As regular readers will know, I often base my blogs on real-world cases I’ve seen during the preceding week. And this week provided a couple of particularly interesting examples.
It’s very common in clinic for patients to be nervous about taking a statin. These drugs are among the most widely prescribed and most extensively studied medications we have — yet they seem to attract a disproportionate amount of bad press. It’s certainly true that some patients experience side effects (about 8% of people), but the public rarely hear about the far larger number of people who quietly benefit from them. To be clear, I wouldn’t take them myself if I had significant side effects (we have lots of other options these days) but that isn’t all that common in real life.
Quoting studies is one thing. Real-world examples, I think, can often be far more powerful when speaking with patients, and when patients speak with friends and loved ones. So, I wanted to share two.
The first is a lady in her mid 60s. She is exceptionally fit, exercises regularly, and pays close attention to her diet. She had no meaningful past medical history, and no symptoms. Despite that, a CT scan of her coronary arteries showed significant coronary artery disease. That discovery prompted her to start a statin, which she had definite reservations about taking.
Before all of this — and entirely off her own initiative — she had arranged some private blood tests, including a high-sensitivity C-reactive protein (hs-CRP). I’ve written about hs-CRP before, but in essence it’s a marker of systemic inflammation. It’s non-specific, but elevated levels are associated with increased cardiovascular risk.
Interestingly, her hs-CRP was relatively high before starting treatment. There was no obvious alternative explanation.
After being on a statin for a period of time, she repeated the test. It had fallen significantly.
Nothing else had changed — not her weight, not her exercise, not her diet. The most plausible explanation was the introduction of the statin.
We know from research that statins don’t just lower LDL cholesterol; they also have anti-inflammatory effects. But it was striking to see such a clean, real-world example.
Given her understandable concerns about starting medication, this provided reassurance. It supported her decision — not just theoretically, but personally.
The second case was a gentleman also in his early 60s with type 2 diabetes. Five years ago, after an episode of chest pain (which turned out not to be cardiac), he had undergone a CT coronary angiogram. That scan showed a small amount of “soft plaque” in one of his coronary arteries. He had no angina, but the finding was enough to prompt him to start a statin.
Fast forward five years, and he wanted to reassess where things stood.
We repeated the scan. The radiologist’s report was clear: there had been no progression of coronary disease.
Of course, we can’t know what might have happened had he not taken the statin. But what was particularly interesting in this case was that the original soft plaque had ‘remodelled’. It had become more calcified — in other words, more stable.
We often think of calcified plaque as something that appears later in life. In his early 60s, this degree of stabilisation was notable. Statins are known to promote plaque stabilisation and reduce inflammation within the vessel wall. Again, this is something we read about in trials and mechanistic studies — but it was genuinely satisfying to see it so clearly reflected in a real patient.
He was understandably pleased.
These two examples don’t replace the evidence base. But they bring it to life.
The second theme of this week’s blog is more personal.
This weekend I travelled back to Warwickshire, where I grew up, to see my dad — and to visit my mum, who now lives in a dementia nursing home. I hadn’t seen her for a couple of months.
It was emotional.
She is beautifully looked after. She was nicely dressed, her hair had been done, and she appeared physically comfortable. But she didn’t know my name. She didn’t know my wife’s name. She repeated a few familiar stock phrases but wasn’t able to hold a conversation in any meaningful way.
And yet, she seemed pleased to see us. Cheerful, even.
Dementia is a condition she would never have wanted for herself. It’s certainly not something I would ever want for me.
Seeing her again was a powerful reminder that prevention matters — not just for heart attacks and strokes, but for cognitive health too. If you haven’t read them already, I’ve written previously about dementia risk and the modifiable factors that can help stack the odds in our favour.
There are no guarantees. But there are choices.
It was emotional for my dad as well. Knowing she is safe and cared for brings comfort. But it remains, for our family, a deeply sad and difficult chapter — one you wouldn’t wish on anyone.
I think what links both halves of this blog is this:
We don’t always see the immediate benefit of prevention. Sometimes it feels abstract. But occasionally, in clinic or in life, you glimpse it clearly — in a stabilised plaque, a reduced inflammatory marker, or in the fierce motivation to protect your future self.
And those glimpses matter.