We explore the science of Set Point Theory and answer questions like how dieting or bariatric surgery impacts set point, and if we can change our set point.
A lot of people ask me about the validity set point theory, variations on set point, and whether or not our weight is set in stone. Today we will get into the science of this popular weight regulation theory and answer some common questions about changing your weight.
What is Set Point Theory?
While Instagram and YouTube influencers may promise you otherwise, our body weight is largely determined by genetic factors and when not manipulated, it’s believed it hovers roughly around a predetermined set point. Set point theory is often thought of like a thermostat where temporary increases or decreases in calories will be accompanied by regulatory mechanisms in the body to maintain a genetically preferred weight.
According to research, our bodies have a set point weight that is encoded into our DNA, or more specifically, encoded in the brain. This hypothesis was tested back in the 1950’s where scientist Gordon C. Kennedy proposed that consuming fat sent messages to the brain to help regulate body expenditure and intake.
Physiological Adaptations to Weight Loss
When we decrease our caloric intake, there are compensatory mechanisms in place that reduce the energy output to “balance” things out. For example, we may push ourselves less hard in the gym (physical activity declines), we may just move or fidget less unconsciously (our non-exercise activity thermogenesis/NEAT declines), we may absorb more calories from food (thermic effect of food decreases), and we weigh less so our body needs fewer calories to sustain that lower weight (resting metabolic rate decreases.)
Specific to body fat, this is often called the “lipostatic model of body fat regulation” which states that no matter the input, the output will remain consistent. The lipostatic model of body fat regulation was further explained when leptin was discovered in the late 1900s.
Leptin, our satiety hormone, is stored in fat stores, so when we lose weight, our fat stores shrink and our normal healthy signals that we’ve had enough to eat become silenced. So, we eat more, and more and more as our body fights to regain its preferred weight.
Ghrelin, our hunger hormone, is inversely related to calorie intake, meaning when we eat fewer calories than what our body needs, this hunger hormone revs up and increases our appetite. Studies show that people who try to lose weight and keep it off end up producing more ghrelin then they did before losing weight. This is our body’s attempt to increase appetite so you eat more and regain the lost fat.
Cortisol, our stress hormone, which is often released under severe caloric restriction or excessive exercise. Increased cortisol can slow metabolism and impair the ability to sustainably lose weight. Some studies have even shown that women who consume low calorie diets have higher cortisol levels and report more feelings of stress compared to women who do not restrict their diet.
Insulin is the hormone responsible for regulating our blood sugar levels by assisting the cells in absorbing glucose for energy. Insulin sensitivity (aka. the degree to which the cells respond to insulin and the uptake of glucose) is negatively associated with cortisol. That means when cortisol increases due to severe caloric restriction, the cells don’t respond as efficiently to insulin. This results in higher blood sugar levels, as glucose is not being absorbed by the cells.
Psychological Adaptations to Weight Loss
Psychological adaptations play a vital role in regards to set point theory, as well. In the very famous Minnesota Starvation Experiment conducted during WW2, lean healthy men were restricted to half of their caloric needs and forced to walk at least 5 miles each day. This semi-starvation experiment took place over a six month time period and not surprisingly resulted in the volunteers losing weight (25% of their baseline) and body fat. The volunteers also experienced extreme fatigue (the body’s attempt to pull back on caloric output), uncontrolled hunger (because their leptin was low), and a total obsession with food. When they were allowed to eat ad libidum again (normally without restriction), they gained the weight back and ended up at a higher weight and body fat percentage than prior to the experiment.
So, to simplify, the evidence suggests that when you cut calories and lose weight, metabolic rate declines, movement declines and hunger signals increases to compensate. Likewise, when you increase calories to gain weight, metabolic rate increases, movement increases and hunger decreases to compensate. This is the general ideology in support of the set point theory.
Unfortunately, it would appear that this isn’t a precise science as metabolism may decline more than what you would expect for the change in body weight. This is most likely a survival mechanism to safeguard against body and fat mass loss and can be supported through results from contestants on a popular reality T.V. show, The Biggest Loser. When contestants were brought in for their final weight in, not only did they lose an extreme amount of weight, but their leptin levels were also incredibly low and their metabolism was also reduced. When contestants were weighed again 6 years later, they gained back the weight and then some, AND their metabolism and leptin levels were still abnormal for their body weight. In fact, while it would be expected that one’s metabolism would be reduced after their body weight is reduced, they found that the metabolic decline was an additional 500 calories lower than what would be expected. In other words, if you needed 2500 calories to maintain 150 lbs, and it would be (hypothetically) expected you would need 2000 calories to maintain 130 lbs, they actually found that they could only consume 1500 calories to maintain that 20 lb weight loss. They also were starving all the time so you can imagine how hard it was to keep any amount of weight off. So to answer hypothesis of the Minnesota Starvation Experiment: “it is possible to conduct a rehabilitation diet without developing added fat deposits?” The current evidence suggests that weight re-gain for a lot of people may be unavoidable.
Set point theory criticisms
Set point theory has been critiqued as it doesn’t explain the increasing prevalence of obesity that we see in westernized societies. If the biological drive to maintain a particular body weight was so strong, why wouldn’t we weigh what we did as a society 50 years ago? It also doesn’t explain why obesity is greater in lower socioeconomic communities, or after particular life changes (like marriage or going to college). We also know that there are a lot of physical and psychological disorders that can cause massive weight changes (i.e. depression, eating disorders, cancer, IBD etc.), all of which are not addressed by set point theory. Finally, it would seem that while we do have homeostatic mechanisms in place to help us maintain our comfortable weight, it seems to be asymmetrical. In other words, it seems to favour weight gain over weight loss, likely as a survival mechanism to safe guard against a future “famine”.
Settling Point Theory
Settling point theory, on the other hand, aims to explain the differences between individuals and their body weight and levels of body fat. Developed by obesity researcher James Hill, settling point theory proposes that changes in body weight are more related to the patterns of diet and activity that people “settle into” over time as habits and how that intersects with their genetic dispositions, nutrition knowledge and environment. Basically, it sees that there is at least one parameter involved that essentially throws the homeostasis off. So being served and eating larger portion sizes of delicious foods, or having tools (like a car) to reduce energy expenditure may impact where the body weight will settle.
Settling Point theory criticisms
The settling point theory is based on the idea of a passive feedback system feedback between the size of the body stores and aspects of expenditure. Passive feedback, unlike a negative and positive feedback, is based on the system of settling at a point, which is based on the level of unregulated boundaries of either the input or output (calorie intake vs expenditure). For example, if an individual’s body fat percentage were to increase due to the increase in caloric intake, the energy expenditure would also increase in order to offset the input.
It should be noted, however, that settling point theory can only work under certain boundaries placed on the input or the output. For example, the input is not always based around caloric intake – it could be based on physical activity, or a combination.
Another criticism, is that it conflicts with the findings of the Minnesota Starvation Experiment. To recap, normal, healthy individuals were placed on an extremely low calorie diet with high amounts of exercise over a six month period of time. The test subjects had lost over 25% of body weight, which, according to the settling point theory, the subjects should have reached a plateau weight. However, when the subjects were released back to their normal routines prior to the experiment, they rapidly increased body and fat mass. This was thought to be due to the subjects overeating and being inactive. However, when the experiment was later reevaluated, the hyperphagic (overeating) response was likely due to the psychobiological response to being extremely food deprived for so long.
The settling point theory has been critiqued by the very clear homeostatic evidence of research like the Minnesota Starvation Experiment, and others that have tied metabolism shifts to changes in body weight and fat loss. Other studies that were conducted were focused on the basal metabolic rate (BMR), which were analyzed across age and health groups (i.e. children, individuals with eating disorders, overweight individuals on weight-reducing diets etc.) One study found that obese subjects had a higher basal metabolic rate but predictions of BMR were lower than expected, whereas the semi-starved subjects had a lower BMR but predictions of BMR were higher than expected.
Also, the settling point theory does not explain why some people can eat a lot of “high calorie” foods and not gain weight, while others do gain weight if consuming higher calorie foods.
General Model of Intake Regulation
The General Model of Intake Regulation combines these two theories and takes into consideration uncompensated (primarily environmental) and compensated (primarily physiological) factors. Compensated factors have negative feedback loops to control body weight with increased or decreased intake, but uncompensated factors influence intake but are not affected by intake. In other words, we may have a strict set point weight or food intake level, but any change in the system can create a new level to defend. It predicts that a sustained long-term change in the environment can trigger a sustained change in body weight, and how much the body changes weight would depend on each individual’s genetic responsiveness to that environmental trigger.
General model of intake regulation criticisms
This theory may explain how genetics and environment interact, but it only focuses on intake, not expenditure as compensated factors. This theory has been described as “informative, but incomplete”. Also, behavioral genetic data has shown that there are simply too many independent genetic influences where many factors can influence an individual’s intake.
The Dual Intervention Point Model
The Dual Intervention Point Model suggests we don’t just have one set point, it’s more of a set point range. Outside the upper and lower intervention points, the control mechanisms get switched on, and within the boundaries, there is only weak physiological control. In other words, if your set point range is 120-135 lbs, you can influence where you fall in that range by eating more or less, or moving more or less, but these efforts will be more likely to be thwarted if you try to get down to 100 lbs or up to 160 lb.
Some experts use evolution to explain why we may be better at protecting our lower intervention point but not our upper one since the lower intervention point would help prevent starvation, and our upper one would prevent predation. But nowadays, we don’t really have the same predators our ancestors had, so this drive may not be as strong. The variability in individual’s ability to maintain the upper intervention boundary is built into this model.
This model may help explain why we may easily go up or down 5-10 lbs after a holiday or life event, but we have a hard time maintaining massive changes in weight. Since everyone’s upper and lower intervention boundaries are different and variable is breadth, it helps explain why some people’s weight seems to be more tightly regulated than others. We all know someone who can eat ANYTHING and stay the same weight, while others have an extra beer on the weekend and gain weight.
Criticisms of the Dual Intervention Point Model
Like the general model of intake regulation, the dual intervention point model has been described as “incomplete”. Critics suggest that there is no explanation for why the model has a lack of concern to all the states between the different thresholds. For example, one review suggested: “in the dual intervention point model, the animal acts to avoid starvation if the lower threshold is reached, and acts to avoid predation if the upper threshold is reached. In between the thresholds, the animal is indifferent to the level of reserves.” This may not hold true in the real world, as current fat reserves may impact future fat reserves and pose a future threat. To sum up, the dual intervention point model is deemed incomplete without predicating a more ‘flexible’ situation where any level of fat reserves is of concern.
How to know what your set point range is?
Regardless of which theory you subscribe to, we can all appreciate that our weight has at least some genetic component and we may find value in knowing where that natural weight is. If your weight has been relatively stable your adult life, you haven’t engaged in a lot of diet behaviour, and you feel energetic and are in good health, there’s a good chance you are where your body wants to be.
Some signs that you are likely not at your natural or set point weight include:
- You have food rules or rituals that dictate when you eat and what you eat outside of just listening to your body’s cues.
- Your weight fluctuates frequently and significantly based on changes to your routine
- You feel preoccupied with food and guilt for eating something that you feel is “bad”
- You have symptoms like low libido, fatigue, coldness, low energy, irritability, menstrual irregularity or extreme hunger
Can You Change Your Set Point?
This is definitely up for debate and probably one of the major reasons why there are so many competing theories when it comes to set point weight. There is a lot of evidence to suggest that being able to change your set point dramatically may be difficult. When we look at research on “obese” patients who lose large amounts of weight, it is often found that they are unable to maintain that weight loss. What is more likely based on the research and based on these statistics is something closer to the Dual Intervention Point Model, where we are more likely to be able to shift our weight within the upper and lower intervention boundaries, but less likely to be able to jump well below or above that for an extended period of time.
Does Dieting Increase or Decrease Your Set Point?
As we have already discussed, weight loss diets have been shown to decrease metabolism and leptin levels, while increasing ghrelin levels. Therefore, when an individual begins to return to a ‘normal’ eating pattern, weight gain and fat gain is expected. However, research has shown in the Minnesota Starvation Experiment, “that after re-feeding it may take more than a year for the fat mass to decrease to within 5% of the initial value”. Therefore, it is possible that extreme dieting and short-term weight loss may not increase or decrease your set point permanently, however, that it may take some time.
Can Bariatric Surgery Change Your Set Point?
Body weight has been shown to not only be affected by intake and expenditure, but by biological factors as well. Research has suggested that in order to permanently change one’s set point, a person must change the biological factor that controls their weight. Bariatric surgery is performed by altering the size or shape of the digestive organs, which of course, will have an impact on caloric intake. But it may also alter the gut hormone levels (like GLP-1) that are in control of hunger and satiety sensations. While we don’t have human research to support this impact, studies where lab mice were both over and underfed after RYGB and sleeve gastrectomy, were shown to fight to defend their lean body mass.
In regard to weight regain post-surgery, bariatric surgery is considered to have the lowest weight regain rates for long-term weight loss. However, while RYGB is considered the “gold standard” of weight-loss surgeries, it comes with a ‘high price’ of weight regain statistics. A long-term study group of patients who had RYBG found that 93% maintained at least 10% weight loss, 70% maintained 20% weight loss, and 40% maintained 30% weight loss after 12 years post-op. Another study showed that around 59% of patients regain 20% or more of the weight they lost after RYGB surgery.
This would refute the set point changing permanently, because if set point was changed permanently, one would expect no weight regain over time after weight loss surgery.
Bottom Line on Set Point Theory
In summary of the various theories discussed, it’s clear that we have yet to uncover a perfect theory to explain body weight changes over time. What we do know is that body weight clearly has a genetic component and the relative impact of environment, gut microbiome, lifestyle behaviours and other factors is clearly what is up for debate.
What theory do you subscribe to when it comes to set point? Leave me a comment below with your thoughts!
Contribution by Brooke Porter
Abbey Sharp is a Registered Dietitian (RD), regulated by the Ontario College of Dietitians. She is a mom, YouTuber, Blogger, award winning cookbook author, media coach specializing in food and nutrition influencers, and a frequent contributor to national publications like Healthline and on national broadcast TV shows.