To rule out the possibility of human error, my thyroid function was retested a few days ago, with a test for antibodies added to rule out or confirm autoimmune thyroid disease. Here’s the result:
I didn’t explain these numbers very well in my previous post. The thyroid sets the pace for your body’s metabolism. If your body were a computer, the thyroid would be the computer master clock that sets the pace for how fast instructions are to be executed. If you are hypothyroid, your clock is running too slow. If you are hyperthyroid, you are over-clocked. In the first three of these columns are TSH, T4 and T3, chemical messengers in your body that attempt to regulate clock speed; in the final column is the antibody test:
- TSH – is a messenger from the pituitary gland to the thyroid trying to tell it to speed things up. My TSH level is way high, so my pituitary is cranking TSH out big-time, trying to bring things up to speed.
- T4 & T3 – are the messengers from the thyroid to the rest of the body that do the actual pace setting. These last levels are just barely within the normal range.
- TPO AB – this test would measure the antibodies leftover in the blood from any previous autoimmune attack … Nope, no antibodies here!
So what’s going on? Because the lab work has established essentially no antibodies, most likely the problem is not the usual suspect, Hashimoto’s. What we know is that the signal is there to turn up the heat, but my thyroid can’t/won’t listen.
As I mentioned in my previous post, there is speculation in the low carb community that outrageously raised cholesterol might be due to euthyroid sick syndrome via low-carb induced hypothyroidism. I definitely had hypothyroid symptoms during the last year when I was losing weight (2011) – cold, low energy. Could my low carb, calorie restricted diet coupled with higher than average exercise be creating the thyroid insufficiency?
A PubMed search returned this from a study of the effect of calorie restriction on thyroid function:
Perfect! The three groups in the study were:
- CR: 28 subjects who were following a calorie restricted diet for 3-15 years
- EX: 28 body fat-matched exercising subjects who were eating Western diets
- WD: 28 sex-matched sedentary subjects who were eating Western diets
At 68, I’m a little older than anyone in the study group. My BMI at 20.4 and %BF at 7.6% fits right between the means of the CR group and the EX group – so that matches up. My T3 (at 62 and then 50) and free T4 (at 0.6 and 0.8) are both at the very low end of the CR group – so that matches, too. But, the disturbing part is my TSH (at 77 and 93). Ooops! Nothing like that from the CR group in the study!
What about low carb inducing lab values like line? Could that be the problem? PubMed search turned up this:
Dietary carbohydrate content is a major factor determining endocrine and metabolic regulation. The aim of this study was to evaluate the relation between thyroid hormone levels and metabolic parameters during eucaloric carbohydrate deprivation. We measured thyroid hormone levels, resting energy expenditure (by indirect calorimetry) and urinary nitrogen excretion in six healthy males after 11 days of three isocaloric diets containing 15% of energy equivalents as protein and 85%, 44% and 2% as carbohydrates. In contrast to the high and intermediate carbohydrate diets, carbohydrate deprivation decreased plasma T3 values (1.78 +/- 0.09 and 1.71 +/- 0.07 vs. 1.33 +/- 0.05 nmol/l, respectively, P < 0.01), whereas reverse T3, T3 uptake and free T4 levels increased simultaneously compared to the other two diets. TSH values were not different among the three diets.
So, it’s not the low carb or the CR. Looks like that’s enough to kill the thought that there’s nothing wrong with my thyroid. I started taking thyroid meds yesterday.
While I’m on the subject of hypothyroid, I want to explore more what’s the story on the hypothyroid – high cholesterol connection? I’m particularly interested in information as to which comes first – thyroid issues or cholesterol issues. Searching, I found a post from a medical student posting at SDN reporting on information from UpToDate. Here’s the whole post:
HYPOTHYROIDISM – Many hypothyroid patients have high serum concentrations of total cholesterol and low-density-lipoprotein (LDL) cholesterol, and some have high serum concentrations of triglycerides, intermediate-density lipoproteins, apoprotein A-1 and apoprotein B.
With respect to serum high-density-lipoprotein (HDL) cholesterol concentrations, high, normal or low values have been reported in different series.
The excess risk of coronary heart disease observed with hypothyroidism has been thought to be due, at least in part, to the characteristic lipid abnormalities (including high LDL).
Pathophysiology — The primary mechanism for hypercholesterolemia in hypothyroidism is accumulation of LDL cholesterol due to a reduction in the number of cell surface receptors for LDL, resulting in decreased catabolism of LDL. A decrease in LDL receptor activity has also been described.
Other mechanisms also may affect the serum cholesterol concentration in hypothyroidism:
•LDL oxidation is significantly increased in hypothyroid patients, the degree of which is directly related to the serum LDL cholesterol concentration.
•Diminished secretion of cholesterol into bile has been demonstrated in hypothyroid rats.
•Reduced cholesteryl ester transfer (the net transfer of cholesterol from HDL to LDL and very-low-density-lipoprotein [VLDL]) in hypothyroidism may minimize the increase in serum LDL cholesterol concentrations.
A different mechanism, reduced lipoprotein lipase activity, is responsible for the development of hypertriglyceridemia in hypothyroidism. The rate of synthesis of triglycerides is normal.
All patients with hypercholesterolemia (and hypertriglyceridemia) should be screened for hypothyroidism (and other secondary causes of hyperlipidemia) before being given specific lipid-lowering drug therapy. If hypothyroidism is present, the patient should be treated for three to four months with T4. If the serum lipid concentrations are not then normal, specific lipid-lowering therapy may be indicated. Patients in the latter group presumably have hypothyroidism superimposed upon primary hyperlipidemia.
SUBCLINICAL HYPOTHYROIDISM — Most patients with subclinical hypothyroidism have normal serum lipid concentrations. However, some have slightly high serum total and LDL cholesterol and lipoprotein (a) concentrations. Serum HDL cholesterol concentrations are low or normal in patients with subclinical hypothyroidism.
HYPERTHYROIDISM — Patients with hyperthyroidism have changes in lipid metabolism generally opposite to those described above for hypothyroidism. Serum total, LDL and HDL cholesterol concentrations tend to be low, as do serum apoprotein-B concentrations. Fatty acid clearance is increased, but lipolysis is increased even more, resulting in high serum fatty acid concentrations.”
That’s pretty clear. High cholesterol is secondary to hypothyroid and is expected to come down with thyroid meds. So, at least in all this, there’s good reason to expect to see my high cholesterol drop. Cool! I get labs rechecked in 2 months; I’ll keep y’ll posted. Of course, if they don’t, there’s reason to expect “primary hyperlipidemia”. Meanwhile, I’ve been checking my heart rate for the past 48 hours. It’s been 60 bpm every time I’ve checked. I’m curious to see if/ by how much the meds change that.
More about Interpreting Thyroid Tests: