PCT: A Clinician's View Part III: Post-Cycle Supplements - In Practice

[dinoiii]

PCT: A Clinician’s View PART III Post-Cycle Supplements: In Practice

Author's Note: If you have yet to visit the PRIMER or PARTS I and II of this series, please do so at the following addresses before proceeding:

Primer
http://www.discountanabolics.com/forum/showthread.php?t=2012
Part I: PCT Demystified
http://www.discountanabolics.com/forum/showthread.php?t=2035
Part II: Post-Cycle Supplements: In Theory
http://www.discountanabolics.com/forum/showthread.php?t=2076

INTRODUCTION

One of the more feminine-like qualities I possess is the daily ritual of perusing through the “Living/Today” sections (title = dependent upon area of country I am in) of the newspaper to find my horoscope. Is it an act that holds much bearing on my life? Well, not exactly. It just seems to preach about a life better than mine – well, that is roughly 90% of the time. Ten percent seems like its right on the money and the “correct” ones tend to come in spurts – yesterday and today falls in the ten percent.

Yesterday: A dream compels you. If it weren’t so lovely, you would
feel like a slave to its ruthless demands. You focus on the delicious
possibility, so nothing you do feels like work.

Today: Challenge conventional attitudes – your fresh thoughts are
needed. You shine in the eyes of family and friends. Now, what
must you do to impress yourself?

2 excerpts from Holiday Mathis of
Democrat & Chronicle (Rochester, NY)

The dream simply begins with the PCT: ACV series which has received a lot of attention for me. I am lucky that it really is a passion in expressing my thoughts on such a topic. I feel this could be a never-ending book. The challenging of conventional attitudes (if not already apparent) will come fast and furious during this installment. I am actually not 100% impressed yet though. The latter part of the year will potentially offer that peace.

Last time, we looked at the various theoretical models implying how they may impact the construction of a post-cycle dietary supplement regime. Today, we see how these items (extracted straight from the paper onto which they have been hypothesized) translate into the real world. While dosages and the like are considered here, a true undertaking of application of these doses to various cycles will be looked at more in-depth in part VII of this series.

[Author’s note: No particular supplement is being marketed in this article as all of them. I have zero financial interest in any of the supplements that follow. In the same sense, I do NOT use ANY manufacturer’s brand name products in the paragraphs that follow – rare in this industry].


SUMMARY OF STEROIDOGENIC THEORY

Keeping the science to a minimum (there’s plenty in the paragraphs and sections that follow), it is imperative that we revisit the multiple pathways of testosterone action in recap-summary formation as to better establish the forthcoming real-world results of adequate post-cycle supplementation.

Normal Steroidogenic Testicular Synthesis Pathway (> 95%, Complete):
LH --> stimulate Leydig Cells of testis to produce Testosterone (primary pathway in males)

Normal Steroidogenic Adrenal Synthesis Pathway (< 1%, Incomplete):
ACTH --> stimulates Zona Reticularis Cells of adrenal gland to produce Testosterone (primary pathway in females, secondary pathway in males)...keep in mind that 90% of DHEAS comes from Adrenal secretion for later discussion, however. Cortisol will take on an indirect role here as well later.

Normal Steroidogenic Peripheral Conversion Synthesis Pathways (< 4%, Incomplete)

Inactivation Pathway:
Testosterone --> hepatic oxidation & conjugation / renal excretion

Amplification Pathway (prostate / skin, 5-10%):
Testosterone --> 5-alpha-reductase --> DHT --> Androgen Receptor

Direct Pathway (muscle):
Testosterone --> Androgen Receptor

Diversification Pathway (brain / bone, 0.1%):
Testosterone --> Aromatase --> Estradiol --> various metabolic pathways --> Estrogen Receptors (i.e. - E1, E2)

[dinoiii]

ANTI-ESTROGENICS

(1) Aromatase Inhibitors

EVIDENCE-BASED EFFICACY: Unfortunately, studies performed by individuals without vested interest are NON-EXISTENT!!! Some wonderful hypotheses have been constructed, however, and on paper, they are not without merit – but my curiosity got the better of me as to how serum lab values would respond to use of various items suggested last time. While this in-house study is still underway, preliminary data suggests that the serum changes seen are those of average 3-fold increases in estradiol and subsequent increases in testosterone are NON-existent.

Choose-your-own Adventure style
Two-fold introduction to the model:

Step 1a) Decrease Aromatase --> Subsequent transient increase in T [If you want to reproduce results of classically-defined research, you can stop now, otherwise Go to Step 2a]

Step 1b) Decrease Aromatase --> Subsequent transient decrease in E [If you want to reproduce results of classically-defined research, you can stop now, otherwise Go to Step 2b]

Step 2a) Prior Affinity for AR leaves new T no where to go [If you are frustrated, you can return to path 1b and see how that adventure ends, otherwise make your way to Step 3a]

Step 2b) Decreased E --> Decreased SHBG [If you are frustrated, you are likely not alone, to see the demise of this pathway, move on to Step 3b]

Step 3a) Newly Increased T lends itself to become Free T (can overwhelm to increase SHBG oputput with prolonged output) – normally, this may be good but now, you continue negative feedback, no HPT axis recovery [SUPPRESSION = UNSUCCESSFUL PCT]

Step 3b) Decreased SHBG --> Increased Free E and Free T normally, this may be good but now, you continue negative feedback, no HPT axis recovery [SUPPRESSION = UNSUCCESSFUL PCT] - author’s note: this decrease in SHBG is actually a transient effect, after an average of 2.5 weeks of use, SHBG seems to super-compensate offering higher levels of bound hormone product. This model needs to undergo further study.

FORMS & DOSAGES: Without evidence-based backing, I am unable to recommend a dose at this time.

POTENTIAL SIDE EFFECTS / INTERACTIONS: AT/ATD are strong cytochrome P450 3A4 inhibitors (Ki values < 0.2 microM via in vitro human microsome studies). 3A4 is the workhorse of the P450 system. It accounts for 30% of P450 activity in the liver and 75% of the P450 activity in the small intestine (wait a minute – this is where ATD-type supplements are absorbed). Because so much P450 activity is due to 3A4, it comes as no surprise that 3A4 performs the bulk of oxidative drug metabolism in humans. This makes 3A4 arguably the most important human P450 enzyme to understand. Until the mid-1990’s, the literature included references to 3A3or 3A3/4. It is now understood, however, that 3A3 is not a separate P450 enzyme but a transcript variant of 3A4. Subsequently, the list of drugs and supplements that are metabolized by 34A IS CONSTANTLY GROWING! 3A4 being a high-capacity/low-affinity enzyme if inhibited means you get spill-over of the drugs to the low-capacity/high-affinity subset [namely in the enterocytes of the gut (recalling the high percentage of 3A4 activity in the gut): 2D6, 2C9, and 2C19]. In English, this means you have the potential for immense toxicity in other drugs metabolized by this cytochrome enzyme.

I will center our discussion here on the supplements that have inhibited metabolism when concurrently used with AT/ATD preached about as classic adjuncts during PCT. In the late 1990s, several 3A4-related casualties occurred, and the drugs were removed from the US market by manufacturers. These cases are reminders of the potentially serious nature of 3A4 inhibition.

INTERACTION #1: Red Yeast Rice (RYR) – a classically-described HMG Co-A reductase inhibitor and also anti-inflammatory and down-regulator of LDL receptors has the potential to cause Rhabdomyolysis (see my For the Love of Science and Medicine, Part II article for some clinical studies for evaluation) and extreme hepatotoxicity. I have already stated in Part II and previous articles/posts that RYR has absolutely NO business in a PCT regime following a C17 alkylated PH/PS/AAS. RYR coupled with either of the 3A4 inhibitors AT/ATD potentiates the aforementioned effects, so I amplify my response to the nth degree and ask with use of AT/ATD-containing products, you fully omit this item.

INTERACTION #2: Hawthorn Berry – a classically-described blood pressure modifying agent and this is attributed to its calcium and beta-blockades as well as its ACE inhibition and diuretic action. This rather safe supplement on its own with a great track record becomes a different animal when combined with 3A4 inhibitors. It can actually drop your blood pressure to a level that would in itself be dangerous. The key here is that if you opt to throw this compound in solely at the time of cessation of PH/PS/AAS that may have elevated your blood pressure – a decline of more than 25% at such a rapid rate can be deadly!

INTERACTION #3: Any sympathomimetic agent. While better avoided in the first place during PCT, people have considered certain agents that act through various andrenergic grounds and they too become MORE potent with AT/ATD.

CAUTION: Nolvadex, a commonly-puported “must-have” by many authorities during PCT. This is an obvious display of their ignorance and blatant disregard for drug-drug interaction as Nolvadex (discussed at greater length in part IV) is metabolized through the 3A4. Now, in addition to people starting at dosing parameters as high as 40mg (which is a highly unnecessary dose even for the heaviest of cycles) with a 7-day half-life, you have increasing toxic levels in addition to what you have already put together. Retinopathy or liver toxicity anyone?

(2) Estrogenic Channeling Agents

Indole-3-Carbinol (I3C)

EVIDENCE-BASED EFFICACY: I have written extensively in various posts on my support of this compound versus its DIM metabolite as well as any other compound in the post-cycle realm from the category of “dietary supplement.” Perhaps the single-most important mechanism of action of I3C is modulating estrogen metabolism. That’s right, tell your friends – ALL ESTROGEN IS NOT CREATED EQUAL. Estrogen receptors are located on the surface of virtually every type of tissue in the human body. Guys, you too, are not off the hook as this applies to you as well.

The body modifies (metabolizes) estrogens through two mutually exclusive pathways, which lead to compounds with dramatically different biological activities. Estradiol is the primary estrogen in circulation (as the example used above in Diversification Model) and one of the most active. It is metabolized to a number of other chemicals, all with some degree of estrogenic activity.

Key here, are the enzymes 2-hydroxylase and 16-alpha-hydroxylase. Several years ago, scientists hypothesized that a preference towards the 2-hydroxylase pathway and the subsequent generation of 2-hydroxyestrone (2-OHE1), results in less toxic metabolites in the circulation, which was subsequently gone on to support a decreased number of breast cancer outcomes if this were the dominant pathway (later, this proved true for prostate cancer as well). It was also around that same time that the hypothesis of greater estrogenic metabolism via the 16-alpha-hydroxylase enzyme would yield greater amounts of the more potent 16-alpha-hydroxyestrone (16alpha-OHE1) and a larger number of estrogen-dependent cancers would likely be the result.

Summary of ORDET study of 2000 (always nice fancy acronyms)
Participants: 10,000 Italian women
Duration: > 5 years
Measured Items: Diet, other breast cancer risks
Findings: Increased level 2-OHE1:16alpha-OHE1 at beginning of study associated with less risk of breast cancer development.

This simply set precedent, mind you – although there is a 1% risk for men to develop breast cancer, posting this study is merely the landmark to establish the importance of greater 2-OHE1:16alpha-OHE1 ratios being desired for decreased estrogen-sensitive cancer risk. This is very important information to someone embarking on post-cycle supplementation.

Summary of Prostate Cancer Study
Although there was a failure to achieve statistically significant results in this study, elevated 2-OHE1 urinary levels indicated a decreased risk of prostate cancer, whereas an increased 16alpha-OHE1 urinary level showed an increase of prostate cancer 2-times that of men with the highest levels of 2-OHE1.

I3C modulates these pathways shifting the conversion of estradiol metabolism to favor the 2-hydroxylase pathway and the subsequent 2-OHE1:16alpha-OHE1 ratio is INCREASED, which correlates with a decreased risk of various estrogen-sensitive cancers. A potential caveat worth further exploration is the increase in production of yet another estrogen exhibited by some studies (4-hydroxyestrone – this is very potent). These increases were NOT significant, however, and as you will see and have seen in my various posts, are put out by people with vested interest in other products. There are multitudes of studies that actually show a concurrent DECREASE in 4-OHE1, so the mixed results tend to leave me questioning those trying to prove their various products superior. Catch my drift?

In addition, and certainly not something studied, but the data seems to suggest shifts from the more potent (2-OHE1) to less potent (16alpha-OHE1) in a time when there is the potential for increased conversion (and this goes out to all of my aromatase-inhibitor-loving friends) – namely, during the post-cycle period would also contribute to a shift in dose-response curves to the right (and that is for my pharmacologically-inclined friends). We’ll see in the pharmaceutic exploration (parts IV + V) that this is NOT the entire picture – unfortunately, I can only address these items one by one in a certain time allotment.

FORMS & DOSAGES: 200mg to as high as 400mg has been studied and based on available evidence, this is what I would be hard-pressed not to suggest at this time. There is no upper-limit established, but even while in the post-cycle realm, I would beg you to adhere to a max of 400mg per day as this is simply what has been supported to date.

POTENTIAL SIDE EFFECTS / INTERACTIONS: Although it may seem obvious that a substance consumed over 1000s of years by millions worldwide is inherently safe, it has been challenged recently by those with vested interest in its metabolite DIM. I have expressed my concern at the challenges DIM supporters have offered and it is just plain bad science. Numerous cell culture, animal, and human studies have demonstrated I3C’s safety and tolerability, along with its targeted ability to SUPPRESS estrogen-receptor-sensitive (breast, cervical, and important for this discussion – prostate) cancer growth (sorry Dr. Z), and induce programmed cell death in a variety of tumors, including those associated with breast, prostate, endometrial, leukemia, and colon cancers.

As an aside, the cytochrome P450 enzymatic system discussed above in the AT / ATD section within both the liver and intestinal track is actually STRENGTHENED by use of I3C – something that could prove especially beneficial to C17 alkylated users.

CAUTION: Be careful of “research” supporting concurrent use of DIM – usual vested interest is a hand-in-hand with the funding of such studies.

[dinoiii]

PRO-TESTOSTERONE

DHEA

EVIDENCE-BASED EFFICACY: Although DHEA is promoted as a miracle supplement that can do everything from bolstering flagging libido, controlling weight, and improving mood to preventing or treating many of our most lethal diseases, there is LITTLE or NO evidence that it can do ANY of these things in humans. Most of the research to date has been done in animals, and human studies involved only small numbers of volunteers. Still, some of the results have been intriguing and hold promise that DHEA may eventually live up to some of its hype. SUPPLEMENT MANUFACTURERS HAVE MADE “EVENTUALLY” NOW!

I, for one, am sick of this supplement! Because the studies are scant, I will discuss the ACTUAL science and practice evidence that is known. DHEA circulates primarily in the blood as DHEAS, a sulfated version which is NOT, in itself, biologically active. When blood tests for DHEA are done, the test results do not usually discriminate between the 95% that is DHEAS and the 5% that is DHEA. Radioimmune assay of saliva, however, can be used to measure the concentration of the biologically active hormone, DHEA. Most not having this done really have ABSOLUTELY NO BASIS FOR INGESTION of this supplement AS THE SULFATED CONCENTRATION TELLS THEM NOTHING USEFUL. Sulfatase and Sulfokinase concentration tests are currently in the planning stages of development which may give us a better idea of serum conversion data between the reservoir DHEAS and active transformed byproduct DHEA.

FORMS & DOSAGES: DHEA marketed as a nutritional supplement is available in tablet, capsule, and cream forms. The usual recommended dosages range from 5 to 25 mg a day. Originally, DHEA was sold mostly as a non-prescription weight-loss aid. In the late 1980s, the FDA ordered that DHEA be classified as an unapproved drug that could be obtained only by prescription or participation in a clinical study. In 1994, it was reclassified as a nutritional supplement that could be sold in health food stores and other outlets. When it came under fire again during 2004’s Anabolic Steroid Control Act, I was pulling for it to actually be canned if any prohormone product was to go. Unfortunately, the cockeyed truly ANYTHING-BUT-SCIENTIFIC COMMUNITY known as legislators and lobbyers alike fought for its safety versus other compounds – well, if that doesn’t explain why government has little, if any, business in dietary supplement legislation, I am not sure what does. Alas, we live in an age where science seems to mean so little these days. And so I digress...

POTENTIAL SIDE EFFECTS / INTERACTIONS: DHEA may spur the growth of hormone-dependent cancers of the breast in women and prostate in men. Animal studies have found that it may also raise the incidence of liver cancer, but it is not known if humans face the same risk.

Dinoiii’s tip(s):
I DO NOT BELIEVE DHEA to have a true place in dietary supplementation in the first place, especially within steroidogenic pathways in the post-cycle time frame.

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Tribulus Terrestris

I, unlike others before me using bad research questioning its efficacy, like this supplement in the post-cycle domain, especially when we will see some problems with hCG in the next part of this series (always consider concurrent pharmaceutics and rationale). I know what anti-trib propaganda will suggest and I have covered a partial retort in my “Tribulus Terrestris: Worthless or Unjustifiably Chastized” article as well as my PCT: ACV II article, so I will not add to that argument at this time.

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Nettle (Urtica dioica)

EVIDENCE-BASED EFFICACY: Traditionally, this agent was used to treat hypertension throughout much of Europe. It has recently been the focus of many pharmacological studies (in vivo) designed to determine the nature and extent of its beneficial effects.

As previously discussed in this series, globulins like SHBG actively inhibit the level of free testosterone by binding to it, thereby rendering it biologically inactive. Research has found, however, that nettle extract has greater affinity for SHBG than does testosterone. As a result, SHBG binds more readily to constituents of the nettle extract, successfully counteracting its effect and thereby increasing the level of free testosterone. What an exciting incidental finding! Though this is not the only positive rationale for its use nor perhaps even the most important – health-wise in the post-cycle period for bodybuilders.

What is known by many in Europe as the “Nettle Effect,” shows some stunning biological ramifications. For example, researchers in Italy – within a series of in vivo studies determined that nettle has direct positive effect on cardiac action. In their study, they found they found that when pre-contracted endothelial tissue is injected with nettle extract, it elicits vasodilation. The researchers concluded that nettle can produce hypotensive responses through a vasorelaxing effect. This suggests that nettle can improve the symptoms of angina and reduce objective measures of myocardial ischemia in men with coronary artery disease.

As I discussed in the last article of the PCT: ACV series, nettle root also may benefit prostate gland health. In Germany, nettle has been used for decades in the treatment of BPH (discussed later in this article and the last of this series). DHT is proposed to be one of the contributing factors to prostate growth (of course, under dictation of the evil step sister estrogen as you learned in the last part of this series). Much the same as its effect on testosterone’s binding to SHBG, nettle inhibits the binding of DHT to its receptor sites on the prostate gland.

FORMS & DOSAGES: Treatment of BPH: 600-1,200 mg daily. But for all testosterone fans desiring an elevation in free levels, multiple doses over the course of the day (considering half-lives, roughly 4 hours) may still offer convincing rationale proposed by one supplement company in its beta-version.

POTENTIAL SIDE EFFECTS / INTERACTIONS: Although allergic reactions to oral stinging nettle are rare, fresh nettles can cause a rash if they come into contact with the skin. Should a similar reaction start to appear at higher frequency in oral users, now would be the time with numerous supplements cropping up with this item in them in the post-ASC act of 2004. The oral does pose some minor gastrointestinal upset in some people but overall, it appears very safe.

Dinoiii's tip(s): I would advise AGAINST its use with non-steroidal anti-inflammatory drugs (NSAIDs, such as Aspirin, Ibuprofen, etc...) as it has the potential to enhance their effects which could subsequently lead to an upper GI bleed via NSAID-induced ulceration.

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I am just covering the major Post-Cycle Points regarding the next two minerals:

Magnesium

Post-cycle considerations here lie heavy in its primary role in enzymatic activation. It is second to potassium in terms of intracellular concentration.

Human Body concentration:
21-28 grams of magnesium

Intracellular Magnesium breakdown:
~ 60% in bone
~ 26% in muscle
~ 14% in soft tissue and body fluids

Potential Sources of Post-Cycle Magnesium Deficiency:
- Multi-Vitamin Use (namely, high calcium – always question the producers of a supplement that contain both calcium and magnesium)
- liver disease (especially concerning for increased number of C17 alkylated use)
- exogenous progestin use

Deficiency Issues to consider:
- heart disease
- high blood pressure
- insomnia + concurrent daytime fatigue
- mental confusion
- irritability
- muscle spasms / cramps
- loss of appetite ( + interesting sequelae that may follow)
- predisposition to stress (see later why this may expedite a particular reconditioning of ACTH)

Zinc

Although severe zinc deficiency is relatively rare in developed countries, this is NOT necessarily the case in heavily-trained athletes. It is believed that many zinc deficiencies go unnoticed and the number of zinc deficiencies is grossly underestimated leaving many athletes with a marginal deficiency. Zinc is in every body cell and is a component in over 200 enzymes. In fact, zinc functions in more enzymatic reactions than any other mineral. A couple of the associated effects of zinc deficiency worth noting in the peri/post-cycle time frame that may see benefit are testicular atrophy and male sexual function likely modulated by zinc’s role in testosterone production. Although testosterone is not the only hormone modulated by zinc to promote proper function. You can tack thymic hormones, insulin, and growth hormone on to that list and they all have important roles in proper post cycle runs.

One final thing – perhaps you have found yourself with some post-cycle acne. There are a few studies that support the use of zinc supplementation to fend this off. Subsequent testosterone regeneration that offers up an outbreak as well may very well be avoided.

Dinoiii’s Tip(s):
To all my multi-vitamin lovers: look to the back of your bottles – should you see concurrent listings for calcium, copper, iron, manganese, OR molybedenum alongside zinc as I have warned you of in my BodyOpus: Reloaded article, you could be robbing your body of this important nutrient – not a good thing coming off a cycle!

[dinoiii]

ANTIOXIDANTS

Alpha Lipoic Acid (ALA, lipoic acid, thioctic acid)

EVIDENCE-BASED EFFICACY: This sulfur-containing vitamin-like substance plays an important role as the necessary cofactor in two vital energy-producing reactions involved in the production of cellular energy (ATP). Lipoic acid, while not considered a vitamin, is an accessory nutrient where a relative deficiency can occur in certain situations, PCT being one of them. It has a well-known antioxidant role.

The racemic mixture is an approved drug in Germany for the treatment of diabetic neuropathy (nerve disease). Several double-blind studies have shown supplementation with 300 to 600 mg daily does improve neuropathy thought to be attributed to its antioxidant properties (which also has shown positive results with compromised antioxidant defense systems in HIV/AIDS research with subsequent serum level elevations in vitamin C, gutathione, and T-helper lymphocytes). Within the diabetic literature, there is also great rationale to support its improvement in blood sugar metabolism, increase insulin sensitivity, improve blood flow to peripheral nerves, and actually stimulate the regeneration of nerve fibers. All of the aforementioned effects have certain tendencies to appear in some people on cycle and post, especially with increased work loads (increased weights with use of exogenous anabolic product).

What’s more? The liver is protected from free-radical damage (to a limited degree, of course) and promotes detoxification reactions. Preliminary studies suggest a possible role in the treatment of hepatitis and cirrhosis of the liver, but more clinical research is needed to confirm these effects.

FORMS & DOSAGES: For general antioxidant support, the recommended dosage remains a measly 20 to 50 mg. I think general antioxidant for a very well-documented, safe antioxidant dose centers more in the 100 mg dosage of the racemic. Diabetic neuropathy and liver disorders were shown to see efficacy at doses ranging from 300-600 mg daily (HIV/AIDS, this dose is cut in half and taken 3 times per day, therefore 150-300 mg three times per day). How can this data be extrapolated and applied to PCT? Concominant liver toxicity and muscle strain with oxidation warrants consideration in varying doses. There is a volume of distribution factor to consider here, however.

Low End of Liver Toxicity Continuum (non-C17 alkylated)
Racemic Mixture Dosing Parameters (general antioxidant):
< 180 lbs. 100-200 mg / 2 times daily
180 – 200 lbs. 200-300 mg / 2 times daily
> 200 – 220 lbs. 300-400 mg / 2 times daily
220 – 240 lbs. 400-500 mg / 2 times daily
240 – 260 lbs. 500-600 mg / 2 times daily
> 260 lbs. 600 mg / 2 times daily

High End of Liver Toxicity Continuum (C17 alkylated)
Racemic Mixture Dosing Paremeters (general antioxidant + Liver protectant):
< 180 lbs. 400-500 mg / 2 times daily
180 – 200 lbs. 500-600 mg / 2 times daily
> 200 lbs. 600-700 mg / 2 times daily (levels beyond this become increasingly less
cost efficient)
* Author’s Note: Please subtract Liver Protectant Additions for C17 alkylated if choosing additional liver protectants. Revert to non-C17 requirements.

POTENTIAL SIDE EFFECTS / INTERACTIONS: Generally regarded as safe, however, hypoglycemic reactions can occur. Due to blood sugar modifications, possible interactions are likely with other glucose modifying agents and this compound may be better left alone at the higher end of dosing.

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Carnitine

EVIDENCE-BASED EFFICACY: While touted as an agent with the potential benefit of aiding impaired fat utilization and energy production with the ability to transport long-chain fatty acids into the mitochondria, its efficacy in this domain has NOT been supported. It is likely that the science here suffers from the various attempts of applying it to oral supplementation.

Nonetheless, clinical research concentration still offers great support for several other items of importance, namely things worth considerable consideration in the post-cycle realm: cardiovascular disease, enhancing physical performance, improving sperm count and motility, cognitive research (namely, Alzheimer’s Disease and age-related senility), kidney disease, and hemodialysis. We will address some of these results from the literature.

For what is approaching the last 20 years, research into the area of cognitive function has proven itself quite significant. A normal reaction that occurs on a daily basis in humans at a copious rate, is one that sees the coupling of acetic acid and L-carnitine forming acetyl-L-carnitine (ALCAR). There are not many places that look into direct comparison of L-carnitine versus the acetylated version – so I am unable to offer estimation into how much more effective the acetylated version is, however, study design usually uses that rationale in attempt to support its use vs. the basic L form.

I don’t want to get heavy into the science on this one, but a minor delving into it is imperative to see what conclusions can be drawn and how aging research can be applied to PCT. ALCAR resembles the neurotransmitter acetylcholine (Ach) which is involved simply in memory and proper brain functioning. In various conditions, there is a decline in Ach utilization. The close structural similarity led researchers to explore the use of ALCAR in Alzheimer’s patients first, followed closely by the aging brain. Results have been extremely encouraging. Cognitive decline or loss of focus and attention is seen readily in post-anabolic use. A hypothesized rationale has TO DATE, not been offered, but I will offer a reason I think this to be the case.

There is some research showing that exogenous testosterone in the aging male leads to improved memory and shows wonderful replicability with Alzheimer’s patients, though it could unfortunately be eons before the FDA approves such an indication. I am willing to place money on the withdraw of exogenous testosterone and subsequent suppression of pituitary gonadotropins (namely LH in this scenario) to be at least, in part, responsible for what I officially dub the phenomenon of POST-CYCLE SENILITY! Now, it is transient in nature and certainly not to an Alzheimer’s, nor age-related senile senility level – but a true anecdotally-reported phenomenon with mental decline coupled with loss of focus in the post-cycle realm. It warrants true future exploration.

Cardiovascular side effects are not something new to the seasoned steroid user.

A Summary of Cardiovascular positives suggested in studies:

• CARDIAC SIDE of the coin: Normal heart function is critically dependent on adequate levels of carnitine. Spanning the huge spectrum of various heart diseases, an association can be made to true morbidity through impaired energy production and low carnitine concentrations. Such disorders as Angina pectoris, congestive heart failure, mitral valve prolapse, and even recovery from an acute myocardial infarction are offered hope through oral carnitine supplementation.
• VASCULAR SIDE of the coin: studies show average decreases in elevated cholesterol and triglyceride levels that span all domains. While recent research shows cholesterol may not be a huge consideration (please see my cholesterol controversy series), triglycerides continue to plague people’s lipid profiles.

FORMS & DOSAGES: All forms produced in capsules, tablets, and liquid. ALCAR, propionyl-L-carnitine, and L-carnitine. [Author’s Note: No studies have been performed on what is touted as “Carnitine Ethyl Ester” – recall from other posts, esterification is simply en vogue now and in this instance, HIGHLY UNWARRANTED – Good try though!]

Dinoiii’s Basic Research Translation Recommendations (clear-cut examples to follow in part VII):
• ALCAR: up to 2 grams per day during the entire duration of PCT for prevention of POST-CYCLE SENILITY.
• Propionyl-L-carnitine (PLC): 1.5-2 grams per day during cycle + PCT for both Angina pectoris and congestive heart failure (CHF)!!!
• L-carnitine: 500mg per day during cycle + PCT for heart attack (acute MI) and cholesterol prevention.
• L-carnitine: 1-2 grams per day with the use of progestin-derivative AAS.
• L-carnitine: 1 gram per day PCT for kidney disease + hemodialysis (which diuresis applies to bodybuilder’s of continued nephron – functional unit – strain).
• L-carnitine: 300 mg 3 times per day for liver protection (again, more support would likely lend itself for those involved with heavy C17 alkylated use).
• L-carnitine: 3 grams per day for a minimum of 4 months prior to cycle for potential low sperm count and decreased sperm motility.

Each Carnitine Conglomerate Plan should be individualized to the particular cycle and cannot be simply applied to all cycles by way of blanket statements. This ensures the inability of marketing such a supplement with success as I would call manufacturers’ bluff on the rationale supporting such a supplement!!! There are some other secret items you will have to wait for the book for as this is not the entire story, but I am giving up quite a bit for free.

POTENTIAL SIDE EFFECTS / INTERACTIONS: Synergistic effects (i.e. – cardioprotective, nephroprotective) shown to thwart side effects of classic chemotherapeutics demonstrating cardiotoxicity (namely, Doxorubicin and Daunarubicin) as well as EPO drugs in anemia and hemodialyzed patients. There are no adverse effects that have been demonstrated with either food derivatives NOR dugs.

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ACES

While there is a plethora of research I could easily apply to the Post-Cycle realm when talking about Vitamin A, Vitamin C, Vitamin E, and Selenium and their antioxidant role, it remains beyond the scope of this writing due to the extensive level of research and my not being able to do an adequate job in the space I have devoted to it. I will say that I think it imperative in the post-cycle realm to consider these items and NOT IN THE REALM OF A MULTI-VITAMIN offering too much potential for cross-reaction and subsequent deficiency (as displayed in detail in part II) at a time when deficiency is simply unacceptable.

[dinoiii]

HEPATOPROTECTANTS (Liver-Protectants)

N-acetylcysteine (NAC)

EVIDENCE-BASED EFFICACY: This natural-occurring derivative of the amino acid cysteine. Cysteine, glutamic acid, and glycine form the antioxidant glutathione. In PCT: ACV Part II, you learned of the evolution of this compound in post-cycle use and how the literature on acetaminophen didn’t necessarily translate into use within the post-cycle time frame. From PCT: ACV Part I, however, we can likely begin to see the unfolding of our game of dominoes.

There were 1,174 deaths (adjusted value based on autopsy) and in excess of 18,500 in the hospitalized realm associated with overdose of acetaminophen (Tylenol, paracetamol) in 2004. Overdose with acetaminophen is capable of injuring the kidneys, heart, and central nervous system, but its most pronounced effect happens with the liver as you saw in part II based on various metabolites. Brief recap: Ingestion of acetaminophen and its N-oxidation yields toxic metabolites (namely, N-acetyl-p-benzoquinone imine, aka NAPQI) that deplete liver glutathione stores and subsequently damage the liver. This action of NAC is QUITE SPECIFIC and has been mistranslated in the supplement world on a number of accounts. First, this specificity to acetaminophen OD is really attributed to overwhelming the 2E1 cP450 enzyme and in science speak this is solely a reaction that isn’t a terrible concern in human dosing. We challenge it, however, when going above the set daily upper-limit of 4 grams of acetaminophen and overwhelm it at 10 grams – much becomes dependent upon our inner abilities as either fast or slow acetylators as well ... But I am really trying to keep this as non-scientific as possible (the extreme science can be found in my upcoming book). What’s more is that extremely high doses are needed in the medical realm, and this is through IV infusion, not an oral capsule as many OTC supplements are sold!

Now, I know what you’re thinking. Nah Dana, I’m still taking my high dose self-prescribed acetaminophen. You just have not convinced. Ok, perhaps we can look at a bit more of the evidence-based data in attempts to do that (plus see in-house study below). I like NAC’s ability as an antioxidant, a free-radical scavenger – if you will. Heck; that is after all how it’s marketed. Preliminary human studies show it may not be as useful as less expensive antioxidants though such as vitamin C. Extrapolation from data on individuals with hereditary deficiencies of glutathione synthesis show better response to vitamin C (3 g per day) than to NAC (800 mg per day). The same may be true in normal individuals, though it obviously hasn’t been studied. There is evidence that NAC supplementation at higher dosages (> 600 mg) may act as a PRO-oxidant, however, the same caveat applies to many purported antioxidants – I just have supplied you with the value. One study found that NAC given orally to six volunteers at a dosage of 1.2 grams per day for four weeks, followed by 2.4 grams per day for an additional two weeks, it actually DECREASED oxidative stress by 83% and REDUCED glutathione concentrations by 48%! Until this issue is resolved, I would be hard press to recommend more than 600 mg per day in healthy individuals, and that number may be pushing the envelope a tad.

Curious how many people have done their homework here or simply assumed the role of a domino?

Other studies show minor support in the realm of bronchial and lung disorders, but terrible results when considering HIV/AIDS patients. It is probably needless to say that NAC has not been studied in the post-cycle realm (until this piece, of course – see below!).

FORMS & DOSAGES: I think adequate oral dosing (keeping in mind our upper limit established in the aforementioned paragraphs) hovers around 200 mg – up to (yet, not exceeding) three times per 24-hour period. This info is imperative to follow closely when in post-cycle phases.

POTENTIAL SIDE EFFECTS / INTERACTIONS: N-acetyl cysteine shows interactions with the following drugs: carbamazepine (Tegretol), nitroglycerine, and several classes of chemotherapy drugs. While this info may not seem important to you in the realm of bodybuilding if you are not on any of the drugs I just mentioned, keep in mind nitroglycerine behaves in a way similar to byproducts of arginine supplementation and the two are better left alone and not used concurrently. Potential side effects to develop with arginine and NAC include: headache (#1), nausea, vomiting, and other gastrointestinal symptoms.

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SAMe (S-adenosyl-methionine)

I will not tell a lie! Anyone familiar with my writing understands that this is my absolute favorite hepatoprotectant and this is NOT unsubstantiated and I have absolutely no vested interest here as this is simply not marketed well – i.e. – there is simply no money in my bringing a product like this to the market as you can already get some VERY cheap brands (in my attempt to head off the potential boo’s and hiss’). The thing I like the most is that is has an impeccable safety profile. This is NOT something that can be said about a lot of supplements.

Pharmacology – SAMe is formed in the body already by combining the essential amino acid methionine to adenosine triphosphate (ATP). Over 50 biochemical reactions in the body draw upon this compound. It functions close with folic acid and vitamin B12 in methylation (addition of a methyl group – which is one central carbon atom with its outer electron shell requirements fulfilled with 3 hydrogen bonds – to another molecule, namely metabolites of steroid metabolism in this case) reactions. SAMe is many times more effective in transferring methyl groups than other methyl donors.

Shhh – I know a secret! SAMe is also required in the manufacture of all sulfur-containing compounds in the human body, INCLUDING glutathione (which we have spoken about at lengths thus far in its role within the liver – important for C17 alkylated users) and various cartilage components, INCLUDING chondroitin sulfate.

EVIDENCE-BASED EFFICACY: In extrapolating the data here, we visit SAMe’s positive effects in depression, liver disorders, migraine headaches, AND osteoarthritis – all of which are reported sides to a degree with PH/PS/ and certain AAS use.

My vote goes to SAMe as the most-effective dietary antidepressant (although admittedly, a strong argument could pit St. John’s Wort and this toe to toe and it would likely come down to the score card – you wouldn’t see a KO by any stretch of the imagination). Now, in studies SAMe has shown BETTER results than prescription antidepressants with less sides! There is more importantly, for our discussion, some hugely positive results in regard to relief of anxiety and depression associated with drug detoxification and rehabilitation. How does it do - become an effective antidepressant, that is? It increases levels of serotonin, dopamine, AND phosphatidylserine (wait a minute, can it too be anti-catabolic???). Serotonin and dopamine, in fact, see improved binding to their respective receptor sites.

Several liver disorders show phenomenal effect in response to SAMe therapy. These include: cirrhosis, Gilbert’s Disease/Syndrome (not incredibly terrible disease, I have it and my bilirubin levels have dropped since beginning use of SAMe – former elevations during periods of stress in my own serum levels are a thing of the past), oral-contraceptive induced liver damage (which may be data that extends across ALL progestin use – which obviates rationale for its use with certain PH/PS/AAS).

It doesn’t stop there! One of the absolute key functions of SAMe in the liver is the INACTIVATION OF ESTROGENS!!!!!!!!!!! Clinical studies have shown that SAMe is quite useful in protecting the liver from damage and improving liver function in conditions associated with estrogen excess – WHO DOESN’T SEE MY POINT??????? Admittedly, this estrogen excess is with oral contraceptive use, pregnancy, and PMS in the study sense, but application has proven interesting in my own in-house study here (see below).

SAMe has been shown to offer benefits in the treatment of more-severe liver disorders, including cirrhosis. One of the greatest risks of chronic liver diseases such as chronic hepatitis is liver cancer (hepatocellular carcinoma / hepatoma – being the worst case). Supplementation with SAMe appears to be very much indicated in these patients in the attempt to reduce the risk of liver cancer. Animal studies have shown a significant protective effect for supplemental SAMe against liver cancer in animals exposed to liver cancer.

SAMe has shown tremendous efficacy in the battle against osteoarthritis. A deficiency of SAMe in the joint tissue, just like a deficiency of everyone’s well-accepted glucosamine, leads to loss of the gel-like nature and shock-absorbing qualities of cartilage. As a result, one of the proposed mechanisms of pathophysiologic etiology of osteoarthritis is SAMe deficiency.

SAMe has been studied in a total of 21,524 patients in detailed clinical trials. In these studies, SAMe has demonstrated reductions in pain scores and clinical symptoms similar to those achieved with non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, indomethacin, naproxen, and piroxicam. While these drugs are associated with significant risk of toxicity, side effects, and actual promotion of the disease process in osteoarthritis, SAMe offers similar benefits without the same risks of side effects. Can you imagine how this information can all be applied to bodybuilding lifestyles and the essence of weight-bearing issues with heavy poundages post-cycle (due to obvious strength increases and adjustment) or not?

FORMS & DOSAGES: SAMe is available in capsules and tablets. Commercially, it was brought to Europe in 1975, however it took 13 additional years for it to show up here in the United States. The recommended normal dosage is too low for someone post cycle. I recommend an enteric-coated 400 mg up to two times per day in the post cycle realm (this cannot be overstated in post-cycle time frame surrounding C17 alkylated products!). You may consider titrating up in dosing and there are interestingly enough no volume of distribution effects here to consider.

Don’t let your head spin in trying to figure out labeling. I’ll do it for you. SAMe is sold with added compounds for stabilizing the molecule and preventing degradation. These compounds include: tosylate, disulfate tosylate, disulfate ditosylate, and 1,4-butanedisulfonate (Actimet), and they’re usually written immediately after SAMe’s chemical name on the bottle (see dinoiii’s tip below).

POTENTIAL SIDE EFFECTS / INTERACTIONS: Individual’s with Bipolar Disorder (manic depression) should not take it. Why? It’s antidepressant effects discussed earlier could induce a manic phase. Be advised. Adverse effects are usually of the mild gastrointestinal variety (i.e. – nausea, diarrhea, etc...) which is why I recommend enteric coating as it tends to decrease these potential sides.

Dinoiii’s tips:
(1) Typically, the stabilizing compounds I mentioned earlier (tosylates, et al) weigh as much as the SAMe molecule itself. Consequently, a tablet containing 200 mg of SAMe disulfate tosylate contains ONLY 100 mg of SAMe. Most, but not all labels are likely to make this clear.
(2) Don’t let companies fool you here – there have been many independent lab testing done on various SAMe brands...if you ever have a question on a brand that matched up to label claims (only less than 50% do!) just let me know.

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[dinoiii]

Silymarin

So, we see this term thrown about, but not too often do we hear, what in the world is this, but somehow, I am sure not many of you know (but your secret’s safe with me). I will allow you now to act smart in front of your friends free of charge with your silymarin knowledge. In short, silymarin is a fancy, shmancy name for a mixture of flavonoid components (i.e. – silybin, silidianin, and silichristine) from milk thistle. The concentration of silymarin is highest in the fruit, but it is also found in the seeds and leaves. Milk thistle extracts standardized for silymarin usually find their way into your favorite supplements at about a 70-80 percent concentration.

Fancy Shmancy, maybe. However, silymarin is at least ten times more potent in antioxidant activity than vitamin E and also increases the liver’s own antioxidant, glutathione (which we have spoken about at great lengths thus far in this series) by OVER 35%!

EVIDENCE-BASED EFFICACY: Positive effects have been seen with 70-80% concentration in treating several types of liver disease, including hepatitis and cirrhosis. The therapeutic effect of milk thistle extracts in these disorders has been confirmed by biopsy as well as by clinical and laboratory data.

Although milk thistle extract has shown benefits in treating acute and chronic viral hepatitis, the results with milk thistle extract are most impressive when looking at studies evaluating its effectiveness in alcohol- or toxic-chemical-induced hepatitis, which is why it applies readily to the post-cycle time frame. For example, in one double-blind study in workers exposed to toxic toluene and/or xylene vapors for five to twenty years, milk thistle extract (Thisilyn) was shown to significantly lower levels of AST and ALT, while significantly improving other blood measurements, such as platelet count, white blood cell count, and percentage of lymphocytes compared to other white blood cells (but it’s use can also create an inaccurate picture for clinician’s, so we must be wary in our question asking during history taking).

Even in cirrhosis of the liver, milk thistle extract has shown some benefits. Although not all studies have shown significant effects, in one controlled study the four-year survival rate was 58% in the milk thistle group compared to 39% in the control group.

There have been no studies to date examining the potential of milk thistle to treat gallstones through it’s ability to increase bile solubility (gallstones form when bile components fall out of solution). When there are drastic body re-composition events, namely fat loss – this is ABSOLUTELY AN IMPERATIVE POINT as gallstones have a tendency to readily form.

FORMS & DOSAGES: Milk Thistle is available as bulk and dried seeds, as tea bags, as a tincture, as a fluid extract, and as a solid extract in tablet and capsule forms. Extracts standardized for silymarin content are preferred as it is the component proposed to be responsible for the extract’s mechanism of action (recall bioflavinoid complex discussed earlier). There is some preliminary data to suggest combinations of Silybin, the key component in silymarin within milk thistle, and phosphatidylcholine would help aid absorption. It is too early to tell and the data available was thus far only published by those with vested interest, so I cannot say definitively. The regular version standardized should be good enough anyway – so why get fancy?

The goal of therapy here will be based on silymarin content. If using the dried seeds, a much lower dose is necessary to see positive effects of the compound.

POTENTIAL SIDE EFFECTS / INTERACTIONS: The earliest side noted is a looser stool (due to increase of bile output). Aside from that, it tends to be a rather safe supplement with a great track record.

If you are taking the following drugs: thyroid hormone, acetaminophen, butyrophenones, phenothiazines, phenytoin, and even alcohol, I advise AGAINST the use of milk thistle as it has a tendency to drive down efficacy of these agents.

Dinoiii’s tip(s):
(1) If loosened stool side effect occurs, it is a good idea to take some sort of fiber source (i.e.- guar gum, pectin, psyllium, and/or oat bran) with your milk thistle dose if it is desired to continue to use the product. This will help aid bile binding preventing irritation.

-----------------------------------------IN-HOUSE STUDY -------------------------------------

Houser, D. The Efficacy of Various OTC Hepatoprotectants in the Post-Cycle time frame following use of C17 alkylated PH/PS – a double-blind, placebo controlled look. (2004) [Unpublished to date-see below]

Study Group: 34 clients in Post-Cycle Therapy after the use of upper-limit dosing of various C17 alkylated PH/PS products. The breakdown of the in-house participants was as follows:

Group A: 15 Solitary M1T (Dosing Parameters: 20 to as high as 60 mg per day x 6-10 week cycles).
Group B: 7 M1T + MD (Dosing Parameters: 12 to as high as 30 mg per day of each x 4-12 week cycles).
Group C: 12 MD + MOHN (Dosing Parameters: 12 to as high as 20 mg per day of each x 4-18 week cycles).

Group A

Study Participants:
5 participants – 600mg NAC
5 participants – 400mg enteric-coated SAMe
3 participants – 600mg NAC + 400mg enteric-coated SAMe
2 participants – placebo-control

“Cliff-Notes” Summary: 4 of 5 participants in SAMe-only group and all 3 participants in NAC + SAMe group had an average 5-day faster return to baseline of AST/ALT elevations than NAC and placebo-control. The addition of NAC in the dual-coverage group seemed to offer no additional benefit without statistically significant results between the two. NAC + placebo-control groups saw no statistically-significant changes in AST/ALT levels. Results seem to suggest SAMe is superior, at least in the post-cycle realm, to NAC in returning transient LFT elevations to baseline INDEPENDENT of cycle length. The essential caveat was the unanswered question in regard is why one of the SAMe-only participants mimicked results of NAC and placebo. Author’s Note: A current follow-up series of serum studies in specific regards to this individual are underway as we speak in hopes of offering answers.

Group B

Study Participants:
3 participants – 600mg NAC
3 participants – 400mg enteric-coated SAMe
1 participant – 600mg NAC + 400mg enteric-coated SAMe
(Author’s Note: not enough participants in this arm for placebo-control)

“Cliff-Notes” Summary: Similar results to Group A were seen in this arm. The SAMe-only and SAMe + NAC participants saw an average 3-day faster return to baseline of AST/ALT elevations. The faster return to baseline of transient LFT elevations was again INDEPENDENT of cycle length. It is truly unfortunate that there was no ability to gain a placebo-control group here, but M1T + MD in a concurrent run was not one of the most popular cycles when these PH/PS products were still being marketed legally. With the support of the first and third arms of the study, some definite inferences can be made. It would appear that the SAMe inclusion is what offered aid in the post-cycle realm for expedited returns to baseline LFT.

Group C

Study Participants:
4 participants – 600mg NAC
4 participants – 400mg enteric-coated SAMe
2 participants – 600mg NAC + 400mg enteric-coated SAMe
2 participants – placebo-control

“Cliff-Notes” Summary: Once again, the SAMe-only and SAMe + NAC participants saw an average 8-day faster return to baseline (inferences about the strength of PH and subsequent elevation in transaminase can likely explain the difference 5 vs. 3 vs. 8 respectively for the three arms) SPECIFICALLY in cycles under 8 weeks. Cycles that extended beyond this time frame tended to exhibit results that were not statistically significant when compared with either the NAC-alone or placebo-control groups. Of note, 2 participants in this arm did NOT see LFT elevation (1 in NAC only and 1 in NAC + SAMe groups). This is likely to be attributed to one of two things: specificity to elevation to particular PH/PS run or irregularly low-level baseline LFTs (of which has not been explored to date due to lack of participant follow-up).

* Author’s note: All information gathered here was done prior to the October 2004 ban. Due to legal issues, follow-ups for replicability are thwarted by the Steroid Control Act of that year. The aforementioned 3-arm study will appear in an upcoming book with complete lab values verified by Quest Diagnostics reports.
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Summary of Hepatoprotectant Use in PCT: Despite certain supplement companies’ claims, the attempts to replicate NAC results in oral (PO) form have been less than stellar and shows these particular supporters simply either not doing their homework or just attempting to “kitchen sink” their products with a bell and whistle. You can get away with very cheap brands quality-tested, but it is imperative to be careful in choosing which brand to go with. Fortunately enough, many brands of SAMe have been tested independently and it would appear this to be the OFFICIAL dinoiii agent of choice at this time, especially post-C17 alkylated oral use.

Quality Dose: 400mg enteric-coated SAMe (keeping in mind concentration of stabilizers we learned about above) two times per day (bid) + Milk Thistle (dose accordingly).

[dinoiii]

PROSTATE HEALTH

As a male, you are likely to be bombarded by information pertaining to clinical syndromes surrounding the prostate. It is imperative that you seek the help of an examining physician to make a definitive diagnosis and steer clear of not trying to self-dianose. The following three items have shown some positive report in the literature surrounding PREVENTATIVE measures and thus are considered here.

Saw Palmetto (Serenoa rapens)

EVIDENCE-BASED EFFICACY: Numerous double-blinds have shown an extract of the berries from this Florida-native palm tree to be efficacious in the realm of treating benign prostatic hyperplasia (BPH), a significant concern when introducing exogenous androgens into the male human body. Newer data suggests that this may be an even larger concern in the post-cycle realm considering the increasing support for both estrogen and DHT as two sources of the seven accepted contributing mechanisms of action to date. While it usually takes a reported average of 4-7 weeks to see results, planning accordingly would imply the need for this supplement in a pre-cycle preventative mode.

FORMS & DOSAGES: Crude form available in bulk as dried berries and in tea bags. Also available are tinctures, fluid extracts, fat-soluble extract in a soft gel cap, hard gel cap, and tablets. Dosage will depend on standardization (see later).

POTENTIAL SIDE EFFECTS / INTERACTIONS: The caveat here is that there is a case-report of saw-palmetto induced hepatitis (presented to the American College of Physicians in 2005 by one of my colleagues, however, this has NOT been reproduced nor published in a peer-reviewed journal to date as far as I am aware though the presenter of the aforementioned case is preparing a subsequent article.). Nonetheless, it stands to reason that this area would need to be further explored before making definitive recommendations especially when considering recovery from a C17 alkylated product. Aside from this, rather detailed toxicology studies in rodents and clinical trials in humans have shown a tremendous track record in the way of safety and current use of the product alongside a basic LFT studies would offer good indication of what may necessitate further exploration from a clinical standpoint.

Dinoiii’s tip(s):
(1) It is imperative to keep in mind that an overwhelming majority of studies used fat-soluble saw palmetto extracts standardized to 85-95% fatty acids and sterols so replication may require the use of such standardized forms in your own practice. The aforementioned individual with the saw-palmetto-induced hepatitis could NOT report if there was standardization to the formula he used. The results remain suspect.
(2) Prostate-Specific Antigen (PSA) serum studies remain a poor deliniating factor between BPH and Prostate cancer. However, elevated levels usually imply some form of increased tissue (see Part II for specifics). Saw Palmetto remains unable to modify PSA serum values that would correspond to symptomatic improvement, which may imply yet another to-be-determined mechanism of action to add to the seven current.

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Pygeum (Pygeum africanum)

EVIDENCE-BASED EFFICACY: 36 clinical studies, 14 of which, double-blind have shown efficacy [author’s note: this efficacy has unfortunately been limited by the number of objective measures – urine flow rate (ml/sec), residual urine content, and prostate size - used in many, yet not all, of them] with regards to improvement of many of the symptoms surrounding BPH (nocturia: nighttime urinary frequency, difficulty in starting urination, and incomplete bladder emptying).

An area that may be worth exploring is something not replicated in the saw palmetto groups. That being the additional benefits seen with improvements in erectile dysfunction, an obvious concern for some people in the post-cycle realm considering hormonal flux. A question to ask is whether or not this is attributed to a vascular mechanism or hormonal? Additionally, there is minor evidence to suggest some potential benefit in the realm of male infertility. This last one is likely ONLY to be effective in cases where prostatic secretion and its contribution to the total ejaculate is significantly reduced.

FORMS & DOSAGES: Clinical studies have been done on Prunuselect, a fat-soluble extract standardized to contain 14% triterpenes. Its availability is either in as a stand-alone in soft gel form or as a soft gel or capsule in various multi-ingredient products on the market. A few liquid multi-ingredient formulas have started popping up on the market as of late.

POTENTIAL SIDE EFFECTS / INTERACTIONS: Most common side effect remains GI upset (nausea, vomiting, abdominal pain, diarrhea, constipation).

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ERECTILE DYSFUNCTION ALLEVIATION

Yohimbe (Pausinystalia johimbe)

Only one additional comment need be made at this time as I delved into thorough discussion of this compound in the last part of this article series.

POTENTIAL SIDE EFFECTS / INTERACTIONS: Yohimbine can cause many side effects, including anxiety, tremors, insomnia, a rise in blood pressure, palpitations, nausea and vomiting, and hallucinations. Taken in high doses, it can cause a SEVERE drop in blood pressure (recall: AUTOREGULATION posts I have spoken at length about), weakness, and paralysis. Some states have banned the nonprescription sales of yohimbine (even as a yohimbe extract), and the FDA has ruled it unsafe as an over-the-counter product in the past.

[dinoiii]

ANTIHYPERTENSIVES

Unless you have a firm grip on how PS/PH/AAS have affected your blood pressure (BP), the following supplements are potentially better left alone until you establish a true baseline set of values (systolic and diastolic).

Hawthorn Berry

EVIDENCE-BASED EFFICACY: Considerable research, both in animal and human studies, supports the claims about hawthorn’s heart benefits. For example, double-blind studies of hawthorn versus placebo have shown improvements in people with heart failure, demonstrating better heart function, less shortness of breath, and fewer palpitations. In a study of thirty patients with congestive heart failure, half were given a placebo and the other half given twice daily capsules of hawthorn extract standardized to contain 15 mg procyanidin oligomers per 80 mg capsule. After 8 weeks, the hawthorn group had statistically significant improvements in heart function and lower blood pressure, with no adverse reactions observed. In a study of 78 patients with the same level of heart failure, those given 600 mg of standardized hawthorn extract were able to exercise much longer than those who received the placebo [now, before every supplement manufacturer gets excited and says boy, we got to market that – the same results have NOT been duplicated in non-heart failure patients]. Based on numerous studies, German health authorities have approved of hawthorn for treating mild heart failure, stable angina, and the slow heart rhythms known as bradycardia.

Less evidence, in animals only, is available to support hawthorn’s potential benefits in lowering cholesterol, triglyceride, and blood sugar levels. Similarly, no human research supports its use in treating insomnia, although it is known that high doses can markedly slow down the nervous system.

FORMS & DOSAGES: Hawthorn is available in many forms, including dried leaves, berries, and flowers, and in elixirs, extracts, infusions, capsules, and tinctures. Usually taken 2 or 3 times a day, the dosage depends on the type of preparation and source material. An infusion dose can be made with a teaspoon of chopped leaves and flowers. Tinctures may be recommended at 4 to 5 ml per dose. Flower extracts, standardized to contain 1.5 percent vitexin-4’-rhamnoside, may be prescribed at 100-250 mg per dose. It may take UP TO 3 MONTHS to note improvement; hawthorn may be taken indefinitely to treat chronic heart failure and other disorders.

POTENTIAL SIDE EFFECTS / INTERACTIONS: Toxic problems with hawthorn are NOT commonly seen and usually only have shown the potential of appearing when overdosed. In such cases, dangerously low blood pressure and sedation may occur. However, because of its potent effects, it should be used with care and only under the supervision of physicians experienced in its impact (unfortunately this is very few). In particular, its use with other heart medication is a serious problem. We’ll use beta-blockers as an example. Because beta-blockers lower blood pressure by reducing cardiac output, simultaneous use of hawthorn may produce a mild RISE in blood pressure (remember, how much I have spoken at length about autoregulatory effects). In contrast, hawthorn can markedly INCREASE the effects of digitalis and other herbs containing cardiac glycosides to enhance their effects. When used with prescription heart drugs, the dosage of the LATTER can be lowered. It should be noted that hawthorn will NOT stop an angina attack.

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Celery

Its diuretic action of the active ingredient (3-n-butyl phthalide) may be left for late PCT time if you are opting to use concurrent cell volumizers.

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CoQ10

EVIDENCE-BASED EFFICACY: Several well-regarded studies indicate that adding CoQ10 supplements to the conventional regimen for treating cardiomyopathy and congestive heart failure show MORE improvement than with medications alone. In a study involving more than 2,500 heart patients in Italy, 80% experienced reduced symptoms (shortness of breath, swelling of the legs and feet, difficulty sleeping) after 3 months of taking CoQ10. It is also a standard treatment of congestive heart failure in Japan. However, the American Heart Association and the American College of Cardiology do NOT advocate CoQ10 as a treatment for heart disease. In any event, CoQ10 should NOT be taken as a substitute for prescribed medication to treat heart failure or any other cardiovascular disease, and if you do take it as part of an overall treatment program, be sure to tell your doctor that you are taking it.

Several studies are underway to investigate whether Co Q10 may help slow the progression of degenerative nerve diseases, such as Parkinson’s and Alzheimer’s, as well as fibromyalgia. Though claims abound concerning CoQ10’s ability to slow aging, reduce fatigue, and improve the quality of life for AIDS patients, promote healing of periodontal disease, and even aid weight loss, more study is needed to document whether it really works in these instances.

FORMS & DOSAGES: CoQ10 typically comes in tablet or pill form, but is also available as a liquid or softgel capsule. It’s even found in some skin creams. Doses thought to be effect for heart disease range from about 100 to 360 mg / day. One small study found that people with cardiomyopathy who took 100 mg or CoQ10 per day, in addition to regular therapy, showed significant improvement compared to those who received a placebo. In another study, a significant number of patients given CoQ10 were able to reduce the number of heart medications they were taking.

POTENTIAL SIDE EFFECTS / INTERACTIONS: There are NO reports of side effects from CoQ10 supplements.

Dinoiii’s Tip(s):
(1) Take your CoQ10 supp with a MINIMUM of a teaspoon of oil mixed in a protein shake. This should aid + increase its absorption potential.
(2) If taking either a beta-blocker or statin drug OR red yeast rice supplement, there is a potential of dramatic decreases in CoQ10 levels in the body. People who take either of these medications (while NOT advised to be on PH/PS/AAS in the first place) should consult with a health care provider to see if CoQ10 supplementation is advisable.

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Garlic

EVIDENCE-BASED EFFICACY: Researchers have been studying the effects of garlic on the body for years, and hundreds of studies have been published suggested how garlic works and trying to pinpoint the specific properties of the herb that are responsible for its metabolic and disease-fighting effects. Many positive results have been found in animal studies, but the findings have NOT been duplicated in controlled clinical studies in humans. For example, garlic has been fed to hypertensive rats and dogs, with statistically significant reductions in blood pressure. Other animal studies suggest that garlic’s sulfur-containing compounds inhibit the stiffening of the aorta in an aging population. But human studies have NOT been so conclusive. Although many researchers believe that garlic has definite health benefits, is NOT known how much must be consumed to be effective. Nonetheless, population studies in Italy and Spain, where large amounts of garlic are consumed, have found that atherosclerosis is uncommon, despite a high-fat diet, although its becoming more common in large cities even there.

Compounds in garlic have been shown to have anti-clotting properties when mixed with blood platelets in a test tube. In one laboratory study, ajoene prevented the formation of blood clots in dogs undergoing open-heart surgery. Other studies have found that ajoenes and dithiins may possess anti-tumor and anti-fungal activities, and thus may help prevent cancer and various yeast infections.

Researchers are also investigating the antioxidant properties of compounds in garlic, which may also help prevent cancer. Sixteen separate animal studies suggest that garlic inhibits the development of tumors, even in those exposed to carcinogenic materials such as carbon tetrachloride, isoproterenol, and heavy metal poisoning. But other studies found that, in rats, garlic does NOT inhibit tumor growth once cancer has developed.

FORMS & DOSAGES: Garlic is available in many forms – fresh bulbs that can be bought in any produce market as well as pills and extracts. Many experts believe that the most benefits are obtained from the whole garlic, preferably raw or very lightly cooked. When pills are taken, the recommended daily dosage is 300 mg of powder per day, the equivalent of the allicin in one or two whole cloves.

POTENTIAL SIDE EFFECTS / INTERACTIONS: Garlic is notorious for causing an unpleasant breath and body odor. This problem can be lessened by taking deodorized garlic pills, but even in pill form, large dosages of 900-1,200 mg a day can cause a garlicky body odor. Some people also experience an upset stomach, heartburn, and other intestinal problems, even when they only eat a small amount of garlic. Because of its anti-clotting properties, high doses of garlic should NOT be used by anyone taking blood-thinning medications OR who have bleeding problems.

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Taurine

EVIDENCE-BASED EFFICACY: This amino acid is involved in the regulation of heartbeat, maintenance of cell membrane stability, and prevention of brain cell overactivity. It has been shown in small double blinds to be effective in heart failure prevention, lowering blood pressure, and seizure reduction in people with poorly-controlled epilepsy. Larger studies would be appreciated to better assess the therapeutic value here.

FORMS & DOSAGES: Every version short of an ethyl ester – oh, wait a minute – as we speak it is likely on the way. 2g taken up to 3 times a day is what is shown in the aforementioned studies to be efficacious dosing.

POTENTIAL SIDE EFFECTS / INTERACTIONS: None known.

[dinoiii]

CHOLESTEROL/DYSLIPIDEMIA-MODIFYING AGENTS

Wow! This particular category needs addressing. While there are some negative cholesterol modifications (i.e. – decrease HDL, etc...) while during cycle, post-cycle, when an inherent ABSOLUTE NEED for steroidogenic substrate predominates, the use of cholesterol-modifying agents should be used with ABSOLUTE DISCRETION. Couple this with my Cholesterol Controversy series and the lipid outcomes may simply require monitoring them through serum studies. Our driving back substrate is the rationale for these modifiers.

[Author’s note: in the case of familial dyslipidemia syndromes, the use of such agents is better-warranted at the discretion of your primary health care giver / endocrinologist]

PRIMARY GOAL: LOW HDL CORRECTION

Niacin (Vitamin B3) + My Anti-Flush Protocol

EVIDENCE-BASED EFFICACY:

FORMS & DOSAGES: Niacin (nicotinic acid or nicotinate), inositol hexaniacinate, niacinamide. Niacin and inositol hexaniacinate are useful in blood cholesterol modification, while niacinamide has shown some positives in arthritis literature and a few very old studies with improvements in early-onset type 1 diabetes.

Niacin is available as pure crystalline niacin and in sustained- or timed-release preparations. Because of the risk of liver toxicity (namely following the use of C17 alkylated PH/PS/AAS), sustained release niacin should not be used in the post-cycle time frame (sometimes a time-released version is snuck into multi-vitamin formulas – be very careful). Inositol hexaniacinate yields slightly better results orally than standard niacin but is much better tolerated in terms of flushing and, more important, long-term side effects.

POTENTIAL SIDE EFFECTS / INTERACTIONS: Because niacin can cause liver damage, periodic checking of LFTs is still recommended every 3-4 months of therapy to assess damage. Telling your physician that you are taking niacin is a good way to have him monitor alongside you changes as they should occur.

Dinoiii’s tip(s):
(1) Remember here again, LFT’s – despite their connotation are NOT liver-specific. You must also make your doctor aware of your weight lifting lifestyle as a concurrent CPK should be drawn. Muscle breakdown, which is not abnormal for you may cause slight elevation of these levels.
(2) What’s an anti-flush protocol? Standard Niacin 50mg or less + Inositol hexaniacinate 500mg – should fend off the harmless yet


PRIMARY GOAL: HIGH LDL REDUCTION

Red Yeast Rice

EVIDENCE-BASED EFFICACY: ONLY two of the more than two dozen clinical studies using red yeast rice were done in the United States; the rest have been done in China. Taken as a whole, the studies have found that red yeast rice can lower cholesterol by 16 to 26 percent as well as lower triglyceride levels and raise beneficial HDL cholesterol. A recent study found that red yeast rice lowered blood cholesterol an average of 40 points over a twelve-week period compared to just 5 points in people who only made dietary changes. Benefits are greatest in people with total cholesterol levels above 200, the cutoff point of desirable cholesterol set by the American Heart Association.

FORMS & DOSAGES: The standard dose is two 600 mg capsules twice a day. It is sold in capsule form at pharmacies and health food stores, and it costs ONLY a fraction of what prescription statin drugs cost. Red Yeast Rice is recommended for people with borderline-high cholesterol levels (200 – 240) and NO other risk factors for heart disease. A low-fat diet is also recommended while taking the supplement. To avoid stomach upset, it should be taken with fluid or fluids.

POTENTIAL SIDE EFFECTS / INTERACTIONS: Minor side effects reported include heartburn, bloating, and dizziness. Because of its similarity to statin drugs, which should NOT be taken with niacin, erythromycin, cyclosporin, fibrates or other statin drugs, the same cautions should be applied to red yeast rice. Red yeast rice could cause some of the same side effects as statin drugs, including elevated liver enzymes (which is what you are trying to return to normal in the post cycle period), damage to skeletal muscle, and a possible increased risk of cancer! Individuals with severe liver or kidney damage need avoid this compound like the plague. NO ONE UNDER THE AGE OF 21 SHOULD TAKE RED YEAST RICE.

Dinoiii’s tip(s):
(1) Cholestin is the ONLY red yeast rice product that is standardized and that has been shown to be effective in clinical trials.

__________________________________________________ _

Guggulipid

EVIDENCE-BASED EFFICACY: This guggul derivative gained approval as a lipid-lowering drug in India in 1986, although as stated in Part II, the herbal use dates back numerous centuries. Numerous studies in animals AND humans over the past 40 years, conducted by researchers in India and elsewhere, have demonstrated the ability of guggul to lower cholesterol and triglycerides. Research was prompted by exploration of the association between obesity and atherosclerosis in ancient Ayurvedic texts. This led to animal studies showing that it lowered both weight and cholesterol levels in rabbits (I know, I know what you’re thinking – you don’t have the same size ears nor a button tail...of course – but bear with me – this was landmark at the time). Further studies showed similar results in humans.

In one study involving 50 patients with coronary artery disease, those who took 10-15 grams of guggul daily for three months showed an average 25 percent drop in total cholesterol and a 30 percent reduction in triglyceride levels. In another study, 22 patients with high blood cholesterol and other lipids were given 1,500 mg of guggulipid daily. Cholesterol levels began to drop within 2 weeks and were significantly reduced in 59 percent of the patients at the end of six weeks. Among responders, serum cholesterol and triglyceride levels and triglyceride levels were lowered 24.5 and 27.3 percent respectively. One could question if the “non-responders” would have seen better results in either a longer-term study or increased dose – if a shorter span were to be effective due to volume of distribution data potentially challenging efficacy. One of these questions was answered. In a multicenter trial involving 205 patients, 1,500mg of guggulipid daily for 3 months (obviously, longer than the 6 weeks used in the previous report) resulted in a 23.6 percent lowering of total cholesterol and a 22.6 percent decline in serum triglycerides in 70 percent of patients treated. In yet another study, the effects of guggulipid on cholesterol and triglyceride levels were found to be similar to those of clofibrate, a popular cholesterol-lowering drug.

Preliminary studies also support guggul’s antioxidant properties and ability to inhibit blood clots, although more research is needed to get me to buy into how accurate these latter effects are. Similarly, although the oldest uses of guggul as an anti-inflammatory agent for such conditions as arthritis, less research has been done in this area as scientists have been focused on its potential cardiac benefits. Thus, only a few animal studies have been done in demonstrating its anti-inflammatory value and it is NOT known whether this will translate into clinical benefits in humans.

FORMS & DOSAGES: Although guggul is available in its crude resin form, clinical studies have involved capsules and tablets that are purified to remove the insoluble components and standardized for guggulipid or guggulsterone concentration. Indeed the guggulipid dosage is usually based on guggulsterone concentration. Most commonly prescribed in clinical trials has been 25 mg of guggulsterones (or 500 mg of product standardized for 5% guggulsterone content), to be taken THREE TIMES DAILY. A comparable dose of the crude gum guggul powder would be 4 to 16 g per day divided into 3 doses.

POTENTIAL SIDE EFFECTS / INTERACTIONS: The only side effects associated with guggul are TRANSIENT and MINOR gastrointestinal problems such as nausea and diarrhea and, less commonly, restlessness, headache, and hiccups. Such problems are less likely when purified guggulipids are given, rather than the crude resin – which is consistent with MOST supplements today. Use in someone who is already taken other medications/supplements MUST be fully evaluated – especially with antihypertensives. Why am I saying this? In one study, for example, guggul reduced peak plasma concentration of propoanaolol and diltiazem – drugs used commonly to treat high blood pressure and heart disease.

There has been discussion as of late regarding guggulsterones cytotoxic nature as well as interaction of with the androgen receptor. First, the cytotoxicity is very specific and actually a good thing. This specificity is through myeloid precursor cells via inhibition of proliferation of HL60 and U937. From the research group in question: “These growth inhibitory effects correlated with externalization of phosphatidylserine and loss of mitochondrial membrane potential, suggesting that these isomeric steroids induce apoptosis in leukemia cells.” This study was the first of its kind to show anti-leukemic effects offering us hope at another chemotherapeutic agent. If you haven’t guessed this is a positive finding.

On to talk of the androgen-receptor binding. First of all, it should be noted that the studies here are funded by a particular competitive drug company (in various drug categories that span many of the aforementioned positives of guggul we have talked about here) and are somewhat tainted in that regard. Additionally, the binding pretty much spans many nuclear receptors and has been demonstrated solely in vitro. It is uncertain whether any outward physical signs are to ever be reported as with MANY years of supported use and positive effect, and clearly further study is needed but hopefully that of the independent variety.

For now, no hypogonadal signs clinically, a definitively higher binding capacity to other receptors – namely mineralocorticoid, and the plethora of good effects already stated topped off by anti-leukemia action leaves this a very strong supplement to consider. Its purported estrogen agonistic effect may be a bit frightening to many in the immediate post-cycle realm, but all ER’s are not identical (just as estrogens) and its affinity for the sub-alpha receptor is NOT seen with the sub-beta. For various reasons, progesterone stimulation (another purported action) kept at a minimum during PCT could offer benefits in an entirely different regard.

[dinoiii]

ANTI-CATABOLICS

7-oxo DHEA (3-acetoxyandrostat-5-ene-7,17-dione) / 7-ketoDHEA

DHEA finds conversion into some 150 metabolites (that we are currently aware of), each with unique actions within the body. One of the reasons my aforementioned comments about the mother-compound DHEA on how I think it is a prohormone that should in fact be banned are worrisome is due to the likely subsequent banning of potentially-useful metabolites. In the early get-go, 7-oxo, TM’d as 7-keto products seem to hold the most promise supported by the literature. I like its seemingly absent conversion to estrogen or testosterone and its anti-catabolic properties (which are purported to control and/or reduce body fat.

The rationale supplied for use of this compound in the post-cycle era, however, through cortisol suppression, I have never understood effectively as stated in Part II and in various posts. Exogenous androgen introduction tends to universally suppress the adrenal gland via feedback inhibition of ACTH. Recall that ACTH subsequently imparts action on production of various adrenal hormones, in this case cortisol being one. For how this effect is seen here, I offer the following “simplified” model:

Step 1: “On” cycle = exogenous androgen introduction, not only leading to subsequent endogenous shutdown of the Leydig cell production of testosterone through feedback inhibition of the pituitary’s production of LH, but also a negative feedback that mimics adrenal cortical (zona reticularis) overproduction of androgenic outflow offering negative feedback tie-in to ACTH pathways.

Step 2: “Off” cycle (PCT) = cessation of exogenous androgen introduction in a still suppressed ACTH (albeit partial) environment (hypOadrenalism) and subsequent low-level cortisol production, amongst other adrenal byproducts.

Step 3: ACTH regeneration BEFORE LH regeneration (due to partial vs. complete negative feedback mechanisms). The question we set out to answer was when this becomes clinically significant. The answer appears to be more complex than the time I would like to offer here, however, I will summarize a few key points:

(1) Half-life of the exogenous compound seems to play a role on ACTH regeneration (which may seem “common sensical”, but how many automatically have assumed immediate catabolism?).
(2) Many factors (dietary as well as other) seem to impart a role on anti-catabolic nature of post-cycle time frame (again, perhaps another “common-sensical” point, but how often is it seen that people go from a hypERcaloric state while “on” cycle into a state of immediate hypOcalorism?).
(3) Another in-house study has given us some answers into regeneration-time frames. Oveall, the 3-week mark post-cycle appears preliminarily to be a time of universal cortisol up-regulation. The first two weeks are assumed to remain in suppression almost independent of the type of agent used. Use of substances such as 7-oxo / 7-keto compounds seems better left out of post-cycle planning for that immediate 2-week time frame.

[author’s note: complete in-house study results will too appear in upcoming book release!]

[dinoiii]

Conclusion

As we come to the conclusion of this part of the PCT: ACV series, you may be caught up in the science or you may be dazed by what you are going to do with all that extra NAC you made sure you stocked up on. Below I have summarized my thoughts on the various supplements presented here. Again, this is an incomplete list of supplements but some of the more common used. If there are additional questions regarding any particular agent, add comments below.

Summary of “PCT: ACV-approved” supplements:

Anti-Estrogenics
1. Aromatase Inhibitors (AT/ATD): - -
2. Estrogen Channeling Agents (I3C): ++++

Pro-Testosterone
1. DHEA: -
2. Tribulus Terrestris: ++
3. Stinging Nettle: +++
4. Magnesium: ++
5. Zinc: ++

Antioxidants
1. ALA: ++++
2. L-carnitine: ++++
3. ALCAR: +++
4. PLC: +++
5. ACES: +++

Hepatoprotectants
1. NAC: -
2. SAMe: +++++
3. Silymarin: +++

Prostate Health
1. Saw Palmetto: +++
2. Pygeum: +
3. Boron: +++

Erectile Dysfunction
1. Yohimbine HCl: -

Antihypertensives
1. Hawthorn Berry: +++, - (w/ cP450 3A4 inhibitors)
2. Celery: - (immediate post-cycle or w/ cell-volumizers)
3. CoQ10: +++++
4. Garlic: ++
5. Taurine: ++

Cholesterol / Dyslipidemia – Modifiers
1. Niacin / Inositol Hexaniacinate Anti-Flush Protocol: +++
2. Red Yeast Rice: -
3. Guggulipid: ++
4. Policosonol: ++

Anticatabolics
1. 7-oxo / 7-keto: - (immediate post-cycle), + (roughly 3-weeks post-cycle)

Others - not discussed
1. Corosolic Acid: +++
2. Fenugreek: +
__________________________________________________ ______________________
Key:

- = evidence-based efficacy lagging, innumerable potential for side effect or interactions, alternatively inappropriate for the post-cycle time frame

+ = some in vitro / hypothetical evidence to support its rationale, further research needed for general use as well as PCT use

++ = quality in vitro / some in vivo, post-cycle rationale requires further research

+++
or
higher = good in vivo studies + at least one double-blind regarding scenarios that mimic PCT considerations, the more stars above this point is due to the more quality research support
__________________________________________________ ______________________

Outside of taurine, many aminos (BCAAs, EAAs) and EFAs, CLA, Sesamin as well as glucose in the post-cycle realm are talked about at length in part VI of the series to follow. For now, it’s time to turn our attention to the world of pharmaceutics. The discussion that follows is NOT for the weak at heart – as stated earlier: the usual suspects (nolvadex, clomid, hCG, arimidex, etc...) will all be covered at length. Stay tuned.

[dinoiii]

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[TheKoos]

The + - ratings in the conclusion are very nice.

Well done.

I hope that part four does not take as long as part three did :)

Thank you for the information.

Koos

[Sonny]

Outstanding Work !

[Trans_Isomer]

Now we have to wait till part VI?

[Batman]

Nice write up, D. You might want to start clearing out your PM box, as I'm sure the questions will be coming in rapidly! Thanks for taking the time! BTW, when is the book due out? Any idea yet?

[dinoiii]

Yeah, the PM situation. I try and keep up with it. There are appx. 400 emails to go along with that. My posts will be restricted to the weekends over the next 4 weeks unfortunately from St. Louis, MO (not that I have anything against those from that area mind you!).

As far as the books. A name has officially gone through Trademarking for a complete training/diet series slated for fall release. The Supplement text I have described in the past is slated for a similar release. Both are schedule-dependent and I am a victim of time right now.

[dinoiii]

Questions directly pertaining to this article series will take priority and you can email them to me @
absivs_revenge@hotmail.com
there is an entire folder I will devote to them.

simply entitle them: "PCT:ACV III" and I will give them direct attention!

[Note: Website will be up within 2 months and this email will change.]

[garb]

once again dinoiii, you outdone yourself.......awsome post

[Dizzle1]

What is your background, are you a Dr., med student, where did you go to school? I find your infromation very interesting. Many of my clients are going off their medication and switching to herbal supplements and their health is increasing,what is your take on this,and if you agree what herbal therpies have you seen that are bringing about a better helath in people.

[italionstallionl]

Good post dinoiii. I found some things to be new info, and some confirmed what i already thought. Overall very helpful and a good read

[Jswoll]

A wealth of info as always, I will have questions D and I expect priority treatment since I am Jswoll--the most important individual ever!, but really bravo, well worth the wait and I think I mean this for every reader, we appreciate you taking the time and effort to share this, I'm sure it took a great deal of time to compile and write, thank you. GIVE ME MORE!

[dinoiii]

While I have attempted to keep my bio at a minimum - others had alternative plans for that during the last year. You will get a full bio soon (inclusive of the info you question Dizzle1), but it likely will not be surprising if you read this forum enough - I have been challenged plenty in the past. There has been a reason I have been somewhat allusive, likely leading to this kind of interrogation. For the time, I am happy I have stimulated your interest to the level you are continuing to question.

As far as a switch from meds --> herbal remedies. I think there is an adjunctive role that the two play. Unfortunately, you look at the allopaths and you get condeming of naturopaths and vice versa. In the process - the patient suffers. If the oath that I signed onto (i.e. - first do NO harm) is adequately adhered to, the patient should be the first consideration, NO?

That being said...when considering which herbals have been of benefit (i.e. - by me, defined as either decreasing morbidity or mortality or better - both), there are quite a few truly defined - I would hope you could be a little more specific - hehe, its an article in and of itself.

[Jswoll]

While I have attempted to keep my bio at a minimum - others had alternative plans for that during the last year. You will get a full bio soon (inclusive of the info you question Dizzle1), but it likely will not be surprising if you read this forum enough - I have been challenged plenty in the past.
You won't ever find me challenging ya, D; Frankly, I'm happy if you ain't in the same mental institution as I am;) But that's the thing about forums, you shouldn't have to put up your credentials just to speak (especially if you want to remain annonymous), it should be up to the reader to discern right from wrong, from those speaking from medical experience and true knowledge, if you can't tell then your not paying attention to the nitty gritty detail. Peace.

[dinoiii]

While I thank you for the support, I have not been exactly hiding credential - its all on here. I am taking a break from the medicine gig in July to pursue the supplement division full fledged (again, this is not new info).

What I am planning will revolutionize and again - this is far from hype. At that time with books and the whole nine, you all will get a very involved bio and a bit of rationale into that which I have not gone into on here, but I have bided time to a degree with just a huge lot on my plate at present.

In May, I will get the Master's (May 13th for all keeping score)....this is new info. Everything else I have been over ad nauseum - P-E-R-I-O-D!

I am entertained by those that attack versus care about the info placed in front of them. If someone cares to challenge what they have read in the article, I'd be more than happy to go a few rounds.

[TheKoos]

I hope DA is the first place your supplements and books will be available as they are released. If this is not the case I would love to know where and when, when the time comes. Good luck with this part of your career.

Koos

[Jswoll]

And remember Swoll gets his 4 free!

[shuttaLCD]

And remember Swoll gets his 4 free!


Ahh.. thanks man i never knew you were paying for mine..


LOL


Yea,

Bust of luck to you Dinoiii. Cant wait to see what the future will bring.. (mabye a revolutionizing supp...???)


-Shutta

[italionstallionl]

If someone cares to challenge what they have read in the article, I'd be more than happy to go a few rounds.

I cant debate you on this, due to my lack of knowledge, but I do have a question on I3c.

Do you think it has a strong enough effect on HPTA to be suggested solely for PCT use after a longer cycle with heavy shutdown? I always thought the goal was to stimulate HPTA to a high degree to get test back up to maximum natural output, which is why clomid is often called a "better" option for the initial phase of PCT, and Toremifene is "better" than clomid.

[Dizzle1]

I'm not questioning your background, if you're not a med student or Dr. I would be suprised by the wealth of knowledge that you have. My client was telling me about switching the water molecules in regular H2O and making it some super drink, ever heard of this?

[dinoiii]

Rapid fire response:



Shutta:
Actually, 8 "revolutionizing" supps to boot!!! and then there are 5 which are kind of staples.

Stallion:
I3C question - It seems that the mechanism of action includes a decrease in the feedback of estrogen (by way of default) on the HPTA.

Dizzel1:
Perhaps it is last year's occurence that leaves me somewhat bitter in the medical realm - again, its all on here.



I can only say you will soon see (actually we are coming down to the wire - late March/April website anticipation - summer subsequent intros).

[dinoiii]

Wanted to add a link for Milk Thistle that I posted some time ago - this is based on some email feedback:

http://www.discountanabolics.com/forum/showthread.php?t=1771&highlight=Milk+Thistle

[Jswoll]

Rapid fire response:

Shutta:
Actually, 8 "revolutionizing" supps to boot!!! and then there are 5 which are kind of staples.


8, really, remember Swoll=freebies; come on D, email me some secret details I just got to know I'll keep my mouth shut [He says like a little boy looking on in curiousity at the presents under the tree on Christmas morning]. I call beta-tester/guinea pig #1!

[dinoiii]

"Beta-testing" would assume we didn't already have 2 years of research to boot with the products though.

[Jswoll]

"Beta-testing" would assume we didn't already have 2 years of research to boot with the products though.
Shut up D, you're ruining my free sups scam!

[dinoiii]

There will be some opportunities to earn free supps. How's that sound?

[dinoiii]

Well, I am interested in what vested interest group has considered this a terrible read (i.e. - via star rating...) :) Boys will be Boys! No comments from them either, I must chuckle.

[Cyber Ninja]

Well, I am interested in what vested interest group has considered this a terrible read (i.e. - via star rating...) :) Boys will be Boys! No comments from them either, I must chuckle.

Doc,

I say we open this up to forum member voting and see who believes your post's are useful and who doesn't. I for damn sure know that what you post up here works. Thanks for your advice during my first stack cycle.

- J

[kappaz]

dinoiii-

What are your thoughts on Thermolife's new product for Liver Protection [Liver Longer]?

Amount Per Serving:
Tauroursodeoxycholic acid (TUDCA): 250mg
Directions: As an adult dietary supplement take one (1) tablet twice daily with meals.

[dinoiii]

Ursodeoxycholic acid is an endogenous bile salt, the molecule used in the Thermolife product simply conjugates a taurine molecule to it - actually making it more hydrophilic (literally water-loving with an alternative excretion route). Now, there has been some purported efficacy in various studies on liver function - however, its more promising effect may actually be in stroke patients and the like.

Anyway - the bile acids are a troublesome sell via oral route, but the taurine conjugate has shown some promise, unfortunately anything that is up on the ball again is in the early study stages still looking for participants - any study out prior had vested interest groups doing the funding.

Overall: the compound looks sincerely interesting and more study will tell us some things. For now, I am not sure what the cost of the thermolife product is but if it isn't that high - you could always compliment a good hepatoprotectant routine...BUT SAMe (although pricey for some if bought with enteric coat), Milk Thistle and NAC already show pretty good efficacy and likely continue to be good places to put your money if you have to chose one versus the other because the data is simply already there with no vested parties to boot.