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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 |

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.

One 20 minute exercise session reduces key inflammatory protein 5%.

[…]This activation process during exercise produces immunological responses, which include the production of many cytokines, or proteins, one of which is TNF -- a key regulator of local and systemic inflammation that also helps boost immune responses. "Our study found one session of about 20 minutes of moderate treadmill exercise resulted in a five percent decrease in the number of stimulated immune cells producing TNF," said Hong.[…]

Individuals hospitalized with acute mania have increased exposure to antimicrobial medications - Yolken - 2016 - Bipolar Disorders - Wiley Online Library

Overall, a total of 18 of the 234 (7.7%) individuals hospitalized for acute mania were prescribed antibiotics as opposed to seven of 555 (1.3%) controls. The prescription of antibiotics was associated with being on an inpatient unit as opposed to being in the day hospital, and having increased mania symptom severity but not with other clinical ratings, demographic variables, or psychiatric medications. Hospitalization for other psychiatric disorders was not associated with the recent prescription of antimicrobial medications. The urinary tract was the most common site of infection in women, while the respiratory tract and mucosal surfaces were the most common sites in men.

Columbia researchers find biological explanation for wheat sensitivity | EurekAlert! Science News

In the new study, the CUMC team examined 80 individuals with NCWS, 40 individuals with celiac disease, and 40 healthy controls. Despite the extensive intestinal damage associated with celiac disease, blood markers of innate systemic immune activation were not elevated in the celiac disease group. This suggests that the intestinal immune response in celiac patients is able to neutralize microbes or microbial components that may pass through the damaged intestinal barrier, thereby preventing a systemic inflammatory response against highly immunostimulatory molecules. The NCWS group was markedly different. They did not have the intestinal cytotoxic T cells seen in celiac patients, but they did have a marker of intestinal cellular damage that correlated with serologic markers of acute systemic immune activation. The results suggest that the identified systemic immune activation in NCWS is linked to increased translocation of microbial and dietary components from the gut into circulation, in part due to intestinal cell damage and weakening of the intestinal barrier.

A Medical Mystery of the Best Kind: Major Diseases Are in Decline - The New York Times

Something strange is going on in medicine. Major diseases, like colon cancer, dementia and heart disease, are waning in wealthy countries, and improved diagnosis and treatment cannot fully explain it. Scientists marvel at this good news, a medical mystery of the best sort and one that is often overlooked as advocacy groups emphasize the toll of diseases and the need for more funds. Still, many are puzzled. “It is really easy to come up with interesting, compelling explanations,” said Dr. David S. Jones, a Harvard historian of medicine. “The challenge is to figure out which of those interesting and compelling hypotheses might be correct.”

Reconceptualizing major depressive disorder as an infectious disease | Biology of Mood & Anxiety Disorders | Full Text

In the first study of this kind, germ-free (GF), specific pathogen-free (SPF), and gnotobiotic mice were compared in their response to restraint stress [36]. GF mice exhibited higher levels of plasma ACTH and corticosterone and had lower levels of brain-derived neurotrophic factor in the cortex and hippocampus, compared to SPF mice. The elevated stress response of GF mice was normalized with administration of the bacterium Bifidobacterium infantis. Another rodent study showed that administration of B. infantis in rats reduced the levels of IFN-γ, TNF-α, and IL-6 following mitogen stimulation and altered tryptophan, 5-HIAA, and DOPAC levels in the frontal cortex and amygdala [37]. Administration of the Lactobacillus rhamnosus strain in mice was shown to alter GABAergic expression in the brain: elevating GABAB1b mRNA in the cingulate and prelimbic cortices, while reducing it in hippocampus and amygdala, among other regions [38].

Is depression a kind of allergic reaction?

Both cytokines and inflammation have been shown to rocket during depressive episodes, and – in people with bipolar – to drop off in periods of remission. Healthy people can also be temporarily put into a depressed, anxious state when given a vaccine that causes a spike in inflammation. Brain imaging studies of people injected with a typhoid vaccine found that this might be down to changes in the parts of the brain that process reward and punishment. There are other clues, too: people with inflammatory diseases such as rheumatoid arthritis tend to suffer more than average with depression; cancer patients given a drug called interferon alpha, which boosts their inflammatory response to help fight the cancer, often become depressed as a side-effect.

Anti-inflammatory chemical may be a new tool for depression therapy

In further explaining the significance of the findings, UC Davis researcher Karen Wagner said: “The rapid antidepressant action of the sEH inhibitor in these murine (mouse) models of depression is truly noteworthy because current antidepressants used in humans and animal models take weeks to have full effects.” The researchers also discovered that postmortem brain samples of patients with psychiatric diseases, including depression, bipolar disorder and schizophrenia, showed a higher expression of sEH than controls. The researchers found that pretreatment with TPPU prevented the onset of depressionlike behaviors in mice after induced inflammation or repeated social-defeat stress. Mice lacking the sEH gene did not show depressionlike behavior after repeated social-defeat stress.

Why your muscles get less sore as you stick with your gym routine: Unexpected immune system cells may help repair muscles -- ScienceDaily

"T-cells, up until recently, were not thought to enter healthy skeletal muscle," said lead author and grad student Michael Deyhle. "We hadn't planned on measuring them because there's no evidence that T-cells play a role in infiltrating damaged muscle tissue. It's very exciting." The presence of the T-cells suggests that muscles become more effective at recruiting immune cells following a second bout of exercise and that these cells may facilitate accelerated repair. In other words, the muscle seems to remember the damaging insult and reacts similarly to when the immune system responds to antigens--toxins, bacteria or viruses. The group was also surprised to find inflammation actually increased after the second round of exercise. Hyldahl, his students and many physiologists have long thought inflammation goes down after the second bout of exercise, contributing to that "less sore" effect. Instead, the slightly enhanced inflammatory response suggests inflammation itself probably does not worsen exercise-induced muscle damage. "Many people think inflammation is a bad thing," Deyhle said. "But our data suggest when inflammation is properly regulated it is a normal and healthy process the body uses to heal itself." Adds Hyldahl: "Some people take anti-inflammatory drugs such as Ibuprofen and Aspirin after a workout, but our study shows it may not actually be effective. The inflammation may not be directly causing the pain, since we see that muscle soreness is reduced concurrent with increases in inflammation."