Alternative Medicine News

Study: Laughter Aids Healthy Blood Vessel Function.

Researchers at the University of Maryland School of Medicine in Baltimore have shown for the first time that laughter is linked to healthy function of blood vessels. Laughter appears to cause the tissue that forms the inner lining of blood vessels, the endothelium, to dilate or expand in order to increase blood flow.

Researchers used laughter-provoking movies to gauge the effect of emotions on cardiovascular health,

When the same group of study volunteers was shown a movie that produced mental stress, their blood vessel lining developed a potentially unhealthy response called vasoconstriction, reducing blood flow.

That finding confirms previous studies, which suggested there was a link between mental stress and the narrowing of blood vessels. . Researchers note that the endothelium has a powerful effect on blood vessel tone and regulates blood flow, adjusts coagulation and blood thickening, and secretes chemicals and other substances in response to wounds, infections or irritation.

It also plays an important role in the development of cardiovascular disease.

"The endothelium is the first line in the development of atherosclerosis or hardening of the arteries, so, given the results of our study, it is conceivable that laughing may be important to maintain a healthy endothelium, and reduce the risk of cardiovascular disease," says principal investigator Michael Miller, M.D., director of preventive cardiology at the University of Maryland Medical Center and associate professor of medicine at the University of Maryland School of Medicine.

"At the very least, laughter offsets the impact of mental stress, which is harmful to the endothelium." The study included a group of 20 non-smoking, healthy volunteers, equally divided between men and women, whose average age was 33. The participants had normal blood pressure, cholesterol and blood glucose levels.

Each volunteer was shown part of two movies at the extreme ends of the emotional spectrum. They were randomized to first watch either a movie that would cause mental stress, such as the opening scene of "Saving Private Ryan" (DreamWorks, 1998), or a segment of a movie that would cause laughter, such as "King Pin" (MGM, 1996).

A minimum of 48 hours later, they were shown a movie intended to produce the opposite emotional extreme. Before seeing a movie, the volunteers fasted overnight and were given a baseline blood vessel reactivity test to measure what is known as flow-mediated vasodilation.

For that test, blood flow in the brachial artery in the arm was restricted by a blood pressure cuff and released. An ultrasound device then measured how well the blood vessel responded to the sudden increase in flow. Volunteers watched a 15-minute segment of the movie while lying down in a temperature-controlled room. After the movie was shown, the brachial artery was constricted for five minutes and then released.

Again, ultrasound images were acquired. Changes in blood vessel reactivity after the volunteers watched a movie lasted for at least 30 to 45 minutes. A total of 160 blood vessel measurements were performed before and after the laughter and mental stress phases of the study.

There were no differences in the baseline measurements of blood vessel dilation in either the mental stress or laughter phases. But there were striking contrasts after the movies were seen.

Brachial artery flow was reduced in 14 of the 20 volunteers following the movie clips that caused mental stress. In contrast, beneficial blood vessel relaxation or vasodilation was increased in 19 of the 20 volunteers after they watched the movie segments that generated laughter.

Overall, average blood flow increased 22 percent during laughter, and decreased 35 percent during mental stress. Several volunteers had already seen "Saving Private Ryan," says Dr. Miller, but even so, some of them were among the 14 with reduced blood flow.

"The magnitude of change we saw in the endothelium is similar to the benefit we might see with aerobic activity, but without the aches, pains and muscle tension associated with exercise," says Dr. Miller.

"We don't recommend that you laugh and not exercise, but we do recommend that you try to laugh on a regular basis. Thirty minutes of exercise three times a week, and 15 minutes of laughter on a daily basis is probably good for the vascular system." Dr. Miller says this study was not able to determine the source of laughter's benefit. "Does it come from the movement of the diaphragm muscles as you chuckle or guffaw, or does it come from a chemical release triggered by laughter, such as endorphins?" he asks.

Dr. Miller says a compound called nitric oxide is known to play a role in the dilation of the endothelium. "Perhaps mental stress leads to a breakdown in nitric oxide or inhibits a stimulus to produce nitric oxide that results in vasoconstriction," says Dr. Miller.

(EDITOR'S NOTE: The Mayo Clinic has noted that l-arginine, an amino acid, "is a precursor of nitric oxide, which causes blood vessel relaxation (vasodilation), and that preliminary evidence suggests that arginine may be useful in the treatment of medical conditions that are improved by vasodilation, such as angina, atherosclerosis, coronary artery disease, erectile dysfunction, heart failure..." L-arginine is available over-the-counter in pills and capsules.)

The current study builds on earlier research Dr. Miller conducted on the potential benefits of laughter, reported in 2000, which suggested that laughter may be good for the heart.

In that study, answers to questionnaires helped determine whether people were prone to laughter and ascertain their levels of hostility and anger.

Three hundred volunteers participated in the study. Half of them had suffered a heart attack or had undergone coronary artery bypass surgery; the other half did not have heart disease.

People with heart disease responded with less humor to everyday life situations than those with a normal cardiovascular system. Dr. Miller says certain factors in the earlier study may have affected the results. For example, he says it may be that people who have already had a coronary event are not as laughter-prone as those who do not have heart disease. He says the current study sought to eliminate that uncertainty by using volunteers whose cardiovascular system was healthy. The results of the brachial artery blood flow measurements, which are precise and objective, appear to make the connection between laughter and cardiovascular health even stronger, according to Dr. Miller.

Other researchers in the study included Charles Mangano, R.D.M.S; Young Park, M.D.; Radha Goel, M.D.; Gary Plotnick, M.D. and Robert A. Vogel, M.D., all from the University of Maryland School of Medicine. The study was supported by a grant from the National Institutes of Health and a Veterans Affairs Merit award to Dr. Miller.                                                                    Top | Home

"A Snail-Like WHO Needs
a Shakeup"

Bill Gates speaks during a press conference prior to addressing the 58th World Health Assembly at the United Nations in Geneva, Switzerland, in May.

May 25, 2005) -- When delegations from 192 nations gathered last [month] in Geneva for the 58th annual World Health Assembly, the buzz in the hallways had little to do with the agency that the assembly governs, the World Health Organization. Instead, everyone was talking about Bill Gates.

As the WHO director-general, Dr. Lee Jong-wook of South Korea, droned his way through the opening keynote speech, about 2,000 heads craned to see Gates take his seat in the United Nations' august Palais des Nations. Soon after, the Microsoft founder announced that the Bill & Melinda Gates Foundation would increase its donations for research into "breakthrough" medicine from $200 million a year to $450 million and would up its support for the search for an AIDS vaccine by $400 million. He got a standing ovation from an awestruck, star-struck crowd.

It's hard not to cheer wildly. The Gates Foundation has given $4.2 billion to global health initiatives over the last 9 1/2 years, and you'd be hard-pressed to find any global health effort based in the United States that isn't getting Gates' money directly or via a secondary agency. (Full disclosure: The foundation partially funds the Global Health Program, which I run at the Council on Foreign Relations.)

But although Gates' money sets the agenda for a great deal of public health policy, it's important to remember what it isn't doing and won't do -- the job of the WHO and the World Health Assembly.

The Gates Foundation, which has to answer only to its board, is adamant about its decision to primarily fund the search for cures and new treatments, rather than broader efforts to fight disease. It's a controversial position. An article in the British medical journal The Lancet recently took Gates to task, suggesting that trying to combat malaria, for instance, without also addressing problems like hygiene and water delivery could backfire.

In contrast to the agile, focused -- but unaccountable -- Gates Foundation, the WHO is governed by its often-embattled member states and lumbers along at a snail's pace, burdened by an obvious lack of clarity about its mission.

The problem isn't money, although more would help. The core budget of the WHO is just $400 million, but it doesn't operate on that sum alone. More than 70% of its budget comes from wealthy-nation donors supporting specific programs, which brings real spending to about $1.5 billion a year. (Still not a big number; it's roughly the same as the annual budget of the New York City Department of Health.)

But because the WHO is so reliant on that wealthy-donor "soft money," its mission is swayed -- in too many directions -- by those countries' agendas, ideologies and pet projects. In a world of globalized health threats, this is nuts. The WHO has to be able to put its resources where its experts can empirically show they are most needed.

Last week alone there were 16 disease outbreaks in 13 countries, including deadly Ebola and Marburg viruses, polio, meningitis and, most ominous of all, avian flu. Scientists fear that it could mutate and cause a contagious killer pandemic.

Yet right now, the entire global alert and response operation for epidemics at the WHO is -- brace yourself -- five people, out of roughly 6,000 employees.

The Gates Foundation isn't going to deploy emergency response teams around the world, send scientists in spacesuits wading into Marburg outbreaks or lead a global response to pandemic flu. That's the WHO's job.

The delegates to the World Health Assembly have the power to remake the WHO. Instead of shifting personnel and funds from Geneva headquarters to regional offices, the WHO should establish a smart, mobile global health force, based in Geneva, that can respond to crises around the world. Wealthy nations should be urged -- shamed -- into funding it, for the sake of their own survival.

And instead of beefing up mini-WHO bureaucracies around the world, the agency should fix public health systems in poor countries -- training personnel, funding labs and communication systems so that local healthcare workers can respond to new disease outbreaks.

Bill and Melinda Gates deserve a global standing ovation. But the delegates at the World Health Assembly cannot afford to be even temporarily blinded by Gates' star power and generosity. Could they hear what he said as they cheered?

"The world is failing billions of people," he warned. "There is no bigger test for humanity than the crisis of global health."
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A Snail-Like WHO Needs a Shakeup
An avian flu pandemic could kill millions
Insomnia Linked to Depression in Elderly

Alternative Medicine News:
Laughter Aids Healty Blood Vessel Functions

An avian flu pandemic could kill mi llions.

When we think of major threats, the first to come to mind are nuclear proliferation, rogue states and global terrorism. But another kind of threat is lurking, one from nature, not humans - an avian flu pandemic. An outbreak could cause millions of deaths and threaten the security of governments around the world. A FLU pandemic could cause hundreds of millions of deaths, according to a warning published in The New England Journal of Medicine.

With vaccine production based on 1950s technology and the system for distributing vaccine “broken, both technically and financially”, the world is ill-prepared for such a pandemic, Michael Osterholm, Professor of Public Health at the University of Minnesota, said. Such a pandemic is inevitable, he said. All that was at issue was when it would begin. It could be caused by the avian flu circulating in Asia or by another strain of the virus.

But only if such a pandemic were a decade away, and a Manhattan Project aimed at producing vaccine for everyone in the world were launched now, would it be possible to make a difference.

If the pandemic struck this year or next, vaccine production could not meet the need and even antiviral drugs would be in short supply. The 1918-19 Spanish flu killed 50 million to 100 million people, Professor Osterholm said, although the figure of 20 million to 40 million is more often cited. If the same death rate obtained in a new pandemic, with the world population greatly expanded, the death toll would be upwards of 360 million. In a separate commentary in the British Medical Journal, a British GP wrote that governments must stop burying their heads in the sand. Nigel Higson, a Hove GP, said that the Asian tsunami would pale into insignificance when compared with an influenza pandemic. Hundreds of millions would die if the world did not act. He said that governments must fund the rapid development of a vaccine against the H5N1 strain of flu as well as stockpile antiviral drugs. Dr Higson said: “GPs and other prescribing practitioners must learn the practicalities of treating epidemic or pandemic influenza and be prepared to prescribe appropriately in all cases of true influenza, to gain experience with the available drugs as well as encouraging increased pharmaceutical company capacity.”

Avian flu, spreading from birds to human beings, has killed more than 50 people in Asia since 2003. Dr Osterholm said that the increasing rate of transmission to human beings is a warning sign.


 

 

 

Insomnia Linked to Depression in Elderly

MONDAY, June 27, 2005 (HealthDay News) -- Chronic insomnia may provoke and perpetuate depression among the elderly, two new studies claim. One study found that elderly patients with a history of depression were more likely to continue being depressed over the course of a year if they also suffered from persistent insomnia.

The second study suggested that even without a history of depression, elderly patients -- particularly women -- who struggle with chronic sleeplessness are at a higher risk for becoming severely depressed than patients who report no trouble sleeping. Both studies are the result of work being conducted at the University of Rochester Sleep and Neurophysiology Research Laboratory. They were presented recently at the Associated Professional Sleep Societies annual meeting in Denver.

"The biggest question for us now is can we get to those cases where elderly people have chronic insomnia and treat that -- and prevent or at least delay chronic depression," said Dr. Michael Perlis, the sleep lab's director. Taken together, the findings support the notion that insomnia may be more than a symptom of depression; it may also be a cause. Perlis' team notes that 2 million older Americans suffer from some form of severe depression, characterized by a loss of hope and profound sadness. Another 5 million cope with milder forms of the illness. And prior research suggests that more than 40 percent of the elderly face trouble getting a good night's sleep, the researchers added.

In the Rochester lab's first study, researchers tracked the mental health of more than 1,800 men and women over the age of 65 diagnosed with severe and/or mild depression. After determining whether or not participants had persistent insomnia, the patients were assessed twice, first at the six-month mark and then after one year, for signs of depressive illness. Individuals who suffered from insomnia were almost 11 times more likely to continue being depressed after six months and 17 times more likely to be depressed after a year compared to non-insomniacs.

In the second study --scheduled for publication in the Journal of Behavioral Sleep Medicine -- Perlis and his team focused on 147 men and women over the age of 60 with no history of mental illness at the start of the study. Thirty-four of the patients suffered from persistent insomnia, 47 had less persistent "indeterminate insomnia," while 66 had no sleep troubles. After conducting two tests spread over a one-year period, the researchers found that 12 patients experienced new-onset depression during the course of the year. Half of these newly depressed patients suffered from persistent insomnia, the investigators note, while four had indeterminate insomnia. Two had no trouble sleeping.

Persistent insomniacs most at risk for developing depression were the so-called "middle insomniacs" -- those whose sleep patterns were typically disturbed by waking up in the middle of the night. Overall, elderly patients with persistent insomnia are six times more likely to experience serious new-onset depression than individuals who sleep easily, the authors concluded.

However, they also noted that 10 of the 12 depressed patients were women, and all the patients who became depressed while suffering from a persistent form of insomnia were female.

Perlis said its unclear why elderly women might be at especially high risk for the insomnia-depression connection.

"What we do know is that insomnia is a risk factor for depression, it precedes depression, and it seems to make depression resistant to treatment," he said. "Insomnia is a clear and present danger for depression."

Dr. Gregg Jacobs, of the Sleep Disorders Center at Beth Israel Deaconess Medical Center in Boston, was slightly more cautious.

"It's an interesting finding, and it's provocative, but the number of patients studied is way too small to be meaningful," he remarked. "And although there is evidence from prior studies that insomnia seems to predict new cases of depression, the actual risk is very low."

Perlis and Jacobs agreed, however, that more research is needed to explore whether insomnia itself is directly related to depression or whether it is instead a red flag for other factors that might make a patient more likely to develop both insomnia and depression. Treatments for both conditions were also a topic of discussion at the sleep conference, where Sepracor, the makers of the new sleep medication Lunesta, presented four studies focused on the effectiveness of that drug.

Researchers from the University of Pittsburgh School of Medicine, as well as Wake Forest University Medical Center and Duke University Medical Center announced the findings. Lunesta was approved as a prescription sleep aid by the FDA in April. To date, it is the only sleep medication deemed safe for long-term use of up to six months.

In the first Pittsburgh study, involving 545 men and women suffering from both insomnia and depression, researchers explored how well the prescription drug works when taken in combination with Prozac, an antidepressant.

When compared to patients who took only Prozac, the researchers found those taking both medications over an eight-week period were able to fall asleep faster, sleep longer, and stay asleep with less disruption.

The drug combo also improved sleep quality and depth, while boosting alertness and the ability to concentrate throughout the day. And in a second Pittsburgh study, patients who took Lunesta for a full year experienced improved sleep habits across the board. Patients who took Lunesta for just six months -- after taking a placebo for the prior six months -- experienced a quick and notable improvement in their sleep habits shortly after beginning the Lunesta regimen.

In the Wake Forest study, researchers reported that patients taking this same Lunesta-Prozac combination were more likely to experience reduction or elimination of depression -- and less likely to require an increase in their Prozac dosage -- than patients taking Prozac alone.

Finally, scientists at Duke found that when patients taking both Lunesta and Prozac for eight weeks ceased taking Lunesta for a two-week period, their sleep habits continued to improve significantly.      

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