Psilocybin Tied to Lower Inflammation in Parkinson's Trial

 Is your competent? doctor ready with this to try to prevent Parkinsons after your stroke? Sorry, your doctor doesn't even know of your Parkinson's risk! 

Parkinson’s Disease May Have Link to Stroke March 2017 

Haven't you gotten that INCOMPETENT DOCTOR FIRED YET?

Isn't your doctor already prescribing psilocybin for stroke recovery? Oh NO, you DON'T have a functioning stroke doctor, do you? 

psilocybin (59 posts to May 2014) 

Psilocybin Tied to Lower Inflammation in Parkinson's Trial

Key Takeaways

• Psilocybin therapy was associated with reduced inflammation in a small trial of Parkinson's patients with mood dysfunction.
• An inflammatory index remained lower through 30 days, but mitochondrial stress marker reductions were transient.
• Findings require confirmation in larger randomized controlled trials.

Markers of systemic inflammation and mitochondrial stress were reduced after psilocybin therapy in Parkinson's disease patients with mood dysfunction, a small nonrandomized trial showed.

Relative to baseline, an inflammatory index was significantly lower at all follow-up time points after psilocybin was administered, reported Ellen Bradley, MD, of the University of California San Francisco (UCSF), and co-authors.

The standard mean difference (SMD) was -0.72 (adjusted P=0.003) 1 day after 10 mg of psilocybin, Bradley and colleagues wrote in a JAMA Psychiatry research letter.

One day after 25 mg of psilocybin, the SMD was -0.60 (adjusted P=0.02), and 30 days after 25 mg, the SMD was -0.62 (adjusted P=.047).

The results support the researchers' parent trial, which showed an association between psilocybin therapy and reduced depression, anxiety, and motor symptoms in Parkinson's patients.

"To our knowledge, this is the first report of changes in these types of markers after psychedelic treatment in people with a neurodegenerative disease," Bradley told MedPage Today. "That gives us and other researchers super-interesting biological questions to pursue: What could be producing these changes, are they consistent in larger groups of people, and do they have anything to do with clinical benefits people with Parkinson's might experience with psilocybin?"

This research comes as part of a series of studies examining the biological effects of psychedelics as potential therapeutics for non-psychiatric conditions, said Albert Garcia-Romeu, PhD, of the Johns Hopkins University School of Medicine in Baltimore, who wasn't involved with the study. It also comes on the heels of work showing that psilocybin appeared to block nerve damage related to chemotherapy in mice, he pointed out.

Much of the work looking at psilocybin or LSD has focused squarely on mental health conditions like depression, anxiety, or addiction, Garcia-Romeu noted. "However, this study is in patients with a neurological condition -- Parkinson's disease -- and shows evidence that psilocybin may have impacted biological markers of inflammation and mitochondrial stress," he told MedPage Today.

"These new data suggest biological effects of psychedelics could be driving potential benefits in patients and pave the way for more work to better understand how psilocybin might be a useful therapeutic both in psychiatric and non-psychiatric conditions," he added.

In their open-label trial, Bradley and colleagues studied 12 people with mild-to-moderate Parkinson's disease ages 40 to 75. Participants received 10-mg and 25-mg doses of oral synthetic psilocybin approximately 2 weeks apart.

The researchers collected plasma samples from nine participants at four time points: baseline, 1 day after each psilocybin administration, and 30 days after the 25-mg dose.

The primary outcome to assess systemic inflammation was a proinflammatory index calculated as the mean z score of interleukin (IL)-6, IL-8, tumor necrosis factor alpha, interferon gamma, and high-sensitivity C-reactive protein concentrations. Mitochondrial stress was evaluated with growth differentiation factor 15 (GDF-15) and fibroblast growth factor 21 (FGF-21) measurements.

Components of the index, including IL-6, were significantly lower 1 day after the 10-mg dose but at no other time points. IL-10 was significantly higher 1 day after the 10-mg dose but not at other times.

GDF-15 was significantly lower relative to baseline 1 day after each psilocybin administration, but not from baseline 30 days after the 25-mg dose. FGF-21 was higher 1 day after each psilocybin administration, but this finding was not significant.

This was a small study of psilocybin therapy and results must be interpreted cautiously, noted co-author Aoife O'Donovan, PhD, also of UCSF. "However, the results are highly promising and suggest that more research in this area is warranted," she told MedPage Today. "We are already following this study up with more in-depth analyses of the effects of psilocybin therapy on inflammation and mitochondrial stress in a randomized controlled trial in patients with Parkinson's disease."

Work from Garcia-Romeu's lab also is studying psilocybin in a trial of people with mild cognitive impairment or early-stage Alzheimer's disease and depression. "To date, we've treated 18 individuals in that study, and enrolled 19 of a targeted 20 patients," he said. "We plan to complete the trial and publish our findings next year."

Association between temporal trajectories of inflammatory markers and prognosis in ischemic stroke

 'Associations' TELL YOU NOTHING ON HOW TO GET RECOVERED! You're all fired for incompetence in not creating inflammation prevention protocols!

Association between temporal trajectories of inflammatory markers and prognosis in ischemic stroke

• 

  Jing Xu 1

• X

  Xiaolan Wu 1

• X

  Xiaorong Lu 2

• S

  Shijun Li 1*

• 1. Department of Neurology, Affiliated Dongyang Hospital of Wenzhou Medical University, Dongyang, China

• 2. Department of Patient Services Management, Affiliated Dongyang Hospital of Wenzhou Medical University, Dongyang, China

Abstract

Background: 

The post-stroke inflammatory response is a dynamic and heterogeneous process that cannot be fully captured by single time-point measurements. This study aimed to characterize the temporal trajectories of four inflammatory markers—neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), systemic immune-inflammation index (SII), and systemic inflammation response index (SIRI)—during the acute phase of ischemic stroke and to evaluate their associations with 3-month functional outcomes.

Methods: 

We retrospectively analyzed patients with acute ischemic stroke admitted within 24 h of onset at Dongyang People’s Hospital from January to December 2024. Complete blood counts collected within the first 7 days were used to construct latent class growth models. Model selection was based on Akaike Information Criterion, the Bayesian Information Criterion, entropy, average posterior probability, and minimum class size. Logistic regression was performed to examine associations between inflammatory trajectories and 3-month modified Rankin Scale outcomes.

Results: 

A total of 735 patients were included. Distinct inflammatory trajectories were identified for each marker: three classes for NLR (stable-low, rapid-increase, gradual-decrease), three for MLR (persistent-low, persistent-moderate, persistent-high), three for SII (stable-low, persistent-moderate, marked-decline with rapid-rebound), and four for SIRI (stable-low, gradual-increase, gradual-decrease, rapid-increase). Stable-low patterns constituted the majority across all markers. For NLR, the rapid-increase trajectory consistently predicted poor 3-month outcomes (Model 3: OR 3.492, 95% CI 1.514–10.265). For SIRI, both gradual-increase and rapid-increase trajectories were independently associated with poor prognosis (Model 3: OR 3.894, 95% CI 1.395–10.872; OR 4.264, 95% CI 1.201–15.136). In contrast, MLR and SII trajectories were not associated with functional outcomes after full adjustment.

Conclusion: 

Distinct temporal inflammatory trajectories are observed during the 1 week after ischemic stroke. Increasing trajectories of NLR and SIRI strongly predict poor 3-month outcomes. These findings underscore the clinical importance of monitoring early inflammatory evolution rather than relying on single measurements and provide a novel framework for prognostic assessment in ischemic stroke.

I’m a cardiologist. This is what you need to know about the side effects of statins

Sorry, but cholesterol is not the problem; INFLAMMATION IS! Without inflammation the arteries wouldn't be grabbing cholesterol to pack into plaque. Medical personnel took the shortcut and left the real cause still out there. And solving the correct problem would negate use of statins, Big Pharma will never allow such research to be completed.

Why doesn't your doctor know about this? Your doctor, like mine, will use the excuse that statins reduce inflammation.

Inflammation video explaining it here:

The accent is a bit hard to understand and needs to be rerecorded to a laypersons understanding.

Inflammation In Atherosclerotic Plaque Formation YouTube 

The latest here:

I’m a cardiologist. This is what you need to know about the side effects of statins

Our new series The Expert View brings you specialist health advice from professionals. In this article, we hear from Dr Ricardo Petraco, an internationally recognised consultant cardiologist and researcher based at Imperial College London and the Mayo Clinic in London. He specialises in cardiovascular screening, coronary artery disease and intervention.

Around seven to eight million people in the UK are on statins, and every week I see patients who are either on or considering taking them. More than with any of their other pills, many are worried about side effects. So what are their real risks?

First, an important disclosure: I have no conflict of interest in recommending or prescribing statins. I don’t make money from doing so, and I have no relationship with the pharmaceutical companies that make and sell them to the NHS.

It’s mystifying to me that statins are so vilified, because if you had to pick the one medication in the history of cardiology with the clearest benefit, it would be them.

Statins work by lowering low-density lipoprotein (LDL), the so-called “bad” cholesterol in the blood that leads to heart attacks, strokes and early death. Across the board, people taking a statin are roughly 25-40 per cent less likely to have a heart attack or stroke, regardless of their cholesterol level at the start of treatment. And the myths about the alleged risks – cancer, dementia, cognitive impairment, sexual dysfunction – have all been robustly debunked.

 Related video: New cholesterol guidelines: What you need to know (WCNC-TV Charlotte)

A study led by Oxford Population Health and published in The Lancet in February 2026 pooled 23 blinded trials involving more than 154,000 people. It found no excess risk from statins for 62 of the 66 conditions listed in their package leaflets, including memory loss, depression and sleep disturbances.

However, side effects can happen and some patients have genuine concerns. Dismissing them is wrong. What we should say is: “Yes, there is a small risk of side effects with statins, but let’s talk about it. Let’s weigh that risk against the risk of having a heart attack, and then you can make a rational decision about your treatment.”

Whatever you do, don’t give up on statins because you’re worried about side effects. That daily pill could save your life.

The side effects – should you be concerned?

Muscle aches

It is estimated that around one fifth of patients refuse or stop taking statins because of muscle aches, fatigue or joint pain. Yet true statin-caused muscle ache is uncommon. A 2022 study led by researchers from Oxford Population Health found that “for every 1,000 people taking a moderate intensity statin, the treatment would cause 11 generally mild episodes of muscle pain or weakness in the first year, with no significant excess in subsequent years”. The occurrence is just over 1 per cent, and only at the start.

A lot of complaints around muscle ache are largely down to the “nocebo effect”. That means the symptom is real but the drug is not causing it – the expectation of feeling unwell is. In studies where people don’t know whether they’re taking a statin or a dummy pill, aches are reported at nearly the same rate in both groups.

At Imperial, where I’m based, my colleagues carried out a study in 2020 that recruited 60 people aged between 37-79 who had stopped taking statins because of side effects, and restarted them, but with a twist. Over a year, each patient received bottles containing a statin, bottles containing a dummy pill, and bottles containing nothing at all, rating their symptoms each day via an app. The results were illuminating. Symptoms were nearly identical whether people took the statin or the placebo.

Nonetheless, it does occasionally happen, and it is a genuine concern. If a patient feels that statins are causing aches and pains, we monitor the situation, temporarily stop the statin and restart it to see how they feel. For many, symptoms lessen with time, particularly if you start on a lower dose and increase gradually. And if muscle problems persist, we can find another way to lower their LDL cholesterol. There are always alternatives.

Severe muscle damage

Rhabdomyolysis (severe muscle breakdown) is a genuine but extremely rare side effect of statins. It happens in about one to three people out of every 100,000 taking statins each year, and less commonly still at lower doses. It is more likely if you’re on a higher dose, if you’re taking certain other medications at the same time, or if you have kidney or liver problems or an underactive thyroid.

The problem is that because people occasionally experience muscle aches on statins, they immediately associate this with rhabdomyolysis and become very concerned. Yet the chances of it occurring are negligible, and that small risk needs to be weighed against the benefit.

A 2016 report published in The Lancet remains the clearest quantification: treating 10,000 people for five years with a type of statin called atorvastatin at 40mg would cause about five cases of muscle injury. One of those five might progress to rhabdomyolysis, and 50 to 100 people would report muscle symptoms.

Over the same five years, it would prevent 500-1,000 major vascular events, including deaths and disability from strokes and heart attacks. The benefits outweigh the harms many times over.

Slightly higher risk of diabetes

Taking a statin does slightly increase your average blood-sugar level, and over five years it raises the chance of being diagnosed with diabetes by about 0.5 to 1 per cent – somewhere between one in 200 and one in 100 people.

If you are fit and well, with a normal blood sugar, you will not suddenly become diabetic by going on a statin. It’s the patients who are already borderline – with insulin resistance or obesity – who may be taken over the line from pre-diabetes to diabetes. But those are precisely the patients at highest risk of a future cardiac event, so they are the ones the statin protects most. In these cases, lifestyle interventions such as diet changes, exercise and quitting smoking are recommended alongside taking statins.

Raised liver enzyme levels

With many medications, such as paracetamol, ibuprofen and antibiotics, there is a very small risk of liver failure. With statins, this is not a clinical concern: they do not measurably increase your risk of dying from liver failure.

It’s true that about four in 1,000 people have raised liver enzyme levels on blood tests when they start taking statins, but this usually causes no symptoms and is rarely a reason to stop.

Dementia (and the brain cholesterol myth)

There is a widespread myth that taking statins causes dementia. It is based on the fallacious claim that “20 per cent of your brain is cholesterol and yet your doctor is giving you medication to lower your cholesterol”. Biologically this makes no sense. Your brain cholesterol is produced locally, by specialised cells, and has nothing to do with the cholesterol circulating in your bloodstream in LDL particles.

Cognitive impairment is not a side effect of taking statins – The Lancet’s 2026 review confirmed as much. If anything, there is a theoretical gain, because you are decreasing the chance of vascular damage in the brain. Observational studies suggest that long-term statin use may even reduce your risk of developing dementia, although that is not yet proven.

Recommended

The truth about statins, memory and dementia

Read more

Sleep problems

Clinical trials have shown no consistent association between statins and sleep problems, but this is something patients do worry about. Again, the picture is confounded: people on cardiac medication tend to be older, and to have other conditions that disturb sleep. The statin itself has never been shown to cause them.

A few people taking statins that cross the blood-brain barrier – such as simvastatin or atorvastatin – report vivid dreams or disturbed sleep. This is rare, and although it’s hard to conclude whether the drug is the cause, we pragmatically recommend moving the dose to the morning; and if symptoms persist, an alternative such as rosuvastatin can be tried, as it is known not to cross into the brain so easily.

Erectile dysfunction

Statins causing erectile dysfunction is another common chapter in the book of online misinformation, but the link is unfounded. Sexual dysfunction is common among patients with cardiovascular disease, and some heart drugs, such as beta-blockers, can indeed cause it.

That confuses the picture, as those are the same patients who take statins. But there is no scientific evidence that statins cause sexual dysfunction. In fact, some studies suggest they can help, possibly by improving vascular health which then improves blood flow to the genitals.

Oedema (swollen ankles)

Three weeks after stopping my amlodipine  for high blood pressure the swollen left ankle is still there. Right ankle(good leg) never swelled up. I wasn't warned about edema when I started taking the drug. Now on nifedipine.

Oedema – essentially swollen ankles – does happen, but the numbers are very small and it’s not something we worry about. The 2026 analysis previously found roughly seven extra cases per 10,000 people per year, or 0.07 per cent. For comparison, amlodipine, a blood pressure tablet frequently prescribed alongside statins, causes dose-dependent ankle oedema in 5-10 per cent of users.

As told to Damon Syson

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Why I'm taking statins after avoiding them for nearly a decade

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Correlations of systemic immune-inflammation index and systemic inflammation response index with the risk for early-onset post-stroke depression in patients with minor stroke: a prospective observational study

 

Why are you researching depression rather than preventing it with EXACT 100% RECOVERY PROTOCOLS?  Oh, you've done NO thinking about the proper solution to stroke, have you? My god, everyone in stroke  must not have any functioning brain cells at all!

Correlations of systemic immune-inflammation index and systemic inflammation response index with the risk for early-onset post-stroke depression in patients with minor stroke: a prospective observational study

• W

  Wei Zhao 1†

• 

  Mingzhu Deng 2†

• 

  Zhen Wang 1

• 

  Guohua He 1

• 

  Wei Xu 1

• T

  Tieqiao Feng 1

• J

  Jian Peng 1

• 

  Kangping Song 1

• L

  Ling Xiao 1*

• 

  Fangyi Li 1*

• 1. Department of Neurology, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, Hunan, China

• 2. Department of Neurology, The Second People’s Hospital of Hunan Province (Brain Hospital of Hunan Province), Changsha, Hunan, China

Abstract

Background: 

Inflammation plays a pivotal role in the pathophysiology of post-stroke depression (PSD). However, the relationship between novel systemic inflammatory indices-the systemic immune-inflammation index (SII) and systemic inflammation response index (SIRI)-and early-onset PSD remains inadequately explored.

Methods: 

Early-onset PSD was diagnosed 2 weeks after acute ischemic stroke (AIS). Depression severity was assessed using the 17-item Hamilton Depression Rating Scale (HAMD-17); patients with scores ≥7 were classified into the early-onset PSD group. Spearman rank correlation analysis was performed to evaluate associations of SII and SIRI with HAMD-17 scores across all participants. Binary logistic regression was used to examine the independent associations of SII and SIRI with early-onset PSD. Receiver operating characteristic (ROC) analysis was employed to assess the SII and SIRI capacity to differentiate early-onset PSD.

Results: 

Of the 1,113 prospectively enrolled patients, 372 (33.42%) were diagnosed with early-onset PSD. HAMD-17 scores showed significant positive correlations with SII (r = 0.440, p < 0.001) and SIRI (r = 0.418, p < 0.001). Both SII (OR = 1.762, 95% CI: 1.261–1.946, p < 0.001) and SIRI (OR = 1.672, 95% CI: 1.348–1.932, p = 0.004) emerged as independent predictors of early-onset PSD. The areas under the curve (AUC) for SII, SIRI, and their combination were 0.767, 0.718, and 0.807, respectively.

Conclusion: 

SII and SIRI may serve as independent risk factors for early-onset PSD. These indices offer potential utility for risk stratification and could inform prevention strategies and prognosis management in this patient population.

Scientists may have discovered how to reverse chronic inflammation

 Have your competent? doctor and hospital further this research to the solution that stops this inflammation. Sorry, they aren't competent, are they?

Scientists may have discovered how to reverse chronic inflammation

A newly identified hormone could hold the secret to slowing biological aging—and making cancer treatments far more effective.

Inflammaging is a chronic, low-grade inflammation that develops throughout the body with age. It’s been linked to many leading causes of illness and death, like cancer, metabolic conditions, and cardiac and neurodegenerative diseases. However pervasive, scientists have struggled to fully understand what causes the inflammation—and, perhaps more importantly, how to reverse its impact.

A new study from the Keck School of Medicine at the University of Southern California published in the peer-reviewed journal Nature Communications identified the thymus, a small organ involved in immune system development, as a key player in inflammaging.

The thymus is located just behind the breastbone and produces a key hormone called thymulin, which regulates inflammation. With age, thymulin decreases while inflammation increases, allowing diseases like cancer to progress.

The scientists at USC found that by increasing thymulin levels in mice, their rates of cancer survival improved and it even made immunotherapy treatments more effective.

“This is the first evidence of a substance that is naturally produced in the thymus, declines with age, and has the power to reverse age-related inflammation,” said Fumito Ito, professor of surgery and immunology and immune therapeutics at the Keck School of Medicine and lead author of the study, in a statement.

 Related video: How to calm chronic inflammation through the foods you eat every day (Talking With Docs)

 Past studies have already suggested a link between the thymus and chronic inflammation, but these researchers went further, finding the biological mechanism potentially responsible for the process. One day, thymulin could even be used in clinical trials to treat cancer, among other diseases. responsible for the process. One day, thymulin could even be used in clinical trials to treat cancer, among other diseases.

The study relied, in part, on an uncommon research method: heterochronic parabiosis. This approach requires researchers to surgically join an older mouse to a younger one, so they share blood flow. 

They found that the procedure reduced inflammation in the older mice—suggesting that parts of the younger blood may help reverse age-related decline.

The researchers looked at both human blood samples and mouse models, analyzing the genes involved with both aging and longevity. They found a shortlist linked to cytokines—small protein messengers that regulate inflammation—and found a surprising pattern: Mice that did not have these genes had problems with the thymus.

They found that thymulin is important in the body’s regulation of cytokines—seeing that, additionally, cytokines increase as thymulin levels fall with age.

Although the thymus is best known for producing the T-cells responsible for the immune system’s defense against infections, the findings show it can also account for age-related inflammation.

Looking at older mice with cancer, they found that when thymulin was added, the immune response against tumors was boosted, improving overall survival.

Future implications

These findings raise new questions about the hormone’s role in age-related diseases. Inflammaging is linked to a long list of conditions, including diabetes, cancer, and Alzheimer’s disease. Ito said in the statement that the research team plans to further investigate the role of thymulin in chronic diseases.

Currently, there are many treatments available that are marketed as anti-inflammatory and anti-aging options—but these focus on suppressing the inflammatory pathways or getting rid of aging cells. The potential treatment that Ito and team are creating is different, he told Inc.

Their possible treatment involves “restoring an age-related endocrine signal that normally helps maintain immune homeostasis,” Ito says. “Rather than broadly suppressing inflammation, our findings suggest that thymulin may help restore a physiological regulatory mechanism that is progressively lost during aging.”

This post originally appeared at inc.com.

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