It’s been pretty darn busy these days as we’ve had a lot going on with the LMHR Study, platform development for OwnYourLabs.com, and some recent work on the Lipid Energy Model paper. Now most of my data has come back for the Eating Window Experiment, but I haven’t had the time to do a full write up. That said, I will at least give the preview on my OxPL-apoB data and why I find it so exciting.
What is the OxPL-ApoB assay?
This description I’m taking directly from the Boston Heart Diagnostics website, which is also where I get the assay:
Oxidized phospholipids are found on all apoB-containing lipoproteins, namely, LDL, VLDL, and especially Lp(a). When taken up by the artery wall, oxidized lipoproteins accelerate atherosclerosis, thereby, increasing the risk of myocardial infarctions, strokes, and calcific aortic valve stenosis. Oxidized phospholipids are highly pro-inflammatory and contribute to many diseases of aging. Clinicians can use OxPL-apoB levels to reclassify patients into higher or lower risk categories allowing better personalized care.
(For the remainder of this article, I’ll just refer to OxPL-ApoB as simply “OxPL”)
To be sure, I have a complex opinion regarding the elements described above and how this plays into the larger topic of the immune response. That said, I definitely do think this assay has enormous value and have been literally talking about this for years before it was even available.
Even as long ago as the fall of 2018 I was speculating on this comparative value…
If you’re a bit lost right now, don’t worry, you don’t need to know the biochemistry on this. The big takeaway is that I’ve long waited for this metric as I’ve believed all along it would (1) provide very powerful data on cardiovascular disease risk (and lots of data certainly suggests this), and (2) that in spite of low carb hyper-responders having very high LDL, I’ve long hypothesized their OxPL values would be generally low.
This is an important metric to determine given OxPL loosely correlates with ApoB in typical diet populations, thus I’ve been speculating something quite contrary to the existing data I’ve been able to find in the research to date.
OxPL-ApoB and Risk
One phenomenal scientist who has done incredible work in the field on this is Sam Tsimikas. He has conducted many trials and closely tracked OxPL levels in both humans and animals across many different study designs.
I became much more aware of his work a couple years ago and even found this older tweet with regard to one of my favorite graphs:
The above graph is taken from this study (Tsimikas et al) and has Lp-PLA2 on one axis and the ratio of OxPL over apoB. The OxPL/apoB ratio is something I’m particularly interested in, and its association with cardiovascular risk is unsurprising, but more on that in a later post.
Since gaining access to the OxPL assay at Boston Heart Diagnostics, I’ve used it a total of seven times over two experiments, the OxLDL Replication Experiment and this recent Eating Window Experiment. Here are my OxPL, ApoB, and Lp-PLA numbers for all phases:
The reference range for the OxPL-ApoB assay is <5.0, 5.0-7.5, and >7.5 nmol/L for “Low”, “Borderline”, and “Increased Risk”, respectively. All my metrics to date have been under 5.0 thus far, but this is what I was predicting overall. Interestingly, there is a clear difference between each experiment within this lower range (2.8-3.8 with the Replication Experiment, and 0.9-1.4 with the Eating Window Experiment).
The OxPL-ApoB/ApoB ratio is extremely low at a range of 0.007-0.021 across all tests. And for what it’s worth, I suspect this will prove common among those with the Low Carb Lipid Triad, particularly Lean Mass Hyper-responders. But only wider data collection will help confirm/disconfirm if this will be the case.
Again, this is preliminary, but certainly exciting. I’ve waited a long time to test this assay repeatedly, and I’m happy to see it falling in line with my general expectation given this context. There’s still plenty more variety to look forward to, both in my own experiments and the reported values of others.
Of course, I suspect this confirms a generally lower risk assessment given existing research in this area, but we can’t say for sure either way. Hence the importance of the LMHR Study as well as regular case data coming in from the LMHR community.