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1.
Geriatrics ; 55(7): 48-52, 55-6, 58, 2000 Jul.
Article in English | MEDLINE | ID: mdl-10909406

ABSTRACT

Little is known about the efficacy and safety of substances that are being promoted to consumers as "anti-aging" therapies. Hormones such as DHEA, human growth hormone, and testosterone tend to decline with aging, but the therapeutic value of replacing them to "normal" physiologic levels has not been substantiated by controlled clinical trials. The best source of antioxidants is a balanced diet, although older patients may benefit from vitamin E supplementation. Providing anti-aging medicine in the primary care setting means practicing good medicine. It means talking to patients who request these therapies and understanding why they want them and how much risk they're willing to take.


Subject(s)
Aging/drug effects , Antioxidants/pharmacology , Hormone Replacement Therapy , Antioxidants/adverse effects , Bone Density/drug effects , Bone Density/physiology , Calcium/pharmacology , Diet Therapy , Drug Approval , Hormone Replacement Therapy/adverse effects , Humans , Risk Assessment , Vitamins/adverse effects , Vitamins/pharmacology
2.
Geriatrics ; 55(6): 36, 39-43, 2000 Jun.
Article in English | MEDLINE | ID: mdl-10872344

ABSTRACT

The growth in popularity of so-called "anti-aging" medicine challenges physicians to examine their attitudes about aging. Does one define aging as a predisposition to pathology or as part of the life cycle? Is longevity without the chronic diseases associated with aging a realistic goal? Anti-aging modalities being prescribed by some practitioners include hormone replacement therapies, vitamin and mineral supplements, diet, and exercise. Although diet, exercise, and some vitamin and mineral supplements are well-recognized as preventive measures, unproven hormone, mega-vitamin, and herbal therapies are controversial. Both the patient and the physician bring biases and values to the discussion of anti-aging medicine, and that combination will influence the treatment decisions.


Subject(s)
Aging/drug effects , Geriatrics , Nonprescription Drugs/pharmacology , Aged , Humans , Longevity , Nonprescription Drugs/adverse effects , Physician's Role , Quality of Life
3.
In Vivo ; 14(1): 29-34, 2000.
Article in English | MEDLINE | ID: mdl-10757058

ABSTRACT

Cell senescence limits cell divisions in normal somatic cells and may play a central role in age-related diseases. In this review, we examine the theory that cell senescence underlies and is a pivotal event in human aging and age-related diseases. The model remains completely consistent with what we currently know of cell biology, cell senescence, and the pathology of all human age-related diseases including atherosclerosis, osteoarthritis, immune senescence, skin aging, Alzheimer's dementia, and cancer. Although there is in vitro and ex vivo data to support the model, there is currently no in vivo data supporting the theory. Such data is probably obtainable using available methods and, if confirmatory, would not only have stunning therapeutic consequences, but significant commercial consequences as well.


Subject(s)
Aging/physiology , Cellular Senescence , Humans , Models, Biological
4.
J Pediatr Endocrinol Metab ; 13 Suppl 6: 1477-81, 2000.
Article in English | MEDLINE | ID: mdl-11202224

ABSTRACT

The notion that all aging is ultimately cell aging is a novel hypothesis and one with growing support. Recent studies in genetics and cell biology are consistent with this view. Criticism of the model is largely reflective of inadequate understanding of both the model itself and human pathology. Hutchinson-Gilford progeria is a segmental progeria that may well be an 'epigenetic mosaic' disease in which certain cell lines exhibit early cell senescence, while others are spared. The general cell senescence model of aging offers a consistent and elegant explanation of both human aging and progeria. More importantly, the model is not only testable but implies fundamental, novel and promising therapeutic avenues for both progeria and more typical age-related diseases.


Subject(s)
Aging , Cellular Senescence , Progeria , Aging/genetics , Cellular Senescence/genetics , DNA Helicases/genetics , Humans , Models, Biological , Mosaicism , Mutation , Progeria/genetics , Werner Syndrome/genetics
6.
JAMA ; 279(21): 1732-5, 1998 Jun 03.
Article in English | MEDLINE | ID: mdl-9624027

ABSTRACT

Recent research has shown that inserting a gene for the protein component of telomerase into senescent human cells reextends their telomeres to lengths typical of young cells, and the cells then display all the other identifiable characteristics of young, healthy cells. This advance not only suggests that telomeres are the central timing mechanism for cellular aging, but also demonstrates that such a mechanism can be reset, extending the replicative life span of such cells and resulting in markers of gene expression typical of "younger" (ie, early passage) cells without the hallmarks of malignant transformation. It is now possible to explore the fundamental cellular mechanisms underlying human aging, clarifying the role played by replicative senescence. By implication, we may soon be able to determine the extent to which the major causes of death and disability in aging populations in developed countries-cancer, atherosclerosis, osteoarthritis, macular degeneration, and Alzheimer dementia--are attributable to such fundamental mechanisms. If they are amenable to prevention or treatment by alteration of cellular senescence, the clinical implications have few historic precedents.


Subject(s)
Aging/physiology , Cellular Senescence/physiology , Telomerase/physiology , Telomere/physiology , Animals , Cell Division , Cell Transformation, Neoplastic , Cellular Senescence/genetics , Disease , Humans , Telomerase/genetics
7.
JAMA ; 278(16): 1345-8, 1997.
Article in English | MEDLINE | ID: mdl-9343466

ABSTRACT

Population projections of the aging global society and its fiscal and social impact have depended on assumptions regarding the human life span. Until now, the assumption that the maximum human life span is fixed has been justified. Recent advances in cell biology, genetics, and our understanding of the cellular processes that underlie aging, however, have shown that this assumption is invalid in a number of animal models and suggest that this assumption may become invalid for humans as well. In vitro alteration of telomeres affects cellular senescence, and in vivo manipulation of genes and diet can increase maximum life span in animal models if these discoveries are extended to humans. We may soon be able to extend the maximum human life span and postpone or prevent the onset of diseases associated with aging. Such a possibility requires that we recognize a growing uncertainty in any attempt to project international health care costs into the next few decades. The costs may be significantly lower than projections, if life span increases and age-related disabilities are postponed or less severe, or perhaps higher, if life span increases without altering the onset and severity of disability. An appropriate uncertainty regarding the human life span undermines any attempt to accurately predict health costs in the next century.


Subject(s)
Cellular Senescence/genetics , Life Expectancy , Longevity/genetics , Aging/genetics , Cloning, Organism , Gene Expression , Humans , Life Expectancy/trends , Neoplasms/pathology , Public Policy , Telomere
8.
J Emerg Med ; 2(2): 107-10, 1984.
Article in English | MEDLINE | ID: mdl-6526987

ABSTRACT

Codeine often causes gastrointestinal cramping and pain. Treatment for such symptoms is usually symptomatic and supportive. Although naloxone is commonly used to treat other medical problems due to opiates, its use in treating such cramping has not been previously reported. The authors present four cases in which naloxone (Narcan) was used with success in relieving gastrointestinal side effects that were apparently due to codeine. It is suggested that patients with gastrointestinal symptoms and a history that strongly implicates codeine as the etiology be treated with naloxone.


Subject(s)
Codeine/adverse effects , Gastrointestinal Diseases/drug therapy , Naloxone/therapeutic use , Adult , Colic/chemically induced , Colic/drug therapy , Female , Gastrointestinal Diseases/chemically induced , Humans , Male , Pain/chemically induced , Pain/drug therapy
9.
J Emerg Med ; 2(1): 33-6, 1984.
Article in English | MEDLINE | ID: mdl-6520368

ABSTRACT

Although a great emphasis has recently been placed on training both the medical profession and the general public in cardiopulmonary resuscitation (CPR), studies have demonstrated that retention of resuscitation skills is poor. Although CPR certification is generally valid for a 1- to 2-year period, evaluation of trainees at all levels has demonstrated a marked lack of proficiency over this course of time. This paper reviews the studies that have disclosed this lack of skills retention, as well as proposed solutions and reinforcement techniques. CPR course content and certification criteria must be appropriate to maximize retention as well as learning. To this end a simplification of basic life-support training curricula is recommended.


Subject(s)
Emergency Medicine/education , Memory , Resuscitation , Retention, Psychology , Certification/standards , Humans , Time Factors
11.
J Med Educ ; 58(7): 568-75, 1983 Jul.
Article in English | MEDLINE | ID: mdl-6864745

ABSTRACT

Performance in and knowledge of cardiopulmonary resuscitation (CPR) were assessed in a group of preclinical medical students who had received CPR certification either two or three weeks (group 0), one year (group 1), or two years (group 2) prior to the study. Assessment, ventilation, compression, and complications caused by incorrect technique were evaluated. A written examination was also given. There was significantly higher rate of failure to perform adequate CPR by students in groups 1 and 2 when compared with group 0 (p less than .05). There was no significant difference between the failure rates of groups 1 and 2. The most frequent errors related to chest compression rate and an inability to adhere to the recommended single-rescuer compression-to-ventilation ratio. Written test scores were also higher in group 0 than either group 1 or 2 (p less than .001). Written examination scores were not reliable predictors of CPR skill in individual cases.


Subject(s)
Clinical Competence , Memory , Resuscitation/education , Retention, Psychology , Students, Medical/psychology , Certification , Educational Measurement , Time Factors
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