Hunger Hormones

TAGS: hunger, hormones, Jamie Hale

The following is an excerpt from Knowledge and Nonsense by Jamie Hale.

I’ll briefly mention some hormones (we’ll call them ‘hunger hormones’ to keep it simple) that basically tell your brain how much you’re eating and what your body fat levels are. These hormones include insulin, leptin, ghrelin, peptide YY, neuropeptide Y (NPY), cortico-tropin releasing hormone (CRH), cholecystokinin (CCK), pancreatic polypeptide, glucagon-like peptide 1, and oxyntomodulin.

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 regarding 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 are responsible for relaying information about energy balance from peripheral hormones to various regions of the brain. They 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 sends messages to your brain regarding eating patterns. For example, injecting insulin directly into the brains of animals decreases hunger and appetite. Insulin is very responsive to single meals. It goes 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. It is often misinterpreted as the cause of obesity. A specific level of insulin actually decreases food intake. Insulin is a complex hormone that plays various roles in the body. We’ll discuss insulin in greater detail later in this chapter.


In 1994, the successful cloning of the obesity gene in the mouse and its human homologue led to the discovery of the hormone leptin. Studies have shown that when leptin is exogenously administered to rodents, their body fat, weight, and food intake decreases. When exogenously administered to humans, these findings have not been consistent, which indicates that leptin resistance rather than a deficiency may play an important role in the development of obesity in humans. In some studies, both lean and overweight persons have shown modest weight loss with daily subcutaneous injections of 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.

Injections of leptin have had dramatic weight loss effects in obese children who lack the ability to produce sufficient leptin.

Leptin regulates food intake and energy expenditure primarily through the inhibition of NYP/AGRP neurons and the disinhibition of POMC/CART neurons. Leptin is a hormone that is made in the muscle, stomach, fat cells, and a few other places in the body. It 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 (the 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 percent higher in women and show a further 50 percent rise just before menarche. They then return to baseline levels. Levels are lowered by dieting and increased by inflammation. Women’s bodies also adapt differently to changing leptin levels and their leptin levels drop faster than men’s. Leptin levels change in response to body fat levels. Leptin also changes in response to short-term overfeeding 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 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 that high fat feeding in rats results in leptin resistance. Regarding other dietary macronutrients, neither protein nor fiber intake seems to impact circulating leptin concentrations. When on a diet, your leptin levels can drop up to 50 percent in one week.


In 1999, Kojma and colleagues discovered the hormone ghrelin, an endogenous ligand of the growth hormone secretagogue. Most of the research on ghrelin has focused on its orexigenic and adipogenic properties due to the finding that ghrelin administration increases food intake and body weight in rats. Ghrelin is a hormone produced primarily in the stomach. Its levels are increased prior to a meal and decreased after a meal, and it’s considered the counterpart to the hormone leptin. Patients with Prader-Willi syndrome, a rare inherited condition marked by hyperphagia (increased appetite) and often morbid obesity, exhibit extremely high concentrations of ghrelin. In the mid-nineties, I worked in a Prader-Willi group home. The stories I could tell you about the patients’ appetites are amazing. It seems like they never satisfy their appetite no matter how much they eat. For example, on one occasion, a resident ordered two large pizzas and had them delivered to his window. The staff regulated their food intake due to their insatiable appetites. They would literally eat until they exploded. They weren’t allowed to have money because they would spend it all on food. Anyways, he locked his bedroom door and started eating the pizzas. Before we could get to him, he had eaten the two large pizzas in fifteen minutes. After eating the pizzas, he didn’t vomit or seem to be affected by the large amount of food he had just eaten.

Another client shoplifted food. He would sneak out of the house, go to the local quick mart, and steal any food he could get his hands on.

Once I had to fight a client to get some candy back from him that he had stolen. It was not unusual to find candy wrappers and food remnants hidden underneath clients’ beds. All of the food in the house was locked away so the clients could not have access to it. Prader-Willi syndrome is a very powerful disease, and certain hunger hormones play a large role in this condition. Sorry, I got off track, but I think some readers will find the Prader-Willi information interesting. Okay, back to ghrelin.

The postprandial ghrelin response is affected by the macronutrient profile with carbohydrates being most effective at suppressing ghrelin levels. Although the ingestion of a physiological dose of amino acids has been shown to increase ghrelin concentrations, there is conflicting evidence as to whether a protein rich meal has the same effect. In one particular study, the consumption of 4 grams of a no caloric psyllium fiber was as effective at suppressing ghrelin concentrations in healthy women as a 585 Kcal meal.

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