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 NEUROLOGY NEWS RELEASES
(Embargoed Until: 3 P.M. (CT), Monday, September 11, 2006)
ACCELERATING WEIGHT LOSS MAY SIGNAL DEVELOPMENT OF ALZHEIMER'S DISEASE
SPECIAL ONLINE PUBLICATION — MIGRAINE TREATMENT ALSO APPEARS EFFECTIVE FOR CLUSTER HEADACHES
AMATEUR BOXING LINKED TO BRAIN CELL INJURY
ARCHIVES OF OPHTHALMOLOGY NEWS RELEASES
(Embargoed Until: 3 P.M. (CT), Monday, September 11, 2006)
WEIGHTLIFTING INCREASES PRESSURE WITHIN THE EYE
PROGRESSION OF DIABETIC RETINOPATHY ASSOCIATED WITH POOR BLOOD GLUCOSE CONTROL AND HIGH BLOOD PRESSURE AMONG AFRICAN AMERICANS WITH DIABETES
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EMBARGOED FOR RELEASE UNTIL 3 P.M. (CT), MONDAY, September 11, 2006
Media Advisory: To contact corresponding author John C. Morris, M.D., call Michael Purdy at 314-286-0122.
ACCELERATING WEIGHT LOSS MAY SIGNAL DEVELOPMENT OF ALZHEIMER'S DISEASE
CHICAGO—The slow, steady weight loss associated with aging may speed up prior to the onset of Alzheimer's disease and related dementias, according to an article in the September issue of the Archives of Neurology, one of the JAMA/Archives journals.
Changes that occur with aging, such as reduced appetite and diminishing height, may induce weight loss in older adults, according to background information in the article. Alzheimer's disease has also been linked to age-related weight loss. Those in the late stages of the disease can lose up to 2 pounds per year; those who lose more weight are more likely to progress quickly and to be placed in a nursing home.
David K. Johnson, Ph.D., and colleagues at Washington University School of Medicine, St. Louis, studied weight loss before the development of dementia in 449 healthy adults (192 men, 257 women). At the beginning of the study and then yearly for an average of six years, the participants were assessed for dementia, weighed and asked questions about their medical history.
Over the course of the study, 125 participants developed dementia related to Alzheimer's disease. Those who did weighed about eight pounds less at the beginning of the study than those who did not develop Alzheimer's disease. In addition, "an acceleration in the rate of weight loss was a harbinger of the change from non-demented status to dementia of the Alzheimer's type," the authors write. "Participants lost about .6 pounds per year while without dementia, but one year before the first symptomatic detection of dementia of the Alzheimer's type, the rate of weight loss in individuals doubled to 1.2 pounds per year." This association held when the researchers controlled for other factors that might influence weight loss, including age, sex, health status, hypertension (high blood pressure) and stroke history.
It is unclear exactly why weight loss is associated with dementia, the authors write. Some have hypothesized that individuals with dementia forget to eat, but this is unlikely given the finding that weight loss precedes the onset of memory problems and other dementia symptoms. Depression has also been suggested as a link, but although study participants with dementia were more depressed, depressed patients did not have any changes in body weight compared with those who were non-depressed. "There are reports of mild to moderate changes in taste and smell in healthy aging populations and in populations with dementia, and these factors need to be measured rigorously in future studies," the authors write. "Subtle gustatory changes could result in cumulative decreases in caloric intake or decreases in the quality of food consumed by individuals with dementia of the Alzheimer's type."
If these results are confirmed in larger studies, they conclude, "weight loss may be a preclinical indicator of Alzheimer's disease."
(Arch Neurol. 2006;63:1312-1317. Available to the media pre-embargo at www.jamamedia.org)
Editor's Note: This study was supported by grants from the National Institute on Aging and by the Alan A. and Edith L. Wolff Charitable Trust. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
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, September 11, 2006
Media Advisory: To contact corresponding author Peter J. Goadsby, M.D., Ph.D., e-mail: peterg{at}ion.ucl.ac.uk.
MIGRAINE TREATMENT ALSO APPEARS EFFECTIVE FOR CLUSTER HEADACHES
CHICAGO—Zolmitriptan nasal spray, used to treat migraine headaches, also may be safe and effective in treating painful cluster headaches, according to an article posted online today that will appear in the November 2006 print issue of the Archives of Neurology, one of the JAMA/Archives journals.
Cluster headaches are characterized by attacks of excruciating pain that typically involve one side of the head and last between 15 and 180 minutes, according to background information in the article. Because the pain is so severe, rapid and effective treatments are needed. Medications known as triptans are typically used to treat migraines; some, including sumatriptan and oral zolmitriptan, have been shown to be effective for cluster headaches as well. Zolmitriptan nasal spray is a new formulation that is absorbed through the nasal passages and acts more quickly. One preliminary study has suggested that the medication could be effective for cluster headache.
Elizabeth Cittadini, M.D., The National Hospital for Neurology and Neurosurgery, Queen Square, London, and colleagues evaulated the use of the nasal spray in 92 patients (80 men, 12 women, average age 40 years) with cluster headaches. Without treatment, the patients' headaches lasted at least 45 minutes. Over the course of the study, the participants each treated three headache attacks: one with placebo, one with 5 milligrams of zolmitriptan nasal spray and one with 10 milligrams of zolmitriptan nasal spray, in random order. Patients were assessed at five, ten, 15 and 30 minutes after taking the medication. If their headache did not subside at 30 minutes, they were allowed to take a different drug to relieve pain.
Because some patients dropped out of the study or did not have enough headaches during the study period, 69 patients were included in the final analysis, which was based on 65 attacks treated with 5 milligrams of zolmitriptan nasal spray, 63 attacks treated with a 10-milligram dose and 61 attacks treated with placebo. Patients reported headache relief after 30 minutes in 38 (61 percent) of the attacks treated with the 10-milligram dose, 27 (42 percent) of those treated with the 5-milligram dose and 14 (23 percent) of those treated with placebo. Thirty-one patients (50 percent) taking 10 milligrams of the nasal spray were pain-free at 30 minutes, compared with 18 (28 percent) of those taking the 5-milligram dose and 10 (16 percent) who took placebo.
Although one patient dropped out of the study due to adverse effects-including shortness of breath, vomiting and joint or muscle stiffness-no serious side effects were reported. "The very minimal dropout rate and low number of adverse events reported suggest that intranasal zolmitriptan is well tolerated in patients treating acute cluster headaches," the authors write.
"The data provide evidence that zolmitriptan nasal spray can be used as a first-line abortive therapy, along with sumatriptan nasal spray or inhaled oxygen, in the management of cluster headaches," they conclude.
(Arch Neurol. 2006;63:(doi:10.1001/archneur.63.11.nct60002). Available to the media pre-embargo at www.jamamedia.org).
Editor's Note: AstraZeneca supported this work but did not initiate, design or analyze the study, interpret the data or have any role in the writing of the manuscript. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
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, September 11, 2006
Media Advisory: To contact Henrik Zetterberg, M.D., Ph.D.., e-mail: henrik.zetterberg{at}clinchem.gu.se.
AMATEUR BOXING LINKED TO BRAIN CELL INJURY
CHICAGO—A study of 14 Swedish amateur boxers suggests that they have higher levels of certain chemicals in their cerebrospinal fluid in the days following a bout, indicating injuries to neurons and other cells important to brain function, according to a report in the September issue of the Archives of Neurology, one of the JAMA/Archives journals.
About 20 percent of professional boxers develop chronic traumatic brain injury, according to background information in the article. Some studies have suggested that amateur boxers also damage their nervous systems, but because their shorter bouts allow fewer blows to the head and because they must wear safety equipment, the effects tend to be less severe. These studies have been based on assessment of thinking, learning, memory and other brain functions long after boxing, rather than an immediate test performed soon after a fight.
Henrik Zetterberg, M.D., Ph.D., The Sahlgrenska Academy at Göteborg University, Göteborg, Sweden, and colleagues obtained spinal fluids (via spinal tap) from 14 amateur boxers (11 men and three women, average age 22 years) seven to 10 days after a bout and again three months later, after a rest from boxing. At the first assessment, the boxers reported how many hits to the head they received during the match and underwent physical and neurologic examinations; none showed signs of brain injury. The researchers also tested the cerebrospinal fluids of 10 healthy men who were not boxers as controls. Levels of several chemicals that indicate damage to brain cells (neurons) and their axons, the thread-like extensions of the cell that reach toward other brain cells to transmit electrical impulses, were measured.
Seven to 10 days after a boxing match, the group of boxers had higher average levels of chemicals known as neurofilament light protein and total tau than they did three months later. "The cerebrospinal fluid levels of these proteins increase in disorders with neuronal and axonal degeneration and damage, and the increase is known to correlate with the size of the brain lesion," the authors write. "When applied to the results of this study, the increases in neurofilament protein and total tau probably reflect damage to neuronal axons from hits to the head during a bout." They also had elevated levels of glial fibrillary acidic protein, which indicates damage to the astroglia, specialized cells that surround neurons to insulate and support them. An increase in this chemical was also recently found in patients who experienced severe brain injury, and the levels were linked to the patient's clinical outcome. Levels of all three chemicals were significantly higher in the seven boxers who had sustained more than 15 hits to the head or experienced grogginess during or after a bout, compared with those who had 15 or fewer hits to the head and no grogginess.
Compared with the non-boxers, immediately after a bout the boxers had higher levels of neurofilament light protein and glial fibrillary acidic protein. Three months later, the boxers still had higher levels of neurofilament light protein than the control subjects.
"Amateur boxing is associated with acute neuronal and astroglial injury," the authors conclude. "If verified in longitudinal studies with extensive follow-up regarding the clinical outcome, analyses of cerebrospinal fluid may provide a scientific basis for medical counseling of athletes after boxing or head injury."
(Arch Neurol. 2006;63:1277-1280. Available to the media pre-embargo at www.jamamedia.org).
Editor's Note: This study was supported by grants from the Swedish Medical Research Council and the Swedish Council for Working Life and Social Research. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
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, September 11, 2006
Media Advisory: To contact corresponding author Robert Ritch, M.D., call Jean Thomas at 212-979-4274.
WEIGHTLIFTING INCREASES PRESSURE WITHIN THE EYE
CHICAGO—Weightlifting may cause a temporary increase in pressure within the eye, with higher pressure occurring with breath-holding during a weightlifting exercise, according to a report in the September issue of the Archives of Ophthalmology, one of the JAMA/Archives journals.
Intraocular pressure (the pressure within the eyeball) is generally decreased after aerobic exercise, such as running and biking, and nonaerobic exercise, including weightlifting, according to background information in the article. However, higher intraocular pressure has been reported during the Valsalva maneuver, in which air is forced against a closed windpipe and pressure increases in the chest. This action occurs during coughing, vomiting, playing wind instruments and sometimes weightlifting.
Geraldo Magela Vieira, M.D., Institute of Specialized Ophthalmology and UNIPLAC School of Medicine, Brasília, Brazil, and colleagues measured intraocular pressure during weightlifting in 30 males age 18 to 40 (average age 26) without glaucoma. The participants, who all had normal (less than 21 millimeters of mercury) eye pressure, performed four repetitions of a bench press exercise in two ways. The first time, pressure was measured in the right eye and the weightlifters held their breath during the last repetition. The second time, pressure was measured in the left eye and the participants breathed normally throughout the exercise. Eye pressure was measured during the fourth repetition.
During the first round of exercise, intraocular pressure increased in 27 (90 percent) of the participants, by an average of 4.3 millimeters of mercury. During the second round, pressure increased in 18 (62 percent) of weightlifters by an average of 2.2 millimeters of mercury. The increased pressure could be due to the Valsalva maneuver or a similar motion performed during bench presses; the even higher pressure during the first repetitions "may be due to greater intrathoracic [chest] pressure caused by the air retained in the lungs when the subjects held their breath during intraocular pressure measurement," the authors write.
The authors note that a certain type of glaucoma (normal-tension glaucoma) is more common in individuals who are subjected to frequent changes in eye pressure. "Prolonged weightlifting could be a potential risk factor for the development or progression of glaucoma. Intermittent intraocular pressure increases during weightlifting should be suspected in patients with normal-tension glaucoma who perform such exercises," they conclude. "Patients with normal-tension glaucoma should be questioned as to a history of regular weightlifting."
(Arch Ophthalmol. 2006;124:1251-1254. Available to the media pre-embargo at www.jamamedia.org)
Editor's Note: This study was supported in part by the Joseph and Marilyn Rosen Research Fund of the New York Glaucoma Research Institute. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
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, September 11, 2006
Media Advisory: To contact Monique S. Roy, M.D., call Kaylyn D. Dines at 973-972-7276.
PROGRESSION OF DIABETIC RETINOPATHY ASSOCIATED WITH POOR BLOOD GLUCOSE CONTROL AND HIGH BLOOD PRESSURE AMONG AFRICAN AMERICANS WITH DIABETES
CHICAGO—In a six-year study of African Americans with type 1 diabetes, progression of diabetes-related eye disease was high and related to poor blood glucose control and high blood pressure, according to an article in the September issue of the Archives of Ophthalmology, one of the JAMA/Archives journals.
Type 1 diabetes occurs when the body is unable to produce enough insulin to process sugar (glucose) into energy. Over time, the resulting high levels of glucose in the blood can cause damage to nerves and blood vessels, including those of the eye. Diabetic retinopathy, a type of diabetes-related eye disease, causes more new cases of legal blindness among U.S. individuals age 20 to 64 than any other factor, according to background information in the article. Researchers have previously described the risk factors for development and progression of retinopathy in white patients with type 1 diabetes, but little information is available on the disease in African Americans.
Monique S. Roy, M.D., University of Medicine and Dentistry, New Jersey Medical School, Newark, and Mahmoud Affouf, Ph.D., Kean University, Union, N.J., evaluated the progression of retinopathy in 483 individuals who had originally participated in the New Jersey 725 study of African Americans with type 1 diabetes, which began in 1993. Six years later, the participants underwent a second assessment that included a complete eye examination, clinical interview to gather medical history and sociodemographic information, blood pressure reading and height and weight measurements. Photographs of the retina were taken to assess retinopathy status and blood was drawn to measure cholesterol levels and glycosylated hemoglobin (HbA1C) levels, which measure blood glucose control over an extended period.
Patients were classified at baseline by level of diabetic retinopathy, as having none (196 patients, 40.6 percent), mild (169 patients, 35 percent) or moderate to severe (118 patients, 24.4 percent). Over the six-year period, 72.3 percent of the patients who did not have diabetic retinopathy at the beginning of the study had developed evidence of the condition. Fifty-six percent with diabetic retinopathy at the beginning of the study showed progression of the disease, including 22 percent who had vision-threatening diabetic retinopathy and 15 percent who progressed to proliferative retinopathy, a condition in which excess blood vessels grow in the eye. In addition, 15.9 percent developed macular edema, a swelling in the area at the back of the retina that produces the sharpest vision.
Participants who had diabetes for the longest period of time were most likely to develop diabetic retinopathy and to progress to proliferative retinopathy. Those with high HbA1C levels and high blood pressure at the beginning of the study were more likely to develop progressive diabetic retinopathy, proliferative retinopathy and macular edema. Development of proliferative retinopathy also was associated with older age, kidney disease and more severe retinopathy at the beginning of the study. Macular edema was associated with older age, lower socioeconomic status, more severe retinopathy and higher total cholesterol levels.
"The results show that progression of diabetic retinopathy in African American patients with type 1 diabetes is high," the authors conclude. "Poor glycemic control and systemic hypertension [high blood pressure] are two modifiable risk factors significantly associated with progression of diabetic retinopathy. Because glycemic and blood pressure control in this population are poor, measures to improve medical care and ensure regular dilated eye examination to detect vision-threatening diabetic retinopathy may reduce morbidity from the disease."
(Arch Ophthalmol. 2006;124:1297-1306. Available to the media pre-embargo at www.jamamedia.org)
Editor's Note: This research was supported by a grant from the National Eye Institute and a Lew Wasserman Merit Award from Research to Prevent Blindness, Inc. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
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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