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Journal Digest
Journal Digest
Psychiatric News
Volume 46 Number 13 page 22-22

—€¢ Researchers at the Harvard School of Public Health and Harvard Medical School have concluded from a large longitudinal study that dietary intake of long-chain n-3 fatty acids does not reduce the risk of clinical depression.

They prospectively studied 54,632 women from the Nurses' Health Study who were aged 50 to 77 and free of depressive symptoms at baseline. Information on diet was obtained from validated food-frequency questionnaires. Clinical depression was defined as reporting both physician-diagnosed depression and regular antidepressant medication use.

During 10 years of follow-up (1996-2006), 2,823 cases of depression were documented. Intake of long-chain n-3 fatty acids from fish was not associated with depression risk, whereas alpha-linoleic acid (ALA) intake was inversely associated with depression risk. The inverse association between ALA and depression was stronger in women with low linoleic acid (LA) intake.

"Although these data support the hypothesis that higher ALA and lower LA intakes reduce depression risk, this relation warrants further investigation," said the research team.

Lucas M, Mirzaei F, O'Reilly E, et al. "Dietary Intake of n-3 and n-6 Fatty Acids and the Risk of Clinical Depression in Women: A 10-Year Prospective Follow-up Study." Am J Clin Nutr. 2011. April 6 [Epub ahead of print]. An abstract is posted at <www.ncbi.nlm.nih.gov/pubmed/21471279>.

—€¢ A randomized, controlled clinical trial of cognitive-behavioral therapy (CBT) was undertaken to measure its effects on cardiovascular disease (CVD) recurrence. Researchers found that a CBT intervention program decreased the risk of recurrent CVD and recurrent acute myocardial infarction.

The study included 362 women and men aged 75 or younger who were discharged from the hospital after a coronary heart disease event within the prior 12 months. Patients received either traditional care (170 patients) or traditional care plus a CBT program (192 patients) that focused on stress management, with 20 two-hour sessions during one year.

Outcome variables were all-cause mortality, hospital admission for recurrent CVD, and recurrent acute myocardial infarction. During a mean 94 months of follow-up, the intervention group had a 41 percent lower rate of fatal and nonfatal first recurrent CVD events, 45 percent fewer recurrent acute myocardial infarctions, and a nonsignificant 28 percent lower all-cause mortality than the reference group after adjustment for other outcome-affecting variables.

The researchers believe their work may have implications for secondary preventive programs in patients with coronary heart disease.

Gulliksson M, Burell G, Bessby B, et al. "Randomized Controlled Trial of Cognitive Behavioral Therapy vs. Standard Treatment to Prevent Recurrent Cardiovascular Events in Patients With Coronary Heart Disease." Arch Intern Med. 2011. 171 (2):134-140

—€¢ Researchers at the Medical University of South Carolina Institute of Psychiatry sought to combine the effects of the opioid receptor antagonist naltrexone with gabapentin, an analog of the neurotransmitter gamma-aminobutyric acid (GABA) that has been approved by the Food and Drug Administration (FDA) since 1994 as an adjunctive medication to control partial seizures. "Since gabapentin and naltrexone work on different neurophysiological systems, this combination has some appeal," said Raymond Anton, M.D., and colleagues.

They evaluated 150 alcohol-dependent individuals who were randomly assigned to a 16-week course of naltrexone alone, naltrexone supplemented with gabapentin for the first six weeks, or double placebo. Participants were seen by a health care provider and a therapist providing combined behavioral intervention at weeks 1, 2, 3, 6, 8, 10, 12, and 16 of treatment.

Criteria evaluated included the interval to heavy drinking, number of heavy drinking days, and number of drinks per drinking day. During the first six weeks, the naltrexone-gabapentin group had a longer interval to heavy drinking than did the naltrexonealone group, which had an interval similar to that of the placebo group; had fewer heavy drinking days than the naltrexone-alone group, which in turn had more heavy drinking days than the placebo group; and had fewer drinks per drinking day than the naltrexone-alone group and the placebo group.

The addition of gabapentin to naltrexone improved drinking outcomes over naltrexone alone during the first six weeks after drinking cessation. This effect did not endure after gabapentin was discontinued.

Anton R, Myrick H, Wright T, et al. "Gabapentin Combined With Naltrexone for the Treatment of Alcohol Dependence." Am J Psychiatry. 2011. [Epub ahead of print]

—€¢ A multinational group of researchers representing Sweden, China, Italy, and the United States recently examined the association of midlife overweight and obesity with dementia, Alzheimer's disease, and vascular dementia in late life. The purpose of the study was to verify the hypothesis that genetic and early-life environmental factors contribute to the association between dementia and being overweight.

A total of 8,534 twin individuals aged 65 or older were selected from the Swedish Twin Registry and assessed to detect dementia cases (DSM-IV criteria). Dementia was diagnosed in 350 subjects, and 114 subjects had questionable dementia. Body mass index (BMI) at midlife was determined; 2,541 (29.8 percent) of participants were determined to be either overweight (BMI of 25 to 30) or obese (BMI greater than 30).

Compared with participants without dementia, those with dementia or questionable dementia were older, had a lower level of education and current BMI, had higher midlife BMI, and were more likely to have been diagnosed with diabetes, stroke, or heart disease. Midlife BMI as a continuous variable was significantly associated with an increased risk of dementia as well as questionable dementia after adjustment for potential confounders (including age, gender, and education).

Xu W, Atti A, Gatz M, et al. "Midlife Overweight and Obesity Increase Late-Life Dementia Risk." Neurology. 2011. 76(18): 1568-1574

—€¢ Although the pathologic changes are similar regardless of the age at onset, Alzheimer's disease (AD) has been divided into two clinical forms according to age at onset: early-onset AD (EOAD) (onset at age 65 or younger) and late-onset AD (LOAD) (onset after age 65 years). A retrospective study of patients with pathologically confirmed EOAD published in the May 17 Neurology found that patients with atypical (nonmemory) presentations of AD are frequently misdiagnosed. Although several clinical studies have previously shown that EOAD presents more frequently with atypical clinical manifestations than LOAD does, a purported limitation of those studies is that the diagnosis is made using clinical criteria, often lacking pathologic confirmation.

Researchers selected 40 cases for retrospective review of clinical data (age at onset, family history, clinical presentation, diagnostic delay, and diagnosis) and Apolipoprotein E (APOE) genotype of patients with neuropathologically confirmed (EOAD).

One-third of patients with pathologic confirmed EOAD presented with atypical symptoms, leading the researchers to conclude that patients with nonamnestic presentations often receive incorrect clinical diagnoses.

Balasa M, Gelpi E, Antonell A, et al. "Clinical Features and APOE Genotype of Pathologically Proven Early-onset Alzheimer Disease." Neurology. 2011. 76(20): 1720-1725

—€¢ Psychotic disorders are usually preceded by a prodromal phase, a gradual deterioration of global and social functioning, and the emergence of attenuated psychotic symptoms. Patients experiencing this prodromal phase have a very high risk of developing a full-blown psychotic disorder, but it is not possible to predict, on the basis of their presenting clinical features, which of them are among the 20 percent to 50 percent who will develop psychosis, usually within 24 months. Thus, individuals first seen with prodromal symptoms are said to be at ultra-high risk (UHR) for psychosis.

Neuroimaging studies have suggested that there are detectable volumetric differences between UHR individuals who later develop psychotic disorder and those who do not. An international team of researchers recently evaluated 182 UHR individuals and 167 healthy controls, who were observed clinically for a mean of two years. Forty-eight individuals (26.4 percent) in the UHR group developed psychosis, while 134 did not. Magnetic resonance images were acquired from each participant, and group differences in gray matter volume were examined using optimized voxel-based morphometry.

The UHR group as a whole had less gray-matter volume than did controls in the frontal regions bilaterally. The UHR subgroup who later developed psychosis had less gray-matter volume in the left parahippocampal cortex than did the UHR subgroup who did not. The researchers concluded that individuals at high risk for psychosis show alterations in regional graymatter volume regardless of whether they subsequently develop the disorder.

Mechelli A, Riecher-Rössler A, Meisenzahl E, et al. "Neuroanatomical Abnormalities That Predate the Onset of Psychosis." Arch Gen Psychiatry. 2011 68(5): 489-49522.inline-graphic-1.gif

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