Sunshine and Vitamin D: A Comprehensive Guide to the Benefits of the "Sunshine Vitamin"

Introductíon

With the hundreds of clinical trials published on vitamin D in recent years—I read one study with 132 references—it is obvious that the sunshine vitamin no longer has to play second fiddle to the other vitamins. However, some of the currently available health books either ignore the vitamin or give it short shrift in just a few paragraphs. This has prompted several internationally respected scientists to call vitamin D the most misunderstood and underrated vitamin of all. To muddy the waters still further, other researchers insist that it is a hormone rather than a vitamin. In the meantime, millions of people around the world have a vitamin D deficiency, costing them lots of money, pain, and poor health.

Now that the vitamin has become a superstar, one wonders why it took so long for it to be recognized. As an example, how many life-threatening illnesses might be prevented with vitamin D? To paraphrase Elizabeth Barrett Browning, let us count the ways: osteoporosis, breast cancer, psoriasis, asthma, prostate cancer, multiple sclerosis, osteoarthritis, cardiovascular disease, diabetes, gum disease, colon cancer, Crohn’s disease, scleroderma, rickets, celiac disease, and many others. How many other vitamins—say vitamin B2—have such an impressive résumé? Not many!

When people moved away from the equator and settled in higher latitudes, they lost many of the life-nourishing benefits of the sun—a major source of vitamin D. To compound the problem, the vitamin is only available in a few foods. For example, how many of the following staples are on your grocery list—salmon, cod, eel, sardines, cod-liver oil, and beef liver? Fortunately, in the United States a quart of milk contains 400 IU of the vitamin. The fly in the ointment is that many seniors, young girls, and those who are lactose-intolerant do not drink milk regularly.

In addition, those who live in northern latitudes are bundled up in the winter, so they derive only minimal benefit from the sun. It stands to reason that you get more vitamin D from the sun if you live in San Antonio, Texas, than in Burlington, Vermont, especially during the winter.

I readily agree that it is sometimes difficult to tell the vitamin D players without a program, since there are various formulations and analogs. In dealing with vitamin B1, you are mostly concerned with thiamine, but, with vitamin D, you are faced with 25(OH)D, 25-hydroxyvitamin D, ergocalciferol, 25-hydroxycholecalciferol, vitamin D2, calciferol, 1,25-dihydroxyvitamin D, vitamin D3, and so forth. Hopefully, the fog will clear as you read through this book and/or refer to the glossary.

What about sunscreens? While a suntan is glamorous and ego-boosting, a serious sunburn contributes to melanoma, perhaps the deadliest and most predominant skin cancer. The jury is still out on whether or not sunscreens inhibit the conversion of vitamin D from the sun, as well as how much to use and when to use them. And are dark-skinned people getting enough vitamin D from the sun?

Michael F. Holick, MD, an internationally known expert on vitamin D, offers a partial answer. On a sunny day, he recommends spending five to fifteen minutes in the sun to get your vitamin D and then going inside to apply sunscreen before going outdoors again. Obviously, enough skin has to be exposed to get the benefit from the sun. The traditional deterrent to sunburn is to wear a wide-brimmed hat and protective clothing, but this can interfere with getting enough vitamin D.

Many prominent vitamin D experts insist that the benefits of vitamin D are not being adequately reported in the media. I couldn’t agree more. Reporters have been persuaded by the often-repeated propaganda that too much of the fat-soluble vitamins—like vitamin D—will have us dropping like flies. Obviously, that has not happened, and many people remain deficient in the vitamin.

The media’s interpretation of high doses is hardly scientific, so the public is fed bogus information, either because reporters are inexperienced in writing about nutrition, they are inept, or they are afraid of litigation if someone is poisoned by a vitamin.

As you will read in Chapter 26, experts on vitamin D are more concerned about people not getting enough vitamin D to ward off illness than they are about alleged toxicity. In fact, there seems to be a consensus that the recommended dietary allowance should be five times higher than the current 2,000 IU/day for many people. The literature suggests that 50,000 IU is needed to produce toxicity and this amount is often given as a one-shot treatment for those who are severely vitamin D–deficient. The exception is pregnant women, whose vitamin D intake should be monitored by a health care professional so as not to harm the fetus. However, as reported in this book, many women are deficient in vitamin D, which can impact their and their children’s health.

After completing this manuscript, I learned of a fascinating study, headed by Pamela Goodwin, MD, at the University of Toronto. The study results suggest that breast cancer patients might fare worse if they do not have enough vitamin D in their blood. Data from the study was presented at the 44th Annual Meeting of the American Society of Clinical Oncology, which was held May 30–June 2, 2008 in Chicago.

I hope that this book gives you a reasonably comprehensive overview of vitamin D and will open your eyes as to the usefulness of this very important—and often neglected—vitamin. As insurance against possible deficiencies, you should consider buying a vitamin D supplement, since the one-a-day formulations often do not contain the potency you need.

—Frank Murray

New York

1.

The Sunshíne

Vítamín

Little is known about when vitamin D made its appearance on earth and what its function was, reported Michael F. Holick, MD, of Boston University School of Medicine in Massachusetts. However, it is known that some of the earliest phytoplankton and diatom life forms produced ergosterol (previtamin D2).¹ This includes Emiliania huxlei, which had existed in the oceans for over 750 million years and which had used calcium for its structural support.

When exposed to simulated sunlight, the ergosterol in E. huxlei was converted to previtamin D2, which rapidly isomerized to vitamin D2, Holick said. "Skeletonema menzelii, a diatom that also contained ergosterol, converted it to previtamin D2."

He added that little is known about the biological function of ergosterol, previtamin D2, and vitamin D2 in convertebral species; however, it has been suggested that ergosterol and its photoproducts are an ideal sunscreening system because of their high absorption of ultraviolet radiation. Ergosterol, previtamin D2, vitamin D2, and their photoproducts efficiently absorb the UV radiation that is damaging to DNA, RNA, and protein.

Thus, before the ozone layer—which now efficiently absorbs all UV radiation—evolved, the ergosterol-vitamin D2 system may have played a critical role in protecting organisms from the high energy UV radiation that could have damaged their UV sensitive proteins, RNA, and DNA, Holick continued. It is also possible that, if ergosterol existed in the plasma membrane of early life forms, it altered the membrane’s permeability for calcium when it was converted to the structurally less rigid vitamin D2.

In his concise article, Robert P. Heaney puts into perspective the many health benefits of vitamin D and the role of vitamin D deficiency in increasing the risk of many common and serious diseases, including some common cancers, type 1 diabetes, cardiovascular disease, and osteoporosis.²

I have provided guidelines for the amount of sun exposure needed by people of all skin types to achieve their vitamin D requirement without significantly increasing the risk of skin damage and skin cancer, Heaney continued. Increasingly, the intakes of food fortified with vitamin D, including milk, orange juice, cereals, and oily fish, is a reasonable approach satisfying the body’s requirement. Taking over one multivitamin is counterproductive, since too much vitamin A could be ingested, and this increases the risk of birth defects and osteoporosis. Alternatively, one multivitamin containing 400 IU of vitamin D and a vitamin D supplement containing either 400 or 1,000 IU of vitamin D is appropriate.

The importance of vitamin D—the sunshine vitamin—in human nutrition lies in its role of regulating calcium and phosphorus metabolism, according to the Foods & Nutrition Encyclopedia. The vitamin promotes intestinal absorption of the two minerals and it influences the process of bone mineralization. Without vitamin D, mineralization in bone matrix is impaired, which results in rickets in children and osteomalacia in adults.³

A bone disorder, which we now call rickets, has been known since 500 B.C., but the disease was first properly described in London about three hundred years ago. The word rickets is derived from the Old English word wrikken, meaning to bend or twist.

Vitamin D is unique among vitamins in two respects: (1) it occurs naturally in only a few foods—mainly in fish oils and a little in liver, eggs, and milk— and (2) it can be formed in the body by exposure of the skin to ultraviolet rays of the sun—light of short wavelength and high frequency, hence, it is known as the ‘sunshine vitamin,’ the encyclopedia reported.

During the Industrial Revolution in England in the eighteenth century, rickets became very prevalent in children in the crowded slums. Industrial smoke and high tenement buildings shut out the sunlight. Therefore, as industrial cities grew, rickets spread. Little was known about the sunshine connection, and rickets was blamed on bad home environment and poor hygiene, leading doctors to brand the condition as a disease of poverty and darkness.

In 1824, the Encyclopedia continued, cod-liver oil, long known as a folk medicine, was found to be an important treatment for rickets. However, the treatment lost favor with the medical profession because doctors could not explain how it worked.

In 1890, Dr. Palm, an English physician, observed that when sunshine was abundant, rickets was rare. In 1918, Sir Edward Mellanby of England, demonstrated that rickets was a nutritional deficiency disease. He produced rickets in puppies and then cured them with cod-liver oil. However, he mistakenly attributed the cure to the newly discovered fat-soluble vitamin A.

In 1922, E. V. McCollum at Johns Hopkins University, Baltimore, Maryland, found that, after destruction of all of the vitamin A in cod-liver oil— oxidation, bypassing heated air through cod-liver oil—it still retained its rickets-preventing potency, the Encyclopedia added. This proved the existence of a second fat-soluble vitamin, carried in liver oils and certain other fats, which he called ‘calcium-depositing vitamin.’ While McCollum discovered vitamin D, he did not call it that until after this designation was in common use by others.

In 1924, the mystery of how sunlight could prevent rickets was partially solved by Harry Steenbock, MD, of the University of Wisconsin and A. Hess, MD, of Columbia University in New York, who, while working independently, found that antirachitic activity could be produced in foods and in animals by ultraviolet light. This process, known as the Steenbock Irradiation Process, was patented in his name.

By the 1920s, it had been concluded that rickets could be prevented and cured by exposure to direct sunlight, by irradiation with ultraviolet light, by eating irradiated food, or by consuming cod-liver oil. Later, the vitamin D of fish liver oils was identified as the same substance that is produced in the skin by irradiation, the Encyclopedia said.

In 1932, crystals of pure vitamin D2 (ergocalciferol) were isolated from irradiated ergosterol by Adolf Otto Reinhold Windaus (1876–1959), a German chemist, and Dr. Askew in England; and, in 1936, crystals of pure vitamin D3 (cholecalciferol) were isolated from tuna liver oil by a Dr. Brockmann in Germany. In 1952, the first total synthesis of a form of vitamin D (vitamin D3) was accomplished by R. B. Woodward of Harvard University, for which he received the Nobel Prize in chemistry in 1965, the Encyclopedia continued. (Ergosterol is a crystalline sterol alcohol in yeast, molds, and ergot [fungi], which is converted by UV irradiation into vitamin D2.)

Although about ten sterol components with vitamin D activity have been isolated, only two—known as provitamins D or precursors—are of practical importance from the standpoint of their occurrence in foods: ergocalciferol (vitamin D2, calciferol, or viosterol) and cholecalciferol (vitamin D3). Cholecalciferol is a reflection of its cholesterol precursor. Since these substances are so closely related chemically, the term vitamin D is used collectively to indicate the group that shows this vitamin activity, the publication said.

Ultraviolet irradiation of ergosterol and 7-dehydrocholesterol will produce vitamin D2 and vitamin D3, respectively. Ergosterol is found in plants, whereas vitamin D3 is available in fish liver oils and in the skin. Vitamin D2 and vitamin D3 have comparable efficacy in combating disease.

When the skin is exposed to the UV radiation of sunlight, part of the store of 7-dehydrocholesterol undergoes a photochemical reaction in the epidermis and the dermis and forms previtamin D3, the publication added. Once previtamin D3 is formed in the skin, it undergoes a slow temperature-dependent transformation to vitamin D3, which takes about 3 days to complete. Then, the vitamin D-binding protein transports vitamin D3 from the skin into circulation.

Cholecalciferol, either from the diet or from irradiation of the skin, is transported by a vitamin D carrier protein (a globulin) to the liver, where it is converted into 25-hydroxycholecalciferol—25(OH)D3. From the liver, this substance is transported to the kidneys, where it is converted to 1,25-(OH)2D3, the most active form of vitamin D in increasing calcium absorption, bone calcium mobilization, and increased intestinal phosphate absorption.

The Encyclopedia goes on to say that the active compound—1,25-(OH)2D3— functions as a hormone, since it is a necessary substance made in the body tissues (the kidneys) and transported in the blood to cells within target tissues. The physiological active form of vitamin D3 is then either moved to its various sites or converted to its metabolite forms—24,25-dihydroxycholecalciferol or 1,24,25-trihydroxycholecalciferol.

While most of the research on vitamin D metabolism has been conducted on cholecalciferol, studies by Dr. DeLuca on ergocalciferol suggest that it is metabolized similarly to cholecalciferol and that it is changed to a similar active metabolite in the liver—25 hydroxy-ergocalciferol, or 25(OH)D2.

Vitamin D potency is expressed in international units (IU) and U.S. pharmacopoeia units (USP), which are equivalent, added the Encyclopedia. One IU or one USP of vitamin D is defined as the activity of 0.025 mcg of pure crystalline vitamin D3 (cholecalciferol). The UV light absorption property of vitamin D may be used for the assay of pure preparations free of irrelevant absorption. However, it does not distinguish between vitamin D2 and vitamin D3.

The principal storage sites of vitamin D are the fatty tissues and skeletal muscle, the Encyclopedia said. Some of it is also found in the liver, brain, lungs, spleen, bones, and skin. However, body stores of vitamin D are more limited than the storage of fat-soluble vitamin A.

Vitamin D increases calcium absorption from the small intestine, and a vitamin D deficiency produces large losses of calcium in the feces. Sufficient vitamin D enhances the levels of phosphates in the body because of: (1) improved absorption of phosphorus through the intestinal wall, independent of calcium absorption; and (2) increased resorption of phosphates from the kidney tubules. When sufficient amounts of vitamin D are not available, urinary excretion of phosphate increases and the blood level drops, the publication added.

Vitamin D deficiency is characterized by inadequate mineralization of the bone, according to Recommended Dietary Allowances, a publication of the Food and Nutrition Board of the National Research Council in Washington, D.C. In children, severe deficiency leads to deformation of the skeleton, or rickets. In adults, a vitamin D deficiency results in undermineralization of the bone matrix osteoid. This results in hypocalcemia, which is accompanied by secondary hyperthyroidism that leads to excessive bone loss and, in extreme cases, bone fractures or osteomalacia. The prolonged time required to produce a vitamin D deficiency is attributed to the gradual release of vitamin D–related steroids from fat deposits and the skin.⁴

Since milk and other foods are fortified with vitamin D, rickets is rare in many countries; however, a vitamin D deficiency occurs in some infants who are breastfed without supplemental vitamin D or exposure to sunlight, the elderly, as well as in those with vitamin D malabsorption, the publication added. Abnormalities in calcium balance and bone metabolism can also occur when the conversion of vitamin D to biologically active forms is compromised by disease. As an example, rickets and osteomalacia are often found in patients with kidney failure.

Vitamin D status is reflected in the concentrations of 25(OH)D and 1,25 (OH)2D in the blood, the publication continued. In surveys of healthy people, the mean value of 25(OH)D ranges from about 25 to 30 ng/ml. The concentrations of 1,25(OH)2D range from 18 to 60 pg/ml of plasma in normal children and between 15 and 45 pg/ml in healthy adults. Pg stands for picogram, which is one-trillionth of a gram. Ng stands for nanogram, or one-billionth of a gram.

Processed cow’s milk, which contains 10 mcg of cholecalciferol (400 IU) per quart, contributes most of the vitamin ingested by children, the publication said. Infant formulas are fortified with the same amount as milk. Human milk contains 0.63 to 1.25 mcg of cholecalciferol per liter.

At its birth almost a century ago, nutritional science had to overcome the prevailing view that all disease was caused by external invaders, either bacterial or toxic, explained Robert P. Heaney, MD, of Creighton University in Omaha, Nebraska. He added that we owe much to pioneers like E. V. McCollum, who were convinced—and ultimately convinced the scientific and medical communities—that foods contained substances the body needs for good health, and that not getting enough of them caused disease.⁵

Unfortunately, the medical community’s approach to nutrition is still strongly influenced by the early external invader model, Heaney added. Some of the most prominent contemporary medical nutritional efforts, such as those involving cholesterol, saturated fat, and salt, typify that paradigm. Additionally, scarcely a day passes without finding a report in the general news media or a study linking this or that cancer—or other dire outcome—with consumption of some nutrient. Clearly, the toxicity model continues to capture the attention of the medical community.

He goes on to say that rickets/osteomalacia is generally thought to be brought on by malabsorption of calcium and phosphorus and that this is correct, as far as it goes. As the efficiency of calcium absorption decreases, parathyroid hormone (PTH) secretion increases. The latter stimulates synthesis of calcitriol, which improves calcium absorption efficiency, but evidently not enough to make up the difference, thus leading to still further increases in PTH concentration.

At the same time, he continued, PTH concentrations lower the kidney threshold for phosphorus, which, together with reduced phosphorus absorption, produces hyperphosphatemia. It is this development that impairs osteoblast and chondroblast cell function and leads to disordered metaphysical growth plates and the characteristic histologic features of rickets and osteomalacia.

The modest vitamin D fortification of milk and other foods, coupled with the use of vitamin D supplements in children, has eliminated most cases of Stage 3 vitamin D deficiency in North America, Heaney said. However, these same stratagems have not been sufficient to prevent the lesser degree of deficiency. The vitamin D supplements are pegged to the prevention of Stage 3 deficiency and there still remains a presumption that if one does not have rickets or osteomalacia, then they have sufficient vitamin D.

Only recently have reliable measurements of serum 25(OH)D concentrations been available, and most of the physiology of vitamin D has been worked out before that time and, thus, was unconnected to specific levels of vitamin D repletion, Heaney added. As an example, the Food and Nutrition Board had no difficulty in identifying 25(OH)D as the functional indicator for vitamin D status, but the Board was not able, with the data then available, to assign numerical values to the lower limit of the normal range, or to assign cutoff values for various vitamin D activities.

As a result, he said, current recommendations are usually related to laboratory ‘reference’ ranges—which are inevitably circular, inasmuch as such ranges record what is observed in people who are considered ‘normal’ only because they do not have rickets or osteomalacia. A large body of data relating to parathyroid hormone to circulating 25(OH)D concentrations indicate that the lower end of an acceptable normal range must be about 80 nmol/l. By contrast, the lower end of most reference ranges is closer to 40 nmol/l.

Nutritional scientists often refer to values less than 20 nmol/l as deficient, since they were reproducibly associated with osteomalacia or rickets, and values above around 80 nmol/l as normal. Values in between are considered insufficient, without a clear consensus as to where the boundary might lie between insufficient and normal, Heaney added.

Concerning calcium economy, it now appears that scientific studies, at least for those in North America and the United Kingdom, indicate values below 80 nmol/l are deficient, he said.

"The awkward term insufficiency ought to be dropped, he added. It’s use simply reflected by the usual observations that the index disease for vitamin D was osteomalacia and rickets. If one had it, they were deficient and if they did not, one could not be deficient."

In the 1999 issue of Clinical Pearls, Kirk Hamilton, PA.C., interviewed Reinhold Vieth, PhD, of Mt. Sinai Hospital in Toronto, who stated that vitamin D is perhaps the most misunderstood and underrated of vitamins.⁶

In some ways, vitamin D is like cholesterol, Vieth explained, in that cholesterol is the raw material for making steroid hormones, including sex hormones and cortisol. However, unlike cholesterol, the amount of vitamin D available for hormone production is minute and arbitrary, mostly dependent on UV-B exposure and, to a lesser degree, upon dietary intake.

Vieth goes on to say there are several cancers whose prevalence increases as one heads north in latitude, especially breast, ovarian, and prostate cancers. And multiple sclerosis is more common in regions with less ultraviolet light.

Based on objective, measurable criteria, vitamin D deficiency is by far the most common nutritional deficiency in northern latitudes, especially in those over sixty years of age, Vieth added.

In the winter, half of the people on my hospital’s laboratory staff fall into the insufficient vitamin D category, Vieth said. This situation is at least as bad in the elderly.

He added that it is his contention that vitamin D is not a natural part of the human diet, since it is not present in plants normally consumed by humans and that the best dietary sources are fatty fish like salmon, cod, or halibut. Most of the vitamin D we get from foods was artificially added. As an example, there is essentially