Vitamin K Deficiency Impairs Brain Health and Memory

Understanding how nutrients affect the brain is a growing focus in aging research and a new study has turned the spotlight on vitamin K.
Led by a team from the Jean Mayer USDA Human Nutrition Research Center on Aging (HNRCA) at Tufts University, the recent investigation, published in The Journal of Nutrition, has provided fresh insights into how vitamin K may influence brain health. They found that a diet low in vitamin K led to impaired memory performance, reduced formation of new neurons in the hippocampus and signs of increased brain inflammation.
Nutrition and cognitive aging
Age-related cognitive decline affects millions worldwide, and as life expectancy continues to rise globally, understanding how to support brain health into old age has become an increasingly urgent area of research. While genetic and lifestyle factors play a role, there is growing recognition that nutrition contributes to shaping cognitive trajectories.
Recent research has homed in on specific nutrients that may influence brain function, including omega-3 fatty acids, B vitamins, antioxidants and, more recently, vitamin K. Known primarily for its role in blood coagulation, vitamin K is essential for clinical nutrition. However, evidence is mounting that it may also contribute to cardiovascular health, bone metabolism and neurological function.
Vitamin K exists in two main forms:
- Phylloquinone (vitamin K₁): Found predominantly in green leafy vegetables like spinach, kale, collard greens, broccoli and Brussels sprouts.
- Menaquinones (vitamin K₂): A group of compounds found in animal products and fermented foods and produced in small amounts by gut bacteria.
In the United States, the recommended adequate intake for vitamin K₁ is 120 μg per day for adult men and 90 μg per day for adult women, according to the National Institutes of Health. Despite these recommendations, data suggests that many older adults fail to meet daily vitamin K requirements.
“There is research that indicates vitamin K contributes to brain function and that brain function declines during the aging process,” said lead author Dr. Tong Zheng, a research scientist at the Jean Mayer USDA HNRCA at Tufts University.
Observational studies have linked higher vitamin K intake with better cognitive outcomes in older adults. Data from the Rush Memory and Aging Project showed that individuals with greater vitamin K concentrations in their brains had lower levels of dementia-related pathology, including fewer neurofibrillary tangles.
Neurofibrillary tangles
Twisted fibers made of a protein called tau build up inside brain cells and are commonly seen in Alzheimer’s disease. They disrupt cell function and are associated with cognitive decline.
While dietary patterns rich in vitamin K appear beneficial, the biological mechanisms behind vitamin K’s effects on the brain are still not well understood.
Vitamin K deficiency impairs memory and brain cell growth
Zheng and colleagues designed a 6-month dietary intervention using 60 middle-aged C57BL/6 mice. The mice were split into two groups: one received a standard diet containing adequate levels of vitamin K, while the other group was fed a vitamin K-deficient diet containing only a fraction of the recommended amount. The control diet provided 1 mg/kg of phylloquinone, while the vitamin K-deficient diet contained only 80 μg/kg – a reduction of more than 90%. The focus of the study was specifically on menaquinone-4 (MK-4), the form of vitamin K most prevalent in brain tissue.
After six months, the mice underwent a series of behavioral tests to evaluate learning and memory. In the novel object recognition test, which measures recognition memory by evaluating how much time mice spend exploring a new versus familiar object, the vitamin K-deficient group showed clear impairments. These mice spent significantly less time with the novel object, indicating a reduced ability to distinguish new from familiar stimuli – a hallmark of memory decline.
In a second test – the Morris water maze, which assesses spatial learning and memory – the vitamin K-deficient mice also underperformed. Over multiple trials, they took longer to locate a hidden platform in a pool of water, suggesting difficulties with learning and retaining spatial information compared to their vitamin K-sufficient counterparts.
Beyond behavioral changes, the study revealed differences in brain structure and function. When the researchers analyzed tissue from the hippocampus, a brain region essential for learning and memory, they found that vitamin K-deficient mice had reduced levels of MK-4 and significantly reduced neurogenesis in their brain tissue. These mice showed fewer proliferating cells and immature neurons in the dentate gyrus, a subregion of the hippocampus where new neurons are born even in adulthood.
Neurogenesis
The process of creating new neurons in the brain, especially in areas linked to learning and memory, like the hippocampus.
Dentate gyrus
A part of the hippocampus involved in memory formation and one of the few regions in the adult brain where neurogenesis continues throughout life.
“Neurogenesis is thought to play a critical role in learning and memory, its impairment could directly contribute to the cognitive decline observed in the study,” said Zheng.
The team also identified signs of increased neuroinflammation in the deficient group. A higher number of activated microglia – the brain’s resident immune cells – were seen in the vitamin K-deficient group. While the total number of microglia remained similar between groups, the vitamin K-deficient mice showed simpler, less branched structures – an indicator of a more activated and potentially inflammatory state. Excessive microglial activation is associated with chronic inflammation and has been implicated in neurodegenerative diseases.
Microglia
Specialized immune cells in the brain that help maintain brain health by removing waste and damaged cells; when overactivated, they can contribute to inflammation and neurodegeneration.
Male mice on the vitamin K-deficient diet experienced significantly lower survival rates and less weight gain over the study period compared to both female mice and control males. The researchers found no evidence of bleeding in the vitamin K-deficient mice that died, suggesting the observed mortality may be related to other physiological effects of deficiency.
Supplementing vitamin K is not necessary
This research reinforces the idea that vitamin K may have a role in supporting brain health, particularly in the context of aging. Although the study was conducted in mice, it aligns with findings from human observational studies that associate a higher intake of vitamin K-rich foods with better cognitive outcomes in older adults.
One of the mechanisms highlighted in this study is the potential for vitamin K to help maintain neurogenesis to regulate neuroinflammation.
“Vitamin K seems to have a protective effect,” said Zheng. “Our research is trying to understand the underlying mechanism for that effect so that we might one day be able to target those mechanisms specifically.”
Looking forward, the researchers aim to validate these mechanisms in human studies, investigate how vitamin K interacts with other dietary components and aging processes and explore whether its role in neuroinflammation and cell development could inform future therapeutic strategies.
“We know that a healthy diet works and that people who don’t eat a healthy diet don’t live as long or do as well cognitively. By choreographing animal and human studies together, we can do a better job of improving brain health long-term by identifying and targeting specific mechanisms,” said senior author Dr. Sarah Booth, director of the HNRCA.
Although the team emphasizes the focus of their research remains on achieving adequate vitamin K through dietary sources, not supplementation.
“People need to eat a healthy diet. They need to eat their vegetables,” said Booth.
Reference: Zheng T, Marschall S, Weinberg J, et al. Low vitamin K intake impairs cognition, neurogenesis, and elevates neuroinflammation in C57BL/6 mice. J Nutrit. 2025:S0022316625000306. doi: 10.1016/j.tjnut.2025.01.023
This article is a rework of a press release issued by Tufts University. Material has been edited for length and content.
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