Cancer Risk Reduction

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Cancer Risk Reduction (Diet/Smoking Cessation/ Lifestyle Changes)

Many cases of cancer can be prevented. Generally, people can reduce their risks for developing cancer by making wise lifestyle choices such as eating low-fat, high-fiber diets that include a variety of vegetables and fruits, avoiding tobacco use, being physically active, and minimizing sun exposure. Specific genetic susceptibilities, however, can influence cancer risk associated with certain lifestyle factors, and variation in risk exists among individuals. Guidelines for implementing lifestyle choices to reduce cancer risk have been formulated to help people adopt cancer-protective behaviors.


The risk of developing cancer, a disease that affects many millions of people worldwide, can be reduced markedly by approaches that encourage primary prevention. A landmark report by Doll and Peto in 1981 summarized the evidence relating lifestyle choices, including diet, tobacco use, and sun exposure, as well as other environmental factors (e.g., occupation, ionizing radiation), to cancer risk. The report suggested that 75-80% of cancer cases were potentially avoidable and that dietary factors, tobacco use, and sun exposure were associated with approximately 35, 30, and 1-2%, respectively, of all cancers. Scientists now recognize that the effects of environmental factors, including lifestyle choices, on cancer risk can be influenced by a person's genetic susceptibility.


A. The Diet-Cancer Relationship
A considerable body of evidence--experimental, epidemiologic, and clinical--indicates that dietary factors, both individual food constituents and dietary patterns, play a major role in determining cancer risk. Generally, the evidence supports inverse associations between cancer risk and intakes of vegetables, fruits, whole grains, dietary fiber, certain micronutrients, and certain types of fat (e.g., n-3 fatty acids, particularly n- 3/n-6 fatty acid ratios), as well as direct associations between cancer risk and intakes of excessive calories, alcohol, total fat, and certain types of fat (e.g., saturated fat). To illustrate, epidemiologic studies have provided consistent and convincing evidence for increased cancer risk when migrants from countries with a low-fat, high-fiber diet adopt the high-fat, low-fiber diet characteristic of Western countries. The Western countries also have higher rates of obesity. Of interest is the possible cancer-protective Mediterranean diet, which emphasizes a high intake of vegetables, fruits, whole grains, fish (high in n-3 fatty acids), and olive oil (high in monosaturated fatty acids). Interactions likely occur among many dietary constituents. However, neither these interactions nor their influence on cancer risk is well understood. Thus, at present it is difficult to tease out the specific effects of individual dietary components from diet and cancer research data.      
Randomized, controlled trials (RCTs) offer one of the best means for testing diet and cancer hypotheses developed from the insights provided by epidemiologic and experimental studies. Among specific dietary constituents investigated in RCTs, vitamins A, C, and E, folic acid, calcium, and selenium have shown promise in reducing cancer risk at certain sites (e.g., vitamin E and selenium for prostate cancer). Some diet and cancer trials include efforts to modify certain lifestyle choices other than diet, such as smoking and level of physical activity, that also could influence cancer risk and thus influence study results.

B. Gene-Nutrient Interactions
Cancer risk reduction by dietary modification likely will depend, in part, on increased understanding of both gene-nutrient interactions and the role of genetic differences (polymorphisms) among individuals. Genes involved in carcinogenesis influence metabolic activation/detoxification, DNA repair, chromosome stability, activity of oncogenes or tumor suppressors, cell cycle control, signal transduction, hormonal pathways, vitamin metabolism pathways, immune function, and receptor or neurotransmitter action. Exposure to the same quantitative level of dietary factor(s) or dietary carcinogens can increase cancer risk in one individual but not in another, depending on specific susceptibilities to gene-nutrient interactions. For example, an intake of heterocyclic amines (HAs), produced by grilling of meat, increases the risk of colorectal cancer. However, people with polymorphic forms of the enzymes N-acetyltransferase type 2 (NAT2) and cytochrome P4501A2 (CYP1A2), which cause rapid activation of HAs, have a greater risk of colorectal cancer than people with polymorphic forms that cause a slow activation of HAs. Folate, found in green, leafy vegetables, is also associated with polymorphisms and cancer risk. A specific polymorphism in the gene that codes for methylenetetrahydrofolate reductase--an enzyme critical to DNA methylation and synthesis--can reduce colorectal cancer risk by altering cellular responses to dietary folate and methionine.     
Understanding gene-nutrient interactions and individual differences in genetic susceptibilities may lead to future dietary intervention strategies to reduce cancer risk. Focusing on polymorphisms in intervention studies allows investigators to develop study designs, stratify participants, and analyze results based on genetic differences within the study population. For example, polymorphisms in genes affecting the use of vitamin D confer different levels of risk for prostate cancer--a fourfold increase in risk among individuals with one polymorphism and a 60% reduction in risk among individuals with another. This kind of information is important for researchers designing trials to investigate the role of vitamin D, or its analogs, in prostate cancer risk. As more knowledge is gained about how genetic polymorphisms influence cancer risk through specific dietary constituents or patterns, researchers can refine recommendations for healthful eating regimens to reduce cancer risk.

TABLE I National Cancer Institute Dietary Guidelines

Reduce fat intake to 30% or less of calories
Increase fiber intake to 20 to 30 g daily, with an upper limit of 35 g
Include a variety of vegetables and fruits in the daily diet
Avoid obesity
Consume alcoholic beverages in moderation, if at all
Minimize consumption of salt-cured, salt-pickled, and smoked foods

C. Dietary Guidelines
As research continues into the role of specific dietary constituents in cancer risk, it is important that clinicians and the public be advised about the importance of modifying diets to reduce cancer risk. Since the mid-1970s, various scientific organizations around the world, including the World Cancer Research Fund (WCRF) in association with the American Institute for Cancer Research (AICR), the American Cancer Society (ACS), and the U.S. National Cancer Institute (NCI), have developed dietary guidelines to promote cancer risk reduction as a population strategy.      
The guidelines of the NCI, outlined in Table I, are in agreement with dietary guidelines developed by other organizations. The average American, according to the latest national health assessment, consumes too much fat (too much saturated fat, too little monosaturated fat), too little fiber, and too few vegetables, fruits, and whole grains. This pattern is seen in many developed countries worldwide. People should be encouraged to adhere to dietary guidelines that promote good health. It is incumbent that physicians, nutritionists, and registered dietitians play a key role in advocating healthful diets that have the potential to reduce cancer risk and are beneficial overall.


A. Smoking and Cancer Risk
Lung cancer is the most common cancer in the world, accounting for almost 13% of all cancers (18% for men, 7% for women). Smoking is the single most important lifestyle factor contributing to lung cancer incidence worldwide. In fact, at least 20 carcinogens that are components of tobacco smoke cause lung tumors in either animals or humans. In addition to lung cancer, smoking substantially increases the risk for cancers of the larynx, oral cavity, and esophagus and contributes to risk for cancers of the pancreas, uterine cervix, kidney, and bladder. People may have different susceptibilities to developing smoking-related cancers because of genetic variations in their metabolism of tobacco smoke carcinogens. Furthermore, the adverse effects of smoking on cancer risk can be enhanced by alcohol consumption and by the presence of other environmental carcinogens, particularly radon and asbestos.      
In many areas of the world, particularly in third-world countries, tobacco use is rising. Although it is estimated that as many as 30% of cancers in developed counties are tobacco related, tobacco use in these countries remains high. In the United States, about one-fourth of adults currently smoke, and tobacco use among high school students has increased steadily since the early 1990s. Results of a national 1999 survey show that almost 35% of high school students smoke.      
Nonsmokers exposed to environmental tobacco smoke (ETS), as a result of either household or occupational exposure, inhale and metabolize components of the smoke and thus also may be at increased risk for lung cancer. An analysis of 37 case-control and cohort studies indicated that, for men and women combined, the risk of lung cancer increased by 23% for a nonsmoker who lived with a smoker; also, risk appeared to be directly related to the number of cigarettes smoked by the spouse and the duration of exposure.      
Educational strategies to prevent the start of smoking by adolescents and smoking cessation approaches to stop tobacco use by smokers permanently are among the most effective ways to reduce cancer risk. Although 70% of smokers claim to be interested in quitting smoking, most of them have no immediate plans to quit. When smokers try to quit on their own, relapse in the majority occurs within days, and only about 7% achieve long-term success. However, longterm success rates can be increased to 15-30% if interventions such as pharmacotherapies and intensive counseling are used. A combination of pharmacotherapy and counseling should be used for adult smokers trying to quit, except for light smokers (< 10 cigarettes/day), women who are either pregnant or breastfeeding, or when pharmacotherapy is medically contraindicated.

B. Pharmacotherapies for Smoking Cessation
Nicotine, present in all tobacco products, is an addictive substance. For most users, tobacco use results in true drug dependence. Not all smokers, however, have the same level of nicotine dependence; a high number of cigarettes smoked each day, frequent smoking in the morning, and smoking while ill indicate a high dependence level. Evidence demonstrating that pharmacotherapies can help people addicted to nicotine quit smoking is strong and consistent, and several pharmacotherapies--primarily nicotine replacement therapies (NRTs)--have been approved for smoking cessation by the U.S. Food and Drug Administration (Table II). All currently approved pharmacotherapies approximately double the chances that an attempt to quit smoking will be successful. Abundant evidence confirms that both nicotine gum and nicotine patches are safe and effective aids to smoking cessation. Nicotine nasal spray, which delivers larger doses of nicotine more rapidly than nicotine gum and patches, is also an effective smoking cessation aid. The nicotine inhaler, a plastic rod containing a plug impregnated with nicotine, is designed to combine pharmacologic and behavioral substitution strategies; it results in blood levels of nicotine similar to those from use of nicotine gum. Bupropion, an antidepressant and the only approved nonnicotine pharmacotherapy, appears to be an effective aid to smoking cessation and is safe even when used jointly with NRT. Although bupropion likely does not influence smoking cessation via its antidepressant effect, its mechanism of action is unclear.

TABLE II Pharmacotherapies for Smoking Cessation

Pharmacotherapy Availability Side effects
Nicotine gum Over-the-counter only Mouth soreness Indigestion
Nicotine patch Over-the-counter and prescription Skin reaction at patch site
Nicotine nasal spray Prescription only Nasal/throat irritation
Sneezing, coughing
Nicotine inhaler Prescription only Mouth/throat irritation
Bupropion Prescription only Dry mouth

C. Behavioral Interventions
Behavioral interventions can range from minimal intervention, such as a 3-min intervention during a routine visit to a physician, to intensive group or one-on-one counseling using multiple sessions. In the United States, more than 70% of smokers visit a healthcare setting every year, providing an excellent opportunity for brief advice and counseling. In fact, patients who smoke expect their physician to inquire into their smoking habits and advise them regarding cessation techniques. Studies show that brief physician advice to quit smoking can produce cessation rates of 5-10% each year. Simple intervention strategies that can be used by physicians to help their patients stop smoking are outlined in Table III. Effective counseling is essential to help a smoker who is willing to quit achieve long-term success in smoking cessation. Practical counseling that provides coping strategies and basic information about smoking/quitting, social support offered as part of treatment, and social support arranged outside of treatment (e.g., community resources) all are important components of effective counseling.

TABLE III Synopsis for Physicians: How to Help Your Patients Stop Smokinga

Ask about smoking at every opportunity a. "Do you smoke?" If so, "How much?"
b. "How soon after waking do you have your first cigarette?"
c. "Are you interested in stopping smoking?"
d. "Have you ever tried to stop before?" If so, "What happened?"
Advise all smokers to stop a. State advice clearly, e.g., "As your physician, I must advise you to stop smoking now."
b. Personalize the message to quit. Refer to the patient's clinical condition, smoking history, family history, personal interests, or social roles.
Assist the patient in stopping a. Set a quit date. Help the patient pick a date within the next 4 weeks.
b. Provide self-help materials. Review the materials with the patient, if desired.
c. Consider prescribing nicotine replacement therapy, especially for highly addicted patients (smoke one pack or more a day or smoke within 30 min of waking).
d. Consider signing a stop-smoking contract with the patient.
e. If the patient is not willing to quit now, provide motivating literature and ask again at the next visit.
Arrange follow-up visits a. Set a followup visit within 1 to 2 weeks after the quit date.
b. Contact the patient within 7 days after the initial visit; reinforce the decision to stop and remind the patient of the quit date and the follow-up visit.
c. At the first follow-up visit, discuss the patient's smoking status to provide support and help prevent relapse. Relapse is common; if it happens, encourage the patient to try again immediately.
d. Set a second follow-up visit in 1 to 2 months. For patients who have relapsed, discuss the circumstances of the relapse and other special concerns.

aAdapted from Glynn, T., and Manley, M. (1993). "How to Help Your Patients Stop Smoking: A National Cancer Institute Manual for Physicians." NIH Publication No. 93-3064. Public Health Service.


A. Physical Activity
Regular physical activity is associated with reduced all-cancer mortality through various mechanisms, including altering hormone levels and increasing immune system activity, energy expenditure, and antioxidant activity. Of particular interest is the role of physical activity in reducing weight and body fat and the possible subsequent effect on cancer risk reduction. For example, being overweight or obese is associated with an increased risk of hormone-related cancers.      
Losing weight and body fat reduces circulating levels of estrogen and progesterone, hormones related to breast and colorectal cancer. Studies suggest that moderate physical activity can reduce breast cancer risk in both premenopausal and postmenopausal women. For colorectal cancer, leanness and regular physical activity have been consistently associated with reduced risk in both men and women. Numerous studies have reported that when caloric intake exceeds energy output, there is an increased risk of cancer of the colon, rectum, prostate, endometrium, breast, and kidney.      
The amount of physical activity needed to maintain a healthy weight, lose weight, and promote good health, including reducing cancer risk, is recommended by various organizations in the United States, including the NCI and ACS, to be 30 min of moderate physical activity on most days of the week. This level of activity might include walking briskly (3-4 miles per hour) for about 2 miles, gardening and yard work, jogging, or swimming. The activity does not need to be continuous; the key is to exercise on a regular basis.

B. Sun Exposure
Exposure to sunlight, the main source of ultraviolet (UV) radiation, is implicated as a causative factor in the development of skin cancer--the most common form of cancer, with about 1.3 million new cases each year in the United States. People with red or blond hair and fair skin that freckles or burns easily are at especially high risk for skin cancer. Basal cell and squamous cell carcinomas, both highly curable, account for the majority of skin cancers. However, the incidence of malignant melanoma, the most dangerous form of skin cancer, is increasing. Total worldwide incidence increased about 15% between 1985 and 1990 estimates. In the United States, the lifetime risk of developing melanoma was 1 in 1500 in the 1930s. Now, the risk is 1 in 74, and there will be an estimated 47,700 new cases in the year 2000.      
Abundant evidence has established that skin cancer risk can be reduced by limiting exposure to sunlight and, thus, to UV radiation. Generally, effective protective behaviors include avoiding the sun during midday (especially between 10 AM and 2 PM), wearing protective clothing and broad-brimmed hats, wearing sunglasses, avoiding tanning beds and sun lamps (these are also sources of UV radiation), and using sunscreen that has a sun protection factor (SPF) of 15 or higher, even on hazy or cloudy days.      
The relationship between sunscreen use and melanoma risk is somewhat controversial. Many epidemiologic studies investigating the association between melanoma risk and sunscreen use have found either reduced risk or no clear association. However, findings in others have suggested that sunscreen use is associated with an increased risk for melanoma, leading some to question the advisability of widespread recommendations for its use. It has been hypothesized that people who use sunscreen primarily to avoid sunburn during intentional sun exposure, such as sunbathing, might increase their sun exposure time when using sunscreen, thus increasing their exposure to UV radiation and risk for melanoma. At present, accumulated evidence on sun exposure and skin cancer still warrants using sunscreen as part of an overall sun protection strategy, during both intentional and unintentional exposures (e.g., in gardening or hiking).  

Peter Greenwald
National Cancer Institute, National Institutes of Health, Bethesda, Maryland

Darrell E. Anderson
Sharon S. McDonald
Scientific Consulting Group, Inc., Gaithersburg, Maryland

See Also

enzyme A protein molecule produced by living organisms that catalyzes chemical reactions of other substances without itself being destroyed or altered upon completion of the reactions.

epidemiology The science concerned with the study of factors determining and influencing the frequency and distribution of disease and other health-related events and their causes in a defined human population.

gene-nutrient interaction The influence exerted by genes and nutrients on each other. The action may be unilateral or reciprocal and usually involves the alteration of metabolic pathways or products.

micronutrient A vitamin or mineral that the body must obtain from outside sources. Micronutrients are essential to the body in small amounts because they are either components of enzymes (the minerals) or act as coenzymes in managing chemical reactions.

oncogene Mutated and/or overexpressed version of a normal gene that in a dominant fashion can release the cell from normal restraints on growth and thus, alone or in concert with other changes, convert a cell into a tumor cell.

pharmacotherapy The treatment of diseases or conditions by medicines.

polymorphism The occurrence of different forms (alleles) of a gene (typically greater than 1%) in individual organisms or in organisms of the same species, independent of sexual variations.

primary prevention The identification, control, and avoidance of environmental factors related to cancer development.

randomized, controlled trials A clinical trial that uses a control group of people given an inactive substance (placebo) and an intervention group given the substance or action under study.

sunscreen A substance applied to the skin to protect it from the effects of the sun's rays; sunscreens act by either absorbing ultraviolet (UV) radiation or reflecting incident light. Their effectiveness is rated by their sun protection factor (SPF); e.g., a sunscreen with an SPF of 15 allows only 1/15 of the incident UV radiation or light to reach the skin.

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