Obesity is a chronic disease and a leading cause of diabetes, heart disease, certain cancers and other serious health problems in the United States, with about a third of the population affected. According to the CDC, as of 2008, the medical costs associated with obesity were estimated at $147 billion; the medical costs paid by third-party payors for people who are obese were $1,429 higher than those of normal weight.

Although there are a number of causes linked to obesity, the one  common thread among obese individuals is a disruption in the chemical balance which regulates appetite and satiety, otherwise known as the feeling of being full or satisfied.  The primary chemicals involved in the regulation of food intake and control of appetite are the neurotransmitters dopamine, norepinephrine, epinephrine, serotonin, acetylcholine, glutamate, D‑serine, and histamine.

Traditional approaches to appetite control have for the most part been unsuccessful in changing eating behavior. Many of the proposed treatments, particularly pharmaceutical agents, have significant side effects including death and serious heart valve disease. Most recently the FDA has reconsidered issuing approval for the weight loss drug Qnexa, which is a combination of the appetite suppressant phentermine and the anti-seizure drug topiramate. The side effects associated with this drug are extreme, and include memory loss, elevated heart rates, a higher rate of oral clefts in infants of women taking the drug during pregnancy, and possible cardiovascular problems.

Nervous System and Appetite Control

Food consumption is controlled by the nervous systems through complex feedback systems that respond to signals generated by physical and metabolic stimuli. These feedback systems evolved as a mechanism to ensure that energy stores were readily available during times where they would be needed most by the human body. Maintenance of a stable body weight is highly dependent on a persons “energy economy”, and the ability of a person to keep a balance of energy intake to energy expenditure.

The loss of appetite control in many obese patients reflects a disruption in the neuroendocrine networks that facilitate communication between the brain, adipocytes, and the gastrointestinal tract regarding the state of current energy reserves. Within the hypothalamus, information is communicated through chemical messengers called neurotransmitters regarding the size of energy reserves (body fat) available and is synchronized with information from the gastrointestinal tract about the volume and composition of food ingested. Gut to brain communication determines the amount of energy available and thus the adjustment in the amount needed to maintain sufficient energy reserves. Energy intake is then adjusted through the generation of appetite or satiety cues sent out through the nervous system via neurotransmitters. The hypothalamus establishes a threshold at which food intake must be initiated or terminated to maintain energy balance. This threshold level or “set point” ensures that the amount of food consumed will be sufficient to meet both current and future energy needs.

Amino Acid Deficiency and Obesity

It has been well established in numerous studies that obese patients experience deficiencies in specific amino acids. These key nutrients are the building blocks of life and are responsible for converting into the neurotransmitters needed for the effecient and reliable nervous system communication that regulates food intake. Regulation of appetite and satiety depends on a carefully orchestrated balance between the neurotransmitter-mediated feedback mechanisms that control the desire to eat, thus inappropriate eating behavior can arise from specific nutritional deficiencies that cannot be met by altering diet alone. For many obese individuals, the ability to regulate food intake has been compromised by impaired metabolic processes that increase amino acid turnover rates and deplete stores of neurotransmitters needed to help the brain and stomach distinguish the desire to eat from the need to eat.

Qnexa, Xenical, Alli and most of the appetite control aids available were developed using the current understanding of the way in which chemical processes function to regulate eating behavior. The synthetic nature of these drugs often create more problems than they solve and can often only be tolerated for short periods of time.  The safest and most effective approaches to controlling appetite and satiety, would be those that utilize nutrients which support the synthesis and activities of the specific chemicals involved in these processes rather than those which choose to manipulate chemicals that are either in short supply or nonexistent in an obese patient. The medication class of  medical foods have been developed to address neurotransmitter deficiencies in a number of disease states. For obese patients, these products can restore the balance of neurotransmitters and other ingredients essential to maintaining the central and peripheral feedback mechanisms that regulate appetite and satiety.