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2005 Annual Meeting CALL FOR
ABSTRACTS |
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March 15!
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2005 Annual Meeting SPONSORSHIP and
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information
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2005 Annual
Meeting
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Discussion
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Announcements
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MARK YOUR
CALENDARS: Deadline for
the Abstract submission is March 15.
NEW!
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Student-Only Program!
>>>
Review the latest program updates!
>>>
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Review commentaries on Dr. Andrzej
Bartke's "Why dwarf mice are long-lived and what
does this tell us?"
submitted by Drs. Norm Wolf and Steven
Austad.
>>>
Stay tuned for next month's discussion
led by Dr. George Martin.
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February Spotlight:
Linus Pauling Institute |
2005 AGE Annual Meeting - June 3-6,
2005
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NEW! -
STUDENT
PROGRAM
The American Aging
Association's Student Committee announces a
Student-Only Program
at the 34th AGE Annual Meeting in Oakland, California,
on Saturday, the 4th of June, at 6 pm. The Program -
open only to undergraduate, graduate and first year
post-doctoral students, will include a Data Blitz, a
Round-Table Discussion, and a Student Social, as
follows:
-
The Data Blitz
will be held for the first 90 minutes of the program and
will include nine presentations of 10 minutes each (five
slides per presentation and 5 minutes of Q & A). These
presentations will be chosen by a scientific committee
headed by
Dr. Rafael de Cabo. Selected presenters will
be notified by April 15, 2005 via email, and will be
featured in the AGE News and meeting website.
-
The Round-Table Discussion
will be held for the following 30 minutes of the
program, including some of the top directions in current
aging research, etc. Panelists will include: Drs.
Rozalyn Anderson, Qitao Ran, Sige Zou and Rafael de Cabo.
-
The Student Social, following
the above, will be held at a venue to be announced
soon.
PLEASE NOTE THAT THERE IS
LIMITED SPACE FOR THIS PROGRAM - SO, BOOK EARLY!
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All registrations for the Student Program
will be entered in a draw for a one-year
student membership with the American Aging
Association (please
click here to review benefits);
the winner has to be present at the meeting
and will be announced at the end of the
Round Table Discussion.
|
IF YOU WISH TO BE PART OF
THIS PROGRAM (presenter or audience), please submit your
entry at the
Call for Abstracts page.
PROGRAM UPDATES:
NEW!
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Be sure not to miss a special talk by Dr.
James Harwood of the Center for Scientific Review at NIH who will explain the workings of the new Study
Sections that were formed to review grant
applications in the areas of gerontology and
geriatrics - mark your calendars for Friday, the 3rd of June,
2005, at 6 pm.
- The
Welcome Reception has
been moved to 7 pm,
immediately following the lecture.
-
Dr. Huber Warner (NIH) will lecture on his 21 Years at the
NIA, outlining research directions -
past, present and future - don't miss this
presentation scheduled for Sunday, the 5th of June,
at 4:15 pm.
MEETING LINKS:
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The following
commentaries were submitted by Drs. Norm Wolf
and Steve Austad on
our January discussion led by Dr. Andrzej
Bartke and titled "Why dwarf mice are long-lived and what
does this tell us?" (Review
also
Dr. Bartke's responses to these
commentaries as well as the
discussion paper.)
Commentary submitted by
Dr.
Norm Wolf:
Dr. Bartke has briefly and effectively
summarized the status and importance of the GH-defective
models, a subject to which he has made many
important contributions. The consensus seems to
be that the removal of GH or GHR results in
consequent disappearance of circulating IGF-1
and, this (along with possible reductions in TH
in most models) produces the phenotype of the
models. One aspect that was not discussed and
that I think is of great importance is the quite
recent article by Muraki, Salmon, Miller and
others, including Dr. Barke, himself, reporting
that adult fourth passage fibroblasts from Snell
and GH deficient mice were extremely resistant
to H202, paraquat and other pro-oxidants in
vitro, as well as to a non-oxidant alkylating
agent, MMS. These findings suggest that the
oxidation-resistance characteristics of the
tissues of living dwarf mice are not only the
result of contemporary circulating GH and IGF-1
deletion, but are somehow intrinsic and lasting
in the cells (fibroblasts) after 4 passages in
vitro, due to an induced cellular status.
Apparently, it takes some period of lifespan
before this resistance is induced (it is not
present in mice only a few days old). Also,
given that 4th passage cells retain
this resistance, would this advantage extend the
length of continuing replications for murine
cells in vitro without crisis and
transformation? It is notable that de Cabo and
co-workers have shown that blood serum from CR
rats extends protection from stress to cells in
culture. Is this the same phenomenon and can
serum from the dwarfs do the same?
Commentary submitted by
Dr.
Steven Austad:
Three
thoughts spring immediately to mind on reading
Dr. Bartke’s lucid discussion piece.
First,
I am not quite yet prepared to agree with Dr.
Bartke that aging is retarded in the dwarf mouse
models. Clearly, they are long-lived and
some markers of aging seem retarded.
However, if aging is a progressive and
generalized decline in function, then relatively
few functions have been investigated so far. In
particular, I’m curious as to whether sensory
function, muscle strength and endurance, and
bone mineral density decline more slowly in
dwarfs than in controls. These are of
particular interest because key features of
human Laron Syndrome (LS), which is genetically
identical to the GHR/GHBP-KO mice, are muscle
weakness, osteopenia, and aberrant retinal blood
vessel morphology.
Second, with respect to whether findings from
the mouse studies extend to humans, we already
have hints at a few answers because humans with
LS have been extensively characterized (Laron,
JCEM 84:4397, 1999; Laron, JCEM 89:1031, 2004).
Ultimately, there are likely to be both
similarities and differences in the syndrome
between mice and humans. Data so far are too
sparse to determine whether LS humans live
exceptionally long, but it is quite clear that
they are not exceptionally short-lived. On the
other hand, they do not appear to age more
slowly by external signs. Although obese, they
have thin skin and early wrinkling. In addition
to the muscle weakness and osteopenia mentioned
above, adults frequently develop
hyperinsulinemia, hypercholesterolemia, and
glucose intolerance or diabetes – all associated
with aging in the general population. Also
intellectual performance is lower on average in
LS humans. Not all of these clinical signs may
be related to growth hormone resistance. People
with LS are invariably the product of
consanguineous marriages, so some effects may be
due to homozygosity for deleterious alleles at
other genetic loci. However this constellation
of clinical signs does not seem to be replicated
in mice.
Third,
if aging can reasonably be thought of as
unrepaired damage to cells, tissues, and organs,
we still have only the faintest clue as to the
origin or nature of that damage. In enumerating
four possible mechanisms by which absence of GH
delays aging, only two (reduced ROS production,
enhanced stress resistance) are clearly
associated with cellular damage. That is,
exactly how something like increased IGF-I or
insulin signaling might lead to the sort of
cellular damage we associate with aging is a
mystery.
The
discovery and creation of these long-lived dwarf
mice have given us exciting new opportunities to
address fundamental questions about the
modulation of aging in mammals. It might be
worth remembering, however, that no animal model
of extended longevity has yet to be
characterized that does not also have some
less-than-desirable side-effects. In our focus
on the length of life, let us not forget about
its quality.
back
Dr.
Andrzej Bartke's
Response:
Drs Wolf and Austad brought up many important
issues in their Commentaries. The results of
recent studies of the resistance of fibroblasts
isolated from long-lived mouse mutants to
various forms of cytotoxic stress indicate that
stress resistance is probably a very important
part of the "longevous phenotype" of these
animals. These findings also suggest that the
association of longevity with stress resistance
which is very well documented in invertebrates
applies also to mammals. To answer the question
posed at the end of Dr. Wolf's comments,
preliminary data obtained by Dr. de Cabo
indicate that serum from Ames dwarf mice
resembles serum obtained from calorically
restricted animals by exerting "protective"
effects on cultured cells.
I certainly agree with Dr. Austad that
retardation of aging is difficult to document.
However, there is a rather long list of
physiological characteristics of hypopituitary
or GH resistant long lived mutant mice that
indicate delayed aging of these animals. These
include data reported in the 70s on cartilage
and joint disease and more recent data obtained
by Flurkey and Miller concerning immune
function, collagen characteristics, renal
pathology and cataracts in Snell dwarf mice,
studies of tumor incidence in Ames and Snell
dwarfs by Ikeno and Miller and a series of
studies by Kinney who examined various measures
of cognitive function in Ames dwarfs and in
GHRKO mice. I am tempted to add a personal
footnote here: one of the reasons many years ago
we decided with Holly Brown-Borg and Kurt Borg
to examine longevity of ames dwarf mice was that
they appeared to us to look younger than their
chronological age.
In the human, hyperinsulinemia and insulin
resistance in some GH deficient or GH resistant
individuals is likely related to their obesity.
Growth hormone exerts anti-insulinemic actions
and promotes insulin resistance in both mice and
men but it appears that in the human, lack of
lipolytic effects of GH may override the effects
of reduced GH signal on sensitivity to insulin
action.
As pointed out by Dr. Austad, the mechanisms
linking reduced somatotropic signaling with
extended longevity remain to be identified.
With available data we can only speculate about
the importance of reduced oxidative metabolism
and ROS generation, improved anti-oxidant
defenses, reduced non-enzymatic glycation etc.
Concerning the "costs" of prolonged longevity in
animals with reduced GH or IGF-1 signaling;
IGF1R +/- mice studied by Holzenberger et al
were reported to be only slightly smaller than
normal and fully fertile. Perhaps more
importantly, studies of genetically normal (i.e.
not mutant, gene knock-out or transgenic) mice
demonstarted consistent and significant negative
correlation of adult body size (presumably a
measure of somatotropic signaling) and life
span. Of course, one could bring up an issue of
smaller animals having smaller litters or likely
being at some disadvantage in a competitive
sitution. Perhaps as one of our former
presidents have said, there are no free
lunches.....
back
Growth hormone signaling and longevity.
Why dwarf mice are long-lived and what does this
tell us?
Andrzej Bartke, Geriatrics Research,
Department of Medicine, Southern Illinois
University School of Medicine, P.O. Box 19628,
Springfield, Illinois 62794-9628,
USA, Email:
abartke@siumed.edu,
Telephone 217/545-7962, Fax 217/545-8006.
Email us
your comments on this paper
Hypopituitary dwarf mice, lacking growth hormone
(GH), prolactin and thyrotropin, and GH
resistant “Laron dwarf” mice live much longer
than their normal siblings (Brown-Borg et al.,
Nature 384:33, 1996; Flurkey et al., PNAS
8:6736, 2001,; Coschigano et al. Endocr
144:3799, 2003). Although these
observations were initially received with
considerable skepticism, evidence for extended
longevity of these animals is now undisputable
and evidence that aging is retarded in these
animals is very strong (Flurkey et al. PNAS
98:6736, 2001; Kinney et al. Horm. Behav.
39:277, 2001; Physiol. Behav. 72:653, 2001;
Ikeno et al., J. Gerontol. Biol. Sci. 58A:291,
2003, & unpublished). In Ames dwarf
(Prop1df), Snell dwarf (Pit1dw) and Laron dwarf
(GHR/GHBP-KO) mice, both the average and the
maximal life span is are significantly increased
with an occasional animal reaching an age of
over four years. This is a truly
remarkable age for a laboratory mouse living
under standard laboratory conditions with
constant access to high energy food.
Association of delayed aging with absence of GH
signaling raises a number of important questions
which are being addressed in current studies and
are likely to suggest directions for future
research.
First
of all, it is not understood how absence of GH
action leads to delayed aging and long life.
However, data available to date suggest a number
of possible mechanisms which singly or, more
likely, combined might account for the
“longevous phenotype” of Ames dwarf, Snell dwarf
and GHR-KO mice.
These
include (i) reduced circulating levels of IGF1,
and reduced somatic growth, (ii) reduced
secretion of insulin combined with enhanced
sensitivity to its actions, (iii) reduced body
temperature and generation of reactive oxygen
species (ROS) together with improved antioxidant
defenses, and (iv) increased cellular resistance
to multiple forms of stress. The
involvement and the suggested importance of
these mechanisms is supported by data obtained
in these and in other long-lived mutant mice
(reviewed in Bartke et al., J. Gerontol. Biol.
Sci. 56A, B340, 2001; Exper. Gerontol. 36:21,
2001), as well as by extrapolation of findings
obtained in genetically normal animals differing
in body size (Rollo, Evol. Dev. 55:55, 2002;
Miller et al. Aging Cell 1:22,2002), in normal
animals subjected to caloric restriction (Weindruch
& Sohal, N. Engl. J. Med. 337; 986:1997; Masoro,
Handbook Biol. Aging, Acad. Press 2001), and in
transgenic animals overexpressing GH (Bartke,
Neuroendocrinology 78:210, 2003). However,
it should be noted that evidence supporting
involvement of mechanisms listed above, although
substantial, is indirect being derived from the
studies of the association of various
physiological characteristics with aging and
life span.
In
addition to suggesting likely mechanisms linking
reduced GH and insulin signaling with longevity,
comparisons of long lived mutants to calorically
restricted (CR) animals reveal some interesting
and informative differences. For example,
adiposity is reduced in CR animals but increased
in GHR-KO mice (Bartke & Heiman, in press) while
Ames dwarfs exhibit relatively minor age-related
changes in adiposity (Heiman et al. Endocrine
20:149, 2003). This contrasts with the
situation in fat-specific insulin receptor knock
out (FIRKO) mice in which extension of life span
is associated with extreme leanness (Blüher et
al., Science 299:572, 2003). We suspect
that alterations in the secretory profile rather
than the mass of adipose tissue will prove
important in the control of aging, acting, most
likely, via alterations in insulin sensitivity.
Another important question raised by the
findings in dwarf mice is whether and if so, to
what extent the conclusions from studies in
these animals may apply to the human.
Delayed aging and long life of mice lacking GH
signaling is at odds with the ability of
injected GH to ameliorate some of the symptoms
of human aging and with the enthusiastic
promotion of GH, GH releasers, and various GH-related
products as “scientifically proven” means to
feel younger, look younger, and combat a host of
age-related problems. Moreover, GH
deficiency in the human is considered a risk
factor for cardiovascular disease, and reduced
life span was recently reported in a cohort of
genetically GH deficient individuals (Bessen et
al., JCEM 88:3664, 2003). However,
hypopituitary patients with a mutation
homologous to one of the life extending
mutations in the mouse are not short-lived and,
in fact, can reach a very advanced age (Krzisnik
et al., J. Endocr. Genetics 1:9, 1999).
Furthermore, ablation of the pituitary was
reported to reduce mortality of diabetic
patients, at least during the first 5-10 years
following irradiation (Klein et al., J. Diab.
Complic. 12:246, 1998). While more work is
clearly needed to resolve these controversies, I
believe that it is exceedingly unlikely that a
mechanism involved in the control of aging in
organisms ranging from worms to mice (and
probably operating also in unicellular yeast)
does not play a similar role in the human.
Extension of life by reducing IGF-1/insulin or
homologous signaling appears to represent an
ancient mechanism facilitating survival under
adverse conditions and promoting enhanced stress
resistance and repair capacity at the expense of
growth and reproduction when energy resources
are scarce (Tatar et al., Science 299:1346,
2003). In support of this reasoning,
enhanced sensitivity to insulin which
characterizes long lived dwarf and Laron dwarf
mice (Dominici et al., J. Endocr. 166:579, 2000;
173:81, 2002) was reported also in exceptionally
long-lived people (Paolisso et al., Am. J.
Physiol. 270:E890,1996).
However, the relative impact of reduced actions
of IGF-1 and/or insulin on life span will likely
prove to differ between species. For
example, reduced activity of the somatotropic
axis may be universally related to reduced risk
of neoplasia, but tumors are a much less common
cause of death in humans than in mice.
Conversely, IGF-1 may be protecting against
cardiovascular disease (Shut et al., Stroke
34:1623, 2003) which is a leading cause of death
in humans but not in mice. Moreover, in
comparison to other mammals, and particularly to
mammals of comparable body size, humans are
rather inordinately long-lived and therefore
there may be less “room for improvement” in the
human than in mice, flies or worms.
Ames,
Snell and Laron dwarf mice are clearly outside
the range of normal variation in body size,
longevity, and other characteristics of the
laboratory stocks of house mice. However,
the extreme features of these diminutive animals
offer exciting opportunities to discover and
elucidate physiological mechanisms that control
aging and longevity in genetically normal
individuals and likely apply broadly, including
our own species.
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REMEMBER!
SUBMIT A COMMENT ON THIS TOPIC/PAPER AND ENTER TO WIN
A FREE MEETING REGISTRATION AT THE 34TH ANNUAL
MEETING OF THE AMERICAN AGING ASSOCIATION
(hotel and airfare not included).
Winner will be announced in our April edition
of the Newsletter.
Comments will be published in subsequent
editions of the AGE Newsletter.
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WELCOME TO OUR NEW AGE MEMBERS:
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L. Stephen Coles,
MD, PhD
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Joe Knight, MD:
"My research
interests over the past 20 years have been
in the area of free radicals and aging and
more recently, the effects of lifestyle on
aging, disease, and longevity (2004 book by
World Scientific, "A Crisis Call for New
Preventive Medicine" as well as two prior
books on aging subjects). Before coming to
the University of Utah School of Medicine
(Pathology Dept) in 1979, I practiced
pathology in private hospitals for 12 years.
Although now partly retired (no research lab
but teaching and administration), I still
enjoy attending meetings. The American Aging
Association meeting last year was
outstanding so I figured I would join and
try to attend the meeting each year."
Boguslaw
Lipinski, PhD: "My research interest
is in the relationship between aging and
free radicals. Although it is generally
believed that aging is associated with
oxidative stress, I argue that the reverse
is true."
Maria
Volkova, PhD:
"Originally from St.
Petersburg, Russia, I have been working in
the US for the last four years as a postdoc
at the Laboratory of Cardiovascular Science,
National Institute on Aging, National
Institutes on Health. The focus of my
research is cardiovascular aging,
especially, the molecular
basis
of aging in rodents (rats, mice) on
different models (heart, skeletal muscles,
aorta); modification of aging process by
caloric restriction - candidate genes;
transcription factors potentially involved
in regulation of aging.
The first results were reported as a
platform presentation at Molecular Genetics
of Aging, Meeting in Cold Spring Harbor, NY,
2004:
Novel microarray analysis coupled with
prediction modeling identifies genetic
components implicated in the longevity of
rodents: a bypass genetics approach."
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GRANT/AWARD
OPPORTUNITIES :
-
RESEARCH FELLOWSHIP -
www.hhwf.org
The Helen
Hay Whitney Foundation supports early
postdoctoral research training in all basic
biomedical sciences. To attain its ultimate
goal of increasing the number of
imaginative, well-trained and dedicated
medical scientists, the Foundation grants
financial support of sufficient duration to
help further the careers of young men and
women engaged in biological or medical
research.
Application
forms become available March 15 each
year online at
www.hhwf.org.
Applications must be received by August
15th. Late applications will not be
considered. Contact
hhwf@earthlink.net.
$25,000 PRIZE FOR NEUROBIOLOGY -
www.eppendorf.com/prize2005
The Eppendorf &
Science Prize for
Neurobiology acknowledges the increasing
importance of this research in advancing our
understanding of how the brain and nervous
system function – a quest that seems
destined for dramatic expansion in the
coming decades. This international prize,
established in 2002, is intended to
encourage and support the work of promising
young neurobiologists who have received
their PhD or MD within the past 10 years.
The prize is awarded annually to one young
scientist for the most outstanding
neurobiological research conducted by
him/her during the past three years, as
described in a 1,000-word entrance essay.
Deadline is June 15, 2005.
2005 NIH Director's Pioneer Award
The National Institutes of Health announces the
2005 NIH Director's Pioneer Award, a key
component of the NIH Roadmap for Medical
Research. The award supports scientists of
exceptional creativity who propose pioneering
approaches to major challenges in biomedical
research. The program is open to
scientists at all career levels who are
currently engaged in any field of research,
interested in exploring biomedically relevant
topics, and willing to commit the major portion
of their effort to Pioneer Award research.
Women, members of groups that are
underrepresented in biomedical research, and
individuals in the early to middle stages of
their careers are especially encouraged to
nominate themselves. Awardees must be U.S.
citizens, non-citizen nationals, or permanent
residents.
In September 2005, NIH expects to make 5 to 10
new Pioneer Awards of up to $500,000 in direct
costs per year for 5 years. The
streamlined self-nomination process includes a
3- to 5-page essay, a biographical sketch, a
list of current research support, and the names
of 3 references. Submit nominations on the
Pioneer Award Web site,
http://nihroadmap.nih.gov/pioneer/
, between March 1 and April 1, 2005.
For more information, visit the Pioneer Award
Web site or e-mail questions to
pioneer@nih.gov.
Email
us your program/job posting
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Meeting Announcements:
Email
us your meeting announcement
 March
9, 2005
Sorrento, Italy
CHALLENGING VIEWS 2005
FOR AGE MEMBERS ONLY!!! IF YOU ARE
AN AGE MEMBER HEADING OUT TO SORRENTO FOR THE
2005 International Conference on Alzheimer's
Disease and Parkinson Disease, WE ARE GIVING
AWAY 5 MEETING REGISTRATIONS FOR THE CHALLENGING
VIEWS DEBATES, a unique satellite meeting to be
held on the 9th of March, at the Hilton Sorrento
Palace, beginning promptly at 8:00 a.m. This
meeting, sponsored by the
Neurological Disease Foundation, is part of a series of conferences that
utilize debates to advance the field of research
in Alzheimer's disease and related
neurodegenerative disorders.
CLICK HERE TO CONTACT THE MEETING SECRETARIAT
TODAY (5 meeting registrations will be awarded
on a first come, first served basis).
 May
18-21, 2005
Portland, Oregon
DIET AND OPTIMUM HEALTH CONFERENCE
The Linus Pauling Institute at
Oregon State University will hold its third
international conference on "Diet and Optimum
Health" on May 18-21, 2005, at the Hilton Hotel
in Portland, Oregon. The Conference is
co-sponsored by the Oxygen Club of California. A
highlight of the conference will be the award of
the third "Linus Pauling Institute Prize for
Health Research." This international award is
intended to encourage and recognize excellence
in the field of nutrition and health, and
consists of a medal and $50,000.
Click
here or on LPI logo to access the meeting
website.
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NIH News:
Effective the 2nd of May 2005, all researchers
who have received NIH support for a given area
of investigation are expected to submit to
PubMed Central an electronic copy of any
manuscript publishing results of that research
as soon as it is accepted for publication. This
requirement is a new part of the final policy
the NIH announced last week following a period
of public comment to its proposed policy last
September. The change gives scientists more
flexibility in the timing of sending manuscripts
to NIH, and is part of a larger policy aimed at
making NIH-funded research results more
accessible to the public. For the full text,
visit the
NIH website.
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FEBRUARY
SPOTLIGHT:
 The
Linus Pauling Institute was
co-founded in 1973 by Linus Pauling,
Ph.D., the only individual ever to win
two, unshared Nobel Prizes (Chemistry,
1954; Peace, 1962).
Our mission is to determine the function
and role of micronutrients (vitamins and
minerals) and phytochemicals (chemicals
from plants) in promoting optimum health
and preventing and treating disease; to
determine the role of oxidative and
nitrative stress and antioxidants in
human health and disease; and to advance
knowledge in areas that were of interest
to Linus Pauling through research and
educational activities.
Researchers at the
Linus Pauling Institute investigate the
role that vitamins, micronutrients, and
other dietary constituents, as well as
oxidative and nitrative stress and
antioxidants, play in human aging and
chronic diseases, especially heart
disease, cancer, and neurodegenerative
diseases.
The goals of these
studies are to understand the mechanisms
by which nutrition affects disease
initiation and progression and how
nutritional factors can be used in the
prevention and treatment of diseases,
thereby enhancing human health and
well-being. |
RELEVANT LPI RESOURCES:
LPI Research Report
and the
Micronutrient Information Center
-
To learn more about LINUS PAULING
INSTITUTE, visit their website at:
|
"Age is opportunity no less than youth
itself."
Henry Wadsworth Longfellow |
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RENEW YOUR MEMBERSHIP TODAY AT:
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www.americanaging.org/membership.html
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and take advantage of discounts for the
annual meeting of June!
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