Post COVID Migraine in a Six Day Cycle

When I was getting lot of cramps, I bought a magnesium product that was supposed to be absorbed through the skin. I then spent some time looking at the evidence for transdermal Mg absorption. Turned out, there was not much evidence to support the idea of delivering magnesium via the skin. The evidence is contested, but from what I've seen, the studies suggesting that there is significant magnesium uptake tend to come from organisations with an interest in promoting a transdermal magnesium product.

Myth or Reality—Transdermal Magnesium? 2017


Maybe a warm foot bath helps with blood circulation, or even just extra rest and muscle relaxation, and those things might impact on a migraine?
I also had a look at studies on transdermal absorption when I was initially looking into this and IIRC there were quite a lot of contradictory ones but in the end I landed on it sounding as though there was reasonable absorption particularly if the concentration of Mg in the water is high, and if the water is warm. I didn't look into conflicts of interest, though, so maybe your assessment of the literature was better than mine! :)

However, any impact on blood circulation is going to be very temporary, and I don't find the baths restful - quite the opposite, because I have to remain sitting, and I'm no more relaxed than when I don't have my feet in a bath - I just carry on doing whatever I'd be doing otherwise (eating, reading, watching the TV, writing on the computer). And I find the effects to be cumulative over periods of weeks. So going by my experience, I think there's something in it, but N=1, possible misattribution, etc. etc.
 
Something strange has just happened which is semi miraculous so I thought I ought to make a note about it here.

In relation to the diabetes 2 like symptoms, which I believe are cause by RAS imbalance cause by covid, my legs have been swelling periodically with oedema which is typical of diabetes 2 and is cause by insufficient blood flow due to issues with poor vasodilation, which is exactly what happens when RAS is out of whack because AngiotensinII is not being converted by ACE2 receptors into vasodilating messengers because covid has nobbled all the ACE2 receptors.

I have been troubled by leg oedema for 6 days. So took a look in my diary to study my records of previous occurrences. After trying to look for causes and finding nothing I had an inspiration to look at the end of oedema episodes and see if there were any prospective cures I had not recognised.

Beetroot juice presented itself, which is something I have tried because of its high nitrate content which can in theory facilitate nitric oxide production which can assist vasodilation. I had not recognised it as having had an effect previously though my diary showed that a dose of it was coincident with the end of previous oedema episodes. So I tried it again today and within an hour my leg oedema of six days had gone down and I am quite pleased about this as it was concerning. I was very surprised it worked so well and do not think it is a coincidence.

Just thought I would pass it on in case it can help someone else.
 
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Beetroot juice presented itself, which is something I have tried because of its high nitrate content which can in theory facilitate nitric oxide production which can assist vasodilation. I had not recognised it as having had an effect previously though my diary showed that a dose of it was coincident with the end of previous oedema episodes. So I tried it again today and within an hour my leg oedema of six days had gone down and I am quite pleased about this as it was concerning. I was very surprised it worked so well and do not think it is a coincidence.

Just thought I would pass it on in case it can help someone else.
Interesting, because beetroot gives me killer migraines!
 
Despite working hard to reduce blood glucose and insulin overproduction causing acanthosis nigricans, I am still getting peripheral neuropathy in the medial plantar and lateral plantar nerves (terminal branches of the tibial nerve), creating sensations in my toes.

As previously stated, I believe this is due to covid becoming recurrent, (like many viruses before it, due to my immune dysfunction), resulting in the depletion of ACE2 receptors, leading to excess unprocessed angiotension II, resulting in renin angiotensin system imbalance at default levels of functionality. i.e. insulin resistance, vasoconstriction, proteinurea etc.

I found this blog interesting. It is one of a series of blogs by Lisa Sanders MD at Yale.
Why would COVID-19 cause peripheral neuropathy?
Lindsay McAlpine, MD, a neurologist and founder of the Yale NeuroCOVID Clinic, has conducted research on what is now known clinically as peripheral neuropathy after COVID-19. She notes that there are two main categories of neuropathy following COVID-19 infection. One is the “acute illness mediated type,” in which patients find themselves with sudden, severe neuropathy, generally around the same time as their active illness. The second is small fiber neuropathy, which results from damage to the thinnest, unmyelinated nerves in our body and often begins with burning pain in the feet. It typically arises somewhat later—around two to 12 weeks post-illness.

Peripheral neuropathy in COVID-19 patients has been reported in both axonal and demyelinating forms, according to the medical literature. Researchers suspect that COVID-19 associated neuropathy could be driven by several causes. One might be immune system dysfunction, in which the body attacks itself instead of, or in addition to, attacking viral particles. Or COVID-19 may have hemodynamic effects that interfere with how blood flows through the body’s blood vessels, damaging the nerves and leading to “ischemia” due to restricted blood/nutrient flow, known as critical illness neuropathy.
 
Progress report - Just so people understand, my body mass index score is right at the bottom of the BMI green zone, the lowest it could be without going into the undesirably low values. In fact when I took dandelion tea as a diuretic (to reduce nocturia) my morning weight was below the green zone due to the dehydration. So I feel a bit close to the edge, as it were and have stopped doing that but I am not fat. I look a bit thin and bony to be honest but I am still alive and able to move around. Not as strong as I was though.

I am continuing a ketogenic diet with the emphasis on a good lipid diet, to reduce glucose and even protein stimulated insulin production and hopefully reduce acanthosis nigricans caused by a build up of insulin, as the insulin is probably not being used due to apparent insulin resistance, the most likely cause of which is suppression of GLUT4 translocation to the cell surface etc by a surfeit of Angiotensin II due to the depletion / impairment of ACE2 activity by covid. To recap, in my case it is recurring covid, the cycle seems to have been about four days at its worst, so frequent it is almost continuous. I am hopeful my immune system is taking it more seriously now and I am trying to support it nutritionally but my tests showed a low white blood cell count and low folate, which are symptoms my mother has and she has a diagnosis of non Hodgkins lymphoma, which is not aggressive but still means she is immunocompromised and has to be careful, like me.

So I am doing the best I can under the circumstances. I am not sure if the peripheral neuropathy is improving and I am trying to ensure it does not get any worse as it is very slow to heal. I am using a very expensive 850nm infrared deep heat therapy boot daily to try to help. (EDIT update, this is causing contact dermatitis because the inner face is made out of leather, would you believe it and when my calves are heated and sweating and they touch this they are contaminated with something leaching from the leather and they have developed a rash. May be able to use it with a transparent polythene bag or something like that but not a very user friendly design IMHO.)

Numbness in my calves indicates when I am getting it wrong but it can be improved in the short term if I reduce protein and most importantly cut carbohydrate intake to the minimum possible. My toes seem to be permanently affected but do fluctuate significantly and seem worse soon after eating. Unfortunately they do not improve as obviously in relation to carb restriction. There seems to be a longer term problem there, possibly nerve damage hence the infrared therapy but it is not very severe when it fluctuates towards a better state suggesting the damage is not that bad and the nerves are themselves being obstructed in their function by other factors but not dead.

I am ascribing two causes to my tingling toes. One is the aforementioned vasoconstriction which I hypothesise is exacerbated by carb even though my HbA1c - IFCC standardised: 31 mmol/mol is considered optimal, equivalent to about 5.08%. I surmise that the affects of Angiotensin II build up and lack of its cleavage by ACE2 to produce Angiotensin(1-7) which is a vasodilation signal molecule means my RAS system is biased to vasoconstriction and so even a tiny influence in that direction by normal glucose levels in the blood can make it worse. So I think I am getting carb induced vasoconstriction despite normal glucose and no hyperglycemia evident. This is probably exacerbated by the second problem which is the AngiotensinII induced insulin resistance which causes the build up of insulin >as though< I had hyperglycemia, when I don't and I suspect this prevents adequate nutrition entering the cells comprising the fine nerve endings, disabling them significantly.

So it is like a covid induced faux-diabetes 2.

I tried berberine to activate AMPK transporter but it gave me mouth ulcers as it is an alkaloid, the same reason I cannot eat any nightshade vegetables due to their alkaloid content so I had to stop. AMPK activation inhibits anabolic processes, which is interesting as this has been a feature of my ME since recurring virus and ME began in 1986 as exercise produces no muscle growth, just damage, since then.

This paper not only elucidates the way AngiotensinII blocks GLUT4 translocation but also suggests beetroot (nitrate) may be a double edged sword after all, which I will have to consider.

We found Ang II to block insulin-dependent GLUT4 translocation in L6 myotubes in an NO- and O2 .−-dependent fashion suggesting the involvement of peroxynitrite. This hypothesis was confirmed by the ability of Ang II to induce tyrosine nitration of the MAP kinases ERK1/2 and of protein kinase B/Akt (Akt). Tyrosine nitration of ERK1/2 was required for their phosphorylation on Thr and Tyr and their subsequent activation, whereas it completely inhibited Akt phosphorylation on Ser473 and Thr308 as well as its activity. The inhibitory effect of nitration on Akt activity was confirmed by the ability of SIN-1 to completely block GSK3α phosphorylation in vitro. Inhibition of nitric oxide synthase and NAD(P)Hoxidase and scavenging of free radicals with myricetin restored insulin-stimulated Akt phosphorylation and GLUT4 translocation in the presence of Ang II. Similar restoration was obtained by inhibiting the ERK activating kinase MEK, indicating that these kinases regulate Akt activation.
 
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