Last I heard, the popular science theory about why it’s easier to lose weight than to keep it off is that appetite increases rather than that metabolism slows. Have you heard anything else that looks plausible?
As you would probably imagine, there is a bit of both, though it seems like the hunger portion is more important. Intuitively, any change in metabolic rate is very easily overshadowed in magnitude by increases or decreases in the amount of food eaten. This is why exercising to “burn calories” is ineffective as a means of weight loss. One tall glass of orange juice is equivalent to ~10-15% of your Basal Metabolic Rate (BMR) or to ~30 minutes on a treadmill.
This turned out a lot longer than I expected, but hopefully it will be useful to some people.
There are two primary hormones involved in hunger and weight management, Ghrelin and Leptin, with Leptin being arguably more important because of all of its downstream effects and because it is the one we can control with diet and exercise interventions:
(One important thing to know here is that the important thing is the level of hormonal “Activity”, not the absolute levels of the hormone. Activity is made up of two factors: How much of the hormone you have and sensitivity to that hormone. For example, obese people with chronically high blood sugar are usually insulin resistant. They have high levels of insulin, but it doesn’t do its job properly because they have low sensitivity to insulin. This is caused by chronically high levels of the hormone.)
Ghrelin: Secreted by adipose (fat) tissue, increases hunger. Ghrelin is “entrained” by your eating habits which is why you usually get hungry at about the same time each day. People who are used to eating breakfast feel hungry if they don’t, because your body releases Ghrelin when you expect to eat. More fat tissue leads to higher Ghrelin levels on average. (More fat ⇒ more hungry) Ghrelin is not known to have “resistance” associated with it.
Leptin: Also secreted by adipose (fat) tissue, decreases hunger. Leptin is also entrained by meal patterns, so having a regular eating schedule is likely effective in controlling excess eating. Low leptin leads to both an increase in hunger and a decrease in metabolic rate. (Less fat ⇒ more hungry). Now you would think that being fatter would increase leptin levels as well. It does. Unfortunately, with chronically high levels of leptin, your body adapts and develops “leptin resistance”. This means that leptin is not as effective at controlling hunger when you are overweight. Naturally thin people have low levels of leptin, but they are very sensitive to it, so it still does its job at controlling hunger.
These are both hormonal systems, so the body takes longer to come to equilibrium after interventions. Also, according to “set-point” theory, your body will vary the levels of these hormones in order to maintain a certain weight range. Set point is thought to have a strong genetic component and it is unclear whether a person’s set point can be changed.
However, there are things that can be done to help get your Leptin system back on track. In the long-term, leptin levels are determined primarily by total fat mass. More fat, more leptin. Less fat, less leptin. If you are overweight, you are likely at least somewhat leptin resistant.
In the short term, leptin is influenced by caloric surplus/deficit and macronutrient ratios (primarily carbohydrates).
So, what does this mean and what can we do about it?
Well, an acute calorie deficit crashes leptin in the short term. This is why you get hungry if you don’t eat. Intermittent refeeds (especially carb refeeds) where you eat a caloric surplus one day before going back to your daily deficit can keep your leptin levels slightly higher to help control hunger over the course of a diet.
If you manage to keep a diet going for long enough to lose a significant amount of fat mass, then your natural long-term leptin levels will be lower. This should make you hungrier. However, your leptin sensitivity will also increase until it gets back to a normal baseline. This helps control hunger.
However, research has not shown any way to increase leptin resistance below an individual’s natural baseline sensitivity. That means that if your set-point is higher than the weight you’ve dieted to, your naturally regulated food intake will lead to slowly gaining weight again up to your set point. However, if you get your leptin sensitivity back to normal by losing weight and keeping it off for a while, then the leptin increase caused by acute overeating can help naturally regulate your hunger to help decrease weight gain.
So the takeaways:
Being overweight makes you leptin resistant. This means even though your body is trying to tell you to stop eating, you can’t hear it. Once you lose weight and give your body time to adjust, your body is sensitive to its own signals again which can help naturally regulate overeating and metabolism.
Acute caloric deficits increase hunger (and lower metabolism by a small amount) via decreased leptin. Having periodic refeeds where you eat higher calorie and higher carb one day can help keep leptin levels higher during a diet and decrease hunger.
Your body probably has a natural “set-point” that it will try to adjust to once it can hear its own signals and your leptin system works properly. This may be higher than you want. Long-term behavioral modifications to induce entrainment of meal patterns, regular exercise, eating less calorie-dense foods, and intermittent fasting can be helpful in allowing you to maintain a weight below your set point.
it is unclear whether a person’s set point can be changed.
It is quite clear that people’s set points change over their lifetime—great many people are trim in their 20s and then succumb to the middle-age spread in their 40s. Looks like one can make an argument that in many (but not all) people their set points drift upwards as they age, at least until the 60s when some revert to losing weight, and not only muscle mass but fat as well.
The interesting question, of course, is whether one can “reset” one’s set point to what it was in the 20s.
leptin is influenced by caloric surplus/deficit and macronutrient ratios (primarily carbohydrates)
Any comments (or links) on how low-carb diets in general and ketosis in particular affect leptin?
Right, I mean by specific interventions. For example, dieting down to very low body fat and then maintaining it does not appear to increase leptin sensitivity (much) beyond that of a normal-weight person, nor does exercise.
As far as ketosis and leptin goes, This study indicates that carbohydrate overfeeding increases leptin and energy expenditure, while fat overfeeding does not. This suggests that eating carbohydrates naturally causes you to get full, while fat does not, which is inline with research on satiety and macronutrients. (Keep in mind that fructose is not metabolized like a normal carbohydrate and has different effects on leptin and so may not cause the leptin increase or induce satiety.)
This study indicates that ketosis blunts ghrelin release even in a caloric deficit which could be the reason that people on ketogenic diets (or doing intermittent fasts, which is a fat-burning state) report lower hunger levels. In this situation, leptin is lower which probably reduces metabolic rate a bit (probably not hugely significant), but its effect on hunger is probably balanced out by the change in ghrelin.
If you are doing a ketogenic or low carb diet, if you reach a plateau with weight loss, it could be because your leptin is too low. Doing a carb refeed with glucose (which includes starches), but not fructose, could be beneficial.
Interesting. So this implies that lower hunger in calorie-deficit ketosis is due to low ghrelin which more than compensates for lower leptin… And yes, carb refeeds (usually weekly) are a component of many low-carb diets.
However, research has not shown any way to increase leptin resistance below an individual’s natural baseline sensitivity. That means that if your set-point is higher than the weight you’ve dieted to, your naturally regulated food intake will lead to slowly gaining weight again up to your set point. However, if you get your leptin sensitivity back to normal by losing weight and keeping it off for a while, then the leptin increase caused by acute overeating can help naturally regulate your hunger to help decrease weight gain.
How long is long enough to increase leptin sensitivity?
Anecdotally, people who keep weight off say it requires constant attention, not that they develop a lower set point.
Anecdotally, people who keep weight off say it requires constant attention, not that they develop a lower set point.
This is correct. That’s what I meant by “That means that if your set-point is higher than the weight you’ve dieted to, your naturally regulated food intake will lead to slowly gaining weight again up to your set point.” If your set-point is higher than your weight, then you will still gain weight back if you’re not careful. Once your leptin system is restored to healthy function though, your body is better at regulating its weight. Weight gain at this point is likely to be slow and gradual rather than the rapid “rebound” weight gain that many dieters get if they completely stop their diet without allowing for this system to recover first. Also, since eating a lot makes your produce leptin, if your body is now sensitive to that signal, it will naturally make you less hungry for a little while, whereas if you’re leptin resistant, you feel hungry even when you’ve had enough. This is the benefit. That means that if you follow sensible lifestyle-diet practices even when you’re done with the intense diet phase, you can greatly slow or prevent weight regain. That would be things such as eating whole foods instead of processed foods, fruits and vegetables for fiber, and limit sugar (fructose is the real culprit) and alcohol consumption.
How long is long enough to increase leptin sensitivity?
This one probably varies a lot with the individual. Also, keep in mind that there are different levels of leptin resistance, so recovery follows a curve. From anecdotal reports, it seems that some people can see significant improvement in 4-6 weeks with most people getting significant improvement within 3 months. I think it’s likely that improvements will continue for 6 months to a year depending on the individual.
Last I heard, the popular science theory about why it’s easier to lose weight than to keep it off is that appetite increases rather than that metabolism slows. Have you heard anything else that looks plausible?
As you would probably imagine, there is a bit of both, though it seems like the hunger portion is more important. Intuitively, any change in metabolic rate is very easily overshadowed in magnitude by increases or decreases in the amount of food eaten. This is why exercising to “burn calories” is ineffective as a means of weight loss. One tall glass of orange juice is equivalent to ~10-15% of your Basal Metabolic Rate (BMR) or to ~30 minutes on a treadmill.
This turned out a lot longer than I expected, but hopefully it will be useful to some people.
There are two primary hormones involved in hunger and weight management, Ghrelin and Leptin, with Leptin being arguably more important because of all of its downstream effects and because it is the one we can control with diet and exercise interventions:
(One important thing to know here is that the important thing is the level of hormonal “Activity”, not the absolute levels of the hormone. Activity is made up of two factors: How much of the hormone you have and sensitivity to that hormone. For example, obese people with chronically high blood sugar are usually insulin resistant. They have high levels of insulin, but it doesn’t do its job properly because they have low sensitivity to insulin. This is caused by chronically high levels of the hormone.)
Ghrelin: Secreted by adipose (fat) tissue, increases hunger. Ghrelin is “entrained” by your eating habits which is why you usually get hungry at about the same time each day. People who are used to eating breakfast feel hungry if they don’t, because your body releases Ghrelin when you expect to eat. More fat tissue leads to higher Ghrelin levels on average. (More fat ⇒ more hungry) Ghrelin is not known to have “resistance” associated with it.
Leptin: Also secreted by adipose (fat) tissue, decreases hunger. Leptin is also entrained by meal patterns, so having a regular eating schedule is likely effective in controlling excess eating. Low leptin leads to both an increase in hunger and a decrease in metabolic rate. (Less fat ⇒ more hungry). Now you would think that being fatter would increase leptin levels as well. It does. Unfortunately, with chronically high levels of leptin, your body adapts and develops “leptin resistance”. This means that leptin is not as effective at controlling hunger when you are overweight. Naturally thin people have low levels of leptin, but they are very sensitive to it, so it still does its job at controlling hunger.
These are both hormonal systems, so the body takes longer to come to equilibrium after interventions. Also, according to “set-point” theory, your body will vary the levels of these hormones in order to maintain a certain weight range. Set point is thought to have a strong genetic component and it is unclear whether a person’s set point can be changed.
However, there are things that can be done to help get your Leptin system back on track. In the long-term, leptin levels are determined primarily by total fat mass. More fat, more leptin. Less fat, less leptin. If you are overweight, you are likely at least somewhat leptin resistant.
In the short term, leptin is influenced by caloric surplus/deficit and macronutrient ratios (primarily carbohydrates).
So, what does this mean and what can we do about it?
Well, an acute calorie deficit crashes leptin in the short term. This is why you get hungry if you don’t eat. Intermittent refeeds (especially carb refeeds) where you eat a caloric surplus one day before going back to your daily deficit can keep your leptin levels slightly higher to help control hunger over the course of a diet.
If you manage to keep a diet going for long enough to lose a significant amount of fat mass, then your natural long-term leptin levels will be lower. This should make you hungrier. However, your leptin sensitivity will also increase until it gets back to a normal baseline. This helps control hunger.
However, research has not shown any way to increase leptin resistance below an individual’s natural baseline sensitivity. That means that if your set-point is higher than the weight you’ve dieted to, your naturally regulated food intake will lead to slowly gaining weight again up to your set point. However, if you get your leptin sensitivity back to normal by losing weight and keeping it off for a while, then the leptin increase caused by acute overeating can help naturally regulate your hunger to help decrease weight gain.
So the takeaways:
Being overweight makes you leptin resistant. This means even though your body is trying to tell you to stop eating, you can’t hear it. Once you lose weight and give your body time to adjust, your body is sensitive to its own signals again which can help naturally regulate overeating and metabolism.
Acute caloric deficits increase hunger (and lower metabolism by a small amount) via decreased leptin. Having periodic refeeds where you eat higher calorie and higher carb one day can help keep leptin levels higher during a diet and decrease hunger.
Your body probably has a natural “set-point” that it will try to adjust to once it can hear its own signals and your leptin system works properly. This may be higher than you want. Long-term behavioral modifications to induce entrainment of meal patterns, regular exercise, eating less calorie-dense foods, and intermittent fasting can be helpful in allowing you to maintain a weight below your set point.
It is quite clear that people’s set points change over their lifetime—great many people are trim in their 20s and then succumb to the middle-age spread in their 40s. Looks like one can make an argument that in many (but not all) people their set points drift upwards as they age, at least until the 60s when some revert to losing weight, and not only muscle mass but fat as well.
The interesting question, of course, is whether one can “reset” one’s set point to what it was in the 20s.
Any comments (or links) on how low-carb diets in general and ketosis in particular affect leptin?
Right, I mean by specific interventions. For example, dieting down to very low body fat and then maintaining it does not appear to increase leptin sensitivity (much) beyond that of a normal-weight person, nor does exercise.
As far as ketosis and leptin goes, This study indicates that carbohydrate overfeeding increases leptin and energy expenditure, while fat overfeeding does not. This suggests that eating carbohydrates naturally causes you to get full, while fat does not, which is inline with research on satiety and macronutrients. (Keep in mind that fructose is not metabolized like a normal carbohydrate and has different effects on leptin and so may not cause the leptin increase or induce satiety.)
This study indicates that ketosis blunts ghrelin release even in a caloric deficit which could be the reason that people on ketogenic diets (or doing intermittent fasts, which is a fat-burning state) report lower hunger levels. In this situation, leptin is lower which probably reduces metabolic rate a bit (probably not hugely significant), but its effect on hunger is probably balanced out by the change in ghrelin.
If you are doing a ketogenic or low carb diet, if you reach a plateau with weight loss, it could be because your leptin is too low. Doing a carb refeed with glucose (which includes starches), but not fructose, could be beneficial.
Interesting. So this implies that lower hunger in calorie-deficit ketosis is due to low ghrelin which more than compensates for lower leptin… And yes, carb refeeds (usually weekly) are a component of many low-carb diets.
How long is long enough to increase leptin sensitivity?
Anecdotally, people who keep weight off say it requires constant attention, not that they develop a lower set point.
This is correct. That’s what I meant by “That means that if your set-point is higher than the weight you’ve dieted to, your naturally regulated food intake will lead to slowly gaining weight again up to your set point.” If your set-point is higher than your weight, then you will still gain weight back if you’re not careful. Once your leptin system is restored to healthy function though, your body is better at regulating its weight. Weight gain at this point is likely to be slow and gradual rather than the rapid “rebound” weight gain that many dieters get if they completely stop their diet without allowing for this system to recover first. Also, since eating a lot makes your produce leptin, if your body is now sensitive to that signal, it will naturally make you less hungry for a little while, whereas if you’re leptin resistant, you feel hungry even when you’ve had enough. This is the benefit. That means that if you follow sensible lifestyle-diet practices even when you’re done with the intense diet phase, you can greatly slow or prevent weight regain. That would be things such as eating whole foods instead of processed foods, fruits and vegetables for fiber, and limit sugar (fructose is the real culprit) and alcohol consumption.
This one probably varies a lot with the individual. Also, keep in mind that there are different levels of leptin resistance, so recovery follows a curve. From anecdotal reports, it seems that some people can see significant improvement in 4-6 weeks with most people getting significant improvement within 3 months. I think it’s likely that improvements will continue for 6 months to a year depending on the individual.