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.

Jan 20

Added Sugar Experiment 2 – The Paul Mason Edition

Last year at Low Carb Gold Coast, I had the pleasure of watching an excellent presentation by Dr. Paul Mason where he talked us through hyper-responders and lipoproteins. Naturally, I was loving every second. To my surprise, he addressed the Feldman Protocol as well, with a suggestion of adding carbs to achieve the same outcome.

Here’s a transcript of that portion of the talk (at about 21:54):

Now we’ve all heard about the Feldman protocol.

So essentially what happens is if you have a very high LDL level on a ketogenic diet, it’s been demonstrated, quite nicely, that if you go on a very high fat diet for about three days and have a blood test at the end of it your LDL levels will significantly drop, some would even say “plummet”. And this is why – it comes down to these LDL receptors.

Now these LDL receptors are what actually takes healthy LDL out of the bloodstream it doesn’t work for damaged LDL, remember, it only works for the healthy LDL and the amount of LDL in the blood has an inverse relationship to the number of receptors. If we have more receptors that are able to take the LDL out of the circulation then we’re going to have less in our circulation. It’s only logical. And interestingly, increasing the amount of calories in our diet, which increases our insulin, actually increases the genetic expression of these LDL receptors.

In actual fact, rather than doing a high-fat diet as with the Feldman protocol a lesser amount of carbohydrates would probably do exactly the same thing because of much stronger insulin response.

Now, why does it take three days? Well just because you increase the expression of a gene doesn’t mean that you get an instant effect there’s a lot of steps that you need to go through before you end up with the final product, which in this case is the LDL receptors and it’s this process between genetic upregulation and the final protein synthesis that likely explains the three-day delay between when you increase the amount of energy in the diet and the LDL actually falls.

Paul’s theory is pretty sound. Again, we’re reading a lot of the same literature. But that said, I had already done an experiment that added carbs to a keto diet known as the Added Sugar Experiment. The net effect wasn’t a significant drop in cholesterol.

However, in chatting with Paul since his talk, we theorized there might be a component with the fact the skittles were far more fructose-based and this could be a confounder. So we discussed using something with glucose, dextrose, or maltose.

Bottlecaps to the rescue! Fortunately, many Willy Wonky candies have dextrose as their primary sweetener, so we agreed on using this brand as the intervention.

Study Design

I was just coming off a carnivore diet (more on that in an upcoming presentation and write up). So I worked out being on my “baseline” diet for five days, then following it with 4 days of the baseline with the addition of the Bottlecaps.

[Paul and I discussed this in an ad hoc video before performing the experiment which you can watch here]

Baseline Diet
Baseline Diet + Dextrose

Changes in Glucose on Dexcom G6 (CGM)

The value of continuous glucose monitors (CGM) is that they can give a constant reading on what is happening to your glucose levels at five minute intervals. I was well aware this would likely jump after I added the dextrose.

For reference, here was a typical 24h reading during my baseline diet, before adding the sugar:

Alas, Dexcom offers no y axis in this view, but I can tell you that my line basically hovers between 85 mg/dL and 105 at its peak. Pretty much the flattest line I ever make on the CGM. (Hello, keto!)

Then Day 1 of the added candy hits and I’m running a little late, hitting the first meal at about 11:45. I get this response following the first meal:


You might recall in my end of the Tandem Drop Experiment I was pretty uncomfortable with topping out at 183 mg/dL on my CGM. Nevermind… that was just a warm up…

This is the full 24 hours as shown before I started my meal on the next day:

I topped out at 255 (last arc) and woke up to a 108 the next morning.

As I told Paul, I seriously considered canceling the experiment at least three times on Day 1. I was certainly uncomfortable with these numbers and that can be a confounder in and of itself (such as raising cortisol, et). But ultimately, I decided to move forward.

Side note: I originally thought I topped out at 254 for Day 1, which led me to post this poll on Twitter:

Thus, 76% of people (myself included) would’ve picked an answer below 254.

By Day 4 I had seen a smaller top off at 232 mg/dL, but I’d call that only a marginal improvement.

It is common advice to those on a low carb diet to consider eating lots of carbs in the days leading up to an Oral Glucose Tolerance Test (OGTT) as it will acclimate one to having a less dramatic response with glucose. Given my own results from above, I’m not sure if this would have worked out so well for me in the context of added carbs. But perhaps it would’ve with swapping in carbs for swapping out fat.

Cholesterol Changes

Now on to the Main Event – LDL Cholesterol:

We did indeed see a drop, although not a very dramatic one when compared to baseline. The last day of the baseline came to 313 with the added dextrose at day four clocking in at 265 for a difference of 48 mg/dL or a 15.3% drop.

Our top three comparisons are my first Feldman Protocol (drop of 73 / 28.5%), the Energy Status Experiment (drop of 73 / 30.1%), and Tandem Drop Experiment (first three days – drop of 136 mg/dL / 45.9%).

The Weight Confounder

Alas, there was also another possible reason for the drop in LDL-C. After I added in the Dextrose, I began gaining weight… pretty rapidly, in fact.

Not too coincidentally, I ran into this very phenomenon in reverse with my Weight Gain Experiment from last year. While I was actively losing weight, I saw a tight inverse correlation with my LDL-C rising (Pearson of -0.936!)

Naturally, at higher levels of insulin we have greater inhibition of lipolysis, leading to higher weight retention. As this lowers the free fatty acid pool, we likewise have less VLDL production and thus less downstream LDL. In theory, this could account for some or quite a lot of the lower overall resulting LDL.

Fortunately, I got a Free Fatty Acid test with all my bloodwork, so we’ll have that for a comparison once all the labs are back, which will likely be in a week or two.


There were a number of issues with this experiment that were notable:

  1. Initial anxiety. This was likely due to my reacting to the CGM readings, which subsided after the first day. But worth noting nonetheless.
  2. Mild clumsiness. This was something very unexpected, yet distinctive enough to journal. With each day past the first, I had one or more moments of stumbling or letting things slip out of my hand in a very uncharacteristic fashion.
  3. “Shipping” issues on Day 2. (Yes, I’m using a euphemism here for bathroom problems.) I was quite surprised it happened so quickly, just one day into the intervention. Because of this, I did have to consume magnesium citrate, which did resolve the issue and it didn’t return again for the duration of the experiment.

Would a Longer Time Make a Difference?

Paul wanted to emphasize that he’d prefer I did the experiment for seven days instead of four. And indeed, since my previous interventions three days, it’s possible he could be right that a more dramatic change was up ahead. But frankly, I just didn’t have it in me. It was tough enough to finish out these four days watching my CGM going off the charts. But more problematic would be if I continued to gain weight, which would have been a persistent confounder.

Moreover, if indeed a longer time is needed, this would seem to suggest any of the other protocols above would be more attractive given turnaround time of just a few days instead.

Final Thoughts

  1. Once again, we seem to have further evidence that swapping is preferable to addition with my N=1. More specifically, if you’re going to attempt using carbs to lower your LDL, you might be much better off swapping out the calories from fat to make room for the calories from carbs. How much of this relates back to weight gain may need further research to determine.
  2. It’s possible this experiment reflects issues with carb loading in the days before an OGTT, but there’s a catch. At first glance, it appears that this process didn’t help me acclimate to a higher carb diet. Yet these spikes were always in the context of the dextrose load following a fatty meal. And, of course, it wasn’t consumed all at once, such as in a sugary liquid bolus. Any of these may have contributed to a very different outcome.

[Paul and I discussed the results in a video at the conclusion of the experiment which you can watch here]

I really want to think Paul for working with me on this. While it wasn’t as dramatic as we had hoped, it is worth reemphasizing that this did indeed succeed at lowering my LDL as hypothesized. Further, it suggests there was a difference between the fructose-based sweetener from Skittles (in the original Added Sugar Experiment) vs dextrose-based sweetener from Bottlecaps.

So perhaps Willy Wonka can thank us for giving them a new tagline on how their candy lowers cholesterol, unlike the competitors.

Jan 16

#CholesterolScience Show – With Dr. Peter Lansberg

0:00 Intro

0:26 Peter’s background and history with lipid research

Term used: Familial Hypercholesterolemia (“FH”) is a cluster of genetic abnormalities that result in high total or LDL cholesterol. If someone has Heterozygous Familial Hypercholesterolemia it means they got a copy of an FH gene from one parent only. If they have Homozygous Familial Hypercholesterolemia, they have a copy from both parents. Homozygous FH is considered more severe of the two.

6:20 For people who see their cholesterol rise on low carb, can Peter provide information on whether they should be concerned?

7:00 How big of a problem is heart disease in general?[

Slide mentioned: Slide 2

9:35 The physical progression of atherosclerosis[

Slide mentioned: Slide 3

11:54 Are the steps of atherosclerosis necessarily progressive? Can they be stopped or reversed?

16:15 The complexity of the lipid system – a long way to go to full understanding.[

Slide mentioned: Slide 4

17:20 The work of the Russian researcher Nikolai Anitschkow and what his rabbit study showed about the development of atherosclerosis

Slide mentioned: Slide 6

21:21 What does the research show regarding cholesterol level and heart disease outcomes/risk?

Slide mentioned: Slide 7

23:47 What does Peter say to the criticism that there can be possible cherry-picking for studies on cholesterol lowering and cardiovascular disease?

25:00 Thoughts on CETP Inhibitor trials – why did they fail? What does it mean?

Term used: CETP stands for Cholesterol Ester Transfer Protein. It is a protein which transfers cholesterol and triglycerides between the lipoproteins. There is a class of drugs which inhibits the actions of this protein, ultimately resulting in higher HDL-C and lower LDL-C.

29:30 Is LDL-C a causal factor in atherosclerosis?

33:05 Could there be other underlying problems with Familial Hypercholesterolemia other than high LDL?

Term used: CIMT stands for Carotid Intima-Media Thickness, it is an ultrasound that looks at the thickness of certain layers of the artery in the neck (the carotid). It is used as a measure of risk of heart disease, with thicker IMT being higher risk.

40:54 Caveat: The problems with CIMT measurements

43:16 Dave’s CIMT results – are they significant, and is there a danger of confirmation bias?

47:45 Comparing risk and context.

50:45 Could Lean Mass Hyper-responders be an example of paradoxical responders?

51:26 Case study – “Miss K.”[

Slide mentioned: Slide 9
Converted measurements

57:04 Comparing treated versus untreated people who have Familial Hypercholesterolemia

1:04:03 Devil’s Advocate Intro

1:04:23 Are LDL particles, like macrophages, a part of the immune response? In addition is it possible that some of the association between LDL and atherosclerosis is due to this immune response?

Study mentioned: Epidemiologic studies of coronary heart disease and stroke in Japanese men living in Japan, Hawaii and California: prevalence of coronary and hypertensive heart disease and associated risk factors.

1:10:47 As more evidence emerges to stratify for this triad (high LDL-C, high HDL-C, and low triglycerides), do you likewise predict it will show lower risk for cardiovascular disease?

1:23:45 Many studies tout changes in risk for cardiovascular disease mortality, yet show no difference in all-cause mortality. Doesn’t this run the risk of misleading people to assume overall benefit where there is none?

1:32:30 Audience questions

1:32:42 Are there any CAC scan studies on people from before and after statin therapy?

Term used: CAC stands for Coronary Artery Calcification. It is a CT scan which looks for calcium in the arteries, the score is used as a risk marker for things like heart attack or all-cause mortality, with lower scores being better risk.

1:34:37 Does Peter know how to access databases to test the triad?

1:38:47 Does Peter have any thoughts on how young to start statin treatment in children with Familial Hypercholesterolemia? Is there any information on it interfering with growth, or adverse side effects?

1:44:04 Side effects and statins – is there a problem with using run ins?

1:49:42 Is the increase in residence time of LDL due to modification of the LDL (e.g. glycation, oxidation, etc).

1:50:40 Can LDL be present and not cause plaque?

1:51:31 What does Peter think about Vladimir Subbotin’s work, wherein he disputes that lipid deposition is the initiating factor for atherosclerosis, rather he states that excessive intimal hyperplasia is the initiating factor?

Study mentioned: Excessive intimal hyperplasia in human coronary arteries before intimal lipid depositions is the initiation of coronary atherosclerosis and constitutes a therapeutic target.

1:53:11 What about the impact on heart disease risk of genetic mutations which result in high LDL without affecting the cells ability to uptake lipids/lipoproteins (e.g. glycogen storage disease)?

2:01:18 Credits and Outro

Twitter: @Lansberg

Website: lansberg.org

Jan 12

Peter Lansberg, Carnivore Conundrum, and Caving Up

Peter Lansberg, MD PhD coming to #CholesterolScience

I’m honored to have Dr. Peter Lansberg join me 9am PST this Monday (14th) on my channel to talk about all things lipids. He is actually the first practicing Lipidologist to jump on and I’m sure we’ll have a lot of great discussion.

As always, you can post questions to Dr. Lansberg either by comment down below or on twitter using the hashtag, #CholesterolScience. And of course, keep it fun and friendly.

Carnivore Conundrum

My carnivore experiment has certainly been an adventure, although not entirely the one I had in mind. Alas, there have been a handful of things within the experiment that seem to have kept it from being an autonomous experience. All of this I’ll have in the write up.

For now, just know that the 30 days will end on the 15th. And while I was originally thinking of doing an addendum experiment to follow, I’m now having second thoughts. More on all this in the final write up.

Caving Up to Write a Paper

While I’ve already been tapering down social media a bit lately, I may be dropping off a fair amount more. My intense focus is needed to complete some important writing, much of which you’ll know about eventually.

Jan 12

The Official Volunteer Sign Up

Moving forward, this will be our official thread for letting us know if you are interested in helping out.

Jan 09

#CholesterolScience Show – With Dr. David Diamond

0:00 Intro

0:30 David Diamond’s health and history – how did he get to where he is now?

3:22 Dr. Diamond’s previous research involving stress and nutrition, and further investigation of the impacts of a “high fat” versus “ketogenic” diet

Study mentioned: Combination of high fat diet and chronic stress retracts hippocampal dendrites.S

6:00 Further investigation into Dr. Diamond’s high triglycerides on a standard American diet, and how he tackled the problem

9:40 David’s current bloodwork and other health markers

11:47 The curiosity of people who change their committed mind

14:30 David’s thoughts on the data on mortality in Norway during WWII

20:50 Morrison study – were improvements from the diet, or the lifestyle?

Study mentioned: Reduction of mortality rate in coronary atherosclerosis by a low cholesterol-low fat diet

23:20 Do ketogenic diets have to be high meat diets? What is an ideal human diet?

25:56 Dean Ornish – changing lifestyle, lowering stress and its impact on health.

Slide mentioned: Slide 2

30:00 What does David say to randomized control trials of vegan vs omnivorous diets being “too hard”?

32:57 Dave’s experience with vegans who have high triglycerides

35:00 Are plant foods and fiber inherently healthy?

38:40 The use “overuse” of paradox in the medical and nutrition field – the paradox of high fat/high meat consumption in indigenous populations and low rates of heart disease

44:07 Devil’s Advocate intro

44:26 Wouldn’t it be fair to say that there’s enough evidence that LDL, in itself, causes heart disease?

Study mentioned: Inborn coagulation factors are more important cardiovascular risk factors than high LDL-cholesterol in familial hypercholesterolemia.

Study mentioned: Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review.

Study mentioned: Mortality among patients with familial hypercholesterolemia: a registry-based study in Norway, 1992-2010.

54:50 The vast majority of experts agree on the need to lower LDL – shouldn’t we trust the experts?

Statement mentioned: Statin Safety and Associated Adverse Events: A Scientific Statement From the American Heart Association

58:55 Submitted questions intro

59:00 How do PCSK9 inhibitors work?

1:04:19 Is two years sufficient to see outcomes from cholesterol lowering therapy? What do the current studies show for effectiveness?

Slide mentioned: Slide 3

1:11:50 What about all-cause mortality and cholesterol levels?

Study mentioned: Familial Hypercholesterolemia: A Genetic and Metabolic Study.

1:14:40 Discussion on the effects of cholestyramine for use in cholesterol lowering

Slide mentioned: Slide 4

Study mentioned: Corn Oil in Treatment of Ischaemic Heart Disease

1:24:24 Can a Low Carb High Fat diet lower the proportion of small dense LDL in people with Familial Hypercholesterolemia?

1:28:28 What are David’s thoughts on taking statins while on keto?

1:35:00 If LDL isn’t a strong indicative marker of risk, what does David suggest people look at instead?

1:35:57 Is it how often your blood sugar spikes per meal, or just that it spikes?

1:38:10 Thoughts on curcumin and berberine to reduce blood sugar and cholesterol?

1:39:34 Do people on Low Carb High Fat/keto have slightly fatty livers?

1:44:00 Outro and how to reach David Diamond

Twitter: @LDLSkeptic

Facebook: David Diamond

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