All cells have within them a biological clock that determines the maximum number of times they can divide. This is called senescence and takes place after about 70 cell divisions in young cells and far less in older cells. However, cells rarely reach natural senescence. Instead, they often die long before their time for another reason: failure to fully replicate DNA.
DNA is made up of 4 types of small building blocks called nucleotides. Arranging these nucleotides properly is the essence of DNA replication during cell division. A cell will automatically self-destruct if the finished product of DNA replication is not perfect. However, the process itself is less than perfect often resulting in mismatched nucleotides that are discarded and replaced before the final product is complete. The body is more than prepared for this contingency by keeping plenty of spare parts (nucleotides) nearby. All chromosomes contain redundant, long and repetitive sequences of DNA nucleotides. These spare parts, called telomeres, are the key to health rejuvenation and anti-aging.
Telomeres are located at the tips of the DNA strand, what Dr. Mehmet Oz visualizes as the little plastic part on the end of a shoelace. Cells with long telomeres (lots of spare parts) flawlessly replicate their DNA. Those with short telomeres do not. A strong correlation exists between short telomeres and disease. Every time a cell divides telomeres become shorter, genetic material becomes less stable and diseases are likely to increase.
Embryonic cells start off with telomeres around 15,000 nucleotides long. At birth, the telomeres have decreased in length to approximately 10,000 nucleotides. They continue to shorten throughout our lifetime to an average of about 5,000 nucleotides. Below this number, cells are unable to divide further, and the end result is death from old age. That is, unless telomeres were able to lengthen again. Researchers know there must be a way to regrow or prevent telomeres from shortening since in some cells this is already taking place.
The reproductive cells, sperm and egg, do not have shortened telomeres no matter how old they may be. The key to this phenomenon is an enzyme called telomerase. Cells with plenty of telomerase do not die and in laboratory testing do not manifest disease. The interesting thing is that all cells have the potential to manufacture this mysterious enzyme, but they do not. Like a cell phone resting quietly on the nightstand until its number is dialed, telomerase genes within every cell await the proper environmental signal before being prompted to action. Whatever turns on telomerase, prevents biological aging.
As one might expect, the pharmaceutical industry is working enthusiastically to develop effective drugs designed to lengthen telomeres by increasing telomerase activity within the cells. The research holds promise but is still many decades off. So instead of purchasing a cryogenic chamber in the hopes of being unfrozen and scientifically resurrected at some point in the Orwellian future, it may be best to get busy putting into practice those things already known to increase telomerase activity and by avoiding those that don’t.
Stress on a cell means more frequent division and a faster road to senescence. Lifestyle factors that stimulate disease processes will also shorten telomeres and reduce telomerase activity including: psychological stress, oxidation (free radical damage) and blood sugar imbalances. At the same time, lifestyle factors known to promote health such as aerobic exercise lengthen telomeres. On the whole, telomerase activity can be encouraged with an anti-inflammatory diet, certain nutritional supplements, regular moderate exercise and stress management. These well-known remedies effect genetic expression from outside the cell, having what cellular biologists call, epigenetic influence.
EPIGENETICS How genes express themselves determines everything about the body, including how it looks, functions, and heals. Diseases, as well, are the result of gene expression. For many years, scientists believed that bad genes were the reason for diseases. If a person had a given disease-gene, she was in trouble. If she did not, then the coast was clear. But, not all women with the gene for breast cancer actually developed the disease. Some women are able to keep the gene from turning on.
The Human Genome Project set out to catalog all the different genes within the body. Expecting to find 120,000 or more genes located within the twenty-three pairs of human chromosomes, scientists were more than surprised to discover only around one fifth of that number. This shocking revelation made it clear: Genes were not the exclusive determinant of destiny.
Still reeling from this microscopic earthquake, classical genetic engineers were about to be hit with a tsunami. Science now knows that a single gene has not one but thousands of potential forms of expression. As it turns out, all manner of outer environmental influences, such as stress, nutrition, and emotions, have a profound effect on what the gene does and when it does it. These phenomena are the realm of epigenetics.
From a nutritional perspective, roughly 50 different human genetic diseases arise when the wrong mutant enzymes replace the right B-vitamins, called coenzymes. This disease-promoting cycle is set up when proper levels of B-vitamins are too low and can be remedied when those levels are high. Raising the levels prevents unwanted gene expression, called polymorphisms, the source for many known diseases.
As epigenetic influences lay siege to the body, functional imbalances appear, manifesting as any of the symptoms listed on the Functional Health Assessment. Protecting the cells from without is a path of prevention, rejuvenation and vitality. However, protecting the cells from within slows down biological aging and is therefore the road to longevity. The origin of both aging and illness – that which shortens telomeres - begins with inflammation at the cellular level.