Previously, in Part I, Part II and Part III of this series, we addressed these 5 concepts:

     #1 — What is cholesterol?

     #2 — What is the relationship between the cholesterol we eat and the cholesterol in our body?

     #3 — Is cholesterol bad?

     #4 – How does cholesterol move around our body?

     #5 – How do we measure cholesterol?

In this post we’ll continue to build out the story with the next concept:

     #6 – How does cholesterol actually cause problems?

Asked another way, how does someone end up with a coronary artery that looks like the one in the picture above?

Previously, in Part I and Part II of this series, we addressed 4 concepts:

   #1 — What is cholesterol?

   #2 — What is the relationship between the cholesterol we eat and the cholesterol in our body?

   #3 — Is cholesterol bad?

   #4 – How does cholesterol move around our body?

This week we’ll address the following concept:

   #5 – How do we measure cholesterol?

In this post I’m going to tackle the next set of logical (at least in my mind) questions to follow up on last week’s post, Part I in this series.

Last week we addressed these 3 concepts:

     #1 — What is cholesterol?

     #2 — What is the relationship between the cholesterol we eat and the cholesterol in our body?

     #3 — Is cholesterol bad?

This week we’ll address the following concept:

      #4 – How does cholesterol move around our body?

I’ve been planning to write at length about this topic for a few months, but I’ve been hesitant to do so for several reasons:

1. To discuss it properly requires great care and attention (mine and yours, respectively).
2. My own education on this topic only really began about 9 months ago, and I’m still learning from my mentors at a geometric pace.
3. This topic can’t be covered in one post, even a Peter-Attia-who-can’t-seem-to-say-anything-under-2,000-word post.
4. I feel a bit like an imposter writing about lipidology because my mentors on this topic (below) have already addressed this topic so well, I’m not sure I have anything to add.

But here’s the thing.  I am absolutely – perhaps pathologically – obsessed with lipidology, the science and study of lipids.  Furthermore, I’m getting countless questions from you on this topic.  Hence, despite my reservations above, I’m going to give this a shot.

Many of you have asked this question over the past few months, and I’m sure many more of you have at least contemplated this question at some point.  I know I did.

For the sake of this discussion, let’s ignore the fact that the “historically” lean countries (e.g., France, Italy, Japan) are catching up to our levels of obesity and metabolic syndrome, especially in certain affluent subsets.  After all, we did get a 40 year head start on how to eat poorly.   So, let’s ask the question this way:

How does the average person living in, say, Japan stay leaner and healthier than the average American while still consuming >70% of their caloric intake in the form of carbohydrates?  

I don’t claim to know the answer this question, but I’ve got a few ideas.

Last week I wrote about how carbohydrates are effectively a performance-enhancing substance, at least for certain performances in certain people.  I received many great questions, including some challenging this suggestion, which really pleases me because it demonstrates folks are thinking about tradeoffs and questioning everything.

Is carbohydrate reduction or outright restriction “right” for everyone?  I doubt it.  Besides oxygen and water the list of “universal truths” for human health is pretty short.  Parenthetically, one can still overdose on both oxygen and water – in other words, even these two completely essential compounds can be toxic outside of their ideal ranges.

If you’ve been following this blog and/or this general discussion, you’ve probably asked yourself the question I’m about to pose.  If you haven’t asked it yourself, you’ve likely been asked by someone as you’ve had the discussion with friends or family.  Here’s the question:

If insulin is so important in regulating fat metabolism, why do some people eat whatever they want and not get fat? Conversely, why do some people following the strictest carbohydrate-reduced diet remain fat?

Before getting to this week’s post, if anyone didn’t see the 60 Minutes segment on Sunday about the toxicity of sugar, here is a link to it.  I was pleasantly surprised by what they were able to convey with such time constraints.  In addition to the great work by Dr. Lustig, the very short segment showing Dr. Cantlely, highlighting the role of insulin, insulin-like growth factor, and glucose in cancer, is a preview of what I’ll be writing about in the near future.

Back to the topic of the week: What do anabolic steroids, EPO, and carbohydrates have in common?  I know what you’re thinking…what is he talking about?  I’m going to attempt to make the following case today: carbohydrates do, in fact, enhance some aspects of human athletic performance.  So do anabolic steroids, human growth hormone (HGH), synthetic erythropoietin (EPO), and countless other drugs classified loosely and broadly as “performance enhancing drugs.”  The question is, or at least should be, Is it worth using these substances to enhance your athletic performance?

Before we go any further, though, I want to ask you to suspend one thought – ignore the “legality” of these substances.  For example, if we were going to have a discussion about cigarettes and marijuana, I would ask that we have the discussion based solely on their pharmacologic, physiologic, and pathologic features.  The legal issue is actually arbitrary and, frankly, highly illogical at times.  So, let’s take legality off the table.  Carbohydrates are legal and anabolic steroids are not.  Cigarettes and alcohol are legal and marijuana is not.  Understood, but irrelevant for this discussion.

Many people question the logic of reducing or outright eliminating carbohydrates, given the possible reduction in athletic and physical performance.  I’ve written about the impact nutritional ketosis has had on my physical performance several times, including here, here, and here.

I find myself getting asked this question, or some variant of this question, with increasing frequency as I speak and write about the Alternative Hypothesis I find most compelling surrounding obesity and chronic disease.  One implication of the Alternative Hypothesis, as you probably understand by now if you’ve been reading this blog, is that carbohydrates are actually fattening.  In other words, overweight people are not the lazy, constantly grazing, weak-willed individuals many in the mainstream have led us to believe.  They just eat the wrong foods (rather than simply too much food).

Remember, I was one of those doctors in the mainstream once upon a time.  While I always tried (and hopefully succeeded most of the time) to treat overweight patients with respect, I silently judged them.  Why can’t you just eat less and exercise more?  Only when I realized, despite my diet which rigorously adhered to formal recommendations and my 3 to 4 hours of exercise per day, that even I was getting too fat for comfort, did I begin to question the Conventional Wisdom of why we get fat.  Of course, not everyone (fortunately) was born with my level of genetic susceptibility to insulin resistance (stated another way, not everyone is born with my level of carbohydrate sensitivity).  In my experience, about 10-20% of the population (my lucky wife included) seem resistant to carbohydrates and maintain exquisite insulin sensitivity, almost independent of diet.   Roughly 30-40% of the population are, conversely, very sensitive to carbohydrates and appear to be quite insulin resistant until nearly the last gram of sugar and most carbohydrates are removed from their diets.  Then there is the rest of population, which includes me.  To varying degrees, we’re somewhere between these two groups.

“For the greatest enemy of truth is very often not the lie — deliberate, contrived and dishonest — but the myth — persistent, persuasive, and unrealistic. Too often we hold fast to the clichés of our forebears. We subject all facts to a prefabricated set of interpretations. We enjoy the comfort of opinion without the discomfort of thought.”

- John F. Kennedy, Yale University commencement address (June 11, 1962)

This is one of my favorite quotes.  Unfortunately, it’s a little bit too appropriate for the field of nutrition science.

As I alluded to last week, I’m going to devote this post to a discussion on what I like to call the Scientific Weapon of Mass Destruction: observational epidemiology, at least for nutrition science. I hope some of you have “prepared” for this post, as I had recommended, by reading this article written by Gary Taubes in 2007. It really is required reading to get the most out of what I’m going to talk about in this post.

You’ll recall from last week’s post I did a self-experiment to see if I could learn something about the interplay of exercise and ketosis, at least in myself. To understand this discussion, you’ll want to have read Part I of this post.

However, before getting to this, I want to digress and briefly address two unrelated issues:

1. Some of you (about 67 or 68 as of this writing) have sent me various links to news reports released yesterday reporting on a study out of Harvard’s School of Public Health.  I was planning to eventually write a post about how observational epidemiology is effectively at the heart of the nutritional crises we face – virtually every nutrition-based recommendation (e.g., eat fiber, don’t eat fat, salt is bad for you, red meat is bad for you) we hear is based on this sort of work.  Given this study, and the press it’s getting, I will be writing the post on observational epidemiology next week.  However, I’m going to ask you all to undertake a little “homework assignment.”  Before next week I would suggest you read this article by Gary Taubes from the New York Times Magazine in 2007 which deals with this exact problem.
2. I confirmed this week that someone (i.e., me) can actually eat too much of my wife’s ice cream (recipe already posted here –pretty please with lard on top no more requests for it).  On two consecutive nights I ate about 4 or 5 bowls of the stuff.  Holy cow did I feel like hell for a few hours.  The amazing part is that I did this on two consecutive nights.  Talk about addictive potential.  Don’t say I didn’t warn you…