This week, Peter Attia released Measuring cardiovascular disease risk and the importance of apoB on his blog. I think it’s well worth the read and highly encourage you to finish it first before reading the rest of this article.
One quote in particular sums the article up well:
While I have historically used LDL-P and apoB metrics somewhat interchangeably, one advantage of measuring apoB over LDL-P is that apoB encompasses all of the potentially atherogenic particles: not just LDLs, but VLDLs, Lp(a), IDLs, and potentially chylomicrons. And this point has me relying more and more heavily on apoB today than on LDL-P in my patients and myself.
Generally speaking, particles that are neither LDL nor HDL are considered “remnants” in the literature. (There’s some further distinction regarding Lp(a) and fully lipidated Chylomicrons in rare circumstance regarding this topic, but we’ll cover that in future article).
In other words, we have three categories of lipoproteins as labeled:
- HDL particles (HDL-P)
- LDL particles (LDL-P)
- Remnants (all non-LDL-P, non-HDL-P particles)
Here’s a good summation from Wikipedia regarding Remnant cholesterol:
Remnant cholesterol, also known as remnant lipoprotein, is a very atherogenic lipoprotein composed primarily of very low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL). Stated another way, remnant cholesterol is all plasma cholesterol that is not LDL cholesterol or HDL cholesterol, which are triglyceride-rich lipoproteins. Nonetheless, remnant cholesterol is primarily chylomicron and VLDL from which most triglyceride has been removed, such that each remnant particle contains about 40 times more cholesterol than LDL.
Which Lipoproteins have ApoB?
So which lipoproteins have this ApoB we’re talking about? That’s easy – basically every lipoprotein that isn’t an HDL*.
- HDL particles (has no ApoB)
- LDL particles (has ApoB)
- Remnants (has ApoB)
* [If you want get technical, there’s some differences in opinion in the inclusion/exclusion of lipid-rich chylomicrons and Lp(a), with most leaning toward exclusion.]
I actually wrote an article on remnants two years ago and included it in my presentation at Low Carb Breckenridge a few months later.
Many people (myself included, originally) used LDL-P and ApoB interchangeably given the vast majority of “ApoB-containing Lipoproteins” in our bloodstream at any given time was likely to be LDL particles (LDL-P). My opinion on this definitely changed the more the Lipid Energy Model developed, because I could see how remnants uniquely told a story of the problem that LDL particles could not.
A Simple Boat Analogy
Imagine a fleet of cargo ships that are constantly being deployed and have two jobs:
- Deliver goods, which takes 1 hour
- Patrol and help out, which they do for 72 hours
You wouldn’t be surprised to see about 1 in 73 of these cargo ships having cargo and the rest being generally empty at any given time. Maybe some timing on launch or deliveries offsets this slightly so it’s more like 1 in 50 at times, or 1 in 100 other times.
Now let’s change it. What if you’re not seeing just one cargo ship full of cargo, you see 5. What does that mean?
You investigate further and find that there’s a reduced ability of these ships to deliver their cargo. They’re having a hard time completing their first job — the same job that should’ve been easy and take much less time on turnaround.
Maybe there’s a problem with the docks or rockier waters or the boats themselves. Regardless, you see more boats with cargo undelivered seems to associate with bad outcomes so you start to take notice.
Yet conversely, you notice that no matter how many more total boats you have, there seems to be very few bad outcomes when at any given time there are very few that have cargo — suggesting they are making their deliveries properly.
ApoB “Boats” Failing to Deliver
Most ApoB-containing Lipoproteins like chylomicrons and VLDL have a first job: to deliver their fat-based energy (triglycerides) to cells, and in normal circumstances it should happen very quickly (typically less than an hour). Then a large portion of VLDL will ultimately remodel to LDL particles and remain in the bloodstream for 2-4 days.
So let’s recreate our boat job list from above:
- Deliver triglycerides, which typically takes less than an hour
- Remain in the bloodstream (potentially immune/repair) for 2-4 days
But what do we commonly see in those who are obese, Type 2 Diabetic, or suffering other metabolic derangements?
- High fasting VLDL
- High fasting Triglycerides
- And thus, high overall remnants
I posit the simple explanation in most of these cases is that there is a clearly reduced capability on the part of the existing VLDLs to make their deliveries (job #1), which matches up well with one being past the “personal fat threshold“. There’s little parking left for the triglycerides, so we see an accumulation of fat in tissues that aren’t designed to store it, such as ectopic fat.
This from a great paper that illustrates this dynamic well:
Visceral fat is considered by many to behave as an ectopic fat depot, accumulating triglycerides (TG’s) when body fat storage needs exceed the capacity of subcutaneous fat depots to function normally
Talking LDL-P and ApoB with Attia
For those who managed to make it through the 3.5 hour podcast Peter and I had, you’ll note I kept bringing up this context often when I was outlining my dream request list on data. Peter was seeking to be helpful in talking about what datsets might have what I was looking for.
The Quebec Heart Study, here I printed it up here. I mean, basically it’s showing it has nothing to do with the LDLC once you know the ApoB. Look at the risk.
After some further back-and-forth I managed to clarify better:
Triglycerides, HDL, and preferably LDLP. Now, there is an important distinction we’ve gotta make with ApoB, because ApoB can, in theory, also include remnant lipoproteins.
Peter agreeing on that note for what I’m looking for:
[Full transcript of this portion of the podcast can be found here]
Yeah, LDL-P is more accurate than ApoB.
Thus far, I haven’t gotten ahold of dataset where I can do that stratification, but I certainly appreciate Peter’s interest in talking about it and his consideration in helping out. (An additional aside to Peter’s credit, he further offered to cover a visit to a National Lipid Association conference where I could’ve met with lipidologists on this very topic).
Are LDLs Getting the Blame for Remnants When Viewing only ApoB?
If one has high triglycerides, one almost certainly has high remnants, given they are triglyceride rich — much more so than LDL particles.
And given high triglycerides typically result in lower HDL (that’s a mechanistic discussion for another day), it’s understandable why this dysregulation would further associate with ectopic fat and yes, cardiovascular disease. (This profile is already recognized in the literature as Atherogenic Dyslipidemia)
Which brings us right back to the “Low Carb Cholesterol Challenge“. I believe the reason we’re having trouble finding studies where high LDL is shown to be atherogenic where HDL is high and TG low is that we are seeing low overall remnants, suggesting a more optimal lipid metabolism. One that is likely functioning well by comparison to one with low HDL and high triglycerides. (To date, we still haven’t had the challenge met.)
Moreover, it makes a lot of sense why one could have higher LDL due to longer residence time of remnants — thus having a higher marginal LDL for a negative reason. The tip off for whether this is the case being high VLDL and triglycerides. But this too is a hypothesis that I’m actively testing.
My larger point is that it is certainly my expectation that looking at ApoB by itself would likely show a greater association with cardiovascular disease given it lumps LDL-P with remnants. But I likewise expect we’d see a much stronger association with cardiovascular disease when looking at remnants without LDL-P.
I realized after posting this that I oddly forgot to mention the LMHR Measurement Project and how our current efforts will actually test the very hypothesis I mention above. Shame on me!
Yes, if you — like me — would want to see if those with very high LDL-P and ApoB would see greater cardiovascular risk at a population level in spite of having low remnants and triglycerides, considering contributing to the project as we’re getting closer to reaching our funding goal. Thanks!
Thanks, Dave. This makes so much sense from a ‘system’ standpoint. It seems like it takes an engineer (over a scientist or doctor) to figure that out. I am an engineer also and I just get frustrated with the lack of a holistic view of the way the body operates among the scientific community.
Thanks again for your great work, Dave. Glad to be a supporter (albeit a modest one)!
And thanks for your support! 🙂
Thank you, Dave for all your hard work! I recently had labs and a CAC done and would like some opinions on my results. My doctor wants to put me on a statin and I do not want to go on one. . I’m really not sure how to interpret these numbers.If anyone can shed some light on my results, I would be very grateful.
Apo B 166 mg/dl
Chol/HDL ratio 4.6 calc
TC 375 mg/dl
HDL 81 mg/dl
HDL large 5070 mmol/L
HS CRP 5.1 ( I have Rheumatoid Arthritis–in remission)
LDL Medium 312 nmol/L
LDL Particle Number 2084 nmol/L
LDL pattern A
LDL peak size 229.9 Angstrom
LDL small 186 nmol/L
LDL Cholesterol 276 mg/dl
Lipoprotein (a) <10 nmol/L
LP PLA2 Activity 178 nmol/min/mLH
Non HDL Cholesterol 294 mg/dl (calc)
TG 77 mg/dl
CAC score: 60.4
Left main Artery 0
Left Anterior Descending Artery 60.4
Left circumflex artery 0
Right coronary artery 0
I am 53 years old, extremely active, and zero carb.
Thanks in advance for any insight!
20 years on a statin can yield bad results (as I’ve seen in my mother). How long zero carb? Any prior CAC? How about maintaining for 6 mos or 1 year and redoing the CAC. If no progression, then why take a statin? Also could do carotid measurements and follow that. Dave’s receded on low carb. See his post on that.
Thank you for your response. I was Keto for one year and have been zero carb since August 2019. Never had a prior CAC. My doctor freaked out at my results, but I told him about Dave’s research and that I feel better than I have ever felt in my life. I’m off all RA meds since going zero carb, almost off antidepressants and anti-anxiety meds. I told him I would not take a statin. I started taking Vitamin K2 MK7 (I think that’s what it’s called) to help reduce the CAC score (heard about that from Ivor Cummins).
I’ll take a look at Dave’s post.
Did your Doc offer Zetia and Enduracin? Not statins.
1-Endur-acin (over the counter niacin) is a proprietary wax matrix that does not cause flushing. Take only 1,000 mg a day.
2-After a month if not at non-HDLc goal, add one half tab Zetia (now generic Ezetimibe 10 mg)
3-After another month if non-HDLc not at goal, take full pill of Zetia.
4- After another month if non-HDLc not at goal get Lipitor 10 mg (now generic atorvastatin) take one half tab a day.
5- Now on triple low dose medications, if non-HDLc not at goal increase to full tablet of Lipitor 10 mg.
Get rid of that RA fast with 30 mg of Boron/day.
Would also suggest low/no carb but you already have that. Maybe go carnivore for total elimination of plants or do the Gundry anti-autoimmune diet. Meat has no real Boron content, so you need a boron supplement. We normally get only 2 mg or less since the soil is depleted but we need more, like at least 10 mg, so do 30 mg therapeutically (just one provider on Amazon has 30 mg). Boron is toxic at 40 grams so no worries. Try it. Jamaica has 70% RA and no boron in the soil (200 years of sugarcane growing), whereas Israel has 0.5% RA and very high Boron soil.
You quoted Wikipedia:
Remnant cholesterol, also known as remnant lipoprotein, is a very atherogenic lipoprotein composed primarily of very low-density lipoprotein (VLDL) and intermediate-density lipoprotein (IDL).
“… very atherogenic lipoprotein” bothers me, as it implies a causal relationship (athero + genesis). Is there, to your knowledge, any evidence/plausible mechanism for a causal relationship, or are they merely (again!!) misstating a correlation? I note that the remnants definition does not seem to include oxLDL (if I understand correctly), which may be implicated in the causal chain of atherosclerosis, though not necessarily as the initiator of that chain.
Many thanks for all you and your cohorts are doing in this.
I believe it’s merely a correlation, restated it would likely say “high levels of remnant lipoproteins are highly associated with atherogenesis”. Which would make sense as the situations where you’d have chronically high remnant lipoproteins going around all the time would be the same that you’d expect to see in someone who was sick and more likely to develop heart disease (diabetes, metabolic syndrome, etc). But, no, I don’t think I’ve ever seen strong causal evidence for remnants *causing* heart disease. This type of language, I’ve noticed, isn’t necessarily uncommon in the research – but that’s a larger discussion in itself.
I can’t seem to find anywhere a desired level of remnant cholesterol. What do we want it to be?
https://cholesterolcode.com/low-carb-breck-18-and-an-update-on-remnant-cholesterol/ Has some indicated cut points – there may be something more recent, but I haven’t seen it.
Hi, unfortunately the studies we’ve found so far haven’t included *fasting* remnant cholesterol, which I would personally find quite important – the studies we’ve seen thus far when looking at All-Cause Mortality tend to use non-fasting measures. Although we’re not doctors, it’s probably safe to say, that if triglycerides are low remnants will also be low just as a rule of thumb.
I just got my lip panel back, and I have confusing Apolipoprotein B and remnant cholesterol results.
TG = 0.62 mmol/L
Total C = 7.64 mmol/L
HDL-C = 1.61 mmol/L
LDL-C = 5.75 mmol/L
Apo B = 1.70 g/L (normal is supposed to be 0.8 associeated with CD)
If you run the calculations, my other markers are good:
Remnant-C = 0.28 mmol/L
TG:HDL Ratio = 0.39
Should I be worried about my 1.70 g/L Apo B when my remnant cholesterol is so low? My test was after 18 hours fasted, and a few weeks of carnivore prior (was keto anyway before carnivore). My initial feeling is that my Apo B is just high because my LDL-C is so high from 18
hours fasted. Thanks!
Hi – we can’t really say whether you should be worried or not, as we’re not doctors. As is true for LDL and risk, everyone has to read the research and come to their own conclusions on what they feel comfortable with. As discussed in the post, it’s likely that high apoB in general is reflecting high *remnants* (paired with high triglycerides) and this might be why it’s more predictive than LDL-C alone. But plenty of lipidologists argue that all apoB containing lipoproteins are “atherogenic”. Likely, what I’d do in your situation is read the case made by several perspectives and decide for yourself, since the context of high apoB without metabolic syndrome is – I think – not entirely clear.
Some perspectives from people on the more cautiously pessimistic side would be people like Thomas Dayspring, Peter Attia, and Spencer Nadolsky – all are great resources. 🙂
You may also want to check out the Cholesterol Code facebook group as there is plenty of research papers and discussion there on this very topic!
What would be the reason that after 10 months of keto (80% – 15% – 5%) I had these blood test results:
Apo B 252 mg/dl
Total Cholesterol: 487
and after that I went on keto-carnivore and 3 weeks later I still got the same results:
Total Cholesterol: 446
All other markers are totally fine and I’ve been taking Omega 3 4000mg/day the 3 weeks prior to the last blood test and B3 500mg (for lowering triclycerides).
Could any stress or medium sleeping quality contribute in such results?
Fasting glucose: 70-80mg/dL, ketones: 1,5 – 4,3mmol/L
Thank you in advance for any input.
Hi – we’re not doctors and can’t give medical advice, but I would want to take a closer look at the context behind these tests. For example, higher than expected triglycerides of that level isn’t something I’d want to ignore, and would definitely want to work on figuring out what’s causing it. There are a couple common things that pop up outlined here.
Namely, in this situation, I would suspect coffee sensitivity as much, but would more focus on asking:
1) Were you 12-14 hours water only fasted for the tests? No coffee, no tea, no caffeine, etc
2) Do you consume any liquid fats like MCT oil, melted butter in broth or coffee etc, tallow in broth, things like that?
3) Do you track your food so you can go back over to see if anything stands out as a suspect for e.g. carb leaks or other issues?
4) Do you have additional markers that may lend further context for the numbers?
If none of those pop up as likely/possible, I’d round back around to coffee as a potential suspect. Which could be sussed out via coffee cessation for 10-14 days and re-testing. But I’d want to verify the other possibilities before assuming that’s what it is.
Thank you Huggins for your answer.
Starting from point (4).
I had multiple blood tests but I’ll name these major two:
This was the first ever after 10 months of KETO (80% fat from refrigerated butter and fatty fish/meat, 15% protein from sausages without any carbohydrates, pork meat, salmon, veal liver, 5% carbohydrates from tomatoes, broccoli, asparagus) while I was drinking 2-3 double black teas a day the last 2 months. I fasted water only for 12 hours ( Recurring Test:00 last meal) and I got these numbers @ 8:00 in the morning:
TSH: 1.68 [0.27 – 4.7μIU/mL]
FT4: 1.18 [0.7 – 2 ng/dL]
FT3: 2.2 [2 – 4.4 pg/mL]
Cortisol (F): 12.4 [6.2 – 19.4 μg/dL -morning]
Vitamin D: 48.4g/mL
CRP: 0.30 [< 6 mg/L]
Glucose: 89 [70 – 110 mg/dL]
Apo-A1: 136 [115 – 220 mg/dL]
Apo-B: 252 [60 – 160 mg/dL]
Ca-Calcium: 9.8 [8.4 – 10.1 mg/dL]
P-Phosphorus: 4.0 [2.7 – 4.5 mg/dL]
Mg-Magnesium: 2.0 [1.5 – 2.6 mg/dL]
Κ-Potassium: 4.7 [3.5 – 5.1 mEq/L]
Na-Sodium: 138 [137 – 150 mEq/L]
B12: 832 pg/mL
Ferritin: 156 [30 – 400 ng/mL]
Total Cholesterol: 487 mg/dL
HDL: 49 mg/dL
LDL: 349 mg/dL
Triglycerides: 220 mg/dL
SGOT/AST: 19 [11 – 38 IU/L]
SGPT/ALT: 17 [11 – 43 IU/L]
γ-GT: 12 [10 – 60 IU/L]
After that I stopped eating butter and replaced it with lard, stopped drinking black tea (I never drink coffee), I stopped eating vegetables and cheese products so I went carnivore 85% fat, 15% protein.
I also got:Vitamin B3 – Flush Free – 500 mgOmega 3 Fish Oil Capsules – daily 4000 mg instead of 1000mg daily since October 2019
So after almost a month with the above changes I did another blood test while I fasted with water only for 20 hours. The results are these:
ΗbA1C: 5.3 [4.8 – 5.9 %]
Fe-Iron: 87 [60 – 160 μg/dL]
Glucose: 84.0 [70 – 110 mg/dL]
C-PEPTIDE: 1.8 [1.1 – 4.4 ng/mL]
Homocysteine: 6.8 [5 – 13 μmo/L]
Total Cholesterol: 446 mg/dL
HDL: 46 mg/dL
LDL: 319 mg/dL
Triglycerides: 237 mg/dL
Just before I started KETO I didn’t have any blood tests. My pro KETO cholesterol values are from 2017 and beyond.
I’m also doing OMAD since October 2019 except from the first blood test.
I also did a carotid-vertebral artery triplex which was perfect and a stress echo-cardiography and my heart was working perfect when at stress of 152 heartbeats per minutes.
Lastly I always track what I eat with cronometer except when I’m on holidays.
Thanks for the additional context! It definitely helps narrow things down. One additional question, which may answer a remaining question I have: Would you mind sharing what exactly you were eating (and the form it was in – so say you had 1tbsp of lard with lunch, was it used to cook with, or was it had in tea/broth, etc) in the week leading into the blood test?
It’s definitely interesting that your triglycerides have still been higher than expected with carnivore as well as keto.
My omad menu was (and still is) like this:
6 whole eggs in omelet, 250-300gr of a fatty meat / fish and 90-160gr of lard from the refrigerator (depending on how fatty is the meat /fish).
I’m thinking that the high triglycerides might be for the reason that lately I’m still loosing fat from my body as I can see more vains in some parts of my body, or because from last year until this May my sleeping wasn’t good enough (5 to 6 hours total).
Or maybe my body is just made to work at these values.
Should I also get some vitamin E also?
Thanks for sharing that back, Nikos. It is pretty interesting as nothing there, or in anything else you’ve mentioned, stands out to me as why you’re triglycerides might be higher than expected. Of course I’m not a doctor, and can’t give medical advice, so beyond asking your doctor just to verify they don’t have any ideas, if I were in the same position I’d likely want to keep an eye on it over time and see if – as you suspect – it might settle on its own.
Another possibility, if you really wanted to rule out anything diet related, is to try a mono-food experiment to rule out a sensitivity to anything else in your diet. For example steak, salt, and water only with beef fat and see if they still remain elevated while eating only with that. Sometimes for family/friends Dave suggests something similar with an egg fast (eating only eggs) but because this can be a food some people are sensitive to, steak would also work along the same lines.
Regardless of what you decide to do from here if you get follow-up bloodwork I’d be interested to see what it looks like whether it resolves are stays consistent over time.
I really can’t comment on the vitamin E as I can’t give any advice on supplements or medicine – and I’m not really familiar beyond supplementing in values are low on tests, which I’d want to verify with a doctor.
There is something far more here than Vit E can adjust. Your no-so-good numbers seem to be fat related. I’d experiment with a low almost no fat/high protein diet and see how I felt and how the new numbers trended.
Steak, salt, and water is a very good idea. But if those were my numbers, I start a 10-plus day fast, get tested, and see what happened.
Good to see your hs-crp is excellent. Maybe no need to worry too much… But something is not right. I’d donate blood to dump ferritin as it is ultra reactive with O2. The normal range (30 – 400) is too high with the bottom number at 30; it should be around 20. If you got down to 20, you’d be better off.
Your Trigs/HDL is a very important biomarker, and Not Good at all. That needs to be investigated and fixed fast.
I need to add further information:
My height is: 174cm
I started keto 10 months ago without any metabolic issues, weighting 81kg and now I weight 68kg with 17,8% total fat in my body (DEXA Scan).
I workout 2-3 times a week (HiiT running and resitant training).
Good job!! Keep posting
I’m stumped: in short, all my numbers seem good accept apo-b, which is very high. I don’t consume carbs/sugar that I believe would lead to high levels of oxidised LDL but I wonder if some degree of fatty liver would simply hamper its LDL reception, raising apo-B? Or if could be something else? That possible? TG: 82 mg/DL, HDL: 59, LDL: 146; apo-B: 160. Any thoughts?
Hello – we’re not doctors and can’t give medical advice, but in our own data, and from Dave’s analysis of the NHANES data, shows that apoB tracks very closely with LDL-C, which makes sense as apoB containing lipoproteins includes primarily VLDL, IDL, LDL, and chylomicrons. VLDL, IDL, and chylomicrons should mostly be out of the circulation by 12-14 hours of water-only fasting, with some remaining (also called ‘remnants’ this would be total cholesterol – HDL – LDL = remnants) hence why it likely tracks so closely with LDL (as, on a fasted test, the majority of apoB containing lipoproteins would be LDL). It looks like the reference range (at least from LabCorp) for apoB is pretty tight, with ‘normal’ likely correlating to LDL levels under 100 mg/dL along with low triglycerides, so I would guess (though again I’m not a doctor) your apoB is listed as high because of that tight range, paired with your LDL-C level.
We can’t say whether that’s of concern or not (can’t give medical advice, don’t know your specific history or overall context, not doctors, etc) but we do have this post on apoB that may be of interest. You could also check out the Cholesterol Code facebook group and ask people to share their own apoB with their LDL-C and triglycerides to get a look at how it correlates and see if yours matches up similarly, as well.
Looking over my own data I’m seeing similar apoB levels at LDL-C levels around there, with some fluctuation seeming to relate to triglyceride level – but of course that’s only my data and it may be more relevant to hear from others or you could ping Dave (in the facebook groups or on twitter) for his NHANES analysis since I can’t find it.
[…] Lipid thoughts. […]
Just got my advanced lipid panel results. I’ve been on a keto/low carb diet for over a year. I lost 14 pounds. I admit I haven’t been strict but trying every day. I know my primary doctor will recommend statins. I need help understanding these results.
Total Cholesterol: 254
LDL particle number 2,178
LDL small 306
LDL medium 502
HDL, Large 7,6581
LDL pattern: A
LDL peak Size: 220.5
Apo B 121
Lipoprotein a <10
What do I do with all this information?
Sometimes putting your results into the report tool can be helpful, as it provides comments we’d likely made in case they’re of interest. Of course we can’t give medical advice, as we’re not doctors. That report is pasted below.
In addition, some further comments on patterns popping up here:
From what we’ve seen in ourselves and others, generally LDL-P is LDL-C x10 +/- 15% or so in generally metabolically healthy people, so for an LDL-C of around 174 I’d expect LDL-P to be roughly up to 1959 nmol/L. Yours falls slightly outside of this generally expected pattern but (again from what we’ve seen) this can be due to a couple of factors – for example of the LDL-P and LDL-C were tested separately instead of together (due to there being a range of standard error for each test), fasting below 12 hours, significantly over 18 hours, generally not being water-only fasted (e.g. consuming coffee, tea, or caffeine during the 12-14 hour fasting period directly prior to the test), and sometimes strenuous exercise in the time leading up to the test – are ones people have shared with us.
From what we’ve seen, small LDL tends to be 30% or less of total LDL-P in seemingly generally metabolically healthy people, which do you fall into.
Additionally, if you’ve seen your total, and LDL-C rise while on a keto/low carb diet you may fall into the pattern of a Standard Hyper-responder.
We can’t say whether this profile is of concern or not (as we’re not doctors), but we can offer some resources to explore different perspectives on the topic. For example there’s this presentation from Dave looking at high LDL in the context of high HDL and low triglycerides from a cautiously optimistic perspective, plus this post from Dr. Nadolsky looking at the same topic from a cautiously pessimistic perspective.
For those who decide they are not comfortable with it for the longterm, or would just like to confirm it is dietarily induced, the most consistently effective method (presuming it is dietarily induced) that we’ve seen demonstrated by people thus far is to decrease fat and proportionally increase carbs (e.g. isocaloric carb swapping), which is discussed here. Other options are available, though, of course.
Lastly, here’s the report tool read out…
• • Coffee: • • Cholesterol Rx: false •
–===== CholesterolCode.com/Report v0.9.5.15 =====–
• 1 on years on LCHF (20g to 120g carbs) •
Total Cholesterol: 254 mg/dL 6.57 mmol/L
LDL Cholesterol: 173 mg/dL 4.47mmol/L
HDL Cholesterol: 64 mg/dL 1.66mmol/L
TG Cholesterol: 72 mg/dL 0.81mmol/L
Atherogenic Index of Plasma: -0.312 mg/dL >>> Lowest Risk Third
—-> Go to https://tinyurl.com/ycccmmnx for more on AIP
Framingham Offspring: 0.7 Odds Ratio >>> Low Risk
—-> Go to https://tinyurl.com/y5fc5adl for more on this Framingham study
Jeppesen: >>> Lowest Risk Third
—-> Go to https://tinyurl.com/y63xp7lj for more on the Jeppesen study
Cholesterol Remnants: 17 mg/dL >>> 0.16 mmol/L >>> Low Risk
—-> Go to https://tinyurl.com/y84u92wm for more on Cholesterol Remnants
——CONVENTIONAL MARKERS AND RATIOS——
Friedewald LDL-C: 176 | Iranian LDL-C: 155
TC/HDL Ratio in mg/dL: 3.97
TG/HDL Ratio in mg/dL: 1.13 | TG/HDL Ratio in mmol/L: 0.49
**This does not constitute medical advice**
• Your triglycerides of 72 mg/dL are typically considered optimal.
• We would consider your HDL of 64 mg/dL as strong.
• We’d consider your LDL cholesterol as in range for what we’d call a “Standard Hyper-responder”. This is common for many going on a low carb diet. For more on hyper-responders, visit cholesterolcode.com/hyper-responder-faq. For a deeper explanation on our proposed mechanisms for this when powered by fat, see CholesterolCode.com/model.