Recovery Michigan

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The enzyme is called cytosine monophosphate kinase 2 (CMPK2) and it activates NLRP3, an inflammation-triggering molecule, or inflammasome.

Scientists already knew that finding a way to block NLRP3 without affecting other inflammasomes could lead to new treatments for many inflammatory conditions.

"Dysregulated NLRP3 inflammasome activity results in uncontrolled inflammation, which underlies many chronic diseases," note the authors.

But without a clear understanding of the molecular pathways involved in triggering NLRP3, it was not possible to design drugs that specifically block it.

During the state of inflammation, there is a sharp rise in a hormone called interleukin 1 beta (IL-1B). The hormone is important for many cell events that occur during inflammation, including proliferation and death.

Inflammasomes control the production and release of IL-1B. NLRP3 is most active in this process. It senses diverse stimuli from noxious threats to tissue changes. These range from silica dust and asbestos to the microcrystals of uric acid that cause inflammation in gout.

In their study, Prof. Michael Karin — from the University of California, San Diego — and team focused on CMPK2 and the key role that the enzyme plays in triggering NLRP3 in sparking production of IL-1B and the subsequent development of chronic inflammatory conditions.

CMPK2 is a nucleotide kinase. Drug developers have already "successfully targeted" some of the enzymes in this group.

Prof. Karin suggests that CMPK2 blockers could reduce pain, inflammation, and tissue damage in osteoarthritis and gout, as well as slow the development of Parkinson's and Alzheimer's diseases.

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Physicians on the front lines of health care today are sometimes described as going into battle. It’s an apt metaphor. Physicians, like combat soldiers, often face a profound and unrecognized threat to their well-being: moral injury.

Moral injury is frequently mischaracterized. In combat veterans it is diagnosed as post-traumatic stress; among physicians, it’s portrayed as burnout. But without understanding the critical difference between burnout and moral injury, the wounds will never heal and physicians and patients alike will continue to suffer the consequences.

The term “moral injury” was first used to describe soldiers’ responses to their actions in war. It represents “perpetrating, failing to prevent, bearing witness to, or learning about acts that transgress deeply held moral beliefs and expectations.” Journalist Diane Silver describes it as “a deep soul wound that pierces a person’s identity, sense of morality, and relationship to society.”

The moral injury of health care is not the offense of killing another human in the context of war. It is being unable to provide high-quality care and healing in the context of health care.

Most physicians enter medicine following a calling rather than a career path. They go into the field with a desire to help people. Many approach it with almost religious zeal, enduring lost sleep, lost years of young adulthood, huge opportunity costs, family strain, financial instability, disregard for personal health, and a multitude of other challenges. Each hurdle offers a lesson in endurance in the service of one’s goal which, starting in the third year of medical school, is sharply focused on ensuring the best care for one’s patients. Failing to consistently meet patients’ needs has a profound impact on physician wellbeing — this is the crux of consequent moral injury.

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Monthly public policy newsletter from the Mental Health Association in Michigan (MHAM).

Court Prevents Kentucky Medicaid Work Requirement from Starting

A federal court has prevented Kentucky from starting its federally approved Medicaid work requirement waiver.

The court did not say a Medicaid work requirement is legal or illegal under Medicaid law. Rather, it said health care is an integral purpose of the Medicaid mission, and the federal Centers for Medicare & Medicaid Services (CMS) did not adequately assess what the impacts of Kentucky’s work requirements would be on beneficiaries’ health care.

Kentucky’s Governor immediately announced cuts to Medicaid services in the state, claiming they couldn’t be fully sustained in light of the court ruling. CMS then announced it was starting over with a new public comment period on the Kentucky proposal, signaling apparent intent to re-assess the impact of a Kentucky waiver on enrollees’ health care coverage. If this is followed through, CMS and the State of Kentucky would presumably submit a new analysis to the court. Would a “better” analysis allow the work requirements to start? That is unknown.

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Professor Jianfeng Feng and Professor Edmund Rolls from Warwick’s Department of Computer Science, with Dr. Wei Cheng from Fudan University, found functional connectivity between the areas of the brain associated with short-term memory, self, and negative emotions – causing sufferers to dwell on bad thoughts and leading to a poor quality of sleep.

This research could lead to better sleep quality for people with depression, and opens up the possibility of new targeted treatments.

Analysing data from around 10,000 people, the researchers examined the neural mechanisms underlying the relation between depression and quality of sleep.

In the brains of those living with depressive problems, they discovered a strong connection between the dorsolateral prefrontal cortex (associated with short-term memory), the precuneus (associated with the self) and the lateral orbitofrontal cortex (associated with negative emotion).

Depression and sleep problems often go hand-in-hand. About 75% of depressed patients report significant levels of sleep disturbance, such as difficulty of falling asleep and short duration of sleep (insomnia). People with insomnia also have a higher risk of developing depression and anxiety than those who sleep normally.

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Lexapro belongs to a class of drugs known as selective serotonin reuptake inhibitors (SSRIs). Serotonin is a chemical messenger or neurotransmitter that affects mood. SSRIs help to restore the natural balance of serotonin in the brain.

Doctors consider SSRIs to be one of the safest types of antidepressants. However, some people taking Lexapro may experience one or more of the following side effects:

• insomnia
• sexual problems, affecting ejaculation and sexual desire
• fatigue
• sleepiness
• dizziness
• increased sweating
• nausea
• constipation
• dry mouth
• trouble sleeping
• infections

In this article, we look at the risks of drinking alcohol while taking Lexapro or other antidepressants, including how alcohol may worsen their side effects.

Doctors usually do not recommend drinking alcohol while taking Lexapro or any other antidepressant. This guidance is because alcohol can make depression worse and can counteract the benefits of a person taking antidepressants.

People who drink alcohol while taking Lexapro may feel more depressed or anxious, and these symptoms may then become more challenging to treat.

This worsening scenario is potentially dangerous as it can lead to some people having an increase in suicidal thoughts.

Drinking alcohol may also worsen some of the side effects of Lexapro or other antidepressants, including drowsiness and dizziness. This is because alcohol can also cause these side effects.

Thanks and a hat tip to Maria S....

https://nyti.ms/2JU273l

The deodorants, perfumes and soaps that keep us smelling good are fouling the air with a harmful type of pollution — at levels as high as emissions from today’s cars and trucks.

That’s the surprising finding of a study published Thursday in the journal Science. Researchers found that petroleum-based chemicals used in perfumes, paints and other consumer products can, taken together, emit as much air pollution in the form of volatile organic compounds, or V.O.C.s, as motor vehicles do.

The V.O.C.s interact with other particles in the air to create the building blocks of smog, namely ozone, which can trigger asthma and permanently scar the lungs, and another type of pollution known as PM2.5, fine particles that are linked to heart attacks, strokes and lung cancer.

Smog is generally associated with cars, but since the 1970s regulators have pushed automakers to invest in technologies that have substantially reduced V.O.C. emissions from automobiles. So the rising share of air pollution caused by things like pesticides and hair products is partly an effect of cars getting cleaner. But that breathing room has helped scientists see the invisible pollutants that arise from a spray of deodorant or a dollop of body lotion.

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Researchers in Germany have found further evidence to support the idea that Parkinson's could be an autoimmune disease.

Autoimmune diseases arise because the immune system attacks healthy organs, tissues, and cells instead of protecting them.

There are at least 80 different known types of autoimmune disease, including rheumatoid arthritis, multiple sclerosis, lupus, and type 1 diabetes.

Although the idea that Parkinson's could be an autoimmune disease is not new, the biological evidence to back it up is only just emerging.

In 2017, for instance, a study from the U.S. revealed how pieces of a protein that builds up in the dopamine cells of people with Parkinson's can trigger a deadly immune attack against the cells.

More recently, scientists have linked the use of drugs that subdue the immune system to a lower risk of developing Parkinson's disease.

In the new study, researchers from Friedrich-Alexander-Universität (FAU) in Erlangen-Nürnberg, Germany, have shown that T helper 17 (Th17) cells — a type of immune T cell — attack dopamine cells derived from people with Parkinson's disease but not those derived from people without it.

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A new study published in Biological Psychiatry finds that the reduced cortical thickness and brain surface area are correlated with a schizophrenia diagnosis but that these differences may be explained by the widespread use of antipsychotic medications.

The researchers report that “effect sizes were two to three times larger in individuals receiving antipsychotic medication relative to unmedicated individuals.”

In fact, the researchers found that participants with a schizophrenia diagnosis, who were unmedicated, were not significantly different from healthy control subjects regarding cortical thickness.

The researchers found that individuals with a schizophrenia diagnosis had thinner cortices than control subjects in specific areas, and thicker cortices than controls in other areas. However, when participants were grouped based on their medication use, the researchers discovered that unmedicated participants with schizophrenia showed no statistically significant differences from healthy control subjects.

The effect size for reduced cortical thickness was twice as large for participants taking second-generation antipsychotics. For those taking first-generation antipsychotics, the effect size was three times larger when compared to unmedicated participants.

In these analyses, researchers controlled for possible confounding variables, such as age at schizophrenia diagnosis, duration of symptoms, the severity of symptoms, current age, and gender. However, even after controlling for severity of symptoms, people diagnosed with schizophrenia taking antipsychotics had significantly reduced cortical thickness, while those who went unmedicated were not significantly different from healthy control subjects.

The researchers did find that the brain surface area was lower on average for participants diagnosed with schizophrenia than for control participants and that this finding was not explained by medication use. However, they also note that this finding involved a much smaller effect size than their other results—indicating that there was significant overlap in surface area between the groups.

The researchers write that future studies on brain differences should take care to include medication use as a potential confounding factor. They suggest that this could be a contributing factor to why even after several hundred studies of cortical thickness and surface area in schizophrenia, no consensus has yet emerged.

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A group of Japanese researchers has discovered that neural inflammation caused by our innate immune system plays an unexpectedly important role in stress-induced depression. This insight could potentially lead to the development of new antidepressants targeting innate immune molecules. The findings were published in the online edition of Neuron.

The research team then developed a method to selectively block the expression of TLR2/4 in the microglia of specific areas of the brain. By blocking the expression of TLR2/4 in the microglia of the medial prefrontal cortex, they managed to suppress depressive behavior in response to repeated social defeat stress. They found that repeated stress induced the expression of inflammation-related cytokines IL-1α and TNFα in the microglia of the medial prefrontal cortex via TLR2/4. The depressive behavior was suppressed by treating the medial prefrontal cortex with neutralizing antibodies for the inflammation-related cytokines.

These results show that repeated social defeat stress activates microglia in the medial prefrontal cortex via the innate immune receptors TLR2/4. This triggers the expression of inflammation-related cytokines IL-1α and TNFα, leading to the atrophy and impaired response of neurons in the medial prefrontal cortex, and causing depressive behavior.

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Until recently, medical professionals believed that only a minority of patients could recover from schizophrenia. But now, new Norwegian research suggests that more than half of the study participants are doing well.

After four years of treatment, 55 per cent of the young people were partially or fully recovered, and fully ten per cent of those who are fully recovered no longer use medication.

"Having such a high proportion be well-functioning shows that schizophrenic patients have a greater potential to get well than previous research has shown," says Professor Anne-Kari Torgalsbøen at the University of Oslo’s Department of Psychology.

She believes too much pessimism has been associated with this diagnosis.

"The results of this study give hope not only to patients and their relatives, but also provide inspiration for everyone who treats young people with psychotic disorders," she says.