Good Foods Boost Moods

New research reveals that some common foods enhance moods with a striking similarity to valproic acid, a widely used prescription mood-stabilizing drug.

“Molecules in chocolate, a variety of berries and foods containing omega-3 fatty acids have shown positive effects on mood. In turn, our studies show that some commonly used flavor components are structurally similar to valproic acid,” said Karina Martinez-Mayorga, Ph.D., leader of the research team, which presented its findings at a meeting of the American Chemical Society.

Valproic acid, which is sold under brand names such as Depakene, Depakote and Stavzor, is used to smooth out the mood swings of people with manic-depressive disorder and related conditions, she said.

“The large body of evidence that chemicals in chocolate, blueberries, raspberries, strawberries, teas and certain foods could well be mood-enhancers encourages the search for other mood modulators in food,” she added.

While people have recognized the mood-altering properties of food for years, Martinez-Mayorga’s team is looking to identify the chemical compounds that moderate mood swings, help maintain cognitive health, improve mental alertness and delay the onset of memory loss.

Her study involved the use of techniques associated with chemoinformatics ― the application of informatic methods to solve chemical problems ― to screen the chemical structures of more than 1,700 food ingredients for similarities to antidepressant drugs and other agents with reported antidepressant activity.

She noted her team plans to move from analyzing the database to actually testing the flavor/mood hypothesis experimentally. The end result may be dietary recommendations or new nutritional supplements with beneficial mood effects, she said.

“It is important to remember that just eating foods that may improve mood is not a substitute for prescribed antidepressive drugs,” Martinez-Mayorga cautioned.

She added that eating specific foods and living a healthful lifestyle can generally boost moods for people who don’t require medication.

Karina Martinez-Mayorga, Ph.D., who described research done while working at the Torrey Pines Institute for Molecular Studies, is now with the Chemistry Institute at the National Autonomous University of Mexico.

Source: The American Chemical Society

Strawberries dipped in chocolate photo by shutterstock.

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Bipolar Patients with History of Pot Use Show Better Cognitive Skills

Individuals with bipolar disorder who also have a history of marijuana use demonstrate advanced neurocogitive skills compared to bipolar patients with no history of use, according to research published online in the journal Psychiatry Research.

Researchers from Zucker Hillside Hospital in Long Island, NY, along with colleagues at the Mount Sinai School of Medicine and the Albert Einstein College of Medicine in New York City compared the performance of 50 bipolar subjects with a history of marijuana use to 150 bipolar patients with no history of use with a series of standardized cognitive tests.

Patient groups were similar in regards to age, racial background, and highest education levels achieved. Bipolar patients with a history of marijuana use had similar age at onset as did study participants who had not smoked marijuana.

During the study, researchers discovered that participants with a history of smoking marijuana exhibited better neurocognitive performance than that of non-users, but there was no major difference on estimates of premorbid IQ.

“Results from our analysis suggest that subjects with bipolar disorder and history of (marijuana use) demonstrate significantly better neurocognitive performance, particularly on measures of attention, processing speed, and working memory.”

“These findings are consistent with a previous study that demonstrated that bipolar subjects with history of cannabis use had superior verbal fluency performance as compared to bipolar patients without a history of cannabis use. Similar results have also been found in schizophrenia in several studies,” said the authors.

“These data could be interpreted to suggest that cannabis use may have a beneficial effect on cognitive functioning in patients with severe psychiatric disorders. However, it is also possible that these findings may be due to the requirement for a certain level of cognitive function and related social skills in the acquisition of illicit drugs,” they said.

Source:  Psychiatry Research

 

 

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Cocoa May Slow Cognitive Impairment of Aging

If there is a more pleasurable way of staving off the cognitive impairment of aging than drinking cocoa, perhaps only red wine drinkers have found it.

Flavanols are naturally occurring antioxidants found in abundance in cocoa plants. They help the body deal with free radicals that trigger negative changes in body chemistry and help prevent blood clots.

Now, a new study led by Giovambattista Desideri, M.D., study lead author and associate professor of internal medicine and public health at the University of L’Aquila in Italy, suggests ingesting cocoa flavanols daily may improve mild cognitive impairment.

Experts say that more than six percent of people aged 70 years or older develop mild cognitive impairment (MCI) annually. Moreover, MCI can progress to dementia and Alzheimer’s disease.

Researchers say flavanols may aid brain health by protecting neurons from injury, enhancing metabolism, and facilitating neuronal interaction with the molecular structures responsible for memory. They are also found in tea, grapes, red wine and apples and have been associated with a decreased risk of dementia.

Indirectly, flavanols may help by improving brain blood flow.

In the study, 90 elderly participants with mild cognitive impairment were randomized to drink daily either 990 milligrams (high), 520 mg (intermediate) or 45 mg (low) of a dairy-based cocoa flavanol drink for eight weeks.

Researchers controlled participants’ diet to eliminate other sources of flavanols from foods and beverages other than the dairy-based cocoa drink.

Cognitive function was examined by neuropsychological tests of executive function, working memory, short-term memory, long-term episodic memory, processing speed and global cognition.

Researchers found:

• Scores significantly improved in the ability to relate visual stimuli to motor responses, working memory, task-switching and verbal memory for those drinking the high and intermediate flavanol drinks;
• Participants drinking daily higher levels of flavanol drinks had significantly higher overall cognitive scores than those participants drinking lower-levels;
• Insulin resistance, blood pressure and oxidative stress also decreased in those drinking high and intermediate levels of flavanols daily. Changes in insulin resistance explained about 40 percent of the composite scores for improvements in cognitive functioning.

“This study provides encouraging evidence that consuming cocoa flavanols, as a part of a calorie-controlled and nutritionally-balanced diet, could improve cognitive function,” Desideri said. However, he warns that the beneficial findings may have been influenced by a variety of factors.

“The positive effect on cognitive function may be mainly mediated (influenced) by an improvement in insulin sensitivity. It is yet unclear whether these benefits in cognition are a direct consequence of cocoa flavanols or a secondary effect of general improvements in cardiovascular function.”

Furthermore, the study population was generally in good health without known cardiovascular disease. Thus, it would not be completely representative of all mild cognitive impairment patients.

In addition, only some clinical features of mild cognitive impairment were explored in the study.

“Given the global rise in cognitive disorders, which have a true impact on an individual’s quality of life, the role of cocoa flavanols in preventing or slowing the progression of mild cognitive impairment to dementia warrants further research,” Desideri said.

“Larger studies are needed to validate the findings, figure out how long the positive effects will last and determine the levels of cocoa flavanols required for benefit.”

The research is reported in the American Heart Association’s journal Hypertension.

Source: American Heart Association

Woman drinking cocoa photo by shutterstock.

How Drugs for Schizophrenia Sow Seeds of Resistance

A new study has identified why certain drugs have mixed success in treating schizophrenia; effective at first, but with chronic administration becoming less and less so.

In the study, reported online in the journal Nature Neuroscience, scientists investigated the external genetic reasons (called epigenetic factors) that cause treatment-resistance to atypical antipsychotic drugs.

Use of antipsychotic drugs is the standard of care for schizophrenia. Researchers at Mount Sinai School of Medicine report that 30 percent of individuals with schizophrenia do not respond to currently available treatments.

Researchers discovered that, over time, an enzyme in the brains of schizophrenic patients, analyzed at autopsy, begins to compensate for the prolonged chemical changes caused by antipsychotics, resulting in reduced efficacy of the drugs.

“These results are groundbreaking because they show that drug resistance may be caused by the very medications prescribed to treat schizophrenia, when administered chronically,” said Javier Gonzalez-Maeso, Ph.D., lead investigator on the study.

Researchers found that an enzyme called HDAC2 was highly expressed in the brain of mice chronically treated with antipsychotic drugs, resulting in lower expression of the receptor called mGlu2 and a recurrence of psychotic symptoms. A similar finding was observed in the postmortem brains of schizophrenic patients.

In response, the research team administered a chemical called suberoylanilide hydroxamic acid (SAHA), which inhibits the entire family of HDACs. This treatment prevented the detrimental effect of the antipsychotic called clozapine on mGlu2 expression, and also improved the therapeutic effects of atypical antipsychotics in mouse models.

Previous research conducted by the team showed that chronic treatment with the antipsychotic clozapine causes repression of mGlu2 expression in the frontal cortex of mice, a brain area key to cognition and perception.

The researchers hypothesized that this effect of clozapine on mGlu2 may play a crucial role in restraining the therapeutic effects of antipsychotic drugs.

“We had previously found that chronic antipsychotic drug administration causes biochemical changes in the brain that may limit the therapeutic effects of these drugs,”said Gonzalez-Maeso. “We wanted to identify the molecular mechanism responsible for this biochemical change, and explore it as a new target for new drugs that enhance the therapeutic efficacy of antipsychotic drugs.”

Mitsumasa Kurita, Ph.D., a postdoctoral fellow at Mount Sinai and the lead author of the study, said, “We found that atypical antipsychotic drugs trigger an increase of HDAC2 in the frontal cortex of individuals with schizophrenia, which then reduces the presence of mGlu2, and thereby limits the efficacy of these drugs.”

As a result of these findings, Gonzalez-Maeso’s team is now developing compounds that specifically inhibit HDAC2 as adjunctive treatments to antipsychotics.

Source:The Mount Sinai Hospital/Mount Sinai School of Medicine

Gene Related to Autism Behavior ID’d in Mice Study

In a new mouse study, University of California, Davis, researchers have found that a defective gene is responsible for brain changes that lead to the disrupted social behavior that accompanies autism.

Investigators believe the discovery could lead to the development of medications to treat the condition.

Prior research had determined that the gene is defective in children with autism, but its effect on neurons in the brain was not known.

The new studies in mice show that abnormal action of just this one gene disrupted energy use in neurons. The harmful changes were coupled with antisocial and prolonged repetitive behavior — traits found in autism.

The research is published in the scientific journal PLoS ONE.

“A number of genes and environmental factors have been shown to be involved in autism, but this study points to a mechanism — how one gene defect may trigger this type of neurological behavior,” said study senior author Cecilia Giulivi, Ph.D.

“Once you understand the mechanism, that opens the way for developing drugs to treat the condition,” she said.

The defective gene appears to disrupt neurons’ use of energy, Giulivi said, the critical process that relies on the cell’s molecular energy factories called mitochondria.

In the research, a gene called pten was modififed in the mice so that neurons lacked the normal amount of pten’s protein. The scientists detected malfunctioning mitochondria in the mice as early as 4 to 6 weeks after birth.

By 20 to 29 weeks, DNA damage in the mitochondria and disruption of their function had increased dramatically.

At this time, the mice began to avoid contact with their litter mates and engage in repetitive grooming behavior. Mice without the single gene change exhibited neither the mitochondria malfunctions nor the behavioral problems.

The antisocial behavior was most pronounced in the mice at an age comparable in humans to the early teenage years – a period in which schizophrenia and other behavioral disorders become most apparent, Giulivi said.

The research showed that, when defective, pten’s protein interacts with the protein of a second gene known as p53 to dampen energy production in neurons.

The interaction causes severe stress that leads to a spike in harmful mitochondrial DNA changes and abnormal levels of energy production in the cerebellum and hippocampus — brain regions critical for social behavior and cognition.

Investigators report that pten mutations previously have been linked to Alzheimer’s disease as well as a spectrum of autism disorders.

The new research shows that when pten protein was insufficient, its interaction with p53 triggered deficiencies and defects in other proteins that also have been found in patients with learning disabilities including autism.

Source: University of California – Davis Health System

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Stress, Depression Reduce Brain Volume Thanks to Genetic ‘Switch’

Scientists have known that stress and depression can cause the brain to retract or lose volume, a condition associated with both emotional and cognitive impairment. Now, a new study discovers why this occurs.

Yale scientists have found that the deactivation of a single genetic switch can instigate a cascading loss of brain connections in humans and depression in animal models.

Researchers say the genetic switch, known as a transcription factor, represses the expression of several genes that are necessary for the formation of synaptic connections between brain cells. The loss of connections, in turn, can contribute to loss of brain mass in the prefrontal cortex, say the scientists.

“We wanted to test the idea that stress causes a loss of brain synapses in humans,” said senior author Ronald Duman, Ph.D. “We show that circuits normally involved in emotion, as well as cognition, are disrupted when this single transcription factor is activated.”

In the study, the research team analyzed tissue of depressed and non-depressed patients donated from a brain bank and looked for different patterns of gene activation.

The brains of patients who had been depressed exhibited lower levels of expression in genes that are required for the function and structure of brain synapses.

Lead author and postdoctoral researcher H.J. Kang, Ph.D., discovered that at least five of these genes could be regulated by a single transcription factor called GATA1.

When the transcription factor was activated in animal models, rodents exhibited depressive-like symptoms, suggesting GATA1 plays a role not only in the loss of connections between neurons but also in symptoms of depression.

This finding of genetic variations in GATA1 may help researchers identify people at high risk for major depression or sensitivity to stress.

“We hope that by enhancing synaptic connections, either with novel medications or behavioral therapy, we can develop more effective antidepressant therapies,” Duman said.

Source: Yale University

Face in the Mirror More Distorted in Schizophrenia

Individuals with schizophrenia experience more intense perceptual illusions while gazing into a mirror than do healthy people, according to a new study.

The new research also showed that patients with schizophrenia were more likely to believe the illusions they see in the mirror were real.

The research highlights the underlying ego dysfunction and body dysmorphic disorder found in schizophrenia.

According to the researchers, gazing at one’s own reflected face under low light can lead to ghostly experiences called “strange-face in the mirror” illusions. No study has previously focused on mirror gazing in schizophrenic patients, who already experience delirium, hallucination and self mis-attribution.

Stefano Zago of the University of Milan conducted the study to compare strange-face apparitions in response to mirror gazing in 16 patients with schizophrenia and 21 mentally healthy controls.

Subjects took a 7-minute mirror-gazing test, after which they filled out a specially designed questionnaire asking them to describe their strange-face perceptions.

The results show a number of differences between patients with schizophrenia and mentally healthy controls.  Patients on average reported a greater total number of strange faces than controls, at 2.8 versus 1.5.

The types of strange faces also differed between patients and controls. Hugely deformed features were seen by all schizophrenia patients and 71% of controls, archetypal faces by 50% of patients and 19% of controls, and monstrous faces by 88% of patients and 29% of controls. Patients’ archetypical and monster faces were typically described as satanic beings.

Furthermore, patients tended to report greater intensity in the strange faces and were more likely to say that they felt real than controls.

Of note, mentally healthy participants felt dissociative experiences during the strange-face illusions and never identified with them.

Overall, the research suggests that strange-face illusions in schizophrenia can be caused by ego dysfunction, body dysmorphic disorder, or by misattribution of self-agency, said Zago.

The research is published in Schizophrenia Research.

Source:  Schizophrenia Research