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Hello everyone.

Greetings from Dallas where it is bright and sunny, but cold.

I may have spoken too soon early last week about the efficiency of UPS. Now they’ve delayed an order on me. Fortunately, it wasn’t anything time dependent, so it really isn’t a big deal, but it is just more grist for the shittification-of-everything mill.

I think it all started with Covid.

Back then deliveries were delayed all the time with the excuse that shortages of drivers and workers due to Covid slowed everything down. And everyone seemed to understand. Covid has been over for years now, but shippers in general seem to be following Covid rules. Just give them an excuse, and we can delay all we want.

Amazon used to be Johnny on the Spot with its Prime deliveries. Always within two days. Now Prime comes any old time, and no one seems to bitch about it, despite paying the Prime fees for expedited delivery.

The item I had coming was supposed to be here in three days. It was sent from Miami late on 1/15 and—according to my tracking number—was scheduled to be delivered on Saturday morning 1/18. Given the short time, I would guess it was being flown, but I suppose it could get from Miami to Dallas in a couple of days on a truck.

The package did not arrive on Saturday. Instead I get a notice it will be delayed due to “extreme weather.” The South had been hit with a cold snap, but not ice and snow yet at the time this was shipped. All the snow came after it arrived. There was neither ice nor snow in Dallas and certainly not in Miami, so if went via UPS plane, that should not have mattered.

It finally arrived late Tuesday, 1/21, at 8:52 pm, after I had received a notice it was to arrive before noon. I think all these companies just figure that since Covid, everyone will just accept their excuses and say, Oh well…

Everything shuts down in the South when a single flake of snow is predicted to fall. Saw this a few days ago and realized how apropos this really is.

Addendum: Last Saturday I found a book on Amazon that I thought might provide some answers to a topic I’ve been pondering. It said if I ordered in the next 3 hrs 40 minutes, I could get it on Sunday. The next day. There is a giant Amazon distribution center about five miles from our house, so we often get deliveries on Sundays. I ordered the book. Here it is Thursday afternoon, and still no delivery. More shittification.

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On another note…

Last week’s Arrow was a bit different in both the content and the response. When I finished it and handed it off to MD to vet, I told her I didn’t think it was all that good. When she finished with it, she told me she thought it was great. She said, “I think people will like it.”

She was right. I got the highest polling numbers by far that any Arrow has ever received. Most of them are in the low to mid-80s, in terms of percent favorable. Some drift down into the high 70s. But I’ve never had one in the 90s.

Plus, I got many favorable poll responses and comments. More than usual.

But there was a downside. First, this issue had the least opens of any Arrow I’ve ever sent out. Usually I get about a 50 percent open rate, which may seem low, but is really good for a weekly newsletter. Last week’s got a 39.64 open rate, which is the lowest ever. It couldn’t have anything to do with the content, because it has to be opened to even see the content.

And not only that, I had the most unsubscribes I’ve ever gotten: 28. I usually get ~15 each week. Used to drive me crazy until I realized that people get new email addresses, or leave their jobs and lose their work email addresses. A lot of reasons, but last week’s was almost double the norm.

Plus, there were four spam reports. I get a spam report once in a blue moon. Almost never. I don’t send The Arrow out to anyone who hasn’t subscribed to it, so I suspect those spam reports are a way of expressing a dislike for what I wrote. Same with the unsubscribes.

Must be a handful of folks on my list who are heavily invested in the religion of climate change. If those are the ones who unsubscribed and reported me as spam, all I can say is AMF.

Also, in last week’s Arrow, there was a line that ended without a word as shown below.

Here what it should have read.

I know I wrote the word “guano,” and I know MD would have picked it up if it weren’t there when she vetted it. Somehow the platform axed the word. Sorry about that.

Metabolic Flexibility

The standard definition of metabolic flexibility is the ability to adapt fuel oxidation to fuel availability. In other words, it is the ability to burn what you eat.

In my view, the standard definition is not quite correct. I guess it is correct in terms of the ability to adapt fuel oxidation (burning) to availability, but it doesn’t provide or explain a mechanism. I think a better mechanistic explanation would be exquisite insulin sensitivity. The more insulin sensitive one is, the better metabolic flexibility one has.

Let me give you an example.

For the most part, kids have exquisite insulin sensitivity. Much better than adults, for sure. Now let’s say you’re on a car trip with a couple of kids under, say, seven years old. You make a pit stop, everyone hits the restrooms, then you grab something to drink and hit the road.

In no time, one, or all, of the kids are whining to stop. They have to pee. They had small drinks while you had a big one—maybe even a big coffee, which is a diuretic—and you don’t have to pee. What’s the deal?

The kids have terrific insulin sensitivity. You don’t.

When the kids throw back their sugary drinks, be they soft drinks or fruit juices, their insulin levels shoot up quickly, and since they are extremely sensitive to the effects of insulin, the sugar they consumed gets driven quickly into their cells. Their insulin levels then drop quickly. They are left with an amount of excess fluid that hits their kidneys. Their Insulin levels are low, so there is no signal to the kidneys to retain sodium and fluid. Their bladders fill, and they commence to whine.

In your case, you don’t have near the insulin sensitivity that they do. If you, too, had a sugary drink, your blood sugar went up just like theirs did, but yours didn’t come back down nearly as quickly. And while your blood sugar is elevated, so is your insulin. Your insulin then, among other actions, signals your kidneys to retain fluid. Which you do.

When your insulin finally drives all the excess sugar into your cells, it finally falls slowly back to normal. And then you have to pee. But this all happens much, much more slowly to you than it does to them.

When people eat a lot of carbs, especially refined carbs, over a lifetime, they tend to become insulin resistant to some degree. And their metabolic flexibility declines. I’m pretty sure this happens to everyone to some extent, but to a much greater extent in some than others.

If your insulin is chronically high because you snack on carbs all day—probably a significant portion of the American population—you will probably carry some excess weight, as do about 75 percent of Americans.

Let’s get into the weeds a bit as to how all this works.

In those so genetically wired, increased carb consumption, especially refined carbs, will end up beginning to develop insulin resistance. It goes in this order.

First comes resistance in skeletal muscle. It is the first major tissue that develops insulin resistance. About 70 percent of the excess glucose ultimately goes into the skeletal muscle. As the glucose accumulates in the muscle, the majority is converted to glycogen (the storage form of glucose) and the remainder is burned as fuel.

Fatty acids also enter the muscle tissue and as they accumulate, it begins causing the muscle to become insulin resistant.

As the muscle becomes more and more insulin resistant it begins to shunt glucose to the liver, which itself will ultimately develop insulin resistance. An insulin-resistant liver increases i lipogenesis, which means the liver begins converting the excess glucose it is taking in into fat (triglycerides). Triglycerides then skyrocket. Which is why people with insulin resistance almost always have elevated triglycerides.

During this process, the adipose tissue is sucking up both dietary fat and the fat being produced in the liver—all under the stimulation of insulin. The insulin resistance created in the muscle drives fat into the fat cells.

The consequence is increased fat cell size and obesity. And, in many people, type 2 diabetes.

The above is obviously a simplistic discussion of what really happens. I wrote it that way to provide kind of a broad strokes overview of what happens without getting into all the biochemistry and physiology.

I looked high and low, but couldn’t find a graphic anywhere that described it all in basic terms. Then I remembered a program I had heard about just a few days ago. It’s called Napkin, and if you feed it words, it generates multiple images for you. I signed up for it (it’s free, but probably not for long), and entered the text I wrote above. It generated a bunch of images. The one I liked best was this one.

As I was scrolling through the 15-20 images Napkin created for me, I also came upon this one.

I like this one a lot because it shows the vicious cyclic nature of the entire process. If you follow the circle around, you come to the excess fat accumulation, which drives increased carb consumption.

This is basically the definition of the carbohydrate-insulin model. As your insulin goes up, it drives fat into the fat cells and traps it there. While insulin is elevated, it’s difficult to get fat out of the fat cells even when your body needs the fuel. This low fuel in the blood hits the hypothalamus and stimulates hunger. You eat to replenish the fuel, and the cycle cranks on.

If you cut the carbs, it runs in reverse. Insulin goes down, and your insulin resistance diminishes. Ultimately, if you follow through and continue your low-carb diet, you can regain your metabolic flexibility. You probably won’t get it to the level it was when you were six years old, but you’ll make it a lot better.

What does that mean?

It means you’ll be able to eat some of the carby stuff you really like without facing adverse consequences. But you can’t do it all the time. If you do try to do it all the time, you’ll be right back to where you started before you know it.

I wrote this whole bit above as kind of a prologue to answer the questions I’m getting about the Lumen, which measures your respiratory quotient (RQ). The RQ basically tells you what you’re burning at the time you take the test. The test takes maybe 20 seconds, so you can do it whenever you want.

I’ve had all kinds of questions from people asking why they’re burning glucose when they’re basically eating a low-carb diet. Based on my own experiences, I found the measurements all over the place at first. But as I worked on my dietary experiment over the holidays and then even fasted for three days, I’ve found the measurements to show I’m burning more and more fat.

I think the Lumen people are incorrect in how they encourage people to eat more carbs to ensure carb burning is efficient. Or that it doesn’t get blunted, which they seem to think happens.

In my view, carbs are toxic. Your body wants to get rid of them, so they always get burned first. And when I say “toxic,” I’m not engaging in hyperbole. They really are toxic.

There is a whole literature on glucose toxicity. I just ran a PubMed search and found there had been over 25,000 papers published on the subject. You read all over the place that carbs are great because they give you quick energy. That’s because the body wants to get rid of them as quickly as possible, not because they’re a super food.

It takes a while to become really low-carb or keto adapted. It takes no time whatsoever to become carb adapted. If you’ve been on a high-carb diet for years, then switch to a low-carb diet, you don’t feel all the great. It takes a while to make the enzymes to rev up all the fat-burning pathways. You’ll burn whatever carbs you eat on your new low-carb diet first.

If, on the other hand, you’ve been on a low-carb diet for a year, say, and you throw back a brownie, you’ll still burn those carbs first. The body wants to get rid of them.

So, if you’ve got a Lumen, when you first get it, you’ll find your readings are all over the place. If you bear down on a low-carb or ketogenic diet, you’ll find yourself burning more and more fat more consistently.

One of my long-time readers, who is an engineer, sent me a graph she put together. She had written me before saying she thought the Lumen was inaccurate, because the readings didn’t seem to correlate with what she had been eating. But once she actually plotted it on a graph, she discovered that when carbs were high, she burned carbs, and when carbs were low, she burned more fat.

There are a couple of other things to be aware of if you’re using a Lumen. As I wrote above, it measures the RQ, but it doesn’t read it out like an RQ. And RQ goes from 1 if your burning pure carbs to ~0.7 if you’re burning pure fat. The Lumen is calibrated to tell you the percentages of fat and carb you’re burning at the moment you take the test.

But there are other fuels you can burn that have different RQs. And burning those can affect your Lumen readings.

For example, acetoacetate, which is a ketone, has an RQ of 1, just like a pure carb.

Beta-hydroxybutyrate, the main ketone you produce once you’ve become ketone adapted has an RQ of 0.89. Our good friend alcohol, which the body does indeed burn as a fuel, has an RQ of 0.67.

As you can see, if you throw all these into the mix, you can have readings all over the place. And if you are keto adapted and producing a lot of beta-hydroxybutyrate, your Lumen reading will probably show a little more carb burning than is really being burned.

Knowing the above numbers should help you tweak your numbers in a more accurate direction.

If you use a Keto-Mojo, it won’t tell you how much carb you’re burning, but it will give you a glucose reading and a ketone reading (beta-hydroxybutyrate). There is more fiddling required with a Keto-Mojo, plus a finger stick and all that. But you do get accurate ketone and blood sugar readings. So, it depends upon what you’re looking for whether you want one of these or the other. Or both. Or none.

This whole section on metabolic flexibility is just a prelude to a paper I want to tell you about that is pretty eye opening. At least if your eyes haven’t been opened to this kind of thing yet.

A few years ago, a group wanted to see how much improvement subjects would have following a “healthy” diet versus the Standard American Diet. So they did a randomized, controlled trial.

Before we get into it, I’ve got to bitch about one of my linguistic pet peeves. I am losing the battle on this one (actually the battle has been lost for years), but I keep trying.

The word healthy describes a state of being. As in, I am healthy. My dog is healthy. The forest is healthy. A diet can’t be healthy. All the components are dead. Dead plants and/or dead animals. Definitely not healthy. Healthful is an adjective modifying a noun.

So, if you are presented with a fresh medium rare ribeye steak and some fresh green beans, that is a healthful diet. Not a healthy diet. Healthy describes a state of being. It isn’t an adjective. The ribeye is from a dead cow, so it can’t be healthy.

But healthy has been word-napped from its rightful meaning and put into service as an adjective. Everyone, and I mean everyone, even those who should know better, all use healthy now to mean healthful when they speak of diets.

Even the authors of the paper we’ll be discussing titled “Effects of a whole diet approach on metabolic flexibility, insulin sensitivity and postprandial glucose responses in overweight and obese adults – A randomized controlled trial.”

Here is the abstract:

The researchers put two groups of overweight/obese subjects on one of two diets for six weeks after a two-week run-in period. 19 of the subjects, ranging in age from 50 to 70, were randomized into the ‘healthy’ diet (HD) group while 21 in the same age range were randomized to follow a typical Western Diet (WD).

Unfortunately, although the lead author sent me the paper, she did not include the two supplements, one of which described the two diets. So all I have to go on is a general description of the two diets from the body of the paper.

So the idea of a healthy (healthful) diet in the minds of these researchers is the same as your standard dietitian or nutritionist: a lot of fruits and vegetables, whole grains, fish, and PUFA. And low in the much despised saturated fat. The WD was, well, the typical Western diet. Kind of the opposite in many ways.

The paper did provide a breakdown of the macronutrient composition.

As you look at this table, the healthy diet (HD) is on the right and the WD is on the left.

I’ve isolated the columns with the actual study meals in red rectangles. If you look at the items I’ve underlined, you should notice a couple of things. First, the WD contains about double the saturated fat as does the HD. And the HD contains over two times as much linoleic acid, an 18-carbon polyunsaturated fat. I didn’t mark it, but the HD contains over double the fiber compared to the WD. Strangely enough, the carb content of the HD is less than the WD, and is all from fruits and vegetables. But the percentages of both are pretty high. No low-carb effect on either one.

So, you’ve got overweight folks randomized to two diets, one of which almost every nutritionist and dietitian would say is a “healthy” diet, while the other is not.

What was the outcome?

According to the authors:

And, not only that, “but unexpected increases in the postprandial glucose profile were observed during a 5-h mixed meal challenge.”

Kind of blows the old healthy diet out of the water.

I would bet that had they compared the WD to a low-carb, higher-saturated-fat, lower PUFA diet, the WD would have been blown way out of the water. You’ve got to get the carbs down to improve insulin sensitivity, i.e., metabolic flexibility to any substantial degree. If you are overweight…I should add that. People who are normal weight or thin, can often—but not always—tolerate more carbohydrate without losing their metabolic flexibility.

I gave a talk once years ago on the effects of saturated vs poly-unsaturated fats in terms of fat storage. It’s kind of technical, but you can watch it here if interested. As I mentioned last week, I think saturated fat is a health food.

Butter, Butter, Butter

Last week I put up a photo of a Land O’Lakes butter box MD was getting ready to throw away. On it, the ingredients were listed as sweet cream and natural flavoring.

I wondered what kind of natural flavor would be added to butter. I figured it was some sort of butter flavor, but I was wrong. In tracking it down, I discovered that Land O’Lakes adds lactic acid to their butter. I wondered why.

So I dug a bit deeper and discovered I didn’t know all that much about butter. I thought butter was butter. But I was wrong.

There are basically two different types of butter: Sweet cream butter and cultured butter. Sweet cream butter comes in salted and unsalted varieties.

Sweet cream butter is made the way I thought all butters were made. It is churned from pasteurized fresh sweet cream.

Cultured butter is made differently. A bacterial culture is added to the sweet cream, and after 24-48 hours of fermentation has taken place, the cream is churned. Cultured butter, found more commonly in Europe, has a stronger flavor.

Sweet cream butter contains ~80 percent butter fat. Cultured butter has a higher percentage of butter fat. Sometimes up to 90 percent.

In terms of flavor, sweet cream butter has a mild, neutral flavor, sometimes with a touch of grassy notes. Cultured butter has a more complex, tangy, even tart taste due to its fermentation.

Cultured butter typically has a more yellow hue compared to sweet cream butter, primarily due to its longer churning process.

Sweet cream butter is ideal for low-temperature cooking, everyday baking (cookies, bread, muffins, etc. not that we do a lot of that), and general cooking as in sautéing and frying.

Cultured butter is better for pastries, pie crusts, croissants, etc. And it’s better for spreading on bread, scones, croissants, etc. And it works better for anything for which its distinct flavor adds to the mix.

But what about the lactic acid in Land O’Lakes?

Well, the cultures used to ferment the cream which will ultimately become cultured butter produce lactic acid. Many companies—Land O’Lakes, for one—that don’t want to go to the expense and trouble to make cultured butter simply add some lactic acid to their standard sweet cream butter.

According to everything I read, the addition of the lactic acid improves the taste a bit, but does not really come close to replicating the taste of real cultured butter.

I don’t believe it is harmful in the way a number of other additives are. It’s just the company’s inexpensive way to try to make its butter punch a little higher. If you want to read more about the difference, read here, here, here, and here.

An Effective, Inexpensive Treatment for Cancer?

A few weeks ago, I got fed the segment below on my X(Twitter) feed. It’s Mel Gibson on the Joe Rogan podcast.

I had, of course, heard of ivermectin, but I hadn’t heard of fenbendazole. Based on the name, I knew it had to be some kind of anti-parasitic drug, but that’s all I knew about it. I didn’t even know it wasn’t a drug made for humans. It’s strictly for animals.

I typically blow these kinds of things off, because they always seem to come to naught. Even the new anti-cancer drugs I read about almost every day in the many medical newsletters I follow end up not working. I read about them and what a huge impact they’re going to make on the so-called war on cancer. Then they disappear, never to be heard of again.

Fenbendazole is dirt cheap. The oncology departments of large hospitals and hospital chains provide a huge percentage of total revenue, mainly from chemotherapy. If somehow an off-patent drug such as fenbendazole could actually treat cancer, or even be used as part of a multi-drug regimen to treat cancer, it would cut billions of dollars from overall health care costs.

For this reason alone, I was a bit intrigued by the whole thing, so I decided to take a look. I wondered if there were any actual studies on fenbendazole. If there were studies, what did they show? Does the stuff work? If so, how does it work? How can an anti-parasitic drug work to kill cancer? What is the mechanism, if there really is a mechanism?

Fascinating stuff.

Let’s dig in.

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