I needed to disable self sign-ups because I’ve been getting too many spam-type accounts. Thanks.
Paul Saladino pushing VitA hard.
Quote from tim on October 26, 2023, 4:45 pmThe thread discussion was about the problem of B6 being casually singled out for everyone to focus on, not about if B6 deficiency can ever occur or not.
Actually, the thread was about Paul Saladino pushing Vitamin A until you veered off on B6 and other people started talking about balding lol
@jaj was pointing out a particular and interesting connection between B6 and Vitamin A metabolism, even suggesting that supplementing B6 may not be advisable despite apparent deficiency. Maybe you should actually listen to what Meri Arthur has to say about B6 instead of cutting @jaj down and implying that Arthur is just another influencer.
Also, a carnivore diet is not inherently deficient in anything if sufficiency is defined by health status/fitness, as it should be. The only modern study on the carnivore diet essentially showed improvements in health outcomes across the board. I'm not claiming it was a stellar study design, but it's the only published research aside from the study on Stefansson and his colleague (which vindicated such a diet as unproblematic for at least the duration of a year). Every other study you might try to use to suggest there are deficiencies on a carnivore diet is riddled with confounders, first and foremost being that the subjects WERE NOT ON A VERIFIED CARNIVORE DIET for any significant length of time. You are inappropriately extrapolating from one set of conditions to another. Even "carnivore diet plus fruit" is not a carnivore diet because there are additional variables at play. We lack controlled studies on the subject, plain and simple, so unless you man it up and try it yourself you should probably just STFU with your armchair opinions on the matter.
In case you felt the post I tagged you in on was disparaging that wasn't my intention and I didn't comment on the hypothesis you presented. I was clarifying the nature of the B6 discussion taking place in the thread and then sharing my thoughts on B6 to everyone.
Thanks @wavygravygadzooks. I appreciate your support. I’ve learnt so much over the past few months. I have much to share. However, I don’t come on forums because negative responses upset my nervous system. And calming my nervous system must be my priority.
However, occasionally I get pushed into reacting as I just don’t like people to have false information. B6 is an incredibly important B vitamin, possibly the most important in terms of how a deficiency can upset metabolism, if I had to pick one. But maybe I’m just biased as B6 deficiency has really messed me up! Meri thinks it’s very common in vA toxicity, not rare. I think she is right.
B6 toxicity is a very interesting topic but I don’t believe it’s a plain toxicity. I think it’s either a failure of B6 to get into cells (Carolyn Ledowsky), and therefore a build up outside cells and a deficiency within them. Or an inactivation of B6 which builds up (see Meri theory) and therefore a functional deficiency. The treatment protocol for B6 toxicity is fascinating and has many parellels to the one I’m using for deficiency. Much more to know in this area. At no point did I suggest supplementing B6.
Edit: However, on the topic of supplements Klinghardt treats pyroluria first (says people don’t recover unless this is addressed first) in his protocols, using B6 as part of his supplement protocol.
https://www.townsendletter.com/July2017/krypto0717.html
Sure thing, I wanted to make sure you knew someone appreciated your comment since you're not on here much these days. You've pointed out some interesting ideas over the years and Meri Arthur's stuff seems novel and intriguing. I also feel a bit guilty that I may have caused you undue strife with my own commentary a while back...sorry about that.
Thanks @wavygravygadzooks. I appreciate your support. I’ve learnt so much over the past few months. I have much to share. However, I don’t come on forums because negative responses upset my nervous system. And calming my nervous system must be my priority.
Yet here you are thanking the user with the longest history of disrupting thread conversations with all sorts of nonsense including personal attacks. Imagine getting so upset about someone online that wasn't even deconstructing your message, just simply pointing out that your disagreement didn't logically follow the nature of the discussion.
It's clear that you are still very salty about me owning you in the carnivore vs omnivore debate earlier this year and got triggered (as you normally do) by carnivore diet criticism in this thread.
Maybe you should actually listen to what Meri Arthur has to say about B6 instead of cutting @jaj down and implying that Arthur is just another influencer.
Since you and @jaj who both claim to be scientists are referencing her instead of citing credible sources let's take a look at her recent article published on hormonesmatter.com
No doubt you will frame my frank criticism of this article as an attack on this researcher so let me just state that she sounds like an interesting and intelligent person. I love technical biochemical breakdowns and have been looking forward to this space attracting more that can do this. However, we are here to improve our understanding of Hypervitaminosis A and you are forcing me into a corner to critically analyse her work.
Oxalate: A Potential Contributor to Hypervitaminosis A
Meredith Arthur, MS, RD, LD
We have many backup pathways in the human body. When one pathway is broken, another pathway can pick up the slack. If that second pathway is broken, that is when disease occurs. Oxalate is a potential second pathway breaker in individuals with underlying mitochondrial disorders. As a dietitian, I have found many of my clients, especially those with Autism Spectrum Disorder (ASD) or other neurodevelopmental syndromes, are struggling with oxalate, which then impairs their ability to metabolize vitamin A. My clients have symptoms of vitamin A deficiency and have retinoic acid deficiency, but because of poor NADH/NAD recycling actually have retinol and retinaldehyde toxicity; a conundrum to be sure, until one understands the connections between oxalate, NAD, and vitamin A metabolism.
To start with the links cited in her article do not back up her thesis. A poorly constructed hypothesis is presented with no evidence to back it up. The "case evidence" published provides no evidence either.
"My clients have symptoms of vitamin A deficiency and have retinoic acid deficiency"
The essential retinoids are retinal in the retina and various homologues of retinoic acid, that's it. So writing VAD and retinoic acid deficiency doesn't make much sense unless both xerophthalmia and symptoms of retinoic acid deficiency are present.
But what are the symptoms of retinoic acid deficiency? They are poorly defined and they are really only easily observable during reproduction.
In addition to causing birth defects at high doses in animals, deficiency of vitamin A can result in incomplete pregnancies and birth defects [24]. A spectrum of birth defects has been observed similar to those found from excessive vitamin A consumption in a number of species, including the pig, rat, rabbit, cattle, and sheep [24]. These findings suggest that there may be an optimum level of maternal retinol consumption above and below which abnormalities may occur. A comparison of birth defects observed from excessive vitamin A consumption and vitamin A deficiency is shown in table 1.
https://journals.sagepub.com/doi/pdf/10.1177/156482650102200304
Low RA levels can occur during liver disease but what biomarkers or symptoms is Arthur looking at to confirm this is occurring in any specific patient?
"but because of poor NADH/NAD recycling actually have retinol and retinaldehyde toxicity"
Even during advanced liver disease retinoic acid synthesis is not inhibited:
In the liver tissues with NASH, RA-metabolism-related genes were examined by real-time reverse transcription–polymerase chain reaction (Fig. 3).22 High expression levels of LRAT, DGAT1, and DGAT2, as well as CES1, imply that mutual conversion between retinyl esters and retinol is active in the liver tissues of NASH. Additionally, upregulation of CRBP1, ADH1, ADH2, ADH3, RDH10, RDH11, DHRS3, and DHRS4 is also observed, suggesting that oxidation of retinol to retinal is actively performed. ALDH1 and ALDH3 were highly expressed. Taken together, conversion of retinol to retinal, and subsequently to RA, is enhanced in the NASH liver tissues. While we found high expression of all the RA-metabolism-related genes analyzed in this study, expression of the target genes was variable; expression of CRBP1, CYP26A1, and PEPCK was increased, but expression of RARα2 and TGase2 was decreased, while expression of RARβ2, ADH3, and Btg2 remained unchanged. On the contrary, expression of CYP26A1 was extremely high, suggesting that degradation of ATRA is very active. These data suggest that metabolism of RA is very active in NASH, and continuous active state of RA metabolism causes subsequent loss of RA in the liver tissues with NASH, which may contribute to the progression of steatohepatitis to liver cirrhosis and HCC.
https://onlinelibrary.wiley.com/doi/10.1111/jgh.12031
So even though RA levels can be low during liver disease it's not due to inhibition of RALDH, it's due to upregulation of both retinoic acid synthesis and catabolism.
Briefly, nicotinamide adenine dinucleotide (NAD), derived from dietary niacin or vitamin B3, is a necessary cofactor in multiple enzymatic reactions involved in mitochondrial energy production. It is recycled endlessly back and forth between its oxidized and reduced forms NAD and NADH, respectively. The oxidized form NAD+ is required for the conversion of retinol to retinaldehyde and then to retinoic acid, the bioactive form of Vitamin A. With poor NADH/NAD recycling retinol and retinaldehyde are not converted to retinoic acid, and thus build up in the cell, presenting signs of both deficiency and toxicity simultaneously.
Hypervitaminosis A disrupts liver physiology in so many ways and there are many complex aspects to investigate. Why choose to specifically theorize that this is an important pathology in vitamin A metabolism? Especially when the science shows that retinoic acid production tends to be upregulated in liver disease?
The culprit behind this perplexing reaction, I believe, is oxalate damage to the NADH/NAD pathways via its interaction with an enzyme called lactate dehydrogenase (LDH). The chemistry in this pathway is a bit complicated, so bear with me. To help with the chemistry, I created a graphic (Figure 1.) to illustrate the pathways in question.
What is Oxalate?
The root of the dysfunction described above, I believe, begins with increased dietary oxalate and poor oxalate elimination. Oxalate is a component of plants that is impossible for the body to completely break down. It is a poison in large amounts. We absorb it at variable rates, but some of us make it in our bodies from vitamin C and glycine. Excess vitamin C becomes oxalate through direct degradation and without enzymes. Usually this occurs in vitamin C intake over 2000mg, but it can happen at lower doses as well. I never recommend vitamin C to “bowel tolerance” as this likely represents the death of the intestinal cells due to oxalate poisoning. Glycine is metabolized to oxalate in a B6 and thiamine deficient state, but when there is adequate B6 and thiamine, glycine does not become oxalate.
I've previous discussed in this forum how oxalate toxicity tends to be more an effect than a cause. This is especially true with Hypervitaminosis A. A healthy gut doesn't hyperabsorb oxalate. Oxalate is endogenously produced in larger amounts in those with liver dysfunction and liver dysfunction leads to gut dysfunction (and vice versa) which leads to dietary oxalate hyperabsorption. Hypervitaminosis A induces liver dysfunction, B vitamin deficiencies/lack of bioavailability, increased collagen turnover resulting in increased hydroxylated amino acid turnover and vitamin C requirements, gut permeability, SIBO and dysbiosis that all lead to either increased endogenous oxalate production or increased exogenous oxalate absorption.
Oxalate is the most important kidney stressor. Grant's diet contains oxalate but lower gut permeability and improved liver function due to avoiding vitamin A combined with minimal intake of collagen and vitamin C probably means his endogenous oxalate production is very low and his absorption is low too. If he had just avoided oxalate instead of vitamin A to try to improve his NAD recycling because that might improve a hypothesized simultaneous vitamin A deficiency/toxicity that would have been more effective, really? Nah.
You made a hypocritical (and false) assertion that I disrupt threads with tangential logical arguments, without addressing the substance of those threads, when that is precisely what you have done here, multiple times.
(1) You failed to address my points about the available research on "carnivore" diets (the only studies available indicate health maintenance and/or improvements with no discernible deficiencies). Instead, you claimed that I was "salty" about getting "owned" by you in our previous debate about humans as carnivores. You pivoted away from addressing substance and relied on an ad hominem attack. Hypocrite +1
(2) You failed to address Meri Arthur's discussion about B6 and Vitamin A, choosing instead to criticize an article of hers focused on oxalates. While I do agree with some of your criticisms of that article (e.g. lack of clear connection to concepts via references, lack of evidence for retinoic acid deficiency in her clients), you are making a logical fallacy by attacking one set of ideas, using that to denigrate the person generating the ideas, and then using that denigration to refute a different set of ideas without considering them independently from the first set. Hypocrite +2
(3) This thread was about Paul Saladino pushing Vitamin A until you redirected it (i.e. "disrupted") toward a discussion of B6. Hypocrite +3
RE: deficiencies on a carnivore diet. Here's another line of reasoning for you: If a carnivore diet is inherently deficient in nutrients for humans, why do other carnivores not suffer deficiencies? Human physiology and digestive anatomy is remarkably similar to that of felids and canines. In fact, mammals in general share very similar physiology and micronutrient requirements; they vary greatly in the means of obtaining those micronutrients. The primary difference with regard to micronutrient needs in humans and other carnivores is a slight difference in the ability to generate some micronutrients endogenously (e.g. taurine, ascorbic acid). The difference in gluconeogenesis for macronutrient needs is irrelevant when humans have sufficient access to fat. There are large differences in morphology, but this is most relevant to prey acquisition, which humans accomplish via exogenous use of tools. In fact, by using tools, humans have access to a much greater variety of prey than any other carnivore and can derive nutrition from more parts of those prey than other carnivores. Where is there any indication that humans would have nutrient deficiencies on such a diet? The RDAs fabricated from people eating plant-based diets? Poorly constructed and reductionist nutrition studies of people not eating a carnivore diet? Other mammals contain in themselves almost the exact proportion of nutrients that exist in our own bodies, in essentially the same form that exist in our own bodies. It is the exact opposite with plants. If humans have the means to acquire and digest the bodies of other mammals (and we most certainly do), there is crystal clear logic for attempting a modern version of a carnivore diet. Now that lots of people are implementing a modern carnivore diet, we have a rapidly growing base of evidence that our logical reasoning pans out in the real world.
RE: hyperabsorption of oxalates and downplaying their role in disease. Hyperabsorption means absorption beyond some "normal" threshold. One does not need to hyperabsorb oxalates through the digestive tract in order to cause problems. "Normal" levels of absorption on a high-oxalate diet, or with acutely high oxalate consumption, are plenty sufficient to fuck somebody up. Not only that, but regular ingestion of oxalates has the potential to degrade the intestinal environment and lead to hyperabsorption. If you're smart enough to look outside the human species and the confines of PubMed articles, you'll quickly notice that herbivores whose entire lives revolve around detoxifying plant compounds must also generally avoid concentrated sources of oxalates...animals with digestive systems much more robust than our own to oxalates will die from excessive oxalate consumption. So, no, oxalates are not going to be "more of an effect than a cause" in many cases, as you suggested.
I could be wrong, but I'm guessing you don't have any real clientele to speak of, Tim. I would also guess that you've not practiced a lot of animal husbandry or observed wild animals much. Your whole world of nutrition seems to revolve around inhaling PubMed articles and regurgitating "facts" you've gleaned from them on internet forums. With no real-world experience and no credentials, you've become a deluded, self-aggrandizing armchair nutritionist who loves to hate on other nutritionists that actually have experience treating clients. Your defense always lies in some literature citation without you realizing the limitations of what you're citing because you're not an experienced scientist. I'm not saying you're not correct in many of your assertions, but you've got a severely bloated sense of authority derived from a distorted sense of scientific comprehension.
Quote from wavygravygadzooks on October 28, 2023, 2:43 pmYou made a hypocritical (and false) assertion that I disrupt threads with tangential logical arguments, without addressing the substance of those threads, when that is precisely what you have done here, multiple times.
(1) You failed to address my points about the available research on "carnivore" diets (the only studies available indicate health maintenance and/or improvements with no discernible deficiencies). Instead, you claimed that I was "salty" about getting "owned" by you in our previous debate about humans as carnivores. You pivoted away from addressing substance and relied on an ad hominem attack. Hypocrite +1
(2) You failed to address Meri Arthur's discussion about B6 and Vitamin A, choosing instead to criticize an article of hers focused on oxalates. While I do agree with some of your criticisms of that article (e.g. lack of clear connection to concepts via references, lack of evidence for retinoic acid deficiency in her clients), you are making a logical fallacy by attacking one set of ideas, using that to denigrate the person generating the ideas, and then using that denigration to refute a different set of ideas without considering them independently from the first set. Hypocrite +2
(3) This thread was about Paul Saladino pushing Vitamin A until you redirected it (i.e. "disrupted") toward a discussion of B6. Hypocrite +3
RE: deficiencies on a carnivore diet. Here's another line of reasoning for you: If a carnivore diet is inherently deficient in nutrients for humans, why do other carnivores not suffer deficiencies? Human physiology and digestive anatomy is remarkably similar to that of felids and canines. In fact, mammals in general share very similar physiology and micronutrient requirements; they vary greatly in the means of obtaining those micronutrients. The primary difference with regard to micronutrient needs in humans and other carnivores is a slight difference in the ability to generate some micronutrients endogenously (e.g. taurine, ascorbic acid). The difference in gluconeogenesis for macronutrient needs is irrelevant when humans have sufficient access to fat. There are large differences in morphology, but this is most relevant to prey acquisition, which humans accomplish via exogenous use of tools. In fact, by using tools, humans have access to a much greater variety of prey than any other carnivore and can derive nutrition from more parts of those prey than other carnivores. Where is there any indication that humans would have nutrient deficiencies on such a diet? The RDAs fabricated from people eating plant-based diets? Poorly constructed and reductionist nutrition studies of people not eating a carnivore diet? Other mammals contain in themselves almost the exact proportion of nutrients that exist in our own bodies, in essentially the same form that exist in our own bodies. It is the exact opposite with plants. If humans have the means to acquire and digest the bodies of other mammals (and we most certainly do), there is crystal clear logic for attempting a modern version of a carnivore diet. Now that lots of people are implementing a modern carnivore diet, we have a rapidly growing base of evidence that our logical reasoning pans out in the real world.
RE: hyperabsorption of oxalates and downplaying their role in disease. Hyperabsorption means absorption beyond some "normal" threshold. One does not need to hyperabsorb oxalates through the digestive tract in order to cause problems. "Normal" levels of absorption on a high-oxalate diet, or with acutely high oxalate consumption, are plenty sufficient to fuck somebody up. Not only that, but regular ingestion of oxalates has the potential to degrade the intestinal environment and lead to hyperabsorption. If you're smart enough to look outside the human species and the confines of PubMed articles, you'll quickly notice that herbivores whose entire lives revolve around detoxifying plant compounds must also generally avoid concentrated sources of oxalates...animals with digestive systems much more robust than our own to oxalates will die from excessive oxalate consumption. So, no, oxalates are not going to be "more of an effect than a cause" in many cases, as you suggested.
I could be wrong, but I'm guessing you don't have any real clientele to speak of, Tim. I would also guess that you've not practiced a lot of animal husbandry or observed wild animals much. Your whole world of nutrition seems to revolve around inhaling PubMed articles and regurgitating "facts" you've gleaned from them on internet forums. With no real-world experience and no credentials, you've become a deluded, self-aggrandizing armchair nutritionist who loves to hate on other nutritionists that actually have experience treating clients. Your defense always lies in some literature citation without you realizing the limitations of what you're citing because you're not an experienced scientist. I'm not saying you're not correct in many of your assertions, but you've got a severely bloated sense of authority derived from a distorted sense of scientific comprehension.
What you're saying doesn't make sense. Vitamin C is metabolized to oxolate in the body. The body does not produce vitamin C but in carnivores it does. Carnivores do not have a deficiency because they eat guts, not just muscle meat. Carnivores can take livers because they internally metabolize vitamin C, therefore they can detoxify vitamin A effectively. Herbivores, like wild animals, have little vitamin A in their liver. Those lions eat farm animals and get fat and sick. Farm animals, cereals, make detoxification of vitamin A deficient and their livers toxic. the livers of wild animals are safe. Livers of animals with a lot of fat such as fish, seals, pigs are not safe since they have much more vitamin A stored by fat.
You made a hypocritical (and false) assertion that I disrupt threads with tangential logical arguments, without addressing the substance of those threads, when that is precisely what you have done here, multiple times.
(1) You failed to address my points about the available research on "carnivore" diets (the only studies available indicate health maintenance and/or improvements with no discernible deficiencies). Instead, you claimed that I was "salty" about getting "owned" by you in our previous debate about humans as carnivores. You pivoted away from addressing substance and relied on an ad hominem attack. Hypocrite +1
I'd say others here might agree with me so "salty" and "owned" might be more of an observation than a personal attack.
(2) You failed to address Meri Arthur's discussion about B6 and Vitamin A, choosing instead to criticize an article of hers focused on oxalates. While I do agree with some of your criticisms of that article (e.g. lack of clear connection to concepts via references, lack of evidence for retinoic acid deficiency in her clients), you are making a logical fallacy by attacking one set of ideas, using that to denigrate the person generating the ideas, and then using that denigration to refute a different set of ideas without considering them independently from the first set. Hypocrite +2
It's the only published article by her I knew about so I critically analyzed it. If she has published an article or has any forum posts anywhere about B6 please link them and I'll analyze them.
(3) This thread was about Paul Saladino pushing Vitamin A until you redirected it (i.e. "disrupted") toward a discussion of B6. Hypocrite +3
Sheesh, you're still going on about that. Relax. Saladino's tweet literally mentioned B6 so it was hardly an irrelevant thing to discuss.
RE: deficiencies on a carnivore diet. Here's another line of reasoning for you: If a carnivore diet is inherently deficient in nutrients for humans, why do other carnivores not suffer deficiencies? Human physiology and digestive anatomy is remarkably similar to that of felids and canines. In fact, mammals in general share very similar physiology and micronutrient requirements; they vary greatly in the means of obtaining those micronutrients. The primary difference with regard to micronutrient needs in humans and other carnivores is a slight difference in the ability to generate some micronutrients endogenously (e.g. taurine, ascorbic acid). The difference in gluconeogenesis for macronutrient needs is irrelevant when humans have sufficient access to fat. There are large differences in morphology, but this is most relevant to prey acquisition, which humans accomplish via exogenous use of tools. In fact, by using tools, humans have access to a much greater variety of prey than any other carnivore and can derive nutrition from more parts of those prey than other carnivores. Where is there any indication that humans would have nutrient deficiencies on such a diet? The RDAs fabricated from people eating plant-based diets? Poorly constructed and reductionist nutrition studies of people not eating a carnivore diet? Other mammals contain in themselves almost the exact proportion of nutrients that exist in our own bodies, in essentially the same form that exist in our own bodies. It is the exact opposite with plants. If humans have the means to acquire and digest the bodies of other mammals (and we most certainly do), there is crystal clear logic for attempting a modern version of a carnivore diet. Now that lots of people are implementing a modern carnivore diet, we have a rapidly growing base of evidence that our logical reasoning pans out in the real world.
The carnivore vs omnivore debate finished months ago. Move on.
RE: hyperabsorption of oxalates and downplaying their role in disease. Hyperabsorption means absorption beyond some "normal" threshold. One does not need to hyperabsorb oxalates through the digestive tract in order to cause problems. "Normal" levels of absorption on a high-oxalate diet, or with acutely high oxalate consumption, are plenty sufficient to fuck somebody up. Not only that, but regular ingestion of oxalates has the potential to degrade the intestinal environment and lead to hyperabsorption. If you're smart enough to look outside the human species and the confines of PubMed articles, you'll quickly notice that herbivores whose entire lives revolve around detoxifying plant compounds must also generally avoid concentrated sources of oxalates...animals with digestive systems much more robust than our own to oxalates will die from excessive oxalate consumption. So, no, oxalates are not going to be "more of an effect than a cause" in many cases, as you suggested.
Hence why I said "more of an effect than a cause" rather than "always an effect, not a cause".. If someone is eating a pound of almonds every day then yes it can be a cause.
I could be wrong, but I'm guessing you don't have any real clientele to speak of, Tim. I would also guess that you've not practiced a lot of animal husbandry or observed wild animals much. Your whole world of nutrition seems to revolve around inhaling PubMed articles and regurgitating "facts" you've gleaned from them on internet forums. With no real-world experience and no credentials, you've become a deluded, self-aggrandizing armchair nutritionist who loves to hate on other nutritionists that actually have experience treating clients. Your defense always lies in some literature citation without you realizing the limitations of what you're citing because you're not an experienced scientist. I'm not saying you're not correct in many of your assertions, but you've got a severely bloated sense of authority.
That whole paragraph is just a personal attack.. Seethe.
I prewarned everyone that you'd do this. You backed me into a corner forcing me to critically analyze your reference then when I do you frame me as "a deluded, self-aggrandizing armchair nutritionist who loves to hate on other nutritionists that actually have experience treating clients". Despite my warning you still did it. Classic!