Since March is National Nutrition Month, and because I’m still on my pediatrics clerkship, I thought “What better time to write about childhood obesity?”
In recent years, childhood overweight and obesity statistics have received a good deal of media attention, but this has done little to slow their rise. Data from the National Health and Nutrition Examination Survey shows that nearly 1 in 5 children aged 2-19 are obese. Even more concerning, since 1980 obesity rates have tripled in the 6-11 and 12-19 age groups.
Our individualistic society has decided that obesity is a personal failure – something that’s completely the fault (and under the control) of the patient – but it’s not as simple a decision to smoke a cigarette, drive drunk, or get on a motorcycle without a helmet. Obesity is multifactorial, and this fact is only highlighted when dealing with pediatric patients, but the advice we give is two-dimensional: eat less, exercise more.
Unfortunately, we’ve been giving more or less this same advice for decades as the problem continues to worsen. There is accumulating research that obesity causes potentially irreversible metabolic alterations that render our mantra of “diet and exercise” inadequate to reverse the problem. Thus, some would argue that the best way to address the obesity epidemic in America is to prevent obesity in the first place – but in order to do this, we have to understand how we got here.
Contributing to the obesity issue is the fact that we’ve drastically changed the very notion of what it means to feed ourselves: at the grocery store we buy meals, entrees, and side dishes – not ingredients. Worse, the food & diet industries actively work to confuse consumers through marketing and product placement. Sedentary entertainment has vastly expanded in the past several decades, and in many communities, such as the one I currently serve, children have even less opportunities to exercise because their schools have cut gym class or it’s just plain unsafe to go outside. These variables result in obesity being practically inevitable – “the new default,” as one of the physicians I work with recently called it.
So what are doctors doing about it? Research shows that we’re doing a poor job of talking to children and their parents about unhealthy weights – one study revealed that among parents of children with a BMI in the 85th percentile or higher (the numerical definition of overweight in children), only 22% report being told by a doctor or other health professional that their child was overweight. Assuming we even decide to address the issue, we have to give children and their parents a clear message and help them set real goals – I cringe when I see doctors tell parents “Johnny just has to try to eat a little less, and get a bit more exercise.”
Two of the biggest offenders I’ve been able to detect when interviewing children and their parents are liquid calories and portion size, but it’s important not to overwhelm patients when asking them to make lifestyle changes. Therefore, my strongest recommendation to parents is often to limit juices and eliminate sweetened drinks – especially sports drinks and sodas. I’m not a fan of artificially sweetened drinks or “diet” beverages, but in medicine we often have to bargain with patients, and I’d rather see children drinking flavored water than Coke and Gatorade. However, I’d caution parents to consider the impact that training their children to drink only that which is sweet will have on their health in the future.
But things like limiting sugar and teaching portion control are just the tip of the iceberg. We won’t make substantial inroads in reigning in childhood obesity until we attack the problem on multiple fronts. That means improving school lunches, eliminating food deserts, making neighborhoods more exercise-friendly, and plenty of other small changes that, when combined, alter the environment we expose our children to – and this can only happen when we decide as a society that these are the right things to do. Until then, parents and doctors will continue to bear the burden of the uphill battle against childhood obesity.
“Our kids didn’t do this to themselves. They don’t decide the sugar content in soda or the advertising content of a television show. Kids don’t choose what’s served to them for lunch at school, and shouldn’t be deciding what’s served to them for dinner at home. And they don’t decide whether there’s time in the day or room in the budget to learn about healthy eating or to spend time playing outside.”
-Michelle Obama
davebrown9
March 30, 2012
For what it’s worth, I think it’s a mistake to suggest that gluttony and sloth are the central issues when what we have is bad science informing dietary advice and public policy. Consider this:
“The current relentless pressure to convert the entire population to a low-fat, high carbohydrate dietary regime seems to be driven by a curious set of circumstances. It began with an idea aimed at inducing the public to buy and eat foods that are profitable to the agricultural and food industries as opposed to foods that man was designed to eat. With judicious use of public relations, advertising, pseudo science, and political prowess, this idea has grown into a sophisticated and powerful movement that is changing eating habits throughout the world. Concurrently, the national priority aimed at the treatment of the modern nutritional diseases, rather than their prevention, has focused medical research on patentable new drugs rather than on preventive methods…The consequences are sobering. Older adults suffer premature disabilities and shortened life spans; younger adults, and even children, are increasingly affected by early signs of atherosclerosis, obesity, and type-2 diabetes. Enormous prescription drug and medical care costs have nearly reached the point of overwhelming the national budget. And tragically, a growing body of evidence suggests that the bizarre and increasingly common behavioral problems among young children and teen-agers are related to the combined effects of high sugar intakes and the virtual absence of omega-3 essential fatty acids in the American diet.” http://books.google.com/books?id=wPrfdvM5V4gC&pg=PA199&lpg=PA199&dq=#v=onepage&q&f=false
Had I authored the above, I would have written, “And tragically, a growing body of evidence suggests that the bizarre and increasingly common behavioral problems among young children and teen-agers are related to the combined effects of high sugar intakes and the ‘excessive amount of omega-6 industrial seed oils” in the American diet.”
At this juncture the low-fat approach to weight control has been thoroughly discredited because, while it’s true that calories do make a difference, appetite, hormonal balance, and cravings are what drive overeating behaviors. Consider, for example, what omega-6s do to appetite when combined, as they often are, with carbohydrates.
“Linoleic acid, which is found in relatively high amounts in soybean, sunflower and corn oil, increased levels of endocannabinoids in mice and caused obesity according to research by scientists from the University of Bergen, Norway, and the National Institutes of Health in Bethesda, USA. Researchers investigated the effects of a 14-week diet high in linoleic acid, an omega-6 fatty acid. They hypothesized that this fatty acid, a precursor of arachidonic acid, from which endocannabinoids are formed, would induce endocannabinoid hyperactivity. Intake of linoleic acid was increased from 1 per cent to 8 per cent of calories of the diet, intended to reflect the increase of omega-6 fatty acids in the food of US Americans during the 20th century. This was mainly due to a dramatic increase in the consumption of soybean oil used for the production of margarines, vegetable oil, fast food, baked goods and other processed foods.” http://www.cannabis-med.org/english/bulletin/ww_en_db_cannabis_artikel.php?id=367
Excessive omega-6 intake, in and of itself seems, to deposit belly fat. Susan Allport’s self experiment hints at the magnitude of this particular aspect of the problem.
“I knew it would be easy to put on five pounds from a month’s worth of eating fast food, as Morgan Spurlock had shown. But I wanted to see what would happen if I just switched the balance of omega-6s and omega-3s in my diet. What would happen if I kept the quantity, and the kind, of food the same, but just changed the essential oils?..at the end of my diet…I had a large, unpleasant wad of belly fat that I could grab in one hand. I was certain I had gained at least 5 pounds…I couldn’t believe it when he said that my weight was exactly as it had been a month before – 56 kilograms or 124 pounds…Later that morning – after all the tests were completed, I learned from Volek just how profound the changes to my body had been. Yes, my weight was almost the same, but what weight I had gained – 5.6 ounces or just under half a pound – was almost entirely fat and in my abdominal area, as the follow-up body scan showed – exactly as I had experienced it. Just as interesting, and the cause, perhaps, of this gain, was that my resting metabolic rate had fallen, by an intriguing five percent” http://www.susanallport.com/newsletter728511.htm
Sadly, the highest nutritional authorities in the land recommend replacing saturated fats with polyunsaturated industrial seed oils. The Harvard School of Public Health:
“Why hasn’t cutting fat from the diet paid off as expected? Detailed research—much of it done at Harvard—shows that the total amount of fat in the diet isn’t really linked with weight or disease. What really matters is the type of fat and the total calories in the diet. (7-15) Bad fats, meaning trans and saturated fats, increase the risk for certain diseases. Good fats, meaning monounsaturated and polyunsaturated fats, do just the opposite. They are good for the heart and most other parts of the body…In place of butter, use liquid vegetable oils rich in polyunsaturated and monounsaturated fats, in cooking and at the table. Olive oil, canola oil, sunflower oil, safflower oil, corn oil, peanut oil, and the like are great sources of healthy fat.” http://www.hsph.harvard.edu/nutritionsource/what-should-you-eat/fats-full-story/
As noted earlier, dietary advice and public policy are informed by bad science. Dietary advice is also informed by misinterpreted science. For example:
Given the large social impact of dietary advice, it is important that the advice have a solid scientific basis. Evidence-based dietary advice should be built on results from all studies available, according to a given methodology. Conclusions should be a valid representation of the summarized results…Results and conclusions about saturated fat intake in relation to cardiovascular disease, from leading advisory committees, do not reflect the available scientific literature. http://www.nutritionjrnl.com/article/S0899-9007%2811%2900314-5/abstract
For nearly six decades scientists have assumed that any effects saturated fats have on cholesterol levels must be pathological. In reality, those effects are physiological and likely beneficial. http://www.eurekalert.org/pub_releases/2011-05/tau-cn050511.php Low LDL cholesterol levels are associated with higher rates of cancer. http://www.theheart.org/article/1375049.do And total cholesterol levels below 200 are associated with increased mortality. http://perfecthealthdiet.com/wp/wp-content/uploads/2011/06/O-Primitivo-Cholesterol.jpg Yet the American Heart Association considers total cholesterol above 200 to be atherogenic.
“The health metrics are part of the 2020 AHA strategy to improve the cardiovascular health of US citizens by 20% and reduce deaths from cardiovascular disease and stroke by 20%. The novel aspect of the 2020 goals is the promotion of cardiovascular health, which includes seven health behaviors and risk factors—smoking status, healthy body mass-index (BMI), diet (based on the healthy diet score), participation in physical activity, and levels of blood pressure (<120/80 mm Hg), blood glucose (<100 mg/dL), and total cholesterol (<200 mg/dL)—that define cardiovascular health. Based on these variables, cardiovascular health is defined as ideal, intermediate, or poor." http://www.theheart.org/article/1371059.do Note: triglyceride levels not mentioned.
Finally, here are comments from a 2002 article by food writer Emily Green who, for whatever reason, put herself on a sensible weight loss regimen and lost 52 pounds in a year.
I have long suspected that the best way to lose weight was to eat rich food in moderation, not diet food in abundance. During the last 52 weeks, I put that idea to the test. And I lost 52 pounds. To my knowledge, not a single low-fat food passed my lips…For me, the result of this diet was not simply weight loss, not simply fresh delight in rediscovering good, simple things; it was vigor. My eyes are brighter, my skin is better and–to the astonishment of my neighbors–I now bound out of the house in the morning wearing a sweatsuit. Which brings the story to the exercise part. I didn't lose weight just by eating all this good stuff and tossing back Pinot Noir. I lost weight eating good, nourishing food that gave me energy to exercise." http://articles.latimes.com/2002/mar/13/food/fo-52-13/2
Jim
March 30, 2012
Hi David,
As always, I appreciate your enthusiasm and dedication to the cause you’ve taken up, but I must make several rebuttals.
I made no claim that ‘gluttony & sloth’ are the central issues of the obesity epidemic (but while we’re on the topic, they ARE issues at the societal level and do contribute to the problem, make no mistake). To the contrary, I asserted throughout the above article that there are a number of issues at the root of the obesity epidemic.
Given this, asserting that the n-6:n-3 imbalance in the Western diet is the root of the problem renders you guilty of the same fallacy committed by those who do believe overeating and inactivity are solely to blame.
You are more than welcome to submit a guest post, as long as assertions are based on the literature and not anecdotal evidence or experiments with an n=1, which I simply can’t endorse.
davebrown9
March 30, 2012
I’m sorry. I should have made it clear that I was attacking the mainstream solution to the so-called obesity epidemic which mainly calls for calorie restriction and exercise. My two major complaints against the establishment is their insistence that saturated fats are a health hazard and that omega-6s are healthy. Warning consumers to restrict saturated fats effectively takes the option of eating saturated fats, as a weight control measure, off the table. http://www.youtube.com/watch?v=vRe9z32NZHY
Really, the best way to bring triglycerides under control, raise HDL, and ensure total cholesterol is in the optimum range, which lies between 200 and 240, is to restrict carbohydrates and omega-6s and increase intake of traditional sources of saturated fat. http://rdfeinman.wordpress.com/2012/02/22/saturated-fat-on-your-plate-or-in-your-blood/
I didn’t say anything about the n-6:n-3 imbalance. I said the problem is too much n-6 period.
Throughout the world, n-6 intake has increased to extraordinarily and historically high levels. http://www.psychologytoday.com/blog/evolutionary-psychiatry/201103/your-brain-omega-3 Global obesity expert Barry Popkin almost put his finger on the problem in a September 2003 article that was published in the Orlando Sentinel. Some excerpts:
“The world’s nutrition problems have changed dramatically in recent years in a way most Americans probably have difficulty fathoming: In most of the developing world, obesity is now a larger problem than malnutrition…What is happening to the diets of the world?..TV, food advertising and other changes have led to diets that are much higher in fat and added sugar…they add a lot of vegetable oil to their dishes. And they consume more meat…the steepest increase is in the use of edible vegetable oils for cooking…edible oil is a most-important ingredient in enhancing the texture and taste of dishes…The edible-oil increase is found throughout Asia and Africa and the Middle East as a major source of change.” http://articles.orlandosentinel.com/2003-09-28/news/0309270148_1_overweight-or-obese-women-were-overweight-south-africa/2
Of course, Popkin also discussed added sugars. The thing is, added sugars are finally being researched and the findings publicized and reported on. The n-6 problem gets almost zero press coverage. How do I know this? I’ve had a Google Alert for “omega-6 lenoleic acid” in place for more than a year.
I included the n=1 Susan Allport experiment utilizing blood tests, body scans, and measurements of resting metabolic rate because there are no trials I know of wherein scientists deliberately lower omega-6 intake to determine the effects on cardiovascular endpoints. However, there is one Mediterranean diet type trial in which omega-6 was inadvertently lowered. From the Abstract: “The experimental group consumed significantly less lipids, saturated fat, cholesterol, and linoleic acid but more oleic and alpha-linolenic acids confirmed by measurements in plasma. Serum lipids, blood pressure, and body mass index remained similar in the 2 groups. In the experimental group, plasma levels of albumin, vitamin E, and vitamin C were increased, and granulocyte count decreased.” http://www.ncbi.nlm.nih.gov/pubmed/7911176
Note this comment from page 7 of a review entitled “Dietary Fat Quality and Coronary Heart Disease Prevention: A Unified Theory Based on Evolutionary, Historical, Global, and Modern Perspectives”:
“The only long-term trial that reduced n-6 LA intake to resemble a traditional Mediterranean diet (but still higher than preindustrial LA intake) reduced CHD events and mortality by 70%. Although this does not prove that LA intake has adverse consequences, it clearly indicates that high LA intake is not necessary for profound CHD risk reduction. http://www.ncbi.nlm.nih.gov/pubmed/19627662
Jim
March 31, 2012
No worries – but again, the focus of this article has nothing to do with dietary fats, and no such recommendations regarding saturated fat have been made at any time in this blog.
We’ve conversed via email and I believe we are generally on the same page, but you must realize the advice I give out here and to my patients has to be tailored to them – the majority of whom do not have a background in nutrition science or even a high school diploma.
Further, if we don’t eliminate food deserts and change what’s served at schools (and I think we would generally agree on what changes need to be made), none of this advice is worth a damn. So, yes, while there is a growing body of research that does support the n-6 inflammatory model, it’s still difficult to have most Americans implement dietary changes in accordance with this because of the environment they’re immersed in.
Regarding “too much n-6, period” – there’s certainly been an increase in the absolute n-6 intake in our post-industrial/Western diet, but there’s also been a decrease in n-3 intake. The literature I’ve read has mostly demonstrated that what’s actually important is the ratio of these fatty acids in the diet. Lowering n-6 intake is one way to alter the ratio, but supplementing n-3 is another, and has been shown in the literature to affect primary cardiovascular endpoints, etc.
In fact, I’m unaware of any literature demonstrating that the problem lies strictly with absolute n-6 content of the diet. That would require demonstrating health benefits with lowering both n-6 and n-3 intake and preserving the ratio – but really, who cares, if we can reap the benefits simply by upping n-3 content in our diets? It’s much, much easier from a public health standpoint to get Americans to increase n-3 intake, as well as to pressure the agriculture/food industries to do the same (as we’ve seen in recent years – think Smart Balance peanut butter and Eggland’s Best Omega-3 eggs). We have to start somewhere.
Here is a review that appears to demonstrate that linoleic acid may not be as crucial as other sources: http://www.nutritionandmetabolism.com/content/pdf/1743-7075-8-36.pdf
And for those interested, here are some other citations for further reading on this topic:
Click to access 1743-7075-8-56.pdf
http://ebm.rsmjournals.com/content/233/6/674.long
davebrown9
April 1, 2012
Thanks for the links to the three articles. You said, “…I’m unaware of any literature demonstrating that the problem lies “strictly” (emphasis mine) with absolute n-6 content of the diet.”
Strictly as a matter of principle, I don’t think it’s possible to supplement oneself out of a problem that involves excessive intake of a dietary component as chemically reactive as n-6 http://www.youtube.com/watch?v=dgU3cNppzO0 or as addictive as added sugars. http://www.businessweek.com/news/2011-11-11/fatty-foods-addictive-as-cocaine-in-growing-body-of-science.html
To me it would seem the below paragraph from the third article by Artemis Simopoulos speaks to the “absolute n-6 content” issue.
Linoleic Acid Increases Low-Density Lipoprotein Oxidation and Severity of Coronary Atherosclerosis.
“Oxidative modification increases the atherogenicity of low-density lipoprotein (LDL) cholesterol. Oxidized LDL is taken up by scavenger receptors that do not recognize unmodified LDL leading to foam cell formation. “Diets enriched with LA increase the LA content of LDL and its susceptibility to oxidation” (emphasis mine). Reaven et al. showed that a LA-enriched diet especially affects oxidation of small, dense LDL. Louheranta et al. showed that as the percent of energy intake from LA increased from the lower quartile 2.9% to the highest 6.4% so did the LDL oxidation. In their study, the average energy from LA was 4.6%. In another small cross-sectional study, enhanced susceptibility of LDL to oxidize was associated with severity of coronary atherosclerosis.”
I suspect scientists will eventually identify multiple damaging effects related to the absolute amount of omega-6 ingested. The rate at which damage from these effects accumulates would logically be determined by the rate at which the individual burns fatty acids for energy. For example, in that “Metabolic responses to high-fat diets rich in n-3 or n-6 long-chain polyunsaturated fatty acids…” paper you linked to, active mice of the lean phenotype were metabolically equipped to metabolize all forms of fatty acid ingested more quickly than the high body weight phenotype. Indeed, the authors said, “It is tempting to speculate that an increase in the antioxidant capacity in DUhTP (lean and active) mice may also lower susceptibility to peroxidation, thus providing further health benefits of dietary n-3 PUFA. This may contribute to the increased running performance in DUhTP mice and support the energy usage phenotype. An increase in the n-6 PUFA content of body tissues was expected with n-6 HFD feeding, however, this was only observed in DU6 (the fat mice phenotype) liver and muscle and not in the DUhTP animals indicating again a genetic component of fatty acid deposition.”
To summarize my current thinking regarding the absolute n-6 content of the diet, I imagine phenotype and the dietary adequacy of one’s food choices would determine the rate at which one deteriorates on high n-6 intake. Interestingly, the Paleo approach, which lowers n-6 consumption by replacing n-6 industrial seed oils with traditional sources of fat, theoretically accomplishes much the same thing, in terms of n-6 reduction, as the low-fat approach advocated by Dr, Dean Ornish. The important thing is to match phenotype to dietary approach so as not to injure ones metabolism.
Something to look forward to: In about three months, Fred and Alice Ottoboni hope to have an update of their 2002 book “The Modern Nutritional Diseases: And How to Prevent Them” ready for publication. Note: My original comment began with a quote from their book.
Jim
April 1, 2012
Certainly to “supplement oneself out of a problem” is not what I suggest on the large scale, but the fact remains that n-3 supplementation alone has been demonstrated to be protective in a number of modalities.
I can tell my patients that walnuts and fish are good for them, and to pick whole foods out at the supermarket, but I will lose the vast majority of them when I start recommending for example that they avoid products made with corn oil. None of them read labels – thus, I can advocate a diet consisting mostly of foods that don’t have labels, but it’s much less practical to have them walking out of the office with a list of things they should be looking for in the ingredients list.
Some of our discussion is beginning to spill over into the esoteric, which is fine, but certainly not the aim of this blog (and especially not this post – the topic of which was childhood overweight and not CHD). Again, if you’d like to present the science and give the average reader some practical advice, I always welcome guest posts.
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