This might turn out to be one of the great discoveries of modern times! Your attention to detail while still focusing on the big picture of what the minutia really means is admirable.
From my understanding after watching this (which could be completely wrong), support your liver. He said d-lactate should NOT be in the blood it should be oxidized in the liver.
The fact that the major source of methylglyoxal is from glycolysis (required for gluconeogenesis), for me it's just another reason to not eat a low carb diet. Also I don't agree with the mainstream that carb itself is the cause for increase of d-lactate, but poor carb choice (grains) resulting in poor digestion, poor carb metabolism, and gut dysbiosis (ibs, sibo) which causes various gut bacteria to ferment foods in the gut resulting in d-lactate production.
If LDHD deficiency causes d-lactate to reach the blood, and d-lactate is neurotoxic, then why did the family with d-lactate dehydrogenase deficiency and gout and high serum d-lactate not have neurotoxic effects?
Great question! Or did the family have some signs of neurotoxicity, but doctors didn't note it because they associated it with high uric acid/gout symptoms?
Nice article! But why so much focus on d lactate when l lactate seems to play major role in sports/performance in general and d lactate is only metabolized in liver? So what is going on with gut producing lactate from fructose- The Gut Shields the Liver from Fructose-Induced Damage.
Is the proton generated in the GAPDH reaction not held on the lone pair found on the NADH (but not on the NAD+)? Thus buffering the acidifying effects of the reaction?
Is there any prospect of high dietary phosphate content protecting against triose phosphate dephosphoylation? i.e. cola drinking having a protective effect?
Speaking of pyruvate, do you have any deeper insights on pyruvate transport, like how does it actually get from the cytosol into mitochondria? As i understand, the MPC complex (mitochondrial pyruvate carrier) uses protons from intermembrane space to shuffle pyruvate into mitochondria, but is the MPC activity itself regulated by something else? For instance, we know that pyruvate dehydrogenase is allosterically regulated by NADH and acetyl-coa while pyruvate dehydrogenase phosphatase is regulated by calcium. So i wonder, does something similar like that happen with the MPC complex too? To me, this looks like another obvious bottleneck.
👋 Trying to buy the ultimate cheat sheet on your website. It says "This store isn’t set up to receive orders yet. Contact the store directly for help." I didn't see a contact you feature so here I am to give you a head up!
Thanks Chris, this is excellent. I suffer from hyperoxaluria and had very high lactic acid levels. Low B1, B6, B9 and B12 as you'd expect. Would love to hear what you think about lysine and arginine in the diet.
I wonder if all plantarum strains produce d-lactate and I also wonder if this is DUE TO or a product of Methylglyoxal breakdown Have you seen the article about high D-lactate in a child with short bowel syndrome. He had extremely high levels of plantarum. His D-lactate was eliminated using specific probiotics. And his PLANTARUM disappeared as well. I wondered if the high plantarum sprung up in response to help breakdown oxalate. I’ll post a link below
In his stool, the D-lactate-producing strains Lactobacillus (L) johnsonii and L plantarum were detected. Therefore, a probiotic cocktail with non-D-lactate-producing bacteria (Pro4-50 D-Lactate Free Multistrain Probioticcapsules [Spectrumceuticals, Sydney, Australia] containing 25 billion colony-forming units [CFUs] of L rhamnosus GG, 15 billion CFUs of Bifidobacterium (B) lactis BS01, 5 billion CFUs of B breve BR03, and 5 billion CFUs of B longum BL03) was introduced into his daily treatment. Since then, the patient remained stable, and there was no additional need for antibiotic therapy for more than a year
I could not post more than one comment above. Here is more This article and others suggest undigested carbs in the colon can cause this too. This child also had SBS but many other conditions can cause this - such as dietary oxalate inhibiting pancreatic amylase. Thiamin deficiency can affect amylase as well. Enlarged parotid glands disappear with thiamine therapy See this excerpt Six months later, although under antibiotic treatment, he developed D-lactic acidosis again. In his stool, the D-lactate-producing strains Lactobacillus (L) johnsonii and L plantarum were detected. Therefore, a probiotic cocktail with non-D-lactate-producing bacteria (Pro4-50 D-Lactate Free Multistrain Probioticcapsules [Spectrumceuticals, Sydney, Australia] containing 25 billion colony-forming units [CFUs] of L rhamnosus GG, 15 billion CFUs of Bifidobacterium (B) lactis BS01, 5 billion CFUs of B breve BR03, and 5 billion CFUs of B longum BL03) was introduced into his daily treatment. Since then, the patient remained stable, and there was no additional need for antibiotic therapy for more than a year. 1library.net/document/y9dn4ljq-lactic-acidosis-successful-suppression-lactate-producing-lactobacillus-probiotics.html
@@lucyloudozarr9349 That's interesting, I haven't looked at the microbiome in that detail as I am more interested in the fact that this is almost entirely unique to SBS and that it's a distraction in the average person from the factors actually influencing their D-lactate flux.
as someone with epilepsy and other neurological diseases, once again i THANK YOU, as you continue to improve the quality of my life!
This might turn out to be one of the great discoveries of modern times! Your attention to detail while still focusing on the big picture of what the minutia really means is admirable.
Well that's motivation to watch the whole video. 😅❤
I just realized this is CMJs first vid in 7 months. He was definitely deep in his cave researching all this time. 😂
Can we get a user friendly video about this more in layman terms and how how we can use tbis information in our quest for health?
I agree. Please consider more vids about d-lactate. I suspect that is the origin of my issues so I'd like to see your take on symptoms and treatment.
From my understanding after watching this (which could be completely wrong), support your liver. He said d-lactate should NOT be in the blood it should be oxidized in the liver.
The fact that the major source of methylglyoxal is from glycolysis (required for gluconeogenesis), for me it's just another reason to not eat a low carb diet. Also I don't agree with the mainstream that carb itself is the cause for increase of d-lactate, but poor carb choice (grains) resulting in poor digestion, poor carb metabolism, and gut dysbiosis (ibs, sibo) which causes various gut bacteria to ferment foods in the gut resulting in d-lactate production.
Hey Chris, great to see you!
If LDHD deficiency causes d-lactate to reach the blood, and d-lactate is neurotoxic, then why did the family with d-lactate dehydrogenase deficiency and gout and high serum d-lactate not have neurotoxic effects?
Great question! Or did the family have some signs of neurotoxicity, but doctors didn't note it because they associated it with high uric acid/gout symptoms?
Nice article! But why so much focus on d lactate when l lactate seems to play major role in sports/performance in general and d lactate is only metabolized in liver? So what is going on with gut producing lactate from fructose- The Gut Shields the Liver from Fructose-Induced Damage.
Is the proton generated in the GAPDH reaction not held on the lone pair found on the NADH (but not on the NAD+)? Thus buffering the acidifying effects of the reaction?
Is there any prospect of high dietary phosphate content protecting against triose phosphate dephosphoylation? i.e. cola drinking having a protective effect?
Speaking of pyruvate, do you have any deeper insights on pyruvate transport, like how does it actually get from the cytosol into mitochondria? As i understand, the MPC complex (mitochondrial pyruvate carrier) uses protons from intermembrane space to shuffle pyruvate into mitochondria, but is the MPC activity itself regulated by something else? For instance, we know that pyruvate dehydrogenase is allosterically regulated by NADH and acetyl-coa while pyruvate dehydrogenase phosphatase is regulated by calcium. So i wonder, does something similar like that happen with the MPC complex too? To me, this looks like another obvious bottleneck.
That’s a great question. I haven’t come across anything on that and I’m sure we have more to learn.
👋 Trying to buy the ultimate cheat sheet on your website. It says "This store isn’t set up to receive orders yet. Contact the store directly for help."
I didn't see a contact you feature so here I am to give you a head up!
Thanks Chris, this is excellent. I suffer from hyperoxaluria and had very high lactic acid levels. Low B1, B6, B9 and B12 as you'd expect.
Would love to hear what you think about lysine and arginine in the diet.
Is it a bad idea to take sulphoraphane and/or eat broccoli sprouts if you have hypothyroidism?
Yes. Eat some carb, your thyroid needs it.
I think the bowel nosode Gaertner is helping me somewhat with this.
Calling it a shuttle does not matter as much as the functionality of the movement of organic acids
I wonder if all plantarum strains produce d-lactate and I also wonder if this is DUE TO or a product of Methylglyoxal breakdown
Have you seen the article about high D-lactate in a child with short bowel syndrome. He had extremely high levels of plantarum. His D-lactate was eliminated using specific probiotics. And his PLANTARUM disappeared as well.
I wondered if the high plantarum sprung up in response to help breakdown oxalate. I’ll post a link below
In his stool, the D-lactate-producing strains Lactobacillus (L) johnsonii and L plantarum were detected.
Therefore, a probiotic cocktail with non-D-lactate-producing bacteria (Pro4-50 D-Lactate Free Multistrain Probioticcapsules [Spectrumceuticals, Sydney, Australia] containing
25 billion colony-forming units [CFUs] of L rhamnosus GG,
15 billion CFUs of Bifidobacterium (B) lactis BS01,
5 billion CFUs of B breve BR03, and
5 billion CFUs of B longum BL03) was introduced into his daily treatment.
Since then, the patient remained stable, and there was no additional need for antibiotic therapy for more than a year
I could not post more than one comment above. Here is more
This article and others suggest undigested carbs in the colon can cause this too.
This child also had SBS but many other conditions can cause this - such as dietary oxalate inhibiting pancreatic amylase. Thiamin deficiency can affect amylase as well. Enlarged parotid glands disappear with thiamine therapy
See this excerpt
Six months later, although under antibiotic treatment, he developed D-lactic acidosis again.
In his stool, the D-lactate-producing strains Lactobacillus (L) johnsonii and L plantarum were detected.
Therefore, a probiotic cocktail with non-D-lactate-producing bacteria (Pro4-50
D-Lactate Free Multistrain Probioticcapsules [Spectrumceuticals, Sydney, Australia] containing
25 billion colony-forming units [CFUs] of L rhamnosus GG,
15 billion CFUs of Bifidobacterium (B) lactis BS01,
5 billion CFUs of B breve BR03, and
5 billion CFUs of B longum BL03) was introduced into his daily treatment.
Since then, the patient remained stable, and there was no additional need for antibiotic therapy for more than a year.
1library.net/document/y9dn4ljq-lactic-acidosis-successful-suppression-lactate-producing-lactobacillus-probiotics.html
@@lucyloudozarr9349 That's interesting, I haven't looked at the microbiome in that detail as I am more interested in the fact that this is almost entirely unique to SBS and that it's a distraction in the average person from the factors actually influencing their D-lactate flux.
@@lucyloudozarr9349 Have you tried those probiotic strains to reduce d-lactate?
Yo, that's cray-cray!