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COMMENTARIES |
VA Puget Sound Health Care System, Seattle, Washington.
Address correspondence to William R. Hazzard, MD, Geriatrics & Extended Care, VA Puget Sound Health Care System, S-GEC182, 1660 S. Columbian Way, Seattle WA 98108. E-mail: william.hazzard{at}med.va.gov
Ever since James Fries (1) framed the central argument for "Preventive Gerontology" (a neologism coined shortly after the publication of his article) (2) and its goal of squaring the human survival curve in his classic 1980 New England Journal of Medicine article entitled, "Aging, Natural Death, and the Compression of Morbidity," I have followed with great fascination the impressive accumulation of evidence for the efficacy of aggressive preventive measures to enhance both vitality and longevity across the entire human life span. Increasingly, this evidence reflects findings in studies that have included persons of truly old age, even some who are approaching or have even surpassed the maximal average age at death under Utopian conditions projected by Fries at 85 ± 4 years, the "barrier to immortality" for our species. Indeed, in the Special Article in this issue, Aronow (3) recommends revisions of NCEP-III guidelines to extend hypolipidemic preventive treatment to octogenarians and nonagenarians based upon his study of residents of a long-term care facility and review of the recent literature in this field.
In his original hypothesis [considerably expanded in the Successful Aging movement (4)], Fries placed primary emphasis upon maintenance at all ages of a healthful lifestyle (in a healthy environment). This was to be accomplished principally through enhanced education, continuing social engagement, robust physical activity, avoidance of substance abuse and environmental hazards, and optimal nutrition (both qualitatively and quantitatively).
However, fueled by the breathtaking advances of biomedicine in recent decades, the platform of Preventive Gerontology for midlife and beyond has shifted ever more toward identification of predisposing disease risk factors, aggressive disease detection at clinical and subclinical stages, and interventions to control those risk factors and disease progression by maintaining key indices of health within acceptable boundaries, especially by pharmacological means. Given the primacy of cardiovascular disease (CVD) as the leading cause of death among adults, and its exponential escalation with advancing age, this effort has focused upon a tetrad of potentially modifiable risk factors that arguably account for up to 80% of CVD deaths: cigarette smoking, hypertension, dyslipidemia, and diabetes. The latter three cluster in the worldwide contemporary epidemic of the metabolic syndrome driven by increasing overweight and obesity, a shift that threatens to nullify the remarkable gains in health and longevity of the late 20th century (widely attributed to the major decline in cigarette smoking during that era).
Five trends of the past 40 years have proven especially powerful in generating the current momentum in Preventive Gerontology in its close conjunction with Preventive Cardiology.
First, the dramatic, ongoing revolution in pharmacology has offered increasingly powerful and acceptably safe agents to intervene upon biomarkers of CVD risk. These drugs have exquisitely targeted key points in physiological regulation such as the low-density lipoprotein (LDL) receptor and the central role of hepatic hydroxymethyl glutaryl coenzyme A (HMG CoA) reductase in the control of LDL cholesterol levels. This trend can be expected to continue and indeed to accelerate as the goals of intervention become individualized to the genome of a given patient in the not-too-distant future.
Second, the ascendancy of chronic disease epidemiology, randomized, controlled clinical trials (RCTs), and evidence-based medicine has provided clinicians and public health leaders with powerful tools to define an ambitious agenda of Preventive Gerontology/Cardiology for the second half of the human life span.
Third, the cumulative results of epidemiological studies and RCTs in support of early, aggressive, and demonstrably effective interventions have been critically examined by expert panels such as the NCEP (I, II, III, ...) and JNC (1–7, ...), commissions reconvened every few years to review latest advances and accumulated evidence in this field and issue updated recommendations. Such periodic reviews have inexorably "raised the bar" of intervention strategies by: 1) creating progressively more ambitious target levels to achieve acceptable control of the risk indices (e.g., lower LDL or non-high-density lipoprotein [HDL] cholesterol, lower blood pressure, lower fasting glucose and HgbA1C levels); such target levels have become especially low in persons at increased risk of disease complications, notably diabetics and also, more recently, patients with renal impairment; and 2) broadening the age criteria for intervention to both earlier and later in the life span.
Fourth, these ambitious recommendations, in turn, have been effectively transmitted to professionals via consensus conferences and expansive, carefully orchestrated professional educational campaigns. They also have been communicated to an eager and anxious public by a large, aggressive, and often medically sophisticated media. Both dissemination processes have generated ever more demand for the pharmaceuticals used in the clinical trials, agents increasingly marketed directly to consumers in remarkably effective manner.
Fifth, all of these advances have occurred as the American population has continued to age progressively, an inexorable trend permitted in no small part by the triumphs of CVD research and development, treatment, and prevention. Collectively, all of these forces conspire to push the recommended age of intervention ever upward.
However, barring true breakthroughs in longevity from virtual elimination of deaths from the leading causes of death (notably CVD) (5) via new marvels of genetic engineering, the "Barrier to Immortality" for our species appears to remain immutably fixed at or near the limit estimated by Fries, and the gap between the present average age at death and that maximum, although narrowing, appears to be doing so at a diminishing rate. Thus, as reflected in the article by Aronow, the trend is for the Compression of Morbidity hypothesis to be increasingly tested by powerful pharmacological and other technological interventions applied ever closer to the upper boundary of the human life span—even into that final life phase of life so familiar to geriatricians dominated by multiple comorbidities, disability, frailty, and decline.
Here, we as clinicians may feel caught in a bind between the expanding promise of technology to extend the lives of our patients "forever" and our sense of an ever-narrowing window of opportunity for them to receive the full benefit of those interventions (and to escape their ever-present risks). Nevertheless, this technological trend is likely to persist and even gather greater momentum as the fruits of the Human Genome Project become fully applied to drug discovery and development. Thus, our role as advocates for our patients in deferring their decline until there is no further opportunity for further "compression of morbidity" will continue to challenge us. Nevertheless, when it becomes clear to us that their "barrier to immortality" is crumbling, we can be counted on to ease their transition to comfort-centered care in a compassionate, seamless fashion, a cardinal, indeed defining, skill in our role as expert geriatricians.
References
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