Set point
chulipa
Posts: 650 Member
I’ve just been hearing and reading about it. How can it be true when people are losing weight and keeping it off. If it is true and only weight loss surgery can change your set point than I guess we need to have weight loss surgery or just give up
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Replies
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We had a good conversation about set point theory last month:
https://community.myfitnesspal.com/en/discussion/10822721/set-point-weight-theory
Many people made the point that brains/behaviors were stickier than weight. In other words, change your habits and the weight will come off.17 -
Here's a recent discussion:
https://community.myfitnesspal.com/en/discussion/comment/45687454#Comment_456874543 -
There was recently a lively thread on this topic. https://community.myfitnesspal.com/en/discussion/comment/45695198#Comment_45695198
Basically, science says, "sure, DNA plays a role, but behavior and Western diets play a bigger role." I love this quote in the abstract of a 2010 NIMH study:- There is evidence for the idea that there is biological (active) control of body weight at a given set point. . . . However, regulation may be lost or camouflaged by Western diets, suggesting that the failure of biological control is due mainly to external factors. . . . Searching for the genetic background of excess weight gain in a world of abundance is misleading since the possible biological control is widely overshadowed by the effect of the environment. (emphasis added)
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We all three posted the same thread.
We pay too much attention.8 -
Funny0
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If set point was really a thing, then a lot of immigrants shouldn't gain weight when they start living in the US.
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If set point was a thing then I'd not gain weight because I really wanted to eat a pack of crisps or liquorice each evening, but because my body made me do it.4
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Did someone ask about set point theory? I think fat point therapy would be better. Lol
Anyways, this is such a large freaking topic to discuss. The brain effects our adiposity, but habit can help dictate weight. We know the brain is central for weight homeostasis because you can give people drugs or make lesions on the brain and effect energy intake. Leptin is most likely the culprit as the key hormone that drives long term appetite. What's odd is obese people have loads of leptin. I think there is a leptin point on the hypothalamus that regulates our appetites, but environment over rides our natural satiety centers. Make a rat obese on an american diet and the.n switch it to a more "natural" diet and they lose most of the excess adipose tissue, but not all? Why? Hmmmm...1 -
I am somewhat convinced by the idea that one can become leptin resistant too. Exercise is one of the things that is theorized to help increase leptin sensitivity.1
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Leptin resistance and insulin resistance explain a lot about why some people's cells take up the hormones streaming in their bloodstreams while other people's cells do not, despite an abundance present. I'm not familiar with the rat study you cite, but once someone develops hormone resistance, it can have a lasting impact.
Separately, is there a reason there seem to be an increasing number of threads on this topic lately? Is "set point" back in the news or something? This idea has been around for decades but has never to my knowledge garnered evidence to support it.2 -
Leptin resistance and insulin resistance explain a lot about why some people's cells take up the hormones streaming in their bloodstreams while other people's cells do not, despite an abundance present. I'm not familiar with the rat study you cite, but once someone develops hormone resistance, it can have a lasting impact.
Separately, is there a reason there seem to be an increasing number of threads on this topic lately? Is "set point" back in the news or something? This idea has been around for decades but has never to my knowledge garnered evidence to support it.
https://pubmed.ncbi.nlm.nih.gov/19401758/
Note, that the control rats and the post obese rats were eating nearly the same calories on the ad lib diet, but the post obese rats maintained 40% more body fat than the never obese controls. Why? Leptin resistance maybe? We know that leptin also helps control how much energy we burn.1 -
Can someone tell me what "set point" is?1
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What's NOT said though is the actual activity level of the groups. Like people, leaner people have a tendency to be more physically active so even if they were eating the same amount of calories, were they burning off also a higher rate than the obese group?psychod787 wrote: »Leptin resistance and insulin resistance explain a lot about why some people's cells take up the hormones streaming in their bloodstreams while other people's cells do not, despite an abundance present. I'm not familiar with the rat study you cite, but once someone develops hormone resistance, it can have a lasting impact.
Separately, is there a reason there seem to be an increasing number of threads on this topic lately? Is "set point" back in the news or something? This idea has been around for decades but has never to my knowledge garnered evidence to support it.
https://pubmed.ncbi.nlm.nih.gov/19401758/
Note, that the control rats and the post obese rats were eating nearly the same calories on the ad lib diet, but the post obese rats maintained 40% more body fat than the never obese controls. Why? Leptin resistance maybe? We know that leptin also helps control how much energy we burn.
A.C.E. Certified Personal and Group Fitness Trainer
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Oops wrong post... sorry.1
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yeah, I don't believe hormone resistance is set in stone. I think the body wants homeostasis and at a healthy weight leptin and insulin resistance are not going to remain unless there's some underlying other pathology.
Maybe the leptin "resistance" takes a few months to balance out - that makes sense. It's a huge stress on the body to lose a lot of weight and there's likely a correlation between cortisol and leptin/insulin. Why wouldn't there be?
I'm with ninerbuff on that rat study.1 -
What's NOT said though is the actual activity level of the groups. Like people, leaner people have a tendency to be more physically active so even if they were eating the same amount of calories, were they burning off also a higher rate than the obese group?psychod787 wrote: »Leptin resistance and insulin resistance explain a lot about why some people's cells take up the hormones streaming in their bloodstreams while other people's cells do not, despite an abundance present. I'm not familiar with the rat study you cite, but once someone develops hormone resistance, it can have a lasting impact.
Separately, is there a reason there seem to be an increasing number of threads on this topic lately? Is "set point" back in the news or something? This idea has been around for decades but has never to my knowledge garnered evidence to support it.
https://pubmed.ncbi.nlm.nih.gov/19401758/
Note, that the control rats and the post obese rats were eating nearly the same calories on the ad lib diet, but the post obese rats maintained 40% more body fat than the never obese controls. Why? Leptin resistance maybe? We know that leptin also helps control how much energy we burn.
A.C.E. Certified Personal and Group Fitness Trainer
IDEA Fitness member
Kickboxing Certified Instructor
Been in fitness for 30 years and have studied kinesiology and nutrition
Sorry, should have posted the full text. It was noted at the end of the study, energy expenditure in the post obese animals was in line with the controls.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2670508/0 -
Ok I googled it. That theory does not make any sense. Your preset weight is hardwired in your DNA and weight loss surgery is best to get past the preset weight is absurd. Weight loss surgery like anything else forces the body to take in less calories. Hence you will lose weight. This sounds like some money making thing.5
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But is the energy expenditure by percentage to body weight or did the rats do the same exact physical expenditure?psychod787 wrote: »
What's NOT said though is the actual activity level of the groups. Like people, leaner people have a tendency to be more physically active so even if they were eating the same amount of calories, were they burning off also a higher rate than the obese group?psychod787 wrote: »Leptin resistance and insulin resistance explain a lot about why some people's cells take up the hormones streaming in their bloodstreams while other people's cells do not, despite an abundance present. I'm not familiar with the rat study you cite, but once someone develops hormone resistance, it can have a lasting impact.
Separately, is there a reason there seem to be an increasing number of threads on this topic lately? Is "set point" back in the news or something? This idea has been around for decades but has never to my knowledge garnered evidence to support it.
https://pubmed.ncbi.nlm.nih.gov/19401758/
Note, that the control rats and the post obese rats were eating nearly the same calories on the ad lib diet, but the post obese rats maintained 40% more body fat than the never obese controls. Why? Leptin resistance maybe? We know that leptin also helps control how much energy we burn.
A.C.E. Certified Personal and Group Fitness Trainer
IDEA Fitness member
Kickboxing Certified Instructor
Been in fitness for 30 years and have studied kinesiology and nutrition
Sorry, should have posted the full text. It was noted at the end of the study, energy expenditure in the post obese animals was in line with the controls.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2670508/
A.C.E. Certified Personal and Group Fitness Trainer
IDEA Fitness member
Kickboxing Certified Instructor
Been in fitness for 30 years and have studied kinesiology and nutrition
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I really dislike mouse studies and spending my time reading them - but this one fed them for only 12 weeks for that experiment and used that data.
I really think it took me about a year post weight-loss to reach my (now) maintenance calorie number. Prior to that one year time frame, I had to eat quite a bit less to maintain. I was eating at Myfitnesspal's recommended maintenance calories, I was super hungry and I had to stick there or gain. It was pretty miserable that first year. I probably would have had less discomfort but I lost about 70 pounds in a year. That big leap likely didn't give my hormones time to catch up/balance. That's just my guess based on my experience. Plus...mice.
After the year, I was able to raise my calories, and again about a year and a half later.
I now eat a good 500-700 calories per day to maintain my weight above what I ate at the end of my weight loss. My exercise and daily activity level is very nearly the same. It's been 12-13 years and I maintain on a lot higher calories than MFP suggests.
12 weeks just doesn't feel long enough to me...based on my N=1 experience.10 -
Given that it takes MONTHS just to change your body in general, I agree.cmriverside wrote: »I really dislike mouse studies and spending my time reading them - but this one fed them for only 12 weeks for that experiment and used that data.
I really think it took me about a year post weight-loss to reach my (now) maintenance calorie number. Prior to that one year time frame, I had to eat quite a bit less to maintain. I was eating at Myfitnesspal's recommended maintenance calories, I was super hungry and I had to stick there or gain. It was pretty miserable that first year. I probably would have had less discomfort but I lost about 70 pounds in a year. That big leap likely didn't give my hormones time to catch up/balance. That's just my guess based on my experience. Plus...mice.
After the year, I was able to raise my calories, and again about a year and a half later.
I now eat a good 500-700 calories per day to maintain my weight above what I ate at the end of my weight loss. My exercise and daily activity level is very nearly the same. It's been 12-13 years and I maintain on a lot higher calories than MFP suggests.
12 weeks just doesn't feel long enough to me...based on my N=1 experience.
A.C.E. Certified Personal and Group Fitness Trainer
IDEA Fitness member
Kickboxing Certified Instructor
Been in fitness for 30 years and have studied kinesiology and nutrition
2
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