INFLAMMATION | +50 articles

[mr peabody]

Potential new drug candidate to “beet” inflammatory diseases

Genetic Engineering & Biotechnology News | 2 Nov 2020

Researchers discover beetroot peptide may serve as potential therapeutic candidate against inflammatory diseases and neurodegenerative diseases.

Beetroot is a vegetable packed with essential vitamins, fiber, and has been linked to many health benefits such as increased white blood cells, reduction of blood pressure and inflammation, and more. Now, researchers at MedUni Vienna’s Institute of Pharmacology isolated a peptide from beetroot that is able to inhibit an enzyme that is responsible for the breakdown of messenger molecules in the body. Their findings suggest the beetroot peptide may be a potential drug candidate used to treat inflammatory diseases.

The recent study titled, “Discovery of a Beetroot Protease Inhibitor to Identify and Classify Plant-Derived Cystine Knot Peptides,” is published in the Journal of Natural Products and led by Christian Gruber, PhD, associate professor and pharmacologist at MedUni Vienna.

“By analyzing thousands of genomic data, our team was able to define a number of new cysteine-rich peptides and assign them phylogenetically in the plant kingdom. In this process, our attention was drawn to a possible function as so-called ‘protease inhibitors.’ The beetroot peptide can therefore inhibit enzymes that digest proteins,” explained Gruber.

The beetroot peptide has been found to inhibit prolyl oligopeptidase (POP), a proline-specific serine protease that cleaves several neuroactive peptides. This peptidase has been implicated in neurodegeneration, as well as in the modulation of the inflammatory response.

POP participates in several aspects of the central nervous system (CNS), including learning, memory, and mood. Currently, several POP inhibitors have already been evaluated in preclinical trials as potential drugs for the treatment of natural memory deficits that occur with aging or the pathological memory loss characteristic of Alzheimer’s disease.

“…in future studies, this group of plant peptides called ‘knottins,’ such as those found in beetroot, could potentially provide a drug candidate for treating these diseases,” Gruber noted.

By combining genome mining with sequence analysis, the researchers discovered a novel trypsin inhibitor peptide, bevuTI-I, from beetroot. BevuTI-I not only inhibits the prototypic serine protease trypsin but is the first reported POP inhibitor from this family of peptides.

The knottin peptide family, which comprises at least 243 unique sequences may be the starting point to isolate and characterize further POP inhibitors.

“Although beetroot counts as a very healthy vegetable, it would be unreasonable to hope that dementia could be prevented by regular consumption of beetroot,” stressed Gruber. “The peptide only occurs in very small quantities and it is not clear whether it can as such be absorbed via the gastrointestinal tract.”

“We are searching through large databases containing genetic information of plants and animals, decoding new types of peptide molecules and studying their structure, aiming to test them pharmacologically on enzymes or cellular receptors (such as one of the prominent drug target classes, the so-called G protein-coupled receptors) and finally analyzing them in the disease models,” explained Gruber.

Their study highlights the great potential of plant protease inhibitors and other related plant species as a valuable source for peptide-based drug discovery for targets involved in diseases such as neurodegenerative disorders and immune system related diseases.

Potential New Drug Candidate to "Beet" Inflammatory Diseases

Researchers discover beetroot peptide may serve as a potential therapeutic candidate against inflammatory diseases.

www.genengnews.com

 

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Dr. Atilla Szabo

Psychedelics and diseases with chronic inflammation*

by Deana Fedaie

Research is being done into the use of LSD as an immunotherapy to treat mental illnesses.

The recent association established between the 5-HT receptors and psychedelics have sparked renewed interest in the use of LSD and other psychedelics as immunotherapies. Szabo calls this the “Biomedical Renaissance of Psychedelic Research,” which they date to have started in the early 2000s. It is understood by the vast amount of research that the mechanism of action of LSD and other psychedelics begin by triggering neurotransmitter receptors in the brain, which creates altered cognition and perception in the user. The immune and nervous systems had not been vastly studied in relation to each other until recently, but it is now understood that immune cells have neuroreceptors associated with them (Beck, 2013).

The 5-HT1 and 5-HT2 receptors have a high expression profile in the lymphoid tissues of mammals and are associated with different immunological processes, including anti-tumor and anti-viral immune responses. Immune homeostasis is also regulated by neuroendocrine regulation of inflammation that happens through serotonin. The ability of psychedelics to enhance immune response or inhibit functions related to inflammation pose psychedelics as possible remedies to treat diseases with chronic inflammatory etiology and pathology, including atherosclerosis, rheumatoid arthritis, type I diabetes, multiple sclerosis, schizophrenia, Alzheimer’s disease, and depression (Szabo 2015).​

 

[mr peabody]

Treating neurodegenerative disorders with cannabinoids

by Cornerstone Wellness | 17 Sep 2014

Neuroinflammation is known to play a significant role in essentially all neurodegenerative processes. Diseases such as Alzheimer’s, Multiple Sclerosis (MS), Huntington’s Disease, and Parkinson’s Disease all involve hyperactive microglia, which are the live-in macrophages of the brain, spinal cord, and central nervous system. Macrophages are immune cells that capture and dissolve foreign substances, germs, and cancer cells within the body. The microglia in the brain and spinal cord form the first line of immune defense in the central nervous system. Unfortunately, in the case of aforementioned diseases, these cells have become overactive causing them to secrete excess substances, such as cytokines (cell signals that regulate cell group growth and response), glutamate, and harmful free radicals. This excessive production of chemicals causes inflammation, which leads to further cell death.

Cannabis and the family of chemicals it produces are known to act on two major cell receptor types named CB1 and CB2 respectively. The CB1 receptor is most commonly found in neurons throughout the brain. The psychedelic effects of cannabis come from this receptor’s function, which re-wires the way neurons signal each other. The CB2 receptor on the other hand, is found throughout the body, especially within the immune system cells. The effects of activating the CB2 receptor are more myriad, but within the immune system specifically four groups of effects have been identified:

1. Induction of apoptosis or forced cell death

2. Suppression of cell proliferation

3. Induction of regulatory T cells

4. Inhibition of pro-inflammatory cytokine/chemokine production and increase in anti-inflammatory cytokines

The last of these effects is the basis upon exploring using cannabinoids to halt the progress of neurodegenerative disorders. The idea is that if cannabinoids can prevent excess production of cytokine, inflammation will decrease, and the resultant cell death around that inflammation will not occur. This would go a long measure toward slowing progression of neuro-inflammatory diseases. However, it is important to note that tempering inflammation would still not allow the brain to recover to its pre-disease state and slow neural damage would inevitably continue to occur. Likewise, modern medicine currently utilizes a variety of treatments in these diseases as more or less palliative care.

Based on these observations, research groups worldwide have been testing specific cannabinoids and other CB2 agonists with various models of neuro-inflammatory disease, generally in rodents.

The following is a general review of effects noticed, grouped by disease:

Alzheimer’s Disease – In Alzheimer’s cannabidiol has been shown to “reduce the transcription and expression of pro-inflammatory molecules in the hippocampus of an in-vivo model of induced neuroinflammation”. The hippocampus is the part of the brain that controls conversion of memory from short to long-term and controls spatial navigation. In Alzheimer’s, it’s one of the first areas of the brain to suffer damage and why patients have memory problems. Another agonist, which has the name SR141716A, also prevents amnesia induced by certain peptides, so these both promise a future in treating the disease.

Parkinson’s Disease – In this disease, the agonist WIN55,212-2 has been shown to protect mouse neurons from the neurotoxin MPTP, which is the chemical which leads to the death of dopaminergic neurons and causes Parkinson’s Disease.

Multiple Sclerosis (MS) – Although the cause of MS is unclear, researchers have determined that both genetic susceptibility and environmental trigger play a role. Some patients develop their symptoms of MS after contracting a virus. Likewise, testing rodents injected with a virus that intentionally lead to animal models of MS provided ground to investigate the effects that CB2 agonists might have on MS in humans. As is, cannabis concentrate is already prescribed under the name Sativex to alleviate neuropathic pain, spasticity, and overactive bladder symptoms associated with MS. Although some agonists did increase symptoms, several, including THC, delayed onset and reduced severity of symptoms. Three agonists, WIN55,212-2, ACEA, and JWH-015 were shown to improve motor function by attenuating microglia and immune cell infiltration into the spinal cord.

Exactly how these effects are achieved is still unknown. Although it is presumed that the effects of the CB2 agonists (any molecules that can activate CB2 receptors, including cannabinoids) stem from CB2 receptor activation, other theories have been proposed. One research group at the University of Bari has explored the extra-cannabinoid receptor binding activity of cannabidiol (CBD). Researchers there found that CBD can surprisingly communicate with the nucleus of the cell directly through interaction with nuclear hormone receptors. There are several possible chemical pathways through which cannabinoids can achieve their effects, beyond CB2 receptors. Further research will illuminate these pathways.

https://cornerstonecollective.com/ho...der-treatment/​

 

[mr peabody]

UC Berkeley scientists propose radical new theory that AD memory loss and cognitive
dysfunction are due to a leaky barrier between the blood stream and the brain.

Drugs that quell brain inflammation found to reverse dementia

UC Berkeley | Neuroscience News | Dec 29 2019

Older mice given anti-inflammatory medication were better able to learn new tasks and became almost as adept at learning as mice half their age.

Drugs that tamp down inflammation in the brain could slow or even reverse the cognitive decline that comes with age. In a publication appearing today in the journal Science Translational Medicine, University of California, Berkeley, and Ben-Gurion University scientists report that senile mice given one such drug had fewer signs of brain inflammation and were better able to learn new tasks, becoming almost as adept as mice half their age.

“We tend to think about the aged brain in the same way we think about neurodegeneration: Age involves loss of function and dead cells. But our new data tell a different story about why the aged brain is not functioning well: It is because of this “fog” of inflammatory load,” said Daniela Kaufer, a UC Berkeley professor of integrative biology and a senior author, along with Alon Friedman of Ben-Gurion University of the Negev in Israel and Dalhousie University in Canada. “But when you remove that inflammatory fog, within days the aged brain acts like a young brain. It is a really, really optimistic finding, in terms of the capacity for plasticity that exists in the brain. We can reverse brain aging.”

The successful treatment in mice supports a radical new view of what causes the confusion and dementia that often accompany aging. More and more research shows that, with age, the filtration system that prevents molecules or infectious organisms in the blood from leaking into the brain — the so-called blood-brain barrier — becomes leaky, letting in chemicals that cause inflammation and a cascade of cell death. After age 70, nearly 60% of adults have leaky blood- brain barriers, according to Friedman’s magnetic resonance imaging (MRI) studies.

An accompanying paper by the two researchers and Dan Milikovsky of Ben-Gurion University shows that the inflammatory fog induced by a leaky blood-brain barrier alters the mouse brain’s normal rhythms, causing microseizure-like events — momentary lapses in the normal rhythm within the hippocampus — that could produce some of the symptoms seen in degenerative brain diseases like Alzheimer’s disease. Electroencephalograms (EEGs) revealed similar brain wave disruption, or paroxysmal slow wave events, in humans with epilepsy and with cognitive dysfunction, including Alzheimer’s and mild cognitive impairment (MCI).

Together, the papers give doctors two biomarkers — leaky barriers detectable by MRI and abnormal brain rhythms detectable by EEG — that can be used to flag people with blood-brain barrier problems, as well as a potential drug to slow or reverse the consequences.

“We now have two biomarkers that tell you exactly where the blood-brain barrier is leaking, so you can select patients for treatment and make decisions about how long you give the drug,” said Kaufer, a member of UC Berkeley’s Helen Wills Neuroscience Institute. “You can follow them, and when the blood-brain barrier is healed, you no longer need the drug.”

Blood-brain barrier

Scientists have long suspected that a leaky blood-brain barrier causes at least some of the tissue damage after brain injury and some of the mental decline that comes with age. But no one knew how.

In 2007, however, Friedman and Kaufer linked these problems to a blood protein, albumin. In 2009, they showed that when albumin leaks into the brain after trauma, it binds to the TGF-β (TGF-beta) receptor in brain cells called astrocytes. This triggers a cascade of inflammatory responses that damage other brain cells and neural circuits, leading to decreased inhibition and increased excitation of neurons and a propensity toward seizures.

They also showed in mice that blocking the receptor with an antihypertension drug, losartan, prevented the development of epilepsy after brain trauma. Epilepsy is a frequent consequence of concussions like those sustained by soldiers from roadside bombs.

Subsequent studies revealed leakiness in the barrier after stroke, traumatic brain injury and football concussions, solidly linking albumin and an overexcited TGF-β receptor to the damage resulting from these traumas.

In their new studies, Kaufer and Friedman showed that introducing albumin into the brain can, within a week, make the brains of young mice look like those of old mice, in terms of hyperexcitability and their susceptibility to seizures. These albumin-treated mice also navigated a maze as poorly as aged mice.

“When we infused albumin into the brains of young mice, we recapitulated aging of the brain: the gene expression, the inflammatory response, resilience to induced seizures and mortality after seizures, performance in a maze. And when we recorded their brain activity, we found these paroxysmal slow wave events,” Kaufer said. “And all were specific to the site we infused. So, doing this is sufficient to get an aged phenotype of this very young brain.”

When they genetically engineered mice so that they could knock out the TGF-β receptor in astrocytes after they’d reached old age, the senile mouse brains looked young again. The mice were as resistant to induced seizures as a young mouse, and they learned a maze like a young mouse.

Serendipitously, a Palo Alto, California, medicinal chemist, Barry Hart, offered to synthesize a small-molecule drug that blocks the TGF-β receptor in astrocytes only, and that could traverse the blood-brain barrier. When they gave the drug, called IPW, to mice in doses that lowered the receptor activity level to that found in young mice, the brains of the aged mice looked younger, too. They showed young brain-like gene expression, reduced inflammation and improved rhythms — that is, reduced paroxysmal slow wave events — as well as reduced seizure susceptibility. They also navigated a maze or learned a spatial task like a young mouse.

In analyzing brain tissue from humans, Kaufer found evidence of albumin in aged brains and increased neuroinflammation and TGF-β production with age. Friedman developed a special type of MRI imaging — dynamic contrast-enhanced (DCE) imaging — to detect leakage in the blood-brain barrier and found more leakage in people with greater cognitive dysfunction.

"Altogether, the evidence points to a dysfunction in the brain’s blood filtration system as one of the earliest triggers of neurological aging," Kaufer said.

Kaufer, Friedman and Hart have started a company to develop a drug to heal the blood-brain barrier for clinical treatment and hope that the drug will help reduce brain inflammation — and, thus, permanent damage — after stroke, concussion or traumatic brain injury, and eventually help older adults with dementia or Alzheimer’s disease who have demonstrated leakage of the blood-brain barrier.

“We got to this through the back door — we started with questions about plasticity having to do with the blood-brain barrier, traumatic brain injury and how epilepsy develops,” Kaufer said. “But after we’d learned a lot about the mechanisms, we started thinking that maybe in aging it is the same story. This is new biology, a completely new angle on why neurological function deteriorates as the brain ages.”

Drugs that quell brain inflammation reverse dementia - Neuroscience News

Older mice given anti-inflammatory medication were better able to learn new tasks and became almost as adept at learning as mice half their age.

neurosciencenews.com

 

[mr peabody]

Previous research has shown that microglial cells are activated in several neurological diseases
such as Alzheimer’s, Parkinson’s and stroke.

Immune cells behind the depression experienced in those with inflammation

Linköping University | Neuroscience News | 25 Jan 2021

Microglia appears to play a key role in inflammation-associated depression.

Special immune cells found in the brain, microglia, play a key role in the processes that make you feel uneasy and depressed in correlation with inflammation. This is the conclusion of a study using mice carried out by researchers at Linköping University, Sweden. The results have been published in the scientific journal Immunity, and suggest that microglial cells contribute to the negative mood experienced during several neurological diseases, and maybe also depression.

David Engblom’s research group at Linköping University has spent many years looking at why inflammation in the body, such as a common cold or influenza, causes us to feel poorly and despondent, and why we feel like retiring into our shell. The activity of the immune system influences nerve cells in some way. However, normal cells of the immune system are not able to get into the brain: it is sensitive and must be protected. Instead, the brain has its own special immune cells: microglial cells.

Previous research has shown that microglial cells are activated in several neurological diseases, such as Alzheimer’s disease, Parkinson’s disease and stroke. People who are affected by these conditions also often fall into a negative mood. Other previous research has suggested that inflammatory processes also play a role in the development of depression. This led the researchers behind the new study to examine more closely whether microglial cells are involved in regulating mood during inflammation.

“The study showed that animals feel sick and uneasy when we activate the microglial cells. We demonstrate that two signal molecules, interleukin-6 and prostaglandin E2, are particularly important in these processes. It’s not surprising that these signal substances are central, but we were a bit surprised that it is the microglial cells that release these molecules,” says David Engblom, professor in the Department of Biomedical and Clinical Sciences (BKV) at Linköping University.

During inflammation, many processes are initiated in several cell types. One of the challenges in determining the role played by a specific cell type in the body, therefore, is to isolate its effects. In this study, the scientists used a technique known as chemogenetics, which enabled them to switch on the activity specifically in microglial cells in mice.

The researchers activated the microglial cells when the mice were being kept in a certain type of surroundings. The mice subsequently avoided this type of surroundings, which the researchers interpret as showing that the animals disliked the experience. The mice also became less interested in a sweet solution, which they normally find very tempting.

In order to investigate whether the microglial cells are an important link between the immune system and mood, the researchers investigated what happened when microglial cells are inhibited. When the microglial cells were not available for activation, the mice did not feel poorly, even when they had inflammation. This reinforces the idea that these cells are necessary for the process.

“Our results show that the activation of microglial cells is sufficient to create aversion and negative mood in mice. It’s natural to suggest that similar processes take place in several human diseases. It’s not unlikely that activated microglia contribute to the discomfort and depressed mood in people with inflammatory and neurological diseases,” says David Engblom.

If further research demonstrates that the biological mechanism described in the study functions in the same way in humans, it may be possible in the long run to reduce symptoms of depression by inhibiting this mechanism.​

Immune Cells in the Brain Are Behind the Depression Experienced in Inflammation - Neuroscience News

Microglia appear to play a key role in inflammation-associated depression.

neurosciencenews.com

 

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Researchers unlock the profound anti-inflammatory properties of cannabis*

by Mark Taylor | Benzinga | Aug 23 2019

A new study deciphers for the first time the cannabis plant's biological blueprint for producing two molecules thought to have anti-inflammatory properties, a discovery that could pave the way for expanded use of cannabis as medicine.

That study, which is published in the August 2019 issue of the journal Phytochemistry delineates for the first time the biosynthesis pathway outside of the actual cannabis sativa plant that allows reproduction of the molecules cannflavin A and cannflavin B.

Those cannflavins belong to the class of plant flavonoids, plant chemicals found in almost all fruits and vegetables, known as flavones, which occur in several plant lineages.

The study shows the medicinal versatility of the cannabis plant: Beyond the intoxicating ingredient THC and therapeutic oils that often contain cannabidiol (CBD), there exist many other specialized metabolites requiring further research.

The researchers at Guelph University in Ontario, Canada, unlocked the blueprint for producing the cannflavins, which were discovered in a 1985 study and were found to display “potent anti-inflammatory activity in various animal cell models.”

The new information in the Phytochemistry study opens a pathway to figure how to engineer plant metabolism to make medicine from the cannflavin A and B enzymes.

Tariq Ahktar, lead author and assistant professor of plant biochemistry at Guelph's Department of Molecular and Cellular Biology, told Weedmaps News that “for almost 30 years nobody touched these molecules or worked extensively on them. We thought it was a good time to look at these very promising molecules more closely.”

Ahktar said his laboratory utilizes plant chemistry and genomics to determine how plants produce certain molecules and compounds that have medicinal or industrial uses.

He said the cannaflavins A and B were discovered in the United Kingdom more than 30 years ago by researcher Marilyn Barrett. Her study also introduced the name cannflavin. Barrett's research also showed that cannflavins A and B have nearly 30 times the power of aspirin to inhibit inflammation in cells.

Yet that discovery is just the beginning. Ahktar explained that the two cannflavins are present in cannabis in very low amounts.

“So if you want to gain the anti-inflammatory benefits, you would have to consume copious amounts of cannabis, which is both unlikely and impractical,” he said, necessitating the need to reproduce the molecules outside of the cannabis plant.

He said cannflavins are “definitely encouraging news” for people suffering from acute and chronic pain, who have few effective alternatives to opioids, which work by blocking the brain's pain receptors. These cannflavins appear to take a different path by attacking cells that encourage inflammation, a primary cause of much pain.

Ahktar said that for decades American and Canadian researchers have been unable to research the medicinal properties of cannabis because of prohibitions against the cultivation and sale of the plant, still considered illegal by the U.S. federal government. Ahktar said his team has demonstrated a biochemical pathway for commercial producers to allow the production of cannflavins A and B from yeast, bacteria, plants, or other means.

“That way you don't have to grow huge fields of cannabis to obtain the benefits,” he said, noting that the Guelph researchers have patented the genes and licensed their research to Toronto-based Anahit International Corp., to biosynthesize those molecules.

The ability to “hack” other plants or microorganisms to produce their medicinal compounds offers great potential benefits to science and industry. Dr. Jeff Chen, Director of the University of California, Los Angeles (UCLA) Cannabis Research Initiative, spoke at the July 2019 Microscopes and Machines conference in Los Angeles about using biosynthesis as an alternative that is more scalable, consistent and continuous than plant farming to produce cannabinoids and other beneficial compounds.

Chen cautioned that science has a long way to go to find the most efficient method of producing the cannabinoids and other beneficial compounds. Patients, however, haven't been waiting.

Ahktar said he spoke with many patients who used cannabis successfully to treat a range of conditions and swore it improved their pain levels and reduced inflammation.

“That got me thinking that there is something else besides CBD contributing to these benefits and it didn't take me long to find Barrett's research,” he said. “My primary focus is to help people with pain.”

Ahktar cautioned that “we are a long way from being able to offer cannflavin products on store shelves. This is not my business or interest. I don't know if this would be marketed as a natural product or undergo clinical trials for drug testing.”

As researchers focus on how cannabis can be used to relieve pain, they're also gaining new insights about the process of inflammation.

He said today neither researchers nor consumers can purchase pure cannflavins A and B.

“Now that we have a mechanism for reproducing this, we can start producing it and performing side by side comparisons with existing pain relievers and test their relative efficacy.”

The study comes amid an ongoing opioid crisis in the United States. According to the U.S. Centers for Disease Control and Prevention (CDC), U.S. healthcare providers prescribed more than 214 million prescriptions for opioid pain in 2016, with an estimated 11 million people misusing prescription opioids that year. More than two-thirds of the 63,632 drug overdose deaths in 2016 involved prescription or illicit opioids. From 1999 to 2017, almost 218,000 people died in the United States from overdoses related to prescription opioids.

Gregory Gerdeman, chief scientific officer for the St. Petersburg, Florida-based medicinal cannabis cultivator 3 Boys Farm and a neuroscientist who has studied the effects of cannabis on the brain for 22 years, said the takeaway from the study is that herbal cannabis takes a multifaceted approach to combating inflammation and that it may offer a greater therapeutic value than the THC or CBD alone.

“It also may point to potential drug development,” Gerdeman said. “I believe in herbal cannabis as a medicine. I think it already offers a very promising strategy for replacing opioids. We now know how the plant synthesizes cannflavins A and B and we're living in an age in which pharmaceutical companies are creating genetically modified cannabis that could allow drug factories to reproduce these molecules outside of the cannabis plant. This study shows how the science of cannabis as a medicine is being taken seriously today in the medical and pharmaceutical worlds. It was not that way in 1997 or even in 2007.”

He called cannabis the “queen of medicinal plants,” adding, “We have many secrets yet to learn from her.”

Gerdeman cautioned, however, that the Canadian study did not explore the precise role of cannflavins A and B in fighting inflammation or the molecules' potential therapeutic effects.

“The assertion from a 30-year-old study that these cannflavins offer anti-inflammatory effects 30 times the strength of aspirin requires much more research and study to validate. It would be premature to say that using isolated cannflavins as a drug would be desirable or without safety concerns.”

*From the article here :

Researchers Unlock What Gives Cannabis Its Anti-Inflammatory Qualities

A new study deciphers for the first time the cannabis plant's biological blueprint for producing two molecules thought to have anti-inflammatory properties, a discovery that could pave the way for expanded use of cannabis as medicine.

finance.yahoo.com

 

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Is the Gut the Driving Force of Systemic Inflammation?

Robert Martindale, MD, PhD, works in the ICU as a general and trauma surgeon. In this video Martindale discusses inflammatory-based diseases (heart disease, cancer, chronic respiratory disease, diabetes) as a global burden.​

 

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Toronto man treats Guillain-Barré syndrome with psilocybin mushrooms*

by Sam Riches | Regina Leader-Post | 22 Mar 2021

Guillain-Barre syndrome is a rare inflammatory disorder in which your body's immune system attacks the nerves. Weakness and tingling in your extremities are usually the first symptoms. These sensations can quickly spread, eventually paralyzing your whole body.

Michael Reynolds knew he was in trouble when he started losing the feeling in his fingertips. A musician and multi-instrumentalist, Reynolds had recovered from a case of Guillain-Barré syndrome, a disorder where the immune system attacks the nervous system, about a decade earlier.

Reynold’s initial case led to a five-week hospital stay, followed by six months in a wheelchair, and lasting nerve damage. He was treated with intravenous injections of immunoglobulins — proteins produced by the immune system that attack infecting organisms — and physiotherapy.

After several months of treatment, he made a significant recovery. But then the numbness in his hands returned.

He started cancelling gigs as his condition quickly worsened. Within a week he had almost no feeling left in his fingers. “It was affecting my playing really severely,” Reynolds tells The GrowthOp. “My drumsticks were flying out of my hands. I was very, very worried.”

Frustrated by traditional treatments and previous health care experiences, Reynolds started researching natural remedies. He’d had success using medical cannabis to manage pain symptoms in the past, so when a friend on Facebook suggested he try psilocybin, the ingredient in magic mushrooms, he decided to give it a shot.

After consuming his first dose of psilocybin, the feeling in his fingers started to return. So he took them again the next day, and then again the next day. Each time, he consumed about a gram and a half of mushrooms, a relatively low dose.

“Then it pretty much resolved,” he says. “My hands had full gripping strength. I had a proper feeling in my hands again.”

Since then, he’s managed his symptoms with a few annual doses of psilocybin, he says. He does not have a legal medical exemption, so he’s reliant on sourcing the mushrooms from the illicit market.

At a psychedelics conference several years ago, Reynolds shared his story and asked if anyone was aware of any research regarding psilocybin’s impact on Guillain-Barré syndrome. He wasn’t surprised to hear the answer was no.

“It’s a very niche thing,” he says. “And there’s not a lot of research on it.”

However, afterward, he was approached by a man with terminal cancer who was also taking psilocybin medicinally and growing his own supply. “He didn’t really have a long time left so he was just growing them and giving them to people for free,” Reynolds says.

The man offered Reynolds some of his mushrooms but that supply has since run out. He expresses some frustration about having to acquire psilocybin on the illicit market but he’s had continued success with the therapy.

“The world needs to know that this works,” he says.

Guillain-Barré syndrome is a relatively rare disorder with many unknowns. Most who develop GBS make a full recovery but some symptoms, like vision issues and difficulty swallowing, can persist. In severe cases, it can lead to respiratory failure and death.

According to the National Institute of Neurological Disorders and Stroke, GBS affects about one person in 100,000 each year and can occur at any age.

The cause of the disease is unknown and there is no known cure, though cases usually follow a respiratory or gastrointestinal viral infection.

A study published in the journal Pathogens late last year cited the only known case of COVID-19 triggering a recurrence of GBS, but there have been many reports of an association between COVID-19 and the disorder.

Dr. Michael Verbora is the medical director at Field Trip Health, a Toronto-based company that develops and delivers psychedelic therapies. He hasn’t used psilocybin to treat GBS clinically or encountered it in medical literature, but he says he’s not surprised to hear it could provide relief from symptoms of GBS.

“There are very good plausible mechanisms by which a disease like Guillain-Barré could get better through a psychedelic drug that has anti-inflammatory and antioxidant effects in the brain,” he says. “There’s not a lot of research on it but it makes a lot of sense to me.”

Dr. Verbora compares Guillain-Barré to multiple sclerosis in that both diseases eat away at the nerve lining, though GBS patients recover, and multiple sclerosis is a chronic condition.

“Inflammation takes place in the brain and it’s an immune reaction. And the proteins, the myelin sheath on the nerve cells, get digested and it affects your whole nervous system,” Dr. Verbora says. “So your peripheral nervous system doesn’t work. You can get sensory changes and motor changes. You can get paralyzed from the neck down.”

"Theoretically, through its anti-inflammatory properties, psilocybin could reduce inflammation in the brain and counteract the effects of an autoimmune reaction like Guillain-Barré Syndrome," Dr. Verbora explains.

He adds that he knows patients with Guillain-Barré who find cannabis, and its anti-inflammatory properties, to be helpful.

“It has similar anti-inflammatory effects on the brain tissue,” he says. “But again, unfortunately, the gap in knowledge and research is still there with these plants and botanicals.”

"Field Trip is actively researching treating inflammatory issues with psilocybin," he says, "along with a number of autoimmune conditions that might benefit from psilocybin and similar drugs."

“Guillain-Barré is probably not going to go anywhere. So it would be really interesting to study, not just this, but any type of neurological disorder,” he says. “It’d be really interesting to know if these anti-inflammatory molecules on the brain have long-term therapeutic effects.”

Reynolds says it’s been several months since his last dose of psilocybin. In addition to treating his GBS, he says psilocybin has also helped to ‘“significantly lessen” his Tourette syndrome.

“The thing that I hope people realize is that there are some neurological uses for psilocybin that they need to look into,” he says.

To his frustration, his own doctor, who he sought out because he wrote a book about natural remedies, appeared unmoved by his experience with psilocybin.

“He didn’t really respond,” Reynolds says, adding that he "didn’t press further on the subject as he feared his quality of care might drop."

Until the medical community offers a better treatment option, Reynolds plans to continue consuming small amounts of mushrooms a few times a year. Since 2016, he says he hasn’t involved a doctor in his treatment of the disorder.

“Guillain-Barré is one of those things where it’s rare enough that there’s no priority on it at all,” he says. “I just want people to know. This is too important to keep to myself.”

*From the article here :

This Toronto man is treating a rare neurological disorder with psilocybin mushrooms

Guillain-Barré syndrome, a disorder where the immune system attacks the nervous system, has no known cause or cure.

leaderpost.com

 

[mr peabody]

Sunflower extracts were to some extent used in traditional medicine for their
anti-inflammatory and analgesic properties.

Sunflower seed peptide could treat pain, inflammation

Medical University of Vienna | NeuroscienceNews | 28 June 2021

Summary: Synthetically optimizing a peptide commonly found in sunflower seeds could help provide relief for gastrointestinal pain and inflammation, a new study reports.

A naturally occurring peptide in sunflower seeds was synthetically optimised and has now been identified as a potential drug for treating abdominal pain or inflammation (in the gastrointestinal tract, abdominal area and/or internal organs).

That is the finding of an international study led by Christian Gruber from MedUni Vienna’s Institute of Pharmacology (Center for Physiology and Pharmacology), which was conducted jointly with the University of Queensland and Flinders University in Australia and has now been published.

The scientific aim of the study is to find analgesics that are only active in the periphery and do not cross the blood-brain barrier, as an alternative to commonly used synthetic opioids.

Gruber explains the background: “Morphine was one of the first plant-based medicines and was isolated from the dried latex of poppies more than 200 years ago. It binds to opioid receptors in the brain and is still regarded as the main pillar of pain therapy. However, there is a high risk of opioid addiction, and an overdose — as a result of this strong dependency — inhibits the breathing centre in the brain, which can result in respiratory depression and, in the worst case, in death.”

For this reason, researchers throughout the world are trying to make analgesics safer and to find active drug molecules that do not have the typical opioid side-effects.
Sunflower extracts were to some extent used in traditional medicine for their anti-inflammatory and analgesic properties. In the current study, the scientists from Austria and Australia, primarily PhD student Edin Muratspahic, isolated the plant molecule that may be responsible for this effect.

Medicinal chemistry methods were then used to optimise the so-called sunflower trypsin inhibitor-1 (SFTI-1), one of the smallest naturally occurring cyclic peptides, by ‘grafting’ an endogenous opioid peptide into its scaffold.

A total of 19 peptides were chemically synthesized based on the original SFTI-1 blueprint and pharmacologically tested.

“One of these variants turned out to be our lead candidate for as potential innovative analgesic molecule, especially for pain in the gastrointestinal tract or in the peripheral organs. This peptide is extremely stable, highly potent and its action is restricted to the body’s periphery. Its use is therefore expected to produce fewer of the typical side-effects associated with opioids,” point out Gruber and Muratspahic.

The mode-of-action of the peptide is via the so-called kappa opioid receptor; this cellular protein is a drug target for pain relief, but is often associated with mood disorders and depression.

The sunflower peptide does not act in the brain, hence there is much less risk of dependency or addiction. Furthermore, it selectively activates only the molecular signalling pathway that influences pain transmission but does not cause the typical opioid side-effects.

The data of the animal model in the current study are very promising: the scientists see great potential for using this peptide in the future to develop a safe medication — which could be administered orally in tablet form — to treat pain in the gastrointestinal tract, and this drug could potentially also be used for related painful conditions, e.g. for inflammatory bowel disease.

Using Nature’s blueprint

The research of this MedUni Vienna laboratory led by Christian Gruber exploits the concept of using Nature’s blueprint to develop optimised drugs.

“We are searching through large databases containing genetic information of plants and animals, decoding new types of peptide molecules and studying their structure, with a view to testing them pharmacologically on enzymes or membrane receptors and ultimately utilizing them in the disease model,” explains Gruber.

Finally, potential drug candidates are chemically synthesised in a slightly modified form based on the natural blueprint, to obtain optimised pharmacological properties.

Drug Relieves Persistent Daydreaming, Fatigue, and Brain Sluggishness in Adults With ADHD - Neuroscience News

Lisdexamfetamine, a drug known to stimulate brain activity, reduces symptoms of sluggish cognitive tempo in adults with ADHD.

neurosciencenews.com

 

[mr peabody]

Scientists find link between Bipolar Disorder and Neuroinflammation

by Ed Cara | GIZMODO | 4 Mar 2021

Scientists may be closer to understanding how the brain can function differently in people who have bipolar disorder. In a new study, researchers say they’ve found evidence that certain brain cells trigger inflammation more easily in those who have bipolar disorder, and that these wayward cells can be linked to decreased neural activity that could be harmful to our mental health. The findings, published on Thursday in Stem Cell Reports, could hint at a new way to treat bipolar disorder someday, though more research is still needed.

Scientists have been studying the connection between inflammation and mental illness for some time, including bipolar disorder. People with bipolar disorder experience uncontrollable mood swings that can leave them severely depressed one moment and manic the next. People with bipolar disorder are known to be more likely to have other conditions associated with chronic inflammation, such as hypertension and diabetes. Some studies have also shown that bipolar disorder patients can have higher levels of proteins that goad the body into becoming inflamed, especially when they’re in the middle of a manic episode. These proteins include interleukin 6 (IL-6), which plays many roles in the body, such as guiding the body’s acute response to infection.

In their new study, researchers at the Salk Institute for Biological Studies, the University of California, San Diego, and the Institute of Psychiatry and Neuroscience of Paris decided to look at a specific type of brain cell, the astrocyte. These are star-shaped cells in the brain that carry out a number of important functions that help support neurons. One of these functions include being part of the chain of command that triggers inflammation in the brain and surrounding nervous system, which is meant to help the brain respond to injury or infection. The researchers theorized that this generally useful process can go awry in people with bipolar disorder, and that astrocytes can have a part in this dysfunctional inflammation.

“Due to a growing understanding of the role of neuroinflammation in psychiatric disorders, we asked whether altered inflammation-driven signaling in astrocytes was associated with bipolar disorder,” study author Fred Gage, president of the Salk Institute for Biological Studies, said in an email.

Gage and his team used stem cells derived from six people with bipolar disorder as well as four controls without bipolar disorder, then had them develop into astrocytes that were studied in the lab. (They had figured out how to create these cells from earlier research.) Compared to the control group, the astrocytes from patients with bipolar disorder were noticeably different. The cells had higher expression of their IL-6 gene and as a result, they secreted more IL-6 than the control astrocytes. When they exposed neurons to these astrocytes, the team saw decreased levels of neural activity, compared to the astrocytes from the controls. And when the researchers introduced an antibody that suppressed IL-6 into the mix, the neurons were less hampered by the astrocytes, further implicating IL-6. Lastly, the blood of bipolar disorder patients also contained more IL-6 than controls.

“Our study suggests that normal function of astrocytes is affected in bipolar disorder patients’ brains, contributing to neuroinflammation,” co-author Renata Santos, a researcher at the Salk Institute as well as the Institute of Psychiatry and Neuroscience of Paris, said.

The findings are certainly intriguing, but the researchers warn there’s still a long road to go before we can confirm a clear, causal link between impaired astrocytes, IL-6, and bipolar disorder, much less something that could lead to meaningful new treatments. Lab-grown astrocytes might be different from those found in our brain in important ways, for instance. (One difference is that these cells are less mature.) And since the brain is plenty complicated, there are likely other aspects of our biology, including in the brain, that could play an important role in causing bipolar disorder.

“Our findings elucidate aspects of the understudied role of astrocytes in neuroinflammation in psychiatric disorders, with relevance for altered IL-6 and inflammatory signaling in bipolar disorder patient astrocytes,” lead author Krishna Vadodaria, a research associate at the Salk Institute, said.

Scientists Find Link Between Bipolar Disorder and Neuroinflammation

Scientists may be closer to understanding how the brain can function differently in people who have bipolar disorder. In a new study, researchers say they’ve found evidence that certain brain cells trigger inflammation more easily in those who have bipolar disorder, and that these wayward cells...

gizmodo.com

 

[mr peabody]

Rapid antidepressant effects of Ayahuasca apparently related to its anti-inflammatory activity*

by Eric Dolan | PsyPost | 18 Feb 2021

The antidepressant effects of the psychedelic brew known as ayahuasca appear to be related to anti-inflammatory activity, according to new research from scientists in Brazil. Their findings, published in the Journal of Psychopharmacology, provide new insights into the biological mechanisms behind the observed antidepressant effects of the substance.

Ayahuasca, a concoction used for centuries by indigenous Amazon tribes, contains the powerful psychedelic drug dimethyltryptamine (DMT) and monoamine oxidase inhibitors. The brew is typically prepared using leaves from the Psychotria viridis shrub and the bark of the Banisteriopsis caapi vine.

The authors of the new study were interested in examining the effects of alternative treatments such as ayahuasca because of the widespread prevalence of depressive disorders.

“Major Depression Disorder (MDD) is one of the most prevalent mood disorders, reaching about 350 million people worldwide. One third of patients with depression do not show a satisfactory response to antidepressants leading to a large proportion of patients developing recurrent MDD with multiple depressive episodes,” said study author Nicole Leite Galvão-Coelho, a professor at the Federal University of Rio Grande do Norte.

In the study, the researchers briefed 28 patients with treatment-resistant depression and 45 healthy controls about the physiological and psychological effects associated with ayahuasca. The participants were then randomly assigned to received either a single oral dose of ayahuasca or a placebo substance.

The placebo substance was a brownish liquid that mimicked the look and taste of ayahuasca. In addition, the placebo contained zinc sulphate, which induces nausea — a common side effect of ayahuasca.

After consuming their dose, the participants stayed in a comfortable room at a hospital for about six hours, where they listened to curated music playlists.

The researchers collected and analyzed blood samples from the participants immediately before dosing and again two days later. They were particularly interested in two blood inflammatory biomarkers: C-reactive protein and interleukin 6.

Galvão-Coelho and her colleagues observed significant antidepressant effects among patients who received ayahuasca. These improvements in depressive symptoms were associated with reductions in inflammation.

Patients with treatment-resistant depression tended to have higher C-reactive protein levels compared to the control group at baseline. The researchers found that C-reactive protein levels were reduced in both patients and healthy controls 48 hours after consuming ayahuasca, but not after consuming the placebo.

“Besides changes in emotions, MDD also induces biological changes. A better comprehension of these biological changes can help in the development of more efficient treatments. For instance, treatment-resistant depression has been associated with mild chronic systemic inflammation. In this study, a single dose of ayahuasca, and not the placebo, reduced both depressive symptoms and systemic inflammation of treatment-resistant depressive patients two days after the treatment,” Galvão-Coelho told PsyPost.

“The commercial antidepressants when work spend about 15 days to start the first effects on reduction of depressive symptoms. Regarding their anti-inflammatory action there is not a consensus of how they are acting.”

Patients and controls showed similar levels of interleukin 6 at baseline and there was no change after treatment.

“Although ayahuasca does not lead to compulsive drug-seeking behaviors or induce physiological toxicity, it does induce acute and mild sympathetic activity. Therefore, patients with cardiovascular disease and who have mania or psychosis must not use it,” Galvão-Coelho cautioned.

“The next step in this field is to test multiple sessions of ayahuasca associated with psychotherapy as treatment for depression. The studies with psychedelics for mental disorders have shown promising results, but we need a bit more understanding to turn them into an accessible treatment.”

The study, “Changes in inflammatory biomarkers are related to the antidepressant effects of Ayahuasca“, was authored by Nicole Leite Galvão-Coelho, Ana Cecília de Menezes Galvão, Raíssa Nóbrega de Almeida, Fernanda Palhano-Fontes, Isaac Campos Braga, Bruno Lobão Soares, João Paulo Maia-de-Oliveira, Daniel Perkins, Jerome Sarris, and Draulio Barros de Araujo.

*From the article here :

Rapid antidepressant effects of the psychedelic ayahuasca linked to changes in inflammatory biomarkers

The antidepressant effects of the psychedelic brew known as ayahuasca appear to be related to anti-inflammatory activity, according to new research from ...

www.psypost.org

 

[mr peabody]

Hemp oil for pain, inflammation*

by Debra Rose Wilson, Ph.D. | MedicalNewsToday | 14 Feb 2019

Many people use hemp or CBD oil as a form of natural pain relief, especially if the pain is a result of inflammation.

Those who do not want to take over-the-counter or prescription pain medications may turn to a high-quality hemp oil for relief.

A 2018 review notes that CBD, one of the main compounds in full-spectrum hemp oil, and other cannabinoids show promise for the treatment of many types of pain.

There is very little risk of intoxication from hemp oil as all forms of hemp oil come from food-grain strains of hemp. The authors of a study in the journal Cannabis and Cannabinoid Research note that food-grain strains of hemp must contain less than 0.3 percent tetrahydrocannabinol (THC). THC is the compound that causes the so-called “high” of marijuana.

Hemp oil is not the same as cannabidiol (CBD) oil. The production of CBD oil uses the stalks, leaves, and flowers of the hemp plant, which contain a higher concentration of CBD, another potentially beneficial compound in the plant.

Hemp seed oil comes from the small seeds of the Cannabis sativa plant. The seeds do not contain the same levels of compounds as the plant itself, but they still have a rich profile of nutrients, fatty acids, and useful bioactive compounds.

Full-spectrum hemp oil that also contains plant matter may add other effective compounds, which may help with certain health issues, such as inflammation.

Takeaway and future research

The research on hemp oil is still relatively new, particularly in the United States and other places where restrictive laws have prevented researchers from fully exploring the potential of cannabis plants until recently.

As CBD comes into more common use in an increasing number of areas, research into the potential benefits of full-spectrum hemp oil may expand. As a result, scientists may find more evidence to support the potential benefits of the plant or even reveal new benefits. In any case, the future of research on hemp oil looks promising.

There is also still a small risk of THC getting into the system, even from hemp seeds, which normally contain no THC. The THC could be present as a result of contamination with other plant matter. The results of a 2017 study show that some commercial brands of food-grade hemp seeds can have a THC concentration that is as much as 1,250 percent higher than the legal limit.

It is essential to ensure that hemp seed oil comes from a reliable manufacturer. The seeds and oil should be free of plant matter that may add additional compounds, such as THC.

*From the article here :

What are the best hemp oil benefits?

The potential benefits of hemp oil include improved heart, skin, and brain health. Research is ongoing, and it might uncover additional benefits. Learn more about the benefits of hemp oil here.

www.medicalnewstoday.com

 

[mr peabody]

Is inflammation the driver of Alzheimer’s?*

Science News | May 2 2018

A new research study by scientists in Australia and the US provides an explanation for why clinical trials of drugs reducing proteins in the brain that were thought to cause dementia and Alzheimer's have failed. The study has opened the way for potential new treatments with existing drugs.

Published online in the journal Human Molecular Genetics, the researchers assembled evidence from a wide range of human studies and animal models of dementia-related diseases to show that inflammation is a major cause, not just a consequence.

They show that many genes linked with dementia regulate our susceptibility and response to inflammatory damage.

"For decades, scientists have thought that dementia and Alzheimer's Disease are caused by protein aggregates forming in the brain. But recent clinical trials of drugs that reduce the aggregates have failed," says project leader Professor Robert Richards, from the University of Adelaide's School of Biological Sciences. He is working in collaboration with the University's Adelaide Medical School and the National Institutes of Health, in the US.

Inflammation has long been known to increase as dementia-related diseases progress, but only now is it identified as the cause. Previously it was thought to act simply to clean up tissue damage caused by the protein aggregates.

"We know that inflammation has different phases -- early on it can be protective against a threat by actively degrading it, but if the threat is not removed, then persistent inflammation actually causes cell death," says Professor Richards.

The new work turns previous thinking around. The genetic linkages imply that the inflammation comes first -- and the tissue damage second.

"Many genes linked with dementia operate at the level of controlling cellular inflammation. Both internal and external triggers interact with these genes to play a part. Inflammation is the point through which many triggers converge," says Professor Richards.

He likens the brain inflammation to a virus infection. "Inflammation is a very effective defence against foreign agents like viruses. But as we get older and accumulate mutations, our cells can make proteins and DNA products that mimic viruses, and these build up in the system," he says.

"Normally, our cells bar-code their own products to tell them apart from foreign agents. When these bar-codes aren't in place, our cells can't properly distinguish 'self' and 'non-self' trigger molecules. The result is inflammation that escalates and spreads -- hence the term autoinflammatory disease."

Certain types of gene mutation cause these systems to fail earlier or more often, and can increase as we age -- possibly accounting for age-related increased risk of developing dementia.

The good news is that by reducing some elements of inflammation, it may be possible to reduce dementia symptoms.

"With this new understanding of the disease, we now need to test existing anti-inflammatory drugs for their effectiveness in treating dementia," he says.

*From the article here:

New leads on treating dementia and Alzheimer's

A new research study provides an explanation for why clinical trials of drugs reducing proteins in the brain that were thought to cause dementia and Alzheimer's have failed. The study has opened the way for potential new treatments with existing drugs.

www.sciencedaily.com

 

[mr peabody]

Anti-inflammatory and antidepressant effects of psychedelics

Psychedelics represent a new and emerging class of therapeutics for psychiatric diseases such as depression, anxiety, and substance use disorder, among others. Additionally, psychedelics are potent anti-inflammatory agents. The mechanisms underlying these therapeutic effects remain unknown. Preclinical models of asthma and cardiovascular disease have been utilized to investigate anti-inflammatory effects of psychedelics, and have shown potent effects on several aspects of immune system modulation from suppression of proinflammatory cytokines to inhibition of T-cell activation and recruitment. Our data suggest that sub-behavioural levels of certain psychedelics represents a new, steroid-sparing, small molecule strategy for the treatment of peripheral inflammatory related diseases. On the psychiatric front, we have developed a new rat experimental system that recapitulates the long-lasting antidepressant-like effects of psilocybin. In this system, a single administration of psilocybin leads to persistent normalization of stress-induced hippocampal dysfunction relevant to depression and other psychiatric conditions.

Speaker Bio: Dr. Charles Nichols earned his BS at Purdue University, his PhD at Carnegie Mellon University studying developmental neurogenetics in Drosophila melanogaster, and performed his postdoctoral work at Vanderbilt University School of Medicine, Department of Pharmacology, researching mammalian serotonin 5-HT2 receptor neuropharmacology. His research has focused on 5-HT2A receptors and psychedelics for the past 24 years, where he has made several key discoveries. These include identification of specific populations of cell types within the brain that directly respond to psychedelics, the development of animal models to study the antidepressant-like effects of psilocybin, and discovery of the potent anti-inflammatory effects of psychedelics. He is currently a Professor in the Department of Pharmacology and Experimental Therapeutics at LSU Health Sciences Center in New Orleans.​

 

[mr peabody]

8 natural supplements to help fight inflammation

by Zawn Villines | MedicalNewsToday | 15 Aug 2019

Inflammation is the body’s response to irritation, infection, and injury. Short term inflammation protects the body, while chronic inflammation can lead to long term pain and damage, such as in arthritis.

Anti-inflammatory medications help fight pain and chronic inflammation.

However, these drugs are not safe for everyone, and extended use can lead to complications and side effects.

Some natural supplements may help fight inflammation, although not all supplements work for every type of inflammation.

In this article, we describe some of the most effective anti-inflammatory supplements that people may wish to try, depending on the cause of their inflammation.

1. Omega-3 fatty acids

Omega-3 fatty acids, which are abundant in fatty fish such as cod, are among the most potent anti-inflammatory supplements.
These supplements may help fight several types of inflammation, including vascular inflammation. Vascular inflammation is a significant risk factor for heart disease and heart attack.

In one study of 250 people with pain from degenerative disc disease, 59% of the participants were able to substitute fish oil for nonsteroidal anti-inflammatory drugs (NSAIDs).

The right dosage varies with the potency of the supplement. Some products come in pill form, while other manufacturers sell omega-3s as an oil. When using these products, people should always follow the instructions on the packaging.

Like many prescription anti-inflammatory medications, omega-3 fatty acids and fish oil may increase the risk of bleeding. People with bleeding disorders and those taking blood thinners should not use this supplement.

Omega-3 fatty acids are available to purchase online.

2. Curcumin

Curcumin, which is an active ingredient in turmeric, is a plant in the ginger family. Animal studies have suggested that it may help reduce inflammation to speed up wound healing and even reduce cancer risk.

A 2011 study also found that curcumin may help reduce inflammation from obesity-related metabolic conditions. Curcumin altered several inflammatory pathways, reducing insulin resistance, hyperglycemia, and hyperlipidemia.

A typical dosage of curcumin is 400–600 milligrams (mg) three times daily.

Although it is safe to take curcumin with low doses of NSAIDs, higher doses may increase the risk of bleeding. Curcumin also increases the risk of bleeding in people taking blood thinners and those with bleeding disorders.

Curcumin is available to purchase online.

3. S-adenosylmethionine

S-adenosylmethionine (SAM-e) is a substance that the body creates naturally. It plays an important role in the epigenetic regulation of genes.

Epigenetic factors affect gene expression and behavior, turning some genes on or off and changing the effect of others.

Doctors sometimes recommend SAM-e to manage symptoms of depression, osteoarthritis, and certain liver conditions, as inflammation may play a role in each of these.

A handful of clinical trials have suggested that SAM-e may help relieve the pain and inflammation associated with various types of arthritis — sometimes as well as NSAIDs can.

The right dosage depends on the condition a person has. For example:​

• A person may take 200–800 mg twice per day for fibromyalgia.​
• A person may take 800–1,600 mg twice per day for depression.​
• A person may take 600–1,200 mg three times per day for osteoarthritis.​

SAM-e may interact with a wide range of drugs, so people must not take it without first consulting a doctor.

At high doses, SAM-e may cause vomiting, diarrhea, gas, and nausea, so people must not exceed the recommended dose.

SAM-e supplements are available to purchase online.

4. Zinc

Some research suggests that zinc is a potent anti-inflammatory that may support the immune system and reduce several markers of inflammation.

According to a 2014 paper, zinc decreased inflammation and oxidative stress among older adults. Oxidative stress triggers inflammation and may increase the risk of a host of conditions, including cancer.

Zinc also reduced the rate of infections by 66%.

People with zinc deficiency are more likely to have arthritis, suggesting a link between zinc deficiency, inflammation, and pain.

The usual daily dosage of zinc supplements is 11 mg for men and 8 mg for women. Taking more than 40 mg per day can be dangerous.

Zinc may interact with calcium, diuretics, and certain antibiotics, so people must talk to a healthcare provider before trying this supplement.Zinc supplements are available to purchase online.

5. Green tea

Doctors have long suspected that green tea may fight inflammation, because people who live in regions that consume more green tea have lower rates of inflammation-related illnesses.

Research suggests that green tea may inhibit the production of certain inflammatory chemicals. It may also help slow cartilage loss, reducing the symptoms of arthritis.
Most doctors recommend drinking three or four cups of green tea per day, or taking 300–400 mg of green tea extract daily.

Green tea contains caffeine, so it is not safe for those who are sensitive to caffeine. The caffeine may cause stomach problems such as diarrhea.

Some companies make decaffeinated green tea, but researchers do not yet know if this type of green tea is effective for reducing inflammation.

Green tea extract is available to purchase online.

6. Frankincense

Boswellia serrata resin, or frankincense, can ease both inflammation and pain.

It may also help reduce cartilage loss and reverse autoimmune symptoms. It is a fast acting supplement that may help with osteoarthritis pain in just 5 days.

The usual dosage is an extract containing 30–40% boswellic acids, which a person takes in 300–500 mg doses two to three times per day.

Combining frankincense with curcumin may increase its potency, and some research has found that people tolerate this combination better than the NSAID diclofenac.

Frankincense is typically safe, with few side effects. However, some people report stomach pain and gastrointestinal problems such as diarrhea.

Frankincense supplements are available to purchase online.

7. Capsaicin

Capsaicin is the ingredient that gives hot peppers their heat. Substance P, a key component of capsaicin, may reduce the body’s ability to feel and transmit pain.

Some research suggests that capsaicin may help with both nerve and muscular pain.

Several manufacturers offer capsaicin creams that people can apply directly to painful areas. Capsaicin supplements may also help. Again, people taking these should follow the directions on the packaging.

Capsaicin can irritate the skin and eyes, so it is essential to wash the hands thoroughly after use.

Capsaicin supplements are available to purchase online.

8. Cat’s claw

Cat’s claw comes from various uncaria plants, including Uncaria tomentosa and Uncaria guianensis.

Research suggests that cat’s claw may reduce various forms of inflammation. It is especially effective at inhibiting TNF-alpha, an inflammatory chemical in the body.

If using cat’s claw tea, a person may drink a ratio of 1,000 mg of root bark to 8 ounces of water. It is also safe to consume as a powder in capsule form, in daily dosages of 20–60 mg.

Although cat’s claw is generally safe, two case reports suggest that it may cause kidney failure in people with lupus. It may also cause nausea, though some studies suggest that it may also help stomach pain from the NSAID indomethacin.

Cat’s claw supplements are available to purchase online.

Other options

Anti-inflammatory supplements do not work for everyone. In almost all cases, these supplements take time to reverse inflammation.
So, people who need immediate pain relief may want to try other options, either in addition to or instead of anti-inflammatory supplements. Some options include:​

• Over-the-counter (OTC) anti-inflammatory drugs: Medications such as ibuprofen, acetaminophen, and aspirin can help with inflammation-related pain. They may also reduce the swelling of a recent injury.​
• Prescription anti-inflammatory drugs: A wide range of prescription medications can help with inflammation and pain.​
• Anti-inflammatory diet: Some people focus on eating foods that reduce inflammation, while others avoid those that may trigger inflammation. Fried foods, soda, refined carbohydrates, and red meat may cause inflammation, while nuts, blueberries, strawberries, olive oil, tomatoes, and leafy green vegetables may help fight it.​

Summary

Natural anti-inflammatory supplements can help the body fight pain and inflammation. They may even prevent some of the long term complications of chronic inflammation, such as cancer.

Before trying a new anti-inflammatory treatment, even a natural one, it is important to consult a doctor. Natural remedies are often potent medicine that can cause side effects and interact with other drugs.

When they work, however, they may reduce the need to take prescription or OTC medications.

8 natural supplements to help fight inflammation

Inflammation is the body’s defense mechanism, but it can be painful and damaging when chronic. As well as medication, people can try natural supplements to relieve inflammation. Learn more here.

www.medicalnewstoday.com

 

[mr peabody]

iAge: Predicting health based on your “inflammatory age”

Age ain't nothing but a number, but "inflammatory age" may be real.

by Robby Berman | BIG THINK | 16 July, 2021​

• Stanford scientists have found a more accurate way to measure a person's biological age based on a blood protein marker.​
• The marker indicates a person's level of inflammation, which is the driver of many age-related conditions.​
• A person's "iAge" more accurately predicts their health than their chronological age.​

According to biologist David Furman of Stanford University, "Every year, the calendar tells us we're a year older. But not all humans age biologically at the same rate. You see this in the clinic — some older people are extremely disease-prone, while others are the picture of health."

Some have suggested that our epigenome — the sum total of the chemical changes to our DNA — can determine our biological age and predict how soon we are likely to have serious age-related health issues.

Now, Stanford scientists have discovered a different way of ascertaining our future expiration dates: the "inflammatory-aging clock" (iAge). Determining someone's iAge is not only far simpler than performing epigenetic tests. It can also help individuals and their physicians anticipate and confront health issues before they happen.

Good and bad inflammation

One of the things that distinguishes people who remain healthy longer from others is the strength of their immune system.

One of the immune system's primary tools is acute inflammation. This is a "good" process because it is the body's localized, protective response to things like tissue damage, invasive microbes, or metabolic stress. Importantly, it is a short-term response that lasts only as long as needed for the immune system to finish its job.

On the other hand, long-term, system-wide inflammation is "bad." This form of inflammation causes organ damage and is associated with aging. It makes a person vulnerable to a whole range of conditions, including heart attacks, cancer, strokes, arthritis, cognitive decline, depression, and Alzheimer's.

Understanding inflammation as a measure of age

Furman is the director of the 1000 Immunomes Project, "the world's largest longitudinal population-based study of immunology and aging." As such, he had access to blood samples taken from 2009 to 2016 from 1,001 healthy people aged 8-96.

Artificial intelligence (AI) analysis of the samples allowed the researchers to identify protein markers in the blood that most reliably indicated a person's inflammation age. They identified a specific cytokine, CXCL9, as being especially useful. When processed by an algorithm the team devised, it produced a simple inflammation-age value. Comparing this to the patients' histories, it turned out to align with the health of their immune systems and subsequent encounters with age-related disease. CXCL9, produced by the inner lining of blood vessels, is associated with heart disease.

The researchers verified the validity of their system by measuring the iAge of people 65 and older who had had their blood drawn in 2010. When they followed up with these people in 2017, the scientists found that their 2010 iAge turned out to be a more accurate predictor of their health than their chronological age.

Finally, the researchers tested their iAge algorithm with 29 long-lived people from Bologna, Italy — only one of whom had not yet turned 100 — comparing them to 18 average 50-79-year-old individuals. The inflammatory age of all the Bolognese participants averaged about 40 years younger than their chronological age. Furman reports that one 105-year-old man had an inflammatory age of 25.
​

Tick tock

CXCL9 is easy to measure and may have significant clinical applications. Specifically, it highlights the value of addressing chronic inflammation as a way to increase longevity.

Most promisingly, a person's iAge could serve as an important early-warning system. Furman notes, "Our inflammatory aging clock's ability to detect subclinical accelerated cardiovascular aging hints at its potential clinical impact." He adds, "All disorders are treated best when they're treated early."

iAge: predicting health with your “inflammatory age”

Age ain't nothing but a number, but "inflammatory age" may be real.

bigthink.com

 

[mr peabody]

A medical diagnostic center. Experts believe chronic inflammation may damage DNA and lead to heart disease or cancer.

Chronic inflammation is dangerous. You may not even know you have it.

by Marlene Cimons | Washingto Post

People often learn they have it when by developing an autoimmune disease. But the ailment might also play a role with heart disease, cancer, other disorders.

Most of us think of inflammation as the redness and swelling that follow a wound, infection or injury, such as an ankle sprain, or from overdoing a sport, “tennis elbow,” for example. This is “acute” inflammation, a beneficial immune system response that encourages healing, and usually disappears once the injury improves.

But chronic inflammation is less obvious and often more insidious.

Chronic inflammation begins without an apparent cause — and doesn’t stop. The immune system becomes activated, but the inflammatory response isn’t intermittent, as it is during an acute injury or infection. Rather, it stays on all the time at a low level.

Experts think this may be the result of an infection that doesn’t resolve, an abnormal immune reaction or such lifestyle factors as obesity, poor sleep or exposure to environmental toxins. Over time, the condition can, among other things, damage DNA and lead to heart disease, cancer and other serious disorders.

“Unlike acute inflammation, which benefits health by promoting healing and recovery, chronic inflammation is characterized by persistent increases in inflammatory proteins all throughout the body and can damage health and promote several major diseases,” says George Slavich, associate professor of psychiatry and biobehavioral sciences at UCLA, referring to small proteins called cytokines that the immune system releases at the site of an injury to promote recovery.

“People typically don’t know that they have chronic inflammation until it’s too late,” he says.

Individuals often learn they have chronic inflammation when they develop an autoimmune disease, such as Crohn’s disease, lupus, or Type 1 diabetes, since inflammation is a hallmark of autoimmune disorders. But experts believe chronic inflammation also plays a role in developing heart disease, cancer, kidney disease, nonalcoholic fatty liver disease, neurodegenerative disorders, cognitive decline and mental health illnesses, such as depression, post-traumatic stress disorder and schizophrenia.

Scientists are still learning about why chronic inflammation is so dangerous and how it contributes to disease. Meanwhile, they suggest actions people can take to reduce their risk, specifically by changing certain behaviors.

Numerous factors appear to raise the risk of chronic inflammation, among them social isolation, psychological stress, disturbed sleep, chronic infections, physical inactivity, poor diet, obesity and exposure to air pollutants, hazardous waste products, industrial chemicals and tobacco smoke.

Experts believe individuals can reduce their risk by adopting lifestyle changes, including eating a healthy diet, improving sleep, exercising regularly, quitting smoking and finding ways to decrease stress and exposure to environmental pollutants.

“Diet is one of the key factors that influences inflammation in the body,” Slavich says. “Whereas fried foods, red meat, sodas, and white bread and pastries that have refined carbohydrates tend to increase inflammation, fruits, nuts, green leafy vegetables, tomatoes and olive oil tend to reduce inflammation. Therefore, while diet is not the only factor that can be targeted to improve immune health, it is an important one.”

Scientists think chronic inflammation causes oxidative stress in the body, which is an imbalance between the production of dangerous free radicals, molecules that harm healthy tissue in the body, and antioxidants, substances that clean up waste products and neutralize them. This can damage DNA as well as proteins and fatty tissue, which in turn accelerates biological aging.

“Chronic inflammation is involved in not just a few select disorders but a wide variety of very serious physical and mental health conditions,” says Slavich, senior author of a paper signed by scientists from 22 institutions urging greater prevention, early diagnosis and treatment of severe chronic inflammation. “Indeed, chronic inflammatory diseases are the most significant cause of death in the world today, with more than 50 percent of all deaths being attributable to inflammation-related diseases.”

Researchers still don’t understand the exact mechanisms of how certain behaviors influence chronic inflammation, although a few examples are clear. In heart disease, for example, cigarette smoking and air pollution irritate the arteries, which stimulates inflammation.

“The ‘damage accumulation’ theory is a possibility, but the reality is that we do not know whether inflammation is causing these health and functional problems, or whether it’s an indication that some other process is evolving that undermines health,” says Luigi Ferrucci, scientific director of the National Institute on Aging. “The evidence is clearer for cardiovascular disease, since it has been demonstrated that blocking inflammation with specific drugs prevents cardiovascular events. For the other outcomes, it’s still uncertain.”

Chronic inflammation can contribute to cognitive decline and mental health disorders by boosting age-related immune system deterioration, known as immunosenescence, and by promoting vascular and brain aging, which, in combination, degrade neural and cognitive function, experts say.

“Chronic inflammation can also cause threat sensitivity and hypervigilance, which gives rise to anxiety disorders and PTSD, as well as fatigue and social-behavioral withdrawal, which are key symptoms of depression,” Slavich says.

Scientists say more research is needed to identify biomarkers or other substances that suggest the presence of chronic inflammation.

There are probably hundreds of these potential diagnostic tools produced by the immune system, but they remain unidentified, Slavich says.

The most widely used test measures levels of C-reactive protein (CRP) in the blood. CRP, a substance produced by the liver, rises when chronic inflammation is present, although the standard CRP test is nonspecific — that is, it indicates inflammation, but cannot pinpoint exactly where it is. A second, more sensitive test (hs-CRP) suggests a higher risk of heart attack, although it too can be imprecise.

Some doctors screen for CRP as part of routine physical exams and also among people at risk for heart disease and autoimmune conditions. Experts think wider screening could identify more patients. “This isn’t a bad idea,” Ferrucci says.

Another test — this one more specific to heart disease — screens for myeloperoxidase, or MPO, an enzyme released by white blood cells that kills harmful bacteria in inflamed blood vessels. Increases in MPO can be dangerous, causing further damage to arterial walls, which encourages the formation of clots. These, in turn, can block blood flow, leading to heart attack and stroke. MPO also reduces the effectiveness of HDL, the “good” cholesterol, and removes nitric oxide, which is important for the regulation of healthy blood flow.

The good news, however, is that people worried about developing chronic inflammation can take affirmative steps to prevent it.

“If we make people aware of these risk factors, our hope is that individuals will reduce the factors that apply to them,” Slavich says.

Chronic Inflammation is Insidious and Dangerous. You May Not Even Know You Have It.

People often learn they have it when by developing an autoimmune disease. But the ailment might also play a role with heart disease, cancer, other disorders.

getpocket.com

 

[mr peabody]

Inflammation could be a key player in Depression*

Imperial College London | Neuroscience News | 17 Aug 2021

A new study adds to the growing body of research linking inflammation to depression. Researchers found the molecule histamine directly inhibits the release of serotonin in the brain by attaching to inhibitory receptors on serotonin neurons in mice.

The findings, from researchers at Imperial College London and University of South Carolina, add to mounting evidence that inflammation, and the accompanying release of the molecule histamine, affects a key molecule responsible for mood in the brain – serotonin.

If replicated in humans, the findings – which identify histamine as a ‘new molecule of interest’ in depression – could open new avenues for treating depression, which is the most common mental health problem worldwide.

Inflammation – a blanket term describing an immune response – triggers the release of histamine in the body. This increases blood flow to affected areas to flood them with immune cells.

While these effects help the body fight infections, both long-term and acute inflammation is increasingly linked to depression. Inflammation accompanies infections but can also be caused by stress, allergic responses and a host of chronic diseases such as diabetes, obesity, cancer and neurodegenerative diseases.

Lead author Dr Parastoo Hashemi, from Imperial’s Department of Bioengineering, said: “Inflammation could play a huge role in depression, and there is already strong evidence that patients with both depression and severe inflammation are the ones most likely not to respond to antidepressants."

“Our work shines a spotlight on histamine as a potential key player in depression. This, and its interactions with the ‘feel-good molecule’ serotonin, may thus be a crucial new avenue in improving serotonin-based treatments for depression.”

Chemical messengers

Serotonin, often referred to as the ‘feel-good molecule’, is a key target for depression-tackling drugs. Commonly prescribed selective serotonin reuptake inhibitors (SSRIs) inhibit the re-absorption of serotonin in the brain, allowing it to circulate for longer and improve mood.

However, although SSRIs bring relief to many who take them, a growing number of individuals are resistant to their effects. Researchers think one reason for this could lie in the specific interactions between chemical messengers, or neurotransmitters, including serotonin and histamine.

With this in mind, researchers set out to investigate the relationship between histamine, serotonin, and SSRIs.

They created serotonin-measuring microelectrodes and put them into the hippocampus of the brains of live mice, an area known to regulate mood. The technique, known as fast scan cyclic voltammetry (FSCV), allowed them to measure brain serotonin levels in real time without harming the brain, as they are biocompatible and only five micrometers wide.

After placing the microelectrodes, they injected half the mice with lipopolysaccharide (LPS), an inflammation-causing toxin found in some bacteria, and half the mice with a saline solution as a control.

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.

To counter this, the researchers administered SSRIs to the mice, but they were much less able to boost serotonin levels than in control mice. They posited that this is because the SSRIs directly increased the amount of histamine in the brain, cancelling out its serotonin boosting action.

The researchers then administered histamine reducing drugs alongside the SSRIs to counter histamine’s inhibitory effects, and saw serotonin levels rise back to control levels. This appears to confirm the theory that histamine directly dampens serotonin release in the mouse brain. These histamine reducing drugs cause a whole-body reduction in histamine and are distinct from antihistamines taken for allergies, which block histamine’s effects on neurons.

A new molecule of interest

The researchers say that if their work translates to humans it could help us towards eventually diagnosing depression by measuring chemicals like serotonin and histamine in human brains.

They also say the findings open new avenues to explore histamine as a causative agent of depression, including potentially developing novel drugs that reduce histamine in the brain.

Because the work was done in animals, more research will be needed to know if the concepts translate to humans. However, it is not currently feasible to use microelectrodes to make similar measurements in human brains, so the researchers are now looking at other ways to get a snapshot of the brain by looking at other organs which use serotonin and histamine, like the gut.

Pain, which accompanies inflammation, can also change neurotransmitter levels – but previous research shows that in similar models, these changes last a few minutes, whereas the serotonin drop shown in this research lasted much longer, ruling out pain as a reason for the serotonin decrease.

Dr Hashemi added: “Inflammation is a whole-body response and is therefore hugely complex. Depression is similarly complex, and the chemicals involved are affected in myriad ways by both genetic and environmental factors. Thus we need to look at more complex models of depression behaviours in both mice and humans to get a fuller picture of both histamine and serotonin’s roles in depression.”

About this depression research news
Author: Caroline Brogan
Source: Imperial College London

*From the article here :

Histamine and Inflammation Could Be Key Players in Depression - Neuroscience News

A new study adds to the growing body of research linking inflammation to depression. Researchers found the molecule histamine directly inhibits the release of serotonin in the brain by attaching to inhibitory receptors on serotonin neurons in mice.

neurosciencenews.com

 

[mr peabody]

Is Inflammation the driver of Alzheimer’s?*

Science News | May 2 2018

A new research study by scientists in Australia and the US provides an explanation for why clinical trials of drugs reducing proteins in the brain that were thought to cause dementia and Alzheimer's have failed. The study has opened the way for potential new treatments with existing drugs.

Published online in the journal Human Molecular Genetics, the researchers assembled evidence from a wide range of human studies and animal models of dementia-related diseases to show that inflammation is a major cause, not just a consequence.

They show that many genes linked with dementia regulate our susceptibility and response to inflammatory damage.

"For decades, scientists have thought that dementia and Alzheimer's Disease are caused by protein aggregates forming in the brain. But recent clinical trials of drugs that reduce the aggregates have failed," says project leader Professor Robert Richards, from the University of Adelaide's School of Biological Sciences. He is working in collaboration with the University's Adelaide Medical School and the National Institutes of Health, in the US.

Inflammation has long been known to increase as dementia-related diseases progress, but only now is it identified as the cause. Previously it was thought to act simply to clean up tissue damage caused by the protein aggregates.

"We know that inflammation has different phases -- early on it can be protective against a threat by actively degrading it, but if the threat is not removed, then persistent inflammation actually causes cell death," says Professor Richards.

The new work turns previous thinking around. The genetic linkages imply that the inflammation comes first -- and the tissue damage second.

"Many genes linked with dementia operate at the level of controlling cellular inflammation. Both internal and external triggers interact with these genes to play a part. Inflammation is the point through which many triggers converge," says Professor Richards.

He likens the brain inflammation to a virus infection. "Inflammation is a very effective defence against foreign agents like viruses. But as we get older and accumulate mutations, our cells can make proteins and DNA products that mimic viruses, and these build up in the system," he says.

"Normally, our cells bar-code their own products to tell them apart from foreign agents. When these bar-codes aren't in place, our cells can't properly distinguish 'self' and 'non-self' trigger molecules. The result is inflammation that escalates and spreads -- hence the term autoinflammatory disease."

Certain types of gene mutation cause these systems to fail earlier or more often, and can increase as we age -- possibly accounting for age-related increased risk of developing dementia.

The good news is that by reducing some elements of inflammation, it may be possible to reduce dementia symptoms.

"With this new understanding of the disease, we now need to test existing anti-inflammatory drugs for their effectiveness in treating dementia," he says.

*From the article here :

New leads on treating dementia and Alzheimer's

A new research study provides an explanation for why clinical trials of drugs reducing proteins in the brain that were thought to cause dementia and Alzheimer's have failed. The study has opened the way for potential new treatments with existing drugs.

www.sciencedaily.com

 

[mr peabody]

Psilocybin as an anti-inflammatory agent in the treatment of Parkinson’s and Bipolar Disorder*

Silo Pharma | Psilocybin alpha | 8 Jun 2021

Silo Pharma, Inc., a development-stage biopharmaceutical company focused on the use of psychedelics as a therapeutic, is pleased to announce that it has entered into a Scientific Research Agreement (SRA) with the University of California San Francisco (UCSF). This SRA will leverage four other clinical trials being planned by the university, to determine the effects of psilocybin on inflammatory markers of patients who have exhibited Parkinson’s, Bipolar disorder, and chronic back pain.

Eric Weisblum, CEO of Silo Pharma commented “Inflammation is a common mechanism across numerous physical diseases. Inflammation has specifically been implicated in the pathophysiology of Parkinson’s Disease, chronic pain, and bipolar disorder. Psilocybin and related compounds have shown strong anti-inflammatory effects in non-human animals, raising the possibility that reducing inflammation is a possible mechanism underlying psilocybin’s positive treatment effects in multiple disorders. A better understanding of the anti-inflammatory effects of psilocybin has potential to allow for optimization and personalization of psilocybin treatment.”

The study will take place at The Translational Psychedelic Research (TrPR) Program at UCSF. The TrPR brings together scientists and care providers across disciplines to understand how psilocybin, LSD, ketamine, MDMA, and related compounds impact the brain and other organ systems. The goal at TrPR is to accelerate progress towards impactful and accessible psychedelic treatments.

Silo Pharma. Inc. is a development-stage biopharmaceutical company focused on merging traditional therapeutics with psychedelic research for people suffering from indications such as depression, PTSD, Parkinson’s, and other rare neurological disorders. Silo’s mission is to identify assets to license and fund the research which we believe will be transformative to the well-being of patients and the health care industry. For more information, visit www.silopharma.com

*From the article here :

Silo Pharma Announces Collaboration with University California San Francisco to study Psilocybin as an Anti-Inflammatory agent in Parkinson’s and Bipolar Patients - Psilocybin Alpha

Englewood Cliffs, NJ, June 08, 2021 (GLOBE NEWSWIRE) — Silo Pharma, Inc. (OTCQB: SILO) a development-stage biopharmaceutical company focused on the use of psychedelics as a therapeutic…

psilocybinalpha.com