TUESDAY, March 4 (HealthDay News) -- There's no proof that any one of the five drugs available in the United States to treat dementia is better than the others, says an American College of Physicians (ACP) and American Academy of Family Physicians (AAFP) committee that just issued a new guideline on drug treatment of dementia.

The committee reviewed published studies for outcomes such as cognition, global function, behavior/mood, and quality of life/activities of daily living. But the committee said it found only limited high-quality scientific evidence about the effectiveness of the drugs and therefore developed the following cautious recommendations:

• The decision to use approved drugs for dementia should be based on an individualized patient assessment.
• The choice of drugs should be based on tolerability, adverse effect profile, ease of use, and cost.
• There's an urgent need for more clinical research to improve knowledge about the clinical effectiveness of drugs treatment for dementia.

The committee recommended the following kinds of research:

• Evaluate the effectiveness of drug therapy for dementia and assess whether treatments affect key outcomes, such as institutionalization.
• Evaluate the appropriate duration of therapy.
• Head-to-head testing of drugs.
• Test drugs in combination therapy.

The guideline are published in the March 4 issue of the Annals of Internal Medicine.

Currently, there are five FDA-approved drugs for treatment of dementia. These include four acetylcholinesterase inhibitors -- donepezil (Aricept), galantamine (Razadyne, Reminyl, Nivalin), rivastigmine (Exelon), and tacrine -- and one neuropeptide-modifying agent -- memantine (Mamenda).

While these drugs may improve symptoms or slow disease progression, they don't cure dementia or repair brain damage.

"Doctors, patients and family caregivers desperately want information on how to treat this disease," Dr. Amir Qaseem, senior medical associate in the ACP's Clinical Programs and Quality of Care Department, said in a prepared statement. "It is disheartening to find that all we have to work with is these five drugs, and the evidence on these is scant. Consider that in 50 years, one in 45 Americans will suffer from Alzheimer's disease. This is a huge problem."

Most of existing studies of the five approved dementia drugs focused on statistical significance of changes, but clinically important improvement is what matters to patients, caregivers and doctors, the committee noted.

"More research is warranted, because the available evidence concerning these pharmaceuticals' effects on quality of life is mixed, and the clinical significance of many of the findings is questionable," Dr. Kenneth G. Schellhase, an AAFP representative on the committee, said in a prepared statement. "In addition, the duration of existing trials was usually less than one year, providing insufficient information to determine the optimal length of treatment, and few trials compare one drug directly with another."

More information

The Family Caregiver Alliance has more about dementia  .

TUESDAY, March 4 (HealthDay News) -- A rare gene mutation that restricts a particular growth factor may be one of the keys to living to 100 and beyond, a new study suggests.

This mutation, which seems to decrease the activity of insulin-like growth factor (IGF-1), results in short stature but longer life. Exactly why this might lengthen someone's life isn't known, but the researchers say the finding might prove useful in developing anti-aging drugs.

"We found that people of a hundred years old have mutations in a gene that is related to the growth hormone pathway," said lead researcher Dr. Nir Barzilai, director of the Institute for Aging Research at the Albert Einstein College of Medicine in New York City. "We think this is important, because that's what now happens in nature. The pony lives longer than the horse, the small dog lives longer than a large dog. Apparently, it's true for humans also."

Interestingly, this particular mutation has been found mostly among women, he added.

It might be possible, given these findings, to develop drugs that can prevent aging and age-related disease, Barzilai noted. "There are drugs being developed to decrease growth hormone in patients with tumors, because sometimes cancer is dependent on growth hormones," he said. "Maybe we can adopt the strategy to slow aging."

The report was published in this week's online issue of the Proceedings of the National Academy of Sciences.

In the study, Barzilai's team looked for this mutation among a population of Ashkenazi Jews who were 100, and their offspring. They also matched these offspring with people who had no history of longevity in their family. The researchers found this particular mutation was more common among those who were centenarians and their offspring. The same research team reported in December 2006 that a particular gene variant that is linked to longevity is also associated with improved mental function in the elderly.

How long growth hormones need to be restricted to produce the slowing of aging isn't known. "Do you have it during early development in the womb, in puberty, or can you have it at any stage that you wish?" Barzilai asked.

Barzilai noted that growth hormone is a very popular anti-aging therapy. Growth hormone changes the tone of the skin and fat distribution, and increases muscle mass.

"However, this study and other studies suggest that, for the purpose of aging and longevity, growth hormone might do exactly the opposite," he said. "In the short run, growth hormones are going to have positive effects, but certainly in elderly people I would suggest, and this study supports the notion, that we will kill them sooner rather than later."

One expert thinks the findings are intriguing but inconclusive.

"This is an interesting study, which has to be replicated by other researchers using a different dataset, because studies on exceptional longevity often cannot be replicated," said Leonid Gavrilov, a research associate at the Center on Aging at the University of Chicago.

The study found a sex-specific increase in IGF-1; it showed up only among the daughters of centenarians, while sons were not affected, Gavrilov noted. "The study does not suggest any explanation, or even a hypothesis, for this sex-specific effect. General conclusions suggested in this paper may be questionable if they are not applicable to men," he said.

"It may be interesting to put this study in a context of other findings, such as being born to a young mother helps to live to 100 years," Gavrilov said.

More information

For more on aging, visit the National Institute on Aging.

MONDAY, Feb. 25 (HealthDay News) -- While the number of elderly Americans newly diagnosed with heart failure has declined, the number of those living with the condition has increased, new research finds.

The Duke University study analyzed data on 622,789 Medicare patients, aged 65 and older, diagnosed with heart failure between 1994 and 2003. It found that the annual occurrence of heart failure decreased from 32 per 1,000 person-years (years of observation time during which each person is at risk to develop the disease) in 1994, to 29 per 1,000 person-years in 2003.

When the researchers looked at specific age groups, they found a sharper decline among people aged 80 to 84 (from 57.5 to 48.4 per 1,000 person-years), and a slight increase among those aged 65 to 69 (from 17.5 to 19.3 per 1,000 person years).

Between 1994 and 2003, the number of people living with heart failure increased, from about 140,000 to 200,000. More men than women live with the condition.

"The proportion of [Medicare] beneficiaries with a heart failure diagnosis increased from 90 per 1,000 in 1994 to 120 per 1,000 in 2000, and remained at about 120 per 1,000 through 2003," the authors wrote.

The findings are published in the Feb. 25 issue of the Archives of Internal Medicine.

"Although the incidence of heart failure has declined somewhat during the past decade, modest survival gains have resulted in an increase in the number of patients living with heart failure," the researchers concluded. "Identifying optimal strategies for the treatment and management of heart failure will become increasingly important as the size of the Medicare population grows."

Almost 5 million people in the United States have heart failure, which kills more than 300,000 patients a year. Since it's primarily a disease of older people, it places a significant and increasing burden on Medicare, said the study authors, who noted that the number of people age 65 and older hospitalized for heart failure increased by more than 30 percent from 1984 to 2002.

More information

The American Heart Association has more about heart failure  .

THURSDAY, Feb. 21 (HealthDay News) -- Nodding off in front of the television, or anywhere else for that matter, may raise your risk of stroke, a new study from Columbia University shows.

"These authors report a potentially important association between daytime dozing, which should correlate with excessive daytime drowsiness," said Dr. Steven V. Pacia, director of neurology at Lenox Hill Hospital in New York City. "It is not clear why this is a marker of stroke."

The findings were slated to be presented Thursday at the American Stroke Association's International Stroke Conference, in New Orleans.

The authors, from the Columbia University College of Physicians and Surgeons in New York City, suspect that stroke and dozing off may be linked via a condition known as sleep apnea.

According to previous studies, daytime sleepiness is associated with various sleep disorders including sleep apnea. Other studies have linked sleep apnea -- when a person briefly stops breathing while asleep -- with a heightened risk of stroke.

In the study, the New York researchers first assessed the daytime sleepiness of almost 2,200 Manhattanites who had not had a stroke.

Participants were asked to report how often they dozed off during specific situations such as watching TV, having a conversation and stopping briefly in traffic while driving.

Based on these responses, participants were categorized as "no dozing" (44 percent), "some dozing" (47 percent) and "significant dozing" (9 percent). Dozing was defined as unintentionally falling asleep.

In 2.3 years of follow-up, people classified with "some dozing" were 2.6 times more likely to have a stroke than "no dozers," while "significant dozers" were 4.5 times more likely to have a stroke.

Occasional dozers were 1.6 times more likely to have a vascular event (such as a heart attack) compared with no dozers, while significant dozers were 2.6 times more likely to have such an event.

The impact of sleepiness was about the same regardless of gender, race or ethnicity.

The issue deserves further probing, Pacia said.

"The study controlled for obesity, which is often associated with obstructive sleep apnea and drowsiness, but it would be important to study the entire group to determine if sleep apnea was present in the dozing patients," he said.

"Another important factor to investigate would be the presence of silent strokes or other brain abnormalities on MRI in the dozing patients prior to their first clinical stroke," Pacia added. "Finally, medications may be associated with drowsiness and may be markers of concurrent illness in the dozing patient group. Investigating prescription and over-the-counter medications in these patient at risk for stroke may also shed some light on the findings."

In the meantime, said the study authors, physicians might well be advised to assess their patients for sleep problems.

More information

Learn more about stroke at the American Stroke Association  .