Vitamin K

Vitamin K is a fat-soluble vitamin that plays crucial roles in blood clotting and bone health. It exists in two main forms: vitamin K1 (phylloquinone), found primarily in leafy green vegetables, and vitamin K2 (menaquinones), which includes several subtypes like MK-4 and MK-7 produced by bacteria or converted from K1. This essential nutrient functions as a coenzyme for vitamin K-dependent carboxylase, enabling the synthesis of proteins vital for hemostasis and bone metabolism. Key vitamin K-dependent proteins include prothrombin for blood clotting, osteocalcin for bone formation, and matrix Gla-protein (MGP) which may help prevent abnormal calcium deposits in arteries. Unlike other fat-soluble vitamins, vitamin K has limited storage capacity and is rapidly metabolized, making consistent intake important. The body can produce some vitamin K2 through gut bacteria, but dietary sources remain the primary means of maintaining adequate levels. Vitamin K deficiency can lead to bleeding disorders and potentially compromised bone health, while optimal levels support proper coagulation function and may contribute to cardiovascular and skeletal wellness.

Vitamin K deficiency primarily manifests through bleeding disorders due to impaired blood clotting. Early signs include easy bruising, excessive bleeding from minor cuts, heavy menstrual periods, and bleeding gums. Severe deficiency can lead to dangerous internal bleeding, including gastrointestinal or intracranial hemorrhage. In infants, vitamin K deficiency bleeding is a serious condition that can cause life-threatening bleeding, particularly in the brain. Bone-related symptoms may include increased fracture risk and poor bone density, though these develop more gradually. Some individuals may experience fatigue or weakness related to chronic minor bleeding. Deficiency is most common in newborns, individuals with malabsorption disorders, those on prolonged antibiotic therapy, or people with severely restricted diets. Vitamin K toxicity from natural sources is extremely rare since excess amounts are readily excreted. However, synthetic vitamin K supplements in very high doses may cause hemolytic anemia or liver damage. Individuals on anticoagulant medications may experience complications if vitamin K intake suddenly increases, potentially reducing medication effectiveness and increasing clotting risk. Most healthy adults with normal diets rarely experience vitamin K-related symptoms.

Optimizing vitamin K levels primarily involves dietary strategies focusing on vitamin K-rich foods. Dark leafy greens like kale, spinach, Swiss chard, and collard greens are excellent sources of vitamin K1, with just one cup of cooked spinach providing several times the daily requirement. Vitamin K2 sources include fermented foods like natto (exceptionally rich in MK-7), sauerkraut, kimchi, and aged cheeses, as well as organ meats and egg yolks from pasture-raised animals. Since vitamin K is fat-soluble, consuming these foods with healthy fats like olive oil or avocado enhances absorption. Supporting gut health through probiotic foods, fiber intake, and avoiding unnecessary antibiotics helps maintain vitamin K-producing bacteria. Supplementation may be beneficial for those with absorption issues or limited dietary intake. Vitamin K2 supplements, particularly MK-7, may offer advantages for bone and cardiovascular health. Typical supplemental doses range from 90-200 mcg daily, though higher doses may be used under professional guidance. Combining vitamin K with vitamin D may enhance benefits for bone health. Individuals on anticoagulant medications should maintain consistent vitamin K intake rather than trying to optimize levels, and any changes should be made under medical supervision. Cooking methods matter less for vitamin K than other nutrients since it's relatively heat-stable, though minimal processing preserves content best.

For health optimization, vitamin K levels of 0.5-2.5 ng/mL are considered optimal, representing a narrower range within the standard reference values that may better support long-term health outcomes. This range aims to ensure adequate vitamin K-dependent protein function while avoiding potential complications from excessive levels. Research suggests that levels toward the higher end of this optimal range may better support bone health through improved osteocalcin carboxylation and cardiovascular health via enhanced matrix Gla-protein function. Some longevity-focused practitioners target levels around 1.0-2.0 ng/mL, balancing the benefits of adequate vitamin K status with safety considerations. Higher optimal ranges may be particularly beneficial for postmenopausal women and elderly individuals at risk for osteoporosis, as well as those with cardiovascular risk factors who might benefit from vitamin K's role in preventing arterial calcification. However, individuals on anticoagulant therapy require specialized monitoring and should maintain consistent rather than optimized levels. The optimal range concept also considers the synergistic relationship between vitamins K and D, with adequate vitamin D status potentially enhancing vitamin K's benefits for bone and cardiovascular health.

The standard laboratory reference range for vitamin K is 0.2-3.2 ng/mL, representing values found in apparently healthy populations. However, these ranges primarily indicate levels sufficient to prevent overt deficiency rather than optimal health. Values below 0.2 ng/mL suggest deficiency and increased bleeding risk, while levels above 3.2 ng/mL are considered elevated. Reference ranges can vary slightly between laboratories due to different analytical methods and population studies. Age affects vitamin K status, with infants being particularly vulnerable to deficiency due to poor placental transfer and low breast milk content, requiring vitamin K prophylaxis at birth. Elderly individuals may have lower levels due to decreased absorption or medication interactions. Sex differences are generally minimal, though pregnant and breastfeeding women may have altered requirements. Geographic variations exist based on dietary patterns, with populations consuming more fermented foods or leafy greens typically showing higher levels. Seasonal variations may occur due to changes in vegetable consumption. These reference ranges serve as general guidelines, but individual optimal levels may vary based on genetic factors, health status, and specific health goals.

Vitamin K blood testing typically measures serum phylloquinone (vitamin K1) levels, expressed in nanograms per milliliter (ng/mL). This measurement reflects the circulating vitamin K available for biological functions, though it represents only a snapshot of vitamin K status since the vitamin is rapidly metabolized. The test indicates the body's current vitamin K availability for synthesizing clotting factors and other vitamin K-dependent proteins. However, serum levels may not fully capture tissue stores or functional vitamin K status. Some laboratories also measure undercarboxylated proteins like undercarboxylated osteocalcin or undercarboxylated prothrombin, which can provide additional insight into functional vitamin K adequacy. These functional markers may be more sensitive indicators of vitamin K status than serum levels alone. The measurement is particularly important for individuals on anticoagulant medications like warfarin, which interferes with vitamin K function, requiring careful monitoring to maintain therapeutic balance between bleeding and clotting risks.

Multiple factors influence vitamin K levels, with diet being the primary determinant. Leafy green vegetables like spinach, kale, and broccoli are rich in vitamin K1, while fermented foods, aged cheeses, and organ meats provide vitamin K2. Gut health significantly impacts vitamin K status since intestinal bacteria produce menaquinones, making antibiotic use a potential risk factor for deficiency. Fat malabsorption conditions such as celiac disease, inflammatory bowel disease, or pancreatic disorders can impair vitamin K absorption since it's fat-soluble. Medications notably affect levels - warfarin and other vitamin K antagonists deliberately reduce functional vitamin K activity, while some antibiotics can destroy vitamin K-producing gut bacteria. Broad-spectrum antibiotics, certain seizure medications, and mega-doses of vitamins A and E may lower levels. Liver disease can impair vitamin K metabolism and storage. Age-related factors include decreased absorption efficiency and potential dietary changes. Chronic kidney disease may affect vitamin K metabolism. Alcohol consumption can interfere with vitamin K function. Genetic variations in enzymes involved in vitamin K metabolism may influence individual requirements. Dietary fat intake affects absorption, with very low-fat diets potentially reducing vitamin K uptake even with adequate intake of vitamin K-rich foods.

Vitamin K testing isn't routinely performed in standard health panels but may be warranted in specific circumstances. Testing is recommended for individuals with unexplained bleeding disorders, those with malabsorption conditions, patients on long-term antibiotic therapy, or people with restrictive diets. Individuals taking anticoagulant medications like warfarin typically require INR (International Normalized Ratio) monitoring rather than direct vitamin K measurement, as this better reflects functional clotting status. For health optimization purposes, testing every 6-12 months may be appropriate for those with risk factors or specific health goals. The test requires a simple blood draw and doesn't require fasting, though consistency in timing relative to meals and supplements may provide more reliable results. Vitamin K testing may be included in comprehensive micronutrient panels or specialized bone health assessments. Some practitioners recommend testing vitamin K alongside vitamin D, calcium, and magnesium as part of bone health evaluation. Functional tests measuring undercarboxylated proteins may provide additional insights into vitamin K adequacy beyond serum levels alone.