As I often say, I believe looking at LDL cholesterol levels alone is like reading the last chapter in a long book… you need to know all the elements in the story before that point to get an idea of how it ended up there.
Certainly I’ve been focused on the energy model and how being “powered by fat” is very relevant to resulting lipid levels. But I’m also aware of many other factors that impact cholesterol levels as well:
Yet one of the most common suggestions in lowering cholesterol (both total and LDL) is “replace saturated fat with mono and polyunsaturated fat”. This advice appears to have lots of evidence behind it. I’ve both read many studies and heard many stories that back up this advice, although individual results can vary.
In particular, I regularly hear one should “replace butter with extra virgin olive oil” where they can. Given the enormous popularity of both these sources of fat, I decided to set up an experiment to test each in isolation — and it’s going to be a bit ambitious.
This experiment will be a double crossover for four weeks, meaning I will be alternating between two interventions each twice, resulting in a total of four one-week phases. I will attempt to keep all other variables as equivalent as possible throughout: eating times, exercise times/duration, and sleep schedule.
For the extra virgin olive oil (EVOO) I’ll be using Kirkland and for the butter, Kerrygold. Both will be combined with warm water by emulsion blender and then mixed with a meal replacement shake powder (Ketochow). In addition to the shakes
- June 30-July 6 – EVOO
- July 7-13 – Butter
- July 14-July 20 – EVOO
- July 21-27 – Butter
Water and electrolyte beverages will be consumed ad libitum
Exercise will consist of two to three miles a day of walking with moderate, ad libitum upper body exercise (such as pushups).
Sleep will be ad libitum between 12am and 8am.
Blood tests for mornings of June 30, and July 7, 14, 21, and 28:
- Apolipoprotein A-1
- Apolipoprotein B
- C-Reactive Protein
- Complete Blood Count (CBC)
- Comprehensive Metabolic Panel (CMP)
- Fatty Acids, Free (NEFA)
- Ferritin, Serum
- Glucagon, Plasma
- Hemoglobin A1c
- Insulin and C-Peptide
- Lipid Panel
- Lp-PLA2 Activity
- Nuclear Magnetic Resonance (NMR)
- Oxidized Low-density Lipoprotein (OxLDL)
- Reverse T3
- Testosterone, Serum
- Thyroid Panel
- Uric Acid, Serum
- Vitamin B12 and Folate
- Vitamin D, 25-Hydroxy
Endpoints of Interest
There are two categories of interest to me for this experiment: lipid levels and inflammation markers. But more specifically, I’m interested in what will happen with LDL-C/LDL-P/ApoB vs Oxidized LDL (oxLDL).
- I posit the EVOO interventions will have lower relative total and LDL cholesterol levels
- I posit the EVOO interventions will have a greater proportion of oxidized LDL relative to total LDL particle count (oxLDL/LDL-P)
As mentioned above, there are many factors that can influence cholesterol levels, particularly LDL. There is one effect that is rarely discussed in the literature but is of particular interest to me — how much we see particular types of dietary fat result in higher or lower oxidation per LDL particle.
In other words, are we seeing lower levels of LDL cholesterol because LDL particles are getting oxidized and cleared by scavenger receptors at a higher rate? There are many limitations to the experiment in how well it can provide evidence to this answer, but it might open the door.
Regardless, I suspect we’ll have lots of other data from the many other blood markers I’m capturing that may prove quite useful.
Wow, at the range of blood tests. I know Nadir likes adiponectin as a marker as well. But as a fellow APOE 3/4 who doesn’t tolerate dairy (histamine intolerance, NOT lactose intolerant), I’d be more interested in a EVOO vs coconut oil challenge. Coconut or MCT oil seems to send my cholesterol through the roof. I peaked out at ~370 TC in February on a strict keto diet, but have dropped it to “only” 253 after switching to EVOO exclusively. I also added small daily quantities of a legume or oatmeal dish, which probably helped. But my TG/HDL ratio also improved to from 1.1. to ~0.5 (tho’ still not quite qualifying for LMHR status). Of course, my cardiologist says he only looks at TC, not ratios. He pushed statins on me as hard as he could, but settled for recommending me for a CT calcium scan in October.
Interesting on the coconut oil, thanks for sharing! Of course if there’s anyone who wants to try other variations of the experiment and share back the results we’d welcome it. For now this is to test against a control (butter) against EVOO – the experiment is already pretty demanding, so adding another arm would be difficult, and swapping butter for coconut oil wouldn’t work well as a control. So, EVOO vs butter it is.
Regarding your results, I wouldn’t at all be surprised if the carb additions (legumes, oatmeal) would impact (as per the lipid energy model), although the EVOO may be impacting as well (perhaps Dave’s experiment will provide some insight on this).
i drink coconut milk daily in a protein drink and my cholesterol was 600. i dont have a perfect diet but not any worse than others and is better than the common diet. so could it be the coconut milk?
Hi Dave, look forward to seeing results, especially as my cholesterol levels have increased somewhat on a low carb mostly carnivore diet. Then there is the question as to how much that matters.
Just wondered: is a week long enough to see changes in your cholesterol levels?
Kind regards, Nic
In our experience the change in lipids from diet is very rapid (3-5 days depending on what you’re looking at). There are exceptions, of course, for example if you’re coming from a metabolically unhealthy context to a healthy one, losing weight, etc that can cause slower changes over time. But for the sake of this experiment I would expect a rapid change in the space of a week, yes. 🙂
Can’t wait to hear the results
Excited for the results
Thanks — should be interesting…
As we all know that most olive oil is mixed with cheap vegetable oils. Good information on how to find the real thing: https://www.epicurious.com/ingredients/seven-ways-to-tell-the-difference-between-real-and-fake-olive-oil-article
Stick with EVOO from Italy. Especially from a single source in the south or Sicily.
The safest EVOO is from Australia or Chile, the others are more difficult to find abroad that are not mixed or low quality.
As far as Dave has mentioned, the brand he chose was picked due to it being reliable in this regard. From what he has commented on with regards to the flavor, it sounds like what the article describes. 🙂
Oh boy, I am so excited to see the outcome of this experiment! Like you Dave, I am also an ApoE4/E3 carrier, and I found this out near the end of June 2019 after having a blood test and seeing the high lipids and bad ratios.
Just curious on what your ratios are if you care to share. Im 6 mo in to Keto as well and had a recent panel done. TC 342, Trig 42, HDL 91 – I consider this my personal best ratio to date.
Non-fasting lipid panel (June 27, 2019) after eating too many eggs and butter:
Cholesterol: 553 mg/dL
Triglyceride non-fasting: 437 mg/dL
HDL: 125 mg/dL
LDL direct: 302 mg/dL
Non-fasting lipid panel (Jan 2, 2020). This was from having eaten no eggs or butter, and only meat:
Cholesterol: 259 mg/dL
Triglyceride non-fasting: 279 mg/dL
HDL: 76 mg/dL
LDL calculated, non-fasting: 127 mg/dL
Now this is my most recent lipid panel (May 9, 2020) eating only meat, no eggs, no dairy fat, and no added fats:
Fasting lipid panel:
Cholesterol: 223 mg/dL
Triglyceride: 109 mg/dL
HDL: 79 mg/dL
LDL calculated: 122 mg/dL
This is very cool. I wish I could use evoo in my coffee…lol
Sounds exciting. Wish you’d also test suet.
Probably won’t be testing any other kind of liquid fat for a while. I’m only on Day 3 and I can tell it’s going to be a long month.
We appreciate your flexible palate, Dave.
Looking forward to seeing your results. Good luck!
Have you considered the Omega 6 to Omega 3 ratio?
That’s a much longer topic of discussion. But regardless, I’m doubtful that will be very meaningful in this context anyway as the experiment is so short term.
Well you need to use a good olive oil not a store bought put together
I’m seeking to balance high quality EVOO with its wide availability/popularity. This is meant to be a very real world consumer comparison in that regard.
Would love to see what stearic acid does to lipids, and if there is a difference between animal-based or plant-based, as in suet vs cocoa butter.
Interesting research. As an apoe 3/4 I am keen to see the outcome of your study. With Kerrygold (or any butter from grass fed cattle) it is cheaper and more readily available than any exotic and expensive EVOO where you have to research the brand. Keen to see too what it means for those that are primarily on a meat diet (i.e. how to introduce more mono and polyunsaturated fats).
Are you weighting yourself? If theory goes right, you’re going to lose weight on butter or gain weight on EVOO . It’d be nice to get a confirmation to that.
Usually Dave weighs himself for experiments as (as he saw in his weight gain experiment) it can influence the numbers. So I’d suspect so, yes.
You are using bottom-of-the-barrel EVOO and top-of-the line butter. Was this intentional?
Apparently kirklands olive oil is supposed to be pretty reliable quality, and actual olive oil instead of cut with other oils which is what he was looking for. Not bottom of the barrel. Both are supposed to be widely available options people are likely to get.
Dave, could you report your Stragene/SNP analysis so we can have an idea of your baseline physiologic tendencies? Would help a great deal in understanding the results of your tests. Also, where can I find the numeric results?
Apologies if you’ve already reported this elsewhere, I am relatively new to your blog.
Dave, could you report your Stragene/SNP analysis so we can have an idea of your baseline physiologic tendencies? Would help a great deal in understanding the results of your tests.
Apologies if you’ve already reported this elsewhere, I am relatively new to your blog.
I’ll ping him on this – I’m sure it’d be of interest to many people.
Hi Dave a very interesting experiment – eagerly await results and hope it is safe for you.
Lets see if oxLDL and LP(a) move together in the same direction
and if the higher oxLDL has any effect on hsCRP & UricAcidSerum.
In your view in response to what stimulus does the liver increase or decrease apo(a) production … which then binds to create LP(a)? And does apo(a) bind mostly to oxLDL?
My educated guess is that the liver tracks some inflammatory markers and based on these increases or decreases apo(a) production … which then leads to increase/decrease LP(a)
Lets see if your experiment can throw some light on this as well.
Hi GPN –
Dave wouldn’t actually be able to test this himself, as his lp(a) is too low to measure via LabCorp (below their cutoff), therefore changes wouldn’t be able to be spotted.
It is my understanding that lp(a) can act as an acute phase reactant, and certain inflammatory cytokines/signals can increase lp(a) levels so I would not be surprised if you were correct and they did increase apo(a) production. Given my own experiments though, I would not be surprised if there were additional signals on top of this as well though, as I’ve seen it track with LDL-C in a metabolic context (under/overfeeding).
Is this completed? If yes where can one see the findings?
Hi – I’m not sure what you are looking for, specifically. If you’re referring to my experiments with lp(a) I posted a link to one of them – if you’re referring to something else, please let me know.
EDIT: You may be referring to this experiment! Dave ended up delaying it for reasons discussed here – I don’t believe he ever successfully completed it.