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The Complete Guide to Vitamin K: Types, Benefits, and Deficiency

Vitamin K is a fat-soluble vitamin crucial for several psychological processes beyond its conventional link with blood coagulation. There are several forms of vitamin K, but the two main ones are Vitamin K1 (phylloquinone)and Vitamin K2 (menaquinones). We now know more about its vital role in bone metabolism, cardiovascular health, and potentially other areas, including diabetes, cancer, and immune function, via a recent study.

Feature	Vitamin K1 (Phylloquinone)	Vitamin K2 (Menaquinones)
Primary Sources	Green leafy vegetables (spinach, kale, broccoli), some fruits and vegetable oils.	Fermented foods (natto, cheeses), and animal products (liver, egg yolks).
Main Function	Primarily involved in blood coagulation in the liver.	Active in extrahepatic tissues (outside the liver) for bone metabolism and cardiovascular health.
Absorption Location	Small intestine	Colon
Bioavailability	Generally low (around 10%) but increases with fat intake.	Higher, especially for long-chain forms like MK-7.
Half-life	Short; quickly cleared from the blood.	Longer, especially for long-chain forms like MK-7, allowing for better redistribution to tissues.
Distribution	Primarily retained in the liver to help with clotting factors.	Less is retained by the liver; redistributed to tissues like bone and blood vessels.

Types and Sources of Vitamin K

• Vitamin K1 (Phylloquinone):  The main source of vitamin K1 (phylloquinone) is plants, particularly in green leafy vegetables (e.g, spinach, kale, broccoli, chard, and parsley). Also present in various fruits and nuts like kiwi, avocado, blueberries, cashew, and pistachios, as well as some vegetable oils (soybean, rapeseed, and olive oil). The blood clotting pathway depends on K1. Because of its strong connection to the plant tissue, its bioavailability from food can be low (around 10%), but it increases when fat is consumed.
• Vitamin K2 (Menaquinones – MKs): The UBIAD1 enzyme converts K1 to MK-4, the most common form in the human body, in tissue-specific ways, such as in the testes, pancreas, and vessel wall. found in animal products such as liver, egg yolks, and chicken meat. MKs with a long chain (like MK-7, MK-8, and MK-9): mostly present in some animal products and fermented foods (such as natto, cheeses, and sauerkraut). Compared to K1 and MK-4, MK-7 has a much longer half-life and a higher bioavailability in human circulation, making it more readily available for extrahepatic tissues. Synthetic Forms: K3(Menadione) is a synthetic version that is no longer often used because of its toxicity (liver damage, hemolysis). K4: Additional Synthetic versions of vitamin K.

Metabolism and Kinetics

• Absorption:  The colon absorbs K2, whereas the small intestine absorbs K1. Both are transported to the liver through chylomicrons in the lymphatic system. Their absorption requires bile salts.
• Distribution: K1 is primarily retained in the liver for the carboxylation of coagulation factors. Due to its longer half-life, K2, particularly long-chain MKs like MK-7, are less preserved by the liver and are instead redistributed to extrahepatic tissues like bone and vasculature.
• Storage and Excretion: The body only stores tiny amounts of vitamin K. It is rapidly broken down and eliminated through bile and urine.

Recommended Intake and Deficiency

•  Adequate Intake (AI): K1 intake for blood coagulation is often a basis for recommendations, which differ globally. Adult males should consume 120 µg daily, while females should consume 90 µg daily, according to the National Academy of Medicine. The evidence, however, suggests these quantities might not be enough to maintain the ideal carboxylation of all proteins that are dependent on vitamin K, particularly in extrahepatic tissues.
• Prevalence of Insufficiency: Functional vitamin K insufficiency is widespread, with some studies showing deficiency/insufficiency in up to 97% of older adults when measured by undercarboxylated protein markers.

Deficiency causes include not enough dietary intake. Medical conditions impact the body’s ability to absorb fat, such as inflammatory bowel disease, cystic fibrosis, liver disease, biliopancreatic disorders, and celiac disease. long-term use of antibiotics (disturbs the production of K2 by gut bacteria). drugs that disrupt the metabolism of vitamin K, such as warfarin. Due to insufficient placental transfer and low concentrations in breast milk, newborns naturally have low vitamin K levels, which can result in Vitamin K Deficiency Bleeding (VKDB).

Clinical Implications of Vitamin K Status

Bone Health and Fractures Association with Deficiency: In observational studies, low BMD and a higher risk of fracture are linked to low dietary intake of K1 and K2, low serum K1, and high ucOC levels. Fracture Risk: Taking vitamin K supplements, especially K2/MK-4, reduces the risk of hip, vertebral, and non-vertebral fractures, per meta-analyses. Fracture-based studies are still needed to make definitive recommendations. BMD: Mixed results. According to certain studies, K2 (particularly MK-4) considerably raises the BMD of the lumbar spine, especially in postmenopausal osteoporotic women. The impact on BMD of the femoral neck is frequently ambiguous. The effect of K1 on BMD is less reliable. It has been proposed that the effects of vitamin K on bone may involve elements other than BMD, such as bone strength and geometry. Concomitant Therapies: Although the data are mixed, K2 may have additional advantages when combined with other anti-osteoporotic medications (such as risedronate).

Vitamin K Deficiency Bleeding (VKDB) in Newborns

Risk: Because of low vitamin K reserves at birth, limited placental transfer, and low amounts in breast milk, newborns are especially vulnerable to VKDB. Types include Late VKDB (one week to six months, peaking two to eight weeks), Classic VKDB (during the first week), and Early VKDB (within 24 hours). The incidence of cerebral bleeding is significant in late VKDB. Preventive measures: Due to its single administration and higher potency, intramuscular injection of K1 (0.5–1 mg) at birth is recommended over oral dosages. Repeated dosages are necessary for oral prophylaxis.

Diagnosis and Management of Deficiency

Diagnosis: Prothrombin Time (PT): A conventional but non-specific measure, it needs to drop by about 50% in order to be considered abnormal. Des-gamma-carboxy prothrombin (DCP) or PIVKA-II (Proteins Induced by Vitamin K Absence or Antagonist-II): A more sensitive indicator of functional vitamin K shortage, particularly for extrahepatic tissues. Deficiency is indicated by elevated levels. Measuring vitamin K plasma directly is difficult and quite variable. Treatment:Adults: Adults with deficiencies are treated with dietary changes and oral K1 supplements (1-2 mg, up to 25 mg max). Chronic diseases are being investigated with higher K1/K2 dosages. Newborns: Preventive intramuscular K1 injection for newborns. K1 (1-2 mg) administered intravenously or subcutaneously, together with fresh frozen plasma for severe bleeding, is the treatment for VKDB. Malabsorption: High oral K1 dosages (0.3–15 mg/d) or parenteral treatment may cause malabsorption. Hereditary Combined Deficiency of Vitamin K-Dependent Clotting Factors (VKCFD): IV or oral K1 (10 mg, 2-3 times/week) with fresh frozen plasma for severe bleeding or surgery. Toxicity: Excessive dietary consumption of natural vitamin K (K1 or K2) has no known negative effects. With parenteral K1, anaphylactoid responses are uncommon and frequently associated with emulsifying agents.   Note:(Please note that this content is not intended to endorse or promote any specific products or supplements. Any mention of dosages or treatments is for informational purposes and should only be considered under the guidance of a healthcare professional. If you are taking blood-thinning medications like warfarin, it is especially important to consult with your doctor before making any changes to your diet or taking any supplements, as Vitamin K can significantly affect these medications.)