10. Is creatine safe for women, children or the elderly?
11. Creatine risks and side effects?
12. Long-term consequences of creatine use?
13. Does creatine cause cancer?
14. Can creatine help those with Muscular Dystrophy?
Recently, there has been a lot of talk about creatine causing cancer. This concern initially arose from the fact that certain carcinogenic agents (AIAs) are produced in meats when exposed to high temperatures. The connection between creatine and cancer stems from the fact that meats with higher creatine content produce more of these cancer causing agents WHEN COOKED. The French agency for food safety, AFSSA (Agence Française de Sécurité Sanitaire des Aliments), thus alleged that creatine supplementation, since it increases our muscle creatine content, increases our chances of developing cancer. It remains to be clearly demonstrated, however, that these same cancer causing agents are produced within the human body. In other words, in a person that isn’t cooked! Moreover, some experiments performed on isolated tumor cell lines maintained in tissue culture have demonstrated just the opposite. That is, creatine had either no effect, or even suppressed tumor cell growth.
There are also theoretical reasons to believe that creatine supplementation should actually suppress tumor growth. These were explained in a recent issue of the Creatine Newsletter (Issue 30) and extend from the fact that creatine in cohorts with certain B vitamins (folate, B6 and B12) protect our genes from spontaneous breaks and mutations. An excerpt from this newsletter is shown in the box below:
Folate, Cancer & Aging
At the root of all life are nucleic acids, the DNA that comprises our genes. Our genes code for every component that the cell will ever express. That is, the selection of which genes are read will ultimately determine a muscle cell from a brain cell, an active cell from a dormant cell, a growing cell from a degenerating cell, or a young cell from an old cell. In brief, our genes decide who, and what, we are at each point in our existence.
Moreover, methylation determines which genes are read and eventually manifested in the cell. Under-methylation (hypo-methylation) switches the pattern of gene expression to one more commonly associated with cancer. For instance, hypo-methylation of the tumor suppressor gene, p53, leads to a two-fold increase in the incidence of bronchial cancer in male smokers; cigarette smoke severely compromises methylation by degrading cellular folate reserves. Folate deficiency predisposes us to cancer and has been associated with the expression of carcinomas of the colon-rectum, lungs, cervix, esophagus pancreas and breast.
DNA methylation also influences chromosome structure, the cell’s ability to repair damaged DNA as well as overall genomic stability. Expectedly, hypo-methylation also results in inefficient replication of DNA, breaks in the chromosomal linear structure and inefficient repair of damaged chromosomes. Folate-based methylation thus protects our genes from spontaneous mutations and chromosome damage that could lead to cancer and cell death.
An age-related decline in methylation capacity is thought to instigate senescence and the loss of physical capacity in the elderly. Folate-deficiency, producing a premature state of hypo-methylyation, may accelerate the normal aging process.
Folate supplementation will thus slow the progressive loss in mental and physical capacities associated with aging as well as protect against many age-related diseases, such as cancer.
Excerpt from Issue 30 of the Creatine Newsletter.