ASA: Coffee Drinkers Have Lower Stroke Risk

By Todd Neale, Staff Writer, MedPage Today
Published: February 26, 2010
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner   
Earn CME/CE credit
for reading medical news


SAN ANTONIO -- Drinking just one cup of coffee a day -- either regular or decaffeinated -- was associated with a 30% reduced risk of stroke, a large, prospective study showed.

Greater consumption did not heighten the apparent protective effect, according to Yangmei Li, MPhil, of the University of Cambridge in England.

The results, gathered over a mean 12-year follow-up, were not affected by adjusting for several known stroke risk factors, Li reported at the American Stroke Association meeting here.

Coffee drinking has been linked to lower risks of several other conditions, including type 2 diabetes and impaired cognition. (See Tea, Coffee Seem to Protect Against Diabetes and Caffeine May Slow Cognitive Decline in Women)Action Points 
Explain to interested patients that this study could not establish a causal relationship between coffee drinking and stroke risk.


Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered preliminary until published in a peer-reviewed journal.
Studies examining the association with stroke, however, have been mixed, with some showing no relationship and others echoing the lower risk in the current analysis. (See High Coffee Consumption Linked to Lower Stroke Risk for Women)

Li and her colleagues explored the issue using data on 9,978 men and 12,254 women from the U.K. general population who were taking part in the European Prospective Investigation into Cancer (EPIC)-Norfolk.

The participants' mean age was 59 (range 39 to 79).

All were free of known heart disease, stroke, and cancer at the baseline period from 1993 to 1997.

Overall, 17,807 reported drinking some amount of coffee -- 3.1 cups a day on average -- and 4,425 said they never drank any coffee.

Through March 2008, 855 strokes occurred, with a lower risk among those who reported drinking any amount of coffee.

Adjusting for smoking, social class, educational level, body mass index, alcohol intake, physical activity, tea drinking, urinary sodium:creatinine, urinary potassium:creatinine, plasma vitamin C, systolic blood pressure, diabetes, and serum cholesterol did not affect the results.

Although men appeared to derive more of a benefit from drinking coffee than women -- HR 0.62 versus 0.84 -- the confidence intervals overlapped, and it was not clear that they were actually different.

Among current smokers, coffee drinkers had a 61% reduced risk of stroke (HR 0.59, 95% 0.38 to 0.94).

Li noted that the subgroup analyses may have lacked statistical power.

Commenting on the study, Daniel Lackland, DrPH, of the Medical University of South Carolina in Charleston, said the main weakness of the study was the use of self-reported data, which makes it difficult to determine the actual quantity of coffee consumed.

He said that even if the association is confirmed, it would be hard to identify the mechanism underlying it, which would be the next challenge.

Compounds in the coffee itself, something linked to the act of coffee drinking, or social behaviors surrounding coffee drinking could all be involved, he said.

Li could not identify a mechanism either, but suggested that compounds in coffee might benefit by improving insulin sensitivity, inhibiting platelet aggregation, and decreasing endothelial dysfunction. Coffee has also been shown to have some antioxidant properties.

Until a mechanism is established, probably in a large clinical trial, Lackland said, it is unlikely the medical community will be telling patients to drink more coffee to prevent stroke.

"Are you going to see this in the recommendations? I don't think right now," Lackland said.

Blocking Enzyme in Mice Reduces Fat

By Michael Smith, North American Correspondent, MedPage Today Published: February 02, 2010 Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston and Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner Earn CME/CE credit for reading medical news

Action Points   Note that this study, in animals, suggests that interfering with a single enzyme might lead to substantial changes in energy expenditure and body fat. Caution that more research is needed to find a compound that can block the enzyme safely in humans. Blocking a single enzyme leads to increased energy expenditure and loss of body fat -- at least in mice, researchers said. Mice treated with a compound that blocks the so-called Fyn kinase expended 14% more energy than animals treated with an inert compound, according to Claire Bastie, PhD, and colleagues at Albert Einstein College of Medicine in New York City. They also displayed a significant weight loss within 12 hours of receiving the compound, compared with animals given the inert substance, Bastie and colleagues reported in the Feb. 3 issue of Cell Metabolism. "This is a new mechanism to help the body to burn extra energy," Bastie said in a statement. The Fyn kinase has previously been linked to energy use: animals with the enzyme blocked burn more fatty acids and are leaner than their normal littermates, Bastie and colleagues noted. Those animals also had increased insulin sensitivity, the researchers said, but the absence of the enzyme did not block the normal anabolic processes of protein synthesis and muscle growth during the feeding cycle. The findings suggested that drugs blocking the enzyme might have a significant effect on energy balance and weight, they theorized. To test the idea, they turned to wild-type mice and a compound called SU6656, a known inhibitor of the Src family of tyrosine kinases, of which Fyn is a member. The mice spent spent 48 hours getting used to a so-called metabolic chamber, which allows researchers to monitor energy intake and expenditure. Then the compound was administered via intraperitoneal injection. Control animals got injections of an inert substance, the researchers said. The shots were given at the beginning of the light cycle, when the animals are least active. Both groups showed identical carbohydrate use during the dark cycle (when they are most active) that preceded the injection. After the injection, the control animals reduced energy use as their bodies switched to the normal lipid production seen during the light cycle. The treated animals, on the other hand, continued to expend energy at a rate that was significantly greater (P<0.0098) than the controls, although there was no significant difference in physical activity. Because mice eat 80% of their calories during the dark cycle, they have a daily pattern of weight loss and gain, Bastie and colleagues noted, so that 12 hours after the start of the light cycle -- when they had been given the shots -- their weight was lowest. But the SU6656-treated mice had a 40% greater weight loss than the control group, a difference that was significant at P<0.003. Lean mass was slightly reduced in all the animals, Bastie and colleagues said, but without significant differences between groups. On the other hand, fat mass was significantly reduced (P<0.05) in the SU6656-treated mice, they found. The metabolic effect of the inhibitor appears to be specific to Fyn, because it had no effect on mice lacking the enzyme, the researchers noted. Unfortunately, SU6656 itself isn't a good choice for clinical trials of the idea in humans, Bastie said, because the Fyn kinase affects the brain, as well as muscle and fat tissue. "Our next goal," she said, "is to design something extremely specific to muscle and adipose."

Metformin Cuts Obese Teens' Weight

By Michael Smith, North American Correspondent, MedPage Today Published: February 01, 2010 Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner Earn CME/CE credit for reading medical news

The diabetes drug metformin can help obese teenagers lose weight even if they don't have the disease, researchers said. In a randomized, placebo-controlled study that combined nearly two years of treatment and follow-up, the drug was associated with a statistically significant drop in body mass index, according to Darrell Wilson, MD, of Stanford University, and colleagues. But the drug appeared to have no effect on many other aspects of obesity, including fat distribution and insulin resistance, Wilson and colleagues reported in the February Archives of Pediatrics & Adolescent Medicine. The study is the longest and largest to test the effect of the drug, Wilson told MedPage Today. Treatment lasted 48 weeks, with another 48 weeks of follow-up, for 77 randomized volunteers. The researchers enrolled the teens (ages 13 to 17) at six pediatric centers in the U.S. After a one-month run-in, they were randomized to 2,000 milligrams of extended-release metformin or to a placebo. Action Points   Explain to interested patients that this study found that, for obese teens without diabetes, the diabetes drug metformin can help them lose weight. All participants also took part in a lifestyle modification program that included diet and exercise. To be eligible, the participants had to be in the 95th percentile or higher for their age and sex and could not have diabetes, Wilson said. The primary goal was to see if the drug had any effect on body mass index, but Wilson and colleagues also measured body fat using dual-emission X-ray absorptiometry and computer tomography (CT) scanning, and measured insulin resistance using an oral glucose tolerance test. After 48 weeks, they found, those in the metformin group had experienced on average a 0.9-point drop in body mass index, compared with a 0.2-point gain in the control group. The difference was significant at P=0.03. The weight loss is roughly equivalent to three kilograms (6.6 pounds) for a 5' 5" adolescent, Wilson and colleagues said. "It's not a 20-pound weight loss, it's not what the world is looking for in a weight-loss drug," he said. "It was a meaningful weight loss, just not a spectacular one." On the other hand, the researcher reported significant differences in body composition, abdominal fat, or insulin indices. The loss of weight lasted between 12 and 24 weeks after stopping the drug, the researchers reported. After that, the BMI of participants in the active group trended back toward levels of the placebo group. There were no significant differences between the groups in adverse events, which were mostly mild or moderate. Two cases of nausea in metformin-treated volunteers were considered probably related to the study drug. One participant stopped the drug because of the nausea. For clinicians, the study suggests that the drug might be useful in treating some obese adolescents, Wilson said. "We've certainly started some of our patients on it, but it has not unleashed us on a campaign of getting everybody on it," he said.