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Author Topic: Ejackulation and prostate cancer  (Read 4484 times)

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Offline veritas

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Ejackulation and prostate cancer
« on: May 15, 2009, 05:03:23 AM »
 Gentlemen protect yourself against prostate cancer:

 
     HIV Articles - NATAP.org 
 
Back  
    
Ejaculation Frequency and Subsequent Risk of Prostate Cancer - "high ejaculation frequency was related to decreased risk of total prostate cancer."
 
 
  
  Michael F. Leitzmann, MD; Elizabeth A. Platz, ScD; Meir J. Stampfer, MD; Walter C. Willett, MD; Edward Giovannucci, MD
 
JAMA. 2004;291:1578-1586.
 
Sexual activity has been hypothesized to play a role in the development of prostate cancer, but epidemiological data are virtually limited to case-control studies, which may be prone to bias because recall among individuals with prostate cancer could be distorted as a consequence of prostate malignancy or ongoing therapy.
 
"In this prospective cohort study among predominantly white men, higher ejaculation frequency was not related to increased risk of prostate cancer. Our results suggest that high ejaculation frequency possibly may be associated with a lower risk of total and organ-confined prostate cancer. These associations were not explained by potential risk factors for prostate cancer, such as age, family history of prostate cancer, history of syphilis or gonorrhea, smoking, and diet. Although we cannot exclude a possibly greater risk of advanced prostate cancer with higher recent ejaculation frequency, we did not observe a higher risk of advanced prostate cancer for high ejaculation frequency earlier in life."
 
"sexual activity is a complex physiological function, which may relate to prostate cancer risk through several nonandrogenic pathways. For example, frequency of ejaculations may modulate prostate carcinogenesis by altering the composition of prostatic fluid. Frequent ejaculations may decrease the intraprostatic concentration of xenobiotic compounds and chemical carcinogens, which readily accumulate in prostatic fluid.44-45 Frequent ejaculations may also reduce the development of intraluminal prostatic crystalloids,46 which have been associated with prostate cancer in some,47-48 but not all pathology studies.49 Because seminal plasma locally reduces host responsiveness50-52 (possibly by factors produced by the prostate gland53), retained prostatic fluid may diminish intraprostatic immune surveillance against tumor cells.
 
A more speculative possibility linking increased ejaculation frequency with decreased prostate cancer risk is that ejaculation is accompanied by a release of psychological tension during the emission phase,54 which may lower central sympathetic nervous activity when repeated frequently. Prostate epithelial cell division is stimulated by the release of growth factors from adjacent stromal cells that are heavily innervated with 1 adrenergic receptors.55-56
 
In summary, our results among predominantly white men suggest that ejaculation frequency is not related to increased risk of prostate cancer. High ejaculation frequency may possibly be associated with a lower risk of total and organ-confined prostate cancer. It is unlikely that reverse causation, differences in prostate cancer screening behavior, or confounding are entirely responsible for the observed results. Mechanisms other than the link between androgenicity and ejaculation frequency should be evaluated as potential etiological factors underlying the inverse association between ejaculation frequency and prostate cancer."
 
Context- Sexual activity has been hypothesized to play a role in the development of prostate cancer, but epidemiological data are virtually limited to case-control studies, which may be prone to bias because recall among individuals with prostate cancer could be distorted as a consequence of prostate malignancy or ongoing therapy.
 
Objective- To examine the association between ejaculation frequency, which includes sexual intercourse, nocturnal emission, and masturbation and risk of prostate cancer.
 
Design, Setting, and Participants- Prospective study using follow-up data from the Health Professionals Follow-up Study (February 1, 1992, through January 31, 2000) of 29 342 US men aged 46 to 81 years, who provided information on history of ejaculation frequency on a self-administered questionnaire in 1992 and responded to follow-up questionnaires every 2 years to 2000. Ejaculation frequency was assessed by asking participants to report the average number of ejaculations they had per month during the ages of 20 to 29 years, 40 to 49 years, and during the past year (1991).
 
Main Outcome Measure- Incidence of total prostate cancer.
 
Results - During 222 426 person-years of follow-up, there were 1449 new cases of total prostate cancer, 953 organ-confined cases, and 147 advanced cases of prostate cancer. Most categories of ejaculation frequency were unrelated to risk of prostate cancer. However, high ejaculation frequency was related to decreased risk of total prostate cancer. The multivariate relative risks for men reporting 21 or more ejaculations per month compared with men reporting 4 to 7 ejaculations per month at ages 20 to 29 years were 0.89 (95% confidence interval [CI], 0.73-1.10); ages 40 to 49 years, 0.68 (95% CI, 0.53-0.86); previous year, 0.49 (95% CI, 0.27-0.88); and averaged across a lifetime, 0.67 (95% CI, 0.51-0.89). Similar associations were observed for organ-confined prostate cancer. Ejaculation frequency was not statistically significantly associated with risk of advanced prostate cancer.
 
Conclusions Our results suggest that ejaculation frequency is not related to increased risk of prostate cancer.
 
Author Affiliations: Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Md (Dr Leitzmann); Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Md (Dr Platz); Departments of Epidemiology and Nutrition, Harvard School of Public Health, Boston, Mass (Drs Stampfer, Willett, and Giovannucci); and Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, Mass (Drs Stampfer, Willett, and Giovannucci).
 
INTRODUCTION
 
Sexual activity is hypothesized to affect prostate carcinogenesis through numerous etiologic pathways. One of the most commonly postulated mechanisms implicates increased sexual activity as an indicator of higher androgenic activity and thus a marker for a high-risk population.1 Another mechanism proposes that sexual activity represents a marker for opportunity for exposure to infectious agents, although no sexually transmitted infection has been consistently implicated in prostate cancer development.2
 
An alternative hypothesis suggests that a reduced ejaculatory output in otherwise normal men is an etiologic risk factor for prostate cancer. That proposition is based on the theory that infrequent ejaculation increases the risk of prostate cancer because of retained carcinogenic secretions in the prostatic acini.3 A further hypothesis implicates repression of sexuality as a risk factor for prostate cancer and is derived from reports of greater sexual drive coupled with deprived sexual activity4 and greater interest in more sexual intercourse than experienced5 among prostate cancer cases compared with controls.
 
In the United States, 38% of married persons aged 60 years or older reportedly engage in sexual activity between 1 and 4 times per month, and 14% indicate being sexually active at least 5 times per month.6 Although the libido declines with age, sexual activity is common among 70-, 80-, and even 90-year-old men.7 Given that sexual activity is common, including in older men,6-7 and that prostate cancer risk is high,8 any association between these factors would have clinical and public health relevance. A recent meta-analysis9 reported an increased risk of prostate cancer with greater sexual activity (odds ratio, 1.2; 95% confidence interval [CI], 1.1-1.3 for an increase in sexual activity of 3 times per week).
 
Epidemiological data on sexual activity and prostate cancer are almost entirely limited to case-control studies,2, 9-10 which may be particularly prone to methodological bias because information on prediagnosis sexual activity is collected after the diagnosis of cancer. Sexual function may diminish after the diagnosis of prostate cancer and its treatment,11 and recall of past levels of sexual activity among individuals with prostate cancer could be distorted as a consequence of prostate malignancy or ongoing therapy.
 
Prospective data on self-reported sexual activity and prostate cancer are restricted to 2 investigations. These studies12-13 considered age at first marriage, marital status, and number of children as measures of sexual activity and found no association between these factors and prostate cancer. Thus, the relationship between sexual activity and risk of prostate cancer is not clear.
 
To help resolve this issue, we prospectively examined the association between ejaculation frequency and risk of prostate cancer in the Health Professionals Follow-up Study, a large cohort of middle-aged US men. We focused on ejaculation frequency, capturing sexual intercourse, nocturnal emission, and masturbation. Thus, our exposure definition encompasses a wide range of variability in exposure to sexual activity. In addition, we reasoned that by examining ejaculation frequency, the effects of sexual function per se would be more readily distinguishable from effects related to exposure to sexually transmitted agents, which we do not consider in this article.
 
COMMENT
 
In this prospective cohort study among predominantly white men, higher ejaculation frequency was not related to increased risk of prostate cancer. Our results suggest that high ejaculation frequency possibly may be associated with a lower risk of total and organ-confined prostate cancer. These associations were not explained by potential risk factors for prostate cancer, such as age, family history of prostate cancer, history of syphilis or gonorrhea, smoking, and diet. Although we cannot exclude a possibly greater risk of advanced prostate cancer with higher recent ejaculation frequency, we did not observe a higher risk of advanced prostate cancer for high ejaculation frequency earlier in life.
 
Although each of several analytic approaches indicated that high ejaculation frequency was related to decreased risk of total and organ-confined prostate cancer, there are several plausible alternative explanations for our results. We were concerned about the possibility that the observed inverse relationships were due to avoidance of ejaculation among men with early symptoms related to prostate cancer. However, diminished ejaculation frequency as a preclinical consequence of prostate cancer would be expected to be more pronounced among men with advanced prostate cancer than among men with organ-confined prostate cancer, a circumstance that was not supported by our data. In addition, our findings were essentially unaltered when we excluded cases diagnosed in the early years of follow-up. Hence, our results suggest that reverse causation may have accounted for very little, if any of the observed inverse association between high ejaculation frequency and total and organ-confined prostate cancer risk.
 
A further potential explanation for our results is that men with high ejaculation frequency may wish to preserve their sexual function and, thus, undergo less screening tests for prostate cancer, leading to less diagnosis of organ-confined prostate cancer among these men. The fact that men in the highest category of ejaculation frequency underwent slightly fewer PSA screening tests and less prostate biopsies than most men with lower ejaculation frequencies suggests the possibility of modest detection bias. In contrast to this possible explanation, the inverse relationship with total and organ-confined prostate cancer persisted when the analysis was restricted to men with the opportunity to have prostate cancer detected by PSA. Thus, decreased prostate cancer detection among men with greater ejaculation frequency is unlikely to entirely account for our results.
 
Because factors such as diet, smoking, physical activity, and the quality of personal relationships are strong determinants of sexual function,15-18 a further potential concern was the possibility that the apparent beneficial effect of greater ejaculation frequency on risk for total and organ-confined prostate cancer was due to the existence of a healthy lifestyle related both to ejaculation frequency and to prostate cancer. We observed similar results before and after controlling for a broad range of lifestyle and dietary factors potentially related to prostate cancer risk. In addition, the fact that the age-adjusted and multivariate-adjusted RRs were almost identical makes it unlikely that an unconsidered factor that correlates with these lifestyle and dietary factors could produce such strong confounding. Thus, our results are probably not due to confounding by purported lifestyle or dietary risk factors for prostate cancer.
 
Our results are not likely to be explained by differential measurement error in our assessment of ejaculation frequency between cases and noncases. Notwithstanding, self-reported ejaculation frequency may have contained some inaccuracy because of its sensitive nature and the need for individuals to recall ejaculation frequency in the distant past. It is possible that the oldest men in our cohort (men aged 81 years in 1992) may not have accurately recalled their average monthly ejaculation frequency from ages 20 to 29 years. Moreover, recall of past levels of ejaculation frequency may have been more accurate among men who had the highest ejaculation frequencies than among those with lower ejaculation frequencies. Reported ejaculation frequency rates among men in our study are largely consistent with survey data on sexual activity among US adults.6, 19 Furthermore, our mailed questionnaire on ejaculation frequency was identifiable only by study identification number and not by name, which may have resulted in a more accurate report than in-person interviews. Because these data were collected prior to the occurrence of prostate cancer, the accuracy of reported ejaculation frequency should not differ between men with and without subsequent prostate cancer. Thus, error in the measurement of ejaculation frequency would tend to dampen the results, but would not produce an inverse association. In addition, reporting of other lifestyle factors in this cohort of health professionals has been found to be reasonably accurate.20-21
 
We noted a suggestive decrease in risk of total and organ-confined prostate cancer among men in the lowest category of ejaculation frequency across a lifetime. Whether that finding was due to lower androgenicity among these men remains unknown. The apparent decrease in risk of total and organ-confined prostate cancer among men with a low ejaculation frequency was not due to low prevalence of sexually transmitted infections among these men because adjustment for history of syphilis or gonorrhea did not alter the results.
 
We only evaluated ejaculation frequency during adulthood, but not during adolescence. The peripubertal period may be of etiologic significance with respect to prostate carcinogenesis because prostate epithelial cell differentiation occurs at this critical period.22 If ejaculation frequency during puberty was most important for prostate carcinogenesis, measuring adult ejaculation frequency would fail to capture the relevant period of exposure. However, our findings suggest that ejaculation frequency during mid and late adulthood rather than in early adulthood are etiologically relevant periods for influencing prostate tumors. Because the inverse relation was observed for organ-confined cases but not advanced cases, sexual activity may be hypothesized only to affect slow-growing, early stage prostate cancers. Our results are generalizable to white US men aged 46 years or older.
 
Previous investigations on reported ejaculation frequencies or sexual intercourse and prostate cancer are limited to studies of retrospective design and results are mixed. Nine studies observed a statistically significant1, 23-27 or nonsignificant28-30 positive association; 3 studies27, 31-32 reported no association; 7 studies found a statistically significant4-5,10, 33 or nonsignificant34-36 inverse relationship; and 1 study37 found a U-shaped relationship.
 
Nine4, 24-25,27, 30-32,35-36 of the aforementioned studies found little or no variation in prostate cancer risk according to sexual activity during different ages. However, 1 study35 observed a nonsignificant inverse association between sexual activity before the age of 30 years and prostate cancer, and no relationship with sexual activity in later life. In contrast, 2 other studies38-39 reported a positive association between frequency of sexual intercourse before ages 50 to 60 years and prostate cancer and an inverse relationship for frequency of sexual intercourse after age 60 years. A recent meta-analysis9 of these studies1, 4-5,23-39 reported RRs for sexual activity at 3 times per week of 1.14 (95% CI, 0.98-1.31) during the third decade of life, 1.24 (95% CI, 1.05-1.46) during the fifth decade, and 0.68 (95% CI, 0.51-0.91) during the seventh decade. That meta-analysis9 noted the somewhat inconsistent association between frequency of sexual activity and risk of prostate cancer in previous studies.
 
Several features distinguish our analysis from previous reports on sexual activity and prostate cancer. First, the prospective study design precluded bias attributable to differential recall of sexual activity by men with and without prostate cancer. Second, we focused on ejaculation frequency rather than on frequency of sexual intercourse, which enhanced exposure variability and allowed us to explore the physiological effects of sexual function per se. Third, our analysis included nearly 50% more cases than the number of cases included in any of the previous studies reporting on sexual activity and prostate cancer. Fourth, our study had data on PSA tests, which allowed us to address the possibility of detection bias. Finally, because we controlled for a wide range of medical, lifestyle, and dietary factors, potential confounding by these factors was likely minimized.
 


 
 
 
 

Offline georgep77

  • Member
  • Posts: 148
Re: Ejackulation and prostate cancer
« Reply #1 on: June 19, 2009, 05:04:57 PM »
Gentlemen protect yourself against prostate cancer:

Get rid of prostate cancer and have fun !!!      ;D
Come on Sangamo,  Geovax,  Bionor immuno, ...Make us happy !!!
+ 2008

Offline sharkdiver

  • Member
  • Posts: 1,351
Re: Ejackulation and prostate cancer
« Reply #2 on: June 25, 2009, 10:09:16 PM »
looking for the connection to HIV.....


still looking.....



hmmm yep still looking

Offline veritas

  • Member
  • Posts: 1,410
Re: Ejackulation and prostate cancer
« Reply #3 on: June 26, 2009, 05:01:05 AM »

It seems your looking in the wrong places:


http://www.aidsmeds.com/articles/hiv_aids_prostate_1667_14422.shtml

Pray you don't get it.

v

Offline sharkdiver

  • Member
  • Posts: 1,351
Re: Ejackulation and prostate cancer
« Reply #4 on: June 26, 2009, 09:12:38 AM »
See, now there is a connection.

Offline veritas

  • Member
  • Posts: 1,410
Re: Ejackulation and prostate cancer
« Reply #5 on: June 27, 2009, 04:36:45 AM »


ROTFLMAO!!!!!

 


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