The Blame Game: Nature, Nurture, and Obesity
Who dunnit? That was the essence of the debate between Sadaf Farooqi and John Wilding at the Society for Endocrinology BES Conference in Brighton, UK. Some very smart people have a tough time wrapping their brains around nature, nurture, and obesity. So Farooqi and Wilding took opposite sides of a simple proposition:
This house believes that nature not nurture determines our body weight.
At the outset, a poll of the audience of endocrinologists revealed that 64 percent of the audience disagreed.
The Nature of a Highly Heritable Chronic Disease
Farooqi is a researcher whose work on the genetic basis for obesity won her the 2019 ADA Scientific Achievement Award. She explained decades-old research that showed the highly heritable nature of this disease in identical twins. It’s “fundamentally important” to understanding obesity, she said. But it’s not just one or two genes that make a person susceptible. Single-gene defects to confer obesity are powerful, but rare.
More important, though, is a key bit of evidence published earlier this year. This study, by Amit Khera et al, showed that a polygenic risk score for obesity can quantify the inherited risk for obesity. That risk shows up early in life. In fact, the risk of severe obesity goes 25 times higher for individuals with a high genetic risk score.
Nurture Matters
Wilding made the argument for the environmental factors that activate obesity. Obviously, our genetic nature has not changed in the last four decades while obesity prevalence has exploded. So he trotted out the Obesity System Map of complex interactions of factors fuelling the growth in obesity.
Zing. Susceptible individuals don’t get obesity unless they’re in an environment that permits it. Nobody has obesity in a famine.
The Irresistible Urge to Believe in Free Will
Of course, this is reductio ad absurdum. Nature and nurture both have a part to play in obesity. Individuals are susceptible to a condition the environment triggers. But the truth is that roughly 70 percent of a person’s obesity risk comes from hereditary factors. Some individuals are very biologically susceptible and live with severe obesity from an early age. Others have bodies that are very resistant to carrying excess fat. By the end of the debate, 53 percent of the audience agreed with Farooqi.
Still, many did not. Environmental factors play a big role. The trouble is that we have many supporting actors in that drama. Big soda? Guilty. Big food? Guilty. Big tech? Complicit without a doubt. But the finger-pointing can go on forever because so many factors are adding to our problem.
We have no choice. We must believe in free will if we are to solve the health problems that obesity is creating. Not by blaming the people who are susceptible. Rather, we must do it by bringing objectivity and curiosity about interventions that will work. Both for treatment and prevention.
So far, we’ve barely made any progress. We can do much better.
Click here for more on this debate from Medscape. For perspective on why we believe so strongly in free will, click here.
At Fault, photograph © Art Bochevarov / flickr
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november 24, 2019
November 24, 2019 at 10:03 am, David Brown said:
To me, it makes more sense to view obesity in terms of symptom rather than disease. Like a peanut allergy, obesity is a genetically determined response to some nutrient in food that triggers an unfavorable response.
Despite the fact that myriads of scientists are working on the obesity problem, the cause or causes remain a mystery. But not for all scientists. Annadie Krygsman writes, “Obesity is currently regarded as one of the most alarming pandemic diseases worldwide as it is closely related to, and in many cases causative of, Type 2 Diabetes (T2D), coronary heart disease (CHD), cancer and other pathophysiological disturbances. A cluster of these disorders are linked together under the term Metabolic Syndrome (MetS). These factors include impaired glucose tolerance and/or insulin resistance, dyslipidemia (high plasma levels of triglycerides and low density lipoproteins), central obesity and hypertension. In the USA a recent Health and Nutrition Examination Survey (NHANES) reported that 68.3% of study subjects were considered as overweight (BMI ≥ 25) and 33.9% obese (BMI ≥ 30). The rising incidence of childhood obesity and T2D, high blood pressure, hyperinsulinemia and dyslipidemia are particularly worrisome as these children often mature to be obese adults. This risk of developing obesity and T2D has largely been blamed on the increased consumption of energy dense foods and fat intake, particularly saturated fat, but it is interesting to know that the mean fat intake of the human population has not increased much in the past 50 years. It is true that the vast advancement in technological developments has led to a reduction in physical activity worldwide, but as obesity now involves infants and the populations of developing countries, this obesity pandemic cannot be attributed to this alone. In addition, laboratory and other domesticated animals have also been subject to the increased prevalence of obesity, despite having largely unchanged living conditions for many years.
Krygsman also notes that “The main alteration within the fatty acid profile of the modern diet has been the increased use of vegetable oil, both as a cheaper and more accessible alternative to animal fats, but also as a substitute to animal fats to reduce the intake of SFAs. Vegetable oils, although higher in monounsaturated fatty acids, are very high in omega-6 fatty acids (100-fold larger) compared with animal fat.
https://www.intechopen.com/books/glucose-tolerance/importance-of-dietary-fatty-acid-profile-and-experimental-conditions-in-the-obese-insulin-resistant-
In this video presentation, Chris Knobbe reinforces Krygsman’s contention that the increase in vegetable oil consumption is a major factor driving the increase in obesity and chronic disease. https://www.youtube.com/watch?v=pHnPinYI2Yc
But that’s only half the story. Feeding grains to livestock has altered the fatty acid profile of meat. For example, “Chicken meat is commonly regarded as a healthy type of meat; it is popular, and hence the consumption has increased. Chicken meat is lean, protein-rich and rich also in other important nutrients. However, the fatty acid composition is strongly dependent on the diet fed to the birds. A typical modern poultry diet is rich in cereals having a high ratio between omega-6 and omega-3 fatty acids. This diet is very different from the natural diet for the same species containing more green leaves that are rich in the omega-3 fatty acid alpha-linolenic acid (ALA).”
Feeding cereals to chickens increases the arachidonic acid (AA) content of lean tissue. “The ratio between concentrations of omega-6 and omega-3 fatty acids, especially the AA/(EPA + DHA) ratio, is too high in the western diet, and a lower ratio between omega-6 to omega-3 fatty acids is desirable because it may help to reduce the prevalence and/or morbidity of chronic inflammatory diseases and atherosclerosis. Therefore, we think that all chicken meat available for human consumption should have a favorable ratio between omega-6 and omega-3 fatty acids, especially when considering the long-chain ones, such as AA, EPA and DHA, and a reduction in the concentration of AA in animal products such as meat, eggs and offal is desirable.”
In an attempt to balance the ratio between omega-6 and omega-3 fatty acids, Americans spend about a billion dollars annually on omega-3 supplements. Is this helping matters? Probably not. “Increasing the long chain omega-3 fatty acids EPA and DHA intake through the ordinary diet is also a better strategy than relying on fish oil capsules or fish alone, especially when one wishes to reach the entire population. Intake through ordinary foods will be associated with less risk of EPA and DHA peroxidation during storage, compared with fish oil capsules (since rancidification of foods is very easily detected by consumers and an important reason for not eating the food, while the same may not be the case for fish oil inside a capsule).”
There is a safer way to balance the omega-6 omega-3 ratio. “Combining reduction of the intake of AA with enhancement of the intake of oleic acid will, moreover, also be a better strategy for reducing the total extent of in vivo lipid peroxidation, rather than adding more EPA (with 5 double bonds) and DHA (with 6 double bonds) to a diet already over-abundant in arachidonic acid and linoleic acid. A reduction of the dietary ratio of total polyunsaturated fatty acids to oleic acid will not only make plasma lipoproteins less vulnerable to oxidation, but must also be expected to lead to reduction of the rate of formation of mutagenic aldehydes that arise as secondary products of lipid peroxidation, such as malondialdehyde, crotonaldehyde, acrolein and 4-hydroxynonenal. High rates of production of these mutagenic aldehydes must be expected simultaneously to lead to enhancement of the risk of various forms of cancer, and enhancement of the rate of mitochondrial DNA aging, which could lead to earlier onset of various age associated degenerative diseases perhaps including type 2 diabetes. The degree of fatty acid unsaturation of mitochondrial membrane lipids has been found to be one of those biochemical parameters that are most strongly correlated with longevity, when different species of mammals and birds are compared, with a low degree of fatty unsaturation being correlated with less lipid peroxidation and a longer normal life-span.
https://lipidworld.biomedcentral.com/track/pdf/10.1186/1476-511X-9-37
November 24, 2019 at 1:27 pm, Richard Atkinson said:
The letter above is very interesting and provocative. However, the information should be taken with a grain of salt (forgive the pun), and are hypotheses, not established facts. The sources quoted are for the most part open access articles in substandard journals, hypothesis papers, or website citations from blogs. The two main citations, Krygsman and Knobbe, are not nutritionists and have very few publications listed in PubMed. Krygsman’s paper was in rodents, so the applicability to humans is not clear. However, there are a good number of papers on PubMed, mainly epidemiological, that support the concept of omega 6 fatty acids associated with obesity. It is hard to do prospective, randomized trials in humans, but the importance of the question should stimulate more definitive research and an examination of how we eat.
November 24, 2019 at 4:04 pm, Ted said:
Excellent perspective, Richard. Thank you.
November 25, 2019 at 12:24 am, David Brown said:
@ Richard Atkinson
Thanks for your comment. 42 years ago I began perusing information regarding the nutrition/disease connection. In light of what has been learned thus far, definitive research may already exist. For example, “Eicosanoids are major players in the pathogenesis of several common diseases, with either overproduction or imbalance (e.g. between thromboxanes and prostacyclins) often leading to worsening of disease symptoms. Both the total rate of eicosanoid production and the balance between eicosanoids with opposite effects are strongly dependent on dietary factors, such as the daily intakes of various eicosanoid precursor fatty acids, and also on the intakes of several antioxidant nutrients including selenium and sulfur amino acids. Even though the underlying
biochemical mechanisms have been thoroughly studied for more than 30 years, neither the agricultural sector nor medical practitioners have shown much interest in making practical use of the abundant high-quality research data now available. https://link.springer.com/content/pdf/10.1186%2F1476-511X-10-16