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The reduced cerebral blood flow could have different causes. If someone has excessive vasodilation of blood vessels, blood can pool in the lower part of body and the blood flow to the brain is affected. However excessive cerebral vasoconstriction can reduce cerebral blood flow as well. These...

It mostly came from my experiences of bad reactions to medications and the glucose issues. The researcher Karl Tronstad did a metabolic study showing 3 subtypes, and I have always been curious why some ME patients have POTS and some don't so I tried to come up with the most plausible explanation...

They found norepinephrine correlated with time to failure, and cerebrospinal fluid DHPG, DOPAC and DOPA were all lower. There is a slide on the video that talks about the difference between healthy controls and ME at 9.43. I actually think normetanephrine levels would be a good indicator of...

It would usually go to between 3mmol/l and 4mmol/l , never lower than 2.8mmol/l. There is a picture of my CGM chart at 18.48 in the video.

No I couldn't find published data on it, so I couldn't include it in the written paper but I included it in the video as I thought people would find it interesting. In the Cort Johnson article he said they looked at a huge sample of 750. He might have got that wrong, I'm not sure.

After 10 weeks of taking the medication that increased insulin resistance, I got a sudden improvement in symptoms, all the symptoms related to beta 2 adrenergic receptor downregulation all improved at the same time. At the same time, the medication I had been taking which increases beta 2...

I think your hypothesis is good and I couldn't come up with anything better! I honestly don't know why taking it wouldn't work again, so can't give an opinion on that. I do talk in the video about acetylcholine effect on tyrosine hydroxylase and norepinephrine at about 37 minutes in the video...

I think that in theory I am in the ME1 subtype. I wore a continuous glucose monitor and got frequent hypoglycemias. I took a medication that increases insulin receptor resistance and my hypoglycemias stopped and my symptoms improved 80%. After three months I stopped taking the medication whilst...

I think I answered your first question in my recent reply to Hutan. In the model I refer to a hypovolemic type of POTs. I don't know what is the cause of hyperadrenergic POTS, although some POTS research has found genetic variants in the norepinephrine transporter itself. It's possible that the...

Well it could be either really, depending on your subtype and type of dysregulation. I am pretty sure with me it is cortisol, because when I took a course of glucocorticoids, all my symptoms improved a lot. Glucocorticoids can't be used as a treatment though because they could cause further...

I would need to put some more thought into this, but the more obvious tests would be to test insulin response very regularly after an Oral Glucose Tolerance Test, 5 mins, 10 mins, 15 mins 20 mins etc all the way through until 3-4 hours. Compare to healthy controls, and then if there are...

Response to a deleted post. I can't give medical advice here but you could watch the video to find out more about the hypothetical ME3 subtype. Although it is just a hypothesis which has not been proven by scientific research and which could be wrong.

I am not sure if response to sugar and carbs is going to be the best way to differentiate subtypes. For example I have the ME1 subtype, had bad reactions to large meals of high glycemic index carbs, but when in a hypoglycemic episode, a small sugary snack helped me feel better. Also even the low...

That is really interesting, but I am not sure why that happened!

I think ME1 and ME2 would feel worse from Methylphenidate because it increases extracellular norepinephrine, but ME1 may benefit from Guanfacine as it can reduce extracellular norepinephrine. However it would be better if ME1 can target insulin signaling itself as that is the root cause.

That's interesting! I follow Efthymios on twitter/X and he posts really interesting findings from his AI work. He posts a lot about liver dysfunction and this could be due to liver insulin resistance but also, downregulated beta 2 adrenergic receptors may have a negative effect on the liver as well.

I don't think you would move between subtypes, but you could move in stages through the illness. For example ME1 moving from overactive SNS to downregulated beta 2 adrenergic receptors. Then the insulin resistance in ME2 may get worse over time and contribute to new symptoms. Testosterone...

I also much feel better soon after VERY stressful situations. I think this is the high cortisol overriding the glucocorticoid receptor resistance, which I suggest in the hypothesis.

In the hypothesis, POTS is more a consequence of compensatory tachycardia due to excessive vasodilation. Yes I'm looking forward to the DecodeME results, hopefully it will give us lots of clues.

The Sympathetic Nervous System is made up of noradrenergic neurons which release norepinephrine. This hypothesis suggests ME comprises three subtypes- one involving norepinephrine deficiency & two involving reduced expression of the norepinephrine transporter. In Subtype 3 (ME3) There is a...