High Cholesterol? Your Thyroid Could Be Part of the Problem

Why Hashimoto’s, liver metabolism and inflammation deserve a place in the conversation about cardiovascular health.

I was recently reviewing blood test results with a client who had been told her cholesterol was too high. She was understandably concerned and had already started thinking about what she needed to change in her diet, particularly whether she should be cutting back on foods containing saturated fat.

But as we looked through her health history, something else caught my attention.

She had been experiencing fatigue, constipation and difficulty maintaining her energy, and she had also been diagnosed with hypothyroidism. Yet nobody had really explained to her how her thyroid function might be influencing her cholesterol levels, or whether Hashimoto’s thyroiditis could be the underlying cause of her underactive thyroid.

This is something I come across surprisingly often in clinic. Cholesterol is discussed in isolation, with the focus immediately turning to diet, while other factors that influence how the body produces, processes and clears cholesterol receive far less attention.

And one of the most important organs in this conversation isn’t actually the heart. It’s the liver.

Can hypothyroidism cause high cholesterol? Yes, and it’s a connection that is sometimes overlooked. Thyroid hormones play an important role in how the liver processes and removes cholesterol from the bloodstream, which means an underactive thyroid can contribute to elevated LDL cholesterol even when someone’s diet hasn’t changed.

October is National Cholesterol Month, an awareness campaign organised by HEART UK, and I thought it would be a good opportunity to explore a connection that I believe deserves much more attention: the relationship between thyroid health, cholesterol metabolism and cardiovascular inflammation.

Cholesterol is about more than what you eat

One of the things I find interesting about cholesterol is how quickly the conversation turns to food, when so much of cholesterol regulation actually takes place within the liver.

Cholesterol is essential for life. We need it to build cell membranes and produce steroid hormones, vitamin D and bile acids. Our bodies manufacture cholesterol, particularly in the liver, and regulate how it is transported, used and removed.

The liver also plays a central role in clearing LDL particles from the bloodstream through specialised receptors. And this is where the thyroid becomes particularly interesting.

Thyroid hormones influence how the liver processes cholesterol, including the activity of LDL receptors. When thyroid hormone levels are insufficient, the liver may remove LDL cholesterol from circulation less efficiently.

The result can be an increase in LDL cholesterol, and sometimes total cholesterol, even when someone’s diet hasn’t changed significantly.

This is why hypothyroidism is recognised as a secondary cause of high cholesterol.

It doesn’t mean that every person with high cholesterol has a thyroid problem, or that correcting thyroid function will always normalise their cholesterol. But it does mean that thyroid health deserves consideration before we assume the explanation is entirely dietary.

What does Hashimoto’s have to do with it?

Hashimoto’s thyroiditis is an autoimmune condition in which the immune system targets the thyroid gland. Over time, this can damage thyroid tissue and reduce its ability to produce sufficient hormones.

It’s one of the most common causes of hypothyroidism in the UK. And yet, I regularly encounter people who know they have an underactive thyroid but have never explored whether autoimmunity is involved.

This distinction matters because Hashimoto’s and hypothyroidism aren’t quite the same thing.

Hashimoto’s describes the autoimmune process affecting the gland, whereas hypothyroidism describes insufficient thyroid hormone activity. You can have evidence of thyroid autoimmunity before your thyroid hormone levels become abnormal, and not every case of hypothyroidism is autoimmune.

When thyroid function declines, cholesterol metabolism can change alongside it.

Some studies also suggest associations between autoimmune thyroid disease and markers of vascular dysfunction or inflammation. However, the evidence is less consistent when thyroid hormone levels are normal, and thyroid antibodies alone don’t establish an increased cardiovascular risk.

The strongest, most clinically relevant connection remains the effect of insufficient thyroid hormone on lipid metabolism.

The other side of the story: inflammation and our blood vessels

Long before I began working as a nutritionist, I studied Biochemistry and Immunology, and my dissertation focused on vasculitis, a group of conditions involving inflammation of blood vessel walls.

I remember being fascinated by the relationship between the immune system and the vascular system, and how inflammation could affect structures we often think of simply as the tubes carrying blood around our bodies.

It’s a subject I’ve continued to find interesting throughout my career. When we talk about cardiovascular disease, cholesterol is often presented as though it simply accumulates inside arteries, eventually causing a blockage.

The biology is considerably more complex.

Our arteries are lined with a thin layer of cells called the endothelium. These cells help regulate vascular tone, blood clotting, permeability and inflammatory signalling.

In atherosclerosis, LDL-containing particles can enter and become retained within the arterial wall. Changes to these particles and the surrounding tissue can stimulate an inflammatory response, attracting immune cells that contribute to plaque development.

Over time, plaques may grow, narrow arteries or become unstable, increasing the risk of heart attack or stroke. This is one reason inflammation matters so much in cardiovascular disease.

Vasculitis and atherosclerosis are different conditions, with different underlying mechanisms, but studying vascular inflammation gave me an appreciation of how closely our immune and cardiovascular systems interact.

And importantly, inflammation doesn’t make LDL cholesterol irrelevant. The concentration and duration of exposure to atherogenic lipoproteins remain major drivers of atherosclerotic disease.

When several risk factors come together

Now imagine someone with Hashimoto’s whose thyroid function is not yet adequately controlled. Their LDL cholesterol may be elevated because their liver is clearing it less efficiently.

Perhaps they also have insulin resistance, elevated blood pressure, a family history of cardiovascular disease or changes in oestrogen levels as they approach menopause.

These factors can interact to increase cardiovascular risk.

This is the situation I think of as a potential perfect storm: an unfavourable lipid profile alongside other metabolic and vascular risk factors.

It isn’t inevitable, and having Hashimoto’s doesn’t mean someone will develop heart disease. But it illustrates why I prefer to look beyond a single cholesterol result.

The important question is not simply why cholesterol is high, but what is contributing to that elevation and what the person’s overall cardiovascular risk looks like.

What should you consider testing?

If you have elevated cholesterol, particularly alongside symptoms of hypothyroidism or an existing thyroid diagnosis, there are several areas worth discussing with your doctor.

A full lipid profile. Total cholesterol alone doesn’t tell us enough. LDL cholesterol, HDL cholesterol, non-HDL cholesterol and triglycerides help build a more useful picture of lipid-related risk.

Thyroid function. TSH is generally the first-line test, with free T4 measured when indicated. If you’re already taking levothyroxine, it’s worth reviewing whether your thyroid function is adequately controlled, particularly if symptoms persist.

Thyroid antibodies. Thyroid peroxidase antibodies (TPOAb) can help identify Hashimoto’s as an underlying cause of hypothyroidism. Thyroglobulin antibodies may sometimes provide additional information, although they aren’t routinely necessary. Once autoimmune thyroid disease has been established, repeatedly measuring antibody levels usually doesn’t guide treatment.

Apolipoprotein B (ApoB). This can provide additional information about the number of atherogenic lipoprotein particles circulating in the blood, particularly when triglycerides are elevated or metabolic risk is present. It isn’t necessary for everyone.

Lipoprotein(a), or Lp(a). This is largely genetically determined and can contribute to cardiovascular risk independently of conventional cholesterol measures. A once-in-adulthood measurement may be particularly useful where there is a family history of premature cardiovascular disease.

Blood glucose or HbA1c. These can help identify diabetes or impaired glucose regulation, both of which are relevant to cardiovascular risk.

In selected circumstances, other investigations may be appropriate. For example, high-sensitivity C-reactive protein (hs-CRP) can provide information about systemic inflammation, but it is non-specific and doesn’t diagnose inflammation within the arteries.

In my clinic, I also like to take a more detailed look at cardiovascular and metabolic health using the Doctor’s Data Cardiometabolic Profile.

This provides a broader picture of cholesterol and lipoprotein markers alongside other indicators of cardiometabolic health, helping me understand the different factors that may be contributing to someone’s cardiovascular risk.

I find this particularly useful when working with clients who have hypothyroidism or Hashimoto’s, because I want to understand what’s happening beyond a standard cholesterol result, including how their thyroid function, lipid metabolism and wider metabolic health might be interacting.

For me, it’s about putting the individual results into context, rather than looking at cholesterol as an isolated number. These additional markers can help inform a more personalised approach alongside conventional cardiovascular risk assessment.

What can you actually do about it?

The first step is to make sure any underlying hypothyroidism is appropriately assessed and treated.

For someone with insufficient thyroid hormone, achieving adequate thyroid replacement can improve their cholesterol profile. However, it may not remove the need for cholesterol-lowering medication, particularly when LDL is substantially elevated or cardiovascular risk is already high.

From a nutritional perspective, I would focus on supporting cardiovascular and metabolic health rather than simply trying to eliminate cholesterol from the diet.

Increasing soluble fibre through foods such as oats, beans, lentils and other fibre-rich plants can help lower LDL cholesterol. Replacing some saturated fats with unsaturated fats from olive oil, nuts, seeds and oily fish can also improve lipid profiles.

Regular physical activity, adequate sleep and maintaining good blood pressure and glucose regulation are equally important.

Omega-3 fatty acids can be particularly relevant when triglycerides are elevated, although standard fish-oil supplements shouldn’t be presented as a substitute for LDL-lowering treatment.

For someone with Hashimoto’s, I would additionally consider whether their thyroid medication is being taken consistently and absorbed appropriately. Calcium and iron supplements, for example, can interfere with levothyroxine absorption if taken too close together.

Another thing I often see in clinic is that people with hypothyroidism have only their TSH monitored, particularly if they’re already taking levothyroxine. While TSH is an important marker and usually the main test used to monitor treatment, it doesn’t always provide the complete clinical picture.

I also like to consider free T4 and, where clinically appropriate, free T3, the active thyroid hormone that influences metabolism throughout the body. This can be particularly useful when someone continues to experience symptoms despite a TSH within the reference range, although free T3 isn’t routinely needed and a normal TSH generally indicates adequate replacement in primary hypothyroidism.

If cholesterol remains elevated, it’s worth reviewing thyroid function alongside the wider metabolic picture rather than assuming that a normal TSH automatically explains everything, or that the thyroid must be responsible.

Why understanding the connection matters

What I hope people take from this is not that high cholesterol is harmless, or that thyroid dysfunction explains every abnormal lipid result.

It’s that our bodies don’t operate as separate systems. The thyroid influences liver metabolism. The liver regulates cholesterol. Lipoproteins interact with the arterial wall, while immune and inflammatory processes contribute to the development of atherosclerosis.

Understanding those connections can help us ask more informed questions and identify appropriate ways to reduce risk.

If you’ve been told your cholesterol is elevated and you also have hypothyroidism, perhaps this is an opportunity to review the wider picture with your healthcare professional.

And if you have an underactive thyroid but don’t know whether Hashimoto’s is the underlying cause, that’s another useful question to explore.

The goal isn’t simply to improve a number on a blood test. It’s to understand what is influencing that number and take meaningful steps to protect your long-term health.

Frequently asked questions

Can hypothyroidism cause high cholesterol?

Yes. Thyroid hormones influence how the liver clears LDL cholesterol from the bloodstream. When thyroid hormone levels are insufficient, LDL cholesterol can rise, even without significant dietary changes.

Does Hashimoto’s increase cholesterol?

Hashimoto’s can contribute to elevated cholesterol when it causes hypothyroidism. However, having thyroid antibodies doesn’t automatically mean your cholesterol will be high, particularly when thyroid function remains normal.

Will treating hypothyroidism lower cholesterol?

Correcting hypothyroidism often improves cholesterol levels, although the degree of improvement varies. Some people will still need dietary changes or cholesterol-lowering medication to reduce cardiovascular risk.

Should I have my free T3 tested if my cholesterol is high?

TSH and free T4 are the main tests used to assess thyroid function. Free T3 may occasionally be useful in selected clinical circumstances, but it isn’t routinely required to investigate elevated cholesterol or monitor levothyroxine treatment.

If you’d like to explore more of these connections between thyroid health, autoimmunity, inflammation and everyday symptoms, I’d love to welcome you into my free Facebook community, The Autoimmune Forum.

It’s a space where we explore the science behind our symptoms, share experiences and learn how to ask better questions about our health.

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