Skip to main content

Archived Comments for: Menopausal status dependence of the timing of breast cancer recurrence after surgical removal of the primary tumour

Back to article

  1. This may be due to low DHEA...

    James Howard, independent biologist

    19 October 2004

    It is my hypothesis that reduced dehydroepiandrosterone (DHEA) may trigger cancer (oncogene) initiation (1994). This may be useful in explaining the findings of Demicheli, et al.

    DHEA naturally begins to decline around age twenty, reaching very low levels in old age. I suggest this may explain why more cancer occurs in old age. In the case of Demicheli, et al., it is pertinent to know that surgery artificially lowers DHEA (J Int Med Res. 2002 Jan-Feb;30(1):9-14 and Acta Endocrinol (Copenh). 1987 Sep;116(1):155-60). I suggest that surgery for breast cancer may reduce DHEA and trigger further cancer initiation because of this artificial, premature reduction in DHEA.

    In premenopausal women, surgery for breast cancer reduces DHEA. In women who have oncogenes which are triggered by low DHEA, this would trigger further cancer formation. This would create the first peak in “hazard rate for breast cancer recurrence.” That is, the surgery reduces DHEA which causes initiation of cancer. As these women have had their DHEA artificially reduced and/or are experiencing the normal decline of DHEA, a second peak of cancer formation occurs as a result of use of DHEA by the cancer (see parenthetical material below). This would cause the second peak. Node involvement, I suggest, indicates that these women exhibit increased probability of oncogene initiation as a result of lower DHEA. This situation would “magnify” the size of the two peaks. Increased node involvement would indicate this vulnerability is increased and, therefore, the hazard rate would be higher in the group with more node involvement. Conversely, lack of node involvement would, therefore, indicate reduced effect of low DHEA on oncogene activation. This is indicated by low recurrence hazard in both pre- and postmenopausal women.

    Postmenopausal women exhibit a single peak because their cancer occurs within the decline of DHEA of old age. That is, there is no second peak because these women express oncogene activation of loss of DHEA of old age. Node involvement, in these women, should indicate enhanced vulnerability to oncogene activation by low DHEA. This manifests itself as a skewing towards earlier recurrence hazard with increased node involvement. There is no second peak because they are already in the loss of DHEA of old age.

    (It is also my hypothesis that all tissues, normal or otherwise, utilize DHEA for growth and development and maintenance of the adult form. Once initiated, cancer also depends on DHEA for growth. This would explain why cancer of old age, while more frequent, grows less fast, i.e., less DHEA for growth. Also, cancer, if it can, will absorb DHEA at the expense of the rest of the body. I suggest this produces “cachexia,” or loss of support of sufficient DHEA to maintain the host body.)

    Competing interests

    no competing interests