Vitamin K1 Vs. K2 And How Much To Take With Aspirin?

[RealNeat]

Just found a supplement that combines the K forms as @haidut and @Amazoniac were mentioning.

Advanced Triple K 1,050 mcg (K-1) (MK-4) (MK-7)

Per microlingual tablet:
K1 = 500mcg
K2 (4) = 500mcg
K2 (7) = 50mcg

a few added ingredients: Lactose, calcium phosphate, acacia gum.

What do we think of that dosage?

 

[Amazoniac]

Just found a supplement that combines the K forms as @haidut and @Amazoniac were mentioning.

Advanced Triple K 1,050 mcg (K-1) (MK-4) (MK-7)

Per microlingual tablet:
K1 = 500mcg
K2 (4) = 500mcg
K2 (7) = 50mcg

a few added ingredients: Lactose, calcium phosphate, acacia gum.

What do we think of that dosage?

I think it's civilized dosing to start.

Regading aspirin, the main focus should be on prevention of bleeding, not on stopping it.

--
- Multiple Vitamin K Forms Exist in Dairy Foods

Spoiler: Figure 1: Vitamin K content of different cheeses

Spoiler: Figure 2: Vitamin K content of different milks

 

[RealNeat]

I think it's civilized dosing to start.

Regading aspirin, the main focus should be on prevention of bleeding, not on stopping it.

--
- Multiple Vitamin K Forms Exist in Dairy Foods

Spoiler: Figure 1: Vitamin K content of different cheeses

View attachment 14972

Spoiler: Figure 2: Vitamin K content of different milks

View attachment 14973

So in the food context it seems that whole milk is preferable. Im guessing that RP depends mostly on liver for his Ks considering he drinks reduced fat.

 

[Amazoniac]

..should've included these:

Spoiler: Table 2: Vitamin K contents of regular and Greek yogurt

Spoiler: Table 3: Vitamin K contents of dairy products comparing full-, reduced-fat and fat-free products

 

[GreekDemiGod]

Taking Kuinone has greatly improved my Aspirin tolerance. I can take 3 x 500mg in one day (with meals) and not feel anything bad on the stomach, also no case of nose bleeding or such.

 

[Amazoniac]

- Divergent effects of vitamins K1 and K2 on triple negative breast cancer cells

Vitamin K serves as an essential co-factor in the γ-carboxylation of glutamate to γ-carboxyglutamate (GLA), a post-translational modification mediated by gamma-glutamyl carboxylase (GGCX) and vitamin K oxidoreductases (VKORC1 or VKORC1L1). While both phylloquinone (K1) and menaquinone (K2) support the synthesis of GLA-modified proteins, studies assessing K1 and/or K2 effects in cancer cells have reported minimal effects of K1 and anti-proliferative or pro-apoptotic effects of K2. qPCR results indicated highest expression of GGCX, VKORC1, and VKORC1L1 in triple negative breast cancer (TNBC) cell lines, Hs578T, MDA-MB-231 and SUM159PT, and in advanced stage disease. To assess differential effects of vitamin K, TNBC cells were cultured in media supplemented with K1 or K2. K1 treatment increased cell growth, and enhanced stemness and GLA-modified protein expression in TNBC lysates. Alternatively, lysates from cells exposed to vehicle, K2, or the VKOR antagonist, warfarin, did not express GLA-modified proteins. Further, K2 exposure reduced stemness and elicited anti-proliferative effects. These studies show that TNBC cells express a functional vitamin K pathway and that K1 and K2 exert distinct phenotypic effects. Clarification of the mechanisms by which K1 and K2 induce these effects may lead to relevant therapeutic strategies for manipulating this pathway in TNBC patients.

 

[LeeLemonoil]

- Divergent effects of vitamins K1 and K2 on triple negative breast cancer cells

​

Thanks. Highly intriguing and puzzling.

It might have to do with K1s side-chains.

 

[MayaPapaya]

The ability of K1 to do *anything* in the body will be directly affected by one's ability to convert K1 to K2, and then by the amount of carbon dioxide available. This is because before K1 can affect the carboxylation (activation) of proteins involved in *both clotting and bone calcification* it has to be converted to K2.

So, that's really nice if K1 works for some people, but that's not going to be the case for everyone. That's because K1 is converted to K2 by digestive flora and the endogenous enzyme vitamin K epoxide reductase (VKORC1). There are several polymorphisms in the VKORC1 gene which can affect the downstream activation of both enzymes involved in bone calcification (osteocalcin) and clotting (clotting factors). Taking antibiotics or living in a sterile environment can ameliorate K2 levels in rats.

Aspirin specifically works on this system by increasing bleeding, and also inhibiting VKORC1. So, expecting K1 to work -- well, that's basically cheering it on to compete with aspirin to activate rather than inhibit VKORC1. But taking K2 bypasses VKORC1 entirely, ensuring that a certain amount of K works on the gamma glutamyl carboxylase enzyme to carboxylate (activate) downstream processes, whereas that is going to be lessened in the situation where one is taking K1 alone, expecting it to compete with the inhibitor (aspirin) of VKORC1. (I explained this in two different ways in this paragraph, so hopefully that is not too confusing).

There are also potential polymorphisms in the gamma glutamyl carboxylase gene -- the enzyme that carboxylates the downstream proteins involved in both bone calcification and clotting. So, the rate limiting factors for this step are going to be 1) availability of ****K2***** (not K1), 2) availability of CO2, and 3) active gamma glutamyl carboxylase enzyme.

So, in short, in order to increase the likelihood of aspirin not being problematic, one should be taking K2, and being sure to otherwise support respiration such that there would be enough CO2, and be aware that there could be an extra challenge in the sense of gastrointestinal flora or genetics for some individuals. Those individuals might have indication of this possibility through 1) easy bruising, 2) petechiae or other signs of bleeding, 3) gastrointestinal ulceration, or 4) spitting up blood.

Of course, perhaps there are no actual metabolic roadblocks, and a person is just overdosing on aspirin in the face of a deficiency in vitamin K, which could be from eating a low-fat diet, other other drain on the clotting system (years of PUFA), which would decrease both absorption and dietary availability of the nutrient.

But it seems like a no-brainer to me: supplement aspirin, eat low-fat, and either don't take any K, or take mostly K1, and sure, there may be some ulceration or bleeding problems. Or development of cavities or bone fractures.

A better course of action is probably to supplement K2, eat a moderate amount of fat, and supplement aspirin after establishing this groundwork

I was taking Aspirin 325, and recently slowly increased it to two times a day. Also I take MK7 180mcg x 3 capsules with Vitamin D at lunch, and Mg Pico-Ionic in the evening. So far no bleeding noted. Thank you very much for a very informative post.