Vitamin health benefits,foods burn fat cells,loss weight program philippines,simple diets to follow - Step 1

Author: admin, 08.03.2015
Warfarin functions by inhibiting vitamin K epoxide reductase, which halts the recycling of vitamin K and subsequently prevents the synthesis of vitamin-K-dependent coagulation factors II, VII, IX, and X. Based on the above data, it can be hypothesized that vitamin K supplementation is particularly useful in achieving therapeutic stability in patients with low vitamin K intake. It is clear from the research outlined here that cutting out vitamin K is not the answer for achieving stable anticoagulation.
In summary, patients no longer have an excuse to avoid leafy green vegetables, missing out on all the other nutrients they harbor as well as vitamin K’s role in slowing vascular calcification[10]. It is well known that intestinal microflora produce several vitamins like b12, folic acid and the Vit K.
As a result, for probably the first time since childhood, patients are steered away from all dark green vegetables, which are rich in the vitamin K that blunts the anticoagulant effect of warfarin, lowering the international normalized ratio (INR). Such advice may be setting up patients for a widely variable and difficult to manage INR.  Low-dose vitamin K supplementation may actually improve the stability of anticoagulation therapy. In such patients, daily fluctuations in vitamin K intake lead to significant and proportional changes in INR that can be avoided by oral supplementation.[3] A 2007 study by Sconce and colleagues put this hypothesis to the test in the first randomized, blinded, placebo-controlled trial investigating the effects of vitamin K supplementation in 70 unstable patients over 6 months. Instead, inform your patients of the vitamin-K rich foods and advise them to maintain a steady dietary pattern. Vitamin K will help rather than hinder the chances of achieving long-term stable anticoagulation. Becker’s excellent review of dietary and supplemental vitamin K intake in patients requiring warfarin is most welcome.


Therefore it is quite strange to exclude veggies while our internal microflora produce this vitamin to assist with the coagulation.
However, once one controls for these variables, oral intake of vitamin K persists as an integral factor in anticoagulation stability.
When patients with unstable anticoagulation were given 150 mcg of vitamin K supplementation per day, they spent a greater amount of time within target INR range and had decreased daily variability in INR when compared with placebo.[2] These findings were consistent with other literature including a 2005 trial by Reese and colleagues[7] as well as a 2007 study by Rombouts and colleagues[8] using phenprocoumon (a longer-acting vitamin K antagonist) as the anticoagulation agent.
If a patient has a consistent diet and all other causes of instability have been eliminated, try vitamin K supplementation. Based upon estimates of fresh food availability, the citizens of New York City probably have a high rate of relative vitamin K deficiency.
Vitamin K supplementation can improve stability of anticoagulation for patients with unexplained variability in response to warfarin.
Over-the-counter vitamin K1-containing multivitamin supplements disrupt warfarin anticoagulation in vitamin K1-depleted patients. Patients with unstable control have a poorer dietary intake of vitamin K compared to patients with stable control of anticoagulation. Relationship between dietary vitamin K intake and the stability of anticoagulation effect in patients taking long-term warfarin. Vitamin K1 supplementation to improve stability of anticoagulation therapy with vitamin K antagonists: a dose-finding study. Pharmacology and management of the vitamin K antagonists: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition).


Finally, a recent 2010 study by Gebuis and colleagues looked at patients taking phenprocoumon or acenocoumarol and compared the effects of placebo with 100-, 150-, or 200-mcg vitamin K supplementation. Vitamin K1, which accounts for approximately 95% of our vitamin K intake, is most readily available in leafy green vegetables.
Although the supplementation provided improved stability, there was little difference between the doses.[9] Ultimately, low-dose vitamin K supplementation, regardless of dose, was shown to improve therapeutic stability in patients with unstable anticoagulation with warfarin or its derivatives. Approximately 3 million people living in New York City live in “food deserts,” where there is limited availability of fresh or healthy food.  Patients who reside in food deserts probably have low vitamin K intake and higher variability in warfarin requirements, like the subjects in the articles by Sconce [5] and Kim [6]. Although genotype can aid in determining anticoagulation initiation doses by being plugged into dose-optimizing algorithms, genotype is not a factor in the ability to maintain stability once it is achieved.[6] On the other hand, vitamin K intake still plays an independent role and thus represents a controllable factor that we can manipulate to improve stability.
Alternatively, vitamin K 100 microgram supplements may be had for approximately $4 for 100 tablets. The largest benefit with vitamin supplementation occurred in studies that excluded patients with other obvious reasons for variability of INR (eg, alcohol abuse, medication non-adherence, and changes in concurrent medications).



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