Self-directed thyroid management

Is there an at-home test you can do to gauge thyroid status?

Yes. Measure your temperature.

Unlike a snake or alligator that relies on the sun or its surroundings to regulate body temperature, you and I can internally regulate temperature. The hypothalamus-pituitary-thyroid glands are the organs involved in thermoregulation, body temperature regulation. While the system can break down anywhere in the sequence, as well as in other organs (e.g., adrenal), the thyroid is the weak link in the chain.

Thus, temperature assessment can serve as a useful gauge of thyroid adequacy. Unfortunately, temperature measurement as a reflection of thyroid function has not been well explored in clinical studies. It has also been subject to a good deal of unscientific discussions.

How should temperature be measured? The temperature you really desire is between 3 am and 6 am, while still asleep. However, this is difficult to do, since it would require your bed partner to surreptitiously insert a thermometer into some body orifice without disturbing you. A practical solution is to measure temperature first upon arising in the morning, before drinking water, coffee, making the bed, etc.--immediately.

While traditionalists (followers of Dr. Broda Barnes, who first suggested that temperature reflects thyroid function) still advocate axillary (armpit) temperatures, in 2009 it is clear that axillary temperatures are unreliable. Axillary temperatures are inconsistent, vary substantially with the clothing you wear, vary from right to left armpit, ambient temperature, sweat or lack of sweat, and other factors. It also can commonly be 2-3 degrees Fahrenheit below internal ("core") temperature and does not track with internal temperatures through the circadian rhythms of the day (high temperature early evening, lowest temperature 3-6 am).

Rectal, urine, esophageal, tympanic membrane (ear), and forehead are other means to measure body temperature, but are either inconvenient (rectal) or require correction factors to track internal temperature (e.g., forehead and ear). For these reasons, we use oral temperatures. Oral temperatures (on either side of the underside of the tongue) are convenient, track reasonably well with internal temperatures, and are familiar to most people.

Though there are scant data on the distribution of oral temperatures correlated to thyroid function, we find that the often-suggested cutoff of 97.6 degrees Fahrenheit, or 36.4 C, seems to track well with symptoms and thyroid laboratory evaluation (TSH, free T3, and free T4). In other words, oral temp <97.6 F correlates well with symptoms of fatigue, cold hands and feet, mental fogginess, along with high LDL cholesterol, all corrected or improved with thyroid replacement and return of temperature to 97.6 F.

But be careful: There are many factors that can influence oral temperature, including clothing, season, level of fitness, "morningness" (morning people) vs. "nightness" (night owls), relation to menstrual cycle, concurrent medical conditions.

Also, be sure that your thermometer can detect low temperatures. Just because it shows low temperatures of, say 94.0 degrees F, doesn't mean that it can really measure that low. If in doubt, dip your thermometer in cold water for one minute. If an improbable temperature is registered, say, 97.0 F, then you know that your device is incapable of detecting low temps.

A full in-depth Special Report on thermoregulation will be coming soon on the Track Your Plaque website.

Comments (9) -

  • Dan

    4/2/2009 6:11:00 PM |

    Dr. Davis.

    What do you think of brachial artery reactivity testing (BART).  There's another study (here: http://www.adajournal.org/article/S0002-8223(08)02336-5/abstract) linking high-fat diets to decreases in flow-mediated vasodilation.  I was wondering your thoughts on the likelihood that BART is measuring a significant risk factor for CVD.  

    This is definitely off-topic so apologies.

  • Anna

    4/2/2009 6:14:00 PM |

    As you say, most common thermometers are calibrated to measure fever or elevated temps.

    Look for basal thermometers, often sold for detecting ovulation, so they'll be with fertility and
    "women's products" aisles, but may be used by anyone. Basal thermometers are calibrated low enough to detect the low temperatures of hypothyroidism.

    When I was experiencing infertility 15 years ago, I handed over many months of early morning temperature charts to the specialists, with all my menstrual cycle details.  Routinely, I had temperatures in the 96°F range, unless I was sick or ovulating (98.6F was a fever for me back then).  A spike to 97 indicated ovulation.  No one ever questioned the low temps in terms of my lack of fertility, of course, but the nurses joked about how cold I was.  If I only knew then...

  • Anonymous

    4/2/2009 8:08:00 PM |

    Dr.Davis

    This is very informative.
    What is the best base level of Iodine daily to promote thyroid health?

    Thanks for you great blog!

    Aaron

  • Anonymous

    4/4/2009 4:33:00 AM |

    Using a thermometer to determine thyroid function may be worthwhile, but realistically... how useful is it really?

    By this I mean, say it registers low. Okay, so now you go to your doctor and try to get your thyroid levels measured. A GOOD doctor who knows what they doing (which is rare) will measure Free T3, Free T4, TSH and antibodies.

    Unless your TSH is in the >3 range, along with raised antibodies, the chances of getting treatment is close to nil, regardless of your temperature. And usually most doctors look for TSH >5.

    Perhaps you can find the rare doctor who will treat based on antibodies alone, or the doctor who will consider a TSH >2.5 significant, but prepare to see a lot of doctors in order to find one who will treat.

    And recommending iodine without checking antibodies first, probably is a bad idea. Iodine + Hashimoto's doesn't always work out so well.

  • Monica

    4/8/2009 3:12:00 AM |

    Thanks so much for this information.  I measured waking temps for around 6 months for fertility reasons.  Usually I was in the low to mid 97 range.  Just measuring, evening, it's only 97.9 -- as measured with two different BBT thermometers.  I've lost about 15 pounds on a wheat-free, sugar-free diet, but I have about 20 lbs. more to lose and often wonder why I can't seem to shake the extra weight.  This post has encouraged me to get my thryoid checked.  my mom, grandma, and great-grandma all have/had hypothyroidism.

  • Anna

    4/8/2009 2:59:00 PM |

    Monica,  based on my experience and of others I know, it might take some persistence on your part.  Learn as much as you can about thyroid function and various approaches to treatment; Mary Shomon's thyroid.about.com website and book are a good start.  Good thyroid function is critical for optimum fertility, healthy pregnancies, and healthy babies; several years after we gave up on trying, when hypothyroid symptoms became so pronounced, I read at least 5 books with different angles; if I hadn't I would have given up much too soon and settled for the wrong care.  Check with a few doctors (even out of network and out-of-pocket if you can) if you are told you are fine despite your symptoms or only need synthetic T4; it's worth it (esp if low thoyroid function might be affecting your fertility - I learned too late it probably was at least part of my infertility problem all along).  I got nowhere fast with my PCP of 10 years and the next physician I saw in my network and only a fraction better.  Even once I found better care out of network, it took a lot of tinkering with treatment and dose to finally feel and function closer to normal in the third year of treatment.  Don't get discouraged.

    I know there's a fine line between doctor-shopping to neurotically get what you think you need vs. being a tenacious advocate for your health (I was constantly aware of this).  Despite the dismissal of concerns and frustration I often experienced early on,  I wouldn't accept the constant push to take other meds offered to manage the symptoms just because the doc or lab held to an outdated TSH threshold or couldn't/wouldn't figure it out.  

    Good luck to you.

  • EMR

    2/10/2010 6:37:34 PM |

    Temperature assessment should be a great way to detect the disease.Thanks for the informative article.

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    3/4/2010 6:41:18 AM |

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What's better than a heart scan?

What's better than a heart scan?


Do you know what's better than a heart scan?

Two heart scans. No other method can provide better feedback on the results of your program.

Say you've made efforts to correct high LDL; lost weight to raise HDL and reduce small LDL; added soluble fibers, nuts, and dramatically reduced wheat products; take fish oil, vitamin D, and follow a flavonoid-rich diet. Has it worked?

After a year or so of your program, that's when another heart scan can give you invaluable feedback on whether it's been successful. I tell my patients that it's relatively easy to correct lipid and lipoprotein abnormalities. The difficult part is to know when it's good enough. Is your LDL of 67 mg/dl and HDL of 50 mg/dl good enough? Another heart scan score is the best way I know of to find out.

Variation in plaque growth differs hugely from one person to another, even at equivalent lipoprotein values. Why? Lots of reasons. Humans are inconsistent day to day. Lipoproteins, being a snapshot in time and not a cumulative value, change somewhat from day to day. There's also the possibility of unmeasured, unrecognized factors that influence coronary plaque growth. We may not be smart enough to identify these hidden factors yet. But your heart scan score will incorporate the effects of these hidden factors.

Ideally, we aim for zero growth in plaque (no change in score) or a reduction. But, particularly in the first year, 10% or less plaque growth is still a good result that predicts much reduced risk of heart attack. More than 20% per year and your program needs more work--or else you know what's ahead.
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More on erectile dysfunction

More on erectile dysfunction

Several facts on erectile dysfunction and coronary plaque:


If you have erectile dysfunction, there's at least a 50% chance you also have coronary plaque.

If you have coronary plaque by a CT heart scan, there's a 50% chance you have erectile dysfunction.

If you have symptomatic coronary disease (chest pains, breathlessness, prior heart attack), there's a 90% chance you also have erectile dysfunction.


Coronary disease is characterized by a dysfunctional state of the "endothelium", or inner lining of the coronary arteries. Erectile dysfunction is characterized by dysfunction of the endothelium of the penile circulation. Same phenomenon, different territories. (There are other differences, of course, but the two conditions share this fundamental phenomenon.)


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Comments (8) -

  • Anonymous

    5/15/2007 8:34:00 AM |

    Would you comment on this?

    Implication in contributing to risk of death from heart disease

    A recent Johns Hopkins study testing the addition of L-arginine to standard postinfarction treatment has implicated L-arginine supplementation with an increased risk of death in patients recovering from heart attack.[5] This study has been discussed in some detail in : "Reverse Heart Disease Now" by Stephen T Sinatra MD and James C Roberts MD, publ. Wiley 2006 ISBN 0-471-74704-1 at pp 111 -113.

    http://en.wikipedia.org/wiki/Arginine#Implication_in_contributing_to_risk_of_death_from_heart_disease

  • Dr. Davis

    5/15/2007 11:46:00 AM |

    I actually posted a full discussion of this issue a few months back on the Track Your Plaque website (www.trackyourplaque.com). I still believe what I said then:

    "Should we panic and stop l-arginine based on this report?

    Take a closer look.  We don’t think so. First of all, two of the deaths occurred months after l-arginine treatment was stopped. Two other deaths were due to infections and therefore likely unrelated to heart disease or l-arginine use. This leaves two deaths attributable to heart disease in the l-arginine group.

    "Numbers this small are likely to represent chance statistical effects, especially in view of the small size of the overall trial. In other words, in all likelihood, a larger study would have revealed more reliable numbers not as susceptible to chance effects.

    "What about all the other studies that have looked at l-arginine? We should view this one study in the context of all preceding experiences. No excess dangers have been observed in thousands of participants with coronary disease, angina, peripheral vascular disease, and heart failure over the last decade of investigation.4 Many of the participants with heart failure in these studies were sufferers of prior heart attack, just like the VINTAGE MI participants.

    "Let’s also not forget that l-arginine is a food substance. Do fish, chicken, eggs, and nuts also pose danger? Of course not.

    "As always, each study should be viewed within the broader context of the available scientific and clinical experience. The overwhelming experience, as well as common sense, suggests that the VINTAGE MI Trial is a statistical fluke."

    In other words, I find this so counter to all prior experiences that I think it's a fluke. But, of course, the pharmaceutical industry-friendly media make hay of such reports.

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  • Jack Willson

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Small LDL: Perfect index of carbohydrate intake

Small LDL: Perfect index of carbohydrate intake

Measuring the number of small LDL particles is the best index of carbohydrate intake I know of, better than even blood sugar and triglycerides.

In other words, increase carbohydrate intake and small LDL particles increase. Decrease carbohydrates and small LDL particles decrease.

Why?

Carbohydrates increase small LDL via a multistep process:

First step: Increased fatty acid and apoprotein B production in the liver, which leads to increased VLDL production. (Apoprotein B is the principal protein of VLDL and LDL)

Second step: Greater VLDL availability causes triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, enriching them in triglycerides (via the action of cholesteryl-ester transfer protein, or CETP). Much VLDL is converted to LDL.

Third step: Triglyceride-rich LDL is "remodeled" by enzymes like hepatic lipase, which create small LDL.


Carbohydrates, especially if they contain fructose, also prolong the period of time that triglyceride-rich VLDL particles persist in the blood, allowing more time for VLDL to interact with LDL.

Many people are confused by this. "You mean to tell me that reducing carbohydrates reduces LDL cholesterol?" Yes, absolutely. While the world talks about cutting saturated fats and taking statin drugs, cutting carbohydrates, especially wheat (the most offensive of all), cornstarch, and sugars, is the real key to dropping LDL.

However, the effect will not be fully evident if you just look at the crude conventional calculated (Friedewald) LDL cholesterol. This is because restricting carbohydrates not only reduces small LDL, it also increases LDL particle size. This make the calculated Friedewald go up, or it blunts its decrease. Conventional calculated LDL will therefore either underestimate or even conceal the real LDL-reducing effect.

The reduction in LDL is readily apparent if you look at the superior measures, LDL particle number (by NMR) or apoprotein B. Dramatic reductions will be apparent with a reduction in carbohydrates.

Small LDL therefore serves as a sensitive index of carbohydrate intake, one that responds literally within hours of a change in food choices. Anyone following the crude Friedewald calculated LDL will likely not see this. This includes the thousands of clinical studies that rely on this unreliable measure and come to the conclusion that a low-fat diet reduces LDL cholesterol.

Comments (15) -

  • nitrile exam gloves

    12/8/2009 3:58:05 AM |

    Thanks for the knowledge sharing...it helps to be healthy.

  • x.ds

    12/8/2009 12:02:31 PM |

    Here is a link showing the atherogenicity in mice of different saturated fats in diets with 1% cholesterol. Look at page 1416 of the free full report that can be downloaded here:

    http://www.ncbi.nlm.nih.gov/pubmed/8409772

    On the opposite you can see bread not being atherogenic in baboons here:

    http://www.ajcn.org/cgi/content/abstract/33/8/1869

    By the way you can notice the effect of 0.1% cholesterol at the end of the article = 1 gm cholesterol per kg of food = 5 egg yolks.

    Does it look a lot ? "There is evidence from animal experiments showing that if atherogenic dietary factors are reduced to levels comparable to man's intake, the same vessel changes occur as with higher levels, but more slowly."

    Download the free full report here:

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1938976/

    In this report you can also see butter to be highly atherogenic to swine without additional cholesterol to their diet.

  • Bobber

    12/8/2009 5:06:03 PM |

    What about rice?  Does it also increase small LDL particles?

  • Nigel Kinbrum BSc(Hons)Eng

    12/8/2009 6:54:52 PM |

    @x.ds: Humans aren't C57BL/6J mice (susceptible to diet-induced fatty streak lesions), baboons or pigs.

  • Future Primitive

    12/8/2009 7:34:20 PM |

    @x.ds

    The strain of mice in the first study are predisposed to diet-induced obesity, type 2 diabetes, and atherosclerosis.

    Likewise, here's an interesting quote from the last paper based on a porcine model: "Whenever there are three
    animals from the same litter, they are divided equally among the three groups (ie, "control", "butter", & "egg yolk" groups)  In the present experiment, this occurred once. These three pigs had the most aortic atherosclerosis in their respective groups. The control pig with the most atherosclerosis was the brother of the pigs with the most disease fed egg and butter."  

    The group of pigs with the highest rate of atherosclerosis was the egg yolk group - yet at most we see a vanishingly positive relationship, if any, in a large number of human epidemiological studies of moderate egg consumption and heart disease (too many to list here - many are recent and easy to locate, though).  Do we even have grounds to formulate a hypothesis of egg induced atherogenesis based on human observational studies? I don't know, really - though a casual glance suggests, "no".

    Looking forward to reading the other study you pointed us to when I get the time.

  • Anonymous

    12/8/2009 7:42:17 PM |

    x.ds:

    Often times these animal studies don't translate well when applied to humans.

    Also, like Dr. Davis pointed out in his blog, most (LDL) cholesterol lowering research doesn't use advanced lipoprotein testing like NMR so the data is misleading to say the least.

  • Anonymous

    12/8/2009 9:16:54 PM |

    x.ds:

    It would be nice for a change to see experiments on other than herbivorous (mice) or mostly vegetarian animals (both pigs and baboons on the wild).

  • Dr. William Davis

    12/8/2009 11:48:34 PM |

    Bobber--

    While all carbohydrates increase small LDL, the effect of wheat is the most extravagant.

  • Anon X

    12/9/2009 3:18:19 AM |

    I generally agree with those who deny the universal applicability of experimental results in mice and rats to men. However, I do so with this one caveat; there is one fact I cannot deny: Many women are convinced that most men are rats.

  • LynP

    12/9/2009 4:42:51 AM |

    Doc, does this mean that I ca sorta log my particle size by getting my apoB checked in quarterly labs? I'll never be able to convince primary to do the outright particle size test...yet (working on that). Thnx.

  • Anonymous

    12/9/2009 3:08:55 PM |

    I admit I do not understand VLDL-C. What I would really like to find is a simple range scale. Mine shows up VLDL-C..7  Non HDL ..70
    I do not know if that is good or bad. Is there such a chart showing like,  1 good ... 100 bad ??
    LP(a) shows up by itself and I understand that because there is a range showing bad ..over 30.
    Any help understanding appreciated

  • David

    12/10/2009 2:39:45 AM |

    Dr. Davis,

    I honestly think you are doing God's work and have learned to appreciate the value of heart scans through your site.  However, it still bugs me that so many people in Asia can live off of large quantities of white rice with minimal atherosclerosis.  For instance, this study shows that American Whites have much higher atherosclerosis than Japanese despite the Japanese having much higher LDL-cholesterol, blood pressure, fasting glucose, and smoking rates:

    http://ije.oxfordjournals.org/cgi/content/full/34/1/173


    This other study (below) tries to explain this difference based on the Japanese consumption of fish. However, if you look at the data, those Americans who consume the most fish oil consume about as much fish oil as those Japanese that consume the least fish oil, and yet between these comparable groups in terms of fish consumption, the Japanese still have vastly lower atherosclerosis on heart scans.  And the Japanese American group consumes more fish than the White American group and has more coronary calcium.

    http://content.onlinejacc.org/cgi/content/full/52/6/417


    And here is another study showing much lower CAC in Japanese than in Japanese-Hawaiians even after controlling for a bunch of risk factors including fish intake:

    http://aje.oxfordjournals.org/cgi/content/full/166/11/1280


    Although in this other study looking at only at Americans, the incidence of CAC appears to be similar to that in Japanese - so maybe there was something unusual about the US samples in the other studies?

    http://content.onlinejacc.org/cgi/content/full/49/20/2013

  • Anonymous

    12/10/2009 8:23:46 PM |

    Dr. Davis,
    What is your opinion of the LP-Pla2 test for arterial plaque?  If you've used the test, do any elements of your program reduce levels of this enzyme?

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    11/3/2010 9:44:57 PM |

    However, the effect will not be fully evident if you just look at the crude conventional calculated (Friedewald) LDL cholesterol. This is because restricting carbohydrates not only reduces small LDL, it also increases LDL particle size. This make the calculated Friedewald go up, or it blunts its decrease. Conventional calculated LDL will therefore either underestimate or even conceal the real LDL-reducing effect.

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Heart scan scores dropping like stones!!

Heart scan scores dropping like stones!!

I saw two instances of dramatic coronary plaque regression today.

John, a 53-years old mechanical lift operator, dropped his heart scan score from 479 to 323--a 32% regression of coronary plaque volume!

Eric, a 50-year consulting engineer, dropped his heart scan score from 668 to 580--a 13% reduction.

Both men did nothing special beyond the principles advocated in the Track Your Plaque program. Recall that, without preventive efforts, your heart scan score is expected to increase by 30% per year. Both men are well on their way to freedom from risk of coronary "events".

Two less people to feed the revenue-hungry hospital procedure system! We need many more like them.
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