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Cannabis link to relieving intestinal inflammation explained -- ScienceDaily

The researchers discovered that gut inflammation is regulated by two important processes, which are constantly in flux and responding to changing conditions in the intestinal environment. The first process, identified in previous scientific research, promotes an aggressive immune response in the gut that destroys dangerous pathogens, but which can also damage the lining of the intestine when immune cells attack indiscriminately. The second pathway, first described in this paper, turns off the inflammation response via special molecules transported across the epithelial cells lining the gut by the same process already known to remove toxins from these cells into the intestine cavity. Crucially, this response requires a naturally-produced molecule called an endocannabinoid, which is very similar to cannabinoid molecules found in cannabis. If the endocannabinoid isn't present, inflammation isn't kept in balance and it can run unchecked, as the body's immune cells attack the intestinal lining.

Reward and unease are closely linked in the brain -- ScienceDaily

One of the key components of the reward system is the signal substance dopamine, which acts as a chemical messenger between nerve cells. Dopamine stimulates motivation and causes animals and humans to exert themselves to achieve anything that is experienced as rewarding. When the researchers examined the dopamine-based signalling in the brain, they saw that the dopamine level in normal mice fell in the reward centre of the brain when the animals experienced something unpleasant. In contrast, it increased slightly in the mice that lacked melanocortin 4 receptors. "It seems that this receptor in some way prevents danger signals from activating the reward system. If the receptor is missing, the danger signals will gain access to the reward system and activate it. This means that mice that lack the receptor will seek out things that are associated with danger or discomfort," says David Engblom.

Video: The Underlying Mechanisms of Depression

While it’s likely that there may be more going on with depression than just inflammation by itself, it could be an incredibly useful lens through which to look at promising avenues to potentially treat or prevent it, since controlling systemic inflammation shows promise as being both important for longevity and health in general. Moreover, inflammation can be clinically monitored by well-known biomarkers for systemic inflammation, making it amenable to potentially tracking therapeutic success: the risk of major depression has been shown to increase by 44% for each standard deviation increase in log c-reactive protein.

The immune system and the pathogenesis of depression

During chronic infections and other chronic medical conditions associated with intense immune activation, the sickness behaviour syndrome can develop into a depressive episode. Studies have found that certain cancer and hepatitis c therapies, which often involve the use of cytokines, have been associated with the development of flu-like depressive symptoms. The causal role of the cytokines has been established by the fact that the depressive symptoms appear almost immediately after cytokine administration and disappear shortly after cytokine treatment is terminated.

Link between autoimmune disorders and psychosis confirmed in new study

But rheumatoid arthritis and ankylosing spondylitis are also characterised by higher levels of inflammation, so this would not explain the negative relationships we found with these disorders. Although all autoimmune disorders activate the body’s immune system, the exact response differs depending on the disorder. This might go some way to explaining why we found different relationships for individual autoimmune disorders, and suggests that inflammation cannot be the only mechanism.

When muscles weaken with age -- ScienceDaily

Working with our colleagues from the University of Aachen, we first systematically surveyed the changes taking place in the peripheral nerves of people aged between 65 and 79," Rudolf Martini describes his team's approach. During this, the researchers encountered an increased number of macrophages in the samples. Macrophages are cells of our body's immune system that engulf, digest and dispose microbes, foreign substances, cellular debris, aging cells etc. They set inflammatory responses in motion, help heal wounds and cleanse the tissue. Unfortunately, however, they also cause damage in some diseases. To find out whether this also applies to age-related nerve degeneration, the scientists performed an experiment on mice. "For this purpose, we looked more closely at the nerves of 24-month-old mice which is an advanced age for mice," Rudolf Martini explains. It turned out that the age-related changes in the mice's peripheral nerves are very similar to those in humans. As in their human counterparts, the number of macrophages was increased in the mice. Also, the older animals had less strength than their younger siblings and their motor endplates, the synapses connecting nerves and muscle fibres, were also less intact.

Exercise makes the blood of obese people healthier -- ScienceDaily

The exercise program consisted of three bicycling or treadmill running sessions per week with each session lasting approximately one hour. Blood was collected before and after the exercise training intervention to quantify blood-forming stem cells. The results of the study demonstrated that exercise reduced the number of blood-forming stem cells associated with the production of the type of blood cells responsible for inflammation.

Early source of irritable bowel syndrome discovered -- ScienceDaily

"The gut has its own brain and that has more neurons in the intestines than in the spinal cord. Within your intestines lies a 'second brain' called the enteric nervous system," said Brian Gulbransen, MSU neuroscientist and the study's senior author. "The enteric nervous system is an exceedingly complex network of neural circuits that programs a diverse array of gut patterns and is responsible for controlling most gastrointestinal functions." Accompanying the neurons in this second brain are enteric glia, which are responsible for regulating inflammation. The disruption of neural circuits in the gut by inflammation is considered an important factor in the development of irritable bowel syndrome and inflammatory bowel disease.

Probiotic Shot May Alleviate Brain Stress | GEN

“Given the evidence for reduced immunoregulation and chronic low-grade inflammation in anxiety and trauma-related disorders, microbial interventions that increase Treg, promote immunoregulation, and increase anti-inflammatory signaling may have value in the prevention or treatment of these disorders,” the authors suggest. M. vaccae has previously been shown to increase induction of Treg production and anti-inflammatory cytokines. A previous study by CU Boulder scientists showed that mice given injections of a heat-killed M. vaccae preparation and then placed in housing with an aggressive male exhibited less anxiety-like behavior and were less likely to suffer colitis or peripheral inflammation than control animals. These findings suggest that immunoregulatory and anti-inflammatory treatments can “buffer against the proinflammatory effects of stress,” the researchers point out.  What hasn’t been studied before is whether M. vaccae has a direct impact on stress-induced neuroinflammation.

Boosting the effects of vitamin D to tackle diabetes -- ScienceDaily

The underlying process has to do with transcription -- the way that genes are translated into proteins. Combining the new compound with vitamin D allowed certain protective genes to be expressed at much higher levels than they are in diseased cells. "Activating the vitamin D receptor can trigger the anti-inflammatory function of genes to help cells survive under stressed conditions," says Michael Downes, a Salk senior staff scientist and co-corresponding author. "By using a screening system that we developed in the lab, we've been able to identify an important piece of that puzzle that allows for super-activation of the Vitamin D pathway."

Drinking baking soda could be an inexpensive, safe way to combat autoimmune disease: A daily dose of baking soda may help reduce the destructive inflammation of autoimmune diseases like rheumatoid arthritis, scientists say. -- ScienceDaily

Drinking baking soda, the MCG scientists think, tells the spleen -- which is part of the immune system, acts like a big blood filter and is where some white blood cells, like macrophages, are stored -- to go easy on the immune response. "Certainly drinking bicarbonate affects the spleen and we think it's through the mesothelial cells," O'Connor says. The conversation, which occurs with the help of the chemical messenger acetylcholine, appears to promote a landscape that shifts against inflammation, they report.

Dark chocolate consumption reduces stress and inflammation: Data represent first human trials examining the impact of dark chocolate consumption on cognition and other brain functions -- ScienceDaily

"This is the first time that we have looked at the impact of large amounts of cacao in doses as small as a regular-sized chocolate bar in humans over short or long periods of time, and are encouraged by the findings. These studies show us that the higher the concentration of cacao, the more positive the impact on cognition, memory, mood, immunity and other beneficial effects."

Researchers Watch Brain's Lining Heal After Head Injury - Neuroscience News

“The lining of the brain, with help from the immune system, has a remarkable ability to put itself back together again after injury,” said Dorian McGavern, Ph.D., scientist at the NIH’s National Institute of Neurological Disorders and Stroke and the senior author of the study published in Nature Immunology. “As we learn more about all the cells involved in the repair process, we may be able to identify potential targets for therapy that lead to better outcomes for patients.” The study came about from an observation on MRI scans of adult patients who experienced a concussion or mTBI. Around half of patients with mTBI show evidence of injury to blood vessels in the meninges, which appears on MRI scans as a vascular dye leaking out of the damaged vessels. The meninges are a collection of membranes that line the central nervous system and help protect brain and spinal cord tissue from various forms of injury. Damage to the meninges can cause cell death in underlying brain tissue.

Vitamin D blood test may one day speed bipolar diagnosis in kids: Finding a reliable blood marker could offer help to doctors and parents, study suggests -- ScienceDaily

The clinical part of the pilot study was conducted at Harding Hospital at Ohio State's Wexner Medical Center and included 13 children without mood disorders, 12 children with diagnosed bipolar disorder and 11 children with major depressive disorder. Ziouzenkova said it made sense to look at vitamin D binding protein because it potentially plays a role in brain inflammation. The researchers also looked at inflammatory markers in the blood, but found no significant correlations. Looking for the nutrient vitamin D in the blood, as opposed to the binding protein, appears to have low diagnostic power, she said. "We wanted to look at factors that could be involved in mood disorders on a cellular level and that could be easily found in the blood," Ziouzenkova said. To date, finding a reliable blood marker for bipolar diagnosis has been elusive, she said. Her lab used an intricate technique to evaluate blood plasma, in which they essentially used biological "bait" to fish for inflammatory factors. That helped them identify the vitamin D binding protein as a potential diagnostic target.

Flu may impact brain health -- ScienceDaily

Although influenza is considered to be a respiratory disease, it has been associated with neurological symptoms in some cases. However, the long-term effects of flu on the brain have not been studied. Martin Korte and colleagues investigated three different flu strains (H1N1, H3N2, H7N7) in mice. Two of these strains, H3N2 and H7N7, caused memory impairments that were associated with structural changes to neurons in the hippocampus. The infections also activated the brain's immune cells in this region for an extended period and altered the expression of genes implicated in disorders including depression, autism and schizophrenia. These findings suggest that some strains of the flu may pose a threat to healthy brain function.

Why do healthy children die from the flu? Study offers new insights -- ScienceDaily

The study examined specific immune pathways known to be activated during flu infections in both humans and mice, which makes the findings relevant to children. Coates and colleagues focused on the initial immune response to the flu, using healthy adult and young mice who have not had previous exposures to the virus. They discovered that in the young, more immune cells called monocytes were recruited to the lungs, and that the gene expression profiles of these cells had more inflammatory features, causing greater inflammation and more severe lung injury. "Our findings provide new targets for developing effective medicines to treat the flu in children," says Coates. "We can seek ways to prevent monocytes from coming to the lungs, or we can target monocyte behavior in the lungs to reduce dangerous inflammation."

Grape-derived compounds may promote resilience against depression, researchers find: New study used DNA epigenetic mapping to analyze novel inflammatory mechanisms influencing brain circuitry associated with depression -- ScienceDaily

According to the U.S. Centers for Disease Control and Prevention, each year approximately 16 million individuals in the United States have a major depressive episode. Conventional pharmacological treatments are estimated to produce temporary remission in less than 50 percent of patients, and they are often associated with severe adverse effects. Thus, there is an urgent need for a wider spectrum of novel therapeutics. Depression is associated with a multitude of pathological processes, including inflammation of the peripheral immune system, a set of biological structures and processes in the lymph nodes and other tissues that protect against disease and abnormalities involving synapses, the structures that permit neurons to pass an electrical or chemical signal to other neurons. However, currently available antidepressants are largely restricted to targeting the systems that regulate serotonin, dopamine, and other related neurotransmitters, and these treatments do not specifically address inflammation and synaptic maladaptations that are now known to be associated with MDD. Previous research has found that grape-derived polyphenols have some efficacy in modulating aspects of depression, yet the mechanisms of action had largely remained unknown until now. The new study, led by Giulio Maria Pasinetti, PhD, Saunders Professor of Neurology, and a team of investigators from the Center for Integrative Molecular Neuroresilience at the Icahn School of Medicine at Mount Sinai, found that a bioactive dietary polyphenol preparation -- a combination of three grape-derived polyphenol products, including a select Concord grape juice, a select grape seed extract, and trans-resveratrol -- was effective in promoting resilience against stress-induced depression in mice. Specifically, researchers found that DHCA and Mal-gluc can promote resilience in mouse models of depression by modulating inflammation and synaptic plasticity, respectively. DHCA reduces interleukin 6 (IL-6), a pro-inflammatory substance secreted by T cells and macrophages to stimulate immune response, by epigenetically modulating the non-coding sequence of the IL-6 gene. Mal-gluc modulates histone acetylation of the Rac1 gene and allows transcription activators to access the DNA for increased transcription in the brain, which influences the expression of genes responsible for synaptic plasticity. Researchers also demonstrated that DHCA/Mal-gluc treatment was effective in attenuating depression-like phenotypes in a mouse model of increased systemic inflammation induced by transplantation of cells from the bone marrow of stress-susceptible mice.

What Is Sensory Deprivation And Why Are More Athletes Using It?

Based on the Restricted Environmental Stimulation Technique (REST), floatation therapy triggers a deep relaxation response that is much deeper than normal sleep which enables the individual to reach the elusive Theta state, which is normally hard to achieve. With the elimination of external stimuli, the central nervous system’s workload is reduced by as much as 90%. During this reduction in stimuli, the body naturally regenerates itself and healing is promoted through the parasympathetic response, which also increases T-cell production and may strengthen the immune system. All of this on top of removing gravity, which allows the muscles and joints to completely release tension –  athletes can largely benefit from this type of therapy.

Gaining or losing weight alters molecular profile in humans -- ScienceDaily

Snyder and his colleagues found that even with modest weight gain -- about 6 pounds -- the human body changed in dramatic fashion at the molecular level. Bacterial populations morphed, immune responses and inflammation flared, and molecular pathways associated with heart disease activated. But that's not the end of the story. When study participants lost the weight, most of the rest of the body's systems recalibrated back to their original states, the study found.

Exercise changes gut microbial composition independent of diet, team reports -- ScienceDaily

In the mouse study, changes in the microbiota of recipient mice mirrored those in the donor mice, with clear differences between those receiving microbes from exercised and sedentary mice. "That proved to us that the transplant worked," Woods said. Recipients of the exercised mouse microbiota also had a higher proportion of microbes that produce butyrate, a short-chain fatty acid that promotes healthy intestinal cells, reduces inflammation and generates energy for the host. They also appeared to be more resistant to experimental ulcerative colitis, an inflammatory bowel disease. "We found that the animals that received the exercised microbiota had an attenuated response to a colitis-inducing chemical," Allen said. "There was a reduction in inflammation and an increase in the regenerative molecules that promote a faster recovery." In the human study, the team recruited 18 lean and 14 obese sedentary adults, sampled their gut microbiomes, and started them on an exercise program during which they performed supervised cardiovascular exercise for 30-60 minutes three times a week for six weeks. The researchers sampled participants' gut microbiomes again at the end of the exercise program and after another six weeks of sedentary behavior. Participants maintained their usual diets throughout the course of the study. Fecal concentrations of SCFAs, in particular butyrate, went up in the human gut as a result of exercise. These levels declined again after the participants reverted to a sedentary lifestyle. Genetic tests of the microbiota confirmed that this corresponded to changes in the proportion of microbes that produce butyrate and other SCFAs. The most dramatic increases were seen in lean participants, who had significantly lower levels of SCFA-producing microbes in their guts to begin with. Obese participants saw only modest increases in the proportion of SCFA-producing microbes. The ratios of different microbes in the gut also differed between lean and obese participants at every stage of the study, the researchers said. "The bottom line is that there are clear differences in how the microbiome of somebody who is obese versus somebody who is lean responds to exercise," Woods said. "We have more work to do to determine why that is."

Childhood infection and adult schizophrenia: A meta-analysis of population-based studies

Our meta-analysis indicates an association between childhood CNS viral infection and risk of adult non-affective psychosis.

Bring On the Exercise, Hold the Painkillers - The New York Times

It found that by reducing the production of prostaglandins, NSAIDs change how a body responds to exertion, this time deep within the muscles. For that study, researchers in the department of microbiology at Stanford University looked first at muscle cells and tissue from mice that had experienced slight muscular injuries, comparable to those we might develop during strenuous exercise. The tissue soon filled with a particular type of prostaglandin that turned out to have an important role: It stimulated stem cells within the muscles to start multiplying, creating new muscle cells that then repaired the tissue damage. Afterward, tests showed that the healed muscle tissue was stronger than it had been before.

Vitamin D Speeds Recovery From Tuberculosis, Scientists Report - The New York Times

In a clinical trial of 95 patients on antibiotics, those who also got vitamin D had less inflammation, and the mycobacteria in their lung phlegm cleared up 13 days earlier on average.

Cognitive decline after surgery tied to brain's own immune cells: In mouse study, experimental drug blocks post-operative memory loss -- ScienceDaily

Post-operative cognitive dysfunction was previously believed to be caused by deep anesthesia during surgery. But increasing evidence instead links the condition to an inflammatory reaction in the brain, now understood to be a normal response to tissue trauma occurring anywhere in the body -- even surgeries physically distant from the brain, such as hip replacement, may trigger this response. Studies have shown that when this inflammation is excessive or too persistent, as may be the case in the elderly, the normally protective response can negatively impact cognition. "Previous studies on post-operative inflammation in the brain had focused on whether circulating immune cells invade the brain and contribute to cognitive decline," Koliwad said. "Based on our new research, we now know that the brain's own microglia initiate and orchestrate this response, including the infiltration of peripheral immune cells and the resultant memory loss."

Loneliness actually hurts us on a cellular level - Vox

In 2007, Cole and a team of researchers at UCLA make a breakthrough in a small 14-participant study. The very cells of people who lived through periods of chronic loneliness looked different. More specifically, the white blood cells of people who suffered through chronic loneliness appeared to be stuck in a state of fear. Cole and his colleagues observed two main genetic differences between lonely and non-lonely people. 1) Genes that code for the body’s inflammation response are turned on to a degree not seen in non-lonely participants. “There is a huge hidden epidemic of loneliness, and disenfranchisement from the human race” Which isn’t good. “Inflammation is great at responding to acute injury, but if you have inflammation going chronically, it serves as a fertilizer for chronic diseases like atherosclerosis and cardio vascular disease, neurodegenerative diseases, and metastatic cancer,” he says. “That provides one reasonable biological explanation for why they might be at an increased risk for these diseases.” 2) “At the same time, in almost like a teeter-totter regulatory dynamic, we see down-regulated, or suppressed activity, in a block of genes involved in fending off against viral infections.” Those genes code for proteins known as type-1 interferons, which direct the immune system to kill viruses. This is a bit of a head-scratcher. Increasing the body’s inflammation response in the face of stress makes sense. It’s protective in the short term. But why would our bodies become less willing to attack viruses?

Mindfulness Meditation Helps You Handle Stress Better | Time.com

Not only did the people who learned to meditate report feeling less stressed than people in the other class, but their blood measurements of ACTH, a stress hormone released in the brain and then into the bloodstream, were lower too, as well as markers of inflammation called pro-inflammatory cytokines. But in the control group, people were actually more stressed the second time they did the test, possibly because they knew and anticipated how bad the it would be.