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Cancer of the breast is the most common incident cancer and cause of death from cancer in women. Several epidemiologic studies have reported a significant inverse relationship between the intake of vitamin A and/or provitamin A-rich foods and the incidence of certain cancers, including breast cancer. A large number of studies have been conducted to determine the effect of retinoids (all-trans-retinoic acid, in particular), and to a lesser extent of carotenoids, on breast cancer using cell culture models. In general, the results of these studies demonstrate beneficial effects of all-trans-retinoic acid on different breast cancer cells. This review compares studies conducted in different laboratories using retinoids and carotenoids as treatments for breast cancer cells and suggests what may be the underlying reasons for the differential effects of these compounds on the same cell lines.

A large body of observational epidemiologic studies has consistently demonstrated that individuals who eat more fruits and vegetables, which are rich in carotenoids, and people who have higher serum beta-carotene levels have a lower risk of cancer, particularly lung cancer. In contrast to these observations, two human intervention studies that used high-dose beta-carotene supplements reported an increased risk for lung cancer among smokers. Recently, in vitro and in vivo studies have shed light on the present conundrum regarding the potential chemopreventive activity of beta-carotene; that is, beta-carotene itself may act as an anticarcinogen, but its oxidized products may facilitate carcinogenesis. These studies support the hypothesis that the carcinogenic response to high-dose beta-carotene supplementation reported in the human intervention trials is related to the instability of the beta-carotene molecule in the free radical-rich environment in the lungs of cigarette smokers. This is especially possible because smoke also causes decreased tissue levels of other antioxidants, such as ascorbate and alpha-tocopherol, which normally have a stabilizing effect on the unoxidized form of beta-carotene. Nutritional intervention using a combination of antioxidants (beta-carotene, alpha-tocopherol, and vitamin C) as anticarcinogenic agents could be an appropriate way to rationally and realistically reduce cancer risk.

Until very recently, phytonutrient research was the province of natural product chemists and consisted of primarily anecdotal clinical references. In recent years, an extensive set of qualitative and semi-quantitative dietary epidemiologic data has been developed. This developing base of epidemiologic data is now being supplemented by biochemical, mechanistic, and genetic epidemiology of a more quantitative nature. As we seek to understand the mechanisms that explain a large body of epidemiologic evidence, newer laboratory methods continue to be developed. Though there is a continuing need for even more discriminating nutrition epidemiology to drive the basic research in this area forward, the focus of in vitro, animal and clinical (human) studies must continue to be refined, and appropriate biomarkers for chronic and acute (death) disease end-points must be developed.

Acquired kidney and liver diseases are relatively common diseases that can raise the potential for nutrient intoxication. For example, high-protein diets increase glomerular blood flow and the blood pressure gradient across the glomerular capillary wall in the kidney, which can result in injury to membranes. Likewise, the liver can increase nutrient intoxication because it is involved in the intermediary metabolism of many nutrients, serves as the storage organ for many nutrients, and is important in the biotransformation and excretion of nutrients. In this paper, vitamin A serves as an example to illustrate how kidney disease and liver disease can increase a single nutrient's toxicity.

Risks for gastric cancer in relation to diet and other environmental factors are receiving renewed attention. New developments include the emerging relationship between Helicobacter pylori infection and an increased risk for gastric cancer, and positive results of chemoprevention trials in decreasing gastric cancer risk with the use of beta-carotene and vitamin E supplements. Factors that may enhance risk include consumption of nitrites, nitrates, alcohol, and highly salted, pickled, fermented, or smoked foods. Other environmental factors which may promote cancer are H. pylori infection, inappropriate food storage, metal and cement dust exposure, and cigarette smoking. High intakes of fruits and vegetables or of antioxidants, such as beta-carotene, vitamin E, and vitamin C may decrease risk.

At the request of UNICEF, the authors conducted a rapid nutritional assessment of children from birth to five years of age in southern Iraq during the second half of June 1991. With support from local UNICEF staff, the nutrition team examined 680 children, measuring weight, height, and mid-upper arm circumference and observing clinical signs of anemia, vitamin A deficiency, and dehydration. These measurements and observations were performed in 14 rural, urban, and periurban settings in Basrah and Amarah governorates. Evidence of both acute and chronic malnutrition was found in large numbers of the children examined. However, the acute nutritional signs of impending famine were not evident at the time of the survey. This is true notwithstanding epidemic levels of infectious disease, market prices for basic food items three to 20 times prewar levels, and a reported crisis in mothers' ability to breastfeed. Other signs of impending famine (distress sales of family assets, disintegration of social structures, etc.) may have existed, but were not evident to the team.