I needed to disable self sign-ups because I’ve been getting too many spam-type accounts. Thanks.
A lowers K2, D raises it
Quote from tim on July 10, 2019, 12:28 amChris Masterjohn is trying very hard here to rationalize away these researcher's findings that VA depletes K2.
https://chrismasterjohnphd.com/blog/2009/04/07/tufts-university-confirms-that-vitamin/
The authors made another interesting observation that I had not hypothesized: vitamins A and D appear to increase the turnover of vitamin K and the conversion of vitamin K1 to vitamin K2. In the D group, liver stores of K1 were reduced and kidney levels of MK-4, the form of vitamin K2 that animals synthesize, were increased. All A groups, whether the A was given alone or in combination with D, had reductions in both K1 and MK-4 levels. The authors referred to this as “antagonism” between vitamins A and K, but since vitamin A improved vitamin K-dependent activation of MGP, could it not be that the reduction in K1 was due to conversion of K1 to MK-4 and that the reduction in MK-4 was due to increased utilization and turnover of MK-4? The authors never suggested that vitamin D “antagonizes” vitamin K1, for example, even though its levels were reduced.
The researchers showed clearly that D raises K2 levels (I assume by assisting conversion of K1 to K2) while A lowers them:
https://www.ncbi.nlm.nih.gov/pubmed/19022954
Although all diets contained equal amounts of PK, the kidney MK-4 concentration was higher in the D group (P < 0.05) and lower in the RA group (P < 0.05) compared with the RA+D or control groups.
Chris Masterjohn is trying very hard here to rationalize away these researcher's findings that VA depletes K2.
https://chrismasterjohnphd.com/blog/2009/04/07/tufts-university-confirms-that-vitamin/
The authors made another interesting observation that I had not hypothesized: vitamins A and D appear to increase the turnover of vitamin K and the conversion of vitamin K1 to vitamin K2. In the D group, liver stores of K1 were reduced and kidney levels of MK-4, the form of vitamin K2 that animals synthesize, were increased. All A groups, whether the A was given alone or in combination with D, had reductions in both K1 and MK-4 levels. The authors referred to this as “antagonism” between vitamins A and K, but since vitamin A improved vitamin K-dependent activation of MGP, could it not be that the reduction in K1 was due to conversion of K1 to MK-4 and that the reduction in MK-4 was due to increased utilization and turnover of MK-4? The authors never suggested that vitamin D “antagonizes” vitamin K1, for example, even though its levels were reduced.
The researchers showed clearly that D raises K2 levels (I assume by assisting conversion of K1 to K2) while A lowers them:
https://www.ncbi.nlm.nih.gov/pubmed/19022954
Although all diets contained equal amounts of PK, the kidney MK-4 concentration was higher in the D group (P < 0.05) and lower in the RA group (P < 0.05) compared with the RA+D or control groups.
Quote from collden on July 10, 2019, 5:46 amInteresting, ever since learning that the science on the nutritional needs of VA is so dodgy I've been skeptical about our needs for Vitamin K as well, it seems deficiency of VK is extremely rare and has hardly ever been described in adult humans.
There are very few foods that contain significant amounts of VK that are not also rich in VA, cabbage might be one, so I guess anyone doing a low-VA diet is also doing a low-VK diet.
Interesting, ever since learning that the science on the nutritional needs of VA is so dodgy I've been skeptical about our needs for Vitamin K as well, it seems deficiency of VK is extremely rare and has hardly ever been described in adult humans.
There are very few foods that contain significant amounts of VK that are not also rich in VA, cabbage might be one, so I guess anyone doing a low-VA diet is also doing a low-VK diet.
Quote from tim on July 10, 2019, 7:27 amHi @collden,
Some vegetable oils like olive, soy and canola oil (not arguing soy and canola are healthy) contain a significant amount of K1 and are zero A. Lard is a good source of K2 MK-4. Chicken is a good source of K2 MK-4 due to the supplements they receive.
When you say VK are you thinking of the menaquinones/K2 as well as phylloquinone/K1? My understanding is that K1 deficiency is very rare however I find it plausible that K2 deficiency is common. This could be due to lack of K2 in the diet but also A toxicity. My impression is that from the current level of research done I think it's hard to come to any solid conclusions.
Here's some info I've looked at:
The Prevalence of Vitamin K Deficiency/Insufficiency, and Recommendations for Increased Intake:
Furthermore, with respect to chemical structure and pharmacokinetics which affects bioavailability, metabolism and perhaps impact on health outcomes, there are differences between two distinct forms of vitamin K: vitamin K1 (phylloquinone) and vitamin K2 (menaquinone). These differences led Beulens et al., [4] to suggest that further investigations should be undertaken to determine whether a new daily intake level for vitamin K should consider each of these two forms.
Vitamin K’s bioavailability from food is poor, and this nutrient has small circulating in the blood compared to the other fat-soluble vitamins, is quickly metabolized and excreted, and has low tissue stores. Data indicates that measurements of prothrombin time, typically used to assess vitamin K status, is not a particularly accurate method for doing so, and that measurements of circulating undercarboxylated MGP levels is a more effective method.Use of this more accurate method has shown that some vitamin k deficiency or insufficiency has been seen in 97% of older subjects in a mixed population. Furthermore, research suggests that supplementation with 180μg/day vitamin K2 is associated with improved bone mineral retention and a decrease in arterial calcification.Considering the benefits associated with a higher intake of vitamin K2, and the lack of toxicity, it seems reasonable to suggest that recommendations for vitamin K2 be increased to 180μg/day for adults, up from its current adequate intake levels of 90-120μg/day for women and men, respectively
In the population-based Rotterdam study, [33] which included 4807 subjects, dietary menaquinone intake was inversely related to all-cause mortality and severe aortic calcification, but phylloquinone intake was not related to any of the outcomes. Similarly, in a cross-sectional study [34] among 564 postmenopausal women found that menaquinone intake, but not phylloquinone intake, was associated with decreased relative risk of coronary calcification (p=0.03).
On the Innovix Labs site which sells a lot of K2 I found this:
https://innovixlabs.com/blogs/insights/vitamin-k2-deficiency
'Yeah but,' you say, 'doesn't our gut bacteria convert our abundant K1 into K2?' Maybe. There may be some of that going on too, but when people were given K2 restricted diet, deficiency developed quickly and gut bacteria did not come to the rescue. This means are we still diet-dependent on K2.
This is the reference used for "deficiency developed quickly":
https://www.ncbi.nlm.nih.gov/pubmed/8527227
Abstract
Bacterially produced menaquinones, 2-methyl-1,4-naphthoquinones with an unsaturated polyisoprenoid chain at the 3-position, are biologically active forms of vitamin K that are present in high concentrations in the human lower bowel. Menaquinones are found in human liver and circulate in human plasma at much higher concentrations than previously thought. Numerous case reports of antibiotic-induced, vitamin K-responsive hypothrombinemias have been taken as evidence that menaquinones contribute importantly to satisfying the human vitamin K requirement. However, more recent production of symptoms of vitamin K insufficiency in normal human subjects by dietary restriction of vitamin K argues against their nutritional significance. Current data support the view that menaquinones may partially satisfy the human requirement but that their contribution is much less than previously thought.I don't know if they are referencing something that is not in the abstract but if they are just using the abstract as a reference then I think it's a bit flimsy. It isn't really clear what type of K they are restricting here. I hope this potential misreference isn't fraudulent.
Hi @collden,
Some vegetable oils like olive, soy and canola oil (not arguing soy and canola are healthy) contain a significant amount of K1 and are zero A. Lard is a good source of K2 MK-4. Chicken is a good source of K2 MK-4 due to the supplements they receive.
When you say VK are you thinking of the menaquinones/K2 as well as phylloquinone/K1? My understanding is that K1 deficiency is very rare however I find it plausible that K2 deficiency is common. This could be due to lack of K2 in the diet but also A toxicity. My impression is that from the current level of research done I think it's hard to come to any solid conclusions.
Here's some info I've looked at:
The Prevalence of Vitamin K Deficiency/Insufficiency, and Recommendations for Increased Intake:
Furthermore, with respect to chemical structure and pharmacokinetics which affects bioavailability, metabolism and perhaps impact on health outcomes, there are differences between two distinct forms of vitamin K: vitamin K1 (phylloquinone) and vitamin K2 (menaquinone). These differences led Beulens et al., [4] to suggest that further investigations should be undertaken to determine whether a new daily intake level for vitamin K should consider each of these two forms.
Vitamin K’s bioavailability from food is poor, and this nutrient has small circulating in the blood compared to the other fat-soluble vitamins, is quickly metabolized and excreted, and has low tissue stores. Data indicates that measurements of prothrombin time, typically used to assess vitamin K status, is not a particularly accurate method for doing so, and that measurements of circulating undercarboxylated MGP levels is a more effective method.Use of this more accurate method has shown that some vitamin k deficiency or insufficiency has been seen in 97% of older subjects in a mixed population. Furthermore, research suggests that supplementation with 180μg/day vitamin K2 is associated with improved bone mineral retention and a decrease in arterial calcification.Considering the benefits associated with a higher intake of vitamin K2, and the lack of toxicity, it seems reasonable to suggest that recommendations for vitamin K2 be increased to 180μg/day for adults, up from its current adequate intake levels of 90-120μg/day for women and men, respectively
In the population-based Rotterdam study, [33] which included 4807 subjects, dietary menaquinone intake was inversely related to all-cause mortality and severe aortic calcification, but phylloquinone intake was not related to any of the outcomes. Similarly, in a cross-sectional study [34] among 564 postmenopausal women found that menaquinone intake, but not phylloquinone intake, was associated with decreased relative risk of coronary calcification (p=0.03).
On the Innovix Labs site which sells a lot of K2 I found this:
https://innovixlabs.com/blogs/insights/vitamin-k2-deficiency
'Yeah but,' you say, 'doesn't our gut bacteria convert our abundant K1 into K2?' Maybe. There may be some of that going on too, but when people were given K2 restricted diet, deficiency developed quickly and gut bacteria did not come to the rescue. This means are we still diet-dependent on K2.
This is the reference used for "deficiency developed quickly":
https://www.ncbi.nlm.nih.gov/pubmed/8527227
Abstract
Bacterially produced menaquinones, 2-methyl-1,4-naphthoquinones with an unsaturated polyisoprenoid chain at the 3-position, are biologically active forms of vitamin K that are present in high concentrations in the human lower bowel. Menaquinones are found in human liver and circulate in human plasma at much higher concentrations than previously thought. Numerous case reports of antibiotic-induced, vitamin K-responsive hypothrombinemias have been taken as evidence that menaquinones contribute importantly to satisfying the human vitamin K requirement. However, more recent production of symptoms of vitamin K insufficiency in normal human subjects by dietary restriction of vitamin K argues against their nutritional significance. Current data support the view that menaquinones may partially satisfy the human requirement but that their contribution is much less than previously thought.
I don't know if they are referencing something that is not in the abstract but if they are just using the abstract as a reference then I think it's a bit flimsy. It isn't really clear what type of K they are restricting here. I hope this potential misreference isn't fraudulent.
Quote from tim on July 14, 2019, 2:43 amThe following amounts are the RDA's of the different fat soluble vitamins in micrograms for an adult man:
A: 900
D: 15
E: 15,000
K: 120These differences will be due to different perceived physiological needs and also molecular size. Given the close relationship of A with D and K though I do wonder about the wisdom of those ratios and how that much A will affect D and K.
The following amounts are the RDA's of the different fat soluble vitamins in micrograms for an adult man:
A: 900
D: 15
E: 15,000
K: 120
These differences will be due to different perceived physiological needs and also molecular size. Given the close relationship of A with D and K though I do wonder about the wisdom of those ratios and how that much A will affect D and K.
Quote from bludicka on July 14, 2019, 3:51 am"I've been skeptical about our needs for Vitamin K as well, it seems deficiency of VK is extremely rare... There are very few foods that contain significant amounts of VK"
This was my idea recently too.... With K1 is no problem, there is a large amount in vegetables but MK-4 - these are micrograms found in the foods 1-20 mcg max. 60 mcg in chicken leg, only goose liver has more but as a nutritional supplement it is sold in mg 1-5 mg (it is produced synthetically from tobacco leaves)- these are supraphysiological doses. The same problem with mk-7, the only major source is natto, otherwise the food does not contain it much but supraphysiological doses of mk-7 are sold and many people have problems with mk-7 toxicity from these supplements, it happend to me. When I believed that I needed some ideal ratio of all three fat-soluble vitamins A-D-K, the only one I really needed more was the vitamin D ( and there was a cause) and a very little vitamin K.
Now when I eat a little vegetables, I supplement K1 200mcg 2xa week, later I will add sauerkraut and more vegetables.I think vitamin A antagonizes vitamin E too, every time I take Solgar vitamin E 100 IU, I have a soft skin for a while, but in a few hours, dry skin and hair again.
"I've been skeptical about our needs for Vitamin K as well, it seems deficiency of VK is extremely rare... There are very few foods that contain significant amounts of VK"
This was my idea recently too.... With K1 is no problem, there is a large amount in vegetables but MK-4 - these are micrograms found in the foods 1-20 mcg max. 60 mcg in chicken leg, only goose liver has more but as a nutritional supplement it is sold in mg 1-5 mg (it is produced synthetically from tobacco leaves)- these are supraphysiological doses. The same problem with mk-7, the only major source is natto, otherwise the food does not contain it much but supraphysiological doses of mk-7 are sold and many people have problems with mk-7 toxicity from these supplements, it happend to me. When I believed that I needed some ideal ratio of all three fat-soluble vitamins A-D-K, the only one I really needed more was the vitamin D ( and there was a cause) and a very little vitamin K.
Quote from tim on July 14, 2019, 5:03 amK1 and K2 are a bit like beta-carotene and retinol, K1 is from plants and plays a role in our physiology but isn't as useful as K2 whereas K2 is the active animal form. Some K1 converts to K2 MK-4 in our body but studies have shown no benefit from K1 vs a very significant benefit from K2 supplementation indicating that K2 is likely an essential nutrient in addition to K1. This isn't very surprising given that animal fat which contains K2 was consumed by humans throughout all of known history.
When our D levels are adequate and we are not toxic with A then the conversion of K1 to K2 is increased and less K2 is depleted within the body.
https://lpi.oregonstate.edu/mic/vitamins/vitamin-K
Although vitamin K is a fat-soluble vitamin, the body stores very small amounts that are rapidly depleted without regular dietary intake.
It makes sense to me to consume lard/tallow and chicken for K2 and some cabbage, herb seasoning and olive/vegetable oil for K1.
K1 and K2 are a bit like beta-carotene and retinol, K1 is from plants and plays a role in our physiology but isn't as useful as K2 whereas K2 is the active animal form. Some K1 converts to K2 MK-4 in our body but studies have shown no benefit from K1 vs a very significant benefit from K2 supplementation indicating that K2 is likely an essential nutrient in addition to K1. This isn't very surprising given that animal fat which contains K2 was consumed by humans throughout all of known history.
When our D levels are adequate and we are not toxic with A then the conversion of K1 to K2 is increased and less K2 is depleted within the body.
https://lpi.oregonstate.edu/mic/vitamins/vitamin-K
Although vitamin K is a fat-soluble vitamin, the body stores very small amounts that are rapidly depleted without regular dietary intake.
It makes sense to me to consume lard/tallow and chicken for K2 and some cabbage, herb seasoning and olive/vegetable oil for K1.
Quote from bludicka on July 14, 2019, 5:09 amChris Masterjohn takes daily 1 mg of K2 MK-4 - you will never find such a high dose in natural sources. He is the main proponent of this vitamin and vitamin A too. (https://chrismasterjohnphd.com/blog/2016/12/09/the-ultimate-vitamin-k2-resource/)
"I have a genetic polymorphism in the enzyme vitamin K epoxide oxidoreductase (VKOR), which decreases the rate at which I recycle vitamin K and presumably increases my dietary need for the vitamin. I suspect this is part of why I am so vulnerable to tooth decay when the nutrient density of my diet is suboptimal. I therefore take 1 mg/day of Thorne vitamin K2 as insurance."
https://chrismasterjohnphd.com/what-chrismasterjohn-does/2016/06/20/nutritional-supplements-i-take/
Mk-7 - it can stay in the body for up to four days and gradually builds up to a toxic level. My side effects were heart palpitations and symtoms of acute calcium deficiency.
Lara Pizzorno, the author of "Your Bones," says that about 1/3 of the population has a genetic inability to quickly process MK7, so it builds up in their systems and causes side effects. Those people--and I am one of them--do better using MK4. Apparently, the other 2/3 can use MK7 with no problem. Research on this is new and still underway.
Chris Masterjohn takes daily 1 mg of K2 MK-4 - you will never find such a high dose in natural sources. He is the main proponent of this vitamin and vitamin A too. (https://chrismasterjohnphd.com/blog/2016/12/09/the-ultimate-vitamin-k2-resource/)
"I have a genetic polymorphism in the enzyme vitamin K epoxide oxidoreductase (VKOR), which decreases the rate at which I recycle vitamin K and presumably increases my dietary need for the vitamin. I suspect this is part of why I am so vulnerable to tooth decay when the nutrient density of my diet is suboptimal. I therefore take 1 mg/day of Thorne vitamin K2 as insurance."
https://chrismasterjohnphd.com/what-chrismasterjohn-does/2016/06/20/nutritional-supplements-i-take/
Mk-7 - it can stay in the body for up to four days and gradually builds up to a toxic level. My side effects were heart palpitations and symtoms of acute calcium deficiency.
Lara Pizzorno, the author of "Your Bones," says that about 1/3 of the population has a genetic inability to quickly process MK7, so it builds up in their systems and causes side effects. Those people--and I am one of them--do better using MK4. Apparently, the other 2/3 can use MK7 with no problem. Research on this is new and still underway.
Quote from bludicka on July 14, 2019, 5:17 am"Some K1 converts to K2 MK-4 in our body but studies have shown no benefit from K1 vs a very significant benefit from K2 supplementation indicating that K2 is likely an essential nutrient in addition to K1."
I was taking K2 MK-4 Thorne and Carlson the last years (I switched from mk-7 to mk-4)... I've never seen anything negative and positive... I stopped it completly.
"Some K1 converts to K2 MK-4 in our body but studies have shown no benefit from K1 vs a very significant benefit from K2 supplementation indicating that K2 is likely an essential nutrient in addition to K1."
I was taking K2 MK-4 Thorne and Carlson the last years (I switched from mk-7 to mk-4)... I've never seen anything negative and positive... I stopped it completly.
Quote from tim on July 14, 2019, 5:38 am@bludicka
I am opposed to supplementation of anything except D.
K2 is something that just needs to be in adequate supply on a daily basis throughout your life. I wouldn't really expect to see any obvious results from supplementation for a period. In studies it has shown benefits for heart disease and other problems.
I am opposed to supplementation of anything except D.
K2 is something that just needs to be in adequate supply on a daily basis throughout your life. I wouldn't really expect to see any obvious results from supplementation for a period. In studies it has shown benefits for heart disease and other problems.