They said it couldn’t be done. They said your Lipoprotein (a) level was purely the result of a genetic lottery and if you lose, you lose and there’s nothing you nor your doctor can do to change that. Lp(a) doesn’t play by the rules that apply to anyone else, including all other lipoproteins, you see.
What makes LDL-C come down makes Lp(a) go up!
And that confused everyone championing a LFHC diet for lipid management in the 90s to now!
But recently some brave researchers have stuck their head above the parapet with their proposal that lipid management, especially in the context of cardiovascular risk reduction, might need to be 😲*GASP*😲 personalised! That it isn’t always about LDL lowering and in fact in someone with elevated Lp(a) that would amplify the issue because, I repeat, what makes LDL-C come down makes Lp(a) go up! You heard it here folks! So instead of saturated fat as the saboteur and statins as the salve, the roles are reversed in any attempt to reduce levels of this rogue lipoprotein.
But given that your Lp(a) is for life – any approach to lowering its level has to be lifelong too
So even if we have some nifty tricks (old diets can learn new ones indeed! 😉) to successfully lower Lp(a) we must undertake a critical cost-benefit analysis unique to each individual. Ensuring we’re clear about how much of a reduction is required to produce real change in outcomes; how sustainable (on all levels) this approach is for the individual and what we’ve gained on one hand, we haven’t lost in the other. We need to be alert to swings & roundabouts in order to combine risk mitigation with overall improved health in cardiovascular medicine.
A New Era in Cardiovascular Risk: Lowering Lp(a)
This episode describes in detail all the natural interventions (CoQ10, Carnitine, Gingko, Niacin, Dietary change etc) we can use for lowering Lipoprotein (a). It clears up the confusion regarding how they compare and in particular how and why the degree of efficacy can be patient specific. And why therefore a series of short trials of single agents is the only way to establish their true effectiveness in any given individual but equally, why ‘stacking’ of these will often ultimately be necessary for maximising risk reduction. A case discussion of a successful strategy in a 57Y female marries the research with the real world, as we answer all-important questions: How low can she go? How low to make meaningful change regarding her cardiovascular outcomes? And is what’s required to keep her Lp(a) low, sustainable and health-promoting all round as a ‘forever prescription’?
You can purchase A New Era in Cardiovascular Risk: Lp(a) here. If you are an Update in Under 30 Subscriber, you will this episode waiting for you in your online account. You can become an Update in Under 30 Subscriber to access this episode and the entire library of Update in Under 30 audios and resources here.
Cracking the Case: Uncovering Cardiovascular Risk – Elevated Lipoprotein (a)
How do you conduct a comprehensive cardiovascular risk assessment? It should always include a Lipoprotein (a) result, having been declared the biomarker with the strongest indication of causality in both atherosclerosis & valvular aortic stenosis. But what use is getting this tested, if, when we identify increased risk due to elevated results, we have no means to lower it? Until now. This is a 57 year old female with a striking personal and family medical history, a peachy coronary calcium score, mildly elevated LDL-C but significantly elevated Lp(a). We describe in detail the meaningfulness of this, as one element in our understanding of her overall inter-connected health story and reveal the prescription and approach that got results. We also discuss the challenge that is inherent in both ‘uncovering risk’ in someone while remaining on the right side of hope vs despair and of the nature of CVD risk reduction which requires lifelong management.
You can purchase this Cracking the Case episode: Uncovering Cardiovascular Risk: Elevated Lipoprotein (a) here.
