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Health InfoCom Network News Page 13
Volume 6, Number 9 April 10, 1993
Years of Potential Life Lost Before Age 65 -- United States, 1990 an
1991
====================================================================
SOURCE: MMWR 42(13) DATE: Apr 09, 1993
Years of potential life lost (YPLL) is a public health measure that
reflects the impact of deaths occurring in years preceding a conventional cut-
off year of age, usually 65 years. YPLL is calculated using final mortality
data from CDC's National Center for Health Statistics (1) for the most recent
year available, provisional mortality data (i.e., a 10% sample of deaths) (2)
for the following year, and population estimates from the U.S. Census. This
report summarizes final YPLL data for 1990 and provisional data for 1991.
During 1990, years of potential life lost before age 65 years (YPLL-65)
totalled 12,237,379 in the United States (Table 1). Unintentional injuries
accounted for the largest proportion of YPLL-65 from all causes (17.5%),
followed by malignant neoplasms (15.1%), suicide/{*filter*} (12.2%), diseases of
the heart (11.2%), con{*filter*} anomalies (5.4%), and human immunodeficiency
virus infection including acquired immunodeficiency syndrome (HIV/AIDS)
(5.4%).
From 1989 to 1990, YPLL-65 decreased by less than 1% (Table 1). The
largest percentage decreases were for prematurity (9.2%), pneumonia/influenza
(4.2%), and unintentional injuries (4.1%); the largest increases were for
HIV/AIDS (12.7%) and suicide/{*filter*} (6.5%).
Based on provisional data, unintentional injuries remained the leading
cause of YPLL-65 during 1991, accounting for 17.1% of all YPLL-65, followed by
malignant neoplasms (15.2%), suicide/{*filter*} (12.7%), and diseases of the
heart (11.7%). HIV/AIDS, which accounted for 6.3% of all YPLL-65, replaced
con{*filter*} anomalies as the fifth leading cause of YPLL-65.
Reported by: Applications Br, Div of Surveillance and Epidemiology,
Epidemiology Program Office, CDC.
Editorial Note: Leading causes of death in the United States are ranked by
using absolute counts of death for selected causes of death, thus giving each
death a weight of 1.0. In comparison, YPLL gives a weight to each death
proportionate to its distance from the arbitrarily designated age of 65 years.
YPLL-65 emphasizes deaths at early ages in two ways: 1) by not including
deaths occurring at ages beyond the cut-off, and 2) by giving greater
computational weight to deaths among younger persons. YPLL-65 is calculated as
65 minus the middle age for each age group, times the number of deaths from a
specific cause within that age group, added for all age groups to 65.
Provisional mortality estimates for selected conditions are based on a
10% sample of death certificates and are adjusted for reporting biases (e.g.,
provisional reporting of cause of death) (4). Because 1991 data are
provisional, YPLL estimates based on 1990 final mortality data are not
Health InfoCom Network News Page 14
Volume 6, Number 9 April 10, 1993
compared with 1991 data.
The causes of death with the largest increases in YPLL-65 from 1989 to
1990 are HIV/AIDS and suicide/{*filter*}. The 12.7% increase in YPLL-65 for
HIV/AIDS corresponds to increases in the annual number of deaths from AIDS.
Prevention programs for communities and individuals are crucial for reducing
behaviors that lead to transmission of HIV. The 6.5% increase in YPLL-65 for
suicide/{*filter*} reflects 1.8% and 10.8% increases in YPLL-65 for suicide and
{*filter*}, respectively. Several factors may have contributed to these changes,
including increases in substance abuse, access to handguns, poverty,
urbanization and crowding, and family disruption and disorganization (5). For
prevention of suicide/{*filter*}, CDC has recommended interventions that can be
incorporated in community programs. These include use of school-based
curricula based on non{*filter*} conflict-resolution skills; peer-counseling
programs; enforcement or enactment of local drinking and firearms-control
regulations; crisis-intervention services; and improved recognition and
comprehensive treatment of persons with mental disorders (6,7).
The 9.2% decrease in YPLL-65 for prematurity from 1989 to 1990 reflects a
1.2% increase in YPLL-65 for disorders related to short gestation and
unspecified low birthweight and a 21.5% decrease in YPLL-65 for respiratory
distress syndrome. Recent improvements in medical management of respiratory
distress syndrome may have contributed to this trend (8,9).
References
1. NCHS. Advance report of final mortality statistics, 1990. Hyattsville,
Maryland: US Department of Health and Human Services, Public Health Service,
CDC, 1993. (Monthly vital statistics report; vol 41, no. 7, suppl).
2. NCHS. Annual summary of births, marriages, divorces, and deaths: United
States, 1991. Hyattsville, Maryland: US Department of Health and Human
Services, Public Health Service, CDC, 1992. (Monthly vital statistics report;
vol 40, no. 13).
3. NCHS. Vital statistics of the United States, 1987. Vol 2, mortality, part
A. Hyattsville, Maryland: US Department of Health and Human Services, Public
Health Service, CDC, 1990; DHHS publication no. (PHS)90-1011.
4. NCHS. Annual summary for the United States, 1978. Hyattsville, Maryland:
US Department of Health and Human Services, Public Health Service, CDC, 1979.
(Monthly vital statistics report; vol 27, no. 13)
5. Reiss AJ Jr, Roth JA, eds. Understanding and preventing {*filter*}.
Washington, DC: National Academy Press, 1993:101-81.
6. Hammett M, Powell KE, O'Carroll PW, Clanton ST. {*filter*} surveillance --
Health InfoCom Network News Page 15
Volume 6, Number 9 April 10, 1993
United States, 1979-1988. In: CDC surveillance summaries (May 29). MMWR
1992;41(no. SS-3):1-33.
7. CDC. Position papers from the Third National Injury Control Conference:
setting the national agenda for injury control in the 1990s -- executive
summaries. MMWR 1992;41(no. RR-6):5-7.
8. CDC. Infant mortality -- United States, 1990. MMWR 1993;42:161-5.
9. Long W, Corbet A, Cotton R, et al. A controlled trial of synthetic
surfactant in infants weighing 1250 g or more with respiratory distress
syndrome. N Engl J Med 1991;325:1696-703.
Health InfoCom Network News Page 16
Volume 6, Number 9 April 10, 1993
{*filter*} {*filter*} Lead Epidemiology and Surveillance -- United
States,Fourth Quarter, 1992
========================================================
SOURCE: MMWR 42(13) DATE: Apr 09, 1993
Data from CDC's National Institute for Occupational Safety and Health
{*filter*} {*filter*} Lead Epidemiology and Surveillance program are complete for 1992.
Efforts to expand the number of states participating in the surveillance
system are ongoing as states increase their capacity to monitor {*filter*} lead
levels in both {*filter*}s and children.
Reported by: B Harrell, MPA, Div of Epidemiology, CH Woernle, MD, State
Epidemiologist, Alabama Dept of Public Health. A Osorio, MD, S Payne, MS,
Occupational Health Surveillance and Evaluation Program, California Dept of
Health Svcs. J McCammon, MS, Epidemiology Div, Colorado Dept of Health. CJ
Dupuy, Connecticut State Dept of Health Svcs. M Lehnherr, Occupational Disease
Registry; H Howe, PhD, Div of Epidemiologic Studies, Illinois Dept of Public
Health. K Choquette, MS, R Currier, DVM, State Epidemiologist, Iowa Dept of
Public Health. E Coe, MPH, Health Registries Div, Maryland Dept of the
Environment. R Rabin, MSPH, Div of Occupational Hygiene, Massachusetts Dept of
Labor and Industries. P Dunbar, MPH, Bur of Child and Family Svcs, Michigan
Dept of Public Health. T Ferrara, MD, Occupational Health Program, Bur of Risk
Assessment, Div of Public Health Svcs, New Hampshire State Dept of Health and
Human Svcs. B Gerwel, MD, Occupational Disease Prevention Program, New Jersey
Dept of Health. R Stone, PhD, New York State Dept of Health. M Barnett, MS,
State Health Div, Oregon Dept of Human Resources. J Gosten, MS, Occupational
Health Program, Div of Environmental Health, Pennsylvania Dept of Health. R
Marino, MD, Div of Health Hazard Evaluations, South Carolina Dept of Health
and Environmental Control. T Willis, DM Perrotta, PhD, Environmental
Epidemiologist, Texas Dept of Health. D Beaudoin, MD, Bur of Epidemiology,
Utah Dept of Health. L Hanrahan, MS, Div of Health, Wisconsin Dept of Health
and Social Svcs. Div of Surveillance, Hazard Evaluations, and Field Studies,
National Institute for Occupational Safety and Health, CDC.
Health InfoCom Network News Page 17
Volume 6, Number 9 April 10, 1993
National Preschool Immunization Week
====================================
SOURCE: MMWR 42(13) DATE: Apr 09, 1993
The first National Preschool Immunization Week (NPIW), sponsored by CDC
and members of the Immunization Education and Action Committee of the Healthy
Mothers, Healthy Babies Coalition (including the Children's Action Network and
the American Academy of Pediatrics); public health departments; and other
private and public immunization partners, is April 24-30, 1993. This year's
theme is "Hands Across the Nation for Preschool Immunization." Events will
encourage cooperation between health-care providers and parents to ensure that
children are enrolled with a private physician, public clinic, or other
health-care facility that will screen and track their vaccination needs to
ensure they receive all recommended vaccinations by their second birthday.
Local programs are encouraged to participate in NPIW by tailoring activities
to fit their communities' needs.
NPIW will be held the last week of April each year. It is intended to
stimulate activities at national, state, and local levels that complement
locally developed Immunization Action Plans (IAPs) and help achieve permanent
improvements in the delivery of vaccines to infants and toddlers. In addition,
NPIW is an annual opportunity to assess progress, plan for the future, and
recognize major accomplishments toward achieving the national health objective
for the year 2000 that at least 90% of children are fully vaccinated by their
second birthday (objective 20.11) (1).
Additional information and a listing of some state and local events
planned for the 1993 NPIW are available from state immunization programs or
from CDC's Division of Immunization, National Center for Prevention Services,
1600 Clifton Road, NE, Mailstop E-05, Atlanta, GA 30333; telephone (404) 639-
1867.
Reference
1. Public Health Service. Healthy people 2000: national health promotion and
disease prevention objectives -- full report, with commentary. Washington, DC:
US Department of Health and Human Services, Public Health Service, 1991:521;
DHHS publication no. (PHS)91-50212.
Health InfoCom Network News Page 18
Volume 6, Number 9 April 10, 1993
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cooking.net">food & Drug Administration News
::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::
Biotech Devices:
Replacing Test Animals, Improving Diagnoses
by Ricki Lewis, Ph.D.
from the cooking.net">food and Drug Administration
This is the first of two articles on biotechnology and medical devices.
The young woman hadn't been feeling well. She tired easily, and her
{*filter*}s were sore. When her menstrual period was a week overdue, she bought a
home pregnancy test kit. The next morning, she placed a few drops of her
urine onto an applicator stick, then spent five very nervous minutes pacing.
Finally, a blue spot appeared on the applicator. She broke into a broad
grin--she was pregnant!
A generation ago, when the young woman's mother suspected she was
pregnant, confirming her suspicions wasn't as easy. After two missed
menstrual periods, the doctor sent a sample of her urine to a lab, where it
was injected into a female rabbit. The rabbit was killed, and its ovaries
examined. If they were swollen, it meant the urine contained human chorionic
gonadotropin (HCG)--the very same hormone indicating pregnancy that today is
detected in minutes, and weeks earlier, with a home pregnancy test kit.
A pregnancy test kit is one of the most familiar medical devices made
possible by biotechnology--the use of biochemicals, cells, or other
components of living organisms to make or modify products. Not only has
biotechnology replaced the use of animals in some medical tests, but it now
routinely diagnoses a variety of illnesses faster and more accurately than
standard laboratory procedures.
In a home pregnancy test kit, a protein called a monoclonal antibody
(MAb) binds to HCG, causing a color change. HCG is present in a woman's urine
only during pregnancy. MAb test kits are the most common type of biotech
device regulated by FDA. The agency has cleared for marketing more than 635
biotech devices, a growing subdivision of the broader area of medical devices.
"A medical device is any health-care product that does not achieve its
primary purpose by chemical action in or on the body or by being metabolized
[altered to a different chemical]," says Kiki Hellman, Ph.D., senior
scientist and manager of the biotechnology program at the Center for Devices
and Radiological Health. MAb-based devices are used in vitro (in laboratory
glassware) to detect infections, hormone levels, drug levels (therapeutic and
"recreational"), and cancer cells.
A second major type of biotech device uses a DNA probe, which diagnoses
infectious or genetic diseases by detecting specific sequences of DNA
(deoxyribonucleic acid), the biochemical components of genes. Other biotech
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Volume 6, Number 9 April 10, 1993
devices include new drug delivery systems, replacement cells and tissues that
combine natural and synthetic components, and biosensors (devices that detect
a biochemical reaction and convert it into an electronic signal). Biotech
devices are used in hospital and private labs, physicians' offices, and in
consumers' homes.
Biotech-based diagnostic devices are often more direct than their
conventional counterparts. Monoclonal antibodies and DNA probes rapidly
recognize proteins or genes distinct to a particular disease-causing microbe
or virus. These techniques are also able to spot an errant biochemical that
makes up a very small part of a specimen (such as {*filter*} or urine).
"Biotechnology has provided significant improvement in the specificity
and reproducibility of diagnostic tests," says Hellman.
Biotechnology offers different approaches to a single problem. Consider
detecting the human immunodeficiency virus (HIV). The most widely used test
detects antibodies that a person's immune system manufactures in response to
encountering HIV. If that test (using a technique called enzyme-linked
immunosorbent assay, or ELISA) is positive, the result is confirmed with a
Western blot test, which detects a protein unique to HIV.
Still other HIV tests using biotechnology are experimental. These include
growing the virus; finding other HIV-specific proteins; and using various
gene amplification techniques to make enough copies of HIV's genetic material
in a body fluid sample to detect it. And a biosensor HIV test is being
developed that couples binding of a person's antibodies against HIV to a
change in capacitance (the ability to store charge) of an electrical system.
The aim of these experimental HIV tests is to be more precise and to do
this by directly detecting part of HIV. (In contrast, antibody-based tests
detect the body's response to HIV, which can appear six weeks to a year after
infection.)
Four areas where biotech devices are having an exciting impact are
biomaterials, biosensors, monoclonal antibodies, and DNA probes.
New Materials
Developing replacement body parts has long been a goal of medicine, but
one surrounded by steep obstacles. Donor organs and tissues are exceedingly
scarce, and even when they are available and transplanted, the recipient must
take immunosuppressant {*filter*} such as cyclosporin for life. Yet a synthetic
implant can be toxic or walled off by scar tissue.
"Many of the synthetic materials now used pose all sorts of problems,
such as toxicity and bioincompatability, so there is a push to use more
natural derivatives or biotech-derived materials," says Hellman.
For example, elastin is a naturally occurring connective tissue protein
that is useful in surgery. When applied as a foam, powder or sheet, the
biocompatible protein prevents scar tissue adhesions from forming at the
sites of surgery.
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Volume 6, Number 9 April 10, 1993
Where does elastin come from? Synthesizing it chemically is
time-consuming and costly, yet obtaining elastin, or any biomolecule, from
cadavers introduces the risk of infection. Enter recombinant DNA technology.
Bacteria given human genes encoding elastin produce pure, plentiful amounts
of the valuable protein.
New products resulting from recombinant DNA technology are proteins or
peptides (pieces of proteins), because these are the types of molecules that
genes instruct a cell to manufacture. These {*filter*} and biologics include
insulin (to control diabetes), human growth hormone (to treat some forms of
dwarfism), the immune system biochemicals interferon and interleukin (used to
treat some cancers), and erythropoietin (to treat severe anemia in kidney
transplant recipients).
Protein products require special delivery systems to enable them to
circumvent biochemicals that dismantle them along the digestive tract, such
as stomach acid and protein-digesting enzymes in the small intestine. Several
biotechnology companies are developing biomaterials to surround these {*filter*}
so that they can reach their sites of action.
Bioengineered Tissue
Recombinant DNA-derived proteins combined with synthetic materials can
function as implants. Two companies, Advanced Tissue Sciences in La Jolla,
Calif., and Organogenesis, in Canton, Mass., have a variety of such
bioengineered tissues in development, with a few in FDA-sanctioned clinical
trials.
The basic recipe for a bioengineered tissue is to sculpt a scaffold from
a synthetic material that is accepted in the body, and place cells in or on
it. These cells secrete substances as they normally would, or they may be
genetically altered to overproduce their natural proteins or manufacture
entirely different ones, such as growth factors that might help make the
implant more acceptable to the body.
"The primary goal of our tissue engineering research is to grow these
tissues as replacements for damaged or failing organs. The benefits of this
research could positively impact the lives of patients requiring organ
transplants as well as those who suffer from diseases or injuries," says Gail
K. Naughton, Ph.D., executive vice president at Advanced Tissue Sciences.
Advanced Tissue Sciences' artificial skin, called Dermagraft, has helped
more than 70 burn patients so far in clinical trials. A similar product from
Organogenesis, called Graftskin, is being tested to replace skin lost during
surgery to remove cancers, moles and tattoos.
"Rather than create a new wound by removing skin from another location on
the body, surgeons could use biologically equivalent skin that won't be
rejected and will promote natural healing," says David J. Leffell, M.D.,
chief of surgery at Yale University School of Medicine (New Haven, Conn.),
where Graftskin is being tested.
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Volume 6, Number 9 April 10, 1993
Other tissues on the drawing board at these and other companies include
liver, connective tissue, bone marrow, and {*filter*} vessels. Some bioengineered
tissues are already commercially available for use in toxicity testing, in
place of animals.
A scaled-down version of an engineered tissue, a cell implant, is a new
route to drug delivery, placing cells that naturally manufacture needed
substances precisely where they are needed.
The key advantage of a cell implant is that it is "immunoisolated"; its
packaging enables the cells to secrete without being detected by the immune
system and destroyed. This is done by surrounding cells with a polymer
membrane with holes small enough to allow nutrients in and the therapeutic
protein out, while excluding the large molecules and cells responsible for
immune rejection, according to Seth A. Rudnick, M.D., president of
CytoTherapeutics, Inc. in Providence, R.I.
Prime targets of cell engineers are the beta cells of the pancreas. These
cells secrete insulin, a peptide hormone that enables glucose ({*filter*} sugar)
to enter cells, where it is a source of energy. A cell implant would far
better mimic the body's continual secretion of insulin than once or twice
daily injections and might prevent some of the damage associated with
diabetes caused by the on-again off-again delivery of insulin.
The beta cells lie in a portion of the pancreas called the islets of
Langerhans. Researchers have been trying to transplant "{*filter*}" islet
tissue--just cells--for 20 years, with little success, because the immune
system attacks them. Throughout the 1970s and 1980s, various biotechnology
companies "played with the idea of encapsulating cells to hide from the
immune system. But in two to three months, the capsules broke down," says
Rudnick.
Several companies, including CytoTherapeutics and BioHybrid Technologies
in Shrewsbury, Mass., are working on finding the right mix of casings and
cells to engineer the long-awaited "artificial pancreas." Both companies'
products are in the animal testing stage, and both say they will apply to FDA
for permission to begin clinical trials by 1994. The same companies are
exploring using cell implants in the brain to treat Parkinson's disease and
in the spinal cord to relieve chronic pain.
Biosensors
Biosensors wed nature to electronics. A biosensor consists of a
biological structure that recognizes another biological structure (such as an
enzyme, antibody or receptor), plus a mechanism to transduce, or convert, the
reaction of biological recognition into an observable signal, such as a
voltage change, light emission, or sound.
Many people who have diabetes use a biosensor to monitor their {*filter*}
glucose (sugar) levels, information needed several times a day to determine
the timing of insulin doses. The device, called a glucose meter, resembles a
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Volume 6, Number 9 April 10, 1993
pen and has been on the market since 1988.
The biological component is the enzyme glucose oxidase. A person drips
{*filter*} onto a disposable test strip, and inserts the strip into the pen. The
enzyme binds to glucose in the {*filter*}, producing an electrochemical reaction
that stimulates electrodes attached to a meter in the pen device. The meter
measures the signal, and in 30 seconds, the {*filter*} sugar level flashes on a
digital display.
In the future, people with diabetes may be treated from within, thanks to
combinations of biotechnology devices. Recombinant DNA-derived insulin, or
perhaps transplanted beta cells, may be implanted along with a glucose
biosensor that controls rate of insulin delivery.
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Volume 6, Number 9 April 10, 1993
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Clinical Research News
::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::
Effect of Hormone Replacement Therapy on Body
by M. Wayne Heine, M.D.
Head, Department of Obstetrics and Gynecology
Clinical Research News for Arizona Physicians
Copyright 1992, University of Arizona
Reproduced with Permission
Hormone replacement therapy has been available in some fashion for almost
a century. Even after this length of time there is still confusion and
differing opinion as to its need. With life expectancy increasing, a third of
a woman's lifetime may be spent in a state of estrogen deprivation. With
increasing knowledge regarding menopausal diseases such as heart disease and
osteoporosis, it is hoped hormone replacement therapy will be based on
scientific information.
Vasomotor Instability
Most women starting hormone replacement therapy take it for relief of
"hot flashes," which usually disappear in two years. Hormone replacement
therapy relieves the symptoms effectively.
Reproductive Tract Change
The {*filter*} and bladder are very sensitive to lack of estrogen. The
epithelium becomes thin, dry and more friable. {*filter*}l Ph becomes more
neutral allowing growth of more coli-form bacteria. The bladder and the
urethra also are thinner and more atrophic. This combination results in more
urinary incontinence and bladder infections. These conditions are well
controlled with hormone replacement therapy
Cardiovascular Disease
Heart disease is the number one cause of death in both men and women.
Ovarian function appears to protect against heart disease, but soon after
menopause the incidence of heart disease increases dramatically. Estrogen
affects heart disease directly as there have been estrogen receptors found in
the coronary vessels. Estrogen also increases HDL while lowering LDL.
Several studies show a decrease in CHD to be in the 40-50 percent range. This
may be the most important reason for hormone replacement therapy
Osteoporosis
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Volume 6, Number 9 April 10, 1993
As women live longer, osteoporosis becomes a greater problem. Loss of
estrogen is the leading factor in the development of osteoporosis in women.
Approximately 30-40 per-cent of women will suffer a hip fracture in their
lifetime. Morbidity and mortality is significant with the death rate from hip
fracture as great as {*filter*} cancer in 1989. Weight bearing exercise,
adequate calcium intake and hormonal therapy reduce the incidence of hip
fractures by as much as 70 percent.
Endometrial Cancer
Estrogen is a growth hormone to the endometrium. Therefore, unapproved
estrogen -- given cyclically or continuously -- may result in an increase in
hyperplasia and finally carcinoma. This overgrowth of endometrium can be
controlled by addition of a progestin 12 days each month. The incidence of
endometrial cancer may be equal to or lower than hormone replacement therapy
Hormone Replacement
Therapy and {*filter*} Cancer
After three decades of hormone replacement therapy and birth control
pills, there is confusion as to whether they are associated with {*filter*}
cancer. The most recent meta analysis ranges from 0.9 to 1.06 R.R. The
benefits from hormone replacement therapy far outweigh the potential small
risks even with long term usage.
Conclusion
A woman with estrogen deprivation should be informed of the risk/benefit
of hormone replacement therapy and allowed to make an educated decision
whether hormone replacement therapy is for her.
Health InfoCom Network News Page 25
Volume 6, Number 9 April 10, 1993
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Articles
::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::
Search for best "antioxidants" to protect LDL
points to vitamin E, new study suggests
American Heart Association
News Release NR 93-4066
April 12, 1993
DALLAS, April 12 -- Researchers studying combinations of three
"antioxidant" vitamins report that large doses of vitamin E provide the best
deterrent against biochemical changes in so-called "bad" LDL (low-density
lipoprotein) cholesterol that appear to make it more easily deposited in
artery walls.
Vitamin E "can confer significant protection to LDL from an oxidant
challenge," write University of California scientists Peter Reaven, M.D., and
Joseph L. Witztum, M.D., in one of two reports published today. The results
from their small, preliminary studies appear in the April issue of
Arteriosclerosis and Thrombosis, an American Heart Association journal.
Reaven and Witztum's second study showed that both natural and synthetic
forms of vitamin E "provided equal antioxidant protection to LDL," at least
when taken at the relatively large dose of 1,600 milligrams per day used in
both studies. This is about 160 times the recommended daily allowance of
vitamin E. "Supplementation with either of the forms of vitamin E commonly
available provided equal levels of alpha-tocopherol in LDL and comparable
antioxidant protection," they report.
Both of the new studies relate to a theory the UC San Diego research team
has proposed about the way high cholesterol levels cause atherosclerosis,
commonly called hardening of the arteries. Their theory suggests it's
oxidation of LDL by highly reactive, unstable molecules called oxygen free-
radicals that sets off the damaging process that leads to buildup of fat-
filled cells and subsequent vessel wall injury and arterial blockage.
Arterial blockage is a major cause of the estimated 1.5 million heart
attacks and 500,000 strokes in the United States each year, according to the
AHA.
The first study involved giving eight people 60 milligrams per day of
beta-carotene for three months, then beta-carotene plus vitamin E (1 600
milligrams per day) for another three months, and then beta-carotene plus.
During phase two of this study, the eight people took only vitamin E for five
months. During vitamin E plus vitamin C (2 grams per day) for three months.
each period, samples of LDL were isolated from {*filter*} and measurements of its
susceptibility to oxidation were performed in the laboratory.
The researchers found that long-term supplementation with large doses of
vitamin E, but not beta-carotene, decreased LDL susceptibility to oxidation 30
Health InfoCom Network News Page 26
Volume 6, Number 9 April 10, 1993
to 50 percent. "In fact," they report, "the effect of vitamin E was even more
impressive in phase two when the beta-carotene was stopped."
Because it's water soluble, vitamin C is not incorporated by the fat-
laden LDL particles (water and fat don't mix), but vitamin C may protect
vitamin E's antioxidant capability, Witztum theorizes. "In our study, when we
added vitamin C, the levels of vitamin E and beta-carotene in the {*filter*} went
up."
"Our study is the first to compare the effects of these vitamins, alone
and in combinations, on the susceptibility of LDL to oxidation," Witztum says.
There was a "strong correlation" between the amount of vitamin E they found in
the LDL particles and the measures of LDL oxidation, thus providing
"additional support for a direct (protective) effect."
The second study involved 16 people taking either natural or synthetic
vitamin E for eight weeks. It showed that at high dosages the two forms
confer equal degrees of protection.
Both studies "clearly document that dietary supplementation with large
doses of vitamin E can signficantly increase the LDL content of vitamin E and
that this, in turn, confers significant protection against oxidative stress,"
Reaven, Witztum and their colleagues conclude.
If oxidized LDL proves to be an important cause of heart and {*filter*} vessel
disease, antioxidant vitamin therapy "may turn out to be a very important area
of nutrition research," says Reaven, assistant professor of medicine at UC San
Diego, La Jolla, Calif. Long-term, large-scale clinical trials will decide
antioxidants' ultimate value, he adds.
Neil Stone, M.D., chairman of the American Heart Association's nutrition
committee, says studies of antioxidant vitamins are "exciting" and show how
important good nutrition is in the prevention of heart and {*filter*} vessel
disease. People who follow the AHA's diet -- which includes eating more
fruit, vegetables and whole grains -- are consuming foods high in antioxidant
vitamins, points out Stone, associate professor at Northwestern University
Medical School in Chicago.
But Stone sounds a cautionary note: "Until scientists determine the
correct doses of these vitamins and whether they actually provide any wasting
their money." At present, he adds, the AHA has no plans to recommend the use
of protection, people who buy vitamin pills may be antioxidant vitamin
supplements.
The UCSD scientists also are not ready to recommend vitamin E pills to
the general public. "Because it's still an unproven theory, I don't take
vitamin E in supplementary doses," says Witztum, professor of medicine at
UCSD. "But I do eat a diet rich in vegetables, grains and fruit."
Although several recent reports have linked vitamin intake with reduced
risk of heart disease and stroke, no human studies have yet been published
that show whether or not intervention with antioxidant therapies will slow
down or prevent hardening of the arteries, Witztum points out. He and UCSD's
Daniel Steinberg, M.D., head of the team that originally proposed the LDL
Health InfoCom Network News Page 27
Volume 6, Number 9 April 10, 1993
oxidation theory, have submitted a grant proposal to the federal government to
conduct a trial in patients with coronary heart disease, Witztum says.
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HICN609 Medical News Part 2/4