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History of Food Restriction in Obesity-Prone Animals Confers Survival Advantage

Yesterday, I posted about the observations that the same genes that confer athletic ability by increasing ‘fuel efficiency’ may also promote obesity when such activity ceases. This is in line with the ‘thrifty gene’ hypothesis, that obesity is the ‘natural’ response to genes that conferred survival advantages in our ancestors in the face of famines and increased demands on physical activity.

Interestingly, a study by Abdoulaye Diane and colleagues from the University of Alberta, just published in OBESITY, demonstrates that genetically obesity-prone animals, do in fact have a considerable survival advantage over lean-prone animals, an advantage that is further enhanced, when such animals have previously experienced caloric restriction.

The researchers took advantage of the fact that limiting access to food in mice (by restricting feeding hours) leads to an incremental increase in ‘voluntary’ wheel running associated with reduced food consumption (activity-induced anorexia) and even more running till the animals ultimately exhaust themselves and die.

In their experiments, while food restriction resulted in increased wheel running and reduced food intake in both obesity-prone and lean-prone juvenile mice, the former survived almost twice as long and lost far less of their body weight (percent and absolute values) than the lean-prone mice, which rapidly succumbed to the challenge.

Furthermore, even obesity-prone rats, who were kept lean by restricting their food to the levels of the lean-prone rats (by ‘pair-feeding’), lived longer, suggesting that this was not an advantage conferred simply by greater ‘caloric reserves’.

Interestingly, obesity-prone juvenile mice, who had previously undergone food restriction and regained their weight prior to the challenge, did even better.

Thus, not only was there a clear survival advantage in the genetically obese-prone mice but previous food restriction appeared to confer even more ‘resistance’ to the challenge.

It appear that not only do ‘obesity-prone’ genes allow animals to better cope with the dual challenge of starvation and increased physical activity, but that this ‘metabolic’ prowess can be further enhanced by prior experience with food restriction (weight loss).

Translated to humans, this later finding would suggest that ‘dieting’ makes you even more fuel efficient (which may well explain why dieting increases the risk of subsequent weight gain).

Or as the authors discuss:

“Our results show that juvenile obese-prone rats gain a survival advantage over lean-prone under famine-like conditions, and this advantage is further enhanced by physiological and behavioral changes induced by prior food restriction. In the wild, this survival advantage in young animals, that are the future breeders, would confer increased reproductive success. At a basic level, these results support the “thrifty gene” hypothesis of obesity.”

The authors further conclude:

“Thus, caloric restriction at early ages may predispose obese-prone individuals to become more metabolically efficient. An inducible increase in metabolic efficiency may help to explain the increased obesity in low- and middle-income countries where childhood under-nutrition exists in the context of rapid economic development and rural/urban migration. Thus, the obese-prone phenotype, that is highly deleterious in a food-rich environment, confers a real survival benefit in an unstable and scarce food environment, that is enhanced by prior caloric restriction.”

In summary, if these findings are indeed transferable to humans, they would have several important implications:

1) Genetically obese-prone individuals are better equipped to survive times of scarcity and/or increase physical demand.

2) This ‘survival’ advantage can be further enhanced by previous exposure to caloric restriction (weight loss).

While these findings may also explain the ‘survival paradox’ of obesity, where obese humans with chronic illnesses tend to live longer than skinny people with those illnesses, they also suggest an explanation for why dieting can make you fat.

I certainly do not envy the folks, who have to translate these findings into coherent ‘public health’ recommendations:

a) having genes that promote obesity is actually a survival benefit (if you should happen to encounter a famine)

b) if you are lucky enough to have these obesity genes, you can further increase your survival benefit (to famines) by (periodically?) losing weight

c) however, if you do (periodically?) lose weight, you may also end up getting even more obese – which, although a survival benefit during the next famine, will increase your risk for obesity-related health problems (in case the famine does not come).

I guess you can’t have it all.

Calgary, Alberta

Diane A, Pierce WD, Heth CD, Russell JC, Richard D, & Proctor SD (2011). Feeding History and Obese-Prone Genotype Increase Survival of Rats Exposed to a Challenge of Food Restriction and Wheel Running. Obesity (Silver Spring, Md.) PMID: 22016097


  1. If this is more or less true for humans, we are looking at rather severe obesity consequences for countries who have gone from famine to indistrialization in a short space of time, eg China and India. Maybe we are seeing this phenomonon in their statistics already.

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  2. Which therefore begs the question: Health at Every Size anyone?

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  3. Is it just me, or this one sort of a no-brainer? (meaning very, very obvious)

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  4. VERY interesting…. the unfashionable “thrifty gene theory” should get a new lease on life. i guess the only logical thing to do (if one is confident about the extrapolation of this from mice to humans) is to use the Perfect Health Diet/Eat Fat Lose Fat philosophy of eating “nourishingly” with low food toxicity but not restricting calories! if some pounds come off, good, but if they don’t, one must reconcile oneself to being overweight.

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  5. This is very interesting. Nonetheless, I think that any reference to the application of this study to humans is speculative at best. It is most certainly a possibility, but probably a little early to warrant the changing of public health messaging.

    Further to that, I believe we can attempt to disuade people from losing weight all we like, but at the end of the day I think we have to accept that many who are obese (or even only a few pounds overweight) want to lose weight. Very seldom does telling them that they are at EOSS stage 0/1 or that they are “metabolically healthy” deter them from this quest.

    I think that although we have to understand and appreciate the value of research like the aforementioned study, but we also have to face the reality that most people will still want to lose weight and we’re going to need to get good at it. And we need to address maintenance. Because with or without our help, people are going to do it anyway.

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  6. NewMe, this doesn’t seem to indicate that obesity is a survival advantage, but that the tendency to “top off the tanks” when the opportunity presents itself was a survival advantage in our past. Until the very, very recent past, that tendency in humans did not translate to problematic amounts of excess weight, because we weren’t surrounded by high-fat, high-calorie food 24/7. Now that we are, that genetic propensity is becoming a problem. HAES doesn’t have anything to do with that.

    There is a serious disjoint in the HAES thinking, I think. It seems to me that you and others promote it for two contradictory reasons: The problem of obesity is made worse by focusing on it and calling it a problem so we’ll say it’s not a problem, because if we say it is, the problem gets worse. Although we’re loudly proclaiming that it’s not a problem …

    It just seems like everyone who has finally managed to get a grip on their health and fitness and maintain significant losses are those who have said, “Screw this ‘I’m fat and fit’ stuff, I’m sick of this and I’m dropping this damned weight now.” It seems to me that, if yo-yo dieting makes the non-problem of obesity “worse,” that HAES is merely the other side of the yo-yo’s swing, just as much as skinny-uber-alles.

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  7. What, Janis? How is HAES the side of any swing? It tends to promote a stable weight.

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  8. Oh Janis. I’m getting tired of people thinking that HAES advocates believe that all bonbons are good bonbons and that as long as you’re breathing you’re healthy. Health at Every Size stresses health and activities/habits/behaviours to help keep you healthy or improve your health if that is what you so desire. HAES simply recognizes the fact that engaging in health behaviours will help you to be healthy, but not necessarily slim.

    Dieting, on the other hand, has an abysmal track record: a 95% failure rate, high chances of ending up heavier than before the diet began, the danger of developing disordered eating…Need I go on?

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