Effect of Obesity on Screening Mammography
Effect of Obesity on Screening Mammography
Abstract & Commentary
Synopsis: Among cohorts of increasing obesity compared to normal women, there were higher rates of recall, biopsy, and screening-detected prevalent cancers of the breast, supporting but not validating a relationship between adiposity and breast cancer.
Source: Hunt KA, Sickles EA. Effect of obesity on screening mammography: Outcomes analysis of 88,346 consecutive examinations. AJR Am J Roentgenol 2000;174:1251-1255.
Epidemiological studies have indicated obesity as a risk factor for the development of breast cancer in postmenopausal women, although specific body habitus (shape) may modify such models. Moreover, higher levels of "adiposity" have been associated with larger tumor size and nodal involvement at the time of initial diagnosis, as well as with higher rates of breast cancer recurrence and mortality in all women.
Such studies have not specifically evaluated women undergoing screening mammography or asymptomatic patients. This work reviewed data from a large series of screening patients, assigning them to four categories as follows, based normative values: a) underweight by greater than 10%, 3475 patients; b) ideal weight ± 10%, 39,656 patients; c) overweight by 11-24%, 20,789 patients; d) overweight by 25-39%, 12,345 patients; and e) overweight by ³ 40%, 12,081 patients.
Prevalent detection rates were determined for mammographically identified lesions and by linkage to a local SEER (Surveillance, Epidemiology, and End Results, a national data analysis project) tumor registry; interval cancers and follow-up data were obtained.
An increase in recall rates was identified with progressively increased adiposity: 3.88%, 4.89%, 5.11%, 5.47%, and 5.55%), as well as rate of biopsy: 0.98%, 1.31%, 1.35%, 1.59%, and 1.65%. This increased rate was at least commensurate with the rates of screening detected cancer/1000 women: 3.74, 4.29, 5.34, 4.70, and 6.04. These trends were also reflected in increased median cancer size and more advanced stage of diagnosis.
Detection rates might be improved by assuming that increased adiposity would also be correlated with decreased mammographic density, as denoted by the American College of Radiology BI-RADS system, and indeed this was the case.
A suggested trend showed increased interval cancer rates in underweight women as well as overweight women compared to ideal weight women.
COMMENT BY r. JAMES BRENNER, MD, JD
While much controversy exists regarding diet and breast cancer risk—consider the considerable increased rate of breast cancer among second generation decendents of Japanese women now living in the United States as well as the increasing incidence now seen in Japan (there is no shortage of McDonalds restaurants now in Tokyo)—most epidemiological studies show a relationship between obesity and breast cancer incidence. Biochemical models have been considered that attempt to reconcile this observation. Following menopause, the main source of endogenous estrogen is the conversion in adipose tissue of the androgen precursor androstenedione to estrone. Obesity is associated with decreased production of sex-hormone-binding globulin, which may result in unbound estradiol, the biologically active form of estrogen.
If these theories are correct, then obesity may not only be a direct risk factor for breast cancer, but may also bear a causative relationship to growth and spread. The observations in this study lend credence to this premise.
However, the real answer to this question would be derived by observing similar trends and comparisons for interval cancers, compared to prevalent cancers. In other words, are the tumors in overweight women that develop within a year of a prior normal examination also larger and more aggressive than their counterparts in ideal weight women? Unfortunately, there were too few interval cancers in this study to reach substantive conclusions regarding this aspect of the study. For example, if a higher percentage of stage II cancers would be physically palpated in a smaller breasted woman than a larger breasted (e.g., obese) woman (where the physical examination would be more difficult to feel deeper lesions), then one would expect a higher prevalence at the first screening examination of stage II tumors to be present in an asymptomatic population of obese women. This phenomenon would thus explain the results in this study, without implying a cause-and-effect relationship between adiposity and cancer growth. In other words, the results may be secondary to the difficulty of palpating tumors in a large-breasted woman compared to a small-breasted woman, although I suspect this is not a sufficient explanation for Hunt and Sickles’ results.
As mentioned, this issue can be addressed, but only in a longer, larger study of interval cancers. Data in this study are derived from one of the largest and longest-running databases from a single institution in the country, demonstrating how difficult such determinations can be. Perhaps collaborations among several institutions or databases may provide statistical power to either corroborate or defeat the notion that increased obesity has a direct bearing on the development and/or progression of breast cancer.
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