Volume 6, Issue 1, 2000
The inverse relationship between higher rates of overweight women in lower socioeconomic groups has been established, yet its underlying reasons remain unclear. Possible causes fall into three categories. First, low SES could lead to higher BMI. Lower income is correlated with less education about nutrition and thus poorer diet. However, studies show that deeper cultural, behavioral, and economic factors correlated with lower SES also contribute to high BMI. Second, higher BMI could lead to lower SES. The discrimination theory states that heavier women are less valued and are blocked from earning opportunities and social networks. Third, biochemistry makes an impact in two ways. Genetic predisposition for obesity could explain how low income, high BMI women have low income, high BMI children. Another impact of biochemistry is weight cycling - the theory that episodic food disposition leads to increased rates of weight gain. For all three categories, public policy can play a role. Anti-hunger programs could focus on steady food supplementation instead of crisis intervention, in order to lower BMI. On a deeper level, policy-makers need a deeper understanding of the SES/BMI relationship to accurately address real issues of hunger among families who might appear well-fed. This deeper understanding requires further research.
It is no secret that overweight children grow up to be overweight adults who have increased risk for cardiovascular disease, diabetes, and hypertension. Within the last few decades, children and adolescents have assumed more sedentary lifestyles and poor dietary habits, both of which contribute to the problem of obesity. School-based intervention is the most efficient and successful way to intervene by promoting and encouraging healthy eating habits, ideas and attitudes toward food and its preparation and increased levels of physical activity. Multi-faceted programs that employ a number of different strategies including modified school lunch programs, physical education, classroom-based curricula and family education elements are most likely to succeed if they are introduced to students at a young age and continue through high school. This must be the first step in creating and sustaining a society that supports healthy behavior.
Hypertension has become a serious public health problem in developed countries, yet the vast majority of cases have no known etiology. A recent hypothesis to account for blood pressure elevation in adults implicates low birth weight due to undernutrition in utero as a possible culprit. This hypothesis depends on the concept of "fetal programming," in which alterations in intrauterine physiology provoke long-lasting changes in fetal tissue development and the setting of homeostatic mechanisms. One possible mechanism for the improper setting of the fetal blood pressure homeostat is overexposure to maternal glucocorticoids. Although the studies have obtained somewhat mixed results, experiments on animal models and epidemiological studies of human cohorts have generated intriguing evidence suggesting that low birth weight may indeed precipitate chronically elevated blood pressure.
Based on ecological studies and early epidemiological findings, a link has been proposed between dietary fats/fatty acids and the development of clinically apparent prostate cancer. Several hypotheses have been proposed to explain this link through biochemical mechanisms, although all remain unproven at this time. More recent epidemiological studies have further analyzed the dietary fat/fatty acid and prostate cancer link, and while suggestive, have returned largely inconsistent and inconclusive results. Results from animal and cell-culture models have been equally difficult to interpret, and these models have the additional complication that they may not be appropriate for studying the pathogenesis of human prostate cancer. In conclusion, current knowledge of dietary risk factors for developing prostate cancer is insufficient to recommend any dietary modifications at this time.
Consumption of tea has been associated with health amongst Asian populations for centuries. Epidemiological studies performed in the last two decades have proposed that green teas may be able to exert anti-carcinogenic effects. It is now believed that green tea polyphenols (GTPs) like epigallocatechin-3-gallate (EGCG), with their anti-oxidant properties, are the primary mediators of such an effect. Recent studies performed on cultured cell lines, animal models and some human populations have shown promise in elucidating if and how green tea may be of benefit to us. This paper attempts to consolidate some of the current research in the field and provide an overview of the direction that the research is taking with the ultimate goal of trying to answer the question of whether or not we, as health care consumers, should "buy into the hype". Unfortunately, it appears that at present the data remains inconclusive. Despite the results of a large number of benchtop experiments and the existence of epidemiological studies indicating correlation, the fact remains that direct clinical evidence is still lacking. Until more clinical trials are conducted, it will remain difficult to prove definitively the existence of a causal relationship between green tea consumption and reduced cancer risk.