Diet, nutrition, and cancer (Part V)
July 23, 2006 | 12:00am
(Conclusion) |
C. Adverse imprinting on fastfood restaurant fare in early life.
Expenditure on foods in so-called fastfood restaurants has increased 15-fold over the past 2 decades in the United States. Selections from these popular food outlets are readily accepted by children. Children also learn to prefer energy-dense foods when consumption of those foods is followed by positive postingestive consequences, such as those produced when high-energy-density foods are eaten when hungry. Aside from high energy densities and large portion size for which this class of cuisine is notorious, the features of high-temperature cooking; high fat intake in meats and fried potatoes; sugary beverages and desserts; and the offering of red and cured and salted meats run afoul of at least 5 of the World Cancer Research Fund/American Institute for Cancer Research recommendations for dietary cancer prevention. Experience with such fast foods can also shape long-term food preferences from early in life. Not only is it important to develop a tolerance and appreciation for the widest range of tastes and foods from early in life, but guidance away from the salty, sugary, fatty and meaty fares that typify classic fastfood menus is an important part of education for nutritional health.
D. Cancer prevention: a comprehensive life-course approach
Examining the immediate, underlying, and basic causes of cancer, we cannot yet fully ascertain the direct causal pathway for most human cancers, but we are certain that cancer is not a random event in the human life course. Our present understanding of molecular regulation of gene expression and how environment and genes interact in defining normal and neoplastic cell growth permits us to unravel how the cancer process is initiated and what can trigger expansion of abnormal cell clones, hormones and growth factors mediated by receptor and signal transduction systems end up regulating the expression of genes responsible for cell growth and replication.
This simplified picture allows us to model the interaction of environmental factors, including diet, with the genetic determinants (seldom monogenic, frequent polygenic) that ultimately determine cancer incidence. Much of the present research is centered on clarifying these mechanisms. This is undoubtedly a valid approach from the standpoint of defining how the cancer process works and possibly how to intervene with treatment and preventive strategies. Within the epigenetic factors, diet- and nutrition-related factors play an important role in defining cancer susceptibility. As indicated in an earlier sections of this review, rate of growth, body composition, and diet macro- and macronutrients content are important in defining cancer risk for some sites.
The metabolic consequences of obesity and the concomitant inflammatory response have been linked to altered hormonal profiles, with consequences for normal and abnormal cell growth and possibly for the expansion of tumors. Nutrients also play important roles in defining the immune response, including natural killer cells, metabolic capacity to detoxify chemicals, and response to drugs with carcinogenic potential. Recent evidence also indicates that nutrients interact by themselves or affect the way other chemicals interact with the genetic material, modulating what genes are expressed and to what degree they are expressed. In other cases, such as vitamin K-dependent carboxylation, nutrients modify the expressed protein after translation.
A major proportion of our human and material resources are presently being spent in advancing the knowledge base to understand what cancer is and how the cancer process develops. Undoubtedly, we can rationalize spending even more resources in addressing these issues; however, the question is whether we should in parallel begin to explore the underlying factors and basic causes that condition the exposures that in turn become the epigenetic factors affecting the genetic determinants of cancer. Progress in cancer prevention will most likely come from what we are able to do in addressing these through effective policies and programs rather than from refining our scientific knowledge of the cancer process itself.
The life-course approach to cancer prevention. Start early; act at all stages of the life course. Life-course prevention of cancer should start before conception; mothers should start pregnancy with a healthy weight for their height and avoid excessive or low weight gain during pregnancy. Key micronutrients such as folate, iron, copper, zinc, and vitamins are important for normal embryonic development and fetal growth. Infant growth should be based on optimal health across all stages of the life course; as previously indicated, this has yet to be established. The present bigger-is-better model may increase cancer risk in later life, because bigger is closely linked to fatter. Moreover, recent assessments of the energy needs of children suggest that over the past decades 15 to 20 percent excess energy intakes have been prescribed, contributing to the surge in obesity observed globally and possibly to increased cancer incidence in some parts of the world. Because most of the information presently available on early nutrition and adult cancer incidence is linked to obesity, we focus mainly on this risk condition in examining the life-course approach to cancer prevention.
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