|
by Aftab J. Ahmed, Ph.D.
Systemic Enzymes and Women's Health
Even though we are living better and enjoying robust health more than ever before, at least some of the healthcare challenges still remain formidable. The major public healthcare concern is the management of chronic diseases. Whereas American medicine in the management of acute and emergency conditions is second to none, despite considerable progress in our understanding of chronic diseases, their clinical management leaves some things to be desired. In fact, chronic diseases will be the major challenge facing the healthcare system in the coming decades.
As chronic diseases take years, even decades, to develop, it is understandable that their management would be less susceptible to the so-called “hand grenade” approach to treatment. That is, to throw powerful drugs at the diseased tissue and organ in the hope that the disease symptoms will relent and the disease will be treated, if not cured. This approach, however, is far less effective than originally thought. To a large extent it is due to the complex natural history of chronic?diseases in which a myriad of factors—from genetic predisposition, dietary habits, lifestyle choices to gender, among others—play a crucial role.
A greater appreciation for the intractability of chronic diseases has driven the point home that a far better understanding of their causes has first to be garnered before effective and safe therapies can become available. In light of this, a healthcare trend has taken hold in which individuals are increasingly assuming greater personal responsibility for their own health to hold disease at bay by nutritional and lifestyle strategies.1 Nutritional intervention rests on the premise that long-term preventive measures are better suited to the management of chronic diseases than an all-or-none approach inherent in the so-called “magic bullet” model. In that regard, systemic enzyme supplementation is one of the most important long-term nutritional strategies. This contribution summarizes the benefits of systemic enzymes with specific reference to female breast health.
Systemic enzymes are a viable, long-term nutritional support system that both helps maintain good health and holds age-related frailties and disorders in check. Systemic enzymes correct and fortify the body’s own defenses. The initiated reader is referred to previous articles by the author in recent issues of this magazine to glean various health benefits of systemic enzymes. Essentially systemic enzymes quench the inflammatory response by conscripting the immune system to restore the balance. Additionally, being composed of proteolytic (protein-degrading) enzymes, they break down the so-called immune complexes, which are metabolic debris circulating in the bloodstream, to improve the blood flow. As a corollary, as the blood flow is improved so is the delivery of nutrients and oxygen to?tissues and organs throughout the body. This panoply of benefits attributed to systemic enzymes is best illustrated by what happens in the body as the aging process sets in.2
Broadly speaking, aging ensues as a result of disturbance in homeostasis, which refers to the balance among various networks in the body and their reciprocal interactions. Perturbation of this balance leads to a domino effect whereby, in a manner of speaking, one broken thread could potentially unravel the entire ball of yarn. How profoundly does the breakdown of homeostasis affect health is, perhaps, best illustrated by the action of growth factors. Growth factors are proteins produced in the body in response to specific stimuli, in the requisite amounts, and for well-defined periods of time, to respond to its metabolic needs. Once a metabolic need is met, growth factors specific to it are suppressed. For example, in case of an abrasion or a wound, transforming growth factor-beta (TGF-?) is produced, which functions by healing the wound fairly quickly. After the wound is healed, it retracts from the scene and the smooth commerce of human physiology resumes. There are occasions, however, when even after the wound is healed or, because the wound does not heal, as in malignant transformations, the body keeps producing TGF-? in relatively speaking, copious amounts, which can and does have serious consequences. Thus, if TGF-?, which is central to human growth and development, is produced in amounts more than necessary, it not only gives rise to scar tissue but also impairs the body’s ability to respond to therapeutic approaches.
Take the case of female breast health. There would be hardly anything more worrisome to a woman than to find a lump in her breast. Ordinarily such lumps appear quite normally and regularly only to disappear subsequently of their own accord, leaving no deleterious traces in their wake. Appearance of lumps in the breast tissue, however, is an age-related phenomenon. It is a given that with increasing age the risk of inflammation increases, in part on account of the low-grade autoimmunity, which is a result of metabolic attrition but does not clinically manifest itself. To slake the inflammatory response, which may be due to a lesion, the body produces TGF-? to heal the tissue. Transient lumps in the breast are a manifestation of this healing process. On occasion, however, this healing process does spin out of control as the body loses its ability to “sense” that the production of additional TGF-? is neither required nor necessary. The continued production of TGF-? causes the tissue at the site of the lesion to harden. This “overkill” in healing the wounds is termed fibrosis, which is suggestive of out-of-context, (over) production of TGF-?.
Inflammation of the breast tissue, or cystic mastitis, is benign and is readily amenable to therapeutic intervention. If the inflammation is not promptly brought under control, however, this apparently benign condition could worsen and potentially contribute to abnormal growth in the breast tissue. How does breast tissue become susceptible to disease? Aside from familial history and genetic predisposition, the most important factor in breast pathology is estrogen, the premiere female hormone. Quite like other critical biomolecules, estrogen, too, is a turncoat agent. Not only does estrogen prepare the female body for pregnancy and lactation but it also protects against the build-up of cholesterol in the coronary arteries and the bones against painful fractures caused by loss of calcium. On the other hand, estrogen can also cause and aid the growth of malignancy in the breast. Over the years considerable strides have been made in the management of breast malignancy. Thus, tamoxifen, approved by the Food and Drug Administration (FDA) in 1978, helps block the body’s use of estrogen. There is a downside to the tamoxifen therapy, however. Inasmuch as it helps prevent breast malignancy, its use entails palpable, albeit slight, risk of malignancy in the endometrium, or the lining of the uterus. To avert this untoward side effect scientists and clinicians have been working diligently on the so-called selective estrogen receptor modulators (SERMs). These designer drugs are anticipated to accomplish what was once thought to be impossible. That is, the ability to block the effect of estrogen on the breast tissue without causing unscheduled multiplication of the uterine cells, which are as responsive to estrogen as the breast tissue, and prevent malignancy. Roloxifene, marketed as Evista and approved by the FDA in 1997 for treatment of osteoporosis, is the first SERM presently under consideration.
Tamoxifen, however, becomes ineffective at the advanced stages of abnormal growth in the cell. The insensitivity of the breast tissue to tamoxifen is the result of TGF-?.3 Ample evidence documents that TGF-? is produced in the transformed breast tissue.4 In 1999 researchers at Vanderbilt University Medical School showed that when TGF-? is neutralized (by exposure to specific antibodies elicited against it), the breast tissue becomes re-sensitized to the effect of tamoxifen; in other words, the abnormal growth relents and is inhibited to a meaningful measure.
That is where the benefits of systemic enzymes are most palpable. Systemic enzymes are known to inhibit TGF-? and thus circumvent its pernicious effects on the tissues. How do systemic enzymes accomplish that? Simplistically, once produced TGF-? binds to a carrier protein called alpha 2-macroglobulin (?2-M). Upon their uptake into the blood stream systemic enzymes also bind to ?2-M. The binding site on ?2-M for TGF-? and systemic enzymes is largely overlapping, as schematized in the accompanying diagram. In addition, in order for TGF-? to exert its physiological function, it has to be degraded to its active form. Its displacement from ?2-M to which it is bound in its inactive, precursor form, inhibits its action. Since TGF-? stimulates its own production, the displacement from ?2-M nips it in the bud. A few fairly large-scale clinical studies indicate that inhibition of TGF-? by systemic enzymes not only reverses mammary cystitis but it also, as noted above, re-sensitizes the breast tissue to tamoxifen. As such, systemic enzymes can be seen as an adjunct to standard approaches in the maintenance of breast health.5
There is another aspect of systemic enzyme function that ought to be emphasized. As alluded to initially, the “hand grenade” approach to chronic diseases is by and large ineffective. Therefore for quite some time now the thrust of biomedical research has been to develop drugs that help the immune system fight malignancy. One of the most notable examples, insofar as the breast malignancy is concerned, has been the identification of herceptin (HER-2), a protein that is associated with breast malignancy. Even though HER-2 protein in found in every individual, roughly 30 percent of patients with breast cancer (which translates to roughly 60,000 patients a year) have abundance of this protein. In large amounts this protein induces aggressive transformation of the breast tissue as malignancy spreads fast and furious. The advantage of HER-2 therapy, which utilizes specific drugs to search and destroy this protein, is that it only targets the transformed tissue while leaving the healthy tissue unscathed. Of late HER-2 therapy has generated considerable enthusiasm and hope. It should be mentioned, however, that it might be some time before it becomes a viable therapeutic option.
Despite its advantages vis-a-vis chemotherapy and radiation therapy, HER-2 therapy revisits the targeted approach. It could be argued that global fortification of the immune system would constitute a better approach to maintain breast health, which deploys the entire immune system without the destructive effects of “hand grenades.” Systemic enzymes offer one such modality; they help the immune system mobilize its own arsenal not only to fend off the invading pathogens but also utilize the body’s indigenous repair processes to fend off abnormal growth. Systemic enzymes function at three different levels to help manage age-related transitions insofar as human health and disease are concerned. First they normalize sub-threshold autoimmunity, which is a hallmark of the aging process and may be construed as the toll that decades-long metabolic attrition exacts. Second, systemic enzymes modulate the levels of TGF-? to well within the normal range, which increase with advancing years and can dispose the body to fibrosis. Third, they facilitate more ready distribution of nutrients and oxygen to various tissues and organs, which fosters more robust metabolism. Given that abnormal proliferation of the tissues is an age-related phenomenon, and multiple factors may concurrently contribute to pathology, systemic enzymes furnish a preventive approach to health and well-being deep into the golden years of life.
References:
Ahmed, A. J. “Nutrition and Successful Aging,” Nat. Med. J. Vol. 1, 18. (1998).
Ahmed, A. J. “The Longevity Stakes: Reversing the Effects of Aging,” totalhealth Vol. 21 p. 44. (1999).
Sierra-Rivera, E., Hargrove, J. and Osteen, K. “Differential Regulation of Tamoxifen-Induced TGF-? Expression in Normal Breast and Endometrial Epithelial Cells by Ovarian Steroid Hormones,” Proc. Am. Assoc. Cancer Res. Vol. 40, p. 1872. (1999).
Blobe, G., Schiemann. W. and Lodish, H. “Role of Transforming Growth Factor-? in Human Disease,” N. Engl. J. Med.: Vol. 342, p. 1350, (2000).
Klaschka, F. “Oral Enzymes: New Approach to Cancer Treatment,” Forum Medizin Verlagsgesellschaft, Graefelfing, Germany, (1996).
Acknowledgement: Assistance in graphic rendition by Anthony Provenzanoin is hereby acknowledged.
|
