Is It Really OK to Ignore a Low TSH? What We Actually Know About Thyroid, T3, and Your Heart

Beyond the Thyroid - Episode 55: Is It Really OK to Ignore a Low TSH? What We Actually Know About Thyroid, T3, and Your Heart

A social media poll made a bold claim: low T3 causes atrial fibrillation, and high-dose T3 therapy with a suppressed TSH is the fix. Dr. Dana Gibbs took that claim seriously enough to spend an entire episode on it -- because the stakes are high and the evidence is more complicated than the poll suggested.

In this episode, she walks through what thyroid hormones actually do to the heart, in both directions, and explains why the goal of thyroid treatment is balance -- not maximization.

In this episode you'll learn:

• The full cardiac picture in hyperthyroidism: tachycardia, atrial fibrillation risk, widened pulse pressure, cardiac remodeling, and heart failure
• The full cardiac picture in hypothyroidism: diastolic dysfunction, bradycardia, narrow pulse pressure, increased vascular resistance, and severe complications including myxedema
• The mitral valve prolapse and thyroid connection
• What the evidence actually shows about low T3 and AFib in otherwise healthy outpatients -- and where the research gaps are
• Why levothyroxine often fails to fully restore T3 to normal physiologic levels
• How T3 dosing and test timing can mask supraphysiologic peaks that never show up in routine labs
• Why a suppressed TSH is a clinical signal worth investigating, not a number to optimize around
• What properly timed, comprehensive labs look like -- and when a cardiac workup is warranted
• The bottom line on T3 therapy, cardiac risk, and what "balance" actually means in practice

If you're on T3, thinking about it, or you've been reassured that a low TSH isn't a problem, this episode gives you the clinical context to have a more informed conversation with your doctor.

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Episode Highlights

00:00 Start
00:43 Show Intro and Host
01:46 Poll Breakdown and the Question It Raised
03:47 Thyroid Hormone Basics
05:13 T3 Dosing and Safety
07:10 How Hyperthyroidism Affects the Heart
10:36 How Hypothyroidism Affects the Heart
12:47 Mitral Valve Prolapse and Thyroid
14:58 The AFib Evidence Review
18:36 Levothyroxine and the T3 Gap
19:48 What We Still Don't Know
20:35 What the Poll Really Shows
22:50 Testing Timing and Ratios
25:17 Bottom Line and Takeaways
29:24 Program Invitation
30:37 Final Wrap and Disclaimers

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✉️ Email Dr. Gibbs at drgibbs@DanaGibbsMD.com or visit https://www.danagibbsmd.com/ for more information.


Thank you so much for listening! Tune in on the next episode.


The medical information provided in this episode is intended for informational purposes only and should not be construed as medical advice. Always consult a qualified healthcare provider regarding any medical questions or concerns.

Transcript

0:01

Welcome to episode 55. You know there are a lot of posts with wild health advice out there on social media. Since I started podcasting about thyroid, I seem to get more than my fair share of those in my feed. So, a social media thyroid advocate recently polled her own followers about atrial fibrillation and high-dose T3. Looked like she was fishing for a confirmation of a pet theory of hers that low T3 causes AFib and that driving TSH very low with high doses of T3 will fix that. Oh, I have so many questions. So today, on the podcast, we're gonna look at the heart effects of thyroid hormones, both low and high. Let's get into it. You're listening to the Beyond the Thyroid podcast. I'm your host, Dr. Dana Gibbs. I'm an ENT surgeon and hormone specialist. For years, I struggled with my own unrecognized thyroid problems before and even after I was regularly performing thyroid surgeries. Then, one day, I learned something that turned my health around and opened my eyes to the limits of mainstream medicine in treating more subtle thyroid abnormalities. I spent the next 20 years fine tuning my hormone expertise in disorders like Hashimoto's disease, perimenopause, and stress related illness. Come join me as I share this new approach to hormones that empowers you to take control of your own thyroid and hormone imbalances. Let's dive in. Hey, welcome back to Beyond the Thyroid. If you are new here, I am so glad to have you. I am Dr. Dana Gibbs. I'm an ENT physician, surgeon, and a thyroid sufferer myself. So I saw a social media post the other day from a well-known thyroid influencer, a self-described thyroid advocate, not a doctor, who advocates for a very unconventional and pretty confrontational towards physicians approach to thyroid care. And in this post, she was polling her group, who has atrial fibrillation, and did it start before or after you started your T3? The answer she seemed to be fishing for was simple, low T3 causes AFib and high dose T3 fixes it. So a lot of the people answering her poll were on very high doses of a T3-containing medication with TSH suppressed, not just a little, but way below normal. And no surprise to me, a bunch of them said, yes, they developed AFib after starting T3. But several of them also said they had AFib before they started the T3. The truth here is a lot more nuanced than the story she's telling. So let's look at the evidence and see what it says about TSH and thyroid hormone levels and heart problems. I read a lot of scientific literature trying to dig out what's actually known about the heart effects of low thyroid levels, high thyroid levels, and T3 in particular So I can answer my real question about this post, which is, is it really okay to ignore a low TSH, particularly when it comes to your heart? So a quick disclaimer, this is educational content, not personalized medical advice, so please work with your own physician before you change any of your treatment. So I already discussed bone loss and the other non-cardiac effects that are signaled by low TSH in episode 22. So if you wanna look at those, go take a look, but today we're just gonna talk about heart. First, let's review how thyroid hormone works. So TSH is a hormone made by your pituitary gland in response to low blood levels of thyroid hormone that's detected in your brain. Your brain writes it, sends it to your thyroid gland, and once it's delivered, its job is done. So TSH is the stimulus to your thyroid gland that more thyroid hormone is needed. TSH doesn't do anything to your heart, your muscle, or any other tissue in your body, and the lower it is, the less signal is being sent to the thyroid When your heart responds to thyroid hormone, it's specifically responding to T3, the active form of thyroid hormone, and only 20% or so of your T3 actually comes straight from your thyroid gland. The other 80% comes from conversion, T4 getting turned into T3 in your body's own tissues, whether that T4 originally came from your thyroid or if it's taken in a pill. So if either of those processes is not happening properly, your heart simply won't see enough active T3, no matter what your thyroid gland is doing. And if there's too much T4, there's a fail-safe mode that T4 gets inactivated to reverse T3 by a specific set of enzymes that ramp up to protect you from that hyperthyroidism. When you take T3 directly, which is what this lady's followers were doing, you skip that conversion step. In some cases, that's actually the right call, especially when someone's conversion is genuinely not working. But it comes with a real safety trade-off. That protection against too much thyroid only exists for the conversion step. There is no equivalent break if T3 is coming straight in from a pill bottle. It can be too much all at once right after a dose, or it can just be too much overall, and either way, nothing in your body is standing between that hormone and your heart. So the TSH ends up being the tell because TSH detects both T4 and T3 in your blood, and TSH is a signal that gets turned down or even off when the brain sees too much active hormone circulating. It reacts pretty quickly, but it does tend to lag the free hormone levels when they're taken as a pill. So why does this even matter? Well, doctors have been taught to be afraid of hyperthyroidism, and that is a legitimate fear. Bad things happen when thyroid hormone runs too high, and I'm not asking anyone to dismiss that. Unfortunately, guidelines-based medicine takes that concern and extrapolates it to cover every suppressed TSH, even one that's only slightly below the reference range, even when the active hormone that's driving that TSH level is perfectly reasonable. And because most testing that's done is TSH only, we often don't know really what the hormone levels are. The response is often to leave a hypothyroid patient chronically undertreated, so no added T3, sometimes on inadequate T4 even, because at least the TSH isn't suppressed then. But What hyperthyroidism does to your heart. Let's start with that. This is well-established, and it has some real bad effects. So true hyperthyroidism causes rapid, irregular heartbeats, including atrial fibrillation, something called widened pulse pressure, high blood pressure, and over time, the heart actually changing shape through ventricular hypertrophy because it's being pushed too hard, all the way up to an increased risk of heart failure and risk of death from something called thyroid storm. So thyroid hormone affects your heart two ways. First, there's a genomic pathway where T3 binds the DNA in your heart cells and turns on the genes for growth and repair, and also for a signaling of something called inotropy, which is the contraction strength of the heart, and chronotropy, that's the speed of the heart activity, and also muscle relaxation. So there's also a non-genomic pathway which more directly affects how heart muscles generate energy and how they contract. So if there's too much thyroid signaling, that is hyperthyroidism, the most common cardiac finding is tachycardia, fast heartbeat, usually sinus tachycardia, but frequently flipping over into the more dangerous atrial fibrillation. Thyroid hormone directly relaxes your blood vessels, largely through a chemical called nitric oxide, which increases. It causes resistance to drop, and so does your blood pressure. Your kidneys will then sense that drop and respond the way they'd respond to any drop in blood pressure with their own hormone cascade that pulls more salt and water back into your bloodstream, which raises your blood volume to push your blood pressure back up. So instead of settling into a calm, low-pressure state, you end up with more volume circulating. And then separately, as a direct effect of thyroid hormone itself, your heart becomes more reactive to norepinephrine, so it's beating harder and faster on top of having more volume to move and less resistance to push against. So that less resistance in the blood vessels gives hyperthyroid patients something called a widened pulse pressure, and that's the difference between the systolic, the top, and the diastolic, the bottom numbers on your blood pressure reading. And that extra pumping increases the production of even more of the kidney chemical called angiotensin, and it's a vicious cycle that can end up with a hyperdynamic, overworked heart and what's called high output heart failure. On top of that, excess thyroid hormone drives new coronary blood vessel growth and enlargement of the heart muscle itself, which sounds kinda good, right? But it actually reduces the volume that your heart is able to pump per beat and creates structural remodeling that causes more irregular heartbeats. So about 6% of hyperthyroid patients present with heart failure as their first sign of thyroid trouble, and the fix is straightforward. You restore the thyroid state, you control the heart rate with beta blockers, and you use diuretics if needed, but this is an emergency when it happens. So what does hypothyroidism do to the heart? This is generally less discussed. Hypothyroidism's heart effects are kind of a mirror image in some ways and just as real, even though they get a lot less airtime. The most consistent finding is diastolic dysfunction. The relaxation and filling stage gets small and sluggish, which means your cardiac output drops, your heart rate slows into what's called bradycardia, and peripheral vascular resistance goes up rather than down, so you don't actually get lower blood pressure. So that combination, lower output, tighter vessels, produces narrow pulse pressure. That's the exact opposite of what we were talking about with hyperthyroidism. And in early stages, this means that a hypothyroid person may not tolerate exercise in the way someone whose heart is able to increase its strength of beats and its heart rate does. In severe, long-standing cases, once again, you get left ventricular hypertrophy. That means heart enlargement, enlarged left atrium and pulmonary hypertension, which is high pressure in the arteries leading to your lungs, and even pericardial effusion, and that's fluid in the sac around your heart that actually can compress your heart. There's also a real mechanism behind why thyroid patients feel unusually terrible on beta blockers. So T3 actually increases the number of beta receptors on heart muscles. It's a direct effect. That's part of why a hyperthyroid heart is so sensitive to adrenaline and noradrenaline. So if you flip that around in a low T3 state, the heart already has fewer of those receptors and is less responsive to the adrenaline-type signaling. If you add a beta blocker on top of that, it blocks those very same receptors, the T3 receptors, and then you're compounding a suppression that's already been happening, which is part of why beta blockers can leave an undertreated hypothyroid patient feeling completely flattened rather than just rate controlled. So here's an aside. It's a genuinely interesting and less known finding that I didn't know, and that's that mitral valve prolapse shows up far more often, up to forty percent in people with autoimmune thyroid disease, both Hashimoto's disease and Graves' disease, than in the general population. And across a bunch of different studies, mitral valve prolapse has been found four to five times more in these autoimmune thyroid diseases than in controls where it's only about 5 to 8%. So what is mitral valve prolapse? Your mitral valve is like a one-way door between the two larger left-sided chambers of your heart. It's built from two flaps that are open and are supposed to snap shut together with every heartbeat. In mitral valve prolapse, those flaps are a little too loose, and so instead of closing tightly, one of them will bulge backwards and let blood leak through backwards. So most people who've had it never even know, and it's usually harmless, but it can cause its own skipped beat feelings and palpitations completely separate from anything your thyroid hormone is doing. And it just happens to show up more often in people with Hashimoto's. It's interesting because this association doesn't track at all with how hypo or hyperthyroid somebody is, or their antibody levels, or how long they've had the disease. Some of this might be a detection artifact because people with thyroid symptoms tend to get more echocardiograms, which finds mitral valve prolapse that might have gone unnoticed. But the association has shown up across multiple independent studies, so it's not nothing. The interesting part of this from the standpoint of my influencer is how many of the people who responded to her poll were actually experiencing the effects of mitral valve prolapse and not AFib. Had the people who responded been formally diagnosed? No way to tell. They are two different diagnoses with pretty similar symptoms. All right, so now I'm gonna talk about some of the studies specifically about AFib and T3 because here's where it kind of gets, unfortunately, a little bit nuanced and a little bit sketchy. So let's go through population by population what exists in the literature. So euthyroid Hashimoto's being, meaning someone who's been diagnosed with Hashimoto's who isn't on any thyroid medication yet and does not have an abnormal TSH, there is no data on new onset atrial fibrillation. It hasn't been studied. How about subclinical hypothyroidism where your TSH is high in new onset AFib? Well, there's a small, possibly real increase in risk, but it's not a settled finding, and it's only based on the TSH because they didn't measure the T3 levels. And matter of fact, most studies on different thyroid related diseases don't check T3 levels, So how about low T3 specifically in AFib? There was a real consistent signal, but it was only tested in acutely ill or structurally diseased hearts, people recovering from open heart bypass surgery, people with hypertrophic cardiomyopathy, people who are already being treated for AFib with an ablation. Nobody had really looked at this otherwise healthy outpatient for low T3, but there is a consistent signal with low T3 in these very, very sick people. How about with stents or other less invasive heart issues or procedures? There's no thyroid specific data at all. So new AFib after a stent is driven by age and heart size, not thyroid status. So How about newly diagnosed untreated hypothyroidism? This makes the influencers theory a little bit more valid. In people showing up with brand-new atrial fibrillation, subclinical hypothyroidism, which remember doesn't measure T3 at all, but usually shows low normal to low T3 in my clinical experience, turned up four times more than an overactive thyroid did with newly diagnosed AFib. So that pushes back on this mainstream assumption that it's always too much thyroid hormone driving new arrhythmias. A separate small study did find also untreated newly diagnosed hypothyroid patients had measurable abnormalities in electrical recovery markings on their markers, on their EKG that are known risk markers for arrhythmia, though these are just risk markers, not the same as documented AFib. But for palpitations and extra heartbeats specifically, this does not support the theory. So first, people with subclinical hypothyroidism don't report any more palpitations than people with completely normal thyroid function. So having a low functioning thyroid doesn't on its own make someone more likely to feel their heart skip or flutter. Second, and this is the part that actually surprised me, when researchers put hypothyroid patients on a heart monitor, found their real measurable extra heartbeats, and then treated them with levothyroxine, the extra beats didn't go away. If anything, they got worse in some of the patients, not all. So being hypothyroid didn't cause more irregular heartbeats than normal, and treating with T4 didn't get rid of the abnormalities that they found. Whatever was driving them, it's not simply low thyroid hormone. So that speaks against this lady's theory. So why does that not mean exactly what it looks like it means? So at first glance, that last point, treatment not fixing benign extra beats, looks like evidence against a low T3 mechanism for heart problems. But here's the catch. Starting levothyroxine does not reliably restore T3 to what a normal thyroid gland would produce. There is large-scale study data on this. Levothyroxine patients who are treated run a fifteen to twenty percent lower T3 to T4 ratio than people who are normal controls, even once their TSH is set to look perfectly normal. And about 15% of those treated patients can't get their T3 into the normal range at all on levothyroxine, no matter how high the dose goes. So when the study finds that the treatment didn't remove the irregular heartbeats, that's not necessarily proof that the T3 didn't matter. It just proves my point that levothyroxine alone doesn't fix underlying T3 problems in the first place. All right. After all that research, here's what we still don't know at all. What level of low T3 actually causes AFib or any other arrhythmia or any thyroid symptom at all? Is it anything in the lower half of the normal range the way this particular influencer seems to assume? Nobody knows. Nobody has actually studied it. It's a genuine data-free zone, to borrow a phrase from my friend and colleague, Dr. Rachel Rubin the studies we do have all come from acutely ill or structurally diseased hearts, not from otherwise healthy outpatients with T3 sitting in the lower normal range. So when somebody tells you with total confidence that a specific number is the threshold, they're not really reporting a finding. They're guessing and stating it's a fact. So what's really going on with that social media poll? If you put it all together, here is my honest read of what the poll data is actually showing. Her followers are running very high doses of T3-containing medication and driving their TSH very low on purpose, ignoring it as just a number. A suppressed TSH from too much thyroid hormone is biochemically one indicator of a medication-caused hyperthyroid state, and a suppressed TSH from overtreatment is a well-established mainstream risk factor for atrial fibrillation and heart failure. That's not fringe. It's not novel. It's exactly why endocrinologists push back against overreplacement and the use of T3. So when her group reports AFib after going on high-dose T3, the far more likely explanation isn't low T3 was secretly the problem all along and high doses fixed it. It's the opposite and much more conventional expectation that pushing TSH artificially low with excess thyroid hormone, regardless of what it is, recreates the same suppressed TSH AFib risk pattern we see with any other cause of hyperthyroidism. So let's back up for a second and recall what TSH actually is. It's that pituitary signal that indicates your body's need for thyroid hormone activity. If it's essentially zero, that means it's sensing too much thyroid hormone is already there, usually. It doesn't specify whether that's coming from T3, from T4, from your thyroid gland, from a pill. It's also really sensitive to transiently high levels of either hormone. So a somewhat low TSH by itself isn't proof of hyperthyroidism if your free T and three four are genuinely within the ideal range on average, not just at a convenient testing moment If neither one is running actually high, then you are not hyperthyroid, whatever your TSH happens to indicate. But that's not what's happening in this poll. The doses she's recommending tend to be beyond anybody's daily physiologic T3 requirement. There's no averaging that down into the normal range. There's also a measurement problem baked into how these communities self-monitor. So T3 has a short half-life. That's known. It's at least less than a day. Some people say it's only about six to eight hours. If somebody tests their T3 first thing in the morning before they take a dose, they're capturing a trough level, the lowest point, even lower than their usual low because most people take their meds at 6:00 AM and the lab doesn't open till 8:00 or 8:30. So this is not their average daily exposure to T3. So somebody on a big dose of T3 can have a dangerously high supraphysiologic peak for hours after each dose, while their trough reading still looks reassuringly normal or even kind of low. I have even seen recommendations for people to skip their afternoon T3 dose the day before the test, which is a deliberate practice to spoof the TSH and make the T3 number look lower than it actually is. That practice creates this confusing and false impression of persistent low T3 layered right on top of what's in reality already an overtreatment problem. So the TSH will tend to rise and look more normal as the apparent T3 level falls if you skip doses. So when you're taking T3, here's a practical check that I use that isn't as easy to fool with the test timing as a single T3 level is. No matter what time of day you take the test, if you compare your total T3 to your reverse T3, this key tool is something I use in my practice, though it's not something that's been validated yet by clinical trials outside the ICU, although there are some studies that are pending. In my clinical experience, this ideal ratio falls somewhere between 10 and 14, with reverse T3 sitting at, at least eight nanograms per deciliter, sometimes higher than that. Because both of these numbers move together in response to things like binding protein changes, this ratio holds fairly steady, unlike your free T level, which can look completely different depending on exactly what time you tested relative to your last dose. That steadiness makes it super useful, and it's much harder to accidentally or conveniently make this number look as- reassuring if you're taking too much T3. So what is the bottom line? Here's where I land on this issue. I find myself genuinely sympathizing with this influencer's concern. Why? Undertreated thyroid hormone is also dangerous to your heart. It's not a safer failure mode. It's the mirror image of the same problem because here's what low T3 actually does to your heart, independent of any dramatic arrhythmias. It leaves you without the energy to exercise, which matters because exercise is one of the most protective things you can do for your cardiovascular system. It worsens insulin resistance. It lowers your basal calorie burn and makes it easier to gain weight and harder to lose it. It shifts your lipid panel in the wrong direction, and over years, it contributes to the slow and unglamorous progression of cardiovascular disease that never makes headlines but is exactly what eventually shows up as a heart attack in some people. So the honest picture is not suppressed TSH is all bad and normal TSH is all safe. It's both directions carry real cardiac risk, and the size of that risk depends on whether your actual thyroid hormone levels, not just your TSH, are balanced properly. So these are my own clinical conclusions, and they're backed up by other clinical studies because a large subset of people with thyroid disease genuinely do feel better and function better with T3 in their regimen. And a low-end TSH doesn't have to mean hyperthyroidism. But to avoid potentially serious and permanent heart damage, T3 has to be balanced, not maximized. That means drawing all five labs together, the TSH, the free T4, the free T3, total and reverse T3, drawn with proper timing, exactly between doses, not a random trough level or not the morning after skipping a dose. And if your TSH is below the lower limit of the range, it's a real signal that you need to get more of those different labs This kind of individualized multi-marker optimization is not how mainstream thyroid studies are designed, and it's not how mainstream guidelines-based treatment is done. Most of the literature we just walked through is built around TSH as the single marker in large population cohorts, not individualized care. That's a real limitation of the evidence that's available to us Some practical takeaways here. Suppressed TSH is not just a number that we can ignore. Whether it comes from Graves' disease or a nodule or over-treatment with thyroid hormone, it's a recognized risk factor for cardiac disease, particularly for AFib. If you're on a T3-containing medication, you must test it with proper timing. Timing and the full lab set I use is discussed in a lot of detail in episode 10 and some of the others. If you have palpitations and Hashimoto's, it's reasonable to ask your doctor about getting a cardiac workup, including an echocardiogram along with your thyroid labs because autoimmune thyroiditis is an independent risk factor for mitral valve prolapse and other heart issues regardless of your TSH level. Don't assume that extra palpitations or extra heartbeats are gonna resolve automatically with taking thyroid hormone. The evidence does not support that, and persistent symptoms deserve their own workup. Finally, your heart is genuinely sensitive to thyroid hormone in both directions. Too much or too little carry real risks, just different ways. So the final answer to, is it really okay to ignore a low TSH, is no. Not because low T3 by itself has been proven to cause AFib in otherwise healthy patients, but because thyroid dysfunction, however you get there, high or low, is a recognized marker of cardiac risk, and balance, not maximization, is our goal. At the same time, balance is what gets you back your energy and the focus you used to have. So as we close today, you may be wondering, how can I go from knowing in theory what ideal labs look like to actually moving mine in the right direction so I can regain my energy and mental clarity? Most of my clients come to me exhausted and foggy, forgetting things mid-sentence, feeling like they're losing their edge at work, and hearing, Your labs are normal," when nothing about how they feel is normal. That's why I'm building my new live signature group program, the Thyroid Clarity Checkup, to make the system I use every day with my one-on-one clients accessible to more people. The checkup will take you all the way from getting the exact right labs to having the tools to actually take charge of your own metabolic health. Because thyroid disease may be a lifelong journey, but it should be a footnote, not a defining feature of your life. So if this sounds like something you need, check out danagibbsmd.com/checkup and sign up to get on the priority notification list. Seats are gonna be limited, but if you're on that list, you'll be first to know when I open up the next round. Have a fabulous week, and I will talk to you again soon. Thank you for listening to this episode of Beyond the Thyroid. If you found this information valuable, it would mean so much to me to take a few seconds and give the podcast a five star review. It helps other people who need this information find the show and it's really easy. Just search and click on the name of the show, Beyond the Thyroid, and scroll to the bottom to ratings and reviews. I truly do read and appreciate. Remember, when it comes to hormones, there will always be more to discover, so follow the show so you get the next episode as soon as it's released. And if you or someone you care about needs a caring doctor to help figure out how to heal hormone problems that other doctors have dismissed, check out my website at www. danagibbsmd. com. And if you're not a physician, please keep in mind, while I'm a doctor, I'm not your doctor. The content of this podcast is my opinion and it's for educational and entertainment purposes only. This is not meant to be individual medical advice and you should consult your own physician for any medical issues or diagnoses that you may have. I look forward to continuing this journey with you beyond the thyroid.