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Topics - Cataceous

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A tip of the hat to "Marco N Cognito" over at ExcelMale for posting about this.

Tailor Made Compounding now offers enclomiphene and will ship it to most states. I called to confirm this and it appears legitimate, with FDA inspections, etc. If you can persuade your doctor to give you a prescription then you are good to go—though I did not find out about pricing. Unfortunately for patients of Defy Medical, it appears as though they will not be prescribing it just yet.

For those who are unaware, enclomiphene is the non-estrogenic component of Clomid/clomiphene. There's been a thus-far unsuccessful attempt to have this drug approved for hypogonadism under the name Androxal. Anyone taking or considering taking Clomid should think about enclomiphene as a potentially better option. Some of the unwanted side effects of Clomid are attributable to the zuclomiphene component. In addition, enclomiphene has a short half-life, around ten hours, meaning it's relatively easy to change protocols or stop taking it. Zuclomiphene has a very long half-life, maybe as much as a month, and therefore takes a long time to get out of your system.

Maybe just a bad heart, but doesn't seem worth the risks anyway...

A billionaire diamond trader has died during a penis enlargement operation at a posh Parisian clinic, it was reported.

Ehud Arye Laniado died at the age of 65 in the clinic of an unnamed plastic surgeon on the Avenue des Champs-Elysees in the French capital Paris.

According to local media, complications during surgery proved fatal for the Belgian-Israeli dual national and he suffered a heart attack when a substance was injected into his penis.

It's being reported on ExcelMale that Dr. Crisler has died, cause not yet disclosed. If true this is very sad, and quite a coincidence that we learn of it a year to the day after we lost PeakT.

I posed this question in a thread on ExcelMale, but would like to have a devoted topic here. Negating the question: Couldn't there be one level of estradiol that's best for vascular health, a different level for sexual function, another for prostate health, etc.? Ideally the levels wouldn't differ greatly, but how close do they have to be? The thread on Rouzier's videos got me thinking about this issue. Basically Rouzier is saying estradiol is totally beneficial, and even supplementation to levels over 100 pg/mL is a good thing. For simplicity just say his position is that supraphysiological estradiol is good for longevity. But this is in contrast to clinical and anecdotal evidence showing that sexual function degrades in some men at higher levels of estradiol. So this already contradicts the notion that a particular level of estradiol is best for everything.


In recent years I've had six sensitive (LC-MS/MS) estradiol tests performed by LabCorp. Two of these have come back with results that were half of the correct levels. The first time it happened the doctor and I assumed that the standard immunoassay test was incorrectly high. But later tests revealed that in fact it was the sensitive test that had been incorrectly low. Because of this experience, when a recent sensitive estradiol test result came back at 15 pg/mL, much lower than expected, I had the test performed again with both methodologies. This time the sensitive and non-sensitive results agreed, with values of 31 and 35 pg/mL respectively.

These experiences jibe with statements made by LEF when they were defending their continued use of immunoassay testing in standard panels: the LC-MS/MS test is complicated and easy to mess up.

Counterarguments? It's just one guy and two tests. I sincerely hope they are not screwing up a third of these tests for everyone. The sensitive test is still important to verify the immunoassay result, which can be falsely elevated by other molecules, such as C-reactive protein.

Recommendation? Get both tests if you can afford it. A substantial disparity between them is usually grounds for concern.

The forum was being attacked by some persistent spambots, so we had to take pretty aggressive action to stop them from creating new accounts. Legitimate users who had trouble registering Wednesday or Thursday should try again.

Overall the results are pretty unimpressive.

More than 25,800 people were randomly assigned to one of four groups: one received 2,000 IU of vitamin D a day and a placebo, another took 1g of omega-3 fatty acids a day with a placebo, a third took both 2,000 IU of vitamin D and 1g of omega-3 a day, and the last group received two daily placebos. All volunteers took their assigned nutrients for approximately five years, and researchers logged everything from cancer diagnoses to major heart events including heart attack and stroke, as well as deaths from cancer and heart disease.

The people taking omega-3 fatty acids did not have a lower rate of heart events compared to the people taking placebo.

When they looked at the effects of vitamin D, they also found little difference among those taking the nutrient and those taking placebo when it came to overall heart disease and cancer measures.

They do try a little positive spin:

While they don’t appear to do much overall in this study, fish oil seems to help specific groups of people and the researchers believe that vitamin D may simply take longer to have an effect on cancer rates and deaths.

Detailed summary: https://www.vitalstudy.org/findings.html

Key findings

Vitamin D supplementation
• Did not reduce risk of cancer
• Did not reduce risk of major cardiovascular events (heart attack, stroke, or cardiovascular death considered together)
• Appeared to reduce risk of cancer-related death

Omega-3 fatty acid supplementation
• Did not reduce risk of cancer
• Did not reduce risk of major cardiovascular events in the overall study population, but did reduce risk of these events by 19% in people with low fish intake
• Reduced risk of heart attack by 28%, when heart attack was considered separately from other cardiovascular events; the benefit appeared strongest in African Americans

For the first time, scientists have discovered a confirmed genetic link to erectile dysfunction.

Researchers pinpointed a stretch of DNA where variations made it more difficult for men to perform as expected.

The finger of suspicion points to a gene called SIM1 which could be a target for new impotence treatments.
Besides having a potential influence on men’s erections, SIM1 is thought to play a role in brain development.

The scientists carried out the study by analysing the complete genomes, or genetic codes, of more than 36,000 American and 222,000 British men.

A search was made for genetic differences that occurred more often in men with a history of erectile dysfunction.

Variations in the SIM1 locus, the region of DNA containing the SIM1 gene, was associated with a 26 per cent increased risk of impotence.

A man developed red-tinted vision after taking too much sildenafil citrate. "... the patient had ingested far more than the recommended 50 mg dose."

The latest case report is the first study to show that color vision problems caused by retinal damage can result from a high dose of sildenafil citrate, and that excessive use of the drug may lead to long-term, possibly irreversible, vision problems.

"People live by the philosophy that if a little bit is good, a lot is better,” Richard Rosen, lead author of the study and Director of Retina Services at NYEE, said in a statement. “This study shows how dangerous a large dose of a commonly used medication can be. People who depend on colored vision for their livelihood need to realize there could be a long-lasting impact of overindulging on this drug."

Here's another recent study sent our way by Nelson. It doesn't address the issue of causality, so low T could contribute to poor sleep, or vice versa, or both.


CONCLUSIONS: Among men aged 16-80 in the United States, we found increasing age, impaired sleep and elevated BMI is associated with low testosterone. It is important, therefore, that evaluation and treatment of reduced serum testosterone should also include improving sleep duration in combination with weight management.

This link forwarded by Nelson hits close to home, as a good friend of mine suffered a severe spinal cord injury, leaving him unable to indulge in his passion for bicycle riding. He's a couple years post-injury now, but I'm wondering if testosterone therapy in some form could still be of use, at least making it easier for him to hand-cycle.



Neuromuscular impairment and reduced musculoskeletal integrity are hallmarks of spinal cord injury (SCI) that hinder locomotor recovery. These impairments are precipitated by the neurological insult and resulting disuse, which has stimulated interest in activity-based physical rehabilitation therapies (ABTs) that promote neuromuscular plasticity after SCI. However, ABT efficacy declines as SCI severity increases. Additionally, many men with SCI exhibit low testosterone, which may exacerbate neuromusculoskeletal impairment. Incorporating testosterone adjuvant to ABTs may improve musculoskeletal recovery and neuroplasticity because androgens attenuate muscle loss and the slow-to-fast muscle fiber-type transition after SCI, in a manner independent from mechanical strain, and promote motoneuron survival. These neuromusculoskeletal benefits are promising, although testosterone alone produces only limited functional improvement in rodent SCI models. In this review, we discuss the (1) molecular deficits underlying muscle loss after SCI; (2) independent influences of testosterone and locomotor training on neuromuscular function and musculoskeletal integrity post-SCI; (3) hormonal and molecular mechanisms underlying the therapeutic efficacy of these strategies; and (4) evidence supporting a multimodal strategy involving ABT with adjuvant testosterone, as a potential means to promote more comprehensive neuromusculoskeletal recovery than either strategy alone.

Testosterone, Hormones and General Men's Health / Prostate cancer and TRT
« on: September 17, 2018, 11:04:34 am »
More evidence against the premise that TRT fuels prostate cancer.



Both testosterone deficiency (TD) and prostate cancer (CaP) have increasing prevalence with age. However, because of the relationship between CaP and androgen receptor activation, testosterone therapy (TT) among patients with known CaP has been approached with caution.

In the absence of randomized placebo controlled trials, our study supports the hypothesis that TT may be oncologically safe in hypogonadal men following definitive treatment or active surveillance for CaP.

This is the first of many articles that Nelson Vergel will be sending our way to read and discuss.


Testosterone Replacement Therapy Versus Clomiphene Citrate in the Young Hypogonadal Male.

The use of testosterone to treat hypogonadal symptoms has increased during the past decade. Consequently, one clinical challenge that has arisen is how to approach the young and treatment-naïve hypogonadal patient who is still within his reproductive years and may desire children in the future. Testosterone is known to suppress the hypothalamic-pituitary-gonadal axis resulting in suppressed spermatogenesis. There is a concern that, in some men, prolonged testosterone use may result in permanent spermatogenic failure.

PATIENT SUMMARY: In this review, we discuss the risks and benefits of available treatment options for the young hypogonadal patient for whom future fertility is an important consideration. Fortunately, alternatives such as clomiphene citrate and human chorionic gonadotropin have been shown to increase endogenous testosterone production. However, their efficacy as treatments for hypogonadal symptoms is still under debate.
The article includes an interesting passage on TRT and fertility:
Conflicting evidence exists for the long-term risk to fertility in men on TRT. Data abstracted from trials which sought to utilize TRT as a contraceptive found that sperm concentrations were suppressed to less than 1 x 106 ml-1 within 3.5 months. After discontinuation of testosterone, projected time to recovery (20 x 106 ml-1) was 67%, 90%, 96%, and 100% at 6, 12, 16, and 24 months respectively [9-11]. A recent publication evaluating men who presented to an infertility clinic with a history of TRT use found that only 70% of men achieved sperm recovery (total motile count >5 x 106) and that increased age and duration of TRT use were negative predictors of a patient’s ability to return to fertility [12]. This data is likely overestimates the long-term detrimental effect of TRT on fertility as no information regarding the patients’ ability to produce sperm prior to TRT is available. While a subset of these men was likely infertile prior to TRT therapy, this data serves as a caution to men and practitioners considering TRT within their reproductive years. While the absolute percentage of men who experience irreversible fertility loss after undergoing TRT is not known, there is a significant concern for this side effect in young men who may ultimately desire to father a child.

Testosterone, Hormones and General Men's Health / Natural hCG in men
« on: September 15, 2018, 04:39:39 am »
Starting a new topic on behalf of DanMac:

Cataceous i heard that men naturally produce tiny amounts of Human chorionic gonadotropin (HCG) in their testes, so it's just boosting our Natural supply, can you confirm this is true? i know for fact of course Pregnant Women produce H.C.G absolutely.  But i heard men make small Tiny amounts in Testicles too. Did you hear of this before?

Taken from LiveStrong.com Article here   https://www.livestrong.com/article/247492-what-is-a-normal-hcg-level-in-males/

Male hCG levels are normally less than 5.0 mU per ml. Human chorionic gonadotropin is a hormone that is most often associated with pregnancy in women. However, both males and nonpregnant females produce low levels of hCG throughout their lives as well

One of our members asked this question, and because there are arguments both ways I'd be interested in any added insight.

On one side, we know that guys have been using Clomid extensively as part of post-cycle therapy. It wouldn't be so popular for this purpose if stopping it caused significant problems of its own. On the other side, the estrogenic zuclomiphene isomer of Clomid has a long half life relative to enclomiphene, with one source saying it's 30 days versus 11 hours. The issue here is that when a guy stops taking Clomid there's a pretty long period in which zuclomiphene alone is dominant. And per a reference in Wikipedia "... unlike enclomifene, zuclomifene is antigonadotropic due to activation of the estrogen receptor and is able to reduce testosterone levels in men to near-castrate levels."

Does the effect exist? That is, after stopping Clomid, instead of gradually reducing from the enclomiphene-stimulated state to baseline HPTA operation, does one go below baseline before recovering? Or is the reduction from the stimulated state slow enough that you never go below baseline in spite of the lingering zuclomiphene?

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