Fat or Fiction: The Link Between Obesity and Breast Cancer
One of the most important lessons in scientific training is that it is difficult to infer mechanisms and causes from observed correlations. This rule, which is often summarized in the trite phrase “correlation is not causation”, is the source of scientific modesty, that tendency of scientists to limit the conclusions they draw from their research – at least in their published work. Unfortunately, when scientific findings are communicated in the popular press, that modesty is often thrown out the window. When several potential mechanisms (causes) may explain the same observed correlations, the subtle differences between them are often lost in the broad brushstrokes of the picture painted by science journalists. A good example of this phenomenon can be found in a recent article in the Los Angeles Times: “Pounds may lower risk but only for the young” (Dec 4, 2006).
It has long been observed that obesity and breast cancer are related. The simple story goes something like this: The excess padding around our collective thighs and bellies contains an enzyme, aromatase, which naturally converts testosterone (an androgen steroid) into estradiol (an estrogen). Over one hundred years of evidence shows that estrogens are related to the development of certain types of breast cancer; and thus it seems to follow that more fat means more estradiol and more cancer.
But little in science is so linear. Scores of well-designed research has documented a complex set of relationships between dietary fat intake, body mass index (BMI; weight [kg] / height [m]2), and breast cancer. Eating a high quantity of animal fat is associated with a higher risk of breast cancer among premenopausal women; yet eating a low-fat diet did not reduce risks of breast cancer among postmenopausal women. A high BMI at birth or after menopause increases the risk of breast cancer; a high BMI during adolescence and early adulthood decreases the risk of breast cancer. And although dietary fat does not necessarily result in obesity, they are strongly associated, particularly in the United States. The Times article is a report on a new study by Dr. Karen Michels, a Harvard University epidemiologist, which focuses specifically on the inverse relationship between BMI and breast cancer in young adults.
One existing hypothesis is that the inverse relationship between BMI and the risk of breast cancer in pre-menopausal women is due to differences in hormonal cycles in more obese individuals. Obese women, defined as a BMI > 30, often have irregular or long menstrual cycles or polycystic ovary syndrome (PCOS; a constellation of features often characterized byovulatory dysfunction, hirsutism, and obesity caused by high levels of circulating androgens). These conditions, which are associated with a lack of ovulation and concomitant decreases in estradiol and progesterone, may explain the lower risk of breast cancer. Dr. Michels’ study is the first to test this hypothesis in a large prospective trial.
Using data gathered in the national Nurses’ Health Study II (NHS II), the study team followed 113,130 premenopausal women with a main outcome measure of invasive breast cancer. Body mass index was calculated for each woman at the time of initiation in the survey and every two years thereafter. Accounting for potential confounding factors, including age at first menstruation, family history of breast cancer, number of pregnancies and children, and alcohol consumption, the authors tested the association of BMI and occurrence of breast cancer. Unsurprisingly, since they used the same secondary data as previous studies, they found the same inverse relationship between BMI and risk of breast cancer.
The interesting finding is that their results did not support the hypothesis that differences in ovulation in obese women explain their decreased susceptibility to breast cancer. On the contrary, the authors conclude that “factors related to ovulation, such as menstrual cycle characteristics, infertility due to an ovulatory disorder, and probable PCOS, do not seem to explain the association” between BMI and breast cancer. And with the exception of the glaring failure to control for smoking in their analyses, it looks like good science. It is a well-designed study investigating an important hypothesis.
Yet, as is all too frequent in science writing, what makes it into the headline is what’s most likely to draw in readers (“Being obese is good for you!”), not the actual results of the scientific study. The main finding of the research is not, as reported on in the Times article, the old news that obese young-adult women are less likely to get breast cancer, but the new observation that differences in ovulation in these women can’t wholly explain the reduced risk. In fact, the Times writer even seems to suggest that the opposite is true when she quotes a scientist as saying that "obese and overweight women are not ovulating normally." While this is true enough, she misses the more important point of Michels’ recent study, which is that this fact doesn’t matter as much as we thought. A more relevant synopsis could have been gleaned from simply reading the abstract of the article itself, which states that the inverse trend between BMI and breast cancer risk “was not explained by menstrual cycle characteristics or infertility due to an ovulatory disorder.”
References
Beckman M. 2006 Dec 4. “Pounds may lower risk but only for the young.” Los Angeles Times.
SIN (Science in the News)
Too often, the media’s reporting on scientific findings and issues becomes a professional game of Telephone, with each re-telling adding an extra layer of misunderstanding, miscommunication, erroneous information, and dumbed down simplification. Each week, we will take a recent news story and attempt to excavate the original truth behind the hype, correcting the errors of the media’s coverage, commenting upon reoccurring issues with the science-to-public pipeline, and analyzing the motives and machinery behind these distortions.