Thyroid Health Updates: Treating Hypothyroid, The Gut, & More

Intro:

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Dr Ruscio, DC:

Hey everyone. Welcome back to Dr. Ruscio, DC Radio. This is Dr. Ruscio, DC and today let’s discuss some updates in thyroid health. As you know, we monitor the literature fairly fervidly and I select some studies on an ongoing basis that I feel like are the most relevant. And I wanted to discuss a number of those as they pertain to thyroid with you today. So let’s jump in.

Dr Ruscio, DC:

This first study looked at what organ antibodies are most associated with thyroid disease. And you’ve probably heard the backstory on this, that when an individual has one autoimmune condition they are at risk for others. Now, that being said, one of my quarrels here has always been the fact that educators/gurus, they don’t always do a good job of saying, “yes, that is true, but your association is XYZ percent.” And some of this likely just comes from the human nature observation that the extremes tend to “sell.” And the people who kind of take that more extreme narrative or position will probably do better with selling books and with working for supplement companies as seminar educators and what have you. And that same thing seems to permeate in politics and in a lot of areas. But I think we are having this conversation because you’re looking for not the heretical, absolutest view. But what are some of the nuances, so that you can make and have an assignment of your risk and not just understand “I am at risk” without knowing, “well, is it 1% or is it 30%?” Because this makes a big difference.

Dr Ruscio, DC:

So they looked at 1500 patients with autoimmune thyroid disease and they found the most common antibodies that were associated with this were parietal cell antibodies at 7%. And the parietal cells are in the lining of your stomach and they help you with the release of hydrochloric acid. And we discussed this on the podcast in the past, that this is the most highly associated auto-antibody (at least to my knowledge and we have somewhat thoroughly fact-checked this). So 7%, this is lower on the estimates. I think I’ve heard up to 30% in some of the studies, but it’s important to mention that the highest finding on one study does not mean that’s been across the board. So in this case, I guess, good news, 7% for the parietal cell antibodies.

Dr Ruscio, DC:

And second to that was the glutamic acid decarboxylase, which is found in the pancreas. And these antibodies can call something that, at least a few years ago, was labeled as “diabetes 1.5” or LADA (latent autoimmune diabetes in adulthood), where someone starts looking like they have type one diabetes but in adulthood. And that’s at 2.8%. Quite rare. I tested for this for a few years and it was so rare of a finding that didn’t really seem to be practical in clinical practice.

Dr Ruscio, DC:

Now I want to flag something else here—that there’s these TG, and more specifically these anti-mitochondrial antibodies. The TTG is the tissue transglutaminase and the mitochondrial antibodies are mitochondrial. They were found in less than 1% of individuals. The reason why I think this is so important to flag is I’ve seen more autoantibody labs popping up. And at least from what I’ve seen, people tend to have a whole bunch of things positive. Yet when you look at the prevalence data, it seems to be far less when you’re looking at labs that are used in a research setting, which presumably are validated, then you do see in these direct-to-consumer, non-regulated or non-validated labs. And the reason why this is so destructive is it puts a lot of fear in people’s heads. Now I’ll be the first to endorse newer tests as they become validated, but it’s really the validation that is crucially important.

Dr Ruscio, DC:

Because said flatly, plainly, if someone goes in to see a provider, and they’re probably well intentioned, and they run an autoantibody panel, now the person, every time they have a symptom of, let’s say, fatigue or brain fog or joint pain is thinking, “oh my God, it’s mitochondrial autoimmune causing the fatigue”, “it’s neurological or brain autoimmunity causing the brain fog” and “its joint autoimmunity causing the joint pain.” And that’s almost for certain not the case when looking at some of the data that tries to quantify what your level of risk is. Whereas, we know that when people have IBS, they tend to have fatigue and brain fog. And so there’s no need to put in their head, “you’ve had this smoldering fire of autoimmunity.” Now yes, there are certain auto conditions that we want to diagnose and treat directly.

Dr Ruscio, DC:

But gosh, we just have to be you careful with how we’re framing some of this narrative around autoantibodies. So sorry for the little bit of editorializing there. But I’ve seen quite a number of patients come in very distraught from these labs. And we’ve quickly checked if any of these labs have had validity and they haven’t. And most of them have had some sketchy funding or ties to either gurus or supplement companies or the like. So [I] just want to flag that for you so that you hopefully can prevent going down this road. Okay.

Dr Ruscio, DC:

Now what about some lighter news? Another study looked at the effectiveness of ginger supplementation in relieving persistent hypothyroid symptoms in those who had hypothyroidism. This is a good study. It was a randomized, double-blinded, placebo-control trial. And in 60 hypothyroid patients who are on thyroid hormone replacement therapy but still had some persistent symptoms, they were given either ginger or placebo. And I should mention, they had normal TSH. So the thyroid hormone treatment was successful in normalizing the TSH, but they still had symptoms.

Dr Ruscio, DC:

Debate alert. You know, this is something that some will say, “well, you’ve got to get the levels at this perfect upper end for the T4 and lower end for the TSH.” I have not found that to be true. And our exhaustive review of the literature has not substantiated those claims. So let’s see what this study finds. They found that after 30 days in the ginger group, they had improved total symptoms, decreased body weight, a further improved TSH, lower, fasting glucose, improved triglycerides, and improved cholesterol.

Dr Ruscio, DC:

So it seems that a simple herbal intervention remedied many of the symptoms and/or lab findings that were thought to be attributed to “hypothyroidism.” And a few other details here I want to kind of parse out, outside of some of the metabolic. If you look at the symptoms specifically, you see again, improvements in weight gain, but also improvements in cold tolerance, improvements in constipation, improvements in dry skin, appetite, memory loss, concentration—interestingly, there was an improvement in feeling giddy, I’m not sure who would be upset about feeling giddy or maybe they meant they felt more giddy—but also improvements in dizziness.

Dr Ruscio, DC:

So a number of symptoms improved that I think are important to clarify and disclose. Now, there were also no improvements in hair loss, nail fragility, hearing, hoarseness of speech, depression, or feeling down. So it wasn’t a cure-all, but look at all these improvements associated with just ginger supplementation for 30 days. I feel this to be fairly powerful support for how careful we have to be not to go to this exercise of fine tuning the thyroid medication when patients are in the normal range and still having symptoms. Now, again, there’s debate about what’s the normal range. And it’s my fairly confident belief, because we have put a lot of time into checking this, that the standard ranges are sufficient for the vast, vast, vast majority of people.

Dr Ruscio, DC:

You don’t have to try to drive someone down into the lower half of the TSH range or the upper half of the free T4 range. Now we do leave a time and a place open for trying a combination of T4 with T3 after someone’s gone through gut health interventions. But we want to go through the gut health interventions first, before fine tuning their dose beyond getting someone into the standard ranges or their medication—meaning going to T4 plus T3 combination therapy, things like armor or Nature Throid or adding Cytomel to levothyroxine.

Dr Ruscio, DC:

And this data point of just using ginger. Gosh, you could save someone from having to go on different medications and doing follow up blood work and the whole song and a dance with weight gain, cold intolerance, constipation, dry skin, appetite loss, memory loss, concentration, something to do with gidyness, and improve dizziness. So just want to make sure that people are aware of this so that they don’t go down that path. That seems to be very unfruitful and make sure they say to their provider, “okay, like I’m in the normal range, I understand that you’re jazzed about Cytomel […] but how about I get my house in order here with some gut health, diet and lifestyle interventions first, and then we can circle back to trying the more, exotic or involved method of fine tuning the thyroid.”

Dr Ruscio, DC:

So just be careful not to fall into what can be kind of an emotional ploy. You know, “you’re not feeling well, we got to fine tune the thyroid.” That doesn’t seem to be the approach that works for the majority of individuals. And we see a sizable number of them at the clinic that have been harmed. And we are usually able to clean up that mess surprisingly quickly just by doing the things in the right order of operations, starting with the gut first, before fine tuning of the thyroid. And I’ll carefully distinguish, if someone needs the medication, they should be on it. But the main point here is not to fine tune the medication beyond getting them in the normal range if they’re still having symptoms, but instead go to diet, lifestyle, and gut health.

Dr Ruscio, DC:

The next study looked at lipid profiles in mild subclinical hypothyroidism. And this was a meta-analysis looking at 35 studies in those who had mild subclinical hypothyroidism. So this is a TSH underneath 10. And this is important to clarify, that you can have subclinical hypothyroidism and be just fine. Meaning you can have a TSH above the normal range cutoff—4.5—and still be fine. And they found that having this mild subclinical hypothyroidism was associated with poor cardio metabolic markers; a slight elevation of total cholesterol (12 points), a slight increase of LDL cholesterol (11 points), higher triglycerides (19 points), and lower HDL (1.8 points).

Dr Ruscio, DC:

So there’s this association. And I leave the door open for, potentially, a trial on thyroid hormone in someone who is not hypothyroid—who is the subclinical and has aberrancies in their lipid profile. But I believe (and I’d have to double check this), I believe that a meta-analysis has been performed on using thyroid hormone replacement in this group of individuals and they did not find any reduction either in cardiovascular disease risk or improvements in their cardiovascular profiles.

Dr Ruscio, DC:

Okay. So I couldn’t help myself. I popped over to PubMed and I found a 2020 meta-analysis that examined what impact treatment of both overt and frank hypothyroidism—or I’m sorry, overt and subclinical hypothyroidism—has on lipids. And they found a significant impact when treating hypothyroidism. They also did find a significant impact when treating subclinical hypothyroidism. But the magnitude there was smaller. So, they don’t seem to be too hot to trot on the treatment of subclinical hypothyroidism with thyroid hormone in attempt to normalize lipid profiles.

Dr Ruscio, DC:

So this is why I leave the door open as maybe an end-phase measure for someone who has imbalances in their lipid profile, that’s been non-responsive to diet, exercise, and other interventions. But we also have to weigh that against the fact that giving someone hormone who may not fully need it can potentially cause things like fatigue and insomnia. So I think this is an area that’s still being mapped out. If I’m reading in between the lines here on these authors non-committal conclusion, which was essentially there was a significant improvement on lipids when treating with thyroid hormone those who are hypothyroid, but a much smaller magnitude when you were treating those with subclinical hypothyroid. So do with that what you will. Sorry to get in the weeds here but this is something I’m quite interested in. I’m always trying to find where the truth lies.

Dr Ruscio, DC:

So continuing over to another study: effects of chronic suppression or over-suppression of TSH on psychological symptoms and sleep quality in patients with thyroid cancer. So essentially the context here is people who have had part of their thyroid gland removed due to having cancer—part or all—and then require thyroid hormone. There’s two different ways you can approach the thyroid hormone supplementation as I understand it in this setting. Which is, get their TSH down to normal or suppress it really quite low.

Dr Ruscio, DC:

And what they found in this group—of about 79 controls versus 190 of those on the medication for cancer suppression—that compared to healthy controls, those on suppressive therapy had more symptoms and worse sleep. And those with lower TSH had higher anxiety. So this is in the model to clarify of over-suppression. But it does at least tacitly reinforce some of what we were just covering, which is we want to be careful not to drive TSH too low period. And that using thyroid hormone isn’t without any risk.

Dr Ruscio, DC:

The next study looked at the effect of vitamin D on thyroid function and autoimmunity markers in patients with Hashimoto’s. And this was a meta-analysis of six trials looking at about 300 Hashimoto’s patients. And vitamin D supplementation resulted in a reduction of TPO antibodies by 158 points with no change in TSH, free T4, or free T3. So this might be the best data point available looking at: “can vitamin D treat or improve thyroid autoimmunity?” And what we see is: Yes. And it’s important to clarify that the 158 point reduction is something, but that’s not huge. And so another reason I think, with vitamin D in particular, we want to be careful to avoid the narrative of, “you have Hashimoto’s, make sure you take vitamin D.” I mean, I agree. But I think we need to be careful with how much of a, “you must do this” or “this is essential for Hashimotos” we portray this. And just to understand that this is something that can be helpful, but it’s not necessarily the end-all be-all.

Dr Ruscio, DC:

And here is another study looking at this entity of subclinical hypothyroidism. And to give this entity credit for when a clinician may want to consider treating subclinical hypothyroidism, because there is debate regarding when is the best time to intervene when someone has this mildly elevated TSH. And we discussed on the podcast in the past that in those who are very young, that’s going to make sense. And this is because there’s a natural drift upward in TSH with age. And also in those who are infertile. The other item here, I think we’re going to start adding to our perspective, is in those with a history of cardiovascular disease and a lipid profile that puts them at increased risk. Because this next study, albeit small, 54 patients and 18 of those had subclinical hypothyroidism.

Dr Ruscio, DC:

Those with subclinical hypothyroidism did see an improvement in what’s known as carotid intima medial thickness (which is essentially a measure of cardiovascular health) after they went on thyroid hormone. This was seen in those with frank or overt hypothyroidism, but it was also seen in those with subclinical. So I think the take home here is we’re trying to build this into a framework. Those who have mildly elevated TSH. When does it make sense? When is it heresy? Right? So those who are very young, those who are infertile, and potentially those with cardiovascular disease. And not for those with say unresponsive fatigue and depression. And certainly not those who have normal TSH. But you want to see the TSH, let’s say below 2.5 and this person has 3.1. So there’s some you know, emerging guidelines for how to be thinking about the appropriate and responsible use of thyroid hormone when someone is not frankly hypothyroid and they have this subclinical hypothyroidism.

Dr Ruscio, DC:

And here’s another very interesting study: elevated levels of circulating markers of leaky gut were associated with Grave’s disease. And this study looked at 91 patients who had graves versus 44 healthy controls and they found that those with graves had higher levels of intestinal permeability. And remember Graves is the opposite of Hashimoto’s or hypothyroidism. It’s where someone has a low TSH and high levels of free T4 and free T3. Pathologically so.

Dr Ruscio, DC:

And it’s not surprising that these individuals may have leaky gut because too much thyroid hormone is stressful in the body. It causes a high heart rate. It can cause fatigue. It can cause insomnia, sweating. Now to balance out how quickly you might be thinking, “oh my goodness, if I have subclinical hypothyroid and I had a high cholesterol test one time” or “I’ve had some mildly elevated lipids, should I go out and get on medication?”

Dr Ruscio, DC:

Here’s another study to kind of counter veil that. This study was looking at: how transient is this subclinical hypothyroidism, this mildly elevated TSH (a TSH that’s between 4.5 and 10, or maybe 4.5 and 7). The cutoff or when we do declare this is no longer subclinical and it’s something that should be really addressed is somewhere between a TSH of 7 and 10. Now in this study, they looked at 431 healthy controls versus 225 patients with subclinical hypothyroidism. No treatment was given to either group. Here’s how this played out: at a six month follow up 12% became frankly hypothyroid, 13% stayed subclinical hypothyroid, and 73% went back to euthyroid or normal thyroid. This is one of the reasons why I tend to lean a little bit more cautious with subclinical hypothyroidism because—as we’ve discussed in the past or in the past, the majority of these cases, at least some evidence is finding that and this is one case in point shows us that—subclinical hypothyroidism will go back to normal on time or in time without any other intervention.

Dr Ruscio, DC:

Hi, everyone. If you are in need of help, we have a number of resources for you. “Healthy Gut, Healthy You”, my book and your complete self-help guide to healing your gut. If you’re not a do-it-yourselfer there is the clinic—the Ruscio Institute for Functional Health—and our growing clinical and supporting research team will be happy to help you. We do offer monthly support calls for our patients where I answer questions and help them along their path, health coaching support calls every other week, and also we offer health coaching independent of the clinic for those perhaps reading the book and/or looking for guidance with diet, supplementation, etc. There’s also the store that has our Elemental Diet line, our probiotics, and other gut health and health-supportive supplements. And for clinicians, there is our FFHR—the Future of Functional Health Review—database which contains case studies from our clinic, research reviews, and practice guidelines. Visit DrRuscio.com/resources to learn more.

Dr Ruscio, DC:

Okay. And coming back to subclinical hypothyroidism. There was a study published looking at, “well, can we get any more granularity on when TSH is elevated above 4.5 in elderly people (let’s say over 65/70)?” So you get a better sense for…well, we know that as you get older TSH naturally drifts up. So can we reappraise or be a bit more definitive in when we—or where we—draw the line for saying, “okay, the TSH is now so high that medication should be used?”

Dr Ruscio, DC:

And in this study, interestingly, they actually found as an aside, iodine excess was a notable risk factor for hypothyroidism. So be careful not to over supplement with a high dose iodine supplement for a long period of time. This is one practice in the field that I think needs to be reexamined, of course. We’ve talked about that before, but just to echo that one finding from this paper.

Dr Ruscio, DC:

And that for those who are over 70, a TSH of anywhere from 6-10 may not require treatment. So there’s this range of 7-10, where it’s debatable in terms of you should initiate treatment. Over 7 in someone who’s, let’s say, 40? Perhaps. 10 in someone who’s 65/70? Perhaps not. I think this is a good example of when an entire context should be taken into consideration. And also consider a trial on thyroid hormone medication objectively with setting a neutral expectation and see if you can connect that to a clear symptomatic signal of improvement. So we’d want to do this mid-to-end phase, and presumably get out of the way diet, lifestyle, and gut health foundational work.

Dr Ruscio, DC:

So if someone is like, “eh, you know, it’s my fatigue and I think this is the thing that’s prompting the thyroid hormone,” or maybe you as a clinician are thinking that, you now have a clear and consistent baseline. And you’re sure that the sleep, or I’m sorry that something like sleep, isn’t driving fatigue or IBS or what have you. So if we get all these things right, you should have someone who has minimal symptomatic noise and you only have one or a couple symptoms left, let’s say fatigue and elevations of cholesterol. That is a good time to do a precise trial with a neutral expectation so that you don’t placebo. And that I think is the best way, in total, to handle this. Sorry if this is getting a little bit detailed, but the subclinical hypothyroidism it is a bit in the gray.

Dr Ruscio, DC:

And I should also mention that while the use of thyroid hormone medication in subclinical hypothyroidism has been shown to lead to a small improvement in cholesterol levels (and that’s true, we want to report on that accurately and objectively), I think it’s also important to juxtapose that with: if you’re going to get a small improvement in cholesterol levels, might there be other things consider first that are non-hormone/non-drug? While being open on the one hand, I just want to make sure to weave in [that] there may be some other things that could get you that same level,—that minimal level of improvement—that don’t require putting someone on thyroid medication, presumably lifelong. So that’s, you know, the other side of the toggle here, we want to be considering. Okay.

Dr Ruscio, DC:

And this is a great study; they looked at, essentially, a liquid form of levothyroxin (I’m not sure if this was tyrosine per se or another similar form) in an individual. So this was a single case study of a 51-year-old female with longstanding Hashimoto’s and multiple food and medication sensitivities. They worked her up. Amongst other findings, they found that she had SIBO. And in this individual who was having a hard time with an inability to control her TSH, the use of an oral or liquid oral thyroid medication led to a 7.4 TSH down to a 1.5 after six weeks.

Dr Ruscio, DC:

And then, check this out, improved even further down to 0.56, so almost kind of looked like she was being overdosed. After treatment with Rifaximin—indicating that when addressing the SIBO—thyroid hormone absorption improved. So this was just one case study, but it really powerfully exemplifies what we discussed in another study—wherein the use of probiotic supplementation improved thyroid hormone absorption and allowed people to have better TSH with a lower dose of thyroid—that the gut can be one of these things that leads one and makes it challenging for someone to get and find the appropriate dose of their medication.

Dr Ruscio, DC:

And, you know, on that note, I’m actually quite excited to share/announce that we are working on a gut-thyroid case series wherein we’ve drawn up six cases from our clinic where patients have had similar stories to this. They’ve either been misdiagnosed as hypothyroid, on medication, having symptoms, struggling…We kind of undiagnosed them, took care of their gut, resolved their symptoms. Or correctly diagnosed, on thyroid hormone medication, suffering, work them up, fix their gut, resolve their symptoms.

Dr Ruscio, DC:

And we’re going to publish this in a peer-reviewed journal. And I’m quite excited about it. And this is actually going to be one of the references that we’ll include in terms of like, “Hey, we’re not the only people seeing this.” We’ll reference this case study because there was one case, that was a beautiful case, wherein one [after] a medication, another medication, another medication, [and] a combination of medications, this poor gal couldn’t get resolution symptomatically or normalization of her TSH.

Dr Ruscio, DC:

And then we treated her gut and within weeks symptoms dramatically improve and TSH finally normalizes. Which is one of the reasons why I’ve harped on how important it is to have the appropriate order through which we work. Sorry, there’s an ambulance going by. I’m not sure if you can hear that.

Dr Ruscio, DC:

So let’s move on to another paper. And this was a narrative review. And this is important, in this narrative review of subclinical hypothyroidism in those who are over 65 (now remember again, subclinical hypothyroidism is a mild elevation of TSH between 4.5-10) the studies reviewed found no increased risk of poor outcomes in this group. So when people who are over 65, who had subclinical hypothyroidism, there was no increased risk of cardiovascular disease or cognitive disease if the TSH was between 4.5 and 7.

Dr Ruscio, DC:

And additional data that in these individuals, another kind of cohort, with symptoms of hypothyroidism and cardiac and bone health issues, they were not improved after levothyroxin treatment. And they quote, “this data suggests that treatment with levothyroxin should be considered for TSH concentrations that are persistently above seven or higher and to not initiate treatment with a TSH concentration that is less than seven.” So, again, this is in those who are over 65, so it’s important to contextualize. But I hope if no other point is kind of registering here, it’s that giving someone thyroid hormone, let’s say because their TSH is 4.4 and they have some symptoms and their provider says, “well, you know, this is sluggish thyroid, you should go on medication,” I hope you’re seeing [that] these studies are a part of the evidentiary basis from which I (and we at the clinic) draw our opinion to be much more timid with the use of thyroid hormone.

Dr Ruscio, DC:

So anyway, there’s a lot there to unpack. I know a podcast like this is a little bit more nuanced than perhaps the probiotic or gut health updates. Your feedback would be appreciated, if I’m going too deep and losing people. Please let me know. I’ll also work on trying to summate some of this and maybe have a simple narrative I can frame these things with to make this all stand out a little bit more. But nonetheless, there are a number of updates on thyroid health and I hope you found that helpful. And we will talk to you guys next time. Take care.

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Thank you for listening to Dr. Ruscio, DC Radio today. Check us out on iTunes and leave a review. Visit DrRuscio.com to ask a question for an upcoming podcast, post comments for today’s show, and sign up to receive weekly updates. That’s DRRUSCIO.com.

 

• Screening of Organ-Specific Autoantibodies in a Large Cohort of Patients with Autoimmune Thyroid Diseases
  • 1,502 patients w/ autoimmune thyroid disease
  • Most common autoantibodies other than thyroid antibodies were:
    • 7% Parietal cell antibodies – 7%
    • 2.8% anti-glutamic acid decarboxylase (found in brain and pancreas)
  • tTg-IgA and anti-mitochondrial antibodies found <1%
  • Commentary: There is a notable rate of parietal cell antibodies in those w/ autoimmune thyroid disease. 

 

• Efficacy of Ginger Supplementation in Relieving Persistent Hypothyroid Symptoms in Patients with Controlled Primary Hypothyroidism: A Pilot Randomized, Double-Blind, Placebo-Controlled Clinical Trial
  • 60 hypothyroid patients on thyroid replacement therapy but with persistent symptoms despite normal TSH
  • Randomized to placebo or ginger supplementation (500 mg BID)
  • After 30 days, the ginger group had:
    • Improved total symptom score (8.6 vs 15.8)
    • Decreased body weight (-2.4 vs +1 kg)
    • Improved TSH (-0.9 vs +0.95)
    • Lower fasting glucose (-11.6 vs +7)
    • Improved triglycerides (-57 vs +40)
    • Improved total cholesterol (-19 vs +10)
  • improvements in the mean scores of the weight gain, cold intolerance, constipation, dry skin, appetite, memory loss, concentration disturbance, and feeling giddy or dizzy domains (P < 0.001). 
  • However, no significant improvements were observed in hair loss, nail fragility, hearing, hoarseness, speech, and depression or feeling down (P > 0.05). 
  • Commentary: Ginger supplementation may improve some hypothyroid symptoms and lead to improvement in some metabolic markers.

 

• Lipid profile in mild subclinical hypothyroidism: systematic review and meta-analysis
  • 35 studies
  • Mild subclinical hypothyroidism (TSH <10) was associated with poorer cardiometabolic markers:
    • Total Cholesterol (+12.8 mg/dL)
    • LDL-C (+11 mg/dL)
    • Triglycerides (+19.3 mg/dL)
    • HDL-C (-1.8 mg/dL)
  • No difference in ApoB
  • Commentary: Mild subclinical hypothyroidism is associated with a poorer lipid profile. 

 

• Effects of Chronic Suppression or Oversuppression of Thyroid-Stimulating Hormone on Psychological Symptoms and Sleep Quality in Patients with Differentiated Thyroid Cancer
  • Prospective study of 79 healthy controls, 191 patients w/ thyroid cancer on suppressive thyroid medication (thyroid medication meant to suppress TSH below reference range)
  • Compared to healthy controls, those on thyroid suppressive therapy had:
    • More symptoms
    • Worse sleep
  • Those w/ lower TSH had higher anxiety scores
  • Commentary: Over-suppressing TSH is associated with worse sleep and more anxiety. 

 

• Effects of vitamin D treatment on thyroid function and autoimmunity markers in patients with Hashimoto’s thyroiditis-A meta-analysis of randomized controlled trials
  • 6 RCTs, 258 participants w/ Hashimoto’s
  • Vitamin D supplementation resulted in:
    • Reduced TPO Abs (-158.2)
    • No difference in TSH, fT4, fT3
  • Commentary: Another data point suggesting a benefit of Vitamin D for thyroid autoimmunity. 

 

• Carotid Intima-Media Thickness in Patients with Subclinical Hypothyroidism: A Prospective Controlled Study
  • 54 total participants: 
    • 18 with subclinical hypothyroidism (SCH) 
      •  median TSH 6.15 µIU/ml
    • 18 with overt hypothyroidism (OH)
    • 18 healthy controls 
  • Carotid Intima-Media thickness (CIMT) measured in all participants
  • Levothyroxine given to those w/ SCH
  • Higher CIMT in SCH compared to healthy controls
  • There was a decrease CIMT after levothyroxine treatment in those w/ SCH
  • Commentary: Even w/ a TSH <10, those w/ SCH had:
    • A higher CIMT
    • Reduced CIMT scores after starting levothyroxine
    • This is why research suggests considering levothyroxine in those w/ SCH who have a TSH between 7-10 and are younger. 

 

• Elevated Levels of Circulating Biomarkers Related to Leaky Gut Syndrome and Bacterial Translocation Are Associated With Graves’ Disease
  • 91 patients w/ Graves’ Disease, 44 healthy controls
  • Measured markers of intestinal permeability
  • Graves’ Disease patients had higher levels of intestinal permeability as compared to healthy controls
  • Higher gut permeability levels were associated with:
    • Higher antibody levels
    • Lower TSH, higher fT4/fT3
    • More symptoms
  • Commentary: Another data point for the gut-thyroid connection.

 

• Transient high thyroid stimulating hormone and hypothyroidism incidence during follow up of subclinical hypothyroidism
  • 431 healthy control participants, 225 patients with subclinical hypothyroidism (SCH) 
  • No treatment was given to either groups
  • At a 6 month followup:
    • 12.2% developed frank hypothyroidism
    • 13.4% stayed SCH
    • 73.8% became euthyroid
  • TPO antibodies and a TSH above 6.9 mIU/L was associated with a higher risk of developing overt hypothyroidism.
  • Commentary: The vast majority of those who were SCH became euthyroid WITHOUT treatment. This is an elegant study showing us that many times SCH will correct on it’s own. Also addressing gut health will most likely improve the rate of those who become euthyroid. There is no need to rush treating SCH in the majority of cases. Dr Ruscio and I encourage you to read the featured study from the FFMR+ two episodes ago which lays out a concise set of recommendations of which SCH patients to treat.

 

• Age-specific thyrotropin references decrease over-diagnosis of hypothyroidism in elderly patients in iodine-excessive areas
  • Cross-sectional study of 2,559 participants from iodine-excessive areas and no previous history of thyroid disorders
  • Diagnosed subclinical hypothyroidism (SCH) and overt hypothyroidism (OH) by using both 
    • lab reference ranges (TSH >4.2) and 
    • age-appropriate reference ranges (TSH >11.5 for those >70, 
  • Iodine excess was a novel risk factor for hypothyroidism
    • especially urinary iodine concentrations  ≥ 700 µg/L (OR = 2.5) 
  • Prevalence of hypothyroidism for those >70:
    • OH:
      • Lab reference ranges: 2.37%
      • Age-appropriate reference ranges: 1.78%
    • SCH:
      • Lab reference ranges: 29.6%
      • Age-appropriate reference ranges: 2.96%
  • Commentary: 
    • Iodine excess is a risk factor for hypothyroidism
    • TSH naturally rises with age. This is a great illustration of how SCH may be OVER-diagnosed in an older population. The prevalence of SCH decreased to 10% of the original rate when using an age-appropriate TSH reference range. For those >70 yo, TSH up to 6-8/10 may NOT need treatment. 

 

• Levothyroxine Sodium Oral Solution Normalizes Thyroid Function in a Patient with Hashimoto’s Disease, Gastritis, Diabetic Gastroparesis, and Small Intestinal Bacterial Overgrowth (SIBO)
  • Case study of a 51 year old female w/ long-standing Hashimoto’s with multiple food and medication sensitivities
  • Presented w/ multitude of symptoms: recurrent hives, dry skin, fatigue, weight gain, intermittent constipation and diarrhea, cold intolerance, brain fog
  • Over course of 6 months, TSH was not well controlled on multiple medications (general T4, brand T4, combined T4/T3)
  • Developed projectile vomiting, weight loss,10-20 bowel movements per day
  • Breath test, endoscopy and scintigraphy revealed SIBO, gastritis, gastroparesis, and hiatal hernia
  • Switched to liquid T4
    • TSH decreased from 7.42 to 1.55 after 6 weeks
  • TSH decreased further to 0.56 after being treated w/ Rifaximin
  • Commentary: This case study exemplifies a few things:
    • The gut-thyroid connection: there remains an association between hypothyroidism, SIBO, and gastroparesis symptoms
    • Consider liquid T4 therapy before combined T4/T3: this case study supports the use of our clinical thyroid algorithm of considering oral T4 and working on the gut before combined T4/T3 therapy. 
    • Authors note a meta-analysis of 141 patients that showed that patients with suboptimal TSH on tablet T4 significantly improved TSH by switching to a liquid L-T4 formulation at an unchanged dose

• Dr. Ruscio’s, DC Resources