While there is certainly ample evidence that excessive ultraviolet exposure is a risk factor for the development of melanoma (and may cause premature aging of the skin), there is another side to that coin. When our skin is exposed to ultraviolet light, it produces a crucial chemical compound erroneously called Vitamin D. Without sufficient ultraviolet exposure (and a lack of adequate dietary Vitamin D to make up for the lost endogenous production), a host of systems in the human body cease to function properly, if at all.
Vitamin D History
As the Industrial Revolution took hold in Europe and the previously agrarian population began to move to growing, smoggy cities in order to find industrial jobs, a mysterious affliction began to strike the children of industrial workers in epidemic proportions. Called "rickets", it was characterized by skeletal bones that did not harden but remained cartilaginous.
| What Was The Industrial Revolution?
The rapid industrial growth that began in England during the middle of the eighteenth century and then spread over the next 50 years to many other countries, including the United States. The revolution depended on devices such as the steam engine, which were invented at a rapidly increasing rate during the period. The Industrial Revolution brought on a rapid concentration of people in cities and changed the nature of work for many people.
Children stricken with rickets were slow to crawl and walk and had telltale deformities in their leg bones. Rachitic children also often suffered from painful spasms in their hands and feet, difficulty breathing and persistent nausea. In severe cases, rickets was fatal.
In 1822 a Polish physician named Jedrzej Sniadecki noted an odd geographic distribution of rickets cases in and around Warsaw. Children living in the city itself were much more likely to develop rickets than those living in the outskirts or in the rural areas outside of the city. He concluded (correctly) that rickets was related to lack of exposure to sunshine.1
He published his findings in Polish, however, and they were not widely read. Rickets continued to plague the industrial cities of Europe and the United States for another century. The only other cure that proved effective (but was not widely promoted by the physicians of the day) was the folk tradition of giving cod liver oil to children upon weaning, to provide additional fats. What was not known is that cod liver oil is an excellent source of Vitamin D.
Discovering Vitamin D:
By the end of the 19th century, rickets had become a real problem (in Britain and Scotland especially), and there was great interest in finding a cure. In 1892, British scientist T.A. Palm rediscovered the geographic distribution of rickets that Sniadecki had noted seventy years earlier and in 1919, German scientists showed that rickets could be cured by exposure to artificially produced ultraviolet light.
In 1922 Elmer McCollum, working at Johns Hopkins University in Baltimore identified a fat-soluble constituent in cod liver oil that could cure rickets. Following the alphabetical designation of vitamins A, B and C all isolated earlier, McCollum dubbed this new substance Vitamin D.2
"Recommended Daily Allowance"
Because it can be produced by the human body in response to UV exposure, Vitamin D, also known as cholecalciferol, is not technically a vitamin. The name is still widely used, however and is still somewhat appropriate because of the quasi-essential nature of this nutrient in populations living in areas that do not get sufficient sunlight.
Unfortunately, like many other vitamins, since determining the minimum dose required to ward off diseases of clinical deficiency, this has stubbornly remained as the "recommended daily allowance", which for Vitamin D is 400 IU or 10 micrograms. In northern areas of the United States , especially in the winter, this amount of supplemental Vitamin D is probably less than half of what is required to maintain optimal serum levels.3
Vitamin D Functions
Functionally, cholecalciferol functions more like a steroid in the human body. One of its most important functions is the regulation of calcium absorption and metabolism. Without sufficient Vitamin D, even if there is sufficient dietary calcium available, it will not be properly absorbed and metabolized. Beyond calcium metabolism, Vitamin D is now being recognized as critical to a number of other body systems.4
There is an interesting epidemiological trend that seems to indicate that the incidence of cardiovascular disease, kidney disease, hypertension and certain cancers is directly related to seasonal and geographical variations in ultra violet light exposure. While there are clearly many factors at work, there is growing evidence that a deficiency of Vitamin D levels in response to reduced sun exposure may play a substantial role in these variations.5,6
Disease Inhibitory Effects:
Vitamin D has a powerful inhibitory effect on the growth of many cancers, including, ironically, some skin cancers.7,8 While excessive UV light exposure is a known risk factor for the development of melanoma, a chronic Vitamin D deficiency created by complete avoidance of unprotected exposure to sunlight will very likely lead to a substantially increased risk of developing other cancers or life-shortening disease.
In fact, one rather interesting study published in 2005 estimated that, while the annual economic costs of excessive UV exposure in the United States (mainly the treatment of melanoma) is $6-7 billion dollars, the economic burden associated with premature death and disease directly relatable to vitamin D deficiency was almost 10 times greater.9
This certainly makes sense as the cancers that appear most closely associated with Vitamin D deficiency are colorectal, prostate and breast; some of the most common and deadly forms of cancer in the United States.
Vitamin D is also closely tied to cardiovascular health. As noted earlier, death from cardiovascular disease fits seasonal and geographical variability that suggests strongly that lack of sun exposure is a factor in its etiology. There is also more direct evidence of the role of cholecalciferol in cardiovascular health.
Although much of its cardio-protective effect is probably via improvements in calcium absorption and metabolism, Vitamin D also reduces serum parathyroid levels. While this effect is thought to be central to cholecalciferol 's cancer preventative effect, elevated parathyroid levels are also associated with the development of cardiovascular disease. Although once suspected as a risk factor for cardiac disease, newer research indicates that the risk acute myocardial infarction actually shows a strong inverse relationship to circulating Vitamin D levels.14,15
One of the best known health benefits of adequate Vitamin D intake/production is bone strength.16 Remember that the primary disease of cholecalciferol deficiency is rickets, characterized mainly by extreme abnormalities in skeletal development in children.
Later in life, insufficient Vitamin D intake can lead to osteoporosis or, in extreme cases, a form of adult-onset rickets called osteomalacia. Older men, and especially women, are prone to bone mass loss and fracture. Additional Vitamin D, either in the form of a supplement or from additional sunlight exposure reduces the risk of fractures and falls in elderly people.17,18
Immune System Modulation:
Perhaps one of the most intriguing effects of Vitamin D in humans is immune system modulation. Multiple Sclerosis is a disease characterized by progressive loss of muscular control believed to be caused by the immune system attacking the nervous system. The cause is unknown but it is five times more common in temperate zones than in the tropics.19
| The Central Nervous System.
The human central nervous system consists of the brain and spinal cord. These lie in the midline of the body and are protected by the skull and vertebrae respectively.
This collection of billions of neurons is arguably the most complex object known.
The central nervous system along with the peripheral nervous system comprise a primary division of controls that command all physical activities of a human.
Neurons of the central nervous system affect consciousness and mental activity while spinal extensions of central nervous system neuron pathways affect skeletal muscles and organs in the body.
That the incidence of a disease that follows this familiar pattern of distribution is inversely related to cholecalciferol intake/production should come as no surprise.20,21 Most recently, a huge epidemiological study of over 180,000 women showed that those with the highest serum Vitamin D levels had a 30% lower risk of developing MS and those who consumed more than 400 IU per day saw a 40% reduction.22 Vitamin D is also showing promise as a potential modulator of other autoimmune disorders like lupus and rheumatoid arthritis.23
Vitamin D Sources
The best and safest way to get adequate Vitamin D is to get sensible exposure to natural sunlight on bare skin. Artificial sunlight, such as that produced by a tanning bed, will also induce cholecalciferol in the skin, so long as it provides adequate UVB light.
During the summer months in most of the northern hemisphere, twenty minutes of UV exposure three times a week is all that is required to ensure sufficient Vitamin D production in persons with light skin color. However, there is insufficient solar intensity during the winter to produce vitamin D in northern latitudes like the upper Mid-West and New England.24
Darker skinned individuals also require either higher intensity light or must spend more time exposed to produce the same amount of Vitamin D.25 During the winter months, individuals living in northern areas must get their cholecalciferol via diet or oral supplements.
Vitamin D is found in cod liver oil and is also added to fortified dairy products in the United States . It is also widely available in supplemental form either by itself or as a part of a multivitamin. It is often combined with calcium supplements to enhance absorption.
Because this vitamin is stored in fat and will accumulate, oral supplementation should be limited to no more than 2000 IU per day. Excessive Vitamin D intake can lead to calcification of the organs and, paradoxically, loss of bone density.
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- Mietkiewski E. Jedrzej Sniadecki, 1768-1838. Acta Physiol Pol. 1987 Mar-Apr;38(2):52-65.
- Nutrition classics from The Journal of Biological Chemistry 53:293-312, 1922. Studies of experimental rickets. XXI. An experimental demonstration of the existence of a vitamin which promotes calcium depositor
- Glerup H, Michelson K, Poulsen L, Hass E, Overbeck S, Thomsen J, Charles P, Eriksen EF. Commonly recommended daily intake of vitamin D is not sufficient if sunlight exposure is limited. J Intern Med. 2000 Feb;247(2):260-8.
- Holick MF. Evolution and function of vitamin D. Recent Results Cancer Res. 2003;164:3-28. Review.
- Giovannucci E. The epidemiology of vitamin D and colorectal cancer: recent findings. Curr Opin Gastroenterol. 2006 Jan;22(1):24-9.
- Grimes DS, Hindle E, Dyer T. Sunlight, cholesterol and coronary heart disease. QJM. 1996 Aug;89(8):579-89.
- Garland CF, Garland FC, Gorham ED, Lipkin M, Newmark H, Mohr SB, Holick MF. The Role of Vitamin D in Cancer Prevention. Am J Public Health. 2005 Dec 27
- Osborne JE, Hutchinson PE . Vitamin D and systemic cancer: is this relevant to malignant melanoma? Br J Dermatol. 2002 Aug;147(2):197-213. Review.
- Grant WB, Garland CF, Holick MF. Comparisons of Estimated Economic Burdens due to Insufficient Solar Ultraviolet Irradiance and Vitamin D and Excess Solar UV Irradiance for the United States . Photochem Photobiol. 2005 Nov-Dec;81(6):1276-86.
- Scragg R. Seasonality of cardiovascular disease mortality and the possible protective effect of ultra-violet radiation. Int J Epidemiol. 1981 Dec;10(4):337-41.
- Zittermann A, Schleithoff SS, Koerfer R. Putting cardiovascular disease and vitamin D insufficiency into perspective. Br J Nutr. 2005 Oct;94(4):483-92. Review.
- Med Hypotheses. 2000 Mar;54(3):475-82. Parathyroid hormone may be a cancer promoter - an explanation for the decrease in cancer risk associated with ultraviolet light, calcium, and vitamin D. 13. Kamycheva E, Sundsfjord J, Jorde R. Serum parathyroid hormone levels predict coronary heart disease: the Tromso Study. Eur J Cardiovasc Prev Rehabil. 2004 Feb;11(1):69-74.
- Lund B, Badskjaer J, Lund B, Soerensen OH. Vitamin D and ischaemic heart disease. Horm Metab Res. 1978 Nov;10(6):553-6.
- Scragg R, Jackson R, Holdaway IM, Lim T, Beaglehole R. Myocardial infarction is inversely associated with plasma 25-hydroxyvitamin D3 levels: a community-based study. Int J Epidemiol. 1990 Sep;19(3):559-63.
- O'Brien KO. Combined calcium and vitamin D supplementation reduces bone loss and fracture incidence in older men and women. Nutr Rev. 1998 May;56(5 Pt 1):148-50. Review.
- Meunier P. Prevention of hip fractures by correcting calcium and vitamin D insufficiencies in elderly people. Scand J Rheumatol Suppl. 1996;103:75-8; discussion 79-80.
- Harwood RH, Sahota O, Gaynor K, Masud T, Hosking DJ; The Nottingham Neck of Femur (NONOF) Study. A randomised, controlled comparison of different calcium and vitamin D supplementation regimens in elderly women after hip fracture: The Nottingham Neck of Femur (NONOF) Study. Age Ageing. 2004 Jan;33(1):45-51.
- Merck Manual of Diagnosis & Therapy 17 th Edition
- Clemens TL, Adams JS, Henderson SL, Holick MF. Acta Psychiatr Scand. 1960;35(Suppl 147):132-47. Some comments on the relationship of the distribution of multiple sclerosis to latitude, solar radiation, and other variables. Cantorna MT, Mahon BD.
- VanAmerongen BM, Dijkstra CD, Lips P, Polman CH. Multiple sclerosis and vitamin D: an update. Eur J Clin Nutr. 2004 Aug;58(8):1095-109
- Munger KL, Zhang SM, O'Reilly E, Hernan MA, Olek MJ, Willett WC, Ascherio A. Vitamin D intake and incidence of multiple sclerosis. Neurology. 2004 Jan 13;62(1):60-5.
- Mounting evidence for vitamin D as an environmental factor affecting autoimmune disease prevalence. Exp Biol Med ( Maywood ). 2004 Dec;229(11):1136-42. Review.
- J Clin Endocrinol Metab. 1988 Aug;67(2):373-8. Influence of season and latitude on the cutaneous synthesis of vitamin D3: exposure to winter sunlight in Boston and Edmonton will not promote vitamin D3 synthesis in human skin.
- Lancet. 1982 Jan 9;1(8263):74-6. Increased skin pigment reduces the capacity of skin to synthesise vitamin D3.