Why Diet and Exercise is Not a Treatment for Obesity

If going on a diet or starting an exercise program resulted in persistent weight loss,  we would not have an obesity epidemic.

Unfortunately, as anyone who has tried this knows, maintaining a significant degree of weight loss requires daily dedication, motivation and a limitless supply of will power – nothing short of developing a compulsive obsession.

As readers will recall, the biology of the post-weight loss state is nothing like the biology of someone who has never lost weight. There are countless ways in which the psychoneurobiology, energy physiology and metabolism in anyone who has lost weight are remarkably different from someone ‘naturally’ of that weight.

Simply stated, someone who was 150 lbs and has lost 20 lbs cannot hope to maintain that weight loss by simply eating the same amount of food or doing the same amount of exercise as someone who is ‘naturally’ a 130 lbs.

The 150 lbs person who has lost 20 lbs, to maintain their new 130 lbs, has to actually now live like someone who is ‘naturally’ a 110 lbs; just eating like someone who is 130 lbs but has never lost weight, will simply result in rapid weight regain.

This is why just cutting out a few ‘extra’ calories or walking a few ‘extra’ steps is not an effective or sustainable strategy for maintaining weight loss – for any clinically meaningful weight loss (when indicated) – we are looking at cutting hundreds of calories from the diet and adding hours of serious exercise per week – forever!

A comprehensive and fascinating overview of the fundamental changes that occur with weight loss to ultimately make sustaining this new weight an ongoing challenge, is discussed by Paul Maclean and colleagues from the University of Denver Colorado, in a paper just published in the American Journal of Physiology.

The authors provide a detailed synthesis of data from a wide range of weight loss studies that include studies in clinically overweight and obese adults, in diet-induced, polygenic animal models of obesity, and with dietary (non-surgical) interventions involving an energy restricted low fat diet.

The consistent finding from all such studies is that all individuals or animals in a post-weight-loss state face considerable ‘homeostatic pressure’ that aims to drive their weight back to initial levels.

The paper extensively discusses how changes in biological signals of fat stores (e.g. leptin) elicit profound metabolic and behavioural adaptations – a topic that I dealt with extensively in previous posts.

The key findings of increased hunger and appetite, reduced satiety and substantially increased ‘fuel efficiency’ have very real underlying biological drivers – drivers powerful enough to ultimately wear down even the most persistent dieter.

As the authors point out – persistent dieting is so difficult because it requires maintaining a remarkably large ‘energy gap’:

“Because both sides of the energy balance equation are affected after weight loss, the biological pressure to gain weight is a consequence of both increased appetite and suppressed energy expenditure.

During weight maintenance after weight loss, this energy gap reflects the magnitude of the daily burden that thwarts cognitive efforts to maintain the reduced weight.

Regardless of which side of the energy balance equation is most affected, the energy gap imparts a substantial pressure to eat in excess of the energy requirements.

The magnitude of the energy gap is greatest at the nadir weight after weight loss. Likewise, this energy gap does not dissipate with time in weight maintenance. Rather, studies in DIO (diet induced obesity) models indicate that the magnitude of the energy gap gradually increases the longer they maintain their reduced weight with an energy restricted diet .

The implications from these observations are that the biological pressures may strengthen with time and the amount of lost weight, gradually increasing their perceived influence.”

The paper also extensively discusses some of the lesser known metabolic adaptations to weight loss including profound changes in gut biology that enhance caloric extraction from food as well as alterations in liver function, skeletal muscle and fat tissue that promote weight regain.

While all of this may seem hopeless to readers, the authors actually end on the rather positive note that:

“… only by acknowledging that these homeostatic pressures emerge, we can proactively develop and implement regain prevention strategies to counter their influence. To ensure success, the regain prevention strategies will likely need to be just as comprehensive, persistent, and redundant, as the biological adaptations they are attempting to counter.”

Obviously, it is also important to note, that no ‘weight-loss strategy” actually addresses the many complex reasons why people may gain weight in the first place.

Whoever said that treating obesity was simply a matter of ‘eating less and moving more’ (ELMM) probably also believes that they can live forever by simply breathing less.

AMS
Burlington, Ontario

Maclean PS, Bergouignan A, Cornier MA, & Jackman MR (2011). Biology’s Response to Dieting: the Impetus for Weight Regain. American journal of physiology. Regulatory, integrative and comparative physiology PMID: 21677272