Bring Me Sunshine and Vitamin D by
Until recently any discussion of vitamin D would have been confined to its promotion of calcium absorption in the gut and calcium transfer across cell membranes, thus contributing to strong bones and a healthy nervous system.
But in the last decade new findings suggest it plays a role in many important body systems. In fact most tissues and cells in the body, including heart, stomach, pancreas, brain, skin, gonads, and activated T and B lymphocytes, have vitamin D receptors. Vitamin D has also been found to regulate the action of a number of genes.
Vitamin D, calciferol, is a fat-soluble vitamin. There are two types found in nature. Ergosterol, which is found in plants, gets converted to vitamin D2 (ergocalciferol) in the body. Vitamin D3 (cholecalciferol) is found in animal foods.
The vitamin is also derived from sunlight. During exposure, 7-dehydrocholesterol, which is present in the epidermis, is converted to previtamin D3, which in turn is isomerised by a thermally induced process to vitamin D3.
Previtamin D3 and Vitamin D3 are efficiently absorbed by sunlight and converted to a multitude of other sterols. So the skin can never generate quantities of vitamin D3 excessive enough to cause intoxication. That is why lifeguards and sun worshippers never suffer from vitamin D toxicity.
Vitamin D is biologically inactive. It is, in reality, a prohormone, so it must be converted first in the liver to the form 25-hydroxyvitamin D or 25(OH)D. This is the major circulating form of the vitamin. In the kidney it is converted to 1,25-dihydroxyvitamin D or 1,25(OH)2D, which is the active hormone. This is also referred to as calcitrol.
Ultraviolet (UV) light is divided into 3 bands or wavelength ranges, which are referred to as UV-A, UV-B and UV-C.
The ultraviolet wavelength that stimulates our bodies to produce vitamin D is UV-B. It is also the primary cause of sunburn. However, it also induces special skin cells called melanocytes to produce melanin, which is protective.
The amount of UV-B reaching a given population will depend on latitude, altitude, season of the year, cloud cover and pollution.
Vitamin D is required to maintain normal blood levels of calcium and phosphorus. With sufficient vitamin D the small intestine will absorb on average, 30% of dietary calcium. Without it the small intestine absorbs no more than 10-15%. During growth, lactation, and pregnancy, the efficiency increases to 80%. Deficiency during this period can result in the bone-deforming disease rickets.
Although bone growth stops in adults there is a constant state of bone turnover. Severe vitamin D deficiency in adults results in inadequate blood calcium which gives rise to secondary hyperparathyroidism. This can precipitate or exacerbate osteoporosis.
In deficiency states hormonal adjustment may maintain the serum calcium concentration within the normal range but it causes a loss of phosphorus in the urine. This, and the need for calcium to be diverted to the blood, prevents adequate mineralisation of the osteoid in the bone, which in turn results in osteomalacia (soft bones). The lack of structural support also increases the risk of fracture.
The mineral content of bones tested after birth and at age 9 were shown to be related to blood levels of vitamin D during late pregnancy. Researchers have argued on the basis of such research evidence that bone development in adults is related to vitamin D levels during pregnancy and early childhood.
Muscle Weakness & Pain
Specific receptors for vitamin D have been identified in human muscle tissue. Studies have demonstrated that elderly persons with higher vitamin D serum levels have increased muscle strength and a lower number of falls.
Of 150 consecutive patients referred to a clinic for the evaluation of persistent, non-specific musculoskeletal pain, 93% had serum 25(OH)D levels indicative of vitamin D deficiency.
A clinical observation was reported in the Archives of Internal Medicine in April, 2000. Five patients had severe weakness and fatigue. They were confined to wheelchairs. Blood tests revealed all suffered from severe vitamin D deficiency. They received 50,000IU of vitamin D per week. All became mobile within six weeks.
In a study published in 2003, 122 elderly women were supplemented with 1200mg calcium plus 800IU of vitamin D or calcium alone for 3 months. The vitamin groups’ serum 25-hydroxyvitamin D increased by an average of 71% and they performed dramatically better in tests of muscle strength. They had a 49% reduced risk of falling compared to the calcium only group.
Vitamin D receptors are present in immune cells. Autoimmune responses are mediated by T cells. Calcitrol has been found to modulate T cell responses such that the autoimmune responses are diminished.
The commonest autoimmune diseases including type 1 diabetes, multiple sclerosis and rheumatoid arthritis have all been successfully prevented in mice that were prone to these diseases if they received calcitrol early in life. Incidence of autoimmune diseases tends to be rare near the equator where vitamin D is produced in abundance.
Type 1 Diabetes
In Type 1 diabetes, insulin producing beta-cells of the pancreas are the target of the inappropriate immune response.
In a recent study it was reported that the lower the vitamin D the less likely participants were to produce enough insulin or to show sufficient sensitivity to insulin. It was found that increasing a person's blood concentration of the vitamin from 25 nmol/l to about 75 nmol/l would "improve insulin sensitivity by 60%" which is a greater increase than many anti-diabetes drugs provide.
In another recent study it was shown that vitamin D deficiency is likely to be a major factor for the development of type one diabetes in children.
In a Finnish study, infants who received a vitamin D supplement in the first year of life had an 80% reduced risk of diabetes compared with non supplemented infants. And the risk was reduced by a further 80% if they took 2000IU a day compared with lower dosages.
Similar findings were found in an animal study. When a strain of mice who typically develop type 1 diabetes received 1,25(OH)2D throughout their life, their risk of developing the disease was reduced by 80%.
In MS, the immune response targets are the myelin producing cells of the central nervous system.
Mother rats deprived of the vitamin before birth have offspring with damage to their brains. It shouldn’t be too surprising then that being born in the winter or spring, when vitamin D reserves are at their lowest, is associated a number of nervous system disorders including MS.
Populations studies find that people who live at higher latitudes face an increased risk of multiple sclerosis. This was first noted in 1960 where evidence was presented of a negative correlation between MS prevalence and hours of sunshine. It was later proposed that genetically susceptible individuals may need larger than normal amounts of vitamin D during myelin formation. It was theorised that insufficient vitamin D during childhood might result in defective myelin which would be susceptible to breakdown in later life.
An Australian study found that if children are exposed to UV-B particularly in winter time the risk of MS is reduced.
People with non-melanoma skin cancer, an indication of extended sun exposure, were compared with healthy controls. Their risk of developing MS was reduced by 50%.
In two ongoing studies of 187,500 U.S. nurses, women getting at least 400IU of vitamin D per day were only 60% at risk of developing MS compared with women getting less of the vitamin.
Many studies have found being born in the winter or spring gives a small but significantly increased risk of schizophrenia; the more so in northern latitudes. This may be because normal brain development is altered in deficiency states during pregnancy or early infancy.
The risk is also greater for those brought up in towns and cities. They tend to be less exposed to sunlight, with the risk in London being found to be greater than in the smaller towns of Bristol and Nottingham. This might be explained by greater air pollution which reduces exposure to UV-B.
A higher than expected incidence of schizophrenia is found in black immigrants and their families in the UK. This could be because dark skin is much less efficient at producing vitamin D than white skin.
Northern countries have higher levels of heart disease, and more heart attacks occur in the winter months.
Yet Alpine areas have much lower mortality at this time of year in spite of being much colder in the winter than the UK. However these areas are at a much higher altitude and so get increased exposure to UV-B.
A study in New Zealand found that heart attack patients had lower blood levels of vitamin D than the control group throughout the year.
Blackpool gets 27% more sunshine hours than Burnley with 9% fewer deaths from heart disease. This inverse correlation has been found for 3 other English towns that were studied.
Eskimos have a low incidence of heart disease despite low UV-B levels. But their diet is rich in fish which is abundant in vitamin D.
Vitamin D also has a role in arterial calcification, and young adults with vitamin D deficiency were found to be at greater risk of congestive heart failure than their vitamin D-sufficient counterparts.
Recent research points to heart disease as an inflammatory process. A marker for this is C-reactive protein. This is regulated by cytokines which are suppressed by calcitrol in a dose dependent manner.
Vitamin D deficiency has been clearly linked with Syndrome X which refers specifically to a group of health problems that can include insulin resistance, diabetes type 2, abnormal blood fats, overweight, and high blood pressure. Asian immigrants in the UK have four to five times the incidence of diabetes than whites.
Vitamin D was found to be effective in mice models in down-regulating renin and angiotensin - enzymes involved with water and electrolyte balance - thereby decreasing blood pressure. It may also have an impact on blood pressure through its role in calcium metabolism.
Population studies link hypertension with higher latitudes and lower levels of serum vitamin D. In 1979 a study showed that people living at higher latitudes in both the United States and Europe were at higher risk of hypertension.
Afro-Americans have more hypertension than white Americans. They also have lower blood vitamin D levels .
Other studies suggest an inverse relationship between serum 1,25(OH)2D levels and blood pressure. One randomised controlled trial found those taking 1600IU of vitamin D with 800mg of calcium for 8 weeks had a significant 9% drop in systolic blood pressure compared to those taking calcium alone.
Hypertensive patients exposed to UV-B radiation for 3 months had a >180% increase in circulating concentrations of 25(OH)D and a 6mm Hg decrease in their diastolic and systolic blood pressures; results similar to what would be expected if the they took blood pressure medication. A similar control group exposed to UV-A saw no such drop.
Obesity & Weight Problems
People who are obese are chronically deficient in vitamin D. The vitamin is efficiently deposited in body fat stores and is not bioavailable.
Many diseases are associated with obesity, which is a growing problem. Yet UV-B stimulates the production of melanocyte stimulating hormone (MSH), an important hormone in weight loss and energy production. Could lying flat on your back in the sun help you to lose weight? As astonishing at that may sound, it could be true.
MSH acts on the brain to control the effects of the hormones insulin and leptin which regulate body fat and hunger. In a study where subjects were given MSH, they lost 1½ kilos of body fat in just 4 weeks.
Another study found that vitamin D deficiency was an independent predictor of obesity.
Polycystic Ovarian Syndrome was corrected in 7 out of 14 women who recovered their periods with supplementation of vitamin D and calcium and 2 of these became pregnant.
Infertility is associated with low vitamin D. Vitamin D supports production of oestrogen in men and women.
Those with PMS including migraine have been shown to be deficient in vitamin D with reduced bone mass. Symptoms have been eliminated with calcium and vitamin D supplements.
Low blood concentrations of vitamin D were linked to gum disease in a study of 11,200 men and women. The rate of loss in tooth-gum attachment was 25% higher among those with the least vitamin D compared to those with the most vitamin D.
Lack of Vitamin D makes us more vulnerable to infection
We have already seen that vitamin D has profound effects on the immune system. Immune cells have vitamin D receptors. Vitamin D can transform white blood cell monocytes into macrophages. And within macrophages inactive D3 can be converted to calcitrol.
Vitamin D deficiency increases the risk of TB. Those with TB have less of the vitamin in their blood than healthy controls.
In days gone by people were sent to a sanatorium to recover with sunshine. Dr Finsen won the Nobel Prize in 1903 for showing how TB of the skin could be cured with UV radiation. Nobody seems to remember any of this however.
The condition of the skin can improve dramatically with exposure to the sun or a sun ray lamp or creams containing vitamin D.
A study published in 1997 “showed that a tested commercial nonprescription tanning unit improved both psoriasis severity and health-related quality of life. Commercial tanning bed treatments may be a useful approach in patients unable to obtain office-based ultraviolet treatments.” (J Invest Dermatol. 1997 Aug;109(2):170-4)
Another study states: “recent advances in investigation have shown that vitamin D also functions as a regulator of cellular growth and differentiation in various tissues. The skin is not an exception from such effects of vitamin D; it is regarded as a site of its activation and action. Evidence has accumulated showing that the active form of vitamin D and its analogs suppress growth and stimulate the terminal differentiation of keratinocytes. In psoriatic lesions, epidermal keratinocytes exhibit hyper-proliferation and impaired differentiation triggered by inflammation. Therefore, it is quite reasonable that vitamin D is effective on psoriasis. Indeed, within the past decade, analogs of vitamin D3 have been used as topical therapy for psoriasis.” (J Dermatol. 2003 Jun;30(6):429-37)
As early as 1941 it was observed that people living at higher latitudes of the USA had a higher risk of dying from the most common cancers than did people living in lower latitudes.
This was confirmed in the late 1980s and early 1990s when several investigators reported increased risks of dying from colon, prostate, and breast cancer in people living at higher latitudes in both the United States and Europe.
In fact 16 cancers have been linked with low intensity UV-B.
25% of deaths from breast cancer in women in Europe have been attributed to their lack of UV-B.
Both sexes have a higher risk of dying of cancer if they have minimum exposure to sunlight.
Men exposed to little sunlight develop prostate cancer up to 5 years earlier than by those exposed to more sunlight throughout their lives.
African American males have both the lowest serum 25(OH)D concentrations and the highest prostate cancer incidence of any population group in the United States.
An important function of calcitrol is its ability to down-regulate cells that are dividing too rapidly. Normal and cancer cells that have a vitamin D receptor i.e they have the ability to make 1,25(OH)2D, often respond to 1,25(OH)2D by decreasing their proliferation and enhancing their differentiation (specialisation) and maturation so that they stop growing, and eventually succumb to programmed cell death. Cancer cells, in contrast, remain immature, rapidly divide, and are immortal.
It isn’t just population studies that link cancer with vitamin D depletion. Clinical studies are also showing that vitamin D deficiency is associated with breast, prostate, colon and cancer of the ovaries.
Diane Feskanich of Brigham and Women's Hospital in Boston and her co-workers compared blood tests from 193 cancer patients with those of age-matched women who were free of cancer. They reported that women in the highest 25-D group with about 100 nmol/l, had only about half the cancer risk of women in the lowest group, averaging 40 nmol/l.
Although the warning to stay out of the sun over the last decade was designed to reduced the incidence of melanoma, the reality is that the incidence of this cancer continues to rise in spite of people avoiding the sun or covering themselves up with sun lotion.
The advice may be having the opposite effect. Firstly melanomas may only be partly caused by the sun. They can occur on parts of the body like the soles of the feet that are seldom exposed to sunlight. The cause of melanoma is far from clear.
Secondly vitamin D stimulates the immune system. People who avoid the sun may be more prone to skin cancer as well as all the diseases mentioned so far.
Thirdly, people may spend more time in the sun if they are ‘protected’ with sun lotion.
Although they may be screened from UV-B, they are not well protected against UV-A. This may cause damage over time.
Casual Exposure Is Good Enough?
In spite of all the new evidence for these roles, the official position is that adults get enough vitamin D. Just casual exposure to sunlight on the hands and face is considered to provide sufficient quantities of the vitamin to meet our needs.
The only groups advised to use supplements are those over 65, pregnant or lactating women, and children up to the age of three. The former are recommended to take 400IU (10mcg) a day. Breast fed babies are recommended drops to provide 340IU a day. From age 6 months to 3 years this is reduced to 280IU a day.
The recommendations to avoid or limit exposure to the sun were established over a decade ago to reduce the incidence of skin cancer, which had been rising for many years. In spite of all the new research findings over this period and the fact that the incidence of melanoma, the most serious type of skin cancer, has continued to increase (24% in the last 5 years) since these guidelines were established, no change in these recommendations have been made.
Sources of Vitamin D
Vitamin D is found in a restricted number of foods. The best source is oily fish. Although more people may well be consuming this with the benefits of omega 3 fatty acids becoming better known, nevertheless it is still not widely eaten. Indeed we are instructed to restrict our intake because of pollution!
Dairy foods are reasonable sources but of course we are instructed to limit intake because their cholesterol content is supposed to increase the risk of heart disease. Margarine is fortified with the vitamin during processing. In the USA and some other countries it is also added to milk.
Liver is another good source but is not widely eaten. In January, the Scientific Advisory Committee on Nutrition recommended that liver should not be eaten more than once a week because of the risk of bone fractures from excess retinol.
It seems we must restrict all foods that contain this vitamin.
Vitamin D content of Foods (mcg per 100g)
Cod Liver Oil 210.0
Vegetable Oil 0
Calves liver 0.25
Lambs liver 0.50
Pigs liver 1.13
Grilled herring 25.0
Fried mackerel 15.4
Tuna in oil 5.8
Because of the limitation of vitamin D in the food supply, we rely on the sun to provide the vast majority of our vitamin D needs.
Vitamin D Daily Reference Intake
Before 1997, the recommended dietary allowance (RDA) of vitamin D for infants and children was 10 mcg (400IU). That is the amount of the vitamin found in a teaspoon of cod liver oil; an amount that was found to effectively and safely prevent rickets.
The adult RDA was put at 200IU, half the children’s dose, for no particular reason. It was not based on its effect on the serum 25(OH)D concentration. It appears to be completely arbitrary.
The newly revised daily reference intakes maintain these recommendations, although there was a big increase for those aged over 70.
Stages of Vitamin D Status
Dr Zittermann (British Journal of Nutrition Vol 89(5), May 2003, pp 552-572), puts vitamin D (25(OH)D nmol/L) status into 5 ranges: deficiency (below 12.5), insufficiency (12.6 - 50), hypovitaminosis (51 - 100), sufficiency (101 - 250), and toxicity (251+).
In deficiency there is severe hyperparathyroidism, calcium malabsorption, bone diseases such as rickets in children and osteomalacia in adults, and myopathy.
Insufficiency results in mild hyperparathyroidism, low intestinal calcium absorption rates, reduced bone mineral density, and perhaps subclinical myopathy.
In hypovitaminosis, body stores are low and parathyroid hormone levels can be slightly elevated.
In sufficiency, there is no disturbance of vitamin D dependent functions.
In toxicity, too much calcium is absorbed leading to hypercalcaemia.
Vitamin D Status in the UK
In the winter, children average 52nmol/L which just pushes them from insufficiency into the hypovitaminosis range. Although in the summer this rises to 80, it still remains in this range. Children with dark skin have levels throughout the year ranging from 36 - 42, which puts them in the insufficient range.
The situation with teenagers and young adults is often worse than with children. For instance in France, adolescents average 21 in winter and 71 in summer. In Germany, young adults average 30 in winter and 70 in summer. Since these countries have a more southerly latitude than the UK and their summer holidays begin earlier than in the UK, it is quite likely that the figures for UK adolescents and young adults would be even worse.
Elderly people in the UK average 23 and 35 in the winter and summer respectively, which puts them at great risk.
This was recognised in a recent paper (BMJ. 2005 Mar 5;330(7490):524-6) which concluded: “Vitamin D deficiency among elderly people is much more common than previously recognised. It constitutes a serious public health problem for residents of old people's homes, nursing homes, and long stay wards and housebound people in the community. The consequences include muscle weakness, body sway, and a tendency to falls and fractures, as well as osteomalacia.”
“Exercise is one evidence based approach to preventing falls, but not all elderly people are able to access or take up exercise training owing to disability and other factors. Treating elderly housebound people with 800IU daily of vitamin D (or equivalent, such as 100,000IU every 4 months) should also be seriously considered.”
How Much Sun Exposure?
The UK National Radiological Protection Board (NRPB) claim in their 2002 report that “short periods outdoors as normally occur in everyday life will produce sufficient vitamin D and additional or intensive exposures will not confer further benefit.” This appears to be based on just one study of 10 elderly people during a single English summer.
Reinhold Vieth, an internationally recognised expert on vitamin D takes a different view. He calculates that such short exposures on the hands and face as the NRPB recommend will only supply between 200IU and 400IU during the summer months, an amount that will leave a substantial proportion of the population deficient.
In the tropics one only needs to spend ten minutes in the sun to achieve maximum synthesis of pre-vitamin D in the area exposed directly to the sun and thereby maximum production in the body.
Michael Holick, one of the world’s foremost authorities on vitamin D (who was sacked from his post last year at Boston University for suggesting that people seek out a few minutes of unblocked sunlight a couple of times per week) has demonstrated that the amount of vitamin D synthesised at different latitudes can be quite substantial.
At midday in Boston (latitude 42ºN) 50% more pre-vitamin D can be synthesised compared to Edmonton, Canada (latitide 52ºN). The latter has almost the same latitude as London, England.
In Britain (latitude 51ºN - 61ºN) the ultraviolet band isn’t strong enough for 6 months of the year between October and March to promote any vitamin D synthesis (this is extended by 4 - 6 weeks in Scotland).
Since the half life of vitamin D in the body is no more than 6 weeks, deficiencies are likely to be well established in many people by late winter or early spring.
Babies born during this period are particularly vulnerable to vitamin D deficiency and are at greater risk of the health problems covered earlier. Also, since vitamin D is low in milk, breast-fed babies who are kept out of the sun may be at even greater risk.
This was pointed out in a paper in The Lancet in 2003. It told of how rickets is reappearing because of extensive breastfeeding without supplementation especially where mothers are deficient. They also pointed to avoidance of the sun because of cancer fears, and the high prevalence of immigrant groups in temperate climates.
Vieth, as well as other experts have suggested that optimum health would be achieved with a daily vitamin D input of 2000IU. For a white person in England in the middle of summer, to achieve these levels would require them to sunbathe for 20 minutes three times a week between 11.00am and 3.00pm.
Dark skinned people take up to six times as long to make the same amount of vitamin D as those with white skin. To achieve the same result, a person with dark skin would have to sunbathe for 6, one hour sessions a week.
According to professor Holick: “People don't realise that 90 to 95% of your vitamin D requirement comes from exposure from sunlight, and if you always wear sun block and never have direct sun exposure you will become vitamin D deficient, and at high risk of developing many serious chronic diseases.”
Sunlight & Skin Cancer
The most serious form of skin cancer is melanoma. 7000 people are diagnosed each year. The annual death rate in the UK is 1,750. There are other types of skin cancer that people die of each year which account for another 200 deaths.
It is assumed that melanoma is caused by the sun, but the mechanism for this is unclear. Adults and children who work and play outdoors have less melonoma than those who work or play more indoors. People who recall being sunburned and who are only exposed irregularly to the sun have a higher risk of melanoma especially if they have fair skin.
If the sun was the cause of melanoma one would expect most cases to occur on the hands and face. In fact in white people most cases occur on men’s backs and women’s upper legs. In black people they occur on the lower legs and soles of the feet.
Two-thirds of melanoma are deemed to be caused by excessive sun exposure. However other methods of analysis put this at 10 - 15%.
Other risk factors for melanoma include excess body weight, lack of exercise and poor diets. The increase in melanoma over the last two decades parallels many other types of cancer.
One of the world's foremost authorities on the subject of skin cancer is dermatologist A. Bernard Ackerman, MD. He states that the link between melanoma and sun exposure has not been proven. Sunburns, even the painful or blistering kind sustained early in life, do not necessarily lead to cancer. The research is inconsistent and fails to make the case.
Sunscreens do not protect against melanoma. He points to a recent editorial in the Archives of Dermatology, which also concludes that there is scant evidence to support this crucial dogma (Bigby 2004).
He challenges the tenet that the more intense a person's exposure to the sun, the greater their risk of melanoma. Although we are told that the incidence of melanoma increases in populations that live nearer the equator, the correlation is not that simple. Epidemiological data on melanoma, says Dr. Ackerman, are imprecise and inaccurate. The data simply “cannot demonstrate cause and effect.” He advises people not to make the mistake of thinking that by avoiding sunlight or using sunscreen they will be protected against deadly melanoma. This, he says, is a myth.
Dr. William B. Grant, who heads the Sunlight, Nutrition and Health Research Center in San Francisco, agrees that sunscreens fail to protect against melanoma. He points out that sunscreens primarily block the shorter wavelength UV radiation, whereas it is the longer wavelength UV that poses the greater risk for melanoma.
Dr. Grant feels that while there is some evidence pointing to a link between sunlight and melanoma, it is not a simple cause and effect relationship. Many other factors should be taken into account. For example, while it is true that melanoma rates increase with increasing latitude, it is also true that occupational exposure to UV radiation is associated with a reduced risk of melanoma. Conversely, for those of northern European ancestry living south of their latitude of origin, melanoma rates are much higher than they are in their countries of origin.
Dr. Grant also points out that there is substantial evidence that dietary factors, particularly vitamin D, can have a significant effect on the risk of developing melanoma. He points to the work of Millen and colleagues, of the National Institutes of Health, showing that diets rich in vitamin D and carotenoids, and low in alcohol, may be associated with a reduction in risk for melanoma. Therefore, Dr. Grant feels that diverse factors including diet, skin type, the presence, number and type of moles, and ethnic, ancestral and geographic origin also have a major influence on melanoma risk. To say that sunlight causes melanoma is at best an oversimplification and at worst a distortion of the scientific evidence.
Of the 1.3 million people who will be diagnosed with cancer this year in the USA, nearly 600,000 will die. Dr. Grant estimates that about 47,000 of these deaths will result from internal cancers that could have been prevented by adequate UV exposure and consequent vitamin D synthesis.
Dr Ackerman also points out that the definition of melanoma has changed over the past few decades, leading doctors to diagnose, remove and cure lesions that until recently would not have been called melanoma. This puts in doubt whether there really is an ‘epidemic’ of melanoma.
More than 60,000 cases occur annually in the UK. Fortunately the vast majority are easily treatable. However in a small number of cases they can leave disfiguring scars and several hundred deaths result from these cancers.
The most common is basal cell followed by squamous cell. The latter has been linked to sunlight but there is some doubt about the former. These skin cancers occur commonly in the elderly and some research suggests that excess body weight and high fat diets are risk factors.
The message to “keep out of the sun” is a decade out of date. It doesn’t take into account new research findings on vitamin D that show it to be vital to our immune and many other body systems.
In formulating a public health policy, you have to look at all factors and not just isolate a single issue. Restricting sun exposure may or may not reduce the number of deaths from skin cancer. Even if lives are saved they will be few in number. Compare that to the lives saved from colon cancer, breast cancer, prostate cancer, and possibly 13 other cancers. Compare that to those who’s lives might be saved from autoimmune diseases, fractures and cardiovascular disease.
Dermatologists should not be determining national policy on this issue. Many other specialists should be allowed to put forward evidence from their own speciality. Whatever happened to the new evidence-based criteria for dealing with health issues? If such evidence were allowed, evidence which points to the substantial benefits that derive from optimal vitamin D intake, then the current policy would surely be scrapped.
The National Cancer Institute published two studies in February (see Addendum). In one, a history of high UV exposure was associated with reduced risk of non Hodgkin’s Lymphoma. The greater the exposure, the lower the risk.
In the other study, those with early onset melanoma who had been sunburned, had high intermittent sun exposure and sun damaged skin were less likely to die than those who kept out of the sun.
These studies prompted an editorial in the Journal. They looked at some of the evidence and concluded that sunlight is a beneficial influence on the incidence and outcome of cancer, probably via vitamin D synthesis.
Unfortunately, dermatologists have backed themselves into a corner on this issue and prefer to maintain the “keep out of the sun” mantra rather than look at the research evidence or wider issues. If they won’t back down, then pressure must come from elsewhere. Let’s hope we don’t have to wait for an acute epidemic of vitamin D deficiency diseases before there is a change of policy.
“There’s no such thing as a healthy tan” is a simple health message to put across. But it’s wrong. A sensible sun policy is not easy to put across because it must take into account differing skin types, presence of moles, ethnicity, family history and lifestyle factors. That is a real problem, but surely not an insoluble one.
This article was first published in Enzyme Digest No. 67/68, New Year/Spring 2005
Sun exposure and mortality from melanoma
528 subjects with cutaneous melanoma were followed up for 5 years. Data, including measures of intermittent sun exposure, perceived awareness of the skin, skin self-screening, and physician screening, were collected during in-person interviews and review of histopathology and histologic parameters for all of the lesions. During the period 58 died of melanoma and 24 from other causes.
Results: sunburn, high intermittent sun exposure, skin awareness histories and solar elastosis (a marker of sun damage) were statistically significantly inversely associated with deaths from melanoma.
Conclusion: sun exposure is associated with increased survival from melanoma.
Journal of the National Cancer Institute Vol. 97 No. 3 February 2nd, 2005 p. 195 – 199
Comment: Mortality from melanoma was approximately half as much among those with significant solar elastosis as those without.
The authors speculate whether an effect of sun exposure on melanoma survival is plausible biologically. “Sun exposure is necessary for the syntheisis of 25-hydroxy vitamin D3 in the skin which, when converted to 1,25(OH)2 D3, the primary ligand for the vitamin D receptor, has anti-proliferative and proapoptic effects. It would be reasonable to speculate therefore that the apparently beneficial relationship between sun exposure and survival from melanoma could be mediated by vitamin D.”
However they put forward another possibility. That the sun induces melanization and increases DNA repair capacity.
Ultraviolet radiation exposure and risk of malignant lymphomas
3,740 patients from Denmark and Sweden diagnosed with malignant lymphomas and 3,187 controls provided a detailed history of UV exposure, skin cancer and other risk factors.
Results: there was a consistent statistically significant negative association between various measures of light exposure and risk of non-Hodgkin’s Lymphoma. A high frequency of sunbathing and sun burns at age 20 and at 5 - 10 years before the interviews and sun vacations abroad were associated with 30 - 40% reduced risk of non Hodgkin’s Lymphoma. These inverse associations increased as levels of sun exposure increased. There was a similar but weaker association with Hodgkin’s Lymphoma.
Conclusion: a history of high UV exposure was associated with reduced risk of non Hodgkin’s Lymphoma. The positive association between skin cancer and malignant lymphomas is therefore unlikely to be mediated by UV exposure.
Journal of the National Cancer Institute Vol. 97 No. 3 February 2nd, 2005 p. 199 – 209
Comment: The Journal’s editorial, commenting on these two papers, was entitled “Sunlight and Reduced Risk of Cancer. Is The Real Story Vitamin D?” They refer to a number of other related studies and hypothesise that vitamin D may be a critical mediator in the relationship between sunlight and cancer. Solar radiation may have a beneficial influence on both the incidence and outcome of cancer.
In terms of what kind of public health message to make regarding safe levels of sun exposure, they could find no simple answer. A high rate of skin cancer is attributable to UV. Melanomas represent a tiny fraction of these but can be fatal. Each of us has to look at our pigmentation, proneness to sunburn, family and medical history.
They point out that substantial numbers of people in northern latitudes are deficient in vitamin D during the winter months and mention best food sources of the vitamin. They even say that supplements are available although they fall short of recommending them.
Recent developments in vitamin D deficiency and muscle weakness among elderly people
Higher plasma concentration of calcidiol (an intermediate metabolite of the vitamin D group that is formed in the liver) is associated with muscle strength, physical activity, and ability to climb stairs. Lower concentrations are associated with falls among the elderly. Trials support this, with incidence of falls halved and improved musculoskeletal function with supplements of 800IU of vitamin D plus calcium.
Among elderly housebound, frequency of severe vitamin D deficiency was 8.3% for those aged 65 - 74, 14.5% for those aged 75 - 84, and 17.4% at 85+. As well as age and housebound status, vitamin D deficiency is ten times higher in African-American than white women in America.
When vitamin D supplements fail to work it is because of inadequate dose. 400IU a day is ineffective in reducing frequency of fractures. High dosages are safe. Lowest level at which adverse effects found was a serum calcidiol concentration of 200nmol/L corresponding to a daily intake of 40,000IU. 800IU therefore has a 50-fold margin of safety.
Conclusion: vitamin D deficiency in the elderly is much more common than previously recognised. Treating elderly housebound with 800IU a day or 100,000IU every 4 months should be seriously considered.
British Medical Journal Vol. 330 No. 5th March, 2005 p. 524 – 526
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