7 ways to raise TSH without reducing thyroid dose

You’ve just come to your doctor for your annual check-up. Either you feel fine and you want to get a renewal of your current thyroid prescription, or you feel rather hypothyroid and you’re hoping to get an increased dose.

But your doctor has been trained to say this: “Your TSH is below reference (or too low in reference). I’m going to have to reduce your thyroid medication.” The current therapy guidelines say so.

Your heart sinks. You predict months or a year of increased brain fog and fatigue.

But have hope! There could be a way to escape from perpetual underdose.

• If you believe something else besides excess thyroid hormone is lowering your TSH, science says you could be right.
• If you believe there’s something you can do to increase your TSH by the time of your next test, science says you could be right about that, too.

If an obedient guideline-following doctor or a TSH-obsessed doctor is not willing to learn about the vulnerability of TSH, you, the patient, may want to try to manage your own TSH to more likely fall within the guidelines that are so often rigidly adhered to.

(Sigh. It is so backwards to be focusing on the lower boundary of the TSH reference range during thyroid therapy. Thyroid hormones and the entire body’s response to them should be the main focus of therapy. But because our broken medical system believes that wagging the tail (TSH) will wag the dog, some patients are left with no other option but “TSH test result management.”)

In this post, learn seven ways you may be able to prop up a lazy TSH to prevent a harmful thyroid dose decrease.

I’ve also added a BONUS 8th way to raise TSH (added January 16th, 2022).

1. Recognize how many nonthyroidal factors can lower TSH.

It’s going to be more difficult — or it may be impossible — to coax the TSH to rise if these factors powerfully weigh your TSH down at the same time.

• Biotin. Health products for skin, hair, or multivitamins or B-complex vitamins can contain them. Biotin is a substance used in the chemical analysis of your blood sample, so if biotin levels are higher than expected, they can cause technical interference at the lab. Biotin’s effect is to falsely lower TSH numbers and raise FT3 and FT4 numbers (Block-Galarza, 2018)
• Pregnancy. During pregnancy, TSH can be reduced by hCG hormone secreted by the placenta. This is the hormone that pregnancy tests measure, and it is especially high in the first trimester. See “Pregnancy thyrotoxicosis vs just a low TSH due to hCG hormone.” This is why the 2017 ATA thyroid guidelines for pregnancy tell people not to panic over a low TSH:

“A reduction in the lower TSH reference range is observed during pregnancy in almost all studies. In a small percentage of women, TSH can be undetectable (<0.01 mU/L), and yet still represent a normal pregnancy.

In addressing the clinical importance of a reduced serum TSH during pregnancy, it is important to note that subclinical hyperthyroidism has not been associated with adverse pregnancy outcomes.

Therefore, a maternal TSH concentration that is low but detectable is likely not clinically significant.”

ATA Thyroid and Pregnancy Guidelines, Question 2. (Alexander et al, 2017)

• Vitamin A. Dosing 25,000 IU can significantly lower TSH by boosting the effect of T3 in pituitary and hypothalamus receptors. Vitamin A and its relatives is likely to have some effect even at lower levels than 25,000/day (Farhangi et al, 2012). A similar effect occurs with acne medications like Accutane that contain Isotretinoin (Sharma, 2006), which is a retinoid, a vitamin A derivative.
• Fasting or dieting of certain types. Intermittent fasting might be okay, but you may see your TSH fall if you severely reduce total calories, cut back on protein calories, or change the type of fats you eat, or lower your leptin levels (Izadi et al, 2014). Lower leptin will lower hypothalamic TRH, which lowers TSH (Flier et al, 2000).
• “Drugs that lower TSH” — See the scientific article by Haugen, 2010. The most common offenders are glucocorticoids like hydrocortisone or prednisone — a lot of the chemical names end in “-one.” See a short list of glucocorticoids . See also the Synthroid monograph by Mylan, “Drug Interactions”, page 11. These lists are the tip of the iceberg.
• Central hypothyroidism. You could have a disability in the organs that secrete TSH. Check out my recent article on diagnosing central hypo while on therapy.
• TSH-disrupting chemicals and foods. Some endocrine disruptors focus on TSH, while others interfere with thyroid hormones. The TSH-specific chemicals are Phthalate, Perchlorates, BPA, Pesticides, PBDE. Bioactive foods: Caffeine, Fatty acids DHA and EPA (in fish oils), and Resveratrol (in red wine). Science is still evolving. See this recent article to find out whether they lower or raise TSH and by how much per dose (Oliveira et al, 2019).
• Euthyroid doses of T3-dominant therapy, including desiccated thyroid therapy. Lower TSH is often a local side effect on the hypothalamus and pituitary, not necessarily a sign of excessive T3 and T4 levels in blood. Test Free T3 and Free T4 to see where they really are. Learn from Robert Utiger, “the father of the TSH test,” about how TSH responds differently in these therapies, plummeting quickly just before we achieve euthyroid levels.
• TSH-receptor stimulating antibodies. See “The TSAb stimulating antibody can lower TSH despite euthyroid status. You might not know you have these antibodies pushing down TSH if you have little to no thyroid gland for them to stimulate. These antibodies may be found in Graves’ disease patients even after a total thyroidectomy with normal FT3 and FT4 levels. They are also found in some Hashimoto’s patients, and in some patients with autoimmune Atrophic Thyroiditis. See “Overlooked: How many Hashimoto’s patients with TSH-Receptor antibodies?”

Don’t obsess over this list too deeply. Do not go to extremes and starve yourself of vitamin A. Realize that science can only see a fraction of what can interfere with TSH.

Takeaway: TSH is a vulnerable, volatile, hypersensitive hormone.

TIP: If you want to raise TSH, do what you can to reduce factors that push TSH down. Some of the factors may involve a long term change of lifestyle or avoidance of a chemical for weeks before the test.

TIP: If you can’t reduce or eliminate essential medications or remove unavoidable factors, make sure your doctor is aware of their TSH-lowering effects. Many physicians don’t know that low TSH can be caused by factors in addition to hyperthyroidism (thyrotoxicosis).

2. TSH can be higher in the early morning, before breakfast.

Book your lab test as early in the morning as possible.

Actually, TSH can be highest at 3 AM, but no laboratories are open to test your blood at that time of night.

Let’s look at how much TSH can fluctuate in a single day in two different people. (These people are not taking thyroid medication.) TSH is the first graph below. I provide the other graphs to show the effects of TSH rhythm in people with healthy thyroids.

Reference ranges that go with these graphs:

• TSH 0.35–3.5 mU/L | FT4 10.3–21.9 pmol/L | FT3 3.5– 6.5 pmol/L

If you have a TSH like the patient #27 on the left, your high rhythmicity uses 2.5 mU/L (79.3%) of the population reference range every day. Your TSH could be 1.0 and 3.5 on the same day. 

It’s hard to know if you are a person with high rhythmicity or low rhythmicity, but there’s usually some degree of rhythm.

Here’s another graph from an earlier study (Brabant et al, 1990). They tested TSH every 10 minutes on a single day in ONE person. The peaks and valleys are very extreme and frequent.

CONTEXT: In the person depicted in the graph, “Sleep was allowed between 2300-0700 h with an average duration of 6h40 ± 0h40/rhythm. Meals were given at 0730, 1200, and 1730 h.”

There’s a new article out that studied TSH tests at 7am and 9am and recommended testing in the fasted state. It can lower the TSH if you eat 400 kcal breakfast OR have 75g glucose intake before your thyroid test:

“Compared with the fasting state, the TSH level at 2 h after the calorie intake was decreased by about 30%” …

“If the reference range of TSH used in the laboratory was from fasting blood samples, it would be better to evaluate the TSH level in fasting blood obtained in the morning compared with random or postprandial samples.”

(Dong et al, 2022)

TIP: Make an early morning appointment for your blood test. Don’t have breakfast or even a very sweet drink before your test.

TIP: If you do night shift work or sleep abnormal hours, consider how your circadian rhythm might shift. TSH might be lowest at a different time during the day than is shown in the graphs above.

3. TSH can be higher the morning after sleep deprivation.

Safety notice: Please do not drive or operate equipment while sleep-deprived!

The 1990 study by Brabant and team tested the effect of sleep deprivation on TSH. They tested 3 conditions in 6 healthy males:

• acute sleep withdrawal (SW) during the 24 h of testing,
• normal sleep (S), and
• sleep after a night of sleep withdrawal (SAW).

The main thing that changed was the height of the peak TSH.

TIP: Your TSH may be higher if you did NOT get a good night’s sleep just before a morning blood test.

TIP: Don’t test TSH as you are recovering from sleep withdrawal.

4. TSH may be higher 12+ hours post-dose

It depends on what thryoid medication(s) you are dosing and how much you are taking.

The graphs below, from Saravanan et al, 2007, show two lines from the same group of patients under two types of experimental conditions.

1. Experimental condition A: “T4 alone.” While taking more than 100 mcg of T4 only on a stable TSH-normalizing dose, patients had their blood tested every 2 hours for 24 hours.
2. Experimental condition B: “T3/T4.” Then the same group of patients had 50 mcg of their T4 dose taken away, and doctors replaced it with only 10 mcg of T3 dosed 1x a day. What a mistake! This replacement wasn’t enough, as you will see. After they “stabilized” at that level of underdose, they did the same 24-hour blood tests.

Then they combined the two experimental conditions’ data on the same graph for comparison.

NOTE: These graphs’ time flow does not begin at midnight. The X axis at 0.0 is the time of a single daily dose. The 24.00 means twenty-four hours after a dose.

In the graphs above, reference ranges are fT3: 2.8 – 7.1 pmol / L | fT4: 10.0 – 24.0 pmol / L, | TSH: 0.3 – 4.0 mU / L.

As you can see, the “T3/T4” data shows TSH very wobbly, but even the “T4 Alone” data shows TSH changes. In the graphs, you can see these principles in people whose TSH is within or above reference range during thyroid therapy:

• If you are dosed with T4 hormone (Levothyroxine, Synthroid, Eltroxin), you can lose a lot of your natural TSH fluctuation. TSH will be relatively flatter, but it can still increase 12+ hours post dose.
• If you are dosed with a little T3 hormone (less than 10 mcg/day — note that 1 grain/60 mg of desiccated thyroid / NDT contains about 8-9 mcg of T3), your TSH may recover 14 hours post-dose. But TSH can fluctuate significantly, especially if you are underdosed like these people and you are taking your T3-containing medication only once a day like these people.

On the T3-T4 combo they tested, the average TSH was 6.0 for part of the day. This protocol rendered the average patient hypothyroid. Obviously the experimental T3-T4 combo was an underdose. They took too much T4 away and gave too little T3 in exchange for it. They didn’t even bother to help patients avoid a high FT3 peak and a long, low FT3 valley by spreading out their T3 into 2 doses of 5 mcg each.

(NOTE: It’s a disappointment to see this major dosing error committed by seasoned thyroid scientists, but we can still be grateful that they published the outcomes of their error. If they had looked into the science before the 1980s, they would have seen that estimated pharmaceutical equivalency of LT4 to LT3 is not 5:1 but closer to 3:1. See Pharmaceutical equivalency of levothyroxine (LT4), liothyronine (LT3) and desiccated thyroid“).

Tip: Test 12+ hours post dose to increase chances of a higher TSH. Don’t take your thyroid medication after 8pm if you have an 8am blood test the next day. Take your thyroid pill after the blood draw.

Tip: IF dosing T3 medication or NDT, avoid testing during the post-dose Free T3, and try to spread out your daily dose to reduce its TSH-suppressive side effects. (See our post on managing Free T3 peaks and valleys.)

5. TSH can be higher if you don’t eat a meal right before the lab test.

Caution: Longer term fasting or calorie restriction can LOWER your TSH (Flier et al). Therefore, this tip is NOT about fasting or reducing calories on a chronic basis.

This is only about the timing of a single meal (Breakfast) in relationship to a blood test.

In 2014, Nair and team did a study on “postprandial state” (just after eating breakfast) and TSH levels. The experiment was simple:

• First, “Phlebotomy [blood sampling] was performed after an 8-12 hour overnight fast between 7:30-8:30 am for free T4 and TSH measurements.”
• Then, “the patients returned 2 hours after breakfast for their samples to be rechecked between 10:30-11:00 am on the same day.”

Before and during the experiment, nobody was taking thyroid hormones.

Results: TSH was significantly higher before breakfast. TSH was significantly lower after breakfast. Their T4 levels were unchanged.

Among the people tested, there were three subgroups. Before the experiment, Group A had normal TSH and FT4 levels, Group B had high TSH but normal T4. Group C had overt hypothyroidism, high TSH and low T4.

Averages:

• Group A: pre-breakfast TSH 2.42, post-breakfast TSH 1.79
• Group B: Pre-breakfast TSH 7.53, post-breakfast TSH 5.35
• Group C: Pre-breakfast TSH 66.93, post-breakfast TSH 61.22

Is this effect simply caused by the TSH circadian rhythm? Maybe. They should have tested other meals, not just breakfast, because TSH can have a steep decline between 6am and 12pm in people not taking thyroid medication.

TIP: Delay breakfast until after your early morning lab test to increase chances of a higher TSH.

6. On thyroid therapy, TSH can be higher mid-menstrual cycle or when dosing estrogen.

A study in two pre-menopausal women taking Levothyroxine monotherapy discovered that the mid-month rise in Estrogen created a significant rise in TSH levels. (Benvenga et al, 2017)

The blood test was taken every day of the month at 8 – 8:30 AM over 36 months (3 years). They found a monthly rise and fall in TSH in two women aged 30 and 32 years.

Woman A on left, Woman B on right:

This happens because estrogen peaks just before ovulation mid-cycle. Day 0 is when the menstrual flow begins.

It is well known in thyroid science that higher estrogen (estradiol) levels can increase TSH because it increases circulating levels of the most important T3- and T4-carrying plasma protein, “TBG” (Thyroxine Binding Globulin) (See Tahboub & Arafah, 2009). See tip #1, above, on low TSH in pregnancy.

When TBG rises, it increases the percentage of T4 and T3 that is bound to TBG, and decreases the percentage of “Free” hormone. Only “free” thyroid hormone can enter cells.

• In women with healthy thyroid glands, there is not much of a difference in TSH because the body adapts: their thyroid gland can add more thyroid hormone to blood to keep Free T3 and T4 levels relatively steady.
• However, in patients who can’t produce extra thyroid hormone from a thyroid gland, we can lose FT3 and FT4 without changing our thyroid dose. Even a tiny decrease can amplify the TSH. That’s part of the reason why, when estrogen peaks mid-month in females who have TSH that is unsuppressed, TSH can rise.

In addition, Benvenga and team explain in a follow-up article that a rise in estrogen can have a direct role in raising TSH:

“a contribution to the increased serum TSH may come from a direct, TBG-unrelated effect of the estrogens on the hypothalamus-pituitary-thyroid axis”

(Benvenga et al, 2018)

Liver cirrhosis can worsen this effect because TBG is secreted by the liver (Benvenga et al, 2018).

Even though their case study data come from some very specific case studies, they provide an extensive annotated bibliography of past scientific research on Estrogen-TSH relationships. They concluded:

“Because either autoimmune or post-thyroidectomy hypothyroidism is relatively common, and so is chronic liver disease, their coexistence may not be rare.

In patients with such coexistence, surveillance for possible undertreated hypothyroidism is suggested.

(Benvenga et al, 2018)

The main challenge is that it’s difficult to predict what day of the month the estrogen peak plus TSH peak will occur for each person.

You might be able to predict it better if you measure basal body temperature, like people do when using the “rhythm method” to increase or decrease chances of pregnancy. You might have a monthly pattern that repeats, like these women. There are now smartphone apps available to track temperature on graphs to predict when ovulation occurs.

TIP: Take your blood test mid-cycle if you are a menstruating female to raise the chances of obtaining a higher TSH.

TIP: If you dose medication including estrogen / estradiol, be aware that it is a TSH-raising medication at the cost of lowering your Free thyroid hormone levels. Some foods also contain phytoestrogens that mimic this effect to a lesser degree.

7. On thyroid therapy, TSH can be higher in the coldest months of the year.

In 2017, Gullo and team did a study of a huge number of people’s seasonal TSH, Free T3 and Free T4 levels.

They compared people with healthy thyroid glands not taking thyroid hormones (BLUE) vs. people after a thyroidectomy who were taking thyroid hormones (RED).

Look what happened to the people who were on the same dose of thyroid hormone all year long.

This study was done on patients in Sicily in this climate:

• August daily temperature is between 19.3°C and 33.1°C
• January daily temperature is between 5.2°C and 15.5°C

What would the results be like in Scotland, or North Dakota, or Canada, or Norway, or Finland where the cold months will be colder?

They also found that thyroidless people on thyroid therapy lost a lot of Free T3 hormone in winter, while people with helathy throids gained Free T3 in Winter.

See posts with fuller data sets and discussion of Gullo et al, 2017:

• “In Winter, everyone gains T3 except thyroidless patients on T4”
• “Winter T3 loss: Why it matters to thyroid patients.”

TIP: If you test TSH once a year, test in the coldest month of the year. If you get TSH tested and your dose adjusted in summer, you may need a really big sweater to stay warm in the winter.

8. BONUS: Milk thistle dosing.

Here are some relevant TSH-boosting details from our new post added January 16, 2022, “Milk thistle alters thyroid hormone transport.”

Silychristin derived from milk thistle is an endocrine disruptor. It inhibits T3 and T4 entry into cells via a transmembrane transporter called MCT8.

The MCT8 transporter is important to many aspects of health. Almost every tissue listed in the Human Protein Atlas expresses the genetic mRNA for this transporter. It is a major portal for T4 and T3 to enter hypothalamus, pituitary and thyroid tissue. Therefore, it is a transporter that enables the hypothalamus-pituitary-thyroid axis to function.

In 2016, scientists found that milk thistle’s silychristin (SC) is the most potent inhibitor of MCT8 known to science. At concentrations used in clinical settings, it can directly compete with T3 and T4 transport into cells. (Johannes et al, 2016) …

Johannes emphasized that SC was “even more likely” to have an effect than MCT8-inhibiting anticancer drugs called Tyrosine Kinase Inhibitors (TKIs).

“Because TKIs have significant effects on the TH [thyroid hormone] axis with plasma levels, even 1 order of magnitude below their IC50 (7), an in vivo effect of SC is even more likely.”

(Johannes et al, 2016)

An earlier study by members of the same research team showed that TKIs can cause TSH to rise in people without thyroid function on LT4 therapy by hindering TH transport into the pituitary and hypothalamus (Braun et al, 2012).

Johannes reported that SC is more potent than TKIs by “one order of magnitude,” which means 10 times more potent.

If TKIs can raise TSH in treated patients without thyroid function, SC is even more likely to do so.

Much like fast-release synthetic liothyronine (LT3) thyroid hormone dosing, SY is fast acting within 1-3 hours, and it has a fast clearance rate. In comparison, LT3 achieves its peak around 3 hours post-dose.

SC’s fast clearance rate is not a bar to therapeutic benefit. The peak concentration and half-life of SC is only part of the equation. The overall effect of this substance on the human body depends partly on downstream events such as T3-signaling upregulation of D1 enzyme in liver. D1 has a half-life of 12 hours (Maia et al, 2011).

The effect of SC may endure long after its blood concentration falls, so it is reasonable to hypothesize the following:

Dysregulations of the TH axis are not always resulting in overt and acute states of disease, but a constant dysregulation will likely lead to adverse effects in the long run.

(Johannes et al, 2016)

Who is most likely to be at risk of adverse effects?

One of the longest-term effects SC may have is on the brain development of a fetus. This is why it was wise for Johannes and team to study astrocyte (brain) cells and compare them with MCT8-rich kidney cells:

SC might significantly block TH import into target cells, causing metabolic and developmental dysregulations. By its high specificity, this will happen in an organ- or even cell type-specific manner, eg, in astrocytes.

Several rat studies report beneficial effects on oxidative stress markers in the young and adult brain, implying that SY is able to cross the blood-brain barrier and enter the central nervous system (30, 31).

Because THs are, for example, important for proper development of the human brain, the use of SY during pregnancy should be discouraged until the proof of its safety.

(Johannes et al, 2016)

Johannes’s concern about the safety of SY dosing in pregnancy was cited and echoed in Barbara Demeneix’s 2019 article in the European Thyroid Journal. It was titled “Evidence for Prenatal Exposure to Thyroid Disruptors and Adverse Effects on Brain Development.” She concluded:

“TH disruption in utero may contribute to an increased risk of neurodevelopmental disease, learning difficulties, and IQ loss.”

(Demeneix, 2019)

Because SY can affect both the “young and adult brain,” according to Johannes’ passage quoted above, one should not only be cautious about pregnancy, but also be careful about the way it may change thyroid hormones’ influence on depression, or neurological degeneration in dementia and Alzheimer’s. (See “Low-normal FT3 increases Alzheimer’s Disease risk).

No studies of milk thistle (that I’m aware of) have examined its effects during hypo- or hyperthyroidism, but in light of the impact of TKIs, it makes sense for Johannes and team to add this:

Also, people with manifested diseases of the thyroid gland, eg, hypo- or hyperthyroidism, are at risk by regular consumption of SY-containing preparations.

(Johannes et al, 2016)

Read more about the potency of SY at various doses in the full post: Milk thistle alters thyroid hormone transport.

CAUTION: Milk thistle may be unsafe during pregnancy and during severe thyroid hormone dysregulation. It may also interact with other health conditions such as heart failure or depression, and various medications. See the recent post on Verywell Health, “What is milk thistle?” by Cathy Wong, October 22, 2021, and scroll down to “Possible side effects.”

TIP: The short half-life of silychristin in milk thistle’s SY mixture may require dosing it within 3 hours before a lab test. There are no clinical trials published yet, so we have no idea how much TSH will rise, if at all, during a certain thyroid therapy protocol, given a certain baseline TSH level and a certain SY dose.

TIP: To minimize adverse effects, try a small dose first (i.e. silymarin extract at <200 mg). Observe its effects on your body within the next 6-12 hours. Then wait at least a day for your body to recover and to notice any short term rebound effects. Then try a slightly larger dose and do the same monitoring. Track vital signs such as heart rate and body temperature, and notice changes in mental function and other symptoms.

NOTE: None of these tips constitutes medical advice. See our disclaimer: Terms of use

Is it worth it?

I’ve just listed 7+1 ways to increase chances of a higher TSH. It all adds up to this list.

Take your TSH blood test:

1. After removing or reducing as many TSH-depressive factors as possible,
2. As early in the morning as possible,
3. After being sleep-deprived the night just before the test,
4. At least 12 hours after taking thyroid medication,
5. Before breakfast on the day you test,
6. If you are a pre-menopausal female, mid-cycle,
7. In the colder months of the year if you live in an extreme climate.
8. BONUS: Milk thistle

THIS IS RIDICULOUS, ISN’T IT?

Why would any thyroid patient be motivated to go to such lengths to try to inflate their TSH or avoid its suppression?

It’s because our medical systems often threaten to reduce our thyroid hormone supply based on a low TSH alone. Raising TSH can be a way to protect our own bodies from a harmful underdose within this broken system.

Many health care professionals do not realize that a low TSH does not “cause” thyrotoxicosis. Only excess thyroid hormone supply has the power to do this. Nor is a low TSH “specific” to the pathology of thyrotoxicosis, since central hypothyroidism and TSH secretion interference can happen for many reasons.

If you step back and think about it, isn’t it amazing that TSH can vary as much as shown in the graphs above in response to some tiny nonthyroidal changes?

• TSH is a volatile, vulnerable hormone. It fluctuates based on factors way beyond your thyroid hormone levels. TSH fluctuations can sometimes be huge even while our thyroid hormone dose does not change throughout the day, month, or year.
• TSH often behaves very differently in thyroid-disabled people taking thyroid hormones compared to people who are not on thyroid therapy. Learn more about the TSH-T3 disjoint in thyroid therapy. The data show our TSH-T3 relationships are extremely abnormal even on standard LT4 therapy
• TSH behaves very differently when dosing different combinations and ratios of T4 and T3 thyroid hormones, so it discriminates against patients by their pharmaceutical use and their peripheral metabolic handicaps.

Isn’t it unfair that our doctors have been given the power to starve us of thyroid hormone for a year just because our TSH is having a bad day?

Why should we be hormonally punished for the fact that our TSH is in its summertime low, or because we took the lab test at 3pm, or on the day after sleep deprivation, or within 3 days before beginning a menstrual cycle?

Why do medical systems grant this volatile TSH hormone the sole right to judge whether we have “adequate” dosing during thyroid therapy?

Mini history lesson: Narrow-minded scientists in the 1980s and 1990s put this moody hormone TSH on a pedestal. They presumed, using a theory of biochemical mimicry (or, what I have called biochemical bigotry), that the TSH hormone’s 95% statistical reference interval in thyroid-healthy populations is the sole judge of thyroid status in all thyroid-disabled individuals. In Lord of The Rings-like fashion, “They sought ONE lab test to rule them ALL.”

But isn’t it interesting thyroid scientists are willing to make exceptions to permit a low TSH in some cases?

• In people with a prior diagnosis of central hypothyroidism,
• In early-term pregnancy, and
• In people being treated with TSH suppression after a high-risk thyroid cancer. In this population, TSH suppression is not associated with harm to bones in men or in premenopausal women (Brancatella & Marcocci, 2020).

A smart, evidence-based doctor should learn to recognize TSH secretion interference. If the patient’s low TSH does not match their normal FT3 and FT4 measured 12+ hours post dose, it ought to be a clear case. It should also be clear case when TSH is being “tricked” by an extremely high or low FT3:FT4 ratio induced by hormone dosing. When in doubt, use the free endocrinology research app SPINA-Thyr to detect pituitary TSH secretion interference before therapy or on LT4 monotherapy (it is not trustworthy during T3-inclusive therapy).

Unfortunately, we are not all blessed with “good thyroid doctors.” Many physicians don’t know that even the 2012 ATA thyroid guidelines ask for clinicians’ independent judgment in their introductory disclaimer. Too many physicians have been afraid to question TSH’s god-like authority by pointing to the evidence. In many cases, patients’ abnormal TSH on therapy has been to discipline physicians. See “How thyroid guidelines are being used to punish doctors.”

Physicians must defend their careers. We patients must defend our health.

We and our physicians can both be victims of TSH and the medical system that idolizes it, or we can use science to try to understand and master TSH.

References