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The findings conclude that gut bacteria, found in the intestinal tract and stool, are associated with brain inflammation in cirrhotic patients and animals known as hepatic encephalopathy (HE). HE can lead to fatigue, the inability to concentrate, mental confusion and death.

“HE is an epidemic in patients with liver disease and cirrhosis,” said Bajaj, associate professor in the Department of Gastroenterology, Hepatology and Nutrition in the VCU School of Medicine. “Bacteria can result in inflammation in the systemic circulation, which in turn could inflame the brain.”

Bacteria have been discovered in our guts that depend on one of our brain chemicals for survival. These bacteria consume GABA, a molecule crucial for calming the brain, and the fact that they gobble it up could help explain why the gut microbiome seems to affect mood.

Philip Strandwitz and his colleagues at Northeastern University in Boston discovered that they could only grow a species of recently discovered gut bacteria, called KLE1738, if they provide it with GABA molecules. “Nothing made it grow, except GABA,” Strandwitz said while announcing his findings at the annual meeting of the American Society for Microbiology in Boston last month.

GABA acts by inhibiting signals from nerve cells, calming down the activity of the brain, so it’s surprising to learn that a gut bacterium needs it to grow and reproduce. Having abnormally low levels of GABA is linked to depression and mood disorders, and this finding adds to growing evidence that our gut bacteria may affect our brains.

In this study, the researchers found that this effect vanished when they surgically removed the vagus nerve – which links the gut to the brain – suggesting it somehow plays a role in the influence gut bacteria can have on the brain.

Researchers at the University of Iowa have found alcohol abuse is linked to discrimination.

“We’ve had this idea that discrimination is associated with heavier drinking and drinking-related problems, but we didn’t have a clear understanding of the evidence underneath that,” says Paul Gilbert, assistant professor of the Department of Community and Behavioral Health at the UI College of Public Health and lead author of the study. “I wanted to uncover what we know and how we know it. What does the science actually say?”

The paper, “Discrimination and Drinking: A Systematic Review of the Evidence,” was published online in June in Social Science & Medicine.

Naloxone, a fast-acting medication used to block the effects of opioids, can be successfully coprescribed to patients receiving opioid analgesics for chronic pain in primary care. Naloxone coprescribing was associated with reduced opioid-related emergency room visits, suggesting that adopting this practice could reduce opioid-related adverse events. The findings are published in Annals of Internal Medicine.

Unintentional opioid overdose is a leading cause of injury-related death in the United States. Many interventions to curb opioid-related morbidity and mortality have not proven effective, but targeted distribution of naloxone to those likely to witness or experience an opioid overdose, mainly illicit drug users, has been associated with substantial reductions in opioid overdose mortality in communities where this practice is implemented. In San Francisco, implementation and expansion of a targeted naloxone distribution program was associated with a temporary decline in heroin-related deaths. However, the number of deaths attributed to opioid analgesics taken for chronic pain continued to climb. Limited research suggests that prescribing naloxone to these patients when they receive their opioid prescriptions could decrease overdose.

Psychiatric researchers have discovered a genetic link between depression and Type 2 diabetes.

Both depression and Type 2 diabetes are chronic health conditions and both have a major impact on public health. Diabetesis a complex disorder and having depression can have a serious impact on an individual's ability to manage their diabetes on a regular basis.

Scientific studies have consistently shown a two-way epidemiological association between the two conditions. People with depression may be up to 60% more at risk of developing type 2 diabetes and those with Type 2 diabetes around 15% more at risk of developing depression, leading psychiatrists and scientists to try and discover how the two illnesses may be linked to each other.

The mechanisms underlying the apparent association between the two conditions are still unclear, although common biological pathways have been implicated in the development of both.

Building on this, Dr Carol Kan, a member of the Royal College of Psychiatrists and her team from the Institute of Psychiatry, Psychology and Neuroscience at King's College London have been investigating the extent to which the co-occurrence of depression and depression could be due to interactions between genetic and environmental risk factors using two approaches; twin data and genome wide association studies (GWAS).

Dr Kan said:

"We are still in the early days, but we have demonstrated significant genetic overlap between Type 2 diabetes and depression in three twin registries. Larger scale studies will further help us to address this complex research question."

In a study appearing in JAMA, Christiane E. Angermann, M.D., of University Hospital Wurzburg, Germany, and colleagues examined whether 24 months of treatment with the antidepressant escitalopram would improve mortality, illness, and mood in patients with chronic heart failure and depression.

Previous meta-analysis indicates that depression prevalence in patients with heart failure is 10 percent to 40 percent, depending on disease severity. Depression has been shown to be an independent predictor of mortality and rehospitalization in patients with heart failure, with incidence rates increasing in parallel with depression severity. Long-term efficacy and safety of selective serotonin reuptake inhibitors (SSRIs), which are widely used to treat depression, is unknown for patients with heart failure and depression.

For this study, 372 patients with chronic heart failure with reduced ejection fraction (a measure of heart function) and depression were randomly assigned to receive escitalopram or matching placebo in addition to optimal heart failure therapy. During a median participation time of 18.4 months (n = 185) for the escitalopram group and 18.7 months (n = 187) for the placebo group, the primary outcome of death or hospitalization occurred in 116 (63 percent) patients and 119 (64 percent) patients, respectively. There was no significant improvement on a measure of depression for patients in the escitalopram group.

"These findings do not support the use of escitalopram in patients with chronic systolic heart failure and depression," the authors write.

Behaviors caused by traumatic experiences in early life are reversible. Researchers from the University of Zurich and ETH Zurich could demonstrate that environmental enrichment allows trauma-related symptoms in mice to be reversed. This is the first evidence that positive environmental factors can correct behavioral alterations which would otherwise be transmitted to the offspring. The symptoms and their reversal are associated with epigenetic regulation of the glucocorticoid receptor gene.

Traumatic experiences in childhood increase the risk of developing behavioral and psychiatric disorders later in life. It is also known that the consequences of a trauma can likewise be observed in the children of people affected even if those children have themselves not experienced any trauma. However, childhood trauma in some conditions can also help individuals deal better with difficult situations later in life. This ability, too, is passed onto following generations. These findings have recently been uncovered by Isabelle Mansuy, Professor of Neuroepigenetics at the University of Zurich and ETH Zurich, during investigations carried out in mice.