‘Touched with Fire’ explores bipolar disorder

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The movie “Touched with Fire” (also the title of Kay Redfield Jamison’s book) is coming out on Feb. 12th. The synopsis and comments of film maker Paul Dalio are hopeful, especially this “If I had any hope at all that there was any chance, any possibility that I could be happy and full of creativity, and even better than I was before, which now is the case, I would fight.” Hope, that is the one thing we all need and the one thing that sustains us, whether we have bipolar disorder or not.

http://www.gettysburgtimes.com/life_entertainment/lifestyles/article_5f834327-ca43-59d2-b098-1881987d1fc3.html

“Set to be released on Feb. 12, Paul Dalio’s new film, “Touched with Fire,” depicts Dalio’s personal experiences with bipolar disorder. The title of the film is taken from Kay Redfield Jamison’s 1996 book, “Touched with Fire,” which explored how many of the greatest artistic minds in history had bipolar disorder. Jamison herself acknowledges having bipolar disorder since early adulthood. Dalio explains that the book helped him see himself not just as an individual with a “defect” but as having a gift that taps into something that most people can’t. “Touched with Fire” takes Dalio’s personal experiences with bipolar disorder and uses two characters, Carla and Marco, to contrast the different emotions Dalio has felt toward bipolar in his life. The love story between these two characters is a metaphor for Dalio’s “love-and-hate relationship with bipolar: the way they bring out the romance in each other, but also the devastation in each other, and the way they have to reconcile those two things.” He stated, “The journey that I went through that I think a lot of people with bipolar go through is that you get it and you’re lost, but then you easily romanticize that fire ultimately to your own destruction. It ultimately takes most people repeated devastations to let go of the mania. What I wanted to do was have that journey of how they learned that they can have real meaningful emotions and sustain them. My hope is that people are able to watch the film and see where Marco and Carla make mistakes and know that they don’t have to make them themselves.”

One of the biggest themes throughout the film is the relationship that the two main characters must manage with their parents and offers glimpses into each person’s actions. Dalio describes how his family would frequently talk him out of suicide when he was in the midst of a depressive episode. “It was very draining on them, but they really struggled to try and give me hope. The best a family can do is to give hope to their family member, but ultimately it has to come down to the individual. The loss of hope – in my own experience – was the only time I had thoughts of suicide. If I had any hope at all that there was any chance, any possibility that I could be happy and full of creativity, and even better than I was before, which now is the case, I would fight.” Dalio stated that his goal for the film was to show a truthful situation between individuals and “well-intentioned parents.” “The truth is, even well intentioned parents, don’t always know what to do. They are dealing with a situation that there is no perfect guidebook for. My hope was to create characters that the audience could see themselves in. If there were any well intentioned parents in the audience, that they could not only see themselves in the parents, but also through their children’s eyes. That they could at least be able to understand their children enough so they could understand where they are coming from so that they can communicate with them.” Dalio’s final thoughts include describing bipolar disorder like a pendulum, and using exercise, meditation, and a low-sugar diet along with his prescribed medications to help manage the emotional swings. According to Dalio, “True happiness is having an appreciation of the darkest and brightest emotions and being able to experience both of them equally.””

Significant Number Of Young People With Undiagnosed Bipolar Disorder

img_6229This article talks about giving antidepressants to depressed people who actually have bipolar disorder. This is a very dangerous thing to do as you can push someone who has bipolar disorder into full blown mania by giving them antidepressants without a mood stabilizer. The 10% stats are for the UK, but I am sure it’s the same here in the US. In fact, I was just such a “casualty.” I went into a severe depression in the end of 1985, I was then prescribed antidepressants without any mood stabilizer, and in February of 1986, I started becoming manic, not knowing what was happening to me, I didn’t report my symptoms to my doctor. In the end of February, 1986, I started becoming full blown manic, out of touch with reality, and in the beginning of March, I was hospitalized. This was in New Orleans, LA, in Touro Infirmary. I was in the hospital for a month, finally being discharged when my psychotic (out of touch with reality) symptoms were gone. I will wonder forever what would have happened if i had not been put on just antidepressants. What if my doctor had put me on Lithium along with the antidepressants, would I then never have manifested bipolar disorder? What if… can’t live there. Must live in what is in this very moment and live as well as I can, because what ifs are a waste of time. The only thing that matters is the reality of what is happening now and we must come face to face with it and live with it with strength and equanimity. I may never know why somethings happened, and there’s no point in blame or anger… they did, and I simply have to accept that they happened and go on from here to make as good a life as I can for myself.

http://www.science20.com/news_articles/significant_number_of_young_people_with_undiagnosed_bipolar_disorder-164556

Around 10% of UK primary care patients prescribed antidepressants for depression or anxiety have undiagnosed bipolar disorder, a study has found.

Researchers from Leeds and York Partnership NHS Foundation Trust and the School of Medicine at the University of Leeds interviewed young adults from general practices in a study1 published in the British Journal of General Practice(BJGP).

Bipolar disorder often presents with depression and can be difficult to diagnose. People who have had periods of symptoms of high mood (such as increased energy and activity, increased confidence, over-talkativeness or being easily distracted) often don’t recognise these as significant and don’t tell their doctor about them.

This can lead to inappropriate treatment, such as the prescription of antidepressants without mood-stabilising medication, which might increase the risk of mood remaining unstable.

The study found that among people aged 16-40 years prescribed antidepressants for depression or anxiety, around 10% had unrecognised bipolar disorder. This was more common among younger patients and those who reported more severe episodes of depression. The study recommends that healthcare professionals should review the life histories of patients with anxiety or depression, particularly younger patients and those who are not doing well, for evidence of bipolar disorder.

Dr Tom Hughes, Consultant Psychiatrist at Leeds and York Partnership NHS Foundation Trust and the University of Leeds, said: “Bipolar disorder is a serious problem, with high levels of disability and the risk of suicide. When it is present in depressed patients it can easily be overlooked. Under-diagnosis and over-diagnosis of illnesses bring problems. Our General Practitioners are the greatest part of the best nationwide health service in the world. We hope this study will be of some help to them and to their patients in helping the better recognition of this important and disabling condition.”

Professor Roger Jones, Editor of the BJGP, said: “Dr Tom Hughes and his colleagues from Leeds and York Partnership NHS Foundation Trust recommend that general practitioners look carefully at patients with depression and anxiety disorders, particularly younger patients and those who are not doing well with their treatment. By reviewing life histories for evidence of symptoms this could provide people with better treatment and quicker recovery.”

The Martian

martianJust saw it. The beginning where Mark Watney gets left on Mars, horrifying! Have I been left behind on Mars? The feeling of watching this man realize he is alone on a planet millions of miles away from Earth, how was that so familiar? Of course, it is the same feeling I have felt when I am in the throes of a manic or severely depressed episode! Abandoned in a desert, no help in sight. Quite sucks your breath out of your lungs. Yes, being left alone on Mars is very much akin to bipolar disorder (BPD). Surviving it requires intelligence, ingenuity, persistence, luck, and eventually help from the outside.

I was watching Matt Damon, playing Mark Watney, and I was so in tune with what he must be feeling. Alone, abandoned, injured, yet he had his wits about him and he survived. That is what we, who have BPD, need. But, awfully enough, bipolar takes our mind/brain/wits from us as well. But we survive, just with the thinking we have left, we survive. The thing to do is to never let it get so far that you cannot think logically or real-ly. With BPD, prevention is worth its weight in gold.

That is what life with bipolar d/o is like, like being abandoned on Mars. it’s that difficult, when you are in an episode, it is just that difficult. It takes superhuman strength to survive. So I congratulate all of us who suffer from this nasty disease and who have survived its ravaging effects over and over again!

 

 

Changing Brain Connectivity May Prevent The Development Of Bipolar Disorder

“Siblings who did not exhibit the disorder were the resilient ones that exhibited similar abnormalities in connectivity of brain networks related to emotional processing. They also showed more changes in neuroplasticity to prevent the development of the disorder.”

http://www.counselheal.com/articles/19319/20160108/changing-brain-connectivity-prevent-development-bipolar-disorder.htm

By changing the wiring in the brain, it is possible to prevent bipolar disorder in patients, according to scientists at the Icahn School of Medicine at Mount Sinai.

Bipolar disorder is an issue in the brain that leads to mood and energy fluctuations, activity levels and the ability to carry out everyday tasks. It is also “highly heritable”, according to researchers.

The Depression and Bipolar Support Alliance  states that bipolar disorder affects close to 5.5 Americans who are above 18 years, or 2.6 percent of adults.

Scientists employed functional magnetic resonance imaging (MRI) in order to map connectivity patterns in brains of individuals who showed symptoms of bipolar disorder. They also examined their siblings without the illness and finally “unrelated healthy individuals”.

“The ability of the siblings to rewire their brain networks means they have adaptive neuroplasticity that may help them avoid the disease even though they still carry the genetic scar of bipolar disorder when they process emotional information,” said lead study author Sophia Frangou, MD, PhD, Professor of Psychiatry at the Icahn School of Medicine at Mount Sinai, in a news release.

Siblings who did not exhibit the disorder were the resilient ones that exhibited similar abnormalities in connectivity of brain networks related to emotional processing. They also showed more changes in neuroplasticity to prevent the development of the disorder.

“A family history remains the greatest risk factor for developing bipolar disorder and while we often focus on risk, we may forget that the majority of those who fall into this category remain well,” added Frangou.

“Looking for biological mechanisms that can protect against illness opens up a completely new direction for developing new treatments. Our research should give people hope that even though mental illness runs in families, it is possible to beat the odds at the genetic lottery.”

The study was published in the journal Translational Psychiatry.

mood and energy fluctuations, activity levels and the ability to carry out everyday tasks. It is also “highly heritable”, according to researchers.

The Depression and Bipolar Support Alliance  states that bipolar disorder affects close to 5.5 Americans who are above 18 years, or 2.6 percent of adults.

Scientists employed functional magnetic resonance imaging (MRI) in order to map connectivity patterns in brains of individuals who showed symptoms of bipolar disorder. They also examined their siblings without the illness and finally “unrelated healthy individuals”.

“The ability of the siblings to rewire their brain networks means they have adaptive neuroplasticity that may help them avoid the disease even though they still carry the genetic scar of bipolar disorder when they process emotional information,” said lead study author Sophia Frangou, MD, PhD, Professor of Psychiatry at the Icahn School of Medicine at Mount Sinai, in a news release.

Siblings who did not exhibit the disorder were the resilient ones that exhibited similar abnormalities in connectivity of brain networks related to emotional processing. They also showed more changes in neuroplasticity to prevent the development of the disorder.

“A family history remains the greatest risk factor for developing bipolar disorder and while we often focus on risk, we may forget that the majority of those who fall into this category remain well,” added Frangou.

“Looking for biological mechanisms that can protect against illness opens up a completely new direction for developing new treatments. Our research should give people hope that even though mental illness runs in families, it is possible to beat the odds at the genetic lottery.”

The study was published in the journal Translational Psychiatry.

mood and energy fluctuations, activity levels and the ability to carry out everyday tasks. It is also “highly heritable”, according to researchers.

The Depression and Bipolar Support Alliance  states that bipolar disorder affects close to 5.5 Americans who are above 18 years, or 2.6 percent of adults.

Scientists employed functional magnetic resonance imaging (MRI) in order to map connectivity patterns in brains of individuals who showed symptoms of bipolar disorder. They also examined their siblings without the illness and finally “unrelated healthy individuals”.

“The ability of the siblings to rewire their brain networks means they have adaptive neuroplasticity that may help them avoid the disease even though they still carry the genetic scar of bipolar disorder when they process emotional information,” said lead study author Sophia Frangou, MD, PhD, Professor of Psychiatry at the Icahn School of Medicine at Mount Sinai, in a news release.

Siblings who did not exhibit the disorder were the resilient ones that exhibited similar abnormalities in connectivity of brain networks related to emotional processing. They also showed more changes in neuroplasticity to prevent the development of the disorder.

“A family history remains the greatest risk factor for developing bipolar disorder and while we often focus on risk, we may forget that the majority of those who fall into this category remain well,” added Frangou.

“Looking for biological mechanisms that can protect against illness opens up a completely new direction for developing new treatments. Our research should give people hope that even though mental illness runs in families, it is possible to beat the odds at the genetic lottery.”

The study was published in the journal Translational Psychiatry.

A genome-wide association study of kynurenic acid in cerebrospinal fluid: implications for psychosis and cognitive impairment in bipolar disorder

 

A variant of the SNX7 gene and its reduced expression, is associated with levels of a protein called kynurenic acid aka KYNA (an end metabolite in tryptophan metabolism.) This is associated with the psychotic (out of touch with reality) symptoms and cognitive impairment seen in bipolar disorder and schizophrenia. Interestingly, this pathway involves signaling via the immune cells (glia) of the brain! Another immune cell connection to mental illness! And KYNA could be targeted for drug development, as reducing it should lead to a decrease in psychotic symptoms as well as cognitive impairment.

http://www.nature.com/mp/journal/vaop/ncurrent/full/mp2015186a.html

Abstract

Elevated cerebrospinal fluid (CSF) levels of the glia-derived N-methyl-d-aspartic acid receptor antagonist kynurenic acid (KYNA) have consistently been implicated in schizophrenia and bipolar disorder. Here, we conducted a genome-wide association study based on CSF KYNA in bipolar disorder and found support for an association with a common variant within 1p21.3. After replication in an independent cohort, we linked this genetic variant—associated with reduced SNX7 expression—to positive psychotic symptoms and executive function deficits in bipolar disorder. A series of post-mortem brain tissue and in vitro experiments suggested SNX7 downregulation to result in a caspase-8-driven activation of interleukin-1β and a subsequent induction of the brain kynurenine pathway. The current study demonstrates the potential of using biomarkers in genetic studies of psychiatric disorders, and may help to identify novel drug targets in bipolar disorder.

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Introduction

Elevation of brain kynurenic acid (KYNA) is a consistently found biochemical aberration in schizophrenia and bipolar disorder (BD).1, 2, 3, 4, 5, 6, 7 Brain KYNA is mainly produced in astrocytes as an end-metabolite of the kynurenine pathway of tryptophan metabolism. This pathway is highly inducible by inflammatory stimuli,8 and we have previously reported that cerebrospinal fluid (CSF) levels of the proinflammatory cytokine interleukin (IL)-1β are markedly increased in patients with BD or schizophrenia, although the majority of other cytokines measured in this study were undetectable.9, 10

KYNA is a neuroactive metabolite that antagonizes the glycine co-agonist site of the N-methyl-d-aspartic acid receptor (NMDAR).8 Administration of synthetic NMDAR antagonists causes psychotic symptoms in healthy individuals,11 and exacerbates psychotic features in patients with schizophrenia.12 Psychotic symptoms are core features of schizophrenia, and more than half of patients with BD will experience psychosis in their lifetime.13 Supporting that KYNA might be specifically involved in the pathophysiology underlying psychotic symptoms, we have found higher levels of CSF KYNA in BD-I patients with a history of psychosis compared with those who had never experienced psychosis.14 KYNA also noncompetitively antagonizes the cholinergic α7 nicotinic receptor, and animal studies indicate that increased brain KYNA might cause cognitive deficits.8 In rats, increased brain KYNA causes behavioral responses analogous to impaired set-shifting in humans,15 an index of executive function. Set-shifting dysfunction as measured by the trail making test (TMT) is indeed a feature of schizophrenia and euthymic BD,16, 17 especially in BD patients with a history of psychosis.18

Family history is the strongest risk factor for BD, but an important obstacle for progress in psychiatric genetics is that psychiatric syndromes—based solely on symptom clustering—do not necessarily reflect specific underlying biological dysfunctions and may be insufficient to delineate heritable phenotypes.19 Indeed, epidemiological and molecular genetic studies have blurred the diagnostic boundary between schizophrenia and BD by demonstrating that these disorders have partly shared genetic causes.20, 21 Complementary approaches to unearth causal genetic mutations are therefore needed. One approach is to focus on biomarkers, that is, measurable key components in biological pathways between genotype and disease.22 For this purpose, the use of CSF KYNA may be particularly rewarding given its biological links to distinct subdomains of pathology present in both BD and schizophrenia.

In this study of euthymic BD patients, we found CSF IL-1β and KYNA to be associated with a history of psychosis and set-shifting impairment. CSF levels of KYNA were also strongly associated with the dopamine metabolite homovanillic acid (HVA). We conducted a genome-wide association study (GWAS) against CSF levels of KYNA in BD that revealed a genome-wide significant association with the single-nucleotide polymorphism (SNP) rs10158645 within 1p21.3, a finding that was replicated in an independent cohort of BD patients. Furthermore, we analyzed this SNP in relation to CSF HVA, a history of psychosis (followed by a replication in a large data set of 565 BD patients) and set-shifting ability. As the minor allele in rs10158645 was associated with decreased expression of sorting nexin 7 (SNX7), we attempted to decipher the biochemical chain of events using a multipronged approach including causal inference analyses of clinical data, post-mortem data and cell culture studies. These experiments converged on the proposal that decreased SNX7 expression is linked to increased CSF KYNA concentration and ultimately psychosis and set-shifting difficulties in BD through caspase-8-driven activation of IL-1β.

 

Ebselen, a mimic of Lithium may be able to be used as a treatment for bipolar disorder: Effect of the Putative Lithium Mimetic Ebselen on Brain myo-Inositol, Sleep and Emotional Processing in Humans

http://www.nature.com/npp/journal/vaop/naam/abs/npp2015343a.html

Lithium remains the gold standard in treating bipolar disorder but has unwanted toxicity and side effects. We previously reported that ebselen inhibits inositol monophosphatase (IMPase) and exhibits lithium-like effects in animal models through lowering of inositol. Ebselen has been tested in clinical trials for other disorders, enabling us to determine for the first time the effect of a blood-brain barrier penetrant IMPase inhibitor on human central nervous system (CNS) function. We now report that in a double-blind, placebo-controlled trial with healthy participants, acute oral ebselen reduced brain myo-inositol in the anterior cingulate cortex, consistent with CNS target engagement. Ebselen decreased slow-wave sleep and affected emotional processing by increasing recognition of some emotions, decreasing latency time in the acoustic startle paradigm and decreasing the reinforcement of rewarding stimuli. In summary, ebselen affects the phosphoinositide cycle and has CNS effects on surrogate markers that may be relevant to the treatment of bipolar disorder, which can be tested in future clinical trials.

Proteins Could be Potential Bipolar Disorder Biomarkers

This is really big! For the first time, doctors are reporting that a group of 6 proteins may be able to be used  to diagnose bipolar disorder. This mental illness, though it affects millions of people, has no diagnostic test. It would make it so much easier to treat people with bipolar disorder if they could definitively be diagnosed first. An example is me. When I became severely depressed n 1985, I was put on antidepressants without any mood stabilizers. This caused me to go into a full blown manic phase. Somewhere no one wants to be. If this diagnostic test had been available then and I would have been put on mood stabilizers right from the beginning, my bipolar 1 may never have been unmasked. Do you know what a difference that would have made in my life? A whole hell of a lot of difference. I hope they develop this test and people who are in the process of developing bipolar disorder can be correctly diagnosed with the help of these 6 protein test. I won’t benefit from the test, but I am  inordinately happy for the people who will, whose lives will be happier and healthier because of it. 
http://www.psychiatryadvisor.com/mood-disorders/protein-bipolar-depression-immunoassay-mood-disorder/article/458539/
Diagnosing bipolar disorder may become easier now that researchers have discovered a group of proteins that could be used as biomarker to identify the mood disorder.Mark Frye, MD, head of psychiatric and psychology at the Mayo Clinic, Rochester, Minn., and colleages examined 272 protein from 288 patient blood samples. Of the study participants, 46 were diagnosed with bipolar I depression, 49 with bipolar II depression and 52 with unipolar depression. They were compared against a control group of 141 subjects without any mood disorders.

A total of 73 proteins were found to differ among the four groups studied. However, there was a significant difference in six proteins in those with bipolar I depression compared to the control group, the researchers reported in the journal Translational Psychiatry, an indication they could be used as biomarkers.

“The potential of having a biological test to help accurately diagnose bipolar disorder would make a huge difference to medical practice,” Frye said in a statement. “It would then help clinicians to choose the most appropriate treatment for hard-to-diagnose individuals.”

The researchers noted their work is “one of the first studies to assess the feasibility of high throughput multiplexed immunoassay technology (272 proteins) trying to distinguish different types of mood disorders,” thought they added the results need to be replicated in a larger study.

Negative Symptoms

SCHIZO

This is a graphic for negative (meaning things that are absent or missing, such as affect, pleasure, speaking, and activity) symptoms of schizophrenia, but these very symptoms are also present in the depressive phase of bipolar disorder. And these can also be erroneously attributed to laziness, “just not trying enough”, or unwillingness, but they are due to illness.

Schizophrenia, bipolar disorder and major depression share genetic risk factors: Study

DSCN6809

From the article below. Again, immune involvement. “The researchers found strong associations between mechanisms related to immune function and changes in processes when genes are turned on and off. The findings confirm known mechanisms as well as revealing new ones that pertain to the development of psychiatric disorders.”

I know when I am in full blown mania and out of touch with reality, there is no difference between me and a person who has schizophrenia. The thing is that my getting to that point can be prevented by taking Lithium (for me), whereas a person with schizophrenia has a lot more trouble coming out from delusions, hallucinations and back in touch with reality.

http://www.belmarrahealth.com/schizophrenia-bipolar-disorder-and-major-depression-share-genetic-risk-factors-study/

Schizophrenia, bipolar disorder and major depression have been found to share a genetic risk factor, according to a new study. Aside from the recent research, many previous studies also showed a genetic link between all three mental disorders. Below are synopses of the health studies that reveal the connection they all possess.

Study on shared genetic risk factors for schizophrenia, bipolar disorder and major depression

Research published in Nature Neuroscience from the Louisiana State University Health Science Centers revealed a genetic risk factor that is shared between schizophrenia, bipolar disorder and major depression. Lead researcher, Nancy Buccola, and her team examined data from 60,000 participants, including those with schizophrenia, bipolar disorder, major depression, autism, attention deficit disorders as well as individuals without any diagnosed conditions.

Study on shared genetic risk factors for schizophrenia, bipolar disorder and major depressionThe researchers found strong associations between mechanisms related to immune function and changes in processes when genes are turned on and off. The findings confirm known mechanisms as well as revealing new ones that pertain to the development of psychiatric disorders.

Treatments are available for many mental disorders but many patients do not obtain relief from such treatments. Buccola stated, “The PGC is a collaboration of some of the finest psychiatric genetic researchers in the world who are working together to understand the biology that underlies psychiatric disorders. This knowledge is critical in developing more effective and personalized treatments. I feel fortunate to make even a small contribution to this important work.”

Previous study shows schizophrenia and bipolar disorder cause dendritic spine loss in brain

Alternative research has found that schizophrenia and bipolar disorder both play a role in dendritic spine loss in the brain. The findings suggest that the two disorders share similar pathopsychological features.

Dendritic spines play a role in many brain functions. To achieve their results, researchers looked at individuals with schizophrenia, bipolar disorder, and individuals not affected by either disorder.

Spine density was reduced in those with bipolar disorder and those with schizophrenia, when compared to the control group. Furthermore, there was a significant reduction in spines per dendrite in both bipolar individuals and schizophrenics.

Lead researcher, Glenn T. Konopaske, M.D., said, “The current study suggests that spine pathology is common to both [schizophrenia] and [bipolar]. Moreover, the study of the mechanisms underlying the spine pathology might reveal additional similarities and differences between the two disorders, which could lead to the development of novel biomarkers and therapeutics.”

Bipolar disorder is often misdiagnosed as major depressive disorder (MDD)

Bipolar disorder is often misdiagnosed as major depressive disorder (MDD)Research has shown that bipolar disorder is often misdiagnosed as major depressive disorder (MDD). In bipolar disorder, individuals experience intense lows in mood and euphoric highs. In major depressive disorder, individuals experience steady, intense lows in mood. Because episodes of low mood can last for days or even weeks in those with bipolar, it can lead to a misdiagnosis of major depressive disorder. Researchers are closing in on an objective to help distinguish between the two conditions in order to reduce misdiagnosis.

Current diagnostic methods involve interviews with the patient, but this can be subjective and misleading. Researchers decided to combine techniques together in order to create a more accurate diagnostic method. The techniques used are gas chromatography-mass spectrometry and nuclear magnetic resonance, which analyze the urine of patients with MDD and bipolar disorder in order to uncover biomarkers of each disorder. These biomarkers will allow doctors to improve diagnosis by 89 to 91 percent.

Depression in patients with schizophrenia

One study found that a quarter (25 percent) of those with schizophrenia also have course-related depression. Depression in schizophrenia patients is related to a reduction in social and vocational functioning and also increases the risk of a psychotic relapse.

Depression in schizophrenia often has poor outcomes; patients have more suicidal thoughts, suicide attempts, and suicides.

It can be difficult to diagnose depression and schizophrenia separately as the “negative” symptoms related to schizophrenia can present themselves like depression. Negative symptoms refer to social withdrawal, low motivation and energy, difficulty experiencing pleasure or having interests and an impaired thought process; all symptoms seen in depression as well.

For the many similarities presented in both schizophrenia and depression, not only is distinguishing between the two difficult, but depression can often be seen in many schizophrenic patients as well.

From all the presented studies we see many links and associations between schizophrenia, bipolar disorder and depression. By continuing to make these links, we can obtain a better understanding of these mental disorders, which could greatly assist in developing more specific treatments that could offer more patients greater relief.

Lower availability of omega-3 fatty acids in the body associated with bipolar disorder

Omega-3 fatty acid can exist in two forms in the blood, 1) free, 2) bound to protein. It is the free form of omega-3 fatty acids that can cross the blood brain barrier. The ratio of free omega-3 fatty acids to bound fatty acids is lower in people with bipolar disorder (BPD). This means that we, people with BPD, have lower levels of these fatty acids available to be transported to our brains.

Fatty acids are very important as they form the cell membranes of all cells. This is especially important in the brain, as they form cell membranes of neurons as well. And neurons, the cells of the brain, are the ones that have ion channels in their membranes that allow Na+ and K+ to pass through creating ionic gradients across the cell membranes, allowing action potentials, which lead to nerve impulses, which is how information, emotions, sensory information, motor directives, everything is disseminated.

Omega-3 fatty acids also play an important role in the inflammatory response. (Another immune system/brain connection!)

This study is important, and they are going to further study the effect of this lower concentration of fatty acids, and hopefully come up with dietary recommendations for omega-3 fatty acids for people with BPD.

http://www.sciencedaily.com/releases/2015/11/151124082456.htm

People with bipolar disorder have lower levels of certain omega-3 fatty acids that cross the blood-brain barrier compared to those who do not, according to researchers from Penn State College of Medicine and the National Institutes of Health. The finding could have implications for dietary interventions for the disorder.

Fatty acids are a major area of interest in bipolar disorder and depression because of their biological importance in the brain. Studies have shown that fatty acid supplementation may be useful for unipolar depression, but the data has been more mixed for bipolar disorder.

The researchers, led by Dr. Erika Saunders, associate professor and chair of psychiatry at Penn State College of Medicine, compared fatty acids in 27 people with symptomatic bipolar disorder and 31 healthy control subjects. The group measured levels of different forms of the polyunsaturated fatty acids omega-3 and omega-6. They also collected self-reported information on fatty acid consumption and bipolar medication use. Their results were published in the journal Bipolar Disorders.

Free fatty acids are able to cross the blood-brain barrier, while fatty acids bound to proteins are not. In study subjects with bipolar disorder, the ratio of a free-circulating omega-3 fatty acid called EPA to bound EPA was lower than in other people.

“This means that the availability of omega-3 in the body is lower in bipolar subjects,” Saunders said.

Omega-3 fatty acids are a large component of brain-cell membranes and are important for cell-to-cell communication in the brain. In the study, the ratio of free to bound EPA correlated with clinical bipolar symptoms, specifically mania and tendency towards suicide.

Fatty acids also play an important role in the immune system and the inflammatory system.

“Omega-3 and omega-6 fatty acids can shift the balance of inflammation, which we think is important in bipolar disorder,” Saunders said.

However, the researchers did not find altered ratios of omega-3 to omega-6 fatty acids in bipolar subjects.

Although the researchers did find lower levels of omega-3s in patients with bipolar disorder that correlated with symptoms, Saunders said it’s too early to advise dietary changes or omega-3 supplementation.

Omega-3 fatty acids are abundant in fish, vegetable oils, nuts — especially walnuts, flax seeds, flaxseed oil and leafy vegetables.

There was no difference in self-reported fatty acid consumption between bipolar and healthy patients.

“Is that because we only included certain foods in the survey? Or is it because people couldn’t accurately recall what they were eating?” Saunders said.

Another possibility the researchers are considering is that there are differences in how healthy people and people with bipolar disorder convert fatty acids from one form to another. Drugs that treat bipolar disorder are known to affect these conversions, but no association was found between fatty acid levels or ratios and self-reported medication use in the study.

Saunders is currently investigating if modifications in dietary intake of fatty acids could be useful in bipolar disorder.

“We are actively pursuing the next step in this line of inquiry to get to the point where we know what changes in diets are going to help people with bipolar disorder so they can have another option beyond the medications that are currently available,” she said.

A number of trials have turned up no benefit of omega-3 supplementation in bipolar disorder, a brain disorder that causes manic episodes of elevated mood, energy and cognition, and major depressive episodes of lowered mood, energy and cognition. Bipolar disorder affects between 1 and 4.4 percent of the population.

“I think our work, along with the work of others, shows that this is an important area for us to continue to study,” Saunders said. “It’s complicated and hard to study, and there are a lot of factors, but it’s an area we need to keep pursuing.”

Most research on fatty acids in bipolar disorder measures levels of fatty acids in cell membranes. Saunders’s group instead looked at circulating fatty acids in the blood, which is a better indication of dietary intake. Fatty acids in the blood are also the type that crosses the blood-brain barrier to enter the brain.


Story Source:

The above post is reprinted from materials provided by Penn State Milton S. Hershey Medical Center. Note: Materials may be edited for content and length.


Journal Reference:

  1. Erika FH Saunders, Aubrey Reider, Gagan Singh, Alan J Gelenberg, Stanley I Rapoport. Low unesterified:esterified eicosapentaenoic acid (EPA) plasma concentration ratio is associated with bipolar disorder episodes, and omega-3 plasma concentrations are altered by treatment. Bipolar Disorders, 2015; 17 (7): 729 DOI:10.1111/bdi.12337