Thread by @Bradgolf1216

GPCR Autoantibodies circulating the blood triggering neuroinflammation of the autonomic nervous system and small fiber nerves that control the body’s functions for daily living. Breaching Blood Brain Barrier and Gut Barriers to induce more neuroinflammation and dysfunction.

These same autoantibodies triggering microclots to form in some people. The autonomic dysfunction altered the baroreceptor reflex and now the body compensates by either altering blood pressure or heart rate in order to get blood back to the heart.

The dysfunction leads to narrowing of the small vessels and altered red blood cell shape which causes hypoxic conditions in tissues and without proper oxygen perfusion the body cannot maintain proper aerobic metabolism to make a majority of the body’s energy (ATP).

The neuroinflammation on the cranial nerve of the ear from autoantibodies I predict can cause the tinnitus. Random anti inflammatory medications do almost nothing for this mechanism.

Blood vessels must now work harder to get blood back up to the heart and brain. This will lead to chronic venous insufficiency and bulging veins. This is due to the increased pressure in the veins.

The breached BBB now allows autoantibodies nearby to trigger inflammation in the brain. Notice the findings of the hypothalamus dysfunction and brainstem dysfunction/volume changes. These all function in part by GPCR receptors so the circulatory autoantibodies attack the ANS.

This neuroinflammation in the brain will alter blood flows on a continuous basis. You can hook a dysautonomia patient up to an ICU line and watch the blood continuously change up/down instead of being consistently supplied with blood like a healthy person.

Without healthy blood flows in the brain, this creates hypoxic conditions and brain fog/cognitive dysfunction sets in. Without the proper blood flow, hypometabolism sets in the brain which can be identified via a particular PET Scan used in certain laboratories.

Autonomic dysfunction also causes the brain’s neurotransmitters to be dysfunctional such as cortisol, dopamine, serotonin, etc. Sometimes they are high, low, in range but they are not always functioning correctly in dysautonomia patients.

Small fiber nerve damage/dysfunction alter the way our body responds to temperature and pressure changes. We can’t regulate our body temperature well in extreme weather environments and beware of barometric pressure changes as symptoms can flare.

The Autonomic Nervous System has a part called the Enteric Nervous System which controls the vast majority of GI functions from mouth to anus. It works closes with the GI reflexes including the gastrocolic reflex which is stimulated after eating.

This reflex is overactive after a large or high fat/spicy meal in most dysautonomia patients. Also the Migratory Motor Complex (MMC) in the GI system is dysfunctional. This complex is in charge of our GI motor patterns. This can be affected by autonomic dysfunction.

Since Fibromyalgia can accompany ME/CFS/POTS, I feel the study injecting the blood of a fibromyalgia patient into mice gives us important clues on how autonomic dysfunction may be working. pubmed.ncbi.nlm.nih.gov/34196305/

There is something in the blood of all of us (most likely autoantibodies gpcr and non-gpcr) that is triggering all of these symptoms. I believe BC 007 will improve/go into remission the symptoms caused by the autonomic dysfunction.

I believe there are other non-gpcr autoantibodies at play in some patients such as the ones causing small fiber neuropathy that need to be addressed. Maybe an aptamer can be developed that will inhibit those specifically.

BC 007 will most likely have to be given more than once such as after an infection or after a traumatic event because sometimes these autoantibodies will return after these events. Genetic predisposition to immunity dysregulation is from changes to the genes.

So since we can’t change the genes back, we must attack the mechanisms and drivers of the disease. GPCR autoantibodies are known drivers of many diseases including some peoples prediction of it driving dysautonomia in lc patients.

I would like for the BC 007 trial to test patients with 1) Trans cranial doppler test for cerebral blood flow 2) 10 min Poor man’s tilt table test (from laying down to standing) 3) 12-T MRI to check BBB, PET scan to check for Hypometabolism, CPET test.

They should bring in people that understand autonomics to help with the study if they haven’t already. BC 007 will be huge for the LC/Pots/ME/CFS communities and even potentially helping fibromyalgia and other chronic illnesses related to autoantibodies.

I am hoping we all can eventually get clinical access to functional assays to test for these GPCR Autoantibodies. Good Day Mate 👍🏻

#LongCovid #pwME #POTS