Metabolic adaptation during dieting

A plateau on a diet is often explained by a “slowed metabolism,” and there is a grain of truth in this. The editorial team broke down what metabolic adaptation is, what mechanisms lie behind it, how pronounced it is in ordinary people and athletes and what can actually be done.

What metabolic adaptation is

Anyone who has been on a long diet is familiar with the situation: the first weeks the weight comes off steadily, and then, with the same eating, the movement slows down or stops. Partly this is explained by simple arithmetic — a smaller body spends less energy. But studies show that expenditure drops more than can be explained by the loss of weight alone. This “excess” decline is called metabolic adaptation, or adaptive thermogenesis.

The classic work on this topic was published by Leibel, Rosenbaum and Hirsch (1995) in the New England Journal of Medicine. Participants who reduced their body weight showed a drop in total energy expenditure greater than predicted for their new mass and body composition, while those who gained weight showed the opposite — an increase. The body seems to “defend” the previous weight.

Even earlier, in the Minnesota Starvation Experiment led by Ancel Keys, it was described how prolonged substantial calorie restriction lowers the basal metabolic rate, spontaneous activity and increases the obsession with food. This work still remains a fundamental source on the psychophysiology of a prolonged deficit.

For athletes this topic is especially relevant: they often bring their body-fat percentage down to values lower than “comfortable” for the body, and it is exactly then that adaptation manifests most strongly. A detailed review of this question in the context of sport was offered by Trexler, Smith-Ryan and Norton (2014).

What energy expenditure is made up of

To understand where exactly adaptation “hides,” it is worth breaking down daily energy expenditure into components. The basal metabolic rate is the energy for maintaining vital functions at rest; it makes up the largest share in most people. The thermic effect of food is the expenditure on digestion. Then — the energy of planned training and the so-called NEAT: all unplanned activity, from walking to gesturing.

With a prolonged deficit all components decline. The basal metabolic rate falls because of the loss of mass and, additionally, because of hormonal changes. The thermic effect of food decreases simply because the person eats less. Training “costs” less, because a lighter body needs less energy for the same work, and the muscles become more efficient.

The most variable component is NEAT. People on a diet unconsciously move less: they walk less, sit more often, stand up less often. This change can be substantial and at the same time imperceptible to the person, so a pedometer is one of the most useful tools of control during cutting.

Rosenbaum and Leibel (2010) in their review emphasize that adaptive thermogenesis after weight reduction persists as long as the weight remains reduced. That is, it is not a temporary “glitch” but a new state of regulation that has to be worked with.

Hormonal and neural mechanisms

A key role in metabolic adaptation is played by leptin — a hormone produced by fat tissue. Its level falls as fat reserves decrease and, even faster, with calorie restriction. For the brain this is a signal of an energy deficit: appetite rises, energy expenditure and the activity of the sympathetic nervous system decline.

• Leptin— decreases, increases hunger and contributes to a reduction in energy expenditure;
• Ghrelin— the “hunger hormone,” in many people it rises on a diet;
• Thyroid hormones— active T3 may decrease with a prolonged deficit;
• Sex hormones— in men testosterone may fall, in women the cycle may be disrupted;
• Cortisol— may rise against the background of stress, lack of sleep and intense training.

These changes make evolutionary sense: in conditions of food scarcity, a body that saves energy and searches harder for food had a better chance of surviving. The problem is that in modern conditions the same mechanism hinders holding onto the achieved result.

It is important to distinguish adaptation from pathology. A decrease in T3 or testosterone against the background of a diet is for the most part a physiological reaction that recovers with the return of normal calories. Self-“treatment” of these changes with hormonal drugs is dangerous and has no medical justification.

In female and male athletes with prolonged low energy availability, relative energy deficiency in sport (RED-S) has been described, which affects bones, hormones, immunity and the psyche. Metabolic adaptation is one of its components.

How strong the effect can be

The magnitude of adaptation is very individual and depends on the duration and depth of the deficit, the initial body-fat percentage and genetics. In most people on moderate diets it is relatively small — on the order of a few percent of daily expenditure. In lean athletes on prolonged preparation and in people with extreme weight loss it can be significantly larger.

The most famous example is the study by Fothergill and colleagues (2016) of participants in the TV show “The Biggest Loser.” Six years after the competition their basal metabolic rate remained substantially lower than predicted for their mass — on average by several hundred kilocalories per day, even in those who had partly regained weight.

At the same time, one should not transfer these data to an ordinary athlete directly. The show’s participants lost a very large mass in a short time under extreme conditions. For a person on a moderate cut, adaptation is usually much more modest and, after the diet ends, partly recedes.

The widespread notion of a “damaged metabolism,” in which a person cannot lose weight even on very low calories, is not supported by science. More often the cause of a stall is inaccurate food tracking, a decrease in NEAT and water retention, not a “broken” metabolism.

What can be done in practice

It is impossible to completely avoid metabolic adaptation, but it can be softened. The first tool is a moderate deficit and a slow rate: the less aggressive the diet, the weaker the compensatory reactions and the better the muscles are preserved, which are the main “consumer” of energy at rest.

The second is high protein and strength training. They preserve lean mass and maintain energy expenditure. The third is control of NEAT: the daily number of steps is a simple and objective indicator that helps to notice an unconscious decline in activity in time.

The fourth tool is diet breaks. In the MATADOR study (Byrne et al., 2018) men with obesity who alternated two weeks of a deficit with two weeks of maintenance calories lost more fat and held the result better than a continuous-diet group. The data for athletes are less clear-cut, but the very idea of planned pauses looks rational.

The fifth is sleep and stress. Lack of sleep increases hunger and lowers spontaneous activity, so without normal sleep any dietary strategy works worse.

Finally, the end of the diet should be planned. A gradual increase in calories after cutting allows a partial recovery of the hormonal background and energy expenditure without a sharp gain of fat.

Editorial conclusions

Metabolic adaptation is a real physiological phenomenon: with a prolonged deficit, energy expenditure drops more than the loss of mass predicts. The main mechanisms are a decrease in leptin, thyroid hormones, sympathetic activity and NEAT.

For most people on moderate diets the effect is small, and the myth of a “broken metabolism” is exaggerated. A moderate deficit, high protein, strength training, control of steps and diet breaks help to soften adaptation.

Any hormonal disturbances against the background of a diet require assessment by a doctor, not self-medication.

We also recommend our articles on the reverse diet after cutting, the basic principles of nutrition during cutting and RED-S in athletes.

References

1. Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med. 1995;332(10):621–628.
2. Rosenbaum M, Leibel RL. Adaptive thermogenesis in humans. Int J Obes (Lond). 2010;34 Suppl 1:S47–S55.
3. Trexler ET, Smith-Ryan AE, Norton LE. Metabolic adaptation to weight loss: implications for the athlete. J Int Soc Sports Nutr. 2014;11:7.
4. Fothergill E, Guo J, Howard L, et al. Persistent metabolic adaptation 6 years after "The Biggest Loser" competition. Obesity (Silver Spring). 2016;24(8):1612–1619.
5. Byrne NM, Sainsbury A, King NA, Hills AP, Wood RE. Intermittent energy restriction improves weight loss efficiency in obese men: the MATADOR study. Int J Obes (Lond). 2018;42(2):129–138.
6. Keys A, Brožek J, Henschel A, Mickelsen O, Taylor HL. The Biology of Human Starvation. Minneapolis: University of Minnesota Press; 1950.