Does testosterone therapy lowers prostate cancer risk?

Discussion:

(too old to reply)

Taka

2016-04-13 05:17:49 UTC

One of the major concerns among doctors and patients with testosterone therapy is its allegedly negative effect on the prostate.[1] However, according to the current ISA, ISSAM, EAU, EAA, ASA clinical guidelines, there is no conclusive evidence that testosterone therapy increases the risk of prostate cancer or benign prostatic hyperplasia.[2]

The guidelines also state that there is also no evidence that testosterone treatment will convert subclinical prostate cancer to clinically detectable prostate cancer.[2]

Despite this, many men are being denied testosterone therapy because of undue fears that it would cause harm to the prostate. Here I summarize the results from a study that investigated incidence of prostate cancer with testosterone therapy for up to 17 years.[3]

KEY POINTS

* In the study population who had been treated with testosterone therapy fro up to 17 years, there were 11 cases of prostate cancer, translating into a proportion of 1.08%.[3]

* This prostate cancer incidence (1.08%) is much lower than that reported in the general population of men who are not on testosterone therapy:

- The Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial on prostate-cancer mortality reported a prostate cancer incidence of 7.35% among 38,345 US men aged 55-74 years who were followed for 7 years.[4]

- The European Randomized Study of Screening for Prostate Cancer (ERSPC) reported a prostate cancer incidence of 9.6% among 72,891 men aged 50-74 years who were followed for 11 years.[5]

* This study shows that testosterone treatment with Nebido® for up to 17 years does not increase the risk of prostate cancer [3], which supports previously presented new insights on the testosterone - prostate relationship, and the saturation limit of androgen-dependent prostate growth.[6, 7]

* Testosterone therapy has no clinically significant adverse impact on prostate cancer incidence among men regardless of administration method.[8]

What is known

Medical students and doctors have been indoctrinated since the 1940s that high testosterone levels supposedly promote the development of prostate cancer, that low testosterone is protective, and that the administration of testosterone to a man with subclinical or existing prostate cancer would speed up its progression.[9] This fear is also the most common reason for doctors' reluctance to prescribe testosterone replacement therapy, even in hypogonadal men [1, 10]. This belief deprives many hypogonadal men of important health benefits, which unnecessarily causes severe harm due to the well documented detrimental health consequences of testosterone deficiency, which I covered in a previous article "Adverse health effects of testosterone deficiency in men".
However, a growing number of studies refute this old testosterone-prostate belief.

What this study adds

In the study by Haider et al, 1,023 hypogonadal men with total testosterone was ≤12.1 nmol/L (350 ng/dL) and symptoms of hypogonadism received testosterone therapy with testosterone undecanoate (1000 mg) (Nebido®) in intervals of 12 weeks following an initial interval of 6 weeks, for up to 17 years. Age at baseline was 41-58 years.

The notable result in this study is that the incidence of prostate cancer among men who had been treated with testosterone therapy using Nebido® for 17 years was lower than the incidence of prostate cancer that is seen in the general population of men who are not treated with testosterone therapy; only 1.08% [3] compared to 7.35 to 9.6%.[4, 5] The results from this study are consistent with findings from another study that investigated prostate outcomes after treatment with testosterone patches for 6 years, which also documented the prostate safety of testosterone therapy.[11]

This 17-year long study with Nebido® clearly demonstrates that testosterone therapy does not increase risk for development of prostate cancer. It also supports previous observations showing no association between endogenous testosterone levels and prostate cancer [12, 13], and meta-analyses which conclude that there is no clinically significant adverse impact on prostate cancer incidence among men on testosterone therapy, regardless of the administration method.[8, 14]

There is also no correlation between testosterone therapy and increased aggressiveness of prostate cancer at diagnosis.[15] A systematic review of testosterone therapy and potential prostate cancer risk among men with and without a history of prostate cancer found that no study demonstrated that testosterone therapy for hypogonadism increased prostate cancer risk or worsened Gleason grade of detected cancer in treated vs. untreated men.[16] Withholding testosterone therapy in hypogonadal men, also in men who have been successfully treated for prostate cancer, is not justified.[17]

Despite the widespread belief that testosterone therapy is contraindicated in hypogonadal men with known or suspected prostate cancer [18], there is no convincing evidence that the normalization of testosterone levels would increase risk for progression of prostate cancer.[6, 7] In view of the current available evidence, clinicians are compelled to consider these new data and abandon the old-school indoctrinated line of thought. [7]

According to Dr. Morgentaler, a leading clinician and researcher specializing in testosterone therapy and prostate safety, the negative view of testosterone with regard to prostate cancer should be recognized for what it is - guilt by association.[19] Dr. Morgentaler also urges clinicians to turn conventional wisdom upside-down by correctly stating: "Finally, after 7 decades of circumstantial evidence pointing us in the wrong direction, perhaps it is time to consider the once unthinkable: a testosterone therapy trial of sufficient size and duration to determine whether normalization of serum testosterone in older men may reduce the risk of prostate cancer, particularly high-risk prostate cancer."[20]

References:

1. Gooren, L.J. and H.M. Behre, Diagnosing and treating testosterone deficiency in different parts of the world: changes between 2006 and 2010. Aging Male, 2012. 15(1): p. 22-7.

2. Wang, C., et al., Investigation, treatment, and monitoring of late-onset hypogonadism in males: ISA, ISSAM, EAU, EAA, and ASA recommendations. Eur Urol, 2009. 55(1): p. 121-30.

3. Haider, A., et al., Incidence of Prostate Cancer in Hypogonadal Men Receiving Testosterone Therapy: Observations from Five Year-median Follow-up of Three Registries. J Urol, 2014.

4. Andriole, G.L., et al., Mortality results from a randomized prostate-cancer screening trial. N Engl J Med, 2009. 360(13): p. 1310-9.

5. Schroder, F.H., et al., Prostate-cancer mortality at 11 years of follow-up. N Engl J Med, 2012. 366(11): p. 981-90.

6. Morgentaler, A. and A.M. Traish, Shifting the paradigm of testosterone and prostate cancer: the saturation model and the limits of androgen-dependent growth. European Urology, 2009. 55(2): p. 310-20.

7. Khera, M., et al., A new era of testosterone and prostate cancer: from physiology to clinical implications. European Urology, 2014. 65(1): p. 115-23.

8. Cui, Y. and Y. Zhang, The effect of androgen-replacement therapy on prostate growth: a systematic review and meta-analysis. European Urology, 2013. 64(5): p. 811-22.

9. Khera, M., et al., A new era of testosterone and prostate cancer: from physiology to clinical implications. Eur Urol, 2014. 65(1): p. 115-23.

10. Atan, A., et al., Serum testosterone level, testosterone replacement treatment, and prostate cancer. Adv Urol, 2013. 2013: p. 275945.

11. Raynaud, J.P., et al., Prostate-specific antigen (PSA) concentrations in hypogonadal men during 6 years of transdermal testosterone treatment. BJU International, 2013. 111(6): p. 880-90.

12. Muller, R.L., et al., Serum testosterone and dihydrotestosterone and prostate cancer risk in the placebo arm of the Reduction by Dutasteride of Prostate Cancer Events trial. European Urology, 2012. 62(5): p. 757-64.

13. Roddam, A.W., et al., Endogenous sex hormones and prostate cancer: a collaborative analysis of 18 prospective studies. Journal of the National Cancer Institute, 2008. 100(3): p. 170-83.

14. Fernandez-Balsells, M.M., et al., Clinical review 1: Adverse effects of testosterone therapy in adult men: a systematic review and meta-analysis. J Clin Endocrinol Metab, 2010. 95(6): p. 2560-75.

15. Kaplan, A.L. and J.C. Hu, Use of testosterone replacement therapy in the United States and its effect on subsequent prostate cancer outcomes. Urology, 2013. 82(2): p. 321-6.

16. Shabsigh, R., et al., Testosterone therapy in hypogonadal men and potential prostate cancer risk: a systematic review. International Journal of Impotence Research, 2009. 21(1): p. 9-23.

17. Rinnab, L., et al., [Testosterone replacement therapy and prostate cancer. The current position 67 years after the Huggins myth]. Urologe. Ausgabe A, 2009. 48(5): p. 516-22.

18. Bhasin, S., et al., Testosterone therapy in men with androgen deficiency syndromes: an Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology and Metabolism, 2010. 95(6): p. 2536-59.

19. Morgentaler, A., Guilt by association: a historical perspective on Huggins, testosterone therapy, and prostate cancer. J Sex Med, 2008. 5(8): p. 1834-40.

20. Morgentaler, A., Turning conventional wisdom upside-down: low serum testosterone and high-risk prostate cancer. Cancer, 2011. 117(17): p. 3885-8.

SOURCE: http://www.agelessforever.net/anti-aging-news-blog/incidence-of-prostate-cancer-after-testosterone-therapy-for-up-to-17-years

Taka

2016-04-13 05:24:14 UTC

Permalink

Post by Taka
One of the major concerns among doctors and patients with testosterone therapy is its allegedly negative effect on the prostate.[1] However, according to the current ISA, ISSAM, EAU, EAA, ASA clinical guidelines, there is no conclusive evidence that testosterone therapy increases the risk of prostate cancer or benign prostatic hyperplasia.[2]
The guidelines also state that there is also no evidence that testosterone treatment will convert subclinical prostate cancer to clinically detectable prostate cancer.[2]
Despite this, many men are being denied testosterone therapy because of undue fears that it would cause harm to the prostate. Here I summarize the results from a study that investigated incidence of prostate cancer with testosterone therapy for up to 17 years.[3]
KEY POINTS
* In the study population who had been treated with testosterone therapy fro up to 17 years, there were 11 cases of prostate cancer, translating into a proportion of 1.08%.[3]
- The Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial on prostate-cancer mortality reported a prostate cancer incidence of 7.35% among 38,345 US men aged 55-74 years who were followed for 7 years.[4]
- The European Randomized Study of Screening for Prostate Cancer (ERSPC) reported a prostate cancer incidence of 9.6% among 72,891 men aged 50-74 years who were followed for 11 years.[5]
* This study shows that testosterone treatment with Nebido® for up to 17 years does not increase the risk of prostate cancer [3], which supports previously presented new insights on the testosterone - prostate relationship, and the saturation limit of androgen-dependent prostate growth.[6, 7]
* Testosterone therapy has no clinically significant adverse impact on prostate cancer incidence among men regardless of administration method.[8]
What is known
Medical students and doctors have been indoctrinated since the 1940s that high testosterone levels supposedly promote the development of prostate cancer, that low testosterone is protective, and that the administration of testosterone to a man with subclinical or existing prostate cancer would speed up its progression.[9] This fear is also the most common reason for doctors' reluctance to prescribe testosterone replacement therapy, even in hypogonadal men [1, 10]. This belief deprives many hypogonadal men of important health benefits, which unnecessarily causes severe harm due to the well documented detrimental health consequences of testosterone deficiency, which I covered in a previous article "Adverse health effects of testosterone deficiency in men".
However, a growing number of studies refute this old testosterone-prostate belief.
What this study adds
In the study by Haider et al, 1,023 hypogonadal men with total testosterone was ≤12.1 nmol/L (350 ng/dL) and symptoms of hypogonadism received testosterone therapy with testosterone undecanoate (1000 mg) (Nebido®) in intervals of 12 weeks following an initial interval of 6 weeks, for up to 17 years. Age at baseline was 41-58 years.
The notable result in this study is that the incidence of prostate cancer among men who had been treated with testosterone therapy using Nebido® for 17 years was lower than the incidence of prostate cancer that is seen in the general population of men who are not treated with testosterone therapy; only 1.08% [3] compared to 7.35 to 9.6%.[4, 5] The results from this study are consistent with findings from another study that investigated prostate outcomes after treatment with testosterone patches for 6 years, which also documented the prostate safety of testosterone therapy.[11]
This 17-year long study with Nebido® clearly demonstrates that testosterone therapy does not increase risk for development of prostate cancer. It also supports previous observations showing no association between endogenous testosterone levels and prostate cancer [12, 13], and meta-analyses which conclude that there is no clinically significant adverse impact on prostate cancer incidence among men on testosterone therapy, regardless of the administration method.[8, 14]
There is also no correlation between testosterone therapy and increased aggressiveness of prostate cancer at diagnosis.[15] A systematic review of testosterone therapy and potential prostate cancer risk among men with and without a history of prostate cancer found that no study demonstrated that testosterone therapy for hypogonadism increased prostate cancer risk or worsened Gleason grade of detected cancer in treated vs. untreated men.[16] Withholding testosterone therapy in hypogonadal men, also in men who have been successfully treated for prostate cancer, is not justified.[17]
Despite the widespread belief that testosterone therapy is contraindicated in hypogonadal men with known or suspected prostate cancer [18], there is no convincing evidence that the normalization of testosterone levels would increase risk for progression of prostate cancer.[6, 7] In view of the current available evidence, clinicians are compelled to consider these new data and abandon the old-school indoctrinated line of thought. [7]
According to Dr. Morgentaler, a leading clinician and researcher specializing in testosterone therapy and prostate safety, the negative view of testosterone with regard to prostate cancer should be recognized for what it is - guilt by association.[19] Dr. Morgentaler also urges clinicians to turn conventional wisdom upside-down by correctly stating: "Finally, after 7 decades of circumstantial evidence pointing us in the wrong direction, perhaps it is time to consider the once unthinkable: a testosterone therapy trial of sufficient size and duration to determine whether normalization of serum testosterone in older men may reduce the risk of prostate cancer, particularly high-risk prostate cancer."[20]
1. Gooren, L.J. and H.M. Behre, Diagnosing and treating testosterone deficiency in different parts of the world: changes between 2006 and 2010. Aging Male, 2012. 15(1): p. 22-7.
2. Wang, C., et al., Investigation, treatment, and monitoring of late-onset hypogonadism in males: ISA, ISSAM, EAU, EAA, and ASA recommendations. Eur Urol, 2009. 55(1): p. 121-30.
3. Haider, A., et al., Incidence of Prostate Cancer in Hypogonadal Men Receiving Testosterone Therapy: Observations from Five Year-median Follow-up of Three Registries. J Urol, 2014.
4. Andriole, G.L., et al., Mortality results from a randomized prostate-cancer screening trial. N Engl J Med, 2009. 360(13): p. 1310-9.
5. Schroder, F.H., et al., Prostate-cancer mortality at 11 years of follow-up. N Engl J Med, 2012. 366(11): p. 981-90.
6. Morgentaler, A. and A.M. Traish, Shifting the paradigm of testosterone and prostate cancer: the saturation model and the limits of androgen-dependent growth. European Urology, 2009. 55(2): p. 310-20.
7. Khera, M., et al., A new era of testosterone and prostate cancer: from physiology to clinical implications. European Urology, 2014. 65(1): p. 115-23.
8. Cui, Y. and Y. Zhang, The effect of androgen-replacement therapy on prostate growth: a systematic review and meta-analysis. European Urology, 2013. 64(5): p. 811-22.
9. Khera, M., et al., A new era of testosterone and prostate cancer: from physiology to clinical implications. Eur Urol, 2014. 65(1): p. 115-23.
10. Atan, A., et al., Serum testosterone level, testosterone replacement treatment, and prostate cancer. Adv Urol, 2013. 2013: p. 275945.
11. Raynaud, J.P., et al., Prostate-specific antigen (PSA) concentrations in hypogonadal men during 6 years of transdermal testosterone treatment. BJU International, 2013. 111(6): p. 880-90.
12. Muller, R.L., et al., Serum testosterone and dihydrotestosterone and prostate cancer risk in the placebo arm of the Reduction by Dutasteride of Prostate Cancer Events trial. European Urology, 2012. 62(5): p. 757-64.
13. Roddam, A.W., et al., Endogenous sex hormones and prostate cancer: a collaborative analysis of 18 prospective studies. Journal of the National Cancer Institute, 2008. 100(3): p. 170-83.
14. Fernandez-Balsells, M.M., et al., Clinical review 1: Adverse effects of testosterone therapy in adult men: a systematic review and meta-analysis. J Clin Endocrinol Metab, 2010. 95(6): p. 2560-75.
15. Kaplan, A.L. and J.C. Hu, Use of testosterone replacement therapy in the United States and its effect on subsequent prostate cancer outcomes. Urology, 2013. 82(2): p. 321-6.
16. Shabsigh, R., et al., Testosterone therapy in hypogonadal men and potential prostate cancer risk: a systematic review. International Journal of Impotence Research, 2009. 21(1): p. 9-23.
17. Rinnab, L., et al., [Testosterone replacement therapy and prostate cancer. The current position 67 years after the Huggins myth]. Urologe. Ausgabe A, 2009. 48(5): p. 516-22.
18. Bhasin, S., et al., Testosterone therapy in men with androgen deficiency syndromes: an Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology and Metabolism, 2010. 95(6): p. 2536-59.
19. Morgentaler, A., Guilt by association: a historical perspective on Huggins, testosterone therapy, and prostate cancer. J Sex Med, 2008. 5(8): p. 1834-40.
20. Morgentaler, A., Turning conventional wisdom upside-down: low serum testosterone and high-risk prostate cancer. Cancer, 2011. 117(17): p. 3885-8.
SOURCE: http://www.agelessforever.net/anti-aging-news-blog/incidence-of-prostate-cancer-after-testosterone-therapy-for-up-to-17-years

Well let me put it this way, Monica, yo comparing the hypogonadal men to start with to normal men. Would the Eunuchs get prostate cancer if yo start feeding them testosterone at the normal age of andropause? Yo better re-do those trials and start injecting the hypogonadal men the testosterone at their normal age of puberty, i.e. as teenagers. Cancer takes decades to develop...

Taka

Taka

2016-04-21 01:53:00 UTC

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The 20-year public health impact and direct cost of testosterone deficiency in U.S. men

Recent evidence strongly suggests that testosterone deficiency is a predisposing factor for various chronic illnesses, including cardiovascular disease, diabetes and osteoporosis.[1-3]Testosterone deficiency has also been implicated as a modifiable disease risk factor for various chronic diseases in otherwise well patients.[4-7]

Cardiovascular disease, diabetes and osteoporosis-related fractures consume a significant portion of the $2.3 trillion in annual U.S. health expenditures. The economic impact of diabetes is estimated at $503 billion, $152 billion for cardiovascular disease, and $6 billion for osteoporosis-related fractures.[8-10]

Thus, the total burden of these diseases is over $660 billion, representing approximately 29% of all U.S. health care expenditures in 2008. Since testosterone deficiency is a potentially modifiable risk factor for these and other medical conditions, it may be responsible for substantial financial and quality-of-life burden on the U.S. health care system.[11]

A study was conducted to specifically quantify the cost burden imposed by consequences of testosterone deficiency ...[12]

STUDY METHOD

Incidence, prevalence, and mortality of cardiovascular disease, diabetes, and osteoporosis-related fractures were collected for men ages 45-74 from six national databases and large cross-sectional studies. Relative risk (RR) rates were determined for these medical conditions in patients with testosterone levels below 300 ng/dL. The prevalence of TD was determined for this cohort of men.

RESULTS

Actual and adjusted (normalized for testosterone deficiency) rates of cardiovascular disease, diabetes, and osteoporosis-related fractures in U.S. men aged 45-74, were calculated.

It was determined that, over a 20-year period, testosterone deficiency is projected to be involved in the development of approximately 1.3 million new cases of cardiovascular disease, 1.1 million new cases of diabetes, and over 600,000 osteoporosis-related fractures.

In year 1, the attributed cost burden of these diseases was approximately $8.4 billion.

Over the entire 20-year period, testosterone deficiency may be directly responsible for approximately $190-$525 billion in inflation-adjusted U.S. health care expenditures.

Testosterone deficiency was implicated in almost 1 million deaths and approximately 3 million cases of cardio-metabolic diseases over a 20-year period.

CONCLUSION

More and more research is emerging showing that testosterone deficiency may be a significant contributor to adverse public health. This study clearly demonstrates that testosterone deficiency imposes a substantial public health burden on the U.S. health care system.[12]

These findings suggest that management of sub-optimal testosterone levels in middle-aged and elderly men is an appropriate consideration for the prevention of several significant chronic diseases, especially cardiovascular disease, diabetes, and osteoporosis-related fractures.

Treatment of sub-optimal testosterone levels would not only realize substantial health care cost savings, but, but would also confer invaluable relief from suffering on a personal level in affected men.[13-16]

SOURCE: http://www.agelessforever.net/anti-aging-news-blog/the-20-year-public-health-impact-and-direct-cost-of-testosterone-deficiency-in-u-s-men

-------------------

Another gem from the clit dick babe Monica Mollica... Well, in the World full of seed oils in our food chain, T will surely suppress and "cool down" the overactive immune system being seemingly helpful as any similar steroid will do. But T will additionally help to rid the body of excessive prostaglandins via the sexual route. Just ride the bitch till the wheels fall off, huh?

Taka

P.S.: Yo should go check Monty how he got rid of his severe osteoporosis, it was not any steroid like T or VitD...

Taka

2016-06-02 08:16:54 UTC

Permalink

Post by Taka
The 20-year public health impact and direct cost of testosterone deficiency in U.S. men
Recent evidence strongly suggests that testosterone deficiency is a predisposing factor for various chronic illnesses, including cardiovascular disease, diabetes and osteoporosis.[1-3]Testosterone deficiency has also been implicated as a modifiable disease risk factor for various chronic diseases in otherwise well patients.[4-7]
Cardiovascular disease, diabetes and osteoporosis-related fractures consume a significant portion of the $2.3 trillion in annual U.S. health expenditures. The economic impact of diabetes is estimated at $503 billion, $152 billion for cardiovascular disease, and $6 billion for osteoporosis-related fractures.[8-10]
Thus, the total burden of these diseases is over $660 billion, representing approximately 29% of all U.S. health care expenditures in 2008. Since testosterone deficiency is a potentially modifiable risk factor for these and other medical conditions, it may be responsible for substantial financial and quality-of-life burden on the U.S. health care system.[11]
A study was conducted to specifically quantify the cost burden imposed by consequences of testosterone deficiency ...[12]
STUDY METHOD
Incidence, prevalence, and mortality of cardiovascular disease, diabetes, and osteoporosis-related fractures were collected for men ages 45-74 from six national databases and large cross-sectional studies. Relative risk (RR) rates were determined for these medical conditions in patients with testosterone levels below 300 ng/dL. The prevalence of TD was determined for this cohort of men.
RESULTS
Actual and adjusted (normalized for testosterone deficiency) rates of cardiovascular disease, diabetes, and osteoporosis-related fractures in U.S. men aged 45-74, were calculated.
It was determined that, over a 20-year period, testosterone deficiency is projected to be involved in the development of approximately 1.3 million new cases of cardiovascular disease, 1.1 million new cases of diabetes, and over 600,000 osteoporosis-related fractures.
In year 1, the attributed cost burden of these diseases was approximately $8.4 billion.
Over the entire 20-year period, testosterone deficiency may be directly responsible for approximately $190-$525 billion in inflation-adjusted U.S. health care expenditures.
Testosterone deficiency was implicated in almost 1 million deaths and approximately 3 million cases of cardio-metabolic diseases over a 20-year period.
CONCLUSION
More and more research is emerging showing that testosterone deficiency may be a significant contributor to adverse public health. This study clearly demonstrates that testosterone deficiency imposes a substantial public health burden on the U.S. health care system.[12]
These findings suggest that management of sub-optimal testosterone levels in middle-aged and elderly men is an appropriate consideration for the prevention of several significant chronic diseases, especially cardiovascular disease, diabetes, and osteoporosis-related fractures.
Treatment of sub-optimal testosterone levels would not only realize substantial health care cost savings, but, but would also confer invaluable relief from suffering on a personal level in affected men.[13-16]
SOURCE: http://www.agelessforever.net/anti-aging-news-blog/the-20-year-public-health-impact-and-direct-cost-of-testosterone-deficiency-in-u-s-men
-------------------

Holly Molly, just tell me Monica, why are not the pre-pubertal kids suffering all these maladies of Testosterone deficiency as the andropaused men??? What is protecting them, high melatonin, hGH or what? Isn't it the gonads doing all the bad things in the absence of testosterone as they are not developed yet before the puberty? Go check some Castratos.

http://io9.gizmodo.com/what-did-it-mean-to-be-a-castrato-1732742399

Taka

Taka

2016-06-02 10:03:13 UTC

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Just for reference:

Testosterone Ranges in Boys

According to the ranges I found it lists anything below 9ng/dl as normal for a 9 year old. Looking at the minimums for the age group above and below 9 year olds it lists the minimums as 2-3 ng/dl so your son may be a little on the low side.

I'm not extremely familiar with testosterone interactions in children, but in adults being on the low side of the range can still present symptoms. The ranges are developed by looking at where 95% of the population lies.

It's based on a false assumption that 95% of the population is perfectly healthy, which isn't always the case. Getting close to the bottom of the range may present symptoms of low T as well, however many doctors won't acknowledge this.
Puberty and Penis Size

Once a boy hits puberty his penis size grows due to increased testosterone. This is mostly governed by the testosterone metabolite DHT (dihydrotestosterone) which causes the majority of androgenic features in males (body hair, lowered voice, acne, etc...)

After puberty, penis size is no longer influenced by DHT, so there is a critical window for growth to take place (11-17 years old). Otherwise you'd see adult men trying to increase their penis size this way, which unfortunately doesn't work. :)

Most doctors won't treat micro penis with testosterone/DHT until the later ages of puberty (13.5-17 years old).
Male Child to Adult - Serum Total Testosterone

Premature (26-28 weeks): 59-125 ng/dl

Premature (31-35 weeks): 37-198 ng/dl

Newborn: 75-400 ng/dl

1-7 months: Levels decrease rapidly the first week to 20-50 ng/dl, and then increase to 60-400 ng/dl between 20-60 days. Boy's testosterone levels then decline to prepubertal range levels of 3-10 ng/dl by seven months.

7-9 years: Less than 9 ng/dl

10-11 years: 2-57 ng/dl

12-13 years: 7-747 ng/dl

14-15 years: 33-585 ng/dl

16-17 years: 185-886 ng/dl

18-39 years: 300-1080 ng/dl

40-59 years: 300-890 ng/dl

60 years and older: 300-720 ng/dl
Androgen Deficiency may Cause Micro Phallus

"Androgen deficiency that develops early in childhood has few consequences, but if it occurs when puberty is expected, secondary sexual development is impaired.

Such patients have poor muscle development, a high-pitched voice, inadequate phallic and testicular growth, a small scrotum, sparse pubic and auxiliary hair, and absent body hair.

They may develop gynecomastia and grow to eunuchoidal body proportions (arm span exceeds height by 5 cm; pubic to floor length exceeds crown to pubic length by > 5 cm) because fusion of the epiphyses is delayed and long bone growth continues."

Reference: Androgen Deficiency during 2nd and 3rd Trimesters may cause Micro Phallus.
Average Penis Growth throughout Puberty

"The penis, measured in the stretched flaccid state, increases from an average length of 6.2 cm in pre-puberty to 12.4 +/- 2.7 cm in white adults and to 14.6 cm in black and 10.6 cm in Asian men"

"Penis growth at puberty generally starts between the ages of 11-14.5 and finishes between the ages 13-17.5"

SOURCE: http://www.menshormonalhealth.com/boys-testosterone-levels.html

SEE ALSO: http://www.healthline.com/health/low-testosterone/testosterone-levels-by-age#Adolescence3

Taka

2016-06-02 01:31:02 UTC

Permalink

Aspirin for prevention of cancer

Accumulating research supports use of aspirin for cancer prevention.[9, 30-35] The evidence for an anti-cancer effect of aspirin is strongest for colorectal cancer, but rapidly accumulating data supports that aspirin also offers protection against development and/or progression/severity (i.e. incidence and mortality) of other common cancers [36], such as breast cancer [37-41] and prostate cancer.[42-45]

Cancer is the second most common cause of premature death worldwide, after heart disease, and its prevalence is increasing because of the aging population, as well as an increasing prevalence of risk factors such as obesity and physical inactivity.[46] Every year, there are 1.5 million new cancer cases and 560 000 cancer deaths in the US.[47, 48] During a lifespan, 41% of the US population will develop cancer and 21% will die from cancer.[47]

In light of the high and rising burden of cancer, aspirin’s potential anti-cancer effects need to be taken into consideration when evaluating the risk-benefit of aspirin use. Daily low dose aspirin (as low as75 mg) reduces deaths due to several common cancers, both during and after the study completion, and benefit increases with duration of aspirin use.[30] Specifically, in long-term studies (4 years or more) investigating the use of aspirin for primary and secondary prevention of cardiovascular disease, when compared to placebo, aspirin reduced 20-year cancer mortality by 20-30%, due mainly to fewer deaths after completion of the trials.[30] This suggest that aspirin has a long-term carryover effect and that it may take a long time to see the full benefits of aspirin on cancer related outcomes.

Amore recent analysis of cancer outcomes included 77,549 patients (40,269 randomly assigned to aspirin and 3, 280 to placebo) from previous studies of aspirin use and prevention of cardiovascular disease.[9] After a minimum of 5 years of follow-up, it was found that aspirin groups had 12% fewer cancer deaths compared with placebo groups. In studies of daily low-dose aspirin in primary prevention (i.e. healthy people) aspirin reduced cancer incidence from 3 years onwards by 25%, in both men and women.[9]

What aspirin dose and form should you take?

Low-dose aspirin is in range of 75 mg/day to 150 mg/day, and is commonly the dose that is used for primary prevention of cardiovascular disease. Notably, the cardiovascular disease risk reduction achieved with low aspirin doses (75 mg/day) are similar to those obtained with higher doses (650 mg/day).[28] This may be because the successive daily administration of only 30 mg of aspirin is sufficient to result in virtually inactivation of platelet COX-1, and thus blockade of platelet thromboxane production (the substance made by platelets that causes blood clotting and constriction of blood vessels).[77] However, there is no study using the 30 mg dose.

For cancer prevention, daily aspirin doses as low as 75 mg have been demonstrated to be protective [30, 33, 60], but a larger dose between 300 to 650 mg per day may confer greater cancer protection.[17, 61-63] People who have a family history of cancer may want to try a minimum daily aspirin dose of 325 mg. However, it should be noted that the protective gastric adaptation to aspirin is delayed and/or less effective when higher aspirin doses are taken (such as those doses used for anti-inflammatory purposes).[12]

When it comes to cancer prevention, duration of use may be more important than the actual dose.[9, 33, 63]. This is not surprising, as for most cancers, the time from carcinogenesis to clinically detected disease is at least 10 years.[63]

What form of aspirin should you take? It is commonly believed that enteric-coated and buffered (effervescent) forms of aspirin are less likely to cause GI bleeding than plain aspirin tablets. A study that investigated this found that the risk for GI bleeding plain, enteric-coated, and buffered aspirin at average daily doses of 325 mg or less were comparable.[64] At doses greater than 325 mg, the relative risk was – counterintuitively - larger for buffered aspirin than plain aspirin (there were insufficient data to evaluate enteric-coated aspirin at this dose level).[64] Another study that compared enteric-coated aspirin and plain aspirin found that the risk of stomach bleeding and/or perforation was the same for both.[10] When comparing buffered aspirin with plain aspirin, buffered aspirin does not cause less gastrointestinal symptoms compared with plain aspirin.[65]

MORE: http://www.agelessforever.net/anti-aging-news-blog/aspirin-can-it-save-you-from-heart-disease-or-cancer

s***@gmail.com

2016-06-04 07:52:09 UTC

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so another myth of male "bad because testosterone" that won't die, this oddly is the feminist line that testosterone is evil, has this bled into popular science.

Taka

2017-08-20 02:06:44 UTC

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Why I do what I do…

I am a former fitness model. Former because I’m now focusing on my professional career as a medical writer and following my mission in life, which is to help educate doctors on the latest medical research findings (I write continuing medical education (CME) material for health care professionals) and empower people to take control of their health. Here I will tell you why...

But I stay in modeling shape all year round even though I don’t pose for the cameras any more for a living. I am constantly being asked in the gym “how do you stay in shape all the time” and “when is your show”… so I felt l wanted share my story in writing because I think it can help many people who are struggling with sticking to regular exercise and healthy eating, as well as those who are undergoing life tradegies…

My motivation

The reason I stay in shape all the time, even after having retired from fitness modeling, is that I am living my passion for health and fitness. I train because I love working out and because I find enjoyment in working out. I never trained “to get ready for a photo/video shoot”. Photographer’s used to love that they could schedule a shoot with me with short notice because they knew “she is always in shape”.

I’m “always in shape” (this is how people express it) because I have an intrinsic motivation for fitness and health promotion. Since childhood I was admiring athletes and wanted to become an athlete. I started to lift at an age of 13 and instantly fell in love with the iron in the gym. This was a profound eye opening experience for me because nobody in my family is an athlete and I wasn’t sure I could become an athlete. A few years later when I noticed how my body responded and how my performance skyrocketed, I excitedly realized that I really do have athletic capability. This further strengthened my intrinsic motivation for working out.

When talking about motivation, if I ask you “how strong is your motivation on a scale from 1 to 5” most people could probably answer easily. But if I ask “what quality is your motivation”, people go “huh”?

I am going to write much more about the mechanics of motivation and motivational quality in upcoming articles. Here I just want to point out that the reason most people are struggling to stick to an exercise program and healthy eating is that their motivation is extrinsic.[1, 2] In other words, their motivation is controlled to different degrees by external factors. When the reason people workout is extrinsinc – for example, they do it to get in shape to please somebody or to get attention etc. – exercising won’t fulfill their basic psychological needs for autonomy, competence and relatedness.[1, 2] This kills persistence and paves the way to unhappiness and unhealthy “dieting” practices, and explains the high drop-out rates in exercise programs.[1, 2]

My father’s fatal heart attack at 48…

My childhood admiration for athletics laid the foundation for my intrinsic motivation for fitness and performance. The foundation for my intrinsic motivation for health is more tragic… three days before my 7th birthday I lost my father in a sudden fatal heart attack. He was only 48… he was living a very unhealthy lifestyle. He never got a second chance. This experience had a profound impact on my development, values and life choices. I ended up with a Master Degree in Nutrition and health promotion, which has given me an invaluable insight into how exercise and nutrition impacts health.

Cardiovascular disease - aka heart disease - is the leading global cause of death; heart disease (including Coronary Heart Disease, Hypertension, and Stroke) remains to be the No. 1 cause of death in the US.[3] Cardiovascular disease accounts for 1 of every 3 deaths in the US; about 2,200 Americans die of cardiovascular disease each day, an average of 1 death every 40 seconds.[4]

My father’s death could have been prevented if he exercised and had healthier food habits. This is why I have a very strong passion for health promotion and am on a mission to help empower and inspire people to take control of their health. I want to be a good role model and live what I preach.

My family history of breast cancer

I have a long family history of breast cancer, which like heart disease, can be prevented.[4] My mother recently underwent bilateral mastectomy and is a breast cancer survivor. One in 8 women in the United States will develop breast cancer in her lifetime [5] and regular exercise is a strong protection against breast cancer development.[4, 6] Another boost to my intrinsic motivation for health promotion!

My near death experience… acute brain surgery

2003 I had an acute brain surgery, which was a near death experience… Apparently I have an anatomical difference in my sinuses that makes me susceptible to ear infections… and brain infections. My diagnosis was cerebral abscess, which is a life threatening condition.[7] I was hospitalized for 2 months…

I must have had an angel watching over me; while still hospitalized I started to study for my final exam in college at the University of Stockholm/Karolinska Institute, Sweden. I graduated 1 year later - at an age of 24 - with a Master Degree and the next year I moved to the US to start PhD level coursework at Baylor University in Texas. The older I am getting, the stronger I’m feeling I have a purpose in life and that there’s a reason I am alive…

Me today

After I retired from modeling I had an interesting experience… I am now enjoying my workouts so much more because I feel I go to the gym because I want to (i.e. I feel completely autonomous), not because I have to (as when I was modeling and under external pressure to look a certain way). I workout seriously because I enjoy it, to prevent cardiovascular disease and breast cancer. And to celebrate being alive! I am grateful for everything I have been though because it strengthened my psyche and changed my outlook and direction in life.

I’m thinking, there’s a clue here… if I can feel this enjoyment from working out and living the health/fitness lifestyle, there must be a way I can help others feel the same... I started to study health psychology and found an impressive line of research on the self-determination theory [1, 2]… I was awestruck how well it explained my own experiences!

The take home message to everybody who is struggling to stick to an exercise program and healthy eating: “change your mind and your body will follow”. Don’t make “get in shape” your primary goal. Exercise for your health and well-being. For your own good. Not for external pressures. Stop looking for the “most effective exercises”; find the exercises you enjoy. Because even the most effective exercises won’t do you any good if you hate them and won’t stick to them. Don't make "get in shape" your end goal; make "get in shape" a means (one of several) to a far more valuable and profound ultimate end goal (such as taking control of your health and increasing your healthspan, be a good role model for others and contribute to make this world a better place).

Set up the game - on your own terms - to win! Start do regular blood work and health checkups and monitor improvements in your lipids (cholesterol and blood fat), glycemic control, blood pressure etc etc. Don’t obsess about the bathroom scale, go get a DEXA body composition analysis and focus on what really matters. For health promotion, you want to lose fat and gain muscle. DEXA will tell you how well you’re doing in that regard. Your body weight in itself in isolation provides no useful information whatsoever, and can very misleading. Women are particularly susceptible to fall for external pressures and become enslaved by their body weight and the number on the bathroom scale.

Also, as I explained in a previous article, sticking to an exercise program will carry over and make you more successful in other areas in life that require self-control and “willpower”, such as healthy eating, stress reduction, brain function, sexual function etc etc.

In upcoming articles I will tell you more about motivational quality, give you validated questionnaires so you can check yourself where you stand and what your “motivational risk factors” are, and help you transform your extrinsic motivations for exercising and healthy eating into a more intrinsic motivational form that is enduring. When that happens, when the focus is on more profound outcomes than merely a superficial body, you will “get in shape” – and importantly – stay in shape, automatically. My body and appearance is a bi-product of me living my passion and walking my talk! Stay tuned…

www.FitnessMindPower.com

References:

1. Deci, E.L. and R.M. Ryan, The "What" and "Why" of Goal Pursuits: Human Needs and the Self-Determination of Behavior. Psychological Inquiry, 2000. 11(4): p. 227-268.

2. Ryan, R.M. and E.L. Deci, Self-Determination Theory Basic Psychological Needs in Motivation, Development, and Wellness. 2017: Guilford Press.

3. Benjamin, E.J., et al., Heart Disease and Stroke Statistics—2017 Update: A Report From the American Heart Association. Circulation, 2017.

4. Howell, A., et al., Risk determination and prevention of breast cancer. Breast Cancer Res, 2014. 16(5): p. 446.

5. DeSantis, C., et al., Breast cancer statistics, 2013. CA: A Cancer Journal for Clinicians, 2014. 64(1): p. 52-62.

6. Friedenreich, C.M. and A.E. Cust, Physical activity and breast cancer risk: impact of timing, type and dose of activity and population subgroup effects. Br J Sports Med, 2008. 42(8): p. 636-47.

7. Muzumdar, D., S. Jhawar, and A. Goel, Brain abscess: an overview. Int J Surg, 2011. 9(2): p. 136-44.

SOURCE: http://www.agelessforever.net/anti-aging-news-blog/why-i-do-what-i-do

Taka

2017-08-20 02:25:02 UTC

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Post by Taka
SOURCE: http://www.agelessforever.net/anti-aging-news-blog/why-i-do-what-i-do

Well, yo got a fabulous physique out there, Moni, but yo aren't gonna fool anyone that this is done without *roids... Or are yo one of the few myostatin mutants on this planet? I-don't-think-so. Given the heart disease and cancer history of yo family and even yo middle ear "infections", this is all likely due to the arachidonic acid overload syndrome. The weight training can keep it at bay for some time, but yo end up badly after the reproductive hormones wear out and yo immune system suddenly realizes all that accumulated damage... Do yo have any kids? Yo still young so there may be some time left to reverse that deadly lifetrack... Do some genetic tests (get yo whole genome sequenced, it's pretty cheap lately) and learn some real life science at RayPeat.com lady! May I also recommend changing the gym and yo mates to
http://www.functionalps.com/blog/

Taka

Taka

2017-08-20 03:10:56 UTC

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Post by Taka

Post by Taka
SOURCE: http://www.agelessforever.net/anti-aging-news-blog/why-i-do-what-i-do

May I recommend these 2 services to unravel yo true genetic potential?

http://www.zymoresearch.com/services/epigenetic-aging-clock

https://www.dantelabs.com/collections/our-tests/products/whole-genome-sequencing

Taka

2017-08-23 00:20:05 UTC

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Post by Taka

Post by Taka
SOURCE: http://www.agelessforever.net/anti-aging-news-blog/why-i-do-what-i-do

May I recommend these 2 services to unravel yo true genetic potential?
http://www.zymoresearch.com/services/epigenetic-aging-clock
https://www.dantelabs.com/collections/our-tests/products/whole-genome-sequencing

If yo continue at yo present course, Molly, yo most likely end up dying of prostate cancer.... Having the susceptibility genes and growing that devil's tissue with *roids... PhD won't help here.

Taka

2017-08-23 04:13:35 UTC

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Post by Taka

Post by Taka
SOURCE: http://www.agelessforever.net/anti-aging-news-blog/why-i-do-what-i-do

May I recommend these 2 services to unravel yo true genetic potential?
http://www.zymoresearch.com/services/epigenetic-aging-clock
https://www.dantelabs.com/collections/our-tests/products/whole-genome-sequencing

If yo continue on the present course, Molly, yo most likely end up dying of prostate cancer.... Having the susceptibility genes and growing that devil's tissue with *roids... PhD won't help here.