PCT: A Clinician's View Part II - Post Cycle Supplements, In Theory

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ERECTILE DYSFUNCTION ALLEVIATION

Yohimbe (Pausinystalia johimbe)

Yohimbe is the only botanical to boast FDA approval as a remedy for ED. Ironically, in spite of this unusual government approval for an herb, U.S. research on yohimbe’s effects on human males is still in its infancy. The active substance is yohimbine, an alkaloid in the bark of the tree of the same name (Paustinystalia johimbe), a native plant of tropical West Africa. The inner shavings of the bark act as a stimulant and aphrodisiac. The tree, which grows predominantly in Gabon, Nigeria, and the Cameroons, grows from 20-50 feet tall, and has leaves from 3-5 inches in length. The seeds are winged.

Pharmacologic properties of this indole alkaloid, is a alpha-2 selective antagonist. It doesn’t have what I would call an established clinical role, but theoretically, it could be useful in autonomic insufficiency by promoting neurotransmitter release through blockade of presynaptic alpha-2 receptors. An easy way to remember the autonomic control over penile function is through the following pneumonic:

 Parsympathetic = Point (Erection)
 Sympathetic = Shoot (Ejaculation)

It is perhaps evident why it is suggested that yohimbine aids male sexual function, but lets look at the evidence. Yohimbe is traditionally used by many Bantu-speaking tribes in a matrimony sacrament. It is used in mating rituals that have been known to last for up to 10-15 days (Holy BeJesus, is it a wonder it has obtained such a wonderful reputation). It has been used for 70 years as a treatment for both male and female sexual difficulties. Although yohimbe enjoys a reputation as an aphrodisiac among traditional practitioners, modern scientists have not been able to prove any effects on sexual drive in humans. The herb has been shown to increase sexual arousal and performance in male rats, but the effect in human males is yet unsubstantiated.

Yet, one study from Rhode Island showed that yohimbe increases blood flow to the penis. In clinical trials, the active ingredient in the herb was tested on men impotent for less than two years. An improvement rate of 81 percent was reported for those who took a moderate dosage of the active ingredient for one month. More than 60 percent of the men who had experienced only partial erections and had failed at normal intercourse at least 50 percent of the time experienced fuller, longer-lasting erections and overall improved sexual function.

Earlier studies reported 70-85 percent “good to excellent” results with impotent patients. In the 1980’s, a highly regulated landmark Canadian study showed that the active ingredient in the herb could be a significant aid for restoring potency in impotent diabetic and heart patients. This widely reported study purported a success rate for serious impotency cases of 44 percent.

In a 1994 Italian study, impotent inpatients were followed for eight weeks. Half received active tablets of yohimbe, half received placebos. The yohimbe group showed a 71 percent positive recovery rate; the placebo group showed a 22 percent recovery. You may think that perhaps this implies something more about the essential etiology (or be a potential weakness shining through form the study) in that 22 percent, however when the placebo group was given the yohimbe tablets, their success rate climbed to 74 percent! Coincidental?

In an additional 1994 double-blind study, eighty-two men with erectile dysfunction had a high incident of diabetes and vascular disease underwent a thorough evaluation. After one month of treatment with a maximum of 42 mg oral yohimbine hydrochloride daily, 14 percent of the men experienced full restoration of sustained erections. Twenty percent reported a partial response, and 65 percent reported no improvement. Only three men reported a positive effect from the placebo group. Not impressive results, but still statistically significant.

Yohimbe can be taken in capsule or liquid forms. Pure yohimbine hydrochloride (despite luxurious claims of marketing) requires a doctor’s prescription. You may see yohimbe in a health food store or on an on-line supplement site in bark or extract form, but some of these may or may not have yohimbine in them. A standard dose is 15-20 mg per day, but higher doses, up to 42 mg, may sometimes be necessary. The effects of the herb, unfortunately takes two to three weeks to manifest themselves. The trick here is that much of your PCT time frame may have elapsed and any erectile dysfunction may have subsided in this same time frame offering rationale to question when you should initiate therapy if at all.

I would find the answer a little more gray. I would opt out of use of this product for about 3 weeks into post-cycle time. If, at that time erectile capabilities continue to manifest, yohimbe supplementation or yohimbine therapy can be considered.

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ANTIHYPERTENSIVES

Blood pressure tends to be one of the larger concerns for some while on cycle. The following supplements, while unable to discuss them all here mimic many drugs of the various pharmaceutic classes and can be used to get the blood pressure back in line with baseline.

Supplements that can act as Diuretics

Hawthorn Berry
Vitamin B6
Taurine
Celery
GLA
Vitamin C
Potassium
Magnesium
Calcium
Protein
Fiber
Coenzyme Q10

• One potential caveat here is that if concominant use of cell volumizers is being employed, use of the aformentioned set of items may best be avoided.

Supplements that can act as Central Alpha Agonists

Taurine
Potassium
Zinc
Celery
Sodium Restriction
Protein
Fiber
GLA/DGLA
Vitamin C
Vitamin B6
Coenzyme Q10
Garlic

Supplements that can act as Direct Vasodilators

Omega-3 fatty acids
MUFAs (omega-9’s)
Potassium
Fiber
Garlic
Flavonoids
L-arginine
Taurine
Celery
Magnesium
Calcium
Soy
Vitamin C
Vitamin E
Coenzyme Q10
ALA

Supplements/Foods that can act as Calcium Channel Blockers

ALA
Hawthorn Berry
Celery
Vitamin C
Vitamin B6
Magnesium
NAC
Vitamin E
Omega-3 Fatty Acids (EPA and DHA)
Calcium
Garlic

Suplements/Foods that can act as Angiotensin Converting Enzyme Inhibitors (ACEIs)

Hawthorn Berry
Garlic
Seaweed
Tuna, Sardines
Bonito Fish (dried)
Pycnogenol
Casein
Hydrolyzed Whey Protein
Sour Milk
Gelatin
Sake
Omega-3 Fish Oils
Chicken Egg Yolks
Zein
Dried salted Fish
Fish Sauce
Zinc
Hydrolyzed Wheat Germ Isolate

Supplements/Foods that can act as Angiotensin II Receptor Blockers (ARBs)

Potassium
Fiber
Garlic
Vitamin C
Vitamin B6
CoQ10
Celery
GLA and DGLA

Supplements/Foods that can act as Beta Blockers

Hawthorn Berry



While it is obviously impossible to cover all the aforementioned agents in an adequate light, there are a few worthwhile notes to make on a few within this class of agents.

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Hawthorn Berry

Hawthorn berry is an herb that was used by the ancients to treat sleep and digestive problems. Modern studies indicate that it may also lower blood pressure and cholesterol, dilate the coronary arteries, reduce the incidence of irregular heartbeat, and otherwise combat hypertension, cardiovascular disease, and related ailments.

The versatility of this supplement is something that I offer the first nod to it. As I noted above, one of its modes of action is that it acts as an ACE inhibitor; that is, it works by inhibiting the angiotensin-converting enzyme that would otherwise cause constriction of the arteries. Hawthorn berry also contains various flavanoids, which have effects similar to beta blockers, calcium channel blockers, and diuretics. It contains rutin, magnesium, chromium, catechin, and several other phytochemicals, all of which work to combat high blood pressure.

Celery

Back in the nineteenth century, celery was considered a delicacy – an exotic and expensive vegetable to be served only at fancy dinners in specially-designed celery dishes. You could actually purchase celery gum and celery soda, and the Sears & Roebuck catalogue sold a celery elixir as a treatment for nervous ailments. Although celery’s popularity plummeted when it became cheap enough for everyone to afford, recent findings about its health benefits are liable to make it much more interesting.

In studies with animals, a component of celery oil called 3-n-butyl phthalide reduced blood pressure significantly. In a Chinese study, blood pressure fell significantly in 14 of 16 hypertensives who were given celery.

We don’t now all the ways celery can help us, but we do know that it contains a substance called apigenin, which among other things, helps lower blood pressure. Celery also acts like a diuretic or ACEI, helping rid the body of excess fluid, which may be the one way it reduces elevated blood pressure.

CoQ10

A relatively recent randomized, double-blind placebo controlled trial reported on the efficacy of CoQ10 in the war that rages on between 76 men and women with isolated systolic hypertension. For 12 weeks, the patients were either given 60 mg/day of the CoQ10 or a placebo. At the end of 12 weeks, the patients taking the CoQ10 showed a mean reduction in their systolic blood pressure by approximately 18 points (9)!

Garlic

Multiple reports have shown that both fresh garlic and garlic supplements can slightly lower total cholesterol and triglyceride levels (10). An article in the prestigious Journal of Hypertension examined the results of seven randomized, placebo-controlled studies on garlic’s effects on hypertension (11). The authors of the study found that garlic supplements, in the dose of 600-900 mg/day (which is roughly equivalent to two to three cloves of fresh garlic), reduced systolic pressure from 7.7 to 11.1 points and diastolic pressure by 5.0 to 6.5 points.

Taurine

This amino acid gets the dubbing as the amino the body doesn’t use to make protein. Instead, it circulates freely throughout the brain, retina, and heart muscle. Studies have shown that taurine can lower blood pressure and heart rate, while decreasing irregular heart rhythms and the symptoms of congestive heart failure. In a study of nineteen people with hypertension, giving each person 6 grams of taurine per day for 7 days reduced the systolic pressure by 9 mm Hg and the diastolic by 4.1 mm Hg (8).




SPECIFIC DOSING PARAMETERS NEXT TIME!

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CHOLESTEROL/DYSLIPIDEMIA-MODIFYING AGENTS

The most predictable and universal effect of oral AASs, and one that has stimulated considerable research, is a decrease in the HDL fraction of cholesterol. The HDL-C2 fraction and accompanying A1 are most affected. The fall in HDL cholesterol is shortly preceded by increased activity of hepatic triglyceride lipase activity (HTLA), leading to the hypothesis that the decline is due to induction of HTLA. T and androstenedione also lower HDL. In contrast to the oral AAS, ND is not clearly associated with a decrease in HDL. In addition, AASs often increase the LDL cholesterol fraction, thus the combined effect is an increased LDL/HDL cholesterol ratio. Since a low HDL cholesterol and elevated ratio are risk factors for cardiovascular disease, the possibility that athletes and medical patients have an increased risk for cardiovascular disease has been considered.

Androgens have been implicated in myocardial infarction, atrial fibrilation, stroke, pulmonary embolism, hypertension, cardiomyopathy, sudden death and other disorders associated with the cardiovascular system; however, there is NO uniform hypothesis or mechanism that unites these observations. An autopsy was conducted on nine males who died suddenly while consuming high doses of AASs. A myocardial infarction was demonstrated in only ONE case; thus, except for the temporal relationship between AAS consumption and sudden death the mechanism for sudden death is not known and apparently does NOT involve infarction. The many ways in which AASs might influence the cardiovascular system have been reviewed.

Now, a caveat of the aforementioned material must be noted. There is a few pieces of literature that suggest that T actually LOWERS LDL and Lp(a). These studies have since been refuted and were not done with examination of typical dosing parameters used by bodybuilders during cycle.

Either way, it is most often exhibited that the cholesterol levels return to normal with cessation of the AAS, but there have been reports of a particular cycle beginning a cascade of detrimental lipid events, the pathogenic models of which are quite complex and for that reason remain beyond the scope of this article. Should you, however, become one of these latter reports, we will discuss the two most commonly suggested supplemental protocols for correction of various scenarios – described in “primary goals” that follow.

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PRIMARY GOAL: LOW HDL CORRECTION

Niacin (Vitamin B3) + My Anti-Flush Protocol

The niacin or nicotinic acid form of vitamin B3 has been known to be an effective method for improving blood cholesterol levels since the 1950s. In the 1970s, the famed Coronary Drug Project demonstrated that niacin was the only cholesterol-lowering agent to actually reduce overall mortality (this information has since been updated with the advent of other agents).

-------------PHARMACOLOGIC SCIENCY STUFF--------

Nicotinic acid reduces plasma VLDL by inhibiting VLDL synthesis (20-80% over 1-4 days); it markedly decreases plasma triglyceride levels. As the substrate, VLDL concentration is reduced, the concentrations of IDL and LDL also fall, thereby reducing plasma cholesterol levels. HDL levels increase significantly.

The precise mechanism of inhibition of VLDL synthesis is unclear. Lipolysis in adipocytes is inhibited, reducing the major source of fatty acids for hepatic triglyceride biosythesis; VLDL catabolism is increased by an elevation in the activity of lipoprotein lipase; and a slight decrease in hepatic cholesterol synthesis is observed.
-----------------------------------------------------

Niacin typically lowers LDL cholesterol levels by 16-23 percent while raising HDL cholesterol levels by 20-33 percent. While niacin is available in the form of a prescription (Nicobid, Nicolar – discussed in latter parts of this series), it is likely a lot cheaper in the supplemental form, but the dose must be ramped up accordingly.

Niacin is available as a pure crystalline niacin and in sustained- or time-released preparations. Because of the significant risk of liver toxicity, sustained-release niacin should be AVOIDED, especially with the use of C17 alkylated orals! Contrary to the preachings of certain authorities, “no-flush” brands are neither synonomous nor homologous with the phrase “sustained-release.”

Inositol hexaniacinate yields slightly better results than standard niacin but is much better tolerated in terms both of flushing (the #1 side effect) and, more important, long-term side effects (hyperglycemia, GI disturbances, peptic ulcers, renal effects with elevated plasma uric acid levels, and macular edema).

Inositol Hexaniacinate (also referred to as hexanicotinate) is a special form of niacin composed of six nicotinic acid molecules bound to and surrounding one molecule of inositol, an unofficial member of the B vitamin group. Inositol hexaniacinate has been shown to exert the benefits of niacin without flushing or other side effects. It has been used in Europe for over 30 years not only to improve cholesterol levels but also to improve blood flow in the treatment of intermittent claudication and Raynaud’s phenomenon. Double-blind studies have verified the beneficial effects of this form of niacin in these peripheral vascular disorders.

While a third form of niacin is widely available, the aforementioned two offer the best cholesterol-modifying effects, whereas niacinamide is useful in arthritis and early onset type I diabetes. We will explore the dosing parameters of the protocol in subsequent parts of this series.

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PRIMARY GOAL: HIGH LDL REDUCTION

Red Yeast Rice

The red yeast (Monascus purpureus) fermented on rice has been used in China for its health-promoting effects for over 2000 years. This yeast is the source of a small group of compounds known as monacolins that can lower cholesterol levels by blocking a key enzyme in the liver. In fact, the cholesterol-lowering drug Mevacor, the trade name for the compound lovastatin, also known as monacolin K, one of the key monocolins in red yeast rice extract.

The marketing of Cholestin (an extract of red yeast fermented on rice, standardized for monacolin content) as a dietary supplement in the United States has caused quite a controversy since 1997. Because it contains a natural source of a prescription drug, the FDA and the maker of Mevacor, Merck, tried to prohibit the sale of Cholestin and other red yeast rice extracts as a dietary supplement. The FDA’s ruling against Cholestin was temporarily reversed in March 1999, but two years later the FDAs ruling was upheld. Nonetheless, many red yeast rice products remain on the market.

These products, like their prescription counterparts, clearly are effective in lowering cholesterol levels. Over twenty clinical trials conducted in China involving thousands of subjects have shown red yeast rice extract to effectively lower high blood cholesterol levels by roughly 20 percent while raising protective HDL cholesterol by about 18 percent. A study conducted at the UCLA Center for Human Nutrition under the direction of David Herber, MD, has also demonstrated positive results. The double-blind, placebo-controlled study consisted of 83 healthy subjects with a cholesterol level between 200 and 239 mg/dl. Subjects were treated with 2.4 g of red yeast rice extract (Cholestin) supplying 9.6 mg of monacolins per day or a placebo. Both groups were instructed to maintain a diet of 30 percent fat with less than 10 percent saturated fat and less than 300 mg of cholesterol. On average, cholesterol decreased in the Cholestin group from 254 to 208 mg/dl by eight weeks, with no change in the placebo group.

While these results sound pretty good and from the outside looking in offer seeming support for this compound, the post-cycle time frame is NOT the time to employ potential use of this type of product.

First, it is a huge strike with those trying to use it with liver protectants post-C17 alkylated products. Liver enzyme elevations are reported as the number one side effect (3.4%). While this may not be a concern in the normal circumstance, the post-cycle period remains a unique time of recoup for all body organs – the liver perhaps having endured the biggest beating. Second, the development of muscle pains – perhaps indicative of a rare, but serious side effect known as rhabdomyolysis, are clearly evident in a few select cases (1%) of the general population. It is difficult to discern between post-workout DOMS and actual muscle pain due to this condition.

Red Yeast Rice like other statin drugs reduces the levels of Coenzyme Q10 at an alarming rate. With already depleted levels in many bodybuilders, this could play the role of a significant detriment to the well-being and attempts at regaining homeostatic environments seen prior to the cycle’s initiation. Niacin products at a dosage of 500 mg three times per day potentiates the effects of Red Yeast Rice and if employing either, it is strongly advised to avoid concurrent therapy. Interestingly enough, I will report a case of hepatic sides in an unknowing post-cycle patient using a Multi-Vitamin (containing Niacin products) and self-medicating with Red Yeast Rice later in this series. In addition, there are far too many drug-herb interactions – perhaps beyond the scope of this article to discuss, but it is wise to discuss the use of this product with your own examining physician if you are taking ANY prescription medications. I personally strongly advise AGAINST use of Red Yeast Rice at any point on or around a cycle.


Guggulipid

Guggulipid is the resin or sap from Commiphora mukul (the mukul myrrh tree). The mukul myrrh tree, which grows in India, is really more of a shrub. As early as 1971, the positive effects of guggulipid (also known as gugulipid, guggul, and guggulu) on cholesterol were reported by Kapoor and colleagues in the proceedings of the Seminar on Disorders of Lipid Metabolism, held in New Delhi, India.

The active ingredients in guggulipid appear to be two plant sterols called Z-guggulsterone and E-guggulsterone. In elegant study by Singh and colleagues, these two steroids were shown to increase the uptake of LDL cholesterol by the liver. This, in turn, significantly lowers the LDL cholesterol in the bloodstream. Guggulipid has been shown to lower both LDL cholesterol (by about 12 percent) and triglycerides (by about 15 percent). Some studies have even shown some HDL improvement with guggulipid.

Guggulipid is used extensively in Ayurevedic medicine. Ayurvedic medicine uses drugs extracted from herbs, as well as diet, meditation, and exercise to treat disease. In India, guggulipid is sold as a drug, whereas in the United States, it is available in health-food stores. The typical dose of guggulipid is 25mg three times per day with meals. This changes considerably in PCT.

Most people have no side effects with guggulipid. There are a few cases of reported mild nausea, diarrhea, and headaches. Generally, these mild sides resolve with continued use. If you choose to use guggulipid, I think it is essential for you to let your doctor know. While it appears that the literature on guggulipid is solid science, the studies have typically been small. It is possible that guggulipid has side effects that have not yet been determined. We will see how this pans out in practice in the next part of this series.

Policosonol

Policosonol is a mixture of fatty substances isolated and purified from the wax of sugar cane (Saccharum officinarum). Policosonol has exceptional clinical documentation demonstrating efficacy, safety, and tolerability in lowering cholesterol and triglyceride levels. The clinical studies have included comparative studies versus conventional cholesterol-lowering drugs (i.e. – lovastatin, pravastatin, simvastatin, gemfibrozil, and probucol). In these studies, policosonol in dosages ranging from 5 to 20 mg per day has resulted in significant improvements in cholesterol and triglyceride levels, with effects typically noticeable in the first 6-8 weeks of use. At a daily dosage of 10 mg of policosnol at night, LDL cholesterol levels dropped by 20-25% within the first few weeks of therapy. At a dosage of 20 mg, LDL levels typically dropped by 25-30%. HDL cholesterol levels typically increased by 15-25% after only 1-2 months of use. The combined LDL reduction and HDL increase produced dramatic improvements in the LDL-to-HDL ratio.

In addition to its effects on cholesterol levels, policosonol also exerts additional positive effects in the battle against atherosclerosis (hardening of the arteries). It prevents excessive platelet aggregation without affecting coagulation (WHICH MAY PROVE VERY PROMISING DURING A CYCLE AND AFTER), prevents smooth muscle cell proliferation into the lining of the artery, and exerts good antioxidant effects in preventing LDL oxidation and subsequent arterial damage.

Great news for bodybuilders! This compound was not available in the United States until very recent as it is manufactured in Cuba. Alternatively, there is a suspect version of it that has been available from Natural Factors out of Canada.

Fish Oils / Various Other Sources of EFAs

This will be discussed at length during dietary discussions of article series.

Lecithin

All quality studies attempting to show cholesterol-lowering effects have simply NOT PANNED OUT! I would avoid this product in reduction of cholesterol levels for this rationale.



So, you may point out that I seem to be against cholesterol as the culprit of disease based on my Cholesterol Controversy series. I see it more imperative to keep in mind here that changes in cholesterol values during a cycle are variants from baseline through exogenous introduction of hormonal byproduct. It is an attempt during PCT to regain homeostatic balance and following your baseline levels of lab work to this point is IMPERATIVE!

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PSYCHIATRIC EFFECTS

I am indifferent to this topic. I find the psyche imperative to discuss with the use of something potentially psychotropic. Most people I am familiar with DO NOT experience remarkable psychiatric effects while receiving AASs, although some report a general sense of well-being and invigoration – more likely induced by the way they are “supposed” to feel. AASs have been used to treat depression with VARIABLE results (27, 28) and with LESS efficacy than tricyclic antidepressants.

The hypothesis that T promotes aggressiveness in males is NOT supported by very many adverse reports arising from studies of T as a male contraceptive. Furthermore, supraphysiologic doses of T enanthate (600 mg/week) administered to healthy males for 10 weeks did NOT produce significant changes in mood or anger inventories, or in an observer mood inventory administered to spouses of significant others (29). A similar study reported marked hypomania in 2 out of 56 subjects (30), roughly the incidence of hyomania in the general population.

One study of AAS users found NO significant mood disturbances (31), however, reports of serious behavioral and psychiatric sequelae including aggressiveness, hostility, and even homicide associated with AASs are increasing (32, 33, 34). A structured psychiatric interview of high-dose users found a high incidence of aggressive behavior, affective syndromes, and psychotic symptoms (35). A double-blind, fixed-order, placebo-controlled study of the effects of placebo, 40 mg of MT, 240 mg of MT, and placebo withdrawl for 3 days each on mood and behavior in healthy, non-AAS users revealed both positive (euphoria, energy, sexual arousal) and negative (irritability, mood swings, violent feelings, hostility) mood changes during high dose MT (33). In addition, 1 of 20 subjects developed acute mania. The possibility that higher dose users develop an addiction with physical dependence and a withdrawl syndrome has been proposed (36).

Fortunately, there are some inferences that can be made at this time. The psyche is quite the strange beast. The variability of results is very representative of the potential variation – however, the inclusion of incidence rates being as low as they are would lend me to believe the psychiatric effects are self-induced in many cases should they show up – again, because it is perhaps an appropriate time for select individuals to act out because it is expected of them while on cycle. The addiction and physical withdrawl is, however, a very real subject even in placebo research (steroids aside), which is why I acknowledge it. The aforementioned paper on dependence and withdrawl only used 8 subjects, so I find it hard to make generalizations of the population as a whole. Further research is certainly warranted.

The case for the addition of a supplement here to offer placebo alleviation is perhaps warranted – but I will forego discussion at this time outside of stating take your pick: Kava, Melatonin, Valerian, Gotu kola, St. John’s Wort, 5-HTP, DLPA, and SAMe. None really stand out and some may be detrimental in the post-cycle period. A couple of these products find different uses and will be discussed with that in mind later in this series.