Thank you Kitt O’Malley (kittomalley.com) for tweeting this.

This is horrifying, any hits to the head can cause chronic traumatic encephalopathy or CTE. The hits don’t have to cause concussions, any hits to the head can cause damage which may or may not be evident immediately.

Football coaches of young kids who play football should read this article as well as NFL players, coaches, and officials. These debilitating, often invisible at first, and sometimes deadly injuries really need to be checked. A sport should not cause the death of its players. 😢😢

http://www.latimes.com/science/sciencenow/la-sci-sn-cte-head-hits-20180118-story,amp.html?__twitter_impression=true

So, this winter, I didn’t really go through my yearly and very dreaded hypomanic phase. It’s been quite a miracle, and for this I am endlessly grateful. The reason was medication of course. A combination of Lithium and Seroquel. Although I am a little sluggish and my muscles ache a little bit, the yearly being out of touch with reality didn’t happen! The Daily emotional breakdowns did not happen. The being totally dysfunctional did NOT happen.

Anxiety still happened but those other things did not!

Amazing what the right dose and combination of meds can do!

So for me, winter in my manic mood and summer is my depressed mood, exactly the opposite of seasonal affective disorder. So I am moving towards depression now. However, I am hoping that since the hypomanic mood didn’t really occur, neither will the depressed mood. As we all know, the intensity of mania in one direction is matched by how intense the depression will be in the other direction.

Oh I have s bit of a pitchy stomach from Seroquel, but nothing that a rigorous ab regimen won’t take care of.

All in all, it’s been an unbelievably stable winter! I can’t tolerate too many meds but these two, Lithium and Seroquel, that I can tolerate are mega bosses.

Hoping for stable moods, happiness and love in the lives of all who visit here and even all who don’t.

💕🙏💐🙏💐💕

This is quite fascinating! Hmmm I’m going to try and see about my allergies which I developed when I moved out of Buffalo. Interesting, very interesting!

https://www.bphope.com/blog/could-emotions-trigger-allergies/

The intense emotions associated with bipolar may cause allergies to flare up.  Pinpointing a traumatic experience and talking it out may help.

Photo: PeopleImages/Getty Images

By Lynn Rae

For this blog post, I am going to take you back in time to the 1970s.  I am going to show you that allergies are really our emotions in disguise, in my experience.

I was a teenager.  I rebelled against authority, but only in small ways.  My mother still ruled and I was afraid of her wrath if I did anything wrong.  Smoking cigarettes was the cool thing to do at that time.  It began innocently enough for me.  I was only 12 and a friend came to our cottage with me.  I tried smoking, but couldn’t inhale.  But I was hooked.  I kept trying to smoke and I was going to learn to inhale.  By the time I was 16 I was smoking regularly, perhaps 2-8 cigarettes a day.

Then I met the man, who was to become my husband. He smoked a pack a day. By the time I was 19, I was smoking that much too.  I really don’t know why I enjoyed it so much.  It is only in the last few years I have come to understand that all my emotions went up in smoke.  I smoked when I was happy, sad, mad or glad.  I smoked to celebrate the beginning and end of the day.  I smoked on my coffee break and lunch hour from work.  If I was angry with my husband or some other family member, the first thing I did was reach for a cigarette.  With every inhale and exhale, my problems seemed to disappear.

By the time my son was 3, he was fascinated with cigarettes and the ashtray.  One thing I didn’t want was for him to become a smoker.  A hypocrite was something I was not!  I quit smoking in the spring of 1988 when I was pregnant with my daughter.  For three days, I lay on the couch in the fetal position having withdrawal.  It was tough, but I was determined to quit for my kids’ sake.  Exactly six weeks after I quit smoking, I was visiting a farm and my nose started running.  It wouldn’t stop.  I went through a box of tissues in 24 hours.  I went to see my doctor.  He said I had allergies.  I shook my head in disbelief.  How could this be?  I quit smoking to get healthy and this is what I get?  I took allergy pills and/or a needle for a few years.  Every time I walked by the perfume counter in a store I would start to sneeze.

Over a 15-year period my allergies eventually subsided.  I didn’t need to take medication for them anymore.  During this time, I was diagnosed with depression, then bipolar disorder.

This is when the real work on myself began.  I read over 200 self-help/motivational books, attending workshops and support groups, left my marriage and began to rebuild my life.

Since 2005 I have had very few problems with my allergies acting up.  Also by 2005, I had resolved every issue I had with people in my life to the best of my ability.  I knew that getting out of toxic relationships and/or jobs was the key to my well-being.  As a side effect, my allergies cleared up as well.

Fast forward to the summer of 2008.  I met a man and fell in love with him very quickly.  However, he was never available.  I didn’t want to believe he was married, but the signs were all there.  But there was something about this man that captivated me.  I wanted him more than I have ever wanted a man.  But all I got was the leftovers.

A few months later he was going away on business.  I told him when he got back he had to decide; it was her or me.  Finally, I had to accept that we would never be together.  When I tried to accept this fact, my sinuses started acting up.  I hadn’t been bothered by allergies for four years.  My nose just ran and ran and ran over a 24-hour period.  I couldn’t sleep, I was so stuffed up.  I tried working, but had to come home.  I could hardly breathe.  I took some over-the-counter medication, but it didn’t help.  I told my girlfriend how I was feeling.  She let me talk and talk and talk.  When I finally was all talked out, my allergies eased up.

Now fast forward to 2015.  I was slightly hypo-manic and decided to contact him.  I hadn’t thought about him in years, but for some reason I needed him again.  Once again, we started up a relationship.  However, by this time he had left his wife a year earlier.  Of course, I was daydreaming about how we would one day live together.  When, once again, I realized he was just using me, and my allergies acted up.   It was only when I could let him go that my sinuses cleared up again.  I have seen over and over again that when I am really upset about something, my nose gets stuffed up.

You see, when we smoke, we are smoking all our emotions away.  When I quit smoking in 1988 there was nowhere for my emotions to go because I didn’t know how to talk to people about what I was feeling.  We didn’t talk about problems in our family; problems got swept under the rug hopefully to be forgotten about and go away on their own.  It was only when I learned to talk about anything and everything that was bothering me that my allergies disappeared.  They only rear up once in a while, but don’t last for more than a day or two because I can usually pinpoint what the issue is and talk in out with a trusted friend.

If you are bothered by allergies, go back to when they started.  What triggered them?  Do you agree or disagree with my opinion about why we get allergies?

https://www.bphope.com/blog/irritated-angry-and-aggressive-bipolar-disorder/

My friend and fellow blogger, Julie Fast (info below) wrote this article. And it is truer than true. The intensity behind our anger, the strength, is unbelievable! And yes medications that control mood can be very helpful but sometimes, anger will slip by. Vigilance, behavior modification and medication are all needed to put this genie back into its bottle.

Unfortunately, aggressive irritation is, quite often, a symptom of bipolar disorder.

Aggressive irritation is a unfortunate symptom of bipolar disorder. It often comes with a down swing or a mixed episode where you’re manic and depressed at the same time.

We all experience irritation- that’s a normal part of life. Getting cut off on the free way- rude people- crowds and long lines at the supermarket can make us irritated. We may mutter under our breath and give a lot of dirty looks when we get in these situations.

Bipolar aggressive irritation is different- it has a lot of strength behind it. Instead of just getting irritated when we get cut off on the free way- we yell and scream, honk the horn and if it’s particularly bad- actually chase down the person with our car. Oh yes, this happens!

If someone is rude to a person in an aggressive irritated mood swing- they had better watch out- we may say, “What the @$@#$#@ are you looking at! You have a problem with me!” And we will move in on them and practically growl.

Bipolar aggressive irritation is different– it has a lot of strength behind it

Some other signs of this aggressive irritation: throwing things- such as wanting to throw my $%#%% computer across the room when the internet won’t work!  Or feeling my head and neck jerk because I’m so angry at something.

This is NOT good stuff, but it’s common.

If you love someone with bipolar, especially a man in his 20s, this may be all too familiar.

Here is some good news. Medications can work wonders with irritation.  Then behavior modification has to become a part of life.

When I get irritated, angry and aggressive, I have learned to calm myself down- and at least stop myself before I take my aggression too far!

Julie

Julie A. Fast is the author of Loving Someone with Bipolar Disorder, Take Charge of Bipolar Disorder, Get it Done When You’re Depressed and The Health Cards Treatment System for Bipolar Disorder. She is a columnist and blogger for BP Magazine and won the Mental Health America journalism award for the best mental health column in the US. Julie was also the recipient of the Eli Lily Reintegration award for her work in bipolar disorder advocacy. Julie is a bipolar disorder expert for the Dr.Oz and Oprah created site ShareCare. Julie is CEU certified and regularly trains health care professionals including psychiatric residents, social workers, therapists and general practitioners on bipolar disorder management skills. She was the original consultant for Claire Danes for the show Homeland and is on the mental health expert registry for People Magazine. She works as a coach for parents and partners of people with bipolar disorder. Julie is currently writing a book for children called Hortensia and the Magical Brain: Poems for Kids with Bipolar, Anxiety, Psychosis and Depression. You can find more about her work at www.www.JulieFast.com and www.BipolarHappens.com

This research shows that schizophrenia may NOT be the result of abnormalities in neurons, but actually abnormalities in cells that support neurons. These cells are Glial cells or Glia. Glia includes two major types: astrocytes and oligodendrocytes.  Astrocytes are the brain’s principal support cells, while oligodendrocytes are responsible for producing myelin, the fatty tissue that, like the insulation on electrical wires, wraps the axons that connect different nerve cells.   The source of both these cells is another cell type called the glial progenitor cell (GPC).

When the production of glia is abnormal, there is less connectivity and nerve impulses are not optimal.

When glial cells from schizophrenic people are turned into pluripotent stem cells and then Glial progenitor cells and injected into brains of neonatal mice, these mice show all the symptoms of schizophrenia, they were more fearful, anxious, anti-social, and had a variety of cognitive deficits. While mice who were implanted with glial cells that were from normal people did not show these symptoms.

So this a very interesting finding, that the support cells may well be involved in the development of schizophrenia!

This could lead to new, and hopefully better, ways of treating people with schizophrenia.

Please read below for more details.

https://www.urmc.rochester.edu/news/story/5101/faulty-support-cells-disrupt-communication-in-brains-of-people-with-schizophrenia.aspx

New research has identified the culprit behind the wiring problems in the brains of people with schizophrenia.  When researchers transplanted human brain cells generated from individuals diagnosed with childhood-onset schizophrenia into mice, the animal’s nerve cell networks did not mature properly and the mice exhibited the same anti-social and anxious behaviors seen in people with the disease.

“The findings of this study argue that glial cell dysfunction may be the basis of childhood-onset schizophrenia,” said University of Rochester Medical Center (URMC) neurologist Steve Goldman, M.D., Ph.D., co-director of the Center for Translational Neuromedicine and lead author of the study which appears today in the journal Cell.  “The inability of these cells to do their job, which is to help nerve cells build and maintain healthy and effective communication networks, appears to be a primary contributor to the disease.”

Glia are an important family of support cells found in the brain and play a critical role in the development and maintenance of the brain’s complex interconnected network of neurons.   Glia includes two major types: astrocytes and oligodendrocytes.  Astrocytes are the brain’s principal support cells, while oligodendrocytes are responsible for producing myelin, the fatty tissue that, like the insulation on electrical wires, wraps the axons that connect different nerve cells.   The source of both these cells is another cell type called the glial progenitor cell (GPC).

Astrocytes perform several functions in the brain.  During development, astrocytes colonize areas of the brain and establish domains in which these cells help direct and organize the network of connections between nerve cells.  Individual astrocytes also send out hundreds of long fibers that interact with synapses – the junction where one neuron’s axon meets another’s dendrite.  The astrocytes help facilitate the communication between neurons at the synapses by regulating the flow of glutamate and potassium, which enable neurons to “fire” when they are communicating with each other.

In the new study, the researchers obtained skin cells from individuals with childhood-onset schizophrenia and reprogrammed the cells to create induced pluripotent stem cells (iPSC) which, like embryonic stem cells, are capable of giving rise to any cell type found in the body.  Employing a process of first developed by the Goldman lab, the team manipulated the iPSCs to create human GPCs.

The human GPCs were then transplanted into the brains of neonatal mice.  These cells out-competed the animal’s own native glia, resulting in mice with brains comprised of animal neurons and human GPCs, oligodendrocytes, and astrocytes.

The researchers observed that human glial cells derived from schizophrenic patients were highly dysfunctional.  The development of oligodendrocytes was delayed and the cells did not create enough myelin-producing cells, meaning signal transmission between the neurons was impaired.

The development of astrocytes was similarly tardy so that the cells were not present when needed and were thus ineffective in guiding the formation of connections between neurons.  The astrocytes also did not mature properly, resulting in misshapen cells that could not fully support the signaling functions of the neurons around them.

“The astrocytes didn’t fully mature and their fibers did not fill out their normal domains, meaning that while they provided control to some synapses, others had no coverage,” said Martha Windrem, Ph.D., with URMC’s Center for Translational Neuromedicine and first author on the study.  “As a result, the neural networks in the animals became desynchronized and uncoordinated.”

The researchers also subjected the mice to a series of behavioral tests.  They observed that the mice with human glial cells from individuals diagnosed with schizophrenia were more fearful, anxious, anti-social, and had a variety of cognitive deficits compared to mice transplanted with human glial cells obtained from healthy people.

The study’s authors point out that the new research provides scientists with a foundation to explore new treatments for the disease.  Because schizophrenia is a unique to humans, until now scientists have been limited in their ability to study the disease.  The new animal model developed the by the researchers can be used to accelerate the process of testing drugs and other therapies in schizophrenia.  The study also identifies a number of glial gene expression flaws that appear to create chemical imbalances that disrupt communication between neurons.  These abnormalities could represent targets for new therapies.

What is resilience? It’s the ability to bounce back after an adverse event. Like a rubber band snaps back to its real shape after being stretched to the limit.

We have resilience. Some of us have more, some of us have less. At times we have lots of it, at other times, we have a little bit.

Sometimes we may be seriously resilience challenged and sometimes we may be blessed with lots of it.

Of course, no matter what happens in our lives, what matters is how we react to it. Easy to say. Sometimes we may feel we don’t have any control over our reaction to an event, that the event is so awful that all we can do is break down. But… but we always have control over how we react. Maybe not the initial reaction, but certainly the ensuing reaction, after we think about what has happened and how it affects us. At that point we can decide how to react and push ourselves towards resilience, towards getting over it, towards being strong and tall.

Ok people take out the flour, butter and eggs, put on your gloves and start baking, cooking, all of these will make you feel better, more in control and happier even the next day! And there really is a journal called The Journal of Positive Psychology! Happy baking, cooking and creating! ‘Tis the season 🎄

https://www.smithsonianmag.com/smart-news/feeling-down-scientists-say-cooking-and-baking-may-help-you-feel-better-180961223/?utm_source=facebook.com&utm_medium=socialmedia

Cooking or baking has become a common cure for stress or feeling down, but there might actually be some science to why small creative tasks might make people feel better. According to a new study, a little creativity each day can go a long way towards happiness and satisfaction in the bustle of daily life.

The study, published in the Journal of Positive Psychology, suggests that people who frequently take a turn at small, creative projects report feeling more relaxed and happier in their everyday lives. The researchers followed 658 people for about two weeks, and found that doing small, everyday things like cooking and baking made the group feel more enthusiastic about their pursuits the next day, Daisy Meager reports for Munchies.

“There is growing recognition in psychology research that creativity is associated with emotional functioning,” Tamlin Conner, a psychologist with the University of Otago in New Zealand and lead author on the study tells Tom Ough for The Telegraph. “However, most of this work focuses on how emotions benefit or hamper creativity, not whether creativity benefits or hampers emotional well-being.”

By following detailed diaries kept by the study subjects, Connor found that in addition to feeling happier, people who worked on little creative projects every day also felt they were “flourishing”—a psychological term that describes the feeling of personal growth. That could mean that the good feeling that comes with pulling a freshly-baked loaf of bread out of the oven could carry over into the next day, making that baker more likely to keep on with their little acts of creative cooking, Ough writes.

This isn’t the first time researchers have drawn a line connecting making food with positive feelings. In recent years, psychologists have started spending more time exploring cooking and baking as a therapeutic tool to help people dealing with things like depression and anxiety, Meager reports.

“When I’m in the kitchen, measuring the amount of sugar, flour or butter I need for a recipe or cracking the exact number of eggs—I am in control,” baker John Whaite, who won “The Great British Bake Off” in 2012, told Farhana Dawood for the BBC. “That’s really important as a key element of my condition is a feeling of no control.”

For people like Whaite, who was diagnosed with manic depression in 2005, baking can help their mood by providing small tasks to focus on in a manner similar to meditation. In order to put together a good meal, cooks have to be constantly in the moment, adding ingredients, adjusting the heat of the stove and tasting their food to make sure everything will come out alright—all of which can be helpful techniques in treating some forms of mental illness, wrote Huma Qureshi for The Guardian in 2013.

“A lot of us turn to baking when we’re feeling low,” Melanie Denyer, the founder of the Depressed Cake Shop, a bakery designed to draw awareness to mental health conditions, tells Dawood. “Some of us even started baking because they were ill and needed something simple as a focus.

Baking may not be a be-all-end-all cure for mental illness, but anyone in need of lifted spirits should consider pulling out the flour and warming up the oven.

GABA, an inhibitory neurotransmitter is involved in intrusive thoughts, rumination and even hallucinations. If the levels of GABA are low in the hippocampus, then it will be difficult to control our thoughts. GABA, GABA, my kingdom for GABA!

https://www.technologynetworks.com/neuroscience/news/brain-mechanism-that-inhibits-unwanted-memories-uncovered-293915

Scientists have identified a key chemical within the ‘memory’ region of the brain that allows us to suppress unwanted thoughts, helping explain why people who suffer from disorders such as anxiety, post-traumatic stress disorder (PTSD), depression, and schizophrenia often experience persistent intrusive thoughts when these circuits go awry.

We are sometimes confronted with reminders of unwanted thoughts — thoughts about unpleasant memories, images or worries. When this happens, the thought may be retrieved, making us think about it again even though we prefer not to. While being reminded in this way may not be a problem when our thoughts are positive, if the topic was unpleasant or traumatic, our thoughts may be very negative, worrying or ruminating about what happened, taking us back to the event.

“Our ability to control our thoughts is fundamental to our wellbeing,” explains Professor Michael Anderson from the Medical Research Council Cognition and Brain Sciences Unit, which recently transferred to the University of Cambridge. “When this capacity breaks down, it causes some of the most debilitating symptoms of psychiatric diseases: intrusive memories, images, hallucinations, ruminations, and pathological and persistent worries. These are all key symptoms of mental illnesses such as PTSD, schizophrenia, depression, and anxiety.”

Professor Anderson likens our ability to intervene and stop ourselves retrieving particular memories and thoughts to stopping a physical action. “We wouldn’t be able to survive without controlling our actions,” he says. “We have lots of quick reflexes that are often useful, but we sometimes need to control these actions and stop them from happening. There must be a similar mechanism for helping us stop unwanted thoughts from occurring.”

A region at the front of the brain known as the prefrontal cortex is known to play a key role in controlling our actions and has more recently been shown to play a similarly important role in stopping our thoughts. The prefrontal cortex acts as a master regulator, controlling other brain regions – the motor cortex for actions and the hippocampus for memories.

In research published today in the journal Nature Communications, a team of scientists led by Dr Taylor Schmitz and Professor Anderson used a task known as the ‘Think/No-Think’ procedure to identify a significant new brain process that enables the prefrontal cortex to successfully inhibit our thoughts.

In the task, participants learn to associate a series of words with a paired, but otherwise unconnected, word, for example ordeal/roach and moss/north. In the next stage, participants are asked to recall the associated word if the cue is green or to suppress it if the cue is red; in other words, when shown ‘ordeal’ in red, they are asked to stare at the word but to stop themselves thinking about the associated thought ‘roach’.

Using a combination of functional magnetic resonance imaging (fMRI) and magnetic resonance spectroscopy, the researchers were able to observe what was happening within key regions of the brain as the participants tried to inhibit their thoughts. Spectroscopy enabled the researchers to measure brain chemistry, and not just brain activity, as is usually done in imaging studies.

Professor Anderson, Dr Schmitz and colleagues showed that the ability to inhibit unwanted thoughts relies on a neurotransmitter – a chemical within the brain that allows messages to pass between nerve cells – known as GABA. GABA is the main ‘inhibitory’ neurotransmitter in the brain, and its release by one nerve cell can suppress activity in other cells to which it is connected. Anderson and colleagues discovered that GABA concentrations within the hippocampus – a key area of the brain involved in memory – predict people’s ability to block the retrieval process and prevent thoughts and memories from returning.

“What’s exciting about this is that now we’re getting very specific,” he explains. “Before, we could only say ‘this part of the brain acts on that part’, but now we can say which neurotransmitters are likely important – and as a result, infer the role of inhibitory neurons – in enabling us to stop unwanted thoughts.”

“Where previous research has focused on the prefrontal cortex – the command centre – we’ve shown that this is an incomplete picture. Inhibiting unwanted thoughts is as much about the cells within the hippocampus – the ‘boots on the ground’ that receive commands from the prefrontal cortex. If an army’s foot-soldiers are poorly equipped, then its commanders’ orders cannot be implemented well.”

The researchers found that even within his sample of healthy young adults, people with less hippocampal GABA (less effective ‘foot-soldiers’) were less able to suppress hippocampal activity by the prefrontal cortex—and as a result much worse at inhibiting unwanted thoughts.

The discovery may answer one of the long-standing questions about schizophrenia. Research has shown that people affected by schizophrenia have ‘hyperactive’ hippocampi, which correlates with intrusive symptoms such as hallucinations. Post-mortem studies have revealed that the inhibitory neurons (which use GABA) in the hippocampi of these individuals are compromised, possibly making it harder for the prefrontal cortex to regulate activity in this structure. This suggests that the hippocampus is failing to inhibit errant thoughts and memories, which may be manifest as hallucinations.

According to Dr Schmitz: “The environmental and genetic influences that give rise to hyperactivity in the hippocampus might underlie a range of disorders with intrusive thoughts as a common symptom.”

In fact, studies have shown that elevated activity in the hippocampus is seen in a broad range of conditions such as PTSD, anxiety and chronic depression, all of which include a pathological inability to control thoughts – such as excessive worrying or rumination.

While the study does not examine any immediate treatments, Professor Anderson believes it could offer a new approach to tackling intrusive thoughts in these disorders. “Most of the focus has been on improving functioning of the prefrontal cortex,” he says, “but our study suggests that if you could improve GABA activity within the hippocampus, this may help people to stop unwanted and intrusive thoughts.”

This article has been republished from materials provided by Cambridge University. Note: material may have been edited for length and content. For further information, please contact the cited source.

Schmitz, TW et al. Hippocampal GABA enables inhibitory control over unwanted thoughts. Nature Communications; 3 Nov 2017; DOI: 10.1038/s41467-017-00956-z

This team has identified 7 causes for bipolar disorder. They don’t think any one gene is responsible as one has never been identified. Also people with bipolar disorder are much more likely to suffer from migraines than non diseased counter parts. This includes me, I’ve had migraines since I was 13 and was diagnosed with bipolar disorder at 25 years if age. Also childhood trauma is a factor. Fascinating article. Below for your reading pleasure.

https://m.medicalxpress.com/news/2017-12-years-bipolar-disorder-team.html

Bipolar disorder is characterized by transitions between depression and mania. Credit: Wikipedia

Nearly 6 million Americans have bipolar disorder, and most have probably wondered why. After more than a decade of studying over 1,100 of them in-depth, a University of Michigan team has an answer – or rather, seven answers.

In fact, they say, no one genetic change, or chemical imbalance, or life event, lies at the heart of every case of the mental health condition once known as manic depression.

Rather, every patient’s experience with bipolar disorder varies from that of others with the condition. But all of their experiences include features that fall into seven classes of phenotypes, or characteristics that can be observed, the team reports in a new paper in the International Journal of Epidemiology.

The team, from U-M’s Heinz C. Prechter Bipolar Research Program, collected and analyzed tens of thousands of data points over years about the genetics, emotions, life experiences, medical histories, motivations, diets, temperaments, sleep patterns and thought patterns of research volunteers. More than 730 had bipolar disorder, and 277 didn’t. Three-quarters of them are currently active research participants in the Longitudinal Study of Bipolar Disorder.

Using those findings, the team has developed a framework that could be useful to researchers studying the condition, clinical teams treating it, and patients experiencing it. The team hopes it will give them all a common structure to use during studies, treatment decisions and more.

“There are many routes to this disease, and many routes through it,” says Melvin McInnis, M.D., lead author of the new paper and head of the program based at the U-M Depression Center. “We have found that there are many biological mechanisms which drive the disease, and many interactive external influences on it. All of these elements combine to affect the disease as patients experience it.”

The Prechter program, funded by gifts from many donors, is named for a late Detroit automotive pioneer who fought bipolar even as he built a successful business.

Long-term funding from this program has made it possible to build a massive library of data from the “Prechter cohort” of patients, which is two-thirds female, and 79 percent white, with an average age at enrollment in the study of 38 years. On average, participants had had their first depressive or manic episode when they were 17, and many had other mental health conditions.

Seven classes and the key findings that shaped them

The seven phenoclasses, as the U-M team has dubbed them, include standard measures doctors already use to diagnose and track the progress of bipolar disorder.

In addition, they include:

• changes in cognition, which includes thinking, reasoning and emotion processing;

• psychological dimensions such as personality and temperament;

• measures of behaviors related to substance use or abuse – called motivated behaviors;

• aspects of the person’s life story involving family and intimate relationships and traumas;

• patterns of sleep and circadian rhythms; and

• measures of how patients’ symptoms change over time and respond to treatment.

Some of the key findings made in the Prechter cohort by the U-M team include:

• Migraine headaches are three and a half times more common among people with bipolar disorder than those without. Eating disorders, anxiety disorders and alcohol problems are also more common in those with bipolar, as is metabolic syndrome.

• More people with bipolar disorder have a history of childhood trauma than those without the condition, it is associated with changes in self-control and attention.

• People with bipolar disorder had higher levels of saturated fats in their diets, and the research also found associations between levels of certain fat molecules in the blood of patients and their mood or level of symptoms.

• Looking at the microbes living in the gastrointestinal tracts of patients and comparison volunteers, the researchers found lower levels of a key bacteria type, and less diversity of microbes in patients taking antipsychotic medications.

• Poor sleep appears to play a key role in bipolar disorder, with links found to severity of depression and mania in female, but not male, participants with the condition. Other gender differences also emerged in other aspects of the study.

• People with bipolar disorder who have a strong neurotic tendency in their personalities are more likely to have severe illness, especially among men.

• A range of cognitive abilities – including memory, executive functioning and motor skills – were poorer in participants with bipolar than those without, in general. The study found a particular link between the cognitive abilities of people who carried a particular genetic trait and were taking newer antipsychotic medicines.

• Two genes, called CACNA1 and ANK3, appear to play a role in susceptibility to developing bipolar disorder. But many genetic variations have been found to be associated with bipolar risk, and more recent findings have explored the role of having a mix of these variations in the chances a person will develop bipolar.

• Stem cells grown from skin samples taken from participants, and then coaxed to grow into nerve cells called neurons, have proven useful in studying cellular aspects of bipolar disorder. For instance, neurons derived from bipolar patients’ cells were more excitable than comparisons – but calmed down when exposed to lithium, a common treatment for bipolar. Also, the cells show differences in how they interact and function.

• Key features of speech patterns predict mood states and may be useful outcomes measures to predict the need for intervention to prevent episodes of mania or depression.

Even though bipolar disorder tends to run in families, the long-term study has revealed no one gene that ‘carries the day’ to explain it, says McInnis, who is the Woodworth Professor of Bipolar Disorder and Depression in the U-M Medical School’s Department of Psychiatry.

“If there was a gene with a strong effect like what we see in breast cancer, for instance, we would have found it,” he explains. “We hope this new framework will provide a new approach to understand this disorder, and other complex diseases, by developing models that can guide a management strategy for clinicians and patients, and give researchers consistent variables to measure and assess.”

He adds, “Bipolar disorder has a lot to teach humankind about other illnesses, because it covers the breadths of human mood, emotion and behavior like no other condition. What we can learn in bipolar about all these factors will be directly applicable to monitoring other disorders, and personalizing the approach to managing them.”

More information: Melvin G McInnis et al, Cohort Profile: The Heinz C. Prechter Longitudinal Study of Bipolar Disorder, International Journal of Epidemiology (2017). DOI: 10.1093/ije/dyx229

The Prechter Bipolar Research Program is still recruiting participants for its long-term study, and accepting donations from those who want to help the research move forward. More information is available at www.prechterprogram.org

Urea has been pinpointed as the cause of at least two, if not all, kinds of dementia. Amazing! A common metabolite of the body can cause dementia. Hopefully ways to prevent this will be forthcoming shortly.

https://www.technologynetworks.com/neuroscience/news/increased-urea-levels-in-brain-linked-with-dementia-295066

An international team of scientists have confirmed the discovery of a major cause of dementia, with important implications for possible treatment and diagnosis.

Professor Garth Cooper from The University of Manchester, who leads the Manchester team, says the build-up of urea in the brain to toxic levels can cause brain damage – and eventually dementia.

The work follows on from Professor Cooper’s earlier studies, which identified metabolic linkages between Huntington’s, other neurodegenerative diseases and type-2 diabetes.

The team consists of scientists from The University of Manchester, the University of Auckland, AgResearch New Zealand, the South Australian Research and Development Institute, Massachusetts General Hospital and Harvard University.

The latest paper by the scientists, published today in the Proceedings of the National Academy of Sciences, shows that Huntington’s Disease – one of seven major types of age-related dementia – is directly linked to brain urea levels and metabolic processes.

Their 2016 study revealing that urea is similarly linked to Alzheimer’s, shows, according to Professor Cooper, that the discovery could be relevant to all types of age-related dementias.

The Huntington’s study also showed that the high urea levels occurred before dementia sets in, which could help doctors to one day diagnose and even treat dementia, well in advance of its onset.

Urea and ammonia in the brain are metabolic breakdown products of protein. Urea is more commonly known as a compound which is excreted from the body in urine. If urea and ammonia build up in the body because the kidneys are unable to eliminate them, for example, serious symptoms can result.

Professor Cooper, who is based at The University of Manchester’s Division of Cardiovascular Sciences, said: “This study on Huntington’s Disease is the final piece of the jigsaw which leads us to conclude that high brain urea plays a pivotal role in dementia.

“Alzheimer’s and Huntington’s are at opposite ends of the dementia spectrum – so if this holds true for these types, then I believe it is highly likely it will hold true for all the major age-related dementias.

“More research, however, is needed to discover the source of the elevated urea in HD, particularly concerning the potential involvement of ammonia and a systemic metabolic defect.

“This could have profound implications for our fundamental understanding of the molecular basis of dementia, and its treatability, including the potential use of therapies already in use for disorders with systemic urea phenotypes.”

Dementia results in a progressive and irreversible loss of nerve cells and brain functioning, causing loss of memory and cognitive impairments affecting the ability to learn. Currently, there is no cure.

The team used human brains, donated by families for medical research, as well as transgenic sheep in Australia.

Manchester members of the team used cutting-edge gas chromatography mass spectrometry to measure brain urea levels. For levels to be toxic urea must rise 4-fold or higher than in the normal brain says Professor Cooper.

He added: “We already know Huntington’s Disease is an illness caused by a faulty gene in our DNA – but until now we didn’t understand how that causes brain damage – so we feel this is an important milestone.

“Doctors already use medicines to tackle high levels of ammonia in other parts of the body, Lactulose – a commonly used laxative, for example, traps ammonia in the gut. So it is conceivable that one day, a commonly used drug may be able to stop dementia from progressing. It might even be shown that treating this metabolic state in the brain may help in the regeneration of tissue, thus giving a tantalising hint that reversal of dementia may one day be possible.”

This article has been republished from materials provided by The University of Manchester, UK. Note: material may have been edited for length and content. For further information, please contact the cited source.

Reference:

Handley, R. R., Reid, S. J., Brauning, R., Maclean, P., Mears, E. R., Fourie, I., . . . Snell, R. G. (2017). Brain urea increase is an early Huntington’s disease pathogenic event observed in a prodromal transgenic sheep model and HD cases. Proceedings of the National Academy of Sciences, 201711243. doi:10.1073/pnas.1711243115