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this post was submitted on 31 Mar 2024
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When you are overweight, it is not a case of just eating less. Eating less has very different physical and psychological effects for someone who is overweight than for someone who is not.
If you are interested in learning something about this, you can check out the setpoint theory of body weight. In short, the body has a setpoint for which weight it should be. If you are overweight, this setpoint is at a higher weight than if you are not. If your weight gets below the setpoint, your metabolism will slow down and your appetite will go up and the body starts to try and do everything to go back to this higher weight. That is why most people are not able to lose more than 10% of their weight in the long term. Often, when they gain the weight back, they gain back even more than they lost and the setpoint might even go up further. It is a neverending struggle for most people. Medication like Ozempic affect this mechanism so it becomes possible to lose weight.
If you want, you can find a lot of scientific papers about this. There is quite a lot of research on this and the setpoint theory is well accepted within the medical field specialised in dealing with weight problems, I believe.
In addition, Ozempic is not only a fat loss medicine. It is also used by people with diabetes to lower their glucose.
The set-point theory is junk science propagated by the HAES movement. Human bodies can't escape the laws of physics, if you eat less energy than you expand you'll lose weight unless your body somehow evolved the ability for photosynthesis or nuclear power.
No, it is not junk science. Research about it is published in many serious scientific journals. Just check out Scopus or something. You cannot say that it is junk science just because you do not like the results.
You also seem to not understand it. It does not say that you can escape the law of physics. It also does not say that in my explanation. It says that you energy expenditure goes down if you get below the setpoint. So, eating less becomes less effective. At the same time, you appetite will go up. This makes it very difficult to maintain the weight loss and this is why many people fail to keep the weight off in the long term.
Criticism of any research is possible, of course. However, just saying it is junk and misrepresenting what the theory actually says are not good arguments.
If you disagree, then what is your explanation of why most obese people tend to not keep more than 10% weight off over time without medication or surgery? What scientific evidence is there for that? I would be very interested in hearing about alternative research on this topic.
When you gain weight, once the fat storage cells reach capacity, your body makes more of them. When you go into ketosis, burning stored fat, the cells don't die. They shrink. So once you go off your diet they will happily plump back up again. This is why your weight will yo-yo.
Losing weight and keeping it off should be done through dietary change, regular exercise, and commitment. That's true even if fat cells are physically killed or removed as part of treatment. Anything else yields temporary results or requires a lifelong legal drug habit.
The fat storage cells definitely play a role as well. One of the ways in which the mechanism I discussed works is via leptin, as leptons regulate energy expenditure. Leptin is primarily produced by adipocytes. So, I believe that is where the connection is. This paper says some interesting stuff about it: https://doi.org/10.1242/dmm.008698.
The issue that I was discussing is that most people do not succeed with keeping the weight off. Most obese people do not manage to lose significant weight in the long term as they tend to regain the weight. We need to look at why that is to solve it. The research on setpoints offers at least a partial explanation. However, if you know about research that further explains this, I would be very interested. (Some sources if you are interested: https://pubmed.ncbi.nlm.nih.gov/17469900/, https://pubmed.ncbi.nlm.nih.gov/11684524/, https://pubmed.ncbi.nlm.nih.gov/19175510/)