I often joke that I have to live schizophrenically between Scientist Dave and Human Dave (the professional lab rat). Today both of them are extremely happy.
What is a CIMT?
CIMT stands for Carotid Intima-Media Thickness test. Here’s a brief description that puts it well:
The carotid intima-media thickness test (CIMT) is a measure used to diagnose the extent of carotid atherosclerotic vascular disease. The test measures the thickness of the inner two layers of the carotid artery—the intima and media—and alerts physicians to any thickening when patients are still asymptomatic.
It’s an ultrasound taken on each side of the neck to make this measurement and typically requires a visit to the doctor’s office to be done by a specialist.
Since my CIMT climbed considerably following the Weight Gain Experiment, I’ve been publicly hypothesizing for over half a year that I expect it will drop again while being on a ketogenic diet and averaging well above 200 mg/dL of LDL cholesterol (LDL-C) and over 2,000 in LDL particle count (LDL-P). Save my half of the Tandem Drop Experiment in September, I’m actually quite confident I’ve been running at these levels throughout this period and have additional CardioChek data to show for it (see below).
The data I have here is quite astonishing. In fact, after getting the first CIMT taken on December 13th, I decided go get a second one a week later on the 20th. I knew there’s be some variability, but I wanted to be sure both of them were well below the previous reading.
Above I’m showing a screen shot from the Dec 20th reading. Below I include both along with the average.
This is the Second Reversal
It can’t be emphasized enough why this is such a milestone. We’ve observed my regressing the CIMT from the very first one I had up until November 2017, all while averaging very high LDL-C and LDL-P. My Weight Gain experiment dropped my LDL-C and LDL-P to 130 and 1,130, respectively, but brought my CIMT to new heights on both sides. Now after this experiment and returning to high LDL-C and LDL-P we see the drop again.
Certainly one can bring up that weight gain alone might track with CIMT increasing and I think there’s definitely some merit in that. However, my CIMT from November 2016 to 2017 was regressing even though I was actually gaining weight (from around 175 to 185lbs). And secondly, my current weight (196) stands at over 10lbs more than all my previous scans save the last one in May. In short, I think weight matters, but by how much is much more debatable in my data set.
I’ve gathered quite a bit of evidence over three years, but I put this well into the highest category of consideration.
These aren’t just transient blood markers, these are actual physical measurements. And thus far, the pattern is especially compelling.
Am I certain this will continue? No. As always, my opinion goes where the data takes me. And if the data changes course in a significant way, I’ll adjust accordingly.
Yet for those who keep asking me why I can be more comfortable with a high LDL-C/LDL-P while also maintaining a high HDL-C and low triglycerides, this is most influential evidence to date.
N=1 to become N=Many?
My sincere hope is that more people follow this example and take regular CIMTs, preferably every six months. This goes doubly so if they are Lean Mass Hyper-responders. If you do, please report that data back to us, positive or negative.
It’s now my pleasure to finally update this chart with the new data. (Just in time for the holidays too!)
I’d love to obtain follow up CIMTs now that I’ve stopped all lipid medications. Unfortunately, after the doc I was seeing wouldn’t really tell me the results of my second CIMT, just that “it’s still bad” and you still need to continue taking a statin, and should obtain prior authorization from insurance to pay for Repatha, I left the practice. I understand that inter-rater reliability is not high for CIMT, so if I obtain another CIMT, I’d almost be starting over.
I think you were Smart to leave that practice as it sounds they lack communication. I think some doctors are afraid that their patients will become more health savy than they are.
I got mixed results. While having LDL-C over 200 and LDL-P over 2000 for most of 2018, the CIMT in my left side decreased, while that in RHS increased. Both tests were done at the same lab.
mean L mean R max L max R
January 2018 0.575 0.4 0.654 0.462
November 2018 0.486 0.502 0.539 0.539
In 2018, my small dense LDL and oxLDL were very high (described in detail here: https://decodinghumanbody.wordpress.com/2018/12/02/correlation-between-oxidized-ldl-and-small-ldl-n1/).
They have come down lately. Hopefully, I will have better results next year.
Very interesting. Yes, please continue to share back the data.
When I had my CIMT done in August I was told it indicated low risk and I had nothing to worry about. When I suggested a follow-up test down the road to determine if there would be any changes happening I was told that in cases like mine there would be no follow-up testing. The insurance covered testing can only be ordered by a specialist and I cannot afford independent testing. The sceptic in me knows that I was given the test for the purpose of finding problems that would convince me to start Statin/PCKS9 Inhibitor drugs which the cardiologist was very enthusiastic about. Although it now should be evident that I am in perfect health I am still considered recalcitrant for turning down drug therapy especially when the $16,000 monthly cost would be covered by insurance.
By $16,000/month I’m guessing it was a PCSK9i.
It’s true, it would be good to do follow up CIMTs at higher frequencies. But perhaps you can request them at lease once yearly.
My LDL-C is 183 LDL-P 2409 CAC Score >900. If I can regress my CIMT, would that correlate with a lowering of the CAC Score? Nice work Dave.
Hi Phil — I’m not sure about regressing CAC. You may want to ping Ivor Cummins on this as he is much move versed in these studies. http://www.thefatemperor.com/
Your hypothesis seems to be gaining more ground with these results Dave.Something I’ll do when it becomes readily available in Botswana next year. I’ll use it to supplement the CAC I had earlier this year.
Great. And as always, feel free to share back the data.
Is the thickness merely inflammation?
I certainly feel it’s a component at a minimum, yes.
Your right increased 10% in a week. Any thoughts on how big the error bars should be on these measurements?
I’ve always suspected it could be 30-60 um. But I haven’t been able to look into it very much as I’d need studies that match that particular model. As always, this is why I like high frequency testing as it becomes more obvious just how high the standard deviation may be.
Dave, do you know the margin of error for the test? I would think that your left side is within the margin of error for your last two tests though a 10% increase on your right is interesting. That suggests that maybe CIMT fluctuates.
Right — see above. No question, I definitely think CIMT fluctuates along with some margin of error. But there’s also the positioning of the device and angle as well. Again, this is why I like frequent testing to help tease out further.
You should probably be asking for the other side of the equation, too. That is, those people with low LDL and low LDL-P to see if they have progression, say, while on a high carb diet. I assume the answer would be “Yes”, but it’s hard to know.
Not sure on CIMT in particular, but I’d be interested in finding out.
I understand the reasoning around LCHF leading to increased baseline LDL. More boats needed, etc. If so, then why does a rapid change in fat see the inverse LDL change ?
A sudden demand for more boats means less boats ? Huh? sorry to take you back 2 years ago…
Is there a post or video you have done that is specific on this?
BTW – LCHF for 6 years – my numbers:
Sure — see this video: https://www.youtube.com/watch?v=0LuKwsz9Woc
And your profile is near a LMHR. If you haven’t already, read this page: https://cholesterolcode.com/lmhr/ and consider checking out our LMHR Facebook group: http://facebook.com/groups/leanmasshyperresponder
OK, thanks ! I think I’m squared away on that part of this. Can you fill in another gap ? The VLDL are created in the liver (because Trigs can’t travel alone in the aqueous medium), but the adipose tissue has the inventory of stored fats (as Trigs). To utilize stored fat, first fatty acids are released by adipose tissue and transported by the bloodstream – to the liver ? and then packaged into lipids so they can be transported in bloodstream (aqueous) to cells that need the energy? If not, where is the liver getting the fatty acids to make Trigs? Why all this re-packaging if the fatty acids are already circulating in the blood? Would monitoring serum fatty acids also be revealing about metabolic status? (Maybe I need a basic text…)
Free fatty acids released from adipose will attach to albumin (a carrier protein) and either (1) get taken up by nearby tissues, generally or (2) get taken up by the liver, then repackaged into VLDL. My energy model posits that there is more need to recirculate VLDL-TG when there is less overall adipose mass (less supply locally, thus more demand globally).
Had a CAC of 833 May or 2017. I’m setting up follow up hopefully this week and will be having my first CIMT done. Since being Keto more than 2 years I don’t know what my CIMT will be. But thanks Dave for doing this. It is very encouraging. Am hoping my CAC levels have dropped. I do not take BP or Statin drugs.
[…] might have surprised you too, but this was entirely expected. And if you haven’t already, consider reading this before you […]
You may find this of interest regarding the impact of a ketogenic diet on CIMT: https://www.sciencedirect.com/science/article/pii/S0261561417313997
Dave, can I ask what the units are in your CIMTs? I called a local imaging center to inquire about getting the test. They said intima thickness info was included in the Carotid Doppler test I had last year. My report says:
Right common carotid artery:
— PSV of 89 cm/s
Right proximal internal carotid artery:
— <40% stenosis with PSV of 150 cm/s with mild, smooth, homogenous plaque
Right external carotid artery:
— PSV of 94 cm/s with mild, smooth, homogenous plaque
Right vertebral artery:
— PSV of 39 cm/s, antegrade Doppler flow
Left common carotid artery:
— PSV of 92 cm/s
Left proximal internal carotid artery:
— <40% stenosis with PSV of 124 cm/s with mild, smooth plaque
Left external carotid artery:
— <40% stenosis with PSV of 140 cm/s with mild, smooth, homogenous plaque
Left vertebral artery:
— PSV of 39 cm/s, antegrade Doppler flow
Obviously I have some plaque side-to-side, but not front to back. And I had to look up what 'PSV' means (peak systolic velocity). This Carotid Artery Stenosis webpage from the Cleveland Clinic is useful, including charts showing the test ranges.
The report also gives ratios between ICA (internal carotid artery) & CCA (common carotid artery):
Right: ICA/CCA Ratio: 1.69
Right: ICA/CCA Values: 150/89
Left: ICA/CCA Ratio: 1.35
Left: ICA/CCA Values: 124/92
Which suggests the ratios are meaningful, like systolic/diastolic in blood pressure. I'd be curious to learn more.
But basically I don't know how to compare your 500-600-ish numbers to the PSV numbers in my report. Do you know the units used in the CIMT? Or is there another resource where I could cross-correlate my numbers to your self-testing?
Thank you for your great work!
I haven’t had a chance to get into PSV measurement yet, but I believe they aren’t exactly 1:1 comparison in that each is apply the physics differently to capture the measurement. I’m looking to get more advanced measurements myself once I can find a better shop around here to help me out with that.
PSV and CIMT are completely different measures. PSV measures blood flow velocity and CIMT measures the thickness of the wall of the vessel. No way to move between the two measures. Sorry.
I sure wish Cardiologist would get on board. I have a Zero Risk CAC but my Cardiologist insists on Statins again and when I asked him about the CIMt to check for soft plaque as well, his response was he’d never heard of it and there’s no test that he’s aware of and rewrote script for Zetia, or I had the choice of infection since I have pain so badly with them. My body rejects injections as well. I do Keto/Carnivore. I think he was annoyed with my questions since he knew nothing.
He may know of it as a Carotid Intima-Media Thickness test, similar to a carotid doppler but measuring the thickness of the intima-media from the ultrasound image. My doctor also didn’t know of it by the term CIMT either, so I had to specify.
Most doctors I meet want the best for their patients, and give advice based on this goal, but it’s the patient’s job to decide if they feel this advice helps them reach their health goals based off of their understanding of the research available. Hopefully you can help explain your position to your doctor, so he can help you address your concerns with the resources he has available. 🙂
Dave, I asked my doctor for CIMT and received a result from carotid ultrasound measuring peak systolic and diastolic velocities. Are these results useful or is CIMT preferred?
Sorry, presses the flag by mistake.
I don’t believe either one of us has experience with that test, although a quick search looks like it’s checking for stenosis (stiffening of the artery) which may be handy information to keep on hand. You should be able to go back and ask for a “Carotid intima-media thickness test” next time if you still want it – I had to give the full name and not just acronym for my doctor to order it properly.
Thanks. Just wondering if it’s necessary with all my other tests being good.
It’s really your decision, especially as far as if you’d find it useful or not – I opted for a baseline just so I could track it over time, that way if it every comes up as odd I knew where I started from. But if it’s not something you’re interested in, it is up to you! 🙂
Wow – great study. Thank you for all you & your crew do.
What exactly did you Standard American Diet entail?
What about the link between snoring and increased cimt? Perhaps the dietary changes are contributing to a reduction in snoring?
Although this is a bit of a guess on my part, as I haven’t looked into it, I’d guess that the environment that leads to one (e.g. CIMT/poor metabolic health) leads to the other (snoring). I did see this a while back, which may be relevant, although it’s discussing sleep apnea and not snoring specifically.