Jul 18

The Trifecta Tour

For the next couple weeks I’ll be taking a lot of planes, trains, and automobiles…

The Tour begins

Yes, while the Mrs holds down the fort at home, I’ll be bouncing around the U.S. doing three presentations in 8 days:

  1. Ancestral Health Symposium in Bozeman, MT, where I will speak on the 19th
  2. Ketofest in New London, CT, where I’ll speak on the 22nd
  3. Low Carb USA in San Diego, CA, where I speak on the 27th

Although those arrows make it look easy, I’ll actually have to navigate a bunch of connecting flights, train and road trips throughout as both Bozeman and New London aren’t near a major airport of any kind. Meh!

But wait… there’s more…

While in San Diego:

Needless to say, it’s going to be a pretty intense couple of weeks.

Siobhan’s Speaking Debut

Also at Ketofest, Siobhan Huggins will be giving her first full presentation, “LDL: Primed to Protect (Cholesterol’s role in defense and repair) ” this coming Sunday at Ketofest. Spoiler alert — I’ve gotten a sneak preview and it’s going to be fantastic!

So Heads Up, Internet – We’re Busy!

With all this in mind, don’t be surprised if both my and Siobhan’s activity here at Cholesterol Code and on social media in general is drawn down for the week.

Jul 09

I’m Booked to Appear on Peter Attia’s New Podcast

No, that’s not a misprint. I’ll be joining Attia in a couple weeks at his offices in San Diego to record an episode that I’m sure will have a lot of people talking.

This has actually been determined for a while, but I was planning to keep it on the down low until closer to the appearance. Naturally, the podcast with Peter and Ron Krauss got a lot of people both requesting I respond and pressing for Peter to have me on the podcast.

So for the record, when I sent out this tweet:

Note the booking and this tweet were up before the Krauss interview got posted. No need to ping Peter anymore — he was ahead of you all along!

Without question, I’m extremely excited to chat with him about the Lipid Energy Model and it’s relevance to lipoprotein and cholesterol homeostasis. I’m confident it will be unlike any podcast I’ve been on before and I’ll apologize in advance for what may be a lipid geekfest.


Jul 04

High Triglycerides on Low Carb – And What to Do About It

Triglycerides (TGs) are effectively fat-based energy. And if you’re on a low carb, high fat diet (LCHF), you are likely eating them every day, along with storing them as such in your own fat cells. The “tri” is for the three fatty acids grouped in each one to a glycerol backbone.

So a common question I get is, “Hey, if we’re powered by triglycerides on LCHF/Keto — then why do my blood tests show my triglycerides have gone down since I started?”

Simple… your usage has gone up. Way up! And that’s a good thing!

Generally speaking, you want to aim for having your triglycerides below 150 mg/dL at a minimum, and preferably below 100 mg/dL for optimum health. I consider this universal, by the way. It doesn’t matter if you’re on a LCHF/Keto, Vegan, Paleo, Mediterranean, or Bob’s Special Custom Juice and Burger Diet. If you have high triglycerides, it suggests a problem — and certainly a problem I pay attention to more than any other marker.

Steps to Take

Here is my general checklist:

  1. Confirm you water-only fasted for 12-14 hours before your cholesterol test. (No food, no coffee, just water) The more outside that window you are, the more it can increase your TGs (especially if near a fatty meal).
  2. You have a coffee sensitivity. I know, I know, I hate to be the bearer of bad news. But we’ve found a surprisingly large number of low carbers who see their triglycerides stubbornly high from what appears to be coffee alone. Note this is just a fraction of the coffee drinkers as most of them appear to be doing fine.
  3. You may have “carb leaks”. Get serious about tracking your food. Be really, truly, absolutely sure you’ve accounted for all carbs in the diet. Common unaccounted-for leaks include sauces, spices, beverages, alcohol, and many things labeled “0g Carb” that actually aren’t (rounded down in some nutrition labels) such as some brands of Heavy Whipping Cream. Sometimes you want to use a glucometer to detect what is actually higher carb than you thought. Bottom line: many who have even moderate carbs while on a LCHF diet can see their TGs spike because it’s still too much of an energy surplus.
  4. Cut out refined/liquid/concentrated forms of fat. Drop bulletproof coffee, oils, fat shakes, fat bombs, etc. Move toward as much fat from real food sources as possible.

These above steps I’ve worked with family and friends on when TG is high and it’s had a very high success rate, save two people.

Jun 29


This thread is dedicated to questions for CholesterolCode.com. Again, we are not doctors or medical professionals and nothing we say here constitutes medical advice.

If you have a question that doesn’t involve your specific cholesterol numbers, feel free to comment to this thread below.

On the other hand, if you do have a question about your cholesterol numbers (total, LDL, HDL, and/or triglycerides), then do the following:

  • Fill out the Report Tool below
  • Copy/Paste the text of the report into your comment along with your question.

Jun 26

Cholesterol Endgame?

Something exciting is happening.

There’s a special group of people that may be answering one of the most powerful medical questions of our time.

The Hypothesis

A hypothesis was made several decades ago, well before I was born. This “Lipid Hypothesis” suggested cholesterol in the blood independently caused heart disease.

From Wikipedia:

The lipid hypothesis is a medical theory postulating a link between blood cholesterol levels and occurrence of heart disease. A summary from 1976 described it as: “measures used to lower the plasma lipids in patients with hyperlipidemia will lead to reductions in new events of coronary heart disease”.[1] Or, more concisely, “decreasing blood cholesterol… significantly reduces coronary heart disease”.[2]

More cholesterol, more heart disease. Simple.

It has since morphed and changed a bit. Now some point to Low Density Lipoproteins as the problem (LDL-P, the “boats”) while others still insist it is the cholesterol found inside them (LDL-C, the “cargo”). Regardless, if you have a lot of LDL-C, you likely have a lot of LDL-P, so it is pretty much the same for most people anyway.

This is “deadly” and “needs immediate treatment” to lower the LDL-C/-P with prescription drugs. Even with the newer guidelines putting less emphasis on LDL, there’s no lack of insistence by doctors around the world on taking drugs to lower it when at high or even moderate levels. In fact, what was considered high has been continually dropped (from 130 mg/dL to 100, and now to 70). Naturally, this has resulted in more and more drugs prescribed.

Case Closed… or is it?

Last year we had a massive Consensus Statement from the European Atherosclerosis Society. In very declarative language, they state the evidence is quite overwhelming and clear: LDL is the bad guy.

Interestingly, this appears to be in the wake of many papers that are pointing to several new channels with higher associations to CVD such as Remnant Cholesterol, something I’ve written about here before.

In fact, even this EAS statement didn’t get very far before it got a paper that sought to show its many problems from the Karger group, A Critical Review of the Consensus Statement from the European Atherosclerosis Society Consensus Panel 2017.

There’s even been a quiet subtraction of LDL as a target for treatment in the new guidelines from 2013 AHA/ACC.

So what’s going on here? Is LDL a problem or not?

HDL High and Triglycerides Low? Then No, LDL Does Not Appear to be a Problem

When looking at only LDL, then one can find a weak correlation with CVD/CHD. But when looking at LDL alongside HDL and triglycerides (TG), it becomes nearly meaningless. HDL & TG together are just a far stronger measurement compared to LDL alone.

Over the last 4 months, I’ve been pinging LDL-lowering experts, organizations, and social media at large for studies showing high LDL is giving high CVD to normal, non-treated people who have high HDL and low triglycerides. Can’t find any studies. Not one. I even turned it into a hashtag campaign on Twitter: the #LCCholesterolChallenge. Or you’ve seen the graphic I’ve posted to help attract attention to the challenge.

Instead, I’ve found compelling studies that show the opposite — that high HDL and low triglycerides are associated with low CVD and low all-cause mortality.

Take this Framingham Offspring study, where I even marked it up to showcase where I (and many other hyper-responders) stood in the risk category. (Colored markings and overlay mine)

In other words, if you grab everyone who had a moderately low TG (less than 100), a moderately high HDL (more than 40 for men, 50 for women) — then even if their LDL was above 130, their risk was nearly identical to someone with LDL of below 100 (0.7 and 0.6, respectively).

But it gets better…

In this observational cohort study of 2906 men aged 53 to 74 years free of IHD at baseline, we see this relationship in perfect display. (Colored markings mine)

You see how on the left we have people with an LDL of 170 or less vs those with an LDL of 170 or more? That’s literally just 20 mg/dL away from one of the two criterions for a diagnosis of familial hypercholesterolemia! In other words, and LDL of 170 will likely get your doctor talking to you about multiple drugs to lower your cholesterol.

Yet there it is in black and white — the group on the left is nearly the same as the group on the right. If you’re in the dark grey bar with HDL of 57 or more and a TG of 97 or less, you’re at nearly identical risk for ischemic heart disease whether above or below LDL of 170. But worse, if you’re hanging out in the white bar and take your lipid-lowering drugs to drop below 170 with no change in your HDL of 46 or less and TG of 142 or more, you’ve made effectively zero impact.

So Why Doesn’t the Medical Community Focus on HDL and Triglycerides?

Good question. I wish I knew the answer.

Sure, there’s plenty of fodder for the cynical answer here: there isn’t a pharmacological solution to it. And yes, there appears to be some support for this given all the trials that chemically alter the lipid system to bring up HDL and reduce LDL, such as CETP inhibitors, have failed spectacularly. But weirdly, this has led to a new train of thought insisting maybe HDL isn’t so beneficial after all. (Note: I couldn’t possibly disagree more with applying the assumptions of a population who had their lipid systems chemically altered through drugs to that of the general population without supporting evidence.)

Enter the Lean Mass Hyper-responder

About a year ago I wrote about this emerging profile that was becoming very central to my research. It represents a kind of endpoint to very high fat-adaption as shown in higher circulation of VLDLs, resulting in high LDL. As a class, these individuals have the highest LDL-C and LDL-P of everyone in the low carb community.

Yet they defy expectations of what we’d imagine with high LDL — the insulin-resistant, junk food couch potato. Rather, they are typically lean, fit, and have very low fasting insulin. Many of whom insist this is the best they’ve ever felt and performed in their life. I see their bloodwork on a near daily basis and it is stunning how many of them have great metabolic markers, extremely low inflammation, CIMT, and CAC scores.

I called this profile “Lean Mass Hyper-responder” (LMHR) and I had no idea how just how many of them there were when I wrote the article. Now I know they are a sizable population in the low carb community.

Many LMHRs are concerned about their cholesterol and are taking steps to change it. However, many others are completely fine with it and have no interest in living any other way. (For the record, we try to help everyone meet their goals and urge community respect for their decision, whatever it may be).

Collision Course

So clearly, the ideal group of individuals to test the Lipid Hypothesis are those who are:

  1. Free of all major CVD risks, such as hypertension, hyperinsulinemia, high waist circumference, high triglycerides, and low HDL (to name a few).
  2. Have extremely high LDL-C and LDL-P

And here we are. If the Lipid Hypothesis is indeed an independent risk factor, then LMHRs should be showing signs of progressive atherosclerosis and higher mortality from heart disease — and rapidly, for that matter. There’s nowhere left to move the goalposts.

I think once we get a decent sample size of LMHRs and a solid follow up period of time, we’ll have a strong answer to that question.

You can probably guess what I’m predicting.

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