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

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

- article originally published on-line on February 10, 2006

Dana Houser, MD, MHSA, CISSN

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.


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)

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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?

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(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.

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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!

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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.