Vitamin K may be one of the most consequential nutrients for brain health that most people have never thought twice about. Research from the Rush Memory and Aging Project found that higher brain concentrations of vitamin K, specifically in its MK-4 form, are associated with a 17 to 20 percent lower chance of developing dementia or mild cognitive impairment. Those same elevated MK-4 levels correlated with reduced Alzheimer’s pathology, fewer neurofibrillary tangles, lower Braak staging, and less Lewy body presence. For a nutrient most clinicians associate strictly with blood clotting, these findings represent a significant shift in how we should think about dietary priorities for aging brains. What makes this particularly urgent is the scale of potential deficiency.
When researchers use sensitive biomarkers like undercarboxylated matrix Gla protein rather than crude clotting tests, subclinical vitamin K deficiency or insufficiency has been observed in up to 97 percent of older subjects in some mixed populations. That is not a typo. The gap between what we measure and what the body actually needs appears to be enormous. Consider someone eating a standard Western diet with few leafy greens and no fermented foods. They may pass every routine blood test while their brain quietly lacks a nutrient it depends on for maintaining neuronal membranes, regulating inflammation, and clearing toxic proteins. This article covers what vitamin K actually does inside the brain, the recent research connecting it to dementia risk, which forms matter most, where to find them in food, the limitations of current evidence, and what a practical approach to improving your intake looks like.
Table of Contents
- Why Is Vitamin K Considered an Overlooked Nutrient for Brain Health?
- What the Latest Research Says About Vitamin K and Dementia Risk
- How Vitamin K Protects Against Alzheimer’s Pathology
- Getting Enough Vitamin K From Food: K1 vs. K2 and What Your Brain Actually Uses
- The Deficiency Problem Most Doctors Are Not Testing For
- Vitamin K and the Gut Connection
- Where the Science Goes From Here
- Conclusion
- Frequently Asked Questions
Why Is Vitamin K Considered an Overlooked Nutrient for Brain Health?
vitamin K has lived in the shadow of its single best-known function for decades. Medical training emphasizes its role in synthesizing clotting factors, and that narrow framing has shaped both clinical practice and public awareness. Meanwhile, neuroscience researchers have been quietly building a case that vitamin K plays multiple independent roles in the central nervous system. The protein Gas6, which depends on vitamin K for its activation, is directly involved in neuronal cell survival, the growth of both neurons and glial cells, chemotaxis, and mitogenesis. Without adequate vitamin K, Gas6 cannot function properly, and the brain loses a key signaling molecule that helps keep its cells alive and communicating. Equally important is vitamin K’s role in sphingolipid synthesis. Sphingolipids are bioactive lipids found in high concentrations in brain cell membranes, where they maintain structural integrity and facilitate cell-to-cell communication, growth, differentiation, and the regulation of programmed cell death.
When sphingolipid metabolism is disrupted, neuronal membranes deteriorate, and the downstream effects touch everything from synaptic transmission to inflammatory signaling. Compare this to the attention given to omega-3 fatty acids for brain health, which have a well-funded public profile. Vitamin K’s contributions to brain membrane composition are arguably just as fundamental, yet most brain health guides barely mention it. A 2025 review published through Taylor and Francis examined the epigenetic potential of vitamin K2 specifically, finding that it may modulate DNA methylation, histone modifications, and microRNA expression in ways that directly impact brain function and neurodegeneration. This adds an entirely new layer. Vitamin K is not just a structural player or a cofactor for a single protein. It may be influencing gene expression patterns that determine whether neurons survive or degenerate over time.
What the Latest Research Says About Vitamin K and Dementia Risk
The Rush Memory and Aging Project remains one of the most compelling pieces of evidence. This longitudinal study followed community-dwelling older adults and measured actual brain tissue concentrations of MK-4 post-mortem, rather than relying on dietary questionnaires or blood levels alone. The direct measurement matters. It showed that people with higher MK-4 in their brains had meaningfully lower odds of dementia and less Alzheimer’s-related pathology across multiple markers. This is not a food frequency study guessing at intake. It measured what was actually present in the organ that matters. In April 2025, a Tufts University study brought animal model evidence that sharpened the picture further. Researchers found that vitamin K deficiency in middle-aged rodents increased brain inflammation and impaired neural cell proliferation in the hippocampus, the region most critical for learning and memory. Deficient mice performed worse on the novel object recognition test, a standard measure of memory function.
The timing of this study is relevant because it focused on middle-aged animals, suggesting that deficiency does not need to accumulate over a lifetime to cause measurable harm. The damage may begin well before old age. However, a critical limitation applies to all of this work. The Rush MAP findings are associational. Higher brain MK-4 correlated with better outcomes, but correlation does not prove that supplementing vitamin K will prevent dementia. There may be confounding variables, such as people with higher vitamin K levels also eating healthier diets overall, exercising more, or having genetic advantages in nutrient metabolism. The Tufts rodent study is mechanistic and controlled, but mice are not humans. No large-scale randomized controlled trial has yet demonstrated that increasing vitamin K intake reduces dementia incidence in people. This is where the science stands honestly: promising, biologically plausible, but not yet proven as an intervention.
How Vitamin K Protects Against Alzheimer’s Pathology
The specific mechanisms by which vitamin K2 may counter Alzheimer’s disease have been cataloged in a 2024 review published in Frontiers in Aging Neuroscience. The findings are striking in their breadth. Vitamin K2 reduces apoptosis induced by beta-amyloid, the toxic protein fragment that accumulates in Alzheimer’s brains. It limits oxidative stress, reverses microglial activation, suppresses neuroinflammation, and improves vascular health to the brain. Each of these mechanisms addresses a different aspect of Alzheimer’s pathology, which is part of what makes the vitamin K connection so intriguing. It is not acting on a single pathway. Take microglial activation as a concrete example. Microglia are the brain’s resident immune cells.
In a healthy brain, they clear debris and damaged cells. But in Alzheimer’s, they become chronically activated, releasing inflammatory cytokines that damage surrounding neurons, creating a destructive feedback loop. Vitamin K2 appears to dial down this overactivation. For someone whose parent developed Alzheimer’s and who wonders whether diet can make any difference at all, this is one of the more concrete biological mechanisms connecting a specific nutrient to a specific disease process. Perhaps the most forward-looking development came in October 2025, when researchers reported the creation of breakthrough synthetic vitamin K analogues that combine vitamin K with retinoic acid. These compounds demonstrated roughly three times greater potency in inducing neural progenitor cell differentiation into neurons compared to natural vitamin K, by activating the mGluR1 receptor. This is not a dietary supplement finding. It is pharmaceutical development that could eventually lead to Alzheimer’s treatments. But its foundation is the recognition that vitamin K’s neuronal effects are real and potent enough to build drugs around.
Getting Enough Vitamin K From Food: K1 vs. K2 and What Your Brain Actually Uses
The recommended adequate intake for vitamin K is 120 micrograms per day for adult men and 90 micrograms per day for adult women, according to the Food and Nutrition Board. Meeting that threshold is straightforward if you eat leafy greens. A single cup of cooked turnip greens or collard greens delivers about 145 micrograms, exceeding the daily recommendation on its own. Kale, spinach, chard, broccoli, and Brussels sprouts are also rich sources. But here is the critical nuance: these foods provide vitamin K1, or phylloquinone. The brain preferentially accumulates MK-4, a form of vitamin K2, regardless of which dietary form you consume. Your body converts K1 into MK-4, and this conversion happens in the brain itself. So eating K1-rich greens does contribute to brain MK-4 levels.
However, vitamin K2 can also be obtained directly from food. Natto, the Japanese fermented soybean dish, is the richest known source at roughly 150 micrograms per tablespoon, about twice the daily adequate intake. Other K2 sources include liver, Jarlsberg cheese at 74 micrograms per 100 grams, blue cheese at 36 micrograms per 100 grams, chicken, and sauerkraut. The tradeoff here is practical. Most Western adults are far more likely to eat a spinach salad than a serving of natto, which has a strong flavor and sticky texture that many find challenging. Cheese provides K2 but also comes with saturated fat and calories. The most reliable approach is probably a combination: regular consumption of dark leafy greens for K1 conversion, supplemented by whatever K2-rich foods you find palatable. Someone who eats a large salad with spinach or kale most days, adds sauerkraut to meals a few times per week, and occasionally includes quality cheese is covering more bases than someone relying on any single source.
The Deficiency Problem Most Doctors Are Not Testing For
The statistic that up to 97 percent of older subjects in some study populations show subclinical vitamin K deficiency or insufficiency when measured by sensitive biomarkers demands explanation. Standard clinical assessment of vitamin K status typically relies on prothrombin time, a clotting test. If your blood clots normally, you are considered vitamin K sufficient. But clotting is the body’s highest priority use of vitamin K. The liver gets first access to circulating vitamin K for clotting factor production, and it takes relatively little to maintain that function. The brain, bones, and vasculature may be starved of vitamin K long before a clotting test shows anything abnormal. This is where undercarboxylated matrix Gla protein comes in. When vitamin K is insufficient, MGP cannot be fully carboxylated, and the undercarboxylated fraction rises. This biomarker reveals a level of insufficiency invisible to standard testing.
The implication for brain health is sobering: millions of older adults may have technically normal lab results while their brains lack the vitamin K needed for sphingolipid synthesis, Gas6 activation, and the anti-inflammatory processes described earlier. If you ask your doctor about vitamin K status, you will likely be told you are fine based on clotting tests. That answer may be incomplete. A significant warning applies to anyone taking warfarin or other vitamin K antagonist blood thinners. These drugs work by deliberately blocking vitamin K’s clotting activity. Patients on warfarin are routinely told to keep vitamin K intake consistent, and some are told to avoid K-rich foods entirely. This creates a direct conflict with brain health goals. Anyone on anticoagulant therapy should not change their vitamin K intake without consulting their prescribing physician. The newer direct oral anticoagulants like apixaban and rivarelbaan do not interfere with vitamin K and may be worth discussing with your doctor if brain health is a concern, though that decision involves many other clinical factors.
Vitamin K and the Gut Connection
An often-missed aspect of vitamin K status is the role of gut bacteria. Certain intestinal bacteria synthesize vitamin K2, particularly longer-chain menaquinones. This means that gut health and vitamin K status are intertwined. Someone who has taken repeated courses of broad-spectrum antibiotics, for example, may have disrupted their gut microbiome enough to reduce endogenous K2 production.
The same applies to people with chronic digestive conditions that impair fat absorption, since vitamin K is fat-soluble and requires dietary fat for uptake. This adds another variable to the deficiency problem. Two people eating identical diets may have different vitamin K status based on the composition of their gut microbiome. Fermented foods like sauerkraut, kimchi, and yogurt may pull double duty here by both providing some K2 directly and supporting the gut bacteria that produce it endogenously. It is one of the clearer examples of how brain health, gut health, and diet converge on a single nutrient.
Where the Science Goes From Here
The development of synthetic vitamin K analogues with three times the potency of natural vitamin K for neural cell differentiation signals that the pharmaceutical world is paying attention. If these compounds advance through clinical trials, they could become targeted therapies for Alzheimer’s disease, moving vitamin K from the nutrition column into the pharmacology column. The 2025 epigenetics review also opens a new front, suggesting that vitamin K2’s influence on gene expression could be harnessed in ways we are only beginning to understand. What the field still needs most is a large, well-designed randomized controlled trial testing whether vitamin K supplementation in middle-aged or older adults reduces the incidence of cognitive decline or dementia.
Until that trial happens, the evidence remains compelling but circumstantial. The biological mechanisms are clear, the observational data is consistent, and the animal studies support causation. For individuals making dietary choices today, increasing vitamin K intake through food carries virtually no risk for people not on anticoagulants, and the potential upside is considerable. This is one of the easier bets in preventive brain health.
Conclusion
Vitamin K has earned a place in the conversation about brain-protective nutrients. The evidence connecting it to dementia risk, Alzheimer’s pathology, neuroinflammation, and neuronal survival is substantial and growing. The Rush Memory and Aging Project’s finding that higher brain MK-4 levels correspond to a 17 to 20 percent lower chance of dementia, combined with the Tufts research showing that deficiency actively harms hippocampal function in middle-aged animals, builds a case that is hard to dismiss. The widespread nature of subclinical deficiency makes this relevant to nearly everyone over 50. The practical steps are straightforward.
Eat dark leafy greens daily. Include fermented foods when possible. Pay attention to fat intake since vitamin K needs it for absorption. If you are on blood thinners, talk to your doctor before making changes. And keep an eye on the research. The synthetic vitamin K analogues in development could eventually offer targeted treatment options for Alzheimer’s, but the dietary foundations you build now may prove to be among the most important things you do for your brain in the years ahead.
Frequently Asked Questions
How much vitamin K do I need per day for brain health?
The established adequate intake is 120 micrograms per day for men and 90 micrograms for women, but these recommendations were set based on clotting function, not brain health. Given that subclinical deficiency appears far more common than clinical deficiency, some researchers suggest current guidelines may be too low for optimal neurological function. A cup of cooked collard greens or turnip greens exceeds the daily recommendation.
Is vitamin K1 or K2 better for the brain?
The brain preferentially accumulates MK-4, which is a form of vitamin K2. However, the body converts dietary K1 into MK-4, so eating K1-rich leafy greens does contribute to brain levels. Eating a variety of both K1 sources like spinach and kale and K2 sources like natto, cheese, and sauerkraut is the most practical approach.
Can I take vitamin K supplements for brain health?
Vitamin K supplements are available and generally safe for people not on anticoagulant medications. However, no randomized controlled trial has yet proven that vitamin K supplementation prevents cognitive decline in humans. Food sources remain the best-supported approach. Anyone on warfarin or similar blood thinners should not take vitamin K supplements without medical guidance.
Does vitamin K deficiency cause dementia?
The current evidence does not prove a direct causal link. What the research shows is a strong association between lower brain vitamin K levels and higher rates of dementia and Alzheimer’s pathology, and that vitamin K deficiency in animal models impairs memory and increases brain inflammation. Causation has not been established through human intervention trials.
What are the best food sources of vitamin K2 specifically?
Natto, a Japanese fermented soybean product, is by far the richest source at approximately 150 micrograms per tablespoon. Liver, Jarlsberg cheese at 74 micrograms per 100 grams, blue cheese at 36 micrograms per 100 grams, chicken, and sauerkraut are also meaningful sources. Gut bacteria also produce some K2 endogenously.
Can warfarin users safely increase vitamin K intake?
Not without medical supervision. Warfarin works by antagonizing vitamin K, so increasing intake can reduce the drug’s effectiveness and raise the risk of dangerous blood clots. Patients on warfarin should maintain consistent vitamin K intake and discuss any dietary changes with their doctor. Newer anticoagulants that do not interfere with vitamin K may be an alternative worth discussing.
