The Odds and Implications
by Aftab J. Ahmed, Ph.D.
 ver the past several years the moniker “anti-aging” has become a part of the health care lexicon. While its misplaced connotations have fueled exaggerated expectations in some quarters, it has also unwittingly fostered the realistic recognition that quality of life may be a more practical health care goal after all. Thus, greater numbers of Americans appear
more concerned about maintaining their health in the latter years of their natural life.
In part, this may be a result of placing overly optimistic stock in developing technologies
to extend life, as if they were a given.
The fact of the matter is that the potential of most of such developments lurks as a promising halo on the distant horizon. Nonetheless, the excitement, and subsequent frustration, about some of the trends—such as the telomerase therapy—does not deter enthusiasts from pinning their hopes on methodologies as technology-intense and fledgling as reproductive/therapeutic cloning, tissue engineering and stem cell research.1
Despite its usefulness in having stimulated some serious research, the term “anti-aging” has been more effective in confusing the distinction between longevity and life extension. In fact, antiaging by definition is more a promise and an expectation. Whereas longevity is the
natural life span, its prolongation by artificial means, beyond the constraints that limit
the number of years, is life extension.
Neither the technology nor sufficient understanding of the basic aging process is on hand to justify the attempts to prolong the human life span at this time. The challenges and impediments in such endeavors ought to be more fully aired. For example, extension of life beyond a certain point would necessitate a drastic reengineering of the skeletal plan of the human body. Thus,
to avert arthritis, bones and joints supporting them would have to be sturdier, the spine would have to be maintained at an optimal angle and the nape of the neck would have to be stronger.2 Such considerations alone would make life extension a daunting challenge. If the prize of youthful immortality remains presently elusive, healthy aging may be a more pragmatic goal, irrespective of what the average and maximum longevity in the future might be.
Aside from the limitations of the skeletal blueprint, other constraints determine longevity as well, including the role of gender. In general, women tend to live longer than men, especially in technologically advanced societies.3 Epidemiological and demographic data support the fact that the life span of men is shorter.4 Traditionally, this has been attributed to the risk-prone behavior among males, such as motor vehicle accidents, suicide and alcohol consumption. Even though male demise coincides precisely with the onset of puberty,
risky behavior does not account for male-bias in mortality rates.
A recent report offers a credible alternative explanation for the early demise in men. Briefly,
shorter male life span may be due to men’s susceptibility to infections.5 Human demographic data support the idea that males are more prone to a host of parasitic and infectious diseases. In the United States, United Kingdom and Japan, men are twice as likely to succumb to parasitic infections than women. More importantly, it should be emphasized that, contrary to widely held belief, overall male mortality does not correlate with puberty, rather, it typically occurs later in life. Taken together these data suggest that women live longer because they tend to have a greater degree of immunocompetence than men. That is, women have a better overall ability to avoid deleterious effects of various pathogens.
One explanation for low immunocompetence in males is that masculinization depends upon testosterone. It should be noted that it is precisely the reason why body-builders, and those taking raw steroids, are frequently stricken with opportunistic infections. While it is not yet known how testosterone might cause immunosuppression, it is plausible that reduced
immunocompetence may minimize the risk of the male immune system to produce antibodies against “self,” as happens in autoimmunity.
Is gender the destiny, then? Not necessarily. Since the human immune system launches an almost fearsome response to infecting pathogens, it is in order to briefly review how pathogens are neutralized. The immune response is the result of a concerted effort by the T and B cells. Whereas the B cells produce antibodies, the T cells produce an array of substances (including cytokines) to thwart the infection. The story, however, is slightly more involved and intriguing. Before the T and B cells join the fray, another type of immune cells raises the alarm in the immune system. These are called dendritic cells, which function both as sensors and messengers and, as such, are literally the early warning network present in just about all tissue of the body.
When a pathogen infects the body, it is “fingerprinted” by dendritic cells. In so doing, they “mature” and migrate to the nearest lymph node, carrying the bits and pieces of the offender. Inside dendritic cells, these bits and pieces (antigens) are diced into even shorter fragments, and are loaded onto a specialized set of proteins (MHC class I and II), whose function is to take these fragments to the cell surface and present them to T cells. The T cells register this information and are activated to eliminate the pathogen by producing a battery of cytokines. In addition, T CELLS not only disarm the pathogen directly but also summon and organize additional
immune cells as well. Among these are the B cells, which are potentiated by activated T cells
to start producing antibodies.
Many different cell types can present antigens to T cells already activated. It is dendritic cells, however, that are indispensable in the original activation of T cells. Accordingly, in immuno-speak, dendritic cells are called professional antigenpresenting cells ( APCS ). For good reason, then, there is significant interest in unraveling their machinations, and considerable research resources are invested in this effort. An understanding of dendritic cell function should provide therapeutic/corrective tools to better counter infectious diseases. Infectious diseases are a clear and present danger experiencing a universal upsurge, especially as drug-resistant bacteria abound.
Presently, however, nutritive intervention with systemic enzymes appears to effectively induce “maturation” of dendritic cells. If in vitro infected cells are challenged with systemic enzymes, in a remarkable sequence of events the dendritic cells mature and effectively fend against the pathogen. By the same token, if malignant cells—say, from an aggressively growing gynecological tumor—are exposed to systemic enzymes, the rate of their multiplication is retarded. Since unbridled growth is a hallmark of transformed cells, it is pertinent to suggest that the rate of growth is reduced as a function of systemic enzyme dosage.6
These findings imply that systemic enzymes provide a promising nutritive regimen to help dendritic cells mature. As a result, systemic enzymes not only control a trenchant pathogen in
tumorigenesis but also should be effective in holding at bay an occasional exposure to an offending microorganism. Systemic enzymes, however, also modulate the immune response in more ways than maturation of dendritic cells. It may well be a corollary of dendritic cell maturation, but systemic enzymes tweak T cells to restore the balance in favor of anti-inflammatory cytokines to calm the inflammatory response. In addition, upon entry into the blood stream, systemic enzymes bind to a cellular “ferry” that in effect mobilizes macrophages, the foot soldiers of
immune response. As such, systemic enzymes modulate the immune system in all phases of its response in face of an imminent infectious threat.
It should be emphasized that systemic enzymes are gender-neutral; that is, their health benefits are just as effective in males as females. In terms of susceptibility to infections, while the odds appear male-driven, the question is necessarily forced: “Why do males bear greater burden of parasitism?” Further, does this susceptibility reflect “maleness” per se? Interestingly, male proneness to parasitism has little to do with the gender. Thus, in species where females are larger, they suffer the greater burden of parasitism. Simply put, it is a matter of size. The larger body size in males provides greater surface area for pathogens to find a home and thrive. Combined with the conclusions from past epidemics, future research should elucidate mechanisms that cause unusually high susceptibility to infections in larger mammals, which happen to be
males in most species.7
This cursory overview underscores the challenges inherent in extending the life span. Extension of life is neither trivial nor that readily achieved as the breathless enthusiasm of its proponents might suggest. Accordingly, additional mechanisms will have to be explored and understood before a meaningful discussion of life extension is deemed even tentatively plausible as a possibility. In the interim, it would be more pertinent to frame the discussion around issues that could potentially improve the quality of life, such as the role of aging in disease, maintenance and restoration of functional integrity in the elderly and the role of the genetic makeup in determining longevity. In other words, a devolution of the loaded term “anti-aging” in
favor of a more practical concept, such as age management, may be a far more appropriate strategy to better offset the ravages of old age.8 Caloric restriction, an example of an “antiaging” regimen, is an unpalatable alternative to many and not necessarily because of lack of
self-discipline. Likewise, castratos live longer and, because of testosterone ablation, are less
likely to fall prey to infections. Yet, castration has not caught on as a viable life extension proposition. Such drastic approaches notwithstanding, sensible lifestyle habits are considerably
more likely to bear fruit in the long run along with meaningful supplementation with nutritives such as systemic enzymes.
Aftab J. Ahmed, Ph.D. is vice president, director of research and development and business development at Marlyn Nutraceuticals, Inc.
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Selected references:
- Ahmed, A. “‘Anti-Aging’: The Elusive Mermaid,” J. I. Med. Assoc. (1998). Vol. 30, p. 178.
- Olshansky, S., Bruce, C. and Butler, R. “If Humans Were Built to Last,” Sci. Am. (2001). Vol. 284, p. 50.
- World Health Organization, World Health Organization Statistics Annual, 2002.
- United States Life Tables www.ccdc.gov/nchs/data/nvsr/nsvr48/nsvr48_18.pdf, 1998.
- Moore, S. and Wilson, K. “Parasites as a Viability Cost of Sexual Selection in Natural Populations of Mammals,” Science (2002). Vol. 297, p. 2015.
- Zavadova, E., Savary, C., Templin, S., Verschraegen, C. and Freedman, R. “Maturation of Dendritic Cells from Ovarian Cancer Patients,” Cancer Chemother. Pharmacol. (2001). Vol. 48, p. 289.
- Kreeger, K. “Sex-Based Longevity,” The Scientist (2002). Vol. 16 (10), p. 34.
- Ahmed, A. “Genes, Longevity, and Functionality ” in preparation, J. Theo. Biol., 2002.
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