Aging: The Running Thread


The anti-aging movement, as it were, has come to an interesting impasse. Two strands are clearly at work. Thus, mega-doses of vitamins, sundry herbs, and hormones are touted as panacea to "reverse" aging (see the BusinessWeek cover story of the March 20, 2006 issue; Simultaneously, high-tech genetic techniques are being used to develop drugs that purportedly restrict the effects of caloric intake. In a sense, it is a rather odd impasse, indeed.

Caloric restriction has been shown primarily in insects and animals to prolong life and, to an extent, offset the ravages of disease. Its extrapolation to the human condition is fraught with conceptual difficulties, however. It is for good reason, then, that researchers working on the genetics of aging have scaled back the claims on the usefulness of a "pill" to extend lifespan. Rather, it is postulated that a drug for caloric restriction would have an impact solely on the disease process. For the knowledge as to what causes aging is virtually nonexistent.

It is quite plausible that genetic and molecular causes of aging and age-related diseases would be connected, but what causes aging is not at all understood. Nonetheless, control of the aging process eventually could provide a powerful means to treating chronic diseases, but that is not in the cards yet. As such, the extension of caloric restriction as a tool to manage chronic diseases as a group is rather untenable at the moment. In the first place, the underlying molecular processes common to aging and chronic diseases need elucidation. Caloric restriction would merely allow management of late-stage presentation of some chronic diseases, at best.

The main question is: What could potentially set off the disease process? Answering that question would also yield clues as to what might cause aging itself. A vast body of information is at hand to hypothesize that cellular attrition may cause injury to the various tissues and organs. It is injuries and suchlike that set the stage for the organ malfunction, which then presents itself as a frank disease.

As noted in the column "Info You Can Use" (page 5), low-grade attrition to the bodily organs causes lesions that must be repaired. Repair is ordinarily accompanied by an inflammatory response, which typically subsides after the injury heals. Repetitive lesions, however, successively raise the threshold of the inflammatory response. In other words, inflammation packs a tad greater punch than the last time around. This escalation puts inflammation center-stage in the onset, perpetuation and aggravation of chronic diseases. Since the stimuli for lesions cannot possibly be controlled, a two-fold effect essentially unfolds: One, inflammation becomes more intense with time; and two, in each cycle repair mechanisms bring greater firepower to the fore. One obvious result is fibrosis of the tissue. The second is that such rapid-fire response with each lesion causes the tissue to literally wither on the vine, and senescence ensues.

How does this happen at the molecular level? One of the major molecular agents responsible for the inflammatory response and repair is transforming growth factor-beta (TGF-?). As mentioned previously, with each round of attrition, TGF-? is produced more copiously and persists for longer periods of time. The result is that the tissue tends to over-repair and, hence, fibrosis ensues. With fibrosis, the tissue hardens, leading to its impaired function. Consequently, molecular processes in the affected tissue become skewed.

Since an organ does not exist in isolation in the body, it affects other tissues with which it must communicate. This state of affairs practically causes a logjam, the cellular consequences of which have not even begun to be asked, let alone studied. Irrespective of that, however, the underlying cause(s) of inflammation and fibrosis and compromised function of the affected tissues by TGF-? are fairly well documented. Hence, a molecular road map is in place.

It would be a daunting task, though, to design therapeutic agents that would specifically target age-related attrition and lesions. To achieve that objective, considerably more work would have to be done. Accordingly, the question is what remedies might be available to at least mitigate the effects of the unavoidable age-related attrition. Systemic enzymes have been shown to normalize the TGF-? amounts to well within the healthier levels without totally removing it from circulation. Ablation of TGF-? would be undesirable, as it carries out many beneficial functions as in wound healing, to name but one. For details of the effect of systemic enzymes on TGF-?, visit

Complexity of the aging process should be evident in the cursory details given in this issue of ROSE. In spite of the significant strides made, aging remains largely a riddle. As such, extravagant claims to extend human life span to 150 years or more are misplaced and misleading. Continuing research has made one thing quite clear, however: It is quite possible to manage.

The recognition has taken hold that aging and healthcare problems in its wake require a continuous response. Compared to the episodic management of chronic diseases of yesteryears, age-related transitions necessitate continuous attention. Since it imposes constraints on healthcare, the need to preventive nutritive approaches figure prominently in age management. It is for good reason that greater emphasis is placed on the need for physical activity, healthy dietary habits and lifestyle habits.

Numerous nutritives are touted to do wonders for an array of age-related conditions, As people increasingly take personal responsibility for their own well-being, it is indispensable that the choice of nutritives serves their individual healthcare needs. It may be necessary for Some to consult with their primary healthcare providers to arrive at (a) regime(s) best suited to individual needs.

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