Is Pot Smoking a Stroke Trigger?
By Chris Kaiser, Cardiology Editor, MedPage Today
Published: February 05, 2013
HONOLULU -- Middle age stroke patients were 2.3 times more likely to be pot smokers than healthy middle age controls, according to a study slated for presentation here at the International Stroke Conference (ISC).
"This is the largest case-controlled study ever done to show a possible link to the increased risk of stroke from cannabis," P. Alan Barber, MD, PhD, a professor of clinical neurology at the University of Auckland in New Zealand, told MedPage Today in an interview.
The study will be formally presented at the conference on Wednesday. The ISC released the information after an Australian publication reported the finding based on an embargoed press release.
Barber's interest in the topic arose when he encountered a 30-something stroke patient who had none of the typical risk factors associated with stroke such as hypertension or diabetes -- but the patient smoked pot.
He and his colleagues then searched the literature and found similar case reports associating marijuana smoking with stroke in younger adults who did not have typical risk factors.
"At that point, we decided to test all young stroke patients for the presence of cannabis in their urine," Barber said. "We found a high proportion of positive tests in the first 40 patients, so we expanded the study."
The current study comprises a cohort of 160 patients (100 of them men) with an average age of 45 (range 18 to 55) who had a stroke or TIA. Most patients (94%) had an ischemic stroke; only 6% had a TIA.
For a control group, the ethics committee allowed the researchers to use a matched cohort of 160 patients who had not had a stroke and who had had urine tests for various reasons.
The problem with the controls, Barber said, was that researchers knew only their age, sex, and ethnicity. The fact that they weren't able to adjust for tobacco use was a big limitation of the study, he said.
Nevertheless, Barber and colleagues found that 16% of stroke patients were positive for cannabis compared with 8% of controls.
"That was surprising to us, that one in six stroke patients also had cannabis in their system," he told MedPage Today.
When researchers performed a logistic regression analysis adjusted for age, sex, and ethnicity, the only factor associated with increased risk of ischemic stroke or TIA was the use of marijuana (OR 2.30, 95% CI 1.07 to 4.95).
"The study provides the strongest evidence to date of an association between cannabis and stroke," Barber said, "but the association is confounded because all but one of the stroke patients who were cannabis users also used tobacco regularly. We could not find out to what extent -- if at all -- controls used tobacco."
However, Barber said he believes the stroke risk is from marijuana use and not tobacco.
"We think causality is plausible, because some of the patients had a stroke within days of using the cannabis. We know cannabis causes palpitations such as atrial fibrillation, and atrial fibrillation is strongly associated with stroke. We also know that cannabis causes constriction of brain vessels," Barber said.
He said his next step is to conduct a similar study where he is able to adjust for tobacco use.
The results of the study are particularly important, he said, because pot smoking is generally considered benign, and several states in the U.S. have legalized it in one form or another.
"Whether marijuana is legal or not is up to regulatory authorities, but it's important to pause and think that there may be risks associated with smoking marijuana," he concluded, adding that further research is needed to explore these risks in more detail.
Lesser Degrees of Excess Weight Do Not Increase Mortality
Miriam E. Tucker
Jan 01, 2013
Severe obesity is associated with an increased risk for death from all causes, but lesser amounts of excess weight either do not increase the risk or may be protective, according to the results of a systematic review and meta-analysis.
The findings were published in the January 2, 2013, issue of JAMA by Katherine M. Flegal, PhD, from the National Center for Health Statistics, Centers for Disease Control and Prevention, Hyattsville, Maryland, and colleagues.
In an accompanying editorial, Steven B. Heymsfield, MD, and William T. Cefalu, MD, both from the Pennington Biomedical Research Center, New Orleans, Louisiana, caution against relying on weight alone to stratify risk.
The analysis used body mass index (BMI) categories drawn up by the National Heart Lung and Blood Institute (NHLBI) as follows: underweight, BMI less than 18.5 kg/m2; normal weight, BMI from 18.5 to less than 25 kg/m2; overweight, BMI from 25 to less than 30 kg/m2; and obese, BMI of 30 kg/m2 or more). The category for obesity was further subdivided into grade 1 (BMI, 30 to <35 kg/m2), grade 2 (BMI, 35 to <40 kg/m2), and grade 3 (BMI, 40 kg/m2 or more) obesity.
The researchers analyzed 97 published studies, identified through PubMed and EMBASE searches, of which 41 were from the United States or Canada and 37 were from Europe. Others were from Australia (7 studies), China/Taiwan (4 studies), Japan (2 studies), Brazil (2 studies), Israel (2 studies), India (1 study), and Mexico (1 study).
In all, the studies included more than 2.88 million participants and more than 270,000 deaths. All of them investigated the relationship between BMI and all-cause mortality and provided hazard ratios (HRs) for standard BMI categories (although some used slightly different ranges for the lowest BMI categories).
Compared with the normal-weight group, the HR for the overweight group was 0.94, with a 95% confidence interval of 0.91 to 0.96. For all grades of obesity together, the HR was 1.18 (95% CI, 1.12 - 1.25), but when the obesity categories were broken down separately, grade 1 was not associated with increased all-cause mortality (HR, 0.95; 95% CI, 0.88 - 1.01).
Obesity grades 2 and 3, in contrast, were associated with greater mortality risk, with an HR of 1.29 for the 2 grades combined (95% CI, 1.18 - 1.41).
"Relative to normal weight, obesity (all grades) and grades 2 and 3 obesity were both associated with significantly higher all-cause mortality. Grade 1 obesity was not associated with higher mortality, suggesting that the excess mortality in obesity may predominantly be due to elevated mortality at higher BMI levels. Overweight was associated with significantly lower all-cause mortality," the authors write.
In a subsequent analysis that excluded 34 studies that were considered possibly overadjusted (ie, adjusted for factors such as hypertension that are considered to be part of the causal pathway between obesity and mortality) and 10 studies that were considered possibly underadjusted (ie, neglected to adjust for factors such as age, sex or smoking), results for the remaining 53 adequately adjusted studies did not significantly alter the results.
Moreover, an analyses of contributors to heterogeneity, including study adjustment levels, whether BMI data were measured or self-reported, age group, and slight differences in BMI categorization, did not reveal a significant effect of heterogeneity on the overall meta-analysis conclusions.
Fits in With Previous Studies
Dr. Flegal and colleagues note that their findings are consistent with previous studies that have also shown lower mortality among overweight and moderately obese patients. Possible explanations also have included earlier presentation of heavier patients for medical care and increased likelihood of receiving aggressive risk factor treatment, cardioprotective metabolic effects of increased body fat, and beneficial effects of higher metabolic reserves.
In their accompanying editorial, Dr. Heymsfield and Dr. Cefalu comment that relying on weight alone is not enough, as individuals with the same BMI can differ widely from one another in factors affecting health and mortality.
"Sole use of BMI as a health risk phenotype aggregates people with substantial differences in nutritional status, disability, disease, and mortality risk together into similar BMI categories," they point out.
Recognizing that, the NHLBI also recommends using the additional marker of waist circumference to help quantify risk, they note.
In addition, the NHLBI's classification of normal as a BMI between 18.5 and 25 kg/m2 obscures the fact that people with a BMI between 18.5 and 22 kg/m2 have been found to have higher mortality than those with a BMI between 22 and 25 kg/m2. Lumping them together raises the mortality rate for the normal-weight group, which could explain why their observed mortality is similar to grade 1 obesity.
However, the editorialists also point out that there does appear to be a protective effect of the overweight or low-obesity BMI categories for people chronic conditions such as heart disease, diabetes, and older age — the so-called "obesity paradox."
"Even in the absence of chronic disease, small excess amounts of adipose tissue may provide needed energy reserves during acute catabolic illnesses, have beneficial mechanical effects with some types of traumatic injuries, and convey other salutary effects that need to be investigated," they add.
Clinically, this means that "[n]ot all patients classified as being overweight or having grade 1 obesity, particularly those with chronic diseases, can be assumed to require weight loss treatment. Establishing BMI is only the first step toward a more comprehensive risk evaluation," Dr. Heymsfield and Dr. Cefalu conclude.
Vitamin C Supplements May Increase Kidney Stone Risk
Lara C. Pullen, PhD
Feb 05, 2013
Men who take ascorbic acid supplements daily (approximately 1000 mg) were at increased risk for first incident cases of kidney stones (rate difference, 147/100,000 compared with men who do not take ascorbic acid supplements). This represents a dose-dependent, 2-fold increased risk for kidney stone formation.
Laura D.K. Thomas, MSc, from the Institute of Environmental Medicine, Division of Nutritional Epidemiology, Karolinska Institutet, Stockholm, Sweden, and colleagues published the results of their large, population-based prospective cohort study online February 4 in JAMA Internal Medicine.
The study was performed in the Cohort of Swedish Men and included 48,850 men aged 45 to 79 years. The authors estimated, but were not able to accurately assess, the dose of vitamin C consumed by the men in the study.
The authors controlled for age, education level, body mass index, tea and coffee use, smoking status, hypertension, and diabetes mellitus. They did not control for dehydration, immobilization, use of loop diuretics, corticosteroids, or vitamin D.
They found high-dose (1000 mg) vitamin C to be associated with a single new kidney stone per 680 high-dose users per year. They found no association between multivitamin use and kidney stone risk (relative risk, 0.86; 95% confidence interval, 0.62 - 1.191).
The study included only men, and the authors note that the results may not be generalizable to women.
In an accompanying editorial, Robert H. Fletcher, MD, from Harvard Medical School in Boston, Massachusetts, discussed the benefits and risks of vitamin supplementation. He began his editorial by describing the original purpose of vitamin supplementation, which was to avoid vitamin-deficiency diseases such as pellagra, rickets, and scurvy. Since that time, however, vitamin supplements have been consumed with the intention of preventing or treating chronic diseases.
Treatment with vitamin C, for example, began in the 1700s as a response to the scurvy experienced by sailors who spent months at sea. In the 1900s, the Nobel Laureate Linus Pauling, PhD, proposed that vitamin C was an effective treatment for the common cold, cancer, and cardiovascular disease. Dr. Pauling's enthusiasm for vitamin C inspired numerous clinical trials that were unable to support the use of vitamin D to prevent mortality.
Recently, evidence has been accumulating that vitamin C supplementation may also be unsafe in that it promotes the formation of kidney stones. Results from the current study are consistent with other studies that have linked vitamin C supplementation and kidney stone formation.
The research was funded by the Swedish Research Council/Research Infrastructures and the Karolinska Institutet. The investigators and Dr. Fletcher have disclosed no other relevant financial relationships.
JAMA Intern Med. Published online February 4, 2013. Abstract
Honolulu, Hawaii — More evidence that smoking cannabis is associated with an increased risk for stroke has come from a New Zealand study.
The first case-control study to investigate this association, presented at the American Stroke Association's International Stroke Conference (ISC) 2013, found that patients with ischemic stroke/transient ischemic attack (TIA) were twice as likely to have recently used cannabis as age-, sex-, and ethnicity-matched controls.
"Cannabis is generally perceived as having few serious adverse effects, but this study suggests that this may not be the case," lead author Alan Barber, PhD, MD, from University of Auckland, New Zealand, concluded.
For the study, Dr. Barber and colleagues tested urine for cannabis within 72 hours of hospital admission in 160 patients with ischemic stroke/TIA aged 18 to 55 years and 160 controls (patients admitted with nonstroke diagnoses, matched for age, sex, and ethnicity).
Dr. Alan Barber
The cannabis screen was positive in 25 (16%) of the stroke/TIA group vs 13 of 160 (8%) control participants. Logistic regression analysis found an odds ratio of 2.30 (95% confidence interval, 1.07 - 4.95).
Dr. Barber said the 16% rate of cannabis use in the stroke patients "took us by surprise." Cannabis users were more likely to be male, tobacco smokers, and Maori. No other illicit drugs were detected.
He explained that he and his colleagues conducted the study after a young woman presented to their emergency department with a stroke after smoking cannabis. "We looked in the literature and found several other case reports, and so decided to do a study."
Dr. Barber said a causal association between cannabis and stroke is plausible, given that cannabis use has been shown to increase sympathetic and decrease parasympathetic activity and to increase heart rate; it is also associated with supine hypertension and postural hypotension, as well as increased cardiac output. It also reduces the oxygen-carrying capacity of blood and may lead to accelerated atherosclerosis, along with cerebral vasoconstriction.
He noted that cannabis use has been associated with a 5-fold increased risk for myocardial infarction in the 60 minutes after use and with atrial fibrillation and sudden unexplained cardiovascular death.
A problem with the study, Dr. Barber said, was that tobacco use confounded the result; 24 of the 25 stroke patients who tested positive for cannabis were also smokers. "We couldn't tease apart the confounding effect of tobacco, but what we can say is that a lifestyle that includes cannabis use appears to double your risk of stroke."
Dr. Barber explained that the ethics committee of this study did not give permission for any more information other than age, sex, and ethnicity to be revealed about the control patents, given that cannabis was an illicit drug. "That made controlling for confounding factors impossible. We are going to ask them again if we can go through the control patients' notes for this additional information so we might be able to establish a causal effect."
Nevertheless, Dr. Barber believes cannabis has an effect on stroke over and above that of tobacco. He referred to a study conducted in 1974. That study randomly assigned patients with angina to placebo, nicotine, or cannabis cigarettes; time to angina on exercise was reduced by 8% with placebo, 23% with nicotine, and 50% with cannabis.
He concluded, "Future research should determine if the association we found is independent of tobacco." But he warned that even though this may prove difficult given ethical strictures and risk of bias with studying an illicit drug, "the high prevalence of cannabis use in this cohort, as well as moves to decriminalize cannabis makes this research imperative."
Dr. Kyra Becker
Asked for comment on these findings, Kyra Becker, MD, professor of neurology and neurological surgery at the University of Washington School of Medicine and co-director of the University of Washington Stroke Center at Harborview, Seattle, said that to her, the findings were not anticipated.
"To me it's actually quite surprising," she told Medscape Medical News. "It's something that I didn't anticipate, and certainly it's something that we don't screen for in our young stroke patients. I'm very intrigued and I'd like to see the follow up studies to actually prove the causation, and why cannabis would actually increase the risk of stroke."
She pointed out that, ironically, some data suggest cannabis is actually neuroprotective in the acute phase of stroke, the difference between the effect on the vessels and the effect on the neurons. "So at the time of stroke, if you get cannabis in your system it actually protects and limits the amount of brain injury," she said, similar to the observed effects with estrogen.
Larry Goldstein, MD, professor of neurology at Duke University Medical Center and director of the Duke Stroke Center, Durham, North Carolina, was cautious. "The thing to keep in mind is that there are very limited data on these patients," he said. "It was done retrospectively so there is undoubtedly residual confounding and factors that weren't measured that might be important."
Dr. Larry Goldstein
In addition, a high relative risk doesn't mean a high absolute risk, and the absolute risk is not clear from this kind of observation.
"It raises a signal that might need to be paid attention to, but I think more work needs to be done before we understand what that risk is, and whether it's real or not after you fully control for other factors," he concluded.
Thanks for this information.
I know thre needs to be more studies on this, but it is good to have the warning. I actually find it terribly disturbing and I hope it is a false alarm...though it seems unlikely to be.
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