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ShanMan's progress
Quote from tim on September 14, 2023, 9:12 pmEarly stage in life
Diet: Tried to be "low fat". Fast food, meat / potatoes, milk / cheese, pizza (especially buffet's with ranch / garlic butter), lots of soda (Dr Pepper)I doubt your original diet was that problematic, probably just far too high in dairy fats which is the most common way to get subclinical Hypervitaminosis A in my opinion. Most of our instinctive food choices tend to be far better than our information based ones but dairy products are quite new evolutionarily and perhaps we don't always have the same level of instinctual awareness around them compared with other foods.
And, I completely stopped the fish oil at the end of November when I became persuaded Vitamin A could be an issue, and could not find a reasonable source that would describe how much Vit. A was in typical fish oil.
Low just like fish. Fish oil should probably be avoided but not because of vitamin A. It's only fish LIVER oil that must be strictly avoided due to vitamin A content.
I'm not yet convinced we need to be taking external DHA/EPA as long as we get very little PUFA, but every once in a while get a small amount of ALA. So, I do have a couple walnuts from time to time.
Then have a look at DHA levels in long term vegans (or fruitarians eating no seed oils). ALA in small amounts will not result in significant EPA/DHA production. ALA in large amounts is unhealthy.
Our ancestral diet contained lizards, snakes, insects, eggs and animal brains as well as fish. It's unwise to remove the only food group left in the modern diet that is a guaranteed source of not just DHA but also iodine and selenium.
When dietary PUFA decreases, SCD1 increases and more stearic acid is converted to oleic acid to maintain an adequate fuel octane level. So oleic acid and linoleic acid move in opposite directions. It is an inverse relationship. One goes up when the other goes down.
Quote from tim on September 14, 2023, 9:12 pmEarly stage in life
Diet: Tried to be "low fat". Fast food, meat / potatoes, milk / cheese, pizza (especially buffet's with ranch / garlic butter), lots of soda (Dr Pepper)I doubt your original diet was that problematic, probably just far too high in dairy fats which is the most common way to get subclinical Hypervitaminosis A in my opinion. Most of our instinctive food choices tend to be far better than our information based ones but dairy products are quite new evolutionarily and perhaps we don't always have the same level of instinctual awareness around them compared with other foods.
And, I completely stopped the fish oil at the end of November when I became persuaded Vitamin A could be an issue, and could not find a reasonable source that would describe how much Vit. A was in typical fish oil.
Low just like fish. Fish oil should probably be avoided but not because of vitamin A. It's only fish LIVER oil that must be strictly avoided due to vitamin A content.
I'm not yet convinced we need to be taking external DHA/EPA as long as we get very little PUFA, but every once in a while get a small amount of ALA. So, I do have a couple walnuts from time to time.
Then have a look at DHA levels in long term vegans (or fruitarians eating no seed oils). ALA in small amounts will not result in significant EPA/DHA production. ALA in large amounts is unhealthy.
Our ancestral diet contained lizards, snakes, insects, eggs and animal brains as well as fish. It's unwise to remove the only food group left in the modern diet that is a guaranteed source of not just DHA but also iodine and selenium.
When you stop consuming polyunsaturated fats, they are released into the body. This causes stearic acid to fall from adipose tissue. stearic acid is very important. When there is a lot of polyunsaturated fat, linoleic acid, oleic acid and stearic acid are needed to counteract the effect. Linoleic acid poisoning takes four years on average. That is why the carnivore diet works high in saturated fats and oleic acid.
@el wrote:
When dietary PUFA decreases, SCD1 increases and more stearic acid is converted to oleic acid to maintain an adequate fuel octane level. So oleic acid and linoleic acid move in opposite directions. It is an inverse relationship. One goes up when the other goes down.
All we really need to know about fats is to minimize intake of seed oils, avoid trans fats, avoid fish oil but include fish in the diet.
@el wrote:
When you stop consuming polyunsaturated fats, they are released into the body. This causes stearic acid to fall from adipose tissue. stearic acid is very important. When there is a lot of polyunsaturated fat, linoleic acid, oleic acid and stearic acid are needed to counteract the effect. Linoleic acid poisoning takes four years on average. That is why the carnivore diet works high in saturated fats and oleic acid.
How exactly does linoleic acid exert toxicity in the body? The most well known way is by oxidization by a free radical and then itself going on to oxidize cholesterol. That's not good but it doesn't tend to dramatically affect one's health like Hypervitaminosis A does.
There are too many problems to list with the Carnivore Diet. The most important one is that we are not carnivores, we are omnivores that cook and process our food, that is what our dentition and digestive system has evolved for. If you are interested in my thoughts on the Carnivore Diet please see this thread:
https://ggenereux.blog/discussion/topic/carnivore-and-bile-acid-malabsorption/?part=44
When dietary PUFA decreases, SCD1 increases and more stearic acid is converted to oleic acid to maintain an adequate fuel octane level. So oleic acid and linoleic acid move in opposite directions. It is an inverse relationship. One goes up when the other goes down.
It's a bit more complex than that. The consumption of PUFA (and MUFA) may indeed be a driver of SCD1 and D6D/D5D activity. I have only recently become aware of this factor. And, I am kicking myself for the years of EVOO consumption which could be from 5% to 20% (or even higher) Linoleic acid. But, I don't think the amount of Linoleic acid matters. It was the fact it was mostly MUFA and PUFA.
And, to that end, beef tallow is not that far off.
Quote from tim on September 14, 2023, 9:12 pmEarly stage in life
Diet: Tried to be "low fat". Fast food, meat / potatoes, milk / cheese, pizza (especially buffet's with ranch / garlic butter), lots of soda (Dr Pepper)I doubt your original diet was that problematic, probably just far too high in dairy fats which is the most common way to get subclinical Hypervitaminosis A in my opinion. Most of our instinctive food choices tend to be far better than our information based ones but dairy products are quite new evolutionarily and perhaps we don't always have the same level of instinctual awareness around them compared with other foods.
I think the biggest aspects were an early life overload of VitA without the necessary fiber and with too much opposition from wheat - CCK inhibition (WGA), Glyphosate (Contributing to aldehydes), etc.
And, I completely stopped the fish oil at the end of November when I became persuaded Vitamin A could be an issue, and could not find a reasonable source that would describe how much Vit. A was in typical fish oil.
Low just like fish. Fish oil should probably be avoided but not because of vitamin A. It's only fish LIVER oil that must be strictly avoided due to vitamin A content.
I tend to agree that fish oil that excludes fish organs should be relatively low(er) in Vit A. But, it still is substantial. In any case, the fish oil that I took for my mTBI was one of the few I could find without Vitamin E because I was wanting to somewhat limit the amount of tocopherol, at the time.
https://www.walmart.com/ip/Spring-Valley-Omega-3-Fish-Oil-Softgels-Lemon-500-mg-60-Count/825345207
It very much caused my voice and throat to BURN. (Unlike my previous Fish oil sources in the past)
I'm not yet convinced we need to be taking external DHA/EPA as long as we get very little PUFA, but every once in a while get a small amount of ALA. So, I do have a couple walnuts from time to time.
Then have a look at DHA levels in long term vegans (or fruitarians eating no seed oils). ALA in small amounts will not result in significant EPA/DHA production. ALA in large amounts is unhealthy.
Our ancestral diet contained lizards, snakes, insects, eggs and animal brains as well as fish. It's unwise to remove the only food group left in the modern diet that is a guaranteed source of not just DHA but also iodine and selenium.
There is a great amount of disagreement as to what an "ancestral diet" was.
I have seen the stories that support elements of what you stated. I have seen the stories and evidence that early homo sapiens (who lived in AFRICA) had a diet rich in fibrous starch. And, that evidence is supported by the large amount of amylases we have in our saliva (and, similarly the co-evolved canines, oddly enough)
Regardless, ancestral is only one dimension. We also need to look at the way the underlying cells evolved and how things like SCD1 gets triggered. I like Fire In A Bottle's "onion of life" thoughts here in organizing the layers of signaling.
https://www.youtube.com/watch?v=ZYcWd3amv-Y
And, this really tracks to making sure that enough NAD+ is available, and enzymes (such as AOX, ALDH, etc.) are de-acetylated. This seems to prefer glucose and glycolysis to support. FAO (Fatty acid-oxidation) is not oxidative enough, and relying on gluconeogenesis from amino acids to generate glucose is extremely inefficient.
@shannon wrote:
I have seen the stories that support elements of what you stated. I have seen the stories and evidence that early homo sapiens (who lived in AFRICA) had a diet rich in fibrous starch. And, that evidence is supported by the large amount of amylases we have in our saliva (and, similarly the co-evolved canines, oddly enough)
Just to clarify I wasn't claiming that the ancestral diet was predominantly those foods just that it contained those foods.
Yes grains, tubers, roots, fruits, legumes, plant saps (like maple and birch) and honey have always been part of our diet.
Some recent findings:
Quote from tim on September 15, 2023, 7:55 pm@shannon wrote:
I have seen the stories that support elements of what you stated. I have seen the stories and evidence that early homo sapiens (who lived in AFRICA) had a diet rich in fibrous starch. And, that evidence is supported by the large amount of amylases we have in our saliva (and, similarly the co-evolved canines, oddly enough)
Just to clarify I wasn't claiming that the ancestral diet was predominantly those foods just that it contained those foods.
Yes grains, tubers, roots, fruits, legumes, plant saps (like maple and birch) and honey have always been part of our diet.
Some recent findings:
The Body Fat Saturation Of Starch Eaters; Linoleic Acid Dysregulates SCD1
Quote from El on September 16, 2023, 5:02 amQuote from tim on September 15, 2023, 7:55 pm@shannon wrote:
I have seen the stories that support elements of what you stated. I have seen the stories and evidence that early homo sapiens (who lived in AFRICA) had a diet rich in fibrous starch. And, that evidence is supported by the large amount of amylases we have in our saliva (and, similarly the co-evolved canines, oddly enough)
Just to clarify I wasn't claiming that the ancestral diet was predominantly those foods just that it contained those foods.
Yes grains, tubers, roots, fruits, legumes, plant saps (like maple and birch) and honey have always been part of our diet.
Some recent findings:
https://fireinabottle.net/the-body-fat-saturation-of-starch-eaters-linoleic-acid-dysregulates-scd1/
That's right, and if you follow his work further you will find that even OLEIC will contribute to linoleic and further dysregulate.
Oleic is still high in Tallow.
Does the Stearic change the behavior? I don't know....
In any case, this discussion has prompted me to bring back a bit of fat in my meat. I do wish there was a way to semi-isolate stearic acid in a column of fat (or siphon off oleic / linoleic)
Hi @shannon Thanks for taking the time to share your progress here. May I ask why you are skeptical of zinc picolinate? I remember @wavygravygadzooks made a great post about how his thinking was that it (zinc picolinate) worked "too well" on the ND forum. I can't remember the specifics about what he said, I thought I would be able to go back and re-read but he was unfortunately silenced/deleted from there as a dissenter. Thanks in advance.
I don't recall all the details of what I wrote a while back, but the gist was that zinc picolinate is highly absorbable but not necessarily highly bioavailable after absorption, based one or more studies cited by Chris Masterjohn in his video discussion of zinc supplements. One potential reason might be that picolinic acid remains tightly bound to zinc and does not readily permit utilization by the body.
Part of what led me to look into this was that I had done a serum zinc and Spectracell Micronutrient Test at the same time. My serum zinc levels were right at the upper edge of the reference range, which made sense because I'd been eating a ton of red meat for over a year and I'd been supplementing zinc on top of that. But my Spectracell MNT results indicated I was horribly deficient in zinc inside my cells. Several alternative practitioners I'd seen really believed in the accuracy of the Spectracell test, so I couldn't decide whether that test was actually just complete bullshit, or whether it was indeed possible to simultaneously have high serum levels and intracellular deficiency. I had been supplementing primarily with zinc picolinate, so I came up with the hypothesis that the body might recognize high levels of zinc in the blood with a bunch of zinc picolinate floating around not getting used, and subsequently deplete other more usable forms of zinc in the process of reducing the total amount of serum zinc. Put another way, zinc picolinate might encourage the turnover and loss of more usable forms, simultaneously encouraging serum overload and intracellular deficiency.
dipSmith claimed that zinc picolinate increased zinc levels in the hair and was therefore working to benefit the rest of the body. I told him the fact you see it in the hair doesn't mean it's getting used in the cells. There's evidence to suggest that unused minerals get dumped into the hair as a route of excretion, so it's possible the zinc picolinate is just getting dumped and/or is encouraging more usable forms to get dumped. dipSmith makes a ton of his own idiotic ASSumptions (as he wrote it) that he warned others not to make.
This all goes to demonstrate just how unreliable HTMA and serum levels of nutrients can be in judging intracellular nutrient levels. I really wish there were more validation for the Spectracell method, but at this point it looks like it's been mostly in-house and/or non-peer-reviewed studies by the company itself used to market their tests.