Curious on y'alls thoughts on this. I spoke to a ayurveda person (ayurveda is where Ashwagandha and Bacopa come from) and he was like for thousands of years we put the herbs into food and ate it long-term and not made extracts out of it. Should we have skepticism over extracts with this logic maybe?

I am promoting modern science, not modern medicine. I agree that the pharmaceutical industry has largely failed everyone, and so have many doctors, to be honest. It's about profit over health most of the time. Even the doctors that are not in it for the money are part of a system that prioritizes seeing more patients in a short amount of time than they should be. That doesn't mean we write off modern science altogether, and group it with the pharma industry, though. Using modern scientific techniques to understand traditionally used botanicals is the only way to optimize and improve the benefits. Let's take your case and feverfew as the example.

First off, your TBI side effects sound like they are in part mediated by dysregulated nitric oxide, particularly iNOS. TBI up-regulates inducible nitric oxide synthase in cerebral arteries, paradoxically causing both excessive nitric oxide (NO) production and impaired NO-mediated vasodilation through uncoupling of endothelial NO synthase (eNOS). This creates a state where blood vessels respond abnormally to vasoactive stimuli. This is why orgasms set things off for you. This is also likely why you get worse symptoms if you don't use your sleep apnea machine. Obstructive sleep apnea causes repetitive cycles of apnea or hypopnea, resulting in oxygen desaturation and carbon dioxide accumulation. During apneic events, oxygen saturation can drop significantly, with some patients experiencing hundreds of desaturation events per night. Hypoxia triggers cerebral vasodilation as a compensatory mechanism to maintain oxygen delivery to brain tissue. Simultaneously, hypercapnia (elevated CO₂) potently dilates cerebral blood vessels. This combination causes increased intracranial pressure and activates pain-sensitive structures, including the meninges and their vascular supply. Your symptoms are vascular in nature. Intermittent hypoxia (IH) from OSA activates inflammatory cascades similar to those seen in TBI. IH upregulates hypoxia-inducible factor (HIF-1α), nuclear factor-κB (NF-κB), and pro-inflammatory cytokines. In animal models, OSA-induced IH increases hippocampal neuroinflammatory factors (IL-1β, IL-6, TNF-α), activates microglia and astrocytes, and promotes pyroptosis. This is a form of inflammatory cell death. Just some backstory to the mechanisms behind your issues.

You say that NOW Foods' feverfew is the only thing that helps. Well NOW's feverfew is NOT a non-extracted whole herb. It's a standardized extract. This is what I mean by saying modern science improves traditional practices. NOW's product is an extract standardized to 0.5% to 0.7% parthenolide. This is a sesquiterpene lactone, and the primary bioactive in feverfew. Parthenolide exerts potent anti-inflammatory effects by directly inhibiting the NF-κB signaling pathway, a master regulator of inflammation. Mechanistically, parthenolide binds to cysteine residues of IκB kinase (IKK), preventing phosphorylation and degradation of IκBα. Without IκBα degradation, NF-κB remains sequestered in the cytoplasm, unable to translocate to the nucleus and activate pro-inflammatory gene transcription. This mechanism directly addresses the chronic NF-κB activation seen in TBI-induced neuroinflammation. Parthenolide also potently inhibits iNOS expression and NO overproduction. This is a perfect example of modern science furthering our understanding of a traditional Ayurvedic practice. You are getting these effects precisely because NOW Foods created a standardized extract for you.

So let's take this a step further. What else could help you? For one, palmitoylethanolamide would be something I would suggest taking daily. PEA activates peroxisome proliferator-activated receptor-α (PPAR-α), producing great anti-neuroinflammatory effects. It has direct evidence in neuroinflammatory conditions and TBI-related pathology. I take our PEA every day, as does my mom and many people on our staff. Another one that would be good is our CoQH-CF. Ubiquinol, the reduced (antioxidant) form of CoQ10, addresses mitochondrial dysfunction and oxidative stress through dual mechanisms: electron transport chain support and direct free radical scavenging. Within mitochondria, CoQ10 shuttles electrons between Complex I/II and Complex III of the electron transport chain, directly participating in ATP synthesis. The ubiquinol form provides additional antioxidant capacity, protecting mitochondrial membranes from lipid peroxidation—a major consequence of TBI-induced oxidative stress. To go with that, I would say our OptiNAD+ would be great as well. This will help the mitochondrial function with the CoQ10. But in addition to that, a recent study showed that NMN itself had direct neuroprotective effects in a rat TBI model. Then of course magnesium is a must. I would personally suggest magnesium pidolate, as that has direct evidence direct TBI benefits in studies.

My suggestions:

OptiNAD+- https://nootropicsdepot.com/optinad/

CoQH-CF- https://nootropicsdepot.com/coqh-cf-ubiquinol-supplement/

PEA- https://nootropicsdepot.com/palmitoylethanolamide-capsules-400mg-micronized-pea-natural-inflammation-and-pain-support/

Magnesium pidolate- https://nootropicsdepot.com/magnesium-pidolate-capsules/

I would keep taking the NOW feverfew, as you know that is helping. Add these others in for improved effects. Let me outline the mechanisms of each so you can see it all.

OptiNAD+

* Restores NAD+ depleted by TBI-induced PARP-1 activation
* Direct TBI evidence (NMN reduces neuroinflammation via NF-κB suppression)
* Stimulates mitochondrial biogenesis for long-term recovery
* Immediate energy boost (NADH component) + sustained benefits

CoQH-CF (Ubiquinol)

* Completes the electron transport chain (OptiNAD+ provides NADH at Complex I, CoQ10 shuttles electrons to Complex III)​
* Direct antioxidant protection of mitochondrial membranes​
* Preserves nitric oxide bioavailability (relevant to vascular dysfunction)​

Palmitoylethanolamide (PEA)

* PPAR-α activation produces profound anti-neuroinflammatory effects
* Direct evidence in spinal cord injury (similar pathology to TBI)​
* Modulates microglia to neuroprotective M2 phenotype​
* Analgesic properties for pain management (CB2 receptor)
* Blood-brain barrier protection​

Magnesium Pidolate

* Primary form used in headache research​
* Pyroglutamic acid (pidolate) enhances brain delivery​
* NMDA receptor modulation (reduces glutamate excitotoxicity)​
* Pain management specifically for head-originating pain​

Here is how I would dose it:

Morning:

* OptiNAD+: 2 capsules
* CoQH-CF: 1 softgel (100 mg ubiquinol)
* Magnesium Pidolate: 3 capsules (1,650mg, 120mg elemental magnesium)
* PEA: 1 capsule (400 mg)
* Feverfew: Continue existing dose

Evening (12 hours after morning dose:

* Magnesium Pidolate: 3 capsules (1,650mg, 120mg elemental magnesium)
* PEA: 1 capsule (400 mg)

If you try this regimen, please let me know how it works for you!