Valvoja: Valvoja
Ilmeisesti siitä samankaltaisuudesta on kuitenkin jonkin verran näyttöä, mielenkiintoista luettavaa, mutta en nyt tarkemmin viitsi alkaa perehtyä viitteisiin..tapsaattori kirjoitti: ↑elo 22, 2021, 16.00 Tuo vertaus rasvan määrän ja ruumiinlämmön säätelyn yhtäläisyyksistä/samankaltaisuuksista on kyllä mieletön.
https://slimemoldtimemold.com/2021/07/1 ... nadequate/ kirjoitti: There is one theory of obesity which is almost entirely satisfying, based around the body’s ability to regulate its adiposity.
A house has a thermostat. The owner of the house sets the temperature to 72 degrees F. The thermostat detects the temperature of the house and takes action to drive the temperature to the set point of 72°F. If the house is too cold, the thermostat will turn on the furnace. If the house is too warm, the thermostat will turn on the air conditioning.
The human body has a lipostat (from the Greek lipos, meaning fat). Evolution and environmental factors set body fatness to some range — perhaps a BMI of around 23. The lipostat detects how much fat is stored and takes action to drive body fatness to the set point of a BMI of 23. If your body is too thin, the lipostat will drive you to eat more, exercise less, sleep more, and store more of what you eat as fat. If your body is too fat, the lipostat will turn on the air conditioning. Just kidding, the lipostat will drive you to eat less, move and fidget more, and store less of the food you eat as fat.
According to this theory, people become obese because something has gone wrong with the lipostat. If the owner of a house sets the thermostat to 120°F, the house will quickly become too hot, and it will stay that way until the set point is changed or the furnace explodes. Something similar is happening in obesity. The set point has been moved from a healthy and natural level of adiposity (BMI of about 23) to an unusually high level (BMI 30+), and all the regulatory systems of the body are working in concert to push adiposity to that level and keep it there.
The lipostat model is supported by more than a hundred years of evidence. By the 1970s, Dr. Michel Cabanac and collaborators were publishing papers in the journal Nature on what they called the “ponderostat” (pondero = weight). This was later revised to the adipostat (adipo = fat), and eventually, as we call it here, the lipostat.
Modern neuroscience and medical review articles (those are three separate links) overwhelmingly support this homeostatic explanation. In animals and humans, brain damage to the implicated areas leads to overeating and eventual obesity. These systems are well-understood enough that by targeting certain neurons you can cure or cause obesity in mice. While we don’t approve of destroying neurons in human brains with hyperspecific chemical techniques, the few weight-loss drugs approved by the FDA largely act on the brain (hopefully without destroying any neurons).
The lipostat explains why diet and exercise work a little, why they don’t work well enough to reverse obesity, and why even people who lose weight on diets generally end up gaining that weight right back.
