Is normal TSH too high?

4. June 2008 William Davis (30)
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
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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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Vitamin D and autism

17. August 2007 William Davis (1)
This has nothing to do with coronary plaque reversal, nor directly with the Track Your Plaque program, but I found Dr. John Cannell's discussion about the possible relationship between vitamin D and autism so compelling that I thought I just had to pass it on.

So, below are Dr. Cannell's latest thoughts. He takes some criticisms along with praise. I think we owe him a lot for continuing to doggedly promote the benefits of vitamin D.




Vitamin D Newsletter


August, 2007



Dear Dr. Cannell:

I saw an article from a Toronto newspaper about autism and vitamin D. I am currently searching for a vitamin D specialist in the Washington D.C. area to perform a medical work up on my daughter to look for vitamin D-related disorders. The reason I am in search of a vitamin D specialist is that I believe I have stumbled upon a complex relationship in my daughter involving her foot pain, vitamin D, and her autism.

In April 2006, a few weeks after my 3-year-old profoundly autistic daughter began refusing her daily PediaSure drink, she began having excruciating foot spasms lasting from 10-30 minutes at a time, several times a week. She would throw herself on the floor, curl her toes, slam her heels against the floor, and rub the tops of her feet against the carpet, all while screaming the entire time. These were horrible for her to endure, and horrible for my wife and myself to watch. This went on for a year.

From what I read, the symptom was perhaps like foot spasms associated with carpopedal syndrome or tetany. But her blood work did not support that at all. Calcium level was normal (10.2 mg/dL); 25-Hydroxy-vitamin D low (23.5 ng/ml); 1,25 dihydroxy-vitamin D normal (24.7). Despite some vitamin D deficiency, I was assured by medical professionals that nothing supported a vitamin D cause of these particular spasms, so vitamin D was dismissed. Because her calcium level was normal, they told me she did not have tetany, and vitamin D could not be the cause of the pain.

All medical consultants were stymied. I made another research effort and found a 2003 article on WebMD that stated vitamin D has been found to have some link to basic, unexplained muscle and bone pain. By chance, vitamin D was the next supplement we had at home to begin giving my daughter to treat her autism. So, in April 2007 we began giving my 4 year-old profoundly autistic daughter Vitamin D supplements. Her foot spasms which had plagued her for a year diminished within days and disappeared within three weeks. She has not had a spasm in over two months.

In addition, we noted clear improvements in her autistic condition which appear to be from the vitamin D supplements. Eye contact went from zero to fantastic. Her vocalizations increased markedly (still only babbling; she remains completely nonverbal). She appears even happier than previously (she has always been a somewhat happy child). (Please note that my wife and I have tried many dietary supplements over the past 1.5 years guided by a doctor and dietician who both specialize in autism. We honestly state that this is the only thing that has ever had a positive effect on my daughter. We have seen nothing else work.)

My daughter and vitamin D have a complicated relationship. By all counts, looking at her lab work and general condition, vitamin D should have played no role in those excruciating foot fits. And yet it is apparently exactly what is involved in them. And, my wife and I believe at the same time her autistic condition has improved from the vitamin D. The foot fits and her autism appear linked; it was not just a coincidence that this autistic child has those mysterious foot spasms, and the link appears to be vitamin D.

And so I wonder if this is just the tip of the iceberg, if perhaps there is more to know about my child's relationship with vitamin D and what that might mean for her autism. Does she have a specific vitamin D-related disorder? If so, might direct treatment of it also improve her autism further? These are the questions I would like to pose to a vitamin D specialist who could perform a medical work up on my daughter. Please let me know if you know of anyone in the Northern Virginia/Washington DC area. Also, where is the best place to get vitamin D? Thank you for your time.

Sincerely,
Paul, Washington, D.C.



Dear Paul:

I know of no such specialist in the Washington area, indeed no vitamin D/autism expert exists in the world. As far as a specific "vitamin D disorder," linking her spasms, autism, and vitamin D, the world's English language medical literature contains no description of such a disorder. From your daughter's case, it sounds as if PediaSure was her only regular source of vitamin D. If so, her spasms began two weeks after stopping the small amount of vitamin D contained in PediaSure. The spasms continued for a year, ending a few days after you started giving her vitamin D again, this time in the form of a supplement. Several weeks after restarting vitamin D, both you and your wife noticed an improvement in her autism. To my knowledge, this "case report" - your daughter's - is the first ever published.

As no medical literature has ever been published on any of this, all you can do is give her enough vitamin D to get her 25-hydroxy-vitamin D, known as 25(OH)D, into high normal ranges and then wait and hope. Vitamin D's extraordinary mass-action pharmacology implies that simply providing more substrate ([25(OH)D] will help children with low enzyme activity produce more activated vitamin D (calcitriol) in their brains. The vitamin D theory of autism is not simply that vitamin D deficiency in gestation or early childhood causes the disorder. Instead, the theory holds that a quantitative or qualitative abnormality exists in the enzyme system that activates vitamin D.

It could as simple as the normal variation in the enzyme, an enzyme whose activity would vary in a normal or Gaussian distribution, much like height. Some people are tall, some are short, most are in the middle. The same may be true of the enzyme that forms activated vitamin D (calcitriol), some children have a lot of enzyme and some only a little; most are in the middle. As the substrate [25(OH)D] the enzyme metabolizes fell over the last 20 years with sun-avoidance, more and more children on the low end of the enzyme curve are effected by marginally low 25(OH)D levels, explaining both its genetic basis and exploding incidence.

At this point, all your daughter needs is a physician willing to periodically measure her 25(OH)D. Then you can safely supplement your daughter with doses higher than the current Upper Limit for children (2,000 IU/day). You did not tell me your daughter's weight but, assuming she weighs about 30 pounds, even without 25(OH)D blood tests, you can safely give her 50 mcg/day which is 2,000 IU per day. In fact, the U.S. government says this dose is safe for children over the age of one. Life Extension Foundation sells 250 of the 1,000 IU capsules for about ten bucks with powdered vitamin D inside. The powder is tasteless and dissolves easily in juice. Bio Tech Pharmacal, of Fayetteville, Arkansas, told me they were going to be making a 1,000 IU capsule. Or you can get 1,000 IU capsules in a pharmacy or at Costco and crush them. A Canadian firm is now making vitamin D liquid, called Ddrops, with 1,000 IU per drop, but their mail order web site is not yet easily accessed. Beware of cod liver oil; do not use it because vitamin A inhibits the actions of activated vitamin D, and due to the potential for low-grade vitamin A toxicity.

Remember, more and more researchers now believe autism is a progressive, inflammatory, disorder. That is, the inflammation probably progressively destroys brain tissue as the child ages. As I said in my recent paper, I think there is a chance that vitamin D may have a treatment effect in young autistic children if given in adequate doses, due to its anti-inflammatory properties, and its ability to upregulate glutathione, the master antioxidant that also chelates (binds) and then helps excrete heavy metals like mercury. Unfortunately, I see no way, even if the vitamin D/autism theory turns out to be true, that vitamin D can regenerate brain tissue. However, if it stops the inflammation, and cell death, the brain could then begin to develop and learn. These are big ifs. However, you have nothing to lose by trying, the worst that will happen is that it will not help and vitamin D will be added to the long list of false-hope treatments.

Actually, there is a worse possibility. Say the parents of a three-year-old autistic child decide today that vitamin D is nonsense, another false hope, and that I'm a quack. They decide not to give vitamin D supplement their autistic child, who is probably - like your child - vitamin D deficient. Then, it turns out five years from now that scientific evidence shows vitamin D does indeed help. By that time, the child will be eight and will have suffered additional, irreparable, brain damage. In my mind, that is more tragic than another false hope.



Dear Dr. Cannell:

After that article appeared in the Toronto paper, I started my four-year-old son on 1,000 IU of vitamin D two weeks ago. So far the only thing I noticed is that after about ten days, he didn't seem so miserable. The thing that has always broken my heart is that look of sadness and suffering on his face. After about two weeks of vitamin D, I noticed he seemed less miserable. I wouldn't say he looks happy now but that look of misery seems to be gone. Will it come back? I'm not sure I can take it if it comes back. What else might happen? Also, last summer we noticed he seemed to get better, but then he got worse in the fall. We never thought about it until we read about vitamin D.

Susan, Toronto, Canada




Dear Susan:

I don't know. I think all parents have had their heart pierced by that look at one time or another. I would advise increasing the dose to 2,000 IU per day, making sure it is cholecalciferol and not ergocalciferol, and having your doctor order a 25(OH)D every two months to see if he needs higher doses. You want to get his blood level up to between 50 ng/ml and 80 ng/ml (In many countries outside of the USA, that would be reported as between 125 and 200 nmol/L.) and keep it there, summer and winter, and that may take more than 2,000 IU/day in the winter. If vitamin D has a treatment effect, it will take many months to see its full effect. As you noted, if the theory is correct, autistic children who spend time outdoors in the summer should show some seasonal improvements - if they don't wear sunblock and they expose enough of their skin to generate significant amounts of vitamin D.



Dear Dr. Cannell:

I resent you calling autism a tragedy. My son is not a tragedy and I'm glad he was born and is in our lives. He is our joy. Autism is not a tragedy.

Emma, London, England.




Dear Emma:

I'm glad he is your joy and I believe you. I'm new to the autism field and was not aware how much thought and speech control exists in the discussion of the disease. Nevertheless, I have a few politically incorrect questions. If autism is a joy, I assume you would like other parents to have an autistic child? If autism is such a joy, why is there a huge industry forming to prevent and treat it? At the risk of sounding insensitive - apparently one of the most serious charges leveled in the autism debate - autism is a tragedy. As I pointed out in my paper, research shows that having an autistic child, puts the family under more emotional stress than having a child with a fatal illness.



Dear Dr. Cannell:

Who are you to write an article on autism? You didn't even publish it in a medical journal. You are not with a university. You have not published very much. You have no expertise on autism. No autism experts support your theory. There is no evidence to support the theory. Shouldn't you leave this to experts before you give parents more false hopes?

Mary, Trenton, New Jersey.



Dear Mary:

You are right, I am a nobody; just ask my ex-wife. In the Toronto Globe, I explained why I have not yet submitted the paper. As far as giving false hopes, I've thought about that charge. Right now, regardless of what advocacy groups say, autism is rather hopeless. That is, no treatment, including vitamin D, has been shown to materially affect the clinical course of autism. As a psychiatrist, my observation is that people would rather live with a false hope than with no hope.

Furthermore, if autistic children began taking vitamin D, the worse that can happen is that a period of false hope will followed by dashed hopes and then parents will be back to hopelessness. In the meantime, they will have made their child vitamin D sufficient. Vitamin D deficiency is a serious problem in childhood.
Postgrad Med J. 2007 Apr;83(978):230-5.

The Telegraph, Why is Vitamin D So Vital?

As far as the theory having no support from experts, Dr. Richard Mills, research director of the National Autistic Society in England, was quoted in the Telegraph article on the autism/vitamin D theory: "There has been speculation in the past about autism being more common in high-latitude countries that get less sunlight and a tie-up with rickets has been suggested - observations which support the theory."

Finally, you said there is no evidence to support the theory. I assume you meant there is no proof. The first statement is absolutely false, the second absolutely true. As I detailed in my paper, there is a lot of evidence to support the theory. In fact, if anyone can come up with an autism fact, that the theory cannot explain, I'd like to know about it. Even the announcement of a link between television viewing and autism supports the theory. Furthermore, the TV/autism link is actually evidence of a treatment effect. That is, if autistic children who play outside in the sunshine more - watching less TV - have less severe illness, it may be due to the Sun-God, who bestows her precious gift of calcitriol into the brains of children playing outside in her sunlight but not into the brains of children watching TV inside in the darkness.
Natl Bur Econ Res Bull Aging Health. 2007 Winter;(18):2-3.

As far as proof the theory is true, there is, of course, none. In medicine, proof means randomized controlled human trials, the gold standard for proof. However, proof is the last step, not the first. First comes evidence, then comes a theory, then comes researchers disproving those theories. It works that way. Sometimes we never get to the last step, proof. For example, please point me to a single randomized controlled human trial proving cigarette smoking is dangerous? Instead, the convincing evidence of smoking's dangerousness lies in epidemiological studies, not randomized controlled trials. Proof, or disproof, of the autism vitamin D theory will take years, years during which young autistic brains will continue to suffer irreparable damage. Perhaps vitamin D' powerful anti-inflammatory actions will help prevent that damage, perhaps not.

It's something of a Pascal's wager, betting on vitamin D instead of the existence of God, risking your child's brain instead of eternal damnation. "If you believe vitamin D helps autism and turn out to be incorrect, you have lost nothing -- but if you don't believe in vitamin D and turn out to be incorrect, your child will suffer irreparable brain damage."

John Cannell, MD
The Vitamin D Council
9100 San Gregorio Road
Atascadero, CA 93422

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. This newsletter is not copyrighted. Please reproduce it and post it on Internet sites. Remember, we are a non-profit and rely on donations to publish our newsletter and maintain our website.

Michael Pollan Podcast

15. August 2007 William Davis (3)
I just found this great podcast of an April, 2006 National Public Radio (NPR) interview with Omnivore's Dilemma author, Michael Pollan:

Author Michael Pollan: 'The Omnivore's Dilemma'

available at http://www.npr.org/templates/story/story.php?storyId=5342514

The Science Friday segment is a great encapsulation of all the fascinating spins this wonderfully insightful author has on human eating habits and the developing distortions of food choices, much magnified by the food manufacturing industry.

One of my favorite comments from Pollan: "The USDA should be called "The Department of Corn," referring to the ubiquitous dissemination of corn products into livestock and human foods that has increasingly led to the enormous health problems we're all facing in 2007.

Are you addicted to fructose?

13. August 2007 William Davis (1)
Try a little experiment:

Side by side, try a yogurt made with fructose or high fructose corn syrup as one of the first ingredients on the label along with a yogurt made without fructose.

Yoplait and Dannon brands, for instance, fit the bill for fructose. Several brands do not use fructose products. Many of these are the unflavored or unsweetened versions. You may therefore have to add some blueberries, strawberries, or some other fruit for some flavor. ( I doubt that you would add high fructose corn syrup.) Add nuts, seeds, flaxseed, or oat bran to either.

Many people who do this will notice a peculiar effect: The fructose or high fructose corn syrup containing product is, to most, delicious. It also triggers a desire for more. You can't have just one--you've got to have another, or you've got to eat something else.

The non-fructose containing product is more likely to generate satiety, a feeling that you've had enough.

If you experience this effect, the solution is simple: avoid fructose and high fructose corn syrup. I believe that the most worrisome health effect of fructose is this hunger-increasing aspect, difficult to document, perhaps impossible to measure, but a great boon to the food industry who practice an "eat more" philosophy to increase revenues year after year.

Perhaps you will also see weight drop (since you will be more satisfied), see triglycerides drop (since fructose raises triglycerides), and maybe obtain all the downstream benefits of reduced triglycerides (higher HDL, less small LDL, less VLDL, more rapid clearance of post-prandial lipoproteins).

Most people who follow this idea gain better control over appetite, lose weight, and do better in health, including in their Track Your Plaque program.

Chicken Little

11. August 2007 William Davis (1)
Clinical studies can be designed in a number of ways. The ease and cost of these studies differ dramatically, as does the confidence of the findings.

The most confident way to design a clinical study is to tell neither the participants nor the investigator(s) what treatment is being offered, then to administer treatment or placebo. Neither the people doing the research nor the participants know what they are receiving. Of course, there needs to be some way to find out what was given at the end of the study in order to analyze the outcome.

This is called a “double-blind, placebo-controlled” clinical study. While not perfect since it tends to examine a treatment phenomenon in isolation (e.g., the effects of a single drug in a select group of people), it is the best sort of study design that is most likely to yield confident results, both negative and positive. This sort of design is followed, for instance, for most prescription drugs.

There are pitfalls in such studies, of course, and some have made headlines lately. For instance, beyond tending to examine single conditions in a select group of participants, a double-blind, placebo-controlled study can also fail to uncover rare effects. If a study contains 5000 participants, for instance, but a rare complication develops in 1 person out of 20,000, then it’s unlikely such an ill-effect will be observed until larger numbers of people are exposed to the agent.

Another pitfall (though not so much of study design, but of human greed) is that study outcomes that are not favorable can be suppressed by simply failing to publish the results. This has undoubtedly happened numerous times over the years. For this reason, a registry has been created for all human clinical trials as a means to enforce publication of outcomes, both favorable and unfavorable.

Despite its weaknesses, the double-blind, placebo-controlled study design remains the most confident way to show whether or not some treatment does indeed yield some effect. It is less prone to bias from either the participant or the investigator. Human nature being what it is, we tend to influence results just to suit our particular agenda or interests. An investigator who knows what you are given, drug or placebo, but owns lots of stock in the company, or is hoping for special favors from the pharmaceutical company sponsor, for instance, is likely to perceive events in a light favorable to the outcome of the study.

Now, most studies are not double-blind, placebo-controlled studies. These are notoriously difficult studies to engineer; raise lots of ethical questions (can you not treat a person with an aggressive cancer, for instance, and administer a placebo?); often require substantial numbers of participants (thousands), many of whom may insist on payment for devoting their time, bodies, and perhaps even encountering some risk; and are tremendously expensive, costing many tens of millions of dollars.

For this reason, many other study designs are often followed. They are cheaper, quicker, may not even require the active knowledge or participation of the group being studied. That’s not to say that the participants are being tricked. It may simply be something like trying to determine if there are more heart attacks in people who live in cities compared to rural areas by comparing death rates from heart attack from public records and population demographic data. Or, a nutritional study could be performed by asking people how many eggs they eat each week and then contacting them every month for 5 years to see if they’ve had a heart attack or other heart event. No treatment is introduced, no danger is added to a person’s established habits. Many epidemiologic studies are performed this way.

The problem is that these other sorts of study designs, because they generate less confident results, are not generally regarded as proof of anything. They can only suggest the possibility of an association, an hypothesis. For real proof to occur, a double-blind, placebo-controlled may need to follow. Alternatively, if an association suggested by a study of lesser design might, by reasons of a very powerful effect, be sufficient. But this is rare. Thalidomide and catastrophic birth defects are an example of an association between a drug and fetal limb malformation that was so clear-cut that no further investigation was required to establish a causative association. Of course, no one in their right mind would even suggest a blinded study.

Where am I going with this tedious rambling? Lately, the media has been making a big to-do about several studies, none of which are double-blind, placebo-controlled, but were cross-sectional sorts of observations, the sorts of studies which can only suggest an effect. This happened with Dr. Steve Nissen’s study of Avandia (rosiglitazone) for pre-diabetes and risk for heart attack and the recent study suggesting that cancer incidence is increased when LDL cholesterol is low. Both were observations that suggested such associations.

Now, those of you following the Heart Scan Blog or the www.cureality.com website know that we do not defend drug companies nor their drugs. In fact, we’ve openly and repeatedly criticized the drug industry for many of its practices. Drugs are, in my opinion, miserably overused and abused.

But, as always, I am in the pursuit of truth. Neither of these studies, in my view, justified the sort of media attention they received. They are hypothesis-generating efforts—that’s it. You might argue that the questions raised are so crucial that any incremental risk of a drug is simply not worth it.

Despite the over-reaction to these studies, good will come of the fuss. I do believe that heightened scrutiny of the drug industry will result. Many people will seek to avoid prescription drugs and opt for healthy changes in lifestyle, thus reducing exposure to costs and side-effects.

But beware of the media, acting as our Chicken Little, reporting on studies that prove nothing but only raise questions.

200 point drop in heart scan score

11. August 2007 William Davis (0)
Some of the math-savvy will have noticed that we often report drops in CT heart scan scores on a percentage basis. Unfortunately, it this were a competition (which, of course, it is not), this would be unfair.

A score of 50, for instance, that drops "only" 25 points would represent a 50% drop in score.

But someone with a score of 1050 who drops his or her score the same quantity, or 25, will have dropped their score less than 5%.

In other words, the magnitude of your starting score determines how large a percentage drop you achieve, even when the absolute, or real, quantity of plaque reversal is the same as someone who begins with a lower score.

I qualify this discussion in this vein because of Grady's story. Grady, a soon-to-retire attorney, started with a heart scan score of 1151. On the Track Your Plaque program, he saw his score drop nearly 200 points--200 points!

But, if we gauged Grady's success just on a percentage basis, he dropped his score only a measly 17% or so. (Imagine the headlines if this program were sponsored by a drug manufacturer. The Track Your Plaque program proudly has nothing to do with the drug industry.)

Of course, the Track Your Plaque program is not a competition. It is an effort to help everyone possible, the more the better. Even if Grady failed to set a new Track Your Plaque record gauged on a percentage basis, he will have achieved an extraordinary advantage in health: the virtual elimination of the dangers of heart disease.

With this drop in score, Grady's risk for heart attack plummets from a spine-chilling 25% per year to nearly zero. (I know of NO other program that can claim such a track record.)

Grady's full story will be reported in the August, 2007 Track Your Plaque newsletter. To subscribe or to just view when it is posted, go to www.cureality.com website, click on the upper right hand corner What Does My Heart Scan Show? graphic, which then takes you to the page to view the newsletter. Or, Track Your Plaque Members can just go to the Library and click on newsletter archives.

How tough is the Track Your Plaque 60-60-60 target?

9. August 2007 William Davis (3)
One of the basic requirements that stack the odds in your favor of stopping or dropping your CT heart scan score is to achieve basic lipid targets of 60-60-60.

In other words, we generally see best results when LDL is reduced to 60 mg/dl, HDL raised to 60 mg/dl, triglycerides reduced to 60 mg/dl. Now, these are not absolute requirements. Someone can have a spectacular drop in heart scan score even with an HDL of 56, LDL of 71. But the "Rule of 60" provides a useful target that is easy to remember, packs real power, and is clearly beyond that achieved with conventional approaches.

People often ask, "Just how tough is it to get to these targets?"

It's really not that tough. Interestingly, whenever I tell my cardiologist or primary care colleagues that I advocate these 60-60-60 targets, they declare that it's tough, perhaps impossible, except for the most highly motivated.

I agree that it requires motivation. A cigarette-smoking, TV-addicted, 70-lb overweight, chip- and pretzel-eating couch potato is not going to achieve them.

On the other hand, you don't have to be a marathon running vegetarian to do it, either.

Most people, in fact, engaged in the Track Your Plaque program achieve the 60-60-60 targets---or exceed them. It's not uncommon, for instance, for HDL to skyrocket to 80 or 90 mg/dl with many of our strategies. (Of course, if your starting HDL is 20 or 25 mg/dl, 80 or 90 is not possible with current technology.)

But it certainly does require more than the "Take Lipitor and stick to your low-fat diet" approach that is the mantra repeated in the vast majority of medical offices across the U.S. For instance, reducing LDL to 60 mg/dl when starting at 170 mg/dl will require addition of oat bran and other soluble or viscous fibers; raw almonds and walnuts; perhaps the use of Benecol butter substitute; reduction or elimination of wheat products if small LDL comprises a substantial proportion of LDL particles. Reducing triglycerides requires the generous use of omega-3 fatty acids from fish oil. Attention to vitamin D must be a part of the effort.

So, yes, it is not as simple as the conventional approach. But the results are far superior in reducing or eliminating heart attack and in dropping your heart scan score.

But it can be done. We do it every day.

Vitamin D2 belongs in the garbage

8. August 2007 William Davis (15)
It happened yet again.

Mel came to the office. CT heart scan score: 799--quite high, enough to pose a real threat very soon. Thus, no time to lose in instituting an effective prevention program.

We do the usual--identify the six causes of coronary plaque; begin fish oil, show him how to correct his plaque causes. You've heard it before.

Vitamin D blood level in March: 17 ng/ml--severe deficiency.

Vitamin D replacement needs to be a part of his coronary plaque control program. So I suggested 6000 units per day of an oil-based preparation of vitamin D3 (cholecalciferol). Conveniently, there is a Vitamin Shoppe outlet across the street from my office. I just point and tell people to go across the street.

Mel did just that. However, he also informed his primary care physician about his vitamin D deficiency. His primary physician promptly told him he needed to take a prescription form of vitamin D and not to bother with just a supplement.

So Mel stopped his vitamin D capsules and started taking vitamin D prescription "medication." Mel figured, naturally, that if it requires a prescription, it must be better. Unfortunately, Mel and his doctor failed to pass the change in strategy onto us.

So, four months later, Mel got repeat vitamin D blood level: 19 ng/ml.

I've seen this too many times. The prescription form of vitamin D is nonsense. There's hardly any effect on blood levels of vitamin D3 at all. The body's conversion of this non-human form of D is extremely inefficient and therefore virtually useless. While it raises the blood level of vitamin D2 (ergocalciferol) and thereby total D (D3 + D2), there is negligible effect on the real human and active form, D3.

How and why this preparation got through the FDA process to obtain approval as a drug is beyond me, though I am not a defender of FDA practices and politics.

This notion that "if it's a prescription, it must be better" is a fiction perpetuated by the drug industry. The same principle gets tossed around with fish oil, hormones like estrogens and testosterone, and others. Often, the principal difference between prescription and non-prescription is patent protection. Patent protection provides profit protection. Selling a product without patent protection can be risky business. It's certainly less profitable.

As always, getting at the truth is sometimes the most difficult job of all. Prescription vitamin D belongs in the garbage. Vitamin D capsules (gelcaps) do the job and do it well, over and over, with reliable, consistent and substantial rises in blood levels of 25-OH-vitamin D3. I take 6000 units per day (3 2000 unit capsules) that cost me $5.99 for a bottle of 120 capsules, or about $4.50 a month.

And nobody--nobody--pays me to say this. I say it because I believe it's true.

Angioplasty vs. Track Your Plaque

5. August 2007 William Davis (10)
What does angioplasty have over the Track Your Plaque program?

Well, first of all, the Track Your Plaque program has a lot to boast about. What other approach can claim to have reduced heart disease 30, 40, 51, and now 63%? That's as close to a cure that's ever--EVER--been achieved. Statin drug manufacturers can talk about an occasional 1, 2, or 5% reversal. We're talking 10 times more.

The Track Your Plaque program also uses as little prescription medication as necessary. Fish oil, vitamin D, coenzyme Q10, niacin--some of the frequent tools used for plaque reversal in our program. Yes, we do use prescription medications, but only when there is truly a benefit and nutritional strategies have failed to achieve the goals we're seeking. We do not endorse shotgun prescription approaches conceived of by some marketing department at a pharmaceutical company.

So what possible advantage can coronary angioplasty have? Why don't more people embrace a program like Track Your Plaque that has already proven itself enormously effective?

Because angioplasty is easy. There's little worrying ahead of time. Just wait for the symptoms or other problem to appear, go to the hospital and get your procedure. You can live the free and easy life beforehand--no exercise, no diet efforts, no nutritional supplements. Just be sure to go to the hospital when suspicious symptoms strike. (Of course, you gamble that you survive the appearance of symptoms, a process 30-50% of people fail to survive.)

That means you can eat all you want, drink all you want, save the money you otherwise might have thrown away on supplements, pocket the monthly costs of an exercise club membership, etc. Go to the hospital when you experience the sensation of an anvil on your chest or of suffocation, let the emergency room do their thing, meet your cardiologist, go to the catheterization laboratory, get two or three stents, go home the next day!

Why bother with a prevention program, especially one that requires involvement, learning, and effort like Track Your Plaque?

Because it's your way to stack the odds enormously in your favor of 1) surviving the appearance of symptoms, 2) avoiding the prospect of heart procedures, which are not as clean and easy as they often seem, 3) have a longer lasting durability than a stent which could buy you a couple of years before your next procedure or heart catastrophe, and 4) it's the right thing to do for the sake of the huge societal cost of heart disease.

Many of you have the equivalent of a cure for heart disease at your fingertips. Unless you have a soft spot in your heart for hospitals, cardiologists, or the pharmaceutical or medical device industry, there isn't a choice.

Plaque is like money

3. August 2007 William Davis (0)
In case anyone missed this in the June, 2007 Track Your Plaque Newsletter, I'm again posting how we calculate the annual rate of score increase, should it occur.

For instance, say your score in January, 2005, is 100. In November, 2006, you undergo another scan and the score is 140. Obviously, your score has increased an undesirable 40%. But what is the annual rate of score increase, the amount of increase per year?

In this example, the annual rate of score increase is 19%--not anywhere near as bad as the 40% that can scare the heck out of you.

Obviously, the best rate of heart scan score increase is a negative number, i.e., a drop in score from, say 100, to 60. You might even eliminate the need for this calculation altogether if you drop your score.

Nonetheless, whenever there is a score increase over an uneven period of time, a fraction of year(s), this is the method we use to annualize the calculation. The equation we use is a modified form of the annual compound interest equation using continuous compounding, since that’s how coronary atherosclerotic plaque grows--just like money. The difference is, of course, is that while you might want more money, you certainly don't want more plaque.

You will need a calculator for this calculation, one with an exponential “y to the power x” function. For ease, calculate "1/t first, then use it as the “x” exponent on your yx function and "(score 2 / score 1)" as the "y".


Annual rate of plaque growth (APG) = ( score 2 / score 1 ) 1/t - 1

Multiply the result by 100 to yield a percent.


“Score 1” is your 1st heart scan score, “score 2” is your 2nd (or any subsequent heart scan score); “t” is the amount of time between the two scans expressed in years in decimal form. Time between scans should be expressed in years or fractions of years. To obtain the time interval in fractions of years, simply divide the number of months between scans by 12 (e.g., 18 months / 12 = 1.5 years ; 22 months / 12 = 1.83 years).

It’s not as tricky as it looks. For example, if your first heart scan score is 300 and your next scan 16 months later (or 16/12 = 1.33 years) is 372, then:

Annual rate of plaque growth (APG) = ( 372 / 300 ) 1/1.33 - 1 = 0.175

Multiply 0.175 x 100 = 17.5% annual rate of plaque growth


Some scan centers will do the calculation for you as part of a repeat scan. However, the equation can be used if you're left on your own, or if you go to a different scan center. If this is too much effort, perhaps it's just another reason to add to the list of reasons to drop your heart scan score!

Triglycerides: What is normal?

1. August 2007 William Davis (2)
In The Track Your Plaque program, we advocate decreasing triglycerides to 60 mg/dl or less.

That's the level of triglycerides that minimize the presence of triglyceride-containing undesirable lipoproteins causing plaque, such as small LDL, VLDL, and the after-eating persistence of IDL (intermediate-density lipoprotein, a bad player). (The enzyme, cholesteryl-ester transfer protein, or CETP, is responsible for exchanging one triglyceride molecule for one cholesterol molecule between HDL and other lipoprotein particles. Thus, an excess of triglyceride availability permits CETP to operate unrestrained, creating more undesirable lipoproteins. This was the basis for Pfizer's now defunct CETP inhibitor, torcetrapib.)

Of course, this triglyceride target is far below that of the conventional guidelines. The Adult Treatment Panel-III of the National Cholesterol Education Panel suggests a triglyceride level of 150 mg/dl is okay.

In my view, a level of 150 mg/dl is highly abnormal, permitting the persistence of multiple lipoprotein particles and virtually guarantees plaque growth. In short, triglycerides of 150 are awful.

Curious thing: Successful participants in our program, i.e., people who achieve desirable weight, reduce processed carbohydrate junk foods and saturated fat sources, and aim for the 60-60-60 targets for conventional lipids, commonly end up with triglyceride levels of 25-50 mg/dl.

We have seen many people drop their heart scan scores just by achieving a triglyceride level of 60 mg/dl or less. So achieving a lower level below 60 is not necessarily a requirement for coronary plaque regression.

But it makes me wonder if a triglycere level of 30s or 40s is the level for perfect health. These are levels ordinarily regarded as impossibly low. When colleagues see the numbers we readily and routinely achieve, they declare that the numbers are spurious, temporary, or just flukes. "No way you can do that all the time!"

This level also seems to, in virtually all cases, eliminate the triglyceride-containing undesirable lipoproteins small LDL, IDL, etc., and allow full conversion of HDL into the healthy, large fraction.

Should we move the Track Your Plaque triglyceride target to below 45 mg/dl or even lower? I don't think so, but it makes me wonder.