Recent quotes:

Consumption of coffee or caffeine and serum concentration of inflammatory markers: A systematic review - PubMed

Fifteen studies (8 involving coffee and 7 caffeine) were included. Increased adiponectin levels were found in four of seven trials comparing filtered coffee/caffeinated coffee with placebo or comparing its levels at baseline and after consumption of medium or dark roasted coffee, but no change was seen in caffeine trials. None of the five studies assessing the effects of coffee found changes in C-reactive protein (CPR), but one out of three trials found decreased CPR levels in response to caffeine. Interleukin (IL)-6 was increased by caffeinated coffee compared with placebo in one of four coffee trials, and by caffeine in three out of five studies. Caffeine increased IL-10 levels in two of three trials. These data suggest a predominant anti-inflammatory action of coffee but not of caffeine consumption. Moreover, the proinflammatory and anti-inflammatory responses to caffeine point to its complex effects on the inflammatory response.

Microbiome Study Provides New Clues to Common Pathology of Inflammatory Conditions | MedPage Today

Patients with axial spondyloarthritis (SpA), acute anterior uveitis (AAU), and Crohn's disease had a low concentration of Lachnospiraceae compared with a control group of patients with back pain and no inflammatory disorders. The most striking difference was a low abundance of Fusicatenibacter among nonsteroidal anti-inflammatory drug (NSAID) users in the control group versus the patients with the inflammatory conditions. The analysis also revealed disease-specific differences in microbiome diversity.

Wheat Gluten Spurs Brain Inflammation - Neuroscience News

The research indicated that gluten, when added to the diet of mice, caused inflammation in the hypothalamic region of the brain. Mice models are deemed valuable for studying human physiology due to similarities in various systems, suggesting potential implications for humans. While the exact reason for the inflammation is still unknown, one theory suggests that indigestible components of gluten may trigger an immune response similar to that seen in celiac patients.

Alzheimer’s: Inflammatory markers are conspicuous at an early stage: Evidence of damage and also neuroprotective processes long before symptoms of dementia manifest -- ScienceDaily

n recent years, it has become evident that the brain's immune system and related inflammatory processes -- also known as "neuroinflammation" -- significantly contribute to the development of Alzheimer's disease. In view of this, the scientists analyzed various immunological biomarkers that are characterized by good detectability in the cerebrospinal fluid and reproducible results. "It was already known that these markers indicate immune processes in the context of Alzheimer's disease. However, how these markers relate to brain volume, cognitive performance and other parameters had not been studied as comprehensively as we have now," explains Prof. Michael Heneka, who led the current study during his long-time tenure at DZNE and UKB. Since the beginning of this year, he has been director of the Luxembourg Centre for Systems Biomedicine. "We have found that some of these inflammatory markers are conspicuous even when there are no symptoms of dementia yet," Heneka says. "Based on the data we have so far, we can't specify the lead time at this point. But my estimate is that it is at least ten to twenty years."

Brain tissue inflammation is key to Alzheimer's disease progression

For the first time ever, the researchers showed in living patients that neuroinflammation—or activation of the brain's resident immune cells, called microglial cells—is not merely a consequence of disease progression; rather, it is a key upstream mechanism that is indispensable for disease development.

Histamine boosts inflammation, alters serotonin

Brain serotonin levels dropped within minutes of LPS injection, whereas they remained the same in control mice, demonstrating how quickly inflammatory responses in the body translate to the brain and affect serotonin. LPS is unable to cross the protective blood-brain barrier and could therefore not have caused this drop directly. On further examination they found that the histamine in the brain was triggered by the inflammatory response and directly inhibited the release of serotonin, by attaching to inhibitory receptors on the serotonin neurons. These inhibitory receptors are also present on human serotonin neurons, so this effect might translate to people.

Another way 'good' cholesterol is good: Combatting inflammation -- ScienceDaily

The researchers found: HDL anti-inflammatory capacity was significantly higher in people who remained healthy (31.6%) than in those who experienced a cardiovascular event (27%); The association of anti-inflammatory capacity with cardiovascular events was independent of the established biomarkers of HDL cholesterol and C-reactive protein levels, and was also independent of cholesterol efflux capacity; For every 22% increase in the ability of HDL particles to suppress inflammation in endothelial cells, participants were 23% less likely to have a cardiovascular event during the next decade; The amount of protection from increased HDL anti-inflammatory capacity was higher in women than in men; and Risk prediction was improved by adding HDL anti-inflammatory capacity to the Framingham Risk Score, or by replacing HDL cholesterol levels with this new measure of HDL function.

Could playing host to hookworms help prevent aging? -- ScienceDaily

They reveal how the loss of helminths has so far been linked to a range of inflammatory diseases, including asthma, atopic eczema, inflammatory bowel disease, multiple sclerosis, rheumatoid arthritis and diabetes. Some studies have shown that natural infection with helminths can alleviate disease symptoms, for example in multiple sclerosis and eczema, while other studies in animal models suggest that intentional infection with helminths could have benefits against disease. The safer, and perhaps more palatable, option is the concept of using helminth-derived proteins to achieve the same therapeutic benefits. This was tested recently in mice and shown to prevent the age-related decline in gut barrier integrity usually seen with a high-calorie diet. It also had beneficial effects on fat tissue, which is known to be a major source of inflammageing.

Dietary interventions may slow onset of inflammatory and autoimmune disorders -- ScienceDaily

During an immune response, T cells flood the affected area to help the body fend off pathogens. Jones, Larochelle and their teams found dietary methionine fuels this process by helping "reprogram" T cells to respond to the threat by more quickly replicating and differentiating into specialized subtypes. Some of these reprogrammed T cells cause inflammation, which is a normal part of an immune response but can cause damage if it lingers, such as the nerve damage that occurs in multiple sclerosis. The researchers also found that significantly reducing methionine in the diets of mouse models of multiple sclerosis altered the reprogramming of T cells, limiting their ability to cause inflammation in the brain and spinal cord. The result was a delay in the disease's onset and slowed progression.

What drives inflammation in type 2 diabetes? Not glucose, says new research - ScienceBlog.com

The team was surprised to find that glycolysis wasn’t driving chronic inflammation. Instead, a combination of defects in mitochondria and elevated fat derivatives were responsible.

Inflammation might be the root of preventable disease | Harvard Magazine

Because these compounds have not yet been synthesized as pharmaceuticals, maintaining healthy levels of SPMs is best supported by foods rich in the essential fatty acids EPA, DHA, and arachidonic acid. “There’s a reason they are called ‘essential,’” says Serhan. “You can only get them from your diet.” Fish contains all three, although arachidonic acid is also present in chicken, eggs, and beef, and EPA and DHA can be obtained from certain plant sources and algae. It’s ironic, he points out, that veterinary science has ensured that lab animals (and even pets) in the United States eat better than most people do, because animal food is fortified with omega-3s. Most Americans, he believes, don’t eat enough of them.

Inflammation might be the root of preventable disease | Harvard Magazine

Think about how over-the-counter anti-inflammatories such as ibuprofen and acetaminophen work. They block a particular signal. But Serhan discovered that aspirin works differently (and in a multi-faceted way): rather than blocking inflammatory signals, it attenuates them. In addition, it has mild anti-coagulant properties that are beneficial in atherosclerosis. And perhaps most importantly, aspirin stimulates the production of at least two classes of health-promoting SPMs. In work published as this magazine went to press, Serhan and colleagues showed that aspirin stimulates the production of a distinct type of SPM that fights cancer tumors in mice, and another SPM that inhibits cancer tumor formation in the first place

Inflammation might be the root of preventable disease | Harvard Magazine

“Chronic inflammation is uniformly damaging and is absolutely causal to the process, because if you interfere with it, you can reverse the pathology.” And this ability to control such diseases simply by reversing inflammation is a biological response, dating far back to the time of a common ancestor, that has been retained across diverse species of animals to the present day, he says, pointing to experimental evidence: “If you can make Drosophila [fruit fly] diabetic, and then block the inflammatory response systems, you can cure diabetes in Drosophila, the same way you can reverse it in the mouse, in primates, and in humans, provided that you do it with the right tools. Of course, the higher the organism, the more complex these pathways are, so it takes more effort to define the precise mechanisms to manipulate.”

Inflammation might be the root of preventable disease | Harvard Magazine

He is the physician-scientist who first demonstrated that a molecule called C-reactive protein (CRP), easily measured by a simple and now ubiquitous blood test, could be used like a thermometer to take the temperature of a patient’s inflammation. Elevated CRP, he discovered years ago, predicts future cardiovascular events, including heart attacks. Although nobody knows what it does biologically, this marker is downstream from IL-1beta, and thus provides a reliable yardstick of that pro-inflammatory pathway’s level of activation.

Study links fluorescent lighting to inflammation and immune response - Neuroscience News

“In this report, we show genome-wide changes of gene expression patterns in skin, brain and liver for two commonly utilized fish experimental models (zebrafish and Japanese rice fish, also known as medaka), and a mammalian (mice), following exposure to 4,100 K ‘cool-white’ fluorescent light,” Walter said. “In spite of the extreme divergence of these animals (i.e., estimated divergence of mice and fish about 450 million years), and drastically different lifestyles (i.e., diurnal fish and nocturnal mice), the same highly conserved primary genetic response that involves activation of inflammation and immune pathways as part of an overall acute phase response was observed in the skin, brain and liver of all three animals. Follow-up studies to further define this response in mice are underway.”

Pure Omega-3 prescription drug markedly reduces first, repeat and total CV events: New data show 4 gram dose of icosapent ethyl may be new, cost-effective way to prevent CV complications among patients with elevated triglycerides who have heart disease or diabetes -- ScienceDaily

Compared with placebo, icosapent ethyl cut the combined rate of first and subsequent cardiovascular deaths, nonfatal heart attacks or strokes, procedures for coronary artery disease such as stenting, or hospitalizations for unstable angina (the study's primary endpoint) by 30 percent, demonstrating the drug may be more protective than previously reported. Earlier analyses of the Reduction of Cardiovascular Events with Icosapent Ethyl-Intervention Trial (REDUCE-IT), which were primarily focused on the first occurrence of a major adverse cardiovascular event, found a 25 percent reduction. This latest analysis aimed to determine the extent to which the drug reduced the total burden of (first and subsequent) cardiovascular events. "In looking at the totality of events -- not just the first ones, but subsequent ones too -- we see that the drug provides even greater reductions in ischemic events. By looking only at first events, we underestimate the true underlying treatment benefit offered," said Deepak L. Bhatt, MD, MPH, executive director of interventional cardiovascular programs at Brigham and Women's Hospital, professor of medicine at Harvard Medical School and the study's lead author. "From a patient's perspective certainly, and from a physician's point of view, icosapent ethyl's impact on total events is what matters most."

Inflammation links heart disease and depression -- ScienceDaily

This finding was given further support by the next stage of the team's research. They used a technique known as Mendelian randomisation to investigate 15 biomarkers -- biological 'red flags' -- associated with increased risk of coronary heart disease. Mendelian randomisation is a statistical technique that allows researchers to rule out the influence of factors that otherwise confuse, or confound, a study, such as social status. Of these common biomarkers, they found that triglycerides (a type of fat found in the blood) and the inflammation-related proteins IL-6 and CRP were also risk factors for depression. Both IL-6 and CRP are inflammatory markers that are produced in response to damaging stimuli, such as infection, stress or smoking. Studies by Dr Khandaker and others have previously shown that people with elevated levels of IL-6 and CRP in the blood are more prone to develop depression, and that levels of these biomarkers are high in some patients during acute depressive episode. Elevated markers of inflammation are also seen in people with treatment resistant depression. This has raised the prospect that anti-inflammatory drugs might be used to treat some patients with depression. Dr Khandaker is currently involved in a clinical trial to test tocilizumab, an anti-inflammatory drug used for the treatment of rheumatoid arthritis that inhibits IL-6, to see if reducing inflammation leads to improvement in mood and cognitive function in patients with depression. While the link between triglycerides and coronary heart disease is well documented, it is not clear why they, too, should contribute to depression. The link is unlikely to be related by obesity, for example, as this study has found no evidence for a causal link between body mass index (BMI) and depression.

Blood clot discovery could pave way for treatment of blood diseases -- ScienceDaily

Amongst other unwanted effects, free radicals play a role in the build-up of blood clots, which in turn are considered a key driver in the a development of a range of conditions, including heart disease, stroke, dementia, and inflammation-related conditions such as arthritis. The new technique is outlined in research published in Haematologica. The technique combines electron paramagnetic resonance, a cutting-edge method for detecting free radicals, with blood cell aggregometry, an established technique for measuring blood clotting. The team has successfully used the technique in mice and in human cells. They aim to better understand how blood cells function, which will help to develop new drugs against blood clotting diseases or to test the risk of clotting diseases in patients.

New scan technique reveals brain inflammation associated with post-treatment Lyme disease syndrome -- ScienceDaily

Results of the study, published in Journal of Neuroinflammation, suggest new avenues for treating the long-term fatigue, pain, sleep disruption and "brain fog" associated with PTLDS, the researchers say. "There's been literature suggesting that patients with PTLDS have some chronic inflammation somewhere, but until now we weren't able to safely probe the brain itself to verify it," says Jennifer Coughlin, M.D., associate professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine, and one of the first authors of the study report. Lyme disease is a bacterial infection transmitted to humans through tick bites. An estimated 300,000 people in the U.S. are diagnosed with Lyme disease each year, and their infections can be successfully treated with antibiotics. Doctors diagnose PTLDS if treated patients report fatigue and brain fog for at least six months after treatment. Little is known about what causes PTLDS or how to treat it, and while studies have shown that people with PTLDS have elevated markers of inflammation -- such as the chemokine CCL19 -- in their bloodstreams, it has not been clear where that inflammation may be occurring. Over the last decade, Coughlin and her colleagues optimized a positron emission tomography (PET) imaging technique in which specially labeled molecules -- or radiotracers -- bind to a protein called translocator protein (TSPO). In the brain, TSPO is released primarily by two types of brain immune cells -- microglia and astrocytes -- so levels of TSPO are higher when brain inflammation is present.

Forget the Blood of Teens. Metformin Promises to Extend Life for a Nickel a Pill | WIRED

He was confident that metformin was good enough for the job. He has maintained this confidence ever since he read a 2014 study that reviewed the fate of 90,400 type 2 diabetics taking either metformin or another medication. The metformin patients in the study not only outlived the diabetics taking the other drug—a not especially surprising result if metformin is a superior treatment—but also outlived the nondiabetics studied as a comparison.

What if the Placebo Effect Isn’t a Trick? - The New York Times

The findings of the I.B.S. study were in keeping with a hypothesis Kaptchuk had formed over the years: that the placebo effect is a biological response to an act of caring; that somehow the encounter itself calls forth healing and that the more intense and focused it is, the more healing it evokes. He elaborated on this idea in a comparative study of conventional medicine, acupuncture and Navajo “chantway rituals,” in which healers lead storytelling ceremonies for the sick. He argued that all three approaches unfold in a space set aside for the purpose and proceed as if according to a script, with prescribed roles for every participant. Each modality, in other words, is its own kind of ritual, and Kaptchuk suggested that the ritual itself is part of what makes the procedure effective, as if the combined experiences of the healer and the patient, reinforced by the special-but-familiar surroundings, evoke a healing response that operates independently of the treatment’s specifics. “Rituals trigger specific neurobiological pathways that specifically modulate bodily sensations, symptoms and emotions,” he wrote. “It seems that if the mind can be persuaded, the body can sometimes act accordingly.”

Endurance Exercise Training Has Beneficial Effects on Gut Bacteria Composition - Neuroscience News

“We found that phospholipids and cholesterol in VLDL particles decreased in response to exercise. These changes are beneficial for cardiometabolic health because VLDL transports lipids from the liver to peripheral tissues, converts into ‘bad’ LDL cholesterol in the circulation, and thus has detrimental cardiovascular effects.” Exercise training also decreased Vascular adhesion protein-1 activity, which can have beneficial anti-inflammatory effects especially on vasculature, though the underlying mechanisms could not be determined in this study. Whether Akkermansia mediates the health benefits of exercise is under further investigation

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.