This blog is part IV in a series of blogs covering the issues presented at the 2018 Dysautonomia International Conference in Nashville, Tennessee.
This is the fourth blog on issues presented in the 2018 Dysautonomia International Conference.
As if we needed another syndrome. Chronic fatigue syndrome (ME/CFS), postural orthostatic tachycardia syndrome (POTS), fibromyalgia (syndrome), irritable bowel syndrome (IBS) are old-timers in the ME/CFS/FM world. In the last couple of years, mast cell activation syndrome (MCAS) and Ehlers Danlos Syndrome (EDS) joined the party. Sjogren’s Syndrome (SS), which was all over the Dysautonomia International conference, may be a late entry, and now it seems we can add antiphospholipid antibody syndrome (APS) – which is apparently very common in POTS – to the list of syndromes that play together in these interrelated diseases. It’s also another autoimmune disease.
In fact, Dr. Hughes, the U.K. rheumatologist who discovered the syndrome, said that if you’re dealing with POTS, you’re very likely dealing with APS, which is also called “Hughes Syndrome”, as well.
Antiphospholipid Antibody aka Hughes Syndrome
APS is not some niche researcher’s fantasy; it’s a well-recognized systemic autoimmune disease which increases the clotting factors in our blood, producing “sticky blood”, which then impedes blood flows.
Antiphospholipid syndrome causes increased blood clotting. Several studies suggest clotting issues may be present in chronic fatigue syndrome and fibromyalgia.
APS occurs when increased levels of antibodies attack the phospholipids or fats in our cells and in the lining of our blood vessels. (You can have the antibodies without having the disease.)
Like other systemic autoimmune diseases, APS can cause a wide range of symptoms that seem disturbingly like those found in ME/CFS. They include chest pain, shortness of breath, pain, redness, warmth, and swelling in the limbs, cold hands, chronic headaches, upper body pain, nausea, brain fog (memory problems, can’t find way home, forget words), balance problems, heart valve problems and a lacy-looking red rash on the wrists and knees. (Notice no mention of post-exertional malaise, though.)
The NIH’s National Heart and Lung Institute reports that APS can cause many health problems including heart attack, stroke, pulmonary embolism and kidney damage. Dr. Hughes reported that APS is commonly found in teenage migraine, stroke, heart attack and teenage epilepsy but is often – more than 30 years after its discovery – undiagnosed.
It affects 1-5% of the population and more often strikes women than men. One third of strokes occurring in younger people (<50 years) are believed due to APS. If you suffer from migraines and cold hands, he suggested that you may have APS. If you have APS, it’s likely you have another autoimmune disease as well.
Dysautonomia, Postural Orthostatic Tachycardia Syndrome (POTS) and Antiphospholipid Antibody Syndrome (APS)
Most of the focus in APS has been on its connection to stroke, clots and pregnancy, but Schofield proposes that its effects on autonomic neuropathy (damage to the autonomic nerves) can be just as devastating.
Dr Schofield – who has pioneered research into APS and POTS – first published evidence of APS in POTS in a small 2014 study. (No ME/CFS or FM studies have been done – but see Dr. Berg’s work below.) A 2015 exercise study, which showed evidence of impaired aerobic capacity and autonomic control, suggested APS could also be misdiagnosed as chronic fatigue syndrome (ME/CFS).
A 100-person 2015 study found APS antibodies in 7% of POTS patients while Schofield’s 38-person 2018 study found that 76% of participants in a retrospective IVIG trial in autoimmune dysautonomia (many of whom had POTS) had APS antibodies.
In her 2014 study, “Autonomic neuropathy-in its many guises-as the initial manifestation of the antiphospholipid syndrome” Dr. Schofield outlines two ways APS might be smacking POTS patients. Either the clotting caused by APS is damaging the autonomic nervous system fibers lining the capillaries; or the antiphospholipid antibodies are binding to and damaging the small fiber neurons.
A POTS / ME/CFS Mimic?
Schofield and others have shown that APS antibodies can be found in POTS patients, but Dr. Hughes proposed that APS may be being misdiagnosed as POTS as well. APS can produce symptoms (dizziness, vertigo and other neurological symptoms) similar to those found in POTS. In fact, Hughes reported that some cases misdiagnosed as POTS cleared up when the anticoagulant therapy used in APS was introduced.
A 2015 exercise study which showed evidence of impaired aerobic capacity and autonomic control provided the intriguing suggestion that some people diagnosed with chronic fatigue syndrome (ME/CFS) might actually be suffering the effects of APS – a treatable disease.
Treatment
Blood thinner, anti-inflammatory, and vasodilator – heparin is often used to treat APS. Dr. Holtorf reportedly uses it in his ME/CFS/FM patients.
Dr. Hughes first tries aspirin, then, if necessary, two weeks of low molecular weight heparin. If that doesn’t work out, he moves on to Coumadin – a harsher drug. The anticoagulant therapy does not cure APS but it can stop the clotting process and clear up the symptoms it causes. Hughes noted one “POTS” patient who did not respond to POTS medications but did respond to heparin and his POTS cleared up.
Dr. Schofield reported that anti-coagulation in combination with IVIG can result in “meaningful clinical improvement” in patients with autoimmune dsyautonomia.
The Gist
Antiphospholipid antibody syndrome (APS) is an autoimmune disease which causes increased clotting
It’s primarily associated with stroke, heart disease and problems in pregnancy, but Dr. Schofield believes it may be contributing to dysautonomia’s such as POTS
Dr Schofield believes APS may be impeding blood flows in the small capillaries and/or contributing to the small fiber neuropathy found in POTS.
Because APS can cause similar symptoms to POTS and ME/CFS some people diagnosed with those diseases may actually have APS – which is treatable
Treatment involves anticoagulants such as aspirin, heparin or coumadin
Around 2000 Dave Berg published several studies suggesting that an APS-like condition was present in ME/CFS, FM, GWS and related diseases.
Berg produced a treatment protocol which used heparin and immune factors to remove the fibrin depositions and pathogens he thought were present
With Berg’s retirement interest in coagulation and ME/CFS faded but recent studies suggest red blood cell and coagulation problems may exist in fibromyalgia.
Testing
Positive antibody results in combination with the right clinical picture are enough to make a diagnosis.
Two types of antiphospholipid antibodies are found: 1) anticardiolipin antibodies (IgG, IgM, and IgA); and 2) something called the lupus anticoagulant, which is directed against beta-2-glycoprotein I (IgG, IgM, IgA) in the blood and prothrombin, and plays an important role in clotting.
Dr. Schofield, who is making something of a career of finding newer, more effective antibody tests in POTS, found that prothrombin-based antibody testing (aPSPT antiphosphatidylserine-prothrombin, aPT antiprothrombin) was far more effective in identifying possible APS patients in POTS.
Testing can also include a panel of blood clotting tests (dilute Russel Viper venom time (dRVVT), lupus aPTT, mixing studies, the hex phase phospholipid test, and the platelet neutralization procedure).
The “Sticky Blood” Chronic Fatigue Syndrome (ME/CFS) / Fibromyalgia Connection
Around the year 2000, several studies suggested that a kind of coagulatory offshoot of APS was happening in ME/CFS. Three studies, one of them very large, suggested that ME/CFS and fibromyalgia patients had hypercoagulated or thickened blood, which David Berg speculated was reducing nutrient and oxygen flows to their tissues.
Berg, who ran Hemex Labs, believed an infection was triggering – or had triggered – antibodies, which ultimately produced the thickened or sticky blood which was clogging up the small capillaries in the body.
Berg also believed his hypothesis could account for the fascia/trigger joint problems in fibromyalgia. In an interview with Dr. Mazlen found on the website “CFS Remission”, he described what he believed was going on:
“The inability to clean up the blood vessel walls once fibrin is formed…The model simply says…they (fibromyalgia patients) form antibodies to whatever their invading pathogen is, (then) the immunoglobulins knock off the protective proteins on the endothelial cell’s surface.
“This exposes phosphatidyl serine in the capillaries to the flowing blood, and that allows the coagulation proteins to bind and so all of a sudden we’re generating thrombin in the small vessels in the capillaries throughout the body.
“So, if we take a muscle and pull it down to a ligament or a tendon and wrap that with the fascia, that fascia is only 5 or 6 cells thick, that’s where the capillary blood flow is and so if you coat the insides of that capillary with fibrin, not a blood clot, but fibrin, then the nutrients and oxygen do not pass through to that ligament or tendon on the other side and all of a sudden it says “ouch” and we’ve got a trigger point, a defined trigger point as in fibromyalgia.”
Berg’s ME/CFS/FM Treatment Protocol
Like Dr. Schofield, Dr. Berg believes blood flows through the small blood vessels are being impaired.
In a Town Hall meeting in 2000, Berg presented a treatment protocol designed to stop the coagulation problems and then clean up the infections he believed were hiding in the coagulated areas:
- Provide heparin for 6 months (Berg described heparin as an anticoagulant, anti-inflammatory, antiplatelet, vasodilator, and NO production increaser).
- Add Bromelain at the beginning for 4-6 months for patients that have an increased Lp(a) or PAI-1.
- Add Transfer Factor after 30 days of heparin for 2-3 months.
- Add antibiotics 30 days after heparin.
- Continue to use heparin for another 2 months, just in case. If there are still a few pathogens left after these therapies, they will attempt to reactivate the coagulation cascade again, to generate Soluble fibrin &/or fibrin deposition. So by continuing heparin, this will prevent cascade reactivation and the immune system will be able to clean up the remaining pathogens.
Berg sounded like he was on a roll. He had a protocol he thought would work and described a typical response to heparin:
“I swam three laps and then worked in my yard. Oh am I going to pay for it tomorrow but only with sore muscles that haven’t been used in so long. Today, when I came in the house I gave in to my urge that I’ve had for the last 2 days to go skipping down the hall. I did it 3 times. How funny I looked. Like a little kid just learning to balance and learning to skip. Now I have to retrain my muscles but my mind still remembers how. That little girl in me got the biggest kick out of skipping again and it’s been years.”
Aftermath
Berg’s retirement in the early 2000’s apparently ended further efforts to establish his findings. A small study (n=17) in 2006 failed to find evidence of hypercoagulation. From what I can tell, nothing more has been done. Pathogen tests since then have failed to find evidence of the infections Berg believed were present, but inflammation could conceivably do the trick, and possible blood issues have continued to pop up in ME/CFS, fibromyalgia and related diseases.
Two 2017 studies found evidence of increased red blood cell deformity and rapid platelet aggregation as well as increased platelet distribution width – a marker of coagulation – in fibromyalgia. A small 2018 Gulf War Syndrome study found evidence of red blood cell deformability issues.
Just as Berg thought with ME/CFS over 15 years ago, Dr. Schofield believes antibodies in POTS and other autoimmune autonomic diseases are blocking blood flow in the capillaries. Ron Davis’s group is exploring whether red blood cell deformability problems are having a similar effect.
Could red blood cells be causing problems in all these diseases? Anything that restricts blood flow in the capillaries could lead to hypoxia and hamper energy production. Vermoulen’s exercise test results suggested reduced oxygen availability was causing the energy production problems he found in ME/CFS. We should learn much more about this with Dr. Systrom’s studies which the Solve ME/CFS Initiative is helping to fund.
More on Berg
- Perhaps the best explanation of Dr. Berg’s hypothesis and findings can be found here.
- Find out more about David Berg and hypercoagulation on Ken Lassesen’s CFS Remission site.
2018 Dysautonomia International Conference Blogs
- 2018 Dysautonomia International Conference I: Small Fiber Neuropathy, POTS, MCAS and Vagus Nerve Stimulation
- The 2018 Dysautonomia Conference Pt. II: Could You Have a Spinal Fluid Leak? An ME/CFS, POTS, FM Perspective
- Dysautonomia International Conference Pt III: The Autoimmunity Revolution in POTS
I’ve known about the “sticky platelet” problem for years. I figured it out when my favorite lab technician couldn’t get a blood draw on me after 10 tries. It was like trying to drink molasses out of a skinny straw. It just wouldn’t flow!
I started taking Nattokinase supplements, and in two weeks we got a perfect draw on the first try. I’ve been taking it ever since, and it does make a big difference. If you’re leery of taking yet another medication, and want to go natural, nattokinase is a great place to start.
Thanks for sharing that. Other than being able to get a blood draw, how does nattokinase help?
Nattokinase is derivative of fermented soy that has an enzyme that is a blood thinner.
I take Lumbrokinase for my diagnosed APS, along with an aspirin every third day, and some gingko for the platelet aggregation. Lumbrokinase is a very powerful, natural anti-coagulant. Much stronger than Serrapeptase or Nattokinase.
An allergist/immunologist (now deceased) who diagnosed me in 1984 was doing research with a professor of immunology from our local university. They treated me with a form of non-anticoagulent heparin and transfer factor. This greatly relieved the extreme chemical sensitivity that I had at the beginning. Also, if I had one of the devastating headaches I had for many years, a shot of heparin would relieve it almost immediately. The form of heparin I was given was not available in the U.S. and was obtained from Germany under an orphan drug provision.
Wow. Chemical sensitivities affected. That’s amazing.
I’ve had the same problem but my Rheumatologist says it wont cause think blood just blood clots.
There is a wonderful formula by Arthur Andrew called Nattovena that isolated the enzyme (Nattokinase). I found it at Azure for .28 a capsule if you buy the large bottle.
https://www.azurestandard.com/?a_aid=3da1e127f2
I have CIRS and am investigating if it is free from mycotoxins as I believe Natto, fermented soybeans the food from which Nattokinase if derived has mycotoxins.
All my clotting lab tests have come back elevated for 18 months including recently, Platelet Factor 4 at over 2,000 when the range is 0-75.
Antiphospholipid antibodies were negative, but I have a Factor 2 clotting SNP.
Aspirin isn’t possible due to a corn allergy and doesn’t heparin set off MCAS? I’ve been on Lumbrokinase and nattokinase, which don’t seem to do much, so am wondering if there are other alternatives besides Coumadin and Xarelto?? Would IVIG help?
And does anyone know about the signigicance of Platelet Factor 4?
You might want to try 4 grams or more daily of EPO-evening primrose oil, Efamol’s efalex brain formula recommended. I have been taking 10 of those which adds up to a bit over 4 g. daily after cfs relapse in jan 2018 after type A influenza and it seems to have made great difference to many symptoms related to blood flow and oxygen to cells. Can tell more when at computer. Too hard to type on phone. I got idea from reading leslie o. Simpson’s book Ramsey’s disease. See pp 186-187 and 207 among others. Book and efamol’s efalex available from amazon thankfully. Ordered from my bed and delivered to my door. Amazon is more useful to us than most doctors. Should we give them a “CFS Friendly” award? Lol
Hi Ruth – is it the GLA needed or the DHA…thanks…
Jane, it put my reply to you after the next comment so just look down further. Ruth
Why not comudain? Asking because I take it due to APS. I don’t like my side effects, but would like to research more on other natural medication.
I infected heparin for two years (usually with antibiotics) when I first got ill and Berg’s theories were floating around. I tested positive for APS multiple times and for clotting factors from Hemex. I did improve some over that time but don’t know much much was due to that protocol. The purple feet etc went away and some symptoms lessened, but POTS and other significant CFS symptoms have frustratingly never left.
Hi Jane, that’s a good question and I wondered about that myself but don’t know answer and it may be another constituent too that I just saw something on but will have to refind to give details correctly. Since this exact product was also recommended to me by a person who works with vets with PTSD here in SATX, many of whom also have CFS and FM, I decided to just stick with exact formula. I had taken it previously but at amt recommended on bottle which is only 40% of amount recommended in Ramsays Disease book. When I upped dosage it made a huge difference. Hope this helps a bit. And I will try to find that other info that I saw recently and post it here as reply to this reply. If you want to email me directly on my gmail you can add my middle name of anne to my first name as well as my last name of Ross. Hope that fools the email grabbing software, lol.
Thank you, Ruth!
I use Vascuzyme. Has a lot of different enzymes in it. Take that in morning and Serrapeptase at night. Seems to work. I had a positive Lupus Anticoagulant at one time. Have Factor VIII and Collagen Binding. So yes, too thick blood can definitely play a part.
Issie
This is so interesting. I have a positive ANA for Lupus. I am also heterozygote for Factor five Leiden. Had never thought my clotting factors could play a part in my fibromyalgia.
I think I might try an aspirin daily to see if it helps.
I’m positive for the anti-cardiolipin antibody and was told to take 325mg aspirin daily for many years. My last test was low positive and my ASA was decreased to 81mg/day. I have Fibromyalgia & POTS. I’ve never had a known clot, or miscarriage (as many do with Hughes Syndrome). I also have a skin disorder, generalized granuloma annulare, it’s believed to be autoimmune. I believe this is all connected.
The connection of miscarriage to Hughes syndrome is interesting. They may have CIHHV6, which i was already wondering about reading this blog. Cort, what do you think about possibility of HHV 6 connection? I saw in some EU research, i think German, that autopsy of group of stillborns and spontaneous abortions all showed the inherited CIHHV6 and none of induced abortions did. Do you have ref for connection between hughes syndrome and miscarriage? Thanks.
Dr. Hughes said the detection of APS has been able to drop the rate of pregnancy related complications including miscarriage. The connection appears to be well founded
Here’s an overview from Medscape – https://emedicine.medscape.com/article/261691-overview
This is really interesting. I have granuloma annulare, I have had a PE and two miscarriages. Icant seem to get pregnant. I have never been diagnosed with APS but from all the research I have done, I am beginning to believe I may have it.
Yes it is all connected, through diet, chronic dehydration (=lack of various good salts), and EBV.
Various undiscovered strains and mutations of the Epstein-Barr and/or HHV-6 viruses are being found to be behind almost ALL ‘autoimmune’ and chronic diseases.
Mental Recognition of this helps boost the natural immune system and speed healing.
Any doctor who tells people their body is being ‘bad’ and is giving them immune suppressants or cortisone to hide symptoms is doing them a great disservice! A few months down the road, the (now unsuppressed) disease will only get worse.
Cort recently published a link to the April 2018 published study connecting EBV directly to 7 chronic diseases (incl. MS and Lupus) and to 94 chronic diseases and cancers via transcriptions.
So more research is needed to cover all HHV viruses.
It does make a LOT more sense that the body is attacking a pathogen and not itself, especially when antibodies and inflammation are present.
“If it walks like a duck, talks like a duck,…”
– I want to add ” And If it is dark out, the duck is still a duck.”
The cure? Do not feed the virus. i.e. Do not eat things the labs often use to grow viruses for millions of vaccines, like eggs, or simple sugars.
The semi-dormant virus lives (hides?) in the extra mucus in the liver and elsewhere in the body, so eat no mucus producing foods, like dairy and gluten.
EBV loves to also break down and eat heavy metals and toxins (which once made EBV beneficial), and then it produces neurotoxins (and sometimes dermotoxins) that then get eliminated by the liver and kidneys.
These days there are so many toxins out there that our liver gets overwhelmed. The virus and toxins spill over elsewhere in our bodies. Eventually the liver gets scarred, clogged, and ‘fatty’. We feel tired and gain weight, and the other symptoms vary person-to-person, with no two identical. It is like the story of the 5 blind men describing an elephant.
So what to do?
Avoid all additional toxins and chemicals, including most patented drugs and non-natural cosmetics, lotions, and sunscreens (zinc sunblock is ok).
Take aspirin or Motrin only for occasional aches’n’pains, since it has the side effect (besides easier bleeding) of halting proteoglycan production, which keeps cartilage from regrowing and thus makes osteoarthritis worse, especially in the hips and knees.
Consult a good licensed holistic doctor and nutritionist. They should be familiar with all of this, what drugs can be stopped, and what supplements should be started.
Eat much MORE organic vegetables, fruits, berries, and herbs with anti-viral properties.
Avoid processed vegetable oils and canola oil. Avocado & Coconut are OK.
To get back on topic:
Omega 3 oils (5gms/day) via low mercury fish, fresh flaxseed oil, and/or high quality capsules, are a natural blood thinner without the side effects of ‘mystery bruising’ or greatly increasing your chances of having an aneurysm-type stroke (bleeding of the brain).
The weakened cell structure and bruising on the ‘outside’ from blood thinners also goes on in the inside.
…So if you are bruising easily, or get weird little dark red blotches for 2 weeks or so, and Whole Food Vit C + zinc is not curing it, blood thinners are not good for you.
Books:
‘Life-Changing Foods’ by health guru Anthony William
JJ Virgin (and others) do something simular by removing many (but not all) inflammatory and mucus-producing foods, so the diet and recipes can easily be modified as needed to make it anti-viral, too.
Most ‘healthy eating’ diet plans make the mistake of including (unfermented/GMO) tofu, greek yogurt (dairy), cheese (dairy), DDT- or arsenic-laced rice, and/or eggs, which is why CFS people who eat ‘healthy’ don’t get healthy.
Hi Susan, your comments are interesting. I developed a measles like rash on my tummy and a couple days of colitis a few months back while still struggling to recover fully from influenza and in looking up the rashes, I came across roseola viruses which were discovered after I already had CFS and I didn’t pay much attention. Since I had been drinking lots of coffee while trying to finish some research reports, I promptly added 3g. lysine daily to try to block arginine, and the rash, which I had had for month, resolved In about a week and also blurring in my eyes improved. I have had these visual problems for several years and opthalmologists and neurologist couldn’t figure it out I think you are correct that there are many more things connected here but finding the precise way they are connected is certainly a challenge. Looks like a connect-the-dots with many of the numbers left out. Since we patients are the ones suffering with the dots, I guess we have to help connect them if we want it done in our lifetime. Happy connecting! Ruth
Hi Susan,
Interesting you mention HHV-6 next to EBV. Reading this blog I was wandering “what do these auto-antibodies try to react to”? I am not convinced they’re just chasing something that is not there.
I have problems with poorly digested proteins and/or poorly folded ones. That is a candidate for me. Doctor Bergs’ use of Bromelian has a slight resemblance of my partial ongoing improvement by eating papaya with protein rich meals. But Bromelian, just like Papain, only breaks down proteins. Would they help with lipo-proteins too?
If auto-antibodies cover endothelial cells and damage them, it could mean leaked lipo-proteins. But still: why would the body attack those? That leads to the question: do auto-antibodies on edothelial cells do the damage themselves, or do they provoke a local immune response bombarding them with ROS/peroxide? If so, it would break down the cells walls and release lipo-proteins passing through a “cloud” of ROS. Pro thrombotic and inflammatory chemicals would leak out of them too and travel through this cloud too. All of them risk damage and as such need to be cleaned up by the body… by aid of the immune system and it’s auto-antibody’s?
RBC passing slowly through these damaged/narrowed capillaries pass through this cloud/storm of ROS too, damaging them and causing loss of flexibility. When healthy RBC have a diameter already smaller then healthy capillaries, good bending of RBC is vital. Simultaneous reduction in capillary diameter, damaged/rougher blood vessels and less flexible RBC is a recipe for very poor and slow flow of blood/RBC/oxygen through this cloud of ROS/peroxide. All this ROS puts a heavy strain on anti-oxidants including glutathione. Less glutathione leads to more protein misfolding, requiring more auto-immune response to break these down. But depleted anti-oxidants let RBC/hemoglobin acts as emergency scavengers of ROS. And for every molecule of ROS/peroxide attached to hemaglobin (becoming methemaglobin) 3 more positions for oxygen binding (total of 4 including the position taken up by ROS) are long-time blocked for transporting oxygen. If this situation perseveres a high percentage of RBC oxygen carrying capacity is semi-permanently blocked, resembling a “mild” form of CO poisoning. That on top of highly reduced blood/RBC stream through the capillaries. That should cripple both functioning and self-healing.
What’s the relation to HHV-6 and EBV? Both increase ROS production from endothelial cells and some types of immune cells https://hhv-6foundation.org/latest-scientific-news/hhv-6-induces-oxidative-stress-and-chlamydial-persistence.
Many of these syndromes seem to be linked to each other by extreme self reinforcing oxidative stress responses and crippled ability of the body to defend against them or reverse the vicious circle IMO.
Susan you use pseudo science to explain your theories and treatments.
I have had ME/CFS and FM since 1986, and was diagnosed with antiphospholipid syndrome in 2008 and POTS long before that. Aspirin, even baby aspirin, destroys my stomach and so did Coumadin. I have to be careful with soy products (which the nattokinase contains) because of thyroid replacement therapy and estrogen receptor positive breast cancer issues. I take Vitamin E, Tumeric, Olive Oil (alternating with Cod Liver Oil and Coconut Oil,) and CoQ10 Ubiquinol, and find these keep my APS under control. My guess is that many ME/CFS and FM patients also have undiagnosed APS.
Did the supplements significantly lessen your fatigue?
“Significantly” is a big word in our ME/CFS & FM world! I don’t know that anything significantly lessens the fatigue, but every little bit helps!
And many of us find the things you take to be essential to our own health (or a reasonable approximation of health). So there’s guilt by association at the least.
Dear chfrazzle. Hang in there; together we are going to figure this thing out. What reduced my fatigue the most was the 4 grams of EPO taken as 10 efalex brain formula per day. Have taken this for almost 6 months. Noticed some improvement, e.g., much less fatigue and some less neuropathy, in first couple weeks. If i stop for couple days or cut dose the fatigue comes creeping back. I think it was about $35 at amazon for 240. So 24 days supply at my rate of 10 daily based on recommendation in dr leslie Simpson’s book Ramsay’s Disease(pp 186-7, 207) Not bad cost for big difference it makes for me but i have to remember to reorder before i run out next time. Lol. But luckily it also hugely helps my cognitive symptoms. Else i wouldn’t even be typing this.
I have only been diagnosed with APS. Had 2 early pregnancies one 6 weeks and 1 13 weeks early, a miscarriage in between all in my 30’s. I have the red lacey marks on arms and legs. I have had 7 documented TIAs and 1 big stroke. Always had headaches that I thought were migraines but since the TIA issues wondering if it was more undocumented TIAs. Still get muscle spasms in legs from time to time. Have been on Warfarin for many years now. Wondering if I have an associated disease that has been undiagnosed? MS was ruled out. Was heavily tested but not sure on all of them. I have been affected by other auto immune problems as a teen, wondering if I need more testing? Any of your thoughts would be appreciated.
Pat S,
What do you mean when you say that “these keep my APS under control” – what symptoms/signs do you have that you attribute to APS and what have you gotten relief from?
Thanks,
Sounds very similar to this story from a couple decades ago.
http://lassesen.com/cfids/familyhistory.htm
Ken played a big role in getting Dr. Berg’s story out. Anticoagulant treatment played a major role, as I remember, in one of Ken’s ME/CFS remissions.
If someone has APS Hugh Syndrome then they do not have CFS they were misdiagnosed all along & it could be that Ron Davis’s new blood test
marker could be linked to thickness in the blood so maybe anti clotting drugs work but not APS unless he has found some new strain or a
medicine that works better…He already said the 2 medicines found work, maybe it is linked to the blood thickness or clotting in East African
Sleeping Sickness now…I have heard APS rules out CFS it is not the same illness at all & also if someone has Radiation Sickness in urine
samples they no longer meet the CFS criteria they also were misdiagnosed
He Ken has Autism Spectrum disorder so I question his ME/CFS diagnosis
I don’t know the person your soaking but if this person (Ken) is on the Autism spectrum there’s a very good chance he has both. My trigger for ME/CFS was the Polio/DTP vaccine. It caused encephalitis then crashed my adrenals and have lived with chronic exhaustion ever since. Autism is linked to vaccine injuries though they won’t do studies on this either. You can search “encephalitis post vaccination” and there are NIH reports on this. I believe this is why it’s so hard to reverse. Vaccines are made to permanently stay in your body and so are a lot of the bio-weapon viruses. Lymes and HINI are under investigation at the Pentagon as released bio-weapons (easy to research as well) and I would bet my life on it that Covid was created for this purpose as well and is causing the same debilitating symptoms and the spike proteins in Covid are in these vaccines so your injecting the same poison if you take these shots. The Polio/DTP vaccine was my trigger and my life was stolen from me after trusting it was safe. Be careful and mindful and research beyond the usual before putting anything virus related in your body via a shot. Biggest mistake of my life was trusting without truly researching.
I was prescribed Eliquis after developing a large blood clot from my pic line that I was using to infuse lactate ringers for POTS and ME. Due to mast cell reaction and anaphylaxis from heparin and aspirin.
My Neuro suspected Hughes syndrome as I have hemiplegic and basilar migraines and 3 pre term births. Labs came back negative.
Since the addition of Eluquis to my suppliments I no longer have daily migraines that can leave me paralyzed for days.
Between the Eliquis and anti viral I go from bed ridden to able to work on my feet at least one day a week with just one day of rest to recover.
I still believe I have ME with the Hughes as I still have PENE but it is certainly managing better, and the lack of paralyzing migraines is amazing. But they can’t officially dx the Hughes as my labs are not showing it.
Doesn’t matter as my Dr are allowing me to stay on it past my 6 month prevention as it is obviously my body needs it to function and I have anaphalaxis reactions to all the other migraine meds they have used. We were at the sorry.
Thank you Cory for another great article!!!
Interesting. As you know, Cort, I have been years making a recovery from FM following my own protocol as the result of reading and self-experimentation. I continue to get better.
But once I started to get better and more active, I had a DVT in a calf muscle after injuring it, 3 years ago. I think part of my FM always has involved vulnerability to torn muscles, I had a lot of these and ended up avoiding activity that led to them. But as I have got better, I have been pushing the boundaries more, and got a torn muscle about once a year, up till about 14 months ago, and haven’t had one since.
The hypothesis that the symptoms of FM are caused by hypercoagulation in the micro vessels is interesting, it fits with my own belief about what is going on when I try to exercise. But adhesions in the fascia contribute to the problem, even if they come later than the hypercoagulation, which may be the initial trigger for problems. The adhesions may be the result of disabled mobilization of toxins out of the area due to the micro vessel blockages.
Anyway, while I have continued to improve, 6 months ago I got another DVT, in the lower leg on the other side, with no explanation this time. So I have been told to take anti-coagulants permanently.
My gut feeling about why this proneness to DVT’s has been manifesting only since I have got better and become more active, is that exercise of the prolonged nature that I am getting involved in now, may be dehydrating me enough that the blood is getting thicker anyway. Both times I got a DVT, was following 3 hours + of group bicycle ride (the first time I had had a DVT “after a muscle injury” but the injury had healed enough for me to do the riding again, so maybe the injury was not a cause of the DVT after all).
I will be prone to dehydration and energy metabolism “issues” because I exist on a very low-carb diet, and this has implications for hydration. I overcame the tendency to cramping that was a horrible obstacle in my protocol at the outset, by using Magnesium “oil” rubbed in through the skin, on the calf muscles etc, and also by eating Konjac pasta and bread made with flax seeds, which gave me very-low-GI soluble fibre. And of course drinking a lot of water, and oral electrolytes.
Reading this now about a blood coagulation angle to FM, is of course very interesting to me. I don’t know what to do further with this information, but I am also very interested in Berg’s hypothesis that there are micro-infections as a result of the coagulation in the micro vessels. Gary Moller, naturopath and sportsmedicine specialist, suggested something like this to me years ago, and insisted I try a combination of Nattokinase and Artemisia Annua (a natural antibiotic). He may have been onto something, but it didn’t “fix my FM” at the time and I couldn’t afford to keep it up.
Ha! Isn’t that something how you appear to fit this profile. I’m glad to learn from yours and other comments about nattokinase.
The fascia liquid contain proteins that resemble a lot commercial two component glue/sealers. As it makes little sense to me the fascia liquid also contains the second component for the reaction, I hypothesize that it is produced in the muscle/blood vessel cells.
When the cell wall is deteriorating by for example physical stress or auto-antibodies, the two components would seal the wound and close injury. As with that yellowish liquid that seals superficial skin scars that do not cause bleeding, removing/peeling it by mechanical force only causes a new one to be bigger, thicker and less elastic.
A sudden drop in pressure could cause increased leaking of leaky membranes as well. Did you happen to be pressure-change sensitive back then?
As to DVT: do you happen to spend considerably less effort on mobilizing/improving the feet? Shoes are very good at immobilizing the feed. That has not only a strong impact on “deconditioning” the feet muscle but also many muscle and tendons of the lower legs. The same immobilizing may have caused less physical injury, making the feet look like they are OK when they may be not. They are very prone to gravity. I doubt the constant temperature environment they live in helps blood flow as well.
Thrombosis does not always originate from where it manifests. Bicycling may put a very repetitive strain on some insufficiently recovered muscles/tendons.
As to Nattokinase, that happens to be another enzyme breaking down proteins…
Thank you, Cort, for taking the time to write this article and for being such a strong advocate. I read the part about testing and I was wondering if anyone could be so kind to share what exactly they have been tested for so that when I present it to my physician, I will have all of my bases covered. Thanks in advance.
Hopefully this is one group of tests that physicians are familiar with and will get done. I haven’t had them done but I was really intrigued by the mention of the low SED rate – a typical finding for me – which I’ve never had a possible explanation for.
FYI ketogenic diet helps improve cardiolipin which is important to the membrane of mitochondria. there are theories that it can be degraded by certain types of polyunsaturated fats in the diet. The blog hyperlipid has some discussion of this. The supplement NT factor provides phospholipids directly and it is the only supplement along with immunocal platinum and aspirin I have found to help. Interesting stuff.
Another fascinating article Cort, thank you. I’m always nearly as interested in the comments as the content, and blown away by everyone’s knowledge! How do so many of you have access to specialist testing and medics? In UK it seems that if we’re lucky enough to be referred to a specialist and diagnosed with M.E., P.O.T.S., Fibromyalgia, Allergies with Anaphylaxis, I.B.S. etc, that’s it – as far as investigations go. From time to time in subsequent years, if we’re desperate enough to seek out an appointment with the GP, they might do routine blood tests, but when these come back ‘normal’, we’re all out of options and it’s back to the struggle: ‘keep up the Midodrine, Gabapentin, Epipens, salt, fluids’.
If Hughes could be an issue for many people with P.O.T.S., I’m wondering where Midodrine fits in? Would it not be contra-indicated for those people, as it helps constrict the blood vessels? Is testing for these elusive antibodies accessible in UK, or is it limited to patients involved in special research studies?
I do better vasodilating. Constricting with too thick blood is a recipe for diaster. I have to be careful how much though or I get too much pooling. I dont take soy products and natto is out. But the enzymes in Vascuzyme work well for me. I can’t use aspirin either as I have MCAS and it causes a mast cell degranulation with me.
Issie
Cort:
As one of the few ‘athletes’ with CFS on this website, I am interested in CFS/EBV, energy production, and oxygen transportation.
Are the deformities of the red blood cells the same as found with active Mono (=EBV in the bloodstream), where many of the red cells disappear (autophagy?) and white cell numbers skyrocket?
Or is it different here?
If the red cells were suddenly ‘deformed’, then of course the body would clear them out.
I have read that EBV, and many other pathogens, find oxygen toxic, so if they can somehow decrease the oxygen levels around them, they will do it. So is crunching red blood cells just a standard EBV survival trick?
I used to be very athletic and compete in gymnastics until 21, and then Powerlifting at the State and National level until 52.
Now with a CFS Index level of 2 or 3 and in my late 50s, I rarely leave the house.
When feeling slightly better, I bicycle twice a week with group of older retirees around my area at 200′ elevation. I find bicycling easier than walking.
However, on even ‘easy’ (4% grade) hills, my muscles often feel starved of oxygen. My riding partners keep asking if I am OK, as I desparately gasp for more & more air. They are all breathing fairly normally on the same hill.
Per blood tests, my body has developed a super high oxygen carrying capacity, as though I was always training at 7,000 ft. altitude. Lance Armstrong would be jealous of my natural EPO levels! My iron levels and EKG are fine. I should be flying up those hills.
However, all that blood oxygen is not going into my muscle cells.
My legs never get any burning feeling from lactate build up. However, everything else aches afterwards for days.
Still, after 3 years of cycling once or twice a week, I have not improved much.
Novice ‘Normals’ improve about 10%/wk for either speed, distance, and/or elevation gain.
Only change for me over the 3 years is that my HR (183 bpm?) comes back down faster afterwards, and I can recover after the ride in 2 or 3 days instead of 4 or 5.
The oxygen is ‘right there’ in my blood, but not going into the cells.
Why??
…Is it from deformed red cells, sticky cells, chronic dehydration (as in not enough different mineral salts), scarred liver, missing nutrients, exhausted adrenal glands, an epigenetic mutation, or what?
Since Exercise Intolerance is the thing that makes CFS differ (and worse?) from the other EBV based diseases, the answer would help a lot of people:
Why isn’t that one basic glycosis reaction happening?
There must be someone who has studied this and has an answer!
I was quite athletic but you were the real deal 🙂
One more option for oxygen not getting through – sludgy blood in the capillaries or fibrin deposition in the capillaries aka Berg.
Lots of interesting questions. The one good bit of news is that energy production is getting a good bit of research from our very small research community. (If only it was getting a lot more). Basically every energy production study finds SOMETHING wrong.
My guess is that energy production is where ME/CFS splits off from POTS, FM and other associated diseases. They all feature reduced energy production but it’s accentuated in ME/CFS. PEM is not even mentioned in these other diseases and is, of course, a core feature of ME/cFS.
Hi Susan,
As Cort said: poor bloodflow in the capillaries will be a big part.
I believe another big part is that ME patients have very high ROS/peroxide production. When anti-oxidants can’t keep up then RBC/hemoglobin play a back up role and scavenge ROS/peroxide. Hemoglobin then converts to methemoglobin https://en.wikipedia.org/wiki/Methemoglobin.
“20-30% metHb – Anxiety, headache, dyspnea on exertion
30-50% metHb – Fatigue, confusion, dizziness, tachypnea, palpitations
50-70% metHb – Coma, seizures, arrhythmias, acidosis”
When it’s too high one has https://en.wikipedia.org/wiki/Methemoglobinemia
“Hypoxia occurs due to the decreased oxygen-binding capacity of methemoglobin, as well as the increased oxygen-binding affinity of other subunits in the same hemoglobin molecule, which prevents them from releasing oxygen at normal tissue oxygen levels.”
“Signs and symptoms of methemoglobinemia (methemoglobin level above 10%) include shortness of breath, cyanosis, mental status changes (~50%), headache, fatigue, exercise intolerance, dizziness and loss of hairlines.”
“Patients with severe methemoglobinemia (methemoglobin level above 50%) may exhibit seizures, coma and death (>70%).[2] Healthy people may not have many symptoms with methemoglobin levels below 15%.”
“However, patients with co-morbidities such as anemia, cardiovascular disease, lung disease, sepsis, or presence of other abnormal hemoglobin species (e.g. carboxyhemoglobin, sulfhemoglobin or sickle hemoglobin) may experience moderate to severe symptoms at much lower levels (as low as 5–8%).”
When increasing exercising, oxidative stress increases much. If blood flow in capillaries is poor to very poor this will coexist with severe tissue hypoxia. Combined they can easily create a “methemoglobin storm”. It’s basically barely better than “mild CO poisoning”. For muscles https://en.wikipedia.org/wiki/Myoglobin can form similar metmyoglobin.
https://www.survivingmold.com/community/erik-johnson
“Dr. Peterson had told me, “Your erythrocyte sedimentation rate is zero. Most doctors are taught that the lower, the better. But a ZERO sed rate is TOO LOW, this is an abnormality.” Dr. Cheney has been saying for years that his CFS patients consistently have such a low erythrocyte sedimentation rate.
Looking back in my medical records from Dr. Cheney, much to my amazement, I saw that I HAD a zero sed rate. But this was before I got the weird flu. Indeed, it was even before the outbreak began.
I had one of the classic abnormalities of Myalgic Encephalomyelitis back when so far as I knew, I was just reactive to mold, and had NONE of the signs or symptoms of ME.
By chance, I appear to have been caught in a precursor state before the virus that went through Lake Tahoe made my illness apparent.
So imagine my shock when Dr. Ritchie Shoemaker told me that his biotoxin patients have a low sed rate.
If this is a consistent finding in mold illness, it appears that we need to consider that by failing to examine the circumstances where the CFS clusters arose, the entire CFS research community chased viruses down a dead end alley, and missed the chance to identify a common denominator hiding in plain sight.”
I had no idea this was so widespread. That’s an eye-opener for me. Thanks.
I have never had any issue with my Sed Rates, all came back in Normal ranges & in the last decade I have monitored these as well all being normal nothing wrong.I’m sure this is not in everyone & it may be some
have a totally different illness or infection all along & do not have CFS…I have seen countless told they have ME/CFS Fibro only to learn decades later they had something else…ME/CFS is a wastebasket label, always
has been this way, when they can’t find things wrong with you they throw CFS at you…Look at the recent NIH study one told he had Major Depression another told all along he had Parkinson’s not CFS…Why I hat
this Label Name…Maybe Sed Rate goes with certain Genetic diseases that have gone not properly diagnosed & missed in many…I hope some of my tests finds something in Genetics…Even the latest GSD Team
from Alabama found Parkinson’s, we need to seperate what people have…
For me CIRS has played a huge part in my health. Treating it and lyme has brought much more relief than anything else I’ve done.
Issie
Let’s hope Dr. David Systrom’s research on exercise intolerance will uncover some of the mysteries of ME/CFS. He has found during the iCPET (invasive cardio-pulmonary exercise testing) that ME/CFS patients present with “preload failure”, meaning there is an inability of the big veins (leg muscles) to squeeze down and push blood back up to the heart.
They have also found abnormality in systemic oxygen exchange/uptake of oxygen in the skeletal muscles. Along with these findings, they are also finding the SFPN (small fiber peripheral neuropathy in approximately 50% of ME/CFS patients.
So vascular dysregulation and /or intrinsic mito dysfunction where muscles are not taking up O2 normally? Could Autoimmune inflammatory processes be a contributing factor to thickened blood?
Let’s hope they unravel the “why’s….soon!
My right side only calf muscle swells up when I stretch it out it becomes hard like a rock & huge then the pain becomes bad & the only way I can stop it is standing
back up from a lying position & keep tapping my foot on the floor & it returns to a normal size…I have heard this can also happen in EDS from stretching…Prior to
becoming Sick I never ever had to do stretching like others commencing any form of exercises I even found it off people had to stretch each time they started any
Sports I still to this day do not believe the diagnosis of Fibro in me is right I still think it is EDS all along & is the proper diagnosis for ME/CFS Fibro labels…I was very
disappointed recently on the NHS here in the UK when I was seen by a top Genetic Doctor, I wanted the full EDS Panel but she said No but I will be doing one at a
Private lab to find my answers I know in HSD or EDS 3 there are ‘crossovers’ highly likely they have 2 types of EDS so I will persist without them on my own…
Coagulation and other sources of poor (capillary) blood flow may cause a strong increase in receptors of all kind in capillaries and nearby tissue.
With crippled blood flow, the flow of many messenger molecules per second to a certain location may be strongly reduced. In order to achieve a proportionate/sufficient reaction to these messenger molecules it would be natural to increase the amount of local receptors.
If so, this could create potential problems:
* With increased receptors one introduces a certain “amplification” of signals. In technical systems stronger “amplification” increases risk of instability and erratic behavior considerably.
* Blood flow through these capillaries varies, for example while exercising (increased local supply), digesting meals (diverting supply) or by day/night rhythms. With increased amount of receptors this would make the local reaction to messenger molecules/stimuli continuously oscillating between underreacting and overreacting. This is both wasteful (energy and bio molecules) and a potential explanation to being oversensitive to stimuli, pain, food, chemicals, visual and auditory stimuli, caffeine, adrenaline… and relates to calcium ion channels regulation and similar. It could also explain how our bodies “seem to have lost their ability to regulate processes well”.
* Maybe part of the body or immune systems sees this abnormal quantity of receptors as unusual/getting out of control and decides to “trim” some by attacking it / producing anti-autobodies to it.
* That potential immune reaction could create enough trouble to further impede local blood flow.
HI I stumbled across this and realize I need to find a way to get checked with APS and I feel a lot of cardiac symptoms and my home oximeter levels are low 90’s and I have watched my heart rate go up and down the oximeter . I already have had diagnosis of mold illness. I’m extremely tired and feel pain and heaviness in my lungs. so glad I came across this discussion. How do I continue to follow with you folks?
I have APS und RA have anyone Tipps what should i take (Supplements)??? I dont take an Medics
From what I understand, Vitamin B12 deficiency can play a role in red blood cell malformation: enlarging the red blood cells, effecting their ability to fold thus making it so they can’t fit through the capillaries, blocking blood flow, leading to nephropathy, even causing abnormal PAP smears because the cells are malformed.
Ironically, folic acid supplementation (which was government mandated to be added to our food) can shrink the red blood cells. This masks the pernicious anemia signs that doctors insist must show up in blood tests before they would consider ordering B12 tests for patients.
(See YouTube: “Diagnosing and Treating Vitamin B12 Deficiency”)
I wonder how much of the problems with the blood cells is undiagnosed B12 deficiency? Did the Dr.s involved in the research know that normal serum B12 results don’t rule out B12 deficiency? Did they test homocyctine or methylmalonic acid levels to see if the B12 was functioning in the body the way it should?
While B12 deficiency may not be the entire problem, how can anyone have normally functioning red blood cells if they are deficient in Vitamin B12?
I recently tried a different form of B12. It’s working so much better for me. I didn’t do well on the methyl form. Some of us with methylation issues may need to change sources.
Issie
On top of the horrendous CFS/ME and Fibro – my heart is now behaving erratically.
The doctors reckon it’s because my blood is much thicker than normal and needs thinning. They’ve prescribed “Lixania”. (Quite an expensive drug) Fortunately, because I reside in the UK, I get it free via the NHS. I’ve been taking the drug since May of this year. So far – it hasn’t helped to change the behaviour of my heart or reduced the CFS symptoms. However, because erratic heartbeats can cause strokes, I will need to continue taking the drug.
Interesting article as always Cort. It makes me wonder! I have had macrocytosis mildly for a long time and no notice is taken of it. But recently had a second blood clot in my leg and am being treated now with rivarobaxan. The first more serious episode was both a DVT and pulmonary emboli which were treated with Heparin and Coumadin for many months. Usual blood testing for clotting disorders showed no reason for this and I have never heard of A PS. SO maybe time to take a look!
You are definitely researching in the right direction.
In 1988 developed trigeminal neuralgia. By 1996 it was apparent I had an avascular necrosis of jawbone putting pressure on nerve. Lovenox didn’t improve pain, coumadin did. Study published by Gruppo, Glueck, Bouquot, McMahon in 1996 about 55 jaw pain patients with multiple clotting disorders causing jawbone ischemia. Journal of Lab and Clinicsl Medicine May 1996). I was one of the 55 patients in study.
I had elevated Lp(a), elevated acl antibodies, homocysteine gene, elevated Factor XI.
Since then it’s been downhill. Currently have nonischemic heart failure(never had occluded coronary), vasculitis, Common Variable Immune Deficiency due to defective B lymphocytes treated with IVIG, varying degrees of chronic kidney failure, nonhodgkins lymphoma 2000, use oxygen at night with Bipap, severe GI issues, severe fatigue, on 5 th pacemaker-biventicular defibrillator, mild pulmonary hypertension, mild hypothyroidism, sjogrens, mild diabetes, history respiratory failure with liver and kidney failure, mild glaucoma.
I was in a study for CFS around the year 2000. I tested positive for RNaseL dysregulation. Im not sure if that has anything to do with sticky blood. I also have enlarged red blood cells, and have anemia off and on. My Endo’s do not seem concerned about the enlarged red blood cells.
I have most of the autoimmune issues mentioned on this website. I am new to this website but in doing research for APS (my brother recently dx) I also came across molecular hydrogen. From what I understand it helps cell membrane, cell hydration and cell oxygen levels. Just washing my hair makes me SOB. I had APS/lupus labs drawn last Monday but don’t know the results yet. Was also looking at natto/nattokinase for natural blood clot buster. A few people mentioned that they cannot take soy but it has been my understanding that fermentation destroys the bad side effects of soy. I have also been thinking dehydration since I get so many cramps and spasms in my legs, feet and back but drink plenty of water. Hence the research to cell hydration and molecular hydrogen (all natural). My genetic snps also seem to point me in this direction.
Kathy fif you get your results on APS/Lupus back yet?
Sorry typo did you get results back?
What you take now? Natokinase?
Hi Kathy, did your tests come back on APS/Lupus for sticky blood in Hughes Syndrome? thanks
Where are these doctors that would know how to treat these conditions? Are there any near southern MD? In Maryland? Northern va? My daughter has been suffering greatly with POTS or that’s what they say, for over 4 years. Many symptoms, most seem like they can be vascular and serious but the experts we’re talking to just says it’s pots but no solutions . No treatment except compression socks and a few meds that didn’t help. I’ve been suffering from FM and chronic fatigue for over 30 years. Help for Halie would be appreciated ?
Nina, Dr. Nsah at Peninsula Cardiology in Salisbury, Maryland is knowledgeable on how to treat POTS. A little further south in Virginia Beach at Pembroke Medical through Bayview Medical Associates is Dr. Janine Frank. She’s an internist but extremely knowledgeable on how to treat POTS. A lot of her patients have POTS, myself included. Good luck.
Does anyone have any updates on this topic? I just started Nattokinase. I was diagnosed with Long haul covid and also had a positive APS result but have not been back. Having trouble finding a doctor that will take me seriously and knows what Long Covid is. I am also doing cod liver oil as well. I cannot do blood thinners as I react badly to everything.