In 1990, Dr. Claude Bouchard and colleagues published a simple but fascinating study demonstrating the importance of genetics in body fatness (1). They took advantage of one of the most useful tools in human genetics: identical twins. This is what happens when a single fertilized egg generates two embryos in utero and two genetically identical humans are born from the same womb. By comparing identical twins to other people who are not genetically identical (e.g., non-identical twins), we can quantify the impact of genes vs. environment on individual characteristics (2).
Dr. Bouchard and colleagues recruited 12 pairs of male identical twins, determined how many calories each person needed to eat to maintain weight, then overfed each person by 1,000 kilocalories per day for 84 days. Although every participant gained weight and fat, "individual changes in body composition and topography of fat deposition varied considerably." Weight gain ranged from 9 pounds (4.3 kg) to 29 pounds (13 kg), despite the fact that all subjects were eating the same calorie excess! This is a really striking result if you think about it. Even after minimizing variability in half of the energy balance equation (energy in), there remained large differences in the amount of weight and fat people gained. Some were able to effortlessly "burn off" most of the excess calories.
However, weight gain within pairs of twins was much more similar than weight gain between pairs of twins. In fact, even the distribution of the gain was far more similar within pairs than between them. If one twin gained 15 lbs around the midsection, the other usually gained about the same amount of weight, and in the same place.
This suggests that a person's genetic makeup determines how well his body naturally 'resists' fat gain during overeating, and also where his body tends to store fat. Some people are genetically predisposed to gaining fat, and others are genetically predisposed to gaining fat in unhealthy places.
Dr. John de Castro and colleagues have taken this research even further. In a large and ambitious study (resulting in a number of papers; here are a few: 3, 4, 5, 6), his group recorded the dietary habits of identical and non-identical twins to quantify the genetic contribution to a range of eating-related variables. Here's a little snippet from one abstract that drives home the main point (3):
Significant heritabilities were also found for the amount of food energy ingested daily, as well as its macronutrient, alcohol, and water content. Linear structural modeling analysis showed that 65% of the variance in energy intake was attributable to heredity. In addition, the pattern of intake, meal frequency, size, and meal macronutrient, alcohol, and water composition, were also found to have strong heritabilities.
In other words, nearly every major aspect of food behavior is strongly impacted by genes*. Other papers from the same study showed that genes have a strong influence on the amount of food it takes to feel full, how likely it is that the sensation of fullness will terminate a meal, the perception of palatability, how much influence palatability has on calorie intake, cognitive dietary restraint, and almost every other measurable characteristic.
This is just a small taste of the literature that demonstrates convincingly that genetics plays a major role in obesity. Twin studies (and similar designs) overall have found that genes explain about 70 percent of the differences in body fatness between people (8). This suggests that when it comes to obesity, it's important to pick the right parents.
What Can We Learn From Obesity Genetics?
Genetics has a lot to teach us about obesity. First, as described above, genetic makeup is a major influence on body fatness and virtually all of its determinants. Your genes determine, to a large extent, how likely you are to become obese, or how hard you'll have to work to remain lean if you're genetically predisposed to obesity. This is one of the reasons why it's unfair to judge obese people for their fatness. Of course behavior does matter, but a) most obese people were dealt a more challenging hand than most lean people, and b) behavior is also strongly heritable, so even that isn't freely chosen.
Beyond the moral/philosophical implications of this research, there's also a strong scientific reason to care about the genetics of obesity: it points to the biological processes that determine body fatness, and it can do so in a relatively unbiased fashion. Genetics is an important tool for understanding how body fatness is regulated, including in humans. I'll discuss this in the next post. This brings us to the third reason for caring about obesity genetics: if we know what biological processes are involved, we can attempt to target them to prevent or reverse obesity, and perhaps individualize treatments. This could involve diet, lifestyle, surgery, and/or drug therapy.
* This statement will sound funny to geneticists because everything we do is strongly impacted by genes. Genes are required for having a body, a brain, and expressing behaviors at all. I've simplified the language for a general audience, but really what we're talking about is the extent to which genetic variability within our species can account for variability in individual characteristics within our species. A more accurate way of saying the sentence I've asterisked would be "individual variability in nearly every major aspect of food behavior is strongly accounted for by genetic variability."
I think it would be interesting to tease out the relative contribution of nuclear to mitochondrial genes in determining one`s susceptibility to obesity. Seeing whether the mother has a bigger influence on offspring`s risk would be a way of doing this. This would be one way of testing whether or not obesity is a mitochondrial disease, as some assert.
That's a good idea for an experiment, although most mitochondrial genes are encoded in the nuclear genome. The hypothesis has already been tested in other ways though. Humans and rodents that are genetically deficient in fatty acid oxidation do not generally become obese. Mice with a genetic deficiency of FA oxidation are often leaner than normal mice. Affected humans do sometimes accumulate fat in lean tissues (e.g. muscle, liver), but they don't end up with a body composition that resembles common obesity (large amounts of subcutaneous and visceral fat) more often than average, as far as I can tell from my reading.
The most common symptom of mild cases is faintness during fasting. It is treated by consuming low-fat high-carb foods frequently.
The fact that even a severe genetic deficiency of FA oxidation, far worse than what is seen in common obesity, doesn't generally cause obesity in humans or mice, puts this hypothesis on thin ice.
Bouchard just put out an interesting RCT over-feeding trial on factors related to FM gain.
"When compared with the six highest BE gainers, the six lowest gainers exhibited higher thermic effect of a meal (TEM) and plasma levels of total testosterone, cortisol, estradiol, androstenedione and androstenediol sulfate (all P<0.05). High baseline levels of total TEM, testosterone and androstenediol sulfate were associated with lower FM gains, whereas high baseline levels of FT4 and estrone were found in low-FFM gainers.CONCLUSION:Although none of the variables exerted individually an overwhelmingly strong influence on overfeeding-induced changes, baseline FFM, maximal oxygen uptake, muscle oxidative capacity, androgens and leptin levels were the most consistent significant biomarkers of the responsiveness to chronic overfeeding.International Journal of Obesity advance online publication, 18 June 2013; doi:10.1038/ijo.2013.77."
I have two comments that challenge the interpretation of these findings:
(1) Twins are not just similar genetically. They have very nearly identical early environments. They were exposed nearly identically in the womb (including to caloric excess and many other things), and had similar diets and exposures in childhood. So this isn't really a test of the effect of genes. It's a test of a whole bunch of things at once. It says that a lot of what determines your body's ability to handle excess calories is determined by your genes AND childhood environment.
(2) How do you rectify the interpretation of these findings with the fact that just 100 years ago obesity was relatively rare? Today there are large groups of people that have great trouble losing weight even when facing very large monetary incentives, and yet 100 years ago that wasn't true. It can't be that the human genome has changed that much in 100 years, so it suggests something else is at work.
Twin studies typically compare identical twins reared in the same household to non-identical twins reared in the same household, controlling for the confounders you mentioned. Also, there are studies that compare twins raised together to twins raised apart.
That being said, it is true that the Bouchard study didn't control for the home environment. However, given the research as a whole, I think it's safe to interpret this effect as largely genetic.
Regarding the second point you raised, I'll address it in a later post.
I'm not an expert, but I would think the answer to #2 would have something to do with the food choices available to people now, as compared to those 100 years ago.
I'm betting that the reason obesity has risen dramatically is because the environment has changed much faster than our genes have evolved. While many have robust enough genetics to handle this rapid environment change, many people do not. I'm looking forward to Stephan's take on this question.
CLB said: "How do you rectify the interpretation of these findings with the fact that just 100 years ago obesity was relatively rare? It can't be that the human genome has changed that much in 100 years, so it suggests something else is at work."
One thing that has changed drastically during the past century is the fourfold increase in intake of omega-6 linoleic acid (LA) while during the same period intake of omega-3 fatty acid has decreased. Increased intake of LA results is increased tissue levels of arachidonic acid (AA). Arachidonic acid is the backbone of the most commonly studied endocannabinoids ananadamide and 2-AG which activate the same receptor activated by marijuana. Tissue levels of ECs increase in proportionate to the increase in tissue AA.
The endocannabinoid system consists of the ECs, primarily anandamide and 2-AG, the receptors CB-1 and CB-2, and enzymes that synthesize and degrade the ECs.
It has been found that dietary LA elevates ECs and induces obesity by (1) reducing energy expenditure by causing hypothyroidism (PMID 22912404)and (2) by increasing food intake.
The EC anandamide is degraded by the enzyme fatty acid amide hydrolase (FAAH)whereas the the EC 2-AG is degraded by monacylgglycerol lipase (MGL)
Genetic mutations in FAAH are associated with obesity in humans. Those who are genetically deficient in FAAH will tend to become obese and this tendency will be greatly exacerbated by following USDA dietary recommendations to decrease intake of animal fats and increase consumption of vegetable fats.
The activity of FAAH increases with increasing obesity but the activity of MGL does not increase with obesity.(PMID 21813022) If a rat (or a person) becomes obese, reducing tissue arachidonic acid (AA) by consuming omega-3 fats can result in normalization of anandamide but will not reduce 2-AG. Thus, once you get fat you tend to stay fat because of elevated 2-AG. Those deficient in FAAH really have a problem losing weight because both anandamide and @-AG will remain high once a person becomes obese.
The endocannabinoid system is immensely complex and I am sure there must be many other genetic complications in addition of FAAH deficiency.
Any idea what happens to those extra calories in the low response group? Do they simply not digest some of the extra energy, do they get more active or fidgety, do some other metabolic processes become less efficient?
I believe NEAT accounts for most, if not all of extra calories being burned off in the obesity resistant individuals.
Not only is the heritability of obesity high, it is as high as the most heritable traits there are. Indeed, in the modern world, obesity is as heritable as height (0.8, the same as IQ).
What's better, the "shared environment" component of obesity is 0. That is, 100% of the similarity between parents and children, relative to others in their group, is due to shared genes. Adopted children do not resemble their adoptive family one bit. (This is true for all traits.)
All Human Behavioral Traits are Heritable | JayMan's Blog
Taming the “Tiger Mom” and Tackling the Parenting Myth « JayMan's Blog
Should Parents Lose Custody of Obese Kids? | JayMan's Blog
Also see this paper for a review of the behavioral genetic evidence:
Heritability of body mass index in pre-adolescence, young
adulthood and late adulthood
But, one point where many commenters get confused is that once they learn that the heritability of obesity is high, that assume that this implies that genes are responsible for the change in obesity over time, which is quite wrong. Heritability is only a measure of how much traits correlate with genes in a given environment. A change in environment can produce a change in phenotype (body weight) without a change in genotype. In addition to my own discussion of this in the above links, Jason Collins discusses this:
Genetics and the increase in obesity - Evolving Economics
As to the cause of the rise in obesity, or even the cause of obesity itself in any given individual (beyond the connection with genes), we are presently quite clueless. I've written a post based on your writings discussing your palatable foods hypothesis:
Fun Facts About Obesity | JayMan's Blog
But we need to be honest: this is just speculation among much speculation. As Gary Taubes notes (see Gary Taubes on Obesity and Bad Science | JayMan's Blog), current scientific investigation is underpowered to determine conclusively what the cause of the rise in obesity is. We need to be mindful of this when discussing the matter.
Indeed, to demonstrate how unclear the cause of obesity is, it should be noted that, in the U.S., lab animals – who live under completely controlled dietary and "lifestyle" conditions – have been getting fat too:
David Berreby – The obesity era
The above article discusses many hypotheses, all of which suffer from the same problem of being unable to be properly tested. This is great scientific mystery that endures, one which the coming years should yield interesting insight.
Rob is correct, at least one other study has suggested that "non-exercise activity thermogenesis" (NEAT), basically unconscious movements and tone in postural muscles, mostly account for the ability of some people to burn excess kcals.
You're stealing my thunder here! Haha.
Regarding Taubes's comments, anyone can take the ultra-skeptic view and say we don't know squat, but I disagree. We have a huge amount of imperfect evidence, just like we do in every other field of biology that has given us useful insights despite imperfections. We can throw out all research on HIV, on cancer, on influenza, on cognition, and on thousands of other topics because it's messy, or we can say "this is not perfect, but as a body of literature it is meaningful and useful".
Genes didn't evolve in a 100 years, but the plethora of cheap, tasty, high calorie foods did. Some people are better equipped genetically to handle that (via increased subconscious energy expenditure, for example). Evolution hasn't evolved rapidly enough to deal with this issue in most peopl.e
"Regarding Taubes's comments, anyone can take the ultra-skeptic view and say we don't know squat, but I disagree. We have a huge amount of imperfect evidence, just like we do in every other field of biology that has given us useful insights despite imperfections. We can throw out all research on HIV, on cancer, on influenza, on cognition, and on thousands of other topics because it's messy, or we can say 'this is not perfect, but as a body of literature it is meaningful and useful'."
I certainly wouldn't be one that would advocate making the perfect the enemy of the good, but it's still important to recognize the limitations of what we do know.
There are many facts that don't lend themselves to easy explanation, particularly by the "default" hypothesis, or even by newer ones like Taubes's (with carbs being the culprit). While it may be practical to run with these hypotheses at times, where it comes to the matter of treating obesity, they don't seem to be horrendously helpful. This may be because we're wrong, or perhaps obesity doesn't lend itself to treatment. Time will tell.
Personally, I believe that when a person is healthy, the brain adjusts the rate that calories are burned to maintain a stable body weight with a fluctuating calorie intake. When too many calories are consumed, extra calories are burned off through metabolic inefficiency. When too few calories are consumed, fewer calories are burned through metabolic efficiency. (Appetite and hunger are also adjusted.)
Here’s an example of what I mean. There was an interesting study that evaluated the metabolisms of the contestants on the Biggest Loser. Despite their incredible weight loss, by the end of the competition the average contestant was burning about 500 fewer calories a day (as compared to their metabolism at the start of the competition). Essentially, because they were restricting calorie intake and engaging in excessive amounts of exercise in an attempt to "burn off" their extra stored calories, they actually managed to induce a starvation response, which made their metabolisms super-efficient. But, because these contestants were exercising intensely for about 4-6 hours a day during the competition, they were able to continue to create the calorie deficit necessary to lose weight every week despite their new increased metabolic efficiency.
But here’s the interesting thing: Most of the contestants in the competition gained back all the weight they lost once they left the Biggest Loser ranch, despite many of them continuing to exercise and restrict calorie intake (this happened to the winner of the second season). The big difference between the ranch and home was that these contestants were no longer burning a ton of extra calories by exercising intensely for 4-6 hours a day.
So, while these former contestants were technically creating a calorie deficit on paper with a restrictive diet and some light exercise, their new super-efficient metabolism produced enough of a calorie surplus to allow them to slowly gain back their weight.
I believe that this can explain why some of the subjects in the study mentioned above could have gained different amounts of weight while consuming those extra 1,000 calories each day. Each subject had a metabolism operating at different speeds, and these speeds could be influenced by their genetics, level of health, and/or environment. This would also be true for identical twins, where genetics (and epigenetics) clearly plays a part.
How do obesity-prone genes fit in with Food Reward theory?
"...current scientific investigation is underpowered to determine conclusively what the cause of the rise in obesity is. We need to be mindful of this when discussing the matter." (emphasis mine)
That's the problem with the Taubes', Lustigs etc of this world. They all focus on "the one, true cause", when there are in fact many causes, some affecting some people more than others, due to genetic differences. See Determinants of the Variability in Human Body-fat Percentage. , which I've recently tweaked.
I do not think that a person in good health can always maintain caloric balance such that they reside at a normal weight. There are plenty of metabolically healthy people who do gain unwanted weight because of their genetics, environment, and lifestyle choices.
The reason people from Biggest Loser end up burning less calories than their lean counterparts while also in a lean state is because of becoming leptin deficient due to their weight sitting far below their body's set point.
However I disagree that they will regain the weight despite continuing their efforts to exercise and eat healthy. I think a small amount of regain explains this, but those that gain it all back must be reverting back to their old lifestyle. The first problem is they are instructed on how to lose weight quickly, not to maintain it. Maintenance is the hardest part because it requires new habits that are sustainable. Most of us live in an environment that is counter-productive towards being healthy. Combine that with the power of being leptin deficient and the odds are the person will make the wrong choices and the weight will come back.
"non-exercise activity thermogenesis (NEAT)--mostly accounts for the ability of some people to burn off excess kcal."
NEAT is related to thyroid function. A recent study showed that rats expended greater NEAT when rendered hyperthyroid.
According to the study, "over the 14 day period, daily neat increased in the hyperthyroid rats from 8.1 to 19.2 kcal per day but did not increase in controls.--In conclusion, hyperthyroidism is associated with increased spontaneous physical activity and NEAT."
It is reasonable to expect that hypothyroidism will reduce NEAT.
In humans, genetic mutations in fatty acid amide hydrolase (FAAH) are associated with obesity and reduced energy expenditure caused by deficiency of FAAH, the enzyme that degrades the endogenous cannabinoid amandamide (AEA). Deficiency of FAAH results in elevation of AEA which causes hypothyroidism, reduced energy expenditure and obesity.
Excess intake of linoleic acid (LA) also elevates AEA and causes hypothyroidism reduced energy expenditure and obesity. A recent ecological study found a strong correlation between the apparent consumption of foods high in LA (soybean oil, shortening, and poultry) and the rise in obesity in the United States during the 20th century. (PMID 22334255)
Identical twins generally share more than just genetics, including a gut biome inherited from the same mother during birth and all kinds of other nurture elements as a result of being raised by the same parents in the same household. I'd be interested to know how much of the differences are as a result of true genetic variability rather than the combination of genetic variability and childhood environment. Separated twin c-section births maybe?
Comparing identical vs. non-identical twins controls for both in utero and shared household environment effects.
Quite true. Clearly, Americans went through a genetic transformation since the 1980s, when they became fat. And Asians and Europeans who visit America for extended periods and become fat also go through a genetic transformation when they reach our shores, and then transform back when they return home and become thin again (this is a well known phenomenon).
And since behavior is genetically conditioned as well, with no or very little room for personal choice, clearly, no one should be blamed for this. It's not like genes play a complex role in determining behavior, one giving us plenty of flexibility and the ability to choose from a range of options, no, our genes are simple determinants.
Facetiousness aside, the modern form of determinism and the modern form of materialism where everything is just genes and only crude material causes get a hearing is not just silly, but probably a huge factor in perpetuating obesity. Obesity is not caused by tasty food. Thin countries like Japan and France eat very tasty (high reward and high palatability) food, and even lots of junk food. And before you say that the French diet is not "extravagant" - no, it is not, but it includes large amounts of VERY tasty food, food that is much tastier than the bland, simple far eaten in primitive societies. And the massive amounts of junk food lining the shelves of Japanese 7-11's (Japan has more than 30 kinds of KitKat alone!), and the Mos Burgers everywhere, get eaten by SOMEONE.
I was only able to get and stay thin when I once and for all ceased looking for the explanation in material factors - i.e the "kinds" of food I was eating, which I found had almost no impact on my appetite. It was almost entirely how MUCH I ate, and I had to find that "sweet spot" where I was not too hungry but was still losing weight, and I simply could not eliminate that nebulous, vague, hazy, and non-material quality called self-control. Waiting in vain for the kinds of foods I was eating to magically result in reduced appetite kept me fat as I cycled through every kind of diet or food fad invented so far.
In the end, the only thing that worked was the non-material factor of will-power, together with not eating too little nor too much, a difficult and fine art. But of course, such a thing isn't scientific in the same way that Physics is, and Physics is the standard by which anything pretending to intellectual respectability is judged by these days, leaving people ignorant of urgent and important truths and intellectually impoverished. Solutions that can't be measured using math simply don't get a hearing.
By encouraging people to ignore the factor of will-power and self-control - something that needs cultivation and building up and that is woefully neglected in our modern culture - leaves them helpless. It does not matter how "low reward" the diet is, they will stay fat as they neglect the one power that can save them. Although intuition and learning the ability to eat just enough but not too much, which is individual to each person and requires listening to feelings and ignoring calories (why is it the countries that think they know all about calories are the fat ones, where the ones that ignore calories are the thinnest?), is also key, and also scorned. No, we must have a mathematical formula.
Modern explanations of obesity come from a desire to banish anything that cannot be mathematically measured from the realm of explanation, from a belief in a crude and simple genetic determinism, and in a belief in material factors over psychological factors.
Isn't it time we accept that the approach based on Physics isn't working here, that we need to pay attention to "intangibles" like cultural values and the cultivation of self-control?
I disagree that healthy individuals cannot maintain a healthy weight automatically. If you look at traditional populations (e.g., Kitivans, Masai), you’ll find that they have no problem with obesity or excessive weight (by BMI) so long as they don’t eat much Western food. And there are a few traditional populations that put a lot of time and effort into gaining weight and usually only succeed in the short-term. This is because once the brain of a healthy person selects a body weight that it likes (determined by genetics and physical activity), it will aggressively defend this weight over the long-term.
And I get that vulnerability to obesity is largely determined by genetics (and epigenetics), but if people are destined to become obese, how come obesity was almost non-existent in the US more than 100 years ago? Why has the rate of obesity in the US accelerated after the 1980s? Why are almost all traditional populations who don’t enjoy a Western diet and lifestyle thin? Why do previously-thin traditional populations suddenly start to have problems with their weight (and health in general) once they transition over to a Western diet and lifestyle? And why do many previously overweight/obese individuals who change their diet to a more traditional one (e.g., Paleo, Primal) usually experience effortless weight-loss without calorie counting?
I ask these questions because it seems to me that many experts think that obesity is somehow just a matter of finding the willpower to consciously restrict calories. But that is actually crazy if you think about it. Calorie intake is not controlled consciously; it is controlled unconsciously (primarily by the hypothalamus). That means that if you have to force yourself to starve to lose a couple of pounds, there are bigger health problems that have to be addressed.
I believe that if someone is struggling with excessive fat weight, they will only be able to permanently lose this extra weight by finding the cause of their long-term calorie surplus (e.g., amped hunger signals, lowered metabolism, leptin insufficiency/interference/resistance, excess consumption of hyper-palatable foods, etc.). If they don’t solve this problem, then they will struggle unsuccessfully to lose their extra weight for the rest of their life.
Hi Stephan, I had the same question as Geoff earlier.
I do understand how comparing differences between identical twins and fraternal twins teases out the impact of genetics vs "everything else", including maternal gut flora and epigenetic factors.
But from a practical perspective, "everything else" is what needs to be addressed clinically to impact obesity.
For example if genes (largely uncontrollable) contribute 70% of the difference, does gut flora contribute 20%? How much does sleep-stress contribute? Micronutrient-deficiency?
It is essential to understand which of those levers are most critical.
I'm getting tired of addressing this argument that a strong genetic influence on body fatness is contradicted by the rapid increase in obesity in the US. Why don't you just hold your horses until I'm finished with the series...
This argument that French and Japanese (or Thai, or Indian, or whoever else) eat super-rewarding/palatable food all the time and are lean is nonsense, and I'm getting tired of correcting this over and over. My father is French and I've spent a lot of time in France. I cook French-inspired food in my own home almost every day. Everyday fare in the home is not the same as what you get in a French (or Japanese, or Thai, or Indian) restaurant. It tends to be tasteful, simple, home-cooked food.
But there are many factors in obesity, and being surrounded by calorie-dense palatable food is only one of them. The Japanese and French are more active than Americans, and have a different culture of meals and snacking. French people aren't surrounded by food all the time, and snacking is considered poor form unless you're a child. In France, overeating and over-drinking are also culturally unacceptable. It's bad manners to say you're stuffed. People say they've "eaten well" or "eaten enough" to indicate they don't want more food.
French people also eat a lot of raw vegetables and fruit. Growing up, my grandparents would start lunch with raw fruit and often a raw vegetable (e.g., cantaloupe, or raw artichoke/radishes/fava beans dipped in salt). There was some type of salad almost every lunch and dinner. Dessert was usually fruit, sometimes with yogurt, and very occasionally ice cream or cake. We got pastries for breakfast once a week or so. Of course there was no soda, though we did drink "syrop" sometimes, a flavored syrup that's added to water.
Americans have this perception that French people eat pastries, quiche, and duck a l'orange all day... give me a break!
Stephan -- I liked your description of the differences in (for example) French culture surrounding food and meals that might explain some of the differences between the obesity rate there compared to the U.S. The French aren't nearly as fat as we are. However, am I wrong or is it also true that the French are fatter than they used to be! Yes, they've maintained cultural advantages on this issue that have helped, but they are also suffering from the same things that have caused the obesity epidemic here, just to a lesser extent.
You're absolutely correct. If we want to know the reasons for French leanness, we need to look at the traditional diet/culture, not so much the current one. People eat at restaurants much more now, including fast food. McDonald's is actually quite popular. People don't have time to cook as frequently and traditional male-female roles are changing just like they did in the US decades ago.
Thanks for the responses on NEAT, it's fairly fascinating. If nothing else it's inspired me to stop wearing my hoodie in my office.
I was wondering what you think would happen if you took identical twins of obese parents, separated them at birth, and left one with their obese parents in America and put the other with a healthy traditional family in Japan. Would the child in Japan be thinner by the time they are an adult? How much variability could one expect?
So how is this research evaluated in the ability of significant numbers of people to lose weight?
Bryan Mayo said: "how come obesity was almost non-existent in the US more than 100 years ago? Why has the rate of obesity in the US accelerated after the 1980s?"
The increase in obesity during the pas century is largely due to changes in the foods that are available.
Food company scientists have been busily working to improve the palletability of foods to increase sales and profits. Food scientists have also been busy developing animals feeds to reduce costs and increase feed efficiency (weight gain per calorie of food intake.)
Major breakthrough was the development of the soy bean oil and soy chow for animal feed. Soy bean oil, which was almost nonexistent a century, now comprises more than 80% of vegetable oils. The demand for soy beans has not been driven by the demand for soy bean oil, however, but by the demand for soy cow for animal feed.
Soybean oil is about 51% n-6 linoleic acid (LA)and 7% n-3 linolenic acid (ALA). It has been estimated that dietary LA has increased from 2.3% of energy intake in 1909 to about 8% today which about half the increase attributable to LA in soybeans.
LA is the precursor to arachidonic acid (AA). The increased intake of n-6 LA without a corresponding increase in n-3 results in increased liver n-6 AA which causes an increase in food efficiency (weight gain per calorie) due to reduced energy expenditure. Because of higher food efficiency, soy chow is now the feed of choice for milk cows, laying hens, and chicken, beef and pork production.
Beef, pork, chickens and eggs and dairy products from soy fed animals have greater LA content than those products from animals fed on grass. Humans who consume these foods therefore have greater intake of LA and therefore increased food efficiency, and therefor gain more weight per calorie of food intake.
A good example of the increased LA content of foods of soy fed pigs is lard. For many years the producers, Research Diets, of the lard based high fat diet (HFD) D12492 has been used in animal experiments have published the LA content of the diet as 15% of the fat content based on USDA data. Two years ago the company tested the D12492 feed and found that the actual LA content to be twice as great as what they had previously published based on USDA data, or 30% of total fat content.
LA content of foods from animals. Diets based on foods from grain fed animals will therefore result in greater weight gain (greater food efficiency)than a similar diet, with the same calorie content, of food from grass fed animals.
The USDA dietary guidelines contribute the problem of excess LA intake by recommending substituting vegetable fats for animal fats.
Some studies have shown that the genetic susceptibility to obesity is attenuated among physically active people. Recent studies also have found that there is a stronger genetic connection to overweight among people who drink more sugar-sweetened beverages (http://www.nejm.org/doi/full/10.1056/NEJMoa1203039) or eat more saturated fats (http://www.ncbi.nlm.nih.gov/pubmed/22049296). I admit, these findings are only preliminary, but intriguing.
The NiHonSan study and the study of Pima Indians in Mexico vs. Arizona showed that the obesity rates become much more prevalent on a population level with migration to a very different environment and dietary pattern, suggesting that "the genes load the gun, the environment loads the trigger" as Francis Collins said.
Some have attributed this to "thrifty genes", but that is evidently a controversial concept.
I would expect to see higher weight variability in that case, and if you did a twin study on them, the heritability estimate would be significantly lower than 70%. The more homogeneous the environment, the higher the heritability estimate will be and the lower the environmental contribution to weight variability will be.
You (and Francis Collins) have got it right in my opinion.
How does this argument fare from an evolutionary perspective. It is quite hard to find pictures or accounts of obese individuals in more native cultures, who have not traded for flour or sugar. The pre agricultural lifestyle of foraging and hunting generally meant that any caloric consumption required a caloric expenditure. I have never seen any evidence of obesity in any HG society. I would argue that this began when we started living in large numbers together thanks in part to agriculture and the advent of "easier" obtainable food. As food became more industrialized and available it seems we started "growing" our waist as well. Purely anecdotal and mostly observational however I have not seen anything to the contrary. Your thoughts?
Erik I agree with you to a point. It could certainly be that those who are able to maintain what for most would be a chronic positive energy balance is the outlier. We all know the one who can eat any and all they want and not gain weight, or so it seems.
Perhaps everyonel (with rare exceptions) would respond to chronic positive energy balance that results in adipocyte hypertrophy, which is pathological, resulting in disregulation and potential multiple diseases! This being the result of a chronic diet that consists of foods with high energy density and low nutrient content and low volume. I propose that most humans subjected to this will end up obese and those individuals or even populations that don't are the outliers.
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