The Arrow #180

Hello friends.

Greetings from Montecito.

Back after a hectic and jam packed weeklong visit to Boulder, CO, our old stomping grounds. We were pretty much scheduled in from dawn to dusk, so I’ve been way behind on emails and everything else. Playing major catch up.

For whatever reason, last week’s Arrow provoked a lot of feedback. I had more poll responses than ever. And more “Totally sucked” votes than ever. Usually there are one or two who hate whatever I write, but this time, when I checked it a few minutes after sending, I had received 9 “Totally sucked” votes. Fortunately, that’s all I got. I figured at least 9 readers were pissed about my section on politics. As it ended up, I got more votes than ever for last week’s effort. And the vast majority were four or five stars, so I’m happy.

Let’s take a look at a few poll responses. As I think I wrote last week, if one person takes the time to type out a question or comment, I figure there are a lot more people out there wondering the same thing. So, I’ll answer those I can.

A handful of people sent me long medical histories and requests for answers to their own personal medical conditions. For medico-legal reasons, I can’t answer these kinds of questions. I can’t treat people over the internet. If people describe a problem they’re experiencing, and it’s one I think a lot of people would benefit from knowing about, I’ll answer it generically.

But do not take what I say as medical advice. Always check with your own physician. He/she knows you much better than I.

Poll Responses

I’ll get my two major screwups out of the way early.


This reader gave me a 4-star rating instead of a 5-star rating for last week’s Arrow and tells me why.

I would have given you 5, but you switched MVX to MXV and had to go back had to reread it all to make sure about what MXV was, if not just a mistake.

You were kind. I would have given me no better than a 2-star, if that. I don’t know what happened. I wrote MVX for about the first half of that section, then inexplicably changed to MXV. The correct representation is MVX. Why I transposed the V and X, I haven’t a clue. My bad. Sorry about that. I know how aggravating it is to think you’ve missed something and then go back and reread a time or two only to realize it was the author who messed up.

Coagulopathy vs Hypercoagulability

I shot from the hip on this one and screwed it up. In the text I wrote coagulopathy, which in my aging brain I just put coagulo- which means basically blood clotting together with pathy, which means disease of. A disease of blood clotting. So either way, overly clotting or failure to clot ought by nomenclature rights to be a ‘coagulopathy’ because it is a disorder of clotting. But that’s not exactly how it is classed and had I thought about it for a minute, I would have remembered that coagulopathy is a specific term meaning blood that doesn’t clot well. What I should have written is hypercoagulability, which specifically means a condition in which blood is more prone to thrombose or clot.

Mike, my MS4 (fresh from taking his Step 2 exam) tells me your use of coagulopathy is incorrect. What you really mean is hypercoagulability. Coagulopathy means lack of clotting. Otherwise, we really enjoyed your blog this week. He is also going to subscribe.”

The senior med student son of one of my readers pointed out my mistake. All I can say in my defense it that I knew this, too, when I was a 4th year med student and had just finished my boards. Thanks for the correction.

Elevated Ferritin Levels

I received a long poll response from a lady who has a condition I’ve seen often. And that I have myself.

I am a 69-y-o woman with a perplexing result on a recent set of blood tests. My ferritin level was sky-high (943 ng/ml; only other time I was tested for ferritin was 2013, result normal at that time).

Ferritin is a ubiquitous, intracellular protein that plays a crucial role in storing, solubilizing, and regulating the body's iron levels to prevent deficiency or overload. Ferritin stores iron in the cells—primarily in the liver, the spleen, and bone marrow—in a soluble form that doesn’t cause problems. The ferritin releases iron if the body needs it and accumulates it if a measure of iron overload exists.

As I’ve written repeatedly when discussing vaccines, sanitation has been a boon to mankind. Up until relatively recently (the early to mid 1900s), most people lived in squalor to some degree. It wasn’t until the latter part of the 1800s before Koch came up with his eponymous postulates that basically put the germ theory solidly on the map. This lack of sanitation and the shitty (literally) conditions under which most people lived constantly kept their immune systems stretched thin. It didn’t take much for a measles virus to add to the burden and, in a lot of cases, overwhelm the already maxed out immune system and kill the patient.

Sanitation was an enormous boon to mankind in a plethora of ways. But it did have its downside as well.

If you plow through the anthropology and archeology and primatology literature as I have, you’ll find that most of our primate relatives are crawling with parasites. Early man was doubtless crawling with parasites, too. I would bet that prior to WWII, just about everyone in rural America had pinworms and Giardia (a type of parasite that comes from drinking contaminated water) and more.

Most parasites feed off their host by sucking blood. As a consequence, over evolutionary time, we hosts developed a way to retain and store iron to keep it away from parasites. In fact, parasites need iron to live, so we humans have evolved to sequester iron when we get infested with them.

The system worked well until sanitation came along. Now almost no one in the Westernized world co-exists with parasites. A kid here and there will get pinworms, but not nearly as often as they used to. And when a kid gets pinworms, all it takes is a dose of chewable medicine to get rid of them. Of course, the entire family has to take the medicine and get wormed as well or it can pass from person to person and persist.

Thanks to sanitation we no longer have the parasites, but we still have all the protective mechanisms to store iron. And too much iron can be a problem. It is highly reactive if it gets loose, and it can get stored in organs where it shouldn’t be. Now instead of fighting to retain each scrap of iron it comes across, our body has way too much. We evolved a way to grab iron and hold on to it, but we haven’t evolved a way to get rid of it when we have too much.

I didn’t mention above, but early man, given his lifestyle, probably got a lot of injuries in one way or another. These injuries would cause him to lose some blood, so, again, the forces of natural selection drove our physiology to hang on to iron like crazy. We had no need to get rid of iron. The parasites and the more dangerous lifestyle took care of that.

Now the only way to get rid of excess iron is to bleed… or rather to give blood. Which is a win-win. The donor gets rid of excess iron and the recipient gets a lifesaving substance. You can also get rid of iron by chelating it, but it’s vastly easier and more charitable to just donate blood.

So, getting back to ferritin…

Along with holding iron in a soluble form inside the cells, ferritin is an acute phase protein. It is released by the liver during inflammation. It sucks up the loose iron and sequesters it in the cells so it won’t be available for any bugs that might need it to survive and thrive.

High levels of ferritin usually indicate some sort of inflammation is in the works. Usually when the inflammation gets under control, the ferritin levels go down. As we discussed last week, visceral fat can accumulate macrophages and stimulate an acute phase response during which the liver releases ferritin.

But another situation can cause greatly elevated ferritin, and that is hemochromatosis. It is a genetic disorder in which its sufferers cling onto a lot of iron and it ends up getting packed in their organs and ultimately kills them if they don’t get rid of the excess.

From 0.4-0.6 percent of folks of European origin have hemochromatosis. But a lot more have one of the genes for it. Those who have hemochromatosis have both genes for the disease and are called homozygous for the disorder. Many more have only one of the genes and are heterozygous.

I, myself, am heterozygous for it. Which is why I give blood often. It keeps my ferritin levels down.

To determine if you are either homozygous or heterozygous for the condition, you can get a lab test to tell you.

Most people who get checked won’t have either gene. So, most folks won’t have to worry about it.

But it doesn’t hurt to give blood even if you don’t have the genes for it. If you are following an animal-protein-based diet, you’ll be getting plenty of easily absorbable heme iron, so don’t worry too much about anemia. If you go to give blood at the Red Cross or wherever, someone there will check to make sure you are not anemic before they will draw your blood.

Donating is a healthful thing for you to do and may even save someone’s life. As I wrote above, it is a true win-win. And since it’s free, it’s a win-win-win.

Visceral fat…How to Lose It

I received a number of poll replies and an email or two from folks wondering how best to lose visceral fat.

The good news is that for most people visceral fat is the easiest fat to lose. It comes off first.

Subcutaneous fat —that is fat under the skin — is the normal, natural storage depot for fat in humans. It’s the depot that fills up first. Once it is filled, then excess fat starts getting crammed into the visceral compartment (e.g., the abdomen) and even into organs, which is not a good thing. As I wrote, since this fat is invading places it shouldn’t be found, the body views it as a foreign body, much like a huge splinter. The immune system mounts a response, macrophages charge in, and the entire immune response cascade begins.

You can see the difference between subcutaneous fat and visceral fat below.

And here:

Here is yet another graphic I use in presentations to show the macrophage infiltration of visceral fat. All of these macrophages are sending chemical signals to recruit more macrophages to the battle. And to send a message to the liver to help.

Since visceral fat is fat where it doesn’t belong, the body typically seeks to get rid of it first under any kind of diet. In my view, a low-carbohydrate diet removes it the quickest simply because such a diet reduces insulin levels the most rapidly. Then, since the body doesn’t have to deal with partitioning the carbohydrate load it would in a higher-carb diet, it can focus on burning fat. And typically the visceral fat gets burned first. (It’s not just my saying this as a function of my low-carb bias, even the Cleveland Clinic—a bastion of mainstream medicine—agrees with me.) You should also make sure you have adequate protein on your low-carb diet as protein itself burns extra calories.

The other way you can help to remove visceral fat is to do high intensity interval training and/or strength training. You’re not going to rid yourself of visceral fat in any meaningful way by taking a stroll around the block a few times per week. Such a stroll brings other benefits, so no need to stop strolling if you enjoy it. But you need to work pretty hard in order for exercise to help ditch the fat quickly.

I like to combine strength training with high intensity interval training. I can tell you at the outset that it is not fun. I dread it, but I do it. And I always feel a thousand times better after I do it. It’s a good thing to have done.

If you want to build and maintain muscle mass, you’ve got to continuously increase the resistance. It’s easy to go to the gym and do a couple of sets of various lifts and feel like you’ve done something, but it doesn’t do you a lot of good unless you continue to increase the resistance, that is the weight or the effort, so that you’re really working.

I use the band system I’ve written about before. I have a set of ‘lifts’ I do at every session. I increase the number of reps until I can’t do any more. Then when I can finally do 40 reps in one constant session, I move up to a larger band and start with fewer reps. I then work up from there, rinse, and repeat. MD can attest that toward the end of my reps as I approach failure, I am practically screaming. [The bride does so attest.] And I fall over on the bed and pant at about a million breaths per second (a bit of an exaggeration, but that’s what it feels like to the panter). Since I increase either reps or size of band, I know I’m making progress, doing more work over time.

A zillion years ago when I was in SCUBA instructor school one of our lecturers was a big time diver and an exercise physiologist from UCLA. He was always going on about Specific Adaptation to Imposed Demand (SAID), a term I’ll forever associate with SCUBA diving. But it applies to everything.

Whatever specific demand we put on ourselves, we end up adapting to. Back in Arkansas I would see roofers out in the middle of the day carrying piles of shingles and working away in the hot, humid summer. I knew that if I tried to do that, I would collapse in about 20 minutes. But if I ended up doing it day after day, I would adapt to that imposed demand and be able to do it like they did. It would take a lot of adapting, however, before I reached their ability to do it for an eight hour day.

It’s the same with strength training. If you struggle to lift a certain weight or stretch a particular band, you will ultimately adapt and be able to do it easily if you persist in the effort. You will have developed a bit more strength and aerobic capacity than you started with, but you won’t continue to improve if you stick with that same demand. To keep improving you have to increase the demand you put upon yourself.

And by continuously increasing the demand, you will more quickly rid yourself of visceral fat. You’ll burn calories like crazy. As long as you’re keeping your carbs low, you’ll end up primarily burning fat. You’ll burn glucose when you’re in the heaving and panting stage, because that is anaerobic. During anaerobic training the only source of energy available is glucose. But in order to access this glucose, you’ll drop your insulin level quickly, which also allows fat to get out of the fat cells. And it will burn during recovery.

As I wrote previously, a quote I heard from I don’t remember whom is what keeps me motivated.

“The only time you can coast is when you’re going downhill.”

Determining Visceral Fat Accumulation

There are a couple of ways to determine how much visceral fat you’re toting around. An expensive method and a free method.

There are a number of scans out there you can get that will accurately show you how much visceral fat you are sporting. They are relatively expensive and require you to go to a scanning center to get them. These are scans that will provide images similar to the ones showing the visceral fat in the section above.

You can also do it free by determining your waist-to-hip ratio, which, surprisingly is pretty accurate. Since your viscera are in your abdominal area, it stands to reason that a lot of visceral fat accumulated there will increase your abdominal circumference. And the bigger the circumference the more the risk.

Here is how you do it accurately.

To accurately determine your waist-to-hip ratio (WHR), follow these steps:

Measure your waist circumference:

  • Stand upright and breathe out normally

  • Use a tape measure to measure the smallest circumference around your abdomen, usually just above the hip bones/belly button

  • Make sure the tape is snug but not compressing the skin

  • Record this measurement in inches or centimeters

Measure your hip circumference:

  • Identify the widest part of your hips/buttocks

  • Wrap the tape measure around this widest point, keeping it parallel to the floor

  • Record this measurement in inches or centimeters

Calculate your WHR:

  • Divide your waist circumference by your hip circumference

  • For example, if your waist is 32 inches and hips are 40 inches, your WHR = 32/40 = 0.8

While taking these measurements, do so after an exhalation and make sure the tape is pull taut, but not indenting the skin. Also, either look in a mirror or have someone help you to ensure the tape is parallel and not askew.

Here is a graphic showing how to do it. This is obviously a female, but it works the same in males. (Before you take me to task, I realize in this picture it SAYS waist at the narrowest point but any fool can see that it’s narrower a couple of inches higher than the picture shows. It’s just the best I could find on short notice.)

Once you have your initial waist-to-hip ratio, you can monitor how it changes as you lose visceral fat.

The numbers I like to use are a little different than on the graphic above. I like to see the WHR of males come in below 0.90. And for females to come in below 0.85.

The waist-to-hip ratio change is vastly more important than scale weight change. I know it’s easy to pop on the scales and see changes versus having to go through the effort to do the measurements of you waist and hips. But, if done correctly, the WHR tells you a lot more about your health status than a simple change in weight.

Muscle weighs significantly more than fat. Remember, fat floats in water, while muscle doesn’t. A given weight of muscle has a lot less volume than the same weight of fat. If you gain an amount of muscle that weighs the same as the amount of fat you lose, you won’t see any change on the scale, but you will see a significant change in your WHR and the way your clothing fits.

If you’re losing more muscle than you are fat, you may end up seeing a loss of scale weight, but determining your WHR may show an increase. You do not want this to happen. If it does, you should make sure you’re getting enough protein and up the strength training.

The WHR is an invaluable tool for determining what’s going on in terms of both muscle and fat. Much, much more valuable than the scale.

Total Cholesterol Level Is Too High

A poll responder asked about cholesterol levels. I don’t know if this is a male or female, but it doesn’t matter.

47 years old and resting heart rate of 60, low blood pressure (usually 115/70). My numbers: Cholesterol: 332 (up from 247 one year ago). Triglycerides 35 (down from 56 one year ago), HDL: 90 (up from 85 one year ago), LDL 235 (up from 151 one year ago), A1C: 5.2 (down from 5.4 one year ago)

This person’s doctor is concerned over the total cholesterol level. The respondent says the doc recommends soluble fiber and/or plant sterols to get the total cholesterol level down. Given the total and LDL cholesterol numbers, I’m surprised the doc hasn’t gone into statin panic mode. Most would seeing those numbers.

Let’s delve into these numbers a bit to see what we can figure out.

First, total cholesterol is a meaningless number. Back in the old days, that’s really all that could be measured, so that’s what everyone looked at. Over time, the various cholesterol fractions were teased out, and cardiologists seized upon LDL-cholesterol as the culprit driving heart disease. As we all know, the idea that any of the various subfractions of cholesterol cause heart disease is speculative at best. It’s called the lipid hypothesis, and although many take it as a fact, as of now, it is still a hypothesis, because causality has never been proven.

Total cholesterol is the sum of all the other cholesterol subtractions. So LDL, VLDL, IDL, and HDL all add up to the total cholesterol number. As LDL is considered the so-called “bad cholesterol,” HDL is considered the “good cholesterol.” Cardiologists like to see HDL as high as possible while keeping LDL as low as possible. An HDL of 90 mg/dl that the respondent above reports should be great news for his/her doc. Which may be why said doc isn’t rushing to the statins.

So if total cholesterol is elevated because HDL is elevated, one would think this would be a good thing. But not if all one is focused on is total cholesterol, a meaningless number.

The subject above also has a triglyceride level of 35, which is exceptionally low. And wonderful! The ratio of triglycerides to HDL is fairly predictive of who is at risk for heart disease or more specifically for having a heart attack. Much more predictive, in my view, than LDL or total cholesterol levels. Generally, a TGL/HDL ratio of 3 or under is considered good. Anything above can cause a bit of concern. If you’re just looking at lipids.

This person has a TGL/HDL ratio of 0.39 (35/90), which is really low, way, way below the 3 threshold for being problematic.

The other issue is that in almost all cases, the LDL-cholesterol measurement in a lipid panel is calculated. That’s right. The LDL isn’t measured—it’s calculated. It can be measured directly, but it’s a more complex and costly test. So, when you get an LDL level, it is usually calculated using one of a number of formulas.

The original formula was called the Friedewald equation named after the lead author of the paper that described it. Here’s how it works.

LDL cholesterol = Total Cholesterol - HDL-cholesterol - Triglycerides/5

Since there are a bunch of fractions of cholesterol besides HDL and LDL, Friedewald determined that those other fractions not specifically mentioned in the equation would total to the value for triglycerides divided by 5. His equation worked well, but only within a narrow range of triglyceride levels. A triglyceride level of anything over 400 would invalidate the equation.

If you ever gotten a lipid panel back saying your LDL couldn’t be calculated, that’s why. Your triglycerides were over 400.

Over the years since Friedewald came out with his calculation, a couple of new calculators have been developed that are more accurate with triglyceride levels over 400.

But no one thinks about how low triglyceride numbers affect these equations. There was a paper from the 2008 Archives of Iranian Medicine, of all places, that looked at how low triglycerides affected the Friedewald equation. As it turned out, low triglycerides made the LDL levels come out higher than the actual measured levels. The Iranian authors of the paper generated their own equation to determine LDL in the face of low triglyceride levels.

Before we get to the Iranian equation, let’s look at the above lab levels and run them through the Friedewald equation to see what we get.

LDL = TC - HDL - TGL/5

LDL = 332 - 90 - 35/5 (7)

LDL = 235

Which is exactly what the lab results showed. So the lab the respondents sent the blood off to used the Friedewald equation.

Let’s use the more complex Iranian equation to see what we get.

LDL (mg/dL) = TC/1.19 + TG/1.9 – HDL/1.1 – 38

LDL = 332/1.19 + 35/1.9 - 90/1.1 - 38

LDL = 279 + 18 - 82 - 38

LDL = 177

As you can see, an LDL level of 177 would have a different effect on most lipophobic doctors than would an LDL of 235 as this respondent’s test showed.

My guess is that if the doc ordering this test had ordered a measured vs a calculated LDL level, the results would have been a lot closer to the 177 than to the 235.

For those interested, I stuck a copy of the Iranian paper in my Dropbox. You can access it here.

Okay, let’s look at one more issue that a lot of people probably wonder about.

High Blood Pressure Won’t Go Down

Here is a partial poll response from a 61 year old man. He weighed ~190 or so at 6 ft tall during college. Then gained over the intervening years to 272 at his heaviest last October. He has a history of yo-yo dieting. He writes

At 18 my blood pressure was 130/80 with the typical white coat syndrome it was always higher than that at doc office. I went on a blood pressure med in 2008 16 years ago and it never really helped a lot but a little. So the second question is based on my last weight loss stint. Jan 1 2024 i got serious and went full carnivore/keto…. I started at 259 lbs and dropped to 226 lbs. Basically the rules were No sugar, NO seed oils, No grains/carbs. Did intermittent fasting as well from one day to 4 days. When i did eat it was usually 1 meal a day occasionally 2 meals but within a 4 to 6 hour window. Any carbs i had were of the green kind usually broccoli, green beans. This was from jan 1 to march 6th I did kettle bells 2 to 3 days a week. Hiked/walked 3 days a week, usually with HIIT somewhere within that hike of doing 30 seconds sprint with 90 seconds cool down. With all this my blood pressure was still high. It would be 150/90 to 160/95 sometimes down to 140/85. And if i sat there and did deep breathing i could get it down to 130/80, and occasionally be in the the mid 120’s over 75 with a lot of calming effort. But I never seem to be able to reproduce that in the doc office. Your comment on inflammation and visceral fat made sense. I was hard core for 2 months, felt great, lost 4 inches off my waist line but blood pressure was still up. How long does it take to come down and can you offer any other tricks for me to try? I fell off the wagon March, April and May and gained 5 lbs back. Was frustrated about blood pressure but am back on the wagon and figure i just gotta keep going.

He’s obviously concerned about his blood pressure.  And why it hasn’t come down after all his dietary and physical activity efforts.

Blood pressure usually responds rapidly to a low-carb diet. But not in all cases. Despite rigorously adhering to a low-carb diet, somewhere between 20-25 percent of people still remain hypertensive. 

When people become insulin resistant and hyperinsulinemic, they tend to retain sodium. When their insulin levels drop after following a low-carb diet, they ditch this sodium pretty quickly. In fact, they ditch too much of it in many cases and have symptoms as a result. Which is why I always encourage my low-carb patients to up their sodium intake. Along with the sodium, they can lose potassium and develop other symptoms. Fatigue, mainly. So I supplement my patients with potassium.

When the body ditches sodium as a consequence of insulin dropping quickly, they lose a lot of water along with it. Typically blood pressure drops at the same time. But not always. There are some folks who follow low-carb to the letter and still have elevated blood pressure.

I’ve had a bunch of patients whose blood pressure didn’t go down to normal on low-carb diets take a magnesium supplement at bedtime. That helped a lot of them. But it didn’t reduce it in all.

Worrying about blood pressure tends to make it go up and stay up. But if you are a worrier about it, it’s difficult to stop worrying. And worriers tend to have white-coat hypertension way more than non-worriers. So it’s difficult to know what the real blood pressure of these people are.

I know how easy it is to worry about it. I’ve always had low blood pressure myself. It typically runs about 100/65. Whenever I go to give blood, they always check it (which is about the only time I ever have my blood pressure checked), and it always comes in low. They always ask me if I’m on medication for blood pressure, and I always tell them, No. 

One time I went in for a blood draw and my BP came in at 130/85, which scared the heck out of me. It didn’t bother the tech at all. But I obsessed on it for days. I finally had someone check my BP, and it came in at the normal 105/68. But  the experience made me realize it’s easy to obsess on something that is an unexpected finding. I’m not sure what I would have done had my BP been higher on the recheck. And 130/85 just isn’t all that high for someone my age. It was just that it was such an elevation from my usual BP.

The blood pressure readings of the respondent aren’t all that high. I’ve had patients walk through the door with no symptoms whatsoever and have blood pressures in the 210/160 range. Those get my attention. But not 130/80 in a 61 year old male.

My suggestion for anyone worried about blood pressure at the 130/80 level would be to take magnesium at bedtime and watch coffee and other stimulant intake. I would get my fasting insulin checked. If it’s elevated, I would have some work to do in terms of carb restriction to get it down. And my other recommendation would be not worry about it. It should come down even more as the excess fat goes away. And if it ever came to it, and I felt the need to take a medicine for high blood pressure, it would be an ACE inhibitor, simply because those drugs are anti-aging drugs as well.

If you want to support my work, take out a premium subscription (just $6 per month)—it’s cheaper than some nasty Starbucks Vente latte gingerbread pumpkin whatever. And a lot better for you. It will run your IQ up instead of your insulin.

Politics Idiocy In Medicine

Let me start out by declaring that men are different than women, no matter how much other people believe that sex is simply a construct. And that one can decide one’s sex. Same with race. Black people are different genetically than white people, who are different than Asians. And on and on. Race is not a construct. It’s a reality. If the genetics of black people make their skins black, then odds are there are other genetic differences as well.

It is well known in medicine that black people have different susceptibilities to disease than do white people. Black folks are more likely to have heart disease and diabetes than are white people. But paradoxically black people tend to have lower LDL levels than white people (which should tell you the lipid hypothesis of heart disease is BS). Black people also have on average higher Lp(a) than do white people. These just skim the surface of the genetic differences between just these two races.

I’m indulging in this discourse because of an article I read a couple of days ago. The degree of insanity this whole DEI movement has encouraged is beyond the pale. When I just thought it was a bunch of Woke college students and professors, I thought this too will pass. But this idiocy has begun to permeate the thinking of people who should know better. And it could cost lives.

I just read an article in STAT, which is a subscription news service that deals with the medical profession. The title of the article that has me so agitated is “Millions fewer people may need statins, a new study suggests. But guidelines have yet to agree.” 

You might think that given my aversion towards statins that I would welcome such an article.

Well, normally I would. And I did have a little frisson of glee when I read the title. But then I read the article. And was totally gobsmacked. How could such idiocy take hold of an intelligent people?

The article began by discussing a familiar scene: a patient discussing the possibility of having to take statins as a result of a routine lab test. Should the doctor recommend a statin to reduce the risk over time?

Then the second paragraph reads

That conversation may happen less often if changes in the risk model presented by the American Heart Association in November translate into new guidelines for prescribing statins. Those guidelines haven’t been recalibrated yet, but a new analysis suggests that the new risk model could mean far fewer Americans — as many as 40% less than current calculators say — would be candidates for cholesterol-lowering drugs to prevent cardiovascular disease.

Wow, now we’re getting somewhere, thinks I. Maybe people are finally seeing the light on the whole statin travesty.

So, I read on.

To reach this conclusion, published Monday in a JAMA Internal Medicine study, researchers analyzed data from 3,785 adults who were 40 to 75 years old and took part in the National Health and Nutrition Examination Survey from January 2017 to March 2020. Their 10-year risk of artery-narrowing cardiovascular disease was computed using the AHA’s Predicting Risk of cardiovascular disease EVENTs (PREVENT) equations from 2023 and then compared to risk estimates using the previous tool from 2013, the Pooled Cohort Equations (PCE) on which current guidelines are based.

Those 2013 equations were widely criticized as overestimating risk. The 2023 version, drawing on billing and electronic health record data from a more diverse real-world population, incorporated current statin use as well as metabolic and kidney diseases.[My bold]

Uh oh.

“…electronic health record data from a more diverse real-world population…”

What could a diversity of population have to do with it? And why would that make any difference in the rationale for prescribing statins?

I read on, then I come to one of the most unbelievable paragraphs I could ever imagine finding in a serious piece of medical writing.

Race, now recognized as a social not biological construct, was excluded in the newer equations. That meant 5.1% of Black adults were computed to be at risk, compared to 10.9% from the previous calculator. For older adults ages 70 to 75, the proportion at risk was 10.2%, down from 22.8%.

“Race, now recognized as a social not a biological construct,”… WTF!

Are they kidding me? This absolutely beggars belief.

What they are saying is basically when we thought black people had more heart disease, diabetes, and higher Lp(a), we did so because we considered race a biological construct. But now that we know race is a social construct, we can ignore the increased risk of the above disorders, because they should be the same for blacks as for whites. And we can lower the risk levels all around. (Regardless of what we see clinically with our own lying eyes!)

And since risk levels are lower for heart disease than they were when we thought blacks were a race instead of a social construct, we can lower the levels of what we consider worrisome.

The benefit is that there will be fewer statin prescriptions necessary.

I thought this may be STAT idiocy, because the authors often appear to be woke, so I took a look at the JAMA paper the article was describing.

And there it was in black and white:

Concerns have been raised that the PCEs, which are derived from 5 cohorts initially recruited between the 1940s and 1980s, may broadly overestimate risk for current populations and that the cohorts underlying calculation of the equations were not reflective of the diversity of the US population. [My bold]

The JAMA article pointed out that Hispanic and Asian were underrepresented, so the risk calculations were overestimated. It goes on to say how black people are overestimated in terms of risk.

Can you believe the abject idiocy of this?

It would be comparable to telling a black person who is having a sickle cell anemia crisis, “Don’t worry, all that excruciating pain you’re experiencing is all in your mind. Same for the fever and shortness of breath. And all the rest that goes with it. Race is a cultural thing, so you don’t have any greater chance of having sickle cell anemia than the white guy across the street.

Or by telling some white guy who has pain, shortness of breath, and swollen hands and feet, Whoa, we need to check you for sickle cell anemia.

It’s insane.

With this kind of idiocy run amok, how can we trust anyone?

Sexes differ. And races differ. And there’s an end on it.

They shouldn’t be treated differently by society, but they may need to be treated differently by the medical profession based on what they’re more or less susceptible or predisposed to.

There is a noxious movement to make studies more equal by mixing the racial and sex differences together in study groups. Therefore the findings will be more relatable to real life. Bullshit.

There are racial differences in disease proclivity. And sexual differences as well. For example, women rarely get heart disease prior to menopause. Men do get heart disease prior to the age at which women hit menopause. Women commonly get breast cancer. Men get it too, but rarely. There are other differences as well.

To perform a decent study, researchers should construct their groups to be randomized by racial and sexual characteristics. In other words, study white males only. Or white females. Or black males. Hispanic males. Asian males. Same with females. Given the genetic differences between the races and between men and women, we can then pinpoint the outcomes much better.

No researcher would ever dream of throwing a bunch of Sprague-Dawley rats in with a bunch of Fischer 344 rats and Zucker rats and hope to generate any worthwhile findings. These rats—as far as I know—can mate and produce offspring, just like the different human races. But anyone trying to bunch them all together for an experiment would get laughed out of the literature.

Yet that’s the new movement in the human research world, because race is a social construct, not a biological one. Tell that to the rat researchers.

We’ve got to end this idiocy somehow.

News You Can Use

Someone sent the short video below to me a day or two ago. It’s brilliant. I have’t had the opportunity to try it out yet, but it looks like it would work like a charm.

When I eat at home or away, I love to add butter to my steaks (if that’s what’s being served) and to any side veggies that might come with my order. About half the time in restaurants when I request extra butter, they bring it in pats on a small plate. The other half of the time, they bring those damnable foil-covered butter pats that are a pain to get open. Especially without getting butter all over your fingers. Or at least my fingers when I do it. You may be better at it than I.

This short video shows a young lady who has it figured out, at least if it is pretty softened up first. I can’t wait to try it myself. But I wouldn’t do it on bread. And I love the Elton John soundtrack.

Nick Norwitz on the MVX Study

A reader sent me this video of Nick Norwitz discussing the MVX study I posted last week. He was as taken with it as I was, but he combines it with another study showing a different take on ApoB. Of course, the study he uses to explain that ApoB really is a risk factor was done in China and underwritten by a number of Chinese funders, including the Chinese government. Which makes the study worthless in my eyes. At best a 50-50 proposition as to whether it is valid. He does do a nice job of demonstrating what ApoB is, which makes the video worthwhile. That and his explanation of the MVX study.

The Mercola Situation and the Latest From Seyfried

I’ve put out some inquiries to people I know who, I suspect, have some insight into the Mercola situation. I haven’t heard from any of them, but maybe I will before next week.

I intended to post on the latest Seyfried paper as analyzed by my friend Bob Kaplan, but I ran out of space. This Arrow is already at Tolstoyian proportions.

I’ll address those two issues next week for sure. I won’t be traveling, so I’ll have a lot more time to dig into things.

Odds and Ends

Newsletter Recommendations

Okay, I’ve got a great newsletter reco for you this week. I recommended it once before, but the link was broken. At least for a while until I figured it out and got it fixed.

The newsletter is Books and Biceps, written by Jon Finkel.

You’ll understand the style and content better by this opening paragraph from an article about Jon, the author, in New Yorker last year.

Jon Finkel’s calling as a book whisperer to burly bros can be traced to the summer of 2005. He was in his mid-twenties, living a version of the Southern California dream: surfing at dawn, writing for fitness magazines by day, and playing beach volleyball in the evening. The courts were in high demand, and he always arrived early and brought something to read. Finkel’s apartment... was too small to accommodate his growing library, so he found himself pushing paperbacks on friends and family as a means of decluttering. His wasn’t a literary crowd. But he found a “hundred-per-cent hit rate,” with a nonfiction book called “Shadow Divers,” by Robert Kurson, about a pair of explorers who discover a sunken German U-boat off the coast of New Jersey. One acquaintance after another devoured the book. Then Finkel got a call from his friend... “Dude, somebody just recommended ‘Shadow Divers’ to me, and it’s the fucking copy you gave me six years ago!” The dog-ears were unmistakable.

The intersection of pumping iron and perusing Plato seems a reach, but in Books & Biceps, Jon Finkel merges the two seamlessly into a powerfully motivating newsletter that encourages gym rats to read (and readers to get fit). His oddball journey combining two such divergent worlds was featured in the article by Ben McGrath in the New Yorker. It's worth it just for the book recommendations, but you can also stay for the strength.

The link to subscribe will definitely be working this time. As you might imagine, I love this newsletter.

And, as always, there is OutlanderMD. This week upcoming the bride tackles the subject of handling a breech birth in the Highlands of Scotland in 1744. Take a look if that strikes your fancy.

Video of the Week

A little different video this week. It’s of a sort of haunting song Nat King Cole made famous 75 or so years ago. I had never heard it until I found out about it from Ted Gioia, one of my favorite Substack writers. The song was written by a weird hippy-oid guy back in the late 1940s named Eden Ahbez, who was kind of a derelict. Ted describes Ahbez’s life and some of the many songs he wrote. Especially interesting—to, me, at least—was how Nat King Cole ended up with the song.

Here is Nat King Cole singing Ahbez’s one great hit: Nature Boy.

Okay, that’s about it. Let me know in the comments or in the poll responses if you enjoy my answers to and elaborations on the questions from readers. Or if you would rather I spend my time analyzing studies.

It’s poll time. Lemme know how I did.

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Keep in good cheer, and I’ll be back next Thursday.

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The information provided in this newsletter and on this site is for educational purposes only and does not substitute for professional medical advice. The author is unable to diagnose, advise, or make medical recommendations for individuals via the internet.

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