Chinese herbalists for centuries have attributed astragalus with immune system boosting properties. In recent years, researchers have started to understand the biochemical basis for why astragalus works. As least some of the immune system benefits appear to be explained by telomere lengthening that rejuvenates aged immune system cells.
Several telomerase enhancing compounds have been isolated from astragalus. These include the telomerase activating compound used in the TA-65 supplement and another that Geron Corporation is calling TAT2 or TAT002. TAT2 is also sometimes referred to as cycloastrogenol, a variant of Astragaloside IV, another compound found in astragalus.
Geron is attempting to develop TAT2 into a treatment for viral infections, particularly HIV and AIDS. Telomerase activating compounds are of a particular help to immune system function in people suffering from chronic viral infections because they help the immune system cells continue to replicate despite being unable to keep their own telomerase production turned on continually.
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Chronic Viral Infections Rapidly Age Immune System
Chronic viral infections such as hepatitis, herpes, cytomegalovirus (CMV) which is an extremely common type of herpes virus affecting about 50% of the population, and human immunodeficiency virus (HIV) put a heavy load on immune system cells that may result in them reproducing much more often than in a person without such infections.
Killer cells in particular, such as CD8 lymphocytes and macrophages, can only destroy a limited number of infected cells before destroying themselves. Estimates vary based upon cell type, but 50 to 100 attacks against pathogens have been mentioned as possible before killer cells start to die.
As a result, killer cells must replicate more quickly in people suffering from chronic viral infections just to keep up with the task of holding chronic infections in check. Eventually, this causes many of the immune cells to reach a senescent state in which they can no longer reproduce and the immune system partially fails, leaving the body poorly defended both against current infections as well as new ones.
“The problem is that when we’re dealing with a virus that can’t be totally eliminated from the body, such as HIV, the T-cells fighting that virus can’t keep their telomerase turned on forever,” explained UCLA AIDS Institute member Rita Effros. “They turn off, and telomeres get shorter and they enter this stage of replicative senescence.”
In a study described in the November 15, 2008 issue of the Journal of Immunology, Dr Effros and her colleagues tested a compound known as TAT2, originally derived from the Chinese herb astragalus, on CD8 T-cells from HIV-infected individuals. They found that TAT2 retarded the shortening of the cells’ telomeres as well as improved their production of chemokines and cytokines that help inhibit HIV replication.
“The ability to enhance telomerase activity and antiviral functions of CD8 T-lymphocytes suggests that this strategy could be useful in treating HIV disease, as well as immunodeficiency and increased susceptibility to other viral infections associated with chronic diseases or aging,” the authors write.
TA-65 Supplement Tied to Immune System Strengthening
A more recent study using TA-65, rather than TAT2, showed similar results in improving telomere length in immune system cells. In a study published in September 2010, TA-65’s effects on CD8 T lymphocyte telomere length shows that the compound appears to work by repairing the most severely damaged telomeres. As treatment progresses, the percentage of CD8 cells with short telomeres significantly decreases whereas the mean telomere length does not change much.
The study found that pre-existing CMV infection was a major predictive factor in the length of immune cell telomeres as well as the effects of TA-65. Patients who were infected with CMV both had larger percentages of very short telomere length lymphocytes before treatment and benefited the most from TA-65 treatment.
It’s possible that the few studies on telomerase activators to date have not been long enough to detect mean telomere length markedly increasing over treatment durations of more than a couple of years. Even if mean telomere length doesn’t increase, it’s reasonably evident that stabilizing telomeres by slowing or halting further shortening would still be a significant step towards avoiding immunosenesence and improving health.
Immunosenescence is believed to be a major explanation for the weakening of the immune system associated with aging. It may be tied to the higher mortality rates from infections and cancers in the elderly. Human biology is so complex that isolating causes and effects is often very difficult to do, but with growing research on immune system aging it seems clear that telomere shortening does explain much of the impaired immune functionality seen with age.
Conditions which chronically activate immune system cells, causing them to eventually die fighting to protect their host, would logically account for the more rapid rate of telomere shortening seen in some people versus others.
Could Other Immune System Triggers Cause Immunosenescence and Diseases of Aging?
While much of the research in this area so far as been directed at chronic viral infections, it appears hypothetically possible that other conditions that cause a significantly increased replicative turnover in immune cells could also lead to immunosenescence via telomere shortening. Besides chronic viral infections, conditions including chronic bacterial infections, recurring exposure to environmental toxins that trigger immune responses, and chronic inflammation are all possible culprits in such accelerated immune system aging.
There’s a possibility that some such factors might be both a cause and an effect of immune system dysfunction. Consider how cells with shortening telomeres are believed to become more likely to mutate and become cancerous. Given this, is it possible that immune cells with overly short telomeres might be more likely to inappropriately pump out inflammatory cytokines and thereby trigger harmful activities by other immune cells? In such a scenario, overproduction of inflammatory cytokines could cause immune cells to suffer a more rapid replicative turnover with no useful purpose, thereby aging the immune system at a higher rate.
Other cells with shortening telomeres could similarly function poorly, further contributing to aging and mortality from diseases of aging. Indeed, it appears there is a correlation between short telomeres and elevated mortality risk from both cardiovascular and infectious diseases.
We aimed to assess an association between telomere length and mortality in 143 normal unrelated individuals over the age of 60 years. Those with shorter telomeres in blood DNA had poorer survival, attributable in part to a 3.18-fold higher mortality rate from heart disease (95% CI 1(.)36-7.45, p=0.0079), and an 8.54-fold higher mortality rate from infectious disease (1.52-47.9, p=0.015). These results lend support to the hypothesis that telomere shortening in human beings contributes to mortality in many age-related diseases.
It appears accelerated telomeric aging triggering or aggravating disease could also be the case for non-infectious diseases. Smoking and COPD (Chronic Obstructive Pulmonary Disease) were found to have high correlations with both shortered telomeres and high elevations of some inflammatory cytokines:
COPD may affect telomere length by inducing systemic inflammation. Respiratory tract inflammation in patients with COPD is considered an exaggeration of the normal inflammatory response to chronic irritants such as cigarette smoke (1). A wide variety of inflammatory mediators is increased in the lung and blood of patients with COPD, even those whose clinical status is considered stable (25). Our data are consistent with these well-established concepts, as circulating levels of the proinflammatory cytokines IL-6, IL-8, IL-1β, and TGF-β were higher in patients with COPD than in control smokers or nonsmokers. In patients with COPD, IL-6 levels were related to the degree of telomere shortening. The association between IL-6 levels and telomere length is consistent with evidence that oxidative stress and inflammation mediate telomere attrition. In the control subjects, we also found a tendency for inflammatory markers to correlate with telomere length, although the relationship was significant only for IL-8. It is noteworthy that the inflammatory cytokine levels differed between smokers and nonsmokers whereas telomere length did not. Differences in cytokine levels, however, were much greater between patients with COPD and control smokers than between control smokers and nonsmokers. These results, therefore, do not disagree with the fact that inflammation may affect telomere shortening; however, they suggest a major role for inflammation severity in telomere shortening.
Research in immune cell aging will likely help provide more definitive explanations of the factors that accelerate immune system aging and what may be done to slow or reverse immune system aging. Perhaps telomere lengthening treatments will be found to be helpful treatments in fighting not only immune system aging but also other common diseases of aging. If so, nonprescription supplements containing telomerase activating compounds such as TA-65 and TAT2 could be very popular in the future, especially if the price can be reduced to levels more like that of increasingly popular supplements like CoQ10 and resveratrol. Such supplements are widely available for much less than $50 per month for common dosages, whereas TA-65 and cycloastrogenol are still upwards of $100 per month.
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