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Mental Health News

Following are the latest news and information resources for the various mental health topics that we cover. We hope you will find the news educational and the links in the resources section useful in helping you to get even more in-depth data.

Differences Between A Panic Attack And Having Panic Disorder

A panic attack occurs when there is an unexpected and abrupt episode of fearfulness, nervousness and endless worrying. It usually happens without forewarning and for no real and valid reason at all. In many cases, panic attacks occur repeatedly and are often triggered by specific situations. One feels being threatened by a certain situation and escaping or fleeing the place is not possible. Panic attacks may happen as part of another mental condition like panic disorder, phobia or depression.

Fear is a normal human response or reaction to certain situations which are potentially dangerous and threatening. But when fear becomes an exaggerated reaction to situations where there are no reasons to be frightened about, it is manifestation of a mental condition known as panic disorder. Panic attacks repeatedly occurring combined with key changes in behavior or chronic anxiety over having more attacks or episodes may develop into a severe mental condition known as panic disorder.

Panic Disorder Symptoms

A person manifesting the following symptoms may be suffering from panic disorder :

Experiencing panic attacks frequently than usual and the panic attacks are not connected or linked to a specific situation.

Anxiety over having another episode of panic attack.

Odd or strange behaviour as a result of the panic attacks.

People with panic disorder are emotionally and physically drained. The memory of severe fear or anxiety felt during a panic attack can make a negative impact on one’s self-confidence. Further frequent panic attacks may interfere with one’s normal daily routine or function.

Anticipatory anxiety – a continuous and non-stop feeling anxious and tense. This anxiety is caused by fear of having follow-up panic attacks.

Phobic avoidance – this is when you start avoiding places or situations or events, believing that they have triggered previous panic attacks. Phobic avoidance in severe cases is likely to develop into agoraphobia or fear of public and open spaces where escape would not be easy and could cause embarrassment or humiliation.

Known Causes of Panic Disorder

The exact cause of panic disorder is not determined to date but several studies and researches have identified the following as what cause panic disorders :

Medical conditions or physical problems such as hyperthyroidism, mitral valve prolapse (a minor heart problem), hypoglycemia, medication withdrawal and use of stimulants.

Genetic links. The condition is passed on to family members by family members.

Life changes or transitions like working for the first time, graduating from college, being pregnant, getting married; and traumatic circumstances like loss of a loved one to death, divorce or losing a job.

Substance abuse. Drugs and alcohol abuse contribute to the onset of panic disorder symptoms.

Abnormal chemicals in the brain. Abnormal activities in the brain causes by some chemical imbalance can cause the panic attack.

Recommended Treatments for Panic Attacks and Panic Disorder

There are treatments available for panic attacks and panic disorder. It can be any of the four treatment options, namely :

Cognitive Behavioral Therapy or CBT. This is considered the most effective way of treating the condition. It helps the persons with panic disorder or experiencing panic attacks to have a different view on the triggers of fear or anxiety. The therapy focuses on identifying and recognizing thought and behavior patterns which have direct contribution to the onset of panic disorder symptoms. The therapy will help the person understand that there is no ‘real’ life-threatening or dangerous outcome from situations or places causing the anxiety. The psychotherapist will painstakingly explain until the person accepts the realistic scenario presented by such feared situations or events or environment. Once it becomes clear to the person that there is no real danger, the anxiety will slowly dissipate.

Exposure Therapy. The psychotherapist will create a safe and controlled environment for exposing the person to the physical feeling or awareness of panic or anxiety. This will give the person the chance to learn important coping techniques when faced with feared situations or places. The psychotherapist may teach some simple exercises to mimic panic or anxiety sensations like head shaking, deep breathing or holding the breath. The person will be able to become less anxious every time these exercises are done. A sense of control is gained by exposing the person to these exercises.

Medication or prescription drugs. Prescription medicines may be used to control or reduce the symptoms of panic attack or panic disorder. But medication should only be used as a temporary treatment option and should be combined with psychotherapy. Antidepressants and benzodiazepines are the common prescribed drugs to help control the symptoms. As in any mental condition, the use of drugs should be under the advice and supervision of the doctor and psychotherapist.

Self-help techniques. These simple techniques are helpful in controlling the symptoms.

Learn about the disorder. The more you know about the disease, the better will be your understanding of your situation.

Avoid triggers like cigarettes, alcohol and caffeine. By keeping triggers away, symptoms are somehow controlled.

Learn breathing control techniques. Breathing exercises calm down the nerves so when anxiety sets in, try deep breathing exercises.

Resort to relaxation exercises when symptoms are showing. Yoga exercises, meditation and other relaxation exercises will enhance the body’s response to relax. They should be part of regular routine.

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Women Face Gender-Specific Challenges In Fighting Addiction And Alcoholism

Men Are From Mars, Women Are From Venus, trumpeted a popular book in the 1990s.

Author John Gray didn’t sell 50 million copies of his book and spark a pop culture fire by telling us anything most of us hadn’t learned by grade school. Men and women are different. Gray just focused on the interpersonal perspective — how we communicate and how these gender differences can lead to conflict.

Here’s another significant way in which the sexes differ: addiction, its aftermath and treatment.

Take alcohol. Men and women metabolize drinks differently.

“Depression is more frequent in women than in men; addiction is more frequent in men than women, but if women have a problem of addiction or alcoholism, there is more likely of having other psychiatric problems like depression. The likelihood they were exposed to trauma is higher,’’ said Dr. Ihsan Salloum, professor of psychiatry and behavioral sciences and chief of the Division of Substance and Alcohol Abuse at the University of Miami Miller School of Medicine.

Women also experience different influences and relapse triggers, according to the Hanley Center, a residential treatment center for women ages 18-46 in West Palm Beach.


The National Institute for Alcohol and Alcohol Abuse estimates that about 5.5 million women drink alcohol at levels that place their health at risk. Double that number for men, said Dr. John Eustace, medical director at the South Miami Hospital Addiction Treatment and Recovery Center. Alcohol abuse can result in liver damage, hepatitis, brain disease, breast cancer and heart disease.

A report from the Substance Abuse and Mental Health Services Administration (SAMHSA) and U.S. Department of Health and Human Services found that in 2012 there were more than 1.7 substance abuse treatment admissions domestically. Alcohol was the most frequently reported primary substance at treatment admission among all racial and ethnic groups. The average age at admission among alcohol-only admissions was 41.

Males, aged 12 and older, represented 67 percent of admissions to these treatment centers in 2012, down from 70 percent in 2002, suggesting that more women were beginning to seek help. For example, 41 percent of the patients at South Miami Hospital’s Addiction Treatment & Recovery Center are women, compared to 10 percent in the 1980s and ’90s, said Eustace.

About two-thirds, 66 percent, of alcohol-only admissions nationwide were non-Hispanic whites, followed by blacks and Hispanics at 13 percent each.

Depression, which can stand alone or be a by-product of alcohol abuse, given alcohol’s depressive effect on the central nervous system, impacted women at twice the rate of men, according to a national drug use and health study by SAMHSA. Among adults aged 18 or older, an estimated 14.8 percent (31.6 million adults) had experienced at least one major depressive episode in their lifetime. Females (10.3 percent) were almost twice as likely as males (5.6 percent) to report a recent past year episode.

Heroin and prescription drug addiction are on the rise among affluent women, according to a 2014 survey from Caron Treatment Centers, parent company of the Hanley Center. Women cited anxiety (65 percent), depression (67 percent) and a critical internal voice (69 percent) as significant factors for their addiction. The top three stressors were relationships with parents and siblings (63 percent), romantic relationships (60 percent) and work (49 percent).


Addiction, for both genders, impacts the brain’s medial forebrain bundle, also known as as the reward target of the body that gets activated whenever an individual engages in an activity perceived as pleasurable, which can include eating and sex. Physical changes to the brain, brought about by the release of dopamine when pleasure centers are tapped, can render people vulnerable to over use.

You eat, you enjoy, you eat again and derive nourishment to sustain life. Similarly, sex feels good, we procreate, the species survives. But drugs —and alcohol is a drug — causes the brain to release dopamine in a disproportional quantity compared to regular pleasurable activity like eating, having sex or exercising. The brain is not built for such over-stimulation and as a result the pleasure centers of the brain require a larger hit to derive the same sensation and addiction can take root.

Genetics is a risk factor but there is not a sex link gene to determine whether a person becomes addictive or not, Eustace said. “The risk for addiction, in general, is higher if there is a first-order relative that is identified. A female grandparent doesn’t mean the girls are more at risk. It’s equal between the male and the female,” he said.


A woman’s physiological make-up makes her stand apart from her male counterparts, even when their size doesn’t differ by much.

“An ounce-and-a-half of alcohol is going to be metabolized differently in women than men regardless of their size,” said Eustace.

Take two 135-pound individuals, a man and a woman. Give each a glass of alcohol.

“Women physiologically have less of a chemical called alcohol dehydrogenase. That is the chemical that immediately begins to break alcohol down into a less toxic, less neurobiologic chemical. So when the woman takes that ounce-and-a-half of ethyl alcohol it’ll be metabolized much slower. Now, if they take another ounce-and-a-half an hour later, rather than starting the process over like the men, there’s going to be an accumulative effect.,” Eustace said.

Weight equality aside, still other factors come into play. The “volume of distraction,” Eustace said.

“The same 135-pound person, the male is more likely to have more percentage of body muscle than fat. What that’s important is that alcohol gets distributed in fat and water substances more so than muscle and alcohol dehydrogenase is much more prevalent in muscle tissue than in fat or water. So right away, the male who takes an ounce-and-a-half will start to digest it both in their stomach and in their muscles, whereas in a woman it will be distributed in a larger volume and slower metabolism so the risk of a toxic effect of the drug goes up more in women than men.

And more often, men are bigger than women. “Because of this, there is less distribution of alcohol in the body and because of more fat content women might be exposed to a higher percent of alcohol in the brain compared to men,” Salloum said.

“That’s the physiological and biological reason, it’s not that men are tougher by some macho formula: ‘I can hold my booze and you can’t.’ It isn’t that at all. That would be a sociological mistake,” Eustace said.

Another property of alcohol is that it is a central nervous system depressant.

“Part of its pharmacology is to depress nerve conduction,” Eustace said. This can lead to a toxic effect when overused. The general guidelines suggest that women consume no more than seven ounces of alcohol per week and no more more than four ounces at any one sitting over the course of an evening, he recommends.

Salloum agreed, adding that men’s make-up can tolerate about 14 ounces a week. “Any more than that could be unhealthy drinking,” he said.

For women who drink socially, or for relief of tension, anxiety, the depressant properties of the beverage can become toxic even if the goal is innocent. “That’s part of the seductive nature of the drug,” Eustace said. “That’s where brain disorders, cardiomyopathy, fatty liver, bone marrow suppression, the risk of malnutrition, all come from the toxic effect of alcohol.”


Kevin Bandy, clinical director of Hanley Center, said that when women seek treatment at the venue the majority of them reported depression, anxiety and a critical internal voice, that subconscious inner monologue that says things like, ‘I’m not a good mother. I’m not going to be able to get well. How am I going to meet friends for drinks after work?’

“One interesting thing about gender is that women are able to identify that they have that critical inner voice,” Bandy said. “That voice is not gender specific. I found our study interesting that the women identified it as something that is a trigger for them.”

The concept of having to “hit bottom” before seeking treatment can also be a dangerous exercise for women given the physiological differences in metabolism of drugs and alcohol. “Externally motivated people actually do better in treatment — people who have something to get sober for. They don’t want to lose family. Lose jobs. They are on probation. Those people have better results,” Bandy said, also noting that group therapy, for which women generally gravitate more toward than men, is more effective.

“Group therapy has the highest rate of efficacy for substance abuse treatment. Makes sense. We live, thrive and exist in systems. Group therapy offers us a chance to be part of a system,” he said.

“When people drink heavily they get depressed,” Salloum said. “Heavy drinkers, 80 percent would tell you they are depressed and 30 percent might have clinical depression when you ask in a more structured way. Clinical depression, independent from alcohol, does improve when you get away from drinking, but the depression still needs to be treated.”

Medications, in pill form and injections, which block the opioid endorphins in our systems that lead to cravings are among the treatment options, as well as therapy at recovery centers and ongoing, post-treatment counseling.

Other triggers to recognize and circumvent include surrounding stigmas — ‘Now I’m an addict in recovery. How will I be seen at my place of employment and seen by my peers? How can I go out with my friends? What can I say?’

Said Bandy: “An informed population just understands and tolerates people and accepts them for who they are.”

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Potential Drug Treatment For Alcohol Abuse Studied At USC

The USC School of Pharmacy has provided data suggesting that a common anti-parasitic medicine can be used therapeutically to help people overcome alcohol use disorders.

Megan Yardley, who will receive her PhD from the Department of Pharmacology and Pharmaceutical Sciences this summer, conducted the research as part of her advanced research training with the TL1 program offered by the Southern California Clinical and Translational Sciences Institute (SC CTSI).

Yardley’s pre-clinical investigations indicate that the drug ivermectin (IVM) — used safely for decades to treat parasitic infections in both humans and animals — may also be used as an alcohol-reduction therapy to help alcohol-dependent patients and individuals that abuse alcohol.

The mechanism for this new indication is currently under investigation, but her data from mouse models suggests that IVM is able to reduce alcohol intake in both social and binge drinking by affecting several different proteins in the brain that alcohol acts upon.

The human toll of problem drinking

A reported 18 million people in the United States have alcohol use disorders, although the actual total is likely much larger because many problem drinkers don’t seek help or receive diagnoses. According to the World Health Organization, in 2012 about 3.3 million deaths — 5.9 percent of all global deaths — were attributable to alcohol consumption.

But medical solutions have not been easy to find. The three U.S. Food and Drug Administration-approved drugs for alcohol abuse are rarely effective. Therapy and programs such as Alcoholics Anonymous, without a pharmacological adjunct, are often unsuccessful, with about a 70 percent relapse rate in the first year.

“Despite the widespread serious social and medical harm attributed to alcohol, there is a lack of effective therapies for alcohol use disorders,” Yardley said.

IVM does not appear to have addictive properties and may prove to be a safe and effective new option to help people break their dependence on alcohol, possibly in combination with therapy or behavioral intervention.

“But there are still many questions we need to answer to better understand how alcohol works in the brain to cause problem drinking and how IVM might affect these processes,” Yardley said.

Key support for research

Daryl Davies, an associate professor at the School of Pharmacy who has been studying IVM for the past six years, served as Yardley’s mentor. The SC CTSI supported two of his studies as well as Yardley’s research as a TL1 scholar.

“None of this new clinical research would have happened had it not been for the TL1 program’s support,” Davies said. “We’ve seen that with some effort and creative financing, we can pull together small amounts of money to fund early stages of research and then go after larger funding.”

Yardley will continue to study IVM in a postdoctoral appointment at UCLA, where she will work with principal investigator Lara Ray, an addiction researcher at the UCLA Department of Psychology, who has recently started to collaborate with Davies on IVM research.

Yardley has co-authored several publications on IVM and alcohol use disorders with Davies and other researchers at USC. She collaborated on the recent study with Michael Neely, associate professor in the Department of Pediatrics at the Keck School of Medicine of USC.

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New Data On Relationship OCD

Obsessing over the state of your relationship has finally been given a name; and so-called 'Relationship Obsessive-Compulsive Disorder' not only makes you anxious but could also be ruining your sex life, say scientists.

Constantly questioning whether your partner loves you, whether they're the right person for you, or if you even love them at all, are all telling symptoms of the condition.

Other common behaviors included constantly reassessing and doubting the relationship and thinking about and picking at their partner's perceived physical flaws.

Compulsions can involve going to great lengths to check that your partner is loyal, such as repeatedly calling them, looking at their emails or Internet search histories or endlessly asking them whether they 'really mean it' when they express their love

Those who suffer these symptoms were identified as having relationship obsessive-compulsive disorder (ROCD) by researchers.

And the participants were also found to be less satisfied with their sex lives than those who did not question things irrationally, says the new study.

This lower level of sexual satisfaction was explained by a decrease in relationship satisfaction - in other words, it seems that ROCD symptoms reduce relationship happiness, which, in turn, affects sex life, researchers said.

The findings, which were published online this month in the Journal of Sexual Medicine, could have implications for the treatment of some people with relationship and sexual problems, researchers said.

'ROCD symptoms are often overlooked by family and couple therapists,' said study researcher Guy Doron, of the School of Psychology at the Interdisciplinary Center (IDC) Herzliya in Israel.

'People with ROCD have unwanted thoughts even when there is no rational reason to question the relationship'

Scientists say ROCD is a form of obsessive compulsive disorder - a condition that can bring unwanted thoughts or worries, and repetitive behaviors that are carried out to address those worries, usually to no avail.

With ROCD, obsessions usually fit into one of two categories: Questioning whether you love your partner, or questioning whether your partner loves you, said Steven Brodsky, a psychologist and clinical director who has treated patients with ROCD.

For example, one of Doron's patients said that although he loved the woman he was in a relationship with, he couldn't stop thinking about whether he might be happier with women he saw on the street, or on Facebook.

It's normal to have some of these thoughts in relationships from time to time, Brodsky said, but a person is considered to have a disorder if the thoughts impair everyday life, such as the ability to do his or her job.

Brodsky also noted that people with ROCD have unwanted thoughts even when there is no rational reason to question the relationship (i.e., their partner really does love them).

Ultimately, these symptoms can lead to rocky relationships. 'These relationships can often repeatedly break up and reunite multiple times a week' or month, Brodsky said.

ROCD can also become a self-fulfilling prophecy if the symptoms end up pushing a partner away.

In the new study, 157 men and women in Israel filled out an online questionnaire intended to assess ROCD symptoms. Couples had been together for about 15 years, on average. Although the survey could not diagnose ROCD, afterwards Doron estimated that about 1 per cent had the condition.

The more severe participants' symptoms were, the more likely the participants were to be unsatisfied with their sex lives. ROCD symptoms may undermine the ability of a couple to bond emotionally, and lead to stress and sadness, all of which may interfere with pleasure during sex, the researchers said.

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Single Dose Of Drug Reverses Autism-Like Symptoms In Mice

In a further test of a novel theory that suggests autism is the consequence of abnormal cell communication, researchers at the University of California, San Diego School of Medicine report that an almost century-old drug approved for treating sleeping sickness also restores normal cellular signaling in a mouse model of autism, reversing symptoms of the neurological disorder in animals that were the human biological age equivalent of 30 years old.

The findings, published in the June 17 online issue of Translational Psychiatry, follow up on similar research published last year by senior author Robert K. Naviaux, MD, PhD, professor of medicine, pediatrics and pathology, and colleagues.

Naviaux said the findings fit neatly with the idea that autism is caused by a multitude of interconnected factors: “Twenty percent of the known factors associated with autism are genetic, but most are not. It’s wrong to think of genes and the environment as separate and independent factors. Genes and environmental factors interact.  The net result of this interaction is metabolism.”

Naviaux, who is co-director of the Mitochondrial and Metabolic Disease Center at UC San Diego, said one of the universal symptoms of autism is metabolic disturbances. “Cells have a halo of metabolites (small molecules involved in metabolism, the set of chemical processes that maintain life) and nucleotides surrounding them. These create a sort of chemical glow that broadcasts the state of health of the cell.”

Cell defense

Cells threatened or damaged by microbes, such as viruses or bacteria, or by physical forces or by chemicals, such as pollutants, react defensively, a part of the normal immune response, Naviaux said. Their membranes stiffen. Internal metabolic processes are altered, most notably mitochondria — the cells’ critical “power plants.” And communications between cells are dramatically reduced. This is the “cell danger response,” said Naviaux, and if it persists, the result can be lasting, diverse impairment. If it occurs during childhood, for example, neurodevelopment is delayed.

“Cells behave like countries at war,” said Naviaux. “When a threat begins, they harden their borders. They don’t trust their neighbors. But without constant communication with the outside, cells begin to function differently. In the case of neurons, it might be by making fewer or too many connections. One way to look at this related to autism is this: When cells stop talking to each other, children stop talking.”

Naviaux and colleagues have focused on a cellular signaling system linked to both mitochondrial function and to the cell’s innate immune function. Specifically, they have zeroed in on the role of nucleotides like adenosine triphosphate (ATP) and other signaling mitokines – molecules generated by distressed mitochondria. These mitokines have separate metabolic functions outside of the cell where they bind to and regulate receptors present on every cell of the body. Nineteen types of so-called purinergic receptors are known to be stimulated by these extracellular nucleotides, and the receptors are known to control a broad range of biological characteristics with relevance to autism, such as impaired language and social skills.

In their latest work, Naviaux again tested the effect of suramin, a well-known inhibitor of purinergic signaling that was first synthesized in 1916 and is used to treat trypanosomiasis or African sleeping sickness, a parasitic disease. They found that suramin blocked the extracellular signaling pathway used by ATP and other mitokines in a mouse model of autism spectrum disorder (ASD), ending the cell danger response and related inflammation. Cells subsequently began behaving normally and autism-like behaviors and metabolism in the mice were corrected.

However, the biological and behavioral benefits of suramin were not permanent, nor preventive. A single dose remained effective in the mice for about five weeks, and then washed out. Moreover, suramin cannot be taken long-term since it can result in anemia and adrenal gland dysfunction.

Clinical trial to begin

Still, Naviaux said these and earlier findings are sufficiently encouraging to soon launch a small phase 1 clinical trial with children who have ASD. He expects the trial to begin later this year.

“Obviously correcting abnormalities in a mouse is a long way from a cure in humans, but we think this approach – antipurinergic therapy – is a new and fresh way to think about and address the challenge of autism.

“Our work doesn’t contradict what others have discovered or done. It’s another perspective. Our idea is that this kind of treatment – eliminating a basic, underlying metabolic dysfunction – removes a hurdle that might make other non-drug behavioral and developmental therapies of autism more effective.  The discovery that a single dose of medicine can fundamentally reset metabolism for weeks means that newer and safer drugs might not need to be given chronically.  Members of this new class of medicines might need to be given only intermittently during sensitive developmental windows to unblock metabolism and permit improved development in response to many kinds of behavioral and occupational therapies, and to natural play.”

Co-authors are Jane C. Naviaux, Michael A. Schuchbauer and Susan B. Powell of the UCSD Department of Psychiatry; Kefeng Li and Lin Wang, UCSD Mitochondrial and Metabolic Disease Center and UCSD Department of Medicine; and Victoria B. Risbrough, UCSD Department of Psychiatry and San Diego Veterans Affairs Center for Excellence in Stress and Mental Health.

Funding for this research came, in part, from the Jane Botsford Johnson Foundation, the National Institutes of Health (grant MH091407), the UCSD Christini Fund, the Wright Family Foundation and the It Takes Guts Foundation.

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Lithium, Quetiapine Equally Effective For Bipolar Disorder

A head-to-head comparison of the efficacy of lithium and the second-generation antipsychotic quetiapine (Seroquel, AstraZeneca Pharmaceuticals LP) in the treatment of bipolar disorder shows there are no real differences between the 2 drugs.

Both agents, which were given together with adjunctive personalized treatment (ATP), emerged from the 6-month Clinical Health Outcome Initiative Comparative Effectiveness (CHOICE) trial neck and neck, with the exception of a very few minor differences.

"Despite adequate power to detect clinically meaningful effects, we found no significant differences on most measures," said Andrew Nierenberg, MD, director of the Bipolar Clinic and Research Program at Massachusetts General Hospital and professor, Harvard Medical School, Boston.

"The good news is that most of the patients actually did improve substantially; the bad news is that maybe a quarter ended up doing really well by the end of 6 months, and we don't know if the study had been extended further whether we would see a difference, whether both would continue to improve, or whether they would have relapses or other problems," he added.

The results were presented here at the American Society of Clinical Psychopharmacology (ASCP) 2014 Annual Meeting.

Surprise Findings

One surprise finding was that 24% of lithium patients and 27.3% of quetiapine patients continued receiving monotherapy throughout the study period. "They didn't need anything else, and we thought that everybody would be on multiple drugs."

The main outcome measures were the Clinical Global Impression–Efficacy Index and the Necessary Clinical Adjustments outcome measure, which assessed changes in APT medications.

Both outcome measures were similar in both groups throughout the study period, Dr. Nierenberg said.

The researchers also assessed the Bipolar Inventory of Symptoms Scale, the Framingham Cardiovascular Risk Score (FCRS), functioning, quality of life, suicidal ideation and behavior, and adverse effects.

All measures except the FCRS improved in both groups equally, Dr. Nierenberg said.

"This was another surprise for us, but this was a fairly big population ― the mean BMI [body mass index] was high at 29, and 44% were obese, 48% had abdominal obesity, and 27.3% had metabolic syndrome. So it may have been that they were already at their maximum weight," he said.

There were some slight differences in side effects, which were slightly greater with lithium, Dr. Nierenberg said. "This was also a surprise because we had anticipated that there might be a sedation load from quetiapine, but we did not see this," he noted.

Another area in which quetiapine performed a bit better was in patients who had more manic symptoms, "but the magnitude here is slight, and the P value is .02," he said.

Lithium, on the other hand, produced slightly better results in patients who had anxiety, a finding Dr. Nierenberg called "counterintuitive." There were no differences in any measures in patients who did not have comorbid anxiety conditions.

"One of our hypotheses for this is that these anxious patients may have been placed on benzodiazepines. We will have to analyze our data further to find out. That's something we can do because we have details on every single other drug that was used, when it was started and stopped, the reason why it was used. So our hypothesis is purely speculative, but we can look at this in the future," Dr. Nierenberg said.

Yet another surprise was that patients with bipolar II disorder did better than patients with bipolar I disorder overall. Additionally, patients who had higher suicide risk scores fared worse than patients with a lower suicide risk score.

"We tortured the data enough to pop out a couple of P values, so I think the differences are relatively minor; overwhelmingly, the data are that there's no big difference between the 2 groups," Dr. Nierenberg said.

Most Patients Did Not Do Well

Commenting on the findings for Medscape Medical News, Holly A. Swartz, MD, of the University of Pittsburgh School of Medicine, in Pennsylvania, noted that although both drugs were equally effective, the fact remains that only one quarter of the patients were truly well at the end of the study.

"This means additional treatments or longer treatment durations may be needed to achieve wellness. Although not tested in CHOICE, other treatments for bipolar disorder, such as evidence-based psychotherapies or combinations of treatment that include lithium plus second-generation antipsychotics, may be needed as part of an algorithm designed to achieve wellness," said Dr. Swartz, who was not part of the study.

Nevertheless, CHOICE "has paved the way for future studies that will allow these questions to be asked in real-world settings," she said.

The information generated by CHOICE will be very helpful to clinicians treating people with bipolar disorder, Dr. Swartz predicted.

"Unlike many earlier studies, CHOICE studied a very representative sample of patients; therefore, results from this study are generalizable to most clinical populations.

"Reassuringly, the results suggest that algorithm-based pharmacotherapy centered on either lithium or a second-generation antipsychotic (quetiapine) results in meaningful reductions in symptoms and improvements in functioning over 6 months for individuals with bipolar I and II disorder. Both approaches work, and there does not appear to be an advantage of one strategy over the other. In light of CHOICE, patients and clinicians should consider issues like personal preference, cost, and side effects in the decision-making process about medications."

Landmark Study

Also weighing in with her opinion on the CHOICE results, A. Eden Evins, MD, MPH, William Cox Family associate professor of psychiatry in the field of addiction medicine, Harvard Medical School, and director, Center for Addiction Medicine at Massachusetts General Hospital, Boston, told Medscape Medical News that "effectiveness studies of this kind can provide critically important information to patients, families, and treaters about the comparative effectiveness of available treatments in the real world."

"For people with bipolar disorder, this means these studies closely follow patients who may be taking 3 or 4 other medications along with the treatment being studied. They follow patients for a meaningful length of time ― in this study, 6 months ― and they compare 2 likely 'best choices' for an illness or a symptom rather than comparing with a placebo and thus inform a likely choice that many patients and their treaters are making together every day."

"This study is a landmark study because it gives strong evidence that the second-generation antipsychotic agent quetiapine may be equally effective to the gold standard treatment, lithium, in the treatment of bipolar disorder under many circumstances," she added.

The study was funded by the Agency for Healthcare Research and Quality (AHRQ). Dr. Nierenberg reports financial relationships with AHRQ, American Drug Utilization Review, American Society for Clinical Psychopharmacology, Appliance Computing, Inc, APSARD, AstraZeneca, Bayamon Region Psychiatric Society, San Juan, Puerto Rico, Baystate Medical Center, Belvoir Publishing, Boston Center for the Arts, Brain Cells, Inc, Brandeis University, Bristol-Myers Squibb, Canadian Psychiatric Association, Cephalon, Clintara, Columbia University, Douglas Hospital/McGill University, Elan, Eli Lilly and Company, EpiQ, Forest, Hillside Hospital, IMEDEX, International Society for Bipolar Disorders, Israel Society for Biological Psychiatry, Johns Hopkins University, Johnson and Johnson, Labopharm, Massachusetts Association of College Counselors, MBL Publishing, Medscape Medical News, Merck, Methylation Science, MJ Consulting, Mylan, New York State, National Institute of Mental Health, Novartis, PamLabs, Pfizer, PGx Health, Physicians Postgraduate Press, Ryan Licht San Foundation, Schering-Plough, SciMed, Shire, Slack Publishing, Sunovion, SUNY Buffalo, Takeda, Targacept, Teva, University of Florida, University of Miami, University of Pisa, University of Texas Southwestern, and University of Wisconsin. Dr. Swartz and Dr. Evins report no relevant financial relationships.

American Society of Clinical Psychopharmacology (ASCP) 2014 Annual Meeting. Presented June 16, 2014.

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Internet Use Can Cause Teenage Depression

Are you reading this from home, in a coffee shop, or perhaps sitting on a mountain top in one of Canada’s national parks?

This past spring, Parks Canada suggested offering Wi-Fi Internet access in up to 50 national parks and historic sites across Canada by the summer of 2014. The suggestion was met with substantial criticism from the public, as the national parks serve as a place of seclusion and calm for many Canadians, relieving them from the stress of keeping up with emails and social media. Parks Canada, however, argue that they are merely responding to a demand from their visitors who want to stay in touch while visiting the parks. The topic divided Canada and many valid points were raised on both sides, like the benefits of being able to access Google maps vs. the online distractions getting in the way of connecting with nature.

I have yet to make up my mind, but the vigorous discussion piqued my interest in the health-related aspects of always having online access — particularly mental health. While the impacts of Wi-Fi in national parks are hard to tease out from the studies I found, there are repercussions of heavy Internet use in general. Although nothing concrete can be said about Parks Canada’s suggestion and how healthy or unhealthy it might be, researchers know a fair amount about heavy Internet use in general.

A quick scan of the scientific literature shows that heavy Internet use — defined differently in each study — is strongly linked to mental health problems, especially in young people. But is it simply the number of hours spent surfing the Internet that affects our mental health? Or is it the things we choose to look at online that are potentially harmful? Or perhaps it is merely the time it takes away from doing something else? Does the act of surfing the Internet somehow affect our brains and push them into a more depression prone state?

In 2002, more than 7000 adolescent boys and girls were asked about their Internet habits and their mental health. They were divided into four groups based on number of hours online per week.

Heavy Internet users; more than 2 hours/day

Regular Internet users; several days/week and less than 2 hours/day

Occasional Internet users; less than 1 hour/ week

Non Internet users

The results showed that heavy internet users were more frequently depressed than regular and occasional Internet users. Surprisingly though, those who did not use the Internet at all were just as depressed as the heavy Internet users. Either end of the spectrum seemed to predispose young people to depression, which perhaps tells us that it is our relationship with the Internet more than the Internet itself that impacts our mental health, and that an obsessive relationship, resulting in countless hours in front of the screen, is just as bad as a fearful relationship shying away from all contact with the Internet.

Many teenagers recognize their Internet use as heavy but refuse to call it an addiction. They often display addictive behaviors, however, without knowing it, and both heavy Internet use and Internet addiction are linked to depression and anxiety in the literature (a recognized tool for assessing possible Internet addiction is available here). But which came first, the chicken or the egg? Does it start with mental health problems and end in specific Internet behaviors, or is it the other way around?

This question was posed by a group of researchers in a 2010 study of 13-18 year old adolescents. It concluded that young people who are initially free of mental health problems, but use the Internet pathologically, can develop depression as a consequence. At the beginning of the study, the researchers used the Young’s Internet Addiction Scale to determine whether the Internet use had a pathological nature or not. At the same time, the adolescents were assessed for anxiety and depression. Nine months later, the measurements were repeated. After adjusting for other potentially confounding factors like area of residence, physical activity level, and study burden, the researchers found that the relative risk of depression for those who used the Internet addictively was about 2.5 times higher than for those who were not addicted to the Internet. From this study it appears that the act of surfing the web can actually bring out mental illness in teenagers all on its own.

So what is a safe number of online hours? There probably isn’t one number. In the 2002 study, two hours a day was considered heavy use. But times have changed, and the impact of those two hours might be equivalent to the impact of a much higher number today. There is no finite number we can use to navigate an online world, and we have to use our best judgement when we decide to log on or off. Excessive Internet use —whatever that is — has some very significant ties to poor mental health, and it seems that especially young people are vulnerable.

So should we install Wi-Fi in our national parks? Well, it might compel some teenagers to stay at the campground with their iPads instead of going hiking with the family. But then again, it might also convince them to come to the campground in the first place.

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Confucius And The Age Of Anxiety

One of the greatest innovations of Confucius' teachings was to change the meaning of the Noble Person from one of inherited rank by birth to one of nobility by moral stature. The Noble Person for Confucius was simply a person of moral goodness. This definition has a number of ramifications for our understanding of Confucian teachings within our own time as it is so dominated by feelings of anxiety and fear.

Confucius points to the Noble Person, chün tzu, as the epitome of human development, a person of moral goodness who is described as having fulfilled a variety of the salient Confucian virtues including goodness, jen, righteousness, i, filial piety, hsiao, empathy, shu and other notable moral qualities.

For Confucius few ever measured up to the ideal of the Noble Person, but it remained the ideal of what all humanity should strive for and should attempt to learn and cultivate if the individual and the world are to be transformed to a moral order resembling the cosmic order of the universe itself, the Way of Heaven, T'ien Tao, in Confucian terms.

Given this new-found focus upon the moral qualities of the Noble Person, Confucius spends much time in the major text of his writings, the Analects, Lun yü, describing the nature of the Noble Person. Many of the passages are set up as a comparison between the Noble Person and its opposite, translated something like petty person, hsiao-jen. Some examples will suffice to show the contrast.

"The Noble Person cherishes virtue; the petty person cherishes comfort: the Noble Person cherishes the law; the petty person cherishes favors." Analects IV:11 (Taylor, Analects, p. 27)

"The Noble Person is conversant with righteousness; the petty person is conversant with profit." Analects IV:16 (Taylor, Analects, p. 27)

And one of the passages that I have always been particularly fond of: "The Noble Person is not a tool." Analects II:12 (Taylor, Analects, p. 23)

In the latter passage, not unlike its very modern usage, a "tool" suggests one who does not stand on their own. They will be used in whatever way someone else should desire. To not be a "tool" is to suggest that they stand on their own moral grounds. They are their own person, not someone being used by another.

As such the Noble Person became the paradigm for Confucian learning and teaching across the centuries.

There are several other features of the Noble Person that fit all we have said, but take the conversation in a different direction, bringing into focus one of the most dominant characteristics of our own age, a malaise that we as individuals as well as societies live with and struggle with day in and day out.

We live in an age of anxiety and fear. There is no need for examples. They are virtually ubiquitous in all we encounter in the world. This is not to suggest that there are not real anxieties and fears, but rather that for most a world of anxiety and fear has been created that has little to do with what is actually out there in the world.

So to the question - what does Confucius say about anxiety and fear and what role does it play in his understanding of the Noble Person?

Confucius suggests in Analects VII:36 that it is the petty person who has a high level of distress, ch'i, while the Noble Person is characterized by being peaceful and calm, tang. The peace and the calm of the Noble Person comes from their capacity to have developed their moral nature of goodness and their capacity to act upon that moral goodness in life situations, following their deepest inner nature.

"The Noble Person has neither anxiety nor fear." "Being without anxiety or fear!" said Niu. "Does this constitute what we call the Noble Person?" The Master said, "When interior examination discovers nothing wrong, what is there to be anxious about, what is there to fear?" Analects XII:4 (Taylor, Analects, p. 33)

Confucius treats anxiety, yu, and fear, chü, as internal feelings, but he also turns them toward an internal standard of right and wrong. The issue then is not what one fears as a source of anxiety out in the world, but the degree to which the individual has created the source of fear and anxiety in themselves by how they have constructed the world they inhabit.

From a Confucian perspective the Noble Person is one who addresses whatever anxieties or fears one feels. The critical element is separating the petty person from the Noble Person. Where in the petty person anxiety and fear live with dominating influence upon the life of the individual, in the Noble Person the individual is in touch with his larger self, what for Confucius would be the Way of Heaven, T'ien-Tao, the moral character of the universe itself. In this state of nobility there is no room for fear or anxiety because they are not part of that moral fiber of the universe.

What lesson does this teaching have for us today? Not unlike contemporary therapies that deal with anxiety and fear, Confucius is suggesting that the petty person is not the real self; it has created a self that is far removed from the capabilities of the true self. It has created its own world of anxiety and fear. It is as a therapist might say, not you, but your thoughts that have created the damage. The challenge is to put aside the thoughts, to put aside the petty person and dwell in the capacity that we all have to live in the reflection of our true and noble self, the self that connects us with all things. In this condition there is no room for anxiety or fear because it is simply not part of the Noble Person or the universal Way of Heaven that the Noble Person embodies.

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Assessing and Enhancing the Effectiveness of Antidepressants

With over 2 dozen FDA-approved antidepressants on the market, it is reasonable to ask: which antidepressants are most effective? After decades of clinical experience and literally millions of prescriptions written over the years, it stands to reason that 1 or 2 agents have risen from the pack to outshine the rest.

Unfortunately, clinical experience shows this not to be the case. The general consensus is that despite their different mechanisms of action, all current antidepressants seem to have more or less the same effect. The functional equivalency of antidepressants is highlighted in practice guidelines and, understandably, serves as justification for restricted formulary access to more expensive agents. As a result, most psychiatrists choose antidepressants not on the basis of efficacy, but rather on the basis of insurance coverage, adverse-effect profiles, or particular clinical features of depression (eg, melancholic, atypical, anxious features), for which some differences in efficacy do exist.

Efficacy vs effectiveness

The question of how well antidepressants work for the routine treatment of depression can be answered in terms of efficacy or effectiveness. An efficacy trial asks the question, Does the drug work under ideal circumstances? Although such trials are usually brief (6 to 8 weeks) and interventions are standardized and rarely flexible, they serve as the basis for the FDA’s approval of drugs.

“Effectiveness” concerns the success or failure of drugs in the real world. A true effectiveness study asks the question, Does the drug work under usual conditions? Effectiveness trials enroll a more heterogeneous population, often with comorbid mental illness, substance abuse, or other psychiatric diagnoses, and health care professionals are often free to offer concurrent therapies. As a result, effectiveness trials tend to have more generalizability, or external validity, to real patient populations.

Effectiveness trials help clinicians and policymakers select which medications work best for a given indication in real-world conditions. Surprisingly, despite decades of experience with antidepressants, information on their relative effective-ness is lacking, while health care costs continue to escalate. As a result, more emphasis is being placed on comparative effectiveness research, in which alternative treatments are compared under real-world conditions, and costs and adverse effects are measured in addition to clinical outcomes.

Effectiveness studies

Effectiveness trials are often large, expensive, and time-consuming. They sometimes take the form of a practical clinical trial in which multiple clinically relevant treatment regimens are compared across a large population of subjects. One such landmark study is the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) trial. In this NIMH-funded study, more than 4000 depressed patients in outpatient psychiatry and primary care practices received citalopram for up to 12 weeks; those who did not improve advanced to later phases that offered augmentation with, or a switch to, a second antidepressant or psychotherapy.

Remission rates in step 1 were low (28%) and decreased further with additional steps. Cumulatively, two-thirds of patients entered remission after 4 steps.3 Direct comparison of the effectiveness of antidepressants was not possible because of the overall lack of randomization and poor statistical power.4 Despite the scope and initial aims of the study, no single antidepressant strategy or combination appeared more advantageous than any other.

Other effectiveness trials have yielded similar results. A 24-week trial that randomized patients to sertraline or citalopram found no significant difference between groups.5 Another 24-week trial of 234 patients randomized to receive sertraline or fluoxetine also found no significant difference.6 In a 2001 study, 573 patients were randomized to 1 of 3 SSRIs for 9 months; sertraline, paroxetine, and fluoxetine were equally effective.7 Patients admitted to a German psychiatric hospital for treatment of depression were followed up for 10 weeks, and response and remission rates were 68.9% and 51.9%, respectively, again with no difference among individual antidepressant agents.8 Effectiveness trials, therefore, seem to confirm the conventional wisdom that no single antidepressant works better than—or worse than—any other.

Meta-analyses of efficacy studies

Efficacy trials rarely resemble real-world conditions and, as such, tend to overestimate how well drugs work. Nevertheless, the aggregation of data from multiple efficacy trials can provide a suggestion as to the relative effectiveness of antidepressants.

In 2005, the Agency for Healthcare Research and Quality commissioned an exhaustive review of antidepressants and their use in MDD.9,10 Close to 300 studies were reviewed, many of them randomized efficacy trials that compared one antidepressant with another. There was sufficient evidence to make 4 drug-drug comparisons: 3 found no significant difference between the two drugs, while another found a small reduction (1.25 points) in the Montgomery-Åsberg Depression Rating Scale (MADRS) score in patients taking escitalopram, relative to citalopram. Findings indicate that there were no significant differences in effectiveness of antidepressants, although individual drugs did differ in terms of onset of action and ease of dosing. A 2011 update found a similarly slight benefit of both sertraline and venlafaxine over fluoxetine, as well as confirmation of escitalopram’s slight superiority over citalopram.

In a review of 117 randomized trials involving 25,928 patients, Cipriani and colleagues12 identified slight differences between certain pairs of antidepressants. Known as “network analysis,” this technique permits comparisons of 2 drugs according to how well they perform against a common comparator. Specifically, the authors found that mirtazapine, escitalopram, venlafaxine, and sertraline had slightly greater odds of inducing a response than other antidepressants studied. They also compared relative acceptability of antidepressants (by assessing dropouts) and found the most benefit for escitalopram and sertraline, but differences were slight and of questionable clinical significance.

Because a meta-analysis is only as good as the data on which it is based, these meta-analyses must be considered in light of the very real problem of selective publication. This is the tendency for favorable results to be published, while negative or neutral results are not. In an analysis of 74 antidepressant trials registered with the FDA between 1987 and 2004, Turner and colleagues13 found that nearly half (36, or 48.6%) were negative, and the vast majority of these were either not published or were published in a way that made the drug seem favorable. Likewise, industry-sponsored studies are more likely to favor the manufacturer’s drug, often because of nuances in experimental design.14 While most researchers make every effort to include unpublished results in their meta-analyses, the “file-drawer” phenomenon of unpublished negative results may bias the conclusions of analyses that exclude the inaccessible data.

Enhancing effectiveness

Data appear to confirm 2 stark truths about antidepressants. First, there seem to be no significant differences among them; although future research may uncover patient-specific biomarkers that favor one medication over another, none has yet done so. Second, and somewhat surprisingly, antidepressant effectiveness is quite low. Thus, in the absence of data that can predict the best antidepressant regimen for a patient, enhancing the effectiveness of an antidepressant seems to be the best strategy.

One strategy has nothing to do with antidepressants, but rather involves a reconsideration of what is being treated. Treatment-resistant depression may be better defined as “depression that is resistant to currently available treatments.” Many of these refractory cases may lie on the bipolar spectrum. Study results show that bipolar depression responds poorly to antidepressants, although what counts as “bipolarity” has been the subject of some controversy.

Depression may be multiple conditions, each deserving its own unique treatment approach. Findings suggest that much of the antidepressant response in mild to moderate depression may be due to placebo effect.18 Similarly, patients with a history of trauma may do better with psychotherapy than with medications, while patients with significant anxiety may not respond as well to antidepressants and their depression might resemble a “neurotic” subtype.

Another way to enhance antidepressant effectiveness is to combine antidepressants or use augmentation agents. While combination strategies have intuitive appeal and offer great flexibility, they are not always supported by the available literature. In the Combining Medications to Enhance Depression Outcomes(CO-MED) trial, 665 patients with depression were randomized to receive bupropion plus escitalopram, venlafaxine XR plus mirtazapine, or escitalopram alone. Outcomes at 12 weeks, and again at 7 months, were the same across groups.21 Similarly, while evidence exists for the efficacy of a wide range of augmentation strategies, other analyses have found relatively low effectiveness or excessive cost or adverse-effect burden of some of these approaches.

The more important question may be more about whom we are treating rather than what we treat with. Recent interest in “personalized medicine” seeks to improve depression treatment by using new tools to more accurately identify whom we are treating. It has been estimated that 42% of the variance in antidepressant response can be explained by genetic variation.24 This suggests that nearly half of a patient’s response to an antidepressant may be due to his or her genetic profile. In reality, however, the genetic contribution likely involves an impractically large number of variants, each having a very small effect, that together contribute to the very complex phenotype of antidepressant response. Indeed, 2 meta-analyses, using genome-wide analysis to identify polymorphisms to predict treatment response, found only a 1.2% contribution or no contribution at all.

Another pharmacogenomic approach is to characterize functional variations in patients’ cytochrome P-450 enzymes. Classification of patients as “poor” or “rapid” metabolizers, for instance, may help predict medication choice or dosage. Unfortunately, these approaches are limited. With few possible exceptions, no evidence exists that blood concentrations influence antidepressant outcomes, and there are multiple nongenetic factors that influence drug metabolism, such as diet, other medications, and adherence. Existing studies that show benefit of pharmacogenetic testing are limited because clinicians are unblinded or randomization procedures are poor, a troubling fact given the high rate of placebo response to antidepressant treatment.

Not surprisingly, we can take advantage of patient preferences to enhance treatment outcomes. When patients in a clinical trial receive a treatment they prefer, response rates are significantly higher than when they are randomized to a non-preferred intervention.27 Even when patients’ preferences do not have any bearing on outcome, matching treatments with patients’ preferences increases their willingness to initiate and adhere to a treatment plan.

Clinical trials are often criticized because the ongoing, regular con-tact between patients and clinicians (frequent office visits, abundant personalized attention, etc) may inflate placebo response rates. Indeed, regular contact with health care pro-fessionals has a therapeutic effect in itself, as do patient expectations. When patients in a clinical trial know they will get 1 of 2 active drugs, response rates are one-third higher than when they know they may be randomized to placebo.

Finally, the quality of the therapeutic alliance between prescriber and patient is sometimes a better predictor of patient outcome than which drugs are prescribed. One study found that “effective” prescribers obtained better outcomes with placebos than “less effective” prescribers with active antidepressants.30 Asking “which” medication may be less important than the “meaning” of medication to both clinician and patient. The characteristics of communication between prescriber and patient, whether the patient perceives an internal or external locus of control over the outcome, and a host of other factors may be more important than which drug is prescribed.


The generally accepted view that all antidepressants are essentially equivalent in their effectiveness appears valid. Selection of the right antidepressant, therefore, may rely less on matching a patient to a specific medication, and more on a consideration of adverse-effect profiles or medication availability, or on a redefinition of the phenotype of depression altogether. The recent emphasis on personalized antidepressant prescribing seems warranted, but rather than taking a combination or pharmacogenomic approach to medication selection, clinicians should focus more on a personalized approach, establish realistic (but hopeful) expectations, and use patient preferences and beliefs to optimize outcomes.

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Sleep Disorders Affect 83% Of Children Diagnosed With Autism

If you have a child diagnosed with autism, or who you suspect is on the spectrum, chances are your child is having trouble getting to sleep or staying asleep.  Sleep is essential to support optimal development.  Research at the Arkansas Children’s Research Institute has identified that 90% of children diagnosed with autism have methylation impairments. Methylation impairment can change the way children produce brain chemicals like serotonin, dopamine, GABA, glutamate and norepinephrine. 

With respect to sleep, serotonin is a much need neurotransmitter.  90% of serotonin comes from the gastrointestinal tract.  Up to 85% of children with ASD have digestive problems including constipation, diarrhea, pain and gut flora imbalance.  Serotonin is converted to melatonin with the help of vitamin D.  Vitamin D deficiency is well documented in the autism focused medical research.  Adequate magnesium levels are required for healthy sleep onset and maintenance.  Many children with autism and ADHD have magnesium levels that are lower than normal.  Magnesium deficiency is the 4thmost common nutrient deficiency in North America.  Nutrient deficiencies, digestive problems and methylation impairment combine to negatively impact healthy sleep patterns in ASD.

Children who are experiencing developmental concerns are at a substantially higher risk of experiencing sleep disorders. The children who need sleep the most are having trouble getting to sleep, staying asleep,  having restful sleep are early waking.

Addressing sleep issues in children with autism is multi-faceted.  Many parents have altered routines to accommodate their child’s imbalanced circadian rhythm.  Putting children to sleep much later than same age peers, results in an exhaustion cycle that exacerbates behaviors and sensory overload.  Your child’s body has two ways to get to sleep. One is exhaustion. 

The other one is at their age appropriate bed time which is supported by appropriate melatonin levels.  The melatonin signal is initiated by darkness and regulates the sleep-wake cycle by causing drowsiness.  Limiting TV, iPads and other screens in the evening is important for children with sleep onset insomnia.  Blackout blinds are also crucial to help support the repair of your child’s sleep cycle.  Melatonin production must be stimulated to increase documented low levels experienced by children with an autism diagnosis.  Use of melatonin is an important “band aid” treatment during this time as children’s methylation cycle is supported and repaired.  Other helpful sleep supports include magnesium glycinate, GABA, L-theanine and botanical medicines like valerian, skullcap, lemonbalm, zizyphus and passionflower.

The International Child Development Resource Center performed a systematic review and meta-analysis on melatonin and autism.  Their findings show that most children diagnosed with autism have:

Abnormalities in their melatonin levels

Gene abnormalities that contribute to lower melatonin levels

Show positive changes with respect to sleep duration, onset and night time waking when supplemented with melatonin

Show improvement in autistic behaviors when supplemented with melatonin

Sleep problems in autism usually start at the same age as developmental regression, suggesting a higher vulnerability at this period of life. Healthy sleep patterns are essential to support neuroplasticity and development so it is important to address sleep disorders as soon as possible.  According to the Center of Pediatric Sleep Disorders, studies of melatonin use in children with ASD provide evidence for its effectiveness and safety in the long run.

Melatonin, however, has a larger role to play in development beyond its function as a synchronizer of the biological clock. Melatonin is a hormone that helps in the regulation of the gastrointestinal system.  The gut is 100% responsible for post-natal development. 

In the gut, melatonin, governs intestinal reflexes, motility, the immune function, gut secretions, energy balance, pain regulation and protects against inflammation.  The gut contains at least 400 times more melatonin than the pineal gland  The GI tract produces its own melatonin which suggests it plays a large role in maintaining gut health; both in a healthy digestive tract and in gut disorders. 

Children diagnosed with ASD have alterations in their gut flora in addition to higher prevalence of constipation, diarrhea, reflux and pain.  The balance of good bacteria is not the same as typically developing children.  Melatonin levels change gut flora and improve anti-microbial actions.  With the startling numbers of children experiencing both gut issues and sleep issues, this new research about melatonin’s role in gastrointestinal health could provide clues about treatment and repair of these biological systems.

Other interesting information about melatonin:

Melatonin is also synthesized by the bone marrow cells, white blood cells, mast cells and skin cells

It is a powerful antioxidant

Melatonin helps to protect mitochondria from oxidative stress which damages cells

Melatonin also helps to support glutathione production.  Glutathione is widely considered the most important antioxidant in the    body.  In another study, The Arkansas Children’s Research Institute found that children diagnosed with autism have up to 80% of their glutathione depleted.  Glutathione depletion may be part of the central mechanism for developmental delay because the role it plays in protecting the brain from toxicity

There is research to support that melatonin helps to support healthy immune function by fighting infectious disease including viral and bacterial infections. Finally, Melatonin has shown some promise in modulating the immune function in autoimmune disease.

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Did You Know?

Obesity is Linked to Increased Risk for Psoriatic Arthritis.


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