A personal peer-support worker also improved satisfaction with mental health care.
Peer-supported self-management can help reduce readmission rates in individuals experiencing a mental health crisis, researchers reported.
Interestingly, there were also more adverse events reported among the control group, including two suicides.
"If the finding that repeat periods of acute care were reduced by around a quarter is replicated in routine settings, the burden on the acute care system could be reduced substantially, and service users would have greater opportunities for sustained recovery," the researchers explained. "This trial adds promising evidence for self-management interventions for people with significant mental health problems."
The analysis included 218 individuals randomly assigned to the peer-support intervention group compared with 220 in the control group. All participants were from six crisis resolution teams around England, who were recruited following a discharge by the crisis resolution team. Individuals were excluded if they were considered to be a high risk to others and unsafe for the peer-support workers.
The peer-support intervention included 10 sessions of 1 hour each led by a peer-support worker once a week. All had personal experience utilizing mental health services themselves, and could, therefore, relate to the individuals in the group. The aim was to assist the individual in completing a personal recovery workbook and provide encouragement and coping strategies. The workbook included information on "setting personal recovery goals, making plans to re-establish community functioning and support networks after a crisis, using the recent crisis experience to identify early warning signs and formulate an action plan to avoid or attenuate relapse, and planning strategies to maintain well-being once a crisis had abated," the researchers explained.
The bacteria that live in our gut are as numerous as the cells in our body. As medical research progresses, the influence that these billions of tiny creatures have on our health is becoming ever more apparent.
It comes as no surprise that they might play a role in gastrointestinal issues, but the microbiome's influence flies much further afield.
Most recently, it has become apparent that there is a significant relationship between gut bacteria and mental health issues, such as depression and anxiety.
A recent piece of research, published in The Journal of Physiology, takes a fresh look at how gut bacteria are involved in gut health problems induced by stress. The work was carried out at APC Microbiome Ireland at University College Cork and Teagasc Food Research Centre in Ireland.
The team of scientists was interested in short-chain fatty acids (SCFAs). Gut bacteria produce SCFAs when they digest fiber; the cells of the colon then use SCFAs as their primary source of energy, making them vital for good gut health.
The researchers found that when they introduced SCFAs to the guts of mice, stress and anxiety-based behaviors were significantly reduced.
After demonstrating that SCFAs reduce anxiety, they wanted to understand how these small molecules influenced physical, stress-related gut damage.
Known as a "leaky" gut, high levels of stress over time increase the intestine's permeability. This means that particles, such as bacteria and undigested food, can move more easily into the bloodstream, which can cause damaging chronic inflammation.
The researchers found that by introducing SCFAs, they reduced the gut leakiness caused by persistent stress.
"There is a growing recognition of the role of gut bacteria and the chemicals they make in the regulation of physiology and behavior. The role of short-chain fatty acids in this process is poorly understood up until now."
Fruits, vegetables, and grains naturally contain high levels of fiber. Although this study was conducted on mice, the inference is that a high-fiber diet might prompt gut bacteria to produce more SCFAs — thereby bolstering our gut's natural defenses against the damage caused by stress.
For more than a year, we have been investigating drug and alcohol rehab programs that offer a tantalizing promise: freedom from addiction for free.
In exchange for treatment, people with addiction are required to work full-time jobs and turn over their paychecks to the rehab center. But we found that some of these programs are little more than work camps for private industry.
Now we need your help to keep the investigation going.
At each rehab we dug into, we found unique problems: Former chicken executives who created a rehab to provide chicken plants with labor. A judge who had participants do his yard work. Fortune 500 companies and powerful politicians reaping the benefits of the cheap labor. Participants put to work as caregivers in an assisted living facility, dispensing the very drugs that landed them in rehab.
We have amassed a list of tips about other rehabs that merit more scrutiny. But it would take years for us to do a deep dive on each of them.
So we’re opening up our database of tips to reporters and editors who want to investigate these work-based rehabs in their own communities. And we’ve put together a reporting guide with our pointers on how to investigate programs in your area.
Do you have experience with a work-based rehab? Share your story.
A U.K. panel found humanitarian groups more concerned about their reputations than stopping their own predators from exploiting the world’s most vulnerable women and children.
The sexual abuse of women and girls by international aid workers and peacekeepers has been “endemic” across the sector for years, targeting both staffers and locals, as perpetrators jump virtually undetected among humanitarian NGOs, according to a report by the U.K.’s House of Commons International Development Committee.
The inquiry was ordered in February after serious allegations of sexual misconduct were reported at Oxfam and other NGOs this year. A report came to light in February that Oxfam staff had paid for prostitutes during its Haiti earthquake-relief mission in 2010. The Red Cross announced that same month that at least 21 staff members were dismissed or resigned after “paying for sexual services” in the past three years.
“The exact scale [of the abuse] is currently impossible to define” due to “confirmed under-reporting,” according to the inquiry, which was published on Tuesday.
But atrocious stories are plentiful. In one example from Haiti in 2007: “There is a girl who sleeps in the street...They took her to a man who works for an NGO. He gave her one American dollar and the little girl was happy to see the money. It was 2 in the morning. The man took her and raped her. In the morning, the little girl could not walk.”
These stories are likely “the tip of the iceberg,” the inquiry claims.
“It is particularly horrifying to find evidence of personnel from the aid and security sectors perpetrating these abuses rather than combating them,” the report states. “There seems to be a strong tendency for victims and whistleblowers, rather than perpetrators, to end up feeling penalized.”
Stephen Twigg, a member of parliament and chairman of the committee, told CNN the report laid out “the collective failure over a period of at least 16 years by the aid sector to address sexual exploitation and abuse.”
These are five stories around different kinds of addiction that are illustrated like comic books.
]]>People with depression have low blood levels of a substance called acetyl-L-carnitine, according to a Stanford University School of Medicine scientist and her collaborators in a multicenter study.
Naturally produced in the body, acetyl-L-carnitine is also widely available in drugstores, supermarkets and health food catalogs as a nutritional supplement. People with severe or treatment-resistant depression, or whose bouts of depression began earlier in life, have particularly low blood levels of the substance.
The findings, published online July 30 in the Proceedings of the National Academy of Sciences, build on extensive animal research. They mark the first rigorous indication that the link between acetyl-L-carnitine levels and depression may apply to people, too. And they point the way to a new class of antidepressants that could be freer of side effects and faster-acting than those in use today, and that may help patients for whom existing treatments don’t work or have stopped working.
In those studies, the animals responded to acetyl-L-carnitine supplementation within a few days. Current antidepressants, in contrast, typically take two to four weeks to kick in — in animal experiments as well as among patients.
Nasca’s animal studies suggest that acetyl-L-carnitine, a crucial mediator of fat metabolism and energy production throughout the body, plays a special role in the brain, where it works at least in part by preventing the excessive firing of excitatory nerve cells in brain regions called the hippocampus and frontal cortex.
The new study, also initiated by Nasca, recruited 20- to 70-year-old men and women who had been diagnosed with depression and, amid episodes of acute depression, had been admitted to either Weill Cornell Medicine or Mount Sinai School of Medicine, both in New York City, for treatment. These participants were screened via a detailed questionnaire and assessed clinically, and their blood samples and medical histories were taken. Twenty-eight of them were judged to have moderate depression, and 43 had severe depression.
In comparing their blood samples with those of 45 demographically matched healthy people, the depressed patients’ acetyl-L-carnitine blood levels were found to be substantially lower. These findings held true for both men and women, regardless of age.
Was it hard to concentrate during that long meeting? Does the crossword seem a little tougher? You could be mildly dehydrated.
A growing body of evidence finds that being just a little dehydrated is tied to a range of subtle effects — from mood changes to muddled thinking.
"We find that when people are mildly dehydrated they really don't do as well on tasks that require complex processing or on tasks that require a lot of their attention," says Mindy Millard-Stafford, director of the Exercise Physiology Laboratory at Georgia Institute of Technology. She published an analysis of the evidence this month, based on 33 studies.
How long does it take to become mildly dehydrated in the summer heat? Not long at all, studies show, especially when you exercise outdoors.
"If I were hiking at moderate intensity for one hour, I could reach about 1.5 percent to 2 percent dehydration," says Doug Casa, a professor of kinesiology at the University of Connecticut, and CEO of the Korey Stringer Institute.
For an average-size person, 2 percent dehydration equates to sweating out about a liter of water.
"Most people don't realize how high their sweat rate is in the heat," Casa says. If you're going hard during a run, you can reach that level of dehydration in about 30 minutes.
And at this level of dehydration, the feeling of thirst, for many of us, is only just beginning to kick in. "Most people can't perceive that they're 1.5 percent dehydrated," Casa says.
I write this as both a (former) mental health professional and a consumer. I am a survivor of childhood trauma, who has lived with PTSD (or what I like to call: the-normal-human-reaction-to-being-in-a-really-effed-situation) for many years.
A word about PTSD: post-traumatic stress (disorder) is a normal reaction.
Here are my 6 (kind and humble) suggestions to help you through those moments.
1. Noticing
As I mentioned, if you haven’t yet taken an inventory of your triggers, this is a good place to start. It’s also super hard, so please do this with a therapist, group or friend. Do it in a way that feels safe, and only do a little at a time.
If you are starting to feel unsafe, or are getting physical and mental cues from yourself that you are unsafe (but the stuff around you seems pretty normal), it is time to tune in.
Simply notice.
From my point of view this is THE HARDEST part. I need to know that I’m having a reaction in order to do something about that reaction, but a lot of the time my brain and body trick me in those moments and it can be super hard to know that my anxiety is escalating and I’m feeling triggered.
And more through the link...http://bit.ly/2M4wQwC
]]>When you’re on military exercise, sleep is a luxury. Maybe you can only snatch a few hours each day. So there’s nothing so frustrating as lying in your sleeping bag with your eyes closed, waiting for something to happen.
You’re totally exhausted. You have to be up in three hours for picket. You’re distracted by the noises around you. There’s a rock jutting into your hip bone. Or you’re replaying the day’s events on repeat in your head.
If you don’t sleep, you’ll burn out pretty quickly. You’ll make bad decisions. You’ll let people down and become a liability.
The U.S. Navy Pre-Flight School developed a scientific method to fall asleep day or night, in any conditions, in under two minutes. After six weeks of practice, 96 percent of pilots could fall asleep in two minutes or less. Even after drinking coffee, with machine gunfire being played in the background.
Which means if you follow these steps, falling asleep will be a piece of cake.
The message is, don't bang your head....
More than 8 years of play linked to Lewy bodies, parkinsonism.
People who played football, ice hockey, boxing, or other contact sports for more than 8 years were over six times more likely to develop neocortical Lewy body disease -- and in turn, symptoms of Parkinson's disease and dementia -- than people who played for 8 years or less, reported Thor Stein, MD, PhD, of the Boston University School of Medicine and colleagues in Journal of Neuropathology and Experimental Neurology.
"Other studies have shown that a single traumatic brain injury is associated with an increased risk of developing Parkinson's symptoms and Lewy body disease in the brain at pathology," said Stein. "Our study looks at this in the context of contact sports play, looking at many years of repetitive concussive and sub-concussive hits."
While Lewy bodies can affect a number of different brain areas, "we were specifically interested in looking at the cortex because we think that's where a lot of the injury occurs," he told MedPage Today.
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.
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.
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.
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.
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:
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....
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.
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.
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.
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.
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.
I’m Finally Finding Coping Mechanisms that Work for Me.
Right now, my body and mind are overcome with depression, anxiety, complex PTSD, and severe physical pain. I’m in crisis mode and having difficulty handling life in general. I’ve been crying more often than usual for a long time.
I don’t like to cry in public, but I had times I couldn’t control it. I’m not talking about being at a funeral where it’s acceptable to cry. I’m talking about being upset about something that usually has nothing to do with my current situation. However, if someone is rude to me, being more sensitive than most, my eyes will fill with tears and I can feel my face turn red.
It comes on suddenly and can be as easy as sitting in the waiting room for my doctor appointment and overhearing a conversation that triggers memories and emotions in me. My thoughts instantly travel back to a point in my life where I felt ashamed or scared.
I do my best to shake it off, but once the thought is in there, it continues to dig at me. As my mind relives those traumatic moments, my stomach hurts, I feel dizzy, and my breathing becomes unsteady. Soon, my heart starts racing and I feel a panic attack coming on. I can’t let this happen, especially if I’m alone. It’s so damn humiliating!
I struggle to bring my thoughts back to the present and do my best to distract myself any way possible. If the magazines are interesting, I’ll immerse my attention in an article on how best to clean your toilet, get out stubborn laundry stains, cook chicken, or anything else that will keep my mind occupied.
I’ve tried bringing my own book, but for some unknown reason, I need complete quiet to read anything of true interest, like a novel or a self-help book. I end up reading the same paragraph over several times and still cannot remember what I just read. However, reading mundane topics like cleaning, cooking, and laundry seem to hold my attention.
I’ve had to learn to tune out the radio if the office, or any place else I visit that has one playing, as some songs can trigger emotionally and physically painful situations from my past. When I’m driving, I play my own CD’s. When I was working, everyone had his or her own music playing, which can be distracting and annoying working in close quarters. I brought in a CD player and discs of nature sounds like birds chirping in the woods and waves crashing on beach sand, my favorite.
We’ve rescued a large number of dogs over the past twenty years. Sometimes I try to list them in my head the order in which we rescued them. Sometimes I get to a name and stop because I recall something special or funny about that particular dog. This can leave me in distraction mode for a few minutes, especially if I start thinking about another dog, which is good. The longer my mind remains distracted, the better chance I have of calming myself down and forgoing the panic attack.
Have you ever woken up with an unpleasant dream?
Is it King Jack Skellington from The Nightmare Before Chrismas that’s doing his boring scare and scream routine again?
Did you know there are biological and spiritual explanations for it?
I had a chronic nightmare that went on consecutively in a period of 6 months and my community supported me to heal it in 2 weeks.
Read on and I’ll share the following throughout the article…
What nightmare is
Distinguish nightmares and night terrors
Spiritual and psychoanalytical explanations for nightmares
Biological explanations for nightmares
Sleep study to rule out some of the causes
Cause of my nightmares and what made a difference in healing it
Nightmares are defined as unpleasant dreams that generally occur during rapid eye movement (REM) and lead to awakening with fear, anxiety or other mentally disturbing experiences. [1]
When I looked into the research, it looks like I’m not the only one having nightmares. In fact, around 40% of people experience one nightmare per month. [2]
Most Americans have a general sense that drunken driving isn’t as bad a problem as it was a generation ago. But few realize how much those numbers changed in a relatively short time. When the federal government started counting alcohol-impaired traffic deaths in 1982, there were more than 21,000 a year. By 2011, the death toll was down by 53 percent. States had raised the legal drinking age to 21 and adopted a common rule that a blood alcohol concentration (BAC) of .08 meant “too drunk to drive.” Many states also mandated the installation of interlock devices to prevent those with a history of drunken driving from turning on their ignition unless they were sober. Those laws, coupled with education and prevention campaigns, helped reduce drunk driving deaths to fewer than 10,000 in 2011.
But recently the trend has stalled. The total number of alcohol-impaired traffic fatalities actually rose in both 2015 and 2016. “Drunk driving has been around since the automobile was invented and it’s still the biggest killer on the highway,” says J.T. Griffin, the chief government affairs officer for Mothers Against Drunk Driving (MADD). Indeed, alcohol causes more traffic deaths per year than either speeding or driving without a seatbelt.
10,497: The number of fatal alcohol-impaired driving crashes in 2016, the highest since 2009
The national conversation around addiction has been dominated in recent years by opioids. Certainly, the rapid rise in opioid overdoses, which claimed 42,000 lives in 2016 alone, is a pressing issue for states across the country. The White House has declared a national public health emergency over the epidemic, and governments everywhere are marshalling efforts to combat the crisis.
But the fact is that alcohol kills roughly 88,000 Americans each year, more than double the number of opioid deaths. Almost half of alcohol fatalities come from chronic health problems attributed to excessive alcohol consumption, such as liver cirrhosis, breast cancer and heart disease. Those alcohol-induced deaths are on the rise. Excluding certain acute causes, such as homicides and traffic fatalities, the rate of alcohol-induced deaths increased by about 47 percent between 1999 and 2015.
Deaths from liver disease have increased sharply in recent years in the United States, according to a study published in the British Medical Journal. Cirrhosis-related deaths increased by 65 percent from 1999 to 2016, and deaths from liver cancer doubled, the study said. The rise in death rates was driven predominantly by alcohol-induced disease, the report said.
Over the past decade, people ages 25 to 34 had the highest increase in cirrhosis deaths — an average of 10.5 percent per year — of the demographic groups examined, researchers reported.
The study suggests that a new generation of Americans is being afflicted "by alcohol misuse and its complications,” said lead author Elliot Tapper, a liver specialist at the University of Michigan.
Tapper said people are at risk of life-threatening cirrhosis if they drink several drinks a night or have multiple nights of binge drinking — more than four or five drinks per sitting — per week. Women tend to be less tolerant of alcohol and their livers more sensitive to damage.
An analysis of more than 1,000 people with and without psychiatric disorders has shown that nitrates–chemicals used to cure meats such as beef jerky, salami, hot dogs and other processed meat snacks–may contribute to mania, an abnormal mood state. Mania is characterized by hyperactivity, euphoria and insomnia.
The findings of the Johns Hopkins Medicine study, which was not designed to determine cause and effect, were published July 18 in Molecular Psychiatry. Specifically, it found that people hospitalized for an episode of mania had more than three times the odds of having ever eaten nitrate-cured meats than people without a history of a serious psychiatric disorder.
Experiments in rats by the same researchers showed mania-like hyperactivity after just a few weeks on diets with added nitrates.
While a number of genetic and other risk factors have been linked to the manic episodes that characterize bipolar disorder and may occur in other psychiatric conditions, those factors have been unable to explain the cause of these mental illnesses, and researchers are increasingly looking for environmental factors, such as diet, that may play a role.
Many famous studies of human behavior cannot be reproduced. Even so, they revealed aspects of our inner lives that feel true.
In recent months, researchers and some journalists have strung cables around the necks of at least three monuments of the modern psychological canon:
The famous Stanford Prison Experiment, which found that people playacting as guards quickly exhibited uncharacteristic cruelty.
The landmark marshmallow test, which found that young children who could delay gratification showed greater educational achievement years later than those who could not.
And the lesser known but influential concept of ego depletion — the idea that willpower is like a muscle that can be built up but also tires.
The assaults on these studies aren’t all new. Each is a story in its own right, involving debates over methodology and statistical bias that have surfaced before in some form.
But since 2011, the psychology field has been giving itself an intensive background check, redoing more than 100 well-known studies. Often the original results cannot be reproduced, and the entire contentious process has been colored, inevitably, by generational change and charges of patriarchy.
“This is a phase of cleaning house and we’re finding that many things aren’t as robust as we thought,” said Brian Nosek, a professor of psychology at the University of Virginia, who has led the replication drive. “This is a reformation moment — to say let’s self-correct, and build on knowledge that we know is solid.”
When Nicole Lee's husband was removed from her home after she disclosed a decade of abuse to hospital staff following a suicide attempt, it took her eight weeks to get a shower.
"I had a 10-year, very violent relationship with my ex-husband who was also my disability carer," Ms Lee said.
"That day when the police decided to put an intervention order on him and remove him from the house, I was sent home on my own without anyone considering how I was going to cope."
When Nicole Lee's husband was removed from her home after she disclosed a decade of abuse to hospital staff following a suicide attempt, it took her eight weeks to get a shower.
"I had a 10-year, very violent relationship with my ex-husband who was also my disability carer," Ms Lee said.
"That day when the police decided to put an intervention order on him and remove him from the house, I was sent home on my own without anyone considering how I was going to cope."I
Almost two months later and feeling lost with who to turn to for support, Ms Lee said she approached child protection services to help lift the intervention order, inviting her husband to re-enter her home.
I suspect some of you will recognize this kind of struggle......
Drawing on seven years of his own research and the work of other esteemed Lincoln scholars, Shenk reveals how the sixteenth president harnessed his depression to fuel his astonishing success.Shenk relates Lincoln’s symptoms, including mood swings and at least two major breakdowns, and offers compelling evidence of the evolution of his disease, from “major depression” in his twenties and thirties to “chronic depression” later on. Shenk reveals the treatments Lincoln endured and his efforts to come to terms with his melancholy, including a poem he published on suicide and his unpublished writings on the value of personal—and national—suffering. By consciously shifting his goal away from personal contentment (which he realized he could not attain) and toward universal justice, Lincoln gained the strength and insight that he, and America, required to transcend profound darkness.
If you have any of the herpes infections, get it treated!!!
What amyloid beta normally does in the brain isn’t clear. Robert Moir, a neurologist at the MassGeneral Institute for Neurodegenerative Disease, says that many researchers have cast it as a villainous molecule with no beneficial function. “It’s just bad, bad, bad,” he says. “But it has become increasingly obvious that this isn’t true.” Moir thinks that amyloid beta has a more heroic role, as a foot soldier of our immune system. It protects neurons from infectious microbes—and from herpes viruses, in particular.
Amyloid beta protects against these viruses by latching onto them in large numbers, imprisoning them in self-assembling cages. That’s typically a good thing, but Moir argues that if the process goes on for too long, it builds up to the problematic plaques of Alzheimer’s. According to him, amyloid beta is still at the heart of the Alzheimer’s story, but it isn’t the villain. “In our model, Alzheimer’s is caused by amyloid beta’s reaction to something else, and most likely some kind of infection” like herpes, he says.
Hints that they can already exist. One study published earlier this year tracked the health of about 78,000 Taiwanese people, half of whom had been diagnosed with shingles within a 16-year period. Shingles is caused by a herpes virus called VZV, which also causes chicken pox in children. Among adults, the study found that people with a recent shingles flare-up had an 11 percent higher risk of developing dementia than healthier peers. And strikingly, those who were treated with anti-herpes drugs had a 45 percent lower risk of developing dementia than their untreated peers.
A second Taiwanese study looked at more than 8,000 people who had been recently diagnosed with HSV–1. Over the next decade, those people were 2.5 times more likely to develop dementia than uninfected peers. But again, that risk fell by 80 percent among those who had been treated with anti-herpes drugs. “That’s perhaps the strongest epidemiological data to emerge so far,” Moir says.
Prison employees experience PTSD on par with Iraq and Afghanistan war veterans, a new study from a Washington State University College of Nursing researcher found.
Working conditions in a prison can include regular exposure to violence and trauma, and threats of harm to the workers and their families. Previous studies have shown that prison workers have some of the highest rates of mental illness, sleep disorders and physical health issues of all U.S. workers. But the rate of PTSD among prison workers isn't well understood.
The new study, "Prison employment and post-traumatic stress disorder: Risk and protective factors," was conducted by lead investigator Lois James, Ph.D., assistant professor at the WSU College of Nursing, and co-investigator Natalie Todak, assistant professor at the University of Alabama at Birmingham.
It recently was published in the American Journal of Industrial Medicine and excerpted in Force Science News.
"Prison employees can face some of the toughest working conditions of U.S. workers," said James, "yet limited evidence exists on the specific risk and protective factors to inform targeted interventions."