vitamin (vahy-tuh-min) vita - Latin for "life" amine - Refers to a class of organic compounds that contains amino acids. deficiency (dih-fi-shuh n-see) deficiens - Latin for "failing" or "lacking"
1600s - Although vitamin D deficiency was first recognized as rickets/osteomalacia in the early 1600s, it was only a century ago that vitamin D, the nutritional factor responsible, was discovered. This discovery was made difficult by the fact that the substance could be synthesized in human skin by exposure to UV light and could also be present in the diet in animal-derived (D3) and plant-derived forms (D2). 1920 - Prior to 1920, the frequency of vitamin D deficiency in the general population of industrialized cities was high. The discovery of vitamin D led to the widespread fortification of foods e.g. milk and the virtual eradication of rickets in developed nations. 1632 marked the earliest written record of the word "rickets" as a disease in an English family's domestic receipt book. Shortly after, in 1634, the London Bill of Mortality printed the earliest record of "rickets" as a cause of death. These significant findings have been cited in important reviews by Swinburne (2006), O'Riordan and Bijvoet (2014), and Mays (2017). The recognition of rickets and osteomalacia dates back to the mid-seventeenth century, with Daniel Whistler in the Netherlands (1645) and Francis Glisson in England (1650) making notable contributions. Glisson's book, "De Rachitide," published in Latin in 1650 and translated into English in 1671, featured illustrations of children with bowed legs and skeletal deformities—key indicators of vitamin D deficiency. By the late 1700s, Percival (1789) advocated for the use of cod-liver oil as a treatment for rickets, suggesting the nutritional aspect related to vitamin D. In the early 1800s, Sniadecki (1840) in Poland observed differences in rickets incidence between urban and rural children, hinting at an environmental factor. Speculation arose regarding the potential role of sunlight, fresh air, and exercise in the disease's etiology. At the turn of the twentieth century (late 1800s and early 1900s), a vigorous debate ensued regarding whether rickets resulted from a dietary deficiency or an environmental factor. Researchers like Owen (1889) and Palm (1890) supported the environmental perspective, noting substantial geographical variations in rickets incidence within the UK and between northern and southern regions of China, respectively. In 1890, Theobald Palm put forward a proposition, drawing upon his extensive research as a medical missionary in Japan and China, that sunlight exposure could serve as a preventive measure against the disease. In 1912, Casimir Funk defined various nutritional diseases by conducting experiments with semi-synthetic diets and identifying essential substances he called "Vital-amines" or "Vitamins." In 1919, Sir Edward Mellanby further demonstrated the nutritional aspect of rickets by inducing the disease in beagle dogs through a diet lacking an anti-rachitic factor and successfully curing it with cod-liver oil. In 1922, McCollum et al. discovered that the anti-rachitic substance in cod-liver oil, which they named Vitamin D, was distinct from vitamin A. The connection between nutrition and sunlight exposure in preventing rickets was later investigated by Harriette Chick (Chick et al., 1922) and Harry Steenbock (Steenbock and Black, 1924), resolving the mystery of how both light and diet could cure the disease. In 1924, Steenbock and Black performed a groundbreaking experiment demonstrating that irradiation of certain foods increased their vitamin D activity, leading to a significant advancement in understanding the role of nutrition in rickets prevention. The historical significance of this period was documented by Hess (1929) in a monograph on vitamin D. In the late 1920s, Adolf Windaus elucidated the structure of several sterols, including vitamin D3 and 7-dehydrocholesterol, the precursor of vitamin D3 in the skin, earning him the 1928 Nobel Prize. Following the Nobel Prize, Vitamin D3 was first chemically synthesized in the 1930s, and its metabolism to the active form 1,25-dihydroxyvitamin D3 and its mode of action in calcium and phosphate homeostasis were elucidated in the latter half of the 20th century. Following Steenbock and Black's (1924) discovery, a patent was filed claiming that irradiation of yeast added to milk could increase vitamin D content, leading to the establishment of the Wisconsin Alumni Research Foundation (WARF). The foundation played a crucial role in commercializing university research and funding future studies, benefiting numerous researchers, including Nobel laureates. On the humanitarian front, the fortification of foodstuffs with vitamin D, such as milk, bread, margarine, and even beer, resulted in the near eradication of rickets and osteomalacia in the United States and Canada. This fortification had a significant impact, particularly in regions with limited sunlight exposure during the winter months. In 1998, approximately 50 years after the discovery of vitamin D, researchers, began to unravel the mechanisms by which vitamin D regulates calcium and phosphate levels in the body. It was found that vitamin D, whether obtained from the skin or the diet, exists in an inactive form and requires two metabolic steps to become an active hormone. In 1968, Hector DeLuca, a student of Harry Steenbock, identified the first step in the liver, leading to the formation of 25-hydroxyvitamin D3 (25-OH-D3), which is the predominant circulating form and serves as a measure of vitamin D status. The second step of activation occurs primarily in the kidney, resulting in the formation of the active form of vitamin D known as 1,25-dihydroxyvitamin D3 or calcitriol. Currently, the year 2000 and beyond, synthetic vitamin D analogs have been utilized as therapeutic agents for various ailments including bone disease, chronic kidney disease, and psoriasis. This highlights the extensive involvement of diverse disciplines in the intriguing history of vitamin D.
Vitamin D is an essential nutrient that our bodies need to stay healthy. It helps us absorb calcium from our food, which is important for strong bones and teeth. It also plays a role in the functioning of our muscles and immune system. When we don't get enough vitamin D, we can develop a deficiency, which means our bodies are not getting enough of this important nutrient. This can happen for a number of reasons, including not getting enough sunlight, not eating enough vitamin D-rich foods, or having a medical condition that prevents our bodies from absorbing vitamin D properly. Symptoms of vitamin D deficiency can include tiredness, muscle weakness, and bone pain. In some cases, a deficiency can lead to more serious health problems, such as osteoporosis or immune system disorders. The good news is that vitamin D deficiency can usually be treated with supplements or changes to our diet and lifestyle. If you think you may be deficient in vitamin D, it's important to talk to your healthcare provider. They can help you figure out the best way to address your deficiency and get you back to feeling your best.
- 1. Lack of Sunlight Exposure: Vitamin D is synthesized by the skin when exposed to sunlight. If you don't spend enough time outdoors, you may not be producing enough vitamin D. - 2. Inadequate Dietary Intake: Your body can also get vitamin D from certain foods, such as fatty fish and fortified dairy products. If you don't eat enough of these foods, you may not be getting enough vitamin D. - 3. Malabsorption Issues: Vitamin D is absorbed in the small intestine, so if you have a condition that affects your ability to absorb nutrients, such as celiac disease or inflammatory bowel disease, you may be deficient in vitamin D. - 4. Obesity: Vitamin D is a fat-soluble vitamin, which means it is stored in adipose tissue. People who are overweight or obese may need more vitamin D than others because they have more body fat. - 5. Dark Skin: Melanin, the pigment that gives skin its color, can reduce vitamin D production in the skin. People with dark skin are at a higher risk of vitamin D deficiency, especially if they live in areas with limited sunlight. - 6. Kidney or Liver Disease: Vitamin D is activated in the liver and kidneys, so if you have kidney or liver disease, your body may not be able to produce enough active vitamin D.
The most common treatment for Vitamin D deficiency is through oral supplements that contain Vitamin D. Depending on the severity of the deficiency, a physician may recommend high-dose supplements or injections. In addition to supplements, it's essential to maintain a balanced and healthy diet that includes Vitamin D-rich foods such as fatty fish, egg yolks, and cheese. It's also important to get enough sun exposure as sunlight triggers the production of Vitamin D in the skin. However, it's crucial to protect the skin from harmful UV rays when spending time outdoors. A doctor can recommend the appropriate treatment for individuals based on their specific condition and needs.
- Be physically active outdoors: Engaging in outdoor activities like walking, jogging, cycling, or gardening can help increase your exposure to sunlight. Combine physical activity with sunlight exposure to promote overall health and well-being while supporting vitamin D synthesis. - Maintain a healthy body weight: Vitamin D is a fat-soluble vitamin, and excess body fat can sequester it, making it less available for use by the body. Maintaining a healthy body weight can help optimize vitamin D levels and overall health. - Consider your geographical location: The amount of sunlight and UVB radiation varies depending on your geographical location and the season. If you live in higher latitudes with limited sunlight exposure, particularly during the winter months, you may be at a higher risk of vitamin D deficiency. In such cases, it may be even more important to ensure adequate vitamin D intake through diet, supplements, or other sources. - Regular check-ups and monitoring: If you have a vitamin D deficiency, it's important to work closely with a healthcare professional. They can monitor your vitamin D levels and provide guidance on the most appropriate lifestyle changes, dietary modifications, and supplementation to address your specific needs.
- Fatty Fish: Fatty fish like salmon, mackerel, trout, and sardines are excellent sources of vitamin D. A 3.5-ounce (100-gram) serving of cooked salmon can provide around 400-500 IU (International Units) of vitamin D, which is a significant amount. - Cod Liver Oil: Cod liver oil is derived from the liver of codfish and is a concentrated source of vitamin D. Just one tablespoon (15 ml) of cod liver oil can provide over 1,300 IU of vitamin D. - Canned Tuna: Canned tuna, especially the varieties packed in oil, can be a good source of vitamin D. A 3.5-ounce (100-gram) serving of canned tuna usually provides around 150-250 IU of vitamin D. - Egg Yolks: Egg yolks contain small amounts of vitamin D. However, the vitamin D content can vary depending on the diet of the hens. It's worth noting that most of the vitamin D in an egg is found in the yolk, so make sure to consume the whole egg. - Fortified Dairy Products: Many dairy products like milk, yogurt, and cheese are often fortified with vitamin D. Check the labels to ensure they are fortified, as not all dairy products have added vitamin D. Fortified milk can provide around 100 IU of vitamin D per 8-ounce (240 ml) serving. - Fortified Plant-Based Milk: Some plant-based milk alternatives, such as soy milk, almond milk, and oat milk, are fortified with vitamin D. Similar to fortified dairy products, the vitamin D content can vary, so it's important to check the labels. - Mushrooms: Mushrooms are unique among plant foods because they contain a compound called ergosterol, which can be converted into vitamin D when exposed to sunlight or UV light. Exposing mushrooms to sunlight for 15-30 minutes can significantly increase their vitamin D content.