Niki Cleuet - Thyroid & Women's Health Naturopath

Niki Cleuet - Thyroid & Women's Health Naturopath A Perth-based naturopath specialising in thyroid issues, women's health, fertility & pregnancy care You can also find me on Instagram (.cleuet).

In addition to conditions like Hashimoto's disease, hypothyroidism and Graves' disease, my clinical specialties include menstrual irregularities, pregnancy and postpartum care, and hormonal conditions such as amenorrhoea, PCOS and endometriosis. I work at Perth Health & Fertility, where I treat patients across a broad spectrum of health conditions, with a holistic, results-oriented and evidence-informed approach. In addition to being a naturopath and mother, I am also currently completing a Master of Reproductive Medicine. If you would like to book an appointment or to find out more, please contact me by emailing niki.cleuet@gmail.com, or by calling (08) 9285 0998.

It’s been a long time between posts but I’m back with a big one - TSH testing. If you have a thyroid condition, TSH test...
12/08/2024

It’s been a long time between posts but I’m back with a big one - TSH testing. If you have a thyroid condition, TSH testing will be a mainstay of your monitoring (hopefully along with some other important markers!), so make sure you’re testing it right!

Hello everyone, I have been very absent from social media lately so this is a long overdue 'hello' - just a quick update...
28/05/2024

Hello everyone, I have been very absent from social media lately so this is a long overdue 'hello' - just a quick update to say I have added some extra consulting hours in June, so if you have been hoping for an earlier appointment, the additional time slots are now available through the booking feature on my website: www.nikicleuet.com/bookings.

Excitingly, I also have a little something (thyroid-related) on the horizon which I hope to put out in the coming weeks - stay tuned!

If you'd like to book an appointment, please do so by following the prompts below. If you'd like to know more, please get in touch via the Contact page, or call our clinic on (08) 9285 0998. In clinic and online consultations available.

The phases of a menstrual cycle ❄️🌱🌞🍂
24/11/2023

The phases of a menstrual cycle ❄️🌱🌞🍂

Every day in clinic, I work with women experiencing menstrual cycle irregularities - irregular periods, painful periods,...
20/11/2023

Every day in clinic, I work with women experiencing menstrual cycle irregularities - irregular periods, painful periods, missing periods, heavy periods and so on. Making sure we are on the same page when it comes to terminology is essential.

It is estimated the average woman will have somewhere between 400-500 periods in her lifetime. PLEASE do not put up with symptoms like pain, heaviness, clots or irregular bleeds. Help is available and taking the pill is not your only option. There is so much we can do to understand, investigate and manage your symptoms holistically. Periods should come and go without major disruption to your daily life, so if your period is causing you distress, please reach out x

When someone has Hashimoto’s, we typically expect that they will end up with an underactive thyroid. In this case, they ...
18/11/2023

When someone has Hashimoto’s, we typically expect that they will end up with an underactive thyroid. In this case, they are usually prescribed medications like Thyroxine to bring their thyroid results back into range.

Occasionally however, an individual with Hashimoto’s will swing into hyperthyroidism (an overactive thyroid). There can be a few reasons for this - like postpartum thyroiditis or taking too much thyroid hormone - but one lesser known cause is Hash*toxicosis. Hash*toxicosis is an overactive thyroid that occurs as a result of Hashimoto’s, and not due to external factors like medications or pregnancy.

In Hash*toxicosis, the initial autoimmune attack on the thyroid causes destruction of the thyroid follicles, resulting in a passive letdown of thyroid hormones into the bloodstream. The thyroid isn’t MAKING too much thyroid hormone. It is passively RELEASING thyroid hormone as its cells become damaged and release their contents. As a result, we see an increase in thyroid hormone levels, sometimes to the extent of full blown hyperthyroidism. Although this hyperthyroidism is temporary, it can be severe enough in some cases to warrant treatment.

When I first diagnosed with Hashimoto’s, my thyroid antibodies were in the thousands, and instead of being hypothyroid, my TSH was 0.009. I was subclinical hyperthyroid. One month later, my TSH was 5.96. I had swung into hypothyroidism.

My experience followed the typical trajectory expected of Hash*toxicosis: it is often the first step in the progression into Hashimoto’s hypothyroidism, but unless we do bloods at this point, we don’t always catch it happening. After an initial period of hyperthyroidism, most individuals will become temporarily euthyroid (meaning their thyroid levels appear ‘normal’), before finally progressing into hypothyroidism. At this point, the thyroid is no longer able to sustain normal thyroid hormone production due to the autoimmune process.

Just recently I was going through my old blood tests and thought I might share my journey with Hashimoto’s and Graves’ through my results. Is this something you would be interested in? What has your journey with thyroid issues looked like?

Iodine. I spend A LOT of time talking about this nutrient in consultations, not only to my thyroid patients but to my pa...
16/11/2023

Iodine. I spend A LOT of time talking about this nutrient in consultations, not only to my thyroid patients but to my patients with fertility issues, menstrual cycle irregularities and women’s health issues as well. Iodine is a nutrient we require in tiny amounts but it is a BIG PLAYER when it comes to many aspects of our health. Still, it is a Goldilocks nutrient, and both too much and too little can be problematic! What’s been your experience with iodine? x

09/11/2023

Hi everyone,
Many of you know I run Hashimoto’s workshops and am about to release my Hashimoto’s ebook.

I am wondering if there is much interest for a Graves’ disease workshop?

My thyroid workshops usually run for 60-90 minutes and my goal is for everyone to walk away feeing much more across their condition - understanding what it is, how it is managed and how they can play a more active role in managing their thyroid health holistically. If you would be interested in a Graves’ workshop, please let me know and I’ll look at putting one together.

Niki

If you have Graves’ disease, you might have heard of both TRAb and TSI and wondered what the difference is. Hopefully th...
08/11/2023

If you have Graves’ disease, you might have heard of both TRAb and TSI and wondered what the difference is. Hopefully this post will help clarify things for you:

- TRAb or ‘TSH receptor antibodies’ are a type of antibody that bind to the TSH receptors on the thyroid. When they bind to and stimulate this receptor, they trigger the thyroid to make more thyroid hormone, and thus they are typically discussed in the context of Graves’ disease and hyperthyroidism. But did you know, TRAb can also exert a blocking effect on thyroid function, reducing thyroid hormone production and even causing hypothyroidism? For this reason, the term ‘TRAb’ can actually be subcategorised into TSH-receptor STIMULATING antibodies (the type found in Graves’) and TSH receptor BLOCKING antibodies (which can be found in autoimmune HYPOthyroidism). Interestingly, the standard TRAb blood test does not distinguish between whether these antibodies are stimulating or blocking in nature, and the distinction is largely made based on thyroid function (i.e. if the thyroid is overactive, they are presumed to be stimulating and thus characteristic of Graves’).

- In contrast, TSI refers to thyroid stimulating immunoglobulin; a type of antibody that exerts exclusively stimulating effects on the TSH receptor. For this reason, they are specific to Graves’ disease and are known to induce hyperthyroidism.

Please note: As they are assessing different things, TRAb and TSI levels are not interchangeable (even if they use the same units of measurement). Whether your care provider tests TRAb or TSI, it is helpful to to stick to the same test each time, for the purpose of monitoring the trajectory of your condition.

Do you have any other questions about Graves' disease or your lab test results? Let me know below!

01/11/2023

I'm finalising the Frequently Asked Questions section of my thyroid eBook, which is coming out very soon (watch this space!).

If you have a question you'd like the answer to, leave it down below (or DM me) and I'll see if I can include it.

Niki

31/10/2023

The caption was a bit tricky to read on my previous post, so here it is again. Hopefully a bit easier to read here!

When I work with patients with high reverse T3, they often ask me, ‘so if Reverse T3 doesn’t do anything, why do we even make it?’ And it’s a great question. As far as we know, Reverse T3 has no biological activity. It is considered an inactive metabolite (essentially a by-product) of thyroid hormone metabolism. Let me tell you though, Reverse T3 does have a very important role, and I’ll explain it in just a moment.

But first, let’s remember where reverse T3 comes from. When we make T4 in the thyroid or take medications containing T4, we convert some of it to its active form (T3) and another portion becomes Reverse T3. In fact, chemically, the difference between T3 and Reverse T3 is minor:
—> T3 is essentially a T4 molecule that has had an iodine atom removed from its OUTER ring.
—> Meanwhile, Reverse T3 is derived from a T4 molecule that has had an iodine atom removed from its INNER ring.

And therein lies the difference as to whether it will be biologically active (aka, T3) or not (Reverse T3).

But this brings back to our original question of WHY do we make reverse T3 if it has no known biological role? The answer is simple: It gives us an ‘off switch’.

If we think of the thyroid as the motor of the body, setting the pace of all the processes and systems that keep us alive, T3 is like the accelerator, while reverse T3 is the brake. The more T3 we have, the faster the body’s system. The more Reverse T3 we make, the more we’re slowing things down.

We would never design a car without a brake, and similarly, the thyroid has an in-built system to help slow things down when conditions aren’t favourable. That system is the ability to convert our thyroid hormone into Reverse T3. It gives us an ‘out’, if things are getting too fast.
So what do I mean by conditions that aren’t favourable? Well, for example, we know Reverse T3 increases during prolonged fasting, pregnancy, caloric restriction, chronic illness, inflammation and during times of stress. Why? To conserve energy! To slow the body’s motor and take the foot off the peddle, so to speak. T4 always needs to be converted into something, so being able to ‘shunt’ towards reverse T3 (and consequently, away from T3) allows the body to apply the brake and conserve energy and resources during these metabolically stressful times.

So finally, this brings us to the question of what to do if your Reverse T3 is high? Well, you need to understand that your body is trying to put the brakes on and you need to ask why. Is it chronic stress or persistent, low grade inflammation? Could it be dietary factors, such as nutritional deficiencies, very low carbohydrate diets, prolonged fasting or caloric restriction? Is it related to impaired liver function or perhaps a combination of factors? Whenever we are shunting to Reverse T3, we have to ask WHY? That is the key to addressing the root cause of the issue and rectifying your reverse T3 issues for good. And this is why I spend so much of my time working with my patients to understand the root cause of their thyroid issues - because we have to work from the ground up to build the right foundation for thyroid health and wellbeing longterm!

Niki x

In my last post, I talked about the conversion of T4 to T3 and how we often look for a ‘roughly’ 3:1 ratio. More often t...
25/10/2023

In my last post, I talked about the conversion of T4 to T3 and how we often look for a ‘roughly’ 3:1 ratio. More often than not, when people experience issues in this area, they are experiencing under conversion, meaning they have lots of T4 but not much T3. I’ve covered many of the reasons for poor conversion in my previous posts, and in blogs on my website, but today I want to touch on something that’s not spoken of very often: Over-conversion.

In an over-conversion situation, we’re seeing a T3 that is ‘high’ relative to our T4. For example, we might see a T4 of 10, but a T3 of 5 (compare this to our typical 3:1 ratio, in which we might see a T4 of 15 and a T3 of 5). There’s a lot of T3 going around, relative to the amount of T4 we have in the system. Why?

Well, there can be a few reasons. Two of the more common ones are T3-containing medications and iodine deficiency.

- If you are on a T3-containing medication, such as Tertroxin or NDT, it is common (and in many situations, expected) to see a higher than usual T3 relative to T4, because you are actively taking the T3 component. This does not necessarily indicate a problem with your medication regime or that you are ‘over-converting’ as such; it is simply an artefact of the fact you are taking additional T3.

- Another potential cause is iodine deficiency. We have to remember that T4 and T3 are both made up of iodine: T4 contains four iodine molecules and T3 contains three (hence their names). Typically, the thyroid produces approximately 80% of its hormone in the form of T4 and 20% in the form of T3. When we are low on iodine though, the thyroid is clever and it increases its production of T3 relative to T4. This is clever because T3 is ‘less expensive’ to make in terms of the amount of iodine it requires and so when iodine is low, the thyroid preferentially makes T3, our active thyroid hormone. This is why if I see an unusual conversion ratio in someone who is not taking T3 (in particular, where someone is dramatically over-converting), I start to question iodine adequacy and whether we might need to investigate this area further. Importantly, you should NEVER commence iodine supplementation without first seeking professional advice, as both too much and too little iodine can be problematic for the thyroid (especially in someone with a pre-existing thyroid condition!).

There are a few other causes of a high T3 relative to T4. For example, it can be seen in Graves’ disease. Here, we typically expect to see both T4 and T3 increase, however T3 often does so to a greater extent. At the other end of things, it can also be seen in overt hypothyroidism, due to up-regulation of one of the enzymes responsible for conversion of T4 to T3. This is another compensatory mechanism designed to help maintain thyroid hormone levels for as long as possible. As a final example, testosterone is also known to increase T3 relative to T4, so we tend to expect a slightly higher ratio of T3 to T4 in males.

As you can see, there are many causes of a high T3 relative to T4, both in healthy states and in the case of thyroid disease. Importantly, if you are feeling well, it’s important to understand and consider the numbers, without necessarily getting bogged down in aiming for a perfect ratio. If your conversion is off though and you don’t feel your best, it can help to work with a thyroid savvy health professional to get to the bottom of what’s going on.

Let’s talk about the 3:1 ratio in hypothyroidism. Note: This post is a little complex and is not necessarily essential k...
24/10/2023

Let’s talk about the 3:1 ratio in hypothyroidism.

Note: This post is a little complex and is not necessarily essential knowledge, but it is interesting to know, especially if you are concerned about your thyroid hormone conversion.

If you’ve followed me for a while, you might have seen me mention that in a HEALTHY state, we typically expect to see a ‘roughly’ 3:1 ratio of T4 to T3. What does this look like? Well, if your T4 is 15, you might have a T3 of ‘around’ 5. It might be 4.7, it might be 5.2, but it’s approximately 3:1 (*technically speaking, it’s slightly more than 3:1 in most cases - say a T4 of 15 and a T3 of 4.7 - but 3:1 is a good ballpark).

This is when we have a HEALTHY thyroid, meaning our T3 comes from two places:
- The T3 we make inside the thyroid.
- The T3 we derive from the conversion of T4 in the body (‘peripheral conversion’)

TOGETHER, these two sources of T3 give us the ‘roughly’ 3:1 ratio of T4 to T3.

So what if we don’t have a healthy thyroid? Well, in a medical setting, if the thyroid is underactive, most people will be given Thyroxine, also known as T4 replacement therapy. This replaces the T4 hormone that their thyroid is no longer making. And it does a great job of that. It’s bio-identical and it can be converted into T3 in the body. That said, it does not replace the portion of T3 that comes from the thyroid itself. As a result, we’ll typically see a lower T3 relative to someone who is able to make T3 in their thyroid as well.

Let’s use an example: If you have have had your thyroid removed, you might be on a dose of say 150 mcg Thyroxine daily. As you no longer have a thyroid, you no longer make any T3 inside your thyroid. This means ALL of your T3 comes from conversion of your Thyroxine medication into T3. As a result, it is not uncommon to see a conversion ratio of less than 3:1 (your T4 might be 15, but your T3 might only be 4). It doesn’t necessarily mean your body is not converting well. It may be converting just fine. It’s just that you no longer have that little bit of extra T3 that normally comes from the thyroid. The same is true if your thyroid is very underactive from something like Hashimoto’s, and so even though you haven’t necessarily had it removed, you might still be on a high dose of Thyroxine because it’s essentially a non-functioning gland. As a result, you’re not producing T3 in the thyroid, and so your T3 levels will be lower because your T3 is only coming from conversion in the body.

So what do we do about this?
- Firstly, we still want to support your conversion. Where possible, we want to make sure we’ve addressed the factors that can compromise T4 conversion (such as nutritional deficiency, stress, inflammation and so on) and make sure we’ve given your body the environment and tools it needs to convert T4 effectively.
- Secondly, we need to determine if your conversion is on the lower side simply because we’ve lost the portion of T3 that comes from the thyroid, or if you do really have a conversion issue. Symptoms and a high Reverse T3 (relative to T3) can be important clues here.
- Lastly, in some cases, it may be appropriate to consider a combination therapy of T4 and T3 medication, under medical guidance. Importantly, not everyone needs T3 therapy and many people feel great on just T4 alone (especially if their conversion is supported), but there are certainly cases where people feel better on T3 or a combination of T4 and T3, and this is something that warrants individualised consideration with your prescribing doctor.

I know this is a very complex topic, so if you’d like me to put together a blog post to really break it down, let me know.

Have you got any T3 questions? Ask them below!

From RACGP (https://www.racgp.org.au/afp/2012/august/thyroid-therapy): "But it is useful to note that with therapeutic thyroxine therapy, free T3 levels tend to be slightly lower and free T4 levels slightly higher than normal. This is because the thyroid normally produces all the circulating T4 and 25% of the circulating T3, with most of the T3 produced in the tissues by conversion of T4 to T3. In therapeutic thyroid replacement, only T4 is given and then subsequently converted to T3 in the tissues resulting in lower levels of serum T3. With adequate replacement the TSH will vary around the middle of the normal range, the free T4 will be high normal or high and the free T3 will be low normal or low".

Note: This doesn't mean people will necessarily feel their best with this, it's just what is commonly expected and knowing this can help us manage the situation appropriately.

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Perth, WA
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