Results for : "Vitamin k"
During a recent group meeting, questions were raised regarding supplementing with Vitamin K1 or Vitamin K2 along with anticoagulant treatment. The table below provides a generalized summary of the Vitamin K1 and K2. The forms of Vitamin K in dietary supplements may differ depending on the supplement and the choice of the supplements may affect their absorptive behavior. This creates a challenge in regulating lab values, especially in patient who require anticoagulation therapy.
In summary K1 and K2 counteract the function of the anticoagulant medications. You should consult the physician prescribing the anticoagulant before taking any vitamin K1 or K2. Even as we think of K2 having less to do with coagulation pathways, it is recommended that the patients do not take any vitamin K supplements unless cleared by their physician, since K2 may also affect the anticoagulation treatment. As a patient who is prescribed anticoagulation treatment you should make your prescribing physician aware of ANY changes in your medications or supplements either over the counter or prescribed.
Vitamin K1 is a found in dark green leafy vegetables, asparagus, brussels sprouts, some grains, olive oil, prunes, soy bean oil, and canola oil. The body has limited storage capacity for Vitamin K and uses a recycle system to reuse it.
Vitamin K1 is a fat-soluble vitamin that after Duodenal Switch is not as easily absorbed due to the limiting contact of the food product with the bile until the common channel. Bile is needed to absorb fatty acids and fat-soluble vitamins.
Duodenal Switch patients in need of Vitamin K1 supplements should take “Dry” or water miscible type of Vitamin K1, such as Biotech brand. The patients laboratory studies will determine if a patient requires Vitamin K1 supplement. Duodenal Switch patients should have laboratory studies drawn and evaluated at least on a yearly basis. Vitamin K works in a delicate balance with other supplements and should be monitored by a physician, in at risk people.
Vitamin K1 is most know for it’s coagulation effect and the clotting cascade. Vitamin K1 works with calcium and proteins in order to accomplish coagulation synethesis. Care should be taken with Vitamin K supplementation and anti-coagulation (blood thinners) therapy. Please see your physician regarding any supplementation of Vitamin K and blood thinner medications.
A discovery of Vitamin K dependent proteins has led to research on Vitamin K1 in bone health. Bone matrix proteins, specifically osteocalcin, undergo gamma carboxylation with calcium much the way coagulation factors do; this process also requires Vitamin K. Osteocalcin is a Gla-protein that is regulated by Vitamin D. The calcium binding ability of osteocalcin requires several Vitamin K carboxylations to exert it’s effects on bone mineralization.
In adults, the causes of Vitamin K1 deficiency include the following :
Multiple abdominal surgeries
Long-term parenteral nutrition
Parenchymal liver disease
Inflammatory bowel disease
Medications: Antibiotics (cephalosporin), cholestyramines, warfarin, salicylates, anticonvulsants, Cefamandole, cefoperazone, salicylates, hydantoins, rifampin, isoniazid, barbiturates, and certain sulfa drugs, higher Vitamin E can antagonized Vitamin K)
Disseminated intravascular coagulation (DIC) – Severe
Chronic kidney disease/hemodialysis
Additional information: https://lpi.oregonstate.edu/infocenter/vitamins/vitaminK/
As always, discuss with your physicians and/or surgeon any changes in medications and supplements. This is not meant to be an all inclusive discussion of Vitamin K.
Vitamin A is one of the 4 fat soluble vitamins along with vitamin D, Vitamin E and Vitamin K. It is multifunctional and essential which means that it is not produced by the body. In this article we will touch on aspects of Vitamin A absorption and it’s effect on wound healing as well as its metabolism.
We often think of Vitamin A as the critical vitamin for vision, however it has several other roles that related to immune function, protein synthesis, and cellular communication. Vitamin A deficiency is a concern world wide because of the natural of the side effects. Vitamin A deficiency is the leading cause of preventable childhood blindness in the world according to UNICEF and sometimes it may be undetected until there is irreversible damage.
There are 2 chemical forms of vitamin A in diet:
Retinoids (Preformed vitamin A) This group include retinol, retinyl esters, and retinal they are mostly found in animal sources like liver, egg yolk or fish oils.
Carotenoids (Provitamin A) This group includes beta-carotene, alpha-carotene and lycopene, mainly found in plant sources like leafy vegetables or yellow/orange vegetables and fruits.
1.- Ingested food is digested in the stomach where retinyl palmitates (esters) are released from proteins. Retinol and beta-carotene are absorbed directly into the small intestine where retinyl esters and betacarotene are transformed into retinol . Retinol is the most easily absorbed form of vitamin A.
2.-That retinol absorbed by the enterocytes in the ileum (small intestine) along with bile is then transported to the liver with the help of chylomicrons a protein that transports fat.
3.-Fifty to 80% of the vitamin A is stored in the liver and the remaining is deposited into adipose tissue, lungs and kidneys.
4.-When stored retinol is released from the liver into the circulation to target organs, it is bound to plasma retinol-binding protein (RBP4) a transporting protein produced by the liver that requires ZINC, which is synthesized by the liver; This complex is stabilized by transthyretin (TTR), which reduces renal excretion.
Retinol is a crucial component for reproduction, embryological development, cellular differentiation, growth, protein synthesis, and immunity in the form of retinoic acid and vision in the form of retinal.
One of Vitamin A additional roles is in epithelial health of skin and mucous membranes. It increases epithelial turnover which is crucial during would healing. It also has anti-oxidative effects which prevent cell damage and can prevent or reverse the effects of other damaging agents. In addition to these benefits it has also been associated with increasing collagen, fibronectin, keratinocytes and fibroblast, all important in wound tissue structure. There have been some studies that suggest giving higher doses of Vitamin A in patients with non or slow healing wounds.
It is important to remember that we have documents delayed diagnosis of adult vitamin A deficiency leading to significant night blindness in adults. It is critical that the patients and their primary care physicians are acutely aware of this possibility. In majority of the patients with low vitamin A, post weight loss surgery, aggressive supplementations, including injections need to be considered as a part of the treatment regimen.
We would like to thank Miguel Rosado, MD for his significant contribution provided for this Blog.
Unfortunately, we have been informed that the company we order our Vitamin A injections from will no longer have Vitamin A available. We have contacted several other companies and they also do not have it available. The manufacturer of Vitamin A states that there is a nationwide shortage of injectable Vitamin A and it may be available next year.
Our office has a few vials left and we are hoping that we can get to as many people as possible before we are completely out. We will continue to look for a source of Vitamin A injections. We will let you know when it is no longer available and when we receive a new shipment. Thank you for your understanding and we apologize for this issue.
Information on Vitamin A deficiency here.
You can find our list of recommended supplements here.
Just as a reminder, we have no financial interest in any of the vendors that are recommended on our website. Also, please note that this is not in ANY form or fashion a substitute for the evaluation by your surgeon or primary care physician. This is informational only and is not to be taken as a recommendation for any patients’ condition.
Many people with obesity face infertility issues and seek infertility treatment or procedures. A recent article linked Vitamin D status to improved success rate of IVF (in-vito fertilization) & ICSI (interacytoplasmic sperm injection) in The Journal of Maternal-Fetal & Neonatal Medicine. It is important to check Vitamin D status for infertility treatment.
Here are the researchers results:
- Of the 252 females that completed the ICSI cycle, 42% became pregnant (n = 108).
- The mean vitamin D status was significantly higher in the pregnant group compared to the non-pregnant group (17.74 ng/ml vs 9 ng/ml, respectively; p = < 0.01).
- Vitamin D status was positively associated with both pregnancy (p = 0.001) and endometrial thickness (p < 0.01).
- Higher vitamin D levels was associated with a 21% increase odds of clinical pregnancy (p < 0.05).
The researchers concluded,
“Deficiency of 25-OHD in females hinders the accomplishment of optimal endometrial thickness required for implantation of embryo after ICSI.”
Following weight loss surgery (WLS) there can be improvement of fertility and for that reason we recommend two forms of birth control methods during the first 18-24 months following WLS or until weight loss has stabilized for several months. This helps to ensure the best outcome and health for the mother and infant.
In our office we continue to stress the importance of Vitamin D3 for bone and dental health, pregnancy, breastfeeding and several auto-immune diseases. Vitamin D has also been shown to reduce pre-term birth Duodenal Switch patients require a dry water miscible form of Vitamin D3 due to the fat malabsorption of the DS procedure. There are several past blog posts on the topic of Vitamin D and it’s associated nutrients.
Thank you to Contributor: Mariam Michelle Gyulnazaryan
Vitamins are organic, essential nutrients that are necessary to keep your body in good health. Most vitamins must be obtained through diet because they cannot be synthesized in the body. However, the human body is able to make its own vitamin D in the skin through sun exposure or it can be obtained by food and supplements of Vitamin D3.
Vitamin D is a fat-soluble vitamin that is responsible for regulating muscle contraction, immune function, bone health, and intestinal absorption of magnesium, calcium, phosphate, iron, and zinc. Good sources of Vitamin D include sun exposure, dairy products, fatty fish, fortified orange juice, cod liver oil, mushrooms, and supplements.
There are two types of Vitamin D: D2 (ergocalciferol) and D3 (cholecalciferol). Both types have the same mechanism of action, but different sources and kinetics.
Ergocalciferol is easily obtained through Vitamin D-rich foods in normal anatomy. However, a post Duodenal Switch patient will have less absorption of Vitamin D via food due to fat malabsorption. Ergocalciferol is hydroxylated to ercalcidiol [25(OH)D2] in the liver. Its second hydroxylation takes places in the kidney, where it is converted to the active form of Vitamin D2 known as ercalcitriol [1,25(OH)2D2]. Now in it’s active form, Vitamin D2 can bind to the Vitamin D receptor (VDR) and help the body where it’s needed.
In the epidermis of the skin, precursor 7-dehydrocholesterol (7-DHC) forms cholecalciferol as a result of UVB radiation. Several factors such as increased skin pigmentation, age, and sunscreen application reduce the skin’s production of choleciferol (6). Cholecalciferol is hydroxylated in the liver to become calcidiol [25(OH)D3]. It is then moved to the kidney for further hydroxylation to Vitamin D3’s active form known as calcitriol [1,25(OH)2D3], also called calcifediol. The active form allows binding to VDR for biological activity.
Both forms of Vitamin D have been shown to effectively increase 25(OH)D levels. Research shows that after administering a single dose of 50,000 international units (IU) Vitamin D2 or D3, both experienced a similar increase in serum 25(OH)D concentration. However, Vitamin D2 levels rapidly declined while Vitamin D3 levels remained high (1). Further studies have confirmed that Vitamin D3 is more effective in elevating and maintaining 25(OH)D levels for a longer amount of time (5). Scientists believe the most reasonable explanation for Vitamin D3’s substantial efficacy is its higher affinity to metabolites, which results in a longer circulating half-life than Vitamin D2 making it more potent(4). For a post Duodenal Switch patient, due to fat malabsorption, it is important to use “Dry” Water Miscible form of Vitamin D3.
A 25-hydroxy Vitamin D blood test is the most accurate way to measure levels. A level between 20 ng/mL-50 ng/mL may be considered sufficient, however in our bariatric practice we would like to keep the levels in 60-80 ng/mL. It is worth nothing that recently the reference ranges was increase to 30-100 ng/mL. Treatments of Vitamin D deficiency include frequent sun exposure, fortified foods, supplements, and injectables. in addition to 50000IU of vitamin D on daily basis in emulsified (water soluble) formulary or unto 600,000IU in injection form. The parallel guide for adequate vitamin D supplementation is normalization of PTH levels. Monitoring these levels is imperative in a post bariatric patient.
In conclusion, studies have shown that Vitamin D2 and D3 are not interchangeable. Although they have comparable absorption, Vitamin D2 has a shorter duration of action which makes it less potent than Vitamin D3. Researchers have shown that neither form is harmful to treat Vitamin D deficiency, but they should not be considered bio-equivalent.
1. Armas LAG, Hollis BW, Heaney RP. Vitamin D2 is much less effective than Vitamin D3 in humans. Journal of Clinical Endocrinology & Metabolism. 2004; 89(11) 5387-5391.
2. Creighton D, Ignaszewski A, Francis G. Vitamin D: new d-fence against cardiovascular disease. BCMJ. 2012; 54(3) 136-140.
3. Holick MF, Schnoes HK, DeLuca HF. Identification of 1,25-Dihydroxycholecalciferol, a form of Vitamin D3 metabolically active in the intestine. PNAS. 1971; 68(4) 803-804.
4. Hollis BW. Comparison of equilibrium and disequilibrium assay conditions for ergocalciferol, cholecalciferol and their major metabolites. J Steroid Biochem. 1984; 21(1) 81-86.
5. Houghton LA, Vieth R. The case against ergocalciferol (Vitamin D2) as a vitamin supplement. Am J Clin Nutr. 2006; 84 (4): 694-697.
6. Howick Mf, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, Murad MH, Weaver CM. Evaluation, treatment and prevention of Vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2011; 96(7) 1911-1930.
7. Johal M, Levin A. Vitamin D and Parathyroid Hormone in general populations: understandings in 2009 and applications to chronic kidney disease. CJASN. 2009; 4(9) 1508-1514.
8. Tetley EA, Brule D, Cheney MC, Davis Cd, Esslingen KA, Fischer PWF, Friedl KE, Green-Finestone LA, Guenther PM, Klurfeld DM, L’Abbe MR, McMurry KY, Starke-Reed PE, Trumbo PR. Dietary reference intakes for Vitamin D: justification for a review of the 1997 values. Am J Clin Nutr. 2009; 89(3) 719-727.
9. Tripkovic L, Lambert H, Hard K, Smith CP, Bucca G, Penson S, Chope G, Hypponen E, Berry J, Vieth R, Lanham-New S. Comparison of Vitamin D2 and Vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: a systematic review and meta-analysis. Am J Clin Nutr. 2012; 95(6) 1357-1364.