Why the obesity epidemic?

There is no need to start with statistics showing obesity is spreading globally like wildfire. Everyone knows it for sure. What we have failed to understand is why this is happening only today. People have mainly blamed various components of food and various eating habits along with lack of exercise. The energy intake-expenditure based thinking appears to ignore that our body has many evolved mechanisms of food intake regulation. Why these mechanisms fail to work is the real question. Why our body and brain fails to tell us when to stop eating is what a hypothesis should address, not how much we ‘decide’ to eat at a conscious level. Some recent (https://www.annualreviews.org/doi/citedby/10.1146/annurev-psych-122216-011643) neurobiological work shows that the subconscious regulation mechanisms are stronger than the conscious factors such as your desire, taste, thinking, self-control and the like.

While theories proliferate, obesity proliferates at a higher rate. The reason why we have failed to understand obesity is that obesity researchers are cut off completely from behavioural ecology. Human biology viewed without behavioural evolution makes little sense. Only in the light of evolution, obesity will make sense.

It’s not that evolutionary thinking has not gone into the biology of obesity. The problem is that these biologists have never experienced themselves a life in wilderness and therefore fail to appreciate the conditions in which human (or mammalian in the broader sense) physiology evolved. A hypothesis called ‘thrifty gene’ originated in the 1960s which was a quasi-evolutionary hypothesis. ‘Quasi’ because it was based on arm chair evolution. Not on a thorough understanding of life in the wilderness. In the following decades many variations and versions of the thrift family of hypotheses followed but all of them suffered the same fate. Any thrift family hypothesis assumes that human ancestors underwent many cycles of food abundance and scarcity. Therefore we evolved for overeating in days of abundance and build fat which we burn during periods of food scarcity; something that sounds very logical on the face of it but does not stand a serious scrutiny and hard evidence. There are many problems with the concept of thrifty origins of human obesity. Some of the serious objections are that (i) human physiology does not match that of other species that clearly have evolved mechanisms to cope with feast and famine conditions. (ii) Human obesity is marked by impaired fat utilization mechanisms, not by faster fat building. This directly contradicts the expectation of feast and famine adaptation. (iii) Models of overeating during food abundance do not account for the short term cost of over-foraging and overeating, it also does not account for the thermodynamic efficiency of energy storage and reutilization, which is typically very low. When these factors are taken into account the thrift hypothesis and all its variations fail badly even in a mathematical model. If something works in a mathematical model, it may or may not be there in the real world, but if something doesn’t work in a mathematical model, you can be sure it does not work in reality. (iv) Last but not the least; no clear mechanism of thrift has emerged in spite of decades of search. There were many false alarms which did not sustain.

One who has lived in a wilderness environment and experienced the life of hunter-gatherers can have a much deeper vision. Feeding is necessarily related to foraging and foraging is prone to risks. So feeding is to be optimized against the risk of foraging. All mechanisms of human food intake regulation are optimized for an interaction between nutritional benefits and foraging risk.

I will try to explain here with a little bit of technicality of the model, not mathematically but graphically. A detailed model is published here (. See this figure. There is an optimum food intake for the best physiological state as in the figure ‘a’.  If foraging associated risk wasn’t there any time in our ancestry, we would have evolved mechanisms to ensure the physiological optimum. But if foraging is associated with risk, we have to face a trade-off between what is physiologically good and what is ecologically safe. The new trade-off optimum always lies to the left of the physiological optimum (see B part of the figure). So species that face a foraging related risk should evolve mechanisms for achieving this trade off. Not only that, they might fail to evolve mechanisms to ensure the physiological optimum, since the foraging optimization mechanisms always works before the physiological optimization could work. Something that is never used, may not evolve or degenerate even if it was there earlier.

The interesting thing is that now we know molecular mechanisms by which this foraging optimum is achieved. Leptin is a protein secreted by the fat tissue of our body. More the fat, more is leptin secretion. Leptin gives a signal to suppress hunger. But the action of leptin is crucially dependent on another peptide produced in the brain called CART. CART is expressed in response to risk perception. Whether the risk is because of predator or because of extreme cold or heat doesn’t matter. All potential foraging risks trigger CART expression. And CART and leptin together suppress the hunger sensation. The story does not end there. CART also suppresses risk taking behaviour. CART expression is dependent on leptin levels, such that when leptin in the brain in low, CART expression is reduced. This ensures that when you don’t have stored fat, you are ready to take greater foraging risks. On the other hand when you have enough fat, you will overexpress CART so that you don’t go out for foraging and expose yourself to risk. This is a perfect mechanism to optimize foraging. We modelled the ecological optimum and it turns out that the steady state body weight will be proportional to the inverse square root of risk. We also modelled the leptin CART interaction and it turns out again that body weight will be a function of the inverse square root of risk. So by both proximate and ultimate modelling the result is the same. This is one of the rare examples in evolutionary modelling where the proximate and ultimate converges so nicely.

So we are getting fat not because of any particular food constituent or because we don’t burn enough fat, it is because we have detached feeding from foraging and from risk. Since we hardly face any risk including exposure to extreme heat or cold, our brain does not make sufficient CART so that our leptin levels are ineffective in telling us when to eat and when not. Further the model also explains why some have greater tendency to accumulate fat than others, why we have impaired fat burning and so on. I will not explain these details here. This model explains many known patterns in the obesity epidemic than any previous models have. What is the take home message? The key to control fat is not in what type of food you eat. It is there in your brain peptide levels that are regulated by your behavioural environment. Well, we are not going to go back to stone age life, are we? But we can still bring back the missing components of our hunter gatherer life. Sports activities do precisely the same. Any kind of sports mimics our hunter fighter ancestry. We hit, kick, aim, chase, attack, defend, team up… precisely the same acts. Studies on the brain physiology of sports are limited, but whatever we know indicates that these activities use the same neuroendocrine pathways and thereby are likely to normalize our brain chemistry back to our stone-age physiology. The pro-health effects of sports are not because they burn calories, they are because they bring back the missing behaviours. So engage in active sports and expose the body to the ambient heat and cold as much as it can tolerate. If this normalizes the evolved regulation pathways, you can certainly stop worrying about calories in and eat whatever you like, just listen to the body’s signals as to when and how much.