ADIPOSE TISSUE AND ÆTIOLOGY OF BREAST CANCER

ADIPOSE TISSUE AND ÆTIOLOGY OF BREAST CANCER

1001 Australian series had five-year-survival rates of 83% for everpregnant and 73% for never-pregnant women; our figures are 64% and 67%. Restriction...

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1001 Australian series had five-year-survival rates of 83% for everpregnant and 73% for never-pregnant women; our figures are 64% and 67%. Restriction of our series to cutaneous lesions (89% of the total), or adjustment for stage at diagnosis still did

yield any association between survival and pregnancy history. Both series come from major referral centres and relate to similar time periods. It seems unlikely that treatment practices were much different. The Australian series has a higher proportion of younger and of never-pregnant patients than ours. The survival-rates are better in the Australian series for all groups except never-pregnant women over fifty. The better survival may be due to earlier diagnosis related to the much higher incidence of melanoma in Australia than in British Columbia.3 However, we cannot see why the difference in survival seen in the Australian series is not replicated in our experience, and the inconsistency argues against the general hypothesis put forward by Hersey et al.

BREAST-SIZE AND BRA-TYPE VERSUS BREAST TEMPERATURE

not

Division of Epidemiology, Cancer Control Agency of British Columbia, Vancouver, British Columbia, Canada

J. MARK ELWOOD ANDREW J. COLDMAN

ADIPOSE TISSUE AND ÆTIOLOGY OF BREAST CANCER

SIR,-Professor Beer and Dr Billingham (Aug. 5, p. 296) propose as an explanation for the higher incidence of breast cancer in Caucasian than in Oriental women the more abundant adipose tissue in the breasts of the former. Adipose tissue is known to store lipid-soluble agents such as anxsthetics and, more specifically, studies in animals indicate that fat-soluble carcinogens localise in high concentrations in breast and perirenal fat cells.’ Beer and Billingham view the increased mass of breast fat of Caucasian women as a depot for the prolonged release and local diffusion of carcinogens into the breast alveoli. This hypothesis ignores some basic principles of vascular anatomy and physiology. Following release from breast fat cells, carcinogens first reach the venules and lymphatics surrounding the fat cells, and then enter the general circulation. Upon recirculation to the breast, carcinogens could be directly taken up and secreted by the alveolar epithelial cells as we have proposed.2 There is no need to believe that an excess of breast fat would be more hazardous to breast epithelium than in any other more distantly located fat depots-subcutaneous fat, omentum, and so on-which are also known to store fatsoluble substances. Further, in unpublished epidemiological and anthropometric studies on the possible relationship of breast size, body-weight, and height to breast-cancer risk, we found no support for the hypothesis that breast size is related to breast-cancer risk, if the data are controlled for height and

weight. Department of Epidemiology and International Health,

University of California, San Francisco, California 94143 U.S.A.

NICHOLAS L. PETRAKIS VIRGINIA L. ERNSTER

SIR,-Dr Adami and Dr Rimsten (Sept. 5, p. 677) address multifactorial problem. Consider these findings: women in upper socioeconomic brackets havemore breast cancer than women in lower socioeconomic brackets; women with large breasts have more breast cancer than women with small breasts; nuns have more breast cancer than non-nuns; and Taiwan women, who nurse only on one side, have little cancer in that breast, but a great deal in the other. The common denominator in these women seems to be overheated glandua

3. Everall, J. D., Dowd, P. M. Lancet, 1977, ii, 286. 1. Gamal, E B., Carroll, K. K., Plunkett, E. R. Cancer Res. 1968, 2. Petrakis, N. L. Natn. Cancer Inst. Monogr. 1977, 47, 161.

28, 384.

lar breast tissue. I tested this hypothesis by tactually noting breast temperatures of 550 women patients within 30 s (if wearing bras) after bra removal. I found that women in upper socioeconomic brackets tended to wear heavier, more expensive bras, making their breasts hotter than lighter-bra-wearing or braless women in lower socioeconomic brackets. Large, braencased breasts were hotter than smaller ones, but braless breasts-large, medium, or small-were cool. In addition, I found that nuns bind their breasts, flattening them; this coupled with black, heat-absorbing clothes overheats their breasts. And, of course, nursing Taiwan women have one breast exposed often, making it cooler than the one remaining at a constant hotter temperature. It is well known that undescended testes have a high cancer incidence due to glandular tissue overheating. Also, testicular cancer increased markedly after men began wearing hotter, jockey-type underwear. I suggest a similar mechanism as one factor in breast cancer-i.e., if one keeps the breasts hot, they develop more cancer than if one leaves them cool as Nature in-

tended. Several years ago, when feminists burned their bras, it seemed peculiar; however, they may have been decreasing the risk of breast cancer. Perhaps doctors should encourage them, or at least recommend net or other cool bras when women insist on wearing them. Department of Internal Medicine, Southern California Permanente Medical Group, Los Angeles 27, California, U.S.A.

JOHN M. DOUGLASS

ROLE OF PINEAL GLAND IN ÆTIOLOGY AND TREATMENT OF BREAST CANCER

SIR,-Idisagree with the hypothesis proposed by Dr Cohen colleagues (Oct. 14, p. 814) and suggest, in fact, that the

and

reverse

may be true: breast

cancer

is related

to

increased

pineal-gland activity. Hyperoestrogenism is important in breast cancer and the pineal gland may suppress ovarian activity. The strongest evidence supporting a link between breast cancer and pineal hypofunction is that relating to pineal calcification. However, much of the supporting evidence on the incidence of pineal calcification is based on studies of radiologically detectable calcium in the gland. Radiology is an insensitive method of detecting calcification; radio-opacities probably indicate individual areas of dense calcification in the gland and do not give a measure of the total calcium content. Quantitative measurements of pineal calcification show that the overall level of calcification is remarkably constant during adult life and that there is no definite increase with age.’ Furthermore, there is no evidence that calcification of the pineal gland is associated with degeneration of the parenchyma.2 In addition it has been suggested that calcification, rather than being an indicator of 1. Tapp, E., Huxley, M. J. Path. Bact. 1971, 105, 31. Wurtman, R. J. in Endocrine Pathology (edited by J. 117. Baltimore, 1968.

2.

M.

Bloodworth);

p.