For decades, we’ve been told by the “authorities” that high cholesterol is bad and that high cholesterol causes heart disease. It’s such an established belief in medicine that it even has a name – the Diet-Heart Hypothesis. Over the years, there’s been conflicting data available for passionate debate on both sides.
Here’s some disruptive research that hasn’t even been published yet, but that was unveiled at the Low Carb Denver conference that I attended in February and was recently released online by the researcher, Dave Feldman.
The Diet-Heart Hypothesis
Specifically, the medical field is targeting LDL cholesterol (LDL-c), the so-called “bad cholesterol”. Sure, there are observational studies demonstrating an association between elevated LDL-c and cardiovascular disease. Quick trip back to 8th-grade science class — I’ll remind you that correlation does not imply causation. There are many potential confounding variables that weaken these studies, making it impossible to make any sort of cause-effect conclusions. These epidemiologic studies are useful only for generating hypotheses — if there appears to be a relationship (a correlation), that suggests that we should do a higher quality study to get the real answer.
There has been a singular focus on reducing LDL cholesterol with aggressive prescribing of statins and other cholesterol medications. Despite these efforts, cardiovascular disease continues to be the #1 killer of Americans.
A study in 2013 found that LDL cholesterol levels were NOT significantly elevated in most individuals who suffered heart attacks (ST-Elevation Myocardial Infarctions, to be precise).
Why? Because it’s just not that simple. Cholesterol is a small piece of a gigantic puzzle.
Over the last several years, the “Keto Diet” (KD) has been a popular trend as a tool for achieving weight loss. Many individuals who follow the KD experience a substantial increase in their LDL cholesterol levels, a supposedly “bad” thing, while realizing favorable decreases in triglycerides and increases in HDL. Despite the weight loss they may have achieved, these individuals are usually being pressured to start cholesterol-lowering medication due to the established beliefs described above.
Questioning the Status Quo
That paradigm is now being questioned . . . with an amazing set of data revealed by Dave Feldman who has passionately studied this so-called Lean Mass Hyper-responder (LMHR) phenotype.
There were 100 LMHR participants. They did a baseline scan to detect the presence of heart disease, with a Coronary CT Angiogram (CCTA) – a study that can detect any plaque formation in the heart, not just calcified plaque which is visible on a Calcium Score (CAC), but also soft plaque (plaque that isn’t calcified). These study participants were on the KD for an average of 4.5 years, with an average LDL of 259.8 mg/dL. [For reference, the cardiology guidelines state that anyone with an LDL-c greater than 190 mg/dL should automatically be placed on a statin. Other decisions are based on risk, often recommending statin therapy for LDL-c above 70 mg/dL.]
Their Total Plaque Score (TPS) at baseline was < 10 (out of a possible score of 45), with most of them being 0 (ZERO). That means that coronary artery plaque was almost nonexistent in these individuals. Remember that conventional medicine says that these individuals should have coronary artery disease, according to the Diet-Heart Hypothesis, after being exposed to extremely elevated LDL cholesterol for nearly 5 years.
Interestingly, there was another study looking at Coronary CT Angiogram (CCTA) data on a similar cohort of individuals, allowing Feldman a unique opportunity to make a comparison of the 2 groups. The baseline characteristics were impressively similar, aside from the difference in LDL-c: 272 mg/dL in the KD group vs. 123 mg/dL in the MiHeart control group.
There was no significant difference in coronary artery plaque burden between the 2 groups.
Also, there was no significant correlation between LDL cholesterol and total plaque.
What does all of this mean?
These results are certainly not the end of the story. There is far more to learn about lipids, cholesterol, metabolic health, heart disease, etc.
The important takeaway from this study is that high LDL is not, by itself, a cause of cardiovascular disease. In individuals who are metabolically healthy, elevated LDL cholesterol does not appear to be a significant risk for development of atherosclerotic plaque.
There will certainly be more to come. This longitudinal study will repeat the CCTA to determine whether there has been any development of plaque in these individuals. This preliminary data, however, certainly casts doubts on the validity of the over-simplified Diet-Heart Hypothesis.
I believe that LDL cholesterol is a relevant risk factor, ONLY in the setting of poor metabolic health – 93% of our population. In individuals who are metabolically healthy, however, cholesterol numbers are largely irrelevant. Medicine guidelines need to cater to the majority, and thus we are stuck with this perspective on LDL as long as the collective health of our nation is so poor.