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Breastfeeding for longer 'improves child's intelligence'

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Main Category: Pregnancy / Obstetrics
Also Included In: Pediatrics / Children's Health;  Neurology / Neuroscience
Article Date: 30 Jul 2013 - 5:00 PDT Current ratings for:
Breastfeeding for longer 'improves child's intelligence'

Researchers have discovered that the longer a mother breastfeeds, the more intelligent their child will become later in life.

A study, published in the journal JAMA Pediatrics has provided evidence that breastfeeding in infancy leads to better cognitive development later in life, but it depends upon how long the infant is breastfed.

Researchers from Boston Children's Hospital say previous work has suggested that breast milk can boost an infant's brain as it contains docosahexaenoic acid (DHA), which helps cognitive development. They add that fish intake during lactation is a good source of DHA.

The study authors say: "Nutrients in breast milk, such as n-3 fatty acid DHA, may benefit the developing brain. A major determinant of breast milk DHA content is the mother's diet, and fish is a rich source of DHA.

"In pregnancy, greater maternal fish intake (particularly fish low in mercury contamination) is associated with better childhood cognitive outcomes, but the extent to which maternal fish intake during lactation accounts for the relationship between breastfeeding and cognition has not been reported."

The researchers analyzed 1,312 mothers and children to see the relationship between breastfeeding duration and child cognition at ages 3 and 7 years.

Authors recommend breastfeeding until at least 12 months, and certainly past 6 months

Children were measured on whether they were breastfed milk only, received mixed feeds, weaned or were never breastfed. For 1,224 of the participants at age 3, the mean duration of any breastfeeding, including mixed feeds, was 6.4 months. The mean duration for breastfeeding only was 2.4 months.

Fish intake by mothers during lactation was also analyzed to see how this would affect associations of infant feeding and later cognition.

A series of cognitive tests were carried out, including:

Peabody Picture Vocabulary Test at age 3Wide Range Assessment of Visual Motor Abilities at age 3 and 7Kaufman Brief Intelligence Test and Wide Range Assessment of Memory and Learning at age 7

The results showed that longer breastfeeding duration was linked with higher test scores in the Peabody Picture Vocabulary test at age 3, and higher intelligence on the Kaufman Brief Intelligence Test at age 7.

However, results showed that longer breastfeeding duration was not linked to any improvement in the Wide Range Assessment of Memory and Learning scores.

Children whose mothers had high fish intake during lactation (greater than or equal to 2 servings per week) had stronger results in the Wide Range Assessment of Visual Motor Abilities at age 3, compared with children of women who had lower fish intake (less that 2 servings per week).

The study authors conclude:

"Our results support a causal relationship of breastfeeding in infancy with receptive language at age 3 and with verbal and nonverbal IQ at school age.

These findings support national and international recommendations to promote exclusive breastfeeding through age 6 months and continuation of breastfeeding through at least age 1 year."

Dr. Dimitri Christakis, of the Seattle Children's Hospital Research Institute, has written an editorial in JAMA Pediatrics to accompany the researchers' study, calling for women to be given better opportunities to breastfeed for longer. Dr. Christakis says:

"Workplaces need to provide opportunities and spaces for mothers to use them.

Breastfeeding in public should be destigmatized. Clever social media campaigns and high-quality public service announcements might help with that."

The problem, Dr. Dimitri Christakis adds, "is not so much that most women do not initiate breastfeeding, it is that they do not sustain it."

He continues: "In the US about 70% of women overall initiate breastfeeding, although only 50% of African American women do. However, by six months, only 35% and 20%, respectively, are still breastfeeding."

Written by Honor Whiteman

Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today Visit our pregnancy / obstetrics section for the latest news on this subject.

"Infant feeding and childhood cognition at ages 3 and 7 years: Effects of breastfeeding duration and exclusivity," Belfort MB, Rifas-Shiman SL, Kleinman KP et al, JAMA Pediatrics, 2013. DOI: 10.1001/jamapediatrics.2013.455. Abstract/summary 'online first', July 29

"Breastfeeding and cognition: Can IQ tip the scale?" Dimitri A. Christakis, JAMA Pediatrics, 2013. DOI: 10.1001/jamapediatrics.2013.470. Abstract/summary 'online first', July 29

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Whiteman, Honor. "Breastfeeding for longer 'improves child's intelligence'." Medical News Today. MediLexicon, Intl., 30 Jul. 2013. Web.
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posted by Sultan on 30 Jul 2013 at 8:06 am

" The mothers shall give suck to their offspring for two whole years " ( QURAN: SURAH ABAQARAH:233)

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posted by Samuel Smith on 30 Jul 2013 at 4:59 am

My wife breastfed all three of our children for as long as they wanted, each one to about three years of age. The oldest is now forty and the youngest is 24. They seem to me to above average, but then, I am their father! I thought it was a great experience cause I never had to get up and feed the baby! Also, all three were reasonably healthy in their youth. Frankly, we should remember - that's why God created breasts!

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posted by ben bonarigo on 30 Jul 2013 at 4:55 am

Incomplete and divergent results especially since the Wide Range studies show no significant improvement. This article is an attempt to promote the authors opinion rather than scientific evidence.

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'Breastfeeding for longer 'improves child's intelligence''

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Anti-herpes virus drug treatment may benefit some chronic fatigue syndrome patients

Main Category: Infectious Diseases / Bacteria / Viruses
Article Date: 30 Jul 2013 - 0:00 PDT Current ratings for:
Anti-herpes virus drug treatment may benefit some chronic fatigue syndrome patients

Many experts believe that chronic fatigue syndrome (CFS) has several root causes including some viruses. Now, lead scientists Shara Pantry, Maria Medveczky and Peter Medveczky of the University of South Florida's Morsani College of Medicine, along with the help of several collaborating scientists and clinicians, have published an article in the Journal of Medical Virology suggesting that a common virus, Human Herpesvirus 6 (HHV-6), is the possible cause of some CFS cases.

Over 95 percent of the population is infected with HHV-6 by age 3, but in those with normal immune systems the virus remains inactive. HHV-6 causes fever and rash (or roseola) in infants during early childhood, and is spread by saliva. In immunocompromised patients, it can reactivate to cause neurological dysfunction, encephalitis, pneumonia and organ failure.

"The good news reported in our study is that antiviral drugs improve the severe neurological symptoms, including chronic pain and long-term fatigue, suffered by a certain group of patients with CFS," said Medveczky, who is a professor of molecular medicine at USF Health and the study's principal investigator. "An estimated 15,000 to 20,000 patients with this CFS-like disease in the United States alone may ultimately benefit from the application of this research including antiviral drug therapy."

The link between HHV-6 infection and CFS is quite complex. After the first encounter, or "primary infection," all nine known human herpesviruses become silent, or "latent," but may reactivate and cause diseases upon immunosuppression or during aging. A previous study from the Medveczky laboratory showed that HHV-6 is unique among human herpesviruses; during latency, its DNA integrates into the structures at the end of chromosomes known as telomeres.

Furthermore, this integrated HHV-6 genome can be inherited from parent to child, a condition commonly referred to as "chromosomally integrated HHV-6," or CIHHV-6. By contrast, the "latent" genome of all other human herpesviruses converts to a circular form in the nucleus of the cell, not integrated into the chromosomes, and not inheritable by future generations.

Most studies suggest that around 0.8 percent of the U.S. and U.K. population is CIHHV6 positive, thus carrying a copy of HHV-6 in each cell. While most CIHHV-6 individuals appear healthy, they may be less able to defend themselves against other strains of HHV-6 that they might encounter. Medveczky reports that some of these individuals suffer from a CFS-like illness. In a cohort of CFS patients with serious neurological symptoms, the researchers found that the prevalence of CIHHV-6 was over 2 percent, or more than twice the level found in the general public. In light of this finding, the authors of the study suggest naming this sub-category of CFS "Inherited Human Herpesvirus 6 Syndrome," or IHS.

Medveczky's team discovered that untreated CIHHV-6 patients with CFS showed signs that the HHV-6 virus was actively replicating: determined by the presence of HHV-6 messenger RNA (mRNA), a substance produced only when the virus is active. The team followed these patients during treatment, and discovered that the HHV-6 mRNA disappeared by the sixth week of antiviral therapy with valganciclovir, a drug used to treat closely related cytomegalovirus (HHV-5). Of note, the group also found that short-term treatment regimens, even up to three weeks, had little or no impact on the HHV-6 mRNA level.

The investigators assumed that the integrated virus had become reactivated in these patients; however, to their surprise, they found that these IHS patients were infected by a second unrelated strain of HHV-6.

Further studies are needed to confirm that immune dysregulation, along with subsequent chronic persistence of the HHV-6 virus, is the root cause of the IHS patients' clinical symptoms, the researchers report.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our infectious diseases / bacteria / viruses section for the latest news on this subject.

The USF-led study was supported by the HHV-6 Foundation and the National Institutes of Health.

Article citation: “Persistent human herpesvirus-6 infection in patients with an inherited form of the virus; ” Shara N. Pantry, Maria M. Medveczky, Jesse H. Arbuckle, Janos Luka,Jose G. Montoya, Jianhong Hu, Rolf Renne, Daniel Peterson, Joshua C. Pritchett, Dharam V. Ablashi, andPeter G. Medveczky; Journal of Medical Virology; published online July 25, 2013; DOI: 10.1002/jmv.23685

University of South Florida (USF Health)

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Osteoporosis Prevention Tips for Women

Osteoporosis is a highly prevalent disease among women; half of women over 50 will break a bone due to osteoporosis, according to the National Osteoporosis Foundation. Characterized by thinning of the bone that leads to fractures, the condition is caused by the fact that the body stops rebuilding bone fast enough to replace degeneration as we age. This generally begins in the mid 30's, but it usually doesn't pose any risks until women reach menopause. Men also suffer from osteoporosis, but usually at a much older age.

When a woman hits menopause, her shares of the hormone estrogen decline dramatically. This hormone is responsible for preventing the breakdown of women's bones. Any situation indicating low estrogen levels, including lack of a menstrual period before a woman reaches a natural age for menopause, is a risk factor for osteoporosis. Combined with the sudden drop in estrogen, women also have smaller, thinner bones than men generally. It's important for women to focus on preventative methods.

Below are several measures you can take to help prevent osteoporosis.

1) Take calcium and vitamin D supplements, the latter of which helps the body absorb calcium.

2) Do exercise that subjects the bones to weight-bearing, which encourages rebuilding.

3) Increase your intake of foods that contain calcium. Dairy products aren't the only foods that contain calcium. Kale, collard greens, tempeh, fortified orange juice, turnip greens and blackstrap molasses are all potent sources.

4) Avoid excess salt consumption. Aside from increasing your risk of heart disease, a Japanese study, available at http://www.sciencedaily.com/releases/2013/06/130617110931.htm, found that very high sodium intake correlates with bone fracture risk.

5) Research is currently inconclusive, but the results of some studies suggest that fructooligosaccharides, aside from being fun to say, are good for your bones. These non-digestible carbs may increase your body's ability to absorb calcium. They're found in chicory root, onions, tomatoes, asparagus and wheat.

6) Take steps to avoid insulin resistance, the hallmark of type 2 diabetes. Insulin resistance is common among people who are overweight. A study, found at http://www.sciencedaily.com/releases/2013/06/130617110715.htm, determined diabetics to have weaker bones than non-diabetics. The best ways to prevent type 2 diabetes are to exercise and eat well, maintaining a healthy weight.

7) If you're too young to be experiencing menopause but have stopped getting your period (or never started), see a doctor. If no dysfunction is found, you may wish to begin using birth control to regulate your hormones. The extra estrogen will help keep your bones strong.

As with most health conditions, preventing osteoporosis involves eating right and exercising. Taking simple steps now to prevent this and other conditions will help you live longer and better as you age.

Solutions specific to pregnancy back pain, weight loss and other women specific issues. Please ask questions, give comments or stories related to this article submission for women's issues.

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Children who use gestures tend to perform better on cognitive tasks

Main Category: Psychology / Psychiatry
Also Included In: Pediatrics / Children's Health
Article Date: 30 Jul 2013 - 0:00 PDT Current ratings for:
Children who use gestures tend to perform better on cognitive tasks

In the first study of its kind, SF State researchers have shown that younger children who use gestures outperform their peers in a problem-solving task.

The task itself is relatively simple -- sorting cards printed with colored shapes first by color, and then by shape. But the switch from color to shape can be tricky for children younger than 5, says Professor of Psychology Patricia Miller.

In a new study due to be published in the August, 2013 issue of Developmental Psychology, Miller and SF State graduate student Gina O'Neill found that young children who gesture are more likely to make the mental switch and group the shapes accurately.

In fact, gesturing seemed to trump age when it came to the sorting performance of the children, who ranged from 2 and a half years old to 5 years old. In the color versus shape task, as well as one that asked children to sort pictures based on size and spatial orientation, younger children who gestured often were more accurate in their choices than older children who gestured less. The children's gestures included rotating their hands to show the orientation of a card or using their hands to illustrate the image on the card, for example gesturing the shape of rabbits' ears for a card depicting a rabbit.

"Gina and I were surprised by the strength of the effect. Still, the findings are consistent with a growing body of research showing that mind and body work closely together in early cognitive development," Miller said.

"The findings are a reminder of how strong individual differences are among children of a particular age," she added. "Certain 3-year-olds look like typical 4-year-olds. This likely reflects an interaction of natural talent and particular experiences -- both nature and nurture, as usual."

There is a growing body of research that suggests gesturing may play a significant role in the processes that people use to solve a problem or achieve a goal. These processes include holding information in memory, keeping the brain from choosing a course too quickly and being flexible in adding new or different information to handle a task.

Studies have shown that gesturing can help older children learn new math concepts, for example. "Really, though, there is evidence that gesturing helps with difficult cognitive tasks at any age," Miller said. "Even we adults sometimes gesture when we're trying to organize our tax receipts or our closets. When our minds are overflowing we let our hands take on some of the cognitive load."

O'Neill and Miller observed the children's spontaneous gestures as they performed the tasks, as well as gestures they were encouraged to make to explain their sorting choices. Both kinds of gestures were counted in comparing high and low gesturing children.

Children who did a lot of gesturing did better at the sorting task than those who didn't gesture as much -- even when they did not use gesturing during the task itself, the researchers found. This makes it difficult to determine whether it's the gesturing itself that helps the children perform the task, or whether children who use a lot of gestures are simply at a more advanced cognitive level than their peers. It is a question that Miller hopes to answer in further studies.

Miller said there is "quite a bit of evidence now that gestures can help children think," perhaps by helping the brain keep track of relevant information or by helping the brain reflect on the possibilities contained within a task. "In my opinion, children shouldn't be discouraged from gesturing when they want to gesture during learning," she said. "Adults sometimes -- appropriately -- say to children, 'use your words,' but some children may think this applies to all situations."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our psychology / psychiatry section for the latest news on this subject.

The study, "A Show of Hands: Relations between Young Children's Gesturing and Executive Function," will be published in the August, 2013 issue of the journal Developmental Psychology.

San Francisco State University

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Children's exercise: Hour a day 'not enough'

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FDA approves treatment for major depressive disorder in adults

Main Category: Depression
Also Included In: Regulatory Affairs / Drug Approvals
Article Date: 30 Jul 2013 - 2:00 PDT Current ratings for:
FDA approves treatment for major depressive disorder in adults

Forest Laboratories, Inc. announced that FETZIMA (levomilnacipran extended-release capsules) was approved by the FDA for the treatment of Major Depressive Disorder (MDD) in adults. MDD, also generally known as depression, affects almost 16 million adults in the United States every year. MDD is a serious medical condition, and despite available options, people with MDD often struggle to find a treatment that works for them -- so FDA approval of FETZIMA may be important for adults living with MDD.

FETZIMA is the most recent addition to Forest's growing mental health portfolio. For more than 15 years, Forest Laboratories has been driven by a focus on addressing unmet needs in the area of mental health. Forest's franchise now includes two marketed products for MDD:

VIIBRYD® (vilazodone HCl), launched in 2011, is the first and only selective serotonin reuptake inhibitor (SSRI) and 5-HT1A partial receptor agonist and is indicated for the treatment of adults with MDD.And now FETZIMA, approved in July 2013, is a once-daily serotonin and norepinephrine reuptake inhibitor (SNRI) indicated for MDD in adults.Please see Important Safety Information, including Boxed Warning, for FETZIMA and VIIBRYD below.

Together, these products reflect Forest's research-driven approach toward identifying and developing a range of treatment options for the millions of Americans who live with MDD.

In three placebo-controlled, pivotal Phase III studies of adult patients with MDD, statistically significant and clinically meaningful improvement in depressive symptoms was demonstrated across three FETZIMA dosage strengths of 40, 80, and 120 mg once daily compared with placebo as measured by the Montgomery Åsberg Depression Rating Scale (MADRS) total score (primary endpoint). FETZIMA also demonstrated superiority over placebo as measured by improvement in the Sheehan Disability Scale (SDS) functional impairment total score (secondary endpoint).

FETZIMA is a serotonin and norepinephrine reuptake inhibitor (SNRI) indicated for the treatment of Major Depressive Disorder (MDD) in adults.

FETZIMA is not approved for the management of fibromyalgia. The efficacy and safety of FETZIMA for the management of fibromyalgia have not been established.

WARNING: SUICIDAL THOUGHTS AND BEHAVIORS

Antidepressants increased the risk of suicidal thoughts and behavior in children, adolescents, and young adults in short-term studies. These studies did not show an increase in the risk of suicidal thoughts and behavior with antidepressant use in patients over age 24; there was a reduction in risk with antidepressant use in patients aged 65 and older.

In patients of all ages who are started on antidepressant therapy, monitor closely for worsening, and for emergence of suicidal thoughts and behaviors. Advise families and caregivers of the need for close observation and communication with the prescriber. FETZIMA is not approved for use in pediatric patients.

FETZIMA is contraindicated in patients with a hypersensitivity to levomilnacipran, milnacipran HCl, or to any excipient in the formulation.The use of MAOIs intended to treat psychiatric disorders with FETZIMA or within 7 days of stopping treatment with FETZIMA is contraindicated due to an increased risk of serotonin syndrome. The use of FETZIMA within 14 days of stopping an MAOI intended to treat psychiatric disorders is also contraindicated.Starting FETZIMA in a patient who is being treated with MAOIs such as linezolid or intravenous methylene blue is also contraindicated due to an increased risk of serotonin syndrome.Do not use FETZIMA in patients with uncontrolled narrow-angle glaucoma. All patients being treated with antidepressants should be monitored appropriately and observed closely for clinical worsening, suicidality, and unusual changes in behavior, especially during the first few months of treatment and when increasing or decreasing the dose. Consider changing the therapeutic regimen, including possibly discontinuing the medication, in patients whose depression is persistently worse or includes symptoms of anxiety, agitation, panic attacks, insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia, hypomania, mania, or suicidality that are severe, abrupt in onset, or were not part of the patient's presenting symptoms. Families and caregivers of patients being treated with antidepressants should be alerted about the need to monitor patients daily. Prescriptions for FETZIMA should be written for the smallest quantity of capsules consistent with good patient management, in order to reduce the risk of overdose.Serotonin Syndrome: The development of a potentially life-threatening serotonin syndrome has been reported with SNRIs and SSRIs both when taken alone, but especially when co-administered with other serotonergic agents (including triptans, tricyclic antidepressants, fentanyl, lithium, tramadol, tryptophan, buspirone, and St. John's Wort) and with drugs that impair metabolism of serotonin (in particular, MAOIs, both those intended to treat psychiatric disorders and also others, such as linezolid and intravenous methylene blue). Symptoms of serotonin syndrome may include mental status changes (eg, agitation, hallucinations, delirium, and coma), autonomic instability (eg, tachycardia, labile blood pressure, diaphoresis, flushing, hyperthermia), neuromuscular symptoms (eg, tremor, rigidity, myoclonus, hyperreflexia, incoordination), seizures, and/or gastrointestinal symptoms. If symptoms of serotonin syndrome occur, discontinue FETZIMA and initiate supportive treatment. If concomitant use of FETZIMA with other serotonergic drugs is clinically warranted, patients should be aware of a potential increased risk for serotonin syndrome, particularly during treatment initiation and dose increases.SNRIs, including FETZIMA, have been associated with increases in blood pressure. Blood pressure should be measured prior to initiating treatment and periodically throughout FETZIMA treatment. Pre-existing hypertension should be controlled before initiating treatment with FETZIMA. For patients who experience a sustained increase in blood pressure, discontinuation or other appropriate medical intervention should be considered.SNRIs including FETZIMA have been associated with an increase in heart rate. Heart rate should be measured prior to initiating treatment and periodically throughout FETZIMA treatment. Pre-existing tachyarrhythmias and other cardiac disease should be treated before starting therapy with FETZIMA. For patients who experience a sustained increase in heart rate, discontinuation or other appropriate medical intervention should be considered.SSRIs and SNRIs, including FETZIMA, may increase the risk of bleeding events, some serious. Concomitant use of aspirin, warfarin, NSAIDs and other anticoagulants may add to this risk.Mydriasis has been reported in association with SNRIs including FETZIMA; therefore, FETZIMA should be used with caution in patients with controlled narrow-angle glaucoma. Patients with raised intraocular pressure should be monitored. DO NOT use FETZIMA in patients with uncontrolled narrow-angle glaucoma.SNRIs, including FETZIMA, can affect urethral resistance. Caution is advised when using FETZIMA in patients prone to obstructive urinary disorders.Symptoms of mania/hypomania were reported in 0.2% of FETZIMA-treated patients and 0.2% of placebo-treated patients in clinical studies. As with all antidepressants, FETZIMA should be used cautiously in patients with a history or family history of bipolar disorder, mania or hypomania. Prior to initiating treatment with FETZIMA, patients should be adequately screened to determine if they are at risk for bipolar disorder. FETZIMA is not approved for use in treating bipolar depression.FETZIMA should be prescribed with caution in patients with a seizure disorder.Discontinuation symptoms, some serious, have been reported with discontinuation of serotonergic antidepressants such as FETZIMA. Gradual dose reduction is recommended, instead of abrupt discontinuation, whenever possible. Monitor patients when discontinuing FETZIMA. If intolerable symptoms occur following a dose decrease or upon discontinuation of treatment, consider resuming the previously prescribed dose and decreasing the dose at a more gradual rate.Advise patients that if they are treated with diuretics or are otherwise volume depleted, or are elderly, they may be at greater risk of developing hyponatremia while taking FETZIMA. Although no cases of hyponatremia resulting from FETZIMA treatment were reported in the clinical studies, hyponatremia has occurred as a result of treatment with SSRIs and SNRIs. FETZIMA should be discontinued in patients with symptomatic hyponatremia and appropriate medical intervention should be instituted.

The most commonly observed adverse reactions in MDD patients treated with FETZIMA in placebo-controlled studies (incidence =5% and at least twice the rate of placebo) were: nausea, constipation, hyperhidrosis, heart rate increased, erectile dysfunction, tachycardia, vomiting, and palpitations.

Please also see full Prescribing Information for FETZIMA.

WARNING: SUICIDALITY AND ANTIDEPRESSANT DRUGS

Antidepressants increased the risk compared to placebo of suicidal thinking and behavior (suicidality) in children, adolescents, and young adults in short-term studies of Major Depressive Disorder (MDD) and other psychiatric disorders. Anyone considering the use of VIIBRYD or any other antidepressant in a child, adolescent, or young adult must balance this risk with the clinical need. Short-term studies did not show an increase in the risk of suicidality with antidepressants compared to placebo in adults beyond age 24; there was a reduction in risk with antidepressants compared to placebo in adults aged 65 and older. Depression and certain other psychiatric disorders are themselves associated with increases in the risk of suicide. Patients of all ages who are started on antidepressant therapy should be monitored appropriately and observed closely for clinical worsening, suicidality, or unusual changes in behavior. Families and caregivers should be advised of the need for close observation and communication with the prescriber. VIIBRYD is not approved for use in pediatric patients.

Serotonin Syndrome and MAOIs: Do not use MAOIs intended to treat psychiatric disorders with VIIBRYD or within 14 days of stopping treatment with VIIBRYD. Do not use VIIBRYD within 14 days of stopping an MAOI intended to treat psychiatric disorders. In addition, do not start VIIBRYD in a patient who is being treated with linezolid or intravenous methylene blue.

All patients treated with antidepressants should be monitored appropriately and observed closely for clinical worsening, suicidality, and unusual changes in behavior, especially during the first few months of treatment and when changing the dose. Consider changing the therapeutic regimen, including possibly discontinuing the medication, in patients whose depression is persistently worse or includes symptoms of anxiety, agitation, panic attacks, insomnia, irritability, hostility, aggressiveness, impulsivity, akathisia, hypomania, mania, or suicidality that are severe, abrupt in onset, or were not part of the patient's presenting symptoms. Families and caregivers of patients being treated with antidepressants should be alerted about the need to monitor patients daily. Prescriptions for VIIBRYD should be written for the smallest quantity of tablets consistent with good patient management, in order to reduce the risk of overdose.

Serotonin Syndrome: The development of a potentially life-threatening serotonin syndrome has been reported with SNRIs and SSRIs, including VIIBRYD, both when taken alone, but especially when co-administered with other serotonergic agents (including triptans, tricyclic antidepressants, fentanyl, lithium, tramadol, tryptophan, buspirone, and St. John's Wort) and with drugs that impair metabolism of serotonin (in particular, MAOIs, both those intended to treat psychiatric disorders and also others, such as linezolid and intravenous methylene blue). Symptoms of serotonin syndrome may include mental status changes (eg, agitation, hallucinations, delirium, and coma), autonomic instability (eg, tachycardia, labile blood pressure, diaphoresis, flushing, hyperthermia), neuromuscular symptoms (eg, tremor, rigidity, myoclonus, hyperreflexia, incoordination), seizures, and/or gastrointestinal symptoms. If symptoms of serotonin syndrome occur, discontinue VIIBRYD and initiate supportive treatment. If concomitant use of VIIBRYD with other serotonergic drugs is clinically warranted, patients should be aware of a potential increased risk for serotonin syndrome, particularly during treatment initiation and dose increases. Patients should be monitored for the emergence of serotonin syndrome.

Like other antidepressants, VIIBRYD should be prescribed with caution in patients with a seizure disorder.

The use of drugs that interfere with serotonin reuptake, including VIIBRYD, may increase the risk of bleeding events. Patients should be cautioned about the risk of bleeding associated with the concomitant use of VIIBRYD and NSAIDs, aspirin, warfarin, or other drugs that affect coagulation or bleeding.

Symptoms of mania/hypomania were noted in 0.1% of patients treated with VIIBRYD in clinical studies. As with all antidepressants, VIIBRYD should be used cautiously in patients with a history or family history of bipolar disorder, mania, or hypomania.

Prior to initiating treatment with an antidepressant, patients with depressive symptoms should be adequately screened to determine if they are at risk for bipolar disorder. VIIBRYD is not approved for use in treating bipolar depression.

Discontinuation symptoms have been reported with discontinuation of serotonergic drugs such as VIIBRYD. Gradual dose reduction is recommended, instead of abrupt discontinuation, whenever possible. Monitor patients when discontinuing VIIBRYD. If intolerable symptoms occur following a dose decrease or upon discontinuation of treatment, consider resuming the previously prescribed dose and decreasing the dose at a more gradual rate.

Advise patients that if they are treated with diuretics, or are otherwise volume depleted, or are elderly, they may be at greater risk of developing hyponatremia while taking VIIBRYD. Although no cases of hyponatremia resulting from VIIBRYD treatment were reported in the clinical studies, hyponatremia has occurred as a result of treatment with SSRIs and SNRIs. Discontinuation of VIIBRYD in patients with symptomatic hyponatremia and appropriate medical intervention should be instituted.

The most commonly observed adverse reactions in MDD patients treated with VIIBRYD in placebo-controlled studies (incidence =5% and at least twice the rate of placebo) were: diarrhea (28% vs 9%), nausea (23% vs 5%), insomnia (6% vs 2%), and vomiting (5% vs 1%).

Please also see full Prescribing Information for VIIBRYD.

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Female deaths much less likely to be reported to coroner in England and Wales, UK

Main Category: Women's Health / Gynecology
Article Date: 30 Jul 2013 - 0:00 PDT Current ratings for:
Female deaths much less likely to be reported to coroner in England and Wales, UK

Doctors in England and Wales are much less likely to report a woman's death to a coroner than they are a man's, reveals research published online in the Journal of Clinical Pathology.

Furthermore, women's deaths are less likely to proceed to an inquest, and those that do are less likely to result in a verdict of "unnatural" death than men's, with some coroners particularly likely to favour a verdict according to the sex of the deceased, the research shows.

The authors analysed figures from the Ministry of Justice on the numbers and proportions of deaths reported to all 98 coroners, in each of the 114 jurisdictions in England and Wales, between 2001 and 2010.

These figures were then set in the context of official national statistics on the number of deaths registered in England and Wales over the same period.

Doctors are not obliged to report a death to a coroner, and the legal duty to hold an inquest resides with the coroner, usually prompted by a death in unnatural or violent circumstances, or when the death is sudden, of unknown cause, or happens in prison.

The analysis of the figures showed that coroner reporting rates varied widely across England and Wales.

Plymouth and South West Devon topped the league table, with 87% of registered deaths reported to the coroner between 2001 and 2010, while Stamford in Lincolnshire came bottom, with only 12% of deaths reported to the coroner.

There were no obvious explanations to account for such wide differences, which remained stable throughout the decade, suggesting that local demographics or medico-legal practice had a part to play, say the authors.

Similarly, coroners varied widely in their use of verdicts, which again remained consistent over time, the analysis showed. This is likely to reflect the personal decision making style of the coroner rather than any local patterns in deaths, say the authors.

But when they looked at reporting rates according to the sex of the dead person, a striking gender divide emerged.

While jurisdictions with high reporting rates for men also had high reporting rates for women, and vice versa, male deaths were 26% more likely to be reported to the coroner than female deaths.

Higher reporting rates for men were common across all jurisdictions in England and Wales, and in some areas male deaths were 48% more likely to be reported.

Not only were female deaths less likely to be reported, but they were also less likely to proceed to an inquest.

Female deaths were half as likely to proceed to an inquest as men's, with just 8% going to this stage compared with 16% of all male deaths. And even when female deaths did get an inquest, they were more likely to be given a verdict of natural causes than men (28% compared with 22%).

Among verdicts of unnatural deaths, men were overrepresented in occupational diseases and suicide while women were overrepresented in narrative verdicts - where cause of death is given in the form of a narrative rather than as a single "short form" definition - and accidents, implying that sex of the deceased influences the verdict, say the authors.

Furthermore, some coroners were "gendered," in their approach to inquest verdicts, and more likely to favour a particular verdict when dealing with a death, according to the gender of the deceased.

The government is currently reforming the death certification process in a bid to strengthen arrangements and improve the quality and accuracy of causes of death, but there are some concerns that the move will prompt a fall in deaths reported to the coroner from the present national average of 46% to around 35%, say the authors.

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Happiness is expressed in your genes

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Main Category: Genetics
Also Included In: Psychology / Psychiatry
Article Date: 30 Jul 2013 - 8:00 PDT Current ratings for:
Happiness is expressed in your genes

"If you're happy and you know it..." Researchers have studied how "positive psychology" impacts gene expression in humans.

Steven Cole from UCLA led a team who examined the human genome - some 21,000 genes - in light of two different classifications of happiness:

Eudaimonic well-being - the type of happiness associated with having "a deep sense of purpose and meaning in life"Hedonic well-being - the type of happiness associated with unmitigated self-gratification.

The researchers assessed 80 healthy adults for hedonic and eudaimonic well-being, and they took into account potential negative psychological and behavioral elements. They then drew blood from the participants and mapped the varying biological effects of either hedonic or eudaimonic well-being, using a gene-expression profile known as conserved transcriptional response to adversity (CTRA).

The CTRA is a shift associated with an increase of inflammation and a decrease in antiviral activities with the genes. This response, notes Steven Cole, probably evolved to aid the immune system in the wake of changing patterns, such as microbial threats accompanying shifting socio-environmental conditions - for example, social conflict and contact.

The study showed that people who had high levels of eudaimonic well-being had low levels of inflammatory gene expression and exhibited a strong expression of antiviral and antibody genes.

The opposite was true for people who had high levels of hedonic well-being - giving high inflammation and low antiviral/antibody expression.

Steven Cole and his team have been studying how the human genome reacts to negative psychology, including stress, misery and fear, for the last 10 years.

He notes that "in contemporary society and our very different environment, chronic activation by social or symbolic threats can promote inflammation and cause cardiovascular, neurodegenerative and other diseases, and can impair resistance to viral infections."

This recent study, which was published in the journal Proceedings of the National Academy of Sciences is the first of its kind to study positive psychology effects on gene expression.

Although the study participants with eudaimonic well-being had positive gene profiles in their immune cells and those with hedonic well-being had more adverse profiles, Cole notes that both groups did not feel any different.

Both groups had similar levels of positivity but their genomes responded quite differently.

Cole adds:

"What this study tells us is that doing good and feeling good have very different effects on the human genome, even though they generate similar levels of positive emotion.

Apparently, the human genome is much more sensitive to different ways of achieving happiness than are conscious minds."

A recent study located a happiness gene, which researchers say affects people's satisfaction with life.

Written by Marie Ellis

Copyright: Medical News Today
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“A functional genomic perspective on human well-being,” Steven Cole, et al., Proceedings of the National Academy of Sciences, published online 29 July 2013.

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High blood pressure risk and playing college football linked

Main Category: Hypertension
Also Included In: Sports Medicine / Fitness
Article Date: 30 Jul 2013 - 2:00 PDT Current ratings for:
High blood pressure risk and playing college football linked

College football players, especially linemen, may develop high blood pressure over the course of their first season, according to a small study in the American Heart Association's journal Circulation.

Researchers documented higher blood pressure levels among 113 first-year college players. Only one player had already been diagnosed with hypertension before the season and 27 percent had a family history of hypertension. At post-season, researchers noted:

47 percent of players were considered pre-hypertensive, while 14 percent had stage 1 hypertension.

While previous studies indicate blood pressure elevation during adolescence and young adulthood can increase heart disease and heart-related death later in life, the unique findings of this study suggest early careful monitoring of young football players and timely treatment could improve their heart health later in life.

"High blood pressure is not a good thing at any point in life, but especially during the first two decades," said the study's senior investigator, Aaron L. Baggish, M.D.

"The findings shouldn't scare players," said Baggish, associate director of the Cardiovascular Performance Program at Massachusetts General Hospital. "The earlier in life we can identify and begin treating it the better, and identifying special at-risk groups, like these players, is essential."

From 2006-11, researchers at Massachusetts General Hospital, Harvard Medical School, and Harvard Department of Athletics tracked blood pressure changes among players on the Harvard University team, before and after their first season. Researchers also examined changes in endurance-trained competitive rowers, but found no corresponding increase in blood pressure, suggesting the phenomenon may be related to periodic episodes of intense exertion such as football, Baggish said.

Overall, blood pressure levels averaged 116/64 millimeters of mercury (mm Hg) - which is normal - before the season, but afterward rose to an average 125/66 mm Hg, which is pre-hypertensive.

Players on the offensive or defensive line who gain weight during the season and have a family history of high blood pressure were most likely to have post-season hypertension.

Researchers also noted structural changes in players' left ventricle, the heart's main pumping chamber, which can be a potential indicator of worsening heart health since it can grow thicker if the chamber is overworked. In this study, left ventricle thickening (left ventricular hypertrophy) was more prevalent among football players than endurance athletes, and it was significantly greater among linemen.

"Importantly, left ventricular hypertrophy among football players was strongly associated with resting blood pressure suggesting that heart remodeling in some athletes may be due to what happens off the playing field," he said.

"Considering the popularity of football in the United States, I believe this knowledge of an association with enhanced prevalence of prehypertension and stage 1 hypertension after one season in some players is extremely important," said American Heart Association spokesperson Ernesto Schiffrin, M.D., Ph.D., who is not affiliated with the study. "However, the study should not be interpreted to mean that playing football causes hypertension. Instead, it suggests increased surveillance particularly in those most susceptible: those with a family history of hypertension or playing on the offensive or defensive line."

Professional football players tend to have higher rates of both hypertension and premature death from heart disease, especially linemen, Baggish noted. He and his colleagues are continuing to monitor players identified as at-risk to gain a better understanding of hypertension and heart disease, if and when it develops, as they age.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our hypertension section for the latest news on this subject.

Article: "Blood Pressure and Left Ventricular Hypertrophy During American-Style Football Participation" Rory B. Weiner, MD; Francis Wang, MD; Stephanie K. Isaacs, BS; Rajeev Malhotra, MD; Brant Berkstresser, MS, ATC; Jonathan H. Kim, MD; Adolph M. Hutter Jr, MD; Michael H. Picard, MD; Thomas J. Wang, MD; Aaron L. Baggish, MD. doi: 10.1161/?CIRCULATIONAHA.113.003522. Author disclosures are on the manuscript.

Editorial: "Tackling Cardiovascular Health Risks in College Football Players" Gary J. Balady, MD; Jonathan A. Drezner, MD, doi: 10.1161/?CIRCULATIONAHA.113.004039

The American Heart Association funded the study.

American Heart Association

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High platelet reactivity on clopidogrel predicts stent thrombosis, heart attack, and bleeding

Main Category: Cardiovascular / Cardiology
Also Included In: Medical Devices / Diagnostics;  Blood / Hematology
Article Date: 30 Jul 2013 - 0:00 PDT Current ratings for:
High platelet reactivity on clopidogrel predicts stent thrombosis, heart attack, and bleeding

Patients who receive a drug-eluting stent (DES) and demonstrate high platelet reactivity on clopidogrel are more likely to have blood clots form on the stent and to suffer a heart attack; however, these patients are less likely to develop bleeding complications. One-year results of the ADAPT-DES trial was published online in The Lancet. The findings were first presented at last year's Transcatheter Cardiovascular Therapeutics (TCT) annual scientific symposium.

ADAPT-DES is the largest study ever to explore the overall treatment implications of platelet reactivity on patient outcomes after successful coronary drug-eluting stent implantation. Researchers investigated the relationship between platelet reactivity during dual therapy with aspirin and clopidogrel and clinical outcomes such as stent thrombosis, major bleeding, and other adverse events.

The study enrolled 8,583 patients at 11 sites in the US and Germany who underwent a percutaneous coronary intervention (PCI) with at least one drug-eluting stent between January 7, 2008, and September 16, 2010. Researchers assessed platelet reactivity with the VerifyNow Aspirin, P2Y12, and IIb/IIIa tests. Patients were followed for one year to determine the relationship between platelet reactivity and subsequent events. At one year, stent thrombosis had occurred in 70 patients (0.8 percent), heart attack in 269 (3.1 percent), major bleeding in 531 (6.2 percent), and death in 161 (1.9 percent).

Platelet reactivity units (PRU), an index of platelet inhibition to clopidogrel, were measured by the VerifyNow P2Y12 test. High platelet reactivity, defined as a PRU of greater than 208, was present in 42.7 percent of patients. At one year, researchers found that high platelet reactivity was significantly associated with stent thrombosis (1.3 percent vs. 0.5 percent) and heart attack (3.9 percent vs. 2.7 percent), but was also found to be protective against major bleeding (5.6 percent vs. 6.7 percent). High platelet reactivity was also associated with one-year mortality (2.4 percent vs. 1.5 percent). However, because high platelet reactivity is also associated with other patient risk factors and baseline characteristics, multivariable modeling was also performed; it showed no independent association between high platelet reactivity and mortality.

"Results from the ADAPT-DES registry definitely demonstrate that high platelet reactivity after implantation of drug-eluting stents is an independent predictor of one-year stent thrombosis and heart attack, but it is also protective against major bleeding, both of which impact mortality," said lead investigator Gregg W. Stone, MD. Dr Stone is professor of medicine at Columbia University College of Physicians and Surgeons and Director of Cardiovascular Research and Education at the Center for Interventional Vascular Therapy at NewYork-Presbyterian Hospital/Columbia University Medical Center. Dr. Stone is also co-director of the Medical Research and Education Division at the Cardiovascular Research Foundation (CRF).

"Because of the counteracting effects of ischemia and bleeding, platelet reactivity was not an independent predictor of one-year mortality. Therefore, overcoming high platelet reactivity with more potent antiplatelet agents is unlikely to improve survival unless the beneficial effect of reducing stent thrombosis and heart attack can be separated from the likely increase in bleeding that results from greater platelet inhibition," said Dr. Stone.

Dr. Stone added: "Platelet reactivity on aspirin was unrelated to stent thrombosis, heart attack, or death, but may be related to bleeding. This raises questions as to the utility of aspirin in patients treated with drug-eluting stents."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cardiovascular / cardiology section for the latest news on this subject.

The ADAPT-DES trial was sponsored by CRF with research support from Boston Scientific, Abbott Vascular, Medtronic, Cordis, Biosensors, The Medicines Company, Daiichi Sankyo, Eli Lilly, Volcano, and Accumetrics.

Cardiovascular Research Foundation

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Hope for motion sickness victims: Key neurons identified that sense unexpected movement

Main Category: Neurology / Neuroscience
Also Included In: Public Health
Article Date: 30 Jul 2013 - 1:00 PDT Current ratings for:
Hope for motion sickness victims: Key neurons identified that sense unexpected movement

It happens to all of us at least once each winter in Montreal. You're walking on the sidewalk and before you know it you are slipping on a patch of ice hidden under a dusting of snow. Sometimes you fall. Surprisingly often you manage to recover your balance and walk away unscathed. McGill researchers now understand what's going on in the brain when you manage to recover your balance in these situations. And it is not just a matter of good luck.

Prof. Kathleen Cullen and her PhD student Jess Brooks of the Dept of Physiology have been able to identify a distinct and surprisingly small cluster of cells deep within the brain that react within milliseconds to readjust our movements when something unexpected happens, whether it is slipping on ice or hitting a rock when skiing. What is astounding is that each individual neuron in this tiny region that is smaller than a pin's head displays the ability to predict and selectively respond to unexpected motion.

This finding both overturns current theories about how we learn to maintain our balance as we move through the world, and also has significant implications for understanding the neural basis of motion sickness.

Scientists have theorized for some time that we fine-tune our movements and maintain our balance, thanks to a neural library of expected motions that we gain through "sensory conflicts" and errors. "Sensory conflicts" occur when there is a mismatch between what we think will happen as we move through the world and the sometimes contradictory information that our senses provide to us about our movements.

This kind of "sensory conflict" may occur when our bodies detect motion that our eyes cannot see (such as during plane, ocean or car travel), or when our eyes perceive motion that our bodies cannot detect (such as during an IMAX film, when the camera swoops at high speed over the edge of steep cliffs and deep into gorges and valleys while our bodies remain sitting still). These "sensory conflicts" are also responsible for the feelings of vertigo and nausea that are associated with motion sickness.

But while the areas of the brain involved in estimating spatial orientation have been identified for some time, until now, no one has been able to either show that distinct neurons signaling "sensory conflicts" existed, nor demonstrate exactly how they work. "We've known for some time that the cerebellum is the part of the brain that takes in sensory information and then causes us to move or react in appropriate ways," says Prof. Cullen. "But what's really exciting is that for the first time we show very clearly how the cerebellum selectively encodes unexpected motion, to then send our body messages that help us maintain our balance. That it is such a very exact neural calculation is exciting and unexpected."

By demonstrating that these "sensory conflict" neurons both exist and function by making choices "on the fly" about which sensory information to respond to, Cullen and her team have made a significant advance in our understanding of how the brain works to keep our bodies in balance as we move about.

The research was done by recording brain activity in macaque monkeys who were engaged in performing specific tasks while at the same time being unexpectedly moved around by flight-simulator style equipment.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our neurology / neuroscience section for the latest news on this subject.

To read the full paper in Current Biology click here.

The research was funded by the Fonds de Recherche du Québec Nature et Technologies and Canadian Institutes of Health Research as well as through a National Institutes of Health grant.

McGill University

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Hospital screening tool for suicide risk among self-harmers should be ditched, UK

Main Category: Mental Health
Also Included In: Psychology / Psychiatry;  Medical Devices / Diagnostics
Article Date: 30 Jul 2013 - 0:00 PDT Current ratings for:
Hospital screening tool for suicide risk among self-harmers should be ditched, UK

A screening tool used in general hospitals to detect suicide risk among patients who have self harmed should be ditched, concludes a study published online in Emergency Medicine Journal.

The technique (SADPERSONS Scale) fails to pick up most of those who require admission to a psychiatric unit, community psychiatric aftercare, or to determine those at risk of self harming again, say the researchers.

The SADPERSONS Scale was developed in the USA in 1983 as a means of assessing suicide risk among patients who had self harmed. It is based on 10 major risk factors, but has changed little since it was first devised, say the researchers.

National guidance in England stipulates that all patients who go to hospital after an episode of self harm should be given a full psychosocial assessment. But current pressures in hospitals to meet waiting time targets, combined with a reduction in the availability of mental health services, mean that emergency care staff are increasingly minded to use rating scales to find out which patients can be discharged without a full psychosocial assessment, say the researchers.

They therefore assessed SADPERSONS scores that had been recorded for 126 patients consecutively admitted to one emergency medicine department in a major general hospital in Oxford during the summer of 2011, to see how accurate it was at predicting how these patients were subsequently managed and treated.

This included admission to a psychiatric unit, a proxy for psychosocial assessment; the provision of community psychiatric aftercare; and bouts of repeated self harm in the following six months.

Self harm was defined as any act of poisoning or injury, irrespective of its purpose. Most of the patients (102; 81%) had taken an overdose; around one in 10 (11%) had cut themselves; and the remaining 10 patients (8%) had inflicted other forms of injury on themselves.

Admission to a psychiatric unit was required in five cases (4%) and community psychiatric aftercare in just over half (55%; 70). One in four patients (24.6%) self harmed again at least once.

The SADPERSONS Scale only picked up 2% of those requiring admission to a psychiatric unit, around 6% of those needing community psychiatric aftercare, and just over 6.5% of those likely to self harm again.

The authors point out that for the purposes of suicide prevention, any technique designed to spot potential suicide risk must have a low rate of false negative results - in other words, it must be accurate and not miss most of those at risk of killing themselves.

While the small numbers of patients in this study don't allow any conclusions to be drawn about the Scale's usefulness in predicting suicide risk, the scores did not pick up very accurately those most at risk of further self harm, which is particularly associated with suicide risk, say the study authors.

Twenty three out of 31 of the episodes of self harm occurred within the first three months of the first visit to emergency care. But only two of these patients had high scores on the SADPERSONS Scale; the rest had low to moderate scores, suggesting they were not at high risk.

"The results clearly show that the SADPERSONS Scale has a very limited role, if any, to play in the assessment of patients presenting to the emergency department following an episode of self harm," write the authors.

"Indeed, arguably, our results show that reliance on the scale for determining who should receive a psychosocial assessment or otherwise using it for prediction is not only misleading, it could be dangerous," they add.

The use of rating scales has become increasingly widespread in response to the need to standardise practice for ever increasing numbers of patients. But these tools often overlook individual dynamics, they say.

"A greater focus on clinical judgement is needed, accompanied by the necessary education, training and supervision, if we are to more accurately fully identify and intervene with those who are at greatest risk following self harm," they conclude.

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Innovation in mouse model helps researchers distinguish disease mechanisms and biomarkers

Main Category: Urology / Nephrology
Article Date: 30 Jul 2013 - 2:00 PDT Current ratings for:
Innovation in mouse model helps researchers distinguish disease mechanisms and biomarkers

A team led by researchers at the National Institutes of Health has overcome a major biological hurdle in an effort to find improved treatments for patients with a rare disease called methylmalonic acidemia (MMA). Using genetically engineered mice created for their studies, the team identified a set of biomarkers of kidney damage - a hallmark of the disorder - and demonstrated that antioxidant therapy protected kidney function in the mice.

Researchers at the National Human Genome Research Institute (NHGRI), part of NIH, validated the same biomarkers in 46 patients with MMA seen at the NIH Clinical Center. The biomarkers offer new tools for monitoring disease progression and the effects of therapies, both of which will be valuable in the researchers' design of clinical trials for this disease.

The discovery, reported in the July 29, 2013, advance online issue of the Proceedings of the National Academy of Sciences, paves the way for use of antioxidant therapy in a clinical trial for patients with MMA. It also illustrates the mechanisms by which dysfunction of mitochondria - the power generators of the cell - affects kidney disease. Mitochondrial dysfunction is a factor not only in rare disorders, such as MMA, but also in a wide variety of common conditions, such as obesity, diabetes and cancer.

MMA affects as many as one in 67,000 children born in the United States. It can have several different causes, all involving loss of function of a metabolic pathway that moderates levels of an organic compound called methylmalonic acid. Affected children are unable to properly metabolize certain amino acids consumed in their diet, which damages a number of organs, most notably the kidneys.

"Metabolic disorders like MMA are extremely difficult to manage because they perturb the delicate balance of chemicals that our bodies need to sustain health," said Daniel Kastner, M.D., Ph.D., NHGRI scientific director. "Given that every newborn in the United States is screened for a number of inherited metabolic disorders, including MMA, there is a critical need for better understanding of the disease mechanisms and therapies to treat them."

MMA is the most common organic acid disorder and invariably impairs kidney function, which can lead to kidney failure. The most common therapy is a restrictive diet, but doctors must resort to dialysis or kidney transplantation when the disease progresses. MMA patients also suffer from severe metabolic instability, failure to thrive, intellectual and physical disabilities, pancreatitis, anemia, seizures, vision loss and strokes.

"There are no definitive treatments for the management of patients with MMA," said Charles Venditti, M.D., Ph.D., senior author and investigator in the Organic Acid Research Section of NHGRI's Genetics and Molecular Biology Branch. "This study is the culmination of collaboration with the patient community. It uses mouse modelling, coupled with innovations in genomics and biochemical analyses, to derive new insights into the causes of renal injury in MMA. Our studies have improved our understanding of the basic biology underlying MMA, created a novel animal model for testing interventions and, now, led us to the promise of a new therapy."

The researchers performed the studies using mice bred to carry gene alterations that disrupt the production of the same mitochondrial enzyme that is defective in patients with MMA. These are called transgenic mice. The enzyme, called methylmalonyl-CoA mutase (MUT), is an important component of the chemical process that metabolizes organic acids, specifically methylmalonic acid.

By measuring gene expression in the transgenic mice using DNA microarrays, researchers discovered 50 biomarkers of gene expression that each indicated declining kidney function. DNA microarrays are silicon chips with many spots to which a given molecule may bind. In this case, the DNA microarrays were used to precisely generate, with the aid of a computer program, a profile of gene expression in a kidney cell.

The researchers chose one of the biomarkers, called lipocalin-2, to test how it correlated with kidney function in 46 MMA patients. Plasma levels of this biomarker rose with kidney deterioration in patients with MMA, and may serve as a valuable indicator of MMA kidney disease progression in the clinic.

"The detection of biomarkers through microarray technology is immensely helpful in pointing to downstream pathways affected by the defective MUT activity," said Irini Manoli, M.D., Ph.D., lead author and a physician scientist and staff clinician in NHGRI's Genetics and Molecular Biology Branch. "The biomarkers provide new plasma or serum tests to follow disease progression in our patients."

Having discovered these important biomarkers of kidney function, the authors turned to kidney physiology experts on their team to explore the structural changes that occur in MMA disease. They analyzed the rate at which the kidneys filter waste from the blood. Co-author and renal physiology expert Jurgen Schnermann, M.D., and members of his laboratory at the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), also part of NIH, demonstrated the early and significant decrease in this rate in MMA mice.

With further studies, the researchers identified increased production of free radicals in tissues from the mice, as well as in the MMA patients. Detection of free radicals indicates chemical instability in cells, which the researchers sought to remedy with antioxidant therapy. After treating the mice with two forms of dietary antioxidants, the researchers observed that the biomarkers of kidney damage diminished and the faltering kidney filtration rate tapered off. The findings demonstrated that readily available antioxidants can significantly affect the rate of decline of kidney function in transgenic mice, which replicate the kidney disease of MMA.

"The next step will be to translate these findings to the clinic," Dr. Venditti said. "With a progressive disorder like MMA, we are hopeful that we have achieved a laboratory success that our patients will benefit from in the near future."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our urology / nephrology section for the latest news on this subject.

Irini Manoli, Justin R. Sysol, Lingli Li, Pascal Houillier, Caterina Garone, Cindy Wang, Patricia M. Zerfas, Kristina Cusmano-Ozog, Sarah Young, Niraj S. Trivedi, Jun Cheng, Jennifer L. Sloan, Randy J. Chandler, Mones Abu-Asab, Maria Tsokos, Abdel G. Elkahloun, Seymour Rosen, Gregory M. Enns, Gerard T. Berry, Victoria Hoffmann, Salvatore DiMauro, Jurgen Schnermann, and Charles P. Venditti, "Targeting proximal tubule mitochondrial dysfunction attenuates the renal disease of methylmalonic acidemia", Published online before print July 29, 2013, doi: 10.1073/pnas.1302764110

For information about the MMA clinical trial, go to ClinicalTrials.gov and search with NCT00078078.

Learn more about the study

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Investing in cardiovascular research benefits economy

Main Category: Cardiovascular / Cardiology
Also Included In: Public Health
Article Date: 30 Jul 2013 - 2:00 PDT Current ratings for:
Investing in cardiovascular research benefits economy

Investing in cardiovascular disease research in Canada provides economic and societal benefits to Canadians, according to new research published in CMAJ Open.

"Our main goal was to understand how much "bang" we were getting from our research "buck" and whether investing in cardiovascular disease research is worthwhile from a population health perspective," writes Dr. Claire de Oliveira, scientist and health economist with the Centre for Addiction and Mental Health (CAMH), Toronto, with coauthors.

Cardiovascular disease is the number one cause of hospitalization and death in Canada. For every $69 spent on cardiovascular health care in the country, $1 was spent on research through public and charitable sector funding.

"We found an internal rate of return of 20.6% for investment in cardiovascular disease research by the public and charitable sectors," the authors write. "Thus, for every $1 spent on public or charitable sources, Canadians receive an income stream of about $0.21 per year in perpetuity. Considering a minimum acceptable rate of return of 12%, this investment is quite attractive."

The internal rate of return is "the annual monetary benefit to the economy for each dollar invested in cardiovascular disease research."

Spending on cardiovascular disease research in Canada has increased from roughly $13 million in 1975 to $41 million in 1990 and $96 million in 2005.

The authors hope this study will help funders determine the return on investment and whether they are spending appropriately.

"Our estimates provide evidence that investing in cardiovascular disease research is valuable and that investments in medical research are returned many times over in societal benefits," conclude the authors.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cardiovascular / cardiology section for the latest news on this subject.

Estimating the payoffs from cardiovascular disease research in Canada: an economic analysis

CMAJ Open - doi: 10.9778/cmajo.20130003

Authors: Claire de Oliveira, MA, PhD, Hai V. Nguyen, PhD, Harindra C. Wijeysundera, MD, PhD, William W.L. Wong, PhD, Gloria Woo, PhD, Paul Grootendorst, PhD, Peter P. Liu, MD, MSc, Murray D. Krahn, MD, MSc

CMAJ Open

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Liver function regenerated and survival extended in mice with hepatic failure using human stem cell-derived hepatocytes

Main Category: Liver Disease / Hepatitis
Also Included In: Stem Cell Research
Article Date: 30 Jul 2013 - 0:00 PDT Current ratings for:
Liver function regenerated and survival extended in mice with hepatic failure using human stem cell-derived hepatocytes

Researchers have generated functional hepatocytes from human stem cells, transplanted them into mice with acute liver injury, and shown the ability of these stem-cell derived human liver cells to function normally and increase survival of the treated animals. This promising advance in the development of cell-based therapies to treat liver failure resulting from injury or disease relied on the development of scalable, reproducible methods to produce stem cell-derived hepatocytes in bioreactors, as described in an article in Stem Cells and Development, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the Stem Cells and Development website.

Massoud Vosough and coauthors demonstrate a large-scale, integrated manufacturing strategy for generating functional hepatocytes in a single suspension culture grown in a scalable stirred bioreactor. In the article "Generation of Functional Hepatocyte-Like Cells from Human Pluripotent Stem Cells in a Scalable Suspension Culture" the authors describe the method used for scale-up, differentiation of the pluripotent stem cells into liver cells, and characterization and purification of the hepatocytes based on their physiological properties and the expression of liver cell biomarkers.

David C. Hay, MRC Centre for Regenerative Medicine, University of Edinburgh, U.K., comments on the importance of Vosough et al.'s contribution to the scientific literature in his editorial in Stem Cells and Development entitled "Rapid and Scalable Human Stem Cell Differentiation: Now in 3D." The researchers "developed a system for mass manufacture of stem cell derived hepatocytes in numbers that would be useful for clinical application," creating possibilities for future "immune matched cell based therapies," says Hay. Such approaches could be used to correct mutated genes in stem cell populations prior to differentiation and transplantation, he adds.

"The elephant in the room for stem cell therapy rarely even acknowledged let alone addressed in the literature is that of scalable production of cells for translational application," says Editor-in-Chief Graham C. Parker, PhD, research professor, Carman and Ann Adams Department of Pediatrics, Wayne State University School of Medicine. "Baharvand's groups' landmark publication not only demonstrates but exquisitely describes the methodology required to scale up stem cell populations for clinical application with a rigor to satisfy necessary manufacturing standards."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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New understanding of actin filament growth in cells

Main Category: Biology / Biochemistry
Also Included In: Cancer / Oncology;  HIV / AIDS
Article Date: 30 Jul 2013 - 2:00 PDT Current ratings for:
New understanding of actin filament growth in cells

University of Oregon biochemists have determined how tiny synthetic molecules disrupt an important actin-related molecular machine in cells in one study and, in a second one, the crystal structure of that machine when bound to a natural inhibitor.

The accomplishments - done in the name of fundamental understanding, or basic science - provide new windows on the complexities of cellular structure and suggest a potential future route to therapeutic targeting, said Brad J. Nolen, a professor of chemistry and biochemistry at the UO, who was principal investigator on both studies.

The machinery is the actin-related protein 2/3 complex (Arp2/3), a large assembly of seven proteins that stick together. This complex is critical to cell motility - the ability to move and perform myriad duties - and for initializing the construction of a network of filaments known as the actin cytoskeleton that provides structural support for cells.

"In addition to cells having a lot of actin, they also have a lot of proteins that bind to actin to control its dynamics," said Nolen, who has just completed his second year as a Pew Scholar in the Biomedical Sciences. "And that's exactly what the complex does. It binds to the side of pre-existing actin filaments, where it nucleates the growth of new filaments. The Arp2/3 complex is very highly conserved, like actin. All of your cells are chock full of actin much like a yeast cell. There are very few differences between the molecule in yeast and in human cells."

The cell loses control of the actin cytoskeleton in various diseased states, including certain viral infections, such as HIV and cancer, he said.

Nolen, also a member of the UO's Institute of Molecular Biology, began studying the Arp2/3 complex's role in cytoskeletal network formation during postdoctoral research at Yale University, where he was part of a team that in 2009 identified two distinct classes of molecules that inhibited normal activity of the machinery. The discovery, reported in the journal Nature, opened the way for exploring how the complex works.

Reporting in a recent issue of the journal Chemistry & Biology, Nolen and a team of UO researchers, in a series of biochemical, biophysical and X-ray crystallography experiments, exposed the complex to the two tiny synthetic molecules, which turned off actin-filament initiation as anticipated. More importantly, they were able to capture exactly where the molecules docked, or bound, with the much larger macromolecular Arp2/3 complex.

That binding activity, they found, was enough to block the ability of the machinery to align properly for activating filament production. "We found that these small molecules throw a monkey wrench in this macromolecular machine and lock it into the off state," Nolen said. "By locking it into the off state it prevents it from nucleating branched filaments."

What was seen in the Arp2/3 complex, Nolen said, will help to understand precisely how actin is controlled in cells. "Cell motility requires actin inside the cell to constantly be remodeled," he said. "A lot of studies are showing that the Arp2/3 complex is very important for cell motility. So if we can figure out the Arp2/3 complex works, we can better understand how it affects things like cellular motility and, therefore, how we might affect things like metastasis of tumors.

In the second paper, placed online July 28 in advance of regular publication in the journal Nature Structural & Molecular Biology, Nolen and Quing Luan, a research technician in the UO's Institute of Molecular Biology, report the first crystal structure of the Arp2/3 complex while bound with a natural occurring inhibitor, glial maturation factor, known as GMF.

"We have determined the three-dimensional structure of all of the atoms that make up each of the sub-units of the Arp2/3 complex, and we've created a 3-D picture of where this regulator binds to the complex by using X-ray crystallography," Nolen said. "What this tells us is the structural basis for how GMF regulates the Arp2/3 complex. It binds to the complex and blocks the initiation of Y-shaped branches that create new filaments. It also binds to the pre-existing branches and causes them to pop off, so it is involved in the disassembly of these networks."

There is a difference, he noted, in how inhibitor molecules in the two studies worked. The synthetic versions in the first study, while binding to specific locations, did not block separate filament-building activators from also binding to the complex but instead stopped activation by locking the complex into a non-productive position. GMF while bound to the complex, on the other hand, blocked activators from also locking on.

The different results, Nolen said, could guide future efforts therapeutic delivery of molecules, or drugs, to fight disease-related scenarios in damaged cells. His lab is now working with a computational chemist on the design of molecules that might drive desired alterations in the complex and related actin regulators without unintended consequences of toxicity.

"We are pursuing the potential clinical value," Nolen said. "It's basic research with a potential long-term payoff, or it may never happen. For now what we've provided is a basic-science tool."

"Researchers at the University of Oregon continue to further our understanding of the dynamic processes that inform multi-level health and well-being," said Kimberly Andrews Espy, vice president for research and innovation and dean of the UO graduate school. "By helping to elucidate the complexities of cellular structure, Dr. Nolen's research may eventually lead to more effective targeting of tumors and other diseases."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our biology / biochemistry section for the latest news on this subject.

Byron Hetrick, Min Suk Han, Luke A. Helgeson, Brad J. Nolen, Small Molecules CK-666 and CK-869 Inhibit Actin-Related Protein 2/3 Complex by Blocking an Activating Conformational Change, Chemistry & Biology, doi: 10.1016/j.chembiol.2013.03.019

Co-authors with Nolen on the Chemistry & Biology paper were postdoctoral researcher Byron Hetrick and graduate students Min Suk Han and Luke Helgeson. The National Institutes of Health (RO1-GM092917 to Nolen and F32-GM097913 to Hetrick, the lead author) and American Heart Association (10SDG2610189 to Nolen) supported the research.

The NIH (RO1-GM092917) and Pew Scholars in the Biomedical Sciences program of the Pew Charitable Trusts supported Nolen for the work in Nature Structural & Molecular Biology. Experiments were done at the Argonne National Laboratory's Advanced Photon Source, a U.S. Department of Energy-funded facility operated by the University of Chicago.

University of Oregon

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