In recent years supplement formulations involving the use of creatine have become more advanced and thus more effective. Most new supplement users are not aware of the days when CellTech and Phosphagen HP reigned supreme and if you wanted to save a few bucks, taking your bulk creatine monohydrate with grape juice was something most educated supplement users preferred.
Of course, both the media and medical communities were very skeptical of the ergogenic and health benefits of creatine supplementation once it became popular among athletes. The medical research community tried focusing on the negative aspects such as increased bloating due to water retention and possible stress placed on vital organs such as te liver and kidneys. However, as more and more studies surfaced showing creatine supplementation proved both safe (1) and an effective (2) ergogenic aid in athletes the medical community began to look at creatine in a positive light. Now current research shows benefits of creatine supplementation in those with muscular dystrophy (3), assisting recovery in patients with chronic heart failure (4), those undergoing mild chemotherapy treatment for cancer (5), as well as neuroprotective benefits (6), and also is being recommendended in PHASE III clinical trials for treatments that slow the progression of Parkinson’s Disease (7). These are just a few of the hundreds of studies surfacing showing the benefits of creatine in both healthy athletes and in clinical applications for treatment of disease.
Despite the support creatine supplementation receives in the medical research community, among numerous athletic trainers, and educated supplement users there is still a lot of ignorance among the general public about creatine use and the media loves to prey on this. Just the term supplement seems to be associated with steroids and bulging veins by the general public. Little do they know is that the body actually produces creatine and it is found in red meats and some fish (8). It has also been shown that muscular creatine stores in vegans are on average low and can be corrected with creatine supplementation (9).
As any avid supplement user can attest to, the reputation of supplements like creatine is fragile and at a disadvantage given the long shadow cast by the judgement of media which has in turn influenced the opinion of the masses. Unfortunately, in the race to make more effective preworkout creatine cocktails we have now begun to see the inclusion of a creatine precursor called glycocyamine or more commonly known in the medical research community as guanidinoacetate (GAA). What frightens me is that the inclusion of this chemical could quite possibly shatter the fragile image both creatine and the supplement idustry as whole must maintain before both the media and general public due to possible long term health concerns.
The reason for my worries is that dietary GAA raises plasma homocysteine levels (10). Unfortunately, elevated plasma homocyteine levels have been attributed to a host of diseases including dementia (11), Alzheimer’s disease (11), and coronary heart disease (12). With that in mind there are other factors which can possibly lower homocysteine levels such certain B-vitamins but have unfortunately shown conflicting results as to a true benefit (13). Another more important supplemental factor which has shown to be effective in lowering homocysteine is betaine (14). Combined, both betaine and GAA can even be effective assisting people with cardiac decompensation (arteriosclerosis or rheumatic disease) and congestive heart failure (15). Unfortunately, weighing both the postives and negatives it is clear that relatively small changes in increasing homocysteine levels can have negative health implications in healthy adults (16)
My issue with basing arguments off the Stuart study (15) is that congestive heart failure can be attributed to anaerobic ATP deficiencies (17). This means that smooth muscle creatine saturation levels are most likely low due to some issue with GMAT production or some other issue. So yes, in a unhealthy person the combo of the two might assist with heart function as it will elevate cardiac muscle creatine levels thus buffering ATP deficiencies.
However, the Stuart study (16) also showed that only betaine benefited arthersclerosis without the inclusion of GAA. We know from the Stead (10) study that GAA raises homocysteine levels in healthy subjects. So why do you want to buffer a potentially dangerous substance when it isn’t necessary in creatine responders at raising muscular creatine levels as the Stead study implied?
"Effect of creatine and GAA supplementation…. Muscle creatine was increased by 39% in GAA-supplemented animals and by 46% in the creatine-supplemented group compared with control values. Phosphocreatine was unchanged. Plasma creatine was about sixfold higher in both the GAA- and creatine-supplemented groups. These data indicate that dietary supplementation with creatine or GAA significantly alters both muscle and plasma creatine levels."
To me, a creatine responder, this will not benefit me at all so why trust a ratio to protect me from possible neurological (11,18) and possible coronary artherosclerotic diseases (12,19). I’m sorry I just don’t trust the inclusion of betaine which was based off of a studies of those with creatine deficiencies is going to protect me from possible glycocyamine induced hyperhomocysteinemia, nor is the inclusion of b-vitamins.
I respect my body more than that and is why I have shed some light on the subject in the hopes others will as well. This is the sort of the same ideology I used when I decided never to try PH’s. Why put something in your body that is potentially toxic when it isn’t necessary? Yes, I can use PCT to counteract the negative side effects, but how do I know they are really countering each other in the desired manner and not injuring a vital organ like my liver? In all reality, I don’t know and thus avoid any potential long term health risks by choosing not use them. The same goes for GAA with regards to potential neurological and vascular pathologies down the road. Ultimately, the choice is up to the consumer to use products containing GAA, however this educated consumer will not. To me, greed and poor research methods for supplement formulation does nothing except continue to fan the flames of the ever growing fire destroying the supplement industry’s image in the arena of public opinion. How much warning does the FDA and government have to give before this freedom of choice is taken away permanently?
1. Groeneveld GJ, Beijer C, Veldink JH, Kalmijn S, Wokke JH, van den Berg LH. Few adverse effects of long-term creatine supplementation in a placebo-controlled trial.Int J Sports Med. 2005 May;26(4):307-13.
2.Racette SB. Creatine supplementation and athletic performance.J Orthop Sports Phys Ther. 2003 Oct;33(10):615-21.
3. Pearlman JP, Fielding RA. Creatine monohydrate as a therapeutic aid in muscular dystrophy. Nutr Rev. 2006 Feb;64(2 Pt 1):80-8
4. Kuethe F, Krack A, Richartz BM, Figulla HR. Creatine supplementation improves muscle strength in patients with congestive heart failure.Pharmazie. 2006 Mar;61(3):218-22.
5. Norman K, Stubler D, Baier P, Schutz T, Ocran K, Holm E, Lochs H, Pirlich M. Effects of creatine supplementation on nutritional status, muscle function and quality of life in patients with colorectal cancer-A double blind randomised controlled trial. Clin Nutr. 2006 Aug;25(4):596-605. Epub 2006 May 15.
6. Prass K, Royl G, Lindauer U, Freyer D, Megow D, Dirnagl U, Stockler-Ipsiroglu G, Wallimann T.Improved reperfusion and neuroprotection by creatine in a mouse model of stroke. J Cereb Blood Flow Metab. 2006 Jun 14;
7 Neurology. 2006 Mar 14;66(5):664-71. Epub 2006 Feb 15
8. Sahelian R, Tutle D. Creatine: Nature’s Muscle Builder. Garden City, NY: Avery Publishing Group, 1997.
9. Watt KK, Garnham AP, Snow RJ. Skeletal muscle total creatine content and creatine transporter gene expression in vegetarians prior to and following creatine supplementation. Int J Sport Nutr Exerc Metab. 2004 Oct;14(5):517-31.
10. Stead LM, Au KP, Jacobs RL, Brosnan ME, Brosnan JT. Methylation demand and homocysteine metabolism: effects of dietary provision of creatine and guanidinoacetate. Am J Physiol Endocrinol Metab. 2001 Nov;281(5):E1095-100
11. Seshadri S. Elevated plasma homocysteine levels: Risk factor or risk marker for the development of dementia and Alzheimer’s disease? J Alzheimers Dis. 2006 Oct;9(4):393-8.
12. May HT, Alharethi R, Anderson JL, Muhlestein JB, Reyna SP, Bair TL, Horne BD, Kfoury AG, Carlquist JF, Renlund DG. Homocysteine Levels Are Associated with Increased Risk of Congestive Heart Failure in Patients with and without Coronary Artery Disease. Cardiology. 2006 Aug 28;107(3):178-184
13. Carlsson CM. Homocysteine Lowering with Folic Acid and Vitamin B Supplements : Effects on Cardiovascular Disease in Older Adults. Drugs Aging. 2006;23(6):491-502.
14.. Lawson-Yuen A, Levy HL. The use of betaine in the treatment of elevated homocysteine. Mol Genet Metab. 2006 Jul;88(3):201-7. Epub 2006 Mar 20.
15. Stuart AS Craig. Betaine in human nutrition. American Journal of Clinical Nutrition, Vol. 80, No. 3, 539-549, September 2004
16. Brosnan JT, Jacobs RL, Stead LM, Brosnan ME. Methylation demand: a key determinant of homocysteine metabolism. Acta Biochim Pol. 2004;51(2):405-13.
17. Okuda M. A multidisciplinary overview of cardiogenic shock. Shock. 2006 Jun;25(6):557-70.
18. Reif A, Pfuhlmann B, Lesch KP. Homocysteinemia as well as methylenetetrahydrofolate reductase polymorphism are associated with affective psychoses. Prog Neuropsychopharmacol Biol Psychiatry. 2005 Sep;29(7):1162-8.
19. Gravina-Taddei CF, Batlouni M, Sarteschi C, Baltar VT, Salvarini NA, Bertolami MC, Sousa JE. Hyperhomocysteinemia as a risk factor for coronary atherosclerotic diseases in the elderly. Arq Bras Cardiol. 2005 Sep;85(3):166-73. Epub 2005
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