Food is so fun, available and tasty that many of us have lost that connection between being hungry, and eating! We are, however, actually designed to have internal signals that tell us we are hungry, and should eat, or we are full, and don’t need to consume more calories. Theoretically that system is in perfect balance and we have what is termed energy homeostasis, and we neither lose weight or gain weight. It is possible, that we do have those higher brain centers thinking famines may still come, so pack on extra nutrients. Anything we pack on is fat. We actually only store about 300 spare calories in the form of sugars in the body!
The regulation of this system is in our brain, and it takes in data from both the adipose tissue (our fat), as well as from our gut. Fat cells, called adipocytes produce many molecules that are released into the blood stream and act as fat regulating hormones. GLP-1, cortisol and insulin all have a role in how hungry we are. GL-1 decreases hunger, insulin regulates sugar which tells the brain how much sugar the body needs, and cortisol increases hunger through stress signals.
The main hormone that cause us hunger is ghrelin. That is produced in the stomach and produced to stimulate appetite in our brain which makes us eat more. Leptin tells our body when we have enough fat stores.
So one of the most important hormones that is critical to the regulation of the energy we consume is made by the fat in our body called ‘white fat’ which is the hormone leptin. Obesity, dieting, and lack of exercise, aging, body fat percentages, and genetic tendencies alter the leptin levels in our body.
Menopause is associated with weight changes, and now menopause has been found to alter leptin levels as well. Menopause is associated with lower estrogen, so it has been thought that perhaps the two hormones, leptin in fat and estrogen of menopause, are linked. Based mostly on animal data, women gain upto 22% extra body fat from the withdrawal of estrogen at the time of menopause.
There is also a subtle chronic raising of leptin with the inactivity of aging that may be the ultimate case of the accumulation of body fat at this time of life. So far to scientists the regulation of leptin is mostly a mystery.
In 1994 we discovered that a ob gene mutation can make mice obese. The ob gene regulates the adipocyte production of leptin. Leptin is one of those hormones that has to be in balance, too much or two little leads to obesity.
Deficiency of leptin can cause obesity, presumably by regulating the amount of hunger, therefore the amount of food taken in. However sustained administration or sustained natural elevations of leptin do not seem to produce ever thinner individuals. Confusingly sustained elevation in leptin can cause obesity by producing diabetic and prediabetic metabolic changes, and make those individuals with chronic high leptin have uncontrolled eating behavior (hyperphagia).
The more fat we add the worse our leptin problem, and thus our weight. Obese individuals conversely can have resistance to leptin itself that can aggravate insulin resistance and compound obesity problems. Interestingly, both leptin and estrogen at the right level can reduce food intake, and help women become more lean.
Much research is going into this area of medicine, and hopefully the answers to whether you have signals to lose or gain weight as these questions are answered. The best strategies are to keep hormones in balance, and thus you are more likely to have the hormones of hunger and fat in balance.
For More Information Read: Menopause, Make Peace With Change.