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

This is amazing! Implanting a small bioelectronic device on the Vagus nerve in Rheumatoid arthritic (RA) patients makes markers of inflammation (such as TNF and other cytokines) go down. And not only that, the symptoms of RA are also decreased.

This can be used for other autoimmune and immune diseases as well.

https://www.technologynetworks.com/neuroscience/news/study-shows-vagus-nerve-stimulation-significantly-reduces-rheumatoid-arthritis-284383

Clinical trial data published in the Proceedings of the National Academy of Sciences (PNAS) demonstrates stimulating the vagus nerve with an implantable bioelectronic device significantly improved measures of disease activity in patients with rheumatoid arthritis (RA). RA is a chronic inflammatory disease that affects 1.3 million people in the United States and costs tens of billions of dollars annually to treat. The findings were announced by the Academic Medical Center/University of Amsterdam, the Feinstein Institute for Medical Research and SetPoint Medical.

See Also: Neurostimulation: What is being said in the media and academic literature?

The publication highlights a human study designed to reduce symptoms of RA, cytokine levels and inflammation by stimulating the vagus nerve with a small implanted device.

“This is the first study to evaluate whether stimulating the inflammatory reflex directly with an implanted electronic device can treat RA in humans,” said Professor Paul-Peter Tak, MD, PhD, FMedSci, the international principal investigator and lead author of the paper at the Division of Clinical Immunology & Rheumatology of the Academic Medical Center/University of Amsterdam. “We have previously shown that targeting the inflammatory reflex may reduce inflammation in animal models and in vitro models of RA. The direct correlation between vagus nerve stimulation and the suppression of several key cytokines like TNF as well as reduced RA signs and symptoms demonstrates proof of mechanism, which might be relevant for other immune-mediated inflammatory diseases as well.”

“Our findings suggest a new approach to fighting diseases with bioelectronic medicines, which use electrical pulses to treat diseases currently treated with potent and relatively expensive drugs,” said Anthony Arnold, Chief Executive Officer of SetPoint Medical. “These results support our ongoing development of bioelectronic medicines designed to improve the lives of people suffering from chronic inflammatory diseases and give healthcare providers new and potentially safer treatment alternatives at a much lower total cost for the healthcare system.”

“This is a real breakthrough in our ability to help people suffering from inflammatory diseases,” said co-author Kevin J. Tracey, MD, president and CEO of the Feinstein Institute for Medical Research, discoverer of the inflammatory reflex and co-founder of SetPoint Medical. “While we’ve previously studied animal models of inflammation, until now we had no proof that electrical stimulation of the vagus nerve can indeed inhibit cytokine production and reduce disease severity in humans. I believe this study will change the way we see modern medicine, helping us understand that our nerves can, with a little help, make the drugs that we need to help our body heal itself.”

Learn More: New non-invasive form of vagus nerve stimulation works to treat depression

While focused on rheumatoid arthritis, the trial’s results may have implications for patients suffering from other inflammatory diseases, including Crohn’s, Parkinson’s, Alzheimer’s and others.

Study methodology and results

In the study, a stimulation device was implanted on the vagus nerve during a surgical procedure, then activated and deactivated based on a set schedule to measure response over 84 days, with primary endpoints measured at day 42 using DAS28-CRP, a standard disease activity composite score for RA that includes counts of tender and swollen joints, patient’s and physician’s assessment of disease activity and serum C-reactive protein (CRP) levels.

Of 17 patients with active RA in the study, several patients that had failed to respond to multiple therapies, including biologicals with different mechanisms of action, demonstrated robust responses. The findings indicate that active electrical stimulation of the vagus nerve inhibits TNF production in RA patients and significantly attenuates RA disease severity.

Don’t Miss: The neurons in our gut help the immune system keep inflammation in check

Several patients reported significant improvements, including some who had previously failed to respond to any other form of pharmaceutical treatment. In addition, no serious adverse side effects were reported.

The emerging field of bioelectronic medicine aims to target disorders traditionally treated with drugs and instead uses advanced neuromodulation devices that may offer significant advantages. SetPoint is developing a novel proprietary bioelectronic medicine platform to treat a variety of immune-mediated inflammatory diseases, using an implanted device to stimulate the vagus nerve.

Note: Material may have been edited for length and content. For further information, please contact the cited source.

Just had one of the best experiences of my life at the Louisville Zoo. He came right up to me and did the head butt on the glass, which means basically “Pet me”!!! I am madly in love. I’ll be visiting him often 🐅😄

Why is it that when we are physically ill, as in for example having the flu, we are allowed to rest and recuperate. However when the illness is mental, as for example a mixed episode of bipolar disorder, we are not allowed to rest. We must keep going as if we are not sick at all. If we are housewives, dinner must be on the table when the family gets home. If we don’t make dinner (just an example of work) then why didn’t we? People might say “You don’t look sick, why don’t you do your work?” I have been in a mixed phase, as I generally am in the Fall. I feel terrible, emotional, terribly anxious, weepy, nothing good. Can’t eat. Yet I’m not given much of a chance to rest. I don’t look sick.