JAMA news releases are made available to the public after 3 pm US Central time on the first 4 Tuesdays of each month. the Archives of Journals news releases are made available to the public after 3 pm Central time on Mondays. We also provide a list of previous news releases.
THIS WEEK'S CONTENTS
ARCHIVES OF INTERNAL MEDICINE NEWS RELEASES
(Embargoed Until: 3 P.M. (CT), Monday, June 12, 2006)
MEDITATION MAY IMPROVE CARDIAC RISK FACTORS IN PATIENTS WITH CORONARY HEART DISEASE
COFFEE DRINKING ASSOCIATED WITH LOWER RISK FOR ALCOHOL-RELATED LIVER DISEASE
ARCHIVES OF OPHTHALMOLOGY NEWS RELEASES
(Embargoed Until: 3 P.M. (CT), Monday, June 12, 2006)
REPORTS CHARACTERIZE FUNGAL EYE INFECTIONS AMONG SOFT CONTACT LENS WEARERS
ARCHIVES OF NEUROLOGY NEWS RELEASES
(Embargoed Until: 3 P.M. (CT), Monday, June 12, 2006)
GENE MUTATION MAY INFLUENCE AGE OF ONSET OF PARKINSON'S DISEASE
SPECIAL ONLINE PUBLICATION — ABNORMAL GLUCOSE METABOLISM MAY CONTRIBUTE TO CHRONIC NERVE DISORDER
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EMBARGOED FOR RELEASE UNTIL 3 P.M. (CT), MONDAY, June 12, 2006
Media Advisory: To contact corresponding author C. Noel Bairey Merz, M.D., call Sandy Van at 800-880-2397.
MEDITATION MAY IMPROVE CARDIAC RISK FACTORS IN PATIENTS WITH CORONARY HEART DISEASE
CHICAGO—A relaxation technique known as transcendental meditation may decrease blood pressure and reduce insulin resistance among patients with coronary heart disease, according to a report in the June 12 issue of the Archives of Internal Medicine, one of the JAMA/Archives journals.
Transcendental meditation, derived from the ancient Vedic tradition in India, is taught through a standard protocol involving lectures, personal instruction and group meetings, according to background information in the article. It has previously been shown to lower blood pressure but its effect on other risk factors associated with coronary heart disease, including those linked to the metabolic syndrome, has not been thoroughly examined. The metabolic syndrome refers to a cluster of symptoms that increase cardiac risk, including high blood pressure (hypertension), abdominal obesity, high cholesterol and insulin resistance, which occurs when the body is unable to use the insulin produced by the pancreas to process sugar into energy.
Maura Paul-Labrador, M.P.H., Cedars-Sinai Medical Center, Los Angeles, and colleagues conducted a 16-week trial of transcendental meditation in patients with coronary heart disease. Fifty-two participants (average age 67.7 years) were instructed in transcendental meditation and 51 control patients (average age 67.1 years) received health education. At the beginning and end of the trial, the patients fasted overnight and then gave a blood sample, participated in a medical history review and underwent tests of blood vessel function and heart rate variability. Heart rate variability testing assesses the functioning of the autonomic nervous system, which controls the heart and other involuntary muscles.
Overall, of the 103 participants who were enrolled, 84 (82 percent) completed the study. At the end of the trial, patients in the transcendental meditation group had significantly lower blood pressure; improved fasting blood glucose and insulin levels, which signify reduced insulin resistance; and more stable functioning of the autonomic nervous system. "These physiological effects were accomplished without changes in body weight, medication or psychosocial variables and despite a marginally statistically significant increase in physical activity in the health education group," the authors write.
"These current results also expand our causal understanding of the role of stress in the rising epidemic of the metabolic syndrome," they continue. "Although current low levels of physical activity, unhealthy eating habits and resultant obesity are triggers for this epidemic, the demands of modern society may also be responsible for higher levels of chronic stress." Such stress causes the release of cortisol and other hormones and neurotransmitters, which over time damage the cardiovascular system.
"Our results, demonstrating beneficial physiological effects of transcendental meditation in the absence of effects on psychosocial variables, suggest that transcendental meditation may modulate response to stress rather than alter the stress itself, similar to the physiological impact of exercise conditioning," the authors write. This method of controlling the body's response to stress may provide a new target for the treatment and prevention of coronary heart disease, warranting further study, they conclude.
(Arch Intern Med. 2006;166:1218-1224. Available to the media pre-embargo at www.jamamedia.org)
Editor's Note: This study was supported by grants from the National Center for Complementary and Alternative Medicine, National Institutes of Health; and a General Clinical Research Centers grant from the National Center for Research Resources.
For more information, contact JAMA/Archives media relations at 312/464-JAMA (5262) or e-mail mediarelations{at}jama-archives.org.
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EMBARGOED FOR RELEASE UNTIL 3 P.M. (CT), MONDAY, June 12, 2006
Media Advisory: To contact Arthur L. Klatsky, M.D., call Michelle Ponte at 510-267-5354.
COFFEE DRINKING ASSOCIATED WITH LOWER RISK FOR ALCOHOL-RELATED LIVER DISEASE
CHICAGO—Drinking coffee may be related to a reduced risk of developing the liver disease alcoholic cirrhosis, according to a report in the June 12 issue of the Archives of Internal Medicine, one of the JAMA/Archives journals.
Cirrhosis progressively destroys healthy liver tissue and replaces it with scar tissue. Viruses such as hepatitis C can cause cirrhosis, but long-term, heavy alcohol use is the most common cause of the disease in developed countries, according to background information in the article. Most alcohol drinkers, however, never develop cirrhosis; other factors that may play a role include genetics, diet and nutrition, smoking and the interaction of alcohol with other toxins that damage the liver.
Arthur L. Klatsky, M.D., and colleagues at the Kaiser Permanente Medical Care Program, Oakland, Calif., analyzed data from 125,580 individuals (55,247 men and 70,333 women) who did not report liver disease when they had baseline examinations, between 1978 and 1985. Participants filled out a questionnaire to provide information about how much alcohol, coffee and tea they drank per day during the past year. Some of the individuals also had their blood tested for levels of certain liver enzymes; the enzymes are released into the bloodstream when the liver is diseased or damaged.
By the end of 2001, 330 participants had been diagnosed with cirrhosis, including 199 with alcoholic cirrhosis. For each cup of coffee they drank per day, participants were 22 percent less likely to develop alcoholic cirrhosis. Drinking coffee was also associated with a slight reduction in risk for other types of cirrhosis. Among those who had their blood drawn, liver enzyme levels were higher among individuals who drank more alcohol, indicating liver disease or damage; however, those who drank both alcohol and coffee had lower levels than those who drank alcohol but did not drink coffee, with the strongest link among the heaviest drinkers.
Tea drinking was not related to reduced risk in the study, suggesting that it is not caffeine that is responsible for the relationship between coffee and reduced cirrhosis risk. "Previous reports are disparate with respect to whether the apparently protective coffee ingredient is caffeine; in our opinion this issue is quite unresolved," the authors write.
The findings do not suggest that physicians prescribe coffee to prevent alcoholic cirrhosis, the authors continue. "Even if coffee is protective, the primary approach to reduction of alcoholic cirrhosis is avoidance or cessation of heavy alcohol drinking," they conclude. "Assuming causality, the data do suggest that coffee intake may partly explain the variability of cirrhosis risk in alcohol consumers. Basic research about hepatic coffee-ethanol interactions is warranted, but we should keep in mind that coffee might represent only one of a number of potential cirrhosis risk modulators."
(Arch Intern Med. 2006;166:1190-1195. Available to the media pre-embargo at www.jamamedia.org)
Editor's Note: This study was supported by a grant from the Kaiser Foundation Research Institute. Data collection from 1978 to 1985 was supported by a grant from the Alcoholic Beverage Medical Research Foundation, Baltimore, Md.
For more information, contact JAMA/Archives media relations at 312/464-JAMA (5262) or e-mail mediarelations{at}jama-archives.org.
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EMBARGOED FOR RELEASE UNTIL 3 P.M. (CT), MONDAY, June 12, 2006
Media Advisory: To contact Eduardo C. Alfonso, M.D., call Marla Bercuson at 305-326-6190. To contact corresponding author David G. Hwang, M.D., call Vanessa deGier at 415-514-1592.
REPORTS CHARACTERIZE FUNGAL EYE INFECTIONS AMONG SOFT CONTACT LENS WEARERS
CHICAGO—Fusarium, the fungus implicated in recent eye infections among soft contact lens wearers, is associated with an increasing number of cases of keratitis (corneal swelling and inflammation), according to a report published online today in the Archives of Ophthalmology, one of the JAMA/Archives journals.
Infections caused by fungi can be devastating to both the structure of the eye and the patient's vision, according to background information in the article. Keratitis, or swelling and inflammation of the transparent membrane known as the cornea, has been associated with wearing soft contact lenses, but such infections usually have not been caused by fungi. At the authors' institution in south Florida, only three cases of fungal keratitis associated with contact lenses were seen between 1969 and 1977, two between 1977 and 1982 and five between 1982 and 1992.
Eduardo C. Alfonso, M.D., and colleagues at the University of Miami, Miller School of Medicine, report 34 cases of fungal keratitis among soft contact lens wearers from January 2004 to April 2006. The researchers reviewed all 34 patients' medical records and report the clinical characteristics of the infections, the treatment prescribed and the microbiologic features.
All of the cases were associated with the fungus known as Fusarium. The average age of the patients was 34.9 years with a range of 13 to 92 years; 14 were male and 20 female. None had a history of disease that would predispose them to fungal eye infections. Among the 13 patients who could identify the type of contact lens solution they used, 12 reported that they had used some type of ReNu brand solution. This included two who reported that they had used ReNu MoistureLoc, the solution implicated in recent Fusarium outbreaks in the United States and Singapore, and nine who used ReNu brand without specifying a particular product.
Most patients were originally assumed to have a bacterial infection and were treated with antibiotics. The average time from the development of symptoms to accurate diagnosis was 9.1 days. After the diagnosis of fungal keratitis, patients were treated with topical (applied to the eye) or systemic (taken internally) antifungal medication for an average of 67.1 days. Two cases required surgery. The length of time between the first symptoms and the beginning of antifungal treatment appeared to be related to treatment outcomes; those patients for whom seven days or more passed between symptom onset and treatment had infections that took longer to cure. "Based on treatment experience in this series, it is our clinical impression that earlier correct diagnosis with institution of proper specific antifungal therapy resulted in a speedier resolution of the keratitis," the authors write.
The cause for the increased prevalence of Fusarium keratitis is not known, they continue; more research is needed. Until then, physicians should remain aware of the outbreak. "Ulcerative keratitis in a soft contact lens wearer should suggest possible Fusarium or other fungal species in addition to bacteria, parasites or viruses as causative organisms," the authors conclude. "Clinicians should conduct the necessary clinical and laboratory investigations to establish a specific diagnosis promptly to initiate the most specific, efficacious therapy."
(Arch Ophthalmol. 2006;124:(doi:10.1001/archophthalmol.124.7.ecs60039). Available to the media pre-embargo at www.jamamedia.org)
Editor's Note: This study was funded by an unrestricted grant from Research to Prevent Blindness.
In an additional report published online today in Archives of Ophthalmology, Maria D. Bernal, M.D., and colleagues at the University of California, San Francisco, report on four additional cases of Fusarium in soft contact lens wearers that occurred during five weeks in early 2006. "Our report strongly suggests that the current cluster represents an unusual spike over the background incidence of Fusarium keratitis seen during the prior 30 years at our institution," the authors report. "We, other laboratories, and the Centers for Disease Control and Prevention are currently investigating the fungicidal properties of the contact lens solutions used by these patients and the genotype characteristics of the Fusarium isolates in an effort to determine the underlying cause of the current apparent outbreak and whether the Fusarium species from these cases originate from a common strain."
(Arch Ophthalmol. 2006;124:(doi: 10.1001/archophthalmol.124.7.ecs60006). Available to the media pre-embargo at www.jamamedia.org)
Editor's Note: This study was supported in part by unrestricted grants from Research to Prevent Blindness and That Man May See.
For more information, contact JAMA/Archives media relations at 312/464-JAMA (5262) or e-mail mediarelations{at}jama-archives.org.
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EMBARGOED FOR RELEASE UNTIL 3 P.M. (CT), MONDAY, June 12, 2006
Media Advisory: To contact corresponding author James F. Gusella, Ph.D., call Sue McGreevey at 617-724-2764. To contact editorialist Roger N. Rosenberg, M.D., call Aline McKenzie at 214-648-3404.
GENE MUTATION MAY INFLUENCE AGE AT ONSET OF PARKINSON'S DISEASE
CHICAGO—The number of mutations in a gene previously found to be associated with early-onset Parkinson's disease may influence the age at which the condition develops; even individuals who carry just one mutated copy may be more susceptible to Parkinson's disease, according to a report in the June issue of the Archives of Neurology, one of the JAMA/Archives journals.
Parkinson's disease affects about 1 percent of individuals age 60 years or older and 4 to 5 percent of those age 85 years or older, according to background information in the article. The neurodegenerative disorder is characterized by tremors, rigid movements, difficulty walking and a mask-like facial appearance. Though much about the development of Parkinson's disease remains unknown, family history has been found to significantly increase risk. Researchers have located several genes that may be implicated, including the parkin gene. About 50 percent of individuals with "juvenile" parkinsonism (in which features of Parkinson's disease develop before age 21 years) and 10 to 25 percent of those with early-onset (before age 50) Parkinson's disease have mutated parkin genes.
Mei Sun, M.D., Ph.D., Massachusetts General Hospital and Harvard Medical School, Boston, and colleagues studied 183 families in which two or more members had Parkinson's disease. The families also met one of two other criteria: either one individual in the family developed Parkinson's disease before age 54 years, or two affected siblings had identical versions of the parkin gene. Because siblings inherit one chromosome from their mother and one chromosome from their father, they can share either zero, one or two versions of each gene. At least one member of each family underwent comprehensive genetic screening to determine the number and nature of any mutations to the parkin gene.
Twenty-three (12.6 percent) of the families screened contained at least one member with a mutated parkin gene. Among those families, 10 (43 percent) had at least one member with two different mutations; three (13 percent) had at least one member with two copies of the same mutation; and 10 (43 percent) had at least one member with one mutated parkin gene and one normal parkin gene. Individuals with one mutated gene and one normal gene are known as heterozygotes; researchers had not previously determined whether heterozygotes were at increased risk for Parkinson's disease. Patients with parkin mutations developed Parkinson's disease at an average age of 42.9 years. Among the families who were selected because two siblings shared the same version of the parkin gene, heterozygotes developed Parkinson's disease an average of 11.7 years earlier than those with no mutations, and those with two or more mutations developed the condition 13.2 years earlier than heterozygotes.
"In conclusion, parkin mutations are not rare in this selected subset of familial Parkinson's disease samples (12.6 percent)," the authors write. "Single parkin mutations may increase susceptibility to the disease and decrease the onset age of Parkinson's disease (mean onset age, 49.6 years)." The fact that even heterozygotes developed Parkinson's disease at an earlier age than those with two normal copies indicates that the gene's effect may be stronger than previously recognized, and that screening for mutations in the gene may help identify those at risk of developing the condition.
(Arch Neurol. 2006;63:826-832. Available to the media pre-embargo at www.jamamedia.org)
Editor's Note: This study was supported by the Bumpus Foundation and grants from the U.S. Public Health Service. The DNA samples contributed by the Parkinson Institute, Istituti Clinici di Perfezionamento, were from the Human Genetic Bank of Patients Affected by Parkinson Disease and Parkinsonisms, supported by a grant from the Italian Telethon Foundation.
EDITORIAL: GENETIC STUDIES HELP EXPLAIN PARKINSON'S DISEASE DEVELOPMENT
CHICAGO—Understanding how mutations in parkin and other genes contribute to Parkinson's disease offers valuable clues to the still-mysterious pathways of its development, write Roger N. Rosenberg, M.D., editor,Archives of Neurology, and Uwe Beffert, Ph.D., both of University of Texas, Southwestern Medical Center, Dallas, in an accompanying editorial.
The editorialists note that if the results of this study are confirmed, they write, they "will require a reexamination of the genetic data associated with Parkinson's disease to take into account the possibility that heterozygous mutations in autosomal recessive genes such as parkin and PINK1 affect the susceptibility and age of onset of Parkinson's disease. These findings are provocative and add a new genetic dimension to the pathogenesis of Parkinson's disease."
(Arch Neurol. 2006;63:807-808. Available to the media pre-embargo at www.jamamedia.org)
For more information, contact JAMA/Archives media relations at 312/464-JAMA (5262) or e-mail mediarelations{at}jama-archives.org.
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EMBARGOED FOR RELEASE UNTIL 3 P.M. (CT), MONDAY, June 12, 2006
Media Advisory: To contact Charlene Hoffman-Snyder, M.S.N., N.P.-B.C., call Carol Benson at 480-301-4219.
ABNORMAL GLUCOSE METABOLISM MAY CONTRIBUTE TO CHRONIC NERVE DISORDER
CHICAGO—Abnormal glucose metabolism, which occurs when the body has difficulty processing sugar (glucose) into energy, is twice as common among patients with chronic nerve dysfunction of unknown cause than among the general population and may be a risk factor for the condition, according to a study posted online today that will appear in the August 2006 print issue of the Archives of Neurology, one of the JAMA/Archives journals.
Many older adults experience nerve disorders known as neuropathy, some of which are characterized by symptoms of "burning feet" and other unpleasant sensations in the lower leg, according to background information in the article. Diabetes, genetic disorders, exposure to toxic substances and a condition called amyloidosis in which extra protein-based substances accumulate in the body tissues can all cause neuropathy, but many cases do not have an easily identifiable underlying cause. When laboratory tests cannot determine the cause, the condition is known as chronic idiopathic axonal polyneuropathy; a cause is eventually found in only 7 to 30 percent of these cases.
Charlene Hoffman-Snyder, M.S.N., N.P.-B.C., Mayo Clinic, Scottsdale, Ariz., and colleagues identified 100 consecutive patients (60 women and 40 men) with chronic idiopathic axonal polyneuropathy who were evaluated between January 2003 and January 2005. Patients underwent a complete neurological evaluation and had a fasting plasma glucose test, which measures the levels of glucose in the blood after eight hours of not eating, and a two-hour oral glucose tolerance test, which determines how well the body processes glucose by drawing blood two hours after fasting patients ingest a dose of glucose. "The fasting plasma glucose level alone does not always identify patients with impaired glucose tolerance and neither does the two-hour oral glucose tolerance test always detect patients with impaired glucose metabolism," the authors write. "Both tests are, however, useful to detect hyperglycemia [high blood sugar] and the consequences of disordered glucose metabolism."
According to the two-hour oral glucose tolerance test, 62 patients (62 percent) with neuropathy had abnormal fasting glucose metabolism, including 24 with undiagnosed diabetes. (This compares with 33 percent of patients of similar ages in the general population with abnormal glucose metabolism as previously estimated by the Centers for Disease Control and Prevention in other published reports.) The results of the current study suggest that abnormal glucose metabolism may be a risk factor for neuropathy.
"Conventional thinking among diabetologists is that diabetic polyneuropathies are the result of prolonged hyperglycemia," the authors write. "Like previous studies, this investigation supports the hypothesis that distal axonal polyneuropathies may occur in much earlier stages of abnormal glucose metabolism than previously thought. Recent studies suggest that the neuropathy associated with impaired glucose tolerance may be milder than neuropathies traditionally associated with diabetes mellitus and may be the earliest detectable sign of abnormal glucose metabolism."
(Arch Neurol. 2006;63:(doi: 10.1001/archneur.63.8.noc50336). Available to the media pre-embargo at www.jamamedia.org)
For more information, contact JAMA/Archives media relations at 312/464-JAMA (5262) or e-mail mediarelations{at}jama-archives.org.
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