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Coronary Heart Disease - CHD
Coronary Heart Disease (CHD) is the poster child of health disorders arising from suboptimal cellular methylation. In the United States alone well over 13 million men and women are currently managing CHD, where it represents the leading cause of death. The principal villain arising from imbalances in the methylation cycle and contributing to the development of CHD, is homocysteine. Consequently, serum homocysteine levels are commonly used as a reliable measure of the chances of developing CHD.
Cellular methylation efficiency decreases with advanced age, reflecting an increased risk of developing CHD in the elderly. The effective clinical management of CHD is thus increasing in urgency as the mean age of the human population steadily climbs.
Click here to be directed to a page discussing the possible benefits of creatine use for the elderly.
The development of CHD can be offset by adopting an active lifestyle and by controlling one's diet.
Recent evidence now seems to suggest that creatine supplementation may also help assist in the management of CHD.
Creatine May Lower Serum Cholesterol Levels
Recent studies have shown that creatine may also improve serum cholesterol profiles by increasing the ratio of good cholesterol (high-density lipoproteins or HDL) to bad cholesterol (low density lipoproteins or LDL) in the blood (Reference 1). Interestingly, this beneficial effect of creatine on blood lipid profiles does not always require a concomitant exercise regimen. A surprising fact given that exercise also exerts a strong protective over blood lipid profiles. It is thus that regular exercise in conjunction with moderate creatine use may prove an effective way to combat coronary heart disease from atherosclerosis in later life.
Interestingly, this positive effect of creatine supplementation on blood lipid profiles may be related to the body's methylation status. Methylation is one of life's most important and ubiquitous forms of biochemical regulation. The scope of this biochemical process is all encompassing. Methylation is applied at the levels of our genes as well as is responsible for functionalizing many known growth factors, hormones, neurotransmitters, metabolic mediators (including creatine, adrenaline and carnitine) and structural components of the cell (phospholipids). Indeed, life itself would not be possible without methylation, much less muscle growth.
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The very important biochemical process of methylation depends on a molecule named SAM, which is derived from the essential amino acid methionine obtained from the diet.
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Ironically, despite the profound importance of methylation, exhaustive methylation can lead to the production of a potentially dangerous compound known as homocysteine. Helping neutralize homocysteine may be another area whereby creatine supplementation exerts a positive effect over health (see next section). Most importantly, creatine supplementation has been shown in recent scientific studies to improve the body's methylation status and hence, mitigate the production of homocysteine (see next).
Homocysteine, Methylation and Coronary Heart Disease
To reiterate the previous section, exhaustive methylation, or B-vitamin deficiencies, increase the levels of an amino acid known as homocysteine in the blood stream, which has very unhealthy repercussions. Homocysteine is a byproduct of methionine consumption produced during cellular methylation that needs to be neutralized soon after being produced.
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The first clinical condition showing elevated homocysteine levels (homocysteinemia) was described nearly half a century ago by Carson and Neill (Reference 2). Patients presenting with this metabolic disorder displayed severe developmental abnormalities including mental retardation, skeletal disorders and invasive vascular disease. Noteworthy, the vascular manifestations of this disease includes widespread arterial and venous thrombosis, usually resulting in the death of afflicted individuals while still within their first decade of life. It is now understood that homocysteine is the principal cause of the primary and secondary vascular complications associated with this disease (References 3, 4).
In the general population only a 5 micoMolar increase in plasma homocysteine level results in a 60% and 80% increased risk of developing coronary heart disease in males and females, respectively. Be absolutely clear on this point, your homocysteine levels need to be kept in check at all cost or your health is at risk. And, the best way to do this is to optimize your methylation status (see next section for details).
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Creatine Supplementation May Assist in the Management of Coronary Heart Disease
Recent evidence now indicates that creatine supplementation decreases blood homocysteine levels, an effect downstream of its positive effect of cellular methylation status (References 5, 6, 7; also see figure below). In this respect, creatine supplementation should help protect against the development of heart and vascular disease. This effect of creatine will be enhanced when combined with smart B-vitamin supplementation.
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The Effect of Creatine Supplementation on Serum Homocysteine Levels
Left: Endogenous creatine synthesis consumes SAM (methyl-carrier) and produces homocysteine. Right: Creatine supplementation (by largely bypassing the need to synthesize creatine) spares the body's SAM reserves as well as mitigates serum homocysteine levels. Certain B-vitamins also assist in the clearing of homocysteine from the blood stream. The size of the letters indicates relative concentrations.
GAA = GuanidinoAcetic Acid
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Click here to be directed to a page detailing the basic requirements for correctly combining creatine and vitamin B supplementation.
Click here for a description of the benefits of combining creatine with essential B-vitamins (B12, B6 & folic acid) over nervous system functioning.
Selected Scientific References:
1. Earnest, C. et al. (1998) High performance capillary electrophoresis-pure creatine monohydrate reduces blood lipids in men and women. Clinical Science, Volume 91 (1), pages 113-118.
2. Carson N. A. and Neill D. W. (1962) Metabolic abnormalities detected in a survey of mentally backward individuals in Northern Ireland. Archives of Disease in Childhood, Volume 37, pages 505-513.
3. Nehler, M. R. et al. (1997) Homocysteinemia as a risk factor for atherosclerosis: a review. Cardiovascular Surgery, Volume 5 (6), pages 559-567.
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4. Malinow, M. R. et al. (1999) Homocyst(e)ine, diet, and cardiovascular diseases: A statement for healthcare professionals from the nutrition committee, American Heart Association. Circulation, Volume 99, pages 178-182.
5. McCarty, M. F. (2001) Supplemental creatine may decrease serum homocysteine and abolish the homocysteine 'gender gap' by suppressing endogenous creatine synthesis. Medical Hypotheses, Volume 56 (1), pages 5-7.
6. Stead, L. M. et al. (2001) Methylation demand and homocysteine metabolism: effects of dietary provision of creatine and guanidinoacetate. American Journal of Physiology and Endocrinological Metabolism, Volume 281, pages E1095-E1100.
7. Taes, Y. E. C. et al. (2003) Creatine supplementation decreases homocysteine in an animal model of uremia. Kidney International, Volume 64, pages 1331–1337.
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Click here for a summary of the devastating effects of homocysteine on central nervous system functioning.
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