Sunshine in my eyes can make me cry
Sunshine on the water looks so lovely
Sunshine almost always makes me high—John Denver, 1971
Picture it: a pro-hormone that not only maintains muscular strength but also reduces musculoskeletal pain. Add to that an ability to prevent cardiovascular disease and at least 17 types of cancer and boost immune response, as well as interact with more than 1,000 genes in the human body. Here’s the kicker: It’s a legal, over-the-counter steroid that will never be banned or outlawed and isn’t expensive or hard to find. It may even help maximize life span. Sound too good to be true? Au contraire, my friends, this amazing substance is none other than vitamin D.Since 1822 it’s been known that exposure to sunlight can cure rickets, a disease characterized by bone deformities and an inability to make hardened bone. Cod liver oil seemed to help the then common childhood disease. No one at the time knew why, but exposure to sun seemed to provide a cure.
By the 1930s the curative factor—known as vitamin D—was available in isolated form, vitamin D2, or ergocalciferol, which is made by irradiating plant sterols with ultraviolet light. Vitamin D became a sensation, heralded as the miracle vitamin. Various products were fortified with vitamin D2, including peanut butter, soda pop, hot dogs and bread. The Joseph Schlitz Brewing Company in Milwaukee, Wisconsin, introduced a beer that contained 100 units of D2 per eight-ounce can. It was marketed as “the beer with sunshine vitamin D.”
As other vitamins and nutrients were discovered, the notion of vitamin D providing “miraculous” effects gradually receded. After World War II an excess of vitamin D was added to milk products, causing an outbreak of vitamin D intoxication among infants and young children, leading to a banning of vitamin D fortification of dairy products in Europe that continues to this day.
Until recently, vitamin D was mostly linked to calcium metabolism. Indeed, D is key to the intestinal absorption of calcium. If you have a vitamin D deficiency, the intestine absorbs 10 to 15 percent of the calcium you eat or drink compared to the 30 percent typically absorbed in what the lab coats call a vitamin D–replete state. When you need calcium, such as during growth or pregnancy and lactation, you can absorb 60 to 80 percent of calcium intake—if you also have enough vitamin D.
Vitamin D’s popularity has surged lately, as mounting evidence has suggested myriad benefits associated with it. In 2007 Time listed its benefits as one of the top-10 medical breakthroughs of the year. Interestingly, vitamin D itself does nothing. It is inert until converted to its more active compounds. That was initially demonstrated in 1967. Two years later 25-hydroxyvitamin D, the active form circulating in the blood, was isolated and synthesized. The amount in the blood, which is called calcidol, determines vitamin D status.
To describe calcidol as “active” is actually a misnomer, as it requires one more change to become fully active. In the kidneys and other tissues, calcidol is hydroxylated, or enzymatically converted to 1-a-dihydroxyvitamin D3, also known as calcitriol, the active-hormone form in the body. Indeed, it’s a steroid hormone because it’s derived from cholesterol. Calcitriol interacts with vitamin D receptors throughout the body and modifies the activity of more than 500 genes, which explains the widespread health properties of “activated” vitamin D.
You’d think that vitamin D would be the easiest of all nutrients to obtain, since it can be synthesized in the skin from sun exposure between 10 a.m and 3 p.m. White people in bathing suits who expose themselves to the summer sun for 30 minutes can initiate the release of 50,000 units of vitamin D into the blood within 24 hours. For those with tans, that goes down to 20,000 to 30,000 units; and 8,000 to 10,000 units in dark-skinned people. Using an SPF8 sunblock lotion reduces the production of vitamin D by 95 percent; sunblocks with an SPF of 15 or more reduce it by 99 percent.
Vitamin D is produced when ultraviolet light reacts with 7-dehydrocholesterol in the skin. It’s self-regulating, which means you can’t experience vitamin D toxicity from sunlight. After it’s produced in the skin, vitamin D is pulled into the blood by special vitamin D–binding proteins located in the skin capillaries. The liver then converts it into 25-hydroxyvitamin D.
Several factors influence how efficiently your body produces vitamin D after sun exposure. Aging affects how much of the skin precursor of vitamin D—7-dehydrocholesterol—exists. A 70-year-old has less than 25 percent of the capacity to produce vitamin D as a healthy young adult.1 Since sunscreens block UV rays, those who apply copious amounts of sunscreens can be at risk of having less vitamin D. So can black people, who require five to 10 times more sunlight than whites to produce it. Those who have lots of bodyfat also have a problem. Vitamin D becomes sequestered in fat cells and is used for metabolic needs. The obese can increase their blood levels of vitamin D by only 50 percent compared to those who have normal or lower amounts of bodyfat.2
Living at higher latitudes, which have longer winters, also means you have increased risk of vitamin D deficiency. The turning point occurs at 37 degrees latitude, or about the location of Atlanta, Georgia. Various studies show a link between living at latitudes above that and the risk of high blood pressure and cardiovascular disease. For 90 to 95 percent of people, their main source of vitamin D is sun exposure.
What about vitamin D from food sources? It’s scarce. You can find some in oily fish, including mackerel, salmon and herring, which also supply omega-3 fats. Cod liver oil has 1,360 units per tablespoon. Sun-dried mushrooms give you 400 to 500 units of D per serving. Shiitake mushrooms dried in the sun give you 21,400 units per 100 grams. Eggs contain 20 units—only in the yolk, by the way, which bodybuilders often discard. Eight ounces of fortified milk or orange juice gives you 98 units of D.
One thing to avoid is too much alcohol. Animal studies show that excess alcohol intake increases the activity of enzymes in the kidneys that prematurely degrade the circulating form of vitamin D. So regular intake of alcohol can predispose you to a vitamin D deficiency.3
You could take vitamin D supplements, but that’s controversial too. Many science papers assert that vitamin D2—the form synthesized by exposing plant ergot or sterols to UV light—is far less effective than the D3 form found in food and synthesized from sun exposure. It seems that D2 raises calcidol levels less effectively, binds less to vitamin D–binding proteins in the blood and has a shorter shelf life than D3.4 A more recent analysis, however, showed that vitamin D2 is as effective as D3 in maintaining calcidol.5 Vitamin D3 supplements, by the way, are made by irradiating 7-hydrocholesterol obtained from lanolin, thereby duplicating the process of how humans synthesize vitamin D from sunlight exposure.
Despite the apparent ease of obtaining the vitamin, it’s become increasingly recognized that many people are deficient in it. D-deficient groups include, for example:
• 32 percent of doctors and medical students
• 40 percent of the U.S. population
• 42 percent of young black women of child-bearing age
• 48 percent of girls nine to 11 years old
• 76 percent of pregnant mothers, as well as 81 percent of the children born to them
• 80 percent of nursing home patients
Recent studies show that being deficient in vitamin D can adversely affect life span. The best blood count for calcidol is 30 to 60 nanograms per milliliter, and not maintaining that is linked to cardiovascular disease and cancer, the two leading causes of death. Yet 41 percent of men and 53 percent of American women have less than 28 nanograms per milliliter of blood. In one recent study,13,331 subjects’ blood vitamin D—collected between 1988 and 1994—was analyzed, then tracked through 2000.
6 The group with the lowest D levels had a 26 percent greater rate of death from any cause than those with the greatest blood vitamin D.
Another study found that low levels of D are linked to increased death rates from any cause—and that those low in D had more internal inflammation and oxidative cellular damage.7 Those studies follow the publication of a study that found a relationship between low vitamin D and premature mortality.8
A study of 2,100 female twins, aged 17 to 79, found that higher vitamin D levels were linked to improved genetic measures of lifelong aging and chronic stress. Researchers measured the length of telomeres, which are the ends of chromosomes, in white blood cells. As cells divide, telomeres shorten, and when the telomeres disappear, the cell stops dividing and dies. Longer telomeres are associated with both longer life span and decreased inflammation. The twins who had more blood vitamin D also had longer telomeres.9
Vitamin D and the Heart
While the heart enlarges just like other muscles with exercise, that isn’t considered dangerous, but when it enlarges due to high blood pressure, the eventual result is often heart failure. Vitamin D helps prevent that through suppressing substances produced in the kidneys that cause high blood pressure, as well as through reducing the activity of genes that are linked to heart enlargement. While blood pressure tends to rise with age, which is linked to heart failure and strokes, one study showed that vitamin D reduces that age-associated risk of hypertension.11
Vitamin D helps modulate risk factors associated with cardiovascular disease. For example, it helps control smooth muscle proliferation in arteries that predisposes you to atherosclerosis. Vitamin D also lowers inflammation, another root cause of cardiovascular disease, and prevents thrombosis, the formation of the internal blood clots that are the immediate cause of most heart attacks and strokes. Animals that are specially bred to produce an excess of an enzyme that breaks down active vitamin D develop big-time atherosclerosis.12
A study of 1,739 offspring of participants (average age 59) in the widely cited, long-term Framingham (Massachusetts) heart study found that those with blood vitamin D below 15 nanograms per milliliter had twice the risk for a cardiovascular “event”—heart attack, heart failure or stroke—compared to those who had more blood vitamin D. Even when the researchers adjusted for such traditional cardiovascular risk factors as high cholesterol, high blood pressure and diabetes, the risk was still 62 percent higher in those low on vitamin D. Only 10 percent of the participants showed blood vitamin D in the optimal range.13
Another study found that doubling the blood vitamin D cut heart attack risk by half.14 The subjects were 454 men, aged 40 to 75, who had a history of nonfatal heart attack or heart disease. Data from the men were compared to 900 healthy men who had no history of heart disease. Those who had vitamin D counts of 15 nanograms or less were 142 percent more likely to suffer a heart attack than men with normal—30-nanograms-per-milliliter—levels. That held true even after other factors, such as omega-3 fat intake, family history of heart attack, high blood pressure, diabetes, bodyfat, alcohol intake, exercise and cholesterol were adjusted for.
Next month I’ll discuss vitamin D’s anticancer connection and its effect on bodyfat and bodybuilding.
Editor’s note: Jerry Brainum has been an exercise and nutrition researcher and journalist for more than 25 years. He’s worked with pro bodybuilders as well as many Olympic and professional athletes. To get his new e-book, Natural Anabolics—Nutrients, Compounds and Supplements That Can Accelerate Muscle Growth Without Drugs, visit www.JerryBrainum.com.
References
1 Holick, M.F., et al. (1989). Age, vitamin D, and solar ultraviolet. Lancet. 11:1104-1105.2 Wortsman, J., et al. (2000). Decreased bioavailability of vitamin D in obesity. Am J Clin Nutr. 72:690-693.
3 Shanker, K., et al. (2008). Chronic ethanol consumption leads to disruption of vitamin D3 homeostasis associated with induction of renal 1,25 dihydroxyvitamin D3-24-hydroxylase (CYP24A1). Endocrin. 149(4):1748-56.
4 Houghton, L.A., et al. (2006). The case against ergocalciferol (vitamin D2) as a vitamin supplement. Amer J Clin Nutr. 84:694-7.
5 Holick, M., et al. (2008). Vitamin D2 is as effective as D3 in maintaining circulating concentrations of 25-hydroxyvitamin D. J Clin Endocrin Metab. 93(3):677-81.
6 Melamed, M.L., et al. (2008). 25-hydroxyvitamin D levels and the risk of mortality in the general population. Arch Intern Med. 168:1629-1637.
7 Dobnig, H., et al. (2008). Independent association of low serum 250 hydroxyvitamin D and 1,25-dehydroxyvitamin D levels with all-cause and cardiovascular mortality. Arch Intern Med. 168:1340-1349.
8 Autier, P., et al. (2007). Vitamin D supplementation and total mortality. Arch Intern Med. 167:1730-1737.
9 Richards, J.B., et al. (2007). Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women. Am J Clin Nutr. 86:1420-1425.
10 Pilz, S., et al. (2008). Association of vitamin D deficiency with heart failure and sudden cardiac death in a large cross-sectional study of patients referred for coronary angiography. J Clin Endocrin Metab. 93(10):3927-35.
11 Judd, S.E., et al. (2008). Optimal vitamin D status attenuates the age-associated increase in systolic blood pressure in white Americans: Results from the third National Health and Nutrition Examination Survey. Am J Clin Nutr. 87:136-41.
12 Kasuga, H., et al. (2002). Characterization of transgenic rats constitutively expressing vitamin D-24-hydroxylase gene. Biochem Biophys Res Commun. 297:1332-1338.
13 Wang, T.J., et al. (2008). Vitamin D deficiency and the risk of cardiovascular disease. Circulation. 117:503-511.
14 Giovannucci, E., et al. (2008). 25-hydroxyvitamin D and the risk of myocardial infarction in men—a prospective study. Arch Intern Med. 168:1174-1180.
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
