I’d forgotten how much I love science!

I am so thankful for reading “Scientists Move Closer to Understanding Schizophrenia’s Cause”

http://mobile.nytimes.com/2016/01/28/health/schizophrenia-cause-synaptic-pruning-brain-psychiatry.html?referer=

It reminded me how interesting this is to me and how much I love reading, writing about, and basically just “ingesting” all the science news. And this kind of systems biology, going all the way from the DNA sequence to a gene to a protein to a mechanism for an illness in the neurons and brain to the causation of an illness, amazing, absolutely amazing science! I am inspired! For writing my blog posts, perhaps Writing a PhD thesis (!) or even writing the book I’ve been thinking of writing forever!

Scientists Move Closer to Understanding Schizophrenia’s Cause (Amazing research and information!)

SCHIZOPHRENIAThis is absolutely amazing! Scientists have found out that the cause of schizophrenia is too much synaptic pruning of neurons, “in which the brain sheds weak or redundant connections between neurons as it matures” in the prefrontal cortex. This begins in adolescence and the symptoms of schizophrenia also start in adolescence! “People who carry genes that accelerate or intensify that pruning are at higher risk of developing schizophrenia than those who do not, the new study suggests.”

They knew that the MHC locus was involved in schizophrenia, they pinpointed the exact gene that is involved, the C-4 gene, this is the gene that facilitates the aggressive tagging of connections, thereby accelerating pruning. Wow, this is so amazing! Here it is in a nutshell, why people get schizophrenia! I am totally floored! So floored, I almost forgot to put the reference, but here is is:

http://www.nytimes.com/2016/01/28/health/schizophrenia-cause-synaptic-pruning-brain-psychiatry.html

“Scientists reported on Wednesday that they had taken a significant step toward understanding the cause of schizophrenia, in a landmark study that provides the first rigorously tested insight into the biology behind any common psychiatric disorder.

More than two million Americans have a diagnosis of schizophrenia, which is characterized by delusional thinking and hallucinations. The drugs available to treat it blunt some of its symptoms but do not touch the underlying cause.

The finding, published in the journal Nature, will not lead to new treatments soon, experts said, nor to widely available testing for individual risk. But the results provide researchers with their first biological handle on an ancient disorder whose cause has confounded modern science for generations. The finding also helps explain some other mysteries, including why the disorder often begins in adolescence or young adulthood.

“They did a phenomenal job,” said David B. Goldstein, a professor of genetics at Columbia University who has been critical of previous large-scale projects focused on the genetics of psychiatric disorders. “This paper gives us a foothold, something we can work on, and that’s what we’ve been looking for now, for a long, long time.”

The researchers pieced together the steps by which genes can increase a person’s risk of developing schizophrenia. That risk, they found, is tied to a natural process called synaptic pruning, in which the brain sheds weak or redundant connections between neurons as it matures. During adolescence and early adulthood, this activity takes place primarily in the section of the brain where thinking and planning skills are centered, known as the prefrontal cortex. People who carry genes that accelerate or intensify that pruning are at higher risk of developing schizophrenia than those who do not, the new study suggests.

Some researchers had suspected that the pruning must somehow go awry in people with schizophrenia, because previous studies showed that their prefrontal areas tended to have a diminished number neural connections, compared with those of unaffected people. The new paper not only strongly supports that this is the case, but also describes how the pruning probably goes wrong and why, and identifies the genes responsible: People with schizophrenia have a gene variant that apparently facilitates aggressive “tagging” of connections for pruning, in effect accelerating the process.

Some scientists warned that the history of biological psychiatry stands as a caution against premature optimism. “This work is extremely persuasive,” said Dr. Samuel Barondes, a professor of psychiatry at the University of California, San Francisco, “but any step forward is not only rare and unusual, it’s just one step in a journey of a thousand miles” to improved treatments.

The study, by scientists from Harvard Medical School, Boston Children’s Hospital and the Broad Institute, a research center allied with Harvard and the Massachusetts Institute of Technology, provides a showcase of biomedical investigation at its highest level. The research team began by focusing on a location on the human genome, the MHC, which was most strongly associated with schizophrenia in previous genetic studies. On a bar graph — called a Manhattan plot because it looks like a cluster of skyscrapers — the MHC looms highest.

 

“The MHC is the Freedom Tower” of the Manhattan plot, said Eric S. Lander, the director of the Broad Institute. “The question was, what’s in there?”

The area is a notoriously dark warren in the genome known to contain genes that facilitate the body’s immune response, for example, by flagging invading bacteria to be destroyed. That property had given rise to speculation that schizophrenia might be a kind of autoimmune condition, in which the body attacked its own cells.

But the research team, led by Steven McCarroll, an associate professor of genetics at Harvard, and by Aswin Sekar, one of his graduate students, found something different. Using advanced statistical methods, the team found that the MHC locus contained four common variants of a gene called C4, and that those variants produced two kinds of proteins, C4-A and C4-B.

The team analyzed the genomes of more than 64,000 people and found that people with schizophrenia were more likely to have the over-active forms of C4-A than control subjects. “C4-A seemed to be the gene driving risk for schizophrenia,” Dr. McCarroll said, “but we had to be sure.”

The researchers turned to Beth Stevens, an assistant professor of neurology at Boston Children’s Hospital and Harvard, who in 2007 was an author of a study showing that the products of MHC genes were involved in synaptic pruning in normal developing brains. But how important was this C4 protein, exactly? Very important, it turned out: Mice bred without the genes that produce C4 showed clear signs that their synaptic pruning had gone awry, Dr. Stevens’s lab showed.

Taken together, Dr. Stevens said in an interview, “the evidence strongly suggested that too much C4-A leads to inappropriate pruning during this critical phase of development.”

In particular, the authors concluded, too much C4-A could mean too much pruning — which would explain not only the thinner prefrontal layers in schizophrenia, but also the reason that the disorder most often shows itself in people’s teenage years or early twenties. “The finding connects all these dots, all these disconnected observations about schizophrenia, and makes them make sense,” Dr. McCarroll said.

Carrying a gene variant that facilitates aggressive pruning is hardly enough to cause schizophrenia; far too many other factors are at work. Having such a variant, Dr. McCarroll estimates, would increase a person’s risk by about 25 percent over the 1 percent base rate of schizophrenia — that is, to 1.25 percent. That is not nearly enough to justify testing in the general population, even if further research confirms the new findings and clarifies the roles of other associated genes.

Yet the equation changes when it comes to young people who are at very high risk of developing the disorder, because they are showing early signs — a sudden slippage in mental acuity and memory, or even internal “voices” that seem oddly real. This ominous period may last a year or more, and often does not lead to to full-blown schizophrenia. The researchers hope that the at-risk genetic profile, once it has been fleshed out more completely, will lead to the discovery of biomarkers that could help clarify a prognosis in these people.

Developing a drug to slow or modulate pruning poses another kind of challenge. If the new study shows anything, it is that synaptic pruning is a delicate, exquisitely timed process, and that it is still poorly understood. The team does not yet know, for example, why C4-A leads to a different rate or kind of pruning than C4-B. Any medication that tampered with that system would be a risky proposition, the authors and outside experts agreed.

“We’re all very excited and proud of this work,” Dr. Lander said. “But I’m not ready to call it a victory until we have something that can help patients.”

Genetic variants associated with response to lithium treatment in bipolar disorder: a genome-wide association study

This is exciting! Since responsiveness to Lithium runs in families, it seems logical to think that specific genes are involved that render a person treatable by lithium, a very fortunate person, I might add, as Lithium is the best treatment for bipolar disorder when it works, however it only works for 33% of bipolar people. (I am one of those 33%, and I consider myself very lucky!) Doing genome wide studies to see if there were any genes associated with being treated by lithium, four linked short pieces of DNA (SNP’s) on Chronosome 21 were found to be associated with lithium responsiveness. These 4 SNP’s are part of two genes which code for long non coding RNA sequences. These non coding sequences are important in gene regulation, particularly in the CNS! 

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(16)00143-4/abstract
SummaryBackground

Lithium is a first-line treatment in bipolar disorder, but individual response is variable. Previous studies have suggested that lithium response is a heritable trait. However, no genetic markers of treatment response have been reproducibly identified.

Methods
Here, we report the results of a genome-wide association study of lithium response in 2563 patients collected by 22 participating sites from the International Consortium on Lithium Genetics (ConLiGen). Data from common single nucleotide polymorphisms (SNPs) were tested for association with categorical and continuous ratings of lithium response. Lithium response was measured using a well established scale (Alda scale). Genotyped SNPs were used to generate data at more than 6 million sites, using standard genomic imputation methods. Traits were regressed against genotype dosage. Results were combined across two batches by meta-analysis.

Findings
A single locus of four linked SNPs on chromosome 21 met genome-wide significance criteria for association with lithium response (rs79663003, p=1·37 × 10−8; rs78015114, p=1·31 × 10−8; rs74795342, p=3·31 × 10−9; and rs75222709, p=3·50 × 10−9). In an independent, prospective study of 73 patients treated with lithium monotherapy for a period of up to 2 years, carriers of the response-associated alleles had a significantly lower rate of relapse than carriers of the alternate alleles (p=0·03268, hazard ratio 3·8, 95% CI 1·1–13·0).

Interpretation
The response-associated region contains two genes for long, non-coding RNAs (lncRNAs), AL157359.3 and AL157359.4. LncRNAs are increasingly appreciated as important regulators of gene expression, particularly in the CNS. Confirmed biomarkers of lithium response would constitute an important step forward in the clinical management of bipolar disorder. Further studies are needed to establish the biological context and potential clinical utility of these findings.

Somewhere…

If “The Martian” is a clear illustration of what my illness feels like, then this song is a pure vocalization of what it feels like to be totally well and at peace! Somewhere over the rainbow, absolutely my preferred place of residence 🙂

Panel Calls for Depression Screenings During and After Pregnancy

Dyane at http://www.proudlybipolar.wordpress.com/ this is for you! A major positive development, don’t you think?!

http://www.nytimes.com/2016/01/27/health/post-partum-depression-test-epds-screening-guidelines.html?hp&action=click&pgtype=Homepage&clickSource=story-heading&module=first-column-region&region=top-news&WT.nav=top-news&_r=0

Women should be screened for depression during pregnancy and after giving birth, an influential government-appointed health panel said Tuesday, the first time it has recommended screening for maternal mental illness.

The recommendation, expected to galvanize many more health providers to provide screening, comes in the wake of new evidence that maternal mental illness is more common than previously thought; that many cases of what has been called postpartum depression actually start during pregnancy; and that left untreated, these mood disorders can be detrimental to the well-being of children.

It also follows growing efforts by states, medical organizations and health advocates to help women experiencing these symptoms — an estimated one in seven postpartum mothers, some experts say.

“There’s better evidence for identifying and treating women with depression” during and after pregnancy, said Dr. Michael Pignone, a professor of medicine at the University of North Carolina at Chapel Hill and an author of the recommendation, which was issued by the United States Preventive Services Task Force. As a result, he said, “We specifically called out the need for screening during this period.”

The recommendation was part of updated depression-screening guidelinesissued by the panel, an independent group of experts appointed by the Department of Health and Human Services. In 2009, the group said adults should be screened if clinicians have the staff to provide support and treatment; the new guidelines recommend adult screening even without such staff members, saying mental health support is now more widely available. The 2009 guidelines did not mention depression during or after pregnancy.

“It’s very significant that the task force is now putting forth a recommendation that’s specific to pregnant and postpartum women,” said Katy Kozhimannil, an associate professor of public health at the University of Minnesota. “Policy makers will pay attention to it. Increased screening and detection of depression is an enormous public health need.”

The panel gave its recommendation, which was published in the journal JAMA, a “B” rating, which means depression screening must be covered under the Affordable Care Act.

For years, obstetricians and other health care providers who saw women during and after pregnancy often felt ill equipped or reluctant to ask about problems like depression, anxiety and obsessive-compulsive disorder.

“Ob-gyns thought that if they identify something and don’t have resources to support it, it puts them at significant legal risk,” said Dr. Samantha Meltzer-Brody, the director of the perinatal psychiatry program at the University of North Carolina at Chapel Hill. “Pediatricians have the added caveat that the mom isn’t really their patient — the child is.”

And, she said, many women are reluctant to share symptoms with doctors on their own. If a mother is “feeling so anxious you’re going to come out of your skin or feeling that you’re going to harm your baby, you may think: ‘Oh my God, I’m having these crazy feelings and nobody’s talking about it. I must be a terrible mother.’”

No one screened Melissa Mead, 30, of The Dalles, Ore., during or after her first pregnancy, five years ago. Shortly after her son Brady’s birth, “I experienced postpartum depression, anxiety and O.C.D.,” she said, and “I didn’t know what it was.”

Ms. Mead cried constantly, barely slept, rarely left home and was “scared to death that my baby was going to suffocate,” she said. At her job as an optician, she said that people asked, “‘Isn’t everything so wonderful?’ and I was like ‘I kind of feel like dying on the inside,’ and you don’t want to say that because you’re afraid what people will think of you.”

After a year, she saw a psychiatrist for talk therapy. When her second son, Emmett, was born, and she had more symptoms, including fearing that she would stab herself with a kitchen knife, Ms. Mead tried several medications until one worked. She now volunteers for Postpartum Support International.

The panel’s recommendations do not specify which clinicians should screen or how often, and Dr. Pignone said that “anyone who has a caring relationship with the patient” should “sit down and say, ‘How do we want to do this in our practice?’” For screening methods, the group said that theEdinburgh Postnatal Depression Scale, a 10-question survey, was effective.

The panel said evidence showed that cognitive behavioral therapy was helpful to mothers. It said that the use of some antidepressants during pregnancy could cause “potential serious fetal harms,” but that “the likelihood of these serious harms is low.”

Dr. Pignone also emphasized that “untreated depression has a lot of adverse consequences itself.”

Among them, experts say, are that pregnant women with depression often take poorer care of their prenatal health. And maternal mental illness can affect children, leading to behavioral problems, emotional instability and difficulty in school.

Besides citing evidence that screening accompanied by even minimal counseling helped women with depression, the panel found that screening caused no harm.

“A decade ago there was more concern that screening pregnant and postpartum women for mental health would do more harm than good,” said Wendy N. Davis, the executive director of Postpartum Support International. “Medical providers would say to me, ‘If I screen and she screens positively for depression and anxiety, I’m afraid that it will just make her feel more scared, or there’s more stigma to that label.’”

But, she said, “screening tools actually can give a language for both the providers and the patients to feel comfortable talking about it and prevent the stigma.”

The panel recommended that clinicians have the ability to diagnose and treat women, or to refer them elsewhere.

That is crucial, said Dr. Lee S. Cohen, the director of the Center for Women’s Mental Health at Massachusetts General Hospital. “I applaud identifying women who are ill,” he said. But “will she be appropriately referred, will she get treated whether it’s medication or therapy, and over time does she actually ever get well?”

The only state that requires screening, New Jersey, has had mixed results because too few treatment options have been available. While pediatricians and obstetricians were trained to screen, they were not compensated for screening, a study by Dr. Kozhimannil found.

A dozen other states, including New York, now have laws encouraging screening, education and treatment. And Bill de Blasio, New York City’s mayor, recently announced a goal of universal screening of pregnant and postpartum women, saying it “should be a part of routine care.”

Routine screening could have benefited Jenna Zalk Berendzen, 40, of Cedar Falls, Iowa, even though during her first pregnancy, five years ago, she was studying to be a nurse practitioner and had medical knowledge. She also had a family history of postpartum depression, but had assumed “it’s not going to happen to me,” she said.

A week after delivering a son, Maxwell, depression “hit me very, very severely,” she said. She felt suicidal, and at one point, while her husband and baby were sleeping, “I had in front of me 15 bottles of different kinds of meds,” she said. “I would open the bottles up and I would close them, open them and close them. I didn’t want to die, I just thought, ‘It’s never going to get better.’”

Ms. Zalk Berendzen ultimately found effective treatment, and has since weaned herself to a low dose of medication. She had no symptoms with the 2014 birth of another son, Samuel. She now works in gynecology at UnityPoint Health in Waterloo, Iowa, where, she said, “Within the last year, we’ve started to recognize we need to be screening every woman.”

Zumba!

Finally went to Zumba after more than a month! How fun and joyous, not to mention a kickass workout! The video has one 4 minute song, we do 55 minutes worth of songs in one class! Love my teacher, she’s from Colombia and has all the moves! ❤ Ivonne! Can’t wait, seriously I can’t, wait for my next Zumba class! Puts a smile on my face every time, not to mention muscles on my body! YaaY!

How ECT works by Natasha Tracy

https://plus.google.com/+NatashaTracy/posts/fZmbu8XrgrN​

How Does Electroconvulsive Therapy (ECT) Work?

In the book I’m writing on electroconvulsive therapy (ECT) I’ve had to address the question as to how ECT works. However, in spite of the fact that ECT has been in use since the 1930s we really don’t know how ECT works.

But recently we may have gotten a bit closer to figuring it out.
Electroconvulsive Therapy (ECT) and Brain Derived Neurotrophic Factor
One of the things we have noted is that people who undergo ECT have measurably increased levels of brain derived neurotrophic factor (BDNF) which is critical in supporting healthy cells and cell growth in the brain. This increase in BDNF is something we’ve noticed when people take antidepressants as well. When you think about it, it makes sense that this would be part of why ECT and other therapies work as it combats the shrinking of the brain seen in depression and other mental illnesses.

Electroconvulsive Therapy (ECT) “Reboots” the Brain
And one of the things I have said is that electroconvulsive therapy does not “reboot” the brain. There is just nothing similar to this analogy that we can point to with regards to ECT. Until now, that is.

Recent research shows that functional connectivity in areas of the brain may be up-regulated in people with depression. In other words, there are areas of the brain with too much connectivity. This theory is known as the “hyperconnectivity hypothesis.”
How Does ECT Work in the Brain

This seems counter intuitive when you think of depression but I suppose it’s like anything else, too much of anything can be a bad thing, especially in the brain.
Recently a study was done where functional magnetic resonance imaging (fMRI) measured the connectivity in areas of the brain. And specifically around the left dorsolateral prefrontal cortical region it was found ECT decreased the functional connectivity, and this decrease in functional connectivity seemed to correlate with positive results from the ECT on depressive symptoms.
Thus ECT was found to change the functional architecture of the brain in a way that helped with depression.
Note that the study size was extremely small but that this is typical for studies using technology like fMRIs. Thus, we cannot say this study proves anything but we can say it leads us in a new, and perhaps promising, direction in terms of discovering how ECT works.
Please see Electroconvulsive therapy reduces frontal cortical connectivity in severe depressive disorder for all the details.
Why Does it Matter How ECT Works?
Well, on the one hand, it doesn’t. For the people for whom ECT has worked, how it worked doesn’t matter a lick. However, the end goal for researchers is to figure out how ECT works so that they can retain the therapeutic component of the treatment while reducing the side effects (like memory loss). Maybe this study got us one step closer.

Thank you for nominating me for the Sunshine Blogger Award

Thank you gentlekindness of http://gentlementalannie.com/2016/01/24/awards/ for nominating me for the Sunshine Blogger Award!

sunshine-blogger-award-200

The rules for The Sunshine Blogging Award are:

  • Thank the person who nominated you
  • Answer the 11 questions from your nominator
  • Nominate 11 bloggers and give them 11 questions to answer

My Nominees Are…

http://justplainolvic.com/

https://itsgoodtobecrazysometimes.wordpress.com/

http://bipolarcompass.com/

https://theblahpolar.wordpress.com/

http://thefallingthoughts.com/

https://synapsparkle.wordpress.com/

http://bipolarforlife.me/

http://fightorflights.com/

https://piecesofbipolar.wordpress.com/

https://thefeatheredsleep.wordpress.com/

http://despairtodeliverance.com/

 

 

Answers to My Questions-  Followed by My Questions for my Nominees

1. What do you like to do first thing  in the morning, if you have a choice?

Have coffee, I can’t start the day without coffee, simply doesn’t work.

2. Do you think we should strive to be “normal” or just be ourselves?

I suppose we should try to be as normal as we can be, all the while being as much ourselves as we can be. What is normal anyway?

3. Does anyone know you well enough that you trust them to “give you advice” about your path and your life? If so, who?

Yes, some friends and my sometime therapist. I definitely trust her, she can be objective, and she is highly intelligent and empathetic, so I definitely trust her. I just wish she took insurance so I could speak to her more regularly.

4. Do you feel more connected to the people you interact with on WordPress, or the “real life” people in your life? Or is it even and balanced?

I do feel very connected to the bloggers with whom I have conversations on WordPress! We, most of us, suffer from bipolar d/o or another mental illness, so we understand a lot of things about each other without having to explain a thing, which is really amazingly nice!

5. Do you prefer to be with people the majority of the time, or prefer time alone?

Sometimes I want to be with people, sometimes not. Sometimes being with people makes me very anxious and I have to come home and be solitary.

6. What do you miss about your younger self?

The being young of course. Also the hope for things to turn out well, the time to work on things, time, really it’s having the luxury of time, that’s what I miss.

7. Favorite tv show? or favorite movie?

Favorite TV show is “Downton Abbey” and “Sherlock”. Favorite movie lately might be “Madame Bovary” and all time is “Amadeus!”

Questions for my Nominees…

1. What is your nickname?

2. What do love the most about blogging?

3. What do you like the least about blogging?

4. When did you start your blog and why?

5. How did you come up with the name of your blog?

6. What are your hobbies?

7. Do you like to read? And if so, what genre of books?

8. Do you believe in keeping fit? If so how do you manage it?

9. Do you have pets?

10. Do you like winter or summer?

11. Do you have any fears? If so, how do you soothe them?

A clarification: I am not my illness and my illness is not me.

img_9435In my post called “The Martian” I had said I knew what it felt like to be alone, abandoned, injured, basically what Matt Damon’s character felt when he was left behind on Mars. Yes I know what that feels like but only from the times I’m not feeling well. That is what this illness called bipolar disorder feels like. That is not the real me, that is the ill me. The real me does not feel abandoned or alone or injured. The real me is strong, happy, capable, helpful to others and in control of my life. That is the real me. Unfortunately, the real me sometimes gets drowned by my illness. But the true me is always there, whether camouflaged by my illness or not.  And it is with this real me, the true me, not my illness, it is with the real me that I live my life. The ill parts are simply short voyages into hell from which I do emerge often stronger and wiser than before. As so aptly said in the comments section by my friend Laura Schulman, I am not my illness and my illness is not me, categorically! Just a clarification.