reasonable standard, our current strategy has proven largely ineffective.  “A more skeptical approach,” Wells and Siervo expect, “is likely to bring valuable returns.”

Pediatric endocrinologist Robert Lustig agrees that adiposity is a hormonal predicament.  In his new book, Fat Chance, the child obesity expert indicts simple, super-sweet sugars as the chief culprits, arguing that sucrose and high-fructose corn syrup corrupt our biochemistry and render us hungry and lethargic in ways fat and protein do not.  In other words, Lustig insists that sugar-induced hormonal imbalances cause self-destructive behaviors, not the other way around.

What EB proponents fail to consider, Lustig vies, is the overwhelming and far-reaching metabolic influence of insulin.  In the body it causes energy to be stored as fat; in the hypothalamus it can cause “brain starvation,” or resistance to leptin, the satiety protein hormone released from adipose tissue.  Excess insulin, or hyperinsulinemia, thus causes our hypothalami to increase energy storage (gluttony) and decrease energy consumption (sloth).  Add to this process an increasingly insulin-resistant liver (which drives blood insulin levels even higher), a little cortisol (the adrenal stress hormone), and sugar dependence (or at least habituation), and dieters, Lustig concludes, hardly stand a chance.

Lustig labels fructose a “toxin” because he believes it drives these events, along with a cluster of maladies and diseases referred to as “metabolic syndrome.”  Although the glucose that always accompanies fructose will stimulate an insulin response directly, fructose itself will not.  It will, however, cause liver insulin resistance which, in turn, stimulates the pancreas to release even more insulin.  Again, leptin resistance may follow.  Notable as well is that fructose, unlike other foods, will not decrease the flow of ghrelin—the hunger signaling peptide hormone—from the stomach to the brain.

Thus, Lustig deems the EB model of weight gain a dangerous and unscientific myth.  First, sugar alone proves that all foods are not beneficial nutrients and, thus, that a calorie is not a calorie.   Second, he contends, generally eating less and exercising more is a strategy doomed to failure given the profound and wide-ranging metabolic processes and effects that certain foods tend to generate.

But the most outspoken and persistent critic of EB might be veteran science journalist and co-founder of the Nutrition Science Initiative (NuSI), Gary Taubes.  In a recent Nature editorial, Taubes blamed the current obesity pandemic on both the research community, for failure to fully comprehend the disease, and the food industry, for exploiting that failure (Taubes 2012).  He picks up the theoretical mantle where Lustig leaves it, implicating insulin and condemning fructose, but he expands the list of “nutritional” villains considerably to include all easily digestible carbohydrates that quickly raise glycemic indices.

As Taubes points out, the “hormonal/regulatory defect” hypothesis (H/RD) of obesity is actually nothing new.  A German internist, Gustav von Bergmann, proposed it in the early 1900s and it gained general acceptance throughout Europe prior to the Second World War.  But, of course, much changed after the conflict ended.  Germans and Austrians struggled to redefine themselves, for example, and the lingua franca of science shifted somewhat abruptly from German to English.

Medical practitioners quickly abandoned H/RD for a different idea articulated in the 1920s by University of Michigan physician Louis Newburgh.  “All obese persons are alike in one fundamental respect,” the American had argued. “They literally overeat.”  In attributing excessive weight gain to either a “perverted appetite” or a “lessened outflow of energy,” Newburgh laid an enduring foundation, Taubes contends, for a failed and yet insufficiently tested hypothesis.

Taubes scoured the relevant literature from 1944 onward and isolated nearly100 experiments (results at nusi.org).  In his estimation, however, each study was critically flawed.  All free-living trials, of course, lack control over subjects’ actual consumption.  On the other hand, the more well-controlled experiments lost statistical power due to small sample sizes and short durations.

Some studies severely restricted caloric intake in carbohydrate-limited diets, thus undermining the investigators’ ability to determine whether carbohydrate content can influence weight gain independent of total caloric content.  Others severely restricted control diets, thereby limiting carbohydrate content as well.  Finally, some trials failed to either evaluate low-carbohydrate diets at all, distinguish between macronutrient content, or eliminate habitually lean subjects.

Through NuSI, Taubes (and co-founding physician Peter Attia) plan to fund and facilitate more appropriate studies performed by “independent, skeptical researchers” who are also leaders in the field.  Designed to rigorously test competing hypotheses, experimental diets would consist of vastly different macronutrient composition and, they hope, demonstrate that fat can be lost or gained while total caloric intake remains fixed.

Subjects would be ward-restricted and randomized into two groups.  One would receive a balanced diet, rich in carbohydrates; the second would be severely carbohydrate restricted—ideally to less than sixty grams per day.  Both cohorts would be fed an isocaloric diet matching daily intake to pre-experiment daily expenditure.  Studies would last for at least two months, and energy expenditure, insulin levels, and body composition would be measured at appropriate stages.

Although she admires Taubes’ commitment, Marion Nestle believes that such experiments will be exceedingly expensive and tough to manage and interpret.  Familiar with his and Lustig’s arguments, she maintains that a calorie is still a calorie in the limited context of weight gain.  Like many others, she characterizes the H/RD view of obesity as “reductionist,” or lacking in nuance, because it fails to consider, among other things, the role of behavior.  “Committed, intelligent people,” she told me, “must find ways to deal with a food environment that encourages frequent eating of large portions.”

Of course some of Lustig’s and Taubes’ ideas have been widely accepted for some time—the most direct effects of insulin and leptin, for instance.   The U.S. Department of Agriculture, for example, has recently supplanted its carbohydrate-ridden food “pyramid” with a “plate” relatively lacking in simple sugars and starches.  And even daytime network television doctors now advise audiences to avoid such cuisine.

But these writers’ contention that personal control and responsibility have no practical place in the discussion remains highly controversial.  The evidence is clear—most (but not all) people who attempt to lose weight—and keep it off—will fail.  Less obvious are the reasons why.  Has biology stacked the deck against the overweight and obese to the point of utter hopelessness?  Or is it merely a fact of life that, in any context, the vast majority always fails to overcome exceptionally challenging obstacles?

Overweight or not, we all have a substantial interest in settling these debates.  Obesity rates have doubled in the U.S. and tripled in the UK since the 1980s.  Health authorities have drawn persuasive connections between obesity—or the metabolic dysfunction for which obesity is a marker—and a plethora of horrifying diseases, including cancer.

Indeed, recent studies have advised us that obesity is directly responsible for twenty-one percent of all U.S. healthcare costs (Cawley and Meyerhoefer 2012), more than even smoking (Moriarty, et. al. 2012).  A genuine medical crisis of this magnitude, I would argue, deserves not so much more attention as it does higher scrutiny.  As Taubes urges, Americans in particular can hardly afford not to make the necessary investments.

References:

Cawley, J. and Meyerhofer, C. 2012. The medical costs of obesity: an instrumental variables approach. J. Health Econ. 31(1): 219-30.

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

Moriarty, J.P., et. al. 2012. The effects of incremental costs of smoking and obesity on health care costs among adults. J. Occup. Environ. Med. 54(3): 286-91.

Nestle, M. and Nesheim, M. 2012. Why Calories Count: From Science to Politics. Berkeley: University of California Press.

Wells, J.C.K. and Siervo, M. 2011. Obesity and energy balance: is the tail wagging the dog? Eur. J. Clin. Nutr. 65(11): 1173-89.

Taubes, G. 2011. Why We Get Fat and What to Do About It. NY: Knopf.

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

Obesity Redux: A Response to the Readers.

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 krausekc@msn.com.

In thoughtful response to my recent SI column, “Obesity: What Does the Science Really Say (Or Not Say)?” a number of readers wrote to me or the editor raising crucial issues deserving of an equally considerate response.  As such, and because a great deal of new science has been published on the subject, I’ve chosen to forego the Letters section and address these readers’ concerns here.

One foundational question tends to resurface every few years or so.  It asks whether excess adiposity is in fact a serious health problem, as prevailing medical opinion has dictated for more than a half century, or whether it is just as well or even better to be fat.

A new JAMA study on the topic caused quite a stir this year among both the popular media and public health officials (Flegal, et. al., 2013).  Four American and Canadian researchers led by Katherine Flegal of the National Center for Health Statistics, Centers for Disease Control and Prevention in Hyattsville, Maryland reviewed 97 studies providing a sample size of more than 2.88 million individuals and 270, 000 deaths to calculate all-cause mortality hazard ratios for standard body mass index (BMI) classifications(1).

Flegal’s results caused some lay observers to inquire, as Slate Magazine’s William Saletan did on January 2, “Is Fat Good?”  Her 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.

Interesting data, to say the least.  But how should they be responsibly interpreted?  Unsurprisingly, much of the popular media, along with certain food and drink special-interests, focused on one possible explanation they assumed their audiences and customers would prefer to hear—essentially that overweight as a general proposition can be a positive thing.

On the other hand, certain popular sources failed to report Flegal’s own list of potential explanations, including an “earlier presentation of heavier patients” and a “greater likelihood of receiving optimal medical treatment.”  In such instances, those inclined for whatever reason to favor a positive appraisal of excess adiposity should be prepared and willing as well to endorse an increased need for frequent medical attention.

But the so-called “obesity paradox” is nothing new.  Since the 1980s, it has typically proposed that, although overweight raises a person’s risk of diabetes, heart disease, cancer, and many other chronic illnesses, some people—particularly the ill and those of middle-age or older—might actually benefit from a little, though never a lot of extra weight (Hughes 2013).

Indeed, in an editorial to Flegal’s study, two physicians suggested that slightly elevated BMIs in patients suffering from certain chronic diseases, acute catabolic illnesses, and even traumatic injuries might be sensibly associated with lower mortality (Heymsfield and Cefalu 2013).  If so, it becomes apparent why overweight or even mild obesity could both increase the risk of life-threatening diseases and decrease mortality rates.

But no responsible health care professional endorses excess weight gain generally.  In fact, at least one recent study has linked higher BMIs to not only the aforementioned physical ailments, but to impaired cognition and poorer memory in post-menopausal women as well (Kerwin et. al. 2010).  In addition, other experts continue to warn, for example, that “individuals exposed to maternal obesity during fetal life are at increased risk of becoming overweight or obese children and adults themselves, thus perpetuating the vicious cycle of obesity” (Gillman and Poston 2012).

We should of course remain open to all potential subtleties regarding adiposity and health.  But given the depth and breadth of the evidence associating extreme overweight with all manner of affliction, the primary public-health objective must be to prevent both obesity and pre-obesity(2).

Other readers have questioned or commented on the efficacy of certain popular diets.  It should be acknowledged from the start, of course, that good health is primary and that only diet plans holding nutrition above or alongside weight-loss or weight-maintenance are worth consideration.  In fact, both my research and personal experience lead me to believe that the only truly effective weight-loss diets are also exceptionally healthy ones.

Experts have now established that the typical Western diet—one replete with fried and sweet foods, processed and red meats, refined grains, and high-fat dairy products—is less than ideal, to put it most diplomatically.  A recent British study, for instance, followed 3775 men and 1575 women of middle-age for an average of sixteen years and concluded quite sweepingly that adherence to Western-style cuisine significantly reduces the prospect of “ideal aging,” i.e., remaining free of chronic diseases and retaining high physical, mental, and cognitive functionality (Akbaraly et. al. 2013).

That much resolved, the implied query remains: With what should we replace the typical Western diet?  I recommend that we begin by conceiving of a “normal” diet.  In other words, why not define appropriate nutritional habits (yes, plural) scientifically as ones offering foods and portions that the human species, or perhaps slightly more specific human populations, evolved to consume?  From there, individuals can and must fashion more exclusive diet plans that suit their particular objectives and biological circumstances.

As one reader observed, some inclined toward an evolutionary definition have endorsed the “Paleo” diet, based on the assumed consumption habits of our ancestors who lived from 2.5 million to 10,000 years ago.  Thus, all foods invented during or after the agricultural revolution are unceremoniously expunged from the menu.  On the obviously positive side, Paleo dieters exclude all processed sugars, meats, and grains.  More controversially, however, they eliminate dairy, peanuts, lentils, beans, and peas, for example.

Like many her colleagues, biologist Marlene Zuk has judged the Paleo diet’s logic a fundamentally flawed fantasy (Zuk 2013).  First, says Zuk, we shouldn’t even hope to construct a nutritional plan based on the distant past when so much has changed in recent millennia, including the biology of every species of plant, animal, and human on the planet.

Second, Paleo diet dogma denies its followers the benefits of some exceptionally nutritious fare.  Dairy is rich in calcium, for example, whole grains are packed with fiber and vitamins, and legumes are replete with protein.  Consider the various circumstances of consumption as well.  Why, for instance, should athletes rebuff easily digested sources of carbohydrates that help them recover quickly and safely from especially vigorous exercise?

Finally, the Paleo fixation ignores the heterogeneous nature of our ancestors’ environments and assumes an ideal past that never existed.  The truth is we don’t know exactly how much meat, fish, fruit, or even primitive grains our Pleistocene forbears ate, or at what precise stages of their evolution.  What we do know is that, to survive, they had to be flexible—not doctrinal.

Another reader contemplates the Mediterranean diet, also the subject of recent popular headlines.  One especially noteworthy study, published last February in the New England Journal of Medicine, contrasted the cardiovascular health benefits of one low-fat diet with those of two Mediterranean-style diets—one supplemented with nuts, the other with extra-virgin olive oil (Estruch et. al. 2013).  After following 7447 randomly assigned Spaniards at risk for heart disease, the investigators found that, relative to a low-fat plan, adherence to either Mediterranean plan reduced a patient’s risk of suffering cardiovascular death, myocardial infarction, or stroke by thirty percent.

So exactly what did the Mediterranean dieters eat?  In addition to either nuts or olive oil, participants consumed at least three daily servings of fruit, and at least two servings of vegetables.  Fish was eaten at least three times per week, as were legumes.  The menu offered white, but not red meats and permitted the drinking of wine.  On the other hand, subjects avoided cookies, cakes, and pastries completely, and limited their consumption of dairy and processed meats.

Perhaps most notably and controversially, however, the authors’ data tend to refute the long-standing conviction that fat intake must be reduced to promote cardiovascular health.  So what of vegetarianism, one might reasonably wonder—is its well-documented reputation for good health at least somewhat overblown?

Not according to a group of researchers from Loma Linda University who recently studied 73,308 male and female Seventh-day Adventists (Orlich et. al. 2013).  Participants were categorized as nonvegetarians, semi-vegetarians, pesco-vegetarians (accepting seafood), lacto-ovo-vegetarians (accepting dairy and eggs) or vegans (excluding all animal products).  After an average of six years per subject, 2570 deaths were recorded.

Overall, the group calculated a twelve percent lower adjusted hazard ratio for all-cause mortality in the combined vegetarian versus nonvegetarian categories.  Oddly, the association was far stronger for men (vegan males scored a twenty-eight percent lower hazard ratio than nonvegetarians) and less than statistically significant for women.

When considered in light of the “hormonal/regulatory defect” hypothesis proffered by writers like Gary Taubes and Robert Lustig, recent studies and commentaries offer considerable, though certainly qualified and incomplete, guidance for the obese and severely overweight.

First, though solutions may appear simple, their execution will doubtless prove otherwise.  For those leading an “average” or “typical” lifestyle, thoughtful and significant changes are unavoidable.  Second, ample portions of vegetables and fruits are the mainstays of any successful diet.  Lean unprocessed meats, healthy oils, dairy, and whole grains—though clearly valuable—should probably be conceived of as nutritional supplements, not as staples.  Empty calories, including all sweets and processed grains, should be erased from the menu until personal experimentation reveals them tolerable to whatever extent.  Finally, each individual must fashion his or her own solution.  Even the most successful popular diets should be scrutinized for their respective strengths and weaknesses, and then summarily rejected.

Tragically, the politics of frustration and anger have intruded deeply into the obesity discussion, as yet one more reader has suggested.  Concerned citizens are frequently implored or even coerced to deny the only interventions that have ever succeeded: those which emphasize education, individual experimentation, and personal responsibility.  In their absence, we are encouraged instead to blame a faceless and unoffendable community for the obese person’s choices at the supermarket, restaurant, and home.

Taubes, Lustig, and others claim that personal responsibility is irrelevant.  They allege that the biological obstacles for certain obese individuals are insurmountable and, as such, that no obese person should ever be asked to make informed, rational choices.  Yet, incredibly, each writer’s new book offers dietary instruction.  They advocate as well for continued research into the science of nutrition as it relates to obesity.  Excellent!  One wonders, however, what desirable interventions could possibly result that demand no measure of personal responsibility?

Of course some of us are biologically predisposed to obesity—myself included.  Why should it surprise us that severely excessive adiposity results from any number of physical problems or abnormalities?  And even among the obese, some solutions will prove more difficult than others.  Nevertheless, well-intentioned, science-minded commentators shouldn’t try to convince us that obesity can’t be overcome until the evidence clearly confirms as much.

Impressionable yet intelligent, motivated children deserve far more forthright and inspiring counsel.  In truth, obesity can be and often is effectively confronted, and obese children especially deserve the chance to regard their situation as an opportunity for accomplishment, and not as an excuse for regression to mediocrity.

Notes:

(1) Standard BMI categories, calculated as weight in kilograms divided by height in meters squared, were reported in 1997 from the World Health Organization Consultation on Obesity and adopted in 1998 by the American National Heart, Lung, and Blood Institute.  In her team’s study, Flegal used the latter organization’s current terminology: underweight (BMI of 18.5), normal weight (18.5-25), overweight (25-30), and obese (≥30).  More specifically, she also defined grades 1, 2, and 3 obesity as corresponding to BMIs of 30-35, 35-40, and ≥40, respectively.  All BMI categories are controversial, however, because they fail to differentiate between lean muscle mass and fat mass or subcutaneous fat (less dangerous) to visceral fat (more dangerous).

(2) But for a sociologist’s critical examination of how obesity has come to be defined as a social crisis of epidemic proportions, see Boero, Natalie. 2012. Killer Fat: Media, Medicine, and Morals in American “Obesity Epidemic.” Rutgers University Press.

References:

Akbaraly, T., Sabia, S., et. al. 2013. Does overall diet in midlife predict future aging phenotypes? A cohort study. Am. J. Med. 126(5): 411-419.e3.

Estruch, R., Ros, E., et. al. 2013. Primary prevention of cardiovascular disease with a Mediterranean diet. N. Engl. J. Med. 368: 1279-1290.

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

Gillman, Mathew W., and Poston, Lucilla. 2012 Maternal Obesity. Cambridge University Press. 4-5.

Heymsflield, S.B. and Cefalu, W.T. 2013. Can overweight as defined by BMI actually have a protective association with mortality? JAMA 309(1): 87-88.

Hughes, V. 2013. The big fat truth. Nature 497: 428-430.

Kerwin, D.R., Zhang, Y., et. al. 2010. The cross-sectional relationship between body mass index, waist-hip ratio, and cognitive performance in postmenopausal women enrolled in the Women’s Health Initiative. J. Am. Ger. Soc. 58(8): 1427-1432.

Orlich, M.J., Singh, P.N., et. al. 2013. Vegetarian dietary patterns and mortality in Adventist Health Study 2. JAMA Intern. Med. DOI: 10.1001/jamainternmed.2013.6473. (published online June 3, 2013.)

Zuk, Marlene. 2013. Paleofantasy: What Evolution Really Tells Us About Sex, Diet, and How We Live. NY: W.W. Norton & Company.

Childhood Obesity, Fast Food, and the Overstuffed Elephant in the Room.

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 krausekc@msn.com.  

One in three American children were confirmed overweight or obese in 2009.(1)  Since then, few if any health statistics have been more widely publicized.  Five years later, however, we still don’t seem to understand how we’ve accomplished this for our kids.

Biologists and anthropologists have broadly indicted certain evolutionary mismatches between our contemporary “obesogenic” environment and biological adaptations naturally selected thousands or even millions of years ago (Power and Schulkin, 2009).  These incongruities generally fall into two categories.

First, present-day humans are thought to naturally favor inactivity and, thus, to consistently burn too few calories.  The role of exercise in body composition control is complicated and somewhat controversial.  Regardless, it is not the subject of this column.

Second, Westerners especially are accused of consuming too many total calories or too many inappropriate foods.  Diet’s role in the obesity crisis is far clearer and more convincing.  Indeed, specific culprits—highly refined carbohydrates, in particular—have been identified.

But a much more practical question remains, implicating both personal behavior and public policy.  From what cultural sources does the problem primarily emanate, and in what relative proportions?  In other words, precisely where are American children really getting fat?

Myriad scholars and government officials have vigorously impugned the fast food industry.  And why shouldn’t they?  As the prevalence of overweight and obesity has tripled among American children in the last thirty-five years, the percentage of total energy intake consumed from fast food has risen from two percent in 1978 to thirteen percent in 2006.

Unsurprisingly, fast food outlets continue to stuff their menus with perhaps the poorest nutritional options imaginable.  On average, fast foods are higher in solid fat (23.9 % of total energy) than food from either retail stores (17.6 %) or schools (20.9%).  Compared with non-consumers, kids who eat fast food receive higher levels of total energy, total fat, and saturated fat.  They also consume less fiber, milk, fruit, and vegetables, and more sugar-sweetened beverages and French Fries.

bad food kid

So what’s not to detest about fast food?  Very little or nothing at all, we might agree, but that’s not the question at hand.  Instead, we might ask whether the evidence truly condemns fast food as a proximate cause of childhood obesity and, if not, whether fast food serves only as a relatively unobjectionable scapegoat for a far more likely suspect.

The Centers for Disease Control and Prevention, one of the main operating arms of the U.S. Department of Health and Human Services, has published an authorless online report titled “Incorporating Away-From-Home Food into a Healthy Eating Plan.”  The article focuses on the relationship between childhood obesity and food-away-from-home (FAFH)—including fast food but not school meals.

With about one-third of the average American’s daily calories coming from FAFH, the report opines, “it is important to consider how individuals can fit these items into a healthy eating plan.”  Assumed but not supported in this decree is the conviction that Americans who consume significant amounts of fast food are interested in a healthy diet and, if so, capable of recognizing, preparing, and consistently consuming one.

After reciting the familiar nutritional and proportional shortcomings of FAFH, the report references dozens of studies thought to demonstrate a robust association between FAFH and overweight or obesity.  One study, for example, found that both adult and child fast food eaters consumed more calories, fat, and sodium, and less vitamins, milk, fruits, and vegetables than non-eaters.  Another discovered that states with higher levels of obesity had more fast food restaurants.  Other longitudinal studies associated higher frequencies of fast food consumption among girls, boys, and adults with elevated BMIs or adiposity.

In the end, the CDC cautioned that the available literature had yet to conclusively establish a direct causal link between FAFH and obesity.  Nevertheless, they left readers with a series of nutritional and behavioral prescriptions revealing an unyielding confidence that FAFH per se continues to supply the United States with an increasing number of overweight and unhealthy children.

For example, the report urges fast food consumers to “tailor away-from-home meals to make them as healthful as possible,” and to “control food and beverage portions” by sharing, ordering half-portions, or taking the excesses home.  It finally concludes with a plea to “reduce reliance on away-from-home food.”  But never does the CDC’s report consider whether fast food consumption might be a mere marker for a more instrumental set of bad nutritional attitudes and habits.

In 2010, four researchers at the Economic Research Service of the U.S. Department of Agriculture published a similar, but more involved report, “How Food Away From Home Affects Children’s Diet Quality” (Mancino 2010).  Led by Lisa Mancino, the group purportedly set out, first, to test the now-popular childhood obesity-FAFH hypothesis and, second, to help inform public policy prevention strategies.

Mancino’s analysis was based on data from the 2003-2004 National Health and Nutrition Examination Survey and the 1994-1996 Continuing Survey of Food Intakes by Individuals.  Children ages six to eighteen were included, and FAFH was defined as all commercially prepared food—featuring fast food but not food from schools.  Results were based on both relative caloric intake and diet quality, as measured by the 2005 Healthy Eating Index. Mancino also attempted to control for the impacts of sugar-sweetened beverages and certain personal characteristics such as food access and preferences.

The government’s findings were striking, of course, but far from unexpected.  For all children, Mancino discovered, each FAFH meal added 65 total calories and lowered diet quality scores by four percent compared to meals prepared at home.  Older children between thirteen and eighteen fared significantly worse, receiving 107 additional calories.

Mancino’s report provides Americans with yet another remarkable set of statistics that might well induce effective behavior change assuming two premises: first, that fast food actually causes childhood obesity and, second, that the target population is open to such adjustment.  But do Mancino’s results truly speak to the foundational issue of causation?

She and other officials at the U.S. Department of Agriculture certainly seem to think so.  Her study’s findings, they contend, not only “support the contention that increased consumption of FAFH is a contributing factor in the current epidemic of childhood obesity,” but also “strengthen() the argument that there is a causal relationship between FAFH and increased caloric consumption and decreased dietary quality.”

Again, the possible effects of other food—even food from the most ubiquitous source available to children—were never discussed.  But isn’t it far easier to intuit, for example, that American kids are getting fat and consuming fast food as a result of nutritional habits and attitudes established at home?

A very similar question occurred quite recently to three nutrition scientists led by Barry Popkin at the University of North Carolina at Chapel Hill.  In a new study supported by both the Robert Wood Johnson Foundation and the National Institutes of Health, Popkin’s group attempted to distinguish and compare the independent associations between childhood obesity and either fast food consumption or the remainder of dietary intake (Poti 2014).

Popkin’s cross-sectional analysis included 4466 children ages two to eighteen who participated in the 2007-2010 National Health and Nutrition Examination Survey.  In terms of fast food, the young subjects were classified as either non-consumers, low-consumers (0.1-30% of energy), or high-consumers (>30%).  Popkin’s group also attempted to control for various potential counfounders, including physical activity levels, sex, age, race-ethnicity, and parental income and education.

The authors first note that previous research has focused intensely on fast food as the key contributor to the rising incidence of childhood obesity.  But prior studies, they argue, tended to “control for, rather than explore, the differences between fast food consumers and nonconsumers.”  Indeed, the mere possibility that fast food might not be directly associated with childhood obesity, they agree, had to that point never been tested.

So Popkin set out to address the problem anew by incorporating and analyzing food choices made outside the fast food restaurant.  In other words, to test his hypothesis that a nutritionally imprudent at-home diet actually associates more robustly with overweight than fast food consumption per se, Popkin contrasted the at-home dietary patterns of fast food non-consumers, low-consumers, and high-consumers.

After examining remainder of dietary intake, then, the authors discovered that the children had clustered into two distinct groups.  Roughly half consumed a typical “Western diet,” characterized by higher intakes of sugar-sweetened beverages, salty snacks, high-fat sandwiches, and candy; while the others ingested a “Prudent diet,” marked by higher intakes of milk, fruit, and low-fat mixed dishes.

Popkin’s results defied received institutional wisdom.  First, both fast food high- and low-consumers were significantly more likely to consume a Western at-home diet than non-consumers (63.4 %, 54.2%, and 43.9%, respectively).  Second, children who combined both high-fast food consumption and a Western diet showed significantly higher prevalence of overweight or obesity than Prudent non-consumers (40.4% and 28.0%, respectively).

Absent consideration of remainder of dietary intake, high-fast food consumption was significantly associated with a higher incidence of overweight.  But that association, the authors emphasize, was “attenuated and nonsignificant after adjustment for the remainder of diet.”  On the other hand, “consuming a Western dietary pattern . . . was significantly associated with a higher prevalence of overweight/obesity after control for fast food intake.”

In sum, when both eating behaviors were considered, “the remainder of diet, but not fast food per se, was associated with overweight/obesity.”  In previous obesity studies, Popkin adds—including the 2010 analysis conducted by Mancino and other officials at the U.S. Department of Agriculture—“(a)ssociations between fast food intake and these health outcomes were overestimated.”

The authors close with an aspirational missive to American policy-makers. These new findings, they warn, also “suggest that the effect of public health efforts targeted at fast food restaurants may also be overestimated” and “not sufficient to reduce childhood obesity if the remainder of the diet is not also addressed.”

As always, the research must continue.  Nevertheless, common sense should inform us all that childhood obesity originates, matures, and proliferates in the home.  Children don’t live in fast food restaurants, after all, and restauranteers are not responsible for the teaching of lifestyle values, attitudes, and habits to our kids.  No family has ever been forced to consume ridiculously inappropriate “foods,” or to sit in front of the television set to view obviously manipulative advertisements.  Plainly, no aspect of fast food will ever be the real issue.

On the other hand, should the U.S. government continue to intercede between childhood obesity and its genesis, it should do so efficiently and scrupulously.  And if any government official genuinely desires to affect childhood obesity, then he or she will surely speak the entire truth to the one true political power (and to the party that needs to hear it most)—that is, the American majority.

Endnote:

Recent studies and popular media reports alleging a decline in U.S. childhood obesity may have been mistaken.  Instead, new research finds that all classes of childhood obesity, especially severe obesity, have increased in the last 14 years.  Skinner, A.C. and Skelton, J.A. 2014. Prevalence and trends in obesity and severe obesity among children in the United States, 1999-2012. JAMA Pediatr. Published online April 7, 2014. doi:10.1001/jamapediatrics.2014.21.

References:

Incorporating Away-From-Home Food into a Healthy Eating Plan. Research to Practice Series, No. 6.  National Center for Chronic Disease Prevention and Health Promotion Division of Nutrition, Physical Activity, and Obesity.  http://www.cdc.gov/needphp/dnpa/nutrition/pdf.r2p_away_from_home_food.pdf (last accessed on April 2, 2014).

Mancino, L., Todd, J., Guthrie, J., and Lin, B-H. 2010. How food away from home affects children’s diet quality. Washington, D.C.: U.S. Department of Agriculture, Economic Research Service. (Economic Research Report No. 104).

Poti, J.M., Duffy, K.J., and Popkin, B.M. 2014. The association between fast food consumption with poor dietary outcomes and obesity among children: is it the fast food or the remainder of diet? Am. J. Clin. Nutr. 99: 162-171.

Michael L. Power and Jay Schulkin, The Evolution of Obesity (Johns Hopkins Press, 2009.