Brain and Hunger Hormones by Jamie Hale
Evolution: During most of our evolution being fat up to a point was beneficial. People never knew what food availability was going to be like. Their bodies begin to adapt as they stored the food they consumed efficiently. They basically learned to survive with an abundant amount of food half of the time while literally consuming minimal amounts of food the other half. These circumstances resulted in a body that could slow down metabolic rate for the purpose of survival.
The ability to store body fat helped humans survive through winter by providing their bodies with heat and storing calories. Being fat was necessary to survive. On the other hand being lean meant quick death in times of famine and cold. I often joke with my clients in regards to the above statement ( inside joke: if a famine ever comes lean people will be the first to go, while the majority of society will live forever). In today’s society under most circumstances it is not necessary or recommended to be fat. Being overly fat can potentially lead to serious side effects.
Women have a harder time losing fat on average than men. Numerous factors can contribute to this situation. Women have lower metabolic rates, lower levels of lypolytic hormones, higher levels of lipogenic hormones, and they seem to adapt to weight loss faster than men. From an evolutionary standpoint this all makes sense. Women were responsible for giving birth so they had to be efficient at survival (in relation to storing body fat for heat and energy during winter months when food availability was limited).
Hunger Hormones: I would like to briefly mention some hormones (we will call hunger hormones for simplicities sake) that basically tell your brain how much your eating and what your body fat levels are. These hormones include insulin, leptin, ghrelin, peptide YY, neuropeptide Y (NPY), cortico-tropin releasing hormone (CRH) and , cholecystokinin (CCK). All of these hormones respond to food intake and send messages to your brain to tell you what is going on.
Numerous regions of the brain are involved with the regulation of food intake and energy balance. For our purposes we will only focus on the regions that are considered most important in regards to the hunger hormones. The arcuate nucleus (ARC), which is readily accessible to circulating hormones, is considered the primary hypothalamic site of food-intake regulation. Two main neuronal subsets located in the ARC which is readily accessible to circulating hormones, is considered the primary hypothalamic site of food-intake regulation. Two main neuronal subsets located in the ARC are responsible for relaying information about energy balance from peripheral hormones to various regions of the brain and are classified as either orexigenic (appetite stimulating) or anorexigenic (appetite suppressing). Neurons expressing neuropeptide Y (NPY) and agouti-related protein (AGRP) are orexigenic, while those expressing proopiomelanocortin (POMC) and cocaine- and amphetamine regulated transcript (CART) are anorexigenic.
Insulin: Insulin is released form the pancreas in response to blood sugar levels. Insulin is considered a storage hormone and it’s primary job is to take sugar from the blood and carry it to muscle, and fat cells. Insulin also sends messages to your brain concerning eating patterns. As an example injecting insulin directly into the brains of animals decreases hunger and appetite. Insulin is very responsive to single meals, going up when you eat, and back down after a few hours. It mainly effects short term reactions to food. Insulin levels are relatively easy to control just by making certain food choices. Consumption of fast digesting (high glycemic index) carbohydrates raise insulin quickly but it tends to cause sudden crashes shortly afterwards. Consumption of slow digesting (low glycemic index carbs) raise insulin more slowly and keep levels stable for longer. Keep in mind chronically high insulin levels are detrimental to health and are powerful lypogenic (fat producing) agents . Controlling insulin is very important in regards to the XDL DIET.
Leptin: In 1994 the successful cloning of the mouse obese gene and its human homologue led to the discovery of the hormone Leptin. Studies have shown when Leptin is exogenously administered to rodents their body fat, weight and food intake decrease. When exogenously administered to humans these finding have not been consistent indicating that a deficiency in Leptin resistance could contribute to obesity. In some studies, both lean and overweight persons have shown modest weight loss with daily subcutaneous injections or recombinant methionyl human leptin over several months. All subjects followed weight reduction diets during the trial period. Weight loss in some subjects receiving leptin did not exceed that achieved by subjects receiving the placebo, but when significant weight reduction occurred, it was proportionate to dosage.
Hugely obese children have been found who have an inability to lose weight due to genetic inability to produce leptin. Injections of leptin have had dramatic weight loss effects in these individuals.
Leptin regulates food intake and energy expenditure primarily through inhibition of NYP/AGRP neurons, as well as the disinhibition of POMC/CART neurons. Leptin is a hormone that is made in muscle, stomach, fat cells and a few other places in the body. Leptin is primarily made by the fat cells. Nearly every tissue in the body has some leptin cells. This indicates that leptin plays a huge role in everyday functioning. Leptin (anti-starvation hormone) tells your body what your energy stores are. Generally speaking a decrease in leptin levels means a decreased metabolic rate.
Leptin levels are 40% higher in women, and show a further 50% rise just before menarche; then retuning to baseline levels, levels are lowered by dieting and increased by inflammation. Women’s bodies also adapt differently to changing leptin levels than men’s. Women’s Leptin levels seem to drop faster when compared with men’s.
Your leptin levels change in response to body fat levels. They also change in response to short term over and underfeeding. When energy deficits occur circulating Leptin concentrations decrease while levels increase when overfeeding occurs. Postprandial (after a meal) Leptin concentrations are dependent on meal profile, with high carb low fat meals producing higher Leptin concentrations as compared with high-fat, low carb meals. Twenty-four hour circulating Leptin levels are also reduced in women consuming high-fat, low-carb diets compared with those consuming a high- carb, low fat diet. Research also indicates high fat feeding in rats result in Leptin resistance. Regarding other dietary macronutrients, neither protein nor fiber intake seem to impact circulating Leptin concentrations. Generally speaking when on a diet your leptin levels can drop up to 50% in one week. A properly designed overfeed can heighten leptin levels quickly. Basically leptin levels are rising faster than body fat is being synthesized. This results in resumed fat loss.
On a final note, Leptin is a anti-starvation hormone that tells your brain and body how and when to adapt in the face of reduced calories or increased activity. Anytime you burn more calories than you are taking in your leptin levels drop. Losing weight beyond a certain point tells your body and brain your starving to death and everything needs to slow down to compensate.
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