Few phrases create more anxiety in clinic.

But did you know that cholesterol is only one small part of your overall cardiovascular risk?

In fact, when I entered my own details into QRISK and changed my cholesterol ratio from a healthy level to a much less healthy one, my overall risk increased by only around 0.7%.

That doesn’t mean cholesterol doesn’t matter.

It means context matters.

Age, sex, blood pressure, diabetes, smoking status, thyroid function, menopause and genetics all play a role.

In this week’s video I discuss:

• Why cholesterol is often misunderstood

• Why thyroid patients frequently have raised cholesterol

• The impact of menopause on cholesterol levels

• Why diet is only part of the story

• How QRISK can help put your results into context

Cholesterol is not a moral judgement.

It’s one piece of information within a much bigger picture.

Watch the full video via the link in bio.”

Not because cholesterol doesn’t matter. It absolutely does.

But because we often reduce an incredibly complex picture down to a single number and then frighten people with it.

Every week I see patients who have been told:

“Your cholesterol is high.”

Often that is the…

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Much of the discussion around thyroid treatment focuses on the risks of overtreatment.

We hear about atrial fibrillation.
We hear about osteoporosis.
We hear about the dangers of a suppressed TSH.

These risks are real, particularly in older patients, when actual thyroid hormone levels are genuinely elevated.

But risk in thyroid medicine is bidirectional.

Undertreatment is not neutral.

And if we are going to have an honest conversation about safety, we need to talk about both sides.

Untreated vs Undertreated Hypothyroidism

Is there a meaningful difference?

In thyroid medicine, risk is often discussed in binary terms.

You are either hypothyroid or not.
Treated or untreated.
Safe or unsafe.

Physiology is rarely that tidy.

There is a difference between untreated overt hypothyroidism and undertreated hypothyroidism.

But that difference lies in degree, duration, age and context, and crucially in which hormone we are looking at, because TSH is a signalling hormone.
It is not the active hormone at tissue level.

T3 hormone is.

Untreated Overt Hypothyroidism

Overt hypothyroidism typically means:

• Elevated TSH

• Low free T4

• Often low T3

• Clinical features of deficiency – eg symptomatic

This state has well described systemic effects.

Cardiovascular changes include:

• Increased LDL cholesterol
• Increased ApoB
• Increased triglycerides
• Elevated diastolic blood pressure
• Increased arterial stiffness
• Impaired endothelial function

Thyroid hormone has profound effects on the heart.

When tissue T3 availability is low:

• Cardiac output falls
• Myocardial relaxation slows
• Diastolic dysfunction can develop
• Severe cases may cause pericardial effusion

Large observational studies associate untreated overt hypothyroidism, particularly when TSH exceeds 10 mIU/L, with increased coronary heart disease risk and cardiovascular mortality.

But those studies are not describing TSH as toxic.
They are describing sustained hormone deficiency.

Untreated overt hypothyroidism carries measurable long-term risk.

That is not controversial.

Undertreated Hypothyroidism

Undertreated hypothyroidism is more nuanced.

It may look like:

• TSH mildly elevated or even normal

• Free T4 in the low-normal range

• Free T3 low or low-normal range

• Persistent symptoms

• Ongoing dyslipidaemia

This is where I see many patients.

Biochemically “acceptable.”
Physiologically not thriving.

The evidence here becomes more complex because most large cohort data stratify risk by TSH, not by free T3.

But we know this:

• Lipid abnormalities are common in low thyroid states.
• Arterial stiffness can increase.
• Cardiovascular risk signals strengthen when TSH exceeds 10.
• For TSH 4–6, risk signals are weaker and variable.

What we do not know well is what happens in patients with persistently low T3 but “in range” TSH.

And physiologically, T3 is the hormone acting at the myocardium, the vasculature, and the liver.

A 35-year-old with ApoB elevation, low T3 and a TSH of 3.8 for 15 years is very different from
an 82-year-old with TSH of 6, normal lipids and no symptoms.

Duration matters.
Age matters.
Metabolic context matters.

And T3 matters.

Age Changes the Equation

Older adults often have slightly higher TSH levels that may reflect physiological adaptation rather than pathology.

In this group:

• Mild TSH elevation may not carry significant cardiovascular risk.
• Aggressive dose escalation can increase arrhythmia risk.

In younger adults:

• Decades of dyslipidaemia are not trivial.
• Persistent low T3 over years may influence vascular health.

Risk is dynamic.

It shifts across the lifespan.

The Duration Variable

This is often ignored.

A mildly elevated TSH for three months is unlikely to change cardiovascular outcomes.

A suboptimal T3 state for ten years may.

Risk accumulates through:

• Persistent lipid disturbance
• Endothelial dysfunction
• Vascular remodelling

Endocrine physiology operates over decades.

We should not pretend that “borderline” over 15 years is biologically neutral.

Thyroid Hormone, Mental Health and Behaviour

One area that is consistently underestimated in thyroid discussions is the mental health dimension.

T3 is active in the brain. It influences neurotransmitters, motivation, drive, cognitive speed and emotional regulation.

When T3 availability is low, patients often describe:

• Low mood
• Flatness or loss of interest
• Reduced motivation
• Brain fog
• Poor stress tolerance
• A sense of moving through treacle

In overt hypothyroidism this is recognised.
In undertreated or low T3 states it is often dismissed because the TSH is fine.

But physiology does not read the lab reference range. The brain responds to available hormone.

And this matters, because mental state influences behaviour.

When energy is low and drive is reduced, people naturally:

• Move less
• Exercise less
• Cook less
• Choose convenience foods
• Crave quick carbohydrate
• Struggle with consistency

This is not lack of discipline.
It is low metabolic drive interacting with modern food environments.

Over time this can lead to:

• Weight gain
• Loss of muscle mass
• Reduced cardiorespiratory fitness
• Insulin resistance
• Worsening lipid profiles

Which then feed into:

• Cardiovascular risk
• Sarcopenia
• Falls risk
• Fracture risk

So when we talk about whether mild undertreatment is safer, we have to look beyond cholesterol and TSH.

A chronically low T3 state may subtly shift mood, motivation and physical behaviour for years. That shift can compound metabolic risk more significantly than a laboratory threshold suggests.

This is not an argument for pushing doses high.
It is an argument for recognising that persistent deficiency has behavioural and psychological consequences that affect long term health.

Mental health, metabolic health and thyroid physiology are not separate systems.

They are interdependent.

And if we are discussing safety, we need to include the whole picture.

Thyroid Hormone and Heart Rhythm

Atrial fibrillation is rightly discussed in the context of hyperthyroidism and true biochemical excess.

But rhythm disturbance risk is influenced by:

• Age
• Atrial structural change
• Duration of exposure
• Sustained elevated T3 or T4 levels

It is not created by a suppressed TSH alone.

TSH suppression in a monitored patient does not automatically equal thyrotoxicosis.

The relevant question is whether free T3 or T4 levels are elevated and whether the patient is clinically over-replaced.

Again, context matters.

Bone Health: More Nuanced Than the Headlines

Overt hyperthyroidism increases bone turnover and fracture risk. That is clear.

But bone health is not a single-variable equation.

Fracture risk is strongly influenced by:

• Oestrogen status

• Age

• Sarcopenia

• Physical activity

• Vitamin D status

• Falls risk

· Weight

A suppressed TSH alone does not automatically equal osteoporosis.

Risk is more closely linked to:

• Sustained biochemical excess
• Duration of exposure
• Postmenopausal status

Also, recent research increasingly highlights the muscle bone connection. Bone is a dynamic tissue that responds to mechanical loading. Strength, resistance exercise and muscle mass are powerful drivers of bone remodelling. If chronic low thyroid hormone availability contributes to reduced movement, loss of muscle and physical deconditioning, that may indirectly influence skeletal health over time.

Bone risk cannot be separated from muscle health.

The Falls Factor

Undertreated hypothyroidism increases:

• Fatigue
• Proximal muscle weakness
• Slowed reflexes
• Impaired balance

Falls are one of the strongest predictors of fracture.

Bone risk cannot be separated from muscle function and neurological responsiveness.

Hypothyroidism reduces bone turnover, but reduced turnover is not the same as skeletal resilience.

Again, physiology is multifactorial.

The Real Question

The question is not:

“Is thyroid hormone dangerous?”

The real questions are:

• Is the dose appropriate?
• Are free T3 and free T4 within physiological range?
• Is age being factored in?
• Is duration considered?
• Are lipids and cardiovascular markers monitored?
• Is overt biochemical excess corrected?
• Is persistent deficiency being ignored?

Risk in thyroid medicine is not created by treatment alone.

It is created by imbalance.

Both excess and deficiency carry physiological consequences.

And deficiency is not automatically safer simply because TSH is not suppressed.

The Clinical Principle

The goal of thyroid care is not:

• To fear T3
• To avoid suppression at all costs
• To accept persistent low T3 as benign

The goal is physiological balance at tissue level.

That means:

• Avoiding sustained biochemical excess
• Avoiding chronic under-replacement
• Adjusting targets by age
• Monitoring lipids and cardiovascular markers
• Considering bone health in context
• Interpreting TSH as one marker, not the whole story

Risk in thyroid medicine scales with:

Degree.
Duration.
Age.
Actual hormone levels.
Monitoring quality.

Binary thinking does not serve patients.

Balanced physiology does.

Conclusion

Both excess and deficiency of thyroid hormone carry physiological consequences.
And deficiency is not automatically safer simply because TSH is not suppressed.

In my practice, I am less interested in chasing a number and more interested in whether tissue level thyroid hormone availability is adequate, sustainable and safe for the individual in front of me. That means looking beyond TSH alone, considering T3 carefully, and balancing long term cardiovascular, skeletal and metabolic health over decades, not just over a single blood test cycle.

The aim is steady physiological equilibrium.

Atrial fibrillation (AF) is a common heart rhythm condition where the heartbeat becomes irregular and often faster than normal. Instead of beating in a steady pattern, the top chambers of the heart quiver, which can cause palpitations, breathlessness, fatigue, or sometimes no symptoms at all. It is usually not immediately dangerous, but over time it can increase the risk of stroke, which is why it is important to recognise and treat appropriately.

Patients are often told that taking T3 “causes arrhythmias” or causes damage to the heart. But most of the research this comes from looks at untreated hyperthyroidism, or elderly patients over-replaced on levothyroxine. It doesn’t really tell us what happens in monitored T4 and T3 replacement therapy.

So, we looked at our own data.

We analysed patients receiving thyroid prescriptions issued by the clinic, representing approximately 80% of the active clinic population.

• 887 patients on thyroid treatment

• 743 exposed to T3 in some form (liothyronine or natural desiccated thyroid)

• Average age: 49

These patients were all reviewed regularly and doses adjusted to keep FT3 below 6.8.

What we found:

There were 3 cases of atrial fibrillation.

All three:
• women over 70
• T3 level above range at the time
• biochemical overtreatment

There were no cases in patients within the normal replacement range.

That works out at about 4 in 1,000 patients exposed to T3, and only when levels were too high.

0.4% of our population.

In people around age 50 (our average age) atrial fibrillation affects roughly 1 in 100 people = 1%.
In people over 70, it affects around 1 in 10, even without thyroid treatment = 10%

All of the cases we saw occurred in this higher-risk age group and when levels were above range.

Putting this audit into context:

Our observed rate:

0.4% across monitored T3 patients (all ages combined)

Important nuance:

• Our patients are continuously followed, not a single time-point snapshot

• And AF occurred only in >70s

So effectively:

Under 70s

Observed = 0 cases
Background risk = low but non-zero

Over 70s

Observed = 3 cases in an age group where baseline risk already ~1–2%/year

Meaning our findings are compatible with:

• age + overtreatment risk rather than treatment-specific risk

What this means?

The important distinction clinically is not just seeing a low TSH on a blood test, but whether the actual circulating thyroid hormone levels are physiological or excessive.

Every thyroid hormone treatment including levothyroxine, can cause arrhythmias if the dose is too high, particularly in older people.

In this cohort, when levels stayed in range, we did not see atrial fibrillation.

Why this matters:

Much of the concern around T3 comes from data derived from different clinical populations. In reality the risk appears related to over-replacement.

Careful monitoring and age-appropriate dosing are what make treatment safe.

This isn’t a trial and it doesn’t prove benefit, but real-world safety data matters. Especially when the alternative is extrapolating from untreated hyperthyroidism.

Conclusions:

Ultimately this audit doesn’t prove one treatment is “better” than another, and it doesn’t mean atrial fibrillation never happens with thyroid therapy. What it shows is something simpler: the heart responds to the amount of thyroid hormone it sees, not the label on the prescription.

When doses drift too high, particularly in older patients, arrhythmias can occur with any thyroid hormone. When levels remain within physiological range and are monitored, the risk appears low and consistent with normal background patterns.

So the question isn’t “Is T3 dangerous?” but more “Are levels appropriate and being reviewed?”

That’s where safety really sits.

The choice is ultimately yours, but these vaccines are safe and do not carry extra risk for most thyroid patients, including autoimmune types.

Having Hashimoto’s/Grave’s does not mean you are immunocompromised, i.e. your immune system is not weakened or unable to respond to vaccines because you have an autoimmune disorder.

For clarity, immunocompromised people are those whose immune systems are suppressed due to chemo/radiotherapy, are on immune suppressing medication (such as long term steroids, methotrexate, azathioprine or biologics), some blood cancers or advanced HIV/AIDS.

If you are prone to post viral fatigue or are in the middle of adjusting your thyroid medications you might choose to wait until you feel well, but ultimately if you were to get flu or COVID the repercussions are likely to be far worse then the vaccines itself.

The conclusion?

Vaccines are safe for you to have with thyroid disease and for some, the disease itself could be far worse then the vaccine. The decision of whether to have one is entirely yours. As always, listen to your body and make the decision that feels right for you.