Obesity - the Fat/sugar Dependency Syndrome (Fathead Syndrome)

What is the theory?

1. Obesity is an obsessive-compulsive disease (OCD).

2. Obesity is caused by food (fat/sugar)-dependency .

The synonym "fathead syndrome" relates to how obese people can be on the one hand very clever but also conceited and egocentric and on the other hand rather slow and quite anxious/depressed people. "Fathead" is a colloquial description of both types.

An analogy of "obesity" is "alcoholism".

Alcoholism is now regarded as an OCD due to alcohol-dependency which most importantly affects the brain although the liver and all other organs of the body are affected. People often mistakenly believe that alcohol-dependency primarily affects the liver.

Obesity can be regarded as an OCD due to fat/sugar dependency which most importantly affects the brain although body fat and all other organs in the body are affected. People often mistakenly believe that obesity primarily affects the fat stores. Hippocrates was aware that obesity was often the harpinger of many other diseases.

What are obsessions and compulsions?

Obsession: Compulsive preoccupation with a fixed idea e.g. eating food or an unwanted feeling or emotion, often accompanied by symptoms of anxiety.

Compulsion: An irresistible impulse to act e.g. eating food, regardless of the rationality of the motivation.

How does obesity result in the obsession-compulsion to eat more food?

Obesity as with most other psychiatric diseases is now being regarded as an immunological disease tending to occur in genetically predisposed people in response to an immunogen (in this case excessive fat/sugar) associated with structural and functional changes in the brain. ( see The Tree Model of Brain Disorders)

Why has food become a problem for the immune system?

In the last century the Western diet has transformed from a low sugar, balanced omega-3/omega-6 essential fatty acid diet to a high sugar, high omega-6/low omega-3 essential fatty acid diet. The human body has not yet adapted to these changes and the new diet has not yet been recognised by the immune system as normal. The new diet is more immunogenic i.e. causes more of an immune response by the body.

What is the immune response to food?

After food is eaten it is broken down (digested) in the gut (small intestine). Obese people have different bacterial populations in their gut compared to normal people which may be important in how the food is presented to the gut`s immune system.

The food molecules are absorbed and enter the general blood circulation via the liver. The food then travels to the various organs of the body including adipose tissue (body fat) and the brain.

Food molecules are eaten or ingested (phagocytosed) by white cells called macrophages (big-eaters). Parts of the food molecule are exposed on the macrophage cell surface to other white cells called helper T cells .

The next step of the immune response depends on cells called TREG cells.

TREGS are white cells called CD4+ and CD25+ T cell lymphocytes which are regarded as the regulators of the immune system hence their name of "regulatory T cells" or TREGS.

Reduced TREG activity results in an overactive immune response and inflammation.

In obesity TREG activity is reduced and the helper T cells and macrophages are allowed to promote an excessive immune response with the release of substances called cytokines e.g. tumor necrosis factor or TNF. Cytokines such as TNF result in tissue inflammation.

Fat stores in obese patients are inflamed and contain increased macrophage numbers and increased concentrations of TNF. Patients with severe obesity have higher TNF levels.

What is genetic predisposition?

This is the tendency for an individual to develop a disease because of their genetic make-up. Obesity or food-dependency as with other types of dependency isn't usually associated with one abnormal gene. Mutations in several genes have been discovered e.g. mutations in agouti (Ay) and obese (Lepob) . There is often a family history of obesity or other dependencies e.g. alcohol, drugs, gambling.

Obesity and the brain

The food-dependency model of obesity describes how the high fat/sugar diet in predisposed individuals results in progressive inflammation of the brain and reduction in dendritic spines in the frontal lobes and hippocampus in particular. (see The Tree Model of Brain Disorders)

What is the effect of food on thoughts and feelings in food-dependency syndrome?

People with obesity often found that when they were younger they felt bad and food made them feel good. Good feelings are generally described or grouped as trust, gratitude, acceptance and honesty. Good feelings are associated with greater connectivity to the outside world and the feeling younger and that time is flying by.

However over the years as obesity progressed increasing amounts of food resulted in bad feelings. Bad feelings are generally described or grouped as fear (anxiety), self-pity (depression), resentment (hatred) and dishonesty. Bad feelings are associated with isolation, feeling older and the feeling that time is going by slowly.

This is referred to as crossing the "magic line". However the patient`s brain is unaware of this and continues to need larger volumes of food believing that the good feelings will return. Unfortunately further deterioration in obesity causes further deterioration in bad feelings.

Sometimes heavy eaters will realise this and will cut back on their intake. However others will enter a severe cycle of increased food intake provoking further bad feelings and increasing obsession-compulsion to eat. These people often end up in the morbidly obese category.

How does obesity affect the MRI scan brain volume/function?

Brain volume is reduced in the later stages of obesity. This is expected as reduced brain volume occurs with other types of dependency. The brain volume is reduced due to inflammation and reduction in neuron volume. Following weight loss after bariatric surgery brain volume may increase as the inflammation improves. Further studies are awaited. Functioning MRI scans confirm that obesity is associated with increased activity in the frontal lobes with exposure to images of food.

What is the effect of obesity on nerve cells (neurons)?

The inflammation in obesity results in reduction of dendritic spines in the memory centre or hippocampus (hippocampitis). Obesity has also been associated with reduced IQ . This may be why obese people are called "fatheads".

Obesity may be a risk factor for the development of Alzheimer`s disease as the hippocampitis progresses. Although it is difficult to find studies of frontal lobe dendritic spines in obesity it is anticipated that dendritic spine density of frontal lobe neurons will be reduced in the later stages of the condition (see The Tree Model of Brain Disorders)

Conclusions

Obesity may be regarded as "food (fat/sugar)-dependency" syndrome in a similar way to how we know view other forms of dependency e.g. alcohol or drug dependency.

Food-dependency occurs in genetically predisposed people often with a family history of obesity or other forms of dependency.

Food in these individuals initially promotes brain growth and dendritic spine density in the frontal lobes resulting in reduced fear (anxiety) and self-pity (depression).

However eventually the magic line is crossed and progressive reduction in frontal lobe dendritic spine density due to an excessive immunogenic response (dendritis) results in bad feelings and further obsession-compulsion to eat and obesity.

The abnormal immunogenic response is related to decreased TREG cell activity.

Obesity could be regarded as another TREG syndrome i.e. an abnormal immunogenic response to fat/sugar (immunogen) in a genetically predisposed individual due to reduced TREG cell activity resulting in inflammation of the dendritic spines of frontal lobe and hippocampal neurons (dendritis/hippocampitis).

As with alcohol dependency all organs of the body are affected resulting in increased risk of diabetes, sleep apnoea, coronary artery disease, cancer etc.

Whatr does the future hold?

There are several developments including

1. Continuing reduction in fat/sugar components in processed food. Increasing the omega-3 essential fat component of processed food is expensive.

2. Treatment which increases TREG numbers/activity thereby reducing the inflammatory response results in a reduction in blood glucose and inflammatory cytokines e.g. TNF in body fat.

http://www.pnas.org/content/107/21/9765.abstract

3. Protecting the small intestine from fat/sugar immunogens by surgical insertion of a sleeve of material into the lumen of the duodenum.

However perhaps intermittent admissions for counselling and controlled food intake may be more acceptable in the early stages of food dependency whereas surgery is perhaps the only successful treatment in late dependency - although rarely super super morbidly obese patients do regain insight and miraculously regain health without surgery.

It is interesting that it is not expected that obesity will be officially classified as a psychiatric disease in the near-future i.e. in the DSM V.