Inflammatory bowel disease (IBD) is an autoimmune condition where in most cases there are multiple triggers chronically stimulating the immune system over a long period of time in multiple ways and the immune system gets into overloaded, overwhelmed state and loses its ability to function leading to chronic inflammation causes symptoms such as diarrhea, abdominal pain, and other debilitating symptoms and anemia.

IBD is an autoimmune condition where part of the digestive tract becomes inflamed and ulcerated marked with sores. There is emerging data that Vitamin D supplementation may lengthen the remission in IBD.

According to a study published last month in Nutrients, researchers investigated the intake of vitamin D and vitamin K in patients with IBD. Disease activity was assessed using the Harvey-Bradshaw Index in Crohn’s disease and the Partial Mayo score in Ulcerative Colitis.

This study included 193 IBD patients (100 men and 93 women) between 2016 and 2020. Eighty-nine patients had Crohn’s disease and 104 patients had Ulcerative Colitis. A dietitian obtained food intake by completing a food frequency questionnaire that was adapted from a 22-item quantitative FFQ, previously validated for calcium and vitamin D intake, and integrated with 6 specific questions. These questions were focused on foods with the highest phylloquinone concentration. Green leafy vegetables including spinach, iceberg lettuce, chicory, beets, turnip tops, and rocket salad, as well as eggs, were the main contributors of vitamin K intake.

The research team demonstrated that IBD patients have a significantly lower intake of

vitamin D and vitamin K more so in active disease cases. In addition, the unfavorable metabolic effects of low Vitamin D intake are further amplified by the inadequate sunlight exposure documented in IBD patients. This is clinically significant as sunlight exposure affects the conversion of vitamin D precursors to its activated form and is more important than diet in determining vitamin D levels.

Also, IBD patients avoid vegetables in the fear of worsening diarrhea. Minimizing the intake of insoluble fiber is advisable in stricturing or perforating CD, but restriction is unnecessary in inflammatory CD and UC. This attitude is not uncommon and has significant metabolic implications.

Green leafy vegetables, which are well represented in the Mediterranean diet are the primary

dietary source of vitamin K.

The present study confirms that the diet of IBD patients often lacks vitamin D and vitamin K. Almost half of the patients in this study limited the consumption of vegetables including green leafy vegetables. This led to an inadequate intake of vitamin K1.

Vitamin D supplements are an important part of the therapeutic strategy targeted at IBD patients. Vitamin K supplementation is advised in bone and inflammatory rheumatic disease, chronic renal failure and for the prevention of vascular calcification and cardiovascular disease

however, is it not mentioned in the nutritional guidelines for IBD patients. This attitude

should change to reduce the adjunctive risk factor of osteoporosis in already

high-risk patients, prevent coagulation defects and possibly help modulate inflammatory

responses in IBD. These fat-soluble vitamins have strong interrelationships and should be provided in a supplement together.

Vitamin D deficiency has been linked to many autoimmune diseases, including type 1 diabetes, systemic lupus erythematosus, multiple sclerosis, and Crohn’s disease, with studies finding a higher prevalence of these diseases in those who are deficient in vitamin D

There is plenty of evidence regarding the benefit of vitamin D supplementation on a multitude of health benefits not just with autoimmune disorders. Given the fact that supplementation of vitamin D in its natural form is harmless and inexpensive, many more people should get their vitamin D levels checked regularly and supplement according.

Source: Vernia F, Scotti GB, Low Vitamin K and Vitamin D Dietary Intake in Patients with Inflammatory Bowel Diseases. Nutrients. 2023 Mar 30;15(7):1678.

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