Adding Value to Long-term Care

Reviewed By:
Barry Goldlist, MD, FRCPC, FACP
Director, Division of Geriatric Medicine,
University of Toronto

Adding Value to Long-Term Care
An Administrator's Guide to Improving Staff Performance, Patient Experiences, and Financial Health
D. Lazer and T.L. Schwartz Cassell
Elder Clinical Resources LLC 2000

This text is clearly meant for administrators of long-term care (LTC) facilities, and not for the physicians who take care of the residents in these facilities. The basic tenet of the book, that placement in LTC facilities can be a positive experience, is to be applauded. Placement should not be considered a "failure", but rather the appropriate choice in certain circumstances. This book is a "how to" manual for creating an optimal environment, an approach that will ensure high quality resident care.

Unfortunately, this book will not help most Canadian LTC administrators. The approach they suggest--ensuring an appropriate physical environment, multidisciplinary resident assessment, programming that ensures family involvement, and continuous quality improvement--is hardly ground breaking. It is the standard approach in most Canadian LTC facilities. The best part of this text is the section on how to make use of U.S. funding sources (e.g. Medicaid) in order to achieve these goals. Unfortunately, this advice is not applicable in Canada, and will not help Canadian facilities.

There are several appendices at the end of the text that are useful for monitoring the LTC environment, but once again they are hardly innovative by Canadian standards.

One of the appendices is on how to use simulation to teach caregivers about physical changes associated with aging. This is clearly a useful section, but it is interesting how little clinical information is available in the text itself. For example, the most common reason for institutionalization is a dementing disorder, and one would think that administrators, many without clinical backgrounds, would benefit from understanding the nature of dementia and its causes. The short section on this topic in this book, is incomplete and seriously out of date. Although excellent references are given, I feel the book would be strengthened by a more comprehensive approach.

In summary, this book addresses a worthy and important topic. However, its areas of greatest strength are relevant only to LTC administration in the United States, and will not help Canadian LTC administrators. Most of the other approaches and tools are easily available from provincial LTC associations, and are specifically designed for the Canadian health care environment. Despite its excellent intentions, I really cannot recommend this book to Canadian readers.

Eat Less and Drink from the Fountain of Youth

Caloric Restriction Leads to Extended Life Span

Recently, the World Health Organization published a Longevity Report Card for the world's nations. This latest report card now rates different countries according to the number of years their average citizen can expect to live "disease-free". Although this new measure is still based on statistical assumptions, it provides an additional index to measure the effectiveness of national healthcare systems in extending 'good' health. Canada ranked 12th on the basis of this new measure, a number of notches below its 7th place in the total life expectancy ratings.

The new WHO index does not mean that the average life span (the average length of human life defined in terms of calendar years) has changed in Canada or anywhere else. Better nutrition, public sanitation, vaccination, and antibiotics have increased the average life expectancy, (one's statistical likelihood of living to a certain age), but so far these advances have failed to raise the ceiling on the maximum human life span

What, you might ask, can be done to raise this ceiling? Even more importantly, if we are to take the WHO statistics seriously, what can save the average 72-year-old Canadian from the rapid onset of diseases?

The answer may be startlingly simple: greatly restrict your consumption of calories! Under-nutrition, as opposed to malnutrition, may be the key to slowing down aging. In the recent Scientific American Supplement on Aging, a fascinating article, "The Famine of Youth," discusses overwhelming evidence in support of caloric restriction. As one writer in the Scientific American states, caloric restriction has "proven to increase life span in virtually every species in which it has been tested, from parameciums and worms to spiders, and rodents". This caloric restriction worked even when it was initiated in adult specimens. Not only do they live longer--the onset of most idiopathic diseases of old age in these creatures is delayed. Caloric restriction seems to have a "profound inhibitory effect on tumours," and, moreover, it "delay(s) the age-related deterioration in every major physiological system."

A recent study using gene chips showed that caloric restriction reduced the age-related increase in stress proteins, which are proteins required for the repair or elimination of damaged DNA and proteins. In this issue, we have interviewed Dr. Tomas Prolla (see page 36), who has been working with Dr. Richard Weinduch, at the University of Wisconsin, both of whom are in the forefront of research into the biology of aging. Their studies provided the first cellular markers for aging, a long-desired objective of aging research; they have also shown that caloric restriction retards the expression of these markers. Dr. Weinduch and Dr. Prolla are currently organizing a large study involving 200 monkeys [coordinated in conjunction with the National Institute on Aging (NIA)] to test whether caloric restriction extends life-span in higher primates. Unfortunately, it will be another twenty years or more before we will know whether the life-span in these monkeys has indeed increased. However, all findings to date demonstrate that the early responses to caloric restriction in these animals are comparable to responses in other species, in which the life-span has been significantly increased.

A few short caloric restriction studies have been carried out in humans. It was found that reducing food consumption to approximately 1800 calories per day, for at least six months, resulted not only in a 10-15% reduction in body weight, but also in a 20% drop in blood pressure, a 35% drop in cholesterol levels, and a 31% drop in serum lipid levels. These changes parallel those changes observed in calorically restricted animals.

While it is important to discover whether caloric restriction affects our health and longevity, the significance of this is, of course, not to impose a dietary "famine" on people, but to understand the physiological and genetic mechanisms triggered by caloric restriction. How does it extend life and retard the onset of disease? The goal of this research is to find alternative means of affecting the same mechanisms, in order to fool our cells into thinking that they are being deprived of calories. This would be tantamount to a fountain of youth pill. Dr. Prolla's group is already experimenting with dietary supplements, vitamins, nutraceuticals, and certain drugs to determine their anti-aging effects on various tissues.

Sources

1. Clark,W.R. 1999. A Means to an End. The biological basis of aging and death. Oxford University Press, Oxford.
2. Scientific American Presents. Summer 2000 volume II Number 2.

Handbook of Psychiatry in Palliative Medicine

Reviewed By:
Barry Goldlist, MD, FRCPC, FACP

Handbook of Psychiatry in Palliative Medicine
Edited by: Harvey M. Chochinov and William Breitbart
Oxford University Press, 2000
ISBN # 0-19-509299-6

This multi-authored text 'grew out' of the editor's contribution to the most recent edition of The Oxford Textbook of Palliative Medicine. The authors are well-respected leaders in the field, and do not reside or practice in any one geographic area. Ten of the contributors are from Canada. This broad representation of authors ensures that the information in the book is based on views which are not parochial, but are rather widely acceptable. The textbook covers more than just psychiatric issues. There is a very good chapter summarizing the principles of physical symptom management in the terminally ill, and there are sections dealing with family and staff issues, and ethical and spiritual issues, which are also appropriate in a general textbook of palliative care.

The chapters specifically pertaining to psychiatric care are all very good, particularly the one on diagnosis and management of depression in palliative care. There is also an extensive section on psychotherapeutic interventions and palliative care. Some of these chapters contain very helpful case examples, which can aid the non-psychiatrist in particular.

In summary, this text is well written and thorough, and covers many important aspects of palliative care. Health specialists involved in palliative care are the most likely target of this book, as most physicians involved in palliative care would probably prefer to purchase a more general text, such as The Oxford Textbook of Palliative Medicine. However, any palliative care service or hospice would benefit from having this book available as a reference.

The OMA Deal with Provincial Government: A Mixed Blessing for Family Doctors

Kimby N. Barton, MSc
Assistant Editor,
Geriatrics & Aging

This past month, the Ontario Medical Association governing council and the Provincial Government of Ontario ratified a comprehensive four-year agreement, which will pave the way for the trimming of $50 million annually in medical services from OHIP. In a telephone referendum that took place May 3 to May 10th, 66% of OMA physician members who took part across Ontario voted 'yes' to the agreement (in total 10,603 members voted, a number that represents less than half of the OMA's total membership). The number of Ontarians over the age of 65 has increased by 31% in the past decade and per capita seniors utilize up to five times more health services than the rest of the population. The new agreement is designed to address some of the issues resulting from the need to allocate sufficient resources to treat this aging population.

The agreement provides for a 1.95% increase in physician billing this year and a 2% increase to be implemented in each of the next three years. It also raises thresholds by $10,000, allowing family doctors to bill up to $330,000 a year and specialists up to $410,000 before discounts on their billings kick in.

The parties have also agreed on several initiatives to enhance delivery of needed services to patients and to provide physicians' incentives motivating them to deliver those services. Some of the initiatives include changes to the Schedule of Benefits with respect to home care application, home care supervision, complex care of the elderly and after-hour premiums. Specifically, a 20% premium ($10.30) will be added to the general assessment code for services provided to patients who are 75 years of age or older. This general assessment premium can be charged only once per patient per year. Physicians who submit a home care service request form to the Community Care Access Centre (CCAC), or who provide information in response to an inquiry from CCAC staff can charge a Home Care Application fee ($16.50) or a Home Care Supervision fee ($10.40). Changes have also been made to the Schedule of Benefits for the after-hours premium codes. Physicians may charge a premium for visiting hospital inpatients, for visiting a patient's home or a multiple resident dwelling and for making a special visit to a long-term care institution. Exact fees for these services are listed in Appendix B of the Agreement.

The Agreement has not met with universal acceptance. A release from the Coalition of Family Physicians (COFP) states that the agreement has merely guaranteed that "for the next four years family physicians will fall further behind inflation". The number of allowable non-emergency visits per month to patients in long-term care facilities and chronic hospitals (complex continuing care) were left unchanged. The allowable number of visits was cut in the last agreement and this is a problem for nursing home physicians. There are also concerns amongst specialists and advocacy groups about the possible delisting of several services. "What it means is $50 million less in health-care spending," says Ray Foley, execu- tive director of the Ontario Association of Radiologists. It is rumoured that optometry, physiotherapy, and audiology tests will no longer be insured. If the committee decides to delist hearing tests it means that patients who require audiology testing are going to have to pay for it themselves. Since many patients who visit optometrists and audiologists are senior citizens, it is apparent that improving geriatric care in one area may result in deficiencies in other areas. If you have any comments about the new deal and how it affects your practice, please email us at geriatrics@ribosome.com.

Is Aging a Disease?

Anna Liachenko, BSc, MSc,
Managing Editor,
Geriatrics & Aging

We take for granted that aging is a natural process. We accept this belief, even as we witness the disease-driven ravages of old age. We separate the diseases of old age from the process itself, as if the diseases of old age take place against a backdrop of biological changes that are somehow removed and independent of the diseases themselves. This separation of the two--aging and the classic diseases of the elderly--may be false and may undermine our ability to understand the real nature of aging.

A number of extraordinary new studies may forever jettison this dichotomy between the diseases that seem to characterize old age and the so-called natural process of aging. Some of the diseases that are characteristic of old age are senile dementia, cataracts, arteriosclerosis, cancer, diabetes, hypertension, osteoporosis, etc. We need to ask whether these diseases are a normal part of the aging process. Alternatively , we could pose the more counter-intuitive and, perhaps, more difficult question, "Is aging a Disease"?

Two recent studies offer unprecedented insight into the genetics of aging, along with evidence for a "general and global explanation of the process itself". If correct, these studies are suggesting that a small set of genes involved in cell division might have broad effects throughout the body and cause the wide spectrum of phenotypic, metabolic, physiological and cellular changes that we associate with aging.

These aging studies are based upon a revolutionary new technology, known as microarrays or, as they are called in the popular press, "gene chips". The reference to chips and microchips is not a misnomer. Gene chips are actually based upon the same technological principles and same technologies that are used in making silicon-based chips. Silicon fabrication technology and various photolithographically-layered masks are used to lay down thousands, or even hundreds of thousands of oligonucleotides of DNA on a postage-stamp-size piece of glass; amplified genetic samples can then be hybridized with these pieces of DNA. Using lasers to scan the chips, an enormous amount of genetic information can be ascertained. This technology promises for biology some of the extraordinary economies and efficiencies that have transformed all of electronics. The implications for aging research could be enormous.

Perhaps of even deeper interest to the whole question of whether aging is a disease, is the work performed by the Scripps team, comparing aging fibroblasts with fibroblasts from children suffering from Hutchinson-Gilford's progeria. A rare condition, that is caused by a single gene defect, Hutchinson-Gilford children experience what, phenotypically, seems to be an accelerated form of aging. That a single genetic defect could cause such a wide spectrum of aging-related alterations, has long been a source of curiosity and interest. These children appear old at ten years of age and rarely live past their eighteenth birthday.

The Scripps study seems to confirm that Hutchinson-Gilford patients do not just mimic aging phenotypically, but that they are indeed experiencing accelerated aging. This extraordinary result lays out part of what might emerge as a genetic program that dictates the aging process. Apart from outward manifestations of aging, Hutchinson-Gilford victims experience rapid onset of old skin, hair loss, arteriosclerosis, cancer, osteoporosis and hypertension. These results force us to ask whether these diseases, the diseases that take the largest toll on humanity, are, perhaps, part of the pathophysiology of aging.

These results are fascinating and as genetic chip technologies advance and as more information emerges from the human genome project, deeper insights will become possible into the genetics of aging. Aging, cancer, and many of the most common diseases of old age may indeed be part of a similar genetic complex, that is regulated by a surprisingly small gene set. Molecular medicine in the very near future may begin to address these diseases at the genetic level. With cellular markers for aging we may begin to develop means to modify genes in order to optimize our maximum life span and to lessen the burden of the most common diseases of old age.

Geriatrics & Aging will be at the forefront in reporting these exciting developments. I would be very interested in hearing your thoughts on whether "Aging is a Disease", please e-mail me at: geriatrics@ribosome.com.

Neurodegenerative Dementias

"NEURODEGENERATIVE DEMENTIAS"

McGraw-Hill, 2000
Edited by G.M. Clark and J.Q. Trojanowski

Reviewed by Barry J. Goldlist, MD, FRCPC, FACP

The text from McGraw-Hill, "Neurodegenerative Dementias" is clearly aimed at a very specialized audience--neurologists with a strong interest in dementia and neurodegenerative disorders. I suspect it will satisfy its target audience. It is remarkably up-to-date for such a multi-authored volume. For example, the chapter on Treatment Strategies in Alzheimer's Disease by Rachelle Doody has references from 1999. For the non-neurologist interested in dementia there are many valuable chapters. The book starts superbly with four chapters on normal aging. Although not meant to be comprehensive, these chapters are clear and address all the key issues. The chapters on Alzheimer's Disease which form the core of this text are excellent. The presentations on amyloid deposition and the tau-based neurofibrillary tangles explain difficult concepts clearly. The chapter on treatment strategies, the key chapter for clinicians, is quite comprehensive. Although current therapy is discussed in a restrained manner, the implied possibilities for the future certainly inspire optimism.

From Pediatrics to Geriatrics--Not that Great a Leap

A. Mark Clarfield, MD

Last Scene of all,
That ends this strange eventful history,
In second childishness, and mere oblivion,
Sans teeth, sans eye, sans taste, sans everything

William Shakespeare (As You Like It. II, vii, 157)
(1564-1616)

The Bard, a noted gerontologist, described those at the extremes of life as having much in common. Both are more fragile than their counterparts mired in middle age. Each exhibits an easy perturbation from the physiologic norms of maturity. As has been said about nostalgia: "It ain't what it used to be"; thus with respect to the homeostasis of both the very young and extremely old. Both can swing out from their narrow organ reserves into failure very quickly indeed.

Many analogies can be drawn between the two ends of the age spectrum--some quite credible, others a bit more fantastic. This month's column will touch on some of these in hope that perhaps a few pediatricians will decide to transfer their allegiance and bolster the still slim ranks of Canada's geriatricians.

More and more I am struck by the similarities exhibited by patients at the extremes of life. For one thing, the older person suffering from severe dementia can no more be maintained at home with the help of community services, as good as they might be, than the average two-year-old.

Does Cloning Result in Premature Aging?

A recent study from Japan may help to answer the question of whether cloned mammals age prematurely.¹ Analysis of telomere lengths in Dolly, the cloned sheep, suggested that she might be aging more rapidly than controls.² Dolly was cloned using a technique known as somatic nuclear transfer in which an adult donor cell is implanted into an enucleated oocyte. It appears that Dolly inherited her mother's shortened telomeres and that the telomeres may have been further shortened during the brief in vitro culture of the cells. This suggests that shortened telomeres may not be restored by the nuclear transfer method and raises the question of whether normal animals can be cloned from an aged animal.

To determine how cellular aging might affect aging of cloned animals, the Japanese group took cells from the ear of a 17-year-old bull and grew them in culture for different periods of time. It was expected that cells from short-term culture would be better for cloning than those from longer-term culture. Surprisingly, the developmental competence of embryos derived from cells of long-term culture was actually better than that of cells from short-term culture. These findings suggest that reprogramming may alter the life span of cells and that the age of the donor animal may not relate to the cell's ability to grow and divide in vitro. Currently, the telomeres from the cloned calves, the donor cells and the donor bull are being analyzed, and the health of the young calves is being monitored to determine their biological ages.

Sources

1. PNAS. 2000. 97:990-995.
2. Nature. 1999. 399:316-317.

Hurst's the Heart, Arteries and Veins, Ninth Edition

HURST'S THE HEART, Ninth Edition

Alexander RW, Schlant RC, Fuster V (editors)
McGraw-Hill, New York, 1998

Reviewed by Barry J. Goldlist, MD, FRCPC, FACP

The latest edition of Hurst's The Heart is a massive tome, comprised of 2602 pages of text, and an index of 96 pages. Clearly this is not a book that is meant to be read at once from cover to cover! My first task was to check the list of authors. There are 181 contributors, and they are truly an outstanding group. However, as is common in American texts, only six of these are from outside the USA (one from Belgium, Germany, South Africa and Canada, and two from the United Kingdom). This could be a weakness as the pattern of delivery of cardiac care, especially advanced cardiac care, may differ from country to country. The table of contents mirrors the goals of the text, which are to provide a comprehensive reference source. However, there are a number of topics that could have been added. Part 1, "Basic Foundations of Cardiology", could have included a chapter on how to interpret the burgeoning cardiovascular literature. Although the principles of critical appraisal span all disciplines, the specifics (e.g. methodological pitfalls, appropriate outcome measures, meaning of clinical significance) vary widely from specialty to specialty. Issues concerning coronary artery disease in women are incorporated into various chapters. Considering the huge challenges this area creates for clinicians, it would have been preferable to have a separate chapter on the topic. There is a chapter entitled "Geriatric Considerations in Cardiovascular Therapy", but it focuses exclusively on pharmacology. Topics such as altered presentation, difficulties in diagnosis, and under-treatment are not addressed.

The book itself is well designed. The typeface is clear and crisp, and there are large numbers of excellent and appropriate illustrations. The use of charts to highlight important information is excellent. As in all multi-authored texts, the quality varies somewhat from chapter to chapter, but generally the content is excellent. The chapter on history, physical examination and cardiac auscultation is superb. The chapter on diagnosis and management of heart failure exhibits the major difficulty that textbooks face. It is very well written, but there is nothing in the references more recent than 1997, and thus the authors do not mention the survival benefits of spironolactone, and are less "bullish" on beta-blockers than they would have been today because more evidence has been accumulated.

In summary, this is an excellent text that covers virtually all aspects of cardiovascular disease, and is a first rate reference. However, the fast pace of change in cardiovascular medicine means that clinicians will have to use additional more current sources of information when they manage individual patients.

A Word from the Managing Editor--April

The process of aging is an inexorable and manifest fact of existence. We age, we know it, and we observe it in all of those around us.

It is only recently, however, that the subject of Aging has begun to attract serious scientific and medical inquiry; the reasons for this are manifold. The subject of aging, and its serious study, has been irreparably damaged by centuries of snake-oil salesmen peddling various concoctions for increasing life span (this in itself is perhaps an interesting subject for a retrospective review). The inquiry into the biological basis of Aging has been further confounded by the heterogeneity and complexity of the aging process.

The 'science' and study of Aging has, however, in the last twenty-five years moved from the periphery of formal inquiry to an emerging framework that seeks a place at the centre of biological and medical science. Two important topics in this issue, the aging of the hematopoietic system and cancer are critically elucidated in reference to this framework.

The cover article in this issue is on the aging of the haematopoietic system. This article is a continuation of a series of articles on age-related changes in various organ and physiological systems. All the principal organ systems will be covered in this series and it should serve as an excellent reference for the future. Great attention has been devoted to visually articulating the subject matter. Age-associated decline occurs in all the systems of the body, although some systems are more affected than others. The digestive system, which was dealt with in the last issue, is minimally affected. The hematopoietic system, vital to overall function, is characterized in the elderly by increased marrow fat, decreased blood flow, and decreased ability of hematopoietic stem cells to regenerate. All of these changes lead to decreased hematopoiesis. The recently discovered process for cloning embryonic stem cells and T-cell precursors might provide critical insights and potential tools for regenerating the hemato-poietic system or, even better, preventing its decline.

The focus section in this issue is devoted to the subject of cancer in the elderly. Cancer is very much a disease related to the aging process. As the report of the Canadian Cancer Society states, cancer is primarily a disease of older Canadians, with 70% of new cancer cases and 82% of deaths due to cancer occuring among those who are at least sixty years old. With the increasing number of elderly Canadians, much of the burden of cancer diagnosis falls on the primary care doctor.

Progress in Cancer therapy has been very slow. As Jerome Groopman of Harvard has suggested, it has been based "on serendipity and trial and error more than on any sort of deep knowledge of malignancy or any sort of rational approach to its conquest". Slowly however, the black box of the cancer cell is yielding its secret, and in yielding its secrets, it is revealing some of the genetic mysteries that underlie the aging process itself.

Breakthroughs in understanding cancer may yield fundamental insights into the aging process. This past summer, Robert Weinberg and his team at MIT's Whitehead Institute, published a paper that reveals the process that turns a normal cell cancerous. Only three genes were necessary. Telomerase, an enzyme that regulates telomere length was a key element of this experiment. The result is of seminal significance for the understanding of both the genetics of cancer and the aging process itself. Gradually, the genetics underlying cancer will be teased apart. Diagnostic tests should follow. The elderly, who suffer disproportionately from cancer should be the biggest beneficiary of this process.

'Aging', as a multifarious and complex process--occurring at the genetic and the physi-ological levels, and affecting the individual as a whole--is the overarching scientific metaphor for Geriatrics & Aging. It is a metaphor that provides a point of convergence for disparate scientific, medical and clinical information. It serves as the thematic backdrop and guiding vision, for a publication that is directed at the practical, clinical decision-making needs of the primary care physician. This organizing vision lends coherence to the publication as a whole.

As I close this issue, I would like to reach out to the readers of Geriatrics & Aging and to ask you how we could improve the publication, and how we could make the publication more relevant to you.

Please e-mail me at geriatrics@ribosome.com.