Prostate cancer risk linked to testosterone level

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    Prostate cancer risk linked to testosterone level


    Prostate cancer risk linked to testosterone level


    WASHINGTON (Reuters) -- Men over 50 who have higher levels of testosterone have a higher risk of prostate cancer, U.S. researchers reported Sunday.

    The findings may mean that men should be cautious about a new kind of treatment called testosterone replacement therapy, being tested in older men who see a decline in general health and vigor.

    A study of more than 750 men showed those with the highest levels of free testosterone in the blood were the most likely to have prostate cancer.

    "Since testosterone replacement therapy increases the amount of free testosterone in the blood, older men considering or receiving testosterone replacement should be counseled as to the association until data from long-term clinical trials becomes available," said Dr. Kellogg Parsons, a urologist at Johns Hopkins University who led the study, said in a statement.

    The association between free testosterone and prostate cancer risk in older men was not affected by height, weight, percent of body fat or muscle mass, Parsons told a meeting of the American Urological Association in San Francisco.

    A second study presented at the same conference found that obese men may be more likely to see their prostate cancer come back after surgery.

    Another Johns Hopkins team found that obese men are more likely than men with normal weight to have high levels of prostate specific antigen, or PSA.

    PSA is produced by prostate cells and is overproduced when the prostate becomes cancerous.

    "Our results show that moderately and severely obese men were at an increased risk for high PSA levels after surgery and therefore are likely to have prostate cancer recurrence," said Dr. Stephen Freedland, who led the study.

    His team studied 1,106 patients treated at five Veterans Affairs and military hospitals across the country.

    "Our findings add to the burgeoning list of chronic and deadly diseases associated with obesity and underscore the importance of this major public health problem," Freedland said.

    Obesity is also linked with pancreatic, breast and colon cancer, as well as heart disease and diabetes.

    Prostate cancer affects 221,000 American men a year and kills 29,000.

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    I just heard about this......this morning on the radio. Good read, thanks for the info.
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    Damn. That can't be good.
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    It is true that someone already suffering from prostrate cancer does not want his test levels elevated further. However, I have read enough studies on this topic that I do not believe prostrate cancer or even BPH is related to test levels. They are reporting on one study. Others show that there is no correlation between the two.
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    Higher serum levels of testosterone are not a risk factor for developing benign prostate disease:

    [Endocrine environment of benign prostatic hyperplasia--relationships of sex steroid hormone levels with age and the size of the prostate].

    [Article in Japanese]
    Suzuki K, Inaba S, Takeuchi H, Takezawa Y, Fukabori Y, Suzuki T, Imai K, Yamanaka H, Honma S
    Division of Urology, Shakai Hoken Mishima Hospital.
    Nippon Hinyokika Gakkai Zasshi 1992 May;83(5):664-71

    To determine the influence of endocrine factors on benign prostatic hyperplasia (BHP), the levels of three sex steroid hormones i.e., total testosterone (Total-T), free testosterone (Free-T) and estradiol (E2), were measured in serum of healthy 154 men. Their ages ranged from 18 to 91 years old. In 59 men, prostatic size was estimated by digital examination and was subdivided into three groups: smaller than or equal to walnut size, small hen's egg size and equal to or larger than hen's egg size. Firstly, relationships of sex hormone levels with age were studied. There was a slight decrease in Total-T over 60 years old, a significant decrease in Free-T, and no change in E2 with age. Thus, E2/Total-T and E2/Free-T ratio increased significantly after middle-age. Secondly, relationships of hormone levels with prostatic size were studied. In the larger prostate group, a significantly lower level of Total-T and significantly higher level of E2 were detected. But there was no difference in Free-T. Thus, the prostatic size was correlated positively with E2 level, E2/Total-T and E2/Free-T ratio. These suggest that the endocrine environment tended to be estrogens-dominant with age, in particular, after middle-age, and that patients with large prostates have more estrogens-dominant environments. We conclude that estrogens are key hormones for the induction and the development of BPH.
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    Normal variation in circulating androgen levels does not influence development of BPH, but that variation in estrogen levels might be important.

    A prospective study of plasma hormone levels, nonhormonal factors, and development of benign prostatic hyperplasia.

    Gann PH, Hennekens CH, Longcope C, Verhoek-Oftedahl W, Grodstein F, Stampfer MJ
    Division of Preventive Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
    Prostate 1995 Jan;26(1):40-9

    We assessed the relation of plasma hormone levels and nonhormonal factors with subsequent occurrence of surgical treatment for benign prostatic hyperplasia (BPH) among participants in the Physicians' Health Study. Frozen plasma samples, collected at the study onset, were available for 320 men who developed surgically treated BPH up to 9 years later and for 320 age-matched controls. Plasma testosterone (T), dihydrotestosterone (DHT), androstenedione, estradiol (E2), and estrone (E1) were measured for each case-control pair. In unadjusted analyses, none of the hormones or hormone ratios were associated with BPH; for example, for T and E2 the odds ratios (OR) comparing the highest quintile (Q5) with the lowest (Q1) were 0.74 (95% CI = 0.42, 1.30) and 1.07 (95% CI = 0.51, 2.22), respectively. However, in multivariate analyses controlling diastolic blood pressure, exercise, alcohol, E1, and DHT:T ratio, we observed a strong trend for increasing risk across quintiles for E2 (Q5 vs. Q1 OR = 3.56, P trend = 0.009), and a weak inverse trend for E1 (Q5 vs Q1 OR = 0.51, P trend = 0.07). The excess risk associated with E2 was confined to men with relatively low androgen levels. Three nonhormonal factors previously suspected as risk factors were independently associated with surgical BPH in these data. The OR for a 1-mm Hg difference in diastolic blood pressure was 1.04 (95% CI = 1.01, 1.07). Alcohol use and infrequent exercise were inversely associated with risk of BPH surgery; however, risk estimates were not consistent across categories of exercise and alcohol frequency. Our results indicate that normal variation in circulating androgen levels does not influence development of BPH, but that variation in estrogen levels might be important.
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    Estradiol, not testosterone, is a likely culprit in prostate problems:

    Estradiol causes the rapid accumulation of cAMP in human prostate.

    Nakhla AM; Khan MS; Romas NP; Rosner W
    Department of Medicine, St. Luke's/Roosevelt Hospital Center, New York, NY 10019.
    Proc Natl Acad Sci U S A 1994 Jun 7;91(12):5402-5

    Androgens are widely acknowledged to be central to the pathogenesis of benign prostatic hypertrophy (BPH). However, BPH increases in prevalence as men age, at precisely the stage of life when plasma androgens are decreasing. The decrease in total plasma androgens is amplified by an age-related increase in plasma sex hormone-binding globulin (SHBG) that results in a relatively greater decrease in free androgens than in total androgens. In addition, estrogens have long been suspected to be important in BPH, but a direct effect on the human prostate has never been demonstrated. We present data that are consistent with a role for estradiol, and for a decrease in androgens and an increase in SHBG, in the pathogenesis of BPH. We show that estradiol, but not dihydrotestosterone, acts in concert with SHBG to produce an 8-fold increase in intracellular cAMP in human BPH tissue. This increase is not blocked by an antiestrogen and is not provoked by an estrogen (diethylstilbestrol) that does not bind to SHBG, thus excluding the classic estrogen receptor as being operative in these events. Conversely, dihydrotestosterone, which blocks the binding of estradiol to SHBG, completely negates the effect of estradiol. Finally, we demonstrate that the SHBG-steroid-responsive second-messenger system is primarily localized to the prostatic stromal cells and not to the prostatic epithelial cells. Thus, we have shown a cell-specific, powerful, nontranscriptional effect of estradiol on the human prostate.
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    I have about 20 articles like this one.

    Endocrine therapy for benign prostatic hyperplasia in the 90's.

    Ekman P
    Department of Urology, Karolinska Hospital, Stockholm, Sweden.
    J Urol (Paris) 1995;101(1):22-5

    Endocrine therapy by means of castration for benign prostatic hyperplasia was introduced already in the middle of the 19th century. The technique was never popularized and was abandoned following the introduction of safe surgical techniques. In the second half of this century, small series of various endocrine treatments have been reported, mainly using progestational agents. The hormone dependency of the prostate is unique, since testosterone itself is not very active on the prostate cells but has to be converted to 5 alpha-dihydrotestosterone, which is almost ten times as effective an androgen in the prostate cell. By blocking this conversion, highly specific antiandrogenic effect will be obtained in the prostate but not in other organs of the body. The first 5 alpha-reductase inhibitor, finasteride, has proven effective in reducing prostate DHT. In large clinical trials, it has shown to reduce prostate size, improve urinary flow and reduce symptom score, statistically significantly better than placebo. The effect is sustained over at least 3 years. In a double-blind, randomized, placebo-controlled study over 2 years, patients were similarly improved in the finasteride group, whereas they deteriorated in the placebo group. This indicates that finasteride is able to halt the progression of the natural course of benign prostatic hyperplasia. Benign prostatic hyperplasia, generally believed to be a stromal disease, is potentially dependent on estrogens for its development. By blocking aromatization of testosterone to estrogen in the prostate cells, a hypothetical beneficial effect on the disease process should be gained. Results from phase II-studies have been promising. However, in placebo-controlled studies, aromatase inhibitors did not perform better than placebo.
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    Are you getting the idea I think the science in the original article, linking test to prostate problems is crap? Here is another study. I will quit for now, but there are many scientific studies like these available.

    Aromatase in hyperplasia and carcinoma of the human prostate.

    Hiramatsu M, Maehara I, Ozaki M, Harada N, Orikasa S, Sasano H
    Department of Pathology, Tohoku University School of Medicine, Sendai, Japan.
    Prostate 1997 May 1;31(2):118-24

    The expression and activity of aromatase was evaluated in 19 individuals with benign prostatic hyperplasia (BPH) and 26 prostatic carcinoma (PC) patients to elucidate the possible biological significance of in situ estrogen production in the development of human prostatic disorders. Marked aromatase immunoreactivity was observed in proliferative stromal cells, especially those around hyperplastic glands in 18 (95%) BPH patients and in stromal cells surrounding carcinomatous glands in 18 (69%) PC patient specimens. The percentage of aromatase-positive stromal cells did not differ between BPH and PC. No significant correlation was apparent between the percentage of aromatase-positive cells and either the extent of carcinoma differentiation or surgical stage in the PC patients. Quantitation of aromatase activity by the [3H] water assay yielded values of 27.23 +/- 6.87 and 26.52 +/- 9.12 fmol/hr/mg of protein for BPH (nine patients) and PC (nine patients), respectively. Reverse transcriptase and polymerase chain reaction analysis revealed that the mean aromatase mRNA content was 1.671 +/- 0.82 and 1.11 +/- 0.51 attomole/ng of total RNA (tRNA) for BPH (seven patients) and PC (four patients), respectively. There were no significant differences in aromatase activity or aromatase mRNA concentration between PC and BPH. The alternative use of multiple exons 1 of the aromatase gene was also examined. Predominant aromatase gene transcripts contained exon 1b in three of four of PC specimens and two of three BPH specimens examined, in contrast to the use of exon 1d previously described in normal prostate. Unlike breast and endometrium, therefore, aromatase expression in human prostate was not associated with malignancy. However, overexpression of aromatase, possibly attributable to abnormal gene regulation, may result in estrogen production in situ and play a role in the induction or development of human prostatic disorders.
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    Now that is some research cougar. Good work


    Enzo
  11. PC1
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    Quote Originally Posted by enzo
    Now that is some research cougar. Good work


    Enzo
    Indeed! Great job, thanks for sharing.
  

  
 

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