Interested in thiamine deficiency and COVID, keto diet, renewable energy, building energy efficiency, regenerative agriculture, permaculture, computing, scottis
Please note: my arguments for a connection between the level of thiamine sufficiency or deficiency in the body and outcome following COVID infection are my unqualified speculations, based on the work of Drs Derrick Lonsdale and Chandler Marrs at
https://t.co/l2keKKRhIE
A female client of mine suffers from migraines
I put her on high dosage Riboflavin, TTFD & Benfothiamine. Migraines almost went down to zero/month.
3 months after the high dosage thiamine there was a supply issue for 3 weeks and directly there were relapses of migraines, 3-5 within a time frame of 4-6 weeks
Riboflavin stayed in the stack at 200mg throughout this time. I wondered wether there is some connection (as I didn't intend the thiamine to improve migraines necessarily, rather her neuropathy & fibromyalgia)
I came across this study where they used high dosage thiamine to improve episodic migraine frequency
Pretty interesting
@tnseyfried I wonder if you're aware of the "ketone adjacent" properties of indole-3 propionic acid, produced in the gut by bacterial metabolism of tryptophan? It seems it can suppress glycolysis, block epithelial-mesenchymal transition, and reactivate p53 apoptosis:
https://t.co/FEPlzvIA0A
@tnseyfried I wonder if you're aware of the "ketone adjacent" properties of indole-3 propionic acid, produced in the gut by bacterial metabolism of tryptophan? It seems it can suppress glycolysis, block epithelial-mesenchymal transition, and reactivate p53 apoptosis:
https://t.co/FEPlzvIA0A
All major cancers produce glucose-derived lactate and glutamine-derived succinate as metabolic end products of insufficient oxygen-dependent energy production. The release of lactate and succinate from cancer cells identifies glucose and glutamine as the metabolic drivers of cancer. Consequently, the simultaneous restriction of glucose and glutamine while non-fermentable ketone bodies are elevated (nutritional ketosis) should be a non-toxic therapeutic strategy for managing all major cancers. This strategy could work even better when combined with low dose chemo- and immune therapies. When will the NCI come to know about this?
(https://t.co/Aj7o4apBR7).
@DrGrahamLJ So what, exactly, causes Long Covid? Here's another "podcast" episode, based on my hypothesis (see above), which seeks to explain it:
https://t.co/qVgc0Fy3rl
@DrGrahamLJ So what, exactly, causes Long Covid? Here's another "podcast" episode, based on my hypothesis (see above), which seeks to explain it:
https://t.co/qVgc0Fy3rl
@DrGrahamLJ So what, exactly, causes Long Covid? Here's another "podcast" episode, based on my hypothesis (see above), which seeks to explain it:
https://t.co/qVgc0Fy3rl
Wow, I think I'm hallucinating. Strange voices telling me all about what's been living in my head the last few years.
If you follow me, you might have noticed that I started a thread a while ago setting out my hypothesis on the nature of chronic disease:
https://t.co/P6vhCcm98f
@DrGrahamLJ Now I have had a closer look at the possible role of my hypothesis (see above) in the action of this bacterium. Here is another "podcast" exploring this:
https://t.co/PXH1cOBze5
A lot of mental illnesses can be viewed as a "brain energy crisis".
So, plenty of times, your depression doesn't start in your head, it starts in your mitochondria.
To demonstrate this point, here's for example an ancient enzyme system that not only controls your mood but is also key when it comes to resolving some side effects of psychiatric medications.
Thread 🧵
Every molecule of glucose you eat has to pass through one enzyme to become ATP. That enzyme is pyruvate dehydrogenase. Its cofactor is thiamine.
Glycolysis breaks glucose down to pyruvate. That happens in the cytoplasm and doesn't require thiamine. But pyruvate can't enter the mitochondria as acetyl-CoA without PDH converting it, and PDH can't function without thiamine pyrophosphate in its active site. If thiamine is missing, pyruvate gets shunted to lactate instead. The citric acid cycle starves. ATP production drops. Lactate accumulates.
This isn't just a textbook pathway. Hanninen et al. measured thiamine status in 100 hospitalized heart failure patients and 50 controls. 33% of heart failure patients were thiamine deficient vs 12% of controls. A well-established driver: loop diuretics increase renal thiamine clearance. Nearly every heart failure patient is on one. Thiamine is water-soluble with total body stores of only 25-30 mg. Without daily replenishment, stores can be depleted in as little as 2-3 weeks.
This creates a plausible vicious cycle. Heart failure patients are put on furosemide. Furosemide depletes thiamine. Thiamine deficiency impairs cardiac energy metabolism. Cardiac function worsens. The diuretic dose goes up. More thiamine is lost. Supplementation trials have shown mixed results on ejection fraction, but the metabolic logic is sound and the deficiency is measurable.
Beyond heart failure: diabetes is independently associated with low thiamine status. Alcohol impairs thiamine absorption and increases excretion. Bariatric surgery reduces absorptive surface. High carbohydrate intake increases thiamine demand because carbohydrate metabolism is the pathway most dependent on it.
Thiamine status is not part of standard blood panels. If you're on a loop diuretic, managing blood sugar, or recovering from surgery, it's worth asking about.
Hanninen et al., J Am
Coll Cardiol, 2006.