All posts by william-davis

You can always count on Dr. John Cannell for unique perspectives on vitamin D. I reprint here his unfailingly entertaining and informative Vitamin D Newsletter on whether vitamin D replacement enhances physical performance.

The whole vitamin D "discovery" sometimes worries me. Vitamin D has proven to be an unbelievable, remarkable, dramatic boon to health, including facilitation in dropping CT heart scan scores. Yet the answer was always right in front of us. It worries me that you and I might have the answer to important questions right within our grasp all along--but don't know it. What if the same were true, say, for cancer? That is, a profound answer is right there, but our eyes just pass right over it.

Anyway, we should all keep our eyes open and perhaps you and I will continue to identify the most powerful tools available that return control over heart disease to us and take it away from the perverse, procedural hospital formula that still reigns.

If you haven't done so already, be sure to visit Dr. Cannell's website, www.vitamindcouncil.com.

The Vitamin D Newsletter
March, 2007

Peak Athletic Performance and Vitamin D

"No way doc." I had just finished telling my patient about the benefits of vitamin D, telling him he should take 4,000 IU per day, using all the techniques I had learned in 30 years of medical practice to convince someone proper treatment is important. But, he knew the U.S. government said he only needed 200 IU per day, not 4,000. He also knew the official Upper Limit was 2,000 IU a day. "What are you trying to do doc, kill me?" I told him his 25(OH)-vitamin D blood test was low, only 13 ng/ml. He had read about that too, in a medical textbook, where it said normal levels are between 10 and 40 ng/ml. "I'm fine doc;" adding "Are you in the vitamin business?" I explained I was not; that the government used outdated values; that recent studies indicate ideal 25(OH)D levels are about 50 ng/ml; and that they indicated that he needed about 4,000 IU per day to get his level up to 50. "No thanks doc, I'm fine."

So I tried a different tact. I brought him copies of recent press articles. "Look," I said, "look at these." Science News called vitamin D the Antibiotic Vitamin. The Independent in England says vitamin D explains why people die from influenza in the winter, and not the summer. U.S. News and World Report says almost everyone needs more. Newsweek says it prevents cancer and helps fight infection. In four different recent reports, United Press International says that: it reduces falls in the elderly, many pregnant women are deficient , it reduces stress fractures, and that it helps heals wounds.

He glanced at the articles, showing a little interest in stress fractures. Then he told me what he was really thinking. "Look doc, all this stuff may be important to old guys like you. I'm 22. All I care about are girls and sports. When I get older, maybe I'll think about it. I'm too young to worry about it. I'm in great condition." I couldn't argue. He was in good health and a very good basketball player, playing several hours every day, always on indoor courts.

What could I do to open his eyes? As an African American, his risk of early death was very high, although the risk for blacks doesn't start to dramatically increase until their 40's and 50's. Like all young people, he saw himself as forever young. The U.S. government was no help, relying on a ten-year-old report from the Institute of Medicine that is full of misinformation.

I tired to tell him that the 200 IU per day the U.S. government recommends for 20-year-olds is to prevent bone disease, not to treat low vitamin D levels like his. I pointed out the U.S. government's official current Upper Limit of 2,000 IU/day is the same for a 300 pound adult as it is for a 25 pound toddler. That is, the government says it's safe for a one-year-old, 25-pound, child to take 2,000 IU per day but it's not safe for a 30-year old, 300-pound, adult to take 2,000 and one IU a day. I mean, whoever thought up these Upper Limits must have left their thinking caps at home. Nevertheless, nothing worked. My vitamin D deficient patient was not interested in taking any vitamin D.

What are young men interested in? I remembered that he had told me: "Sex and sports." Two years ago I had researched the medical literature looking for any evidence vitamin D enhanced sexual performance. Absolutely nothing. That would have been nice. Can you imagine the interest?

Then I remembered that several readers had written to ask me if vitamin D could possibly improve their athletic performance? They told me that after taking 2,000 to 5,000 IU per day for several months, they seemed just a little faster, a little stronger, maybe had a little better balance and timing. A pianist had written to tell me she even played a better piano, her fingers moved over the keys more effortlessly! Was vitamin D responsible for these subtle changes or was it a placebo effect? That is, did readers just think their athletic performance improved because they knew vitamin D was a steroid hormone precursor (hormone, from the Greek, meaning "to set in motion")?

The active form of vitamin D is a steroid (actually a seco-steroid) in the same way that testosterone is a steroid and vitamin D is a hormone in the same way that growth hormone is a hormone. Steroid hormones are substances made from cholesterol, which circulate in the body, and work at distant sites by "setting in motion" genetic protein transcription. That is, both vitamin D and testosterone regulate your genome, the stuff of life. While testosterone is a sex steroid hormone, vitamin D is a pleomorphic (multiple function) steroid hormone.

All of a sudden, it didn't seem so silly. Certainly steroids can improve athletic performance although they can be quite dangerous. In addition, few people are deficient in growth hormone or testosterone, so when athletes take sex steroids or growth hormone they are cheating, or doping. The case with vitamin D is quite different because natural vitamin D levels are about 50 ng/ml and, since almost no one has such levels, extra vitamin D is not doping, it's just good treatment. I decided to exhaustively research the medical literature on vitamin D and athletic performance. It took me over a year.

To my surprise, I discovered that there are five totally independent bodies of research that all converge on an inescapable conclusion: vitamin D will improve athletic performance in vitamin D deficient people (and that includes most people). Even more interesting is who published this literature, and when. Are you old enough to remember when the Germans and Russians won every Olympics in the 60's and 70's? Well, it turns out that the most convincing evidence that vitamin D improves athletic performance was published in old German and Russian medical literature.

With the help of my wife and mother-in-law, both of whom are Russian, and with the help of Marc Sorenson, whose book Solar Power is a must read, I finally was able to look at translations of much of the old Russian and German literature. When one combines that old literature with the modern English language literature on neuromuscular performance, the conclusion is inescapable. The readers who wrote me are right.

If you are vitamin D deficient, the medical literature indicates that the right amount of vitamin D will make you faster, stronger, improve your balance and timing, etc. How much it will improve your athletic ability depends on how deficient you are to begin with. How good an athlete you will be depends on your innate ability, training, and dedication. However, peak athletic performance also depends upon the neuromuscular cells in your body and brain having unfettered access to the steroid hormone, activated vitamin D. In addition, how much activated vitamin D is available to your brain, muscle, and nerves depends on having ideal levels of vitamin D in your blood - about 50 ng/ml, to be precise.

Why would I write about such a frivolous topic like peak athletic performance when cancer patients all across this land are dying vitamin D deficient? Like many vitamin D advocates, I have been disappointed that the medical profession and the public don't seem to care about vitamin D. Maybe people, like my young basketball player, will care if it makes better athletes. So, Hey! You jocks! Listen up! I'm talking speed, balance, choice reaction time, muscle mass, muscle strength, squats, reps, etc. Important stuff. Here's the Vitamin D Council's first ever sports quiz.

1. Vitamin D-producing UVB radiation improves athletic performance and may have been widely practiced by German and Russian Olympic athletes in the 1960's and 70's.

True. I found tantalizing evidence the Russians and especially the Germans were on to this during the 60's and 70's when those two nations took turns placing number one and number two in the Olympics every year?

For example, in 1938, Russian researchers reported that a course of ultraviolet irradiations improved speed in the 100-meter dash in college students compared to matched controls, both groups undergoing daily training. Average 100-meter dash times decreased from 13.51 seconds to 13.28 seconds in the non-irradiated controls, but from 13.63 seconds to 12.62 seconds in the irradiated students. Here we see training improved times but training and irradiation improved times much more. Obviously, irradiation or vitamin D would not render the same magnitude of improvements in world-class sprinters, but they would be happy with a few milliseconds.

Gorkin Z, Gorkin MJ, Teslenko NE. [The effect of ultraviolet irradiation upon training for 100m sprint.] The Journal of Physiology of the USSR [Fiziol, z. (RSSR)] 1938; 25: 695-701. (In Russian)

If you want to know what early German thinking was on this, read this summation of the German literature:

"It is a well-known fact that physical performance can be increased through ultra-violet irradiation. In 1927, a heated argument arose after the decision by the German Swimmers' Association to use the sunlamp as an artificial aid, constituting an athletic unfairness, doping, so to speak. In 1926, Rancken had already reported the improving effect of sunlamp irradiation on muscle work with the hand-dynamo-graph. Heib observed an improvement in swimming times after repeated irradiations. In thorough experiments, Backmund showed that a substantial increase in muscle activity happens after radiation of larger portions of the body with an artificial sunlamp; that this performance increase is not caused through local - direct or indirect - effects on the musculature, but through a general effect. This general effect, triggered by ultra-violet irradiation, is caused by a systemic effect on the nervous system." (p. 17)

Parade GW, Otto H. Die beeinflussung der leistungsfahigkeit durch Hohensonnenbestrahlung. Zeitschrift fur Klinische Medizin (Z Klin Med),1940;137:17-21 [In German]

In 1945, two Americans measured the cardiovascular fitness and muscular endurance of 11 male Illinois subjects undergoing training in an indoor physical education class, comparing them to 10 matched controls. Both groups underwent similar physical training. Treatment consisted of ultraviolet irradiation, given in the nude, up to two minutes per session, three times per week, for ten weeks in the late fall and winter. After ten weeks, the treatment group had a 19% standard score gain in cardiovascular fitness compare to a 2% improvement in the control students. To regular readers of this newsletter, it should come as no surprise that the un-irradiated control group reported twice as many viral respiratory infections as the treatment group.

Allen R, Cureton T. Effects of Ultraviolet Radiation on Physical Fitness. Arch Phys Med 1945: 10: 641-44.

In 1952, the German sports medicine researcher, Spellerberg, reported on the effects of wholesale irradiation of athletes studying and training at the Sports College of Cologne - including many elite athletes - with a "central sun lamp." He irradiated the athletes in their bathing suits, on both sides of their bodies, for up to ten minutes, twice a week, for 6 weeks. He reported a "convincing effect" on athletic performance and a 50% reduction in sports injuries. Results were particularly impressive for swimmers, soccer, handball, hockey, and tennis players, as well as for boxers and most track and field athletes. He reported that irradiation leading to burns, further irradiation of athletes having achieved peak performance, and irradiation within 24 hours of competition, all impaired athletic performance. Their results were so convincing, the Sports College of Cologne officially notified the "national German and International Olympic committee." (p. 570)

Spellerberg AE. [Increase of athletic effectiveness by systematic ultraviolet irradiation.] Strahlentherapie 1952; 88: 567-70. [In German]

In 1952, Ronge exposed 120 German schoolchildren to UV lights installed in classrooms and compared them to 120 un-irradiated control children. Over a two-year period - excluding summer vacations - he tested both groups with a series of six cardiovascular fitness tests using a bike ergometer. Un-irradiated children showed a distinct seasonality in fitness, with the highest values right after summer break and the lowest values in the spring. Treated children showed no seasonal differences in physical performance. Differences in work performance between the irradiated and un-irradiated children were most conspicuous in the spring with 56% difference between the two groups. In a final experiment, he gave 30 children in the control classrooms 6.25 mg (250,000 IU) of vitamin D as a single dose in February and found their performance had "increased considerably," one month later but did not report the actual numbers. He concluded that vitamin D, either as a supplement or induced via UV irradiation, improved physical performance.

Ronge HE. [Increase of physical effectiveness by systematic ultraviolet irradiation.] Strahlentherapie 1952; 88: 563-6. [In German]

In 1954, another researcher, at the Max-Planck Institute for Industrial Physiology in Dortmund, Germany, administered three different wavelengths of UV light over 8 weeks to university students. He found that ultraviolet light in the vitamin D-producing UVB range was consistently effective in reducing resting pulse, lowering the basal metabolic rate, and increasing athletic performance. UVA had no effect; interestingly, artificial UVC irradiation (the atmosphere normally completely filters out UVC radiation and thus it's not naturally present on earth) also gave some positive results.

Lehmann G. [Significance of certain wave lengths for increased efficacy of ultraviolet irradiation.] Strahlentherapie. 1954 Nov;95(3):447-53. [In German]

In 1956, Hettinger and Seidel irradiated seven subjects in two different experiments: athletic performance on bike-ergometers and forearm muscle strength. They found that UV radiation induced a significant improvement in both muscle strength and athletic performance.

Hettinger T, Seidl E. [Ultraviolet irradiation and trainability of musculature.] Internationale Zeitschrift für angewandte Physiologie, einschliesslich Arbeitsphysiologie 1956; 16: 177-83. [In German]

Another German researcher, at the Institute for Medical Physics and Biophysics at the University of Gottiingen, studied reaction times (the time needed to recognize a light and switch it off) during October and November in a series of controlled experiments on 16 children and an unspecified number of adults. He first controlled for practice effects (getting better by practicing) and then administered nine full-body UV radiation treatments over three weeks to the two treatment groups, using placebo radiation in the two control groups. UV radiation improved choice reaction time by 25% in children and 20% in adults while reaction time worsened in controls. The improvements in the irradiated groups peaked at the end of the three weeks of UV treatments and reverted to baseline levels three weeks later. In the two control groups, he found distinctly improved reaction times in the sunnier months.

Sigmund R. [Effect of ultraviolet rays on reaction time in man.] Strahlentherapie. 1956; 101: 623-9. [In German]

The next study threw me because it was very well conducted, meticulously designed, and completely negative. In 1963, Berven reported on the effects of ultraviolet irradiation and vitamin D supplementation in a group of 30 Stockholm schoolchildren, aged 10 -11, comparing them to appropriate controls. He found no seasonality of fitness in the control group and no effect from either irradiation or two different vitamin D supplementation protocols (1500 IU of cholecalciferol daily for two months and a single dose of 400,000 IU of ergocalciferol) on performance on a bike ergometer.

Berven H. The physical working capacity of healthy children; seasonal variations and effect of ultraviolet irradiation and vitamin-D supply. Acta paediatrica. Supplementum 1963; 148: 1-22.

However, two things were not right and got me thinking. One, Berven found no seasonality of physical fitness and was the only author who found no such seasonal variations in athletic performance. Second, he found no effect from irradiation, again, the only author. Then I realized he was working with Swedish children in the late 1950's. Supplementation of children with high doses of vitamin D - often as cod liver oil - was routine in Scandinavia in the past, particularly in children. For example, in neighboring Finland, the official recommended daily dose of vitamin D for children - including infants - was 4,000 IU per day until 1964, when authorities reduced it to 2,000 IU/day. (That's right, you read that correctly, 4,000 IU per day for infants, which is too much by the way.)

In 1975, Finnish authorities reduced it to 1,000 IU per day, and, in 1992, to 400 IU per day. I emailed Professor Elina Hypponen who confirmed that the Swedish recommendations were similar to the Finnish ones. Therefore, it seems highly unlikely that many of Berven's Swedish children, studied in 1958 and 1959, all from "families with a good standard of living," were vitamin D deficient. Therefore, this study showed that vitamin D will not improve athletic ability in vitamin D replete people. That's very important because it indicates more is not necessarily better. More is only better if you are not taking enough.

Hypponen E, et al. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet. 2001 Nov 3;358(9292):1500-3.

In the 1960's, three American researchers conducted experiments with university students. Rosentswieg studied the effects of a single six-minute dose of UV light on each side of the trunk in 23 college women, recording changes in various tests of muscle strength at one and five hours. He found a trend towards significance after five hours in white but not African American students. In 1968, Cheatum found that a six-minute administration of UV light, on each side of the trunk, increased the speed of 15 college women in the 30-yard dash. In 1969, Rosentswieg found a six-minute dose of UV light, on each side of the trunk, finding improved performance on a bicycle ergometer in college women. However, unlike the Germans and Russians, I could find no evidence that any of these American findings interested any American professionals involved in the care or training of athletes.

Rosentsweig J. The effect of a single suberythemic biodose of ultraviolet radiation upon the strength of college women. J Assoc Phys Ment Rehabil. 1967 Jul-Aug;21(4):131-3.

Cheatum BA. Effects of a single biodose of ultraviolet radiation upon the speed of college women. Res Q. 1968 Oct;39(3):482-5.

Rosentswieg J. The effect of a single suberythemic biodose of ultraviolet radiation upon the endurance of college women. J Sports Med Phys Fitness. 1969 Jun;9(2):104-6.

2. Athletic performance peaks in the summer when vitamin D levels peak, and is at its lowest in the winter when vitamin D levels are at their lowest.

A. True
B. False

True. The studies below - all I could find in the literature - show tests of physical performance peak in the summer, when vitamin D levels peak, start to decline in early autumn, as vitamin D levels decline, and athletic performance reaches its lowest point in late winter, when vitamin D levels bottom out. However, it is reasonable to assume that any associations between athletic performance and summer season may be due to "reverse causation." That is, improved athletic performance in the summer might be secondary to increased outdoor physical and recreational activity in the warmer weather with an indoor sedentary lifestyle during the colder months. Maybe people have better athletic ability in the summer because they exercise more. If that is true - and using the same logic - athletic performance should not begin to decline until late autumn, because at most temperate latitudes early fall weather is ideal for outdoor physical activities.

However, some of the studies below controlled for seasonal variations in time spent exercising. Furthermore, besides a consistent positive association of summer season with improved athletic performance, the below studies found an abrupt - and unexplained - reduction in athletic performance beginning in the early fall - when vitamin D levels decline - but when the weather is ideal for outdoor activities.

For example, in 1956, German researchers found a distinct seasonal variation in the trainability of musculature, studying wrist flexor strength in 21 German subjects undergoing daily training. They found highly significant seasonal differences with peak performance during the later part of the summer, nadirs in the winter, and an unexplained sharp autumn decline beginning in October.

Hettinger T, Muller EA. Seasonal course of trainability of musculature. Int Z Angew Physiol. 1956;16(2):90-4.

A study of Polish pilots and crew found physical fitness and tolerance to hypoxia were highest in the late summer with an unexplained sharp decline starting in September. The authors hypothesized that seasonal variations in an unidentified hormone best explained their results.

Kwarecki K, Golec L, Klossowski M, Zuzewicz K. Circannual rhythms of physical fitness and tolerance of hypoxic hypoxia. Acta Physiol Pol. 1981 Nov-Dec;32(6):629-36.

Cumulative work ability among 1,835 mainly sedentary Norwegian men during bicycle exercise tests showed an August peak, a sharp decline starting in the autumn, and a wintertime nadir. There were no seasonal changes in body weights, as might be expected if more caloric-demanding recreational activity during the sunnier months explained their results.

Erikssen J, Rodahl K. Seasonal variation in work performance and heart rate response to exercise. A study of 1,835 middle-aged men. Eur J Appl Physiol Occup Physiol. 1979 Oct;42(2):133-40.

Koch and Raschka reviewed the mostly German literature on the seasonality of physical performance, discussing studies indicating that muscle strength and stamina peak in the late summer. The authors then attempted to control for seasonal variations in the time spent exercising by instituting a controlled yearlong training regimen, beginning in December. The training regimen consisted of at least 20 push-ups per day and 2 or 3 long-distances races per week for the entire year. They found the both the number of push-ups and muscle strength peaked in late summer followed by a rapid decline in the fall, and a nadir in the winter, despite continued training. They concluded that seasonal variations in an unidentified hormone best explained their results. In addition, by now we all know that vitamin D is a seasonal hormone, and a steroid hormone precursor to boot.

Koch H, Raschka C. Circannual period of physical performance analysed by means of standard cosinor analysis: a case report. Rom J Physiol. 2000 Jan-Dec;37(1-4):51-8.

3. Vitamin D has direct muscle-building (anabolic) effects.

A. True
B. False

True, but only in vitamin D deficient subjects. Both animal and human studies have found that vitamin D directly affects muscle. That is, vitamin D increases muscle mass.

For example, Birge and Haddad found that vitamin D caused new protein synthesis in rat muscle.

Birge SJ, Haddad JG. 25-hydroxycholecalciferol stimulation of muscle metabolism. J Clin Invest. 1975 Nov;56(5):1100-7.

What about humans? In 1981, Young performed muscle biopsies on 12 severely vitamin D deficient patients before and after vitamin D treatment. They found type-II (fast-twitch) muscle fibers were small before treatment and significantly enlarged after treatment. Sorensen performed muscle biopsies on eleven older patients with osteoporosis before and after treatment with vitamin D. The percentage and area of fast twitch fibers increased significantly after treatment, despite the lack of any physical training.

Young A, Edwards R, Jones D, Brenton D. Quadriceps muscle strength and fibre size during treatment of osteomalacia. In: Stokes IAF (ed) Mechanical factors and the skeleton. 1981. pp 137-145.

Sorensen OH, Lund B, Saltin B, Lund B, Andersen RB, Hjorth L, Melsen F, Mosekilde L. Myopathy in bone loss of ageing: improvement by treatment with 1 alpha-hydroxycholecalciferol and calcium. Clin Sci (Lond). 1979 Feb;56(2):157-61.

Sato reported that two years of treatment with 1,000 IU of vitamin D per day significantly increased muscle strength, doubled the mean diameter, and tripled the percentage of fast-twitch muscle fibers, in the functional limbs of 48 severely vitamin D deficient elderly stroke patients. The placebo control group suffered declines in muscle strength, and in the size and percentage of fast-twitch muscle fibers.

Sato Y, Iwamoto J, Kanoko T, Satoh K. Low-Dose Vitamin D Prevents Muscular Atrophy and Reduces Falls and Hip Fractures in Women after Stroke: A Randomized Controlled Trial. Cerebrovasc Dis. 2005 Jul 27;20(3):187-192 [Epub ahead of print]

These studies clearly show that vitamin D when administered to vitamin D deficient people stimulates the growth and number of those muscle fibers critical to athletic ability, type-2, or "fast twitch," muscle fibers.

4. Many studies have found direct associations between physical performance and vitamin D levels. That is, the higher your vitamin D level, the better your athletic performance.

A. True
B. False

True. I found 13 positive studies of associations between vitamin D levels and various parameters of neuromuscular performance. However, they were all in old people. Of course, old people can be athletes too. Furthermore, age differences in physiology and pharmacology are quantitative, not qualitative. That is, what is true in old people will be true in young people, although the magnitude might be different. Higher vitamin D levels are associated with a wide variety of athletic performance but appear to have the strongest associations with balance, timing, and timed tests of physical performance.

The three largest studies had more than 7,000 elderly subjects. All found evidence of a vitamin D threshold of between 30 - 50 ng/ml, above which further improvements in athletic performance were not seen. Wicherts and her colleagues found a linear correlation between vitamin D and neuromuscular performance; scores were 78% better for those with vitamin D levels greater than 30 ng/ml compared to those with levels less than10 ng/ml.

Bischoff-Ferrari HA, Dietrich T, Orav EJ, Hu FB, Zhang Y, Karlson EW, Dawson-Hughes B. Higher 25-hydroxyvitamin D concentrations are associated with better lower-extremity function in both active and inactive persons aged > or =60 y. Am J Clin Nutr. 2004 Sep;80(3):752-8.

Gerdhem P, Ringsberg KA, Obrant KJ, Akesson K. Association between 25-hydroxy vitamin D levels, physical activity, muscle strength and fractures in the prospective population-based OPRA Study of Elderly Women. Osteoporos Int. 2005 Nov;16(11):1425-31.

Wicherts IS, et al. Vitamin D status predicts physical performance and its decline in older persons. J Clin Endocrinol Metab. 2007 Mar 6; [Epub ahead of print]

Professor Heike Bischoff-Ferrari, now in Switzerland, did the largest study. She and her colleagues found a strong positive correlation and suggestion of a U-shaped curve with athletic performance on one test peaking with vitamin D levels of 50 ng/ml but deteriorating at higher levels. It is interesting to speculate that levels around 50 ng/ml may be optimal for athletic performance as such levels are common in humans living in a "natural" state of sun-exposure, such as lifeguards or tropical farmers.

Bischoff HA, Stahelin HB, Urscheler N, Ehrsam R, Vonthein R, Perrig-Chiello P, Tyndall A, Theiler R. Muscle strength in the elderly: its relation to vitamin D metabolites. Arch Phys Med Rehabil. 1999 Jan;80(1):54-8.

Interestingly, all three studies that looked for an association between mental abilities and vitamin D levels found one. A fourth study, unrelated to athletic function, also found an association. The obvious explanation for these findings is that cognitively impaired patients do not go outdoors as often as higher functioning patients and thus have lower vitamin D levels. However, Dhesi found the association after excluding all but mildly demented patients, making such an explanation more difficult. Flicker and - more recently - Przybelski and Binkley, found the association after controlling for outdoor activities, raising the possibility that the association of vitamin D levels with cognitive abilities is casual. Both the vitamin D receptor and the enzyme necessary to activate vitamin D are present in a wide-variety of human brain tissue. If vitamin D deficiency impairs cognitive abilities, it is likely that such deficiencies will also impair the brain's ability to process the complex circuits needed for peak athletic performance.

Dhesi JK, Bearne LM, Moniz C, Hurley MV, Jackson SH, Swift CG, Allain TJ. Neuromuscular and psychomotor function in elderly subjects who fall and the relationship with vitamin D status. J Bone Miner Res. 2002 May;17(5):891-7.

Kenny AM, Biskup B, Robbins B, Marcella G, Burleson JA. Effects of vitamin D supplementation on strength, physical function, and health perception in older, community-dwelling men. J Am Geriatr Soc. 2003 Dec;51(12):1762-7.

Flicker L, Mead K, MacInnis RJ, Nowson C, Scherer S, Stein MS, Thomasx J, Hopper JL, Wark JD. Serum vitamin D and falls in older women in residential care in Australia. J Am Geriatr Soc. 2003 Nov;51(11):1533-8.

Przybelski RJ, Binkley NC. Is vitamin D important for preserving cognition? A positive correlation of serum 25-hydroxyvitamin D concentration with cognitive function. Arch Biochem Biophys. 2007 Jan 8;

There can be no doubt that higher vitamin D levels are associated with improved athletic performance in the elderly. From what we know of physiology and pharmacology, the same associations should hold true in young people, including young athletes.

5. Numerous studies have found that vitamin D improves physical performance.

A. True
B. False.

True, but, again, most all the studies are in old persons, not young ones, and none of the studies are in world-class athletes. However, there is no medical reason why vitamin D would improve the athletic performance of vitamin D deficient old people but not vitamin D deficient young ones. Eleven studies found vitamin D improved physical performance, mainly on measures of balance and reaction time. The one study of younger subjects showed dramatic physical performance effects in 55 severely vitamin D deficient women.

Sorensen OH, Lund B, Saltin B, Lund B, Andersen RB, Hjorth L, Melsen F, Mosekilde L. Myopathy in bone loss of ageing: improvement by treatment with 1 alpha-hydroxycholecalciferol and calcium. Clin Sci (Lond). 1979 Feb;56(2):157-61.

Gloth FM 3rd, Smith CE, Hollis BW, Tobin JD. Functional improvement with vitamin D replenishment in a cohort of frail, vitamin D-deficient older people. J Am Geriatr Soc. 1995 Nov;43(11):1269-71.

Glerup H, Mikkelsen K, Poulsen L, Hass E, Overbeck S, Andersen H, Charles P, Eriksen EF. Hypovitaminosis D myopathy without biochemical signs of osteomalacic bone involvement. Calcif Tissue Int. 2000 Jun;66(6):419-24.

Prabhala A, Garg R, Dandona P. Severe myopathy associated with vitamin D deficiency in western New York. Arch Intern Med. 2000 Apr 24;160(8):1199-203.

Verhaar HJ, Samson MM, Jansen PA, de Vreede PL, Manten JW, Duursma SA. Muscle strength, functional mobility and vitamin D in older women. Aging (Milano). 2000 Dec;12(6):455-60.

Pfeifer M, Begerow B, Minne HW, Abrams C, Nachtigall D, Hansen C. Effects of a short-term vitamin D and calcium supplementation on body sway and secondary hyperparathyroidism in elderly women. J Bone Miner Res. 2000 Jun;15(6):1113-8.

Bischoff HA, Stahelin HB, Dick W, Akos R, Knecht M, Salis C, Nebiker M, Theiler R, Pfeifer M, Begerow B, Lew RA, Conzelmann M. Effects of vitamin D and calcium supplementation on falls: a randomized controlled trial. J Bone Miner Res. 2003 Feb;18(2):343-51.

Dhesi JK, Jackson SH, Bearne LM, Moniz C, Hurley MV, Swift CG, Allain TJ. Vitamin D supplementation improves neuromuscular function in older people who fall. Age Ageing. 2004 Nov;33(6):589-95.

Sato Y, Iwamoto J, Kanoko T, Satoh K. Low-Dose Vitamin D Prevents Muscular Atrophy and Reduces Falls and Hip Fractures in Women after Stroke: A Randomized Controlled Trial. Cerebrovasc Dis. 2005 Jul 27;20(3):187-192 [Epub ahead of print]

In summary, five converging - but totally separate - lines of scientific evidence leave little doubt that vitamin D improves athletic performance. (I actually left out a sixth line of evidence, something a little more complicated, studies of muscle strength and vitamin D receptor polymorphisms; the two studies I could find were both positive.) Anyway, the scientific evidence that UVB radiation, either from the sun or from sunbeds, will improve athletic performance is overwhelming and the mechanism is almost certainly vitamin D production. Peak athletic performance will probably occur with 25(OH)D levels of about 50 ng/ml, whether from sun, sunbeds, or supplements.

All that is missing is a big-time professional or college team identifying and then treating their elite athletes who are vitamin D deficient. Can you imagine what such performance-enhancing effects would do for basketball players, most of who are African American and who practice and play indoors all winter? Or gymnasts? Or weight lifters?

However, a word of caution. The above studies suggest that taking too much vitamin D (more than 5,000 IU per day) may actually worsen athletic performance. Take the right amount, not all you can swallow. Take enough to keep your 25(OH)D levels around 50 ng/ml, year round. Easier yet, regularly use the sun in the summer and sunbeds in the winter - with care not to burn. Once a week should be about right.

When you think about it, none of this should surprise anyone. Every body builder knows that steroid hormones can improve athletic performance, certainly increase muscle mass. Barry Bonds knows they increase timing and power. Moreover, activated vitamin D is as potent a steroid hormone as exists in the human body. However, unlike other steroids, levels of activated vitamin D in muscle and nerve tissue are primarily regulated by sun exposure. That's right, the rate-limiting step for the cellular function (autocrine) of activated vitamin D is under your control. It depends on how much you put in your both or go into the sun. It's ironic that many athletes now avoid the sun, organized baseball is even promoting sun avoidance and sunblocks. The ancient Greeks knew better; they had there elite athletes train on the beach and in the nude.

The medical literature indicates vitamin D levels of about 50 ng/ml are associated with peak athletic performance. Of course, recent studies show such levels are ideal for preventing cancer, diabetes, hypertension, influenza, multiple sclerosis, major depression, cognitive impairments, etc. But who cares about all that disease stuff old people get, we're talking about something really important: speed, balance, reaction time, muscle mass, muscle strength, squats, reps, etc. And guess who's now taking 4,000 IU/day? Yes he is, and he tells me his timing is better, he can jump a little higher, run a little faster, and the ball feels "sweeter," whatever that means.

John Cannell, MD

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The reason why I've been blogging lightly these past few days is because, as a favor, I'm covering the practice for some colleagues who I'm (very) loosely affiliated with. The time demands have been great.

Nonetheless, it is a good reminder to me just how far wrong conventional cardiology remains. Judging by what I see around me, there is a startling lack of restraint in proceeding to the catheterization laboratory. Curiously, the internists and family practitioners have been brainwashed into accepting this path. I suppose that all it takes is an occasional real "save" for these physicians to develop a fear of ever missing real disease.

What I'm seeing is just how many people presenting with chest pain or similar symptoms end up going to the cath lab. I would crudely estimate 80%. That is, once you make it past the emergency room, there's a four out of five chance that you'll end up with a heart catheterization to "be sure your heart is okay", "make certain you're not going to die of heart disease", "see if there's a ticking time bomb in your chest". You've heard all the clever, scary phrases that get tossed around to scare the pants off you and justify putting catheters in your groin.

Despite the fact that tools for heart disease prevention have improved dramatically, the volume of heart catheterizations continues to grow nationwide.

I find it shocking and unacceptable. We're currently working behind the scenes to help change this situation through education of the public. Persuade a $1 million a year cardiologist that he is overdoing procedures? Unlikely in my experience. Educate the public about the shocking over-reliance on high-revenue procedures? Perhaps more practical.

Garlic May Not Lower Cholesterol
Study Shows No Improvement in Cholesterol Levels From Raw Garlic or Garlic Supplements

Lots of reports continue to hit the press about a small study that hoped to determine whether garlic as whole cloves (4 to 6), an aqueous extract of garlic called Kyolic, or an oil extract called Garlicin (high in allicin), or placebo. No differences in lipid numbers including LDL cholesterol were observed.

(Full text at WebMD at http://www.webmd.com/cholesterol-management/news/20070226/garlic-may-not-lower-cholesterol?ecd=wnl_chl_030507. You may be required to log in or register.)

I believe that the researchers were sincere in their effort to follow an honest, scientfically sound clinical trial design. I'm personally not that surprised. The effect in prior studies has been modest, sometimes none. Does that mean that we should ignore the other studies that suggest there may be modest blood-thinning, anti-inflammatory, blood pressure-reducing, and cancer-preventing properties? No, it does not. Dr. Matt Budoff at UCLA even published a very small study in about 20 people that suggested a slowing of plaque growth by using Kyolic in persons tracked by CT heart scans.

Nonetheless, garlic is, at best, probably no more than a source of small benefits. The biggest fallout from this kind of report, however, is not the neutral results from garlic, but from the open door the drug companies sense when this happens.

If you read the WebMD report, you'll notice all sorts of advertisements from drug companies for statin cholesterol drugs ("Cholesterol health center"; "Understanding Cholesterol Numbers"; "There are two sources of cholesterol: food and family"), Niaspan (which I used to support but have been discouraged by the Kos companies excessively profiteering methods and recent big Wall Street sellout).

It doesn't follow. The failure of one nutritional strategy to reduce LDL does nothave to trigger a run to the drugs. Don't fall for it. Drugs have their place. So do supplements and food choices, which can be very powerful. Drug manufacturers and their marketing people salivate when something like this comes along, an open invitation to say, "If garlic doesn't work, _____ sure does."

Jason came to the office because of chest pain. At 34 years old, he works as manager of a (non-fast food) restaurant, but indulges in lots of the odds and ends. Among his indulgences: Diet Coke.

Every time he'd have a diet Coke, he'd have chest pain. Not drinking diet Coke--no chest pain. If Jason drank coffee, no chest pain. Other foods, no chest pain. Anyway, just eliminating the diet Coke seemed to do the trick. (Aspartame?)

Anyway, that's not why I tell you Jason's story. In the midst of his evaluation, an echocardiogram showed a mildly enlarged aorta, measuring 4.0 cm in diameter. So we obtained lipoproteins. Jason showed lipoprotein(a) and small LDL particles, the dreaded duo. We talked about how to correct this pattern. Among the strategies we discussed was niacin.

But what bothered me was that neither of Jason's parents had a diagnosis of heart disease. Jason had to have gotten Lp(a) from either his mother or father, since you obtain the gene from one or the other parent. You cannot acquire Lp(a). So one of Jason's parents was sitting on a genetic time bomb of unrecognized Lp(a) and hidden heart disease.

Because Jason's paternal grandfather had a heart attack at age 62, only Jason's Dad had the heart scan (though I urged both to get one). Score: 1483. Recall that heart scan scores >1000 carry a risk of death or heart attack of 25% per year if no preventive action is taken. Now, of course, we have to persuade Jason's Dad that a program of prevention--intensive prevention is in order, including a measure of Lp(a).

So that's the curious story of how Diet Coke probably saved Jason's Dad's life. The lesson is that if you or someone you know has Lp(a), think about their children as well as their parents, each of whom carry a 50% chance of having the pattern.

There's a widely-known (among cardiologists) problem with nuclear stress tests. It's called the "false positive." (Nuclear stress tests are known as stress Cardiolites, stress thalliums, stress Myoviews, persantine stress tests, adenosine stress tests)

Stress tests, nuclear and otherwise, are helpful for identifying areas of poor blood flow. If an area of poor blood flow is detected and the area is substantial, then there may be greater risk of heart attack and other undesirable events in the relatively near future.

What "false positive" means is a stress test that shows an abnormality but it's not true--it is falsely abnormal. There are a number of reasons why this can happen. The problem is that this phenomenon is very common. Up to 20% of nuclear stress tests are false positives.

There are indeed situations where there may an abnormality and it is not clear whether it is true or false. This may lead to a justifiable heart catheterization or CT coronary angiogram. But, given the extraordinary number of false positives, there's a lot of gray in interpreting these tests. Hospital staff, in fact, call nuclear medicine "unclear" medicine. It's common knowledge that you can often see just about anything you want to see on a nuclear image of the heart. Abnormalities in the bottom of the heart, the "inferior" wall, are especially common due to the overlap of the diaphragm with the heart muscle, yielding the appearance of reduced blood flow. Defects in the front of the heart heart are common in females with large breasts for the same reasons.

The problem: The uncertainty inherent in nuclear stress tests opens the door to the unscrupulous or lazy practitioner. Any blip, tick, or imperfection on the nuclear images serve as carte blanche to drag you into the hospital for procedures.

This abusive practice is, in my experience, shockingly common for two reasons: 1) It pays better to do heart catheterizations, and 2) Defensive medicine.

What's the disincentive? Only doing the right thing and maintaining a clear conscience. Slim reasons for many of my colleagues--and a lot less money.

If you are without symptoms and feel fine, and a nuclear stress test is advised by your doctor, followed by a discussion of an abnormality, insist on a discussion of exactly what is abnormal, just how abnormal, and what the alternatives might be. If you receive unsatisfactory or incomplete answers despite your best effort, it's time for another opinion.

Magnesium is kind of boring. So most people don't pay too much attention to it.

Magnesium can be important, however. I saw an interesting phenomenon recently. A type I diabetic patient of mine (that is, an adult who developed diabetes as a child), Mitch, was experiencing wide swings in blood sugar: low low's and very high high's (300-400 mg/dl). Mitch's magnesium was only marginally low at 2.0 mEq/L. (Ranges for normal magnesium blood levels are usually 1.3–2.1 mEq/L or 0.65–1.05 mmol/L.) Note that Mitch's blood levels fall within "normal." I do not agree with these "normal" ranges. I shoot for 2.1 to 2.4 mEq/L, which I think is the truly normal range.

In addition to eating plenty of raw nuts and green vegetables, Mitch began supplementing magnesium with magnesium citrate, 200 mg twice a day (our preferred supplement form). He reported that the wide swings in blood sugar were nearly eliminated.

Mitch's dramatic benefit is just a great illustration of how magnesium can help control blood sugar metabolism. A type I diabetic is more sensitive to the effects, but anyone with type II (adult) diabetes, metabolic syndrome, or just a slightly high blood sugar could benefit from magnesium supplementation.

There's a number of ways to accomplish getting sufficient magnesium in your daily regimen. Track Your Plaque members, Be sure to read:

Your water may be killing you at
http://www.cureality.com/library/fl_03-002magnesium.asp

Magnesium: Water to the rescue! at http://www.cureality.com/library/fl_03-010magnesium2.asp

It struck me recently that, for many people, it's not the second but the third heart scan that more commonly shows a reduction in score.

I think this is because many people's reaction to their first heart scan is "This can't be. There's no way my arteries have that much plaque." They then follow a half-hearted program to correct their patterns.

When the second heart scan shows a significantly higher score, that really catches their attention. This is when they finally buckle down and give it their all.

Only the occasional person will, after the first heart scan, seize full control and take their program very seriously. These tend to be highly motivated people.

Don't feel too bad if your second heart scan score shows an increase. Look at it for what it represents: feedback on the adequacy of your program.

Peter started out at age 59 at 248 lbs, standing 6 ft tall (BMI = 33.6!).

Along with his weight, Peter had the entire panel of phenemena of the so-called "metabolic syndrome", or pre-diabetes:

--Triglycerides 238 mg/dl and associated with extremes of excess VLDL and IDL
--High blood pressure
--Blood sugar 115 mg/dl
--High c-reactive protein
--Small LDL particles 99% of total LDL

Interestingly, Peter's HDL was a surprisingly favorable 58 mg/dl (HDL is usually low in this syndrome). However, when broken down by size, he had nearly zero large, healthy HDL (sometimes called HDL2b). Though total HDL was favorable, most of it was simply ineffective.

Peter eliminated snacks and processed foods, particularly bread; increased his reliance on healthy oils and lean proteins; incorporated soy protein; increased vegetables. He added 30 minutes of a rapid walk on a treadmill every day. He added vitamin D to achieve a blood level of 50 ng/dml. He added a magnesium supplement.

Peter has lost 31 lbs. in the last year. Weight 207 lbs., BMI 28.1 (desirable <25). Blood sugar: 96 mg/dl; triglycerides: 56 mg/dl; HDL 71 mg/dl with 35% in the large fraction; small LDL 45% of total. Not perfect, but a damn site better.

Control of metabolic syndrome is an achievable goal for over 90% of people, just with these simple efforts. We haven't yet had a chance to assess the effect on the progression or regression of Peter's heart scan score, but he has, at the very least, spared himself a future of diabetes and all its complications.

This is a "slice" from a normal heart scan in a 58 year old woman. Heart scan score zero. Look at the lungs, the dark areas left and right of the heart in the center. The lungs are also normal. Black represents normal density, healthy lung tissue. The white streaking is just normal lung blood vessels. This person doesn't smoke.

This woman smokes a pack of cigarettes a day and has done so for 45 years ("45 pack-years"). She had a surprisingly low heart scan score (at age 64) of only 71, despite the smoking. However, look at this woman's lungs. It's a little tough to make out, since the computer graphics loses some of the resolution. But you can see the near absence of lung tissue on both sides. This is an advanced phase of the destructive lung disease, emphysema, from smoking. Even if she quit smoking today, the destroyed lung tissue never grows back. She literally has huge gaps or holes in her lungs where lung tissue used to be.

Smoking is among the most destructive, terrible things you can do to your body, short of swallowing strychnine or jumping off a building. Stay as far the heck away from cigarettes as you possibly can. If you are exposed to "secondary" smoke, insist that the person never smoke in your presence. It's not the smell that destroys your lungs or causes coronary plaque (though it is indeed foul), it's the actual smoke.

Do you need to become a vegetarian in order to reduce your heart scan score?

No. Plain and simple. We’ve had many non-vegetarians drop their scores.

That said, are there still advantages to following a vegetarian diet, or some variation on the vegetarian theme?

Yes, there are. Let’s put aside the moral or religious arguments in favor of not eating animals—the need to eliminate killing animals for food, elimination of suffering common in modern livestock practices, Kosher considerations, etc. (Not that there aren’t real arguments here. Our focus for this conversation is not, however, the moral dilemma, but the health argument.)

Some of the most unhealthy people I’ve ever met, mostly males, are proud carnivores who boast of their prodigious capacities to eat meat. Unfortunately, it’s hard to tease out the ill-effects of excessive meat eating, since these same men also tend to be substantially overweight, smoke, drink excessively, and fail to get exercise unless their job is physically demanding. You know the type.

What advantages does a vegetarian obtain? A number of studies have suggested that the reduced saturated fat, reduced exposure to parasites, as well as reduced exposure to the antibiotics and hormones now used routinely in livestock-raising practices, do indeed provide benefits to the vegetarian. Thus, vegetarians tend to be substantially thinner, experience less bowel cancer, have less diabetes and heart disease, and live longer.

(If you are interested in reading or seeing more about just how inhumane modern livestock practices are, take a look at the video, "Meet Your Meat" at meat.org. Be sure not to view this after dinner.)

Of course, some of the disadvantages of eating animal products diminish when free-range livestock are eaten, i.e., livestock not raised in the inhumane cramped, filthy conditions of livestock factories, but in the open, grazing or rooting freely. These animals tend to have different fat compositions and taste different.

The advantages of vegetarianism, however, have blurred in recent years, since many so-called vegetarians have failed to maintain the distinction between naturally-occurring foods and processed foods. So, Ritz Crackers, Oreo cookies, whole wheat bread, and Raisin Bran fit into a vegetarian program, but they’re awful for your health. I’ll occasionally meet a self-proclaimed vegetarian who looks every bit as unhealthy as a conventionally eating American, that is, overweight, pre-diabetic person with a developing heart scan score.

So it is not necessary to be vegetarian to reduce your score. You might consider vegetarianism for other reasons, such as moral considerations, or to reduce your risk for cancer. But it is not necessary to drop your heart scan score. A non-processed food diet? Now that's is worth giving serious consideration.

Lipoprotein(a), Lp(a), can be a tough nut to crack.

Having struggled and wrestled with this genetic pattern for the last 12 years or so in hundreds of patients, I have gained great respect for this difficult to control pattern.

I regard lipoprotein(a) as the number one most aggressive cause for heart disease and coronary plaque known. It can account for heart attacks in men in their 40s, women in their 50s. It can cause heart disease and heart attacks in even the ultra-fit like marathon runners. It accounts for both excessive coronary risk and misleading cholesterol values in slender, healthy-appearing people.

Niacin is the number one treatment choice for Lp(a), followed by testosterone for men, estrogens (preferably human, not horse or other non-human mammal) for women. I then often resort to DHEA, along with adjunctive nutritional agents like raw almonds, ground flaxseed, and others.

Our most recent addition to the Lp(a) treatment list is high-dose fish oil, which appears to exert a significant effect in about 40% of people with Lp(a).

Even with this multi-agent approach, not everybody gains control over Lp(a).

That makes me wonder if someone has Lp(a) at a substantial level of, say, 200 nmol/L or 70 mg/dl (values can differ tremendously, depending on the method of measurement), should we throw everything but the kitchen sink at Lp(a) from the start? Right now, by adding an agent one at a time, it often takes two years to gain control over Lp(a) (if we are going to get it at all).

While many people might find this unpalatable and overwhelming from the starting gate of their program, I do believe it may be a strategy we should consider adopting for full and more immediate plaque control in the Track Your Plaque program. Something to chew on.

Clearly, we need better answers for Lp(a). A "kitchen sink," full-frontal assault might be a way to gain faster control, though not necessarily a superior approach with regards to efficacy and potency.

There are a number of unique, potentially effective therapies for Lp(a) that are worth examining. Given the difficulty of performing clinical trials with non-drug agents (largely a lack of financial support, since nobody gets a financial return with non-patent-protectable agents), I am anxious to put these potential treatments to a test in the Track Your Plaque program Virtual Clinical Trail (VCT). The VCT gives us a quick and relatively easy method to test various potential treatments, with feedback generated in months, rather than years.

Any suggestions on promising agents to test? Of course, they must be widely available nutritional agents, not drugs.

Colleen started with the usual discrepancy between conventional calculated LDL cholesterol of 121 mg/dl and the far more accurate LDL particle number (NMR) of 1927 nmol/L.

Those of you following this conversation or our many conversations on the Track Your Plaque Forum know that a useful and highly reliable rule-of-thumb for converting NMR LDL particle number to LDL is to drop the last digit: 1927 nmol/L becomes 192 mg/dl. (This is, admitttedly, arrived at empirically, not by design. However, it has held up through thousands of NMR analyses and plays out reasonably when you compare distributions of Friedewald LDL and LDL particle number on a population basis.)

In other words, by this simple manipulation, Colleen's Friedewald calculated LDL is off by 58%. This is very common, a phenomenon I witness several times every day.

By LDL particle size, 75% of all Colleen's LDL particle were abnormally small (small LDL particle number 1440 nmol/L). This is a moderately severe small LDL tendency.

So we took all the steps for reduction of small LDL/LDL, including elimination of wheat and cornstarch, exercise, weight loss (which happens inevitably when wheat and cornstarch are eliminated), fish oil, vitamin D, etc.

Another NMR lipoprotein panel showed an LDL particle number of 882 nmol/L and a Friedewald calculated LDL of 87 mg/dl. Using our rule-of-thumb, LDL by particle number is virtually the same as the calculated LDL. This time, small LDL numbered only 237 nmol/L, or 26.8% of the total, a marked reduction.

Isn't that interesting? As small LDL is corrected, the crude Friedwald calculated LDL approximates the more accurate LDL particle number.

It assumes that accuracy of the Friedewald calculation may be more likely to occur as LDL size approaches normal. However, when LDL size is abnormally small--a condition shared by at least 70% of people with coronary heart disease--then the Friedewald LDL becomes increasingly inaccurate.

The opposite can also happen: When all or nearly all LDL particles are large, Friedewald calculated LDL can markedly overestimate LDL particle number. Yesterday, for instance, a patient had a Friedewald calculated LDL of 183 mg/dl, but an NMR particle number of 1110 nmol/L--drop the zero . . . LDL 110 mg/dl. This woman was advised to take a statin drug by her primary care physician, based on the Friedewald LDL. Instead, she proved to have a far lower LDL. She would not have benefitted from taking a statin drug.

As I've warned many times before: Beware the Friedewald calculated LDL.

The last post on vitamin D raised a number of basic questions among readers. So let me discuss some of these questions one by one. All of them raise important issues surrounding the practical aspects of managing vitamin D in your health.

Anne said:

I think it is important to stress that vitamin D supplementation needs to be continued long term.

I have met too many people who have been prescribed 50,000 IU of D2 for 8-12 weeks and then told to stop because their 23(OH)D went over 30ng/ml. I know one person who's doctor stopped and started the D2 3 times.

Thanks for pointing that out, Anne. Excellent point. I also see doctors do this with statin drugs: start it, check a LDL level which is lower, then think that you're done and stop the drug. What the heck are they thinking?

If vitamin D is not being produced by sun exposure and not obtainable through diet, continued supplementation is necessary, essentially for life.

Twinb asked:

How often you think Vit. D levels should be tested after the initial test is done, especially if the levels are drastically low?

We have used every 6 months in the office. Ideally, levels are in mid-summer and mid- to-late winter in order to gauge the extremes of your seasonal fluctuations. While most adults over 40 fail to fluctuate more than 10 ng/ml in the Wisconsin climate (and this summer, after an initial rainy season early, has been flawlessly bright and sunny, in the high-70s and 80s every single day for months), an occasional person fluctuates more widely. The only way to judge is to check a blood level.

Rich said:

Vitamin D dosage effects appear to be quite idiosyncratic.

Yes, indeed it is. Despite using crude rules-of-thumb, like taking 1000 units of vitamin D per 10 ng/ml desired (a rule I learned from Dr. John Cannell, which he offered fully aware of its inaccuracy), many people will surprise you and have levels that make no sense. Testing is crucial to know your vitamin D level.

Richard asked: Where do we get enough vitamin D wihout worring about laboratory tests?

Well, the entire point of the post was that you absolutely, positively cannot just take vitamin D blindly at any dose and hope that your level is ideal, no more than you can blindly take a dose of thyroid and know you have achieved normal thyroid levels. In my view, vitamin D blood levels are an absolute.

Another simple issue: Don't be afraid of vitamin D. It is, in all practicality, no more dangerous than getting a dark tan. (But, as many of you realize, getting a tan is no assurance of raising vitamin D if you are over 40 years old.)

Wouldn't it be great if someone developed a do-it-yourself-at-home skin test for vitamin D? I know of no effort to develop this, but it would be a huge advantage for all of us.

It’s probably the number one most common question I get today:

“How much vitamin D should I take?”

Like asking for investing advice, there are no shortage of people willing to provide answers, most of them plain wrong.

The media are quick to offer advice like “Take the recommended daily allowance of 400 units per day,” or “Some experts say that intake of vitamin D should be higher, as high as 2000 units per day.” Or “Be sure to get your 15 minutes of midday sun.”

Utter nonsense.

The Food and Nutrition Board of the Institute of Medicine has been struggling with this question, also. They have an impossible job: Draft broad pronouncements on requirements for various nutrients by recommending Recommended Daily Allowances (RDA) for all Americans. The Food and Nutrition Board has tried to factor in individual variation by breaking vitamin D requirements down by age and sex, but what amounts to a one-size-fits-nearly-all approach.

Much of the uncertainty over dosing stems from the fact that vitamin D should not be called a “vitamin.” Vitamins are nutrients obtained from foods. But, outside of oily fish, you'll find very little naturally-occurring vitamin D in food. (Even in fish, there is generally no more than 400 units per 4 oz. serving.) Sure, there’s 20 units in an egg yolk and you can activate the vitamin D in a shiitake mushroom by exposing it to ultraviolet radiation. Dairy products like milk (usually) contain vitamin D because the USDA mandates it. But food sources hardly help at all unless you’re an infant or small child.

It all makes sense when vitamin D is viewed as a hormone, a steroid hormone, not a vitamin. Vitamin-no, steroid hormone-D exerts potent effects in tiny quantities with hormone-like action in cells, including activation of nuclear receptors.

It is the only hormone that is meant to be activated by sun exposure of the skin, not obtained through diet. But the ability to activate D is lost by the majority of us by age 40 and even a dark tan is no assurance that sufficient skin prohormone D activation has taken place.

As with any other hormone, such as thyroid, parathyroid, or growth hormones, dose needs to be individualized.

Imagine you developed a severely low thyroid condition that resulted in 30 lbs of weight gain, lose your hair, legs swell, and heart disease explodes. Would you accept that you should take the same dose of thyroid hormone as every other man or woman your age, regardless of your body size, proportion of body fat, metabolism, genetics, race, dietary habits, and other factors that influence thyroid hormone levels? Of course you wouldn’t.

Then why would anyone insist that vitamin D be applied in a one-size-fits-all fashion? (There’s another world in which a one-size-fits-all approach to hormone replacement has been widely applied, that of female estrogen replacement. In conventional practice, there’s no effort to identify need, estrogen-progesterone interactions, nor assess the adequacy of dose, not to mention the perverse non-human preparation used.)

With thyroid hormone, ideal replacement dose of hormone ranges widely from one person to another. Some people require 25 mcg per day of T4; others require 800% greater doses. Many require T3, but not everybody.

Likewise, vitamin D requirements can range widely. I have used anywhere from 1000 units per day, all the way up to 16,000 units per day before desirable blood levels were achieved.

Vitamin D dose needs to be individualized. Factors that influence vitamin D need include body size and percent body fat (both of which increase need substantially); sex (males require, on average, 1000 units per day more than females); age (older need more); skin color (darker-skinned races require more, fairer-skinned races less); and other factors that remain ill-defined.

But these are “rules” often broken. My office experience with vitamin D now numbers nearly 1000 patients. The average female dose is 4000-5000 units per day, average male dose 6000 units per day to achieve a blood level of 60-70 ng/ml, though there are frequent exceptions. I’ve had 98 lb women who require 12,000 units, 300 lb men who require 1000 units, 21-year olds who require 10,000 units. (Of course, this is a Wisconsin experience. However, regional differences in dosing needs diminish as we age, since less and less vitamin D activation occurs.)

Let me reiterate: Steroid hormone-vitamin D dose needs to be individualized.

There’s only one way to individualize your need for vitamin D and thereby determine your dose: Measure a blood level.

Nobody can gauge your vitamin D need by looking at you, by your skin color, size, or other simple measurement like weight or body fat. A vitamin D blood level needs to be measured specifically-period.

Unfortunately, many people balk at this, claiming either that it’s too much bother or that their doctor refused to measure it.

I would rank normalizing steroid hormone-vitamin D as among the most important things you can do for your health. It should never be too much bother. And if your doctor refuses to at least discuss why he/she won’t measure it, then it’s time for a new doctor.

If you’re worried about adding to rising healthcare costs by adding yet another blood test, think of the money saved by sparing you from a future of cancer, heart disease, osteoporosis, diabetes, etc. The cost of a vitamin D blood test is relatively trivial (around $40-50, a fraction of the cost of a one month supply of a drug for diabetes.)

So how much vitamin D should you take? Enough to raise your blood level of 25-hydroxy vitamin D to normal. (We aim for a normal level of 60-70 ng/ml.)

The results of the recent Heart Scan Blog survey in response to the question: MY DAILY DOSE OF EPA + DHA FROM FISH OIL IS revealed:

Zero--I don't take any
17 (7%) of respondents

Less than 1000 mg per day
24 (10%) of respondents

1000-2000 mg per day
91 (38%) of respondents

2000-3000 mg per day
44 (18%) of respondents

3000-4000 mg per day
40 (16%) of respondents

More than 4000 mg per day
20 (8%) of respondents

Based on the above results, I would say that only a minority of respondents are taking an ideal dose of omega-3 fatty acids. Nearly all of us should consider taking more.

Benefits of omega-3 fatty acids (EPA + DHA) from fish oil begin around a dose of 840 mg per day, according to the GISSI Prevenzione Trial of 1999, an 11,000-participant trial. This dose also corresponds to a quantity of omega-3s that have been shown to raise EPA + DHA blood levels and thereby reduce the notoriously high AA:EPA ratio of Americans.

But what dose is sufficient? What dose is ideal?

Well, the answer to a great degree depends on what you are taking the fish oil for. If being taken to reduce triglycerides and triglyceride-containing lipoproteins, like VLDL and the after-eating (postprandial) IDL, then a higher dose will be necessary. (Triglyceride reduction for the genetically-determined very high triglyceride level of familial hypertriglyceridemia is the FDA-approved indication for prescription Lovaza.)

If you are taking fish oil for treatment of ADHD, depression, or bipolar illness, very high doses are often necessary.

But how about maximal reduction of cardiovascular risk and for control or reversal of atherosclerotic plaque?

This conversation is still evolving. But we can learn some important lessons from three populations of the world that are vigorous consumers of fish:

--The Inuits (aka Eskimos) of Greenland and northern Canada
--The Japanese
--The Bantus of Tanzania who live along Nyasa Lake

All three indigenous populations have several-fold greater intakes of fish and omega-3 fatty acids, have higher blood levels of omega-3 fatty acids, and have enjoyed reduced cardiovascular events, reduced atherosclerotic plaque, or improvement in various surrogates of cardiovascular risk (e.g., Lp(a)).

The most recent addition to this conversation is the ERA JUMP Study, discussed in a previous Heart Scan Blog post. In ERA JUMP, despite being heavy smokers and having other markers for greater risk for heart disease, Japanese men living in Japan had markedly less carotid and coronary plaque, as compared to Caucasian men living in PIttsburgh or Hawaiian men of Japanese descent. The difference appeared to be attributable to serum levels of omega-3 fatty acids.

I believe that the trend is here is to increase the amount of omega-3 fatty acids that most of us take. In the Track Your Plaque program, we have been advocating a rock-bottom starting dose of EPA + DHA of 1200 mg per day. However, I believe that this is due for a change.

We will be increasing the minimum dose for plaque regression and control. Please attend our Webinar this evening for a full, in-depth discussion of the rationale behind this important change.

As always, let me remind you that I am not selling, nor ever have sold, fish oil supplements. If I advocate a specific dose, a higher dose, I do so based on my interpretation of the data and experience with patients, not because I am interested in selling brand X of fish oil.

Despite the paucity of scientific documentation of this phenomenon, I am continuing to witness extraordinary increases in HDL cholesterol levels with vitamin D supplementation.

I've touched on the interaction of vitamin D supplementation with HDL in The Heart Scan Blog previously:

Vitamin D: Treatment for metabolic syndrome?

HDL for Dummies

At first, I thought it was attributable to other factors. In real life, most people don't modify one factor at a time. They reduce
processed carbohydrates/eliminate wheat and cornstarch, lose weight, add or increase omega-3 fatty acids from fish oil, begin niacin, increase exercise and physical activity. All these efforts also impact on HDL.

Among the many things I do, I consult on complex lipid (cholesterol) disorders (complex hyperlipidemias) in my office. A substantial number of these people carry a diagnosis of hypoalphalipoproteinemia, a mouthful that simply means these people are unable to manufacture much apoprotein A1, the principal protein of HDL cholesterol particles. As a result, people with hypoalphalipoproteinemia have HDL cholesterol levels in the neighborhood of 20-30 mg/dl--very low. They are also at high risk for heart disease and stroke.

Encourage these people to exercise, attain ideal weight, eliminate wheat and cornstarch: HDL increases 5 mg/dl or so.

Add niacin, HDL increases another 5-10 mg/dl.

Perhaps we're now sitting somewhere around an HDL of 35-40 mg/dl--better, but hardly great.

Add vitamin D to achieve our target serum level . . . HDL jumps to 50, 60, 70, even 90 mg/dl.

The first few times this occurred, I thought it was an error or fluke. But now that I've witnessed this effect many dozens of time, I am convinced that it is real. Just today, I saw a 40-year old man whose starting HDL was 25 mg/dl increase to 87 mg/dl.

Responses like this are supposed to be impossible. Before vitamin D, I had never witnessed increases of this magnitude.

Not all therapies for raising HDL raise the important large (also known as HDL2b) fraction. With lipoprotein analyses, it appears that is principally the large fraction of HDL that rises with vitamin D supplementation.

Why? How?

That I can't tell you. But for those of you struggling with low HDL cholesterols despite your best efforts, vitamin D can make a world of difference.

An interesting corollary: If super-high HDL cholesterols are associated with extreme longevity, as they are with centenarians, does raising HDL to extraordinary levels with vitamin D lead to longer, healthier life, all the way up to age 110 years?

Again, no answers, but an interesting thought. And one I'd bet on. (And I'm not selling vitamin D.)

Here's another thought with regards to time issues with weight loss: reductions in blood pressure (BP).

The previous post talked about how triglycerides initially go up, sometimes way up, when weight drops, only to be followed months later by substantial drops. HDL initially drops in response to the triglyceride fluctuations, only to be followed by a rise.

Blood pressure also shows a curious pattern that is largely dependent on age.

Say someone in their 20s or 30s, for instance, loses 30 lbs (through elimination of wheat and cornstarch, say). BP usually drops within a few weeks, perhaps a month or two at most.

How about someone in their 70s? Say a substantial amount of weight is lost, say 50 lbs over 6 months. BP does indeed drop, but it may require 6 months or longer after weight plateaus for the full effects of BP-reduction to be fully expressed. But it will eventually drop.

Why the age-dependent difference?

It relates to the capacity of arteries to remain flexible and distensible. Over the years, cross-linking of collagen (a structural protein), glycation (glucose molecules attaching to proteins), loss of endothelial responsiveness to generate artery-dilating substances like nitric oxide, and arterial atherosclerotic plaque all all up to making older arteries less able to "relax" and BP to drop.

But given time and the proper effort, BP will eventually drop. Awareness of this time effect can help most people decide better when medications are necessary or if weight loss alone is sufficient to reach BP goals.

Brad needed to lose weight.

At 6 ft tall, he began the program at 291 lbs, easily 80 lbs overweight. He wore virtually all of it in his belly.

He had laboratory numbers to match: HDL 33 mg/dl, triglycerides 225 mg/dl, LDL (calculated) 144 mg/dl, blood sugar 122 mg/dl (fasting--clearly "pre-diabetic"), c-reactive protein 3.0 mg/dl. Among his lipoprotein abnormalities: small LDL representing 80% of all LDL (no surprise).

Readers of The Heart Scan Blog know that these are the patterns of the carbohydrate-indulgent. I asked Brad to eliminate all wheat flour products, all foods made with cornstarch, and follow a diet rich in healthy oils, raw nuts, vegetables, and lean meats.

Brad returned for a discussion about follow-up basic lipids (cholesterol) values four months later--31 lbs lighter, most of it clearly lost from his abdomen. He claimed he felt more energetic and clear-headed than he had in years.

His lipid panel: HDL 34 mg/dl, LDL 122 mg/dl, triglycerides 295 mg/dl. Brad's smile dissolved. "How could that happen? You said losing weight would make my HDL go up and my triglycerides go down!"

Yes, I had said that. But I was oversimplifying.

The truth is that, when there is weight loss, especially profound weight loss like Brad experienced eliminating wheat and cornstarch products, there is mobilization of fat stores. Fat is stored energy. Energy is stored as . . . triglycerides.

So when there is substantial weight loss, there is a flood of triglycerides in the blood, and triglyceride levels in the midst of weight loss can commonly jump up, not uncommonly to the 200-300+ mg/dl range. When triglycerides go up, there is also a drop in HDL (triglycerides interact with HDL particles, modify their structure and make them more readily destroyed, thereby dropping blood levels). Occasionally, substantial weight loss like Brad experienced will drop HDL really low, as low as the 20's.

Once weight stabilizes, this effect can last up to 2 months before correcting. Only then will triglycerides drop and HDL rise. The rise in HDL occurs even more slowly, requiring several more months to plateau.

In other words, weight loss like Brad's causes triglycerides to increase and HDL to decrease, to be followed later by a drop in triglycerides and a rise in HDL.

I know of no way to block this phenomenon. And perhaps we shouldn't, since this is how fat stores are mobilized and "burned off." Fish oil does blunt the triglyceride rise (perhaps through activation of lipoprotein lipase, an enzyme responsible for clearance of triglycerides), but doesn't eliminate it.

I call these changes "transitional" changes in lipids.

Patience pays. A few more months from now, Brad's numbers will be much happier, as will Brad.

The doctor-patient relationship has gone sour.

This probably comes as no surprise to most of you, particularly if you've been following conversations here in The Heart Scan Blog:

Who is your doctor? discussing the emergence of the physician-as-hospital-employee phenomenon that causes your doctor to become the de facto portal (seller?) of hospital services to you, a model fraught with conflicts of interest.

Exploitation of trust, my observation that the enormous gap in heart disease prevention between the woefully ignorant (by necessity) level of sophistication of the primary care physician and the procedure-obsessed cardiologist leads to an exploitation of humans-for-heart-procedures because of the failure to institute genuine preventive efforts.

Bait and switch , a description of how a minor test or symptom can reap a bonanza of medical testing; a $20 "screening" test yields $10's of thousands in hospital procedures. If it were entirely due to the imprecision of medical testing and detection of disease, that might be forgivable. But it often is not: It has become utterly distorted by the profit model.

Lest you think that I am a kook ranting off in some backwoods corner (Milwaukee), here are the comments of New York Times' Health Editor Tara Parker-Pope in a series called Doctor and Patient, Now at Odds:

Lately I've been hearing a lot from patients who are frustrated, angry, and distrustful of doctors. Their feelings speak to a growing disconnect between doctors and patients and worries that drug companies, insurance rules, and hospital cost-cutting are influencing the care and advice that doctors provide.

Research shows that even among patients who like their personal physicians, there is a simmering distrust of the medical system and the doctors who work inside it.

(There's also a series of candid video interviews with people who echo these sentiments.)

There are a number of reasons for this increasing "disconnect," some of them articulated by Ms. Parker-Pope, others detailed in my blog posts.

The solutions, however, will not be found by advancing technology: the newest robotic surgery, a better defibrillator, a new statin drug, the next best chemotherapeutic agent. It will not be found by adding a new wing to the hospital. It will not be found by the reorganization of healthcare delivery achieved by converting primary care and specialty practice into an arm of hospital care. It will not be improved by employing "hospitalists." It will not emerge from legislation controlling insurance company practices. It certainly will not come from increasing marketing dollars spent by drug companies (who make $4 for every $1 spent on direct-to-consumer marketing).

The solutions will come from shifting the idea of care from a paternalistic, "I'm the doctor and I'll tell you what to do" approach, to the doctor-as-advocate-and-supporter of the patient. The physician should act as someone with a particular sort of expertise that can advise a patient.

But a caveat: The patient MUST be informed.

Proper information will not originate with the doctor. It will originate with internet-based information portals and tools that help you understand the issues, often with far greater depth than your doctor could ever provide. The physician needs to accept this role, one of advocate, adviser, but not of being in charge, not of viewing the patient as profit-center, not as an opponent in a power struggle.

Sadly, the last few years in online information portals has been dominated by the drug company-dominated websites like WebMD, nothing more than a deliverer of the conventional wisdom with nothing whatsoever aimed towards empowering patients in a self-directed healthcare model.

Some people call the emerging new empowered and information-armed patient Medicine 2.0. Unfortunately, Medicine 2.0 will first benefit the intellectual upper crust of Americans, the web-savvy and motivated to engage in health issues. But, give it 10 years, and we will witness the effects on an unprecedented broad scale. Part of the Information Age is acceleration of information dissemination. Imagine your children, facile with a computer mouse, posting comments on FaceBook, doing homework with Google and Wikipedia, now turning their attentions to health.

It will be a startling change.

In the meantime, be wary. Be empowered. Think increasingly about self-direction in your health.

In a comment to the Bait and switch post, Jennytoo offered an insightful response:

You are getting to the essence of the problem, and it's not just cardiology that is rife with what is, at bottom, malpractice.

There is little incentive for the profession as a whole to know anything about or promote prevention, and many incentives from hospitals, drug and insurance companies to stick with the status quo or to change it in their corporate favor. The formulaic, conventional statements purporting to be guidelines for prevention that are put out by various interest groups and in such publications as hospital-sponsored newsletters ("eat a 'balanced diet', avoid stress, etc.") are useless sops to the concept of prevention.

It is, and I fear is going to remain, up to motivated individuals, both physicians and patients, to reshape the system, and it's going to be a long frustrating struggle.

It's my personal conviction that if just 4 things were promoted to the public, and people actually practiced them, we could change the health profiles of the majority of people in this country for the better within two years or less. They are:

(1) education on and promotion of a true low-carbohydrate, whole foods, diet,
(2) measurement and supplementation of Vitamin D3,
(3) supplementation with DHA/EPA (found in Fish Oils), and
(4) measurement and supplementation of intracellular magnesium.

I am not a health professional, and others may want to add to this list, but I don't think any strong case can be made against any of the items. The wonderful and hopeful thing is that each of us can implement them ON OUR OWN, and thereby take charge of our own well-being. (The Life Extension Foundation is one organization which provides access to lab tests you can request on your own.)

If you have a physician who is willing and capable of being your partner, you are richly blessed, and that is the ideal we all should hope for. But in the more likely event that you do not have such a physician, and if your physician demonstrates little potential for becoming one, think about firing the one you have and finding another.

Sometimes we are forced by circumstances, particularly urgent ones, to deal with physicians who are not ideal, but the main impetus for change will come from us, the patients, and the expectations we communicate to our individual doctors. In the meantime, we can be self-reliant in our own prevention practices.

Wow. A woman after my own heart.

This post just furthers this line of thinking out loud: How much fish oil is "enough"?

Observations over the last 30 years followed this path: If a little bit of omega-3 fatty acids from fish are beneficial in reducing cardiovascular events, and a moderate intake is even better, is even more better? When have we reached a plateau? When do adverse effects outweigh the benefits?

Some insight can be gained through studies that examined blood levels of omega-3s. Let's take a look at some data from 2002, a comparison of men dying from heart disease vs. controls in the Physicians' Health Study, Blood Levels of Long-Chain n–3 Fatty Acids and the Risk of Sudden Death.

This is a table that shows the blood levels of various fatty acids Group with sudden death vs Control Group:

Several observations jump out:

--The total omega-3 blood content differed significantly, 4.82 vs 5.24% ("Total long-chain n-3 polyunsaturated")
--Total omega-6 content did not differ
--Arachidonic acid (AA) content did not differ
--Linolenic acid content did not differ (i.e., plant sourced omega-3)

The fact that neither omega-6 nor arachidonic acid content differed counters the argument that Simopoulos has made that the omega-6 to omega-3 ratio (intake, not blood levels) is what counts. It also argues against the EPA to AA ratio (and similar manipulations) that some have argued is important. In this study, only the omega-3 level itself made a difference; no ratio was necessary to distinguish sudden death victims vs controls.

Further, quartiles of omega-3 blood levels showed graded reductions of risk:

An omega-3 blood level of 6.87% conferred greatest risk reduction. Depending on the model of statistical analysis, risk reductions of up to 81-90% were observed. Wow.

Taken at face value, this study would argue that:

--An omega-3 fatty acid blood level of 6.87% (or greater?) is ideal
--The omega-3 fatty acid blood level stands alone as a predictor without resorting to any further manipulation of numbers, such as relating EPA and/or DHA to AA levels.

Of course, this is just one study, though an important one. It is also not a study based on any intervention, just an observational effort. But it does add to our understanding.

We will develop these issues further in our upcoming Track Your Plaque Webinar on Wednesday, August 20th, 2008.

John Cannell on Vitamin D

Watch your groin

Garlic and cholesterol--Does everyone now need Lipitor?

Diet Coke saves father's life

Beware the "false positive" stress test

Don't neglect your magnesium

Third heart scan a charm

Metabolic syndrome--cured

Heart Scan Curiosities #6

Should you become a vegetarian?

Kitchen sink approach for Lp(a)

Making Dr. Friedewald an honest man

Some basic vitamin D issues

“How much vitamin D should I take?”

You probably don't take enough fish oil

Vitamin D and HDL

Weight loss and blood pressure

"I lost 30 lbs and my triglycerides went . . . up?"

Divorce court for the doctor-patient relationship?

How much fish oil is enough?