One more time: saturated fats and cholesterol do not cause heart disease!

More fake science in the field of lipidology.

A while ago, the Lancet published a ridiculous study with the snappy title:

'Application of non-HDL cholesterol for population-based cardiovascular risk stratification: results from the Multinational Cardiovascular Risk Consortium.'

https://pubmed.ncbi.nlm.nih.gov/31810609/

Which created headlines around the world - most of which failed to understand the difference between LDL ('bad' cholesterol) and non-HDL cholesterol. Which may, or may not, have been deliberately done.

This study was reported as saying that twenty-five-year-olds should get their cholesterol checked because raised cholesterol is far more damaging at a young age than previously thought.

Then another study came out a few weeks after. It had the even snappier title:

'Association between hyperlipidemia and mortality after incident acute myocardial infarction or acute decompensated heart failure: a propensity score-matched cohort study and a meta-analysis.

https://pubmed.ncbi.nlm.nih.gov/31843818/

You know that title really does not scream 'READ ME!' What is it about medical journals and medical writing, which demands all enthusiasm and interest is sucked out, leaving only the driest of dry husks.

What I first noticed was that it did not appear to make any headlines, anywhere, at all. Of course, making enough noise to be heard in today's jittery, overloaded information world takes a lot of money and effort.

This is why the Lancet study got blanket coverage. Someone, somewhere, will have been paid a lot of money to ensure that it happened.

The money was paid because there are people who stand to make billions and billions from increased cholesterol testing, including younger people, and suggesting that "raised" cholesterol must be 'treated' from an ever-younger age. Perhaps you would like to guess who those people may be.

On the other hand, the study's Association between hyperlipidemia and mortality after incident acute myocardial infarction or acute decompensated heart failure: a propensity score-matched cohort study and a meta-analysis could result in the loss of billions and billions.

Because what they found was that, after an acute myocardial infarction (AMI), and in people with acute decompensated heart failure (ADHF) – normally caused by a previous MI – the higher the LDL level, the lower the overall mortality.

They called a higher LDL level hyperlipidemia (HLP), but it was a high LDL, a.k.a. 'bad' cholesterol.

The 'association' of which they spoke is in the exact opposite direction to that in the Lancet study. Just to repeat their main finding. Those with higher LDL levels lived the longest. Full stop, exclamation mark.

They set the study up to consider the following questions:

'We postulated that if a diagnosis of HLP [Hyperlipidaemia] decreases the mortality after AMI or HF [Heart Failure], then, it also lessens the magnitude of mortality risks associated with other competing comorbidities.

We tested this hypothesis separately in large cohorts of patients hospitalized for incident AMI and acute decompensated HF (ADHF). To compare patients with and with no HLP, we assembled 1:1 balanced groups using propensity score-matching for each study condition.

Our objectives were three-fold:

(1) to estimate the Association of HLP with all-cause mortality among patients with AMI or ADHF,

(2) to determine the extent to which the Association between other competing comorbidities and mortality is modified by HLP

(3) and to provide risk estimates for mortality associated with HLP after incident AMI or HF through systematic review and meta-analyses of published and current study data to place the current findings in the context of published literature.'

Here were the main results. First, for those diagnosed with AMI:

? In matched patients, mortality was significantly lower among patients with Hyperlipidaemia (HLP) versus those with no Hyperlipidaemia (HLP)

? Overall mortality 2182 (50.2%) vs 2718 (62.5%)

? 9 vs 8.6 deaths/100 person-years of follow-up, p<0.0001.

Next for those diagnosed with acute decompensated heart failure (ADHF):

? In matched patients, mortality was significantly lower among patients with HLP versus those with no HLP

? Overall mortality 1687 (58.6%) vs 1948 (67.7%)

? 4 vs 16.3 deaths/100 person-years of follow-up, p<0.0001.

You may have noted that the mortality rate in these patients was very high. For those with ADHF, and lower cholesterol levels (LDL levels), the mortality rate was 16.3 deaths per 100 person-years. That is a sixteen-point three percent death rate per year—one in six.

This, therefore, is a super, exceptionally high-risk population. It is also a super exceptionally high-risk secondary CV prevention population. The exact group where statins are purported to do the most good – through the specific action of lowering LDL levels.

At this point, a short detour. I know any cardiologist reading this will be thinking – or has been taught to think: "Yes, but low cholesterol is a sign of other serious conditions, such as cancer.

Ergo, it is not the low cholesterol that is damaging, it is the other underlying conditions".

This 'fact' been stated for many years – without a single scrap of evidence to support it.

It was Stamler who first came up with this 'apologia' for much contradictory evidence about low LDL levels and increased mortality. Like many things in medicine it is universally believed, without any supportive evidence. It is true that in a very few cases, late stage terminal cancer, and late stage liver failure, the LDL levels can drop. Otherwise … nothing.

However, these researchers made sure they adjusted for this, non-existent, factor anyway.

'Our findings were adjusted for cancer and numerous other Clinical Conditions.'

What were the conclusions of this study? Well, they were exceptionally carefully worded.

'The findings of this study, if validated, should reinforce the importance of HLP in predicting long-term mortality after index AMI or ADHF and potentially provide guidance for subsequent management. HLP can readily be diagnosed and help recognize AMI and HF patients with lower long-term mortality.

In these patients, clinical care should not focus on certain lipid targets; rather, evidence-based secondary prevention strategies should be initiated.

Conversely, patients with AMI and ADHF without HLP may be considered to have increased risk for early mortality and potentially alert providers for close monitoring during hospitalization and after discharge. Both categories of patients would profit from a thoughtfully tailored program with distinctive goals of care for existing CCs.'

Let me cut to the key comment in that passage. That is, the comment regarding those patients who had HLP:

Clinical care should not focus on certain lipid targets

Clinical care should not focus on certain lipid targets

Clinical care should not focus on certain lipid targets

Of course, the comment is couched in such diplomatic language that I am not absolutely sure what is meant by it, although I am pretty sure.

These poor people, who are dreadfully ill, who have suffered the agony of a heart attack, or severe heart failure, fare so much better when they have a high LDL level. So, for pity's sake, I beseech thee in the name of God, do not try to lower their LDL level, you mad fools.

Maybe a touch too emotive? Oh well – after reading too many clinical papers, the temptation to shout becomes irresistible. Creeping around in the grey and lifeless world of the passive voice is not really my style. Science should not be a place of hushed diplomacy. Science should be lively and stimulating, nay argumentative. If you've got something to say, shout it out. Fight for it and debate it properly.

God bless y'all ??

Dr. Serge

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