Recovery Michigan

http://bit.ly/2JyJjqP

The Fragrance-Free Initiative from the University of Colorado Boulder’s Office of Information Technology (OIT) has created a video I really like,  and they have also put together some other resources that can be useful to learn from when creating fragrance-free policies.

The Fragrance-Free Initiative website also has a sidebar with these resources:

FAQ
Offenders/Alternatives
Resources 

It may well be that for the people working there, the Offenders/Alternatives   section works brilliantly, but do keep in mind that it would need revisions to accommodate other people with MCS, MCAS/D,  or fragrance allergies.

The way they’ve listed the Offenders on their site from least to most ‘offensive’  will not  accurately reflect  truth for everyone who experiences adverse effects from the products.  I hope they remove the  category designations, since for some people, what is  most disabling, can be in the site’s ‘least offensive’  category, and no fragrance remain at arm’s length (as was stated somewhere), especially when the people using them move or have a breeze pass them.

https://bbc.in/2Kbsqn7

Human cells make up only 43% of the body's total cell count. The rest are microscopic colonists.

Understanding this hidden half of ourselves - our microbiome - is rapidly transforming understanding of diseases from allergy to Parkinson's.

The field is even asking questions of what it means to be "human" and is leading to new innovative treatments as a result.

"They are essential to your health," says Prof Ruth Ley, the director of the department of microbiome science at the Max Planck Institute, "your body isn't just you".

No matter how well you wash, nearly every nook and cranny of your body is covered in microscopic creatures.

This includes bacteria, viruses, fungi and archaea (organisms originally misclassified as bacteria). The greatest concentration of this microscopic life is in the dark murky depths of our oxygen-deprived bowels.

The human genome - the full set of genetic instructions for a human being - is made up of 20,000 instructions called genes.

But add all the genes in our microbiome together and the figure comes out between two and 20 million microbial genes.

Prof Sarkis Mazmanian, a microbiologist from Caltech, argues: "We don't have just one genome, the genes of our microbiome present essentially a second genome which augment the activity of our own.

"What makes us human is, in my opinion, the combination of our own DNA, plus the DNA of our gut microbes."

https://bbc.in/2FeXoab

The game Hellblade: Senua's Sacrifice has won many awards and fans for its story and the way it depicts psychosis.

It follows Nordic warrior, Senua, on a quest to rescue the soul of her dead lover. She hears voices, and experiences hallucinations throughout, disorientating the player.

Gamers and experts rate its portrayal of the mental illness - but does it go down well with people who have psychosis in real life?

Danny Bowyer first experienced psychosis in his early 20s and has played the game. He explains how he hears voices continually - including while talking to the BBC Ouch team on this podcast.

http://bit.ly/2Kd5Tq3

A response to Benedict Carey and Robert Gebeloff’s New York Times article

In their article, Carey and Gebeloff point to the role of antidepressants as something that was supposed to be a temporary solution for a temporary problem. This rules out the idea that genetics come into play in determining mental illness. This also rules out the idea that things like stress and trauma don’t have long-term effects on a person’s ability to cope with life. Harvard Health claims that, “[m]any researchers believe that early trauma causes subtle changes in brain function that account for depression and anxiety.” What we’re learning about antidepressants, and depression itself, is that for many people, mental illness is not a temporary issue. Mental illness — depression, anxiety — is something that can come down to biology.

What the article suggests is that, like with opioids, patients on antidepressants can’t get off of them. If they try, they suffer through terrible withdrawal symptoms. For some people, this is true. Weaning off of Paxil wasn’t a pleasant experience. For those years that Paxil was working for me, however, the withdrawal experience was worth it. Not only did I not have to up my prescription dosage, but I also was able to find something that worked better for me at helping to manage my anxiety and depression. Can I live without my antidepressants? Sure. But what quality of life would I have? What quality of life would others have, who rely on antidepressants and other psychiatric medications to help balance their emotions?

To frame those on antidepressants as being addicts, unable to wean off of their drug of choice, furthers the stigma against those with mental illness and those who choose to take medication. In demonizing these people, we’re further alienating them. Beyond alienation, we’re ignoring the disgusting way society looks at those who need help. The idea that anyone can just roll out of bed and keep going, no matter what, stems from this American idea that anyone can pick themselves up by their bootstraps. But this doesn’t take into account genetics, biology, and life experience. This outlook offers no compassion to those who need it.

http://bit.ly/2KbTIJR

Meet CrowdSource Rescue, a passion project that grew into something much larger.

Matthew Marchetti was among thousands of Houstonians motoring through the turbulent, murky stormwaters of Hurricane Harvey as the sun set on August 27th, 2017. He was sitting in a stranger’s dinky motorboat, attempting to rescue neighbors and shuttle them to safety. The problem was that he didn’t know where to look — neither did the police and fire departments.

“It was a big ol’ mess,” Marchetti says. As he disembarked to high ground, he phoned his friend Nate Larson, and said, “You know, we should develop a little website. Just for our neighborhood.” His idea was to create an application where a family in distress could quickly submit a call for help containing their location and information, which would instantly appear on a map. A responder could pull the location in order to execute the rescue. Once the family was safe, the information would be taken down so rescuers could focus on those still in need.

This idea — the “little website” — would balloon into something much larger.

Marchetti and Larson built a web-based geolocation service that collected data from social media, centralizing and visualizing the calls for help. It became a clearinghouse for volunteers and their boats, who could then be dispatched to help with rescues. As they worked in their company’s office through the night to build the site, the hurricane’s gusts pounded the windows. Water seeped in from above. The power flickered. But they finished, put about 25 people into the system, and went to bed.

When they woke, their service had blown up: there were over 1,000 entries.

Marchetti says. “We’re going to be on the news tonight… ‘Open developer idiot develops a website that doesn’t rescue anybody.’” The site gained traction as it was shared across social media and through word of mouth. As the storm crested, the amount of rescues swelled. At any given time, there were 40,000 to 60,000 people on the website.

At least 25,000 people were rescued in Houston using the app, Marchetti says. High-density rescue locations — such as a nursing home, an apartment building, or a block with multiple potential rescuees — might have been undercounted. For this reason, the number of rescues could be even higher. “It’s kind of hard to pin that number down concretely, but we’re working with a lot of universities going through that data trying to figure it out,” Marchetti says.

The service — now known as CrowdSource Rescue (CSR) — was meant to fill the deficit of public services during a time of immense, dizzying catastrophe. CSR reduced the redundancy created by reposting and sharing across multiple platforms. It crowdsourced every part of the operation: posting, dispatching, rescuing, and updating. It allowed Houstonians and outside volunteer organizations such as the Cajun Navy to work hand in hand with public officials.

http://bit.ly/2qTrxGJ

Abstract Full article available through link

Current treatment options for depression are limited by efficacy, cost, availability, side effects, and acceptability to patients. Several studies have looked at the association between magnesium and depression, yet its role in symptom management is unclear. The objective of this trial was to test whether supplementation with over-the-counter magnesium chloride improves symptoms of depression. 

An open-label, blocked, randomized, cross-over trial was carried out in outpatient primary care clinics on 126 adults (mean age 52; 38% male) diagnosed with and currently experiencing mild-to-moderate symptoms with Patient Health Questionnaire-9 (PHQ-9) scores of 5–19. The intervention was 6 weeks of active treatment (248 mg of elemental magnesium per day) compared to 6 weeks of control (no treatment). Assessments of depression symptoms were completed at bi-weekly phone calls. 

The primary outcome was the net difference in the change in depression symptoms from baseline to the end of each treatment period. Secondary outcomes included changes in anxiety symptoms as well as adherence to the supplement regimen, appearance of adverse effects, and intention to use magnesium supplements in the future. 

Between June 2015 and May 2016, 112 participants provided analyzable data. Consumption of magnesium chloride for 6 weeks resulted in a clinically significant net improvement in PHQ-9 scores of -6.0 points (CI -7.9, -4.2; P<0.001) and net improvement in Generalized Anxiety Disorders-7 scores of -4.5 points (CI -6.6, -2.4; P<0.001). 

Average adherence was 83% by pill count. The supplements were well tolerated and 61% of participants reported they would use magnesium in the future. Similar effects were observed regardless of age, gender, baseline severity of depression, baseline magnesium level, or use of antidepressant treatments. Effects were observed within two weeks. Magnesium is effective for mild-to-moderate depression in adults. It works quickly and is well tolerated without the need for close monitoring for toxicity.

Duh...

http://bit.ly/2HAzOtR

http://bit.ly/2qQurNe

Manipulating the microbiota with supplemental Akkermansia muciniphila may offer hope for the global and hard-to-treat problem of alcoholic liver disease (ALD), a preliminary U.S.-European study in humans and mice suggested.

One modulator of ALD is the integrity of the intestinal barrier, and this integrity is supported by A. muciniphila, a Gram-negative intestinal commensal bacterium that enhances mucus production. In healthy people, this organism constitutes as much as 4% of fecal microbiota, according to Herbert Tilg, MD, of the Medical University in Innsbruck, Austria, and colleagues.

"We propose that depletion of A. muciniphilareflects an early event in the pathophysiology of ALD, probably by regulating gut barrier function. Recovery of ethanol-induced A. muciniphila depletion by oral supplementation could represent a novel treatment option for patients with ALD," they wrote in Gut.

ALD is the most common cause of liver-related deaths worldwide and is responsible for 5.9% of all global deaths. It encompasses simple steatosis, fibrosis, and cirrhosis, all of which can deteriorate toward acute alcoholic steatohepatitis (ASH) with its high mortality rates.

"Despite our increasing understanding of ALD pathogenesis, treatment strategies remain scarce," Tilg's group stated.

The degree of liver injury varies among individuals with ALD, and researchers increasingly believe that the microbiota plays a role in this variation. They are hopeful that appropriate probiotic supplementation may reduce hepatic injury.

http://bit.ly/2vtCeFu

Epstein-Barr Virus Affects Health in More Ways Than Known

A far-reaching study conducted by scientists at Cincinnati Children’s reports that the Epstein-Barr virus (EBV)—best known for causing mononucleosis—also increases the risks for some people of developing seven other major diseases.

Those diseases are: systemic lupus erythematosus (SLE), multiple sclerosis (MS), rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), inflammatory bowel disease (IBD), celiac disease, and type 1 diabetes. Combined, these seven diseases affect nearly 8 million people in the U.S.

Study results were published today in the journal Nature Genetics. The project was led by three scientists: John Harley, MD, PhD, Director of the Center for Autoimmune Genomics and Etiology (CAGE) at Cincinnati Children’s and a faculty member of the Cincinnati VA Medical Center;  Leah Kottyan, PhD, an immunobiology expert with CAGE; and Matthew Weirauch, PhD, a computational biologist with the center. Critical contributions were provided by Xiaoting Chen, PhD, and Mario Pujato, PhD, both also in CAGE.

The study shows that a protein produced by the Epstein-Barr virus, called EBNA2, binds to multiple locations along the human genome that are associated with these seven diseases.

Overall, the study sheds new light on how environmental factors, such as viral or bacterial infections, poor diet, pollution or other hazardous exposures, can interact with the human genetic blueprint and have disease-influencing consequences.

“Now, using genomic methods that were not available 10 years ago, it appears that components made by the virus interact with human DNA in the places where the genetic risk of disease is increased,” Harley says. “And not just for lupus, but all these other diseases, too.”

The full impact of this study could take years to explore. Here are some of the initial implications:

http://bit.ly/2qOQjbX//

Compared with rats given saline, those that received morphine endured postoperative pain for over 3 additional weeks. Also, the longer the morphine was provided, the longer the rats' pain lasted.

The study also revealed that tapering of morphine dosage makes no difference. As Grace explains, "This tells us that this is not a phenomenon related to opioid withdrawal, which we know can cause pain. Something else is going on here."

The next question to ask, of course, is what drives this counterintuitive effect. Prof. Watkins calls it the result of a "one-two hit" on glial cells.

In the brain, glial cells are more numerous than neurons. They protect and support nerve cells and, as part of their role as protector, they direct the brain's immune response, including inflammation.

The first "hit" occurs when surgery activates glial cells' toll-like receptor 4 (TLR4). Prof. Watkins calls these "not me, not right, not O.K." receptors; they help to orchestrate the inflammatory response. This first hit primes them for action when the second hit occurs.

The second hit is morphine, which also stimulates TLR4. As Prof. Watkins explains:

"With that second hit, the primed glial cells respond faster, stronger, and longer than before, creating a much more enduring state of inflammation and sometimes local tissue damage."

Although the study is in an animal model and will need replic