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Breast cancer.

Breast Cancer

One out of every ten American women will get breast cancer in her lifetime. Every 13 minutes of 1988, another woman will die of the disease. Despite all efforts to better detect and treat it, breast cancer claims lives at the same rate today as it did in 1950.

Leonard Cohen is one of many experts who believe that prevention, rather than treatment, is the best way to stop this frightening killer. One key to preventing breast cancer, says Cohen, is a low-fat diet.

Leonard A. Cohen heads the Section of Nutritional Endocrinology at the Naylor Dana Institute of the American Health Foundation, a private, non-profit research and educational organization. A biochemist and cell biologist, he has conducted numerous animal studies on nutrition and breast cancer. He spoke with NAH from his laboratory in Valhalla, New York.

NAH: Has it been easy for scientists to accept the possibility that diet is linked to cancer?

LC: When I came into this field in 1972, if you proposed to do a study on diet and cancer, you would literally be laughed out of the room by your peers. I wrote a grant back in those days to study dietary fat and breast cancer, and one of the reviewers wrote back, "This will contribute nothing to science, but it will contribute a great deal to the folklore of science."

So it's been a very difficult time over the last ten, fifteen years to get people--not only the public, but the medical establishment, the government, and the American Cancer Society--to take the relationship between nutrition and cancer seriously.

NAH: When did scientists first begin to think of dietary fat as a cause of breast cancer?

LC: Over 40 years ago, a scientist named Albert Tannenbaum, at the Michael Reese Hospital in Chicago, carried out a series of classical experiments showing that if animals are fed high levels of fat in their diet, they develop more breast cancers than if they are fed a low-fat diet. Tannenbaum and others published many experiments in the 1940s and 1950s, but no one paid any attention until about 1967, when Kenneth Carroll at the University of Western Ontario in Canada began to study the problem. Now at least 20 groups around the world are involved in similar lines of research.

NAH: What prompted epidemiologists to compare fat consumption in different countries?

LC: The real breakthrough came when the United Nations Food and Agricultural Organization published its food balance sheets. The FAO compiled data on the export and import of food in about 50 or 60 countries around the world. Carroll took a look at these and noted how very different food intake was worldwide. If you compare 40 countries, you'll find low breast cancer mortality in countries with low fat intake and the opposite in countries with high fat intake (see graph).

NAH: Couldn't the differences in cancer rates be due to something other than diet?

LC: Evidence from Japan suggests otherwise. The Japanese are exposed to as much environmental pollution as we are, and educationally and health-wise, they are close to or above the U.S. level. Yet the Japanese have breast cancer death rates which are only one-quarter of ours. So there has to be something in the Japanese environment other than pollution or industrialization to account for these low rates.

In addition, when Japanese migrate to Hawaii and California, the second generation's breast cancer death rates come up to the rates of Americans. This suggests that the differences are not based on genetics.

On the other hand, one thing about the Japanese is that their diet is one of the lowest in fat in the world. Among farmers and fishermen, it remains around 11 percent of calories from fat, whereas our diet is 40 percent fat, as are the diets of most western countries.

NAH: What other evidence do we have from populations that a high fat diet promotes breast cancer?

LC: Over time, when a low-risk population's fat intake increases, breast cancer mortality also increases. Since World War II, we've seen dramatic increases in breast cancer in Japan, Greece, and Iceland. The people of these countries eat a lot more fat than they used to.

NAH: Do all population studies support the fat-breast cancer link?

LC: No. The data from certain special populations is weak. For example, Mormon women have lower rates of breast cancer than other American women, but they eat as much fat as other Americans. In Britain, nuns in certain religious orders eat little or no meat, but they don't have less breast cancer.

Weakest of all are the case-control studies. That's where researchers ask women who already have breast cancer about their lifelong diets, and compare them to the diets of similar women who don't have breast cancer. Some case-control studies find a fat link, but many do not.

Recently, Walter Willett of Harvard University reported on a prospective study of 89,000 nurses. He collected information on their diets and waited four years to see who would get cancer. Willett found that women who got 40 percent of their calories from fat were no more likely to get breast cancer than those who got 30 percent of their calories from fat.

NAH: How do you explain these contradictory findings?

LC: You have to look at the evidence like a mosaic. If you look only at one piece, you can easily be misled. You have to view the entire body of information to draw conclusions.

One way to explain the case-control evidence and Willett's nurse study is that neither the U.S. nor any other western country has large enough differences in fat intake to make a difference in breast cancer rates. We may have to find people who are eating less than 30 percent of their calories from fat to get below a mysterious threshold where fat is a promoter. In animal studies, we find a threshold somewhere between 25 and 30 percent of calories.

In other words, you may have to eat less than 25 or 30 percent of your calories from fat to reduce the risk of breast cancer. Since the people in these studies ate between 30 and 40 percent of calories from fat, fat appeared to have no effect.

NAH: Is that the only explanation for the contradictions?

LC: Another explanation is that the methods we have to collect information on what people eat are too imprecise to detect a fat-breast cancer link. Case-control studies work fine for comparing smokers with non-smokers because people can accurately report whether or not they smoke and how many packs per day. But food intake is not so easy to recall, and reporting is very susceptible to the "wish bias."

The "food frequency" questionnaires are often not specific about food and quantity. For example, the questionnaire may ask, "how often do you eat green vegetables?" but fail to ask "how often do you eat broccoli?" or "how much broccoli do you eat on each occasion?" Moreover, the questionnaires are based on the assumption that people can remember what they ate in the past. Four-day food records are an improvement, but they don't tell you what people ate years ago.

NAH: Is the fat-cancer theory under attack?

LC: The food industry is very concerned that this will hurt their business. The more enlightened argue that fat is overemphasized, and calories and exercise may be more important than we think. The others argue that dietary fat has nothing to do with cancer.

Other opponents of fat and cancer theory include scientists and physicians who work on chemotherapy and other treatments, and see the fat hypothesis as something that will threaten their research funding. These people have a fundamental belief that we shouldn't put much effort into prevention, yet chemotherapy has been unsuccessful in women who get breast cancer after menopause.

We also have to fight the hard-core nutritionists who spent their research careers studying vitamin deficiencies. They're left out of diet and cancer research and want to defend their role as the voice of nutrition.

NAH: What animal evidence suggests that a high-fat diet promotes breast cancer?

LC: At least 25 independent studies in different countries using different animal models have shown that if you feed animals a low-fat diet (10 to 20 percent of calories) they will exhibit one-third to one-half fewer breast tumors than if you feed them a high-fat diet (40 percent of calories). It is one of the strongest and clearest of all the diet-cancer relationships.

NAH: If you restrict an animal's calories, even a high-fat diet does not promote cancer. Does that mean we could avoid breast cancer just by watching our weight, and forgetting about how much fat we eat?

LC: You can cut an animal's incidence of tumors sharply by decreasing calories by 25 to 30 percent. That was shown over 40 years ago. But animals fed 25 percent fewer calories are extremely anxious and aggressive. They are smaller in stature than animals allowed to eat freely. So you have to question whether these results can realistically be applied to humans. Only one experiment has found that a somewhat more realistic 10 percent drop in calories inhibits tumors, but no one has duplicated it.

What really renders the calorie hypothesis questionable is that some types of high-fat diets promote tumors more than others, despite the fact that both have the same number of calories. If excess calories were solely responsible for a high-fat diet's ability to promote tumors, all high-fat diets would be equally potent tumor-promoters. They're not.

NAH: Which types of fat promote cancer?

LC: In animal experiments, so far we know that olive, fish, and coconut oil are non-promoters. Lard, beef tallow, corn, safflower, and sunflower oils are promoters. Butter, peanut, canola, and soybean oil haven't been adequately studied.

NAH: What do you mean when you say fat is a "promoter?"

LC: The process of carcinogenesis consists of three steps--initiation, promotion, and progression. Initiation occurs over a relatively short period of time, and it is irreversible. This step has already taken place in most adults. That is, most men and women have pre-cancerous lesions in their organs.

In breast cancer, the initiation step appears to occur sometime during puberty, during the development of the mammary gland, and does not appear to be related to diet.

However, these pre-cancerous lesions will not surface as clinically detectable cancer unless they are stimulated by a promoting agent. There are many possible promoters, and they exert their effects over a long period of time. We see fat having its most pronounced effect during this long latent period.

The last stage in cancer, which is the lethal stage, is progression. In this stage, tumor cells metastasize--that is, tumor cells from the original site colonize another organ. If it is a vital organ, such as the lung, liver, or brain, that is what utimately causes death.

NAH: If fat does promote breast cancer, how would it work?

LC: One possibility is through changes in hormones, such as estrogens or prolactins. Or, high-fat diets may suppress the body's immune response so it fails to reject an emerging tumor. Hormone-like substances called prostaglandins may also be involved. When we consume certain fats--called "essential" fatty acids because the body can't make them--they are converted by the body into prostaglandins. These essential fatty acids are found in polyunsaturated vegetable oils, but not in fish or other animal fats. That may explain why corn, sunflower, and safflower oils--which are rich in essential fatty acids--are such good promoters.

One of the peculiar things about breast cancers is that they produce unusually large amounts of prostaglandins, sometimes as much as ten times more than normal breast tissue does. However, at the present time, no one knows whether or how these prostaglandins help breast cancers grow.

NAH: To what extent is breast cancer a matter of heredity or other things we can't change?

LC: We can attribute some of the risk to known factors. You're at greater risk if your mother or sister had breast cancer; if you had your first child after age 25; if you started menstruating at an early age; or if you have had an unusual type of benign breast lump known as atypical hyperplasia. But add up all these attributable risk factors, and you still can't explain who gets breast cancer and who doesn't. That's why the "environmental hypothesis" came about -- to explain this non-attributable risk.

NAH: What else besides fat may affect breast cancer risk?

LC: If you allow animals on a high-fat diet to exercise voluntarily, you do get about one-third fewer tumors. We're now testing to see whether exercise plus a low-fat diet inhibits tumors even further. We also have to determine what kind and how much exercise is necessary.

Rose Frisch at Harvard found that former college athletes were less likely to get breast cancer than non-athletes. Her data suggests that while exercise is not an enormous protector, it seems to have some protective effect.

The trace element selenium and betacarotene, a precursor of vitamin A, may also help prevent breast cancer, but we don't have enough evidence to say for sure.

NAH: How important is it for young girls to eat a low-fat diet? Is there evidence that it's more important to change one's diet early or late in life?

LC: Since the initiating action occurs at puberty, the sooner women eat a low-fat diet and exercise, the better. On the other hand, we shouldn't overlook the effect of diet on the breast during maturity. Elizabeth Boylan, at the City University of New York, recently found that a low-fat diet reduced the number of breast tumors metastasizing to the lung in older mice, but not in young virgin mice. This study suggests that fat may also influence the metastatic process in postmenopausal women.

NAH: What can women who already have breast cancer do to reduce their risk of a recurrence?

LC: The evidence indicates that heavier women have a lower chance of survival, at least among those who get breast cancer after menopause. In addition, Japanese women who get breast cancer after menopause (but not before) have a better survival rate than their American counterparts. This evidence suggests that a low-fat Japanese-type diet protects against recurrence, but we need more studies to answer this question.

NAH: What should women or girls do to reduce their risk of breast cancer?

LC: They should reduce their fat intake to 30 percent of calories or less, get more of their fat from olive oil, eat more fatty fish from unpolluted waters (such as salmon, herring, and sardines), and exercise. Perhaps all of these measures together will offer as much protection as a 20 percent fat diet.
COPYRIGHT 1988 Center for Science in the Public Interest
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Title Annotation:Leonard Cohen believes one way to prevent breast cancer is a low-fat diet
Publication:Nutrition Action Healthletter
Article Type:interview
Date:Mar 1, 1988
Previous Article:Frozen finds: a survey of light meals.
Next Article:Cost killed the trial.

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