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Scurvy, Rancid Fat, and VA "deficiency"
Quote from Rudi on October 31, 2021, 4:38 pmGrant’s post about scurvy made me curious to learn a little more about the topic. I looked around a little more and came by some interesting notes and experiments. If there was a discussion on this earlier, I apologize that I was unable to find it.
The first article [1] that sparked my curiosity was this note saying that James Cook in fact suspected rancid fats to be the cause of scurvy.
Cook considered rancid fat the cause of scurvy. He wrote, " The fat boiled out of the salt beef and pork, I have never suffered to be given to the people, being of the opinion that it promotes the scurvy".
We all know that this was all discarded in favor of the VC deficiency.
The paper then reminds us that rancid fats are VE depleted just when they are needed most:
Rancidification of fat is an auto-oxidation reaction which occurs only when the antioxidant capacity of the fat is overwhelmed. Rancid fats are therefore depleted of vitamin E, the natural lipid-soluble anti- oxidant (7). On the other hand, the body's need for vitamin E increases in order to protect against the harmful effects of lipid peroxides (8). It is interesting to note that vitamin E deficiency was first demon- trated in animals fed a diet containing rancid fat (9).
Of course, VC is not a bystander in this process:
In 1968 Tappell (10) suggested that an interaction could occur between the two anti-oxidant vitamins, C and E, such that the oxidised form of vitamin E, formed during destruction of a lipid free-radical, could be reduced by vitamin C. More recently Slater and Willson (6) have obtained direct evidence for regeneration of vitamin E by vitamin C in the presence of free radicals. In this way, therefore, an increased demand for vitamin E could lead to an increased utilisation of vitamin C; in marginal (sub-clinical) vitamin C deficiency, ingestion of rancid fats could therefore precipitate the onset of scurvy.
Here we should recall that RA depletes VE and VC.
Keeping all this mind, consider this experiment feeding rats rancid lard from 1950’s [2]
When 12 female and 19 male weanling rats were placed on the vit. A-free rancid lard diet, they developed deficiency symptoms within 2 to 3 weeks, such as bloody mucous secretion from their nostrils, reddening of their eyes, and roughened, unclean fur. Death occurred among the emaciated animals 3 to 6 weeks after they had been placed on the diet, and there was no essential difference between males and females
First of all, what the hell kind of a deficiency is that? If I were to guess, the symptoms look awfully similar to the side effects of Accutane to me. Sadly, the experiment was done before the discovery of RA, so there was no way the researchers could have considered this possibility.
The most interesting part of this experiment isn’t their flawed deficiency model, but how they corrected the supposed deficiency. They managed to neutralize the toxin by supplementing the diet in with three different ingredients (separately):
- Cod Liver Oil
- Retinol Palmitate
- Crystalline Beta Carotene
This is undeniable proof that although VA isn’t a vitamin, it was an effective antidote to the poisoning. Anyone cares to speculate on the mechanism used here? If I were to guess, I’d say retinol itself has some VE sparing capacity because it can also act against lipoperoxidation. @ggenereux2014 ?
[1] https://www.sciencedirect.com/science/article/abs/pii/0306987783900786
[2] https://journals.sagepub.com/doi/abs/10.3181/00379727-75-18186
Grant’s post about scurvy made me curious to learn a little more about the topic. I looked around a little more and came by some interesting notes and experiments. If there was a discussion on this earlier, I apologize that I was unable to find it.
The first article [1] that sparked my curiosity was this note saying that James Cook in fact suspected rancid fats to be the cause of scurvy.
Cook considered rancid fat the cause of scurvy. He wrote, " The fat boiled out of the salt beef and pork, I have never suffered to be given to the people, being of the opinion that it promotes the scurvy".
We all know that this was all discarded in favor of the VC deficiency.
The paper then reminds us that rancid fats are VE depleted just when they are needed most:
Rancidification of fat is an auto-oxidation reaction which occurs only when the antioxidant capacity of the fat is overwhelmed. Rancid fats are therefore depleted of vitamin E, the natural lipid-soluble anti- oxidant (7). On the other hand, the body's need for vitamin E increases in order to protect against the harmful effects of lipid peroxides (8). It is interesting to note that vitamin E deficiency was first demon- trated in animals fed a diet containing rancid fat (9).
Of course, VC is not a bystander in this process:
In 1968 Tappell (10) suggested that an interaction could occur between the two anti-oxidant vitamins, C and E, such that the oxidised form of vitamin E, formed during destruction of a lipid free-radical, could be reduced by vitamin C. More recently Slater and Willson (6) have obtained direct evidence for regeneration of vitamin E by vitamin C in the presence of free radicals. In this way, therefore, an increased demand for vitamin E could lead to an increased utilisation of vitamin C; in marginal (sub-clinical) vitamin C deficiency, ingestion of rancid fats could therefore precipitate the onset of scurvy.
Here we should recall that RA depletes VE and VC.
Keeping all this mind, consider this experiment feeding rats rancid lard from 1950’s [2]
When 12 female and 19 male weanling rats were placed on the vit. A-free rancid lard diet, they developed deficiency symptoms within 2 to 3 weeks, such as bloody mucous secretion from their nostrils, reddening of their eyes, and roughened, unclean fur. Death occurred among the emaciated animals 3 to 6 weeks after they had been placed on the diet, and there was no essential difference between males and females
First of all, what the hell kind of a deficiency is that? If I were to guess, the symptoms look awfully similar to the side effects of Accutane to me. Sadly, the experiment was done before the discovery of RA, so there was no way the researchers could have considered this possibility.
The most interesting part of this experiment isn’t their flawed deficiency model, but how they corrected the supposed deficiency. They managed to neutralize the toxin by supplementing the diet in with three different ingredients (separately):
- Cod Liver Oil
- Retinol Palmitate
- Crystalline Beta Carotene
This is undeniable proof that although VA isn’t a vitamin, it was an effective antidote to the poisoning. Anyone cares to speculate on the mechanism used here? If I were to guess, I’d say retinol itself has some VE sparing capacity because it can also act against lipoperoxidation. @ggenereux2014 ?
[1] https://www.sciencedirect.com/science/article/abs/pii/0306987783900786
[2] https://journals.sagepub.com/doi/abs/10.3181/00379727-75-18186
Quote from wavygravygadzooks on October 31, 2021, 5:22 pm@rudi
You guys are doing precisely what you claim the authors of Vitamin A research doing...denying the findings of the research from the outset. You start by saying that Vitamin A is not a nutrient, then wonder how adding it to a deficient diet resolves illness? Maybe it's because it acts as an antioxidant, which is why carotenoids are pretty much ubiquitous in plant parts exposed to UV light, and probably the reason Vitamin A is found in the eyes of animals where UV light is concentrated down to a pinpoint by a lens, and in the skin of humans that is poorly protected from UV by guard hairs? Just maybe?
You guys are doing precisely what you claim the authors of Vitamin A research doing...denying the findings of the research from the outset. You start by saying that Vitamin A is not a nutrient, then wonder how adding it to a deficient diet resolves illness? Maybe it's because it acts as an antioxidant, which is why carotenoids are pretty much ubiquitous in plant parts exposed to UV light, and probably the reason Vitamin A is found in the eyes of animals where UV light is concentrated down to a pinpoint by a lens, and in the skin of humans that is poorly protected from UV by guard hairs? Just maybe?
Quote from Rudi on October 31, 2021, 5:38 pm@wavygravygadzooks I do not deny that VA is universally useless, I simply haven't yet seen good evidence for its general utility. What I absolutely deny is its elevated status as a *vitamin* - a molecule that is absolutely essential to life. The evidence required to prove something is essential should be damn high, and VA is simply nowhere near it. On other hand, there's a rock solid tower of evidence demonstrating its poisonous properties. Now whose position is more rational again?
Maybe it's because it acts as an antioxidant, which is why carotenoids are pretty much ubiquitous in plant parts exposed to UV light, and probably the reason Vitamin A is found in the eyes of animals where UV light is concentrated down to a pinpoint by a lens, and in the skin of humans that is poorly protected from UV by guard hairs? Just maybe?
Ah, back to blind speculation. That's OK, I don't mind exercising my imagination. Plants, as opposed to mammals, rely on sunlight to produce energy. Therefore, it seems logical that a molecule that is so easily excited by sunlight would be useful to them. Animals clearly have less uses for such a molecule. We only rely on sunlight to produce hormones, and we manage to do it just fine without BC. On the other hand, I can imagine plenty of reasons why we might not want molecules that are so unstable under sunlight in our skin.
Now back to the topic of this thread...
PS: plants already have an antioxidant, it is called VE.
@wavygravygadzooks I do not deny that VA is universally useless, I simply haven't yet seen good evidence for its general utility. What I absolutely deny is its elevated status as a *vitamin* - a molecule that is absolutely essential to life. The evidence required to prove something is essential should be damn high, and VA is simply nowhere near it. On other hand, there's a rock solid tower of evidence demonstrating its poisonous properties. Now whose position is more rational again?
Maybe it's because it acts as an antioxidant, which is why carotenoids are pretty much ubiquitous in plant parts exposed to UV light, and probably the reason Vitamin A is found in the eyes of animals where UV light is concentrated down to a pinpoint by a lens, and in the skin of humans that is poorly protected from UV by guard hairs? Just maybe?
Ah, back to blind speculation. That's OK, I don't mind exercising my imagination. Plants, as opposed to mammals, rely on sunlight to produce energy. Therefore, it seems logical that a molecule that is so easily excited by sunlight would be useful to them. Animals clearly have less uses for such a molecule. We only rely on sunlight to produce hormones, and we manage to do it just fine without BC. On the other hand, I can imagine plenty of reasons why we might not want molecules that are so unstable under sunlight in our skin.
Now back to the topic of this thread...
PS: plants already have an antioxidant, it is called VE.
Quote from Даниил on October 31, 2021, 6:09 pmHey, Rudi. Interestingly, they were treated with "massive doses" of retinol. I think the explanation may be that retinol inhibits the conversion of itself into retinoic acid (destroys ALDH cells). But a quick Google search didn't find anything.
I think if the explanation was in the antioxidant activity of VA, large doses would not be required. In addition, it is unlikely that sailors who had scurvy suffered from VA deficiency)
Add: omega 3 definitely do this: https://pubmed.ncbi.nlm.nih.gov/25648304/
Hey, Rudi. Interestingly, they were treated with "massive doses" of retinol. I think the explanation may be that retinol inhibits the conversion of itself into retinoic acid (destroys ALDH cells). But a quick Google search didn't find anything.
I think if the explanation was in the antioxidant activity of VA, large doses would not be required. In addition, it is unlikely that sailors who had scurvy suffered from VA deficiency)
Add: omega 3 definitely do this: https://pubmed.ncbi.nlm.nih.gov/25648304/
Quote from wavygravygadzooks on October 31, 2021, 9:24 pm@rudi
So why do we so consistently find Vitamin A in the eyes of animals?
Even if you don't need much Vitamin A to maintain vision, it is absolutely imperative that you never lose your vision if you depend on it for survival, so it would make sense that the body would have the ability to store nutrients critical for vision for long periods of time.
UV light does oxidative damage to living tissue. Seeing as we evolved as diurnal hunters, we obviously require some protection against that damage. You don't think it makes sense that a fat-soluble molecule like Vitamin A, which is capable of residing in the skin and eyes (areas of the body most exposed to UV damage), would act as an antioxidant to protect from UV damage?
You are aware of what happens when you focus sunlight through a magnifying glass, aren't you? (You can set ants on fire!) Now, imagine that same sunlight being focused onto the back of your eye through the lens of your own eye for 12 hours every single day of your life... Do you see a need for protection?
It's funny when you say "now back to the topic of this thread", as if it were really different from every other thread attempting to disparage Vitamin A under a different pretense. Vitamin A has ruined the last 4 years of my life, and yet here I am defending it because...I'm not blind 😉
So why do we so consistently find Vitamin A in the eyes of animals?
Even if you don't need much Vitamin A to maintain vision, it is absolutely imperative that you never lose your vision if you depend on it for survival, so it would make sense that the body would have the ability to store nutrients critical for vision for long periods of time.
UV light does oxidative damage to living tissue. Seeing as we evolved as diurnal hunters, we obviously require some protection against that damage. You don't think it makes sense that a fat-soluble molecule like Vitamin A, which is capable of residing in the skin and eyes (areas of the body most exposed to UV damage), would act as an antioxidant to protect from UV damage?
You are aware of what happens when you focus sunlight through a magnifying glass, aren't you? (You can set ants on fire!) Now, imagine that same sunlight being focused onto the back of your eye through the lens of your own eye for 12 hours every single day of your life... Do you see a need for protection?
It's funny when you say "now back to the topic of this thread", as if it were really different from every other thread attempting to disparage Vitamin A under a different pretense. Vitamin A has ruined the last 4 years of my life, and yet here I am defending it because...I'm not blind 😉
Quote from Rudi on October 31, 2021, 10:29 pm@daniil
Interestingly, they were treated with "massive doses" of retinol. I think the explanation may be that retinol inhibits the conversion of itself into retinoic acid (destroys ALDH cells)
I'll see if I can come up with some references.
I think if the explanation was in the antioxidant activity of VA, large doses would not be required. In addition, it is unlikely that sailors who had scurvy suffered from VA deficiency)
Interesting, what kind of dose would you expect of another anti oxidant (say VE) for some unit of rancid fat?
Nobody suffered from VA deficiency because there's no such thing :). But even if we were to accept that a "deficiency" exists, according to the experiment, it is easily induced in a few weeks after the consumption of adulterated fats. The conditions at sea would be quite similar to the experiment then in fact.
Interestingly, they were treated with "massive doses" of retinol. I think the explanation may be that retinol inhibits the conversion of itself into retinoic acid (destroys ALDH cells)
I'll see if I can come up with some references.
I think if the explanation was in the antioxidant activity of VA, large doses would not be required. In addition, it is unlikely that sailors who had scurvy suffered from VA deficiency)
Interesting, what kind of dose would you expect of another anti oxidant (say VE) for some unit of rancid fat?
Nobody suffered from VA deficiency because there's no such thing :). But even if we were to accept that a "deficiency" exists, according to the experiment, it is easily induced in a few weeks after the consumption of adulterated fats. The conditions at sea would be quite similar to the experiment then in fact.