Jun 15

Cholesterol Code – Part I : More Fat, Less LDL-C

I’ve thought a lot about how best to get this information out and knowing it will have many possible audiences. So I decided to just put it in a multipart series. This first installment will have some extremely surprising data with regard to dietary fat and its effect on LDL, HDL, and Triglycerides on a low carb / ketogenic diet.

Before we get started I wanted to emphasize two things:

  1. A big THANKS to all the doctors and engineers I swore to secrecy on the deeper data I was sharing. I really appreciate you keeping a lid on this until I had verified and re-verified. (With extra special thanks to the collaboration of Dr. Sarah Hallberg, Dr. Jeffry Gerber, and Ivor Cummins.)
  2. My cholesterol numbers are certainly high, and this might be distracting. I’m well aware of this and it is part of what started this data journey in the first place. But they’ll be more to this story by the time I get to my latest data.

The Brief Backstory

In March of last year, I got a marker for prediabetes from my blood panel, an A1C of 6.1. I was intent on avoiding future Type 2 Diabetes, so I researched and then began a low carbohydrate diet the month after. I lost 35 pounds, it raised my energy levels and seemed to improve my health in almost every way.

However, seven months later in November, I got back my first bloodwork and saw my total cholesterol had gone from 186 to a whopping 357, with LDL-C cholesterol climbing from 137 to 271. Given how incredibly great I felt the entire time, I was in complete disbelief. I heard some low carb dieters had exploding cholesterol, but assumed I wouldn’t, given I didn’t have higher than usual to begin with. From there, I began learning everything I could about Cholesterol Homeostasis.

The Idea

And this is where it got interesting for me. As a senior software engineer, the more I learned about the lipid system, the more I saw a familiar pattern –> a distributed network of objects. I read with particular interest on the assignment and apportionment of apolipoproteins and their potential role as a proxy for an information feedback loop to the liver.

Anyway, I’ll lay the general theory in more detail in a later post. Just know that if true, there should be two key presumptions:

  1. The cholesterol transporting lipid system would prove to be agile — much more so than is typically believed
  2. Discreet patterns should emerge between the diet and serum cholesterol now that disruptive inflammation is lower

So I went about testing these two points with my own blood starting in late November taking regular NMRs (Nuclear Magnetic Resonance – an advanced cholesterol test that directly measures lipoprotein particles and their sizes/classifications). Likewise, I kept meticulous track of my diet and nutrition values, both logging and taking pictures of just about everything I ate and drank. With blood taken every one to two weeks, I would make key changes between tests to see the outcome. Of course I was told over and over again that this was too frequent and that I needed to give the body more time to see results.

Initial Data

Sure enough, in eight tests over just three months I saw rapid changes, enforcing presumption (1). And yes, very discreet patterns did emerge, bringing evidence to presumption (2). In fact, both these behaviors were more pronounced than I could have imagined.

The tightest correlation appeared with total fat in my diet and LDL-C cholesterol. Now hearing this, you might not be surprised given that conventional wisdom seems to agree with the assumption higher fat (especially saturated fat) tracks with higher cholesterol in the blood. But that’s the first big twist — this isn’t a positive correlation, it’s a negative one. And get this –  the strongest time tracking appears to be not months or even weeks, but a three day rolling average.


Let’s use an example to illustrate. Imagine I took a blood test on a Friday morning, which we’ll call Day 0. Tuesday is Day -3, Wednesday is Day -2, and Thursday is Day -1 just before that Friday. If you took the dietary fat average I had between those three days, you get the score in the yellow line above. Put another way – all the days before that Tuesday (Day -3) appear to have very little to no relevance to my LDL cholesterol – I can practically ignore them!

To better show the correlation, I’ll flip the vertical axis of this same graph for the three day average of fat. (I’ll be doing this a lot moving forward)


At this point, I took my data to the Low Carb Vail conference and met with a number of great doctors there. I also had a particularly good conversation with Ivor Cummins who is likewise very versed in the subject as well as being a fellow engineer.

I explained the next obvious step was to do a “reproduction test” and see if I could replay the experiment to get anywhere close to the same results. Except this time, it was going to be even more controlled with a tighter timeline. (And frankly, very unenjoyable!)

Reproduction Test

The plan was to have my blood drawn every single day, five days in a row (Monday-Friday). On the preceding days (Sunday-Thursday), I’d have a specific day of meals that matched the two of the extremes in my testing for LDL-P. The highest LDL-P score (3073) was Dec 19th, when I had just 68g of fat the previous day, which we’ll call the “Low Meal Plan.” The lowest LDL-P score (1967) being on Feb 19th when I had 222g the previous day we’ll call the “High Meal Plan.” All day Friday, Saturday, and Sunday I didn’t have a prescribed meal plan and just ate generally “high” fat. We’ll call this period the “General Meal Plan.”

The pattern would be:

  • Sunday – Low Meal Plan
  • Monday – Low Meal Plan
  • Tuesday – High Meal Plan
  • Wednesday – High Meal Plan
  • Thursday – Low Meal Plan
  • Friday, Saturday, Sunday – General Meal Plan (Uncontrolled)

For the first five days I ate the meals in as close to the same times and in the same order as the days they were modeled after. I also timed the blood test to have the same fasting time since the meal of previous day as well.

I was flying to a developer conference that weekend and hadn’t planned to take another test, but finally decided to add one more after I got there on the following Monday. So the Friday, Saturday, and Sunday meals when I went back to higher caloric intake with higher fat would likewise show as well, though they weren’t as controlled as the previous week.

So what happened? See for yourself:



And again – let’s flip that left axis so you can see the reverse correlation better…


This was especially meaningful, not just because it replicated the same three-day average, but because now we could actually see the changes in successive time to the cholesterol payload. (As an aside, the LDL-P had a more interesting story with this run of days. But again, I’ll detail that in the next post.)

The Intentional Outlier

Any engineer reading this is probably thinking the same thing I was by this point. “If this is an algorithm, then it stands to reason I can crank it up to a new level to generate a new extreme.” Which is exactly what I did.

I scheduled a test for April 8th, and for the three days before, I ramped up my diet to an average of 4,274 calories and 349g of fat per day. Just a little heads up… this is extremely hard to do on a low carb diet.

Let’s display all 15 data points together now with this last one on the end…


And again with the reverse axis…


Sure enough, the April 8th result was the lowest LDL cholesterol score of all the tests. Moreover, it likewise tracked to the correlative envelope of the previous 14 data points, giving the entire series a jaw dropping -.905 Pearson score.

Other Data Points

I could write another five posts on the other data points, but I’ll let the graphs speak for themselves with just a brief statement for each.

Three Day Average Total Fat (inverse axis) vs Total Cholesterol


Generally, I don’t care that much for the TC metric, but I thought I’d include it for those who do. It is worth noting that data point 9 started on 3/7 with a 348 TC, just two days later I peak out at 422, then six days later I’m down to 364. Again, this is one more example of where we are told frequently that these numbers take a lot more time to change when clearly my data suggests otherwise.

 Three Day Average Total Fat vs HDL-C


While the correlation at 0.742 isn’t as prominent as as the -0.905 of LDL above, there’s no question it is still a very strong relationship. The primary divergence is in the first data point going back to 11/24/15, but otherwise it tracks remarkably close – even during the day-after-day reproduction experiment.

 Three Day Average Total Fat (inverse axis) vs Triglycerides


Lastly, we see the trigs are pretty close in correlation as well. Ironically, a 0.6 correlation on at least one metric was what I was originally hoping for when I started this experiment. Yet here’s trigs showing such a strong inverse correlation and it’s the runt of the pack at -0.61. Go figure.

Final Thoughts

While I’m glad both (1) and (2) of my theory above proved to open the door to these emerging patterns, I certainly didn’t think it would be such a perfect inversion of almost everything I’ve read to date with regard to Cholesterol.

My data over 15 data points suggest:

  • The more fat I eat, the lower my Total Cholesterol (87% inverted correlation)
  • The more fat I eat, the lower my LDL-C (90% inverted correlation)
  • The more fat I eat, the lower my Triglycerides (61% inverted correlation)
  • The more fat I eat, the higher my HDL-C (74% correlation)

Coming up in Part II – Particles, Particles, Particles. Results and analysis for my LDL-P, small LDL-P, and Pattern A/B.


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Siobhan HugginsDavidTimiVictoriaDave Recent comment authors

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I am just stating to read the article.

1) thanks for sharing all the details

2) please add a date somewhere at the top, end the article or where it mention ” The Brief Backstory In March of last year”, please change to March 201?

Thanks again


I got the opposite : on ketogenic diet both my total and LDL cholesterol went much higher. Only the triglycerids went down.


I have been doing LCHF diet for almost a year and a half now.
My Cholesterol (mmo/L) is very high;
TC 9.4
HDLC 1.9
LDLC 7.5
TG 0.97

Because of the above I decided to do the particle size test (Lipoprotein Electrophoresis) for LDL.

To my horror the results was bad: Result = I/B
Which means my LDL size is close to the smallest of the usual range.

During the time I was eating allot of cheese (Mature cheddar), eggs and Macadamia nuts.

The results have been done in April 2015 so more than a year ago.


When my doctor told me that cholesterol “bounced”, she wasn’t kidding! Thanks to your work here, I can see it for myself.


hi Dave,

Thanks for such a good post. I am impressed by the level of detail on your data. I too have a similar pattern that yours. My LDL (187) is not so high but my LDL-P ranges close to 2000 and sometimes more. HDL (70) is high and trigs are low (47).

I have ready from Ivor’s posts that there is no real correlation to mortality of ldl-p yet, and that also saturated fat seems to do the trick to lower the ldl-p.

Have had CAC scores 2 years in a row, bot to 0, so on the plaque arena I am happy.

If you don’t mind could you share with me which resources did you use to perform the testing?

Were the tests normally done by doctors appts. I’d assume you did them on your own since insurance companies don’t like paying for repeated tests and definitely insurance companies don’t like paying for the nmr nuclear test. I’d really appreciate if you can share that. May be there is a cheaper option that I don’t know about.

Because like you I am also an engineer and have drawn some correlations through the years (don’t we all love data 🙂

Thanks and excellent work


Thank you for posting. This is really interesting, I look forward to seeing more.

When thinking about lipid profiles and risk for CVD, the reference I often see is the Harvard study showing that the most important number we should be tracking is the Triglycerides/HDL ratio (getting it to about 2.0 or lower). The study indicated that this ratio is 16 times more predictive for a cardiac event.

If that is the case, should we pay any attention to the total cholesterol number? Seems that it would become irrelevant in light of the Trig/HDL numbers but I don’t know.

Timothy K Foxon
Timothy K Foxon

Hi Dave.

Interesting data, as you say, counter intuitive.
I am a hyperresponder also and have been trying to determine risk since I got my first blood test post starting LCHF.

I have “discovered” the following.

LDL levels change because the LDL setpoint changes for the following reasons.

1. Saturated (and maybe polyunsaturated) fat intake increases LDL since chylomicron remnants compete with returning LDL for uptake by the hepatic LDL receptor, so the catabolic rate of LDL declines while production is unaffected.
2. Dietary cholesterol increases LDL since this cholesterol accumulates in the liver and pressures/down regulates the LDL receptors. Same mechanism applies, catabolic rate of LDL decreases.
3. Insufficient intake of linoleic acid (18:2 n6) acts like a gate. Lower than 3% energy saturated fat, particularly lauric acid greatly increases LDL whereas above 7% of energy this activity is dampened (I don’t know why this occurs).
4. Insufficient bile production in liver down regulates the LDL receptor.
5. LDL can be considered as composed of two seperate pools that exhibit metabolic channelling controlled by triglycerides, for simplicity call them pool A and pool B. Pool A is composed primarily of LDLI and LDLII and is not as atherogenic. Pool B is composed of LDLIII/IV and is smaller, denser and considerably more atherogenic. These pools evolve under the control of triglycerides and insulin resistance. As trigs rise CETP and hepatic lipase activity rises and LDL/HDL is first cholesterol reduced and then lipid reduced by VLDL, resulting in small dense LDL and low HDL (since the ApoA1 protein gets shed due to the small size). Thus you can have high LDL that is benign or dangerous depending on your level of trigs. There is a threshold in males about 1.3-1.5 mmol where the changes start to become destructive, below this you are ok, above you start to accumulate small/dense LDL. Atherogenic dyslipidemia is characterized by higher trigs, low HDL but relativeley normal LDL (more particles but less density per particle). So most people in cardiac wards have low/normal cholesterol.

LDL becomes dangerous because it becomes oxidised, small dense has less antioxidant defence so succumbs faster.

Would love to see you debunk any of this or augment it.


Timothy K Foxon
Timothy K Foxon

Hi Dave.

Thanks for your quick response.

The reference for cholesterol and linoleic acid effects is “Saturated Fatty Acids and LDL Receptor Modulation in Humans and Monkeys” K.C. Hayes, P. Khosla, A. Pronczuk. For chylomicron remnant uptake by the LDL receptor it is “https://en.wikipedia.org/wiki/LDL_receptor”.

I think you are correct that chylomicron remnants have a shorter lifespan, however if the effect is strongly pulsatile the pulse in LDL may last much longer (since the plasma residence times of LDL I/II is about 2 days and LDLIII/IV about 5 days so the pulse generated on your day-1 would last past the test point further confusing me). Reference for residence times is “http://atvb.ahajournals.org/content/17/12/3542.long” fig 4. This paper is also the reference for my point 5 (metabolic channeling)

I think it is very strange that your pre/post LCHF experience with LDL is similar to mine but the within LCHF response is totally unexpected. I look forward to your subsequent posts.


Timothy K Foxon
Timothy K Foxon

Hi dave.

Sorry, one more point. The conflict time may well be extended since a high fat meal may take up to 8 hours or so to be digested and you will be producing chylomicrons throughout this time so your conflict window may extend to as long as 9-9.5 hours which is probably enough to raise LDL given your very short response times elucidated in your graphs.


Joan Day
Joan Day

most people do not have ferritin levels tested, but i ask for one. as it has been just a little high over the years, at 308 the end of nov/2015, now june I just had it done it has shot up to 491. I have been doing low carb high [good] fats for around 3 to 4 months, My ketons with urine test was 2..so that was great–but my cholesteral has gone from 5.6 last nov to now 8.22 –my dr is going to flip out for sure. trig moved from 2.54 in nov to 2.22 june so this has improved. My HDL was . 93 last nov and now is .93 –so the good one is not improving and still low, non LDL was 4.66, now up to 7.29, LDL was 3.51 now up to 6.28–and my cholesterol /HDL ratio is far worse, from 6–to 8.8–does anyone know much about he genetic mutation , and perhaps i have it and this is creating the problems. Others see improvements with there good cholesterol and lipids etc. –my bg has improved fasting was 6.1 now good at 4.5, and my A1C/ is gone down to 5.7, from 6.0 last end of nov. 29/15/ I have lost over 34 lbs, and feeling so much better–now this ferritin and cholesterol situation–I think I really need a specialist to help sort this out. but have no idea where i can find one to work with. My gp will be wanting me to take drugs, and i want to see what kind of diet I can use to fix this if it needs fixing.. i would be interested to know how many other people ever check there ferritin levels on high fat low carb diets, and with higher A1C–


You could have hereditary hemochromatosis, you can read about it on my blog
Hereditary Hemochromatosis
What is your age? I’m assuming based on your name you are female which means you have a built in iron reducer until you hit menopause. You want your ferritin levels to be in the range of 50 – 150 for optimal health. Ferritin is also an inflammation marker so it can go up with inflammation. I would definitely look into giving blood with those ferritin levels but I’d also get the gene test to rule out hereditary hemochromatosis.


Great post Dave. In regards s to Tim’s post, I have had total Cholesterol at 11.0 with HDL at 2.2 and tried at 0.7 yet after a subtraction analysis I had some small dense Ldl, – phenotype B. This was after a year of LCHF and training for endurance sports. Previously followed at high carb diet and previous lipid analysts for the past 10 years showed “normal lipid profiles. Total chol 4.2 HDL 1.7 trigs 0.5. Hard to know which way to go for the best of health

Adam Nally, D.O.

Superb . . . Thank you for posting this information.

Dustin Gerken

I comment each time I especially enjoy a post on a blog or I have something to contribute to the discussion. Usually it is caused by the passion communicated in the post I read. And after this article Queen Of Charms |. I was excited enough to post a thought I actually do have 2 questions for you if you do not mind. Is it just me or do a few of the responses appear like they are coming from brain dead visitors? And, if you are posting on other online sites, I would like to follow anything new you have to post. Would you make a list every one of your community sites like your Facebook page, twitter feed, or linkedin profile?

Han Sanson

I have not checked in here for some time because I thought it was getting boring, but the last few posts are good quality so I guess I¡¯ll add you back to my daily bloglist. You deserve it my friend 🙂

Jason Bellotti
Jason Bellotti

Great info, very interesting, I’ve been Keto for about 6 months, just had a second lot of bloodwork done, shows an increase in tg, only .2 from 1.2 to 1.4, my hdl went up .4 from 1 to 1.4 so my ratio went from 2.7 to 2.2 which is good, my total LDL went from 3.5 to 6 in the same time frame, any thoughts on the small tg increase? I’m very active (grapple/bjj regularly) and while I’ve dropped over 20kg on Keto, I’m currently sitting at about 10-12% body fat. Side note, the preceding day to my most recent test I dropped just over a kilo of weight, (mobilized tg theory?)


It would be interesting to see the same experiment on a person who have been eating a non LCHF diet.

Dr. Steven Horvitz


Great blog so far.
Only issue is you write like my engineering friend Ivor ; )

Your results are an N=1 experiment. It raises interesting questions.

I too, when going LCHF had a dramatic rise in all my lipid fractions, other than Trigs which remained normal.
Of course the elevated ldl-c and ldl-p still get my attention, even though I am a physician. Don’t worry, I do not believe in statins.

My question for you is:

Have you had any of the following tested along with the numbers you shared above?

Fasting insulin
Uric Acid
Tsh, free t-4 and free t-3
Apolipoprotein Genotype??? Actually are you and E4 genotype carrier?


LK Taylor
LK Taylor

I am as lost as a fat cell or is that a bug in the rug. I began a no sugar carb about 3 months ago and went to the doctor and cholesterol is up and thyroid is high. I am not a pill popper so figuring out how to get both measures lowered is the plan of the day. More fish possibly!


Hello. And Bye.

Andrea Mikler
Andrea Mikler

Hello Dave,

you have so much knowledge! Could you, please comment on higer HDL than LDL numbers. My total cholesterol was 6.16 with HDL 3.24 and LDL 2.69. Trigs were o.5 mm/l. I am on LCHF for about 4 years now. Normally I would not be concerned as we hear that HDL is the “good” cholesterol. However, I read few opinions (do not remember where) that high HDL is associated with higher mortality from all causes. Any thoughts on this?

Andrea Mikler
Andrea Mikler

Dave, I just noticed you commented on my numbers in part 1 just few days ago. Please, disregard my comment here and thank you so much for your opinion. Thanks for all your research and sharing it with the community :).


Hello Dave, just went through your narrative of the experiment. I was shocked to see my recent blood tests after being on low carb diet. Total Cholesterol 371.1; Triglycerides 100.3; HDL 73.9; LDL 210; Apo A1 177.8; Apo B 198. Before dieting Total Cholesterol 152; TG 81; HDL 31. Reading your notes gave me some solace. I was having high blood sugar previously. Now settled with HbA1C 4.9. Will be continuing this diet. Have increased my fat intake from 120 to 180. Will check blood and post you the results. Your comments on my reports?, please.


Just coming into this with 9 months LCHF behind me and the results of my first blood lipids test. Results very similar to the ones you had that set you off down this road. Total Col – 8.6 mmol/l, 6.3 LDL, 1.6 HDL and 0.6 Trigs. Had a massive argument with my doc over these results because I had stopped taking statins 6 months previously which he wanted to get me on. But onto my question, Considering your study findings that higher fat intake lowers cholesterol then why do you think your (and mine) lipid results jumped when you started LCHF which by definition means your fat intake was higher ?

Nancy Williams
Nancy Williams

Finally found a way to message you as I do not particupdate in Twitter or FB. Are you an APOE4 allelcarrier? Is that why you are a hyperabsorber? Thought you would enjoy the following article:
https://mobile.nytimes.com/2017/07/14/o … an-kennedy


Hi Nancy, looks like your link didn’t paste properly. What article were you trying to link?

I think I remember Dave saying he was APOE 3-4 in a Q&A one time. I haven’t had that tests yet, although I should put 23andme on my wishlist.

Nancy Williams
Nancy Williams

Finally found a way to message you as I do not participate on Twitter or FB. I am so very confused by all these diet experts and their conflicting opinions. I just read a comment in which I learned you are also a 3/4 genotype, like me. I have high cholesterol levels and am a hyperabsorber. I am not an idiot, and I have read your Part I several times; yet, I don’t understand. You began the article saying when on the low carb diet your cholesterol levels were exceedingly high. Are you saying you began a low carb low fat diet initially and then switched to a LCHF diet during your testing period? By eating the saturated fat, your cholesterol levels dropped but when ONLY eating low carb your cholesterol levels climbed? As an APOE 3/4, conventional medicine is dictating I eat very little fat; other medical advice states high amounts of monounsaturated fat only, and others say extremely low saturated fat and no dairy whatsoever. I just lost 30+ lbs on a LCHF diet (most days low carb only) and intermingled with intermittent and extended day fasting. Can you help me correlate the high cholesterol in the beginning of your low carb diet but the low cholesterol during your LCHF testing days?

Thought you would enjoy the following article:



[…] very first post here was on June 15th, 2016. By the end of the year, this site had mustered up 35,614 page views, for a […]

William Aschmetat
William Aschmetat

I am interested in trying this protocol before my next lipid panel. My question is, can a large portion of my fat/calories come from heavy cream? I’ve figured, based on the nutrition label of the brand I use, that a quart of heavy cream has about 288 grams of fat, so about 2600 calories. That would provide roughly half of my fat/calories for the day. I really enjoy heavy cream and would have no problem drinking a quart per day for three days. Does this sound reasonable or should I get my fat from other sources?


Hello, I recently watched your podcast with biohackers lab and found that your situation described me quite well. I am a very typical hyper-responder. I am 17 year old female and started low carb 1.5 months ago, with 3-4 weeks being ketogenic. Here are my details in my most recent of two tests (done last week and not so far apart with similiar results) in mmol/L:
TC: 14
Triglycerides: 0.9
HDL: 2.7
LDL: 10.6
Chol/HDL: 5.1

These results would usually be mind-blowingly concerning, but after watching that video, I am more willing to experiment, rather than just switching to the low fat diet as my doctor recommends. What actions should I take now? Do I need to look into genetics or do a lot of further testing?


Hello, I am 59 years, male.

Healthy, quite fit, no medication. I have been in low carb about 10-15 years, strict ketogenic diet about 4 months. I got my tes results yesterday, and they got me nervous.
fP-Kol 10.9 mmol/l double checked (422 mg/dl)
fP-LDL 9.3 mmol/l double checked (375 mg/dl)
fP-Kol-HDL 1.74 mmol/l (67 mg/dl)
fP-Trigly 1.24 (111 mg/dl)

Fasted 13 hours before test.

(6 months earlier: 9.4 (total), 6.7 (LDL), 2.19 (HDL), 1.2 (trigly)

P-CRP <1

What do you say? Thank you for your great site!

Dave Feldman: The Truth About Cholesterol – Carnivore MD

[…] and experimentation which has revealed some very powerful data (see his Cholesterol Code series Part I, Part II, Part III, Part IV, and Part […]


This is an old post, but I hope you can help me out with a question. You say and show that eating more fat will lower your LDL. But that does not jibe with your real world experience. Before you went on LCHF your cholesterol was lower than it is now, on a high fat diet. In the past, eating Std. American diet, which is lower in fat, you had lower cholesterol. Then you went on a higher fat diet and your cholesterol went up. In fact the higher cholesterol is what alarmed you so much that it spurred you on to doing more research.

So how can you say that eating more fat will drop your LDL? Is there a short term vs long term effect going on?

Siobhan Huggins

Hi! Yes you are exactly right that there’s a difference between the long term and short term effects. You may want to watch some of Dave’s presentations, which more clearly outline this – like this one from Breckenridge.

In short, the difference is mainly this:
The long term effect appears to mainly be one of primarily using glucose for fuel versus primarily using fat for fuel (e.g. high carb versus low carb). The running theory is that this is because relying on fat for fuel also necessarily relies on trafficking fat through the body in the form of VLDL, and chylomicrons (which carry fat as their cargo), in which VLDL remodels to LDL. Glucose does not.
So highly relying on fat for fuel may result in higher LDL compared to relying on glucose for fuel due to this turnover of VLDL resulting in a downstream increase in LDL with higher fat/lower carb – this is a hypothesis, but seems to fit with what we’ve seen so far.

The secondary short term effect mostly seems to rely on primarily relying on fuel from chylomicrons (fat from food you just ate) versus VLDL (mostly fat from storage).
You can think of these two as balancing each other – if you eat a lot of fat, you require less fat from storage, and over a period of three days LDL will tend to go down as the VLDL was needed less. That’s a gross oversimplification but hopefully gets you the main idea.

Hopefully that helps illustrate the difference between the long and short term effects of high fat. But the short term effects help to show that the long term effects may be driven by energy demands – short term gives us hints as to why in some people the long term effects happens. Hope that helps!