The Arrow #200

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Hello everyone.

Greetings from Dallas.

Happy Halloween!

Well, I’ve hit 200 issues of The Arrow. Given my ADD and monkey brain, MD had her doubts that I would make it two weeks with this newsletter, much less 200 weeks, yet here we are. Without a single week missed. Thanks to all of you for being dedicated readers. I really appreciate it. And I really, really appreciate with all my heart those of you who have signed up as premium subscribers. It’s what’s keeping it going.

Last week I posted a few comments from folks who didn’t enjoy my occasional rants. Since then I’ve received a ton of comments and poll responses from people who say they enjoy them. But I more or less asked for those by writing about it. So, I suspect there are probably as many who don’t like the rants as there are those who do.

Those who don’t like them will be pleased to learn that I have nothing to rant about this week. My life has gone swimmingly, other that the typical annoyances we all experience due to the shittification of everything. Those happen routinely now to all of us, so there really isn’t anything unusual about them. It’s just life in America—and I’m sure in many other countries—today.

Comments, Poll Responses & Emails

Poll Workers

Thought you might enjoy this poll response about my comments on the poll workers when MD and I went to vote.

As a long time elections volunteer poll worker and elections officer, a big fat "f#ck you" for bashing the volunteers who are putting themselves out there to get that thankless job done down in your state of Texas.

Except he/she didn’t put the # in the bad word. I guess if these are volunteers (I always assumed they were paid) then I shouldn’t have been as hard on them. They were just feeling their way through that first day. We all queued in line until we got into the actual place where the voting machines were. Then one at a time we were called to come up to a table, where we presented our picture ID and matched our signatures. Then we were given a ballot and sent to the machines to vote.

There were five people sitting behind a long table calling people one at a time to come forward and go through the process. MD got called right before I did. She went to one of the women who got her through in a trice. I got one who took forever. As I watched before we were called, the woman who dealt with MD was cranking people through like crazy. The rest of them together weren’t getting people through as fast as that one woman was. So, call it whatever you want. Incompetence. Slow horses. Whatever. Maybe they improved. And I thank them for their service.

Who ever you are who responded, I’m sorry I ruffled your feathers.

Speaking of voting and the election, I’ll be damn glad when it’s over. I hope it’s a landslide one way or another so it will be over and not linger for weeks.

Gnawing Hunger

I’ve gotten a number of responses from people telling me that they do indeed get gnawing hunger a couple of hours after eating. All I can infer from this is that there really are a subset of people who get incredibly hungry even after having eaten not that long before.

While ruminating over it, I recalled that I had read something about hunger in Georgia Ede’s terrific book Change Your Diet, Change Your Mind. I grabbed my copy and took a look. She didn’t have anything indexed for hunger, but I did remember that she wrote something about it in the part on dairy. So I turned to those pages, and, sure enough, she had written about hunger and binge eating as a result of consuming dairy.

She wrote

Is Dairy Addictive? Most low-carbohydrate and ketogenic diets emphasize heavy cream, butter, and cheese because they are naturally low in carbohydrate, but quite a few of my patients feel "addicted" to dairy products, which can lead to cravings, binge eating, and unwanted fat gain. One reason for this may be that casein stimulates the release of a hormone called IGF-1 (insulin-like growth factor type I), which stimulates growth pathways in our bodies and increases appetite. Casomorphins may also have something to do with it, because they can cross the blood-brain barrier and stimulate opiate receptors in the brain. However, the opiate-like effects of casomorphins are fairly weak compared to drugs like morphine, and (to make matters more complicated) some dairy proteins even have anti-opiate properties. Perhaps the allure of dairy products is that processing methods-even traditional methods like fermentation, churning, and salting-concentrate their ingredients and intensify their flavor profiles. There isn't enough research to be certain about what drives some people to lose control over their appetite and eating behavior when eating dairy products, but if you struggle with overeating, a dairy-free experiment is well worth trying. [My bold]

A woman in her sixties with a long history of overeating consulted with me because she was trying to transition to a ketogenic diet but couldn't make it past day three without intense cravings and urges to binge. The plan she was following allowed for up to four ounces of cheese per day, so she had been enjoying cream cheese as a daily snack. When I suggested she try setting all dairy aside as an experiment, she was easily able to make it past day three, get into ketosis, and enjoy excellent appetite control without making any other changes to her menu.

Whey Proteins. Whey proteins are popular with bodybuilders because they are rapidly digested into individual amino acids, stimulating an insulin surge that supports the growth and repair of muscle tissue after exercise. They are also popular with processed food companies who use them to manufacture "keto-friendly" products such as shakes, chips, cereals, and bars. Although whey protein contains no carbohydrate and doesn't raise glucose levels, it raises insulin levels substantially, so it can turn fat-burning off and reduce ketone levels. In fact, the insulin response to whey is almost as dramatic as the insulin response to pure glucose. (Buyer beware: just because the label says "keto-friendly" doesn't necessarily mean the product is ketogenic or friendly.)[My bold]

I pulled a paper on whey and insulin response and discovered that whey ends up increasing the activity of GIP and GLP-1, two incretins that stimulate an insulin response. We all know GLP-1 from Ozempic, Wegovy, and the other GLP-1 receptor agonist drugs. But GLP-1 as we produce it naturally doesn’t have exactly the same effect. It does have the effect, but we produce an enzyme called dipeptidyl peptidase 4 (DPP 4) that pretty quickly degrades it. The half life of GLP-1 is about 2 seconds while the half life of GIP is about 7 seconds. DPP 4 degrades them quickly, the GLP-1 more so than the GIP. Here is a graphic from the paper:

Whey protein ends up inhibiting the normal degradation of DPP-4, which means GIP and GLP-1 hang around longer. Both of them increase the insulin response. Whey protein contains a lot of branched-chain amino acids, which also stimulate insulin.

Through these mechanisms whey protein intake stimulates insulin release. And we all know what elevated insulin levels do. They run blood sugar down. One of the most—if not the most—powerful stimulus to eat is a rapidly-falling blood sugar level. So, mechanistically we know whey protein can drive insulin up and glucose down. I’m sure there is a wide range over how this happens with a variety of people.

Some will have minimal, if any, increase in hunger after consuming whey, while others may be ravenous. If you are one of the ones who develops ravenous hunger, then it might be worthwhile to give dairy avoidance a try.

Remember, dairy is really one of the only foods found in nature that contains a lot of all three of the macronutrients: fat, protein, and carbohydrate. It is designed to induce rapid growth in infants.

One study Georgia wrote about was done in Denmark (I have not pulled this paper yet, but knowing Georgia as I do, I trust that she is describing it accurately.) Researchers randomized 24 8-year-old boys into two groups. Both groups were instructed to add 53g of animal protein per day to their usual diet. One half of the boys added the protein as 8.8 ounces of lean meat while the other half added it by consuming two liters of skim milk. Skim milk has all the fat removed, leaving only the whey, which contains the whey protein.

After seven days, the fasting insulin levels and insulin resistance of the boys in the meat group remained unchanged, whereas the fasting insulin levels of those in the milk group had doubled, and insulin resistance had increased by 75 percent. [Italics in the original]

Those are impressive findings. Especially when you consider youth is a bulwark against most changes of this type. We can get away with most anything, it seems, when we’re young and healthy. But maybe we only think we get away with it. Our inner young self is experiencing damage that out outer self doesn’t display.

The findings were so impressive to me that I decided after writing the above to pull the paper and take a look. (It’s behind a paywall, but I put a copy in my Dropbox.) One of the things Georgia didn’t mention in her description of the study is that the researchers checked the levels of branched-chain amino acids in the boys, and found them to be the same in both groups. So whatever it was that doubled their insulin levels and increased their insulin resistance, it wasn’t branched-chain amino acids.

I’m sure I’ll get a handful of comments from those experiencing gnawing hunger telling me they don’t eat dairy. My purpose in throwing this out there isn’t to imply that every case of hunger is driven by dairy, but it apparently is in many cases.

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Omega-3 and Omega-6

A number of people commented on my thoughts about O-3 and O-6 PUFA. Here is one from the poll responses:

Two criticisms: The previous names of the military rations were A, B, C, D, E, F, G, H, I, and J. The "K" just came next, although Keys was happy to say that it was named after him. Any time I see flax praised as a super-food, which is often, I try to point out that it is extremely high in estrogen, a case of a plant trying to protect itself from predators who would eat its seeds by messing with their reproductive systems. It causes miscarriages in women and birth defects in male babies. (The oil does not have the lignans unless they are added back.)

First, I’ve heard countless times that K-rations were named after Ancel Keys, because he basically developed them. So I simply repeated that. I looked it up, and I was wrong. This respondent doesn’t have it exactly correct either, but is more correct that I was. The rations were named K-rations not because of Ancel Keys but, according to Wikipedia, which accords with other references I checked, “because it was phonetically distinct from other letter-name rations.”

Some believed the K-ration was named after Dr. Keys or was short for "Commando" (as elite troops were the first to receive it). However, the letter "K" was selected because it was phonetically distinct from other letter-name rations.

Of course, the people from Minnesota (Keys was on the faculty of University of Minnesota) claimed the rations were named after him. But they would, wouldn’t they?

My respondent brought up the fact that flax oil, thought by many to be a superfood, is loaded with estrogens. Which, for some people, can be problematic. I purposely chose the flax oil without the lignans, which is where virtually all of the pre-estrogenic compounds are. If you avoid the lignans, you should be okay.

I wasn’t particularly thinking of flax oil as a food, but as a salad dressing. Flax seed oil by itself tastes like grass, which makes sense, because grasses have a lot of O-3 fats in their membranes. Most seeds have O-6 fats, but flax seeds are the exception.

I think the taste kind of sucks, but when you add a little balsamic vinegar to mix to make a vinaigrette, it doesn’t taste bad. I don’t like to use olive oil, because olive oil, for the most part, is heavily adulterated. I read a study a few years ago that said the amount of “olive oil” sold in a year is about twice as much as the amount of olive oil produced. Which tells you most of the olive oil you find is adulterated.

Canola oil also has a decent amount of O-3 fat in it, but in its natural form is repulsive and must go through a deodorization and decolorization process to be fit to eat. I don’t know what that process does to the quality of the O-3 fats as they are very delicate, so I avoid it. Which pretty much leaves only flax seed oil available if you’re looking for an O-3 oil to make a vinaigrette. There are avocado and macadamia nut oils, which aren’t bad taste-wise, but also don’t have much O-3 fat.

There are a couple of types of fat the body uses. There is storage fat and membrane fat. Saturated fat and monounsaturated fats are primarily storage fats. Omega-3 and omega-6 fats can be stored, but their primary function is in the lipid-bilayer membranes in both animals and plants. The O-3 and O-6 fats in the bilayer membranes that hold the contents of all the cells are incredibly important in making the membrane fluid enough to work optimally. And it is crucial that these membrane omega fats are in the correct proportions.

There is a difference in the bilayer membranes of plants and those of mammals. In the plants, the primary omega-3 and omega-6 fats are of 18 carbons in length. The fats in the membranes of humans and other mammals are 20 and 22 carbon chains.

Which means when we consume plants, we can get the raw materials for the 20 and 22 carbon fats we need, but we need to modify them. We have enzymes called elongases to make the chains longer, and we have desaturases to create more double bonds. Since enzymes are proteins coded for in DNA, there can be genetic differences in ability to elongate or desaturate the 18-carbon chains that come in from plant foods.

When herbivores consume grass, they get 18-carbon-chain fats that they proceed to convert to 20- and 22-carbon chains with the proper degree of desaturation and elongation. If we eat the meat of these herbivores, then we get the 20- and 22-carbon chain fats pre-made for us.

Fish do the same thing; they convert the 18-carbon chain fats in any plants they decide to eat and get 20- and 22-carbon chain fats ready made when they eat smaller fish or other living things. And we get them when we eat them.

In my view, it’s always better to get your 20- and 22-carbon chain omega fats from foods of animal origin, because you don’t have to worry about the conversion from 18-carbon chain fats from plants.

Since most of the added fats we get these days come from seed oils, which come from plants, we get a lot of omega-6 fat that we don’t really need or want. We end up converting these O-6-18-carbon fats to O-6-20-carbon fats, which we don’t really want. We need some, but we don’t need nearly what we’re getting.

It’s the same for the herbivores we eat. If they eat a lot of grain (a seed), they will store a lot of O-6 20-carbon-chain fats. When we eat them, we get that fat pre-made. But we also get a little O-3 fat, too. Just not as much as we would get were the herbivores grass fed.

Having said that, let’s take a look at everyone’s favorite food…

Sardines

I got a number of poll responses, comments, and even an email or two on sardines. Apparently, many people hate them. And wanted an alternative.

But there are many reasons to learn to love them.

Lately, I’ve been eating a tin per every day or two, whereas I used to eat maybe a tin per month, if that.

Would I rather have a slice of my mother’s carrot cake? Absolutely. But the carrot cake has nothing good in it but taste. In fact, it has almost all bad in it. The sardines, on the other hand, are virtually all good. As long as you don’t get them packed in olive or (God forbid) soybean oil. And those are the easiest ones to find. The olive oil, even if it really is olive oil, has a lot of O-6 fat in it. If it’s not really olive oil, which is likely the case, then it will be almost all O-6.

Forget about the taste for a minute. Sardines are great because they are small and haven’t had time to concentrate a lot of mercury. Not so with tuna, salmon, and larger fish. Unless you get fish that have been mercury tested and found to be free of it, you’ll get mercury. Which isn’t that big a deal if you have a little here and there. But if you’re eating a lot of fish, it can be problematic.

Not so with sardines.

Plus, gross as it sounds, with sardines you eat their bones, which provide calcium, boron, phosphorous, molybdenum, vitamin D, magnesium, and a host of trace minerals and other important nutrients.

If you douche the sardines with mustard, as I do, they don’t taste too bad. Especially if you use the mustard that comes with the little seeds still in it. Mustard actually contains a lot of O-3 fat. Granted, it’s 18-carbon chain O-3 fat, but it beats O-6 fat.

I’m fervently of the belief that if you eat anything enough, you’ll learn to like it. You may not learn to love it, but you’ll learn to like it.

I have never seen a study showing what I’m about to tell you, but I have had a LOT of patient experience to go by. MD and I always got dietary histories from our patients, and one of the things we both noticed was that overweight people by and large have limited palates.

You would think it would be just the opposite. You would think that people who love to eat any and all foods would be the ones who were overweight. But that wasn’t the case with our own patient population. It was the opposite, in fact.

Almost none of them came in telling us they loved meat and could gladly eat nothing but meat. Most of them enjoyed high-carb foods, especially high-carb, high-fat foods. Upon questioning, most of them didn’t like the very foods that were good for them. It was a struggle with some folks to come up with diets compatible with their limited food palates.

I would look upon sardines as medicine. And just take it like medicine. Soon, like me, you’ll go from toleration to maybe enjoyment. Especially if you wait until you’re really hungry.

Speaking of which

More On Gnawing Hunger

There is a new study out from the University of Virginia showing that, in women, high-intensity exercise gets rid of hunger. I know that’s not what anyone wants to hear, but, if this study is to be believed, it does work. The higher the intensity the better.

Ghrelin is a hormone that regulates hunger and appetite. Those with higher levels of ghrelin usually have a tougher time losing weight than those with lower levels. A handful of studies have shown that exercise helps reduce ghrelin levels.

The study above shows that intensive exercise suppresses ghrelin levels more than does moderate exercise.

Going back to Dr. Glasser’s work, it makes me wonder if pondering on hunger maybe increases ghrelin levels. I don’t know this for a fact, I’m simply speculating. And refocusing on hard exercise gets the idea of hunger out of the forefront of the mind and reduces ghrelin levels. The study linked above shows the intense exercise reduces ghrelin levels. But does the intense exercise to the job, or does the refocusing from I’m-so-hungry to the exercise do the lowering? I don’t know.

If you are really doing intensive exercise, it’s difficult to think about much else.

Based on the findings in this study, forcing yourself to do a bout of intensive exercise is yet another way of dealing with hunger.

The Lumen

MD and I are getting better and better on burning fat using our Lumen. It takes a bit of trial and error to see what works and what doesn’t. Drinking a lot late at night definitely doesn’t. Being careful with your diet does. Makes a big difference. It helps us be good. Sometimes you think you’re being good, but your device outs you. It’s been an enlightening experience.

I’ve discovered from MD’s workouts that when she does high intensity but not to exhaustion, fat burning is at a max. If she goes over the edge, then she burns almost all carbs. Which is how it works. You go anaerobic, you burn carbs. It has its advantages in terms of overall fitness. But if you want to burn a lot of fat, you’ve got to go as hard as you can, but not until you go anaerobic. It’s fun to have a device like this to fiddle with and really know what you’re burning.

If you want to support my work, take out a premium subscription (just $6 per month). Thanks in advance.

Okay, it’s time for a change of pace.

My Interview On Claryfication

I got a Twitter DM out of the blue from a guy in Springfield, Missouri, the city of my birth, asking if I would give him an interview on his radio program. He’s a homie, so how could I refuse?

As it turned out, James Clary, the host, had solved a bunch of his own health problems with a carnivore diet. He wanted to hear my views on that and on the ancestral diet, so we had a fun conversation.

Just before I went on, MD warned me not to get carried away and talk too fast, which is a problem I sometimes have when I’m really fired up. I heeded her advice, and the interview sounds (to me, at least) as if I’m talking through molasses.

Cancer as a Mitochondrial Metabolic Disease

The Broken Science Initiative is a group MD and I have been a part of from its inception. They had a meeting in Boston not too long ago that, unfortunately, we were unable to attend. At the meeting, Dr. Tom Seyfried, who is also a member, gave a talk on how cancer is a mitochondrial metabolic disease and not a genetic one. Tom always gives a great talk, so enjoy.

Statinators and Cholesterol Deniers

This last week was a busy one for me in terms of statins and my advocacy as a statin denier.

I had an article in one of my many tabs I kept intending to write on, but ran out of space each week. I finally forgot about it, but it still lived on in its own tab buried in with several hundred others.

Then a few things happened almost all at once that got me off the dime.

First, MD got a call from an old friend who had a medical issue. She said she had acquiesced to a statin prescription from her doctor, but she had taken it only sporadically as she felt like crap since starting. MD told her to quit. That statins had never been shown to provide any benefit in terms of all-cause mortality to woman of any age. And that a number of observational studies had shown that older women who had higher cholesterol levels had greater longevity than those with low cholesterol levels.

MD asked her for her labwork that caused her doctor to prescribe her the statin. She dug them out and sent them to MD. Here they are:

This can’t be anything but brain-dead thinking. The doc looks at the lab, sees red (literally) and prescribes without thinking about what he/she is looking at. I don’t know if it was the total cholesterol or the LDL (or both) that triggered the prescription, but whichever, it was crazy. Total cholesterol is made up of all the lipoprotein particles, including HDL. In MD’s friend’s case, her HDL was damn near half of her total cholesterol. It doesn’t take much of a thinking person to figure out the patient does not need a statin. Or any drug, for that matter.

Her triglycerides are low, her HDL is massively high, what’s the problem? There isn’t one. Yet she went out the door with a prescription for a statin that made her feel like shit. It is the shittification of modern medicine.

When I was in medical school statins didn’t exist. There wasn’t any drug that I can recall that was touted as a cure-all as statins are today. The only thing I can think of is that statins must be inculcated into the brains of every medical student so much so that they just give them without thinking.

As I’ve detailed before, all the doctors from the big, prestigious medical schools get recruited by the drug companies to tout their drugs. The academicians have all the academic merit badges, titles, etc. Then these are the docs who end up on all the advisory committees to come up with the standards for the various medical specialties. They all recommend statins as a treatment for anyone who has a total cholesterol over 200 and an LDL over 100 (or whatever the standards are now; I don’t even know for sure.)

As long as a practicing doc adheres to these standards, he/she won’t be sued if a patient so treated has a bad outcome. He/she was just following the standards.

If, on the other hand, a doctor thinks for him/herself and decides the patient, for whatever reason, doesn’t need the statin, and the patient has a bad outcome, then the prescribing doc is in the crosshairs.

And it’s not like people on statins don’t have heart attacks or strokes. They do. They just have them at slightly reduced rates as compared to those not on statins.

But, then, you may be thinking, why not take a statin? After all they do slightly reduce the risk of fatal and non-fatal heart attacks and strokes. What’s the problem?

Well, the problem is that in all the large randomized controlled trials, those on statins don’t live any longer than those not on statins. In other words, those on statins don’t have any decrease in all-cause mortality. They die of heart attacks at slightly lower rates than do those not on statins, but they die at higher rates of other diseases. Going on a statin simply trades one form of death for another.

Ideally, you would want a drug that reduces the rate of death of whatever you’re taking the drug for without increasing your risk of dying of something else. Then you would have a worthwhile drug that would end up showing a decrease in all-cause mortality.

But statins don’t fill that bill. The only group for whom a decrease in all-cause mortality has been shown are men under 65 who have had a heart attack. And even in that group, the decrease is tiny. For men who have never had a heart attack, there is no reduction in all-cause mortality. Same for women of any age.

Yet, they’re doled out like Halloween candy.

I well remember my first encounter with a patient on statins. It was in the mid-1980s and the first statins had become available. This patient was the mother of the pitcher on my men’s over-30 baseball league. He was worried about her and asked if I would see her.

She was 72 years old and mildly, mildly overweight. She had gone to her doctor a few months earlier and was discovered to have a total cholesterol of 795 mg/dl. Which scared both her and her doctor to death. He treated her with Mevacor.

My first reaction would have been to repeat the lab. Labs do make errors. More often than you would think. But he took the lab as what it was and gave her the statin. I did repeat her labs, and they came back as follows:

  • Total cholesterol: 424

  • LDL cholesterol ?

  • HDL cholesterol ?

  • Triglycerides 1828

These were while on Mevacor, so maybe the 795 wasn’t a lab error. Labs are getting better now, but back then it was common not to get LDL or HDL readings when triglycerides are so high.

I also discovered her blood sugar to be elevated. It was 154 mg/dl, which is in the diabetic range. She said the doc who put her on Mevacor didn’t say anything about her blood sugar.

Was it up, and he just hadn’t checked it? Or was he overwhelmed by the 795 total cholesterol and just trying to deal with that first? Or, did the statin she was on cause her blood sugar to go up? Which is one of the issues with statins, particularly among females. That was not known then, though, so it didn’t occur to me.

I told her I didn’t have any experience with that class of drugs, but I did know how powerful diet was in correcting bad lipid values. I told her to stay on the statin, follow the diet I gave her (a low-carb diet), and come back and see me in three weeks. I didn’t want her to discontinue the statin, because since I had no experience with the drug, I was worried about some sort of rebound effect.

We rechecked her labs after her change of diet. They were great. Better than I expected, in fact.

  • Total cholesterol: 186

  • LDL cholesterol: 118

  • HDL cholesterol: 27

  • Triglycerides: 201

I was delighted. She was delighted. Based on these lab changes, I told her to go ahead and stop the Mevacor. She gave me a funny look and said, “I stopped it when I started the diet. I thought that’s what you told me.”

Oh, and her blood sugar was 90 mg/dl.

What this taught me was that diet was vastly more powerful than statins to normalize lipid values. I saw this time and time again over many years. Though I never saw anyone again with a total cholesterol as high as hers, I did see many with hugely elevated triglycerides, way up in the thousands. Those patients always responded to the low-carb diet.

Before we continue this discussion, let me show you a couple of graphics.

The chart shows the decline in deaths from heart disease in the US from 1950 till 2014. As you can see the decline in deaths from heart disease is much like the decline in deaths from infectious diseases we saw in the vaccine graphics. They were on their way down long before statins came on the scene in the mid-1980s. Statins didn’t hit their stride until the 1990s, and, as you can see, they didn’t really change the trajectory of the downward curve.

The main reasons the curve went down are the major fall off in smoking that started in the 1960s after the Surgeon General’s warning came out in 1953 and the vastly improved treatment methods (clot busters and all kinds of life saving technology) developed over the last several decades.

The next graphic shows deaths from heart disease from 2010 to 2022.

The first graph above shows kind of a leveling off at ~2015. This one shows what has happened since. Bear in mind that during this period everyone and his brother has been on a statin. And pretty much nada. No change. Smoking has leveled off at a much lower rate, and no new life saving techniques for heart attack have come along.

I don’t know about you, but it doesn’t look to me like statins have done a whole lot. Don’t get me wrong, statins have reduced the number of fatal and non-fatal heart attacks. That isn’t in dispute. The issue is that statins may be causing other issues—cancer, maybe—that have increased the number of deaths that offset the lives prolonged by statins.

Take a look at this graphic prepared by the CDC showing overall deaths from 1969 to 2020.

The chart was created by the CDC in 2016 projecting the deaths from heart disease and cancer. The statisticians there project that cancer deaths will outpace deaths from heart disease very soon. Make of that what you may.

The whole issue may be confounded by the increase in cancer deaths allegedly driven by the mRNA Covid jabs. But that remains to be seen.

While all this is fresh in your mind, let’s turn our attention to a couple of screeds that appeared on my radar recently. The first one is the one I wrote about at the start of this section. It’s been languishing in my tabs for a few months. The article titled “Cholesterol Denialism is Pseudoscience” appeared in Medscape a while back.

The piece is well worth reading because it encapsulates all the arguments of those mentally deficient enough to be entangled in the cholesterol or lipid theory of heart disease without realizing it is just that: an unproven theory. A hypothesis, not fact.

He starts out discussing Anitschkow’s work on giving rabbits cholesterol back in the early 1900s and discovering that these animals developed plaque in their arteries. It never occurred to Anitschkow or the author of this piece that rabbits are basically herbivores and cholesterol is only in foods of animal origin. (Which brings me to one of my pet peeves: advertisers that prominently proclaim “contains no cholesterol” when what they are selling is a cookie or some other grain-based food.)

From there our correspondent writes

Though Anitschkow's work was largely ignored, it became impossible to ignore the soaring rates of heart disease observed through the 20th century. A cause and solution had to be found. It was the era of the big epidemiologic studies that defined many of the traditional risk factors that define current medical practice. The Framingham Heart Study is the longest-lasting and arguably the most famous such study (and bears the distinction of having coined the term "risk factor"). The Framingham study identified high serum cholesterol, high blood pressure, and smoking as cardiac risk predictors, thus giving birth to the Framingham Risk Score. However, the epidemiologically astute among you would point out that no observational study can prove that an association is causal. High cholesterol might be a useful predictor of cardiac risk but may not necessarily be a factor that needs treatment. If you had said that in the 1960s, your criticism would have been appropriate.

Did it ever occur to the writer that heart disease soared throughout the 20th century, but not the 19th century? Did he ever wonder what changed between the 19th century and the 20th century? ln the 19th century and before, refrigeration wasn’t widely available, so people basically ate what was fresh and available. Meat was a staple. Fresh fruits and vegetables were not except when in season. Meat was always in season. If you google menus from the 1900s, you will find that the dishes served in most restaurants were meat dishes of one sort or another. Bread was a staple as were potatoes and other root vegetables that could be stored.

Well into the 20th century we developed the means to refrigerate and to transport foods via truck and rail. We could finally have fresh fruits and vegetables year round. But suddenly we started dropping like flies from heart disease. What happened?

Widespread smoking started in WWI in men and was picked up by women during the roaring 20s. Nothing drives heart disease quite like cigarettes, and they were smoked in massive amounts during the 20th century up until the mid-1960s when the Surgeon General’s report came out. Smoking rates have been on a long slide since then. As have deaths from heart disease.

As Nina Teicholz and others have reported, both Big Tobacco and Big Sugar foisted the blame for the increase in heart disease onto saturated fat. Ancel Keys piled on with all of his nonsense.

Saturated fat became the villain while smoking and sugar went on their way unscathed by any hints that they might be involved. Despite Keys and others fingering saturated fat in the mid-1900s, the link between saturated fat and heart disease has never been proven. It is still in the hypothetical state.

This author and others like him try to make their case in two steps. First, they say, studies have shown that saturated fat causes an increase in cholesterol levels. That is absolutely true. It’s been shown many times.

Then they follow with elevated cholesterol levels are associated with increased rates of heart disease. Therefor saturated fat causes heart disease. And elevated cholesterol causes heart disease.

And if you don’t look at it too closely, it makes a sort of sense. But when you really dig in, you realize it is a fallacy.

Two studies—the Minnesota Coronary Experiment and the Sydney Heart Study—have shown that replacing saturated fat with polyunsaturated fat significantly reduced cholesterol levels, but showed no decrease in all-cause mortality or in cardiovascular deaths. The researchers who did the work on these two studies decided not to publish them because they didn’t like the results. They were recovered and published years later.

Significant reductions in cholesterol levels did not promote longevity.

The author writes

Run a meta-regression of cholesterol trials involving both statin and nonstatin medications and you see a very linear association. In short, if you lower LDL-C, you reduce cardiovascular risk. The mechanism of lowering is irrelevant. Statins, believe it or not, work by lowering cholesterol.

This is a tautology. He is careful to avoid describing what cardiovascular risk is. If he—as most statinators do—considers a high cholesterol level a cardiovascular risk, then reducing cholesterol lowers cardiovascular risk as defined. But the two studies mentioned above clearly show that reducing cholesterol doesn’t reduce risk as there were more deaths in the study groups than those in the control groups, who had lower cholesterol levels.

You can read the article on Medscape linked above and find all the fallacies right and left.

Then just a couple of days ago, I get yet another. It must be something in the water. Or more likely the great legal victory of Zoë and Malcolm may have the statinators worried, so they’re dashing off these hit pieces referring to those of us who aren’t believers as deniers.

This one is much better produced and comes from Massachusetts General Hospital of all places and is titled “The Cholesterol Deniers.” Guilty as charged.

I’m going to leave this for you to read between now and next Thursday. I’ll go over some of the specifics then. See if you can spot the fallacies.

I fear I’m about to run out of space, and I want to address Malcolm Kendrick’s great post on the big trial in which he and Zoë Harcombe triumphed so mightily. I was going to excerpt it here and there, but I would just end up excerpting the whole thing.

You can read it in its entirety here. He shows email correspondence and lays out well the collaboration and dishonesty of the statinators responsible for the piece in the Sunday Mail that ended up bringing them all down. Couldn’t have happened to nicer people.

Important Announcement

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Odds and Ends

Newsletter Recommendations

Video of the Week

The video of the week this week is a real treat. Or at least it was for me when I came across it. I got dazzled many moons ago by the tales of the great Italian violinist Niccolò Paganini, the world’s first mega musical superstar. I got so dazzled, in fact, that I took up the violin. And as is my wont, I began to delve into the lives of all the great violinists of the past as I, myself, was scrawking along on my own violin. I could play the guitar pretty well at the time, so I figured it would be an easy switch to the violin. Wrong! It was brutal. I finally abandoned it after a) my violin was stolen in a house burglary, and b) I realized I would never be a concert violinist.

Anyway, in all my studying of the great violinists of the past 200 years, I came across Pablo de Sarasate, a Spanish virtuoso who both played and wrote music. His great violin piece in the repertoire of every great violinist is Zigeunerweisen. I knew I would never be able to play that one, but I harbored hope that I might be able to play some of his Spanish dances for violin and piano. One in particular that I really loved titled Zapateado I thought might be in my wheelhouse, but now after watching it performed by Midori, all I can think of is What was I thinking. This short piece as every piece of violin technique worked into it: harmonics, double stops, pizzicato, you name it, it has it. Enjoy!

As if to rub in my realization of how far I was from being able to play this, when the above video ended, I was served up with this video of a little bitty nine-year-old girl playing the heck out of the same piece. Wow!

I should have started earlier.

Time for the poll, so you can grade my performance this week.

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That’s about it for this week. Keep in good cheer, and I’ll be back next Thursday.

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This newsletter is for informational and educational purposes only. It is not, nor is it intended to be, a substitute for professional medical advice, diagnosis, or treatment and should never be relied upon for specific medical advice.

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