Читать книгу Anti-Aging Therapeutics Volume XIII - A4M American Academy - Страница 27

The walnut-sized prostate gland is a mucus-producing organ in males that lies just below the bladder. Growth to functional size is triggered by puberty, and continues until about age 30 when equilibrium is established between cell growth and apoptosis. Normal mid-life hormone changes, when coupled with diets that do not provide adequate nutrition for prostate cell integrity and hormone balance can trigger benign enlargement (BPH) and set the stage for other prostate conditions including prostatitis and PCa. The typical hormone pattern leading to BPH is elevated estradiol combined with elevated dihydrotestosterone (DHT), and typically estrogen dominance. This also sets up the circumstances for chronic prostatitis. While there is substantial evidence that BPH does not develop into cancer, the same underlying factors of cellular environment and integrity set the stage for PCa, and therefore, both can be considered nutritional in origin.

There are several key factors that are known to influence the development of PCa, these include:

•Inflammation: While only a relatively small percent of prostatitis – any form of inflammation of prostate tissue – is caused by bacterial infection, increasing evidence indicates a link to an imbalance in sex steroid hormones in all chronic prostatitis. An elevated level of the inflammatory cytokine interleukin (IL)-8 is a second and critical inflammation factor. IL-8 promotes stromal and epithelial cell proliferation. It is upregulated in both BPH and PCa, and it is also implicated in angiogenesis. IL-8 has been shown to have a pervasive role in promoting tumor cell survival and proliferation for all cancers. Although BPH is not a causal factor for PCa, any form of chronic inflammation of the prostate can now be considered a risk factor for PCa. (Some nutritional approaches have gone further, declaring inflammation the single “driving force” behind PCa and relying on non-nutritive supplements in an attempt to address this issue. However, this does not restore underlying nutritional imbalances which can redress the inflammation, and adds an extra, mostly unnecessary layer of complexity.)

•Prostate cell membrane elasticity: There is substantial evidence from two sides that disruption in the cell membrane’s elasticity that increases rigidity is a precursor for the development of cancer cells. It is also a factor in insulin resistance. On one side, there is evidence to suggest that rigidity leads to focal adhesions and aberrant growth [cancer] by increasing tension in the cell that is normally generated by elevated Rho factor (GTP-binding protein family).^7,8 On the other, ultrasound units that can read the elasticity of cell membranes are now being shown to be accurately able to detect cancer. The primary dietary reason for alteration to a cell’s elasticity and fluidity is an imbalance between B-Sit (B-Sit) and cholesterol in the cell membrane.^9,10

•Membrane permeability and intracellular environment: There are many cell functions dependent upon normal cell membrane permeability. Of interest here is an alteration in the isoprenoid pathway, the alteration of the balance of calcium and magnesium with excessive entry of Ca²⁺ and the release of calcium stores, a critical factor in cancer metastasis, which can be triggered when this imbalance is accompanied by critically low CoQ10 levels in the immediate intracellular fluids.

The nutritional protocol described here, addresses the above issues but also increases PCa cell apoptosis, reduces proliferation, reduces excess estrogen production, supports/restores normal cell reproduction and differentiation, and reestablishes several mechanisms of homeostasis, especially for copper homeostasis. In other words, the B-Sit/AOX Matrix provides the nutritional substructure missing from today’s food supply for the body’s normal, dynamic anticancer functions, and when balanced properly accomplishes this at physiological levels.