Diet and Nutrition
Alcohol and Cancer Risk
Researchers have identified multiple ways that alcohol may increase the risk of cancer, including:
- metabolizing (breaking down) ethanol in alcoholic drinks to acetaldehyde, which is a toxic chemical and a probable human carcinogen; acetaldehyde can damage both DNA (the genetic material that makes up genes) and proteins.
- generating reactive oxygen species (chemically reactive molecules that contain oxygen), which can damage DNA, proteins, and lipids (fats) through a process called oxidation
- impairing the body’s ability to break down and absorb a variety of nutrients that may be associated with cancer risk, including vitamin A; nutrients in the vitamin B complex, such as folate; vitamin C; vitamin D; vitamin E; and carotenoids
- increasing blood levels of estrogen, a sex hormone linked to the risk of breast cancer
- Alcoholic beverages may also contain a variety of carcinogenic contaminants that are introduced during fermentation and production, such as nitrosamines, asbestos fibers, phenols, and hydrocarbons.
Antioxidants and Cancer Prevention
Antioxidants are chemicals that interact with and neutralize free radicals, thus preventing them from causing damage. Antioxidants are also known as “free radical scavengers.”
The body makes some of the antioxidants it uses to neutralize free radicals. These antioxidants are called endogenous antioxidants. However, the body relies on external (exogenous) sources, primarily the diet, to obtain the rest of the antioxidants it needs. These exogenous antioxidants are commonly called dietary antioxidants. Fruits, vegetables, and grains are rich sources of dietary antioxidants. Some dietary antioxidants are also available as dietary supplements
Examples of dietary antioxidants include beta-carotene, lycopene, and vitamins A, C, and E (alpha-tocopherol). The mineral element selenium is often thought to be a dietary antioxidant, but the antioxidant effects of selenium are most likely due to the antioxidant activity of proteins that have this element as an essential component (i.e., selenium-containing proteins), and not to selenium itself .
Artificial Sweeteners and Cancer
Artificial sweeteners, also called sugar substitutes, are substances that are used instead of sucrose (table sugar) to sweeten foods and beverages. Because artificial sweeteners are many times sweeter than table sugar, smaller amounts are needed to create the same level of sweetness.
Artificial sweeteners are regulated by the U.S. Food and Drug Administration (FDA). The FDA, like the National Cancer Institute (NCI), is an agency of the Department of Health and Human Services. The FDA regulates food, drugs, medical devices, cosmetics, biologics, and radiation-emitting products. The Food Additives Amendment to the Food, Drug, and Cosmetic Act, which was passed by Congress in 1958, requires the FDA to approve food additives, including artificial sweeteners, before they can be made available for sale in the United States. However, this legislation does not apply to products that are “generally recognized as safe.” Such products do not require FDA approval before being marketed.
Calcium and Cancer Prevention
Calcium is an essential dietary mineral commonly found in milk, yogurt, cheese, and dark green vegetables. It also is found in certain grains, legumes (including peas, beans, lentils, and peanuts), and nuts.
Calcium is a major component of bones and teeth. It also is required for the clotting of blood to stop bleeding and for normal functioning of the nerves, muscles, and heart.
Chemicals in Meat Cooked at High Temperatures and Cancer Risk
Heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs) are chemicals formed when muscle meat, including beef, pork, fish, or poultry, is cooked using high-temperature methods, such as pan frying or grilling directly over an open flame. In laboratory experiments, HCAs and PAHs have been found to be mutagenic—that is, they cause changes in DNA that may increase the risk of cancer.
HCAs are formed when amino acids (the building blocks of proteins), sugars, and creatine (a substance found in muscle) react at high temperatures. PAHs are formed when fat and juices from meat grilled directly over an open fire drip onto the fire, causing flames. These flames contain PAHs that then adhere to the surface of the meat. PAHs can also be formed during other food preparation processes, such as smoking of meats
HCAs are not found in significant amounts in foods other than meat cooked at high temperatures. PAHs can be found in other charred foods, as well as in cigarette smoke and car exhaust fumes.
Cruciferous Vegetables and Cancer Prevention
- What are cruciferous vegetables?
Cruciferous vegetables are part of the Brassica genus of plants. They include the following vegetables, among others:
o Bok choy
o Brussels sprouts
o Collard greens
- Why are cancer researchers studying cruciferous vegetables?
Cruciferous vegetables are rich in nutrients, including several carotenoids (beta-carotene, lutein, zeaxanthin); vitamins C, E, and K; folate; and minerals. They also are a good fiber source.
In addition, cruciferous vegetables contain a group of substances known as glucosinolates, which are sulfur-containing chemicals. These chemicals are responsible for the pungent aroma and bitter flavor of cruciferous vegetables.
During food preparation, chewing, and digestion, the glucosinolates in cruciferous vegetables are broken down to form biologically active compounds such as indoles, nitriles, thiocyanates, and isothiocyanates . Indole-3-carbinol (an indole) and sulforaphane (an isothiocyanate) have been most frequently examined for their anticancer effects.
Indoles and isothiocyanates have been found to inhibit the development of cancer in several organs in rats and mice, including the bladder, breast, colon, liver, lung, and stomach . Studies in animals and experiments with cells grown in the laboratory have identified several potential ways in which these compounds may help prevent cancer:
o They help protect cells from DNA damage.
o They help inactivate carcinogens.
o They have antiviral and antibacterial effects.
o They have anti-inflammatory effects.
o They induce cell death (apoptosis).
o They inhibit tumor blood vessel formation (angiogenesis) and tumor cell migration (needed for metastasis).
A possible relationship between fluoridated water and cancer risk has been debated for years. The debate resurfaced in 1990 when a study by the National Toxicology Program, part of the National Institute of Environmental Health Sciences, showed an increased number of osteosarcomas (bonetumors) in male rats given water high in fluoride for 2 years . However, other studies in humans and in animals have not shown an association between fluoridated water and cancer .
In a February 1991 Public Health Service (PHS) report, the agency said it found no evidence of an association between fluoride and cancer in humans. The report, based on a review of more than 50 human epidemiological (population) studies produced over the past 40 years, concluded that optimal fluoridation of drinking water “does not pose a detectable cancer risk to humans” as evidenced by extensive human epidemiological data reported to date .
In one of the studies reviewed for the PHS report, scientists at NCI evaluated the relationship between the fluoridation of drinking water and the number of deaths due to cancer in the United States during a 36-year period, and the relationship between water fluoridation and number of new cases of cancer during a 15-year period. After examining more than 2.2 million cancer death records and 125,000 cancer case records in counties using fluoridated water, the researchers found no indication of increased cancer risk associated with fluoridated drinking water .
In 1993, the Subcommittee on Health Effects of Ingested Fluoride of the National Research Council, part of the National Academy of Sciences, conducted an extensive literature review concerning the association between fluoridated drinking water and increased cancer risk. The review included data from more than 50 human epidemiological studies and six animal studies. The Subcommittee concluded that none of the data demonstrated an association between fluoridated drinking water and cancer . A 1999 report by the CDC supported these findings. The CDC report concluded that studies to date have produced “no credible evidence” of an association between fluoridated drinking water and an increased risk for cancer . Subsequent interview studies of patients with osteosarcoma and their parents produced conflicting results, but with none showing clear evidence of a causal relationship between fluoride intake and risk of this tumor.
Recently, researchers examined the possible relationship between fluoride exposure and osteosarcoma in a new way: they measured fluoride concentration in samples of normal bone that were adjacent to a person’s tumor. Because fluoride naturally accumulates in bone, this method provides a more accurate measure of cumulative fluoride exposure than relying on the memory of study participants or municipal water treatment records. The analysis showed no difference in bone fluoride levels between people with osteosarcoma and people in a control group who had other malignant bone tumors .
Garlic and Cancer Prevention
Several population studies show an association between increased intake of garlic and reduced risk of certain cancers, including cancers of the stomach, colon, esophagus, pancreas, and breast. Population studies are multidisciplinary studies of population groups that investigate the cause, incidence, or spread of a disease or examine the effect of health-related interventions, dietary and nutritional intakes, or environmental exposures. An analysis of data from seven population studies showed that the higher the amount of raw and cooked garlic consumed, the lower the risk of stomach and colorectal cancer
The European Prospective Investigation into Cancer and Nutrition (EPIC) is an ongoing multinational study involving men and women from 10 different countries. This study is investigating the effects of nutrition on cancer. In the study, higher intakes of onion and garlic were associated with a reduced risk of intestinal cancer
The Iowa Women’s Study is a large prospective study investigating whether diet, distribution of body fat, and other risk factors are related to cancer incidence in older women. Findings from the study showed a strong association between garlic consumption and colon cancer risk. Women who consumed the highest amounts of garlic had a 50 percent lower risk of cancer of the distal colon compared with women who had the lowest level of garlic consumption
Several population studies conducted in China centered on garlic consumption and cancer risk. In one study, investigators found that frequent consumption of garlic and various types of onions and chives was associated with reduced risk of esophageal and stomach cancers, with greater risk reductions seen for higher levels of consumption .Similarly, in another study, the consumption of allium vegetables, especially garlic and onions, was linked to a reduced risk of stomach cancer.In a third study, greater intake of allium vegetables (more than 10 g per day vs. less than 2.2 g per day), particularly garlic and scallions, was associated with an approximately 50 percent reduction in prostate cancer risk .
Evidence also suggests that increased garlic consumption may reduce pancreatic cancer risk. A study conducted in the San Francisco Bay area found that pancreatic cancer risk was 54 percent lower in people who ate larger amounts of garlic compared with those who ate lower amounts.
In addition, a study in France found that increased garlic consumption was associated with astatistically significant reduction in breast cancer risk. After considering total calorie intake and other established risk factors, breast cancer risk was reduced in those consuming greater amounts of fiber, garlic, and onions .
Obesity and Cancer Risk
Obesity is associated with increased risks of the following cancer types, and possibly others as well:
- Colon and rectum
- Breast (after menopause)
- Endometrium (lining of the uterus)
One study, using NCI Surveillance, Epidemiology, and End Results (SEER) data, estimated that in 2007 in the United States, about 34,000 new cases of cancer in men (4 percent) and 50,500 in women (7 percent) were due to obesity. The percentage of cases attributed to obesity varied widely for different cancer types but was as high as 40 percent for some cancers, particularly endometrial cancer and esophageal adenocarcinoma.
A projection of the future health and economic burden of obesity in 2030 estimated that continuation of existing trends in obesity will lead to about 500,000 additional cases of cancer in the United States by 2030. This analysis also found that if every adult reduced their BMI by 1 percent, which would be equivalent to a weight loss of roughly 1 kg (or 2.2 lbs) for an adult of average weight, this would prevent the increase in the number of cancer cases and actually result in the avoidance of about 100,000 new cases of cancer.
Several possible mechanisms have been suggested to explain the association of obesity with increased risk of certain cancers:
- Fat tissue produces excess amounts of estrogen, high levels of which have been associated with the risk of breast, endometrial, and some other cancers.
- Obese people often have increased levels of insulin and insulin-like growth factor-1 (IGF-1) in their blood (a condition known as hyperinsulinemia or insulin resistance), which may promote the development of certain tumors.
- Fat cells produce hormones, called adipokines, that may stimulate or inhibit cell growth. For example, leptin, which is more abundant in obese people, seems to promote cell proliferation, whereas adiponectin, which is less abundant in obese people, may have antiproliferative effects.
- Fat cells may also have direct and indirect effects on other tumor growth regulators, including mammalian target of rapamycin (mTOR) and AMP-activated protein kinase.
- Obese people often have chronic low-level, or “subacute,” inflammation, which has been associated with increased cancer risk.
Other possible mechanisms include altered immune responses, effects on the nuclear factor kappa beta system, and oxidative stress.
Tea and Cancer Prevention: Strengths and Limits of the Evidence
Among their many biological activities, the predominant polyphenols in green tea―EGCG, EGC, ECG, and EC―and the theaflavins and thearubigins in black teas have antioxidant activity . These chemicals, especially EGCG and ECG, have substantial free radical scavenging activity and may protect cells from DNA damage caused by reactive oxygen species . Tea polyphenols have also been shown to inhibit tumor cell proliferation and induce apoptosis in laboratory and animal studies . In other laboratory and animal studies, tea catechins have been shown to inhibit angiogenesis and tumor cell invasiveness . In addition, tea polyphenols may protect against damage caused by ultraviolet (UV) B radiation , and they maymodulate immune system function . Furthermore, green teas have been shown to activatedetoxification enzymes, such as glutathione S-transferase and quinone reductase, that may help protect against tumor development .Although many of the potential beneficial effects of tea have been attributed to the strong antioxidant activity of tea polyphenols, the precise mechanism by which tea might help prevent cancer has not been established .
Vitamin D and Cancer Prevention
Early epidemiologic research showed that incidence and death rates for certain cancers were lower among individuals living in southern latitudes, where levels of sunlight exposure are relatively high, than among those living at northern latitudes. Because exposure to ultraviolet lightfrom sunlight leads to the production of vitamin D, researchers hypothesized that variation in vitamin D levels might account for this association. However, additional research based on stronger study designs is required to determine whether higher vitamin D levels are related to lower cancer incidence or death rates.
Experimental evidence has also suggested a possible association between vitamin D and cancer risk. In studies of cancer cells and of tumors in mice, vitamin D has been found to have several activities that might slow or prevent the development of cancer, including promoting cellulardifferentiation, decreasing cancer cell growth, stimulating cell death (apoptosis), and reducing tumor blood vessel formation (angiogenesis) .