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Open Access Publications from the University of California


The Global Epidemic of Childhood Obesity: Poverty, Urbanization, and the Nutrition Transition

Childhood obesity is increasing worldwide at rates of epidemic proportion (1, 2). Previously a public health concern of only the modern, industrialized world, this problem now increasingly affects children and adolescents of poor, developing countries. This new and somewhat baffling phenomenon urgently begs the question: How is it that impoverished children around the world become obese? Recent studies suggest that rapid globalization and urbanization account for significant shifts in dietary patterns and physical activity levels that tend to increase risks for obesity in children. Industrialized agro-food systems established by global corporations have made cheap calorie-dense foods, fats, and oils widely available across the world and have caused what researchers call a "nutrition transition". This new global diet has led to increases in fat consumption worldwide (2, 5). Rapidly increasing urbanization has resulted in greater dependence on mechanized transportation and the loss of safe, open spaces for physical activity (2, 5). The combination of increasingly sedentary lifestyles and a lipid-rich diet is documented both in children of poor countries, as well as among impoverished children of the US and other industrialized nations. The global nature of this epidemiological trend indicates that global interventions will be necessary to adequately address the social, economic, and political forces that impact access to healthy food, and voluntary participation in physical activity and consequently lead to increasing rates of childhood obesity worldwide.

Role of Lipids in Osteoporotic Bone Loss

Osteoporotic bone loss is characterized by a marked decrease in osteoblast number and bone forming activity, in the face of an unaltered or slightly increased osteoclastic bone resorption.(3) Recent evidence suggests that hyperlipidemia may contribute to osteoporosis, and that lipid oxidation may be the mechanism underlying this process. Oxidized lipids have been shown to inhibit osteoblastic differentiation in vitro,(14) and in vivo studies have found that a high-fat, high-cholesterol diet reduces bone mineral density.(15) There is also strong epidemiological evidence suggesting that elevated lipid levels may play a significant pathogenic role in age-related osteoporosis in patients. Furthermore, studies have shown that lipid-lowering therapy in osteoporotic patients may reduce fracture incidence and have an anabolic effect on bone formation. These findings suggest that using antioxidants, in addition to regular exercise and a healthy diet, may be an effective method for preventing osteoporotic bone loss.

Two Wrongs Make A Right: Nicotine and Caffeine as Defensive Agents Against Parkinson's Disease

Epidemiological studies have long established that smokers and coffee drinkers experience a decreased incidence of Parkinson's Disease (PD), a progressive neurodegenerative disorder for which there is no cure. Only recently have studies begun to explain these associations through plausible biological mechanisms, which in turn have helped further characterize the onset and progression of PD. Nicotinic acetylcholine receptors are present in dopaminergic neurons in the substantia nigra, and stimulation by nicotine has been shown to alleviate Parkinsonian symptoms as well as decelerate the progressive loss of dopaminergic neurons (10). A2A adenosine receptors are co-localized with dopamine receptors in GABA-ergic neurons in the striatum, and the presence of caffeine as an A2A adenosine receptor antagonist leads to symptomatic and neuroprotective benefits similar to nicotine (17). The elucidation of nicotine, caffeine, and their differing mechanisms of receptor interaction have provided valuable insights into the development of Parkinson's Disease, and may lead to novel preventive treatments and therapies.

Oh How Sweet It Is: The Heart's Love Affair With Chocolate

For many chocolate is not a health food. It has been linked to medical conditions including acne (1) and in most forms it is high in fat and sugar. Recent data, however, has shed light on chocolate's cardio-protective roles. Specifically, cocoa has been found to have flavonoids which are high in antioxidant activity (3). Cocoa's role in platelet activity has also been investigated10 and has been shown to inhibit platelet activity which can further prevent cardiovascular disease. Investigators have also looked at chocolate's fat content and noticed that, although it is high in fat, most of it is in the form of stearic acid which is not well absorbed and excreted as feces (2). Although the data is limited, there is promise that chocolate may provide benefits beyond great taste. Until more research is completed, however, the quantity of chocolate should be limited, but each bite should be relished, not only for its flavor but for its health benefits as well.

Nutritional Management of Children with Congenital Heart Disease

Children and infants with congenital heart disease (CHD) often have disturbances in growth and development. Recent research suggests that this is due mainly to inadequate caloric intake and increased energy expenditure as compared to normal children (1). This presents a significant problem because if left untreated these children can develop permanent disabilities and poorer outcomes after corrective surgery. In order to treat this problem, a systematic approach must be used to identify the specific reasons for this failure to thrive, to develop a strategy for a structured feeding program, and to educate parents as to the best ways to feed their children (2).