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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All posts by william-davis

What to eat: Part I

I've spent a good number of Heart Scan Blog posts detailing what foods to limit or avoid.

The list of unquestionably bad foods to avoid include foods made of wheat, cornstarch, and sugars. Fructose is proving to be an exceptionally bad form of sugar, worse than any other. I've issued warnings about levels of carbohydrates that can be determined by postprandial testing.

In response to several requests to clarify what foods to eat, this post begins a series discussing what foods are good to eat.

I believe that a strong case can be made for eating vegetables in nearly all its varied forms, from cucumbers to peppers to leafy vegetables to eggplant to alliums like onions. The only form we avoid are red and white potatoes due to the blood sugar-increasing effects.

While this seems obvious, I am impressed how many people who follow low-carb diets find themselves following a high-animal product diet with vegetables as the sideline. It should be the other way around: A high vegetable diet with animal products as the sideline.

Vegetables are your principal source of:

1) Flavonoids and polyphenols--e.g., anthocyanins and catechins. All the recently appreciated effects of flavonoids and polyphenols highlight the wonderful effects of compounds originating in plant foods. This includes the anthocyanins and resveratrol in red wine; the catechins and epicatechins cocoa and green tea; the hydroxytyrosol, phenolic acid, and flavonoids of olive oil.

2) Fiber--Fiber is essentially a plant phenomenon, since there is virtually none in chicken, fish, and beef. The benefits of fiber are, I believe, undisputed. Neglecting fiber can, at the very least, lead to a nasty case of hemorrhoids. At the worst, it is related to various cancers, especially colon cancer.

3) Vitamin C--While vitamin C may be old and boring in light of new, exciting discoveries like flavonoids, neglect leads to bad things.

Vegetables are generally classified as carbohydrate foods, since they are low in protein and fat. But this is the source of carbohydrates you do not want to sacrifice in a low-carbohydrate diet. There's just too much good from vegetables.

Notice that I didn't say "fruits and vegetables." This is a fundamental mistake made by many: Oveconsumption of fruits. I've even seen people who follow an otherwise good diet develop diabetes--just from too much fruit.

Vegetables should be the cornerstone of the human diet. But I'll bet you knew that already.

Carbohydrates and LDL

There's a curious and powerful relationship between carbohydrates and LDL particles. Understanding this relationship is crucial to gaining control over heart disease risk.

(Note that I did not say "LDL cholesterol"--This is what confuses people, the notion that cholesterol is used as a surrogate marker to quantify various lipoproteins, including low-density lipoproteins, LDL. I'm NOT interested in the cholesterol; I'm interested in the behavior of the low-density lipoprotein particle. There's a difference.)

Carbohydrates:

1) Increase triglycerides and very low-density lipoprotein particles (VLDL)
2) Triglyceride-rich VLDL interact with LDL particles, making them smaller. (A process mediated by several enzymes, such as cholesteryl-ester transfer protein.)
3) Smaller LDL particles are more oxidizable--Oxidized LDL particles are the sort that are taken up by inflammatory white blood cells residing in the artery wall and atherosclerotic plaque.
4) Smaller LDL particles are more glycatable--Glycation of LDL is an important phenomenon that makes the LDL particle more atherogenic (plaque-causing). Glycated LDLs are not recognized by the LDL receptor, causing them to persist in the bloodstream longer than non-glcyated LDL. Glycated LDL is therefore taken up by inflammatory white blood cells in plaque.

Of course, carbohydrates also make you fat, further fueling the fire of this sequence.

The key is to break this chain: Cut out the carbohydrates. Cut carbohydrates and VLDL and triglycerides drop (dramatically), VLDL are unavailable to transform large LDL into small LDL, small LDL is no longer available to become oxidized and glycated, blood sugar is reduced to allow less glycation. Voila: Less atherosclerotic plaque growth.

Yet the USDA, American Heart Association, and the Surgeon General's office all advise you to eat more carbohydrates. The American Diabetes Association tells you to eat 70 grams or so carbohydrates per meal. (Yes: Diabetes, the condition that is MOST susceptible to these carbohydrate effects.) Follow their advice and you gain weight; triglycerides and VLDL go up; calculated (Friedewald) LDL may or may not go up, but true measured LDL (NMR LDL particle number or apoprotein B) goes way up; small LDL is triggered . . . You know the rest.

The dance between carbohydrates and LDL particles requires the participation of both. Allow one partner to drop out of the dance and LDL particles will sit this dance out.

Strange but true: Part II

Here's the second part of the Heart Scan Blog post I wrote a couple of years back describing the wacky origins of this thing that has so changed the face of heart care in the U.S., the cardiac catheterization.

Heart catheterization: Strange, but true

It's a couple of years old, but this post from March, 2008, remains relevant.

It details the curious origins of heart catheterization, the procedure that has saved some lives, but also been responsible for the proliferation of unnecessary heart procedures.



The modern era of heart disease care was born from an accident, quirky personalities, and even a little daring.

The notion of heart catheterization to visualize the human heart began rather ignominiously in 1929 at the Auguste-Viktoria Hospital in Eberswalde, Germany, a technological backwater of the day. Inspired by descriptions of a French physician who inserted a tube into the jugular vein of a horse and felt transmitted heart impulses outside the body, Dr. Werner Forssmann, an eager 25-year old physician-in-training, was intent on proving that access to the human heart could be safely gained through a surface blood vessel. No one knew if passing a catheter into the human heart would be safe, or whether it would become tangled in the heart’s chambers and cause it to stop beating. On voicing his intentions, Forssmann was ordered by superiors not to proceed. But he was determined to settle the question, especially since his ambitions captured the interest of nurse Gerda Ditzen, who willingly even offered to become the first human subject of his little experiment.

Secretly gathering the necessary supplies, he made his first attempt in private. After applying a local anesthetic, he used a scalpel to make an incision in his left elbow. He then inserted a hollow tube, a catheter intended for the bladder, into the vein exposed under the skin. After passing the catheter 14 inches into his arm, however, he experienced cold feet and pulled it out.



One week later, Forssman regained his resolve and repeated the process. Nurse Ditzen begged to be the subject, but Forssmann, in order to allow himself to be the first subject, tricked her into being strapped down and proceeded to work on himself while she helplessly watched. After stanching the oozing blood from the wound, he threaded the catheter slowly and painfully into the cephalic vein, up through the bicep, past the shoulder and subclavian vein, then down towards the heart. He knew that simply nudging the rubber catheter forward would be sufficient to direct it to the heart, since all veins of the body lead there. With the catheter buried 25 inches into his body, Forssmann untied the fuming Ditzen. Both then ran to the hospital’s basement x-ray department and injected x-ray dye into the catheter, yielding an image of the right side of his heart, the first made in a living human.

Thus, the very first catheterization of the heart was performed.

An x-ray image was made to document the accomplishment. Upon hearing of the experiment, Forssmann was promptly fired by superiors for his brazen act of self-experimentation. Deflated, Forssmann abandoned his experimentation and went on to practice urology. He became a member of the Nazi party in World War II Germany and served in the German army. Though condemned as crazy by some, physicians in Europe and the U.S., after hearing of his experience, furthered the effort and continued to explore the potential of the technique. Forssmann himself was never invited to speak of his experiences outside of Germany, as he had been labeled a Nazi.

Many years after his furtive experiments, the once intrepid Dr. Forssmann was living a quiet life practicing small town medicine. He received an unexpected phone call informing him that he was one of three physicians chosen to receive the 1956 Nobel Prize for Medicine for his pioneering work performing the world’s first heart catheterization, along with Drs. André Cournand and Dickinson W. Richards, both of whom had furthered Forssmann’s early work. Forssmann remarked to a reporter that he felt like a village pastor who was made a cardinal.

Strange, but true.

Rerun: To let low-carb right, you must check POSTPRANDIAL blood sugars

Checking postprandial (after-eating) blood sugars yields extraordinary advantage in creating better diets for many people.

This idea has proven so powerful that I am running a previous Heart Scan Blog post on this practice to bring any newcomers up-to-date on this powerful way to improve diet, lose weight, reduce small LDL, reduce triglycerides, and reduce blood pressure.



To get low-carb right, you need to check blood sugars

Reducing your carbohydrate exposure, particularly to wheat, cornstarch, and sucrose (table sugar), helps with weight loss; reduction of triglycerides, small LDL, and c-reactive protein; increases HDL; reduces blood pressure. There should be no remaining doubt on these effects.

However, I am going to propose that you cannot truly get your low-carb diet right without checking blood sugars. Let me explain.

Carbohydrates are the dominant driver of blood sugar (glucose) after eating. But it's clear that we also obtain some wonderfully healthy nutrients from carbohydrate sources: Think anthocyanins from blueberries and pomegranates, vitamin C from citrus, and soluble fiber from beans. There are many good things in carbohydrate foods.

How do we weigh the need to reduce carbohydrates with their benefits?

Blood sugar after eating ("postprandial") is the best index of carbohydrate metabolism we have (not fasting blood sugar). It also provides an indirect gauge of small LDL. Checking your blood sugar (glucose) has become an easy and relatively inexpensive tool that just about anybody can incorporate into health habits. More often than not, it can also provide you with some unexpected insights about your response to diet.

If you’re not a diabetic, why bother checking blood sugar? New studies have documented the increased likelihood of cardiovascular events with increased postprandial blood sugars well below the ranges regarded as diabetic. A blood sugar level of 140 mg/dl after a meal carries 30-60% increased (relative) risk for heart attack and other events. The increase in risk begins at even lower levels, perhaps 110 mg/dl or lower after-eating.

We use a one-hour after eating blood sugar to gauge the effects of a meal. If, for instance, your dinner of baked chicken, asparagus brushed with olive oil, sauteed mushrooms, mashed potatoes, and a piece of Italian bread yields a one-hour blood sugar of 155 mg/dl, you know that something is wrong. (This is far more common than most people think.)

Doing this myself, I have been shocked at the times I've had an unexpectedly high blood sugar from seemingly "safe' foods, or when a store- or restaurant-bought meal had some concealed source of sugar or carbohydrate. (I recently had a restaurant meal of a turkey burger with cheese, mixed salad with balsamic vinegar dressing, along with a few bites of my wife's veggie omelet. Blood sugar one hour later: 127 mg/dl. I believe sugar added to the salad dressing was the culprit.)

You can now purchase your own blood glucose monitor at stores like Walmart and Walgreens for $10-20. You will also need to purchase the fingerstick lancets and test strips; the test strips are the most costly part of the picture, usually running $0.50 to $1.00 per test strip. But since people without diabetes check their blood sugar only occasionally, the cost of the test strips is, over time, modest. I've had several devices over the years, but my current favorite for ease-of-use is the LifeScan OneTouch UltraMini that cost me $18.99 at Walgreens.

Checking after-meal blood sugars is, in my view, a powerful means of managing diet when reducing carbohydrate exposure is your goal. It provides immediate feedback on the carbohydrate aspect of your diet, allowing you to adjust and tweak carbohydrate intake to your individual metabolism.

LDL glycation

The proteins of the body are subject to the process of glycation, modification of protein structures by glucose (blood sugar). In the last Heart Scan Blog post, I discussed how glycated hemoglobin, available as a common test called HbA1c, can serve as a reflection of protein glycation (though it does not indicate actual Advanced Glycation End-products, or AGEs, just a surrogate indicator).

There is one very important protein that is subject to glycation: Apoprotein B.

Apoprotein B, or Apo B, is the principal protein of VLDL and LDL particles. Because there is one Apo B molecule per VLDL or LDL particle, Apo B can serve as a virtual VLDL/LDL particle count. The higher the Apo B, the greater the number of VLDL and LDL particles.

Because Apo B is a protein, it too is subject to the process of glycation. The interesting thing about the glycation of Apo B is that its "glycatability" depends on LDL particle size: The smaller the LDL particle, the more glycation-prone the Apo B contained within.

Younis et al have documented an extraordinary variation in glycatability between large and small LDL, with small LDL showing an 8-fold increased potential.

Think about it: Carbohydrates in the diet, such as wheat products and sugars, trigger formation of small LDL particles. Small LDL particles are then more glycation-prone by up to a factor of 8. Interestingly, HbA1c is tightly correlated with glycation of Apo B. Diabetics with high HbA1c, in particular, have the greatest quantity of glycated Apo B. They are also the group most likely to develop coronary atherosclerosis, as well as other consequences of excessive AGEs.

No matter how you spin it, the story of carbohydrates is getting uglier and uglier. Carbohydrates, such as those in your whole grain bagel, drive small LDL up, while making them prone to a glycating process that makes them more likely to contribute to formation of coronary atherosclerotic plaque.

High HbA1c: You're getting older . . . faster

Over the years, we all accumulate Advanced Glycation End-products, or AGEs.

AGEs are part of aging; they are part of human disease. AGEs are the result of modification of proteins by glucose. AGEs form the basis for many disease conditions.

Accumulated AGEs have been associated with aging, dementia, cataracts, osteoporosis, deafness, cancer, and atherosclerosis. Most of the complications of diabetes have been attributable to AGEs.

There's one readily available method to assess your recent AGE status: HbA1c.

Hemoglobin is the oxygen-carrying protein of red blood cells. Like other proteins, hemoglobin becomes glycated in the presence of glucose. Hemoglobin glycation increases linearly with glucose: The higher the serum or tissue glucose level, the more glycation of hemoglobin develops. Glycated hemoglobin is available as the common test, HbA1c.

Ideal HbA1c is 4.5% or less, i.e., 4.5% of hemoglobin molecules are glycated. Diabetics typically have HbA1c 7.0% or greater, not uncommonly greater than 10%.

In other words, repetitive and sustained high blood glucose leads to greater hemoglobin glycation, higher HbA1c, and indicates greater glycation of proteins in nerve cells, the lens of your eye, proteins lining arteries, and apoprotein B in LDL cholesterol particles.

If AGEs accumulate as a sign of aging, and high blood sugars lead to greater degrees of glycation, it only follows that higher HbA1c marks a tendency for accelerated aging and disease.

Indeed, that is what plays out in real life. People with diabetes, for instance, have kidney failure, heart disease, stroke, cataracts, etc. at a much higher rate than people without diabetes. People with pre-diabetes likewise.

The higher your HbA1c, the greater the degree of glycation of other proteins beyond hemoglobin, the faster you are aging and subject to all the phenomena that accompany aging. So that blood glucose of 175 mg/dl you experience after oatmeal is not a good idea. 

The lesson: Keep HbA1c really low. First, slash carbohydrates, the only foods that substantially increase blood glucose. Second, maintain ideal weight, since normal insulin responsiveness requires normal body weight. Third, stay physically active, since exercise and physical activity exerts a powerful glucose-reducing effect. Fourth, consider use of glucose-reducing supplements, an issue for another day.

While HbA1c cannot indicate cumulative AGE status, it can reflect your recent (preceding 60 to 90 days) exposure to this age-accelerating thing called glucose.

If your doctor refuses to accommodate your request for a HbA1c test, you can perform your own fingerstick test.

Slash carbs . . . What happens?

Cut the carbohydrates in your diet and what sorts of results can you expect?

Carbohydrate reduction results in:

Reduced small LDL--This effect is profound. Carbohydrates increase small LDL; reduction of carbohydrates reduce small LDL. People are often confused by this because the effect will not be evident in the crude, calculated (Friedewald) LDL that your doctor provides.

Increased HDL--The HDL-increasing effect of carbohydrate reduction may require 1-2 years. In fact, in the first 2 months, HDL will drop, only to be followed by a slow, gradual increase. This is the reason why, in a number of low-carb diet studies, HDL was shown to be reduced.--Had the timeline been longer, HDL would show a significant increase.

Decreased triglycerides--Like reduction of small LDL, the effect is substantial. Triglyceride reductions of several hundred milligrams are not at all uncommon. In people with familial hypertriglyceridemia with triglyceride levels in the thousands of milligrams per deciliter, triglyceride levels will plummet with carbohydrate restriction. (Ironically, conventional treatment for familial hypertriglyceridemia is fat restriction, a practice that can reduce triglycerides modestly in these people, but not anywhere near as effectively as carbohydrate restriction.) Triglyceride reduction is crucial, because triglycerides are required by the process to make small LDL--less triglycerides, less small LDL.

Decreased inflammation--This will be reflected in the crude surface marker, c-reactive protein--Yes, the test that the drug industry has tried to convince you to take statins drugs to reduce. In my view, it is an absurd notion that you need to take a drug like Crestor to reduce risk associated with increased CRP. If you want to reduce CRP to the floor, eliminate wheat and other junk carbohydrates. (You should also add vitamin D, another potent CRP-reducing strategy.)

Reduced blood pressure--Like HDL, blood pressure will respond over an extended period of months to years, not days or weeks. The blood pressure reduction will be proportion to the amount of reduction in your "wheat belly."

Reduced blood sugar--Whether you watch fasting blood sugar, postprandial (after-meal) blood sugars, or HbA1c, you will witness dramatic reductions by eliminating or reducing the foods that generate the high blood sugar responses in the first place. Diabetics, in particular, will see the biggest reductions, despite the fact that the American Diabetes Association persists in advising diabetics to eat all the carbohydrates they want. Reductions in postprandial (after-eating) blood sugars, in particular, will reduce the process of LDL glycation, the modification of LDL particles by glucose that makes them more plaque-causing.


You may notice that the above list corresponds to the list of common plagues targeted by the pharmaceutical industry: blood pressure, diabetes (diabetes being the growth industry of the 21st century), high cholesterol. In other words, high-carbohydrate, low-fat foods from the food industry create the list of problems; the pharmaceutical industry steps in to treat the consequences.

In the Track Your Plaque approach, we focus specifically on elimination of wheat, cornstarch, and sugars, the most offensive among the carbohydrates. The need to avoid other carbohydrates, e.g., barley, oats, quinoa, spelt, etc., depends on individual carbohydrate sensitivty, though I tend to suggest minimal exposure.

Normal fasting glucose with high HbA1c

Jonathan's fasting glucose: 85 mg/dl
His HbA1c: 6.7%

Jonathan's high HbA1c reflects blood glucose fluctuations over the preceding 60-90 days and can be used to calculate an estimated average glucose (eAG) with the following equation:

eAG = 28.7 X A1c – 46.7

(For glucose in mmol/L, the equation is eAG = 1.59 × A1C - 2.59)

Jonathan's HbA1c therefore equates to an eAG of 145.59 mg/dl--yet his fasting glucose value is 85 mg/dl. 

This is a common situation: Normal fasting glucose, high HbA1c. It comes from high postprandial glucose values, high values after meals. 

It suggests that, despite having normal glucose while fasting, Jonathan experiences high postprandial glucose values after many or most of his meals. After a breakfast of oatmeal, for instance, he likely has a blood glucose of 150 mg/dl or greater. After breakfast cereal, blood glucose likely exceeds 180 mg/dl. With two slices of whole wheat bread, glucose likewise likely runs 150-180 mg/dl. 

The best measure of all is a postprandial glucose one hour after the completion of a meal, a measure you can easily obtain yourself with a home glucose meter. Second best: fasting glucose with HbA1c.

Gain control over this phenomenon and you 1) reduce fasting blood sugar, 2) reduce expression of small LDL particles, and 3) lose weight.  

Can you handle fat?

No question: Low-carbohydrate diets generate improved postprandial lipoprotein responses.

Here's a graph from one of Jeff Volek's great studies:



Participants followed a low-carb diet of less than 50 g per day carbohydrate ("ketogenic") with 61% fat.   The curves were generated by administering a 123 g fat challenge with triglyceride levels assessed postprandially. The solid line represents the postprandial response at the start; dotted line after the 6-week low-carb effort.

Note that:

1) The postprandial triglyceride (area-under-the-curve) response was reduced by 29% in the low-carb diet.  That's a good thing.

2) The large fat challenge generated high triglycerides of greater than 160 mg/dl even in the low-carb group. That's a bad thing. 

In other words, low-carb improves postprandial responses substantially--but postprandial phenomena still occur. Postprandial triglycerides of 88 mg/dl or greater are associated with greater heart attack risk because they signify the presence of greater quantities of atherogenic (plaque-causing) postprandial lipoproteins.

A full discussion of these phenomena can be found in the Track Your Plaque Special Report, Postprandial Responses: The Storm After the Quiet!, part of a 3-part series on postprandial phenomena.