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Rachel-2 my vitamin D
It's hard to think of what fat to eat! LOL all of them have some drawback. The animal ones maybe have VA, the vegetable ones some have lutein, like olive, people talk badly here of coconut oil, the ultra processed ones are no longer food...
I eat less fat than ever trying to be lowered VA. However, I do eat fat, including old fashioned lard.
This is why I keep saying we need to to fix our farm feeds so the animals themselves aren't VA toxic.
I had my vD tested at the start of the year, it was 139 nmol/L. About a month before that I took about 350,000 IU over the course of a week to see how it would affect me. I didn't notice much. My vD level will be a lot lower now.
Fun fact: You can produce one billion IU of vD from the lanolin of one sheep's fleece! It's very cheap to produce. It's produced via UV light simulating the way vD is produced naturally so I don't see why supplementing is that different from getting it via sunbathing? It's not like other vitamins that are produced synthetically that have different isomers and enantiomers from what occurs naturally.
I'd be keen for you to share some of that vD info in a thread here.
Did you mean that there are different enantiomers of 1,25(OH)2D with different effects?
I'm glad because there is no way I would ever start eating every few hours just like I would never use steroids. I do make sure I eat plenty of protein twice per day though and I try to maximize my testosterone production through diet and lifestyle. I'm not too concerned with more muscle growth but I'm certain that vA depletion will lead to becoming less injury prone and to greater strength gains, it will help with ligament and bone strength as well.
Yeah very low fat cannot be good. Also, I don't just eat to live I also like to live to eat a little bit.
@josh @jiri @dino With regard to vD it seems to me that things that block VDRs are more of an issue than 25(OH)D levels. 25(OH)D is just the storage form and it acts a bit like retinol, if it is high then excess of the hormone like metabolite 1,25(OH)2D is created and if it is low then not enough is created but there is a decent range where 1,25(OH)2D production is not affected. We don't necessarily need to take that much to get the full benefits of vD without any of the toxic effects.
Holick is enthusiastic about more though:
The current report of Dudenkov et al1 sheds
light on the appropriateness of the Institute of
Medicine recommendation. Dudenkov et al1
evaluated more than 20,000 25(OH)D measurements performed at Mayo Clinic from 2002
to 2011 and related blood levels of 25(OH)D of
more than 50 ng/mL with potential vitamin D
toxicity (as determined by the presence of hypercalcemia). They observed that from 2002 to
2011, there was a more than 20-fold increase in
the number of individuals with serum 25(OH)D
levels of more than 50 ng/mL; however, elevated
serum 25(OH)D levels were not statistically
significantly related to serum calcium values.
This discovery of Dudenkov et al1 is logical
because the body tightly controls the conversion
of 25(OH)D to 1,25-dihydroxyvitamin D, which
is responsible for regulating calcium metabolism
by enhancing intestinal calcium absorption and
mobilizing calcium from the skeleton. A study of
healthy adults who received 1000 IU of vitamin
D3 daily for 11 weeks and who raised their blood
levels of 25(OH)D from 22.2 13 to 33.6 7.5
ng/mL reported that blood levels of 1,25-
dihydroxyvitamin D did not change: baseline,
35.4 13.0 pg/mL; 11 weeks later, 34.3 13.8
pg/mL.14 Dudenkov et al also found that only 1
person with a serum 25(OH)D level of 364 ng/
mL had evidence of clinical toxicity, that is,
hypercalcemia. For comparison, the Endocrine
Society’s practice guidelines on vitamin D state
that vitamin D intoxication is usually not
observed until serum 25(OH)D levels are more
than 150 ng/mL.
Do you have a reference for that?? I'm joking. Well... maybe only half joking.
Abstract
Large white male turkey poults were fed diets with different levels of vitamins A and D to study the interaction of these vitamins with regard to skeletal development. Poults fed a basal diet deficient in both vitamins A and D developed severe lameness, growth depression, mortality and lesions consistent with rickets. Birds fed a diet containing the required level of viatmin D (900 ICU/kg, NRC estimated requirement) and a high level of vitamin A (400,000 IU/kg) also developed severe lameness, growth depression and a rachiticlike condition, characterized by thicker than normal proximal tibial epiphyseal plates and lower than normal bone mineral content. When fed a diet containing the required level of vitamin A (4,000 IU/kg, NRC estimated requirement) and a high level of vitamin D (900,000 ICU/kg), poults developed hypervitaminosis D as evidenced by mild growth depression and renal tubular mineralization. When poults were fed a diet containing high levels of both vitamins A and D growth rate and bone mineral content were similar to control poults fed a diet containing the required levels of vitamins A and D. In addition, lameness and renal tubular mineralization were not apparent in the poults fed a diet containing high levels of both vitamins A and D. It was concluded that there is an antagonistic interaction between vitamins A and D.
Vitamin A (retinol) plays a crucial role in lung development and cell differentiation and signaling the vitamin D pathway. Vitamin D receptor (VDR) must form a hetero-dimer complex with retinoid X receptor (RXR) to regulate gene transcription. 9-cis-Retinoic acid, an active vitamin A metabolite and the ligand of RXR, assists VDR signaling and suppresses the degradation of circulating vitamin D.
The consumption of vitamin A supplements and animal liver that often contains high levels of vitamin A results in elevated concentrations of active vitamin metabolites including 9-cis-retinoic acid in the body. However, owing to its strong affinity to RXR, excess levels of 9-cis-retinoic acid can form RXR–RXR homodimers and interrupt the dimerization of RXR–VDR and VDR-related transcription.
My comments on the turkey study above:
Excess retinoic acid interferes with vD receptors thus causing birds that were getting sufficient vD to develop rickets. When excess retinoic acid is present it is likely that the body typically responds by elevating levels of calcitriol, the active form of vD. Because calcitriol has a short half life this has the effect of accelerating the depletion of calcidiol, the storage form of vD. By increasing the bird's vD intake, consistently elevated levels of calcitriol were produced which effectively competed against elevated levels of retinoic acid and prevented the development of rickets.
There is evidence that vD toxicity is largely mediated by K2 levels. Excess retinoic acid depletes a range of micronutrients including K2. Counteracting excess retinoic acid with vD probably further accelerates the depletion of certain other micronutrients including K2.
It makes sense for those depleting their vA levels to take some vD (if they aren't getting it from UVB exposure), if they do so it is important to also supplement with K2.
There is no way that beef tallow, lard, coconut oil, refined palm oil or olive oil are problematic from a vA perspective.
On a low vA diet it's only dairy fats that need to be avoided.
@tim-2 I agree. If anything fats like that will promote bile production, bile flow and with soluble fiber it is the best way to detox things like vit A.. I think because Grant is on very low fat diet so long. His bile is not moving at all. I wouldn't be surprised if he gets gallstones or something.. It will be very problematic for him to eat more balanced diet with higher amounts of fat.. Btw I eat a lot of chicken/turkey thighs now and it is interesting that sometimes that fat is white and sometimes yellow.. I rinse that meat during cooking in water. So there is very little fat left after cooking.. Factory farming beef fat is always white and it has good fatty acid profile. So I have no problem eating beef fat.. Poultry higher in vit A and PUFA can be problematic..
Do you have a reference for that?? I'm joking. Well... maybe only half joking."
===> I read that like two years ago on her website:
https://people.csail.mit.edu/seneff/
It is burried somewhere there but honestly I don't know in which article(s) because I don't like supplementing anything at all and go to the sun without cream at midday each time I can and (before Corona) travelled a lot and even spent twice a full year in the tropics with a lot of sunbathing so my vitamin D have never really bothered me.
However, as I was interested in Seneff's work 2-3 years ago I read most of her articles and can remember that at least in one of them she went in great depth and detail about vitamin D through sun vs through skin (sun) and that the form was very different etc (the sun gave a form of D-sulfate through cholesterol sulfate and is the true bioavailable one while supplements are only partially or not at all and could be dangerous in some occasions or something like that). I basically told myself "ok fine I don't like supplements anyway" and went on. So if really interested you'd have to seek there within her papers.
Yep fat is important for bile flow, vD vE and vK absorption and it's an important energy source. My understanding is that low fat diets are a major cause of gallstones.
Yeah I just avoid too much chicken skin. Once I'm vA depleted I'll happily eat chicken skin again though, good source of gelatin.
Ok thanks.