Nederland op de 16de plaats in
levensverwachting wereldwijd
Waar je woont maakt een gigantisch verschil
uit betreffende je levensverwachting. In het geval van Swaziland is het gemiddeld slecht
gesteld met de levensduur, 39,6 levensjaren! Daar tegenover staat nog steeds de absolute
topper Japan met 82,6 (79,0 mannen / 86,1 vrouwen) Nederland bekleed de 16de plaats
79,8 gemiddeld (77,5 mannen / 81,9 vrouwen) Opvallend is dat we het veel minder goed doen
dan andere Europese landen. Zwitserland 81,7 jaar, Spanje 80,9, Zweden 80,9, Frankrijk
80,7, Italië 80,5, Noorwegen 80,2 en Oostenrijk eindigt op gelijke hoogte met ons land.
De Nederlandse Antillen eindigen op plaats 60 met een gemiddelde leeftijd van 75,1 jaar,
Aruba 65ste met 74,2 jaar. De gemiddelde leeftijd betreffende de gehele wereldbevolking is
67,2 jaar (65 mannen / 69,5 vrouwen)
Sportupplementen worden steeds gezonder.
Van creatine en BCAA's wisten we al dat ze het leven verlengen, maar nu vertraagt volgens
een dierstudie van de Russian Academy of Medical Sciences ook carnosine [structuurformule
hieronder] het verouderingsproces. Als je beta-alanine slikt, verhoog je de hoeveelheid
carnosine in je spiercellen.
Italiaanse duursporters kennen het
aminozuursupplement BigOne. Italiaanse onderzoekers die BigOnedoor het drinkwater van
muizen mengden, ontdekten dat de dieren daardoor tien procent langer leefden.
Bewerkte voedingsmiddelen kunnen
kans op overlijden verdrievoudigen
Een nieuwe studie laat zien dat bewerkte
voedingsmiddelen, zoals producten van (wit) tarwemeel en met een hoog suikergehalte de
kans op overlijden fors verhogen
Working at the intersection of science and
policy, population researchers examine the causes and impacts of population trends.
Understand how the science has changed and hear about the factors and phenomena that
affect mortality and other human longevity statistics. Population aging and extending the
human life span can challenge public support systems. Learn how the skills of the
demographer are applied to these and other important social and economic issues.
Radio - Bas Zwaan, hoogleraar
veroudering
We worden geboren, we slijten en dan gaan
we dood. Maar waarom? Waarom gaan we dood? Waarom blijven we niet gewoon jong? Waarom
worden sommige levende wezens niet ouder dan een dag, terwijl anderen het meer dan 400
jaar uithouden. Niet de minste vragen waar je je mee bezig kan houden. Bas Zwaan doet dat
dagelijks. Hij is net benoemd tot hoogleraar Erfelijkheidsleer aan de Wageningen
Universiteit.
Japan vs. USA Diet. Why Japanesse
Men and Women Live So Long
Genetische cocktail bepaalt
ouderdom
Amerikaanse onderzoekers vonden bij extreem
oude mensen van over de honderd jaar een aantal specifieke genetische overeenkomsten. Het
onderzoek ondersteunt de stelling dat genen een belangrijke factor zijn om gezond oud te
worden. Het is zelfs de eerste stap naar een betrouwbaar voorspellingssysteem voor hoe oud
je genetisch gezien kunt worden.
Glucosamine- en
chondroïtinegebruikers leven langer
Voorlichters en voedingswetenschappers
verslijten de helft van de Nederlandse bevolking voor gek. Zo'n zes miljoen Nederlanders
gebruikt voedingssupplementen, aldus een onderzoek van de NPN. [evmi.nl 19-05-2010] En die
werken niet. Nee, sterker nog, supplementen maken je alleen maar ongezonder. Zeggen
wetenschappers en voorlichters.
Hoe oud we worden hangt af van veel
factoren, maar één daarvan is het 'methusalemgen', waarvan de bezitters een grote kans
maken om heel oud te worden, zelfs als ze de uitspattingen niet schuwen.
Een 83-jarige yogi claimt dat hij al
zeventig jaar niets heeft gegeten en gedronken. De Indiase Prahlad Jani krijgt naar eigen
zeggen energie door meditatie.
Veroudering remmen zonder honger
dankzij levensverlenger in groene appels
Het organische zuur waaraan groene appels
hun friszure smaak danken verlengt de levensduur. Het wormpje Caenorhabditis elegans [je
ziet er eentje hieronder] leeft gemiddeld 25 langer als het L-malate door zijn voer
krijgen. Dat ontdekten farmacologen van de University of California-San Diego.
BBC, "How to Live to 101" The
quest to live longer has been one of humanities oldest dreams, but while scientists have
been searching, a few isolated communities have stumbled across the answer. On the remote
Japanese island of Okinawa, In the Californian town of Loma Linda and in the mountains of
Sardinia people live longer than anywhere else on earth. In these unique communities a
group of scientists have dedicated their lives to trying to uncover their secrets. Horizon
takes a trip around the globe to meet the people who can show us all how to live longer,
healthier lives.
Goede voeding vertraagt
verouderingsproces
Amerikaanse wetenschappers zien verband
tussen het gehalte aan omega-3 vetzuren in het bloed en de lengte van telomeren en dus
invloed op gezond oud(er) worden. Korte telomeren worden in verband gebracht met kanker,
hart- en vaatziekten, osteoporose en daling van de immuniteit. Telomeren zijn de uiteinden
van chromosomen.
Wetenschappers van het UMC Groningen hebben
een gen ontdekt dat betrokken is bij biologische veroudering in mensen. Zij deden dat in
samenwerking met Engelse collega’s van de Universiteit van Leicester en het
King’s College te London. Dit onderzoek wordt vandaag gepubliceerd in het
vooraanstaande tijdschrift Nature Genetics.
De onderzoekers keken naar de telomeren, de
beschermkapjes van het DNA, te vergelijken met de plastic uiteinden van schoenveters. Bij
de meeste cellen worden telomeren korter bij elke celdeling. Wetenschappers beschouwen
daarom telomeerlengte als een marker voor biologische leeftijd.
“In deze studie hebben we ontdekt dat
individuen met een bepaalde genetische variant kortere telomeren hebben en dus
waarschijnlijk biologisch ouder zijn dan hun kalenderleeftijd”, vertelt dr. Pim van
der Harst van de afdeling Cardiologie UMCG, die een belangrijk deel van het onderzoek in
Leicester en Groningen uitvoerde. “Het effect was behoorlijk, één kopie van de
variant zorgt ervoor dat de telomeren gemiddeld 75 basenparen korter zijn, wat normaal
gesproken drie levensjaren duurt. Van beide ouders kun je deze variant erven en als je er
twee hebt ben je biologisch gezien zeven jaar ouder.”
De nu geïdentificeerde genetische variant
ligt dicht bij het TERC-gen, waarvan bekend is dat het een belangrijke rol speelt bij de
telomeerlengte van stamcellen. De resultaten suggereren dat sommige mensen genetisch
voorbestemd zijn om kortere telomeren te krijgen dan anderen. “Deze genetische
variatie zou dus deels kunnen verklaren waarom mensen in sommige families allemaal veel
ouder worden dan in andere families.”
Bekend was dat de telomeren sneller slijten
door schadelijke factoren, zoals roken. Ook hartfalen en telomeerlengte zijn aan elkaar
gelinkt, vertelt prof.dr. Dirk Jan van Veldhuisen, betrokken bij het onderzoek en hoofd
van de afdeling Cardiologie in het UMCG. “We hebben eerder al aangetoond dat
patiënten met hartfalen kortere telomeren hebben. Nu is het de vraag of gezonde mensen
met deze genetische variant een groter risico hebben op het ontwikkelen van
hartfalen.”
Het onderzoek maakte gebruik van data van
de PREVEND studie. Dit Groningse bevolkingsonderzoek bestudeert of eiwitten in de urine
nier-, hart- en vaatziekten voorspellen. Het onderzoek werd mede gefinancierd door NWO,
via een Veni-beurs van Pim van der Harst, het Interuniversitair Cardiologisch Instituut
Nederland (ICIN), de Nederlandse Hartstichting, de Nederlandse Nierstichting en de
EU-projectsubsidie GENECURE.
Cortisol Is the Major Hormone
Involved In Accelerated Aging
Dr. Michael Borkin, NMD is a pioneer in
hormone and electrolyte research. He specializes in hormone and electrolyte testing and
balancing. For more information contact him at: 888-285-9098 or by email: doctorborkin@gmail.com. His evaluation of
hormones levels in patients provides an in-depth snap shot of the health level and disease
processes. These tests and the unique balancing programs created by the trained doctors
and lab technicians are incredibly valuable for individuals who have used anabolic
steroids, HGH (human growth hormone), insulin, testosterone and progesterone without
understanding the importance of exact supplementation in response to test results. Gross
dosing without testing has caused many people to be biochemically and hormonally out of
balance. Dr. Michael Borkin is also one of the creators of the science of bio-identical
hormones and transdermal (through the skin) creams. Unique creams are created for each
patient to restore hormonal homeostasis. The creams are made up of hormones, hormone
precursors, nutrients, homeopathics, herbs and electrolytes. Specific electrolyte and
nutrient rich supplements help balance each patient's bio-chemistry in all their cells,
including the brain.
Dr. Borkin invested many years in treating
the "Who's Who" of Hollywood and Las Vegas. After studying so many people who
violate the health laws and natural circadian cycle (24-hour light and dark cycle), that
stay up all night and sleep during the day, he became the leading expert on the three
stages of adrenal exhaustion and the terrible consequences of a stressful life. As we all
know, stress kills. Some of the most famous actors, stars and athletes are his patients.
They keep his name as a jealously guarded secret so he will personally have time to work
with them. They want to take advantage of his knowledge and research so he can create and
monitor their special balancing programs. They are desperate to look younger, have more
energy, feel their best and perform at optimal levels.
Dr. Borkin has developed a 24-hour test of
the flood of hormones throughout the entire body, every 4 hours. A patient starts
collecting their saliva at 8 AM. They take a sample every 4 hours until 4 AM the next
morning. By studying the levels of bio-active hormones and electrolytes available in
saliva, doctors learn a great deal about the health and disease processes going on inside
their patients' cells.
Boeken
Gesprek. met Ellen de Bruin over haar boek
Onsterfelijkheid voor beginners. In dit boek onderzoekt de wetenschapsjournaliste van
NRC/Handelsblad de verschillende manieren die mensen in de loop der tijd hebben bedacht om
eeuwig te leven, en daar jong en gezond bij te blijven.
To find the path to long life and health,
Dan Buettner and team study the world's "Blue Zones," communities whose elders
live with vim and vigor to record-setting age. At TEDxTC, he shares the 9 common diet and
lifestyle habits that keep them spry past age 100.
Adviezen mbt aging
CNN's Dr. Sanjay Gupta teams with
anti-aging experts to bring you an in-depth discussion on the search for immortality.
Met zijn 113 jaar is Walter Breuning
officieel de oudste man op aarde. In zijn leven heeft hij veel diëten voorbij zien komen.
Welk dieetadvies kan hij ons geven?
Say Yes to Sex - It Can Help You
Live a Longer Life
Recent studies indicate that more sex can lead to a longer life. One study indicated that
having three or more orgasms a week can extend the life of a man by reducing the risk of
heart disease, stress, cancer and depression.
We know that lifespan can be extended in animals by restricting calories such as sugar
intake. Now, according to a study published in the journal PLoS Genetics, Université de
Montréal scientists have discovered that it's not sugar itself that is important in this
process but the ability of cells to sense its presence. Aging is a complex phenomenon and
the mechanisms underlying aging are yet to be explained. What researchers do know is that
there is a clear relationship between aging and calorie intake. For example, mice fed with
half the calories they usually eat can live 40 percent longer. How does this work? As part
of the PLoS Genetics study, Université de Montréal Biochemistry Professor Luis Rokeach
and his student Antoine Roux discovered to their surprise that if they removed the gene
for a glucose sensor from yeast cells, they lived just as long as those living on a
glucose-restricted diet. In short, the fate of these cells doesn't depend on what they eat
but what they think they're eating. There are two obvious aspects of calorie intake:
tasting and digestion. By the time nutrients get to our cells there is an analogous
process: sensors on the surface of the cell detect the presence of, for example, the sugar
glucose and molecules inside the cell break down the glucose, converting it to energy. Of
these processes, it is widely thought that the by-products of broken down sugars are the
culprits in aging. The study by Rokeach and Roux suggests otherwise. To understand aging,
Rokeach and Roux in collaboration with Université de Montréal Biochemistry Professors
Pascal Chartrand and Gerardo Ferbeyre used yeast as a model organism. At a basic level,
yeast cells are surprisingly similar and age much like human cells, as well as being easy
to study. The research team found that the lifespan of yeast cells increased when glucose
was decreased from their diet. They then asked whether the increase in lifespan was due to
cells decreasing their ability to produce energy or to the decrease in signal to the cells
by the glucose sensor. The scientists found that cells unable to consume glucose as energy
source are still sensitive to the pro-aging effects of glucose. Conversely, obliterating
the sensor that measures the levels of glucose significantly increased lifespan.
"Thanks to this study, the link between the rise in age-related diseases and the
over-consumption of sugar in today's diet is clearer. Our research opens a door to new
therapeutic strategies for fighting age-related diseases," says Professor Rokeach.
Study of protein structures reveals
key events in evolutionary history
A new study of proteins, the molecular machines that drive all life, also sheds light on
the history of living organisms. The study, in the journal Structure, reveals that after
eons of gradual evolution, proteins suddenly experienced a "big bang" of
innovation. The active regions of many proteins, called domains, combined with each other
or split apart to produce a host of structures that had never been seen before. This
explosion of new forms coincided with the rapidly increasing diversity of the three
superkingdoms of life (bacteria; the microbes known as archaea; and eucarya, the group
that includes animals, plants, fungi and many other organisms). ead author Gustavo
Caetano-Anollés, a professor of bioinformatics in the department of crop sciences at the
University of Illinois and an affiliate of the Institute for Genomic Biology, has spent
years studying protein structures – he calls them "architectures" –
which he suggests offer a reliable record of evolutionary events. All proteins contain
domains that can be identified by their structural and functional similarities to one
another. These domains are the gears and motors that allow the protein machinery to work.
Every protein has one or more of them, and very different proteins can contain the same,
or similar, domains. By conducting a census of all the domains that appear in different
groups of organisms and comparing the protein repertoires of hundreds of different groups,
the researchers were able to construct a timeline of protein evolution that relates
directly to the history of life.
The theory that a higher metabolism means a shorter lifespan may have reached the end of
its own life, thanks to a study published in the journal Physiological and Biochemical
Zoology. The study, led by Lobke Vaanholt (University of Groningen, The Netherlands),
found that mice with increased metabolism live just as long as those with slower metabolic
rates. The theory that fast-living animals die young, known as the rate-of-living theory,
was first proposed in the 1920s. The premise is simple: Aging is the inevitable byproduct
of energy expenditure. The faster you expend energy, the faster you age, and the sooner
you die. It remained a prominent theory of aging until recently, when comparisons across
broad animal groups cast doubt on it. For instance, birds have significantly higher
metabolisms than mammals of similar size, yet the birds live much longer. Vaanholt's study
was designed to test the rate-of-living theory among individuals of one species—in
this case, mice. For their experiment, Vaanholt and her team followed two groups of mice
through their entire lives. One group's environment was kept at 71 degrees Fahrenheit (22
degrees Celsius), and the other group's at 50 degrees Fahrenheit (10 degrees Celsius). The
colder group had to expend more energy to maintain body temperature, and according to the
rate-of-living theory, should therefore die sooner than the warm group. But that's not
what happened. "Despite a 48 percent increase in overall daily energy expenditure and
a 64 percent increase in mass-specific energy expenditure throughout adult life, mice in
the cold lived just as long on average as mice in warm temperatures," the authors
write. "These results strengthen existing doubts about the rate-or-living
theory." The finding is consistent with an experiment Vaanholt conducted previously.
That experiment manipulated metabolism in mice through exercise rather than temperature.
Mice that expended more energy over a lifetime through exercise had the same lifespan as
those that did not exercise. Both studies cast significant doubt on a theory that just may
have burned itself out.
In 2004, researchers at the University of North Carolina at Chapel Hill Lineberger
Comprehensive Cancer Center announced a crucial discovery in the understanding of cellular
aging. They found that as cells and tissues age, the expression of a key protein, called
p16INK4a, dramatically increases in most mammalian organs. Because p16INK4a is a tumor
suppressor protein, cancer researchers are interested in its role in cellular aging and
cancer prevention. Now the team has proven that the same biomarker is present in human
blood and is strongly correlated both with chronological age and with certain behaviors
such as tobacco use and physical inactivity, which are known to accelerate the aging
process. In a paper published online ahead of print in the journal Aging Cell, the
researchers reported that they have solved technical hurdles to develop a simple blood
test to detect p16INK4a expression, which is present in cells called T-lymphocytes, also
known as T-cells. "This is a major step toward a practical tool to clinically
determine a person's actual molecular, as opposed to just their chronological age,"
said UNC Lineberger member Norman Sharpless, M.D., the senior author of the study and
associate professor of medicine and genetics at UNC's School of Medicine. They validated
the test by obtaining blood from two groups of healthy human volunteers, totaling 170
subjects, who also filled out a questionnaire about current and past health status and
health behaviors. They found that expression of the biomarker was strongly correlated with
the donor's chronological age and, in fact, increased exponentially with age. In addition,
increased levels were independently associated with tobacco use and physical inactivity as
well as with biomarkers of human frailty.
kanker
Researchers learn how mutations extend life span
A new approach to stimulating immune cells enhances their anticancer activity, resulting
in a powerful anti-tumor response in mice, according to a study by researchers at the
National Cancer Institute, a part of the National Institutes of Health.
Researchers uncover details about
how dietary restriction slows down aging
University of Washington scientists have uncovered details about the mechanisms through
which dietary restriction slows the aging process. Working in yeast cells, the researchers
have linked ribosomes, the protein-making factories in living cells, and Gcn4, a
specialized protein that aids in the expression of genetic information, to the pathways
related to dietary response and aging. The study appears in the April 18 issue of the
journal Cell.
'Life force' linked to body's
ability to withstand stress
Our ability to withstand stress-related, inflammatory diseases may be associated, not just
with our race and sex, but with our personality as well, according to a study published in
the July issue of the journal Brain, Behavior and Immunity. Especially in aging women, low
levels of the personality trait extraversion may signal that blood levels of a key
inflammatory molecule have crossed over a threshold linked to a doubling of risk of death
within five years. An emerging area of medical science examines the mind-body connection,
and how personality and stress contribute to disease in the aging body. Long-term exposure
to hormones released by the brains of people under stress, for instance, takes a toll on
organs. Like any injury, this brings a reaction from the body's immune system, including
the release of immune chemicals that trigger inflammation in an attempt to begin the
healing process. The same process goes too far as part of diseases from rheumatoid
arthritis to Alzheimer's disease to atherosclerosis, where inflammation contributes to
clogged arteries, heart attacks and strokes. The current study found that that extroverts,
and in particular those high "dispositional activity" or engagement in life,
have dramatically lower levels of the inflammatory chemical interleukin 6 (IL-6). Swiss
psychiatrist Carl Jung defined extroverts as focused on the world around them and most
happy when active and surrounded by people. Introverts looked inward and were shy. The
definitions of extraversion and other personality traits were refined by American
psychologist Gordon Allport beginning in the 1930s. He reviewed all adjectives in the
dictionary used to describe personality, and attempted to group them into clusters. Over
the next several decades, researchers statistically analyzed these dictionary terms and
discovered that they tended to cluster into five general dimensions: extraversion vs.
introversion, emotional stability vs. neuroticism, openness vs. closed-minded, agreeable
vs. hostile, and conscientiousness vs. unreliability. These dimensions, known as the
"Five Factor Model" of personality, served to organize hundreds of specific
traits like "activity" for psychologists, similar to the way the Periodic Table
organizes elements for physicists.
Children of centenarians live
longer, have lower risk of heart disease, stroke, diabetes
A recent study appearing in the November issue of Journal of American Geriatrics Society
revealed that centenarian offspring (children of parents who lived to be at least 97 years
old) retain important cardiovascular advantages from their parents compared to a
similarly-aged cohort.
A new idea for how anti-aging
products delay ripening of fruit and wilting of flowers
A research team led by UC Riverside's Michael Pirrung, a professor of chemistry, offers a
novel pathway for how "antiaging" products like EthylBloc and SmartFresh block
ethylene in plants, delaying the plants' demise and allowing people to enjoy their beauty
and products for longer than nature allows.
Identification of Key Protein May
Explain Anti-cancer, Anti-aging Benefits of Dietary Restriction
A protein that plays a key role in tumor formation, oxygen metabolism and inflammation is
involved in a pathway that extends lifespan by dietary restriction. The finding provides a
new understanding of how dietary restriction contributes to longevity and cancer
prevention and gives scientists new targets for developing and testing drugs that could
extend the healthy years of life.
Researchers To Reveal Aging’s
Origins on Global Stage
Four of the biologists who described the underlying causes of aging will soon share their
findings with an international audience during a symposium at the upcoming World Congress
of Gerontology and Geriatrics, taking place from July 5–9, 2009, in Paris, France.
The presentation, titled “Ageing Is no Longer an Unsolved Problem,” is being
supported by the Ellison Medical Foundation and co-sponsored by The Gerontological Society
of America (GSA). Among the speakers will be former GSA President Leonard Hayflick, PhD, a
professor of anatomy at the University of California, San Francisco. He said that the
accumulation of new insights has made it possible, for the first time, to understand the
biological reasons for the aging of animals and humans. “Aging occurs because the
complex biological molecules of which we are all composed become dysfunctional over time
as the energy necessary to keep them structurally sound diminishes. Thus, our molecules
must be repaired or replaced frequently by our own extensive repair systems,”
Hayflick said.“These repair systems, which are also composed of complex
molecules,” he explained, “eventually suffer the same molecular dysfunction. The
time when the balance shifts in favor of the accumulation of dysfunctional molecules is
determined by natural selection — and leads to the manifestation of age changes that
we recognize are characteristic of an old person or animal. It must occur after both reach
reproductive maturity, otherwise the species would vanish.” Hayflick also noted that
these repair and maintenance systems are called “determinants of longevity,”
which is a phenomenon different from the aging process itself.
U-M scientists develop tool to
probe role of oxidative stress in aging, disease
Oxygen, although essential for human life, can turn into an aggressive chemical that is
outright toxic to important molecules inside our cells. This "oxidative stress"
is associated with many diseases, such as Alzheimer's, heart disease and cancer, and has
been suggested to be the culprit underlying aging.
Researchers at the Fritz Lipmann Institute in Jena are establishing Nothobranchius furzeri
as a new model organism for studying aging processes. Nematodes, yeasts, and fruit flies
belong to the most important model organisms used to research biological aging processes.
They yield information about which physiological processes and molecular biological
conditions accelerate or delay aging processes. These model systems for aging research are
now seeing competition from a smart newcomer in the scientific field: the killifish
Nothobranchius furzeri. This African fish has been popular for decades with aquarists and
is known for its short life span. In three months, it completes the life cycle of birth,
reproduction, and death. “We suspect that there is a genetic program behind this
which regulates the life cycle and thus predetermines the aging process,” said Dr.
Alessandro Cellerino of the Leibniz Institute for Age Research, Fritz Lipmann Institute
(FLI) in Jena.
Landmark Study Opens Door to New
Cancer, Aging Treatments - Wistar Institute Researchers Decipher Telomerase Structure
Researchers at The Wistar Institute have deciphered the structure of the active region of
telomerase, an enzyme that plays a major role in the development of nearly all human
cancers. The landmark achievement opens the door to the creation of new, broadly effective
cancer drugs, as well as anti-aging therapies. Researchers have attempted for more than a
decade to find drugs that shut down telomerase—widely considered the No. 1 target for
the development of new cancer treatments—but have been hampered in large part by a
lack of knowledge of the enzyme’s structure. The findings, published online August 31
in Nature, should help researchers in their efforts to design effective telomerase
inhibitors, says Emmanuel Skordalakes, Ph.D., assistant professor in Wistar’s Gene
Expression and Regulation Program, who led the study. “Telomerase is an ideal target
for chemotherapy because it is active in almost all human tumors, but inactive in most
normal cells,” Skordalakes says. “That means a drug that deactivates telomerase
would likely work against all cancers, with few side effects.”The study elucidates
the active region of telomerase and provides the first full-length view of the telomerase
molecule’s critical protein component. It reveals surprising details, at the atomic
level, of the enzyme’s configuration and how it works to replicate the ends of
chromosomes—a process critical to both tumor development and the aging process.
Wine, veg and little meat 'a recipe
for long life'
It has long been heralded as the perfect recipe for a long life but a new study suggests
that not all foods that make up the Mediterranean diet carry the same benefits.
The same chemical reaction that causes iron to rust plays a similarly corrosive role in
our bodies. Oxidative stress chips away at healthy cells and is a process, scientists
know, that contributes to a host of diseases and conditions in humans ranging from
Alzheimer's, heart disease and stroke to cancer and the inexorable process of aging.
'Jumping gene' may contribute to a
premature aging syndrome
Scientists have identified a fusion protein that may contribute to Cockayne syndrome, a
devastating disease characterized by developmental defects, neurodegeneration, severe
wasting, and premature aging. The study is described in an article published March 21 in
the open-access journal PLoS Genetics.
Joslin researchers discover new
effect for insulin
Researchers at the Joslin Diabetes Center have shown that insulin has a previously unknown
effect that plays a role in aging and lifespan, a finding that could ultimately provide a
mechanism for gene manipulations that could help people live longer and healthier lives.
Severely restricted diet linked to
physical fitness into old age
Severely restricting calories leads to a longer life, scientists have proved. New research
now has shown for the first time that such a diet also can maintain physical fitness into
advanced age, slowing the seemingly inevitable progression to physical disability and loss
of independence.
Scientists at the University of Liverpool have developed a new method to help researchers
identify genes that can help protect the body during the ageing process. The team
developed a method of analysing genes in multiple ageing tissue types in both animals and
humans. The analysis, which included more than five million gene measurements, highlighted
the mechanisms used by the body to protect against cellular changes with age that can
result in conditions such as muscle degeneration and cognitive ageing. The new method
could help further understanding into anti-ageing interventions by identifying genes that
indicate biological changes as a result of ageing. Research has suggested that some genes
respond to age-related conditions by increasing key protein levels, allowing the body to
manage the ageing process more effectively. Dr Joao Pedro Magalhaes, from the University's
School of Biological Sciences, explains: "We developed a new algorithm to analyse
microarray data of genes from different species, and combined data from multiple studies
to obtain a picture of how genes respond to ageing in a whole organism. This method is
similar to the way scientists study the molecular characteristics of cancer, but it is the
first time it has been used to research ageing.
Einstein researchers discover gene
mutations linked to longer lifespans
A gene linked to living a very long life -- to 90 and beyond -- is also associated with
short stature in women, according to new research by scientists at the Albert Einstein
College of Medicine of Yeshiva University.
UCLA study finds that broccoli may
help boost the aging immune system
The study findings show that sulforaphane, a chemical in broccoli, switches on a set of
antioxidant genes and enzymes in specific immune cells, which then combat the injurious
effects of molecules known as free radicals that can damage cells and lead to disease.
Drug-free treatments offer hope for
older people in pain
Mind-body therapies, which focus on the interactions between the mind, body and behavior,
and the ways in which emotional, mental, social and behavioral factors can affect health,
may be of particular benefit to elderly chronic pain sufferers. A new study published in
Pain Medicine provides a structured review of eight mind-body interventions for older
people, including progressive muscle relaxation, meditation, hypnosis, tai chi and yoga.
A variation in the gene FOXO3A has a positive effect on the life expectancy of humans, and
is found much more often in people living to 100 and beyond – moreover, this appears
to be true worldwide. A research group in the Faculty of Medicine at the
Christian-Albrechts-University in Kiel (CAU) has now confirmed this assumption by
comparing DNA samples taken from 388 German centenarians with those from 731 younger
people. The results of the study appear this week in the prestigious American scientific
journal Proceedings of the National Academy of Sciences ("PNAS").
Don’t go changing - New
chemical keeps stem cells young
Scientists at the Universities of Bath and Leeds have discovered a chemical that stops
stem cells from turning into other cell types, allowing researchers to use these cells to
develop new medical treatments more easily. Stem cells have the ability to develop into
many other cell types in the body, and scientists believe they have huge potential to
treat diseases or injuries that don’t currently have a cure. Professor Melanie
Welham’s team at the University of Bath’s Department of Pharmacy &
Pharmacology, collaborating with Professor Adam Nelson at the University of Leeds, have
discovered a chemical that can be added to embryonic stem cells grown in the lab, allowing
them to multiply without changing into other cell types.
Recruitment of reproductive
features into other cell types may underlie extended lifespan in animals
In the sense that organisms existing today are connected through a chain of life –
through their parents, grandparents and other ancestors – almost a billion years back
to the first animals of the pre-Cambrian era, an animal's reproductive cells can be
considered to be immortal. These germline cells generate their offspring's somatic cells
– other cells involved in all aspects of growth, metabolism and behavior, which have
a set lifespan – and new germline cells that continue on, generation after
generation. Now in a dramatic finding, researchers from the Massachusetts General Hospital
(MGH) Department of Molecular Biology have found that certain genetic mutations known to
extend the lifespan of the C. elegans roundworm induce 'mortal' somatic cells to express
some of the genes that allow the 'immortality' of reproductive germline cells. Their
report will appear in the journal Nature and is receiving advance online release. "C.
elegans mutants with extreme longevity accomplish this feat, in part, by adopting genetic
programs normally restricted to the germline into somatic cells," says Sean Curran,
PhD, of MGH Molecular Biology, the study's lead author. "We know that germline cells
are more stable than somatic cells – they live longer and are more resistant to
stresses that damage other cells – and understanding the molecular pathways involved
in that stability may someday allow us to devise therapies protective against age-related
decline in other tissues." Curran is a research fellow in the laboratory of MGH
investigator Gary Ruvkun, PhD, whose work focuses on the development, longevity and
metabolism of C. elegans, a tiny worm broadly used as a model for studying basic
biological systems. Ruvkun and other researchers discovered that simple mutations in
genetic pathways conserved throughout evolution can double or triple the lifespan of C.
elegans, and that similar mutations in the corresponding pathways also dramatically extend
mammalian lifespan.
Researchers find connection between
caloric restriction and longevity
Scientists at Harvard Medical School, Cornell Medical School and the National Institutes
of Health have discovered how caloric restriction enables cells -- and many higher mammals
-- to live longer and healthier lives.
Easter Island compound extends
lifespan of old mice
The giant monoliths of Easter Island are worn, but they have endured for centuries. New
research suggests that a compound first discovered in the soil of the South Pacific island
might help us stand the test of time, too. Wednesday, July 8, in the journal Nature, The
University of Texas Health Science Center at San Antonio and two collaborating centers
reported that the Easter Island compound – called "rapamycin" after the
island's Polynesian name, Rapa Nui – extended the expected lifespan of middle-aged
mice by 28 percent to 38 percent. In human terms, this would be greater than the predicted
increase in extra years of life if cancer and heart disease were both cured and prevented.
The rapamycin was given to the mice at an age equivalent to 60 years old in humans. The
studies are part of the National Institute on Aging (NIA) Interventions Testing Program,
which seeks compounds that might help people remain active and disease-free throughout
their lives. The other two centers involved are the University of Michigan at Ann Arbor
and Jackson Laboratory in Bar Harbor, Maine.
A major mystery about the origins of life has been resolved. According to a study
published in the journal Nature, two Université de Montréal scientists have proposed a
new theory for how a universal molecular machine, the ribosome, managed to self-assemble
as a critical step in the genesis of all life on Earth."While the ribosome is a
complex structure it features a clear hierarchy that emerged based on basic chemical
principles," says Sergey Steinberg, a Université de Montréal biochemistry professor
who made his discovery with student Konstantin Bokov. "In the absence of such
explanations, some people could imagine unseen forces at work when such complex structures
emerge in nature."
People everywhere are feeling the stress of a worldwide recession. Our cells, too, are
under continual assault from stress. Hidden from sight, our cells battle challenges such
as their environment, bacteria, viruses, too much or too little oxygen, and physiological
stressors. Molecular systems protect cells under assault, but those systems can break
down, especially with age. To better understand how cells are protected from stress and
damage, a team led by Northwestern University researchers studied the effect of
resveratrol, a beneficial chemical found in red wine, on human cells in tissue culture.
The findings may help explain what happens in neurodegenerative diseases, which are
age-related, when cell protection fails, proteins misfold, lots of damage accumulates and
the system falls apart. The researchers discovered a new molecular relationship critical
to keeping cells healthy across a long span of time: a protein called SIRT1, important for
caloric restriction and lifespan and activated by resveratrol, regulates heat shock factor
1 (HSF1), keeping it active. HSF1 in turn senses the presence of damaged proteins in the
cell and elevates the expression of molecular chaperones to keep a cell's proteins in a
folded, functional state. Regulation of this pathway has a direct beneficial effect to
cells, the research shows.
The bottom-line message from a decades-long study of monkeys on a restricted diet is
simple: Consuming fewer calories leads to a longer, healthier life. A team of researchers
at the University of Wisconsin-Madison, the Wisconsin National Primate Research Center and
the William S. Middleton Memorial Veterans Hospital reports that a nutritious but
reduced-calorie diet blunts aging and significantly delays the onset of such age-related
disorders as cancer, diabetes, cardiovascular disease and brain atrophy. "We have
been able to show that caloric restriction can slow the aging process in a primate
species," says Richard Weindruch, a professor of medicine in the UW-Madison School of
Medicine and Public Health who leads the National Institute on Aging-funded study.
"We observed that caloric restriction reduced the risk of developing an age-related
disease by a factor of three and increased survival." During the 20-year course of
the study, half of the animals permitted to eat freely have survived, while 80 percent of
the monkeys given the same diet, but with 30 percent fewer calories, are still alive.
Begun in 1989 with a cohort of 30 monkeys to chart the health effects of the
reduced-calorie diet, the study expanded in 1994 with the addition of 46 more rhesus
macaques. All of the animals in the study were enrolled as adults at ages ranging from 7
to 14 years. Today, 33 animals remain in the study. Of those, 13 are given free rein at
the dinner table, and 20 are on a calorie-restricted diet. Rhesus macaques have an average
life span of about 27 years in captivity. The oldest animal currently in the study is 29
years. The new report details the relationship between diet and aging, according to
Weindruch and lead study author Ricki Colman, by focusing on the "bottom-line
indicators of aging: the occurrence of age-associated disease and death."
Children's Hospital of Pittsburgh
of UPMC scientists identify enzyme important in aging
The secret to longevity may lie in an enzyme with the ability to promote a robust immune
system into old age by maintaining the function of the thymus throughout life, according
to researchers studying an "anti-aging" mouse model that lives longer than a
typical mouse. The study, led by Abbe de Vallejo, Ph.D., associate professor of pediatrics
and immunology, University of Pittsburgh School of Medicine, and immunologist at
Children's Hospital of Pittsburgh of UPMC, reports that the novel mouse model has a thymus
that remains intact throughout its life. In all mammals, the thymus?the organ that
produces T cells to fight disease and infection?degenerates with age. Results of the study
are published in this week's issue of the Proceedings of the National Academy of Sciences.
"These findings give us hope that we may one day have the ability to restore the
function of the thymus in old age, or perhaps by intervening at an early age, we may be
able to delay or even prevent the degeneration of the thymus in order to maintain our
immune defenses throughout life," said Dr. de Vallejo.
Wistar Institute team finds key
target of aging regulator
Researchers at The Wistar Institute have defined a key target of an evolutionarily
conserved protein that regulates the process of aging. The study, published June 11 in
Nature, provides fundamental knowledge about key mechanisms of aging that could point
toward new anti-aging strategies and cancer therapies. Scientists have long known that a
class of proteins called sirtuins promotes fitness and longevity in most organisms ranging
from single-celled yeast to mammals. At the cellular level, sirtuins protect genome
integrity, enhance resistance to adverse stresses, and antagonize senescence. However, the
underlying molecular mechanisms have remained poorly understood. The team, led by senior
author Shelley Berger, Ph.D., Hilary Koprowski Professor at The Wistar Institute,
demonstrated for the first time a molecular target for a member of this class, Sir2, in
regulation of aging in yeast cells. Sir2 removes an acetyl group attached to a specific
site (lysine at position 16 or K16) on histone H4—histones are proteins that package
and organize the long strands of DNA within the nucleus and also are central regulators in
turning genes on and off. The study reveals that removal of this acetyl group by Sir2 near
the chromosome ends—the telomeres—is important for yeast cells to maintain the
ability to replicate. Researchers found that Sir2 levels decline as cells age, and there
is a concomitant accumulation of the acetylation mark along with disrupted histone
organization at telomeres. Deacetylation of H4K16 by Sir2 and consequent telomere
stability play a major role in maintaining long lifespan in yeast. Since sirtuins
deacetylate many different proteins, these results clarify a key role of Sir2 protein in
control of lifespan. "Some modifications on histones, like this acetylation on
histone H4 lysine 16, are persistent and are maintained through generations of cell
divisions. This DNA-independent inheritance is called epigenetics," Berger says.
"Characteristic epigenetic features have been discovered for various developmental
processes in recent years. Understanding epigenetic changes associated with aging is a
hugely exciting direction in aging research. It will provide insights and ideas not only
for new therapies to regulate cells that have lost control of proliferation, such as
'immortal' cells found in cancers, but also for new strategies to maintain health and
fitness." "We plan to continue to search for new targets of Sir2 and other aging
regulators," says lead author Weiwei Dang, Ph.D., a postdoctoral scientist working
with Berger. "We are designing unbiased screens for other aging targets and
mechanisms in chromatin. Using yeast as our aging model enables us to do many discovery
screens that are impossible with other, more complex organisms. Yet it is remarkable that
many of these chromatin mechanisms associated with yeast could turn out to be relevant
even for aging human cells."
Is red wine the key? Eating to improve brain chemistry? Or a low-cal, low-carb approach?
Or should nutrition be tailored to blood type? Authors have their ideas.
Dietary sport supplement shows
strong effects in the elderly
Beta-alanine (BA), a dietary supplement widely used by athletes and body builders, has
been proven to increase the fitness levels of a group of elderly men and women. The
research, published in BioMed Central's open access Journal of the International Society
of Sports Nutrition, suggests that BA supplementation improves muscle endurance in the
elderly. The research was carried out by Jeffrey Stout, PhD from the University of
Oklahoma, USA, and a team of colleagues. According to Dr. Stout, "This could have
importance in the prevention of falls, and the maintenance of health and independent
living in elderly men and women." BA is an amino acid that, together with histidine,
forms the dipeptide carnosine. Carnosine is found in muscle tissue and makes an important
contribution to the maintenance of intracellular pH, which is vital for normal muscle
function during intense exercise. An increased intake of BA significantly raises muscle
carnosine levels. In this double-blind, randomized controlled trial, 26 elderly men and
women were given a 90-day course of BA supplementation or placebo pills. Their fitness
levels were tested before and after the course. In the treatment group, 67% of the
subjects showed an improvement in their fitness levels, compared to 21.5% of the people
receiving the placebo treatment. The researchers write, "Our data suggest that 90
days of BA supplementation increases physical working capacity in elderly men and women.
These findings are clinically significant, as a decrease in functional capacity to perform
daily living tasks has been associated with an increase in mortality, primarily due to
increased risk of falls."
aging
Glucose Restriction Extends Caenorhabditis elegans Life Span by Inducing Mitochondrial
Respiration and Increasing Oxidative Stress
Accordingly, treatment of nematodes with different antioxidants and vitamins prevents
extension of life span. In summary, these data indicate that glucose restriction promotes
mitochondrial metabolism, causing increased ROS formation and cumulating in hormetic
extension of life span, questioning current treatments of type 2 diabetes as well as the
widespread use of antioxidant supplements.
Growth hormone's link to starvation may be clue to increasing life span,
researchers find
Researchers at UT Southwestern Medical Center have determined that starvation blocks the
effects of growth hormone via a mechanism that may have implications in treating diabetes
and extending life span.
Looking for the Founatain of Youth?
Cut your calories, research suggests
In addition to reducing one's risk for many common diseases, new Saint Louis University
research found that calorie restriction may slow the aging process.
Einstein researchers use novel
approach to uncover genetic components of aging
People who live to 100 or more are known to have just as many -- and sometimes even more
-- harmful gene variants compared with younger people. Now, scientists at the Albert
Einstein College of Medicine of Yeshiva University have discovered the secret behind this
paradox: favorable "longevity" genes that protect very old people from the bad
genes' harmful effects. The novel method used by the researchers could lead to new drugs
to protect against age-related diseases.
Sensory Perception of Food and
Insulin-Like Signals Influence Seizure Susceptibility
Food deprivation is known to affect physiology and behavior. Changes that occur could be
the result of the organism's monitoring of internal and external nutrient availability. In
C. elegans, male mating is dependent on food availability; food-deprived males mate with
lower efficiency compared to their well-fed counterparts, suggesting that the mating
circuit is repressed in low-food environments. This behavioral response could be mediated
by sensory neurons exposed to the environment or by internal metabolic cues. We
demonstrated that food-deprivation negatively regulates sex-muscle excitability through
the activity of chemosensory neurons and insulin-like signaling. Specifically, we found
that the repressive effects of food deprivation on the mating circuit can be partially
blocked by placing males on inedible food, E. coli that can be sensed but not eaten. We
determined that the olfactory AWC neurons actively suppress sex-muscle excitability in
response to food deprivation. In addition, we demonstrated that loss of insulin-like
receptor (DAF-2) signaling in the sex muscles blocks the ability of food deprivation to
suppress the mating circuit. During low-food conditions, we propose that increased
activity by specific olfactory neurons (AWCs) leads to the release of neuroendocrine
signals, including insulin-like ligands. Insulin-like receptor signaling in the sex
muscles then reduces cell excitability via activation of downstream molecules, including
PLC-? and CaMKII.
Shchepinov, however, is the first researcher to link the effect with aging. It dawned on
him that if aging is caused by free radicals trashing covalent bonds, and if those same
bonds can be strengthened using the isotope effect, why not use it to make vulnerable
biomolecules more resistant to attack? All you would have to do is judiciously place
deuterium or carbon-13 in the bonds that are most vulnerable to attack, and chemistry
should take care of the rest.
Insulin regulates the secretion of
the antiaging hormome Klotho
Dr. Carmela Abraham, a professor of biochemistry and medicine at Boston University School
of Medicine, reports this week in the Proceedings of the National Academy of Sciences new
findings on Klotho, an antiaging gene that is associated with life span extension in
rodents and humans. Dr. Abraham's interest in Klotho stems from her studies comparing the
expression of genes in young and old brains.
If you are a mouse on the chubby side, then eating less may help you live longer. For lean
mice – and possibly for lean humans, the authors of a new study predict – the
anti-aging strategy known as caloric restriction may be a pointless, frustrating and even
dangerous exercise. "Today there are a lot of very healthy people who look like
skeletons because they bought into this," said Raj Sohal, professor at the University
of Southern California's School of Pharmacy. He and Michael Forster, of the University of
North Texas Health Science Center, compared the life span and caloric intake of two
genetically engineered strains of mice. The "fat" strain, known as C57BL/6,
roughly doubles in weight over its adult life. That strain benefited from caloric
restriction, Sohal said. The "lean" strain, DBA/2, does not become obese.
Caloric restriction did not extend the life of these mice, confirming previous work by
Forster and Sohal. The results appeared online Jan. 13 in advance of print publication in
the Journal of Nutrition. "Our study questions the paradigm that caloric restriction
is universally beneficial," Sohal said. "Contrary to what is widely believed,
caloric restriction does not extend (the) life span of all strains of mice." By
measuring the animals' metabolic rate, Sohal and his colleagues came to a deceptively
simple conclusion: Caloric restriction is only useful when, as in the case of the obese
mice, an animal eats more than it can burn off.
Researchers unravel key mechanism
of cellular damage in aging and disease
Researchers have taken a first snapshot of how a class of highly reactive molecules
inflicts cellular damage as part of aging, heart disease, stroke, cancer, diabetes, kidney
disease and Alzheimer's disease to name a few. According to a study published today in the
journal Cell, researchers have discovered a tool that can monitor related damage and
determine the degree to which antioxidant drugs effectively combat disease.
The herbal extract of a yellow-flowered mountain plant indigenous to the Arctic regions of
Europe and Asia increased the lifespan of fruit fly populations, according to a UC-Irvine
study.
Happiness does not heal, but happiness protects against falling ill. As a result, happy
people live longer. The size of the effect on longevity is comparable to that of smoking
or not. This is concluded from an analysis of 30 follow-up studies published in the latest
issue of the Journal of Happiness Studies (September 2008).
Eating a Mediterranean-style diet, rich in fruit, vegetables, olive oil and fish, may
reduce the risk of dying from cancer and cardiovascular disease, says a new US study.
Where does the gene activity of
youth go? New findings may hold the key
New evidence may explain why it is that we lose not only our youthful looks, but also our
youthful pattern of gene activity with age. A report in the Nov. 26 issue of the journal
Cell, a Cell Press publication, reveals that a protein perhaps best known for its role in
the life-extending benefits of a low-calorie diet also maintains the stability of the
mammalian genome -- the complete set of genetic instructions "written" in DNA.
There are a lot of great anti-aging and metabolism boosting nutrients: DHA, pantethine,
acetyl-l-carnitine, carnosine, R-alpha lipoic acid, grape seed extracts – the list
goes on and on. In fact, most nutrients help cells function better and thus live longer.
So, why is resveratrol vying for the position as King of the anti-aging nutrients –
with a potent fat-burning twist thrown in for good measure?
For the first time, scientists have proof in human subjects that a derivative of an
ingredient in red wine combats some symptoms of aging. Sirtris Pharmaceuticals announced
the results here on Monday at the JPMorgan Healthcare Conference. Resveratol, naturally
found in red wine, stimulates a gene known as SIRT1, which has been linked with extended
lifespans in rodents. The new study is the first time similar effects have been replicated
in humans.
Middle-aged men want younger women, often touting their intelligence and their high
income; this is shown in research at Gothenburg University and Oxford University that
studied 400 lonely hearts ads to see how men and women choose partners Middle-aged men
want younger women, often touting their intelligence and their high income. This is shown
in research at Gothenburg University and Oxford University that studied 400 lonely hearts
ads to see how men and women choose partners. Research in the theory of evolution includes
a number of accepted theories about how men and women choose their partners. Among the
more established ones is that men place more emphasis on attractive appearance, whereas
resources and social status are more important to women. By examining lonely hearts
advertisements, researchers at the University of Gothenburg and the University of Oxford
have now tested how valid these presumed preferences are when modern individuals choose
partners.
Stowers Institute's Baumann Lab
identifies key step in maturation pathway of telomerase
The Stowers Institute's Baumann Lab has discovered an important step in the maturation
pathway of telomerase, the enzyme that replenishes the sequences that are lost at
chromosome ends with every cell division. The findings were published today in the advance
online publication of Nature.
Smoking, alcohol, low
fruit/vegetables intake, not exercising decreases life 14 years
We examined the prospective relationship between lifestyle and mortality in a prospective
population study of 20,244 men and women aged 45–79 y with no known cardiovascular
disease or cancer at baseline survey in 1993–1997, living in the general community in
the United Kingdom, and followed up to 2006. Participants scored one point for each health
behaviour: current non-smoking, not physically inactive, moderate alcohol intake
(1–14 units a week) and plasma vitamin C >50 mmol/l indicating fruit and vegetable
intake of at least five servings a day, for a total score ranging from zero to four. After
an average 11 y follow-up, the age-, sex-, body mass–, and social class–adjusted
relative risks (95% confidence intervals) for all-cause mortality(1,987 deaths) for men
and women who had three, two, one, and zero compared to four health behaviours were
respectively, 1.39 (1.21–1.60), 1.95 (1.70–-2.25), 2.52 (2.13–3.00), and
4.04 (2.95–5.54) p <0.001 trend. The relationships were consistent in subgroups stratified by sex, age, body mass index, and social class, and after excluding deaths within 2 y. The trends were strongest for cardiovascular causes. The mortality risk for those with four compared to zero health behaviours was equivalent to being 14 y younger in chronological age.
