Pregnancy postponement and childlessness leads to chronic hypervascularity of the breasts and cancer risk.

Epidemiologists have established that women with small families, and particularly nulliparae, are prone to develop breast cancer later in life. We report that physiological mammary hypervascularity may be an intermediate reason against the background that breast-core vascularity is normal in pregnancy but pathological in the vascularisation of cancer. We examined breast 'core' vascularity in nulliparae during their potential reproductive life and in parous women after their last birth but before their menopause. Fifty clinically normal pre-menopausal non-pregnant women (100 breasts) were studied daily for one 'luteal positive' menstrual cycle. Their parity history varied from zero to five babies. Under controlled domestic conditions each wore a special electronic thermometric bra to automatically record breast 'core' temperature changes as a measure of mammary tissue blood flow. In the nulliparae there was a rise of breast vascularity throughout reproductive life. In the parous women, a year or so after each birth, breast vascularity was reset at a lower level than before the pregnancy; thereafter, as in nulliparae, there was progressive increase in mammary vascularity until the menopause.

The luteal heat cycle of the breast in disease.

Wearing a special thermometric brassiere, selected women self-measured their breast surface temperature. These measurements were made during one hour each evening at home for one menstrual cycle under standard conditions of overclothing and room temperature. To stage their cycle they also collected daily samples of saliva in their freezer for immuno-assay of progesterone concentration in the laboratory. A total of 82 women participated, most having young families. This total included four groups, a control group (N = 25) and three 'disease' groups, namely: family history of breast cancer (14); benign breast disease (12); and a 'cancer-associated' group (31) who had had previous cancer surgery. A significant breast temperature rhythm with a period at or about 28 days was found not only in the controls but also in the three groups of breasts designated 'disease'. Nevertheless, consistent rhythm abnormalities were found in all the disease groups. Most evident was a hyperthermia throughout the cycle, a reduction in the rhythm amplitude, and a tendency for the breast temperature rhythm to be manifest 1-2 days earlier in the menstrual cycle.

A non-invasive test for the pre-cancerous breast.

This paper describes a non-invasive, self-measured procedure by which the precancerous breast can be distinguished from the normal breast. The method involves wearing a specially designed thermometric brassiere for 90 min each evening at home through one menstrual cycle. Profiles of progesterone through the cycle, obtained from daily saliva sampling, and determination of the steroid content by radioimmunoassay, are made to allow the status and calendar date timing of the luteal phase to be established. Thus, cycles can be synchronised across subjects. In this study, two types of breast were compared: 50 normal breasts and 41 age-matched precancerous breasts. Differences between the groups were striking in terms of amplitude, phasing and average temperature during the luteal heat cycle. When these parameters and others were used as predictors in a linear discrimination and/or neural net analysis, a sensitivity and specificity of > 90% was achieved.

The luteal heat cycle of the breast in health.

Wearing a special thermometric brassiere, twenty-five normal women self-measured their breast surface temperature. The subjects averaged 39 years of age and all were parous. Observations were made for one hour each evening for one menstrual cycle under semi-standardized domestic conditions. They also collected daily samples of saliva for radioimmunoassay of progesterone concentration. The surface temperature of the breast is relatively cold around mid-cycle; thereafter, and without interruption in averaged data, the temperature increases steadily by about 1 degree C over the 12 days of the luteal phase; around the time of the menses, it falls rapidly. This heat rhythm does not occur in peri-menopausal low progesterone menstrual cycles or in patients where the breast tissue has been irradiated for cancer treatment.

Genesis of breast cancer is in the premenopause.

In Britain and other high-risk countries, about a third of patients with breast cancer are premenopausal at diagnosis. In the remainder, tumour initiation might have occurred in the premenopause, even though the clinical presentation was late in life. This possibility has important implications for breast cancer prevention and screening. The relations between the patient's age and tumour kinetics, prognosis, oestrogen receptors, and environmental X-ray carcinogenesis were studied, together with the age-related protection afforded by pregnancy. The findings support the hypothesis that breast cancer is initiated in the premenopause.