The Straw That Breaks the Camel’s Back
Nothing that raises ApoB is likely a good thing.
“This explains the failures of therapies that raise ApoB, including fibrates and DHA” - Dr. Matthew Budoff, MD @BudoffMD - “X” 2/2/2023.
ApoB represents all atherogenic particles, but LDL is by far the predominant player in atherogenesis. LDL-C is the biomarker for LDL.
As we discuss elsewhere, atherosclerosis takes many years (decades) to develop. The risk of atherosclerosis is commensurate with the cumulative exposure to atherogenic particles.
With the latest diet craze invoking a ketogenic diet and lifestyle as the panacea, or “therapy,” for all one’s ills, there has been an epidemic of LMHR patients arriving at the preventive clinic with, sometimes, astronomically elevated LDL-C levels. This is not likely a good thing, but it largely depends on baseline risk and exposure time to such high levels.
We presently don’t have enough data to inform us on the hazards of this particular dietary impact. Review of current evidence and clinical recommendations on the effects of low-carbohydrate and very-low-carbohydrate (including ketogenic) diets for the management of body weight and other cardiometabolic risk factors: A scientific statement from the National Lipid Association Nutrition and Lifestyle Task Force
What we do know is that LDL is causal to atherosclerosis and casting doubt and misinformation about LDL causality IS harmful.
Flying Under the Radar
Why do these cases go undertreated?
You just never know which inflammatory trigger, from which infiltrating LDL particle is going to be the one that causes that red hot “pimple,” or plaque to rupture and spew it’s gooey contents into the arterial lumen, activating platelets, clotting factors and forming a massive sticky thrombus that instantly plugs the pipe (coronary artery).
In atherosclerosis, LDL is largely what is causing the inflammation - the repetitive infiltration of LDL particles into the intimal layer of the vessel, every second of every day. As inflammation progresses, the architecture of the plaque becomes less and less stable over time, until one day it bursts, like a “zit” on a teenager’s face. If that happens high up in the “widowmaker” artery (Watch The Widowmaker | Prime Video) called the LAD (left anterior descending), a large amount of myocardial tissue living downstream is suddenly deprived of blood and oxygen. This causes ventricular fibrillation (V-fib arrest), where the heart is no longer squeezing or pumping blood, and the person dies instantly.
Nobody wants that for their loved one. Certainly nobody dispensing advice on social media should want that on their conscience.
If, after reading this document, you feel the benefits of a ketogenic diet outweigh your individual risk for future ASCVD and you wish to engage in this lifestyle, please consider our checklist below:
A checklist of targeted recommendations based on published guidelines
Cardiawareness Advocate Checklist:
- Talk to your doctor, ideally before initiating a ketogenic diet
- Begin a formal risk assessment based upon established ASCVD risk factors and available risk calculators
- Obtain baseline lipid panel
- Assess Non-HDL-C or ApoB if triglycerides are elevated (typically > 150 mg/dL)
- ApoB may be assessed at baseline and with changes in diet, lifestyle or lipid lowering therapy. This is typically a separate blood test
- Check Lp(a) - blood test
- Lp(a) is another atherogenic lipoprotein causal to atherosclerosis
- > 125 nmol/L (50 mg/dL - less preferred assay) - associated with heightened risk of premature ASCVD, often presenting as heart attack or stroke
- Coronary Artery Calcium Score A Picture is Worth a Thousand Words - Coronary Artery Calcium Scores
- Age > 40 years with at least 1 risk factor
- May consider screening at younger age if other significant risk factors present such as family history of premature ASCVD
- Follow up with doctor
- Repeat lipid panel with ApoB after 3-6 months or with any other significant lifestyle or clinical changes
- Periodically thereafter, at least annually
Going into detail on the evidence behind the recommendations and history of treatment for this phenotype.
Lean mass hyper-responders (LMHR) refers to a specific phenotype with lower BMI, total cholesterol > 200 mg/dL, HDL-C > 80 mg/dL and TG