Low HDL makes Dr. Friedewald a liar

There's a $22 billion industry based on treating LDL cholesterol, a fictitious number.

LDL cholesterol is calculated from the following equation:

LDL cholesterol = Total cholesterol - HDL cholesterol - triglycerides/5

So when your doctor tells you that your LDL cholesterol is X, 99% of the time it has been calculated. This is based on the empiric calculation developed by Dr. Friedwald in the 1960s. Back then, it was a reasonable solution, just like bacon and eggs was a reasonable breakfast and a '62 Rambler was a reasonable automobile.

One of the problems with Dr. Friedewald's calculation is that the lower HDL cholesterol, the less accurate LDL cholesterol becomes. If it were just a few points, so what? But what if it were commonly 50 to 100 mg/dl inaccurate? In other words, your doctor tells you that your LDL is 120 mg/dl, but the real number is somewhere between 170 and 220 mg/dl. Does this happen?

You bet it does. In my experience, it is an everyday event. In fact, I'm actually surprised when the Friedewald calculated LDL closely approximates true LDL--it's the exception.

Dr. Friedewald would likely have explained that, when applied to a large population of, say, 10,000 people, calculated LDL is a good representation of true LDL. However, just like saying that the average weight for an American woman is 176 lbs (that's true, by the way), does that mean if you weigh 125 lbs that you are "off" by 41 lbs? No, but it shows how you cannot apply the statistical observations made in large populations to a single individual.

The lower HDL goes, the more inaccurate LDL becomes. This would be acceptable if most HDLs still permitted reasonable estimation of LDL--but it does not. LDL begins to become significantly inaccurate with HDL below 60 mg/dl.

How to get around this antiquated formula? In order of most accurate to least accurate:

--LDL particle number (NMR)--the most accurate by far.

--Apoprotein B--available in most laboratories.

--"Direct" LDL

--Non-HDL--i.e., the calculation of total cholesterol minus HDL. But it's still a calculated with built-in flaws.

--LDL by Friedewald calculation.

My personal view: you need to get an NMR if you want to know what your LDL truly is. A month of Lipitor costs around $80-120. A basic NMR costs less than $90. It's a relative bargain.

Menopause unleashes lipoprotein(a)

Faye was clearly frustrated.

At age 52, she was having chest pains every day. A CT heart scan showed a score of zero. A CT coronary angiogram showed no plaque whatsoever.

"Everything went downhill when my menopause started. I gained weight, I started to have chest pains, my blood pressure went up, my cholesterol shot up."

She saw three physicians, none of whom shed much light on the situation. They ran through the predictable sequence of (horse, not human) estrogens, anti-depressants, suggestions for psychological counseling.

But we checked Faye for lipoprotein(a), which she proved to have at a high level of 182 nmol/l. This explained a lot.

A curious and predictable set of phenomenon occur to females with Lp(a) proceeding through the menopause. As estrogen recedes:

--Lp(a) levels rise dramatically.

--Blood pressure goes up, sometimes creating severe hypertension by mid- to late-50s.

--Chest pain can develop, presumably due to "endothelial dysfunction" or "microvascular angina", both representing abnormal coronary artery constriction facilitated by worsening expression of Lp(a).

All too often, these phenomena get dismissed as simply part of the menopausal package, when they are, in fact, important facets of this very important genetic pattern that confers high risk for heart disease.

If any of this rings familiar for you or a loved one, think Lp(a). Though Faye hadn't yet developed any measurable coronary plaque by her CT heart scan score, it was likely on its way, given the surge in Lp(a) expression as menopause unfolded--unless its recognized and appropriate preventive action taken.

Vitamin D must be oil-based

I've talked about this before, but I need to periodically remind everybody:
Vitamin D must be an oil-based capsule, a gel-cap, not a tablet.

Lisa is one of early success stories: a heart scan score of 447 in her early 40's, modest reduction of CT heart scan score three years ago.

However, Lisa had a difficult time locating oil-based vitamin D. There has, in fact, been a national run on vitamin D and I'm told that even manufacturers are scrambling to keep up with the booming demand. So, she bought tablets instead and was taking 3000 units per day.

She came in for a routine check. Lisa's 25-OH-vitamin D3: 17 ng/ml, signifying severe deficiency, the same as if she were taking nothing at all. (Recall that we aim for 50 ng/ml.)

In other words, vitamin D tablets do not work. It is shameful. I see numerous women taking calcium tablets with D--the vitamin D does not work. I've actually seen blood levels of zero on these preparations.

You may have to look, but if you want to enjoy the extraordinary benefits of vitamin D replacement, it must be an oil-based capsule. Carlson's and Vitamin Shoppe have excellent prepartions. They raise blood levels substantially and consistently, and they're inexpensive. We pay $5.99 for a bottle of 120 capsules.

Vitamin D for $200?

What if vitamin D cost $200 rather than $2?

In other words, what if cholecalciferol, or vitamin D3, was a patent-protectable agent that would sell for an extravagant price, just like a drug?

Vitamin D would be the hot topic. There would be TV ads run during Oprah, slick magazine two-page spreads with experts touting its outsized benefits, insurance companies would battle over how much your copay should be.

The manufacturer would host large fancy symposia to educate physicians on how wonderful vitamin D is for treatment of numerous conditions, complete with dinner, a show, and gifts. They would hire expert speakers to speak, scientists to have articles ghost-written, give out knick knacks with the brand label inscribed--just like Lipitor, Actos, Vytorin, ReoPro, Plavix . . .

After all, what other "drug" substantially increases bone density (up to 20% in adult females), enhances insulin responses 30% (equivalent to the TZD drugs, Actos and Avandia), and slashes colon cancer risk?

But it's not a drug. That is both vitamin D's strength and its weakness. It's a strong point because it's natural, phenomenally helpful across a variety of conditions, and inexpensive. It is also a weakness because, at $2 a month, no one is raking in the $12 billion annually that Pfizer makes for Lipitor that allows it to fund an enormous marketing campaign.

Vitamin D is a "discovery" of huge importance for health, including making reductions of CT heart scan scores far more likely for more people. And it comes without a prescription.

What's up with garlic?


Fanatic Cook has posted an excellent summary on the recent negative attention cast on garlic preparations, at least for LDL cholesterol reduction.

Go to http://fanaticcook.blogspot.com to view.

I think Fanatic Cook is right--despite the lack of LDL reducing effects, it doesn't necessarily mean no benefit whatsoever. Anti-coagulation and anti-inflammatory effects, in particular, are well proven.

I do think, however, that it argues more in favor of sticking to whole cloves, rather than supplements. The benefits are also likely small. I would view garlic as a soft advantage for your plaque control program. You can do fine without it. You might do slightly better with it.

Drop the pretense

Most hospitals maintain the "Saint _____" in their names, despite many having little or nothing to do with the church.

Out of 15 hospitals in my area, 13 are named after saints.

In my view, a more honest name would be something like "ABC Medical Enterprises, Inc." The profit motive, aggressive marketing tactics, and high CEO salaries would make better sense then. The trend to convert practicing physicians from professionals acting on behalf of patient welfare into paid employees would also be clearer.

Imagine Walmart were to change its name to "St. Mary's Emporium" Would it modify your perception of their business? I think it would. It would cause many people to believe that maybe their work was, at least in part, charitable and being done for the public welfare. But Walmart makes such pretense--they are in business for profit, just like all businesses.

It's time for the pretense to be dropped. Hospitals are cut-throat profit-seeking operations, operating under the guise of charitable, tax-free institutions. It's the farthest thing from the truth.

John Cannell on Vitamin D

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

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency. If you don't want to get the newsletter, please hit reply and let us know. We don't copyright this newsletter. Please feel free to reproduce it and post it on Internet sites and blogs. Remember, we are a non-profit educational organization. Our pathetic finances are available for public inspection. We rely on donations to publish our newsletter and maintain our website. Send your tax-deductible contributions to:


The Vitamin D Council (www.vitamindcouncil.com)
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Atascadero, CA 93422

Watch your groin

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 and cholesterol--Does everyone now need Lipitor?

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."

Diet Coke saves father's life

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.
Is normal TSH too high?

Is normal TSH too high?

There's no doubt that low thyroid function results in fatigue, weight gain, hair loss, along with rises in LDL cholesterol and other fractions of lipids. It can also result in increasing Lp(a), diabetes, and accelerated heart disease, even heart failure.

But how do we distinguish "normal" thryoid function from "low" thyroid function? This has proven a surprisingly knotty question that has generated a great deal of controversy.

Thyroid stimulating hormone, or TSH, is now the most commonly used index of the adequacy of thyroid gland function, having replaced a number of older measures. TSH is a pituitary gland hormone that goes up when the pituitary senses insufficient thyroid hormone, and a compensatory increase of thyroid hormone is triggered; if the pituitary senses adequate or excessive thyroid hormone, it is triggered to decrease release of TSH. Thus, TSH participates in a so-called "negative feedback loop:" If the thyroid is active, pituitary TSH is suppressed; if thyroid activity is low, pituitary TSH increases.

An active source of debate over the past 10 years has been what a normal TSH level is. In clinical practice, a TSH in the range of 0.4-5.0 mIU/L is considered normal. (Lower TSH is hyperthyroidism, or overactive thyroid; high TSH is hypothyroidism, or underactive thyroid.)

The data from a very fascinating and substantial observation called the HUNT Study, however, is likely to change these commonly-held thyroid "rules."

The association between TSH within the reference range and serum lipid concentrations in a population-based study. The HUNT Study

In this study, over 30,000 Norwegians without known thyroid disease were enrolled. TSH levels and lipid (cholesterol) levels were measured.

In this large and extraordinary observation, increasing TSH levels were associated with increasing levels of LDL cholesterol and triglycerides, and decreasing HDL. At what level of TSH did this relationship start? At TSH levels as low as 1.0!

In other words, there were perturbations in standard lipid measures even with TSH levels ordinarily regarded as "normal," even "perfect."

A subsequent observation from the HUNT Study was even more recently published:

Thyrotropin Levels and Risk of Fatal Coronary Heart Disease: The HUNT Study

Abstract:

Background Recent studies suggest that relatively low thyroid function within the clinical reference range is positively associated with risk factors for coronary heart disease (CHD), but the association with CHD mortality is not resolved.

Methods In a Norwegian population-based cohort study, we prospectively studied the association between thyrotropin levels and fatal CHD in 17 311 women and 8002 men without known thyroid or cardiovascular disease or diabetes mellitus at baseline.

Results During median follow-up of 8.3 years, 228 women and 182 men died of CHD. Of these, 192 women and 164 men had thyrotropin levels within the clinical reference range of 0.50 to 3.5 mIU/L. Overall, thyrotropin levels within the reference range were positively associated with CHD mortality (P for trend = .01); the trend was statistically significant in women (P for trend = .005) but not in men. Compared with women in the lower part of the reference range (thyrotropin level, 0.50-1.4 mIU/L), the hazard ratios for coronary death were 1.41 (95% confidence interval [CI], 1.02-1.96) and 1.69 (95% CI, 1.14-2.52) for women in the intermediate (thyrotropin level, 1.5-2.4 mIU/L) and higher (thyrotropin level, 2.5-3.5 mIU/L) categories, respectively.

Conclusions Thyrotropin levels within the reference range were positively and linearly associated with CHD mortality in women. The results indicate that relatively low but clinically normal thyroid function may increase the risk of fatal CHD.


In other words, the findings of this substantial observation suggest that the ranges of TSH usually regarded as normal contribute to coronary events, cardiac death, as well as lipid patterns. While several other studies have likewise shown a relationship of higher TSH/lower thyroid function with lipid abnormalities and overt heart disease, no previous study has plumbed the depth of TSH to this low level and to such a large scale.

I believe that these findings are enough cause to begin thinking seriously about monitoring thyroid function more seriously to uncover "borderline" TSH increases in the "normal" range. While higher TSH levels predict cardiovascular events, does thyroid replacement at these levels reduce it? Critics will say it's a big leap, but I think that it is worth at least considering.

Stay tuned for a lengthy Special Report followed by a full booklet on these issues on the www.cureality.com website.


Copyright 2008 Wiliam Davis, MD

Comments (30) -

  • Anna

    6/4/2008 6:13:00 PM |

    As a woman with undiagnosed, and worsening hypothyroidism for at least 12-15 years (I've been treated for 2.5 years with much improvement), I'm so glad you posted this.  

    My TSH levels were checked many times while I was experiencing infertility for many years, but the results were always in the upper half of my lab's "normal" range (.5 - 5.5), so my results were never flagged and hypothyroidism was always dismissed, despite classic hypothyroid symptoms that worsened steadily as my TSH crept up over the years (nurses used to joke about my "icy temps".  Of course, the focus was always on the blood lipid tests, as they kept pace with the TSH!  Currently, conventional medicine treats not the patient, but the lab test results, when it comes to hypothyroid issues.  

    I talk to women (late 30s - late 40s) all the time who describe classic hypothyroid symptoms (chronically cold  - even in So Cal, low body temps, constant fatigue, trouble with mental concentration, sleep disruption, not sweating, etc.) and they all say the same thing I said for a decade, "my doctor tested me and he/she says my TSH is just fine".   Frankly, we get tired of telling our doctors we don't feel right anymore and being told "your test results are all normal so there there's nothing wrong with you, here are some samples of anti-depressants, time is up, bye-bye".  I had to find treatment from a doctor outside of my network and without insurance reimbursement initially to get the care I needed to feel better (T4-T3 combo).  It was hard to "keep at it" until I found the right doctor and care, but it made a huge difference in my daily life and that of my family and was well worth the extra effort.  

    I realize hypothyroidism symptoms are also common with other conditions, but I find it ironic that all sorts of Rx are written for serious and potential dangerous drugs to manage these common mid-life symptoms, yet a trial of thyroid hormone is considered too dangerous.  

    Additionally, many primary care doctors and labs seem to be very "behind the times" when it comes to recent thyroid research, AACE and NACL recommendations, not to mention thyroid hormone supplementation options.  My own networks lab is very proud of their brand new, ultra-sensitive machines, but the supervisor of the lab wasn't even aware that the AACE and NACL had recommended lowering the upper level of the TSH reference range several years ago.  He promised to look into the reference range issue and get back to me, but of course he hasn't.

    I won't even get started on the sad state of how thyroid hormone is common prescribed in such a one-option-fits-all manner.

    Untreated and under-treated hypothyroidism is a risk factor for heart disease and is much more common than most people (even doctors) think.  You are doing people a great service in writing about this.  Thanks!

  • PJ

    6/4/2008 11:28:00 PM |

    I've been reading a little on thyroid issues. All the women in my family but me are on thyroid medication. I have refused to have it checked. The thing is, I believe if you treat the body right it will usually heal. The problem is, when I search on the internet for what I can do to improve the health of my thyroid, all I really find is endless amounts of ads and talk about thyroid medications.

    I see the constant prescription of thyroid for low-thyroid as akin to drugs that allegedly will lower cholesterol or something. I know they help people, but why is nobody interested in what might be causing it or how to naturally work at solving it??

  • Stan

    6/5/2008 2:35:00 AM |

    Interesting.  Could an increased TSH be a proxy for insulin resistance? Does insulin resistance mean thyroid hormone resistance as well, necessitating an overproduction of TSH?  Could all the above be a proxy for excessive carbohydrate consumption?   I wonder if that connection (i.e. thyroid and carbohydrates) has ever been studied?

    Stan(Heretic)

  • brian

    6/5/2008 2:16:00 PM |

    Could it be possible that simply isolating TSH levels isn't enough? Shouldn't we look at the system in its entirety?

    If normal levels are still contributing to ill effects, it would seem that a new definition of normal is needed (not what I would personally prescribe) or a view of the whole system to identify what is causing the normal levels to still be related to ill effects.

    As the "Master Gland" of the endocrine system, it would seem to have wide-ranging ability to promote homeostasis. As other hormones enter hypo- or hyper-status, the TSH would have the ability to over-ride and protect the system.

    I'm not an endocrinologist, but it seems to me the isolation of a single hormone in a complex system makes it difficult to identify ranges of normal - as evidenced in this study.

    Love your stuff. Keep up the great work.

    Brian

  • Anna

    6/6/2008 6:54:00 PM |

    Hmmm,  I find the idea that a healthy diet and lifestyle might "heal" hypothyroidism very appealing, but if there is such a way to improve a bona fide hypothyroid condition without thyroid hormone, I have yet to find it, despite reading everything I could get my hands on in both conventional sources as well as alternative.  Certainly, healthy lifestyle and diet are important supporting factors for any person with a thyroid condition,  but I can find no indication that they alone are enough to override an autoimmune attack on the thyroid gland, for instance, or undo many years of insufficient thyroid function.  And believe me, there are plenty of ideas out there for non-Rx treatment of thyroid issues.  I've looked into quite a few of them.

    My TSH levels were checked for more than 12 years, due to infertility and later, fatigue/unusual weight gain.  It was always the first test my former primary doc ran when I said I wasn't sleeping well, was always tired, had trouble concentrating and remembering, and not feeling "quite right", among other things.  She always said my thyroid checked out fine.  So did the reproductive endo I saw (for two rounds of infertility testing). During that time I spent years on a high carb diet (with some weight gain) followed by several years on a low carb diet (with weight loss).  My TSH continued to creep up (though continually in the higher end of the "normal range) and my hypothyroidism symptoms became much worse.  When just dropped from lack of "oomph" and began to research thyroid conditions, I had been on a low carb (little to no grain, starch, or sugar) whole food diet (primarily home prepared) already for several years, which was effectively keeping my impaired glucose regulation in the normal range (without meds) and my weight in a normal range (I think I am first phase insulin insufficient, not insulin resistant, at this point).  No, I don't think low carb caused the thyroid problems, that had started much earlier when I was making homemade pasta and baking whole wheat bread.  I now actually think it probably started at age 29 (17 years ago) when I went through a brief but exceptionally stressful time in my life.  Nothing about my metabolism was the same afterwards when the stressful situation was resolved.  

    I subscribe to a farm vegetable box and get meat and eggs from a local farm.   Believe me, I eat good, real food from good sources whenever I can, instead of industrial, factory farmed food.  Good food alone isn't enough to keep my thyroid happy.

    The vit & supplement dept folks tried to convince me that all I needed was iodine and raw gland products.  Too much iodine can cause problems, too, so that is a tricky way to self-treat.  I don't use iodized salt, but I do use unrefined sea salt and some kelp seasoning.  I tried acupuncture, too.  I tried coconut oil.  

    The only thing that makes a difference for me in any measurable way (both in lab tests and in symptoms and quality of life) is an appropriate dose of  T4 with a small dose of compounded timed-release natural thyroid extract to provide a bit of T3.  A bit of regular, daily sunshine exposure (not enough to burn or tan) helps, too, but as a support, not primary treatment.  Two years in a row, I have had a recurrence of some hypothyroid symptoms at the same time of the year (mid-September) which were alleviated with a minor T4-T3 dose increase, later dropped in the late spring.  There is clearly a seasonal component to my own hypothyroid condition, even living in mild coastal So Cal (my thyroid doctor notices this in many of his Boston area patients, but even more pronouced), perhaps due to reduced daylight hours more than temp changes.  I am finally not dragging myself through the school year (I have 1 elem school age child) and only perking up a bit during the summer.

    If hypothyroidism was like iron or protein deficiency and I could improve the condition with food, I would.  I tried that route when I couldn't get my former primary care doctor to consider it really was my thyroid, as I'm not one to take a medications lightly.  I'm quite open to alternative ideas besides medications, but in my experience, if my thyroid gland isn't producing the levels I need to function well, then my best bet is to supplement with T4 and T3 and take the strain off it (I don't have a goiter, but my gland aches when it is straining to keep up).   I don't even think of the thyroid hormone supplementation as medication, I think of it like a nutrient in which I am deficient and can't make or get another way.  Taking thyroid hormone is in no way like a taking a statin medication that interferes with cholesterol production.  Diet and lifestyle (getting enough sleep and maintaining skeletal muscle strength, especially) are certainly important support components, but simply aren't not enough on their own when the gland just isn't functioning well or the inactive T4 just isn't being converted to the active form, T3, in the body's tissues.  

    There is a lot of evidence that environmental factors over which we have little or no control, are significant factors in the development of hypothyroidism, too.

    Certainly a new definition of "normal" is needed.  I don't even like the term "normal"; I prefer "reference range".  Currently, the reference range my lab uses is akin to measuring a bunch of feet, determining that the size range of the group is size 4-11, lopping off the smallest and largest 2.5% of sizes on either end of the range, and saying that all sizes in between are fine and one should be able to function wearing all the sizes in the ref range.  When I spoke to the lab supervisor about their TSH testing, he was most focussed on the sensitivity and accuracy of the machines (machine a & b should get the same result from the same sample) and he wasn't even aware that there was controversy or a new recommendation concerning the upper half of the reference range.   If the labs can't get it right, how can we expect the primary care doctors who only looked for flagged lab results to get it right?

    But if I wear a size 7 or 8, even if a 10 is "normal", it isn't a good fit for me, is it?  And what if most of the sizes fall between 5-8, but there are a few very large feet that skew the range?  

    Primary care docs seem to think they know all about thyroid conditions, but the ones I have seen clearly don't know very much of the latest research and treat like one-size-fits-all.  Both endos I have seen, as well as the reading I have done, indicate that the vast majority of "normal" TSHs are around or under 1.0 mIU/L.  What they tend not to agree on is resolution of symptoms and if only synthetic T4 is enough or adequate treatment.  Over my thyroid treatment time (about 2.25 years), I have determined I don't begin to have enough resolution of symptoms until my TSH is no higher than 1.0, preferably a bit below.

  • Anonymous

    6/6/2008 8:30:00 PM |

    Stan, You might be interested in reference #9 in the Hunt research study: "The relationship between thyrotropin and low density lipoprotein cholesterol is modified by insulin sensitivity in healthy euthyroid subjects."
    Lynn

  • Anonymous

    6/6/2008 9:04:00 PM |

    Dr. Davis, I started reading your blog a few weeks ago.  I thought the fact that you hadn't addressed the relationship between thyroid health and lipid issues undermined your credibility. You had left a big factor of heart health out of consideration, and I was waiting for the right place to comment about that oversight.  Then lo and behold, here is your TSH blog.

    As a 61 year old woman who has taken thyroid supplementation for 59 years, I have seen an obvious relationship between my thyroid hormone levels and LDL/HDL levels.  It's nice to see the scientific confirmation.  

    Although TSH is now the most commonly used index of the adequacy of thyroid gland function, it is nevertheless a very flawed indicator, as my personal experience and that of many on various thyroid boards attests to.  There are a myriad of factors that interfere with the negative feedback loop.  Inadequate hypothalamus and pituitary function, iodine insufficiency, cortisol insufficiency, selenium insufficiency, thyroid antibodies, and thyroid supplementation can all throw off the feedback loop and make TSH meaningless.  

    A far better test of thyroid health is to directly measure the hormones that the thyroid actually produces, those being thyroxine (T4) and triodo-l-thyronine (T3).  Any blood test is still inadequate, because they don't measure what is happening at the cellular level.  But measuring the biologically active components of what the thyroid produces, the Free T3 and Free T4, plus looking at clinical symptoms, is much more informative than just looking at TSH values.

    And as Anna alluded to, once a person can get a hypothyroidism diagnosis, getting adequate treatment is another sorry story.  Most of the medical community doesn't seem to recognize that the body can only use T4 after it's been converted to T3 and there are places in the body such as the brain that can't convert T4 to T3, T3 must be supplied directly. The usually prescribed T4-only medication (levothyroxine, best known as Synthroid) doesn't do the job.

    If people were correctly diagnosed and treated, I think a lot of antidepressants, statins, other drugs, and doctor visits would be unnecessary.  It's said untreated or undertreated hypo are a gold mine for doctors.

    Lynn

  • Anonymous

    6/6/2008 9:32:00 PM |

    pj,
    As to what may be causing thyroid issues, some factors are within our personal control. Iodine sufficiency (well beyond the 150 mcg RDA), selenium sufficiency, and a health style that lends itself to adrenal health (esp. avoidance of refined foods and overstress) are all within our personal control.

    However, we are exposed to many factors that are are not within our control that harm thyroid function - e.g. fluorides, soy, bisphenol A, and perchlorate in foods and water.  It's not enough to treat the body right if you're damaged by things beyond your control.  

    Thyroid is something the body naturally produces. Drugs to control cholesterol are not, and I don't think taking a form of thyroid that is comparable to what your own thyroid would produce is comparable to taking statins.

    Lynn

  • Anonymous

    6/6/2008 9:36:00 PM |

    Stan,

    Hypothyroid people do have problems processing carbohydrates.  I don't know if it's been studied, but I have seen it recognized.  But I think that even with diminished carbohydrate consumption they still remain hypothyroid.

  • Dr. William Davis

    6/7/2008 3:20:00 AM |

    You know, I sense that we are all zigzagging towards a program of regaining health that uses more and more endogenous (internal, naturally-occuring) substances, such as thyroid hormone, vitamin D, and omega-3 fatty acids, and away from exogenous (external, foreign) substances like statin agents, osteoporosis drugs, and the like.

    Of course, with thyroid issues, the great unanswered question is: Why is this happening in the first place? Why is there such widespread thyroid deficiency? Mineral (e.g., selenium) deficiency, fluoride exposure, pesticide and other organic chemical exposure, etc.?

  • Dr. William Davis

    6/7/2008 3:21:00 AM |

    Thanks, all, for the wonderful articulate and enlightening comments.

  • Dr. B G

    6/7/2008 4:43:00 AM |

    I think these comments demonstrate the potential vast improvements in Hypothyroidism (prevention of and of course tx depending on current structural integrity) that can occur with Track Your Plaque.

    Brian -- from my extensive reviewing of PubMed to find answers to why TYP is so effective, (and Dr. Davis needs a Nobel ;D not joking) it appears that every facet of TYP strengthens steroid nuclear receptors.  I think you are absolutely right. TR (thyroid hormone receptor) does not work alone.  It 'crosstalks' with ALL the other NRs (nuclear receptors).

    Anna -- are you the same Anna in San Diego who's hubby studies apoptosis? Thanks for all your insights if so!

    TRs are immensely supported by the other NRs PPAR, ER (estrogen receptor), GR (glucocorticoid receptor), VDR (vit D receptor) and RXR/RAR (vit A/carotenoid receptors) for the sole purpose of growth, fertility, reproduction and longevity.

    Guess what degrades and reduces the presence of PPAR?
    --movement deficiency
    --strength training deficiency
    --sedentary lifestyles
    --high carb reliant diets
    --wheat due to insulin surges, inflammation, more ox stress, silent/latent CD, etc
    --obesity (fat is an endocrine tissue and the signals it produces kills off PPAR and other NRs)

    Guess what degrades and reduces ER?
    --menopause (which leads to the 'menopot' on the belly)
    --lack of steroid storage forms/ depot in body (secondary to elevated cortisol, vit D defic, etc)

    Guess what degrades GR?
    --'overstress' as Lynn puts it (I *heart* that phrase!)

    Guess what degrades VDR?
    --Vitamin D deficiency (25(OH)D < 50-60 ng/ml)
    --Obesity
    --'Overstress'

    Guess what degrades RXR/RAR?
    --Carotenoid deficiency from poor diet
    --Vitamin A deficiency from poor diet
    --Inflammation


    Why does Track Your Plaque work?

    All the recommendations optimize the functions of all these receptors and their maximal integrity:
    --movement (30-60min minimum daily and more)
    --grain-free Paleo diet (low carb, rich in the trace nutrients discussed here -- iodine,Mg,Zn,Bs,etc)
    --vitamin 'O' for reducing 'over stress' (omg -- that word is GREAT)
    --E2 as needed
    --vitamin D3 as needed
    --vitamin A/carotenoids as needed (see the blog)
    --multiple modalities to reduce internal inflammation/cortisol -- including IF, high vegs intake, fish oil, certain nutritional factors, etc

    Wouldn't you agree?

    -G

  • Dr. B G

    6/7/2008 4:43:00 AM |

    I think these comments demonstrate the potential vast improvements in Hypothyroidism (prevention of and of course tx depending on current structural integrity) that can occur with Track Your Plaque.

    Brian -- from my extensive reviewing of PubMed to find answers to why TYP is so effective, (and Dr. Davis needs a Nobel ;D not joking) it appears that every facet of TYP strengthens steroid nuclear receptors.  I think you are absolutely right. TR (thyroid hormone receptor) does not work alone.  It 'crosstalks' with ALL the other NRs (nuclear receptors).

    Anna -- are you the same Anna in San Diego who's hubby studies apoptosis? Thanks for all your insights if so!

    TRs are immensely supported by the other NRs PPAR, ER (estrogen receptor), GR (glucocorticoid receptor), VDR (vit D receptor) and RXR/RAR (vit A/carotenoid receptors) for the sole purpose of growth, fertility, reproduction and longevity.

    Guess what degrades and reduces the presence of PPAR?
    --movement deficiency
    --strength training deficiency
    --sedentary lifestyles
    --high carb reliant diets
    --wheat due to insulin surges, inflammation, more ox stress, silent/latent CD, etc
    --obesity (fat is an endocrine tissue and the signals it produces kills off PPAR and other NRs)

    Guess what degrades and reduces ER?
    --menopause (which leads to the 'menopot' on the belly)
    --lack of steroid storage forms/ depot in body (secondary to elevated cortisol, vit D defic, etc)

    Guess what degrades GR?
    --'overstress' as Lynn puts it (I *heart* that phrase!)

    Guess what degrades VDR?
    --Vitamin D deficiency (25(OH)D < 50-60 ng/ml)
    --Obesity
    --'Overstress'

    Guess what degrades RXR/RAR?
    --Carotenoid deficiency from poor diet
    --Vitamin A deficiency from poor diet
    --Inflammation


    Why does Track Your Plaque work?

    All the recommendations optimize the functions of all these receptors and their maximal integrity:
    --movement (30-60min minimum daily and more)
    --grain-free Paleo diet (low carb, rich in the trace nutrients discussed here -- iodine,Mg,Zn,Bs,etc)
    --vitamin 'O' for reducing 'over stress' (omg -- that word is GREAT)
    --E2 as needed
    --vitamin D3 as needed
    --vitamin A/carotenoids as needed (see the blog)
    --multiple modalities to reduce internal inflammation/cortisol -- including IF, high vegs intake, fish oil, certain nutritional factors, etc

    Wouldn't you agree?

    -G

  • Anna

    6/7/2008 6:03:00 PM |

    Dr. B G,

    Yup, that's me.

  • mike V

    6/7/2008 7:11:00 PM |

    I support most of Anna's observations. I started off with synthetic T4 about more than thirty years ago. Most doctors I have encountered were taught (and insist on) treating the (TSH) number and not the patient.
    About 12 years ago I became aware of a few studies that suggested the addition of a small amount of T3 was beneficial, especially in mood and mental performance.
    With the help of a couple of  cooperative docs (who had not been aware of this at the time) I tried a small amount of T3 (cytomel or triiodothyronine). This was helpful, and eventually I switched to Armour Thyroid (pork derived) which contains natural T3. This may not be appropriate for everyone since pig thyroids are said to produce a somewhat higher proportion of T3 than human.

    These years of experience now allow me to self "tweak" my dose.occasionaly. Invariably my TSH turns out to be between 1 and 2 when I am feeling at my best.
    Many doctors experienced in the "art" of thyroid treatment now recognize a condition known as "subclinical hypothyroidism". Google it.
    Also, Google "Mary Shomon" She is a well known  thyroid journalist and advocate, who is herself a long term thyroid patient. She frequently interviews (and maintains a list of) doctors who provide specialized thyroid care.
    One final suggestion: don't overlook heredity as a factor. My late mother  and four brothers and sisters have all suffered from hypothyroidism. While many people "get by" with standard thyroid treatment, many (especially women) need careful individual treatment.
    Fortunately for me, my approach seems to have worked well. At 72, I have a zero plaque score, and take no other meds. While I have  generally eaten a healthy diet, I personally have never found diet or supplementation to be a significant influence on my TSH score. Perhaps if you start early  enough?          
    I hope someone will find these comments helpful.
    MikeV

  • donny

    6/7/2008 9:14:00 PM |

    There's an issue of the Vitamin D Council Newsletter where a woman whose mother was taking synthetic thyroid writes in. Her mother started supplementing vitamin d, and her TSH levels went up. The mother's doctor raised the dose for the thyroid, and the woman's mother ended up with hyperthyroid symptoms (the one I remember is increased heartrate.) That got me poking around, and it looks like there are some studies where vitamin d increased TSH output. In people whose thyroids respond to TSH as they should, maybe this is part of why vitamin d increases hdl?
    I've read that vitamin d can increase the output of insulin (this makes a lot of low carb dieters cringe, but 1)some people don't put out enough insulin, and 2)I think it's possible that strategically increased output of insulin, at just the right time, might actually decrease 24-hour insulin under the curve.

  • Dr. William Davis

    6/7/2008 11:09:00 PM |

    Dr. BG opened my eyes to the potential vit D/TSH interaction.

    I believe that there is indeed a real-life effect here (vit D raising TSH). That alone might account for much of the benefit of vitamin D supplementation/normalization.

  • Dr. B G

    6/8/2008 1:57:00 AM |

    Donny -- That's interesting. It's unusual that TSH  would increase. (did they document that free T4 actually decreased, in the newsletter? Perhaps they were only treating a 'lab #' and it was only a transient effect) Though I think that Vit D3 may increase TSH (and worsen hypothyroidism) theoretically if the vitamin D dose or blood level is excessive. It is important to check blood 25(OH)D routinely if one is on supplementation to avoid excessively high doses. Again, at supratherapeutic levels, it can cause the conditions it actually ameliorates --  like calcifications).  And potentially thyroid dysregulation too.

    I didn't know vitamin D can raise insulin! But that makes sense and explains why it's is effective as part of a diabetic treatment.

    In trials, many hormones raise vitamin D blood levels (see below citations):
    --estrogen
    --(genistein (phytoestrogen from soy -- as advised in the TYP plan)
    --thyroid hormones
    --testosterone

    And VICE VERSA! Vitamin D raises the above hormone levels. In fact, after menopause (after the eggs have complete atresed and no longer provide estrogen), estrogen sources come from subcutaneous fat.  After skin activation of vitamin D -- estrogen levels then increase as a function of autocrine regulation (thank goodness!). Vitamin D indeed affects the synthesis of nearly all the other hormones.

    -G

    ++++++++++++++++++++++++++++++++
    Gallagher JC, Riggs BL, DeLuca HF.
    Effect of estrogen on calcium absorption and serum vitamin D metabolites in postmenopausal osteoporosis.J Clin Endocrinol Metab. 1980 Dec;51(6):1359-64.
    PMID: 6255005
    van Hoof HJ, et al.Hormone replacement therapy increases serum 1,25-dihydroxyvitamin D: A 2-year prospective study.Calcif Tissue Int. 1994 Dec;55(6):417-9.
    PMID: 7895179
    van Hoof HJ, et al.Female sex hormone replacement therapy increases serum free 1,25-dihydroxyvitamin D3: a 1-year prospective study.Clin Endocrinol (Oxf). 1999 Apr;50(4):511-6.PMID: 10468912

    Cross HS, et al.Phytoestrogens and vitamin D metabolism: a new concept for the prevention and therapy of colorectal, prostate, and mammary carcinomas.J Nutr. 2004 May;134(5):1207S-1212S. Review.PMID: 15113973

    Weisman Y, et al.Decreased 1,25-dihydroxycholecalciferol and increased 25-hydroxy- and 24,25-dihydroxycholecalciferol in tissues of rats treated with thyroxine.Calcif Tissue Int. 1981;33(4):445-7.PMID: 6271357

    Otremski I, et al.The metabolism of vitamin D3 in response to testosterone.Calcif Tissue Int. 1997 May;60(5):485-7.PMID: 9115169

  • Dr. B G

    6/8/2008 1:57:00 AM |

    Donny -- That's interesting. It's unusual that TSH  would increase. (did they document that free T4 actually decreased, in the newsletter? Perhaps they were only treating a 'lab #' and it was only a transient effect) Though I think that Vit D3 may increase TSH (and worsen hypothyroidism) theoretically if the vitamin D dose or blood level is excessive. It is important to check blood 25(OH)D routinely if one is on supplementation to avoid excessively high doses. Again, at supratherapeutic levels, it can cause the conditions it actually ameliorates --  like calcifications).  And potentially thyroid dysregulation too.

    I didn't know vitamin D can raise insulin! But that makes sense and explains why it's is effective as part of a diabetic treatment.

    In trials, many hormones raise vitamin D blood levels (see below citations):
    --estrogen
    --(genistein (phytoestrogen from soy -- as advised in the TYP plan)
    --thyroid hormones
    --testosterone

    And VICE VERSA! Vitamin D raises the above hormone levels. In fact, after menopause (after the eggs have complete atresed and no longer provide estrogen), estrogen sources come from subcutaneous fat.  After skin activation of vitamin D -- estrogen levels then increase as a function of autocrine regulation (thank goodness!). Vitamin D indeed affects the synthesis of nearly all the other hormones.

    -G

    ++++++++++++++++++++++++++++++++
    Gallagher JC, Riggs BL, DeLuca HF.
    Effect of estrogen on calcium absorption and serum vitamin D metabolites in postmenopausal osteoporosis.J Clin Endocrinol Metab. 1980 Dec;51(6):1359-64.
    PMID: 6255005
    van Hoof HJ, et al.Hormone replacement therapy increases serum 1,25-dihydroxyvitamin D: A 2-year prospective study.Calcif Tissue Int. 1994 Dec;55(6):417-9.
    PMID: 7895179
    van Hoof HJ, et al.Female sex hormone replacement therapy increases serum free 1,25-dihydroxyvitamin D3: a 1-year prospective study.Clin Endocrinol (Oxf). 1999 Apr;50(4):511-6.PMID: 10468912

    Cross HS, et al.Phytoestrogens and vitamin D metabolism: a new concept for the prevention and therapy of colorectal, prostate, and mammary carcinomas.J Nutr. 2004 May;134(5):1207S-1212S. Review.PMID: 15113973

    Weisman Y, et al.Decreased 1,25-dihydroxycholecalciferol and increased 25-hydroxy- and 24,25-dihydroxycholecalciferol in tissues of rats treated with thyroxine.Calcif Tissue Int. 1981;33(4):445-7.PMID: 6271357

    Otremski I, et al.The metabolism of vitamin D3 in response to testosterone.Calcif Tissue Int. 1997 May;60(5):485-7.PMID: 9115169

  • Anonymous

    6/16/2008 3:33:00 AM |

    Very interesting.  All I know is that at the same time that I was diagnosed with Hashimoto's disease with a TSH which had jumped from 2.25 to 6.61, my LDL, which normally hovered around 115, jumped to 180.  After two months of thyroid replacement, my LDL dropped back to 112.  My doctor said the 180 must have been a lab error.  I'm not so sure.

  • janisko

    6/18/2008 4:46:00 AM |

    I am a 60 year old female and was finally diagnosed as hypothyroid almost two years ago when my internist put the symptoms together.

    I was freezing cold at anything below 80 degrees, totally exhausted and was nearly starving myself on low carb to maintain my weight.  This was after losing 70 lbs. and having no trouble maintaining my weight.

    He ran the full thyroid panel, including free T3 and free T4.  My TSH and free T4 were normal but my free T3 was very low and out of range.

    I was immediately sent to one of the top endocrinologists here in Milwaukee.  He ran more tests and even with several low and out of range scores in his hands he told me I was getting old and there's no cure for that!  From there his comments became more absurd but I won't bore you with the details.  I'm sure you've got the picture.

    It took quite some time to find a doctor who practices "outside the box" using both traditional and holistic medicine to get a proper diagnosis.  He treats by symptoms and uses the lab values for reference only.  He says most patients feel best with TSH below 1.0 and medicates based on symptoms.

    Unfortunately, neither Armour Thyroid or Cytomel is working for me and my free T3 continues to drop even lower.  I have now been diagnosed with adrenal fatigue based on cortisol saliva tests, which explains why the thyroid meds aren't working.  All of my hormones are badly out of balance and low.

    Much to my surprise he has recommended most of the same things you do...  low carbing, high-dose vitamin D, DHEA, testosterone, etc.

    The only thing that was normal and excellent was my cholesterol.  By low carbing I got it into excellent territory in 2004, where it stayed until all my hormones went out of balance.  My HDL in the high 70's was even higher than my LDL and my Trigs were in the low 40's.

    Having fought high cholesterol for most of my adult life I was astonished to find that it is now too low at 142.

    We can't look at just TSH and just thyroid.  The entire endoctrine system MUST be evaluated.

    Many of us who are hypothyroid don't respond to treatment because our adrenal glands are not working properly.  Finding appropriate treatment there is even worse than trying to find help with thyroid issues.

    Since both of them have serious long-ranging effects on our heart health they must be properly addressed.  We shouldn't have to beg for treatment and almost become our own physicians.

    My heart scan this week came in with a calcium score of 7.94.  I suspect that my untreated hypothyroid and adrenal fatigue are part of the picture and too many doctors ignore them.

    I am more than thrilled to see that you are finally addressing these issues, which have been ignored for far too long.

    Based on my reading and comments from my internist I continually recommend your blog to anyone and everyone.  Keep up the great work!

  • Anonymous

    3/27/2009 7:05:00 PM |

    Donna said:

    I am a 56 year old female, and was diagnosed with Hashimotos Thyroiditis, along with Graves diasease, giving me a dual diagnosis.  

    I am currently, and have been very frustrated over the last five years, due to the fact that:

    I remain fatigued, have sleep interruption, suffer periodically from muscle pain in my mid-back, as well as my neck, have heart palpitations on and off, and my TSH and Free T4 are close to the top of the reference range, with my T3 being close to the bottom.  I get muscle aches in my back, some so extreme, that in a few cases, I have gone to the emergency room, but they can't find what causes the pain. In addition, I have gained approximately 15 pounds over the last year, and I just get told I should exercise more and eat less.  I have a very restricted diet to begin with, due to a surgeon nicking my pancreatic duct during an ERCP procedure, which blew out six weeks later, giving me acute pancreatitis.  

    My primary care doctor tells me that "thyroid" cannot cause muscle pain, and I disagree with him.

    Last year I saw an ndocronologist, and he thought I had musco-skeletel problems.  The only thing they uncovered was some arthritis in my spine and neck.

    In 2001 I had an I131 Uptake, because my TSH and T4 were opposite of my T3, according to the doctor.  

    Ever since, my weight has just crept upward, no matter how little I eat, how much I exercise or don't exercise.  There is no explanation.

    What would you suggest?  Would it make sense that my TSH, T4 and T3 are doing the same thing again?

  • Christine Agro

    3/31/2009 1:47:00 PM |

    Thank you Dr. Davis for posting this.  As a woman who has managed her own Hypothroidism for more than 20 years now, I am happy to see a western doctor finally state that 'normal' means nothing.

    I can tell you that my body functions best when my TSH is at 1.0 - 1.15.  All of my hypothryoid symptoms disapper.  As soon as it begins to creep up and reaches anything over 2 the symptoms return.

    Because no doctor would actually listen to me I have managed my thyroid naturally for years by taking herbs to balance my hormones and my endocrine system.

    As a Natural Healer (I was also glad to read today's post about becoming our own doctors (I'm paraphrasing - yes.) with a degree in true naturopathic medicine and western herbs I am glad that I had the awareness and personal power to trust and know what my body needed but so many people put blind faith in their doctor and turn over their power.

    Thanks again for posting this article.  I trust that it will be helpful to many who are told they have 'normal' thyroid function yet know something is not right in their own bodies.

    Christine Agro
    The Conscious Mom's Guide
    www.theconsciousmomsguide.com
    blog.theconsciousmomsguide.com

  • Anonymous

    5/5/2009 2:26:00 AM |

    The current accepted range is ridiculous. Fortunately, I found a doctor who believes that the normal level for a 21-year-old girl is around 1.

  • Leanne

    11/12/2009 8:13:40 PM |

    I have had Hypothyroidism since I was 9 years old, I am now a 41 year old woman who has had a complete hysterectomy.  I take Estroven, Vitamin A, D3, B12 and Levothroid (112mcg) I have always noticed even the slightest change in my TSH levels, my hair starts falling out, I get excessively tired, get really dry skin and heart palpitations and I become extra nervous.  I got a blood test the other day because I wasn’t feeling right again… my TSH was 13.60uIU/mL!  My Doctor just had me switch my Levothroid back to 125mcg starting tomorrow. I also have a family history of heart disease.  How dangerous is my situation? I bounce between the two levels of Levothroid about 2 to 3 times a year.  My results so far this year are 2/09 0.86, 7/09 4.78 & 11/09 13.60.  Thank you for the help! I think my doctor thinks I am crazy when I say I can feel it, sometimes I am not even off enough to switch to the next level.

  • sratan

    4/20/2010 3:21:16 PM |

    My TSH levels came in at 7.75 and the T4 (I think) was normal.  I had biopsies done on 3 nodules two years ago and the only recommendation was to follow up with regular check ups.  I don't seem to have any of the symptoms of hypothyroidism - feeling cold, weight gain etc.  I am a regular runner and eat well so I have no idea what I should be asking for in terms of treatment.  Any suggestions?

  • mike V

    9/29/2010 3:06:03 AM |

    For anyone who still has doubt about the importance of getting thyroid right; there's this:

    *Subclinical hypothyroidism and the risk of coronary heart disease and mortality*
    JAMA. 2010 Sep 22;304(12):1365-74.

    http://www.ncbi.nlm.nih.gov/pubmed/20858880?dopt=Abstract

    Regards
    MikeV

  • Anonymous

    10/12/2010 10:15:55 AM |

    I fixed my thyroid naturally by finding a source of natural untreated water (no fluoride or chloride) and taking LOTS of iodine (8 Lugol's drops per day). (My doctor regularly tested iodine levels using a 24hour urine test to see how much of 8 drops is absorbed). After 6 months my doctor told me I could stop taking my thyroid supplememt. I also was taking astragalus and chitosan as a telomerase activator at the time and I think this might have helped regenerate my thyroid activity as well. I also was put onto physiologic doses of cortisol + DHEA, as adrenal dysfunction goes hand in hand with thyroid function, and supporting the rest of the endocrine system helps the thyroid. I could not believe how much iodine I needed; after 6 months it started to taste metallic and I could reduce my dose (8 drops a week).

  • mike V

    10/12/2010 4:05:30 PM |

    Anonymous, 10/12/10

    Interesting.
    I would be interested to learn how long you had been 'hypo', prior to beginning this process, and your age.
    Were there any 'hyper' symptoms before your doc dropped your thyroid med?
    Was your doctor specializing in this approach?
    Thanks
    Mike V

  • buy jeans

    11/3/2010 6:17:12 PM |

    In other words, the findings of this substantial observation suggest that the ranges of TSH usually regarded as normal contribute to coronary events, cardiac death, as well as lipid patterns. While several other studies have likewise shown a relationship of higher TSH/lower thyroid function with lipid abnormalities and overt heart disease, no previous study has plumbed the depth of TSH to this low level and to such a large scale.

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