Creatine & the Elderly : Part 3

Possible Benefits and Precautions of Creatine Use for the Elderly

The Root of Creatine’s Benefit for the Elderly

  1. Reduced Methylation Status Characterizes Old Age
  2. Creatine Supplementation Enhances Cellular Methylation
  3. Creatine Supplementation May Help Postpone Mental Senescence
  4. Precautions of Creatine Supplementation for the Elderly

Creatine May Help Postpone Mental Senescence

An age-related decline in methylation efficiency is responsible for an increase in serum homocysteine levels as we grow older. This situation is given urgency by the fact that homocysteine has been strongly implicated in the development of several common health disorders inflicting the elderly. For instance, homocysteine has been strongly implicated in the mental decline observed with advanced age as well as with the manifestation of certain psychiatric disorders, Alzheimer’s disease, dementia, poor memory and some age-related neuropathologies.

Creatine supplementation, via its positive effect on methylation status should thus help retard some of the more deleterious neurological disorders associated with elevated serum homocysteine levels. Perhaps, the relevance of creatine in combating many age-related neurological disorders explains the observed increase in the mean age of the visitors to this site over the last eight years. Creatine supplementation has clear advantages for the mind and body of the elderly!

Read a description of how creatine supplementation may help offset the development of Alzheimer’s disease and dementia in later life.

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.

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