PubMed · 10578600
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A Martin. 1999-10-15. [Nutriceuticals].. https://pubmed.ncbi.nlm.nih.gov/10578600/
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Trials of nutritional supplements for cancer prevention must overcome a variety of challenges not shared in the usual paradigm of pharmaceutical agents for prevention of cardiovascular disease. Unlike for cardiovascular disease, for cancer we typically do not have well-established causal risk factors as targets for intervention. Also, for most likely cancer interventions, the expected time to achieve an effect is much longer, more variable, and far less well understood than for cardiovascular disease, and the progression of pathophysiology is much harder-or impossible-to follow, in contrast with imaging for progression of atherosclerosis in cardiovascular disease. Also, cancers at various sites have a wide range of etiologies. The optimal age for intervention, best dose, and duration needed to test nutritional agents for cancer prevention are largely unknown, making null findings hard to interpret. Unlike with drugs, baseline nutritional status can be critical. Moreover, because the nutritional agents are often readily available, adherence in control groups in trials can be impaired. Several gene-nutrient and nutrient-nutrient interactions have been identified that could affect trial results. Some studies suggest that particular nutrients may be effective only in subgroups defined by genotypes or by nutritional status of another nutrient. All these challenges must be considered in planning informative trials. Long-term prospective cohort studies, especially with repeated measures and high follow-up, can provide useful data for planning trials as well as the basis for rational recommendations while awaiting trial results or in settings where trials may be infeasible.
Approximately 20-30% of Americans consume multivitamin supplements daily, indicating high public interest in the prevention of cancer and other chronic diseases through a nutrition-based approach. Although several bioactive food components, including vitamins and minerals, have been investigated for their ability to affect cancer risk, few large, randomized, placebo-controlled clinical trials of multivitamins with cancer as the primary endpoint have been performed. The results of most large-scale trials of multivitamin supplements (combinations of > or = 2 vitamins and minerals) to prevent cancer have been mixed. The Linxian General Population and Dysplasia trials found a decreased risk of cancer, particularly stomach cancer, for participants taking a multivitamin supplement, but this was in a borderline-deficient population in China. Two trials, the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study and the beta-Carotene and Retinol Efficacy Trial, found an increased risk of lung cancer among male cigarette smokers or asbestos-exposed persons taking beta-carotene-a surprising result, considering that most epidemiologic studies have suggested that consumption of fruit and vegetables appears to lower cancer risk. To clarify the effects of multivitamin supplements, several large randomized clinical trials are underway, including the Physicians' Health Study II, the Selenium and Vitamin E Cancer Prevention Trial, and a European study, Supplémentation en Vitamines et Minéraux Antioxydants (SU.VI. MAX). Because epidemiologic studies generally evaluate foods rather than specific bioactive food components, a systematic approach to determining how combinations of vitamins and minerals may interact to ameliorate cancer risk is necessary to further our understanding of the potential benefits and risks of supplement use.
Chronic inflammation is associated with a high cancer risk. At the molecular level, free radicals and aldehydes, produced during chronic inflammation, can induce deleterious gene mutation and posttranslational modifications of key cancer-related proteins. Other products of inflammation, including cytokines, growth factors, and transcription factors such as nuclear factor kappaB, control the expression of cancer genes (e.g., suppressor genes and oncogenes) and key inflammatory enzymes such as inducible nitric oxide synthase and cyclooxygenase-2. These enzymes in turn directly influence reactive oxygen species and eicosanoid levels. The procancerous outcome of chronic inflammation is increased DNA damage, increased DNA synthesis, cellular proliferation, disruption of DNA repair pathways and cellular milieu, inhibition of apoptosis, and promotion of angiogenesis and invasion. Chronic inflammation is also associated with immunosuppression, which is a risk factor for cancer. Current treatment strategies for reactive species overload diseases are frequently aimed at treating or preventing the cause of inflammation. Although these strategies have led to some progress in combating reactive species overload diseases and associated cancers, exposure often occurs again after eradication, treatment to eradicate the cause fails, or the treatment has long-term side effects. Therefore, the identification of molecules and pathways involved in chronic inflammation and cancer is critical to the design of agents that may help in preventing the progression of reactive species overload disease and cancer associated with disease progression. Here, we use ginseng as an example of an antiinflammatory molecule that targets many of the key players in the inflammation-to-cancer sequence.