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.
Final Thoughts
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.
So can we order this test and, if so, how? Thanks.
Hi Cindy,
it can be ordered Boston Heart Labs, the test is called OxPL-ApoB.
The first place I’d personally check is whether your doctor can order it, as physicians may have an account with Boston Heart. If not available, you may want to check in in the Cholesterol Code facebook group if there’s a provider in your area you could go through.
We are intending to launch a Boston Heart ordering beta via Own Your Labs in the future but it’s not currently available yet. So the above avenues might be worth exploring if you’re interested in testing it now.
Very cool! So glad to see this and looking forward to your continued release of info as you move forward.
I recall you talking about this before the assay was available. Nice spotting. Looks like a smoking gun. Thanks for the heads up.
I have super high LpPLA2 so I want to order the oxidized LDL test to clarify my risk, following the figure. Is there a third party site where you can order Boston Heart tests?
Hi – the first place I’d check is with your primary care provider as they may have an account (or be willing to set up an account) with Boston Heart so you could order directly through them. If that isn’t available I’d recommend asking in the Cholesterol Code facebook group for potential distributors in your area, as I’m not personally aware of all of them. We are planning to provide through our service Own Your Labs but it’s still currently being set up and isn’t available yet. There’s a sign up for the beta here though.
[…] Feldman digs into a little-used measure of lipoprotein […]
I’ve got aortic stenosis and I am trying to slow it down
Hi Dave, we’re not doctors and can’t give medical advice – but if you had any specific questions perhaps we could provide our thoughts (if relevant), or resources that may be of interest (to discuss with your healthcare team if you wanted to follow-up on them).
I’ve been fending off even my self-identified “Keto docs” for years over elevated LDL, in the context of perfect other markers including pristine HDL and Tryglycerides. The latest pitch for statin therapy is a “high” LP PLA2 activity. Apparently my latest self-identified “Keto doc” (I came to him from a referral service which shall remain nameless) had attended a conference and was very excited about this Cleveland Heart marker.He even provided a Cleveland Heart-branded handout.
Looking into it more closely (I have a close family history of fatal arterial hemorrhage vs arterial blockage; CAC=0) including review of Siobhan’s excellent work, it appears to me that my inflammation elevation is moderate — at worst. But hard to tell on the lab binary reference range ( “optimal” or “high” — WTF!).
BTW, on the Krauss particle analysis, I’m a low risk Pattern A! When questioned, Keto Doc clearly had no idea this was on the lab report in his hand, or what significance this might have to MY CVD risk. I guess the Cleveland Heart (sponsored?) conference failed to cover Dr. Krauss’s work at UCSF.
Your information on the Boston Heart test, and the context to understand it, is very exciting. Keto Doc is re-running the labs as part of my annual “sick care” exam. If it again indicates “arteries on fire” to Keto Doc, I’ll be headed to Boston Heart — one way or another— to investigate further. Given the family history of fatal arterial hemorrhage, this is worth an informed careful analysis.
Thank you for all you do!
Hi Richard, glad to hear you’ve been able to work with your doctor and discuss your own concerns/perspective with them – that’s always great even if at times you disagree on what the best approach is for you and your situation.
As a side note, although we’re not doctors and can’t give medical advice, we’ve personally noticed that Lp-PLA2 activity in our own and others results can track with LDL-P (and thus LDL-C in situation of ‘concordant’ LDL-C and LDL-P which typically occurs with low TG and high HDL). I wonder if this may be what you’re seeing? Not possible to tell without actual levels posted to see if they fall into the pattern we’ve personally seen thus far, so if you want to share the lipid panel results (LDL-C, TC, HDL, TG) and Lp-PLA2 value (and measurement used) I would be able to comment better.
I did carnivore for 30 days and then did a comprehensive lipid panel to see what things looked like. I’m trying to understand it all, and what’s really ok and what isn’t. My mentor who thought carnivore might help my Lyme disparase led me here. I’ve been reading on Apolipoprotein B (162mg/dL) and Lipoprotein (a) (99mmol/L) and am trying to figure out how much trouble I’m in with those numbers?
Hi Dave, this is indeed exciting and I truely appreciate the engineering approach as the guidances to date have been very confusing. I too believe it may prove to be the damaging factor from diet rather than the volume of native ApoB particles and I would be particularly keen to know its(Diet) implication on the Endothelials for which I suspect will be triggered by processed oils and sugars.
I have achieved green lights across the board on many markers without Statins, yet I too still have high LDL-C .. my ApoB/ApoA-1 ratio is 1.0 and LP(a) 47nmol/L, remaining cautious about Statins and their impact on my Liver enzymes, one can only hope.
We unfortunately do not appear to have this test in Australia, but I will watch for your detailed write up for sure and if the test becomes available, I will be on it mate!
Thanks to the Team!