August 08-26 Live Q&A Recording

Curtis Gillespie Sayers

3d • General discussion

Hey everyone,

Here is the recording from today's Q&A!

https://www.skool.com/the-healing-path/classroom/16bfed01?md=ce00248bda6746c9b12416185578c20a

(4:13 – 13:35)

Danielle's Husband John — Nystatin, Clostridia, and the Kidney Connection

• Avoid hammering an assumed infection — aggressive antimicrobials disrupt the microbiome, drive inflammation, and generate toxic byproducts the liver and kidneys can't keep up with, which matters especially given John's kidney picture

• Slow single-ingredient approaches (caprylic acid, or oil of oregano which is stronger) are the gentler route, but nystatin takes priority here because it destroys ergosterol, the yeast cell membrane — like poking a hole in a bucket, the organism physically cannot survive without it

• Fluconazole works differently, entering the yeast cell to inhibit ergosterol formation; medications act far faster than botanicals, which matters when the goal is reducing an immune response quickly in rheumatoid arthritis

• Clostridia is worth considering if nystatin doesn't produce the expected improvement — Candida and Clostridia go hand in hand, though Curtis leans yeast for John since Clostridia would likely produce more neurological presentation

• Foam in the urine is a kidney signal; Dan Shen, Rehmannia, and astragalus support the kidneys, but the infection still has to be cleared or it's an uphill battle

• Beta-glucuronidase (raised by yeast) recycles toxins back into the system — bile packages a toxin like a tied garbage bag in the small intestine, and beta-glucuronidase unties the bow further down; this is why some people show clean stool markers while nothing is actually leaving the body

• Yeast also causes translocation into the blood, which puts the load back on the kidneys

• Sourcing options for nystatin and fluconazole: Push Health (US, often covered by insurance and prescribing 90-day supplies), All Day Chemist, or a sympathetic local prescriber — aim for at least 90 days, not the standard two weeks

(14:51 – 25:32)

Chelsea — Gut Zoomer vs. Organic Acid Test (and Where the Dutch Fits)

• If forced to pick one, the organic acid test wins — it captures mitochondrial markers, glutathione demand, toxin insight, and infections well beyond what a stool test reaches

• The organic acid test measures byproducts rather than testing directly: Candida secretes hyaluronidase, which breaks down hyaluronic acid, producing arabinose — infections are sophisticated at hiding, so byproducts are more reliable than direct detection

• The Gut Zoomer rarely identifies yeast and is only somewhat better at Clostridia; it does give inflammatory markers that hint at infection (eosinophil activation protein suggests parasites or allergens, while S100A12, beta-defensins, and lysozyme suggest yeast)

• Gut Zoomer's real advantages: fat digestion, short-chain fatty acid status, and specific microbial strains — the latter matters because low Akkermansia, Bifidobacterium, or Lactobacillus paracasei allow Candida to become more invasive and drive relapse

• A key limitation: infections can live in blood and tissue rather than the gut (especially post-surgery), which is why 'all disease starts in the gut' doesn't hold up — running both tests gives the full picture

• No test is perfect; Curtis described reading a panel this week showing no yeast or mould where he could still identify it through other markers combined with blood work

• Dutch testing generally comes later — hormones are downstream, and whatever shows up on a Dutch is being driven by what the OAT and Gut Zoomer would reveal; the exception is anyone on hormone replacement or anabolics, where confirming safe estrogen detox pathways matters

• Parallel example: thyroid medication improves labs roughly 90% of the time without improving symptoms, because the problem is conversion rather than TSH

(25:33 – 36:30)

Tina — When GLPs Aren't Working: Genes, Carnitine, and Mitochondrial Fuel

• Run the genes first — non-response is common enough that spending ~$100 to check can save a year of GLP costs; if the gene is there, that person shouldn't be on a GLP at all

• Set clear conditions with clients: someone who can't reach adequate protein shouldn't be running a GLP, and putting that in writing protects both parties

• Carnitine is the go-to next step — it transports fat into the cell, which is where many people are actually stuck; injectable intramuscular is most effective, oral needs higher doses, and acetyl-L-carnitine crosses into the brain for cognitive benefit

• Complex I of the electron transport chain produces the most ATP but is the most vulnerable to toxins and infections; when damaged, the chain bypasses to Complex II and produces far less energy

• Methylene blue can act as an electron donor to bypass that damage — 3 mg is the sweet spot for electron transport support, while higher doses (10–50 mg) create oxidative stress deliberately for antiviral and anti-cancer purposes; caution with SSRIs due to MAO inhibition

• Hydrogen tablets amplify methylene blue (dissolve it into the hydrogen water) and support gut health and SIBO

• Tributyrin is underrated for weight loss and energy — short-chain fatty acids fuel mitochondria and feed the citric acid cycle, and deficiency is near-universal

• The TMAO and deuterium mechanism: gut dysbiosis raises TMAO, which raises deuterium (a heavier hydrogen isotope) that physically plugs ATP synthase and creates mitochondrial dysfunction — these are often the people who react badly to phospholipids like Body Bio PC or NTFactors

• Deuterium-depleted water works but is expensive (~$175 for 8 litres); restoring the gut is the accessible route to lowering it

• Bottom line: people with dysbiosis generally won't lose weight, and a GLP only masks it — which is why the weight returns when it's stopped; Akkermansia supplementation is worth considering since it upregulates GLP receptors

(37:12 – 45:30)

Tina's Client with Crohn's on Remicade — Biologics, Detox, and Uncouplers

• Twenty years on Remicade means significant toxin accumulation — the R-class biologics (Remicade, Rinvoq) affect the P450 enzymes that initiate phase I detoxification, so she's likely storing toxins rather than clearing them

• Glutathione is useful for neutralising, but the bottleneck is initiating phase I — TUDCA is the practical addition

• Biologics also increase infection load (yeast is essentially guaranteed), and the medication blocks the immune response that would otherwise signal it

• The result is impaired ability to use fat as a fuel source and heavy reliance on glucose — which is exactly why the GLP isn't producing results despite good diet and training

• AICAR is a gentler alternative to metformin for insulin resistance, though caution applies: AMPK senses ADP/ATP ratios, so pushing a cell that doesn't want to be pushed can make someone worse

• Metformin isn't inherently bad (it benefits the microbiome and bile) but depletes B12 and can affect testosterone

• BAM-15 explained: a mitochondrial uncoupler that pokes a hole in the proton gradient so the cell must work harder, generating heat and burning fuel — it helps weight loss, but with a damaged Complex I or leaking cytochrome C it can increase apoptosis and oxidative stress

• That same mechanism is why BAM-15 has anti-cancer affinity — cancer cells already sit at a threshold and the added demand pushes them over

• NAD after BAM-15 can amplify problems long-term in this population: the oxidative stress raises CD38 and inflammation, which NAD then feeds, plus senescent cell accumulation when apoptosis is stimulated without clearing the mitochondria

• Practical framing for weight-loss-only clients: TUDCA, glutathione, carnitine, and berberine can all be honestly framed through a fat-loss lens (mitochondria drive fat burning; berberine activates AMPK) to earn buy-in before the deeper conversation

(45:37 – 49:50)

Tina Personally — Nystatin, Fluconazole Duration, and Reading Blood in Stool

• Focus solely on getting nystatin for now — nothing else needs adding until that's in hand

• The single fluconazole pill prescribed for a vaginal yeast infection won't touch invasive gut Candida; that requires at least a month, and fluconazole is harder on the body, which is why Curtis doesn't start there

• Script for requesting it: describe persistent toenail fungus, scalp issues, oral thrush that won't clear despite tongue scraping, and recurrent monthly vaginal yeast infections, framed around the gut being a reservoir for invasive Candida

• Blood in stool interpretation — fresh bright red blood with a history of constipation and straining points to hemorrhoids and hepatic portal hypertension (blood flow can't make it up through the liver)

• Blood accompanied by diarrhoea, or darker blood, points to actual tissue damage in the colon or further up the intestinal tract

• Mucus is simply mucin production coating the intestines in response to damage — and Candida eating away at the gut lining is a direct driver

(50:53 – 58:30)

Why Yeast Is Such a Systemic Problem — The Full Mechanism

• Three ways Candida damages the gut lining: endocytosis (burrowing in, releasing intracellular components that stimulate immune responses and can drive autoimmunity), hyphae formation (roots that dig in and create the leaky gut through which toxins and infections pass), and enzyme release that eats away at the lining directly

• If you have leaky gut, you have leaky brain — they're made of the same materials

• The damaged environment lets lipopolysaccharides rise, which elevate zonulin and pull epithelial cells away from their tight junctions — a double whammy alongside the yeast damage (this is where lorazatide fits, as it inhibits zonulin)

• The autoimmunity mechanism: dendritic cells sit beneath the epithelial lining with sensors poking through; when yeast trips one, the antigen is presented to adaptive immunity, generating antibodies — as the lining degrades, one sensor becomes several, so ordinary foods and supplements start tripping them too

• Candida can secrete beta-amyloid (the antimicrobial peptide that accumulates as Alzheimer's plaque), produces oxalates that damage mitochondria and tissues, and drives the quinolinic acid pathway toward neuronal damage

• Arabinose binds lysine and arginine to form pentosidine, an advanced glycation end product — a direct route from Candida to the 'type 3 diabetes' framing of neurodegenerative disease, and to diabetes itself

• Why doctors miss it: testing is poor, yeast is a billion years old and highly evolved at hiding, and it's part of normal commensal flora — so it gets dismissed or treated for two weeks

• Realistic timeline is one to two years of treatment, which does not mean symptomatic that whole time — it means staying on top of something genuinely invasive

(58:40 – 1:07:15)

Chandler — Why Everything Improves Except the Colon / Methylation Recovery

• The colon is the exit route, so anything passing through irritates tissue that's already an open wound — Curtis uses the image of toxins as sandpaper on a wound, and healing itself mobilises toxins

• The neutrophil-macrophage mechanism: a neutrophil engulfs the yeast pathogen and becomes apoptotic, phosphatidylserine signals a macrophage to engulf it, and it should be dumped to the nearest lymphatic drain — but hyphae can form inside the macrophage and burst out in the colon, seeding that area

• Colonoscopy images and oral thrush endoscopies can look strikingly similar, which supports yeast as a plausible driver of localised colon presentation

• Macrophages can't be measured in blood, which is why monocytes are the proxy (monocytes convert to macrophages in tissue — microglia in the brain, Kupffer cells in the liver)

• The other reason symptoms improve elsewhere while one site persists: organisms defend themselves by burrowing into biofilm and going quiet, releasing fewer toxic byproducts and provoking less immune response — the same pattern as parasites around a full moon, and the reason two-week protocols produce relapse

• Curtis's stance on blood: it's information, not cause for panic, as long as the person is sleeping well, headache-free, and improving overall — it warrants review if unchanged after a month or two on a new protocol

• Methylation does improve as overall health improves — MTHFR produces 5-methyltetrahydrofolate feeding methionine synthase, and B12 fuels that enzyme, but toxins, infections, and inflammation strategically inhibit the whole cycle

• This is why B12 can rise in blood while doing nothing — the enzyme is inhibited, not saturated; genes are not destiny, and epigenetic expression shifts as the underlying drivers are cleared

(1:07:15 – 1:15:10)

Chelsea — Her Daughter's Bald Spot, Blood Work to Request, and Handling Doctors

• A bald spot following a physical injury may be scar tissue, but an open wound is also an easy entry point for infection and instant biofilm formation — the skin heals over and the infection stays, damaging follicles and inhibiting Wnt signalling

• This is the same reason surgery is such a common cause of persistent infection — complete exposure plus immediate biofilm production

• Blood work worth requesting: a full iron panel (serum iron, TIBC, transferrin saturation, and ferritin — never a single marker), C-reactive protein, and a CBC with differential (specifying lymphocytes, basophils, eosinophils, neutrophils, since a total white count alone says nothing)

• A lipid panel is less critical at her age, though checking for low cholesterol is worthwhile since that's its own problem

• Practical route: use the family doctor purely to obtain the dermatologist referral rather than fighting for comprehensive blood work — if the dermatologist finds nothing, the cause is internal

• On non-functional doctors: smile and nod, take the information, stay analytical, and don't write them off entirely — but there's little point trying to change their framework

• Prescriptions you don't intend to fill can simply be accepted (one client must complete eight weeks of antidepressants before insurance covers Exomind) — Curtis is candid that he'll say what's needed to obtain what he wants, while acknowledging others may view that differently

(1:15:47 – 1:21:40)

Kaylee and Danielle — Glutathione Duration, Nystatin Form, and Post-Surgery Constipation

• 100 mg of glutathione once weekly can continue for a very long time — in today's toxic environment that's nowhere near overdoing it; 300 mg weekly is likely fine too depending on the person's stage and circumstances

• The concern isn't suppressing inflammation excessively but depleting the nutrients required to recycle glutathione — and remember oxidative stress is a necessary signalling molecule, not something to eliminate

• Organic acid testing (and blood work) will show whether glutathione is running too high; Sam's 150 mg twice weekly is a safe holding position until his results arrive

• Nystatin oral suspension (swish and swallow rather than spit) does work, but the pill form is preferable where obtainable — a dentist may be an unexpected but viable prescriber route

• Danielle's post-surgery constipation (two bowel movements in two weeks, down from daily) is very common after surgery — driven by the mitochondrial hit and bile disruption

• Increase TUDCA, since bile stimulates the migrating motor complex, and raise magnesium citrate substantially — 300 mg is far too low here, with at least 1000 mg the likely target

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August 08-26 Live Q&A Recording