Increase your Life Span and Health Span

Every once in a while, a paradigm shift occurs that can greatly affect our lives. *The science of Telemerase and the ability to lengthen telomeres is a paradigm shift in aging and health.

*It is believed that telomerase activation will play a significant role in the extension of our healthspans and the early users will be part of the vanguard that will ultimately change the focus of health care from the treatment of specific diseases to true prevention of the maladies and challenges associated with aging.

In our efforts to stay abreast of current science and offer our clients the most advanced diagnostic testing and the most advanced and scientifically proven products, NBH Lifetime Health is now offering TA-65®MD. This is the  first and only telomerase activator tested on humans for safety and efficacy.

Telomeres and Telomerase:  An Overview

Telomere: A repetitive segment of DNA at the ends of all chromosomes that helps keep the structure of the chromosome intact and protects the genes that make up our genome.

Telomerase: An enzyme that synthesizes the specific DNA sequence (TTAGGG) at telomeres.

The only normal cells that have telomerase turned on permanently are eggs and sperm which are called germ line cells. (It has to be this way so that babies are born as babies and not with telomeres that are as short as their aging parents.) All the rest of our cells are called somatic cells.

Cell Death

Normal somatic cells comprise the vast majority of all our cells and they have very low levels of telomerase activity that cannot keep pace with the telomere loss that occurs with normal aging. These cells normally can divide 30 to 50 times before their telomeres become too short and they reach a state of replicative senescence and can no longer divide or function properly. The limited number of times a cell can divide is called the Hayflick Limit. Science showed that that even healthy cells that are growing under ideal conditions stop dividing and ?senesce? and die soon thereafter.

Hayflick proved his theory with enough repetition that eventually the world of science had to listen and named the finite lifespan of cell division after him: the ?Hayflick Limit.  If this limit cannot be overcome, we are all doomed to die from cellular senescence.

For a while there was a debate whether the telomere is the arbiter of this death or merely a marker of the inevitable progression towards it.  However it was proven some 35 years later by other scientists that shortening telomeres do in fact cause cell senescence and death.

Replicative senescence refers to the inability of a cell to further duplicate itself, but cells show senescent changes even before that point. When a cell can no longer divide, it is either senescent or it goes into apoptosis and dies. However even before actual replicative senescence occurs, cells begin to behave abnormally as their telomeres shorten. Obviously when too many cells in an organ system cease to perform their proper function, that organ system can‘t function normally and eventually will fail. This leads to disease and finally death of the whole organism. Replicative senescence happens when telomeres get too short. So you can see how telomere length limits human lifespan.

Let‘s elaborate a bit more about when telomeres get too short. As mentioned, the cell can no longer divide and one of two things happens. *Either it enters an arrested state (senescence) or it commits a kind of molecular suicide known as apoptosis (programmed cell death for the good of the organism). Cell death is the better of the two possibilities; a dead cell gets disposed of and is out of the picture. *But even before this occurs, cells with shortened telomeres are already losing the ability to repair and maintain themselves; the result is abnormal function and disease.

*Senescence is bad news.  Senescent cells are still around, they are by no means dead and gone; they have a life of their own. They no longer perform their intended function and instead pour all kinds of pro-inflammatory substances into the tissue and bloodstream, such as cytokines (including interleukins and tumor necrosis factor-alpha), and enzymes called proteases that chew up proteins, particularly materials such as collagen and elastin, which hold together our organs and our skin.

*Indeed, some scientists believe that it‘s the emissions from accumulating senescent cells that make our skin sag and our hair thin, and that set our immune systems on an inflammatory track linked with cardiovascular disease and cancer.  ?It‘s a toxic thing –a rotten apple spitting out bad stuff, is what Nobel Prize winner Elizabeth Blackburn says about a senescent cell.

Tissues loaded with senescent cells, whether they‘re stem cells or differentiated cells, have a reduced ability to respond to illness and injury –that is, to repair and regenerate tissue in everything from kidneys to blood vessels to skin –a fundamental feature of aging. Non-dividing cells not only emit stuff that degrades tissues and stimulates the activity of pre-cancer cells, they also take up the valuable space of healthy ones and crowd them out. This explains why an increased ratio of senescent CD28- (negative) cells is a marker of an aged and weakened immune system. Here we should note that one of the most important findings to come out of the data from people taking TA-65 for a year was a significant improvement in the ratio and absolute number of senescent CD28- cells.

“Client satisfaction with TA-65 has been so high that most people continue taking TA-65® long after finishing their first year on the product. Although the science of Telomere Biology is a work in progress, an ever increasing number of forward thinking men and women are actively seizing the historical opportunity to do something positive to protect their chromosomes and reverse aging.” Quote from Studies

NBH

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