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Blood-work: A Year in Review, advice needed, and a mea culpa

It is more like EOD and everything I have read or been told by my Doctor indicates that Clomid is very well tolerated across the board and not hepatotoxic at all. My Doctor is a little on the progressive side and knows her shit when it comes to alternative medicine which she specializes in.

The more i think about my Numbers I think the Liver values are raised due to New Years Eve weekend binge drinking, and the SHBG levels are tanked due to hGH use which I guess I over responded too. I don’t yet have a hypothesis for Test levels…this may be function any sort of witchcraft interaction. Hoping Doc can shed light on it.

I DO appreciate everyone’s input, it helps explore the unconsidered and it helps formulate good questions to be ask to the professionals.
 
If insurance covers it that’s cool as heck HCG. Is my go to but it’s available to me hcg will do what clomid can’t for me which is raise fsh and lh but remember what works for me might not for you and vice versa I couldn’t get sperm count up with clomid. But hcg made them boys clank
 
I hear you man. Definitely do whatever works for you. I just mentioned the HCG bc it’s usually the gold standard for TRT. If clomid is working good for you then keep that up.
 
This may be the witchcraft that is leading to my Total Testosterone (TT) numbers dropping…

"Low SHBG increases Free Test (FT)%, not T output. The hypothalamus responds by seeing it as an excess and lowering LH pulses to maintain homeostasis and get back to the FT target it wanted. This decreases total testosterone.

Check out the studies that show that SHBG and TT are positively correlated. So, the higher SHBG, the higher the TT, and the lower the SHBG, the lower the TT (in men without deficiency.)

This is the mechanism by which hypothyroidism or insulin resistance (which cause very low SHBG) lead to hypogonadism (low T.) "

also…

There is no such thing as waste with SHBG. The broscience is that SHBG “stealz ur T”, but the exact opposite is true. SHBG does not metabolize or destroy testosterone. SHBG does not “steal” T and then perform some biochemical magic to make the T vanish from the universe, either.

SHBG prevents the metabolism of testosterone and slows down your overall MCR (metabolic clearance rate) by preventing the liver from destroying testosterone and also prolonging the action of T within cells (SHBG passes into the cell via endocytosis instead of free diffusion.)

SHBG+T has an approximate half-life of 2 hours in serum. Then, the complex dissociates. The T is returned to the bloodstream — intact.

Do you know what wastes your testosterone/other compound? The liver. Get rid of the liver and you’ll enjoy all the benefits of your pinning. Also, stop cellular glucuronidation and you’re “GTG”, as they say.

Decreasing SHBG is the fastest and most guaranteed way ensure free androgens are removed from your body as rapidly as possible.

In healthy men with naturally high testosterone levels, SHBG correlates positively with TT.

When steroids are used, SHBG becomes nearly irrelevant because androgen levels grossly outweigh the binding capacity of SHBG. In a normal, healthy male, there are more SHBG glycoproteins than there are molecules of androgen. In a steroid user, SHBG becomes oversaturated and the liver attempts to address the androgen excess by reducing SHBG concentration to speed up the clearance (removal) of androgens from the body. However, due to the relentless exogenous supply of androgen, the liver’s effort is futile. MCR is maximized and overridden.

Excessive SHBG can interfere with passive diffusion through cellular membranes by limiting the concentration of T in its free moiety. Aromatization slows and both DHT and E2 become excessively bound to SHBG, limiting the immediate action of all major steroid hormones before they are degraded.

Normal SHBG slows MCR, prevents over-metabolization and also enhances cellular uptake and retention by reducing the glucuronidation and efflux of FT from cells and excites the SHBG-R receptor to increase cellular cAMP. SHBG at adequate level preserves testosterone and enhances the action of two pathways: the endocytic pathway and the extracellular (SHBG-R) pathway. (Androgens bind to SHBG which has already bound to extracellular megalin.)

Insufficient SHBG increases MCR (your liver destroys T rapidly), allows for excessive metabolization to DHT and E2, and speeds up (per study!) the breakdown of testosterone in cells. Secondary pathways are starved. This is situation is either genetic, the result of excessive inflammation (or other disease state) or due to an excess of androgen in the body."

Credit: Reddit user Vestpocket
 
Some TUDCA and UDCA information I hadn’t seen…

TUDCA and UDCA are by far the best quintessential treatments for both the prevention of cholestasis, as well as the recovery from it. They are, quite literally, the compounds specific to the treatment and mitigation of oral C17-alpha alkylated anabolic steroid liver toxicity - this cannot be said of any other liver support supplement/compound. In addition to treating cholestasis very effectively, it has demonstrated in studies to also reduce the risk of hepatitis B, where they had significantly decreased the risk of having abnormal serum alanine aminotransferase activity at the end of treatment compared to the beginning.[8] Other studies have also shown that UDCA and TUDCA are beneficial in the treatment necroinflammatory liver disease, such as (and especially for) hepatitis C-related chronic hepatitis in which bile duct damage and some degree of cholestasis are frequently seen at histology, and the study had observed that TUDCA had significantly improved the biochemical expression of chronic hepatitis.[9] In general, TUDCA seems to prevent hepatic cell death.[10]

Dosing of TUDCA and UDCA: 500-1000mg daily for the maintenance of healthy liver function during the use of a C17aa oral during a cycle. 1,000mg or higher daily for the purpose of repairing the liver following heavy hepatotoxicity and hepatocyte damage from cholestasis (and/or for individuals with serious liver disorders).

IMPORTANT: Do not exceed 8 weeks of TUDCA/UDCA use, as it can increase negative cholesterol values and decrease HDL. It is recommended to use these bile salts only during a cycle of oral C17aa anabolic steroids, or for the purpose of liver repair following periods of significant hepatotoxicity from the use of these compounds. Other compounds should be sought after for general year-round liver support.

According to this study (taken from Examine), TUDCA has been shown to decrease HDL levels when taken for extended periods of time. In normal people, this really isn’t a big deal. In people who are constantly using steroids, like blasting and cruising (B&C), it can become counter-intuitive to run TUDCA for no reason due to decreased HDL levels. For example, on a cruise one wants to let their body recover, and ideally see good bloodwork before blasting again. One key reading on the bloodwork is the HDL, as HDL is one marker that almost always drops significantly while taking exogenous steroids in large dosages.
 
NAC info…
Dosing of NAC: As previously mentioned, there are issues in regards to poor oral bioavailability with NAC. IV and inhalation formats of NAC do exist, but are generally prescription-only, depending on which country. However, the oral format of NAC is generally widely available for purchase almost anywhere. Be sure to look for a NAC product that has chelated it to an element or compound to provide greater bioavailability. With that being said, a proper dose for the purpose of maintenance of liver health during a cycle of C17-alpha alkylated anabolic steroids would be in the range of 1,000mg - 2,000mg of NAC per day. NAC can be used year-round as a general liver support, and should be run at 1,000mg per day or less when not utilizing C17-alpha alkylated oral anabolic steroids.

IMPORTANT: Studies have demonstrated that high doses of NAC can cause lung and heart damage in mice[16] due to the fact that NAC is metabolized in the body to S-nitroso-N-acetylcysteine (SNOAC). In large enough amounts, SNOAC leads to significantly increased blood pressure in the lungs and the right ventricle of the heart. This is why it is advised to not exceed the standard dose of 1,000mg - 2,000mg per day while on C17aa oral anabolic steroids. Other than this warning, it should be mentioned that the implications of long-term NAC use (at any dose range) are currently unknown and have not been investigated. This is not to say that long term use is a bad thing, but that we simply do not know if the outcome is indeed good or bad.
 
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