Your LDL cholesterol has increased. A couple of good reasons not to panic.

No one wants to be told their LDL cholesterol (LDL-C) has jumped up. But take a deep breath because it mightn’t mean what you think it means.

It’s been standard practice to estimate heart disease risk from a few key numbers: aside from blood pressure, it’s mainly LDL-C, along with total cholesterol and HDL cholesterol or HDL-C.

The central theme has been ‘good’ (HDL) and ‘bad’ (LDL), though there’s a growing conversation about the need to move on from this.

LDL-C: what is it? And what else should we know about?

We’ve probably all heard that cholesterol is vital, and our cells can’t function without it. It helps our bodies make hormones, bile acids and vitamin D.

To do its work cholesterol needs to move around the body, but since it can’t dissolve in the bloodstream and travel that way, it needs transport.

This comes in the form of a lipoprotein, which is made of lipid (fat) on the inside and protein on the outside.

The illustration shows an LDL (or low-density lipoprotein) particle with its cholesterol (and triglycerides — another kind of fat) inside, looking a bit like an arancini ball or some kind of confectionery.

The blue patch on the outside is a protein carrier called apolipoproteinB (apoB for short).

When I say there’s a conversation about moving on from the idea of good and bad cholesterol, that’s because apoB is considered a far better indicator of cardiovascular disease than the amount of cholesterol inside LDL particles (which is what we currently try to assess with LDL-C).

A better measure than LDL-C

LDL isn’t the only kind of lipoprotein. There’s HDL too, of course, which has a carrier protein called apoA.

But five others, in addition to LDL, have an apoB carrier. These five, like LDL, are atherogenic, meaning they can cause a buildup of plaque.

ApoB attaches to receptors on our cells, allowing any of the lipoproteins it carries to get into those cells. Once inside our arteries they can create a problem, especially if high blood pressure has damaged the walls of our arteries.

To reiterate, any lipoprotein particle (arancini ball) with an apoB protein can be atherogenic. If we have too many of them, we’ll have a greater risk of arterial plaque.

Cardiovascular disease is driven by the number and type of lipoproteins, not by the cholesterol inside them. As some observers have said, the concern is the carrier, not the cargo.

In fairness, LDL cholesterol can be a reasonable indicator of apoB. But not always.

It’s possible for two people to have the same amount of LDL-C, but if one has more particles contacting their artery walls, they’ll have a greater risk of disease.

An example comes from the Women’s Health Study in the US. This is a long-term collaboration on women’s health research between the Brigham and Women’s Hospital and Harvard Medical School in Boston.

A study on cholesterol in women identified four groups: those who measured high on both apoB and LDL-C, those who were low on both, those who were high on apoB but low on LDL-C, and those who were low on apoB and high on LDL-C.

Not surprisingly, the first group (high on both) had the greatest risk of heart disease, and the group who were low on both had the lowest risk.

Of the two other groups, those with high apoB, low LDL were at greater risk than the low apoB, high LDL group. (If you only measured LDL-C and not apoB, you’d come to the opposite conclusion.)

The takeaway? We should know about apoB, and that testing for it is fairly inexpensive (about $70).

Your doctor won’t authorise it, so if you’re keen you’d have to organise it yourself (yes, Google it). Over time this might change given there are calls for it to be added to the measures we currently use.

High LDL-C may not mean high risk of heart disease

We’ve already seen this from the Women’s Health Study, but at the end of last year a UCLA professor and cardiologist named Matthew Budoff surprised a medical audience by outlining the results of his research on men in their mid-50s who’d been on ketogenic diets (i.e. higher fat and very low carb) for an average of almost five years.

Some of this group showed very high LDL-C. But they were lean, their HDL and triglyceride levels were healthy, and they had no more plaque than men of the same age with normal LDL-C.

In this case there was no relationship between LDL-C and the presence of plaque.

Budoff’s research team concluded that these men’s bodies had switched energy sources on this kind of diet and were excreting more LDL-C which showed up in their tests.

What occurs in a narrow subset of people — men on ketogenic diets — might seem irrelevant to the rest of us, but he also pointed to a Danish study of around 11,800 people who’d been identified as having a genetic predisposition for high LDL-C. Despite this, around half of them had coronary artery calcium scores of zero (i.e. low risk of cardiovascular disease).

He rightly pointed out that this needs more study, and that the other half of the Danish study group were at high risk. But high LDL-C, even when it’s genetic, doesn’t automatically mean high risk. In this Danish sample it was about 50:50.

A doctor from the audience asked him what she should do with patients who have high LDL-C but seem otherwise healthy. Get a calcium score, Budoff told her.

If your LDL-C stays high over time that’ll probably be done. (I wrote about coronary artery calcium scores last month, so look at the explanation there if you’re not sure what I’m talking about. Or Google it, of course. 😊)

To sum up, LDL-C isn’t a terrific predictor of heart disease risk. A smart GP won’t react in too much haste if it suddenly increases. They’ll look at the big picture, including your other results, and monitor things over time.

But if you want to cross check your risk level, two options are to get a test for apoB, and get your coronary artery calcium measured. Both are better indicators of risk than LDL-C.

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