Oxidative stress is often portrayed as being similar to 'rust' but a much better analogy is acid rain or a corrosive liquid. Reactive oxygen species (ROS) dont cause a build up - like with rust - instead they eat away at the cell's components and damage structure, including DNA. 1/x The latest paper from Dr. Ron Davis lab shows that in both ME and LongCovid oxidative stress in immune cells is higher than in controls. Importantly ROS was even higher in female patients.
2/xbiorxiv.org/content/10.110…

Current preclinical research indicates that BPC-157 is not only unlikely to cause anhedonia but may actually PROTECT against depressive symptoms.

Anhedonia = inability to feel/experience pleasure (one aspect of depression that is ALSO very common in people who use anti-depressants such as SSRIs).

Here are several lines of evidence (Chat GPT):

Antidepressant Effects in Animal Models

In forced swimming tests (a standard model for assessing depression‐like behavior), BPC-157 administration significantly reduced immobility time in rats. This reduction is comparable to that seen with traditional antidepressants like imipramine, indicating that BPC-157 has robust antidepressant properties rather than depressogenic effects.

These findings suggest that, mechanistically, BPC-157 is protective against the development of depressive symptoms rather than causing anhedonia.

Modulation of Neurotransmitter Systems

BPC-157 has been shown to interact beneficially with several key neurotransmitter systems:

Serotonin: Research demonstrates that BPC-157 can stimulate serotonin release in specific brain regions (e.g., the nigrostriatal area) and even counteract serotonin syndrome. Enhanced serotonin neurotransmission is generally associated with improved mood and is a common target of antidepressant therapies.

Dopamine: BPC-157 also modulates dopamine activity. It counteracts behavioral disturbances (like neuroleptic-induced catalepsy) that are linked to dopaminergic dysregulation. Given that dopamine plays a key role in reward and motivation, its proper modulation by BPC-157 supports a healthy reward system rather than one that would lead to anhedonia.

Other Systems:
Additionally, BPC-157 appears to influence glutamate and GABA systems in a way that promotes overall neural homeostasis.

Together, these actions support a neurochemical environment that is conducive to normal mood regulation and motivation.

Anti-inflammatory and Neuroprotective Actions

Inflammation—both systemic and within the brain—has been strongly implicated in the pathophysiology of depression. BPC-157 is known for its potent anti-inflammatory and cytoprotective effects, including in neural tissues. By reducing brain inflammation, BPC-157 may help prevent or mitigate neuroinflammatory processes that can lead to depressive symptoms.

Mechanistic Rationale

The peptide’s overall mechanism:
**enhancing endothelial function
**promoting angiogenesis
**stabilizing cellular integrity
supports its role as a cytoprotective agent.

Such effects not only improve tissue repair and recovery after injury but also support the overall health of the brain’s neurovascular unit. A well-maintained neurovascular environment is critical for normal neurotransmission and has been associated with resistance to depression and anhedonia.

Summary:
The preclinical evidence suggests that BPC-157 is unlikely to cause anhedonia. On the contrary, by enhancing serotonin and dopamine function, reducing neuroinflammation, and promoting neuroprotection, BPC-157 may actually offer protective and even therapeutic benefits in depressive conditions.

TR: I know there are some Reddit posts with users claiming that BPC caused anhedonia. Sure, it is possible - but based on the above and the mechanisms of action it is just very unlikely - it is much more likely that something else was causing the depression and that BPC actually was minimizing it. I know its hard sometimes to make the right links with interventions but we need to fall back to the mechanisms. If something is likely to be protective - then well....it is not very likely to be damaging. Right? What else were they doing? Do they have histories of depression? The peptide primer (focusing on using peptides for Hypermobility/hEDS and connective tissue issues)

https://x.com/chydorina/status/1656708398753406976

I have seen many cases where the addition of BPC-157 is what stopped the cycle of decline in MECFS.

Management in chronic disease is NOT a "One and Done".

If the trigger is still maintaining the disease, the issue has not be fixed - its just been controlled - and to keep up the desired state of function - you need to keep up the treatment and management.

Does this make sense?

One of the key issues in MECFS and similar conditions is sensitivity and reactivity. There are MANY reasons why we have more side-effects and lower tolerance to medication but a major MAJOR MAJOR one is actually leaky gut itself.

Just like our body freaks out when the endotoxins from bacteria leak out of our gut lining - our body also freaks out when meds leak out into the blood stream.

They are not being processed in the normal way. They get into the body too fast, in too high of an amount, they are processed too quickly, the normal co-factors and processing pathways cant kick in so they do abnormal stuff.

There are many ways that leaky gut impacts reactivity and sensitivity but because LEAKY GUT itself (and the MCAS-leaky gut-microglial feedback loops that maintain it) is an issue - this means that most of us actually feel like we don't respond well or normally to medications. I think actually that most of us would answer this question in the affirmative, especially as severity increases:

Do you feel like you are more sensitive and reactive to medications, supplements, and interventions than people that do not have ME or LC or a similar condition? As we get more severe sensitivity becomes more likely (or so it seems to me) and by the time you hit moderate/severe - it probably feels like every new supplement or medication is a risk.

But why? right? why are we more sensitive? Its actually not just leaky gut - there is a lot more going on - but the THREE processes below are important:

**Depending on ones particular situation they might need many MANY times LESS of a medication to equal the dose that a non-leaky gut person would need. **They might get a huge bolus-like dose (i.e. all at once) versus the slower entry of the substance that non-leaky gut people experience.
**Because of MCAS and autoimmunity our bodies mistake more substances as potentially dangerous.

Regardless of the particulars - the key is to TREAT leaky gut. And keep treating it.

If the pedal is still on the metal (i.e. the triggers of the condition are still present - including MOLD/fungus, LPS, viruses, bacteria, chemicals) you will likely need to Treat Leaky GUT and then MAINTAIN the gut so that leaky gut does not re-occur.

Does this make sense? Management in ME and similar conditions is not a One and Done. It is management.

Here is some advice:
1. Work leaky gut treatment into your general protocol. its an ongoing management issue.
2. Best way to do this IMO is BPC-157. You can cycle on and off.
3. If you are still SICK - the process that drives leaky gut is still operating. This means that we must MANAGE it. Its not a one and done. It can come back.

Because BPC-157 is a great systemic anti-inflammatory it could be the type of intervention that replaces a whole slew of other common interventions for you. If it works for you and you dont react to it - use it as a basis of your treatment protocol - build on it. It will not cure ME but without directly managing leaky gut - it is hard for other interventions to work. BPS-157 can be like the foundation - that helps other interventions be effective (or more effective).

I see many cases where BPC-157 started the shift in baseline increase.

The addition of BPC-157 is often what stops the cycle of decline. I actually first started posting on X (then twitter) because of my experience with peptides in stabilizing #hEDS. They were one of the main game changers for me. I really don't have obvious connective tissue issues the way I once did.

Mixing up ones own electrolyte mix seems to be a major barrier for getting started with Born Free protocol and electrolyte supplementation in general.

With the help of ChatGPT I have put together a more commercially based mix of products that hits all the Born Free targets.

The main potassium core is Dr. Berg's electrolyte mix. We then add Nutri-Align capsules, Now foods Red Mineral Algae, and Himalayan/Celtic Salt and Baking Soda.

It will be many times the cost of buying the bulk powders but if it is easier - and means people will be more likely to use it - then its worth considering. 1/x 2/x

Electrolyte Needs in ME/CFS, Chronic Infections, and Post-Viral Syndromes (versus needs in Healthy people)

Electrolytes play a critical role in cellular energy production, nerve function, hydration, and blood pressure regulation. In ME/CFS and chronic illness, electrolyte imbalances are common due to autonomic dysfunction (POTS, dysautonomia), mitochondrial dysfunction, poor absorption, chronic inflammation, and infections.

People with ME/CFS, post-viral syndromes, and high pathogen loads (bacteria, fungi, viruses, mold toxicity) often require significantly higher electrolyte intake than standard RDAs, particularly sodium, potassium, magnesium, bicarbonate, and phosphate to maintain blood volume, support ATP production, and counteract inflammatory depletion.

Chat GPT

How Do Nutrient, Vitamin, and Mineral needs differ for those with chronic Illness (ME/CFS, LongCovid Post-Viral Syndromes, and persistent infections) than for healthy people?

People with chronic illnesses, especially post-viral conditions like ME/CFS, have significantly altered nutrient demands compared to healthy individuals due to persistent infections, high bacterial and fungal loads, mitochondrial dysfunction, and chronic inflammation. These factors increase nutrient depletion, impair absorption, and alter metabolism, making the standard Recommended Dietary Allowances (RDAs) insufficient for optimal function.

Let's get into the details with Chat GPT

Yesterday's article showing how Ambien/a z-drug ( benzodiazepine type sedative) negatively affects glymphatic clearance needs to be addressed and the potential consequences need to be carefully deconstructed especially in light of how common their use is in MECFS LongCovid and other chronic illnesses.

Its not fearmongering. I do think there is a major issue here and improper use might be one of the most dangerous things we can do in terms of our long-term cognitive health.

Its not just glymphatic clearance that is being negatively affected.

Benzo-type sedatives also affect brain wave patterns. Studies from way back in the 60s showed that they increased beta waves. Its a paradoxical effect - we feel like we are less anxious when we are on them but our brains are actually in fight-flight.

This recent paper on the negative effects of Ambien (which will likely apply to more benzodiazepine type drugs) on glymphatic clearance is a major issue especially in MECFS.

Pretty much the only intervention we know of that can help reduce the severity of PEM crashes from developing when used in moderation and very infrequently has potentially disastrous consequences if used improperly long-term. And this is not even taking into consideration the potential for serious adverse consequences of withdrawal and how difficult it is for people who have been on them for prolonged period to stop.

I was put on benzos (both Clonazepam and Lorazepam) for over a decade, with full physician oversight and was told that I would likely always need to be on them (I started prior to my second bout of MECFS). The reason was constant sympathetic nervous system overactivation (c-PTSD). Tapering and getting off of them took years in my case. I am now at a place where I can use lorazepam infrequently and do so for major crash inducing activities - but I try very hard to keep my use lower than a few times a month.

I would think this issue would be getting WAY more attention than it does - I guess we are all just too afraid to discuss it (let alone think about it) given that it is considered the only option my many people for PEM crashes and sleep.

The risk:benefit however is very seriously on the side of risk - especially when used daily for long periods of time. The bottom line here is that we just dont know how risky this medication might be in terms of long-term cognitive decline - but the literature is stacking up that the risk might be very considerable.

Sleep dysfunction and glymphatic clearance are among the biggest potential issues in MECFS that make recovery difficult. Without proper sleep we cannot heal. Many of us use these medications for sleep as MCAS and histamine and mast cell dysfunction directly affects our circadian rhythms and increases insomnia and its the only thing that helps. I know many of us would be seriously hooped if we didnt have access to benzodiazapines.

Finding alternatives is of paramount importance and should be one of the very top clinical priorities in MECFS and LongCovid research.

We should not be forced into taking a drug that can lead to cognitive decline and dementia (the potential ultimate consequence of dysfunctional glymphatic clearance as is suggested by much of the literature) to help us sleep and help control the severity of PEM.

That this is literally the only option that is available and it is potentially this damaging when used long-term and continuously is frankly completely unacceptable.

Like using chemo to treat cancer, how much unnecessary damage are we doing to ourselves - under the guise of 'treatment'.

I know this issue will be very scary for people to think about and i apologize as I know this will be triggering for a lot of people because there really are no good options.

But, it is too important to sweep it under the rug and we do need to discuss it.

How can we use benzo-type drugs are safely as possible given the potential consequences for glymphatic clearance and long-term cognitive decline should be a big conversation. Is there any safety margin or dose or is their use keeping us stuck in chronic illness and decline.

x.com/chydorina/stat…

https://x.com/chydorina/status/1436064278499381281

Toxoplasmosis infection is one of my opportunistic co-infections and the threat of it getting into the central nervous system (brain) is ever present (it can be a high risk in those that have immunosuppression as well as during pregnancy).

Its not a parasite that can really be successfully treated w/ current pharma drugs - they are not effective on all stages and can be much too hard on altered sick bodies dangerous as the mess with folate metabolism.

I use a Herbal protocol designed by master herbalist Dr. Stephen Buhner (search Buhner toxoplasmosis and you will find it) and I do a 21 day course 2-3 times a year. With addition of a few other herbs its also a good EVB herbal protocol.

I am always looking for alternate ways of keeping the toxo latent and making sure cysts dont grow. Probiotic mixtures that increase SCFAs - seem a useful add-on for anyone dealing with toxoplasmosis.

Probiotic-induced changes in intestinal microbiome inhibits Toxoplasma gondii infection
parahostdis.org/journal/view.p…
Multi-strain mixture composed of:

We need an X prize for a biomarker(s) for #LongCovid.

Currently there are no well accepted clinical endpoints that can be used in clinical trials and this more than anything else is hampering research progress and drug development.

There has got to be a couple billionaires out there who would fund an X prize (or we just tap $1 from every person who has #LongCovid and run a few hundred X prizes). With 200+ million people globally, the demand/resource is there. Plus, it would be a billion dollar company eventually.

Special bonus prize of course for the marker also applying to #MECFS.

Home test/commercial test would be the goal. All we really have right now are 'survey's' - questionnaires were people are asked questions like 'what is your level of fatigue'. This is not acceptable.

"The patients taking the synbiotic reported a significantly superior drop in post-exercise malaise (68.0% on average) at 3-month follow-up as compared to the placebo group (37.5%)."

Small trial finds significant effect of probiotic mixture on PEM with increase of choline in the thalamus, creatine in white/grey front matter, and N-acetyl aspartate before/after

Synbiotic (probiotics+) trial worth mentioning. The trial may have been small (n=32) but the significance of the intervention on PEM was quite high. Interestingly there was no effect on 'fatigue' per se - it was actually Post-exertional malaise where the benefit was found.

What did they do? 3 months of a combo probiotic supplement that included:
- Lacticaseibacillus rhamnosus DSM 32550, -
- Humiome® Lactiplantibacillus plantarum DSM 34532 (formerly known as L. plantarum TIFN101),
- Bifidobacterium lactis DSM 32269,
- Bifidobacterium longum DSM 32946,
- FOS fructooligosaccharides (2.5 mg) - a 'pre-biotic'
- Zinc (5 g).

The effects of 3-month supplementation with synbiotic on patient-reported outcomes, exercise tolerance, and brain and muscle metabolism in adult patients with post-COVID-19 chronic fatigue syndrome (STOP-FATIGUE)

link.springer.com/article/10.100…

You are competing RIGHT NOW for ENERGY with all the parasites and pathogens that are living on and in you. Yes, there are pathogens that can hijack the products of our mitochondria and co-opt ATP production for replication. In the process they will create more inflammatory reactive oxygen species, more systemic inflammation, and more dysfunction.

ENERGY production is a resource, and not one we have enough of a surplus of to share with pathogens - treat whole body pathogen load! Treat what can be treated.

It is possible to have normal oxygen saturation and pathological hypoxia at the same time? In certain conditions like #ME and #LongCovid this is likely what is actually occurring. Some tissues (like brain and muscles) are not getting enough oxygen.

To make matters worse it is possible that epigenetic 'memory' of the sick state is part of what might keep us sick (even when an acute illness ends) - and that changes in oxygen gradients in tissues (pathological hypoxia) is a trigger for these epigenetic changes.

We don't have a definitive answer yet but interactions between inflammation + the immune system + pathological hypoxia (low oxygen) may provide some clues that this is indeed occurring.

It can be hard to wrap ones head around having low oxygen or hypoxia when your smart watch shows normal oxygen saturation.

BUT! It is oxygen USE that is the issue, not that it is there is the first place. When we look at oxygen getting to the brain and oxygen use in the muscles, we see a different story.

It is obvious that hypoxia would interact with the immune response and inflammation and changes oxygen gradients in different tissues.

"These changing oxygen gradients are exaggerated during inflammation, where oxygenation is often depleted owing to alterations in tissue perfusion and increased cellular activity."

Pathological hypoxia also interacts with Mast Cells - causing them to degranulate and release inflammatory meditators. Obviously those that have MCAS might need to pay particular attention to hypoxia as a risk factor to help manage Mast Cells.

If activity also restricts oxygen in brain and muscles this could be one reason why physical activity can lead not just to crashes but also MCAS flares and its maintenance when all other triggers have been removed. (note: mast cells can also release interferon-gamma!!).

Hypoxia potentially interacts with ME and LC disease processes in many ways, affecting inflammation, immune responses including mast cells, and even epigenetics. Hypoxia might induce epigenetic changes in immune cells, such as chromatin remodeling, which can have long-lasting effects leading to 'immune memory' and a change of state from pre-illness that is hard to turn back.

Practically, this means that immune cells exposed to hypoxia may retain a "memory" of this exposure, affecting their response to future infections or inflammatory signals.

"How oxygenation shapes immune responses: emerging roles for physioxia and pathological hypoxia" link in comments: nature.com/articles/s4157…

Screens and Neuroinflammation

We all know that too much screen time can be hard on the eyes and brain, but if you have #ME or #LC it can be a major element of daily life that needs to be managed.

This is because screens both indirectly and directly are related to neuroinflammation - which we already suffer from.

I wish this paper focused less on healthy people/kids and developmental patterns and more on disease conditions and biology - but regardless - I copied the relevant sections on neuroinflammation and circadian cycle disruption (article is paywalled).

This is a topic that really needs to be covered for #ME specifically given our underlying neuro-issues. Using larger screens, blue light blockers, e-ink readers, special eye safe screens, screens with low flicker frequency and checking your tech to make sure if is not one of those units that people complain about are all options. I also wear 'Avulux' migraine glasses.

I upgraded to a 15.6" laptop with a high resolution screen a year ago and this was a great move for me. The smaller the screen is the harder I 'look'.

Search my feed for previous discussions of screen usage: "screens (from:chydorina)"

Interconnections of screen time with neuroinflammation (2024) article link:
link.springer.com/article/10.100…

Have you ever felt like your brain was on fire? This feeling is often linked to "Glutamate Excitotoxicity" - a process where neurons are exposed too high concentrations of the excitatory neurotransmitter glutamate leading to neuronal cell death.

Read paper: "Excitotoxicity Revisited: Mitochondria on the Verge of a Nervous Breakdown" (linked in comments)

Its probably quite common in #MECFS but then again it is super widespread across many neurodegenerative conditions and psychological disorders - which means that it would great to treat it but in and of itself treating it is not going to 'cure' MECFS.

Because it is SO widespread across so many conditions it has been heavily studied and there have been major research efforts to see if interventions could be developed to manage it (see image below).

Unfortunately (or maybe even fortunately as messing with fundamental pathways like this could have major unknown consequences) it has not been very amendable to direct treatment interventions.

There is however a way to help manage dysfunctions in this system. A backdoor so to speak. This is because the problem is not so much the glutamate itself, it is that the mitochondria are doing a poor job of processing it.

So, instead of trying to mess around with the glutamate levels directly or affect the clearance of glutamate we could instead focus on the mitochondria - which we know are struggling in MECFS.

"Therefore, one possibility might be to couple drugs that impact the glutamate responses with interventions that support mitochondrial bioenergetics, for example by promoting mitochondrial biogenesis or supporting intermediary metabolism, impacting both the mechanisms that may contribute to neurodegeneration in these diseases."

Check out the linked paper: it will really flesh out for you why glutamate has been such a heavily researched subject.

The bottom line is that mitochondrial function is probably where we should be focusing our intervention effort.

Methylene Blue, Photobiomodulation (PBM), the NAD pathway, Ellagic Acid and Urolithin a, as well as comprehensive protocols that address energy processing, amino acids, ALCAR and mitochondrial cocktails such as are used in mitochondrial disorders.

The Born Free protocol is also EXPLICITLY designed to modulate mitochondrial function.

Astaxanthin might also be worth looking into for these indications. see paper link below in comments.

Astaxanthin Protection against Neuronal Excitotoxicity via Glutamate Receptor Inhibition and Improvement of Mitochondrial Function (2022) Born Free protocol link: bornfree.life/download/BF_Pr…

Warning!

This makes me a little sick just considering this but I would not be surprised if Auvelity (a mix of dextromethorphan and bupropion) starts being pushed like crazy in #MECFS #LongCovid.

Given the big SSRI - serotonin/LC papers that hit in the last year you can actually see the lead up to these new psych meds being released for LC.

Adding an NMDA receptor antagonist to an anti-depressant is really insidious. If Auvelity worked for LC it would be the "dex" component and not the bupropion. We have known for ages that NDMA receptor antagonists might be helpful - other options are ketamine, memantine, as well as safer stuff like Magnesium, Zinc, L-theanine, NAC.

NMDA receptor antagonists are used for glutamate ecotoxicity (brain on fire) symptoms. We do have glutamate excitotoxicity but it is also present across most neurological conditions and many other diseases including depression. It is not a lever that will 'fix' MECFS in and of itself.

I have been hearing a lot about 'dextromethorphan' lately on X and while it is available OTC in cough syrup - its obviously not helpful to Pharma that needs it to be RX. So? A new drug mixing it with an SSRI (bupropion). If you want to try 'dex' just try the OTV version. Dont give in and get pushed into an SSRI.

Repeat: If you must try 'dextromethorphan' - please just get the OTC drug store stuff. Adding SSRIs just to try in post-viral conditions could have negative consequences. These are not disorders that will be fixed with psych meds.

I first tried "dex" back in 2014. All these interventions just keep going through cycles - we all try them - most fail and many have baseline decreases. It is not a miraculous PEM buster but it can lower glutamate ecotoxicity.

Its obvious the media is going to promote the #$%^& out of this:

What wont fail? Basic foundational optimization: nutrition, minerals, electrolytes, microbiome. Until our biochemistry is less dysfunctional and we actually are getting nutrients from food - nothing is going to work 'properly'. Doing this above is an intervention that will always be worthwhile. It may not make you better in and of itself, but it will set you up for it when 'disease modifying interventions' come down the pipeline.x.com/search?q=dextr…

https://x.com/TheBorisLab/status/1825338425035338038

This is pretty interesting (and actually somewhat surprising). I have known that plasmalogens were going to get major attention in the coming years for a wide range of conditions, from #LongCovid and #MECFS to autoimmune conditions like #MS, neurodegenerative conditions like #Alzheimers #Parkinsons and also cardiovascular conditions but this new paper (out of Australia) suggests that in the coming years we might be seeing a new standard cardiovascular marker based on plasmalogen levels.

I am not surprised by the evidence or usefulness of plasmalogen supplements - suggesting that plasmalogen levels should be used more generally as cardiovascular markers suggests that the potential importance of plasmalogens is really reaching the mainstream.

In this paper they discuss using shark liver oil. I am obviously not a fan of this source (I actually supervised a PhD thesis on shark biology and the consequences of shark fisheries on declines in top down control in oceans when I was a prof). Dr. Goodenowe has pioneered the production of synthetic plasmalogens which I believe are the best choice for a wide variety of reasons.

Development and validation of a plasmalogen score as an independent modifiable marker of metabolic health: population based observational studies and a placebo-controlled cross-over study (2024)

paper is linked in comments paper:
thelancet.com/pdfs/journals/…

Treatments that have helped patients go into remission or improve #MECFS #LongCovid - thanks to HIP!

If you have any experience with any of these interventions please comment and add your experience. This could become a REALLY valuable thread.

Full thread copied to X in images.
1/xforums.phoenixrising.me/threads/list-o… 2/x

Leaky gut and Berberine?

This figure is amazing. Let me explain. Its so obvious when you know what you are looking at.
ZO=Zonulin, Occludin, and Claudin are proteins that are involved in barrier function in the gut. Here they are stained with immunofluorescence. The regular spacing represents intact barrier function.

First line: The control is for 'healthy epithelium'.
Second line: When they add berberine to controls it gets a bit more disorganized.
Third line: When they add pro-inflammatory cytokines IFN-g and tnf-a the barrier function becomes totally disorganized.
Fourth line: When they add berberine to the pro-inflammatory condition it normalizes somewhat.

Berberine is notorious for being not an easy supplement to use, not very bioavailable and can cause side-effects.
Liposomal forms may help to counteract these issues:

Plasmalogens + Photobiomodulation + Medicinal Plants = potentially increased lymphatic drainage

COVID-19 infection is accompanied by amyloid aggravation in the brain associated with the neurological disorders.

Augmentation of lymphatic removal of amyloids from the brain may be a promising therapeutic approach.

"Promising Strategies to Reduce the SARS-CoV-2 Amyloid Deposition in the Brain and Prevent COVID-19-Exacerbated Dementia and Alzheimer’s Disease" (2024) mdpi.com/1424-8247/17/6…

When you look at MECFS management protocols (even ones that have been around for ages like Dr. Sarah Myhill's) one of the first set of recommendations is to address nutrient deficiency and mineral deficiency and heavy metals.

WHY?

Because nutrients and minerals are the co-factors that make our biochemical pathways work properly. Heavy metals are blocks to proper biochemical function. You simply cannot properly treat chronic illness without first repleting minerals and providing the body with the building blocks it needs for biochemical function.

I finally got my first set of Oligoscan results this week. I have been doing parts of the Born Free protocol (@joshual_tm) for a few months now but have been unable to get the CMA or mineral testing so was not able to personalize what I was doing. As of 2 weeks ago I am now doing ~95% of it and am committing to it for at least the next few months. I have also been detoxing mold and heavy metals and was interested to see if my detox pathways were blocked.

I am including the full Oligoscan results below. As 'non-optimal' as they are - I was actually quite pleased with the results and I think they suggest the work I have done the last few months has not been in vain (I was expecting them to be a LOT worse).

I am pretty stoked now to optimize my mineral intake based on actual data and also to be able to do monthly testing. A recent OAT and @biomesight is on the way and a CMA is also in the works.

The one big problem area was LOW ZINC and lowish COPPER. Zinc is probably THE most important mineral across the board for most issues and it is likely driving a lot of the blocks and pathway dysfunctions. Low copper is also an issue and will need to be repleted together. I will be tweaking my nutrient supplements (more D, C, Bs, E, A) and also adding Chromium, Zinc, Mitosynergy transdermal Copper, and more Silica and Molybdenum than I was using before. The mineral deficiency score is driven in part by the low zinc which affects a LOT of the body's biochemical function.

What does the scientific literature say about the risk of neuropsychiatric side-effects and Montelukast?

I am incredibly angry after a google scholar search. The consensus (even with the black box warning) is that it is a SAFE drug and common side effects are related to allergy (see pic below).

BUT!!!!

The X-poll suggests that of ~1/3 of respondents that took the drug had "awful side effects" and from reading the responses we can clearly see these were not your run of the mill mild adverse side effects.

Suicidality and psychosis as a big deal.

So, what is it about the #MECFS #LongCovid population that raises the risk of neuropsychiatric side-effects so sharply?

Because like with most safety issues to do with Pharma - adverse events have been buried as deeply as possible so unravelling this is nearly impossible as no one has done adequate studies.

Even more insidious, one of the studies I read suggested that allergic rhinitis itself drove neuropsychiatric effects - thus placing the blame on the allergy response itself.

Hmm...

So, despite the black box warning - the literature mostly suggests the pattern is NULL - invalid, weak, non-existent.

Once again patients experience gets thrown out the window.

My take on this is that pre-existing neuroinflammation likely increases RISK. This could be due to pathogens and it could also be due to mast cell dysfunction itself. There is obviously something going on here - something probably covered up and thus unravelling this from public data hard to impossible.

At least we can warn each other about risks. I am not giving medical advice about whether to take or not, however safer options for MCAS at least DO EXIST. In my mind Montelukast is not a first line medication for MCAS due to this issue. Ugh...even worse.
link.springer.com/article/10.100…