Exercise Tips for Seniors to Start a Healthy 2009

Most fitness advice is aimed at a general audience.But if you're an older adult, the International Council on Active Aging (ICAA) has some tips for seniors to get started and keep them at the top of their game: Read more

Exercise Benefits Even the Oldest Old

Older adults who get regular exercise may live longer and be at lower risk for physical disabilities, according to an Israeli study. Read more

Good News for Elderly: Happiness Keeps Growing

The longer you live, the happier you're likely to be, a growing body of research shows. Read more

Berry Compound Reduces Aging Effects

In a new study, elderly laboratory animals that ate a diet rich in the berry and grape compound pterostilbene showed a reversal of some of the negative effects of aging on brain function and behavioral performance. Read more

Neighborhood Safety Is Linked to Disability

(HealthDay News) -- Living in unsafe neighborhoods -- or even believing that a neighborhood is unsafe -- can lead to disability among elderly, low-income people, suggests a new study. Read more

As Literacy Improves, So Might Happiness

(HealthDay News) -- Among older adults, the better they're able to read, understand and use health and medical information, the happier they are, suggests a U.S. study. Read more

Health Tip: Before Getting Plastic Surgery

(HealthDay News) -- You should do your homework before you elect to have plastic surgery.

Here are suggestions on how to prepare for the procedure, courtesy of the American Society of Plastic Surgeons:

• Research the surgery until you fully understand its possible benefits and risks.


• Talk to your doctor about what to expect after the surgery, including likely results, how much time it may take you to recover, and what the recovery period will feel like.


• Talk to other people who have had the procedure to gain their insight.


• Don't be afraid to discuss any questions or concerns with your doctor. Be sure the physician knows your complete medical history.


• Make sure the surgeon you select is qualified, properly trained, and certified to perform the procedure.

Antipsychotic Drugs of Little Benefit to Alzheimer's Patients

, (HealthDay News) -- The continuing use of antipsychotic drugs provides no cognitive or neuropsychiatric benefit for Alzheimer's patients, a British study concludes.

Researchers at King's College Hospital in London studied 165 patients who were already being treated with antipsychotic drugs. The patients were divided into two groups -- one continued treatment with the drugs, while the other group stopped treatment.

The patients were assessed six and 12 months later, and the researchers found no differences between the two groups in terms of cognitive decline or in the number of neuropsychiatric problems.

Patients with severe neuropsychiatric problems at the start of the study may have derived some benefit from continued drug therapy, but this difference was not statistically significant, the researchers said.

While these findings suggest that continued use of antipsychotic drugs offers no benefits for Alzheimer's patients, this was a small study, the study authors noted. More research is needed to improve management of these patients, they added.

The study appears in the cuurent issue of PLoS Medicine.

Almost all older dementia patients have some neuropsychiatric symptoms, such as agitation, aggression and psychosis. Antipsychotics are often used to manage or control these symptoms, but there are safety concerns, including increased risk of stroke, sedation, edema, chest infections and parkinsonism. Prolonged use of antipsychotics may also lead to a worsening of cognitive decline.

More information
The U.S. National Institute on Aging has more about Alzheimer's medications.

Age-Related Eye Disease on the Increase

(HealthDay News) -- Twice as many women as men in the United States are diagnosed with vision-threatening eye disease every year, but the numbers are increasing for both genders as the baby boomer generation enters its golden years, a newly updated report shows.

The study, from the Prevent Blindness America and the government-backed National Eye Institute, found that of more than 3.6 million Americans aged 40 and older who suffer from visual impairment, including blindness, 2.3 million are women. Potentially blinding diseases such as glaucoma, cataracts, macular degeneration and diabetic retinopathy strike women in some cases almost twice as much as men.

"Some may be under the impression that losing vision is just a simple part of the aging process, but these numbers include many women in their 40s," Daniel D. Garrett, senior vice president of Prevent Blindness America, said in a prepared statement. "It's never too early to start caring for our eyes, and we strongly encourage women to make eye health a priority for themselves and their families today."

The report shows age-related eye disease has risen for both sexes, but especially among women, who represent more than 1.3 million of the more than 2 million Americans aged 50 and older that have age-related macular degeneration.

And, approximately 6 million women and 3 million men have moderate to severe symptoms of dry eye syndrome, a condition caused when not enough natural tears are produced, according to the National Women's Health Resource Center. Postmenopausal and pregnant women are most at risk because of hormonal fluctuations, and without proper lubrication, their corneas can become damaged.

"Fortunately, there is a simple way for women to protect their vision: Get regular eye care," Garrett said.

More information
Prevent Blindness America has more about eye disease.

Injection Of Human Umbilical Cord Blood Helps The Aging Brain, Study Shows

When human umbilical cord blood cells (UCBC) were injected into aged laboratory animals, researchers at the University of South Florida (USF) found improvements in the microenvironment of the hippocampus region of the animals’ brains and a subsequent rejuvenation of neural stem/progenitor cells.

The research presented the possibility of a cell therapy aimed at rejuvenating the aged brain.

“Brain cell neurogenesis decreases dramatically with increasing age, mostly because of a growing impoverishment in the brain’s microenvironment,” said co-author Alison Willing, PhD, of the USF Center of Excellence for Aging and Brain Repair. “The increase in neurogenesis we saw after injecting UCBCs seemed to be due to a decrease in inflammation.”

According to lead author Carmelina Gemma, Ph.D., of the James A. Haley Veterans Administration Medical Center (VA) and USF, the decrease in neurogenesis that accompanies aging is a result of the decrease in proliferation of stem cells, not the loss of cells.

“In the brain, there are two stem cell pools, one of which resides in the hippocampus,” explained graduate student and first author Adam Bachstetter. “As in other stem cell pools, the stem cells in the brain lose their capacity to generate new cells. A potent stressor of stem cell proliferation is inflammation.”

Prior to this study, the research team led by Paula C. Bickford, Ph.D., of the VA and USF found that reducing neuroinflammation in aged rats by blocking the synthesis of the pro-inflammatory cytokine IL1 rescued some of the age-related decrease in neurogenesis and improved cognitive function.

“We think that UCBCs may have a similar potential to reduce inflammation and to restore some of the lost capacity of stem/progenitor cells to proliferate and differentiate into neurons,” said Dr. Bickford.

The study found that the number of proliferative cells increased within 24 hours following the UCBC injections into the aged laboratory rats and that the increased cell proliferation continued for at least 15 days following a single treatment.

“We have shown that injections of UCBCs can reduce neuroinflammation,” concluded co-author Paul R. Sanberg, Ph.D. D.Sc. director of the Center of Excellence for Aging and Brain Repair. “Our results raise the possibility that a cell therapy could be an effective approach to improving the microenvironment of the aged brain and restoring some lost capacity.”

Citation: Bachstetter, AD, Pabon, MM, Cole, MJ, Hudson, CE, Sanberg, PR, Willing, AE, Bickford, PC, Gemma, C. Peripheral injection of human umbilical cord blood stimulates neurogenesis in the aged rat brain. BMC Neuroscience, 9(1), 2008, 22 (Epub ahead of print).

The USF study was supported by the National Institutes of Health and the VA Medical Research Service.

'Testosterone link' to depression

Older men with lower levels of the male sex hormone testosterone in their blood may be more prone to depression, a study suggests.
A study of about 4,000 men aged over 70 found those with lowest testosterone were three times more likely to be depressed than those with the most.

Researchers suspect the hormone may affect levels of key brain chemicals.

The study, by the University of Western Australia, features in Archives of General Psychiatry.

Research has found that women are more likely to be depressed than men until the age of 65, when the difference between the genders almost disappears.

Testosterone levels decline with age - but there is wide variation.

The Australian team studied 3,987 men over the age of 70. Each gave blood samples and took part in tests to determine whether they were depressed.

In total 203 of the participants were assessed as being depressed.

They had significantly lower levels of both total testosterone, and free testosterone, which is not bound to proteins.

The researchers then adjusted the data to take account of factors such as educational attainment and body fat levels.

They found those men whose level of free testosterone was in the bottom 20% were three times more likely to be depressed than those in the top 20%.

The researchers said further work was required to confirm their findings.

But their work raised the possibility that treatment to boost testosterone levels in older men may be an effective way to treat depression.

Raised death risk

A previous study of 800 men over the age of 50 found that those with low levels of testosterone had a 33% increased risk of death over an 18-year period than those with higher levels.

They appeared significantly more likely to have a cluster of risk factors associated with cardiovascular disease and diabetes.

This raises the possibility that men with low testosterone levels may be prone to depression because they are also more likely to be in poor physical health.

However, the Australian researchers concluded that this could not fully explain the link, and that some other factor must also be in play.

Testosterone replacement therapy has also been shown to help elderly men with mild Alzheimer's disease.

Research has suggested that levels of testosterone in men of all ages are falling.

Professor David Kendall, an expert in pharmacology at the University of Nottingham, said there was a wealth of evidence to show that testosterone levels were linked to mood.

For instance, farmers had long castrated their stock to pacify them.

Research on animals had also shown that removal of their gonads blocked the action of anti-depressants on key mood-controlling chemicals in the brain.

"It would be no surprise that low testosterone reduces mood," he said.

"Testosterone therapy offers a relatively simple intervention, potentially, for some groups of older depressives with hypogonadism (low production of sex hormones)."

Professor Stafford Lightman, a hormone expert at the University of Bristol, said testosterone potentially had many small effects which could raise the risk of depression. For instance, low levels had been linked to poor cognitive performance.

However, he warned that depression, particularly in elderly people, was often the result of many different, inter-relating factors, and warned against placing too much emphasis on one in isolation.

"My view is that low testosterone could be a contributory factor to depression, but probably not a very powerful one," he said.

http://news.bbc.co.uk/1/hi/health/7274481.stm

How to Age-Proof Your Memory

Drink a cocktail, gossip, and other surprising ways to boost your brain power
by Ross Weale

Health magazine contributor Roshini Raj, MD, gives tips to boost your memory on Today, March 3, 2008.



DR. ROSHINI RAJ
Roshini Raj, MD, a Health magazine contributor and part of the magazine's Health Expert Network, is board-certified in gastroenterology and internal medicine with degrees from the New York University School of Medicine and Harvard University. Currently Dr. Raj is an attending physician at NYU Medical Center's Tisch Hospital in New York City. She also serves as an assistant professor at the NYU School of Medicine, and she has a special interest in women's health and cancer screening. She has also published several research articles on colon-cancer screening.

Dr. Raj has discussed health topics on numerous television outlets, including NBC's Today show, ABC's Good Morning America, CNN, FOX News, and Discovery Health. She has been quoted in publications such as the New York Times, the Wall Street Journal, Men's Health, Women's Health, and Fitness on the state of health care and other health news of the day. Dr. Raj is often called upon to explain and demystify complicated health topics.

Most Older Americans Living Longer and Better

(HealthDay News) -- Older Americans are living longer than ever and enjoying better health and financial security, a new report finds.

Yet there continue to be lingering disparities between racial and ethnic groups.

In 2006, there were an estimated 37 million Americans 65 and older -- 2 percent of the population. By 2030, it's estimated at 71.5 million people will be 65 and older -- almost 20 percent of the population, according to the report, Older Americans 2008: Key Indicators of Well-Being.

"This report comes at a critical time," Edward Sondik, director of the National Center for Health Statistics, said Thursday in a prepared statement. "As the baby boomers age and America's older population grows larger and more diverse, community leaders, policymakers and researchers have an even greater need for reliable data to understand where older Americans stand today and what they may face tomorrow."

The report examined five broad areas of well-being: economics, health status, health risks and behaviors and health care.

Even though life expectancy for Americans continues to increase for those 65 years of age, it is lower than in countries such as Canada, France Japan and Sweden. For example, Japanese women 65 years of age live 3.2 years longer than women in the United States. Among men, the difference is 1.2 years, according to the report.

In terms of overall health, key indicators such as smoking rates, flu and pneumonia vaccinations and screening for breast cancer have improved but have leveled off in recent years.

As for chronic conditions, women reported higher levels of arthritis compared with men. Men reported higher levels of heart disease and cancer. Among African-Americans, there were higher levels of high blood pressure and diabetes compared with whites. Hispanics reported higher levels of diabetes than did non-Hispanic whites.

The number of people 65 and older who are obese increased from 22 percent in 1988-1994 to 31 percent in 2000-2006. At the same time, there was no significant change in the number of older people who engaged in physical activity. In fact, most days Americans 65 and older reported spending half their time watching television. Those 75 and older, however, spent more time reading and relaxing and thinking, compared with people 55 to 64 years old.

In addition, as people aged, they spent less time visiting friends or attending social functions. Socializing declined from 13 percent of those 55 to 64 to 10 percent of those 75 and older. And, time spent devoted to sports, exercising, recreation and travel also declined with age, according to the report.

Older people's ability to obtain, process and understand health information or services -- called health literacy -- declined with age. Thirty-nine percent of people 75 and older had below basic health literacy, compared with 23 percent of people ages 65 to 74, and 13 percent of people 50 to 64.

Escalating health-care costs, particularly for prescription drugs, also affected older Americans: From 1992 to 2004, costs rose from $8,644 to $13,052. In 2004, prescription drugs made up 61 percent of out-of-pocket health costs for older Americans, the report found.

These costs are expected to be mitigated by the Medicare Part D prescription drug benefit. From 2006 to 2007, the number of people enrolled in the program increased from 18.2 million to 19.7 million, according to the report.

Despite these rising costs, many older Americans are more economically secure. From 1974 to 2006, the number of older Americans living below the poverty line decreased from 15 percent to 9 percent. In addition, the number of older Americans with higher incomes increased from 18 percent to 29 percent.

However, racial disparities existed, with net worth among whites 65 and older six times that of older African-Americans. And, more older Americans, particularly women, continued to work after 55.

The report was prepared by the Federal Interagency Forum on Aging-Related Statistics, which represents 15 agencies responsible for collecting data on aging. The last report was released in 2006.

One expert thinks that lack of physical activity and lack of social activity are the two biggest factors affecting the health of older Americans.

"It's kind of sad when you think about all the money and all the effort that has gone into physical activity awareness and that the actual amount has not increased over the last 10 years," said Colin Milner, chief executive officer of the International Council on Active Aging. "What that is saying is, we're doing something wrong."

Milner thinks new ways of getting people to be more active are needed. People don't realize that only a little physical activity can have a major impact on their health, he said.

"People see athletic activity, and they say: 'Forget it. I can't do that, I'm old,' " Milner said."We can save roughly $77 billion in health-care costs by increasing physical activity," he noted.

Milner said he's also concerned that older people spend too much time watching TV and becoming socially isolated.

"How long is it going to be before we engineer socialization out of our lifestyle," Milner said. "By 2020, depression will be the second-leading cause of premature death according to the World Health Organization. And now, you're taking socialization out of a lifestyle."

More information
To see the full report, visit the U.S. Federal Interagency Forum on Aging-Related Statistics.

Older Women Have Harder Time Preserving Muscle Than Men

(HealthDay News) -- Keeping in good shape is more difficult for older women than men because it's harder for women to replace muscle that's lost naturally as they age, say U.S. and British researchers.

The study of 29 healthy women and men, aged 65 to 80, found that women were less able to use protein to build muscle mass -- a key difference in the way women's and men's bodies react to food. This may be due to menopause-related hormone changes in women, said the researchers from the Washington University School of Medicine in St. Louis and The University of Nottingham. One possible culprit is estrogen, which is known to be needed to maintain bone mass.

The findings, published in the current issue of the Public Library of Science One, seem to fit with preliminary results showing that older women have less muscle-building response to weight training than older men. This difference is not apparent in younger women and men.

"Nobody has ever discovered any mechanistic differences between men and women in muscle loss before. This is a significant finding for the maintenance of better health in old age," and reducing demand on health-care systems, Michael Rennie, a professor of clinical physiology at the University of Nottingham, said in a prepared statement.

The findings of this new study show that it's important for older women to consume plenty of protein-rich foods such as eggs, fish, chicken and lean red meat and to do resistance training (lifting weights in a gym), the researchers said.

"Rather than eating more, older people should focus on eating a higher proportion of protein in their everyday diet. In conjunction with resistance exercise, this should help to reduce the loss of muscle mass over time. There is also a case for the beneficial hormonal effect of limited HRT (hormone replacement therapy), although this has to be balanced against the other risks associated with such treatment," Rennie said.

The researchers noted that maintaining muscle is essential in reducing the risk of falls, one of the major causes of premature death in older adults. After age 50, people lose up to 0.4 percent of muscle mass per year.

Women are at particular risk for muscle mass decline, because they tend to have less muscle and more fat than men in early and middle age, which means they're already closer to the "danger" threshold of becoming frail when they're in their 50s and 60s, the researchers said.

More information
The U.S. Centers for Disease Control and Prevention has more about healthy aging for older adults.

Low cholesterol linked to stomach cancer risk

People with very low cholesterol levels seem to be at increased risk of developing stomach cancer, Japanese researchers report.

Some studies have linked low cholesterol levels to higher death rates from cancer in general, Dr. Kouichi Asano, of Kyushu University, Fukuoka, and colleagues explain in the International Journal of Cancer. "With respect to gastric cancer, a limited number of studies suggest this inverse association, while others do not."

The researcher looked into this in a study involving some 2,600 residents of Hisayama, Japan, who were followed for 14 years.

Gastric cancers developed in 97 subjects. After accounting for age and gender, stomach cancer rates rose significantly with descending cholesterol level. For example, among subjects with the highest cholesterol levels, the gastric cancer rate was the equivalent of 2.1 cases per 1000 persons per year; among those with the lowest cholesterol, the rate was 3.9 per 1000 person-years.

"Our data suggest that patients with low serum cholesterol should consider regular gastro-intestinal examination for the prevention of gastric cancer," the investigators conclude.

http://news.yahoo.com/s/nm/20080223/hl_nm/low_cholesterol_cancer_dc

Faulty Fountains of Youth

Skin sags. Hair grays. Organs don't work quite like they used to. A gradual wearing out and running down of the body's tissues seems an inherent part of growing older. Rejuvenation of skin, muscles, and other body parts naturally declines with the passing years.

Scientifically speaking, however, this observation is much less self-evident. Some cells in a person's body can resist the tide of aging. Consider the reproductive cells a person carries that will become the cells of newborn children who have 80-plus years of life to look forward to. Generation after generation, these reproductive cells form an unbroken line stretching for millennia.

The reason that an otherwise healthy person grows old and dies remains a mystery. Scientists have suggested several suspects for why people's bodies wear out with age, including accumulated damage to DNA, free radicals, and the shortening of telomeres—the caps on the ends of chromosomes. While each of these factors may play a part, biologists acknowledge that their understanding of aging is incomplete.

Enter stem cells. Scientists have long known that people have small reservoirs of stem cells in some of their tissues, such as bone marrow. These stem cells are distinct from those found in newly fertilized embryos—the more controversial embryonic stem cells. The embryonic type can become any type of cell in the body.

Adult stem cells, in contrast, can normally generate new cells only for the tissue in which they're found: blood cells for blood, intestinal cells for the intestines. As old cells in these tissues are damaged or wear out, nearby stem cells can manufacture new ones to take their place. At the same time, the stem cells produce more copies of themselves, maintaining a seemingly indefinite pool of cells capable of churning out a stream of replacement cells.

Until recently, most scientists thought that adult stem cells existed only in tissues that need to constantly replace their cells, such as skin, blood, and the lining of the intestine. But over the past few years, researchers have found stem cells in many, perhaps most, of the body's organs and tissues. Even the brain, which scientists once thought never replaced its nerve cells during adulthood, is now known to have stem cells that make new nerve cells throughout life (SN: 6/16/07, p. 376).

With the realization that so much of the body contains self-renewing stem cells, scientists began wondering whether changes in these stem cells over time might contribute to aging.

Imagine that, as a person ages, these fountains of cellular youth might start to run dry. As the supply of fresh cells dwindles, tissues would gradually decline and show signs of age. "That was the initial model" of how stem cells could be involved in aging, says Norman E. Sharpless, a stem cell expert at the University of North Carolina in Chapel Hill. And some data support this idea.

Graying of hair, for example, could be caused by a decline in melanocyte stem cells that accompanies aging, as observed by Emi K. Nishimura and her colleagues at Dana-Farber Cancer Institute in Boston. Melanocytes make the hair pigment melanin, so depleting these stem cells eventually causes loss of hair color, the team reported in Science in 2005.

Elderly people also have diminished resistance to disease because their immune systems make fewer of the disease-fighting white blood cells known as lymphocytes. In mice, bone marrow stem cells produce fewer lymphocytes as the mice get older, Derrick J. Rossi, now at Harvard Stem Cell Institute in Cambridge, reported in 2005 in the Proceedings of the National Academy of Sciences.

Yet evidence is mounting that the connection between adult stem cells and aging is more complex. Some kinds of stem cell actually grow more abundant with age. And just as stem cells affect aging, the aging body affects stem cells.
Tinkering with time

To untangle these effects, scientists led by Thomas A. Rando of Stanford University surgically joined pairs of mice like reconnected Siamese twins. The team linked the animals' circulatory systems so that blood from each member of a pair flowed through both mice. One mouse in each pair was old; the other was young.

Scientists knew that the ability of muscle stem cells (also called satellite cells) to repair damaged muscles declines substantially with age. Rando's team wanted to find out whether such declines should be attributed to changes in the satellite cells themselves or to changes in the cells' environment as the animals aged.

"There clearly is an effect of aging on stem cells," Rando says. "But I think the other question is ... are those changes reversible or irreversible?"

Amazingly, the blood of the young mice completely restored the tissue-healing powers of the satellite cells in the older mice, Rando's team reported in 2005 in Nature. Exposure to the young blood reactivated a system of proteins inside the cells called the Notch signaling pathway, which is crucial for triggering the cells' muscle-repair functions. Notch signaling in satellite cells normally declines in old age, but Rando's experiment showed that this decline is a response to changes in the blood, not the result of an inherent wearing out of the satellite cells themselves.

This influence of the cells' environment is possible because all cells receive signals—including hormones and other messenger proteins—from their surroundings, and these signals allow the cells to behave appropriately for their context. So a change in these external messengers in aging mice could diminish the satellite cells' muscle-repair activity.

Stem cells' surroundings also wield an influence in fruit fly testes. Changes in the stem cell–harboring niche inside the testes contribute to a decline in the number of sperm-making stem cells with age, according to research by D. Leanne Jones of the Salk Institute for Biological Studies in La Jolla, Calif., and her colleagues. As the flies grew old, the niche produced less of a protein that activates a gene in the stem cells called unpaired, which triggers self-renewal of the cells, the team reported in the Oct. 11, 2007 Cell Stem Cell.

"We definitely see changes in the environment long before we start to see" signs of intrinsic aging, Jones says. In mice testes as well, "there seems to be evidence for the environment aging instead of the stem cells themselves."

In other cases, though, stem cell aging seems independent of context. Blood-forming stem cells from bone marrow age in an unusual way. When scientists transplant blood stem cells from an old mouse into a young mouse, allow the young mouse to grow old, and then repeat the process for several generations, the stem cells lose none of their ability to make copies of themselves. In fact, in some mouse strains, blood stem cells become even more numerous with age.

But that's not necessarily a good thing. While old age doesn't appear to affect blood stem cells' power of self-renewal, it does gum up their ability to make specialized offspring cells. Ideally, each time a stem cell divides, one of the daughter cells would remain a stem cell, and the other would continue dividing to produce a fresh crop of specialized cells to replenish the tissue. That way, the stem cell's lineage always contains only one stem cell at a time to replace the original, keeping the total number of stem cells constant.

For that number to increase, daughter cells must sometimes both become stem cells, decreasing production of tissue-replenishing cells.

Even when these elderly stem cells do spawn new lines of specialized cells, the process goes awry. Blood stem cells must give rise to a whole family of specialized cells: red blood cells, lymphocytes, monocytes, macrophages, and others. As the stem cells age, something goes wrong in this specialization process, skewing it away from making lymphocytes. So the old-age slump in germ-fighting lymphocytes happens not because the stem cells peter out but because they charge ahead with their specialization machinery slightly broken. In mice, this misbehaving of blood stem cells occurs even when scientists repeatedly transplant the cells into young animals, leading them to conclude that the stem cells themselves become damaged with time.
Fighting death with aging

In trying to understand how stem cells in various organs deteriorate with age, scientists have run up against the perennial nemesis of cell biology: cancer.

"Having all these cells around that can divide all the time is quite dangerous for an organism," Sharpless says. Cells continually accumulate DNA damage, but copying and segregating the DNA during cell division is particularly hazardous. Every time a cell divides, there's some error of replication.

Most of these mistakes get fixed by repair enzymes, but certain lingering errors in DNA can cause a cell to begin growing and dividing out of control, which is how cancer arises. Cells have elaborate tools for detecting DNA damage early and either fixing it or shutting down the affected cell. Recent data suggest that these mechanisms for thwarting cancer could cause the body to cull some of its own stem cell supplies.

For example, researchers led by Sean J. Morrison of the University of Michigan in Ann Arbor found a link between the decline in nerve stem cells in mouse brains and the potent anticancer gene p16. This gene causes cells to enter a dormant state called senescence. Mice bred without p16 retained significantly more of their nerve stem cells into old age than did mice that had the gene, Morrison's team reported in Nature in 2006.

The famous tumor-fighting gene p53 also reins in damaged stem cells in old age. Blocking the activity of p53 in stem cells restored populations of intestinal stem cells in elderly mice, K. Lenhard Rudolph of Hannover Medical School in Germany and his colleagues reported in the January 2007 Nature Genetics.

Whether the bodily declines that come with aging are due to the depletion of stem cells depends on which organ is in question—and on which scientist you ask. Most scientists agree that adult stem cells play an important role in aging; the other thing that they seem to agree about is that this role is complicated. "There's still a tremendous amount of debate about even the [blood stem cell] system, which is one of the best-studied systems," Jones says.

In blood and other tissues with high cell turnover, decline of stem cells may make a greater contribution to the signs of aging than it does in tissues with slower cell turnover.

In skin, which constantly produces new cells, a decline in stem cell vigor is expected by some scientists to play a big part in the sagging and poor elasticity of skin that comes with old age. For organs such as the brain and heart, which retain most of their cells throughout adulthood, signs of old age more likely come from traditional mechanisms of aging acting on the organs' mature, specialized cells.

But even this guideline may be too simple. Alzheimer's disease, a form of dementia that commonly occurs in the elderly, is characterized by plaques accumulating in the brain. Young people's brains make the plaque proteins as well, but some data suggest that immune cells called macrophages patrol the brain and clear out budding plaques. Macrophages are continuously being made by—you guessed it—blood stem cells. So even for organs in which cell renewal by stem cells proceeds very slowly, the declines of old age might be caused by the decline of adult stem cells elsewhere in the body.

Some aspects of aging will likely prove unrelated to stem cells, Sharpless says, but these cells now appear far more important for aging than scientists once thought. "I've stopped trying to predict which symptoms of aging are related to [stem cell] proliferation and which are not," Sharpless says. Scientists "used to be so confident about this 10 years ago. Now I'm prepared to be wrong."



http://www.sciencenews.org/articles/20080209/bob8.asp

Life Expectancy Tied to Education

Published: 03/11/08
TUESDAY, March 11 (HealthDay News) -- Life expectancy in the United States is on the increase, but only among people with more than 12 years of education, a new study finds.

In fact, those with more than 12 years of education -- more than a high school diploma -- can expect to live to 82; for those with 12 or fewer years of education, life expectancy is 75.

"If you look in recent decades, you will find that life expectancy has been increasing, which is good, but when you split this out by better-educated groups, the life expectancy gained is really occurring much more so in the better-educated groups," said lead researcher Ellen R. Meara, an assistant professor of health care policy at Harvard Medical School.

"The puzzle is why we have been successful in extending life span for some groups. Why haven't we been successful in getting that for less advantaged groups?" Meara said.

The answer may lie with tobacco, the study found.

About one-fifth of the difference in mortality between well-educated and less-educated groups can be accounted for by smoking-related diseases such as lung cancer and emphysema, Meara said.

But the disparity in life expectancy is not only a function of education, Meara said. "Those with less education are likely to have lower income. They're likely to live in areas that have their own health threats, either through crime or poor housing conditions. In addition, they may have worse access to health insurance coverage and health services," she said.

The study was published in the March/April issue of Health Affairs.

For the study, Meara's team collected data on people who took part in the National Longitudinal Mortality Study. The researchers used death certificates, plus estimates from Census data, to create two datasets -- one covering 1981 to 1988 and the other from 1990 to 2000.

The researchers found that in both datasets, life expectancy rose but only for people with more than 12 years of education. For those with 12 years of education or less, life expectancy remained flat through the periods.

When the researchers compared data from the 1980s to data from the 1990s, people with more education had almost a year and half of increased life expectancy. But, for people with less education, life expectancy increased by only six months.

In the period of 1990 to 2000, the better educated saw their life expectancy increase by 1.6 years. For the less educated, life expectancy didn't increase in all.

When the researchers looked at gender differences, they found that less-educated women actually had a decline in life expectancy. In 2000, those women with more than 12 years of education by age 25 could expect to live five years longer than less-educated women, the study found.

The challenge, Meara said, is to figure out ways to extend life expectancy of all groups in U.S society. "We need to get a better understanding of how we can extend these great things we're learning about how to lead healthier lives into these groups," she said.

Dr. David L. Katz, director of the Yale University School of Medicine's Prevention Research Center, thinks fighting poverty and improving education are key to increasing life expectancy among less-advantaged Americans.

"Disparities in health are a major challenge in the United States," he said. "The less affluent and less educated are also, invariably, less healthy."

Initiatives that target health disparities are always welcome, but they may not go far enough if they don't relieve underlying discrepancies in educational or economic status, Katz said.

"Despite efforts throughout the 1980s and 1990s to reduce the disproportionate mortality and morbidity burden experienced by ethnic minorities and the socio-economically disadvantaged, those burdens have persisted," Katz said. "And the gap in life expectancy between the more educated and the less has actually widened."

The take-home message is to redouble efforts to eliminate health disparities, Katz said. "Health is not a product of health care per se, but of one's life course and opportunities. Poverty and limited education are enemies to both opportunity and health. Public health efforts must strive against them as earnestly as against the diseases they drag in their wake."

In another report in the same journal issue, Rachel Kimbro, a sociology professor at Rice University, and colleagues found that immigrants with low levels of education fared better in health outcomes compared with native-born Americans, regardless of race or ethnicity.

The researchers said these differences should be taken into account when targeting programs to reach specific groups of people.

More information
For more on health-care disparities, visit the U.S. Agency for Healthcare Research and Quality.

Anti-aging, Stay Young and Healthy, Look Younger

Anti-aging, Stay Young HealthyYou can't stop getting older but you sure can keep yourself for prematurely aging, keep your body healthy and functioning correctly despite your age.

How to stay young, stay healthy and look younger with nutrition.

Strokes among middle-aged women triple

Strokes have tripled in recent years among middle-aged women in the U.S., an alarming trend doctors blame on the obesity epidemic. Nearly 2 percent of women ages 35 to 54 reported suffering a stroke in the most recent federal health survey, from 1999 to 2004. Only about half a percent did in the previous survey, from 1988 to 1994.

The percentage is small because most strokes occur in older people. But the sudden spike in middle age and the reasons behind it are ominous, doctors said in research presented Wednesday at a medical conference.

It happened even though more women in the recent survey were on medicines to control their cholesterol and blood pressure — steps that lower the risk of stroke.Women's waistlines are nearly two inches bigger than they were a decade earlier, and that bulge corresponds with the increase in strokes, researchers said.

In addition, women's average body mass index, a commonly used measure of obesity, rose from 27 in the earlier survey to 29. They also had higher blood sugar levels.No other traditional risk factors like smoking, heart disease or diabetes changed enough between the two surveys to account for the increase in strokes.

In a "pre-stroke population" of middle-age women, a tripling of cases is "an alarming increase," said Dr. Ralph Sacco, neurology chief at the University of Miami Miller School of Medicine.The study was led by Dr. Amytis Towfighi, a neurology specialist at the University of Southern California in Los Angeles, and presented at the International Stroke Conference in New Orleans.

She used the National Health and Nutrition Surveys, a federally funded project that gives periodic health checkups and questionnaires to a wide sample of Americans. Participants are routinely asked whether a doctor had ever told them they had had a stroke, and about 5,000 middle-aged people answered that question in each survey.

Researchers saw that the stroke rate had spiked in middle-aged women but stayed about the same — around 1 percent — in middle-aged men. So they looked deeper at the responses to see if they could learn why.Belly fat stood out, Towfighi said. The portion of women with abdominal obesity rose from 47 percent in the earlier survey to 59 percent in the recent one.

The change in men was smaller, and previous studies have shown that "abdominal obesity is a stronger risk factor for women than men," she said.Men traditionally have had a greater risk of stroke than women, and "women start catching up to men five or 10 years after menopause," said Dr. Philip Gorelick, neurology chief at the University of Illinois in Chicago and chairman of the stroke conference.

The new research means "we need to redefine our textbooks about stroke in women," because they may now be more at risk in middle age than men.Obesity "sets the stage for all the other risk factors to come in" like diabetes and heart disease, Gorelick added.In other news at the conference, two studies found that stroke patients were more likely to die if they went to hospitals on nights or weekends, echoing other recent studies that found similar risks for heart attack and surgery patients.

Michigan State University doctors analyzed 222,500 stroke cases at more than 850 hospitals participating in an American Heart Association quality improvement program from 2003 to 2007.In-hospital deaths were about 6 percent for those who arrived during normal business hours and had strokes caused by a clot, compared with 5 percent of those who entered the hospital after-hours. Deaths were 27 percent for off-hour strokes caused by bleeding in the brain versus 24 percent during normal hours.

A second study of 2.4 million stroke patients in California found death rates of 10 percent on weekends and nights versus 8 percent during weekdays.Despite the poorer outcomes, doctors said no one should ever delay getting help, since any delay raises the risk of death. The best treatments can only be given in the first few hours after symptoms appear.

http://news.yahoo.com/s/ap/20080221/ap_on_he_me/obesity_strokes

Weighty Evidence

Living large can mean dying large, as familiar reminders about obesity's link to cardiovascular disease and diabetes repeatedly emphasize. But those warnings often overshadow another threat from obesity: cancer. Excess weight accounts for 14 percent of cancer deaths in men, and 20 percent in women, researchers estimate. Among all preventable cancer risk factors, only smoking claims more lives.

Obesity's link to cancer should come as no surprise. Signs of that relationship began to emerge 2 decades ago. In the late 1980s, laboratory researchers found connections between cancer and insulin—one of the major hormones that responds to obesity.

While the findings got little attention then, today at least a half-dozen companies are developing cancer drugs that interfere with the hormone's cousin—insulinlike growth factor 1 (IGF-1).
"We've been working on this for 20 years," says Derek LeRoith of the Mount Sinai School of Medicine in New York City. Yet until recently, "nobody ever bought into it." After all, even if a tumor does need insulin, the rest of the body does too. The early research was seen as hardly relevant for disease treatment.

Not so today. If clinical trials find that dampening IGF-1 shrinks tumors in cancer patients, scientists will have not only a new kind of cancer drug but also a new source of insight into the interplay between body weight, metabolism, and cancer. In 2003, a study in the New England Journal of Medicine estimated that if the U.S. population were of a healthier weight, "90,000 deaths due to cancer could be prevented each year." That number may not fall for generations, as obesity rates among even the youngest Americans continue to soar.

Heavy hormones
Lower weight and more physical activity can affect the production of insulin, the hormone that allows the body to soak up fuel. After a meal, food is broken down into glucose, which is the body's main source of energy. Insulin triggers cells to take up and use glucose. As a person gains excess weight, the cells can become resistant to insulin's actions. To compensate, the pancreas begins to produce more insulin, but it can't stay in overdrive indefinitely. Eventually, insulin production will fall and blood glucose levels rise in some people.

The potent hormone IGF-1 and the related IGF-2 are very similar to insulin, helping support rapidly dividing cells, especially during childhood and adolescence. IGF-1 is a powerful driver of cell growth and body size: A toy poodle is a standard poodle with a faulty IGF-1 system.

The link between these insulinlike hormones and obesity is less clear than the connection between insulin and obesity. Although insulin and IGF-1 have individual parking places, or receptors, on a cell, some experiments suggest that at high enough levels, insulin starts to trespass on the IGF-1 receptor, LeRoith says.

In the late 1980s, laboratory researchers demonstrated that IGF-1 might have a role in cancer. Tumor cells were found to contain the IGF-1 receptor. In 1989, experiments with mice showed that blocking the receptor with an antibody could stop tumor growth. Researchers also found that mice bred to lack IGF-1 receptors in all their tissues were born tiny, thereby establishing the hormone's significance in growth. More important for cancer research, cells taken from the miniature mice lacking IGF-1 receptors could not be transformed into tumor cells.

"A cancer cell has to have the IGF-1 receptor," says Renato Baserga of the Kimmel Cancer Center at Thomas Jefferson University in Philadelphia, one of the field's pioneers. "If not, it cannot grow."

At first, results like these were puzzling. Unlike cancer genes that encode other proteins and start down the path to cancer after mutating, the IGF-1 receptor gene wasn't altered in tumors. Also, IGF-1 receptors show up in normal tissues throughout the body. The hormone itself is such a basic substance for animal life that even flies produce it. It was hard to imagine that a normal receptor found in normal cells could have anything to do with cancer.

Then scientists had an idea. Malignant cells may be overly dependent on IGF-1 receptors, on a scale far surpassing the dependence of normal cells. A tumor is like a car—a gas-guzzling Hummer—with a stuck accelerator and no brakes. Even if IGF-1 doesn't spark the ignition, the hormone keeps the gas tank full. Block IGF-1, according to this line of thinking, and the tumor suddenly finds itself running on empty.

Fueling cancer
Still, this notion might have stalled without two other developments. First, epidemiological studies began to find links between cancer and the insulin-IGF axis in people. Then, the entire field of cancer treatment underwent a transformation.

"What got people's attention was the epidemiologic data," says Doug Yee of the University of Minnesota Cancer Center in Minneapolis. In 1998, researchers reported in the journal Science that the risk of prostate cancer among men with the highest circulating levels of IGF-1 was four times as great as the risk among men with the lowest IGF-1 levels. Similar findings quickly followed in breast, colon, and other cancers.

So far, colon cancer has the most consistent association with insulin and IGF-1 levels, says Edward Giovannucci of the Harvard School of Public Health, a coauthor of the 1998 Science study. In 1999, he and his colleagues reported that colon cancer rates were more than twice as high among men who had the highest levels of IGF-1 as they were among men with the lowest IGF-1 levels.

Such findings fit with global patterns of the disease. "If you look at the rates of colon cancer across the world, populations where you expect people to have low insulin invariably have low rates of colon cancer," Giovannucci says. Physical activity and reduced calorie intake can lower insulin levels; populations with more sedentary jobs and calorie-dense diets have higher rates of obesity and higher insulin levels.

"Once you become economically developed, colon cancer rates go up," Giovannucci says. Also, the risks for colon cancer read largely like a list of red flags for type 2 diabetes. Diabetes itself is a risk factor for colon cancer.

Scientists are quick to point out that a higher insulin level isn't the only chemical change that can occur with obesity. Levels of hormones that cause inflammation also rise, as do sex hormones, which can be produced in fat tissue. These and other changes in the body could themselves drive cancer. Or all these fluctuations could work in concert to feed malignancies.

And it might be not only the IGF-1 of middle age that matters, but also the IGF-1 production that orchestrates development early in life. Studies have suggested that babies born at the highest birth weights—and children experiencing early growth spurts—have a greater risk of cancer as adults.

While epidemiologists gathered evidence for a relationship between insulin and cancer, a second, unrelated advance gave the insulin-cancer connection new life: treatment success using antibodies that can attach to precise targets. Antibody-based drugs are large molecules that take the parking space so its rightful owner can't use it. Herceptin, an antibody-based breast cancer treatment, came on the market in 1998, followed by others. Targeted antibodies were suddenly more than theory.

"I think once people got more comfortable making these drugs, the floodgates opened," says Yee. And when pharmaceutical companies started casting for other promising targets for antibody development, the IGF-1 receptor suddenly looked attractive.

"They turned around and said, 'You know, there's this IGF receptor,'" says LeRoith of Mount Sinai. Drug development didn't happen, and perhaps couldn't have, until epidemiology and the technology caught up with the laboratory evidence.

Broad target
Nonetheless, an antibody that interferes with IGF-1 in people raises concerns. Although the full role of IGF-1 in adult tissues is still being worked out, rapidly growing tissues such as those in bone marrow and the intestine might become innocent by-standers of chemotherapy.
"You're going to hit a receptor that's present on every cell in the body, except the liver," LeRoith says.

Also, in a case of molecular friendly fire, the drug might hit unintended targets. Because the insulin receptor and the IGF-1 receptor are cousins—they are actually more than 70 percent alike—some drugmakers worry about the possibility of accidentally interfering with the insulin receptor and making a cancer patient diabetic.

As an endocrinologist, LeRoith isn't as disturbed by these scenarios as some of his colleagues may be. He believes chemotherapy-induced diabetes would be only temporary, and treatable. In the larger picture, it would not be as grave a threat as the cancer itself. Also, he says, chemotherapies already on the market cripple rapidly growing cells in the intestine, bone, and elsewhere. While these drugs do cause notorious side effects, the complications are generally accepted as the price of disease treatment.

So far, though, the experimental drugs haven't caused major problems in early tests. Results of the first human-safety studies are starting to appear, most just in the past few months. The results are encouraging enough that companies are easing into larger studies.

"This was a target that was on everybody's radar screen, but nobody jumped so strongly at it," says Kapil Dhingra of Roche Pharmaceuticals in Nutley, N.J.

They have now. In October, at the International Conference on Molecular Targets and Cancer Therapeutics, researchers from Roche described a study of 34 patients with advanced tumors who received infusions of an experimental drug designed to target the action of IGF-1. Disease in nine patients stabilized. The most common side effects were fatigue, weight loss, and anorexia—complaints that are also often found in patients with advanced cancer. Subjects' blood sugar levels appeared to remain stable.

The trial was designed to test the safety, and not the effectiveness, of the drug. But the researchers noted that it seemed to have a remarkable result in one of the study participants with Ewing's sarcoma, a cancer of children and young adults that Yee in Minnesota had long ago identified as feeding heavily off IGF-1.

"We have a patient, a young woman in her 20s, who really has had honestly one of the best responses I've seen in 20 years," says Razelle Kurzrock of the University of Texas M.D. Anderson Cancer Center in Houston. "When you see something like that in cancer, you've usually hit the molecular target."

Within 6 weeks, the woman's tumor melted away. The results were promising enough that Roche plans to test more patients.

The antibody-based drug that appears to be the farthest along in testing comes from Pfizer Inc., which has moved beyond safety studies into tests that gauge its effectiveness on cancer. Last summer, during a meeting of the American Society of Clinical Oncology, company researchers described results of a trial involving 70 patients with advanced lung cancer. About 46 percent of patients who received the drug in combination with standard chemotherapy improved, compared with 32 percent of those who did not get the anti-IGF-1 drug. Twenty percent of the patients getting the treatment experienced a jump in blood-glucose levels, implying some interaction with insulin. Later this year, the company hopes to report the effects of treatment on patient survival.

Other companies are also working on antitumor antibodies or on smaller molecules that will block the IGF-1 receptor. In the end, researchers say, the drugs may have a role in combination with standard treatments, and trials will probably also find that some tumors are more dependent than others on IGF-1.

"It's not realistic to think that any one target is going to hit all of them," says Kurzrock. Still, she says, "I would say this is going to be a good molecule." If so, a line of research almost lost to the past could one day benefit cancer patients of the future.

http://www.sciencenews.org/articles/20080216/bob9.asp