Introduction to Ghrelin

Ghrelin is widely known as the hunger hormone and is released in the stomach. Similar amounts are released in the brain (hypothalamus) small intestine and pancreas. As it has a relationship with food there is no surprise that it stimulates the pituitary gland to release growth hormone, controls sugars and regulates the insulin within a person’s body. It also prevents muscle weakness and plays a part in bone strength. While all of this is occurring somatostatin must reduce its levels to make sure its inhibitory properties do not interfere with ghrelin’s processes. However, in a healthy individual there is a time when corticotropin releasing hormone must increase to offset these rising levels. (Ghrelin increases). This in turn causes increases in corticosteroid secretion which are anti-inflammatory by nature. Corticotrophin releasing hormone has also qualities that improves memory and selective attention. Serotonin also modulates ghrelin. This is probably because serotonin brings to the table a cyclic side to the human feeding and grazing role. Serotonin is supposed to promote a buoyant mood however this is lost with all that goes on with this debilitating illness.

Introduction to Leptin

Leptin was discovered not that long ago. This being 1994. Leptin is a hormone that the body releases to maintain normal body weight over a long period of time. Blood levels of leptin represent how much body fat there is within an individual. Feeling full is a hallmark of what leptin does to maintain long term health regarding food intake and energy use. Leptin is a calorie counter and inhibits a hunger response when food is not required. Body fat makes and release leptin. Irregularities of leptin levels are problematic. High levels of leptin are associated with neurodegenerative disorders, depression and food addiction. Low levels of leptin can be associated with bacterial infections, excess insulin production and low sex hormone levels. These low leptin irregularities are more of a low somatostatin problem and high dopamine consistency / that is and not

including low sex hormone levels. As discussed, adrenocorticotropic hormone is high in anorexia. This activates stress hormone cortisol which controls the body’s use of fats, proteins and carbohydrates. It also helps with inflammation and ultimately gluconeogenesis. While this is very helpful, sustained high levels can be very damaging. By constricting the intracellular and extracellular transmission channels of a cell the lysosomes become underactive and fail to clean out irrelevant and non-essential matter. This would include lipids and proteins that make up myelin. In comparison to low cortisol the transmission channels are more accessible, and signals are not inhibited in any way or form. This produces less myelin but better access to nerve cells and transfer of information. Overall, this gives better stability in the central nervous system/brain. Poor nutrition stifles this process as lipids and proteins make up myelin. Fundamentally this is a major marker in what causes brain shrinkage.

Theory

While anorexia is about starvation and an unhealthy relationship with food, it is once again about dopamine levels and its rewarding ability in a not so helpful scenario. Once there is an indication to produce more than average levels of dopamine all the brain/body wants is more of it at all costs. With this illness leptin is at an all time low telling the body that it needs food.

Now it takes quite a while to lower leptin levels as body fat releases it and thus reflects the position the anorexic mind has been able to manifest. Leptin regulates growth hormone- releasing factor somatostatin and alpha melanocyte stimulating hormone. Obviously, when it is in higher quantities it suppresses hunger. Importantly leptin inhibits along with insulin ventral tegmental area dopamine neurons. Unfortunately, with starvation there are minimal levels of leptin to reduce buoyant levels of dopamine. The hunger hormone ghrelin which is perpetually high in anorexics activates these areas. The more an individual doesn’t eat the more they are rewarded. This activity becomes deadly as time progresses and intervention is sometimes not enough to turn this illness around. Because leptin regulates somatostatin via the hypothalamus there is a heightened vulnerability. In other illnesses somatostatin can offset some of the dopamine and rein it in. This is why there is a high mortality rate in anorexia nervosa. It must also

be asked if corticotropin is doing its job properly on ghrelin and suppressing hunger in an unhealthy manner. Overall, it seems starvation is the winner.

References: https://www.mayoclinic.org/diseases-conditions/eating-disorders/symptoms-causes/ Eating Disorders: Types, Causes, Treatment & Outlook (clevelandclinic.org)