Cy-BORG
Intelligent Drug and Supplement Info
by Cy Willson

Alpha Male and Erections

Q: Can I mix Alpha Male with prescription drugs like Viagra and other erectile drugs?

A: I wouldn’t recommend using them concurrently. While they may work via different mechanisms, it’s still possible that sildenafil (Viagra) and similar compounds could potentiate the hypotensive effects seen with the other compounds in Alpha Male, which either directly or indirectly, allow for a vasodilatory effect.

If one were to use such compounds concurrently, you’d run the risk of dizziness, headache and fatigue and in some cases, much worse side effects. My advice would be to give either one or the other a try first. Alpha Male would be the easier choice as it of course doesn’t require a prescription and obviously has the added benefit of containing compounds that increase endogenous Testosterone levels.

Should we Resurrect Chromium from the Supplement Graveyard?

Q: Chromium Polynicotinate was hot a few years ago but seems to have fizzled. Now I'm reading about how it can help the body metabolize sugar and help blood lipids, plus there was a new study showing that it decreases carb cravings. So is this stuff worth taking for general health? Is it worth taking when on a low carb diet?

A: Well, I think chromium certainly has its role in our diets and is a very important player in a number of things, just as with other essential minerals. The most important aspect to bodybuilders would be its role in potentiating the action of insulin, or enhancing its effects.

A few important things to consider are that we as athletes or body builders, while excreting less chromium than those who don’t exercise, still excrete a fair amount. Another thing to keep in mind is that the consumption of simple sugars seems to increase excretion of chromium. Finally, cortisol levels and chromium excretion are positively correlated. Combining that with the fact that chromium has very poor oral bioavailability could easily result in a person being deficient if not consuming at least trace amounts in the everyday diet.

One nice thing is that chromium displays triphasic pharmacokinetics, with the elimination half-life (in this case, the phase representing 10% of the amount absorbed) being around 3 years. We again, however, have to keep in mind that the oral bioavailability is only around 0.5-2.8% and the more you take, the lower the bioavailability.

The 2.8% percentage was found in those taking 400 mcg/day, by the way. Anyhow, in those who have poor insulin sensitivity as well as, of course, diabetics, chromium can have some very beneficial effects. However, in normal humans who are euglycemic, I really don’t see any reason to begin supplementing with chromium beyond what you’d obtain in a multi-vitamin/mineral supplement. It was recently shown that in such individuals, excess chromium might even act as a pro-oxidant.

One interesting note is that chromium has shown some promise in terms of a possible treatment for depression. The dosage used was 600 mg/day of chromium picolinate. While I still don’t know if I like the idea of someone taking that amount every day for what could be years, it’s still interesting data. If these people with depression were evaluated and a chromium deficiency were found, we could have a general correlation between the two and thus I’d be more apt to recommend it as a possible alternative treatment.

Anyhow, there’s some limited data that may further support a mechanism for this anti-depressant effect; that mechanism of action being a serotonergic and perhaps a noradrenergic effect as well. While I haven’t seen the study you’re referring to that directly evaluated carbohydrate cravings and chromium, it would actually fit in with the proposed mechanism of action.

In any event, if you’re not suffering from insulin insensitivity or depression, I really don’t see any data just yet to convince me that larger amounts than what’s found in a multi-vitamin/mineral are warranted. However, if you want to give it a try for a short period of time, be my guest. (1-7)

NADH the Cure for Fatigue and Stupidity?

Q: What's the scoop on NAHD? It's supposed to help with fatigue and depression, as well as boost mental clarity. Sounds like something I need because I'm tired, sad and not too bright. Should I try it?

A: I hope you mean NADH. Otherwise, I have no idea. Anyhow, NADH is Nicontinamide Adenine Dinucleotide and in this case, it’s the reduced form. NAD+ should look very familiar to you as it’s one hell of an important molecule. NAD+ acts as a coenzyme for dehydrogenase enzymes, one of those being alcohol dehydrogenase, the enzyme found in your liver that effectively works to oxidize ethanol to form aldehydes, thus "detoxifying" the ethanol.

Unfortunately, or fortunately, however you want to look at it, we humans tend to outgun the alcohol dehydrogenase by consuming more ethanol and effectively elevating blood ethanol concentrations.

Anyhow, the simplest way to view NAD is as an electron carrier. When you consume food or even ethanol for energy, NAD is the redox coenzyme, in this case acting as an oxidizing agent (FAD as well) that essentially rips off that hydrogen and accepts the transfer of electrons via a hydride ion, thus forming NADH.

From there the electrons can be transferred to yet another electron acceptor. This process allows for ATP synthesis. So as you can see, NAD plays a very important role in cellular energy and biochemical reactions. As a side note, niacin (nicotinic acid) and niacinamide (nicotinamide) are precursors to NAD.

Anyhow, moving on to what you were asking about, it may have some promise for those suffering from fatigue and it may even have some benefit in those suffering from chronic fatigue syndrome. It may also have some benefit in those suffering from Parkinson’s disease in addition to dementia stemming from Alzheimer’s, as well as depression. It may also have a hepatoprotective effect, at least in those suffering from viral hepatitis.

While there have been claims that it helps with opiate and alcohol addiction, there really isn’t any data to support that directly. Other than that, researchers have found a positive effect upon cognitive function and sleepiness in those suffering from jet lag when they took 20 mg of NADH.

The reason that NADH is thought to have such positive effects stems from the previously mentioned idea that it increases ATP, but a second mechanism may be a dopaminergic effect. It’s thought that it increases tyrosine hydroxylase (the rate-limiting enzyme in the synthesis of all catecholamines) activity, resulting in greater formation of L-dopa, which provides more substrate for dopamine formation via aromatic amino acid decarboxylase.

Anyhow, if you want to give it a try, you’ll need to take anywhere from 5-20 mg, depending on what effects you’re looking for. For those with chronic fatigue, try 10 mg/day. Those wanting to give it a try for depression should go with 5 mg/day. For dementia, try 10 mg/day and 5 mg/day for Parkinson’s. As mentioned, if you want to give it a try for jet lag, take 20 mg upon landing at your destination.

At this point, I’d say it’s worth a try, but I’m hesitant to say NADH is a wonder supplement.

Steroids Made His Ticker Ache?

Q: I stopped taking steroids a few months ago because of a mild ache in the chest. Have the steroids damaged my heart?

A: That’s interesting as someone very close to me had that same thing happen to him. This person told me they’d begin using certain androgens when every so often, they’d experience what they thought was angina. This person also has a physician in his family, who although not a cardiologist, is still rather knowledgeable. The physician stated strongly that it was likely angina and that the steroid user should permanently cease the use of androgens.

I discussed this with another physician and he quickly pointed out that he thought it was pericarditis. Pericarditis, as the name would indicate, is inflammation of the pericardium (in short, a membrane comprised sac that surrounds the heart). The physician told me he’s actually seen a number of weight trainers between the ages of 20-50 who experience pericarditis from time to time.

Once I was able to ask my friend about his actual symptoms, he described exactly what the second physician mentioned, which was a sharp pain brought on and/or worsened by lying down and by taking a deep breath.

As it turns out, one of the possible causes of pericarditis (microbial infection) was also present in this person. Anyhow, the reason why the second physician almost immediately discounted angina was because of the relatively young age and otherwise healthy condition of this individual. Anyhow, I feel it’s important that people learn the difference between the two so as not to confuse angina with something else and perhaps put the blame on androgens. Refer to http://www.americanheart.org/presenter.jhtml?identifier=4683 for more information.

Last, however, and this is very important, I don’t want people to use this case as an excuse to simply disregard any chest pain (irrespective of androgen use) and simply chalk it up as pericarditis. It’s not a green light for you to start self-diagnosis. If you experience any chest pain, period, consult with your physician as soon as possible.

Eurycoma is One Cool Plant

Q: Tell me about this eurycoma stuff that’s in Red Kat.

A: Eurycoma longifolia Jack is a plant or bush found in Malaysia and Vietnam if not other places. In Vietnam, the plant is locally referred to as "cay ba binh" which means the tree that cures hundreds of diseases. Its bark is used in Vietnamese pharmacopoeia and it’s been used to treat malaria. Amongst other compounds, it contains eurycomalactone as well as other quassinoids; certain alkaloids; and two steroids, b -sitosterol and campesterol.

Anyhow, it’s been shown to increase testicular steroidogenesis or in other words, increase Testosterone production at the testicular level. Aside from this, it’s been shown to increase ATP formation, which can have a number of benefits including a possible vasodilatory effect, which can increase blood flow to various tissues including penile tissue.

All in all, it’s a very interesting plant that contains some very cool molecules. (19-20)

Lance on HRT?

Q: As I write this, the Tour De France is in full swing. So what are these dudes using these days? I heard EPO was old news and there's new stuff out there now. Got any dirt? Also, since Lance Armstrong had testicular cancer, is it a fair assumption that he’s getting legal T replacement, which probably puts his hormonal milieu at a superior level than his "natural" rivals?

A: I’m not really sure exactly what those guys may be using as I’m not really a big fan of bike racing and such. The few people who’ve seen me on one of those bicycles you can rent to ride back through the Tijuana-US border will confirm how hilarious of an experience it was for them.

Speaking strictly in regard to recombinant EPO and analogues like darbepoetin, they’re detectable with certain analytical methods and thus I doubt you’ll see any one using those if increasing erythropoiesis is the goal. For more information on darbepoetin, EPO, etc., see my past column.

Anyhow, what I can tell you is the direction that things are moving in, at least in regard to increasing erythropoiesis and avoiding detection. For example, there are synthetic erythropoiesis proteins (SEP’s) in existence, which are protein conjugates with negatively charged polymers as opposed to the oligosaccharides found on the recombinant EPO molecules like epoetin alfa and darbepoetin alfa. This is significant because it’s those oligosaccharides that are used to help to directly detect their presence in urine. So, these molecules could be used to increase erthyropoiesis but wouldn’t yield a positive. There are also peptide and non-peptide based molecules around that essentially act as EPO receptor agonists.

And finally, there’s the potential for gene doping where you’d transfect the gene that codes for EPO mRNA into the human cells, thus allowing for consequential and substantial increase in endogenous EPO formation. They could potentially inject the plasmid vector containing the EPO gene intramuscularly, or perhaps use another method of delivery.

The significance of this is great. By doing this, you’re increasing the endogenous production of EPO and thus any analytical techniques designed to directly find recombinant EPO or any of its analogues wouldn’t work. In other words, there’s no way they could directly detect anything, as the EPO in your bloodstream is your own.

However, they could indirectly catch you by simply measuring other things like serum EPO concentrations and hematocrit in your blood, amongst other things. One could of course argue that they might have a mutation in a given gene, although DNA analysis could quickly discount or confirm whether the claim or argument has any merit.

So while the evolution of "doping" is very quick, it doesn’t seem that there will ever be a surefire way to "beat the system" indefinitely.

As for Lance Armstrong, I don’t think it’s a fair assumption that he’s taking exogenous Testosterone. Most physicians will argue that even if one testicle is removed, the other can make up for it, so to speak. This can be confirmed by simply evaluating endogenous Testosterone levels once the testicle is removed and determining if the person is hypogonadal or not. So, if they don’t have to put someone on Testosterone for the rest of his life, they most certainly won’t. To the best of my knowledge, he doesn’t use exogenous Testosterone either. Then again, as I said before I’m not a big fan, so I could be wrong. (21-26)

You’re a Fat Bastard Because of Stress

Q: The commercials are driving me bat shit so I gotta ask: do any of these supplements designed to "suppress cortisol" actually have any merit whatsoever? Am I really fat because I'm stressed out?

A: Well, there are some supplements that might reduce cortisol levels. Those being, but not limited to, fish oil, ginkgo biloba and phosphatidylserine.

If you’re a person who’s highly or rather, chronically stressed, then taking such compounds could have a beneficial effect in terms of preventing an excess of cortisol from being produced. Now, will taking compounds that moderately reduce cortisol levels actually allow for a significant reduction of fat mass in normal humans? I highly doubt it.

More importantly, I’m getting tired of people making these generalizations about various hormones and biological molecules. In just about every, if not all cases, you can’t say a particular hormone is "good" or "bad" but rather, you need to take into account what effects it may have at subphysiological, physiological and supraphysiological levels.

For example, with estradiol and cortisol, you don’t want subphysiological levels. Low levels of estradiol will typically leave you with a negative alteration in your blood lipids, alterations in mood or depression, dry skin, poor wound healing and decreased libido, just to name a few side effects.

Having low levels of cortisol might leave you with muscle weakness, decreased responsiveness to beta 2-adrenergic agonists (e.g., clenbuterol or the less selective ephedrine), depressed lipolysis, increased cellular damage when other cells are injured, excessive oxidative damage and perhaps most importantly, a lack of cortisol could allow even a minor respiratory tract infection or a hypersensitivity reaction to cause death.

Without cortisol, we can’t handle physical or mental stress. On the other hand, as we all know, excess cortisol and excess estradiol can also have negative effects. However, our body strives to keep hormone levels exactly where they need to be, despite changing environmental conditions.

Another thing people often forget is the fact that by manipulating one hormone, we must then consider what other effects it may have upon not only other hormones, but what alterations in physiology are seen as well. My main point is that unless you’re a chronically stressed individual with severe anxiety, I really don’t see the point of going out of your way to suppress cortisol as our bodies, despite most peoples’ attitude, tend to do a rather good job at regulating levels via negative feedback controls. That isn’t to say there are going to be exceptions, but the majority of us don’t need to be overly concerned.

If there were one thing I’d recommend taking on a consistent basis for stress and resultant inflammation (among other things), it would be fish oil. My suggestion would be to save your money when it comes to cortisol-suppressing supplements.

Prolonging Life with L-Carnosine

Q: The life extension people have been talking a lot about l-carnosine. They say it "prolongs life." Are they loopy?

A: Well, I don’t know if I’d be so quick to say that any compound will, without a doubt, prolong life. With that being said, it does appear that carnosine is a very potent antioxidant.

One thing I want to touch base on is the fact that most people tend to really oversimplify the role of antioxidants and their effects. There are many factors you have to consider, just as you would with any compound. Questions that need to be asked are how potent is the antioxidant as compared to other compounds? What is its mechanism of action? What’s the oral bioavailability and how much would need to be ingested in order to actually yield positive effects?

I think that by asking those questions, more people would realize that maybe their antioxidant needs aren’t covered with a simple multivitamin in most cases. Anyhow, carnosine provides an antioxidative effect via different mechanisms, making it just that much more potent.

Based on data acquired from Senescence Accelerated Mice, carnosine supplementation prolonged the average lifespan and prevented the senility normally seen in these mice. There’s also other data that would indicate a lack of carnosine could have detrimental effects upon the brain as we age, as well as other tissues. It’s this reduction in oxidative stress that’s thought to be at least one of the mechanisms through which starvation prolongs life in mice.

One of the proposed mechanisms of aging as well as the formation of various diseases is oxidative stress (e.g., heart disease, cancer, stroke, high blood pressure, Alzheimer’s, etc.). Oxidative stress caused by ROS (Reactive Oxygen Species), AKA, ROI (Reactive Oxygen Intermediates) such as hydroxyl radicals, singlet oxygen, superoxide radicals and hydrogen peroxide is something that, contrary to what most people think, we encounter every day as ROS or ROI are continuously produced by living cells throughout various biological processes.

Exercise, injury or technically any type of activity that causes inflammation/cellular damage, infection, hypersensitivity reactions, smoking or smoke inhalation, normal ETC functioning, UV light, ionizing radiation and even certain drugs can all generate ROS enough to where oxidative damage can ensue. Granted, our bodies do contain endogenous antioxidants and antioxidative enzymes (e.g., superoxide dismutase, glutathione peroxidase, carnosine, etc.) to combat this, but often the stress and environmental conditions we encounter every day seem to simply outgun our own defenses.

Over time this oxidative damage adds up. Going back to cortisol, it helps to prevent some of the oxidative damage caused by hypersensitivity reactions, injury/cellular damage and so forth by not only preventing further damage to other cells, but by its overall immunosuppressive and anti-inflammatory effect as well (e.g., preventing or minimizing the respiratory burst from white blood cells).

Looking at the data on l-carnosine, I’d say it’s certainly worth a try at around 1-3 grams per day. However, if using it to prolong life, it’s obviously going to prove difficult to determine whether it was actually efficacious or not any time soon! So, while I’ll have to disagree that any compound has enough data to say that it will definitively prolong a normal human’s life to any significant degree, I will say that it’s an interesting dipeptide worth giving a try if the price is right. (27-36)

L-Carnitine Possibly Superior to Testosterone?

Q: I recently read a study where l-carnitine was said to be "superior to Testosterone" in elevating libido. What’s the dope on this stuff?

A: In the study you’re referring to, they divided subjects up in to three randomized groups. Group I consisted of 40 men (ages 60-72) and they received 160 mg/day of Testosterone undecanoate orally.

Group II consisted of 45 men (ages 61-73) and they received 4 grams of l-carnitine/day consisting of two esterfied derivatives, one being acetyl-l-carnitine and the other being propionyl-l-carnitine. 

Group III consisted of 45 men (ages 61-74) and they were given a placebo that consisted of one 500 mg tablet of starch per day.

They administered the drugs for 6 months and assessed results at months 3 and 6, in addition to 6 months after the trial. What they found was that carnitine proved to be just as, if not more, efficacious as compared to Testosterone with erectile function, fatigue, depression, orgasm and sexual well-being, sexual intercourse satisfaction, etc.

Although, to be fair, consider that Group I was given "replacement" amounts of Testosterone undecanoate, which has a rather low oral bioavailability. However, that seemed to be all they were trying to achieve.

In any event, this data is very interesting and certainly warrants some further study. By the way, coming back to ROS again, it was this group of scientist’s theory that because of carnitine’s antioxidative properties and unique mechanism of action thereof (in part), it would have a positive effect upon the parameters measured. They also made a point to mention that Testosterone supplementation increases carnitine levels in tissues.

One problem I have with this study is the high amount of l-carnitine used. For most people, using that amount each day could be rather cost prohibitive. Aside from that, you’d expect the two esterfied derivatives to have higher oral bioavailability than what you’d get from over the counter versions, so you might need even more l-carnitine to achieve the same results.

On a side note, carnitine supplementation may improve certain symptoms of chronic fatigue syndrome as well. Oh, and it was also shown to increase adenosine and ATP levels in humans, which could technically account for at least the decrease in fatigue as well as the improved erectile function.

So again, while I think I’d like to see some more data, be my guest if you want to give it a try.

On one final note, I hope that people will see the theme and overall importance of antioxidants not only with this question but some of the others I’ve addressed as well. (37-41)

References Cited:

1. Franklin M, Odontiadis J. "Effects of treatment with chromium picolinate on peripheral amino acid availability and brain monoamine function in the rat." Pharmacopsychiatry. 2003 Sep;36(5):176-80.

2. Davidson JR, et al. "Effectiveness of chromium in atypical depression: a placebo-controlled trial." Biol Psychiatry. 2003 Feb 1;53(3):261-4.

3. Anderson RA, Bryden NA, Polansky MM et al: Exercise effects on chromium excretion of trained and untrained men consuming a constant diet. J Appl Physiol 1988; 64(1):249-252.

4. Anderson RA, Bryden NA, Polansky MM et al: Effects of carbohydrate loading and underwater exercise on circulating cortisol, insulin and urinary losses of chromium and zinc. Eur J Appl Physiol 1991; 63(2):146-150.

5. Kozlovsky AS, Moser PB, Reiser S et al: Effects of diets high in simple sugars on urinary chromium losses. Metabolism 1986; 35(6):515-518.

6. Stearns DM, Belbruno JJ & Wetterhahn KE: A prediction of chromium (III) accumulation in humans from chromium dietary supplements. FASEB J 1995; 9(15):1650-1657.

7. Cheng HH, Lai MH, Hou WC, Huang CL. "Antioxidant effects of chromium supplementation with type 2 diabetes mellitus and euglycemic subjects." J Agric Food Chem. 2004 Mar 10;52(5):1385-9.

8. Birkmayer GD, Kay GG, Vurre E. "Stabilized NADH (ENADA) improves jet lag-induced cognitive performance deficit" Wien Med Wochenschr. 2002;152(17-18):450-4.

9. Birkmayer W & Birkmayer GJD: The coenzyme nicotinamide adenine dinucleotide (NADH) as biological antidepressive agent. New Trends Clin Neuropharmacol 1991; 5(1):19-25.

10. Birkmayer GJD: Coenzyme nicotinamide adenine dinucleotide: new therapeutic approach for improving dementia of the Alzheimer type. Ann Clin Lab Sci 1996; 26(1):1-9.

11. Birkmayer GJD, Vrecko C, Volc D et al: Nicotinamide adenine dinucleotide (NADH) - a new therapeutic approach to Parkinson's disease: comparison of oral and parenteral application. Acta Neurol Scand Suppl 1993; 87:32-35.

12. Forsyth LM, Preuss HG, MacDowell AL et al: Therapeutic effects of oral NADH on the symptoms of patients with chronic fatigue syndrome. Ann Allergy Asthma Immunol 1999; 82(2):185-191.

13. Birkmayer W, et al. "The coenzyme nicotinamide adenine dinucleotide (NADH) improves the disability of parkinsonian patients." J Neural Transm Park Dis Dement Sect. 1989;1(4):297-302.

14. Birkmayer GJ, Birkmayer W. "Stimulation of endogenous L-dopa biosynthesis—a new principle for the therapy of Parkinson's disease. The clinical effect of nicotinamide adenine dinucleotide (NADH) and nicotinamide adenine dinucleotidephosphate (NADPH)." Acta Neurol Scand Suppl. 1989;126:183-7.

15. Kuhn W, et al. "Parenteral application of NADH in Parkinson's disease: clinical improvement partially due to stimulation of endogenous levodopa biosynthesis." J Neural Transm. 1996;103(10):1187-93.

16. Dizdar N, Kagedal B, Lindvall B. "Treatment of Parkinson's disease with NADH." Acta Neurol Scand. 1994 Nov;90(5):345-7.

17. Birkmayer W, Birkmayer GJ. "Nicotinamidadenindinucleotide (NADH): the new approach in the therapy of Parkinson's disease." Ann Clin Lab Sci. 1989 Jan-Feb;19(1):38-43.

18. Demarin V, Podobnik SS, Storga-Tomic D, Kay G. "Treatment of Alzheimer's disease with stabilized oral nicotinamide adenine dinucleotide: a randomized, double-blind study." Drugs Exp Clin Res. 2004;30(1):27-33.

19. T.K. Kwan, J.M. Saad , O. Farizaturradiah dan B.H. Koh. 1995. The Effect of Eurycoma longifolia on Rat and Human Testicular Steroidogenesis. Posiding Konvensyen Kebangsaan Tumbuhan Ubatan. FRIM. m/s 201-204.

20. Le-Van-Thoi, Nguyen-Ngoc-Suong. "Constituents of Eurycoma longifolia Jack." J Org Chem. 1970 Apr;35(4):1104-9.

21. Johnson DL, et al. "Amino-terminal dimerization of an erythropoietin mimetic peptide results in increased erythropoietic activity." Chem Biol. 1997 Dec;4(12):939-50.

22. Minuto F, Barreca A, Melioli G. "Indirect evidence of hormone abuse. Proof of doping?" J Endocrinol Invest. 2003 Sep;26(9):919-23.

23. Breidbach A, et al. "Detection of recombinant human erythropoietin in urine by isoelectric focusing." Clin Chem. 2003 Jun;49(6 Pt 1):901-7.

24. Egrie JC, Browne JK. "Development and characterization of novel erythropoiesis stimulating protein (NESP)." Nephrol Dial Transplant. 2001;16 Suppl 3:3-13.

25. Qureshi SA, et al. "Mimicry of erythropoietin by a nonpeptide molecule." Proc Natl Acad Sci U S A. 1999 Oct 12;96(21):12156-61.

26. Gaudard A, Varlet-Marie E, Bressolle F, Audran M. "Drugs for increasing oxygen and their potential use in doping: a review." Sports Med. 2003;33(3):187-212.

27. Babizhayev MA, et al. "L-carnosine (beta-alanyl-L-histidine) and carcinine (beta-alanylhistamine) act as natural antioxidants with hydroxyl-radical-scavenging and lipid-peroxidase activities." Biochem J. 1994 Dec 1;304 ( Pt 2):509-16. 

28. Nagasawa T, Yonekura T, Nishizawa N, Kitts DD. "In vitro and in vivo inhibition of muscle lipid and protein oxidation by carnosine." Mol Cell Biochem. 2001 Sep;225(1-):29-34. 

29. Guliaeva NV. "Superoxide-scavenging activity of carnosine in the presence of copper and zinc ions." Biokhimiia. 1987 Jul;52(7):1216-20. 

30. Boldyrev A, Abe H, Stvolinsky S, Tyulina O. "Effects of carnosine and related compounds on generation of free oxygen species: a comparative study." Comp Biochem Physiol B Biochem Mol Biol. 1995 Nov;112(3):481-5. 

31. Aruoma OI, Laughton MJ, Halliwell B. "Carnosine, homocarnosine and anserine: could they act as antioxidants in vivo?" Biochem J. 1989 Dec 15;264(3):863-9. 

32. Stuerenburg HJ. "The roles of carnosine in aging of skeletal muscle and in neuromuscular diseases." Biochemistry (Mosc). 2000 Jul;65(7):862-5.

33. Boldyrev AA, et al. "Antioxidant systems in tissues of senescence accelerated mice." Biochemistry (Mosc). 2001 Oct;66(10):1157-63.

34. Decker EA, Livisay SA, Zhou S. "A re-evaluation of the antioxidant activity of purified carnosine." Biochemistry (Mosc). 2000 Jul;65(7):766-70.

35. Klebanov GI, et al. "Evidence for a direct interaction of superoxide anion radical with carnosine." Biochem Mol Biol Int. 1997 Sep;43(1):99-106

36. Kohen R, Misgav R, Ginsburg I. "The SOD like activity of copper:carnosine, copper:anserine and copper:homocarnosine complexes." Free Radic Res Commun. 1991;12-13 Pt 1:179-85. 

37. Cavallini G, et al. "Carnitine versus androgen administration in the treatment of sexual dysfunction, depressed mood, and fatigue associated with male aging." Urology. 2004 Apr;63(4):641-6.

38. Vermeulen RC, Scholte HR. "Exploratory open label, randomized study of acetyl- and propionylcarnitine in chronic fatigue syndrome." Psychosom Med. 2004 Mar-Apr;66(2):276-82.

39. Capecchi PL, et al. "Carnitines increase plasma levels of adenosine and ATP in humans." Vasc Med. 1997;2(2):77-81.

40. Harper P, Elwin CE, Cederblad G. "Pharmacokinetics of intravenous and oral bolus doses of L-carnitine in healthy subjects." Eur J Clin Pharmacol. 1988;35(5):555-62.

41. Evans AM, Fornasini G. "Pharmacokinetics of L-carnitine." Clin Pharmacokinet. 2003;42(11):941-67.

© 1998 — 2004 Testosterone, LLC. All Rights Reserved.