One of the critical symptomological problems is exercise, which boils down to both mitochondrial dysfunction and lactic acid. Let's dive a little deeper into lactic acid. Considering all of these, you can build a protocol on top of dry fasting that allows you to exercise again and further ramp up autophagy, muscle endurance, and mitochondrial levels. Some of these strategies can be used for many more autoimmune diseases that include CFS, ME, and POTS.
I will address the theories and supplements needed to address these issues, from a list of long covid helping supplements.
You wouldn't catch this if you did not have a handful of data corroborating this event. Many people I've worked with, including myself, have experienced a sort of mast cell activation that resembles an allergic reaction for a few days after ivermectin use. The first day resembles improved symptoms, followed by a continual improvement of most symptoms, but also includes worsening of allergies / MCAS-style symptoms. Does that necessarily mean everyone is dealing with parasitic infections being killed by ivermectin? Highly unlikely, but without specific research studies, we won't know. However, the fact that an increased number of mast cells was documented in an ivermectin study, helps us realize that there is a recurring pattern appearing there.

Inflammation and GABA
GABA is the main inhibitory neurotransmitter in humans. It reduces neuron excitation in most areas of the central nervous system and blocks impulses between nerve cells in the brain. Low levels of GABA can be associated with anxiety disorders, attention deficit hyperactive disorder (ADHD), and epilepsy.

This research proposes that gamma-aminobutyric acid (GABA), a primary inhibitory neurotransmitter in the central nervous system, may help reduce inflammation in conditions like rheumatoid arthritis (RA).
The model suggests that GABA can reduce the activity of p38 MAPK, a protein that plays a crucial role in inflammatory responses. By doing this, GABA might decrease the production of proinflammatory cytokines—molecules that amplify inflammation—in the joints affected by RA. This is based on evidence that GABA can prevent the release of a proinflammatory cytokine, IL-6, by inhibiting p38 MAPK in certain cells.
There is a strong link to GABA helping out a lot with long covid neurological symptoms. Some of the theories I most strongly subscribe to is the one that covid affects the acetylcholine and glutamate receptors, therefore, causing neuronal death due to 'overexcitation'.
It's very hard to get GABA to the brain though.
Dietary GABA, which is unable to cross the BBB, might act on the brain via vagal afferent neural pathways.
Studies did show however that small amounts of GABA do reach the brain, even from dietary sources, just not a lot. So it's important to learn about the connection and supplements that you can use on top of a proper healing protocol.
How Do We Produce GABA?
GABA is synthesized in the brain from the amino acid glutamate using the enzyme glutamate decarboxylase (GAD), with pyridoxine phosphate (Vitamin B6) as a cofactor. Glutamate is synthesized from the essential amino acid L-glutamine using the enzyme glutaminase.
Image here Treating anxiety sounds pretty simple then. Increase your intake of L-glutamine and you will have more resources to produce GABA, and increase your intake of pyridoxine and you will be able to convert more of the L-glutamine into GABA. Unfortunately, it's not that simple. The reason it's not that simple is that GABA can actually be converted back into glutamate in a process called the GABA shunt, and glutamate is also a neurotransmitter, but which has exactly the opposite effects of GABA.
The Glutamate Paradox
Glutamate is the main excitatory neurotransmitter in our nervous system. It is an important neurotransmitter for memory and learning because of the role it plays in neuroplasticity, but in excessive quantities it can lead to excitation problems such as anxiety disorders. The GABA shunt pathway usually keeps glutamate in check, but there are number of things that can aggravate this pathway. Lack of vitamin B6 is the most significant factor for insufficient conversion to GABA, but auto-immune dysfunctions can also inhibit the GAD enzyme, which catalyses this conversion. Food intolerances such as gluten intolerance, along with hormone replacement therapy, are notably responsible for this inhibition of GABA conversion.
GABA Transaminase Inhibition
GABA begins its conversion back to glutamate through the action of the enzyme GABA transaminase. If this enzyme is inhibited, however, then GABA levels will remain at higher levels. Lemon Balm (or Melissa officianalis) and Rosemary (or Rosmarinus officianalis) contain the compound rosmarinic acid, which has been shown (link to study) to be a GABA transaminase inhibitor. This compound can reduce the rate at which GABA is shunted back to glutamate.
GABA Receptor Agonism
A method of increasing GABAergic effects, especially in the short-term, is by using GABA analogues that agonise GABA receptors. A receptor agonist is a chemical that binds to a given receptor, activating it to produce a biological response. The nootropic drugs phenibut and picamilon are the best known agonists of both GABA-A and GABA-B receptors, but there are also number of natural products that have proven effectiveness as GABA agonists. Passion Flower contains the flavonoid chrysin, which has been shown (link to study) to be a GABA-A receptor agonist. The amino acid taurine has also been shown (link to study) to be a weak agonist at GABA-A receptors.
GABA Reuptake Inhibitor
Reuptake inhibitors inhibit the reabsorption of a neurotransmitter from the synapse back into the neuron after it has performed it's activity. St John's wort (or Hypericum perforatum) contains two compounds—hyperforin and adhyperforin—that have been shown (link to study) to induce noncompetitive reuptake of various monoamine neurotransmitters including dopamine, serotonin and GABA.
Ivermectin and GABA
It means that ivermectin binds to similar receptors that stimulate GABA release thereby increasing GABA in the body. What is a receptor agonist? A drug or substance that binds to a receptor inside a cell or on its surface and causes the same action as the substance that normally binds to the receptor.
This solves a lot of mysteries and anecdotal evidence claiming that Ivermectin has healed things like brain fog and some long covid neurological problems. (On top of other mechanisms like FXR ligand blood glucose control, immunomodulating, ace2 receptor binding, and parasitic cleansing).
If you have long covid and have not tried ivermectin to treat some of the symptoms and return a bit of normal to your life, you are missing out. However, it's also critical in knowing when to use it, how to pulse it, and when to avoid it. Synergizing the right time to take it along with dry fasting is also key and my strategies are based on personal experimentation.
Schedule a meeting with me if you need a supplier that I have used in the past, for cheap 12mg tablets.
Melatonin and Inflammation
Berberine and Inflammation
Berberine might cause sleepiness and slowed breathing. Some medications, called sedatives, can also cause sleepiness and slowed breathing. Taking berberine with sedative medications might cause breathing problems and/or too much sleepiness.
Magnesium and inflammation
Researchers have found that when magnesium levels are too low, there is a profound increase of inflammatory cytokines, along with increased levels of histamine. Inflammation uses up or depletes magnesium levels.

