Two Cognitive Diseases
Fibromyalgia is more than a pain disease – it’s also a cognitive disease. In fact, some studies suggest the cognitive issues can present more problems than the pain. They’ve been prevalent and serious enough to spark the creation of a new term: “fibro-fog”. Unfortunately, not many cognitive FM studies have been done, but those that have been suggest that the same problems with information processing speed found in chronic fatigue syndrome (ME/CFS) exist in fibromyalgia as well.
Cognitive issues are common in FM – but is ADHD present as well?
There’s some evidence that cognitive slowing in FM causes more than mental distress and may contribute to the fatigue and pain FM patients experience as well. The difficulty FM patients’ brains have in switching off their attention to innocuous background stimuli can contribute to mental and even physical fatigue. Plus, the sheer effort it takes to screen out the pain signals in FM in order to concentrate on something can contribute to fatigue. In fact, one study which found increased pain and fatigue after a cognitive task in people with FM suggests that a kind of mental post-exertional malaise exists in fibromyalgia.
Plus, poor sleep, antidepressants, anti-epileptics, and opioid pain relievers can also produce problems with concentration. In short, there’s no dearth of reasons for the cognitive problems present in fibromyalgia. Plus, a recent study found somewhat increased rates of dementia in fibromyalgia.
ADHD?
Cognitive issues clearly exist in both ME/CFS and fibromyalgia, but what about attention deficit hyperactivity disorder (ADHD)? Pairing a hyperactivity disorder with a fatigue and pain disorder might seem strange, but the “wired and tired” problems in both ME/CFS and FM suggest that an odd combination of system hyperactivity and fatigue may be present.
According to the National Institute of Mental Health (NIMH) ADHD is characterized by a difficulty staying on task and sustaining focus, feeling the need to move constantly, and increased impulsive behaviors. People with ADHD tend to miss details, have problems organizing activities, lose things, and are easily distracted. (That pretty much fits me to a tee…)
The reduced information processing speed found in ME/CFS and FM impairs one’s ability to take in information and can contribute to problems like ADHD or ADD (attention-deficit disorder).
Given common complaints of “racing minds”, difficulty concentrating, difficulty following conversations and the wired and tired state, ADHD seems like a natural fit for both FM and ME/CFS. In fact, several past studies have suggested that ADHD is increased in FM, and one found that 30% of children with ME/CFS met the criteria for ADHD.
The Study
Screening for Adult ADHD in Patients with Fibromyalgia Syndrome. Roland van Rensburg, MBChB,* Helgard Pieter Meyer, FCFP(SA),* Sonia Anne Hitchcock, MPraxMed,* and Christian Edward Schuler, MMed (Psych). Pain Med. 2017 Nov 1. doi: 10.1093/pm/pnx275. [Epub ahead of print]
This South African study screened 123 fibromyalgia patients for adult ADHD using the World Health Organization Adult ADHD Self Report Scale v1.1. It also assessed their symptoms.
- Find the WHO’s self-test for ADHD in Health Rising’s Cognitive Resource section.
Remarkably, almost 45% (44.72%) of FM patients screened positive for adult ADHD using the self-test. If that number is accurate, it represents an enormous increase in ADHD prevalence in FM relative to the general population (5.29%/ 7.1% – children/ adolescents; 3.4% – adults). Self-report tests (FIQ-R) suggested that people who had both ADHD and FM were more functionally impaired as well.
Connections
The authors suggested that problems in the dopaminergic system may connect the two diseases.
High rates of mood disorders and an abundance of neuropsychiatric symptoms have lead ADHD to be characterized as a kind of psychiatric disease. The view of ADHD as simply a brain disease is changing, however. Research indicates that ADHD is more than simply a neuropsychiatric disease with strong ties to mood disorders. Slowly but surely, an immune component of the disease is being uncovered.
Some studies suggest the immune system is involved in ADHD.
A recent large study (n=23,645) found an increased incidence of ADHD in autoimmune diseases like Type 1 diabetes, autoimmune hepatitis, psoriasis and ankylosing spondylitis. Another study found that women with psoriasis, Crohn’s disease or ulcerative colitis had an increased risk of ADHD.
Another study found that the children of mothers with immune diseases such as multiple sclerosis, rheumatoid arthritis, asthma, hypothyroidism, and Type 1 diabetes had an increased risk of ADHD. The authors believe that autoimmune disorders in the mother caused an “exaggerated central nervous system inflammatory response” in the child.
Interestingly, given the high rate of hypothyroidism in both FM and ME/CFS, another study found that children of mothers with elevated levels of maternal thyroid peroxidase antibodies had more ADHD symptoms. The authors suggested that antibodies in the mother affected the neuronal development of their children. Some Georgetown University researchers proposed that allergic reactions could contribute to ADHD, ME/CFS and FM.
Treatment
If ADHD is indeed increased in FM and/or ME/CFS, what to do about it? Since most of the approaches below have not been tested in ME/CFS or FM – two diseases with considerably more fatigue and pain than ADHD – it’s hard to tell.
Behavioral Approaches
The Attention Deficit Disorder Association (ADDA) asserts that cognitive behavioral therapy and other mindfulness-based practices are the most effective therapeutic approaches to ADHD. They reported that these practices can help develop “new, workable actions and skills in the present moment” and that ADHD coaching can help “improve organizational skills, time management, goal completion, and productivity.”
There is no cure for ADHD but studies suggest that brain training can help.
Many studies have addressed this approach. A 2017 Mindfulness-Based Cognitive-Therapy (MBCT) program resulted in “a significant reduction of ADHD symptoms and improvements of executive functioning, self-compassion, and mental health.” A “Cognitive-Functional (Cog-Fun) occupational therapy intervention“, designed to improve executive functioning (attention, organizational skills, etc.), reported that it had similar effects in children. A literature review suggested that mindfulness approaches done in conjunction with stimulant medications were the most effective.
Mindfulness-Based Cognitive Therapy (MBCT) seeks to identify and alter problematic thinking patterns and use mindfulness meditation to increase focus, stop the mind from wandering so much and reduce distractibility, and regulate the emotions better. Researchers believe it does this by taking advantage of the inherent plasticity of the brain to improve the functioning of the default mode network, which plays a large role in attention. Approaches like these take work – studies indicated that the more you do them the better effects they have – but the study evidence is pretty clear that they can help (there is no cure for ADHD).
Psychostimulants
Stimulants such as Ritalin, Concerta, Adderall, Adderall XR, Vyvanse, and Focalin XR are commonly used in ADHD, and non-stimulant medications (Strattera, Intuniv, SNRI’s such as Welbutrin, etc.) can reportedly help as well.
Psychostimulants may be able, in some patients, to improve more than cognition. One case study reported that the cognitive scores as well as fatigue and pain scores improved in three patients with chronic fatigue syndrome (ME/CFS). Another case report found that problems with focus, distractibility, hyperactivity and impulsivity, as well as pain and fatigue, improved in a person with FM taking psychostimulants. I know of one person with ME/CFS who said psychostimulants essentially solved his fatigue problems.
Back in 2002 Glenda H. Davis, MD, and Patricia Stephens, CNC, reported that ADHD medications can provide an “unlikely source of relief” by alleviating fatigue, memory fog and mood swings in FM. They cautioned, though, against self-medicating and urged FM patients to seek out good practitioners. The most common psychostimulant, Adderall, which combines amphetamine and dextroamphetamine, can be addictive and can lead to crashes when not used properly.
While noting that psychostimulants can indeed boost energy levels, Dr. Murphree asserts that long term use – which these studies do not address – is “a disaster for most folks, but especially so for those with fibromyalgia and or chronic fatigue syndrome (CFS/ME)”. Stating that taking psychostimulants will stress your adrenal glands, Murphree pointed to a long list of potential side effects, and argued that, “Whipping the exhausted horse harder and harder isn’t the answer – eventually your fatigued adrenals, like the exhausted horse, will give out, no matter how hard you try to stimulate them.”
Dr. Jon Kaiser, another alternative-focused MD, might disagree. Kaiser, who has or had ME/CFS at one time (he improved using rest, pacing, micronutrient therapy, physical therapy, and an aggressive stress reduction program) believes that stimulating drugs in combination with micronutrients can help revive the mitochondrial functioning in ME/CFS patients. Once that mitochondrial wake-up has been achieved, the drug is no longer needed.
Kaiser reported on many ME/CFS/FM patients who improved on his protocol, and ultimately produced the Synergy trial which combined Methylphenidate/Ritalin and a nutrient formula for ME/CFS patients. Patients receiving the drug/nutrient combination reported a significant increase in functionality, but a surprisingly high placebo response rate in some patients essentially nullified the result. (Ten to fifteen patients on the placebo responded so well as to be considered cured (!).)
Stimulant Effectiveness Poll for Fibromyalgia and ME/CFS
A 2010 Cochrane Review examining psychostimulant effectiveness in cancer fatigue reported that, “There is increasing evidence that psychostimulant trials provide evidence for improvement in CRF at a clinically meaningful level”. Another 2015 Cochrane review of studies for people with very serious illnesses reported that modafinil and methylphenidate may help improve fatigue in palliative care. (The review suggested that dexamethasone, methylprednisolone, acetylsalicylic acid, armodafinil, amantadine and L-carnitine should be studied further.) These trials do not address possible long-term effects of the drug.
A meta-analysis found that behavioral therapy, stimulants, and non-stimulant drugs were all at least somewhat effective treatments. (No cure for ADHD is known). The most effective stand-alone therapy was stimulants, and the most effective therapy overall was behavioral therapy combined with stimulants.
Conclusion
More studies are needed but this study’s results – that ADHD appears to be highly prevalent in FM – suggests that we can add another comorbidity to the rather long list of disorders (ME/CFS, migraine, IBS, POTS, depression) associated with fibromyalgia. Whether or not ADHD is clinically present, ADHD-like issues such as poor attention span and problems with organization appear to be common in both diseases. The wired but tired issues in ME/CFS/FM seem to fit ADHD well.
ADHD has been traditionally conceived as a neuropsychiatric disease based in the brain, but more recent evidence suggests that the immune system is involved as well. Various treatment approaches, some of which (stimulants) have been used in both FM and ME/CFS, exist. Both mindfulness and stimulants are effective for some ADHD patients, but no cure has been found. One ME/CFS doctor warned against the long-term use of stimulants while another used them (with micronutrients) as the basis for a treatment protocol.
- Check out the World Health Organization’s self-test for ADHD in Health Rising’s Cognitive Resource section.
- Check Health Rising’s Stimulants for Fibromyalgia and Chronic Fatigue Syndrome resource page.
That’s all I need this problem just keeps getting better and better ( not ) 5 years of misery and no end in sight when will it end .or will I have too end it .May b
Hang in there Mark (and keep following ME/CFS news as well as it may impact people with FM.) I really support checking out things like mindfulness meditation to relieve your mental pain. If you’re depressed – and considering ending it is pretty depressing – please see your doctor! These diseases are tough – and rates of depression, not surprisingly, are high in them. (How could they not be?). Antidepressants can be very helpful in getting you out of a rut.
Toni Bernhard’s “How to Be Sick” is a great way to approach the emotional distress these diseases bring. It’s a Buddhist approach to chronic illness.
The recognition that ADHD rates may be high in FM could have it’s benefits if some ADHD treatments help some.
Good luck and hang in there!
Hi Cory, just a quick comment. I was diagnosed with ME at Brigham and Women’s Mastocytosis Center in Boston.
Mast Cell Activation Disorder/Disease has very similar symptoms only my tests were short by a few points to qualify for the WHO definition of MCAD, thus a diagnosis of ME. Dr. Marie Castells happened to mention that the personality trait she saw most commonly in her mast cell patients was ADHD..yep, guilty as charged.
There are several things to consider about this “disorder” which, in my view isn’t really a disorder but a throwback to primal survival skills which were dependent on quick, imaginative thinking and high awareness of one’s surroundings. First is that today’s society treats those of us who are easily bored with rote memorization as “other” creating a lifetime of stress for not thinking and planning in a structured manner so stress levels (cytokines) are much higher from the getgo. Second, as I have gone from two years in bed to a productive almost normal life within 5 years of initial onset, the most remarkable thing I have experienced is that diet and toxic environmental exposure affects cognitive thinking profoundly. People don’t stop to think that all the chemicals in the body lotions, makeup and sunscreens they apply are absorbed instantly and affect the nervous system, for instance. My thinking was greatly influenced by Thom Hartmann in his books on ADHD about a Hunter in a Farmer’s World and I suggest reading his theories to broaden perspective.
Interesting! I read that ADHD is probably produced in several ways and it looks like MCAS is one of them. Ha! Thanks for the tip on the book 🙂
Cort do you have any more info on the MACAS – ADHD ME connection you mention in this stream please? This is very interesting to me.
Hi Phillida,
I haven’t come across anything recently. There could be more info – I just don’t know.
Hello Mark,
It wasn’t that long ago that I was in bed planning the ending to my life story because I felt like I had lost control over my pain and my life and the exhaustion was too much to bear. Then one day I watched the TED talk but Dr Terry Wahls on YouTube called Minding Your Mitochondria and it changed my life. I figured if she could do it I could too and that was the beginning of how I got control over my illness and started getting better. When I read about Dr Ron Davis and the research he started when his stepson got so sick I was inspired, lots of brilliant people are working on finding a cure, we just have to hang in there. It is not an easy path we have but when we change the way we look at this disorder we can discover unexpected gifts, like strangers who really care.You are not alone.
Thank you for your message. I really needed to hear that today.?
I needed this message today (different “today”) too. I have tried the adderall very, very intermittently as even a very small dose, though helpful at times, just feels as if I am drawing my adrenals. As a result I still have an RX from 3 years ago. I am happy to say that my DO had a good conversation Tuesday where I actually came clean with a more clear picture of what my day to day life struggles are really like. I have after decades backed off the more ugly aspects of my life when crashed. As a result I am going to share with him more information from pieces like these. Even though I have seen him off and on for years I don’t think I had been totally honest in my sharing tending to just hit the high points and getting his remarkable treatment when I can afford to do so.I realize that even the kindest most skilled Doctors have limited knowledge of all of the various conditions and symptoms of chronic (ME/CFS for me) illnesses. He was sympathetic and really didn’t have a true picture. I know from experience that it is almost impossible for anyone who doesn’t have it to comprehend. Heckler, most of the time I myself still forget until it whacks me upside the head again and again.
Cort, thank you for digging into this! I recently read a blurb about this study and thought “makes sense to me”.
I had a history of attention problems throughout my childhood and teen years that I eventually self-medicated with cigarettes and coffee. I was completely unaware that I had innatentive ADD. When I became ill, all my self-medication tricks—that enabled me to have a successful career and business—simply stopped working.
When they stopped working, I was able to quit smoking and limit my coffee to one cup per day but my attention difficulties just got progressively worse.
My daughter has just been diagnosed with Innatentive ADD after being incorrectly diagnosed with anxiety. My sister has a lifelong stutter and auditory filtering troubles; her son has non-verbal autism.
I am looking forward to the day when they uncover the link, the triggers, and how to help us all.
In the meantime, I will mention that eating a ketogenic diet seems to be helping me (finally) with some of my concentration issues. Wish I could get my family on the bandwagon. Life without sugar hasn’t cured my ME/CFS, but I feel better for it.
Thanks again Cort. Really appreciate your work.
There seems to be so many things that have an effect – going Ketogenic seems to help a lot of things, including brain dysfunctions like epilepsy. But it also helps the outright pain levels in FM (in my experience), so what is going on, that it is effective in such quite different things? I have believed for a long time that researchers should be looking back upstream at digestion, renal system and metabolism issues. For some (unlucky) cohort of the population, “sugar” is a poison, period. Being among this cohort seems to correlate with an increased vulnerability to FM at least, along with other triggers like trauma, injury, infection, surgery, toxic substance exposure.
One of the most frustrating things about “mainstream” medical attitudes is that “XYZ can’t be a problem because so many people are perfectly OK with it” – they dismiss the factors I mention because “everyone out there” is eating processed carbs without getting FM, or suffering stress without getting FM, or having surgery without getting FM. So an unlucky (genetic?) vulnerability has no chance of getting identified.
A lot of us discover self-help strategies that work, but it is not a cure or a reversal of our condition; we need to keep self-helping and following our helpful protocol for life, or we relapse. So obviously there is an underlying vulnerability, and that is what research should look for, otherwise we are just developing symptom-suppressing drugs that are no more effective than alternative medicine self-helps.
I agree completely. They need to identify the vulnerability, not just treat the symptoms. And I’ve also noticed a decrease in my FM pain in the absence of carbs. Seems like carbs are causing inflammation for some of us despite an absence of inflammation markers. Go figure.
Thanks, Debbie. I think the explanation is that there are some types of pain that do not produce inflammation. Or possibly the inflammation would be so widespread if it did happen, with dire consequences, the immune system deliberately suppresses it.
“There seems to be so many things that have an effect – going Ketogenic seems to help a lot of things… …so what is going on, that it is effective in such quite different things?”
The question why Ketogenic seems to help sure remains a difficult one to crack.
Lately I started to wonder if the fact that it puts people into a starvation-like hormonal state would play a significant role. A group of both ME/FM patients seems to be helped by partial fasting. Hormonally speaking (insuline, glucagon, epinphrene, norepinephrene, leptin, grehlin…) a Ketogenic diet resembles a fasting state but it offers a lower bar of entry for already weakened patients.
People who have low(ish)-caloric diets are often amongst the healthiest people in the world. Obese people who often, not always, have high-caloric diets however have high rates of inflammatory related diseases.
Another link I still try to follow is the seemingly contradiction between both a Ketogenic and a vegan diet often being helpful. I believe that using the seemingly contradictions can create much insights as they reduce the search space enormously.
I did stumble upon a new possible link.
A) from https://en.wikipedia.org/wiki/Starvation_response I did find: “Triglycerides and long-chain fatty acids are too hydrophobic to cross into brain cells, so the liver must convert them into short-chain fatty acids and ketone bodies through ketogenesis. The resulting ketone bodies… …can be transported into the brain.”
-> this gives the impression that not only ketone bodies but also short-chain fatty acids might be able to cross the blood-brain barrier…
B) from https://en.wikipedia.org/wiki/Short-chain_fatty_acid I did find: “Short-chain fatty acids (SCFAs), also referred to as volatile fatty acids (VFAs),[1] are fatty acids with two to six carbon atoms.[2] Free SCFAs can cross the blood-brain barrier via monocarboxylate transporters.”
-> This may be pretty big, as it clearly is a third source of energy that can pass through the blood brain barrier next to glucose and ketones: Short-chain fatty acids
C) from the same source as B): “Short-chain fatty acids are produced when dietary fiber is fermented in the colon”
=> A, B and C combined give 2 potential methods to supplement glucose as a source of energy for the brain: ketones AND SCFA. One primarily delivered by a hormonal fasting state (including keto diet) and another by having a high fiber diet and the needed gut microbiome to ferment them (vegan diet, people who can digest a vegan diet may have to have such microbiome).
=> In addition it also gives a link between gut microbiome or disfunction and the sources of energy available to your brain.
Phil, I never would have considered that the immune system could be suppressing an inflammation response. That is very interesting…
dejurgen, there was no way for me to reply directly to your response, but I find it very interesting. I was overweight when I got sick, and I stayed that way for the past thirteen years. The only way I could get the scale to move on a normal, no sugar, low carb diet was to eat below 800 calories. I just couldn’t shed any weight.
Now that I’m in ketosis with a primarily vegetarian diet, I’m losing weight on twice the calories. There is definitely something wrong with my insuline, glucagon, epinphrene, norepinephrene, leptin, grehlin… system. I can’t tell you how many times I asked the doctors if they were SURE I wasn’t diabetic.
So, it all adds up to too many variables for my addled brain to figure out. I will check those links. Thanks.
Debbie, that is incredible new information to me – it is possible to be ketogenic and vegetarian? I am finding information on Google about this. You are not the first person I know to have improved on a vegetarian diet – isn’t this extraordinary – some get better on low-carb high-fat ketogenic and others get better on a vegetarian diet? I am wondering whether to try a switch in my own diet and see how I get on, I have been satisfied with the rate of improvement I have already, but hey…trouble is I love my red meat, I can handle going without tasty starchy foods and making up for it with tasty fat and protein foods, but I don’t know if I could handle living on spinach and tofu.
Dejurgen contributes one impressive insight after another to this forum, and he might just have provided the answer on this specific point already. I already owe to him, the insight that inflammation can be suppressed by the immune system if it would be so ubiquitous that it would be harmful.
Hi Debbie, Phil,
For me too it is the first time ever I heard about someone managing going in ketosis on a mostly vegetarian diet. That is quite a feat.
However I still can’t fit it together with “The only way I could get the scale to move on a normal, no sugar, low carb diet was to eat below 800 calories. I just couldn’t shed any weight. … Now that I’m in ketosis with a primarily vegetarian diet, I’m losing weight on twice the calories.”
800 calories is really low to go under in order to lose weight. For some time I’d wandered if the very high caloric needs of most/all? severely ill ME patients combined with their very low weight isn’t more of a lack of gut functioning unable to extract the calories out of food rather than an extreme use of “harvested” calories. What goes in must come out. If those high calories go hand in hand with very low activity and (very often) hypothermia I don’t see the numbers adding up for making the difference by night sweats or sugar and protein dumping in the urine. So the feces/gut bacteria running away with the bulk of calories AND nutrients makes most sense to me.
But here is what does not work out yet: if Debbie now could extract calories by turning hard to use fiber into SCFA then caloric needs should drop further. So this leads me to the follow question for Debbie: is the fact that you go into ketosis confirmed with a reliable test once you got into a stable regime? The reason I ask this is because a recent blog of Cort surprised me by telling that many people who think they are in ketosis are actually not.
I learned from that blog that my try at ketosis probably didn’t get me into ketosis either. I still used one slice of bread a day, a small piece of fruit (low caloric lemon) and a little bit of milk in order to not lose precious gut flora in case it did not work out. That however wasn’t the main problem. Me eating lots of nuts and seeds was as high amounts of protein convert to glucose too in times of need easily staving of ketosis.
So a vegetarian diet and ketosis would leave few foods but low carb vegetables, olives, avocados and plenty of vegetable oil it seems. That would require a very strong gut and be a very restrictive diet but it is possible.
Actually if you wouldn’t reach ketosis but reap the results as if you were that would be great. It would make the case for this “third way” a stronger one and would leave more options for a ME/FM friendly diet at a lower difficulty level.
I myself try to avoid both too high and too low levels (at night) of blood sugar. I learned to avoid the too deep drops at night thanks to someone on this forum saying he’d carb loaded before the night to get better sleep. While very skeptical at first some of his arguments made sense. I don’t go that far but now add a coffee spoon of honey in each cup of weak coffee (caffeine helps with breathing, a nightly weakness of me) I drink at night. It didn’t make me sleep better, but it surprisingly strengthened my resistance. I’m happy with that too ;-).
If I combine all of this I wander if a diet that does stabilizes blood sugar and prevent both too high and too low values could mix well with this potential “third way”. Part of the strength of ketosis or potential SCFA could be that by providing an alternative fuel for the brain the blood glucose levels could be set more freely for the entire body. Without such alternative fuel glucose levels, and with it an entire range of hormones that might help us if “set” at a different level, are locked by the need to block of too high sugar levels in order to avoid diabetes and to prevent too low levels in order not to starve the brain.
It would help building insight if you could tell if actual ketosis is confirmed by a reliable test and what sort of diet you have now. Only needing relatively small amounts of SCFA would be a nicer option then the all or nothing option of ketosis.
Kind regards,
dejurgen
Hi Phil, Hi dejurgen,
Sorry, I didn’t see your responses earlier. My brain’s not 100% today, so I’ll cover what I think seem to be the most curious parts of my statements.
It’s true that I had to get below 800 calories/day to lose weight when eating a normal, balanced diet that included plenty of chicken, fresh veg, little processed food, and few carb-heavy foods. I was at a very stable, immovable weight for years (ladies’ prerogative not share). I rarely ate garbage (cakes, candies, chips), never drank juices, sodas, sweetened teas or coffees. I was not focused on weight loss, so I just continued to eat what I considered a healthy diet and worked towards slowing my declining state.
That said, I had TERRIBLE digestion. Constipation and bloating plagued me. Perhaps I managed to keep the weight on because my body had so much time to nosh on every single molecule of food?? I was diagnosed with Hashimoto’s hypothyroid seven years ago (have been ME/CFS for thirteen) once that was controlled, my weight creeped down a bit. But as to why I couldn’t drop weight on, say, 1,100 cal/day, I honestly cannot guess.
Now, vegetarian ketogenic… I am not strictly vegetarian. I say that my diet is PRIMARILY vegetarian because I get the bulk of my protein from organic, plant-based protein shakes that contain a decent amount of low-carb vegetables in powered form as well. While most people would add something tasty like fruit juice, I add beef collagen and olive oil. All low-carb veg… greens, peppers, celery, etc. are eaten with generous amounts of olive, coconut, or avocado oils. I cannot get myself on the butter and lard train. It just doesn’t sit with me. I also use eggs as wraps for veggies and dig into fatty fish drizzled in oil whenever possible.
I also enjoy pumpkin seeds when I need to fill in my protein/fat ratios. They are IMO the perfect kept snack.
That said, were I to try to gain enough protein through a traditional vegetarian diet (one where protein wasn’t processed out of the veg –like the pea protein that is in my powders) I don’t think it would be possible. Seems to me that all high-protein veg (legumes) are FAR too high in carbs.
I do not think the way I eat could ever go mainstream. But it is definitely ketogenic and I am definitely in ketosis. I use urine ketone strips, which I know are not terribly accurate, but where there is color, there are ketones. My daily net carb never goes above 20. My daily carb count rarely goes over 30.
My digestion finally seems to be normalizing. I started with the liquid diet because I seemed to have started to have slow gastric emptying. It seemed like the perfect time to switch to ketogenic. I’ve been adding cooked veg slowly and now fresh.
You two are way ahead of me on the knowledge curve here, so I’ll leave you with the above info to ponder. I’m just happy that my brain seems to finally be fat-adapted and I am not in constant fog. My muscles, completely deconditioned, seem to be regaining energy, if not yet strength. My neurological symptoms may be too far progressed. So far no luck improving sound sensitivities, difficulty understanding speech at times, and speaking freely or moving at a normal pace.
And with that, I’m pooped! All the best to you both. 🙂
Hi Debbie,
“I was diagnosed with Hashimoto’s hypothyroid seven years ago (have been ME/CFS for thirteen) once that was controlled, my weight creeped down a bit. But as to why I couldn’t drop weight on, say, 1,100 cal/day, I honestly cannot guess.”
=> Would you have had lower body temperature at that time (before controlling Hashimoto) compared to now (since controlling Hasimoto)? Hypothyroid often goes hand in hand with lower temperature and lower body temperature requires quite a few less calories.
“Now, vegetarian ketogenic…”
=> Wow, a diagnose confirmed keto vegetarian! Your response did conflict with some of my ideas. I always hate that, but it’s actually a good thing. Narrowing the search space ;-).
“I do not think the way I eat could ever go mainstream.”
=> Health and digestion wise I think it has good potential, taste and texture wise…
“My digestion finally seems to be normalizing.”
=> That was the spanner in the wheels for me, would have guessed you always had a very efficient gut (considering the 800 calories you got by), but you may have found a diet working around that (maybe the liquid/grinding).
“You two are way ahead of me on the knowledge curve here”
=> Don’t do yourself short. You may be the only living ME/FM patient on the planet able to succeed with a mainly vegetarian keto diet. On plus you managed to do so from a terrible gut situation before. Going for example vegan with terrible gut functioning is problematic and you may have found a way around that too. Practical knowledge is way underrated IMO. Great job!
Debbie’s response conflicted with some of my ideas, so I had to go back to the drawing table. May have found a new angle that potentially reduces a few more oddities. Still fresh idea, but with some potential.
The conflict in my ideas made me unable to draw a straight line from Debbie’s diet to a vegan one. Ideally if both work then a mix in between both should offer benefits too. I hoped to find common ground as it would offer more attractive diet options and maybe an even better optimum. I failed to do so until I included another common element between vegan and keto: purine metabolism.
Purines are a breakdown product from proteins. Purines itself are essential building block of life as they are used in plenty of vital processes, but too much is too much. Then it breaks down by a complex purine breakdown process, see the many steps breakdown process in the first figure in https://en.wikipedia.org/wiki/Purine_metabolism.
Now it becomes a bit murky. Uric acid is described both as a purine itself https://en.wikipedia.org/wiki/Purine and as a breakdown product of other purines https://www.urmc.rochester.edu/encyclopedia/content.aspx?ContentTypeID=167&ContentID=uric_acid_urine.
Whatever, protein consumption creates uric acid. Uric acid is strongly linked to highly inflammation based diseases like diabetes, gout, inflammatory arthritis… Note that diabetes also is an auto-immune based disease. https://en.wikipedia.org/wiki/Uric_acid
My father has and my grandfather had strong and varying episodes of severe to very severe leg weakness AND high uric acid problems with an average diet. I inherited this leg weakness but do not seem to have too high uric acid levels in my blood. Note however that uric acid is an anti-oxidant. I believe ME is a highly oxidative stress disease and Naviaux stated that our cells churn out massive amounts of peroxide in a cell defense reaction. That should drop uric acid levels dramatically. One could say that they are no longer a problem then if they are within normal but not low.
However our blood circulation is crippled too, reducing removal speeds of local wast products. What is worse, during bad episodes our capillaries see a combination of poor oxygen delivery and constricted blood vessels. If this happens during exertion then the local tissue has a combined shortage of blood flow, availability of oxygen in said blood and turns too massive anaerobic functioning. I long believed glucose could not be short with ME/FM. But glucose levels are elevated in “normal diet” patients, and it could be to accommodate this massive local consumption rate under low blood flow conditions when exercising. (Local) glucose consumption per ATP goes up about tenfold compared to aerobic conditions. So glucose may easily be short. Possible body response: turn every available protein molecule into glucose. That is a wasteful process when it comes to energy production. Worse, it likely creates enormous spikes in local purine production and local blood flow is constrained at the same time, so there is no easy way to remove the waste fast enough. Likely result: the local purine levels and uric acid levels go sky high and overwhelm the local detoxification capacity.
Under those conditions AND with the high amounts of lactic acid AND H2CO3 present (both increasing acidity), uric acid should drop out of solution very rapidly. If it were local, it would result in gout. If it is body-wide, invoking body-wide gout-like inflammation would mean near instant death or maybe accelerated sepsis rather then mild sepsis.
This idea has other links. Take a look at the uric acid solution table in https://en.wikipedia.org/wiki/Uric_acid. Higher values mean less solvable, lower values mean the formed salt can stay in far greater quantities in the (local) blood.
This means: potasium, sodium, lithium, calcium and magnesium can keep massive amounts of uric acid in liquid form. It also means: those salts will bind easily to uric acid and be removed from the body. Now that may be why we are in the odd position that extra salt does help us, and IV saline does too. It binds on masse to sodium and gets excreted through the urine, taking water and blood volume with it. It also grabs calcium and deposits it at random places where local uric and lactic acid concentrations are lower. Maybe related to Issie’s surgeon confirmed huge calcium deposits around the body and Phils accumulation of “stuff” in his fascia. May also be related to the few understood relationship between calcification and inflammatory diseases. Low CO2 values due to overbreathing or keto diet help a bit here to as they lower blood acidity. Magnesium ain’t the best here, but it could explain why so many ME/FM patients do better on magnesium
supplements. This last one is a bit of a stretch, but lithium used to be the prime medicine for treating gout, as it is still for some mental illnesses. Could they be purine induced inflammation based? Many anti-depressants work on reducing inflammation too and there is a shift to consider depression a brain inflammation disease.
Now what’s the link between all of it and a keto or vegan diet?
Keto diet:
* has high animal fat and moderate animal protein only.
* has quite likely lower CO2 production per ATP, reducing blood acidity a lot (to too alkali), decreasing local acidity peaks when over exerting.
* has a hormonal hunger/starving state; more then the low amount of blood glucose this hormonal state largely inhibits anaerobic functioning (when starving wasting buckets of glucose for droplets of ATP is bad economy); this does not only reduce lactic acid production but more importantly slows down the extreme pace of conversion of proteins to glucose/purines/uric acid to a relative trickle => far smaller local uric acid overload
Vegan diet:
* one of the more alkali ones, again dropping the base acidity so allowing some larger local rise in acidity before uric acid crystallizes
* alkali diets provide more minerals like sodium, potasium, calcium… that can bind uric acid and remove it through urine
* moderate amounts of vegan based proteins do NOT produce increased purine production https://en.wikipedia.org/wiki/Gout
“Specifically, moderate consumption of purine-rich vegetables (e.g., beans, peas, lentils, and spinach) are not associated with gout”. => It sounds odd as proteins are proteins, but seeds and nuts come with enzymes converting proteins to glucose (in order to unpack seeds to seedlings) so the process may be cleaner; maybe the higher the protein content the more enzymes and that makes seeds and nuts better then grains, with the exception of oath that contains twice as much protein as most grains and is seen to be better accepted with ME patients.
My lifestyle changes:
* improving blood flow, reduces risk of local anaerobic functioning, glucose shortage and poor waste removal; I do so only selectively to not release an inflammatory wave
* improve breathing lowering blood to slightly alkali base levels and reduce the effects of the tidal wave of oxidate stress following the initial problems
* deep diaphragm breathing increases reflow to the hart and drainage to the lymphatic system improving both blood flow and waste removal
* eating plenty of alkali food, see above; in special eating much low carb low caloric celery, often considered the number one anti-rheumatic food but a strong allergenic product!
* pace a lot, avoiding anaerobe functioning
* drink lots of water, helping purine removal and keeping blod volumes up
* keep blood flow, breathing levels and the odd one *blood sugar* above minimum levels at night. If they fall as they do the problem rises. See when gout starts: exercise and at night https://en.wikipedia.org/wiki/Gout; degrading condition and exhaustion after a night are commonplace with ME. Sugar levels drop at night and combined with nightly poor blood flow and breathing may turn on the anaerobe-purine-inflammation machine
* I’ll try a few new ones as a result of these theories ;-)!
There is more: uric acid crystals “like” to block capillaries (and according this theory when blood flow is already under heavy attack).
There are links to Phil’s fascia abnormalities: uric acid crystals “like” to deposit on capillaries, joints, tendons and surrounding tissue (like fascia?)). See also the idea of encapsulating deposited crystals I launched earlier regarding to your question “what could be in these lumps?” See for
“Microscopic tophi may be walled off by a ring of proteins, which blocks interaction of the crystals with cells and therefore avoids inflammation.[30] Naked crystals may break out of walled-off tophi due to minor physical damage to the joint, medical or surgical stress, or rapid changes in uric acid levels.[30] When they break through the tophi, they trigger a local immune-mediated inflammatory reaction in macrophages,” my note: tophi is crystal deposits of uric acid.
It provides a link to physical stress AND medical AND surgical stress both known to be able to initiate ME/FM. When those tophi break trough their encapsulation they also trigger a immune-mediated inflammatory reaction…
Imagine those “thopi” being created in the capillaries and being locally encapsulated creating bumpy AND narrowed=constricted (happens when the same amount of material is bend an zigzaged by local “bumps”- blood vessels. If the encapsulation breaks: inflammatory reaction. If they are to many: body must ditch those capillaries and build replacements OR immune system must attack those encapsulated “thopy” in order to remove them = auto-immune reaction against blood vessels; if successful: thopy breaks and more immune system related inflammatory reaction.
The list of foods to avoid are not unfamiliar for ME/FM patients either: sugar, alcohol… and there is also meat and so seemingly conflicting with keto diet but if you do not eat mainly the fatty parts of meat there is more protein then fat in meat. Yeast is another no; I used to wander why yeast, producing many vitamins, could be so bad.
There is much more, but I’ll end with this one. Doctor Ron Davis asked this question: why would cells be that desperate to throw ATP out of their core? Maybe this could answer that question: https://en.wikipedia.org/wiki/Purinergic_signalling
See the top left picture: ATP is extracellular (thrown out of cells) in the process called “purinergic signalling”. Purines are also a signalling molecule and in its signalling function makes use of ATP. If massive purine is outside the cells then plenty of ATP will be thrown out of the cells as well. See also
“The regulation of vascular tone in the endothelium of blood vessels is mediated by purinergic signalling. A decreased concentration of oxygen releases ATP from erythrocytes, triggering a propagated calcium wave in the endothelial layer of blood vessels and a subsequent production of nitric oxide that results in vasodilation.” => a bit more vasodilation and NO could be welcome under the described massive attack. And it could be a good answer to the original question: why do the cells throw out ATP if they are already faltering.
Actually, much of the Cell Defense Reaction could be seen as a response to sky-high purine/uric acid levels:
* produce massive peroxide, peroxide is a massive attractor of immune cells that may be asked to clean up those thopi and the damage they do to the capillaries hopefully before they get “encapsulated” making problems even worse long term. While the massive peroxide release would further constrict the blood vessels it may be worth the cost.
* throw out large amount of ATP in order to somewhat compensate for the vasoconstriction caused by the peroxide and destruction of NO.
Now the same source states: “Micromolar concentrations of adenosine activate A2A and A2B receptors. This inhibits the release of granules and prevents oxidative burst. On the other hand, nanomolar concentrations of adenosine activate A1 and A3 receptors, resulting in neutrophilic chemotaxis towards inflammatory stimuli.”
=> Saying: throwing out ridiculous amounts of ATP (micromolar) reduces oxidative bursts, so reducing the “normal extreme” release of H202 during CDR to “very high but not extreme” in ME/FM (and sepsis?). So this presents a clear “self constraining” mechanism both setting a limit to vasoconstriction AND offering a potential mechanisms to suppress body-wide “body turned into one big deadly purple balloon” type of inflammation disguising our disease as not very inflammatory.
See also “Like most immunomodulating agents, ATP can act either as an immunosuppressive or an immunostimulatory factor, depending on the cytokine microenviroment and the type of cell receptor.[27] In white blood cells such as macrophages, dendritic cells, lymphocytes, eosinophils, and mast cells, purinergic signalling plays a pathophysiological role in calcium mobilization, actin polymerization, release of mediators, cell maturation, cytotoxicity, and apoptosis.[28] Large increases in extracellular ATP that are associated with cell death serve as a “danger signal” in the inflammatory processes”
The above and my far too lengthy discription of the “methemoglobine poisoning” may discribe a pretty big portion of what could be a fundamental part of a ME/FM like disease. https://www.healthrising.org/blog/2018/01/01/chronic-fatigue-syndrome-chronic-form-sepsis/
Kind regards for anyone if any getting this far 😉
dejurgen
Lenghty comment broken up in parts.
Part 1:
Debbie’s response conflicted with some of my ideas, so I had to go back to the drawing table. May have found a new angle that potentially reduces a few more oddities. Still fresh idea, but with some potential.
The conflict in my ideas made me unable to draw a straight line from Debbie’s diet to a vegan one. Ideally if both work then a mix in between both should offer benefits too. I hoped to find common ground as it would offer more attractive diet options and maybe an even better optimum. I failed to do so until I included another common element between vegan and keto: purine metabolism.
Purines are a breakdown product from proteins. Purines itself are essential building blocks of life as they are used in plenty of vital processes, but too much is too much. Then it breaks down by a complex purine breakdown process, see the many steps breakdown process in the first figure in https://en.wikipedia.org/wiki/Purine_metabolism
Now it becomes a bit murky. Uric acid is described both as a purine itself https://en.wikipedia.org/wiki/Purine and as a breakdown product of other purines https://www.urmc.rochester.edu/encyclopedia/content.aspx?ContentTypeID=167&ContentID=uric_acid_urine
Whatever, protein consumption creates uric acid. Uric acid is strongly linked to highly inflammation based diseases like diabetes, gout, inflammatory arthritis… Note that diabetes also is an auto-immune based disease. https://en.wikipedia.org/wiki/Uric_acid
My father has and my grandfather had strong and varying episodes of severe to very severe leg weakness AND high uric acid problems with an average diet. I inherited this leg weakness but do not seem to have too high uric acid levels in my blood. Note however that uric acid is an anti-oxidant. I believe ME is a highly oxidative stress disease and Naviaux stated that our cells churn out massive amounts of peroxide in a cell defense reaction. That should drop uric acid levels dramatically. One could say that they are no longer a problem then if they are within normal but not low.
However our blood circulation is crippled too, reducing removal speeds of local waste products. What is worse, during bad episodes our capillaries see a combination of poor oxygen delivery and constricted blood vessels. If this happens during exertion then the local tissue has a combined shortage of blood flow, availability of oxygen in said blood and turns too massive anaerobic functioning. I long believed glucose could not be short with ME/FM. But glucose levels are elevated in “normal diet” patients, and it could be to accommodate this massive local consumption rate under low blood flow conditions when exercising. (Local) glucose consumption per ATP goes up about tenfold compared to aerobic conditions. So glucose may easily be short. Possible body response: turn every available protein molecule into glucose. That is a wasteful process when it comes to energy production. Worse, it likely creates enormous spikes in local purine production when local blood flow is constrained at the same time, so there is no easy way to remove the waste fast enough. Likely result: the local purine levels and uric acid levels go sky high and overwhelm the local detoxification capacity.
Under those conditions AND with the high amounts of lactic acid AND H2CO3 present (both increasing acidity), uric acid should drop out of solution very rapidly. If it were local, it would result in gout. If it is body-wide, invoking body-wide gout-like inflammation would mean near instant death or maybe accelerated sepsis rather then mild sepsis.
Part 2:
This idea has other links. Take a look at the uric acid solution table in https://en.wikipedia.org/wiki/Uric_acid . Higher values mean less solvable, lower values mean the formed salt can stay in far greater quantities in the (local) blood.
This means: potasium, sodium, lithium, calcium and magnesium can keep massive amounts of uric acid in liquid form. It also means: those salts will bind easily to uric acid and be removed from the body. Now that may be why we are in the odd position that extra salt does help us, and IV saline does too. Uric acid binds on masse to sodium and gets excreted through the urine, taking water and blood volume with it. It also grabs calcium and deposits it at random places where local uric and lactic acid concentrations are lower. Maybe related to Issie’s surgeon confirmed huge calcium deposits around the body and Phils accumulation of “stuff” in his fascia. May also be related to the few understood relationship between calcification and inflammatory diseases. Low CO2 values due to overbreathing or due to keto diet help a bit here to as they lower blood acidity. Ketones themselves are however acidic. Magnesium ain’t the best here, but it could explain why so many ME/FM patients do better on magnesium supplements. This last one is a bit of a stretch, but lithium used to be the prime medicine for treating gout, as it is still for some mental illnesses. Could they be purine induced inflammation based? Many anti-depressants work on reducing inflammation too and there is a shift to consider depression a brain inflammation disease.
Now what’s the link between all of it and a keto or vegan diet?
Keto diet:
* has high animal fat and moderate animal protein only.
* has quite likely lower CO2 production per ATP, reducing blood acidity (compensating in part for ketones acidity), decreasing local acidity peaks when over exerting.
* has a hormonal hunger/starving state; more then the low amount of blood glucose this hormonal state largely inhibits anaerobic functioning (when starving wasting buckets of glucose for droplets of ATP is bad economy); this does not only reduce lactic acid production but more importantly slows down the extreme pace of conversion of proteins to glucose/purines/uric acid to a relative trickle => far smaller local uric acid overload
Vegan diet:
* one of the more alkali ones, again dropping the base acidity so allowing some larger local rise in acidity before uric acid crystallizes
* alkali diets provide more minerals like sodium, potasium, calcium… that can bind uric acid and remove it through urine
* moderate amounts of vegan based proteins do NOT produce increased purine production https://en.wikipedia.org/wiki/Gout
“Specifically, moderate consumption of purine-rich vegetables (e.g., beans, peas, lentils, and spinach) are not associated with gout”. => It sounds odd as proteins are proteins, but seeds and nuts come with enzymes converting proteins to glucose (in order to unpack seeds to seedlings) so the process may be cleaner; maybe the higher the protein content the more enzymes and that would make seeds and nuts better then grains, with the exception of oath that contains twice as much protein as most grains and is seen to be better accepted with ME patients.
My lifestyle changes:
* improving blood flow, reduces risk of local anaerobic functioning, glucose shortage and poor waste removal; I do so only selectively to not release an inflammatory wave
* improve breathing lowering blood to slightly alkali base levels and reduce the effects of the tidal wave of oxidate stress following the initial problems
* deep diaphragm breathing increases reflow to the hart and drainage to the lymphatic system improving both blood flow and waste removal
* eating plenty of alkali food, see above; in special eating much low carb low caloric celery, often considered the number one anti-rheumatic food but a strong allergenic product!
* pace a lot, avoiding anaerobe functioning
* drink lots of water, helping purine removal and keeping blood volumes up
* keep blood flow, breathing levels and the odd one *blood sugar* above minimum levels at night. If they fall as they do at night the problem rises. See when gout starts: exercise and at night https://en.wikipedia.org/wiki/Gout ; degrading condition and exhaustion after a night are commonplace with ME. Sugar levels drop at night and combined with nightly poor blood flow and breathing may turn on the anaerobe-purine-inflammation machine
* I’ll try a few new ones as a result of these ideas ;-)!
Part 3:
There is more: uric acid crystals “like” to block capillaries (and according this theory when blood flow is already under heavy attack).
There are links to Phil’s fascia abnormalities: uric acid crystals “like” to deposit on capillaries, joints, tendons and surrounding tissue (like fascia?)). See also the idea of encapsulating deposited crystals I launched earlier regarding to Phil’s question “what could be in these lumps?” See for
“Microscopic tophi may be walled off by a ring of proteins, which blocks interaction of the crystals with cells and therefore avoids inflammation.[30] Naked crystals may break out of walled-off tophi due to minor physical damage to the joint, medical or surgical stress, or rapid changes in uric acid levels.[30] When they break through the tophi, they trigger a local immune-mediated inflammatory reaction in macrophages,” my note: tophi is crystal deposits of uric acid. other note: protein scavenging during exercise could potentially break this protective ring initiating more inflammation.
It provides a link to physical stress AND medical AND surgical stress both known to be able to initiate ME/FM. When those tophi break trough their encapsulation they also trigger a immune-mediated inflammatory reaction…
Imagine those “thopi” being created in the capillaries and being locally encapsulated creating bumpy AND narrowed=constricted (happens when the same amount of material is bend an zigzaged by local “bumps”- blood vessels). If the encapsulation breaks: inflammatory reaction. If there are to many encapsulated “thopi”: body must ditch those capillaries and build replacements OR immune system must attack those encapsulated “thopy” in order to remove them = auto-immune reaction against blood vessels; if successful: thopy breaks and more immune system related inflammatory reaction.
We are also found to be short on key Phosphor chemicals used in aerobe mitochondrial breathing. Many purines are phospor bound. Under normal conditions the phospor is recycled leading to few losses. When the purine detoxifying system would be massively overwhelmed it is easy to see the body trying to dump as much purines as it can. In doing so, valuable phospor compounds would get lost.
The list of foods to avoid are not unfamiliar for ME/FM patients either: sugar, alcohol… and there is also meat and so seemingly conflicting with keto diet but if you do not eat mainly the fatty parts of meat there is more protein then fat in meat. Yeast is another no; I used to wander why yeast, producing many vitamins, could be so bad.
There is much more, but I’ll end with this one. Doctor Ron Davis asked this question: why would cells be that desperate to throw ATP out of their core? Maybe this could answer that question: https://en.wikipedia.org/wiki/Purinergic_signalling
See the top left picture: ATP is extracellular (thrown out of cells) in the process called “purinergic signalling”. Purines are also a signalling molecule and in its signalling function makes use of ATP. If massive purine is outside the cells then plenty of ATP will be thrown out of the cells as well. See also
“The regulation of vascular tone in the endothelium of blood vessels is mediated by purinergic signalling. A decreased concentration of oxygen releases ATP from erythrocytes, triggering a propagated calcium wave in the endothelial layer of blood vessels and a subsequent production of nitric oxide that results in vasodilation.” => a bit more vasodilation and NO could be welcome under the described massive attack. And it could be a good answer to the original question: why do the cells throw out ATP if they are already faltering.
Actually, much of the Cell Defense Reaction could be seen as a response to sky-high purine/uric acid levels:
* produce massive peroxide, peroxide is a massive attractor of immune cells that may be asked to clean up those thopi (by releasing massive amounts of peroxide) and the damage they do to the capillaries hopefully before they get “encapsulated” making problems even worse long term. Also, peroxide reacts with anti-oxidant uric acid and hence removes uric acid. I used to see uric acid as the protecting chemical, but Naviaux’s idea of oxidative shielding seems to be more at place here. While the massive peroxide release would further constrict the blood vessels it may be worth the cost.
* massive peroxide production would also “invite” mast cells and glial cells to “carpet bomb” many affected body parts with ROS, again cleaning up uric acid waste. Imagine dirty massive ROS production being the cure to something…
* throw out large amount of ATP in order to somewhat compensate for the vasoconstriction caused by the peroxide and destruction of NO.
Now the same source states: “Micromolar concentrations of adenosine activate A2A and A2B receptors. This inhibits the release of granules and prevents oxidative burst. On the other hand, nanomolar concentrations of adenosine activate A1 and A3 receptors, resulting in neutrophilic chemotaxis towards inflammatory stimuli.”
=> Saying: throwing out ridiculous amounts of ATP (micromolar) reduces oxidative bursts, so reducing the “normal extreme” release of H202 during CDR to “very high but not extreme” in ME/FM (and sepsis?). So this presents a clear “self constraining” mechanism both setting a limit to vasoconstriction AND offering a potential mechanisms to suppress body-wide “body turned into one big deadly purple balloon” type of inflammation disguising our disease as not very inflammatory.
See also “Like most immunomodulating agents, ATP can act either as an immunosuppressive or an immunostimulatory factor, depending on the cytokine microenviroment and the type of cell receptor.[27] In white blood cells such as macrophages, dendritic cells, lymphocytes, eosinophils, and mast cells, purinergic signalling plays a pathophysiological role in calcium mobilization, actin polymerization, release of mediators, cell maturation, cytotoxicity, and apoptosis.[28] Large increases in extracellular ATP that are associated with cell death serve as a “danger signal” in the inflammatory processes”
The above and my far too lengthy discription of the “methemoglobine poisoning” may discribe a pretty big portion of what could be a fundamental part of a ME/FM like disease. https://www.healthrising.org/blog/2018/01/01/chronic-fatigue-syndrome-chronic-form-sepsis/
Kind regards for anyone if any getting this far 😉
dejurgen
WOW! Dejurgen does it again, but topping all previous efforts!!
That hypothesis fits very well with my experience and explains why I have got better with all the things I have been doing, even if my hypothesis about the mechanisms and channels was a bit simplistic. I think it also explains why the only people who get better are those who are doing the right pace of exercise, as well as whatever else they are doing right.
I think Cort should post this as a “new topic”.
Hi Phil,
Thanks for reading so much and for the nice comment. Some part of my thinking this way came in the wake of your question “what could be in those corrugations?” Communicating and sharing experiences and ideas is so important!
I did spot a mistake in “It also means: those salts will bind easily to uric acid and be removed from the body.”
-> Strong acids drive weak acids out of there salts. I expected uric acid to be a stronger acid then H2CO3. Apparently not, uric acid is a pretty weak acid. So it’s acid quality is far less a problem then crystallization in the body. Unfortunately, it makes removal of uric acid by binding to minerals a lot harder as displacing NaHCO3 was my prime candidate but this goes the other direction: H2CO3 would drive uric acid out of its sodium salt.
This problem also gave room for improvement. Just as HCl stomach acid just isn’t automatically created out of its salt, biology can help the process here as well. This is my most likely candidate:
Chemical reactions are equilibrium reactions. Sort of:
2 sodium uric acid salt + H2CO3 2 NaHCO3 + uric acid
with the reaction going much faster from left to right then from right to left. That seems bad. The only way to remove uric acid here is to have far larger amounts of uric acid then H2CO3. In my previous theory we have way too high local uric acid concentrations on one hand, so that works out. On the other hand we are renown for heavily over breathing especially at times of trouble. That lowers CO2 and hence H2CO3 values a lot. That is however not sufficient. There is still too much local H2CO3 around for the reaction to go the wright direction. Now comes into play the RBCs: RBCs store plenty of C02 and H2CO3 inside their cells, potentially separating uric acid rich blood from the bulk of H2CO3 by a cell membrane. This may be sufficient to let go the reaction the wright direction. Over breathing and keto’s lower production of CO2 could come in helping here. Seems that nature, just like me, loves mechanisms that hit two or more birds with one stone.
So, over breathing may have yet another useful function. We’re not nuts after all ;-).
This reaction being an equilibrium reaction also demonstrates that, as soon as uric acid concentrations drop, uric acid could be released from its salt and put back in the bloodstream again. So it provides a means for detoxing, but unfortunately it often only transports uric acid over short distances. If conditions are bad, like reduced body temperature, uric acid and its salt/crystals will be formed a bit away from the place of origin. So the main place of origin sees some relief, but at the cost of spreading the problem. Or could we say: if it keeps on happening for too long at the cost of becoming body wide and near-permanent?
It also points at the importance of NaHCO3 as a salt as it is one of the few at first sight that can mediate this reaction. Calcium and magnesium salts might as well, but drop very quickly out of solution. Calcium is the worst here. Combined with the short distance transport mechanism of for example uric acid bound calcium, it “eats away” calcium at the place of strong inflammation. For example it dissolves bone. And then it litters the nearby regions with calcium deposits that could grow problematic. This is the problem of osteoporosis.
This may well link to the easy calcification of tendons when they are inflamed. Tendons are not made up of stockpiles of calcium so them becoming calcified is not that a logical thing. It also could explain why many of us have low to very low supplemented vitamin D levels: vitamin D may be needed time and again to “re-uptake” calcium from these affected and undesired deposit places. While doing so we burn our reserves. When my disease really kicked in, my doctor seemed to be shocked by how low my vitamin D levels were.
It may also help explain the importance of magnesium supplements and what supplements may potentially be more effective: take for example magnesium carbonates. In the stomach they convert to chlorine salt by reacting to HCl. In doing so they neutralize stomach acid making digestion harder but they also indirectly create NaH2CO3 out of much more available NaCl. That even happens when the magnesium is not reaching our bloodstream but disposed. So even if magnesium has often poor bio-availability it might do the trick by taking chlorine with it. In the blood stream it can help some too.
I did find this one: https://www.ncbi.nlm.nih.gov/pubmed/2845176 “Prevention of uric acid stone formation by sodium bicarbonate in an ileostomy patient–a case report.”
It has it’s downsides as well so don’t go mad on it yet. After all, it’s still a theory too. But once more it may have potential and these ideas could further reduce the mysteriousness of our disease.
I hope you can get your family into a genetic study Debbie! Some important clues lurk in them…
Cort, Our DNA is all over the place! LOL, I do hope it’s doing some researcher some good somewhere.
Glad to hear it! I’ll bet it is 🙂
You said, “SNRI’s such as Wellbutrin, etc” but Wellbutrin is not an SNRI. It is in a class by itself: an NDRI (norepinepherine, dopamine reuptake inhibitor). As such, it tends to have a much more stimulating effect than any other antidepressant on the market. (That may, or may not be a good thing for someone with ME or Fibro.)
Also, while people with ME and Fibro often show signs of ADHD, I think we have to be very careful with treating them the same way that typical forms of ADHD are treated. The cause of the usual form of ADHD is that the brain is unable to block out external distractions because its inhibitory action is lowered. (It’s not working hard enough.) In ME and Fibro, it seems that internal signals (like those for pain & exhaustion) are interfering with other signals, and thus we can’t focus on both. (The brain is being worked too hard.)
So, in typical ADHD, improving the brain’s ability to block extraneous external distractions helps. In ME and Fibro-related ADHD, it would seem that helping to reduce the internal pain & exhaustion signals would go a lot further than adding a treatment that actually adds to the work that the brain has to do. (Stimulating the brain & the adrenals is adding to its workload). And, the typical ADHD treatments can actually wind up wearing us out even further, which would also add to the distractions that our brains are trying to cope with (thus making the ADHD worse).
Further, there is some evidence that ADHD meds can also harm the mitochondria. Since mitochondria are one area that is consistently being looked at as a part of the problem in ME and Fibro, taking something that could further harm them is not goign to be helpful in the long run.
Thanks AuntTammie for clarifying what is going on ADHD. I think that blocking out external signals is a problem in ME/CFS and FM (hence the problems with stimuli many people have) AND I agree that those internal pain and fatigue signals have to be an even bigger issue as well – an issue which people with ADHD don’t have nearly to the same degree.
ADHD is being increasingly recognized as a heterogenous condition just as FM and ME/CFS is – so there could be some overlap – some people with FM and ME/CFS could have an ADHD like condition which might respond to these protocols. Time will tell I guess.
For me stimulants like caffeine actually work really well in lowering my pain levels. Over time, as you suggest, they tend to wear me out, though.
“…In ME and Fibro, it seems that internal signals (like those for pain & exhaustion) are interfering with other signals, and thus we can’t focus on both. (The brain is being worked too hard.)…”
Exactly! So much research that assumes “brain dysfunction first, physical later” is likely to have been a colossal waste of research funding. The incompetence and dishonesty is especially high in the case of FM, where sufferers have palpable deformations in their muscle tissue, recognised by all hands-on practitioners for all time, but “mainstream” researchers do not want to look in this direction. It is “unscientific”, apparently. By this standard, what Galileo could see in his day, would have had to wait for solar exploration modules and photography from outer space, for the “mainstream” science community to accept his hypotheses.
Can one of you wise people please summarize what seems to be the best diet for FM/ME? I have both and am overweight and really struggling here. Although I have a medical background today my cognitive fog is getting in the way of following this discussion but I’m very interested. I would love to shed some of this weight as I think it would help my fatigue.
The difficulty FM patients’ “brains have in switching off their attention to innocuous background stimuli can contribute to mental and even physical fatigue”
Yes, exactly!ADHD, for me is like having “too many browser windows open” and my “RAM gets used up” and everything freezes (overwhelm, paralysis) or goes haywire (cognitive anxiety).
I was diagnosed with ADHD in 1998 and Fibromyalgia in 2015. Executive function issues like working memory, are made worse with Fibro because I can’t seem to filter out somatic or sensory stmulii. This could manifest or be misdiagnosed as as anxiety, OCD, hypochodriasis etc. For me its just a wired brain that noticed too much and a lot of uncertainty kicks in.
Apparently the drug Intuniv (Guanfacine) is suppose to help with this “noise” reduction. Its not covered on my health plan, so I haven’t been able to try it yet.
Wellbutrin, while it helped some depressive symptoms, caused the tinnitus to increase. It turned up the “brain noise.”
I think executive functions play a huge part in all of this. Here is a good resource for ADHD/Executive Functioning Model
http://www.brownadhdclinic.com/add-adhd-model/
The Fibro-ADHD connection is very real for me..and it would be great to learn more about “noise reduction.”
There is another issue of elevated intracranial pressure..especially during yoga inversions or laying down too long which also plays a part in my life…but that’s another thread.
Willow
Thanks for your journalism and focus on these topics, Cort. I certainly relate to the ADD/ADHD symptoms. And many years ago was able to directly connect depression, racing mind (thoughts and emotions) to inflammation, which surprised my at the time doctor, but the connection was clear. I’d like to encourage everyone to hang in. Please don’t give in to ending your life. We are in a time of hope. There has never before been the kind of research happening now by researchers who are motivated to help. More is known about the processes we live with and we are being believed, finally. I am convinced that in the next while (couple of years) we will have effective treatments that improve our quality of life. This is a really really difficult disease to live with. But I encourage us all to hang in, keep looking, and now waiting with expectancy is at last viable. One day at a time, sometimes one moment at a time. We have help now by motivated people who care. Hold the fort. Look for beauty in the immediate present moment, moment by moment. We are not alone.
Thanks Deborah. I wouldn’t be surprised if inflammation is not the source for a large number of people with ME/CFS and FM who have depression as well.
Were you able to use anti-inflammatories or diet or supplements to bring down the inflammation and depression? (A blog on this is on the way by the way)
It’s soooo important, I think, to avoid thinking about what was lost and do this: To “Look for beauty in the immediate present moment, moment by moment.” Just focus on being in the moment – whatever the moment is bringing and often times it’s not so good – but practicing being in the moment is an excellent idea I think.
I commented on here once about the novel “Seabiscuit” by Laura Hillebrand (who has CFS) that the enforced slow pace of life in her case seems to have produced an attention to detail that resulted in absolutely perfect novel writing.
That is great advice Cort. I’ve forgotten about living in the moment glad you mentioned it I will begin practicing this again….. it’s difficult to think about what you have lost if you’re living in the moment…. I had to stop painting, gardening, riding all the things that I love. Hopefully there will be a cure or at least a treatment that helps and I can once again do the things I love. ?
deborah,
You are like me… FM, hypothyroidism, thyroid removed after filled with nodules, periodical symptoms of Sjogren, lupus, Behcet neuropathy……no kidney or heart symptoms yet (or not aware of)…looking healthy with great skin, laughing and not whining (or just a little bit )
I wonder, did you also suffer from migraines before you got the diagnosis “FM”?
What markers of inflammation do you have? Did they ever check the ratio 1,25vit D / 25 vit ?
“…Patients receiving the drug/nutrient combination reported a significant increase in functionality but a surprisingly high placebo response rate in some patients essentially nullified the result…”
We see again and again, some cohort in studies making “mysterious” improvements. In this case it is people receiving the placebo as well as those on the drug! I would like to see studies investigate everything the patients were doing, and see if something correlates with success – unfortunately, researchers are always trying to prove the efficacy of a drug so they are not interested in looking at other factors such as lifestyle, diet, exercise, to find a more complex basis for symptom amelioration.
This comment makes good sense. When is a placebo actually a placebo? They may be taking an inert placebo but what else were the two groups doing? These are not studied or reported. It is sssumed that if the numbers in the study are large enough these other factors will be raNdomly distributed and therefore will not effect results. But this is very rarely the case. Most study groups have far to few subjects to achieve this AND metanlysis as in the large reviews does NOT address this problem.
If I remember rightly, you made a “mysterious” improvement from CFS yourself, didn’t you? And in discussing the bigger picture, I say you got your activity, exercise and pacing exactly right to create the conditions for this, even if by accident. I don’t think anyone who improved, regardless of the co-contributors to improvement (drugs, diet, therapy etc), was either sedentary or overdoing it. I would argue that a patient either being sedentary or overdoing it, guarantees failure of any therapy or treatment at all under our current conditions of knowledge.
Wigers and Finset (2007) is the best study I know of so far, and it should have been regarded as the best indicator for the direction of further research.
Nice write up Cort. I just threw away Adderall – without trying it. Just couldn’t see how more stimulus with an already over active autonomic system could be good for me. My nervous system is already stressed with POTS and FMS, Amongst other things. I agree with others that diet may be a big key here. The microbiome and gut health can affect EVERYTHING. It affects brain function and response, autoimmune system and absorption of everything we ingest – be it food, medicine or supplement. Having the desired response is necessary for our over all health and well being.
Yes, so maybe what I am saying about sugar – it poisons some people but not most people, in a multitude of ways (muscles, brain, organs) – is not sugar per se doing the poisoning, but whatever the digestion is “turning the sugar into” in the case of some unlucky minority.
I believe that in FM at least, a major part of the problem is a kind of toxic sludge lingering in the tissues and around organs, and the body is not mobilising it and excreting it like what happens in normal healthy people. FM symptoms always flare up in the hours following harder-than-usual exertion – so is it the anaerobic, sugar-burning energy metabolism that is the pathway between the sugar (possibly already toxified by the digestion) and the FM symptoms?
It is an obvious connection, that “toxic sludge” could be the cause of the adhesions and corrugations in the muscle fascia, simply by its adhesive properties, when the fascia needs to be well-lubricated and able to slide smoothly. The Chinese in their traditional medicine, interestingly, diagnose what we call FM, as “mucus in the tissues”. The common Chinese medical word usually translated as “dampness” is actually “mucus”.
Phil:I have FM with many trigger points in three quadrants of my body
Five years ago I frequently had cysts on my thumb: the dermatologist opened them with a sterile needle and a thick muceous substance came out.They kept coming back and after a few times I opened them up myself.
A few monts later they were suddenly gone. Don’t know why.
Hi Issie,
Ritaline/methylphenidate also helps against POTS, https://ic.steadyhealth.com/adhd-and-pots-treatment-with-methylphenidate “This medication is a commonly prescribed choice for the treatments of ADHD and POTS since it increases the production of dopamine and norepinephrine in the brain, removing the symptoms of these conditions and some other, similar health problems.”
Apparently norepinephrine does reduce POTS too according the above and both Ritaline and Adderall increase it. So does Symbalta/Duloxetine, one of few official FM medications.
Norepinephrine also is the building block of epinphrine, a very potent enhancer of breathing. Caffeine converts for about 30% into a potent bronchodilator too.
I for one fare well by using low doses of stimulants. What may make it work for me may be my below average breathing ability even for a ME patient, my high tolerance to the side effects and addiction of many stimulants, me still pacing a lot rather than “consuming” the performance benefit stimulants could provide and only using low doses (with better benefit/side effect ratio I believe).
But yes, stimulants use with ME/FM is more then a bit tricky.
Another good topic, Cort, thanks! I want to add that it is helpful for us to distinguish whether or not we might have ADHD or ADD as a symptom pattern. I think that hyperactivity in the sense of having a lot of energy and capacity for activity wouldn’t apply certainly to those in the ME/CFS camp and may not necessarily for those with FM. However, the pain in FM causes distress and one of the ways people have to deal with this is to distract themselves—get busy in some other way so that pain doesn’t take over one’s attention. There is an intensity I have often noticed with those who have FM but I see it as coming from the stress of pain, not sleeping well, the ups and downs coming from a disordered system. But this isn’t about having more energy or being able to do a lot.
What’s common to ADD and ADHD is what’s important—the difficulty being organized, distractability, tangential thinking. What that comes from, according to research is low energy in the frontal lobes, so that stimulating the brain has the effect of enabling the person to be more focussed and organized, actually calmer in terms of kids behavior.
A stimulant like methylphenidate which adds dopamine? enabling neurotransmission will help, but finding the best dose for a patient is very important. It might be a low or very low dose that contributes to a more functional and balanced brain.
For those with hypotension, one of the treatments Dr. Peter Rowe uses are stimulants, and I have read of other clinicians in our field who also do. Extended release form and the lowest effective dose. The stimulant helps with neurally mediated hypotension too, in addition to helping with cognitive function.
@Phil: a bit of topic, but you learned me a lot about fascia so I owe you this one. I asked my PT if I could have stuck and lumpy fascia if my muscle feel smooth. She answered only a specialized PT can. She can’t while she is very good at what she does for me. Maybe it is obvious in extreme cases, but I can’t tell if my fascia are OK or not. She gave me an address of someone specialized but I’ll hold off for now. I like to try when I do not try other things. With successful changes going on I wouldn’t be able to tell the impact of fascia therapy.
Dejurgen; I think the most dramatic way to detect this problem, is with massaging “cups”. Muscle tissue that can feel soft / OK suddenly reveals corrugations when a cup with suction activated, is slidden across it.
But in my case, everything felt wrong anyway, to any massage therapist, the muscles felt like they were riddled with unhealed injuries. I believe that fascia adhesions can be so bad that this is the result. Schleip certainly seems to believe that a lot of what massage therapists can “feel” is fascia-related rather than purely in muscle tissue itself. This is why trying different techniques can suddenly resolve a stubborn chronic injury that was not responding to “ordinary” massage or physiotherapy.
I have thought for a long time that FM involves fascia dysfunction but CFS is something else. Some very unlucky people may have both – or perhaps they have FM and the development beyond a certain point results in the same fatigue dysfunctions as CFS, while the mechanism that causes CFS in “normal CFS patients” may be absent.
I have a question for you now: I have always noticed that my “adhesions” tended to worsen overnight, and if I had “gone anaerobic” the day before, that is when I would be at my worst the next morning. In fact any prolonged immobility following anaerobic exercise, was bad, even sitting. I just assumed this was consistent with an “adhesive” (worsened post anaerobic activity) being given time to work while tissues remained static. But what you are saying earlier, is that eating some of the right carbs prior to bed, (or post exercise?) might prevent this?
The other point is that “muscle strengthening” routines greatly increased the extent of painful lumps in my muscles at the same time as impressive muscle mass developed; again I thought this was merely a matter of “adhesive” being presented with more scope to cause trouble as muscle-fibre bundle surface areas increased (plus the muscle foreshortening as is commonly acknowledged in muscle-building). Could this too be forestalled just by eating the “right” carbs at the right time? Glad of more explanation.
Hi Phil,
“I have thought for a long time that FM involves fascia dysfunction but CFS is something else.”
-> I feel that ME and FM have much in common while still being different diseases. To me, they can flow over into each other.
“I have a question for you now: I have always noticed that my “adhesions” tended to worsen overnight”
-> In my idea nights are though to ME (and FM patients to some extent) in part because the combination breathing/blood flow is dropping under a certain threshold. That brings with it a daily drop in health making it so hard to improve our health even when we live so healthy as possible and pace a lot. In that sense nightly “stalls” are the “forgotten” equivalent of overexertion during the day. It’s a part that is harder to remedy than overexertion as not sleeping doesn’t help either.
“and if I had “gone anaerobic” the day before, that is when I would be at my worst the next morning.”
-> Fits with my idea: you start the night with greater dysfunction of local blood flow and breathing and a pile of waste that only will grow over night. As to speak, you give the nightly ME/FM engine a serious head start.
In fact any prolonged immobility following anaerobic exercise, was bad, even sitting.
-> I have the same; even lying down while sleeping becomes painful. Quite common in ME/FM. Could potentially be those “tophi” with uric acid and minerals binding uric acid that press with their edges to your tissue that is (pus like) weakened by the immune system to get rid of them.
“But what you are saying earlier, is that eating some of the right carbs prior to bed, (or post exercise?) might prevent this?”
-> Please do not intend to use this daily-care procedure as an excuse to push yourself harder into anaerobic area. With your keto diet you have day round low blood sugar and hormones geared to not using sugar as much as possible. Can’t really expect to do well in anaerobic exercise IMO. Largely inhibiting anaerobic metabolism may be a big part of why keto helps…
Let me explain my routine. I do not carb load in the evening unlike the person I learned this trick from. I’ll look up his name and the blog when I can. I only try to reduce the amount of shortage I guess there is at night, to a very rough extent of about 30%.
Why only try and remove part of the expected temporary shortage at night? I believe in a variant of the common 80/20 rule (80% of a project is done in 20% of the time, while the remaining 20% is done in 80% of the time.) The variant is, very roughly: 40% of potential benefits are obtained when handling 30% of the excess/shortage while producing only 20% of the side effects. So it provides better return to effort ratio and having less side effect makes it more accessible. Moreover guessing the size of a problem is very difficult. Aiming for 100% resolving it could be a massive overcompensation doing few good and plenty wrong.
The amount of sugar I use at night is really small. 10 to 15 grams of honey dissolved in my drinks and drunk in several times spread over the worst part of the night helps strengthen my immune system. It requires keen senses to detect a day to day difference, but part of it builds up over time. The effect is thus small but growing and the daily effort is low. So it’s size is too small as to act as an emergency routine at least in this form.
Why such small amounts can work? I do need less then 2000 calories, about 1600. About half of them are carbs or 800. For the 6 worst hours that’s 200. At night metabolism is lower so let me say 160 calories. If I only get 60% of this, I am 40% short. 60% equals to 96 rather leaving 44 short. With 10 to 15 grams I would already risk overcompensating, but I guess anaerobic mechanisms makes the 44 calories short a bit optimistic. IF it would help somewhat while not jumping out of keto diet it may require really low amounts of honey. The effort might well outweigh the benefits as it’ll be a lot harder to get it right on a keto diet.
“The other point is that “muscle strengthening” routines greatly increased the extent of painful lumps in my muscles at the same time as impressive muscle mass developed;”
-> muscle growth is quite an inflammatory process, lowering the threshold for the proposed mechanism. I already asked before, but forgot. Did you eat plenty of protein (possibly meat or powder devout of other nutrients?) during that period as many sporters do when growing muscles fast?
“Could this too be forestalled just by eating the “right” carbs at the right time? Glad of more explanation.”
-> potentially, but too late for you now (unless anaerobic exercise and muscle mass are the only remaining things separating you from normal health) and misfit with keto
What works for me in order of effect to reduce the hypothetical problem: not go anaerobic > pace > learn to breath well / get muscle and blood vessels less constricted > keep breathing and blood flow above minimum threshold at night > keep blood sugar above minimum at night.
In your case I’d consider looking at the potential to replace some animal proteins with vegetarian whole food proteins, if that is realistic. Debbie may be our new expert on this ;-). With years of animal keto diet transitioning slow over months may be required depending on remaining gut flora diversity.
Hi Phil,
looked a bit further into this and found:
https://arthritis-research.biomedcentral.com/articles/10.1186/ar4026
“Patients with anemia had a two-fold increased risk of developing gout over nine years” -> gout is a purine based disease; anemia has a very strong correlation to hypoxia (and with it strong ties to anaerobe metabolism in locations / at times). So IF purine metabolism came into play with FM, reducing anaerobe functioning gets another plus.
https://www.ncbi.nlm.nih.gov/pubmed/22470026
“Flaxseed has been suggested play preventive and therapeutic roles in cardiovascular disease… …HDL-C (High-density lipoprotein cholesterol) increase (p < 0.05) in 47% when compared C group. The LDL-C (Low-density lipoprotein cholesterol), glucose and uric acid were reduced (p < 0.05) 22%, 78% 64%, respectively"
Note this was a study of rats, and the percentage of flaxseed in their diet was impractical, but it points at potential advantages of shifting protein sources more towards vegetarian.
Was diagnosed with ADHD by my healthcare provider after being given a short questionnaire. Was then prescribed ritalin/adderall/vyvanse for several years.
Side effects were horrific at times, but doctors insisted I take stimulants as prescribed if I wanted to function and hold a part time job.
A few years later, after my baseline health had declined and I was no longer able to work even part time, I did in-depth neurocognitive testing ordered by a neurologist.
Afterwards, the tester laughed and said, “Well you definitely DO NOT have ADHD”. So my initial ADHD testing was wrong.
Taking stimulants with ME/CFS did give provide a short term boost in function, but at the cost of horrible side effects and a slow but substantial decline in my baseline health.
Anyone with ME/CFS considering stumulants should be aware of the risk of permanent baseline health decline.
Thanks for sharing your experience, John.
Hi and thanks everyone for a lot of insight and for sharing your experiences.I have ME since about 15 years back, after a giardia infection. My experience with Adderall and Vyvanse is similar as John’s , they helped for a while but depleted me quite rapidly, ending in pretty bad relapses of pain and deep fatigue. I got my ADD diagnose after quite a lot of testing, but don’t really know how it’s separate from brain fog in ME-CFS. My “ADD” gets worse when my other symptoms get worse, pain, shortness of breath, OI, etc. Right now I’m better than I’ve been for many years, even running twice a week which was unimaginable for years and years. But I don’t have normal energy, I have to lie down a lot during the day, working maximum 50%. I get by by keeping a strict high fat meat and leafy vegetables diet, and doing regular coffee enemas. I figured that one way to battle oxidative stress was to get more glutathione, and stimulating bile flow also helps the gut, eg. if there is dysbiosis. It’s helped me enormously. Before I have also experienced improvement by sodium bicarbonate, as a way to eliminate lactic acid. I think I’ve tried all the meds but nothing has given me any long term improvement. I cannot eat any carbs really… sugar, starch, any grains. Even a lot of vegetables can set of my symptoms. FODMAP captures most of my food sensitivities.
Hey Hedy,
I wonder if combining adderall with nutritional supplements aka the Synergy trial would help?
Willow – what a great description. I can so relate to: “too many browser windows open” and my “RAM gets used up” and everything freezes (overwhelm, paralysis) or goes haywire (cognitive anxiety). And to everyone else in this terrific discussion.
I often wonder about a common underlying mechanism for many of our symptoms (brain fuzz, wired and tired or simply tired, altered sugar/fat metabolism, depression, fatigue, etc ) and some of the overlaps in the ME/CFS community (what I have) as well as FMS (pain, muscle changes etc).
One of my areas of curiosity is whether these symptoms, including ADHD-type brain fuzz, are signs of an underlying shift in nervous system functioning towards something akin to a cell danger response ie: those of us with these illnesses are either in prolonged physiological states of relative freeze/hibernation (more the me/cfs end of the spectrum?) or combined fight & flight / freeze (more the FMS & POTS end?).
From a Porges polyvagal theory point of view, this would suggest that we all have some kind of loss of or decreased vagal support from the highest functioning branch of our nervous systems – the ventral vagal aka social nervous system – which is capable of regulating the other two and keeping them for only occasional use. Even altered breathing as you refer to dejurgen (although I don’t know what your exact symptoms are), could reflect a state of relative nervous system imbalance (airways open up in fight / flight and breathing rates increase and the airways narrow in states or more relative freeze, which is similar to the diving reflex in whales and other mammals and which Porges refers to when discussing asthma).
As such, the huge variety of things that help some of us improve and not others (and vice versa), and that don’t work in reliable ways, could be things that support or increase vagal tone (the myelinated social nervous system branch of the vagus rather than the unmyelinated dorsal vagal branch that facilitates “freeze”). Things that calm and soothe, feel comforting or resourcing – from vagal stim to foods to interactions with people who are supportive, to meds to mindfulness, meditation and other mind body practices, to therapies that work directly with the nervous system etc.
Better vagal tone and nervous system balance would then directly influence all the other players, from mitochondria, to the immune system, hormones and more.
I had to finally just stop trying to read all of the long post about diet and the debate of the reason why someone with Fibro. or ME/CFS may have ADHD. Well, it is very simple and basic for me. I have had severe ME/CFS, completely bedridden now for 20 years, and the only way or time that I have enough energy to get up and sit in a chair or even raise my head up off of my pillow so I can watch television, including having mental focus and clarity, is when I take my Adderall. I take 30 mgs twice a day and only then can I even dream of getting up. Well, I never had ADHD in my past and developed it very soon when I came down with this illness and I can tell you this, the main or primary reason, if not the only reason entirely, that I currently have ADHD is because of being so physically and mentally exhausted that I simply do not have the energy or capacity for any mental stimulation and in the same manner that I do not have the physical energy to get up and out of bed. I am so tired that I am just paralyzed both physically and mentally. I probably could focus enough to read, comprehend it and show interest in my photography for example but I just can’t even get there from the cruel, unforgiving and ever present fatigue. But, once this has been overcome, in my case with Adderall, I am just as fresh mentally, as I was in high school. That goes the same for the physical challenges we face too. I believe that my ADHD is caused simply because of the fatigue and exhaustion being so strong. Also, all I could make out of the dietary post about Ketosis is that you must be doing Atkins!?? I am just the complete opposite, I do much, much better in overall general health, weight maintenance, acid reduction eliminating my GERD, etc., but also including my ME/CFS symptoms when I follow a low carb diet. I don’t even pay attention to trying to force my body into Ketosis, I just eat this way most of the time and I have no problem in losing weight but feeling better too. Now, what I also do with the Adderall, I take the Adderall usually 2-4 days in a row, if possible, and then I quit taking it for 3-6 days, giving my body all the time it needs to recover and recuperate from being up and about and stimulated and before I push myself to far and into a much more severe crash. I have been able to do this for several years now and while I am still not able to really be active when up, at least it gets me the heck out of that bed that I have living in for the past 20 years! Now, I will say that all of this works for me, I don’t know nor do I claim to know, anything except what I have learned from this horrible disease pertaining to how it effects me and what I have learned from in my experience. What is really a major problem, that I am currently struggling with, like so many others, is the fact that I have now, after all this time, completely lost all hope where there was no hope to speak of, and that I will ever live a life that has joy, meaning and purpose, ever again. I no longer grieve for all of the joys of life, material things, marriage, children, or independence etc., that ME/CFS robbed and stole from me but I am now in constant turmoil, filled with worry and uncertainty of what is going to happen to me in the future because I will soon be alone with no other living relative to help me, broke and completely disabled with absolutely no way to do anything about it either. I do not want to die, I just am tired of this life, the suffering and do not want to live like this, in a bed, any longer. We need help and all we can look to is science. Well, we know how that has been. Thank you.