Well hey!

Welcome back. I missed you.

In today’s issue:

• One big thing. Heart disease is still our number one killer. It is also the disease you have the most control over, if you understand it. Let’s find out if I can challenge a few of your assumptions.

• You have to check this out. Big speeches and tiny tips to improve your life.

• Tools & tech. Make Google Flights better and maximize your time off.

I’m ready to go if you are!

1️⃣ ONE BIG THING

Gen X Heart Guide: Part 1

What is the right age to truly pay attention to heart disease?

Leading cardiologists now argue the answer is before you're 40.

For my Gen X readers, that means the right age is yesterday.

What does it mean to “truly pay attention”?

Most of us would say: Well, I track my cholesterol, and it’s not too bad. I’ve had an EKG, and my heart seems to beat normally. So, I seem to be in good shape for my age. I keep an eye on things.

I’m going to challenge your thinking… if you'll let me.

Over the next two weeks, I will try to convince you that you could be doing more. Things that won’t take big chunks of time or be overly expensive.

But first, let me back up a step and tell you a story.

I’ve had high blood pressure since my mid-20s. I had a battery of tests to find out why. No reason was found (which is good in this case). It meant the source was genetic. I started taking blood pressure medication. I’ve taken them ever since.

This part of the story is a bit odd. Several years ago, my best friend’s dog died suddenly (we miss you, Peanut). He wasn’t very old, and he was healthy and happy. But out of the blue, his heart gave out, and he was gone. I’m sure many people have stories like this about dogs, friends, and relatives.

It got me thinking. And it led me down a path of deep learning.

Here's the #1 thing I learned: The medical profession is exceptionally good at bringing you back to life and setting you on a healthy path if you have a heart attack or stroke. Up until such an event, most doctors are borderline worthless. Gasp.

I visited a cardiologist at Emory in Atlanta who asked me why I was even in his office. "I can assure you that you will not have a heart attack in the next 10 years. Come back then.”

Most primary care physicians will give you feedback on your cholesterol numbers that is somewhere between misleading and meaningless.

Heart disease remains the number one cause of death in the developed work for men and women. As a member of Generation X, you are of the age that deeper understanding and better testing should be considered mandatory (imho).

Unlike other major disease categories (especially cancer and dementia), we have the tools to see if heart disease is coming our way and the means to counteract it. If we know what they are and we make a choice to use them.

For those who follow Dr. Peter Attia, this mindset will be familiar. It represents the tectonic shift in thinking from Medicine 2.0 to Medicine 3.0 (from treatment to proactive prevention). Watch a 10-minute summary of this here.

But you need motivation and a baseline of knowledge upfront.

That is my goal for this week and next week in this newsletter.

I took everything I have learned over the past three years on this subject and tried to condense it down to what I believe are the core ideas needed to truly understand what’s going on, and the main areas for action.

I decided to split this information into two newsletters. The plan:

• This week’s goal: To give you a foundational understanding of atherosclerosis (the process where your blood vessels get clogged—the primary source of heart disease that leads to heart attacks and strokes) and its connection to cholesterol.

• Next week’s goal: To show you how to act on this knowledge and better understand your blood test results, what other tests you should get, and how to reduce your modifiable risk factors.

I hope you agree this is worth your time. I would love to hear what (if any) parts of this newsletter are new to you, or if there is something you still don't understand. Just hit reply.

This is a fun challenge for me because, first and foremost, I am not a physician. I don't play one on TV, I don't have doctors as friends, and I don't do heart research.

Ready?

Week One: Who the Hell Is Blocking the Street?

You’re a smart person. You pay attention.

Regarding diet and health, one thing we all know a fair bit about is cholesterol.

I thought it could be fun to take a quick quiz. I’ll keep it to one question:

Which of the following statements are true:

1. When it comes to cholesterol, there is “good cholesterol” and “bad cholesterol."

2. The balance between good and bad cholesterol is one of the more important aspects of cholesterol.

3. One way to lower your cholesterol is to avoid foods high in cholesterol.

4. LDL is the worst type of cholesterol.

5. Our arteries may start to clog (atherosclerosis) as early as our 40s.

6. Answers 1, 2, and 3.

7. All of these are true.

As a Gen X reader of this newsletter, you almost certainly grew up thinking most of these are true (at least 1, 2, and 3).

We all remember the great egg takedown. 🥚🥚 This magazine came out when I was 12 years old (1984).

Since those days, you’ve gotten smarter, right? Perhaps you have heard that eating foods high in cholesterol will not increase cholesterol levels in your annual blood test.

As the National Library of Medicine article "The Fifty Year Rehabilitation of the Egg" says, "Half a century of research have shown that egg and/or dietary cholesterol intake is not associated with increased CVD risk.” (CVD = cardiovascular disease.)

Sweet. Eggs are back, baby!!

But hang on. Pick up any packaged food at the grocery store and look at the nutrition label. In bold, there are five major categories: fat, cholesterol, sodium, total carbs, and protein.

Fifty years of research show that cholesterol in food is "not a nutrient of concern for overconsumption," yet it is still on the label.

Why?

Medical research takes a long time to translate into national health guidance.

You don’t have that kind of time.

So, let’s return to my initial question. Which of those statements is true?

The answer: None of them. Those statements are all inaccurate.

Like the little egg mix-up (scramble?), we all grew up with these ideas. So, it makes sense if you still thought a few of them were true. More troubling is that most doctors still use these ideas on the regular.

Let’s see if we can sort this mess out, shall we?

The top-line concern.

The first thing to know is that cardiovascular disease is the leading cause of death in the developed world (for both men and women). “Cardiovascular” means it is related to the heart and blood vessels that carry blood around the body.

The biggest problem in the world of cardiovascular disease is atherosclerosis, which occurs when one of your blood vessels becomes clogged or blocked.

Blood carries oxygen. If a blood vessel in or around your heart gets clogged, your heart doesn’t get enough oxygen to keep working, causing a heart attack. If the problem is a clogged blood vessel supplying oxygen to your brain, this causes a stroke.

OK, so... What is clogging up your blood vessels and causing all this trouble?

It’s cholesterol. But not really. Here’s where things get good.  

The actual problem is the containers that carry cholesterol around in your blood.

Let’s step back and get to know Mr. Cholesterol a bit more.

Who is Mr. Cholesterol?

You see, our poor friend Mr. Cholesterol is tragically misunderstood.

Let me reintroduce him to you. His molecular formula is C₂₇H₄₆O. He is a white, crystalline substance that is odorless and tasteless. He doesn't mean to offend, but due to thoughtless rumors years ago, no one likes him.

Cholesterol is our friend and essential for life. Here are a few examples:

• It is the key ingredient in your cell membranes (the containers that hold cells together).

• It is essential to produce things like testosterone, estrogen, and Vitamin D.

• The Mike drop: Cholesterol is the most important molecule in the brain. The brain contains the highest level of cholesterol in the body. Cholesterol is so essential to the brain that it makes all its own rather than risk relying on cholesterol from the rest of the body.

Cholesterol is so essential to life that every cell in your body produces it.

But not all parts of your body make enough of it. Your liver solves this problem by making plenty of the stuff to go around.

That leaves one final challenge: The cholesterol from your liver needs to make its way around your body to all the other places that need it. Seems easy, right? After all, that’s what your blood vessels do: they shuttle essential things around your body.

But, tenemos un problema!

Our good friend Mr. Cholesterol is a type of molecule known as a lipid, which is just a PC way to say he is a type of fat. Aw, no, don't call him fat. He is "a fat."

The problem is that our blood is basically water. Like Hatfields and McCoys or Kendrick Lamar and Drake, we know that oil and water do not mix.

What Mr. Cholesterol and his buddies need is a disguise of sorts. They need to be wrapped up in a water-friendly cloak so their fat asses can complete their essential mission traveling through your watery blood.

And this is just what happens (thanks evolution!).

All cholesterol travels through the bloodstream in what are called lipoproteins.

It is lipid/fat on the inside (lipo) and protein on the outside. But these traveling containers don’t just carry one cholesterol around at a time. They gather a whole bunch of cholesterol together for the trip, like a big ole lipoprotein bus.

Now, if we go back to my earlier question tied to heart disease:

What is clogging up your blood vessels and causing all this trouble?

The answer is not cholesterol.

The source of the problem is the lipoprotein bus that the well-meaning cholesterol passengers are travelling in—the containers that carry cholesterol around in your blood are the problem.

There are two types of buses.

The next big thing to know is two major categories of buses carry cholesterol through your blood vessels. Two major features distinguish them:

• Their density (how jam-packed are the molecules inside the bus).

• A variation in a single molecule wrapped around the outside of the bus.

Taking those two things together gives us two main categories of lipoprotein buses:

1. Higher density + wrapped in a molecule called “apoA."

2. Lower density + wrapped in a molecule called “apoB” (apoB 100 for any nerds).

Now is a good time to remind you of the passengers inside these two types of buses. It is our friend Mr. Cholesterol. The same molecule, C₂₇H₄₆O, is inside both buses.

Read this twice: there is no good cholesterol or bad cholesterol.

There is only one cholesterol. And that’s Mr. Cholesterol to you!

It is also worth noting briefly here (I will return to this) that there is another passenger inside these buses: Ms. Triglyceride. Here’s a little secret: She is also a fat. 🤫

Here is a bit more scientific view of what these lipoprotein buses look like. You will see the purple cholesterol and triglyceride fats inside and the yellow water-soluble outer shell.

Finally, you can also see the single protein (apoB, for example) in blue wrapped around the outside like a brand that says, "This is an apoB bus."

OK. Now that we know there are two types of buses, let’s expand our understanding in ways that will connect the dots so you can better understand your annual blood test and the things you have heard about cholesterol before.

There are actually more than two types of buses.

Ack! More than two?

Hang with me… it is not that complicated.

Here is the expanded list of buses carrying cholesterol and triglycerides throughout your body:

BUS TYPE ONE: Higher density + wrapped in a molecule called “apoA”:

• Just the one bus here! This is the HDL particle you are probably familiar with. HDL means high-density lipoprotein (a high-density bus carrying fats through the blood). Stupidly called “good cholesterol," these HDL buses generally do not contribute to clogging our blood vessels (but as we will see in time, there is more to the story).  

BUS TYPE TWO: Lower density + wrapped in a molecule called “apoB." There are several types of this apoB bus, and all can cause some degree of trouble:

• VLDL is a very low-density lipoprotein.

• LDL, low-density lipoprotein. This is the particle stupidly called “bad cholesterol” that has made life so hard on our friend Mr. Cholesterol.

• Lp(a), lipoprotein(a), which is said “el pee little a”. Only about 20% of people have this type of bus cruising around. If you have this (and at what level), it is determined by genetics. The bad news: One of these fellas is about 8x as destructive as one LDL particle, so this is one dangerous bus. There will be a whole section on this next week.

Here is a chart showing the various densities and sizes of the buses. Notice the horizontal line dividing the good from the bad particles (at a certain density).

Who is blocking the street?

OK. Let’s finally answer my initial question:

What is clogging up your blood vessels and causing all this trouble?

Why is it that everyone talks about cholesterol in relation to atherosclerosis (blood vessels getting clogged or blocked, which is the top form of heart disease)?

Here’s why:

These buses full of cholesterol (and triglycerides) are constantly cruising along in your blood vessels.

The inside of your blood vessels has a super-thin coating (it is only one cell thick), which allows certain things to pass in and out of your bloodstream.

Under normal operating conditions, this all works fine. The buses zoom down the street with no issues, and there are no backups.

But sometimes, one of the buses crashes into that thin inner wall of your blood vessel and gets stuck there, like getting a bit of popcorn between your teeth and gums. Your immune system senses a problem and sends help. Rather than a tow truck, it sends in cells to eat the entire crashed bus.

This is where things begin to go wrong. Like any bus crash surrounded by emergency vehicles, this crash site begins to snare other buses in the growing mess. So, your immune system sends out a call for even more help.

Soon this whole mess of crashed buses and immune cells form fatty streaks along the inside of your blood vessel (remember that our friends cholesterol and triglycerides are fats).

Over time (many years), your body tries to paper over the crash site so it doesn’t break apart and send a bunch of fatty gunk downstream. First, it covers the fatty streaks in a fibrous substance called plaques (which you have likely heard of).

And finally, over many more years, these plaques calcify, meaning they get a hard outer shell.

When we talk about atherosclerosis causing heart attacks or strokes, two things can happen:

1. The "crash site" size becomes large enough that not enough blood can pass through the blood vessels, which means not enough oxygen getting to your heart or brain. This is what happens when people feel or exhibit early symptoms of chest pain or stroke.

2. The whole crash site ruptures. If this happens, unfortunately, your immune system reacts with the worst possible solution. It treats this internal rupture by sending in blood clotting agents, which quickly expand and block the blood vessel entirely. This is what leads to fatal heart attacks or strokes if someone cannot get immediate help.

A crash in slow motion that begins very early in life.

Now, before you have visions of Da Bears and Bill Swerski's Superfans on SNL eating a sausage and immediately having a heart attack, here are two key things to know about the lifetime progression of atherosclerosis:

• The good news is that any clogging of your blood vessels (from zero to a problem) takes a very long time. This article describes it as a 40- to 50-year process.

• The poorly known news: Lipoprotein buses crashing into the inside walls of your blood vessels starts far earlier in life than most people realize (think: your teenage years).

In this study done during the Korean War, researchers examined 111 soldiers who died on the battlefield. Their mean age was 26. Autopsies concluded: "Signs of coronary atherosclerosis were seen in 78% of the total study group, with >50% narrowing in 20.7% and >75% narrowing in 9%.” More research was done during the Vietnam War, with similar findings.

Let’s get a bit younger. Pediatric studies (PDAY, Bogalusa Heart Study) have found fatty streaks in the aorta in children aged 4-8.

Crazy right? What does this mean?

While the consequences of heart disease are rarely seen before 40, the groundwork for the disease begins far earlier than most of us imagine.

Yet herein also lies a prime opportunity for you, my dear Gen X friend: Now is the time to examine your current risk profile more closely.

There are two ways to do this, each of which I will cover next week:

1. Do you have any blood vessels with any blockages today? How do you know?

2. What modifiable risk factors increase the odds of the lipoprotein "bus crashes" I described above? Plus, how to understand your blood tests and the one blood test your kids should get without fail (if you have any).

If you made it this far, way to go. I know that is a lot for a Sunday morning, but that was the foundation.

I promise Part Two will take all this information and make it actionable next week.

Thanks, as always, for being part of Second Act Creator.

See you next Sunday.