Ketogenic diet for M.E.: Can it really be this simple?

Can it really be this simple? A ketogenic diet…. or supplements like caprylic acid or medium-chain triglycerides… replace glucose metabolism with β-Hydroxybutyrate and acetoacetate, or ketosis.

In myalgic encephalomyelitis (and multiple sclerosis), the ability to break down amino acids like tryptophan is affected by reduced IDO level. IDO isn’t there because it needs interferons like IFN-beta and IFN-gamma, which are essential building blocks of the immune system, which these diseases reduce. The ketogenic (high-fat, low-carb) diet, or ketone bodies in general, bypass this problem.

Evidence points to an effect on brain handling of amino acids, especially glutamic acid, the major excitatory neurotransmitter of the central nervous system. The diet may limit the availability of oxaloacetate to the aspartate aminotransferase reaction, an important route of brain glutamate handling. As a result, more glutamate becomes accessible to the glutamate decarboxylase reaction to yield gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter and an important antiseizure agent. In addition, the ketogenic diet appears to favor the synthesis of glutamine, an essential precursor to GABA. This occurs both because ketone body carbon is metabolized to glutamine and because in ketosis there is increased consumption of acetate, which astrocytes in the brain quickly convert to glutamine.
The ketogenic diet and brain metabolism of amino acids: relationship to the anticonvulsant effect.

The extreme hypersensitivity to sound, and the whirlwind of discombobulated sensations that replaces ordinary thought in severe ME, and causes paralysis, is a type of seizure. GABA is a natural anti-seizure agent in the nervous system. This line of thought says that the neurological manifestations of M.E. are due to a metabolic disorder, which is triggered by imbalances in the immune system.

It is well known by the ME community (not ME/CFS) that this disease features abnormalities in cellular energy utilization.

This review article explores the rationale for using the KD and related dietary treatments in neurological disorders outside of epilepsy, and summarizes the clinical experience to date. An underlying theme of such diet-based therapies is that nutrients and metabolic substrates can exert profound effects on neuronal plasticity, modifying neural circuits and cellular properties to enhance and normalize function. At a fundamental level, any disease in which the pathogenesis is influenced by abnormalities in cellular energy utilization – and this implies almost every known condition – would theoretically be amenable to the KD. It is important to acknowledge that much of the data discussed here are preliminary and anecdotal, and hence need to be validated by well-controlled prospective studies. Nevertheless, that diet and nutrition should influence brain function should not be altogether surprising, and there are already abundant clinical and laboratory data linking defects in energy metabolism to a wide variety of disease states (Waldbaum and Patel, 2010; Roth et al., 2011; Schiff et al., 2011). Thus, the potential for interesting and novel applications of the KD and related dietary therapies is almost limitless (Stafstrom, 2004).
The Ketogenic Diet as a Treatment Paradigm for Diverse Neurological Disorders

Oxidative stress is the first link in the ME chain, ahead of even STAT-1 inhibition. Oxidative stress in increased by exercise, which brings on post-exertional neuroimmune exhaustion. Radioactive contaminants in the body also lead to free radicals and oxidative stress, since radiation causes radiolysis, the splitting of water into hydrogen and oxygen:
Suppression of Oxidative Stress by β-Hydroxybutyrate, an Endogenous Histone Deacetylase Inhibitor

Ketosis reduces the amount of glutamate available for neurotransmitter usage, and is then available for GABA synthesis. Glutamate as a neurotransmitter causes neural excitability, and the hypersensitivity and paralysis in severe ME, and GABA causes the opposite, neural inhibition:
Availability of neurotransmitter glutamate is diminished when β-hydroxybutyrate replaces glucose in cultured neurons

An increasing number of data demonstrate the utility of ketogenic diets in a variety of metabolic diseases as obesity, metabolic syndrome, and diabetes. In regard to neurological disorders, ketogenic diet is recognized as an effective treatment for pharmacoresistant epilepsy but emerging data suggests that ketogenic diet could be also useful in amyotrophic lateral sclerosis, Alzheimer, Parkinson’s disease, and some mitochondriopathies. Although these diseases have different pathogenesis and features, there are some common mechanisms that could explain the effects of ketogenic diets. These mechanisms are to provide an efficient source of energy for the treatment of certain types of neurodegenerative diseases characterized by focal brain hypometabolism; to decrease the oxidative damage associated with various kinds of metabolic stress; to increase the mitochondrial biogenesis pathways; and to take advantage of the capacity of ketones to bypass the defect in complex I activity implicated in some neurological diseases.
Ketogenic Diet in Neuromuscular and Neurodegenerative Diseases

Here we hypothesize that CNS depressants may promote consciousness recovery by reversing a condition of GABA impairment in the injured brain, restoring the normal ratio between synaptic excitation and inhibition, which is the prerequisite for any transition from a resting state to goal-oriented activities (GABA impairment hypothesis). Alternative or complementary mechanisms underlying the improvement of consciousness may include the reversal of a neurodormant state within areas affected by diaschisis (diaschisis hypothesis) and the modulation of an informative overload to the cortex as a consequence of filter failure in the injured brain (informative overload hypothesis).
Silencing the brain may be better than stimulating it. The GABA effect.

24 thoughts on “Ketogenic diet for M.E.: Can it really be this simple?

  1. Had heard that remarked by a commenter on a (previously posted here – am not able to search comments here, hopefully admin can) UK site, where he alleged his surprise how avoidance of certain foodstuffs aided his quality of life. It seemed like an “outlier” at the time, yet it would not surprise me that it was data instead. Would the optimal particular nutritional foodstuffs melange vary from person to person?

    Huh. I missed the extended version the first time through. Seems timely.

    Title: “What is M.E.? Extra extended version”

    Quote: “The terms ‘fatigue’ and ‘chronic fatigue’ were not associated with defining this illness at all” [(Myalgic Encephalomyelitis – M.E.)] ” until the new name (and definition) of ‘Chronic Fatigue Syndrome’ was created in 1988 in the USA (Hyde 2006, [online]). But M.E. and CFS are not synonymous terms.”

    http://www.hfme.org/whatismeextraextended.htm

    “The UK definition of CFS was also arrived at without the vast majority of those involved having had the benefit of examining either individual patients or an outbreak of the illness. Many of them were also psychologists rather than physicians. It was a similar story worldwide. As M.E. expert Dr Byron Hyde writes, ‘The inclusion of psychiatrists in the defining of an epidemic and [what is] obviously a disease of infectious origin, simply muddies the water for any serious understanding of that disease’ (1998, [Online]).

    Why were the renaming and redefining of the distinct neurological disease Myalgic Encephalomyelitis allowed – indeed intended – to become so muddied? Indeed why did Myalgic Encephalomyelitis suddenly need to be renamed or redefined at all?

    Money.

    There was an enormous rise in the reported incidence of Myalgic Encephalomyelitis in the late 1970s and 1980s, alarming medical insurance companies in the US. So it was at this time that certain psychiatrists and others involved in the medical insurance industry (on both sides of the Atlantic) began their campaign to reclassify the severely incapacitating and discrete neurological disorder known as Myalgic Encephalomyelitis as a psychological or ‘personality’ disorder, in order to side-step the financial responsibility of so many new claims (Marshall & Williams 2005a, [Online]). As Professor Malcolm Hooper explains:

    In the 1980s in the US (where there is no NHS and most of the costs of health care are borne by insurance companies), the incidence of ME escalated rapidly, so a political decision was taken to rename M.E. as “chronic fatigue syndrome”, the cardinal feature of which was to be chronic or on going “fatigue”, a symptom so universal that any insurance claim based on “tiredness” could be expediently denied. The new case definition bore little relation to M.E.: objections were raised by experienced international clinicians and medical scientists, but all objections were ignored… To the serious disadvantage of patients, these psychiatrists have propagated untruths and falsehoods about the disorder to the medical, legal, insurance and media communities, as well as to government Ministers and to Members of Parliament, resulting in the withdrawal and erosion of both social and financial support [for M.E. patients] (2003a, [Online]). Influenced by these psychiatrists, government bodies around the world have continued to propagate the same falsehoods with the result that patients are left without any hope of understanding or of health service provision or delivery. As a consequence, government funding into the biomedical aspects of the disorder is non-existent (2001, [Online])”

    “The only way forward, for the benefit of society and every patient group involved, is that:
    1. The bogus disease category of ‘CFS’ must be abandoned completely.”

    “2. The name Myalgic Encephalomyelitis must be fully restored (to the exclusion of all others) and the World Health Organization classification of M.E. must be accepted and adhered to in all official documentations and government policy.”

    “3. People with M.E. must immediately stop being treated as if they are mentally ill, or suffer with a behavioural illness, or as if their physical symptoms do not exist or can be improved with ‘positive thinking’ and exercise – or mixed in with various ‘fatigue’ sufferers in any way or patients with any other illness than authentic Myalgic Encephalomyelitis. ”

    I would add, if relevant: 4. Lobby groups that fundraise for MS to extend their umbrella towards other similar forms of disease, such as M.E

    • “it’s an unholy … vortex … of fraud!” – Max Keiser
      http://www.youtube.com/watch?v=o78jG5BJf18#t=598

      Is M.E. another example of “the Privatization of Risk”?
      Majia and yourself would be more qualified to assess that.
      Of certainty it seems to me that risk in the current financial climate is being actively privatized, in manifold ways, as we ponder the very fact. When the poker chips are nearly free for the fat cats, is not the nature of such gambles towards high-risk high-return and thereby high-stakes poker where the citizen’s share in the (former) partnership is a compounding bill for the failed gambles (with their own potential “outlier” body counts) by players at the table???

      Tip it good, Soltysik-sensei.

    • Quote: “So what you can do to help is to PLEASE help to spread the truth about Myalgic Encephalomyelitis and try to expose the lie of ‘CFS.’ You can also help by NOT supporting the bogus concepts of ‘CFS,’ ‘ME/CFS,’ ‘subgroups of ME/CFS,’ ‘CFS/ME,’ ‘CFIDS’ and Myalgic ‘Encephalopathy.’ Do not support groups which promote these concepts. Do not give public or financial help to our abusers.

      This appalling abuse and neglect of so many severely ill people on such an industrial scale is truly inhuman and has already gone on for far too long.

      People with M.E. desperately need your help.”
      http://www.hfme.org/whatismeextraextended.htm

      Whydo i get the sense that Obamacare didn’t solve inequalities for M.E. sufferers (hoping am wrong).

      http://www.hfme.org/whobenefitsfromcfs.htm
      Quote: “medical insurance companies”

    • Chronic fatigue syndrome is a cluster of symptoms associated with autoimmune diseases like arthritis. Myalgic encephalomyelitis is a neurological disease like multiple sclerosis. I used to have CFS. CFS went away when my lifelong autoimmune disease went away, when I suddenly got ME.

      I have been trying to figure out what the hell is going on. There is no way to communicate with others who have ME online, because there are 10 CFS people for every ME person, and they all say they have ME/CFS, which doesn’t exist.

      CFS features an upgrade in cellular immunity, ME is a devastating deficiency in cellular immunity. Not only are they not the same disease, they are opposite diseases.

      On top of that, I just came down with enterovirus 68 myself.

    • Guess not, you need true ketone esters:

      Oral administration of BHB and AcAc in their free acid form is expensive and ineffective at producing sustained ketosis. One idea has been to buffer the free acid form of BHB with sodium salts, but this is largely ineffective at preventing seizures in animal models and causes a potentially harmful sodium overload at therapeutic levels of ketosis (6). However, esters of BHB or AcAc can effectively induce a rapid and sustained ketosis (7, 21) that mimics the sustained ketosis achieved with a strict KD or prolonged fasting without dietary restriction.

      http://ajpregu.physiology.org/content/304/10/R829

      • “Guess not, you need true ketone esters:…”

        I don’t think that’s a fair statement despite the accurate quotation, Bobby. There are essentially two companies/research camps/patent holders competing to bring a ketone ester precursor to market: TDeltaS (Oxford) in the UK, and Savind (Univ South Florida – USF) in the US. Neither one actually has an esther-based product in the market.

        The only ketone precursor commercially available, as far as I know, is the KetoForce precursor salts through Patrick Arnold’s Prototype Nutrition (though Savind).

        KetoForce is directed at the extreme performance sport crowd. It uses both sodium and potassium salts, unlike the pure sodium salts used in older USF research. It gives a pretty stiff daily dose of either sodium or potassium, but neither is really a problem for a tri-athelete or long-distance runner.

        Dosing for the beneficial ketone effects for ME (vs. performance sports) over days or weeks could be more of an issue. But we’re still just talking ‘a lot’ of sodium and potassium – like ‘junk-food levels’, not an extraordinary or lethal amount. Maybe some ME sufferers would be able to tolerate the levels at beneficial therapeutic doses and others would not.

        The two assertions about the salts in quote from the AJP article – no anti-seizure properties and potential sodium overload – contains footnote (6), which references a 2007 study by Bough and Rho, Anticonvulsant mechanisms of the ketogenic diet. Epilepsia 48: 43–58, 2007. That study,

        http://onlinelibrary.wiley.com/doi/10.1111/j.1528-1167.2007.00915.x/pdf

        seemingly makes no mention of BHB salts at all, unless I’m missing something. Since the AJP article relates to the ‘new and improved’ esther precursor, I wonder if the dismissive tone is intentional.

        I can’t speak to the anti-seizure claim, but there’s little reason NOT to believe the BHB salts in KetoForce do raise blood ketone levels the same as any other precursor would. I’m not promoting it by any means, but at least it’s available. The $25 or so per day cost puts it well outside my financial means for a few week trial just for the heck of it.

        The TDeltaS esther is reported to be in the hundreds of dollars/day theraputic dose range cost for the small quantities they produce now. If they ever do get funding to ramp up, it looks like it will still be fairly expensive – similar to KetoForce. Same problem with the USF/D’agostino esther. Patrick Arnold made a comment that TDeltaS and USF/Savind’s esthers would be targeted to the pharmaceutical markets rather than the sports supplement markets. Cost might very well be the driver behind that.

        The down-side of targeting esthers to the pharma side is that it may be years before they are approved for treatment of any one specific condition, and/or paid for by insurance.

        • I wish I knew more about this issue. Ketone esters should be regarded as GRAS (Generally Recognized As Safe), so there should be all sorts of Chinese manufacturers jumping on it to drive the price down. There must be some shenanigans going on to keep the price up.

          ME, MS, Alzheimer’s and some epilepsy patients need this. It should be regarded as a supplement. I know I really need this. Ketone esters are potentially 10-100 times as powerful as ketogenic diets and coconut oil in promoting ketosis metabolism. The GABA supplements I take (phenibut) have too many side effects.

          • Synthesizing a particular ester at all, much less a *suitable* and marketable ester seems to be legitimately technically challenging. The TDeltaS http://www.faqs.org/patents/app/20130102663 patent discusses the chemical black magic a bit.

            From the material that’s out there, it seems there was limited commercial interest until recently in spending time on development. The two esters mentioned above were just patented last year. I understand why pharma interest has been limited – they don’t seem know the exact mechanisms at work for the potential therapeutic uses. That’s pretty evident in the USF anti-seizure studies. The more you read, the more complex and speculative it becomes. That always makes it a bit dicey for regulatory approval. Aspirin would never make it through regulation to market today.

            It will probably take a lot more interest from the weight loss / athletic supplement markets before the Chinese are interested in bulk production of something and we see affordable products. I won’t comment on the sad state of moral depravity for depending on the sports supplement profit motive vs. motives for therapeutic use to reduce human suffering. I’m just assuming that’s the way it’s going to play out…

            I agree with your comments on the efficacy of precursor esters vs. ketogenic diets for the most part, Bobby. And most certainly for therapeutic use for serious illnesses like yours.

            My interest in ketones and the digestive system are mostly for a potential poor man’s answer to metabolic and immune disorders. KDs are of limited use because, as you have observed, they just don’t produce enough circulating ketone bodies. I have nothing more than a hunch, but I think that there’s a potential to produce higher levels through the diet route than are currently noted. I don’t know if that means ‘high enough’ for theraputic value, but certainly higher than the sub mM values currently reported.

            Those levels make sense from a starvation/survival perspective, not an evolutionary perspective. I wouldn’t think cavemen survived in northern latitudes for four months or so of winter on a few tenths of a mM of ketone, but maybe I’m wrong.

            As I rambled on about in my other post, I think there may be some combination of lower intestine bacteria and some optimal food *for them* that results in nutrients for us that provide an overall higher level of circulating ketones. That is, it’s not as simple as say direct intestinal absorption of MCTs and their eventual conversion in the liver. I know that works, it just doesn’t seem to work fast enough. Maybe a healthy colony of some species of beneficial bacteria and eating tree bark results in symbiotic magic that produces single-digit mM quantities of blood ketones.

  2. Whoa, this is TANTALIZINGLY close to being an effective treatment for ME neurological symptoms. Psilocybin preferentially activates the 5-HT2A serotonic receptors, which activate GABA transmission… it deactivates the default mode network (!) Unfortunately, the party pooper TGF-beta shows up, which screws with the immune end of ME. Still, maybe take psilocybin with a TGF-beta inhibitor?

    http://www.pnas.org/content/109/6/2138.full.pdf+html

    http://blogs.scientificamerican.com/scicurious-brain/2012/02/08/this-is-your-brain-on-psilocybin/

    • So we have these possible treatments for ME:

      1. Ampligen, IL-12, IFN-gamma. They address the cause of the disease, but they are very expensive and may have significant side effects.

      2. Baclofen, phenibut, tiagabine. These increase GABA levels and inhibitory transmission. Great for hypersensitivity, pain, tinnitus. Not so good addressing brain fog, cognitive defects. Sedating & addictive, but should be considered for severe ME.

      3. Ketone esters, ketogenic diet. The diet should help, but ketone esters in pill form should really do the trick by bypassing glucose metabolism entirely. But ketone esters are in the rat testing phase.

      4. Psilocybin and other drugs that are agonists preferentially or only at the 5-HT2A receptors. Must be combined with TGF-beta inhibitors.

      5. Antioxidants, alpha lipoic acid, L-carnitine etc. Important, but I don’t think they’ll do the trick by themselves.

      6. Serotonin antagonists, TGF-beta inhibitors, amino acid formulations, probiotics such as L. rhamnosus and L. casei. Who knows.

  3. The day the reactor exploded, I said to my wife that was the last bottle of milk that my son will drink. And so far that has been the case.

    The radically change their diet about a month after the Greack Thursday melted down as I started to gather more information about how certain foods could remove fallout from our bodies and restore damage.

    There have been a few variants over the last few years. I can’t believe it’s been years now that that thing has been melting down. Assholes.

    Basically the core has been 1.krill oil,
    2. chlorella,
    3. seaweed soup, lots of it, 4. Alpha lipoic acid-r,(I guess this is an important distinction. And not regular alpha lipoic acid, which I understand might cause more damage if there’s fallout. )
    5. Melatonin ( kids too)
    6. Fermented plum juice
    7. Lypo-c
    Then added..

    Coconut oil for all we do..

    Prior to eating this food, although I ate quite well, I was in some sort of pre- disease state as I woke up in the mornings with general inflammation .

    I ate NAC for the first year or so me. This supplement is used to boost glutathione production in the body. I stopped using it however as I was having some lung issues.

    Strangely, I feel better and healthier after the nuclear reactors blew that I did before.

    But I’m feeling bolder these days am and venturing out to eat ‘forbidden’ foods. I guess a lot of feed from Japan is sold in korea.. So I don’t venture to far. Isn’t that just gross?
    Who the frick are these people?

    I hope you can find what you need Bobby. Because we need you.

    ——————————
    I have learned that
    Once these nuke puke bastards die, Their wills will be fixed. And for the that means against love and against my Lord.

    Furthermore…I was taught today that I should not pray for the damned. Nice….

    • Thanks, Iwunder. I changed the way I ate and felt better than I did before, in 2011. But it didn’t last long.

      I started to eat only imported food. I tried to get southern hemisphere food, but settled for European if I had to. I was eating Korean food too… as long as it wasn’t fish, seaweed, or mushrooms, it was better than anything from America.

      The metal taste in my mouth, I found out later, was from inflammation. I had a pituitary tumor, and this made my autoimmune diseases much worse… every time I ate something contaminated with radionuclides, inflammation would start up in the salivary gland area. In February 2013 I started taking hydergine for the tumor. I didn’t get metal mouth anymore. This was part of my downfall, I started eating American food again.

      And yes, you’re right, you should not pray for the damned. Though it is possible that a nuke sociopath sees the light. It has happened before.

  4. The epithelial cells in your large intestine metabolize short-chain fatty acids into ketone bodies. Mucosal flora (healthy gut bacteria) should produce short-chain fatty acids if fed properly – mostly in your large intestine. ‘Proper feeding’ means digestive-resistant dietary starches that make it though the small intestine undigested.

    Dietary ketones may help temporarily with gut bacteria dysbiosis but candidia – for example – will readily and preferentially consume ketones. So will other ‘bad’ gut bacteria. The rapid candidia overgrowth will compound the existing dysbiosis, trap more heavy metals, and result in a worse leaky gut syndrome and immune system degradation.

    This might not happen in a healthy digestive system, so endurance athletes using ketone supplementation for performance reasons wouldn’t notice – maybe it doesn’t happen to them. You may have a profoundly different experience if your digestive system is already compromised.

    I’ve never supplemented with ketones, but have had candida overgrowth (or some kind of general dysbiosis) caused by a few trials of dietary ketosis a while back. The extra energy and mental clarity effects only lasted a few days. This was confounding because it had ‘worked’ fine when I was younger for as long as I wanted to stay in ketosis.

    Much later, many friends using KD with their autistic children were noting the same kind of temporary effect followed by worsening of other GI problems. That frustrated them because they knew others had success with KD. Someone made the connection that it was crucial to start out with healthy, functional gut flora in their child before trying to ‘fix’ something, which makes perfect sense.

    The ‘right’ way to do this seemed to be to tackle any hint of candidiasis first, followed by rehabilitation of the gut and mucosal lining along with proper feeding of the intestinal flora – particularly that of the large intestine – accomplished through dietary resistive starches (RS). The small intestine does not digest RS, so large intestine flora are dependent on them as a food source. Give them enough and they will flourish and get busy making short chain fatty acids, which your intestines will partially metabolize to ketone bodies.

    The poor man’s test for ‘proper’ bacteria balance throughout the digestive system is to eat gassy foods – they have a lot of RS. If you have the proper balance and adequate quantity of well-fed beneficial bacteria, you will not get ANY gas. There are rare genetic exceptions to that. Efficient chain fermentation (through multiple ‘normal’ strains of gut bacteria) of RS to short chain fatty acids does not yield carbon dioxide or methane or any other gas as a byproduct. Efficient chain fermentation and adequate SFCA will keep the intestinal epithelial cells healthy and maximize their natural production of ketones.

    Supplementing at that point may very well be beneficial for ME. I don’t know. My personal N=1 sample of using dietary ketosis for heavy metal toxin- (and probably radiation-) induced CFS-like symptoms will probably never happen. Rehabilitating my gut seems to have made them pretty much disappear. Bonus: I can smell again and have dreams in color after a decade of neither (don’t ask me!).

  5. I started on coconut oil and caprylic acid. I think it is helping with the ME symptoms… but what unpleasant side effects, nausea, and headachy feeling, mostly due to the caprylic acid. It will kill the candida, though. Hopefully it will control the dermatitis which is fungus-related, too.

    • I feel for you, Bobby – herxheimer from candida is the worst. Alcohol, ammonia, aldehydes, neurotoxins… yeast has developed an impressive array of self-defense mechanisms. Ideally, one would tough it out for however long it takes – a few days or a few weeks. Which is easy to say if you’re not already really sick to begin with. I would encourage a less masochistic approach: if it becomes overwhelming after a few days, than give your body a break to clean out the toxins and start up the caprylic acid again a few days later. Herx reactions for the second and subsequent rounds are usually a lot milder. The caprylic acid will eventually kill all of it no matter how many breaks you need to take.

      Everyone on the internet has advice for dealing with the herx, but they seem to be trying to get you to dump even more stuff in your already overloaded body – herbs, vitamins, antioxidants, etc. The only things that seemed to make sense/work for me were things specifically to move the released toxins out of your body as fast as humanly possible.

      – Ginger keeps the stomach and upper digestive tract active and emptying themselves quickly. Ginger tea works for some people. I prefer to gobble spoonfuls of pickled ginger (the pink stuff in the Asian food section) for a stronger effect. Ginger also helps a lot with the nausea.

      – Magnesium to keep your lower digestive tract active if that’s an issue. Even if it’s not, some people prefer to intentionally overdo it anyways. Extremely loose stools are an acceptable trade-off for a week or so to minimize herx – even a little – by getting rid of the released toxins as quickly as possible.

      – Activated charcoal doesn’t help with the alcohol and ammonia, but seems to grab a few of the neurotoxins and seems to help with headaches. Hard to tell with everything else going on. A good thing anyways if you have any heavy metal/radiation toxicity:

      Candida wraps itself in a protective biofilm. It’s a polysaccaride matrix that incorporates metal ions (like magnesium and iron). One hypothesized hiding place for ingested and inhaled radionuclides is in that matrix through substitution. Cesium and Strontium are likely culprits. Biofilms are one of the primary radioactive bioaccumulation routes for simple organisms. Yeast biofilms seem to suck up a fair amount of mercury as well.

      Activated charcoal *may* help pick up some of the stray metal ions released when the yeast dies and the matrix degrades. That has little to do with helping minimize the herx reaction, but you have to like the idea of any released toxic metals (especially cesium) leaving your body once and for all rather than risk reabsorption further down your digestive tract.

      Good luck. I hope you post updates.

  6. In the last 25 years, my arthritis has always gone away in the summer, and comes back around October 15. This changed after Fukushima, becoming year-round.

    Coming down with ME made the arthritis go away. It was replaced with neuropathic pain. It is interesting to speculate what will happen this month. Will the arthritis come back? It always increases IFN-gamma levels. That should make the neurological symptoms subside.

    Or will the arthritis morph into something else, like the psoriasis morphed into eczema and dermatitis? Being disabled with arthritis is like paradise compared to full-blown ME.

  7. After going on a Ketogenic diet to lose weight and having my CFS/ ME/FIBROMYALGIA all but disappear and being able to take up some academic study after losing 25 years of my life to these Illnesses all I can say is there is definitely something here that demands a closer look. I have only had one short bout of Fibro after knee replacement surgery and a few days on a normal diet in hospital. I wouldn’t like to hazard a guess as to which of those triggered it ~ probably both.
    I wish I had known about this years ago!

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