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A startling change occurs around age 65 that decimates our ability to combat infections and malignancies. This catastrophic event decreases naïve T cells needed to ward off new bacteria, viruses, and cancers. At the same time naïve T cells are lost, we accumulate senile memory T cells that emit pro-inflammatory signals that wreak havoc in every organ system.

One of the most deadly of these inflammatory “signals” is a cytokine called interleukin-6 (IL-6). Higher IL-6 levels are associated with a 2-fold greater risk of death. Higher levels are also involved with multiple degenerative processes including frailty that so many elderly suffer.

A common trait of healthy centenarians is that they have unusually low levels of IL-6. People associate immune senescence with weakened immune function. It turns out that impaired immunity is only half the problem. Spiraling levels of IL-6 that attack our healthy tissues are another component of immune senescence that must be addressed.

The encouraging news is that significant dollars are being invested to develop technologies to turn back “on” youthful immune function. These immune-restoration therapies will likely add decades to our healthy life spans. The problem is that many of us can’t wait for bureaucratic delays while our immune systems decline.

Immune senescence is a leading cause of disability and death in aging humans.

By way of example, deaths from pneumonia are rare in youth, but spiral upwards as humans mature. In people over age 65, the top 10 causes of death include influenza, pneumonia, and sepsis. Immune senescence is a major cause of all these maladies.

Cancer, stroke, Alzheimer’s, and heart attack are common diseases of aging. These illnesses are all related to immune senescence. Lately, we hear the term “immune health” as people seek to protect against viral infections. The public does not yet understand what causes our immune system to fail as we age.

More Naïve T Cells Urgently Needed

Immune imbalance occurs when our aging immune system fails to protect against new cancers/infections, and instead generates inflammatory reactions (including increased IL-6) that attack every cell in our body.

A “naïve” immune cell is one that has not yet been activated. Since it is “naïve” (not yet exposed to an antigen), naïve immune cells are primed to effectively respond to new infectious agents and malignancies. Once exposed, naïve immune cells become memory cells or plasma cells specific to the original antigen. As our internal reservoir of naïve immune cells is decreased, we have less ability to respond to new infections/malignancies.

A deficit of naïve immune cells combined with overaccumulation of exhausted memory cells decreases the efficacy (antibody response) of vaccinations. Exhausted memory T cells are associated with increased risks of coronary heart disease, impaired vascular function, and endothelial dysfunction, along with systemic inflammation.

If we are to guard against the ravages of immune senescence, we need to increase our numbers of naïve cells (“virgin” immune cells), while reducing numbers of senile memory cells.

Protecting against Immune Senescence Today

Zinc and DHEA partially restore thymus function, which is vital to transforming bone marrow-derived immune cells into activated T cells. DHEA and fish oil help suppress interleukin-6.

A prime cause of the severe immune dysfunction suffered by the elderly is a marked decrease in naïve T cells and functional natural killer cells, with a concomitant increase in memory T cells.

Publication: International Journal of Cardiology Article title: Immunosenescence and inflammation characterize chronic heart failure patients with more advanced disease. We conclude that CHF (chronic heart failure) patients show a higher degree of immunosenescence than age-matched healthy controls. T-lymphocyte differentiation and IL-6 levels are increased in patients with an advanced clinical status and may contribute to disease impairment through a compromised adaptive immune response due to accelerated aging of their immune system.”

Senile bone marrow loses its ability to produce fresh naïve immune cells, which are launched into the bloodstream to differentiate into mature naïve T and natural killer cells. Bone marrow stem cell antigen-1 represents the body’s main source of naïve T cells in the blood.

Suppressing Deadly Impact of IL-6

One way of describing “aging” is that beneficial factors (such as naïve T cell production) decrease while detrimental ones (like interleukin-6) increase. IL-6 levels are especially high in patients with autoimmune conditions where an out-of-control immune system attacks one’s own tissues. High serum IL-6, as seen in rheumatoid arthritis, for instance, is regarded as a reliable biomarker of high-grade inflammation.

When it comes to “normal” aging, elevated IL-6 contributes to the chronic destruction of our bone, heart valves, neurons, and other tissues, while the DNA damage it inflicts accelerates aging processes and malignant transformation of healthy cells.

INFLAMMATORY MARKERS PREDICT HUMAN MORTALITY A study of community-dwelling people over age 80 was done to investigate whether interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-alpha (TNF-a) levels predict all-cause mortality. Baseline levels of these inflammatory markers were taken and the subjects followed up for a period of four years.

After adjusting for potential confounders, those with high levels of IL-6 were 2.18 times more likely to die, while study subjects with high CRP were 2.58 times more likely to die. While TNF-a by itself did not increase mortality rates, those with all three inflammatory markers above the median had the highest mortality risk during the four-year study period. The doctors who conducted this study concluded: Low levels of inflammatory markers are associated with better survival in elderly, independently of age and other clinical and functional variables.


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