Men who drink alcohol every day have a lower risk of heart disease than those who drink less frequently, suggests research in the British Medical Journal. But the same is not true for women.
This study raises important questions about drinking patterns and heart health among men and women, but an editorial warns that the results should be interpreted with caution and should not be used to justify potentially harmful drinking behaviour.
It is widely known that moderate drinkers have a lower risk of coronary heart disease than those who abstain, but most research in this field has been done on men and little is known about drinking patterns and risk of heart disease among women.
Researchers in Denmark studied over 50,000 men and women aged 50-65 years who were taking part in a national health study. Details on alcohol intake and drinking frequency over the preceding year were collected, and participants were monitored for an average of 5.7 years.
Coronary heart events were recorded and results were adjusted for known risk factors, such as age, smoking, education, physical activity and diet.
A total of 28,448 women and 25,052 men took part in the study. Women consumed an average of 5.5 alcoholic drinks a week and men consumed 11.3. During the study, 749 women and 1,283 men developed coronary heart disease.
Women who drank alcohol on at least one day a week had a lower risk of coronary heart disease than women who drank alcohol on less than one day a week.
However, risks were similar for drinking on one day a week (36% reduced risk), or seven days a week (35% reduced risk), suggesting that the amount of alcohol consumed is more important than drinking frequency among women.
In contrast, for men, risks were lowest for the most frequent drinkers. For example, men who drank on one day a week had a 7% reduced risk, while men who drank daily had a 41% reduced risk. This suggests that it doesn’t matter how much men drink, as long as they drink every day.
To see complete article please go here.
Thursday, November 30, 2006
Wednesday, November 29, 2006
Painkillers may threaten power of vaccines
With flu-shot season in full swing and widespread anticipation of the HPV vaccine to prevent cervical cancer, a new University of Rochester study suggests that using common painkillers around the time of vaccination might not be a good idea.
Researchers showed that certain nonsteroidal anti-inflammatory drugs (NSAIDs), also known as cyclooxygenase inhibitors, react with the immune system in such a way that might reduce the effectiveness of vaccines.
The research has widespread implications: study authors report that an estimated 50 to 70 percent of Americans use NSAIDs for relief from pain and inflammation, even though NSAIDs blunt the body’s natural response to infection and may prolong it.
“For years we have known that elderly people are poor responders to the influenza vaccine and vaccines in general,” said principal investigator Richard P. Phipps, Ph.D., a professor of Environmental Medicine, and of Microbiology and Immunology, Oncology and Pediatrics. “And we also know that elderly people tend to be heavy users of inhibitors of cyclooxygenase such as Advil, aspirin, or Celebrex. This study could help explain the immune response problem.”
The study is available online in the Dec. 1, 2006, Journal of Immunology, and was funded in part by the National Institutes of Health. (See full study here.)
When a person is vaccinated, the goal is to produce as many antibodies as possible to effectively neutralize the infection. To do this, white blood cells called B-lymphocytes, or B cells, spring into action to produce those antibodies. B cells also serve as the immune system’s memory for future protection against the illness.
But Phipps and colleagues discovered that human B cells also highly express the cyclooxygenase-2 (cox-2) enzyme, which is not intrinsically bad unless it is overproduced, causing pain and fever. So, when a person takes a drug to block the cox-2 enzyme – and thereby reduce pain and fever – the drug also reduces the ability of B cells to make antibodies.
“The next step is to figure out the worst time to take drugs that inhibit cox-2 in the context of getting vaccinated. Is it the day before, the day of, or the day after" The timing is likely to be very important,” Phipps said. “But meanwhile, we believe that when you reach for the medicine cabinet to reduce pain at the injection site, that is probably the wrong thing to do.”
The findings are based on laboratory studies of blood samples from people who participated in early clinical trials for the HPV vaccine, and on studies of mice.
For the animal portion of the study, researchers vaccinated normal mice and mice engineered to be cox-2 deficient with a component form of the HPV vaccine. They analyzed the amount of antibodies the animals produced, focusing on the critical virus-neutralizing antibodies. The cox-2 deficient mice made 50 to 70 percent less of these key antibodies.
The same experiment was done on preserved blood samples from people who had been vaccinated against HPV-16, the strain linked to cervical cancer. Scientists reactivated the B cells in the blood samples and watched them churn out antibodies, as expected. But when researchers treated the B cells with a cox-2 inhibiting drug, the cells significantly diminished their production of antibodies – showing that cox-2 is essential for an optimal immune response against HPV 16.
This study is not questioning the effectiveness of the newly marketed HPV vaccine, the Rochester scientists said. They pointed out that in many clinical trials involving thousands of women, the vaccine offered complete protection against the development of cervical cancer. And presumably some of these women were taking NSAIDs at the time.
“There’s no doubt the HPV vaccine showed 100 percent efficacy. Still, our data does suggest that it might be wise to limit the use of NSAIDs when you receive any vaccine,” said co-author Robert Rose, Ph.D., associate professor of Medicine and Microbiology and Immunology at the University of Rochester, and one of the virologists whose work led to the development of the new cancer vaccine.
Scientists do not completely understand the mechanism by which cox-2 influences the immune response in humans. They do believe the response may depend upon the dose and frequency of NSAID use.
The negative effects of blocking cox-2 could be more pronounced in people with compromised immune systems, such as AIDS or cancer patients, the study noted. Moreover, if a vaccine is in short supply and needs to be given in lower-than-optimal doses, taking an NSAID could hamper the immune response even more.
Researchers showed that certain nonsteroidal anti-inflammatory drugs (NSAIDs), also known as cyclooxygenase inhibitors, react with the immune system in such a way that might reduce the effectiveness of vaccines.
The research has widespread implications: study authors report that an estimated 50 to 70 percent of Americans use NSAIDs for relief from pain and inflammation, even though NSAIDs blunt the body’s natural response to infection and may prolong it.
“For years we have known that elderly people are poor responders to the influenza vaccine and vaccines in general,” said principal investigator Richard P. Phipps, Ph.D., a professor of Environmental Medicine, and of Microbiology and Immunology, Oncology and Pediatrics. “And we also know that elderly people tend to be heavy users of inhibitors of cyclooxygenase such as Advil, aspirin, or Celebrex. This study could help explain the immune response problem.”
The study is available online in the Dec. 1, 2006, Journal of Immunology, and was funded in part by the National Institutes of Health. (See full study here.)
When a person is vaccinated, the goal is to produce as many antibodies as possible to effectively neutralize the infection. To do this, white blood cells called B-lymphocytes, or B cells, spring into action to produce those antibodies. B cells also serve as the immune system’s memory for future protection against the illness.
But Phipps and colleagues discovered that human B cells also highly express the cyclooxygenase-2 (cox-2) enzyme, which is not intrinsically bad unless it is overproduced, causing pain and fever. So, when a person takes a drug to block the cox-2 enzyme – and thereby reduce pain and fever – the drug also reduces the ability of B cells to make antibodies.
“The next step is to figure out the worst time to take drugs that inhibit cox-2 in the context of getting vaccinated. Is it the day before, the day of, or the day after" The timing is likely to be very important,” Phipps said. “But meanwhile, we believe that when you reach for the medicine cabinet to reduce pain at the injection site, that is probably the wrong thing to do.”
The findings are based on laboratory studies of blood samples from people who participated in early clinical trials for the HPV vaccine, and on studies of mice.
For the animal portion of the study, researchers vaccinated normal mice and mice engineered to be cox-2 deficient with a component form of the HPV vaccine. They analyzed the amount of antibodies the animals produced, focusing on the critical virus-neutralizing antibodies. The cox-2 deficient mice made 50 to 70 percent less of these key antibodies.
The same experiment was done on preserved blood samples from people who had been vaccinated against HPV-16, the strain linked to cervical cancer. Scientists reactivated the B cells in the blood samples and watched them churn out antibodies, as expected. But when researchers treated the B cells with a cox-2 inhibiting drug, the cells significantly diminished their production of antibodies – showing that cox-2 is essential for an optimal immune response against HPV 16.
This study is not questioning the effectiveness of the newly marketed HPV vaccine, the Rochester scientists said. They pointed out that in many clinical trials involving thousands of women, the vaccine offered complete protection against the development of cervical cancer. And presumably some of these women were taking NSAIDs at the time.
“There’s no doubt the HPV vaccine showed 100 percent efficacy. Still, our data does suggest that it might be wise to limit the use of NSAIDs when you receive any vaccine,” said co-author Robert Rose, Ph.D., associate professor of Medicine and Microbiology and Immunology at the University of Rochester, and one of the virologists whose work led to the development of the new cancer vaccine.
Scientists do not completely understand the mechanism by which cox-2 influences the immune response in humans. They do believe the response may depend upon the dose and frequency of NSAID use.
The negative effects of blocking cox-2 could be more pronounced in people with compromised immune systems, such as AIDS or cancer patients, the study noted. Moreover, if a vaccine is in short supply and needs to be given in lower-than-optimal doses, taking an NSAID could hamper the immune response even more.
Halving daily cigarette quota has no health benefit
Halving the number of cigarettes smoked every day in the belief that it will stave off an early death makes no difference, suggests research in the journal Tobacco Control.
Although reducing consumption may have a place as a temporary measure in smoking cessation, this study proves quite clearly that the only safe way out of the risk caused by smoking is to quit, say the authors.
They base their findings on more than 51,000 men and women, all of whom were aged between 20 and 34 at the start of the study.
Participants were initially assessed for cardiovascular risk factors, and then screened again twice at an interval of three to 10 years, adding up to an average monitoring period of over two decades.
Participants were classified as never smokers; ex smokers, quitters (those who gave up between the first and second check); moderate smokers (1 to 14 cigarettes daily); reducers (more than 15 cigarettes a day, cut by more than half at the second check); and heavy smokers (more than 15 cigarettes a day).
Among men, deaths from lung cancer and cancers associated with smoking were not significantly lower in those who had cut back compared with heavy smokers. But this was not true of women who cut back, where the reverse was true.
And men who cut back only had slightly lower death rates from all causes combined than the heavy smokers during the first 15 years. After that, death rates were comparable.
And there were no significant differences in death rates from specific causes, including early death from cardiovascular disease, among women who cut back their daily consumption, compared with those who continued to smoke heavily.
Women who cut back actually had higher death rates from all causes combined than heavy smokers.
The authors conclude that long term monitoring provides no evidence that heavy smokers, who halve their daily cigarette consumption, significantly cut their risk of early death. They add that people may be misled if they are advised that cutting back will help them stave off disease.
Although reducing consumption may have a place as a temporary measure in smoking cessation, this study proves quite clearly that the only safe way out of the risk caused by smoking is to quit, say the authors.
They base their findings on more than 51,000 men and women, all of whom were aged between 20 and 34 at the start of the study.
Participants were initially assessed for cardiovascular risk factors, and then screened again twice at an interval of three to 10 years, adding up to an average monitoring period of over two decades.
Participants were classified as never smokers; ex smokers, quitters (those who gave up between the first and second check); moderate smokers (1 to 14 cigarettes daily); reducers (more than 15 cigarettes a day, cut by more than half at the second check); and heavy smokers (more than 15 cigarettes a day).
Among men, deaths from lung cancer and cancers associated with smoking were not significantly lower in those who had cut back compared with heavy smokers. But this was not true of women who cut back, where the reverse was true.
And men who cut back only had slightly lower death rates from all causes combined than the heavy smokers during the first 15 years. After that, death rates were comparable.
And there were no significant differences in death rates from specific causes, including early death from cardiovascular disease, among women who cut back their daily consumption, compared with those who continued to smoke heavily.
Women who cut back actually had higher death rates from all causes combined than heavy smokers.
The authors conclude that long term monitoring provides no evidence that heavy smokers, who halve their daily cigarette consumption, significantly cut their risk of early death. They add that people may be misled if they are advised that cutting back will help them stave off disease.
Use folic acid to cut heart disease, say experts
The scientific evidence is strong enough to justify using folic acid as a cheap and simple way of reducing heart disease and strokes, say researchers in this week’s British Medical Journal.
Debate continues over whether raised homocysteine levels in the blood (an amino acid implicated in the development of arterial disease) causes heart disease and stroke, and whether folic acid, which lowers homocysteine, will help reduce the risk of these disorders.
So heart expert, Dr David Wald and colleagues set out to clarify the issue. They examined all the evidence from different studies to see whether raised homocysteine is a cause of cardiovascular disease.
Some studies looked at homocysteine and the occurrence of heart attacks and strokes in large numbers of people (cohort studies), some focused on people with a common genetic variant which increases homocysteine levels to a small extent (genetic studies), while others tested the effects of lowering homocysteine levels (randomised controlled trials).
The cohort studies and genetic studies yielded similar results, indicating a protective effect from lower homocysteine levels, even though they did not share the same sources of possible error. The randomised trials were too small to be conclusive although their results were consistent with the expected protective effects of folic acid.
The conclusion that homocysteine is a cause of cardiovascular disease explains the observations from all the different types of study, even if the results from one type of study are, on their own, insufficient to reach that conclusion, say the authors.
Since folic acid reduces homocysteine concentrations, it follows that increasing folic acid consumption will reduce the risk of heart attack and stroke.
They therefore take the view that the evidence is now sufficient to justify action on lowering homocysteine concentrations, although the position should be reviewed as evidence from ongoing clinical trials emerges.
Debate continues over whether raised homocysteine levels in the blood (an amino acid implicated in the development of arterial disease) causes heart disease and stroke, and whether folic acid, which lowers homocysteine, will help reduce the risk of these disorders.
So heart expert, Dr David Wald and colleagues set out to clarify the issue. They examined all the evidence from different studies to see whether raised homocysteine is a cause of cardiovascular disease.
Some studies looked at homocysteine and the occurrence of heart attacks and strokes in large numbers of people (cohort studies), some focused on people with a common genetic variant which increases homocysteine levels to a small extent (genetic studies), while others tested the effects of lowering homocysteine levels (randomised controlled trials).
The cohort studies and genetic studies yielded similar results, indicating a protective effect from lower homocysteine levels, even though they did not share the same sources of possible error. The randomised trials were too small to be conclusive although their results were consistent with the expected protective effects of folic acid.
The conclusion that homocysteine is a cause of cardiovascular disease explains the observations from all the different types of study, even if the results from one type of study are, on their own, insufficient to reach that conclusion, say the authors.
Since folic acid reduces homocysteine concentrations, it follows that increasing folic acid consumption will reduce the risk of heart attack and stroke.
They therefore take the view that the evidence is now sufficient to justify action on lowering homocysteine concentrations, although the position should be reviewed as evidence from ongoing clinical trials emerges.
Tuesday, November 28, 2006
Adolescent smokers have a greater risk of developing alcohol-use disorders than nonsmokers
Popular and clinical lore support the strong connection between smoking and alcohol consumption.
Adolescent smokers appear to have a greater vulnerability to developing alcohol-use disorders.
Results indicate that smoking “primes” the brain for subsequent addiction to alcohol and possibly other drugs.
Both academic studies and casual observation support the view that smokers tend to drink, and drinkers tend to smoke. New research using nationally representative data from the U.S. finds that smokers – particularly adolescent smokers – clearly have a greater vulnerability to alcohol-use disorders (AUDs) than do non-smokers.
Results are published in the December issue of Alcoholism: Clinical & Experimental Research.
"Smoking and alcohol – separately, or together – account for more than 20 percent of deaths in the United States," said Richard A. Grucza, an epidemiologist at Washington University School of Medicine and corresponding author for the study. "Cigarettes and alcohol are also known to be 'gateway' drugs, that is, the overwhelming majority of illegal drug users begin their use with one or both of these legal drugs."
"We have known about the link between cigarette smoking and alcohol use for a while, but we have not really asked the question, as the authors here asked, whether use of one could increase the vulnerability of becoming addicted to the other," said Kevin W Chen, associate professor at the University of Maryland School of Medicine.
"Ours was the first," added Grucza, "to examine quantity of drinking in relationship to smoking and AUDs. Our central questions were: Can this association be explained by the fact that smokers are heavier drinkers, or is there something else going on? In other words, do smokers appear to be more sensitive to the effects of alcohol?" The short answer appears to be yes.
Researchers examined data from an aggregate of 2002 through 2004 U.S. National Surveys on Drug Use and Health. Randomly selected, household-dwelling adolescents and young adults (n=74,836) were selected from the non-institutionalized and civilian American population and queried about their drinking and smoking practices.
Results indicate that smokers – particularly adolescent smokers –have a greater vulnerability to AUDs than do non-smokers.
"In general, smokers were at more than a 50 percent higher risk, although the differences were larger in younger adolescents and among light drinkers," said Grucza. "For example, among 15- to 17-year-olds who drank fewer than eight drinks in the month before the survey, more than 20 percent reported an AUD, compared with about five percent among the non-smoking group with the same level of drinking. We conclude that, although smokers do drink higher rates of alcohol, this alone does not explain their higher vulnerability to AUDs."
Grucza said that these findings go beyond the popular view that bad behaviors like smoking and drinking to excess simply tend to "go together," especially during adolescence. "It seems that smoking makes the adolescent brain more vulnerable to other addictions," he said. "Addictive drugs all act on a part of the brain that is described as the 'central reward circuitry.'" Once this system is exposed to one drug, the brain may become more sensitive to the effects of other drugs, as demonstrated by a number of rodent studies.
"Studies like this will set up an alert – for those who consider adolescent smoking tolerable – to rethink the issue, or perceive the problem differently," noted Chen. "Although we do not know the exact causal relation between the two, the damage to our health is so severe that we need to create a more objective image to reject both smoking and drinking among adolescents."
"Ours is the first study to … establish a correlation between adolescent smoking and AUDs that cannot be explained by heavier drinking," said Grucza. "Now we, and hopefully others, need to investigate whether or not smoking actually causes adolescents to be more susceptible to AUDs. Our results are in line with an emerging literature that shows adolescence may be a unique window of vulnerability for addictions development. If it is proven that nicotine directly impacts vulnerability to alcoholism and other addictions, then that is a new, strong message to add to the health-education arsenal. However, even if this correlation is completely non-causal, these results can help to identify kids who are at risk for AUDs."
Adolescent smokers appear to have a greater vulnerability to developing alcohol-use disorders.
Results indicate that smoking “primes” the brain for subsequent addiction to alcohol and possibly other drugs.
Both academic studies and casual observation support the view that smokers tend to drink, and drinkers tend to smoke. New research using nationally representative data from the U.S. finds that smokers – particularly adolescent smokers – clearly have a greater vulnerability to alcohol-use disorders (AUDs) than do non-smokers.
Results are published in the December issue of Alcoholism: Clinical & Experimental Research.
"Smoking and alcohol – separately, or together – account for more than 20 percent of deaths in the United States," said Richard A. Grucza, an epidemiologist at Washington University School of Medicine and corresponding author for the study. "Cigarettes and alcohol are also known to be 'gateway' drugs, that is, the overwhelming majority of illegal drug users begin their use with one or both of these legal drugs."
"We have known about the link between cigarette smoking and alcohol use for a while, but we have not really asked the question, as the authors here asked, whether use of one could increase the vulnerability of becoming addicted to the other," said Kevin W Chen, associate professor at the University of Maryland School of Medicine.
"Ours was the first," added Grucza, "to examine quantity of drinking in relationship to smoking and AUDs. Our central questions were: Can this association be explained by the fact that smokers are heavier drinkers, or is there something else going on? In other words, do smokers appear to be more sensitive to the effects of alcohol?" The short answer appears to be yes.
Researchers examined data from an aggregate of 2002 through 2004 U.S. National Surveys on Drug Use and Health. Randomly selected, household-dwelling adolescents and young adults (n=74,836) were selected from the non-institutionalized and civilian American population and queried about their drinking and smoking practices.
Results indicate that smokers – particularly adolescent smokers –have a greater vulnerability to AUDs than do non-smokers.
"In general, smokers were at more than a 50 percent higher risk, although the differences were larger in younger adolescents and among light drinkers," said Grucza. "For example, among 15- to 17-year-olds who drank fewer than eight drinks in the month before the survey, more than 20 percent reported an AUD, compared with about five percent among the non-smoking group with the same level of drinking. We conclude that, although smokers do drink higher rates of alcohol, this alone does not explain their higher vulnerability to AUDs."
Grucza said that these findings go beyond the popular view that bad behaviors like smoking and drinking to excess simply tend to "go together," especially during adolescence. "It seems that smoking makes the adolescent brain more vulnerable to other addictions," he said. "Addictive drugs all act on a part of the brain that is described as the 'central reward circuitry.'" Once this system is exposed to one drug, the brain may become more sensitive to the effects of other drugs, as demonstrated by a number of rodent studies.
"Studies like this will set up an alert – for those who consider adolescent smoking tolerable – to rethink the issue, or perceive the problem differently," noted Chen. "Although we do not know the exact causal relation between the two, the damage to our health is so severe that we need to create a more objective image to reject both smoking and drinking among adolescents."
"Ours is the first study to … establish a correlation between adolescent smoking and AUDs that cannot be explained by heavier drinking," said Grucza. "Now we, and hopefully others, need to investigate whether or not smoking actually causes adolescents to be more susceptible to AUDs. Our results are in line with an emerging literature that shows adolescence may be a unique window of vulnerability for addictions development. If it is proven that nicotine directly impacts vulnerability to alcoholism and other addictions, then that is a new, strong message to add to the health-education arsenal. However, even if this correlation is completely non-causal, these results can help to identify kids who are at risk for AUDs."
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