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By Dr. Mike Roizen

As we stand on the cusp of revolutionary advances in medical science, the quest to understand and potentially reverse the aging process captures the imagination of researchers and the public alike. Among the promising avenues of exploration is therapeutic plasma exchange (TPE), a process that has shown intriguing potential in decreasing biological aging, especially reversing cognitive decline in early Alzheimer’s in AMBAR studies.

Here, I offer a hypothesis on why TPE works, centered around the role of senescent cells in the aging process. Senescent cells are essentially aged cells that have lost the ability to divide and function normally. Interestingly, they are present even in utero, but unlike in later life, they do not accumulate. Up until around age 30, our immune system efficiently clears these senescent cells. However, as we age, senescent cells begin to accumulate, with detrimental effects on surrounding cells. This process is driven by what is known as the senescent-associated secretory phenotype (SASP), which transforms neighboring cells into a more aged, connective tissue-like state.

The evolutionary roots of this mechanism may lie in our ancient past. When early humans faced injuries, such as a spear wound or an animal attack, rapid formation of connective tissue could help stem bleeding and aid survival. While beneficial in those times, this process now contributes to aging, with no compensatory benefit in our relatively safe modern environment.

Recent studies by Dr. Dobri Kiprov and his collaborators at the Buck Institute have unveiled a fascinating insight: six sessions of therapeutic plasma exchange, particularly when combined with immune globulins, can significantly reduce biological markers of aging. One notable finding from their research is the reduction of interleukin-11 (IL-11) levels, a cytokine possibly implicated in the aging process.

This discovery might be analogous to the checkpoint hypothesis, a concept that has revolutionized cancer treatment. The checkpoint hypothesis suggests that cancer cells evade immune detection by sending signals that mask them as normal cells. Jim Allison’s groundbreaking work on checkpoint inhibitors, which earned him a Nobel Prize, demonstrated that blocking these signals allows the immune system to recognize cancer cells as not normal, and attack cancer cells effectively.

Could IL-11 play a similar role in senescent cells, signaling the immune system to ignore them? If so, therapeutic plasma exchange might help by removing excess IL-11, thereby allowing the immune system to target and eliminate these aged cells, contributing to a younger physiological state.

Although this remains a hypothesis, the data from Dr. Kiprov’s studies indicate that therapeutic plasma exchange not only alters epigenetic clocks to reflect a younger biological age but also notably reduces IL-11 levels. Whether or not this precise mechanism holds true, the evidence suggests that TPE could play a substantial role in promoting longevity and youthful vitality.

As we continue to unravel the complexities of aging, therapeutic plasma exchange offers a tantalizing glimpse into a future where we may not only extend life but enhance the quality of those extended years. The journey to fully understand and harness this potential is just beginning, yet the promise it holds is undeniably profound.

Thanks for reading, Michael F. Roizen MD