Quote:
Originally posted by PM_Mama00
You're right it CAN be done, but it's very very hard. ..I stopped drinking pop, stopped eating late at night, starting working out alot, drinking lots of water, started eating low carb (not no carb). Started this a few weeks ago (maybe a month?) and have seen NOTHING.
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Currently, there are 2 genetic mouse models for obesity that many researchers study:
The
ob/ob mouse that is leptin (a protein secreted from adipose tissue which affects the arcuate nucleus of the brain indicating some level of satiation) deficient and there are VERY LOW numbers of humans that actually have a leptin deficiency because it causes a birth defect (I think) only in humans...
And the
db/db mouse that is a leptin receptor-deficient mouse--meaning the leptin must use a "key to unlock the door to get into the brain"--a receptor... I don't think any human has been found with a leptin receptor deficiency--but I could be wrong...
What we are discussing is diet-induced obesity that indirectly affects leptin levels. But leptin levels alone cannot account for the massive increases in WAT in morbidly obese people. To induce obesity in animals, one has to feed a high-fat and high carbohydrate diet with essential vitamins and nutrients... But only a select number of mouse strains are obesity susceptible--most never get fat, ever... Either they don't eat the diet, or the rapidly metabolize the diet.
There is a "convention" of thought that something in WAT suppresses metabolism in the liver and the gut. Something is secreted by the WAT that goes to the brain that shuts off the metabolism in the liver and gut--something to do with POMC and melanocortin levels... What the WAT cranks out is not really understood. But my guess is that it they are free fatty acids which can be strong ligands for many a receptor... It has been shown that fatty acid structured sterols in the liver with the orphan nuclear receptors--such as LXR and RXR regulating cholesterol levels... So, I have no reason why this would not occur in other parts of the body...
Which says, that the genetic pathways to regulated appetite and metabolism is not all just with will-power, it may be truly genetic. It may not be because of straight out mutation in one's genes, but by differences in the genetic structure of the protein--like my protein just works better than yours kinna thing... The single nucleotide polymorphism issue...
Moreover, women are structured in the child-bearing years to maintain a certain weight... Why? Because you don't want the lack of "insulation" and "nutrients" if a woman were to ever become pregnant... I.e. there is no such thing as a cholesterol-free fertilized chicken egg... There IS a reason for that and YES, it is evolutionarily conserved...