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One of the most challenging first steps in autism treatment is getting an early and accurate diagnosis. One blogger I’ve corresponded with recently said she had to be quite aggressive in persuading her pediatrician to run tests on her two year old son to confirm what she suspected: a diagnosis of autism. Early intervention and therapy has meant her son is much more on track to enter school at an age appropriate time.

Now a clinical trial is set to commence that might allow doctors to diagnose autism with a blood test. From Disability Scoop:

In what’s believed to be the largest such effort to date, a clinical trial expected to launch this week will examine the effectiveness of a possible blood test to detect autism. The 20-site trial is slated to include 660 patients in an attempt to identify children with autism as opposed to other developmental delays through a blood test.

The effort is part of a broader movement to find ways to diagnose kids at younger ages. Experts say earlier diagnosis is important because children with autism respond best to therapy when it begins early.
The new study being sponsored by the company SynapDx is based on findings from several research groups including the work of a team at Boston Children’s Hospital who found that they could accurately differentiate between kids with autism and children with other developmental delays in about two-thirds of cases.

Those behind the initial research say it’s a good starting point, but much more work remains before a diagnosis will be able to be made on biomarkers alone, reported The Wall Street Journal on April 23.


Nearly all of us have unwanted fat cells, but it turns out it could hold some good news for those of us with migraines. From the Migrane.com blog:

For several years, a group of Migraine researchers have been looking at a unique hormone secreted by fat cells, which could serve as a bio-marker for Migraine attacks as well as potentially lead researchers to another new way to target future Migraine treatments.

This is good news for Migraineurs!

Fat as an organ

Fat doesn’t just store energy and keep us warm. Although obesity isn’t a risk factor for Migraine, it has been linked to an increase in both frequency and severity of Migraine attacks as well as being an independent risk factor for chronic daily headache (CDH). It is an important comorbid condition that can exacerbate our Migraine disease.

Did you know you have different kinds of fat cells in your body, and that some of them act just like an endocrine gland? Our bodies are so complex and amazing and this interaction helps explain some other frequently comorbid conditions with Migraine disease too. Research has been ongoing for years, leading some scientists to speculate that obesity may actually be a unique endocrine disorder.

First some background

An endocrine gland secretes hormones that alter the way your organs and cells function. Examples of endocrine glands include


A special kind of fat called adipose fat is found primarily in the abdomen and is often known as *belly fat*. Those with larger tummies have more adipose fat. It is often considered to be an unofficial endocrine organ too because of its unique role in the production of special hormones. A part of the brain called the hypothalamus controls the secretion of hormones from adipose fat.

Some of the hormones adipose cells secrete play roles in our body’s energy and inflammatory homeostasis (balance). Homeostasis is good, and it’s really very important in keeping sensitive Migraine brains from being triggered resulting in a cascade of neuronal and other activity that can lead to a Migraine attack.

These hormones are called Adiponectins because they’re made by adipose fat, and there are two different kinds that seem to directly relate to Migraine. High Molecular Weight (HMW) and Low Molecular Weight (LMW). (A third, Middle Molecular Weight or MMW is a building block that contributes to the formation of HMW resulting in increased inflammation)

In this case the thing to remember is this: High is bad. Low is good.

Because some of these hormones play a part in modulating inflammation and insulin sensitivity and therefore energy metabolism, we want them to stay in balance. We want our body to be able to use energy efficiently (good insulin sensitivity), and we want to minimize inflammation that plays a role in Migraine pathogenesis (how a Migraine attack occurs inside our brains) and other painful conditions.

The old research gives us clues

A few years ago, researchers found several points of interest when they looked at adiponectin in patients with Migraine and chronic daily headache (CDH).

Some interesting things they have learned previously that can be applied to Migraine patients:

–At puberty, females have higher HMW than males.
–Estrogen suppresses adiponectin, and menstrual Migraines usually occur as estrogen levels decline during the end of the menstrual cycle. Could adiponectin then play a part in menstrual Migraine?
–Testosterone suppresses adiponectin which may account for the success of testosterone treatment of male cluster headache patients.
–There is hypothalamic involvement in Migraine, and there are adiponectin receptors in the hypothalamus.

The new research builds on the old studies.

In a more recent, but very small preliminary research study of 20 patients, the ratio between HMW’s and LMW’s was higher during pain. The LMW’s increased though as pain decreased.

According to the authors, HMW’s seem to activate pain pathways and inflammation. LMW’s seem to have anti-inflammatory properties. Having a higher HMW:LMW ratio helped indicate which patients would be responsive to Migraine therapy. Knowing this might help doctors diagnose headache disorders with more accuracy, and may help them decide which treatments might be the most likely to be effective in a given patient.

This study utilized placebos – a *pretend*or sham treatment that won’t actually help a Migraine attack. Those getting the placebo didn’t know that’s what they were getting. However, another interesting finding was that those in the placebo group who felt they had relief of their pain also had corresponding changes in their adiponectin levels.

It is hoped that discovering a way to target and lower adiponectin levels, or even more specifically HMW levels, might be possible. This would represent a brand new way to identify and treat Migraine. Hopefully more research will be done on this in the future.


Sources: 1. Peterlin, B. Lee, DO; White, Linda, CRNP; Dash, Paul, MD; Hammond, Edward, MD, MPH; Haythornethwaite, Jennifer, PhD. “Blood Levels of Fat Cell Hormone May Predict Severity of Migraines”. Johns Hopkins Medicine. Available at: http://www.hopkinsmedicine.org/news/media/releases/blood_levels_of_fat_cell_hormone_may_predict_severity_of_migraines. Release Date 3/18/2013 2. Peterlin, B. Lee, DO; “The Role of Adiponectin in Migraine. Migraine Resource Network”. Available at: http://www.migraineresourcenetwork.com/index.php?option=com_content&view=article&id=141&catid=16&Itemid=53. Last Updated: November 17, 2009

This is still Autism Awareness Month, and from the website Autism Speaks comes news of a large scale study that links the use of valproate or valproic acid during pregnancy to some form of autism:

For over a decade, studies have suggested a link between autism and the use of the anti-epileptic drug valproate during pregnancy. Today, the Journal of the American Medical Association (JAMA) published the results of the largest-ever study to address this concern.

The researchers studied the national health registry records of all Danish children born between 1996 and 2006. Out of a total of 655,615 children, 508 were born to mothers taking valproate during pregnancy.

The study found that prenatal exposure to valproate nearly tripled the risk of autism spectrum disorder (ASD). ASD prevalence was 4.4 percent (just under 1 in 20) among the children whose mothers took valproate during pregnancy. This compared to 1.5 percent (1 in 66) across all the children in the study. The researchers emphasized this increased risk remained relatively low – still under 5 percent. They saw a less-pronounced increase in autism risk among children whose mothers had used valproate but stopped before pregnancy.

Of additional interest, the prenatal valproate exposure appeared to change the ratio of boys to girls affected by autism. In the general population, autism affects four times as many boys as girls. Among those exposed to valproate in this study, autism affected just twice many boys as girls. Further research is needed to understand this effect.

The study did not find increased autism risk with other anti-epilepsy therapies. However, these alternatives don’t work for all patients. As such, the researchers emphasized that the increased risk of autism must be balanced against the benefits to women who need valproate to control their epilepsy.

Jakob Christensen, Ph.D., of Denmark’s Aarhus University Hospital led the study. The analysis controlled for factors that might skew outcomes. These included parental age and psychiatric history, prematurity, birth weight and birth defects.

JAMA published a related editorial by neurologist Kimford Meador, M.D., and neuropsychologist David Loring, Ph.D., of Emory University, in Atlanta. They noted that prenatal use of valproate has also been linked to birth defects and mental impairments. As such, they urged doctors to discuss valproate’s risks and benefits with their patients and consider alternative medicines. If no effective alternatives can be found, they recommend using the lowest effective dose of valproate.

“As the largest study to date identifying valproate as a risk factor for ASD, this research contributes to our understanding of environmental risk factors associated with autism,” adds Alycia Halladay, Ph.D., Autism Speaks senior director of environmental and clinical research. “Further research is needed. If scientists can identify the mechanism by which valproate affects risk, then prevention measures may be taken.”

The Epilepsy Foundation has more information on pregnancy and epilepsy medications here.

From DisabilityScoop: 

New research suggests it may be possible to identify children at risk for autism from day one.

By looking at the placenta, researchers say they’ve found key markers that could be used to spot at-risk babies the day they are born. The development could be significant, potentially allowing for early intervention within the first year of life.

In the study published online Thursday in the journal Biological Psychiatry, researchers found that abnormal placental folds and abnormal cell growths called trophoblast inclusions are more common in babies with increased odds for autism.

Researchers at the Yale School of Medicine and the University of California, Davis MIND Institute looked at 117 placentas from babies born to families with at least one child already diagnosed with autism. Such babies are considered to be at risk with previous research showing that parents who already have a child with autism are nine times more likely to have another with the developmental disorder.

The placentas were compared to those from 100 control-infants born to women with only typically-developing kids.

The study found that placentas from children in the at-risk group had as many as 15 trophoblast inclusions while babies in the control group had no more than two.

“I hope that diagnosing the risk of developing autism by examining the placenta at birth will become routine, and that the children who are shown to have increased numbers of trophoblast inclusions will have early interventions and an improved quality of life as a result of this test,” said Harvey Kliman, a research scientist at the Yale School of Medicine and a senior author of the study.

The researchers plan to continue to track the children involved in the study to find out whether or not they are ultimately diagnosed with autism.


Find out more about DisabilityScoop 




The Depression and Bipolar Support Alliance (DBSA) has posted the following statement on the President’s proposed gun control legislation. You can also find it on their website here.


The Depression and Bipolar Support Alliance (DBSA) applauds the inclusion of increased access to mental health care within President Obama’s recent gun control proposal. Greater understanding of and access to mental health screening and treatment, along with necessary clarifications to and investments in the Mental Health Parity and Addiction Equity Act of 2008, are vital for our nation’s health.

Together with millions of Americans, DBSA deplores gun violence and violence in general, and we are invested in the prevention of shocking tragedies like those at Newtown, Aurora, Oak Creek, and Tucson. Yet DBSA is also deeply concerned about the seeming conflation of mental health issues and violence in the media and within public discourse.

As the President’s gun control plan explicitly states, the percentage of people with mental health conditions committing gun violence in America is very small. In fact, people experiencing mental health symptoms are more likely to be the victims of violence than perpetrators, and are more likely to use guns to die by suicide than to use guns against others. Yet much of the current talk about gun control focuses on individuals with mental health conditions and the perception of them as potential threats for gun violence. Such media- and government-endorsed associations between violence and mental health conditions increase prejudice and stigma. So while we wholly support efforts to reduce gun violence, we contend that we as a society must be cautious about restricting the rights of people because of a health condition or disability.

Access to mental health care and gun responsibility laws are important, but we at DBSA additionally contend that a larger conversation needs to take place that focuses on prevention. There are many such programs already in place around the country and around the world, but developing and implementing them broadly are more difficult. We must respond urgently to the unspeakable Newtown tragedy, as the President has done, yet we must also remain committed to the long process of evolving the nation’s access to mental healthcare, the quality of that care, and the attitudes we have about people who need help to achieve wellness.

DBSA looks forward to working within the mental health community and with the public at large to continue an important dialogue about reducing and eliminating violence—and to work collaboratively to improve access to quality mental health care.

Migraine facts

From Migraine.com: Facts about Migraine disease

To view the findings of the full study, Migraine in America 2012, go here.

Well, here’s something I hadn’t heard before. For the past week or so I’ve been in the midst of a wicked spring allergy attack, something new for me. I usually am only bothered by mid- and late summer allergies. And I’ve been wondering why I haven’t felt my usual zing with the coming of spring, especially after such a long winter.

It turns out that seasonal allergies are linked with the onset of depression in bipolar patients.

You’re kidding me. There’s yet another trigger for a bipolar swing?

Apparently, this is so. From Psychology Today:

Spring is usually a happy, hopeful season – think spring fever and spring break. But for some people, the season brings out the opposite feelings. Two likely culprits are seasonal allergies and reverse SAD.

Seasonal Allergies: The Achoo! Effect

Springtime pollen allergies may leave you both sneezy and grumpy. Several studies have now shown a link between allergies and depression. Researchers have also noted that the springtime pollen period seems to coincide with a spike in suicides.

One interesting study led by researchers from the University of Maryland at Baltimore was recently published in the journal Bipolar Disorders. The researchers found that depression worsened during peak pollen periods in people with both bipolar disorder and active pollen allergies. The misery endured by seasonal allergy sufferers – sneezing; runny or stuffy nose; itchy eyes or throat; watery eyes – might be reason enough to get depressed. But in this study, the worsening of depression after high pollen exposure wasn’t fully explained by the severity of people’s allergy symptoms. Something more also seemed to be contributing to their blue mood.

The most likely candidates are cytokines, the chemical messengers of the immune system. Allergy attacks trigger the release of cytokines that promote inflammation. In both humans and animals, high levels of inflammation-promoting cytokines have been linked to something called “sickness behavior.” This pattern of behavior is characterized by increased sleeping, decreased appetite, reduced sex drive, and withdrawal from the environment. In short, it’s an awful lot like depression.

Beyond that, raging allergies make it hard to get a good night’s sleep. And too little or poor quality sleep may also contribute to depression symptoms.

Reverse SAD: Bright Days, Dark Moods

Rain or shine, some people find the weather depressing. A recent study led by researchers at Utrecht University looked at different patterns of mood in response to weather conditions. One group, dubbed Summer Haters, felt in a worse mood as the weather got warmer and sunnier. The researchers speculated that Summer Haters might be at risk for a condition sometimes referred to as reverse SAD.

Seasonal affective disorder (SAD) is a form of recurring depression in which the symptoms start and stop around the same time each year. Typically, they begin in fall or winter and subside in spring. But in about one out of 10 SAD sufferers, the pattern is reversed, with depression returning in the spring or summer. Common symptoms of reverse SAD include insomnia, irritability, restlessness, poor appetite, and weight loss. It’s thought that this form of depression may be a reaction to higher heat and humidity, since traveling to a cooler locale sometimes brings relief.

Unfortunately, the very fact that spring is supposed to be a time of joy and renewal can highlight what’s missing for those who aren’t feelng that way. It’s the “I’m the only one not having fun on spring break” effect, and it’s bound to make someone who’s already down feel even worse.

If you’re in that group, there may be some comfort in knowing that you aren’t the only one. Don’t hesitate to reach out for help if you’re struggling. For some people, April showers bring not only May flowers, but also a trip to the therapist’s or a prescription for antidepressants.

For those of you who are more clinically inclined, there’s this research from NIMH:

Although growing evidence supports an association between allergy, allergens and depression, it remains unknown if this relationship is between “states” (possible triggers) or “traits” (possible vulnerabilities). We hypothesized that patients with recurrent mood disorders who are sensitized to tree pollen (as determined by allergen specific IgE antibodies), in comparison to those who are not sensitized, would report larger negative changes in mood during exposure to tree pollen in spring. We also hypothesized that differences between high and low tree pollen periods in self reported allergy symptoms would correlate positively with differences in self reported depression scores. We present 1-year preliminary data on the first 51 patients with unipolar or bipolar disorder (age: 19-63 years, 65% female, twelve patients were tree-pollen IgE positive). Ratings of mood and allergic disease status were performed once during the peak airborne pollen counts and once during the period of low airborne pollen counts, as reported by two local pollen counting stations. Linear regression models were developed to examine associations of changes in depression scores (dependent variable) with tree pollen sensitization, changes in the allergy symptom severity score, adjusted for gender and order of testing. We did not confirm the hypothesized relationship between a specific tree pollen sensitization and changes in mood during tree pollen exposure. We did confirm the hypothesized positive relationship between the changes in allergy symptoms and changes in subjects’ depression scores (adjusted p<0.05). This result is consistent with previous epidemiological evidence connecting allergy with depression, as well as our recent reports of increased expression of cytokines in the prefrontal cortex in victims of suicide and in experimental animals sensitized and exposed to tree pollen. A relationship between changes in allergy symptom scores and changes in depression scores supports a state-level rather than only trait-level relationship, and thus lends optimism to future causality-testing interventional studies, which might then lead to novel preventative environmental interventions in mood disorders.

Good luck this allergy season, my friends.


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