Set point theory: why your body brings your old weight back

In 1995, a team at Rockefeller University in New York led by Rudolph Leibel and Michael Rosenbaum took a close look. Forty-one adults, 18 of them with obesity, lost 10 to 20 percent of their weight or gained 10 percent under controlled conditions. Those who stayed 10 percent or more below their starting weight used 6 to 8 kilocalories less per kilogram of fat-free mass each day. Those who were 10 percent above it used 8 to 9 kilocalories more.

What this means for you: your body puts on the brakes in both directions. This applied to people with and without obesity, regardless of sex and body fat percentage.

At the University of Melbourne, a team led by Priya Sumithran followed 50 people with overweight or obesity through a ten-week very low-calorie diet. On average, they lost 13.5 kilograms. Afterward, satiety signals such as leptin, peptide YY and cholecystokinin fell, while the hunger hormone ghrelin rose. One year later, many of these changes were still measurable, and the participants were still hungrier than before the diet.

What this means for you: hunger after a diet is not in your head. It has a hormonal signature that can last a long time.

A team led by David Polidori and Kevin Hall of the National Institutes of Health used data from a study of 153 people with type 2 diabetes. A medication made them lose sugar, and with it energy, through their urine, without them directly noticing the deficit. The calculation showed: for every kilogram lost, the participants ate about 100 kilocalories more per day than before. That was more than three times the reduction in energy expenditure.

What this means for you: the stronger opponent appears to be appetite, not metabolism.

A team at Kiel University led by Müller and Bosy-Westphal summarized the data on adaptive thermogenesis in humans. Under controlled underfeeding, this energy-saving mode takes more than two weeks to build up. On average, it amounts to about 120 kilocalories per day, with large differences between individuals. A dampened sympathetic nervous system, less of the active thyroid hormone T3 and low leptin levels probably contribute to it.

What this means for you: the energy-saving mode is real, but usually smaller than feared. In some people, it is considerably stronger.

The New York team led by Rosenbaum and Leibel studied 21 people on an inpatient basis, in groups of three matched for sex and weight. They compared people at their usual weight, people shortly after losing at least 10 percent of their weight, and people who had already maintained such a loss for over a year. Energy expenditure was lower in both weight-loss groups, and to a similar degree.

What this means for you: the energy-saving mode doesn't necessarily disappear after a few weeks. It can still be there after more than a year.

In 2014, Rosenbaum and Leibel summarized twenty years of leptin research in humans. Their conclusion: leptin's most important job appears to be signaling scarcity, meaning a negative energy balance and shrinking reserves. When people at their usual weight receive extra leptin, their weight barely changes.

What this means for you: leptin is more of an alarm for scarcity than a brake against excess weight. That's why excess weight can't simply be treated with leptin.

A rare case from Cambridge shows how powerful this signal is. In 1999, a team led by Farooqi and O'Rahilly reported on a girl whose body had been unable to produce functional leptin since birth. The child had excessive hunger and was severely overweight. During treatment with leptin, she ate less and lost weight.

What this means for you: if the message from fat tissue is missing, the brain reacts as if there were a famine, even when reserves are large.

Ten people were kept as inpatients at a body weight reduced by 10 percent. Afterward, their muscles worked more economically, meaning they used less energy for the same movement. Then they received enough leptin by injection to bring their levels back to the value before the weight loss. Energy expenditure, muscle work, sympathetic activity and thyroid hormones returned to their pre-weight-loss levels.

What this means for you: in some respects, a body that has lost weight behaves like a body with leptin deficiency. The authors speak of a relative leptin insufficiency.

In another study, the same team showed six people with obesity pictures of food in a brain scanner, before and after a 10 percent weight loss. After the weight loss, regions involved in emotion, memory and the evaluation of food responded more strongly. In other regions, including the hypothalamus, the response decreased. With leptin, many of these changes reversed.

What this means for you: after a diet, your brain may evaluate food differently. This is a very small study, but it helps explain why that piece of cake suddenly calls out louder.

A team at the University of Washington in Seattle fed rats and mice a very high-fat diet. After just one to three days, before the animals had gained any significant weight, inflammatory signals appeared in the hypothalamus. Later, signs of gliosis followed, a scar-like reaction of the brain's support cells. In people with obesity, the team found MRI evidence of similar gliosis in the same brain region.

What this means for you: the control center might be altered by diet and inflammation. In humans, this is so far an association from imaging, not proof of cause and effect.

A team at the National Institutes of Health led by Erin Fothergill and Kevin Hall re-examined 14 contestants from the US show The Biggest Loser six years after the finale. During the 30-week show, they had lost an average of 58.3 kilograms, and their resting metabolic rate dropped by 610 kilocalories per day. Six years later, an average of 41.0 kilograms had come back. Yet their resting metabolic rate was still 704 kilocalories below the baseline value. Adjusted for body composition and age, the energy-saving mode amounted to around 500 kilocalories per day.

What this means for you: after extreme weight loss, the body can stay in energy-saving mode for years. Strikingly, those who kept off more weight in the long term also had the stronger energy-saving mode.

The same group looked at what set the more successful contestants apart from the others. Those who had still kept off around a quarter of their weight after six years were 160 percent more physically active than before the show. Among those who had regained weight, it was only 34 percent more. The two groups barely differed in energy intake.

What this means for you: physical activity appears to play a major role in maintaining weight. Whether this is cause or side effect is something a small observational study like this cannot clarify.

A team from Trondheim in Norway and Birmingham, Alabama, led by Catia Martins followed 71 people with obesity. For eight weeks, they ate 1,000 kilocalories a day and lost 14 kilograms on average. Immediately afterward, their resting metabolic rate was 92 kilocalories below the expected value. After four weeks of weight stabilization, this gap had roughly halved, and in a subgroup it was no longer detectable after one year.

What this means for you: a large part of the energy-saving mode might be tied to the ongoing deficit. In this study, it did not predict later weight regain.

In the Minnesota Experiment, men ate a severely reduced diet for months and were then fed back up to health. A team at the University of Geneva led by Abdul Dulloo reanalyzed the data of twelve of these men. The excessive hunger during the recovery phase persisted until not only fat but also fat-free mass had been replenished. The less fat and muscle had returned, the greater the hunger.

What this means for you: your body seems to monitor not only its fat reserves, but also muscles and organs. Because the hunger keeps going until the muscles have been rebuilt too, there can be more fat in the end than before. Experts call this fat overshooting.

A team at the University of Helsinki followed 4,129 Finnish twins from their teens to age 25. Those who had intentionally lost more than 5 kilograms gained weight faster afterward. In women with two or more such diets, the odds of being overweight at 25 were around five times higher than without dieting. Among identical twins, the twin with a dieting history was slightly heavier on average, by 0.4 BMI points.

What this means for you: people who diet often frequently already have a tendency to gain weight. But the twin data suggest that diets themselves might make a small contribution.

A psychologist at Drexel University in Philadelphia summarized the opposing view. According to his analysis, a diet does speed up weight regain. But a dieting history does not make you heavier than you would have become without diets. In people without obesity, it is more an indication of personal susceptibility and of an environment that favors weight gain.

What this means for you: whether diets themselves cause weight gain is scientifically controversial. Less controversial is that the cycle of losing and regaining weight is very stressful for many people.

In the extension of the STEP 1 trial, 327 people were followed for another year without treatment after 68 weeks of semaglutide or placebo plus a lifestyle program. With semaglutide, they had lost 17.3 percent of their weight on average. One year after stopping, when the lifestyle program also ended, around two thirds of that had come back.

What this means for you: as long as a medication dampens appetite, it can override the counter-regulation. This study did not show a permanently reset set point.

In 2011, an international group led by John Speakman of the University of Aberdeen compared the models. The set point model fits biology and genetics well, but does a poor job of explaining why many people's weight has risen since the 1980s. The settling point model explains environmental influences better, but the biological findings less well. The group therefore proposes models that consider genes and environment together.

What this means for you: your weight arises from the interplay of predisposition and everyday life. Neither side explains it alone.

In 2023, John Speakman and Kevin Hall compared seven models of weight regulation. Particularly illustrative is the model with two intervention points: between them lies a zone in which weight can fluctuate without strong pushback. Beyond the limits, physiological counter-mechanisms kick in. The authors themselves emphasize that experiments to decide between the models are lacking.

What this means for you: the idea of a rigid set point is probably too simple. The pushback during weight loss is nonetheless well documented.

In 2017, the Endocrine Society, a large international professional society for hormone medicine, summarized the state of research on how obesity develops. The authors increasingly describe obesity as a disorder of the system that balances energy intake and expenditure. They consider it possible that the level of body fat being defended is shifted upward, whether inherited or acquired. Exactly how this happens, they say, remains to be clarified.

What this means for you: if a set point can shift upward, it's fair to ask whether it can also find its way back down. That's what the next section is about.

A team at the University of Melbourne randomly assigned 200 people with obesity to either twelve weeks of rapid weight loss on a very low-calorie diet or 36 weeks of gradual weight loss. Those who had lost at least 12.5 percent then entered a 144-week maintenance program. In the end, both groups had regained around 71 percent of the weight they had lost. The pace made no difference.

What this means for you: slow is not automatically more sustainable. With the fast program, more people actually reached their goal, although one case of gallbladder inflammation that required surgery occurred in this group. In both groups, the bigger challenge was maintaining the loss.

In the Australian MATADOR study, 51 men with obesity dieted for a total of 16 weeks at about two thirds of their energy requirements. One group ate a reduced diet continuously. The other switched between dieting and a maintenance phase every two weeks and needed 30 weeks to do so. The group with breaks lost more weight, 14.1 instead of 9.1 kilograms on average, and also more fat. Adjusted for body composition, their resting metabolic rate dropped by only about 86 instead of 179 kilocalories per day.

What this means for you: maintenance phases might dampen the pushback. The study was small, included only men, and the figures refer to the participants who went through the entire program.

A team from Pittsburgh surveyed 931 people from the US National Weight Control Registry. All of them had lost at least 13.6 kilograms and kept it off for two years or longer. The longer they had already maintained their weight, the less effort and attention it took, according to their own reports.

What this means for you: maintaining your weight might get easier over time. This is a snapshot based on self-reports, not proof. But it fits with the hope that a new weight can settle in.