Alzheimer's, Dementia & Mental Health
Study Shows Cigarette Smoking Jumps Risk for
Alzheimer’s; All Research Not Trustworthy
Industry-affiliated studies = smoking protects
against the development of AD; independent studies = smoking increases
the risk of AD
Feb. 1, 2010 - A UCSF analysis of published studies
on the relationship between Alzheimer’s disease and smoking indicates
that smoking cigarettes is a significant risk factor for the disease.
The study group also determined that the myth that smoking offers
protection from AD has been perpetuated by tobacco industry-affiliated
studies.
After controlling for study design, quality of the
journals, time of publication, and tobacco industry affiliation of the
authors, the UCSF research team found an association between tobacco
industry affiliation and the conclusions of individual studies.
Industry-affiliated studies indicated that smoking protects against the
development of AD, while independent studies showed that smoking
increased the risk of developing the disease.
Study findings were published online today in the
January issue (19:2) of the Journal of Alzheimer’s Disease. An
abstract of the paper is available at the link below.
“For many years, published studies and popular
media have perpetuated the myth that smoking is protective against the
development of AD. The disease’s impact on quality of life and health
care costs continues to rise. It is therefore critical that we better
understand its causes, in particular, the role of cigarette smoking,”
said Janine K. Cataldo, PhD, RN, assistant professor in the UCSF School
of Nursing and lead author of the study.
According to the Alzheimer’s Association, 5.3
million Americans currently have the disease, and that number will
escalate rapidly as the baby boom generation ages. AD also triples
health care costs for Americans aged 65 and older, the organization
states.
The UCSF team reviewed 43 published studies from
1984 to 2007. Authors of one-fourth of the studies had an affiliation
with the tobacco industry.
The UCSF team determined that the average risk of a
smoker developing AD, based on studies without tobacco industry
affiliation, was estimated to be 1.72, meaning that smoking nearly
doubled the risk of AD. In contrast, the team found that studies
authored by individuals with tobacco industry affiliations, showed a
risk factor of .86 (less than one), suggesting that smoking protects
against AD. When all studies were considered together, the risk factor
for developing AD from smoking was essentially neutral at a
statistically insignificant 1.05.
Previous reviews of the association between smoking
and AD have not controlled for study design and author affiliation with
the tobacco industry, according to Cataldo. To determine if study
authors had connections to the tobacco industry, the UCSF team analyzed
877 previously secret tobacco industry documents.
The researchers used an inclusive definition of
“tobacco industry affiliation” and examined authors’ current or past
funding, employment, paid consultation, and collaboration or
co-authorship on a study with someone who had current or previous
tobacco industry funding within 10 years of publication.
“We know that industry-sponsored research is more
likely to reach conclusions favorable to the sponsor,” said Stanton A.
Glantz, PhD, of the UCSF Department of Medicine and a study co-author.
“Our findings point to the ongoing corrosive nature of tobacco industry
funding and point to the need for academic institutions to decline
tobacco industry funding to protect the research process.”
Judith J. Prochaska, PhD, MPH, of the UCSF
Department of Psychiatry, also is a co-author. The team’s research was
supported by grants from the California Tobacco Related Disease Research
Program, the National Cancer Institute, and the National Institute on
Drug Abuse.
UCSF is a leading university dedicated to promoting
health worldwide through advanced biomedical research, graduate-level
education in the life sciences and health professions, and excellence in
patient care.
Related links:
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Journal of Alzheimer’s Disease (January issue, 19:2)