A study reported in the May 2014 issue of the Journal of Nutrition links higher intake of vitamin K with a lower risk of dying from any cause over a median follow-up of 4.8 years.

The study included 7,216 participants in the PREDIMED study, which sought to evaluate the protective effect of a Mediterranean diet against the risk of cardiovascular disease in older men and women. Annual dietary questionnaire responses completed by the participants were analyzed for the intake of phylloquinone (vitamin K1) and menaquinone (vitamin K2). Over a 4.8 year median, there were 323 deaths, including 81 deaths from cardiovascular disease and 130 cancer deaths.

Adjusted analysis uncovered a 36% lower risk of dying from any cause and a 46% lower risk of dying from cancer over follow-up among those whose vitamin K1 intake was among the top 25% of participants in comparison with the lowest 25%. For those who increased their intake of vitamin K1 over follow-up, the risk of death was 43% lower and for vitamin K2, the risk was 45% less than subjects whose intake was reduced or unchanged. Improvement of vitamin K1 and K2 intake was also associated with a 36% and 59% lower risk of dying from cancer during the follow-up period.

"To our knowledge, this is the first study to evaluate the specific association of both active forms of vitamin K (vitamins K-1 and K-2), and their changes during the follow-up, with cancer mortality, cardiovascular mortality, or all-cause mortality in a prospective longitudinal study of Mediterranean individuals at high cardiovascular disease risk and using repeated measurements of dietary intake," the authors announce. "The results of the present study show, for the first time, an inverse association between an increased intake of both dietary phylloquinone and menaquinone, and cancer mortality or all-cause mortality."

In RA, the immune system mistakenly attacks healthy cells and tissues — predominantly the synovium, the soft tissue between the articular capsule (joint capsule) and the joint cavity of synovial joints. This immune mediated assault leads to the development of pannus, a destructive fibrous tissue within affected joints that erodes cartilage and exacerbates joint dysfunction.

RA damage is engendered by multiple components of the immune system, including antibodies and killer T-cells.

Antibodies are proteins secreted by β-cells that normally recognize and bind to invading microbes such as bacteria and viruses. By attaching to the invading microbe, they activate other components of the immune system to launch an inflammatory response, which destroys the cells.

In RA, antibodies mistakenly recognize "self" cells as invaders. Once antibodies attach to synovial cells in the joint, they attract a variety of immune cells that launch a devastating inflammatory attack. The complex inflammatory process within joints is mediated in large by the cytokines tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). The inflammatory damage is not limited to the synovium, but spills over to the chondrocytes (cartilage cells that cushion joints). This process raises the level of dangerous inflammatory compounds throughout the body, including C-reactive protein (CRP), which is a marker of inflammation and can be evaluated via a high-sensitivity CRP (hs-CRP) test.