T HE obese state is a much maligned one. Those with a religious bent see it as the outcome of the sin of gluttony. Our culture associates obesity with ugliness, laziness and poor self-control. The medical profession defines it as a disease the criteria for diagnosis being if one is 20% or more above his desirable weight, and that extra weight is in the form of stored fat. Most medical investigation has focused on the metabolic, genetic, constitutional and social factors in obesity. Mayer 1 quotes studies which show that 2/3 of obese patients have one obese parent, as well as studies of fraternal and identical twins raised in the same environment which show that only 2% of the identical twins had a difference in weight of more than 12 pounds compared with the fraternal twins, 50% of whom showed a difference of more than 12 pounds. Now these statistics might be successfully argued to point to environmental influences; however the geneticists feel there is a recessive gene responsible for obesity the obese carry genes for both fatness and leanness, while the lean rarely carry the gene for obesity. Also using Sheldon's classif ication of endomorph, mesomorph and ectomorph to study constitution and body build, one notes that the ectomorphs never become fat, and that obese people, in addition to having excess fat also have bigger muscle and bone mass which also contributes to their excess weight. Also, recent investigators 2 feel that obesity is caused by the excessive number of fat cells laid down in infancy in response to overfeedinq the infant. After a medical investigation a patient is usually told there is no hormonal or metabolic factors to explain his obesity, so it must be that the patient just eats too much, which puts the full responsibility for the disease on the patient. It would be more accurate and also kinder to the patient if one said that our current medical instruments cannot identify any such abnormality. This is not to say that emotional factors don't play a major role in obesity, but that if we wish to relate obesity to emotional factors, we must make it through a positive diagnosis, and not through the process of excluding other factors. And we must also be cautious in applying any conclusions we draw from a psychiatric study of a small group of the obese to the obese population at large. We do treat a select group who consider themselves psychiatric patients. Most obese don't. Because of our patients' obvious neurotic conflicts as well as their obvious obesity, one might attribute one to the other. But one can be neurotic and by coincidence be fat, just as one can be neurotic and by coincidence be thin. Psychiatrists studying obesity have used the following models: 1) The psychosomatic model for example there could be a specific or non-specific conscious or unconscious conflict, or a specific or non-specific traumatic event which through the cortical-hypothalamic connections may alter the sensitive feeding and satiety regulatory centers in the ventro-medial area of the hypothalamus, which could be constitutional ly predisposed to poor regulation, and now cannot properly respond to the homeostatic feedback stimuli such as blood sugar levels and nerve messages from the gut. 2) The social reject model where the neurosis is the end result of a person