Fat Soluble Vitamins
The fat soluble vitamins are vitamin A, D, E, and K, and they are associated with lipid transportation and absorption (Gropper & Smith, 2013). Chylomicrons transport fat soluble vitamins, bile is used to absorb them, and they are stored in body lipids (Gropper & Smith, 2013). Each fat soluble vitamin has specific functions, and if enough of the vitamin is not part of the diet, related deficiency symptoms will occur.
Vitamin A
Vitamin A, and the precursors, carotenoids, come from food sources such as liver, dairy, fish, and eggs (Gropper & Smith, 2013). The many functions of vitamin A include formation of rhodopsin for vision, cell differentiation, bone development, and immune function (Gropper & Smith, 2013). Deficiency in vitamin A, which is rare in the United States, results in slowed growth, depressed immunity, and skin issues, but, one of the first symptoms to appear is night blindness (Gropper & Smith, 2013). Vitamin A, in the form of 11-cis-retinal, is found in retinal epithelial cells and becomes covalently bound to the protein opsin (Palczewski, Kumasaka, Hori, Behnke, Motoshima, Fox, Trong, Teller, Okada, Stenkamp, Yamamoto, & Miyano, 2000).These two components make up rhodopsin, which is a necessary component to vision (Palczewski et al., 2000). When light is detected by rhodopsin, a conformation change occurs that breaks opsin from 11-cis-retial and transforms it to trans-retinal, which sends signals to the brain to detect image (Palczewski et al., 2000). This give the human eye the ability to see at night as long as five photons are able to be absorbed (Palczewski et al., 2000). Because of vitamin A’s necessary involvement in the formation of rhodopsin, deficiency of this vitamin will result in lack of formation of rhodopsin, inability for cleavage from opsin, and lack of visibility (Gropper 7 Smith, 2013).
Vitamin D
Vitamin D is mainly associated with bone health, calcium homeostasis, and cell differentiation (Gropper & Smith, 2013).Other than being found in fortified foods and animal products, the body is able to produce vitamin D through a series of processes in the dermis and epidermis (Gropper & Smith, 2013).The steroid 7-dehydrocholesterol that is made in sebaceous glands is secreted onto the skin and absorbs UV light and causes the formation of previtamin D3, but over a relatively short period of time, the unstable bonds rearrange into vitamin D (Gropper & Smith, 2013). Functions of vitamin D include increases in intracellular calcium, uptake of calcium, and gene expression via DNA sequencing (Gropper & Smith, 2013). When calcium is low, parathyroid hormone is released, kidneys stimulate increase in calcium absorption and blood levels, renal-hydroxylase converts the precursor to calcitriol (vitamin D), intestines sense increased blood calcitriol and increase calcium transportation and exportation, which ultimately increases blood calcium levels (Gropper & Smith, 2013). Therefore, deficiencies in vitamin D result in lack of calcium absorption, as well as phosphorus absorption (Holick, 2007). Growing children can be affected when vitamin D is deficient and this can result in low bone calcium deposition, hyperparathyroidism, and rickets (Holick, 2007). Adults can be affected with osteomalacia, which causes bon e pains (Holick, 2007). Vitamin D deficiency may also cause muscle weakness and increase fall risk (Holick, 2007). Inability of vitamin D to reach its corresponding receptor, 1,25-dihydroxyvitamin D, can affect tissues such as the brain, breast, prostate, colon, cells involved in immunity, and cellular regulation of proliferation, differentiation, and apoptosis (Holick, 2007).
Vitamin E
Eight compounds broken into categories of tocopherols and tocotrienols make up vitamin E (Gropper & Smith, 2013). Plant oils are the best dietary inclusion of vitamin E. Vitamin E acts as an antioxidant, with its main function being to scavenge peroxyl radicals and protect the membranes of polyunsaturated fatty acids by free radical cessation (Traber & Atkinson, 2007). By doing so, the polyunsaturated fatty acid membranes maintain lipid domains and fluidity (Traber & Atkinson, 2007). Vitamin E also blocks protein kinase C, which eliminates growth and differentiation of cells, leading to apoptosis (Traber & Atkinson, 2007). Through this mechanism, a deficiency in vitamin E can lead to nerve damage that resulted from either apoptosis or oxidative stress (Traber & Atkinson, 2007).
Vitamin K
Bacteria in the intestine contribute to vitamin K known as menaquinones, but it can also be found in leafy greens, soy beans, and liver in the form of phylloquinones (Gropper & Smith, 2013). The major functions of vitamin K are clotting of blood and mineralization of bone (Gropper & Smith, 2013). Vitamin K dependent processes in blood clotting include activating the X factor (clotting protein) and activating prothrombin to produce thrombin, which finalizes with production of fibrin (Gropper & Smith, 2013). The fibrin forms into a polymer to stop bleeding, therefore, a deficiency in vitamin K will result in severe bleeding and inability to clot (Gropper & Smith, 2013). Vitamin K also helps calcium bind to bone matrixes through bone Gla protein and matrix Gla protein (Gropper & Smith, 2013). Without vitamin K, matrix Gla protein found in cartilage and bone will act to calcify arteries and soft tissue and lack thereof will also cause issues with bone mineralization (Gropper & Smith, 2013).
Treatment and Conclusion
Vitamin A, D, E, and K are fat soluble vitamins with unique functions. Deficiencies in these vitamins can result in a variety of symptoms. Vitamin A and D deficiencies can be eliminated though supplementation, although vitamin A deficiency is rare (Gropper & Smith, 2013). Vitamin E deficiency is also uncommon, and there does not appear to be much toxicity related to vitamin E supplementation, but gastrointestinal issues may arise if exceeding the tolerable upper limit (Groper & Smith, 2013). Vitamin K deficiency is most seen in infants and people on chronic antibiotics, and there does not exist a tolerable upper limit for this vitamin. Overall, it is found that fat soluble vitamins are not often in deficiency, with the exception of vitamin D.
Sources
Gropper, S.S., & Smith, J.L. (2013). Chapter 10: Fat-soluble vitamins. Advanced nutrition and human metabolism (6th ed.)(pp.371-414). Belmont, CA:Wadsworth Cengage Learning
Holick, M.F. (2007).
Vitamin D deficiency. New England Journal of Medicine, 357, 266-281. doi:10.1056/NEJMra070553
Palczewski, K., Kummasaka, T., Hori, T., Behnke, C.A., Motoshima, H., Fox, B.A., Trong, I.L., Teller, D.C., Okada, T., Stenkamp, R.E., Yamamoto, M., & Miyano, M. (2000). Crystal structure of rhodopsin: A G protein-coupled receptor. Science, 289, 739-745. Retrieved from http://science.sciencemag.org/content/sci/289/5480/739.full.pdf?casa_token=d_erakWCSJQAAAAA:XKMwXfWDCpeTX5AjZxphzu7TPt25ZIayGR9_HOEWTiNNszHaVdWTuTP35Vbx4rbytHba0SJDWNscpA
Traber, M.G., & Atkinson, J. (2007). Vitamin E, antioxidant and nothing more. Free Radic Biol Med, 43(1), 4-15. doi10.1016/j.freeradbiomed.2007.03.024
Disclaimer
All programs and articles provided are intellectual property of James Shmagranoff. No copies or redistribution of these is allowed without express permission from James Shmagranoff. James Shmagranoff is not a doctor and nothing contained within this article is to be taken as medical advice. Always follow the directions of your medical practitioner.
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