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In the past three decades, total fat and saturated fat intake as a percentage of total calories has continuously decreased in Western diets, while the intake of omega-6 fatty acid increased and the omega-3 fatty acid decreased, resulting in a large increase in the omega-6/omega-3 ratio from 1:1 during evolution to 20:1 today or even higher. This change in the composition of fatty acids parallels a significant increase in the prevalence of overweight and obesity. Experimental studies have suggested that omega-6 and omega-3 fatty acids elicit divergent effects on body fat gain through mechanisms of adipogenesis, browning of adipose tissue, lipid homeostasis, brain-gut-adipose tissue axis, and most importantly systemic inflammation. Prospective studies clearly show an increase in the risk of obesity as the level of omega-6 fatty acids and the omega-6/omega-3 ratio increase in red blood cell (RBC) membrane phospholipids, whereas high omega-3 RBC membrane phospholipids decrease the risk of obesity. Recent studies in humans show that in addition to absolute amounts of omega-6 and omega-3 fatty acid intake, the omega-6/omega-3 ratio plays an important role in increasing the development of obesity via both AA eicosanoid metabolites and hyperactivity of the cannabinoid system, which can be reversed with increased intake of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). A balanced omega-6/omega-3 ratio is important for health and in the prevention and management of obesity.

In Western societies, energy imbalance is characterized by obesity and sedentary life styles and is associated with increased morbidity and mortality from all causes of cancer, including cancer of the breast, colon and prostate. The interrelationships of energy intake and energy retention, to energy expenditure and physical fitness need further investigation from the physiologic, metabolic, endocrine and genetic aspects of cancer development, since obesity, energy expenditure and cancer have a familial predisposition. The effects of exercise on estrogen and prostaglandin metabolism and their relationship to cancer development require further investigation. Although the exact amount and intensity of exercise that confers benefit is not known, physical activity and physical fitness are inversely associated with all-cause mortality, including cancer. These findings have important public health implications, because about one-third of persons in industrialized societies are quite sedentary, and the prevalence of low physical fitness is quite high. The balance between total energy intake and expenditure may be more important in cancer development than the intake of any given dietary component or energy source. Exercise increases prostacyclin and decreases the aggregation of platelets and possibly decreases the platelet derived growth factors (PDGF). One could speculate that exercise may in turn decrease the probability of developing colon cancer in those who are predisposed to it, since the SIS oncogene is in fact a variant of PDGF.

Obesity is considered to be a major nutritional disorder in the U.S. and in many parts of the industrialized world. The physiology of the obese and their propensity for chronic disease has been of growing interest over the past few years, and an extensive literature has begun to accumulate. Obesity is a heterogeneous disorder. When viewed in the broadest sense, it has been considered a disorder of energy balance. The development of obesity in humans is of complex etiology, involving genetic and environmental components that affect regulatory and metabolic events. The prevalence of overweight and obesity in a population depends on the particular reference or standard of desirable weight selected for use. A trend toward increasing height and weight has been evident among adults for several centuries, and among children as early as the 7th year of life in developed countries. Overweight persons are at increased risk for coronary artery disease, high blood pressure, diabetes mellitus, and cancer. The degree of overweight that carries additional risk without affecting mortality needs to be defined. Overweight most likely contributes in varying degrees to morbidity in different societies, because the risk for most common chronic diseases is multifactorial. In defining overweight and obesity, morbidity, in addition to mortality, ought to be taken into consideration. The multidisciplinary approach to the study of obesity--borrowing concepts and techniques from endocrinology, neurobiology, genetics, and nutrition--should yield new insights into how environmental factors such as diet and physical expenditure interact to influence energy metabolism and body composition.

Many studies indicate that obesity is associated with postmenopausal breast cancer and cancer of the endometrium. The mechanisms by which obesity contributes to cancer risk is not known, although increases in serum estrone from delta 4-androstenedione by the adipose tissue have been implicated in postmenopausal women. Blood estrogens increase with the degree of obesity and aging. In animal experiments the confounding of high fat, low carbohydrate, and high calorie diets needs to be defined. The effects of diet on estrogen metabolism; the relationship of fatty acids from animal, vegetable, and marine sources to tumor formation; and the mechanisms by which energy intake influences cancer risk need to be precisely defined. Any estimate of the contribution of heredity to the burden of human cancer is impossible until we have a better understanding of genetic and environmental interactions.