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My physician told me to absolutely stay away from soy products of any type. There is plenty of evidence that links soy to higher levels of estrogen. In addition, estrogen may not be our friend when it comes to our prostate.
There are so many sources of protein in this world... soy would be my last pick:
Effects of soy in men
A major concern of men is the possible effects of soy on the male endocrine (hormonal) system. While there have been few studies addressing the effects of phytoestrogen in males, what conclusions have been drawn are negative. 3a, 17B- androstanediol glucuronide and androstanediol glucuronide are DHT metabolites and are essential for male secondary sex characteristics as well as the anabolism of skeletal muscle. Obviously decreases in these hormones mean less lean mass, more stored body fat, and a possible retardation of male secondary sex characteristics.
“In males, levels of 17B-estradiol and testosterone were not affected, but levels of 3a, 17B- androstanediol glucuronide (a metabolite of dihydrotestosterone) and dehydroepiandrosterone sulfate were decreased by 13% and 14%, respectively, after 2-4 weeks of daily soya ingestion.” (8)
Androgens vs estrogens in prostate cancer
GP Risbridger
Monash University, Melbourne, Australia.
--------------------------------------------------------------------------------
Androgens and increasing age are established risk factors associated with prostate cancer, Paradoxically, testosterone levels gradually decline with increasing age as the incidence of prostate cancer (PCa) rises in older men. Estrogens have been implicated in PCa as estrogen levels in older men remain relatively unchanged resulting in a decline in the ratio of androgens:estrogens with age. Thus the hormonal regulation of prostate cancer is not limited to a role for androgens and we propose that androgens in combination with estrogens are required for PCa. Our hypothesis is based on the following evidence. The estrogen deficient, ArKO, (aromatase knock out) mice have a life long elevation of androgens; the prostate is enlarged and leads to the development of BPH, but not PCa. Estrogens have systemic actions in the male that include the suppression of testicular androgen synthesis leading to prostatic atrophy. As well, estrogens have local, direct actions on the prostate gland. In many mammalian species, including mice and men, estrogens induce proliferative change to the epithelium leading to squamous metaplasia, an effect that is mediated via the ERalpha subtype. Prolonged exposure to high levels of estrogen initiate an inflammatory response probably mediated via the ERbeta subtype. In the absence of androgens, estrogens do not induce malignancy. We conclude that neither testosterone nor estrogen alone is sufficient to induce malignancy, but a combination of both is required for the development of PCa.
All men will develop prostate cancer if they live long enough. Several recent studies show that a man's susceptibility to prostate cancer may be influenced more by his exposure to the female hormone, estrogen, than to the male hormone, testosterone.
A derivative of the male hormone, testosterone, stimulates the prostate to grow, but a recent article in the medical journal, Prostate, suggests that it does this only after the prostate has been sensitized by the female hormone, estrogen. (1) Men with the highest blood levels of estrogen are the ones most likely to get prostate cancer (2). Blood levels of the male hormones, testosterone and dihydrotestosterone, produced by a man's body are not associated with susceptibility to suffer prostate cancer (2). Prostate cancer is not associated with frequency of sexual activity and there is no evidence that it is caused by taking male hormones or an infection. Athletes who take large doses of male hormones have not been shown to be at increased risk for prostate cancer.
A high fat, low-vegetable diet is associated with an increased risk for prostate cancer, and a low-fat diet that is rich in fruits, vegetables, whole grains and beans is associated with protection against this cancer (3). A study in the British journal, Lancet, shows plant sterols help to shrink an enlarged prostate at least as much as Proscar does, and when given to humans, plant sterols block some of the effects of the female hormone, estrogen.(4) So, eat a low-fat diet that contains fruits, vegetables, whole grains and beans that are rich sources of sterols and other phytochemicals to block human estrogens and oxidant reactions in the body.
Again, there are lots of conflicting studies out there, and I'm not here to preach, but I'm leaning towards staying away from estrogen and getting a CRP test as opposed to watching my cholesterol.
There are so many sources of protein in this world... soy would be my last pick:
Effects of soy in men
A major concern of men is the possible effects of soy on the male endocrine (hormonal) system. While there have been few studies addressing the effects of phytoestrogen in males, what conclusions have been drawn are negative. 3a, 17B- androstanediol glucuronide and androstanediol glucuronide are DHT metabolites and are essential for male secondary sex characteristics as well as the anabolism of skeletal muscle. Obviously decreases in these hormones mean less lean mass, more stored body fat, and a possible retardation of male secondary sex characteristics.
“In males, levels of 17B-estradiol and testosterone were not affected, but levels of 3a, 17B- androstanediol glucuronide (a metabolite of dihydrotestosterone) and dehydroepiandrosterone sulfate were decreased by 13% and 14%, respectively, after 2-4 weeks of daily soya ingestion.” (8)
Androgens vs estrogens in prostate cancer
GP Risbridger
Monash University, Melbourne, Australia.
--------------------------------------------------------------------------------
Androgens and increasing age are established risk factors associated with prostate cancer, Paradoxically, testosterone levels gradually decline with increasing age as the incidence of prostate cancer (PCa) rises in older men. Estrogens have been implicated in PCa as estrogen levels in older men remain relatively unchanged resulting in a decline in the ratio of androgens:estrogens with age. Thus the hormonal regulation of prostate cancer is not limited to a role for androgens and we propose that androgens in combination with estrogens are required for PCa. Our hypothesis is based on the following evidence. The estrogen deficient, ArKO, (aromatase knock out) mice have a life long elevation of androgens; the prostate is enlarged and leads to the development of BPH, but not PCa. Estrogens have systemic actions in the male that include the suppression of testicular androgen synthesis leading to prostatic atrophy. As well, estrogens have local, direct actions on the prostate gland. In many mammalian species, including mice and men, estrogens induce proliferative change to the epithelium leading to squamous metaplasia, an effect that is mediated via the ERalpha subtype. Prolonged exposure to high levels of estrogen initiate an inflammatory response probably mediated via the ERbeta subtype. In the absence of androgens, estrogens do not induce malignancy. We conclude that neither testosterone nor estrogen alone is sufficient to induce malignancy, but a combination of both is required for the development of PCa.
All men will develop prostate cancer if they live long enough. Several recent studies show that a man's susceptibility to prostate cancer may be influenced more by his exposure to the female hormone, estrogen, than to the male hormone, testosterone.
A derivative of the male hormone, testosterone, stimulates the prostate to grow, but a recent article in the medical journal, Prostate, suggests that it does this only after the prostate has been sensitized by the female hormone, estrogen. (1) Men with the highest blood levels of estrogen are the ones most likely to get prostate cancer (2). Blood levels of the male hormones, testosterone and dihydrotestosterone, produced by a man's body are not associated with susceptibility to suffer prostate cancer (2). Prostate cancer is not associated with frequency of sexual activity and there is no evidence that it is caused by taking male hormones or an infection. Athletes who take large doses of male hormones have not been shown to be at increased risk for prostate cancer.
A high fat, low-vegetable diet is associated with an increased risk for prostate cancer, and a low-fat diet that is rich in fruits, vegetables, whole grains and beans is associated with protection against this cancer (3). A study in the British journal, Lancet, shows plant sterols help to shrink an enlarged prostate at least as much as Proscar does, and when given to humans, plant sterols block some of the effects of the female hormone, estrogen.(4) So, eat a low-fat diet that contains fruits, vegetables, whole grains and beans that are rich sources of sterols and other phytochemicals to block human estrogens and oxidant reactions in the body.
Again, there are lots of conflicting studies out there, and I'm not here to preach, but I'm leaning towards staying away from estrogen and getting a CRP test as opposed to watching my cholesterol.
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