How to prevent breast cancer
The most progressive approach women can adopt today in the fight against breast cancer is to concentrate on its prevention. This is particularly important for women who have any family history of breast cancer. Two of the most potent allies women have for preventing breast cancer are seleno-methionine and vitamin E.
This approach must also involve an attitude change. Most people believe free radicals are the main cause of accelerated ageing, cancer and other degenerative diseases. However, the biological research has moved on. So rapid has been its progress that the vista of free radicals has become a blurred picture, replaced by a much more specific biochemical activity.
To date, biologists have shared their understanding of the potentially dangerous activity within cells derived from the breakdown of reactive oxygen, reactive nitrogen and reactive nitrogen oxide products. Recently, an additional group of dangerous products that are active in cells, reactive sulphur products, has also been introduced. It has been suggested that these chemical substances also act as â€˜aggressive oxidising agentsâ€™. Although we do not usually notice changes in the atmosphere, the critical oxidising potential of the atmosphere has actually shifted from a negative minus-five to a positive plus-13 in the past 2.5 billion years. The level of oxygen in the atmosphere is of critical importance. It has been maintained at 21 per cent for millions of years, but a one per cent increase in the concentration of oxygen in the atmosphere can have some negative effects.
In November 2001, the Schrauzer Symposium was held in Baden Baden Germany to discuss selenium and breast disease. Thoughts were expressed concerning the role of oxidation stress — that is the products produced by the breakdown of oxygen and nitrogen — in the initiation of breast cancer and the potentially important role of seleno-methionine to neutralise its influence.
Benign breast disease
Also discussed at the conference was the link between benign breast disease and breast cancer. Benign breast disease is a common breast condition experienced by many young women. The signs and symptoms of this condition include:
- Swelling and tenderness of one or both breasts
- Marked induration (hardened area) of one or both breasts, particularly towards the axillary tail (armpit)
- Development of cysts of variable size and shape, gradually or suddenly
Many women are tolerant of these signs and symptoms. While mammograms can detect breast cancer, they usually don\’t indicate benign breast disease, so women may put up with the discomfort, even if extreme. It is well recognised that various treatments are frequently only partially successful in relieving pain and tenderness associated with the disease. However, it is important to consider the prevention of breast cancer at this stage, irrespective of the person\’s age.
Much confusion has surrounded this condition on account of the large number of technical names given to it around the world. In Australia it is usually referred to as â€˜benign breast diseaseâ€™ or â€˜mammary dysplasiaâ€™. In 1902 it was called â€˜chronic mastitisâ€™ by Cheatle, an English surgeon. Subsequently, he denounced the term as a fallacy and instead described it as \”a dangerous condition frequently associated with cancer\”. Similarly, Willis, a famous Australian pathologist from The Royal College of Surgeons in England, called the condition â€˜cystic hyperplasiaâ€™. He, too, was highly critical of surgeons who were not able to accept that it was frequently associated with breast cancer.
Recently, the condition has been given another name: mammary intraduct epithelial hyperplasia (MIEH). This all-inclusive term describes the basic cellular activity that can result in excessive activity of the cells lining the milk ducts, cyst formation, intraduct cancer, breast cancer or breast destruction.
Breast milk ducts
A basic change in the breast associated with the benign breast disease is the excessive overgrowth (hyperplasia) of the cells lining the breast milk ducts. This change is greatly accelerated following ovulation, in the luteal phase of the menstrual cycle, as the breast prepares for pregnancy and subsequent lactation. It is not oestrogen alone that causes the condition, but also the integrated activity of progesterone released after ovulation into the oestrogen-primed breast duct cell. If pregnancy does not eventuate, the same excessive development of the breast duct epithelial cell is repeated month after month, year after year.
This recurrent cellular activity can result in the formation of small groups of cells undergoing abnormal development. As these groups of cells undergo rapid change, they can go on to form cancer within the ducts, which can spread into the breast itself. On top of the recurrent breast duct cellular activity, damaging oxidative byproducts caused by the biochemical substances are released onto cells that have already been stimulated into activity. The object of early prevention of breast cancer is to neutralise and counteract the activity of these chemical products, the biochemical nature of which subsequently induces the development of abnormal cells in the ducts of the breast.
With more women choosing to have fewer or no children, together with early commencement of regular menstruation and delayed menopause, the risk of breast cancer is significantly increased. This is because the period during which the breast duct cells are exposed to the effects of oxidative stress is increased.
One hundred years ago a woman may have experienced 150 menstrual cycles to menopause; today it is closer to 400. This is a recognised stimulant to the development of breast cancer. It cannot be forgotten that the breast is a very active organ. Indeed, it can be described as a metabolic factory, continually exposed to intense biochemical activity.
Women who lactate following pregnancy experience a long continued cellular activity accompanying milk production. When lactation ceases and weaning occurs, 80 per cent of the breast duct epithelial cells, including cells which may be undergoing premalignant change, die off as a result of a special physiological process which protects the breasts from cancer. In contrast, the breast cells of women who do not become pregnant are continuously subjected to cellular activity. A similar die-off period occurs during the bleeding phase of menstruation, but by comparison it is limited and incomplete. This leaves the same overactive duct cells to be restimulated cycle after cycle. It is recognised that this continual physiological activity can lead to the development of mutant (pre-malignant) cells, from which breast cancer can develop.
A clinical intervention trial conducted over a two-year period indicated that premenstrual changes in the breast are responsive to a daily supplementation of 100mcg of seleno-methionine, taken as a high selenium yeast. Of 135 patients treated — all suffering from very severe symptoms — 107 women experienced complete relief over several cycles. A regular cycle of events occurred following supplementation:
- Loss of pain, tenderness and swelling in the affected breasts over two to three cycles, with return of normal breast consistency over a three- to six-month period.
- There was no resolution of breast cysts nor did any change in mammographic pattern occur during the period under observation.
While the counter activity of seleno-methionine against the activity of free radicals was considered as a potential reason for the sometimes dramatic relief of the symptoms, it was not until 1992 that the potential of the combination of derivatives of oxygen and nitric oxide induced by the inflammatory reaction in the breast was considered as the most likely cause of the oxidant stress within the breast and the associated symptoms. In 1992, it was Professor Joseph Beckman, the principal investigator at the Linus Pauling Institute, who suggested that the capacity of products of oxygen reduction and nitric oxide could combine to produce a highly toxic and dangerous substance called peroxynitrite. Beckman also transferred the emphasis of tissue damage and the capacity of oxidative stress to cause ageing and degenerative disease from \”free radicals\” to reactive oxygen and nitrogen products. Helmut Sies, a German biologist, has since shown that seleno-methionine and selenium enzymes can interact with peroxynitrite to neutralise its dangerous activities.
Results from the intervention trial suggest that seleno-methionine may have a function as a chemopreventive agent. In this case it is important to recognise it is not used simply as a nutritional benefit. It needs to be taken in an amount (100-200mcg) daily, over a specific period, to give adequate protection to the breast. To understand at what time and over which period it must be realised that the changeover from a simple condition such as MIEH to breast cancer can take 10-30 years. The period of flux of agents causing oxidative stress, which have the potential to cause breast cancer, exists from menarche to menopause, say from 12 to 45 years. It is likely that the period 18-25 years of age is the most critical phase for seleno-methionine supplementation; that is, during the period when a women experience most metabolic and hormonal activity.
Seleno-methionine, as high selenium yeast, is available throughout Australia from healthfood shops and chemists. There are two levels of intake that are recommended.
The recommended daily allowance (RDA) is a level of intake required to prevent the development of a selenium-deficient disease. The RDA for most Australian women will be met with a daily supplement of 50mcg of selenomethionine.
Many biologists now advocate a significantly higher level of intake, a supernutritional intake, to prevent the development of chronic diseases. Thus a separate reference dose, RFD, has also been set as a safe level of intake. The RFD is five micrograms of selenium per kilogram of bodyweight per day. For example, 350mcg is recommended for a 70kg individual.
In the management of benign breast disease a daily supplement of 100-150mcg of seleno-methionine should be adequate. It is important that you remain under the supervision of your medical practitioner.
The evidence available suggests the prime strategy of any chemopreventive practice is to prevent and control and physio-pathological inflammation associated with hormonal activity as early as possible and to maintain therapy throughout the phase of oxidative stress. In summary, it can be said that seleno-methionine has a function in the management of the physio-pathological inflammation accompanying oxidative stress induced in the breast during the premenstrual period. To what extent this function may be related to the prevention of more serious diseases remains to be finally determined.
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