Jan 20


Please consider supporting my Patreon. All funding for my research and this site come solely from individuals like you. Thank you!

  • If you know little to nothing about cholesterol->
    • And you want to learn the basics->
      • You can check out my Simple Guide to Cholesterol series. It’s full of illustrations and is written for laypeople. Enjoy!
      • Likewise, I have this video that goes over the basic markers for cholesterol while on a low carb diet. (Pictured to the right)
    • You can enter your cholesterol numbers into our popular Report tool to check them against many risk calculations at the same time.
  • If you’re wanting to know about my research->
    • You want an overview->
    • You want the most recent breakthroughs->
      • 1/2/2018: In this latest video, I demonstrate massive changes to my LDL Cholesterol over 5 stages in a matter of days. LDL 207 to 103 mg/dL in seven days with high carb, up again to 146 on mixed, down again to 113 on high fat. (Pictured to the right)
  • If you have seen your cholesterol rise considerably on a low-carb high-fat diet (like myself):
    • You may want to first visit the FAQ.
    • I would strongly encourage you to read through this blog and my own journey revealing the Inversion Pattern. Key moments were the Identical Diet experiment and the Extreme Cholesterol Drop experiment that I wrapped around the first presentation of my data for the Ketogains Seminar.

Dec 13

#CholesterolScience Show – with Ivor Cummins

Audio Only Version Available

Click here to download the audio only version of the show (thanks, Ivor, for supplying this for our readers!)

Show Notes

0:00 Intro and Greetings

0:35 Ivor’s backstory

2:40 Cholesterol Conundrum – What’s changed since Ivor gave the presentation in 2014?

Video mentioned: Cholesterol Conundrum

3:55 Dave’s thoughts on Ivor’s Cholesterol Conundrum video

4:43 Do LDL particles drive inflammation in-and-of themselves?

5:43 Do LDL particles “BB gun” into the arteries and damage the endothelium (arterial wall)?

7:35 Devil’s Advocate Intro

7:50 Considering the majority of top lipidologists are in general agreement over lowering LDL cholesterol and particle count, shouldn’t Ivor (and other non-experts) concede to this point?

9:55 Even if one were to find a few outlier studies, doesn’t the bulk of the data on LDL cholesterol and particle count more than cover any skepticism of the lipid hypothesis?

Study mentioned: A consensus statement from the European Atherosclerosis Society Consensus Panel

Study mentioned: A Critical Review of the Consensus Statement from the European Atherosclerosis Society Consensus Panel 2017

12:30 Whether CAC is zero or not shouldn’t everyone take steps to prevent heart disease anyway? Wouldn’t you want to discourage a false sense of security from a zero score?

Slide mentioned: Slide 2

19:14 Discussion on no benefit from statins for 0 CAC results

21:37 Concerns over adjustments in the study

22:55 Submitted Questions from Social Media Intro

23:37 What tweaks to keto would Ivor suggest for people with genetically high cholesterol (Familial Hypercholesterolemia)?

26:18 ApoE4 and keto – does anything change if they’re already, in some way, metabolically deranged?

28:52 What is your opinion on keto and saturated fat for people with apoE4? And what is your ApoE status?

30:32 How soon after receiving a CAC Result above 0 should you re-test?

32:00 Is there any strong mechanistic evidence that real world changes in human serum LDL can alter the rate of active or passive movement across the arterial glycocalyx or endothelium without pre-existing damage to the area?

Slide mentioned: Slide 5

35:31 What is LOX-1 and what is it for?

36:48 Could aspects of atherosclerosis be serving a purpose?

37:50 Differences in LDL types in healthy and diabetic people and its effects on endothelial cells

Study mentioned: Low-density lipoprotein in hypercholesterolemic human plasma induces vascular endothelial cell apoptosis by inhibiting fibroblast growth factor 2 transcription.

40:18 Different contexts for high LDL-P – metabolically healthy vs diseased

42:05 What is your opinion on high lipoprotein(a)?

NOTE: Lipoprotein(a) is considered an important cardiovascular risk factor. Like HDL and LDL it is a lipoprotein found in the bloodstream in humans, however it has a unique apolipoprotein: apo(a).

Blog post mentioned: The Big Deal about Lipoprotein(a)

44:25 LP-PLA2 as a risk factor – and what is “high”?

49:17 Why did Ivor call Ancel Keys misinformed?

NOTE: Ancel Keys was a physiologist and researcher, most known for his Seven Countries Study (first presented in 1955), and for popularizing the idea that saturated fat and cholesterol cause heart disease.

55:06 Your thoughts on taking statins on a ketogenic diet?

56:58 How would a person on a whole food plant-based diet lower their cholesterol? And for someone leading a healthy lifestyle is high cholesterol still a risk factor?

1:01:00 Is isolated high LDL high risk?

Slide mentioned: Slide 3

1:05:07 Updated 2018 guidelines

Article mentioned: 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol

1:06:45: Where does the LDL >190 mg/dL cutoff come from?

Study mentioned: Low-Density Lipoprotein Cholesterol Lowering for the Primary Prevention of Cardiovascular Disease Among Men With Primary Elevations of Low-Density Lipoprotein Cholesterol Levels of 190 mg/dL or Above: Analyses From the WOSCOPS (West of Scotland Coronary Prevention Study) 5-Year Randomized Trial and 20-Year Observational Follow-Up.

1:09:55 Could context matter for calculating Total/HDL?

1:11:55 Assuming saturated fat raises LDL, and assuming LDL causes heart disease assuming all other things remain constant can it other factors influence risk?

1:14:54 Questions from Chat Intro

1:15:18 Please tell us about your high ferritin, and how it relates [to health]

1:21:08 The apparent modern pushback against HDL

Study mentioned: HDL and cholesterol: life after the divorce?

Slide mentioned: Slide 4

1:27:45 For Lean Mass Hyper-responders on LCHF/keto if there is temporary systemic inflammation is there reason to lower LDL/apoB to avoid atherogenesis?

1:30:18 Can anything be done to improve particle size and number?

1:33:22 Should you be concerned about isolated low HDL if all other markers look okay?

1:39:57 Keto critics say keto is unhealthy long-term but provide no reasons. Is this because there are no reasons, or if anyone knows a reason please let us know.

1:42:55 Where you can find Ivor

Twitter: @FatEmperor

Facebook: Ivor Cummins

Website: The Fat Emperor

Youtube: Ivor Cummins

1:43:15 A note for Joel Kahn

Slide mentioned: Slide 1

1:46:26 Credits and Outro

Dec 09

#CholesterolScience with Ivor Cummins and Joel Kahn (Rescheduled)

Alas, due to a recent unfortunate event, I had to delay these two great interviews. But both guests were gracious enough to reschedule to this week.

How to Ask Your Question

You can ask questions of either Ivor Cummins or Joel Kahn in advance of the broadcast one of two ways:

  1. Comment to this blog post down below — but keep it short! (Don’t ask multiple questions)
  2. Comment on Twitter using the hastag: #CholesterolScience

Feel free to direct your question to the guest you want to answer. If you don’t, we’ll choose for you.

As always, keep it respectful and fun.

Dec 07

Guest Post: Testing Twins, Keto vs Non-Keto

My name is Chris Bair, and I am the owner of the company Keto Chow, a ketogenic shake supplier. I also have two sets of twins, and when the Keto Chow team went to Low Carb USA (San Diego) earlier this summer, over a meal, I mentioned to Dave Feldman that one of our sets of twins had one doing keto (hereafter referred to as “KT”) for a year and the other not doing keto (hereafter referred to as “NKT”). Dave got really excited (that’s a SEVERE understatement) and wanted to know if we could convince them to get some blood tests to see how their diet was affecting their cholesterol, insulin, glucagon, and other factors. Dave wanted to make sure they had similar activity levels. Both have Fitbits Alta HRs, you can see the raw data from those here (KT) and here (NKT). They are relatively close in activity 169,928 steps for KT vs 158,278 for NKT over a 2 week period before the blood tests. Sleep patterns are noticeably different: the Fitbit on KT recorded 5524 minutes of sleep, the Fitbit on NKT recorded 6388 for the same 2 week period; that’s 92 vs 106.5 hours.

The same 2 weeks leading up to the blood draw, each was taking Dave Feldman style photos of everything they ate, which proved to be the biggest annoyance for both during the experiment and they were looking forward to concluding so they could stop with that. This was to ensure that we had a record of what they were eating and that both stayed pretty much consistent with their food during the 2 weeks before the blood draw. The day of the blood tests came, and KT was worried as she has had issues with blood and fainting – strangely KT had absolutely no problems at all with the blood draw and was done in about 3 minutes. NKT, on the other hand, went pale and ended up needing to lie down before the lab could finish the blood draw. We were very happy that she came out OK, though I doubt she’ll be donating blood anytime soon. 🙂

Before we get to the results I should explain that both parents in our home are quite strict with keto for ourselves. Two of our daughters are also strict about staying keto, though both are more “lazy keto” and don’t track carbs or such – frankly, it’s not really necessary. As young and healthy as our children are, simply the act of cutting out sugar and flour was likely enough to prevent problems in the future. Our other children are not doing keto and will eat candy, pizza, fruit, and such if given the opportunity – though we, as parents, do not buy anything non-keto anymore so it’s usually at school or when visiting.

Now for the data! Dave wanted to get a recording of his first read-through of the blood tests:


Most of the analysis was done by Dave during the video so refer there for commentary. If you prefer to look at the data yourself, you can either read it in tabular format on the “Twins” tab of this spreadsheet (the other tabs are data from previous experiments I’ve done) which also has % difference and absolute value difference columns for comparison, or you can grab the original blood tests in PDF format: KT, NKT. I’ve made some handy graphs (also on that spreadsheet in the “Twin Charts” tab) to illustrate some of the takeaways.

To start, we have a comparison of their NMR Lipid Panels. Nothing here is really a surprise at all, KT has higher numbers for all of the measurements except LDL size which is the same for both, this follows Dave’s hypothesis regarding the lipid system as an energy distribution apparatus. Both are low on HDL but have fantastic Triglyceride levels. Both also have a remnant cholesterol of 8. Dave has explained this better but this number represents energy parked in the blood in VLDL particles and you want this as low as possible since it tends to be a legit indicator of risk; an 8 is fantastic.

Both have really good fasting glucose.

Which should make their nearly identical Hemoglobin A1c not a surprise at all. This number represents the percentage of their red blood cell hemoglobin that has become “glycated” or exposed to glucose. It serves as a way to measure your average glucose over several months, usually 3 months. HbA1c is the test used to diagnose Type 2 Diabetes Mellitus, although elevated HbA1c is a symptom of T2DM, not the cause. Most experts agree that the underlying cause is hyperinsulinemia or chronically elevated insulin levels.


KT’s low fasting insulin doesn’t indicate how close she is to having hyperinsulinemia or her risk of T2DM or Alzheimers – that would require a Kraft test and measuring insulin response to glucose over time instead of once while fasting. NKT’s elevated fasting insulin does indicate that even without eating for 12 hours, her insulin was still elevated. For now, she’s likely to be able to handle that insulin load; but Dave feels that he’d like to see insulin below 10 in the future. This higher number for NKT was one of the few surprises that were in the test, most of the other markers fell in-line with what Dave expected to see based on the other results he has seen from both keto and non-keto subjects.

The other surprise was the low glucagon levels in both. A typical level is 50, and one would expect KT to have higher than normal levels. While hers is higher than NKT, both are abnormally low. Glucagon is something that Dr. Benjamin Bikman presented about at the 2018 Low Carb Breckenridge conference, interesting stuff.

It’s interesting to note the difference in the LDL numbers of the two. Many professionals are of the opinion that LDL is causal in atherosclerosis and would insist that KT has a higher risk of heart disease in the future. The cool thing with this data is that genetically they’re identical, with the same environment, same living conditions, same lack of cholesterol-lowering medication. They actually have almost the same triglyceride numbers too! NKT and KT both are handling the glucose load really well (that’s rather expected, given all the machinery is still new and fully functional). It is important to note the massive difference in their respective fasting insulin. So many of the chronic diseases in modern society are a direct result of too much insulin: chronic hyperinsulinemia. NKT is in danger of hyperinsulinemia causing problems in the future which is something to be truly concerned about.

[NOTE FROM DAVE -> Full disclosure: Keto Chow has supplied both Siobhan and I some of their product for experiments (like the Tandem Drop), but neither this company, nor any other, is an affiliate or in any way compensates CholesterolCode or has any quid pro quo agreement of any kind.]

Dec 05

Guest Appearance on the Diet Doctor Podcast

This may be one of my favorite guest appearances to date. Below are the general times and subjects discussed.

One errata: I mentioned a-tocopherol and shortly after “binding to pathogens” where I was meaning lipoproteins in the same context, not the a-tocopherol itself (it primarily converts ROS to non radical products).

The below outline is lifted from the DietDoctor.com website on this episode:

3:00  Summary of Dave Feldman’s work
5:18  Why do we care about LDL cholesterol?
11:10  About Dave’s apperance on Petter Attia’s podcast
12:10  Phinney and Volek study
16:13  Dave’s three-day protocol
18:20  The accelerant hypothesis
23:10  About the VLDLs
27:38  ApoC-3
32:02  Mendelian studies
38:07  Treating patients
44:40  Dave’s latest experiment
52:30  Last words


Nov 28

A Tragic Event

My apologies, but I’ll need to step away. I’ve gotten some terrible news regarding a very close friend that requires my attention. I’ll expand more once everyone in their life is informed.

I need to cancel the shows with Ivor Cummins and Dr. Joel Kahn for now (hopefully we can reschedule soon). And I probably won’t be very engaged on social media for a little while.

Thank you for your patience.

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