The Arrow #169

Hello friends.

Greetings from Montecito.

I hate to start yet another issue of The Arrow by whining about issues with the platform, but I keep getting complaints about certain aspects. And I know if one or two people complain, that means a bunch of other people have the same issues, but don’t complain.

So…

First, I have had a number of folks telling me they can’t see the graphics. This is almost always a function of the browser they are using. Browsers must be continuously updated to function properly. Before it goes out, I check The Arrow on Safari, Chrome, and Brave. And it works on all of them. All the graphics come through perfectly. MD is the world’s worst at keeping her computer and browser updated, and she occasionally runs into a graphic she can’t see, but even she sees them all on The Arrow, and she doesn’t update till she can’t see something. So, some folks must have not updated either their operating systems or browsers in a long time. So if you don’t see the images, see if you need to update your browser. Or try a different browser.

I was reading comments just this morning on one of the many newsletters I read, and came across one from Substack. It’s from a few months ago. The author I was reading linked to a previous post. At the bottom were comments, including this one:

I had to laugh. I went back and checked. All the links worked fine for me, and apparently for the others who commented on the post. The guy needs to update his browser.

The second issue is that some people each and every week don’t get their issue of The Arrow. I don’t know why this is, but it happens every week. When I look at my stats, I see that I have 11,362 subscribers, yet only 11,349 emails go out. I don’t know why this is, but it has been the same on all three platforms I’ve used. Fewer emails go out than I have in my list of subscribers.

When people email me that they didn’t get their Thursday missive, I always tell them to check their spam folders. Almost always that does the trick. But sometimes it just doesn’t come. I subscribe myself, and once in the 168 weeks I’ve sent out The Arrow, I didn’t get it. And it wasn’t in my spam filter, which, admittedly, I don’t check very often.

If you don’t get an issue, first check your spam filter, then second, you can go to arrow.proteinpower.com and it should be there if it has gone out. As you all know, like tonight, sometimes I’m a little late with it on Thursday night.

Finally, the most heat and pushback I got last week was from people agitated that I referred to MD as the “elderly, grey-headed woman at the far end next to Jay…” A dozen people, at least, took me to task for writing that, and all I can say is that it wasn’t my fault.

After I finish The Arrow, MD goes over it looking for typos, incomplete sentences, sentences that don’t make sense, etc. Once she gives it a thumbs up, I hit send. To keep her on her toes, I always plant something in there that she will find offensive. “You can’t say that,” she’ll scream, while she’s vetting the thing. And she’ll change it. This time, I left it with her, and ran a few errands. When I got back, she said it all looked fine. She had made a few corrections and added a bit here and there.

So, I sent it. I didn’t go back and reread it. I just sent it. Like I always do. This time I was more careful to make sure it went to ALL subscribers, not just the free ones. Other than that, all was normal.

Then I start getting these blistering emails.

I say to MD, “did you even notice the part where I referred to you as the elderly, grey-headed lady? She says, “Yep, I saw it.” I said, “You were supposed to take that out.”

She says, “I thought it was funny, so I left it in.”

So, ladies and gentlemen, boys and girls, it wasn’t my fault. It was simply a test. And one she failed miserably. Or perhaps passed. I’m not sure which.

And, BTW, she may be elderly—depending upon your definition—but she isn’t a typical little old lady. Here is a photo of her she sent to me a couple of days ago, workout hair and all. She gave me permission to put this up. She had just finished off a cardio workout that included intervals of sprinting plus 75 burpees (if you don’t know what a burpee is, look it up; they’re brutal). I hate burpees. I would be lucky if I could do 7.5 of them. (I could probably do 7.5 of them, I just wouldn’t want to.)

She is strong. Like bull.

Speaking of working out…

N=1 With a Terrible Outcome

Unfortunately, I was the 1 on this one.

When MD and I went to the Broken Science Initiative meeting a couple of weekends ago, I decided to do an experiment with me as the subject. It did not turn out well.

I try to lift weights three times per week, and I do so to failure. I have a starting weight, which I lift until I can’t lift it any longer. Once I’ve hit a certain number of reps, I switch to a higher weight and start the progression again. I do as many reps as I can, then work up over time to a large number, then I increase the weight and start again.

I do only three lifts. I always do squats and deadlifts, and then alternate bench press and overhead press. So one day it is squats, bench presses, deadlifts, and the next session in a couple of days is squats, overhead presses, deadlifts. All to failure.

Why to failure?

Because that works all the muscle fibers to the max. There are basically two types of muscle fibers: Type I and Type II. Type I are the so-called slow twitch fibers that are recruited for endurance types of exercise. Type II fibers, the fast twitch fibers, are those that are used for quick athletic maneuvers. Most natural athletes are born with a lot of Type IIB fibers, a subset of Type II fibers that are especially active in sports requiring quick, explosive movements.

All these fibers fail at different rates. The Type I fibers fail first, and the Type IIB fibers fail last.

You might be wondering why anyone would want any muscle fibers to fail irrespective of what kind they are.

When muscle fibers fail, they end up damaged, or at least micro-damaged. During the rest period after failure, they regrow and in doing so become bigger and stronger. Which is the whole point of taking them to failure.

The stress to failure breaks them down. The rest period after allows them to rebuild to a bigger, stronger state. All the real growth takes place during the rest period. The brutal part of the workout—the actual lifting to failure—simply sets the stage. The rest period is when the body rebuilds.

In order to break down Type IIB fibers, you have to take them to failure. But before they fail, you have to take the Type I and Type IIA fibers to failure. Since the Type IIBs fail last, you have to lift till you can’t do another rep. And then you try to do another one, and you simply can’t. It is not pleasant. But it works.

If you do light lifting with piddly-assed weights, you may strengthen your Type I fibers a tiny bit, but that’s about it. You’ve got to go to complete failure to get to the Type IIBs. Which are the ones I want to build. Why? So I can hit a golf ball farther, of course.

And maybe fend off an Antifa attacker if it comes to that.

As I’ve written many times in these pages, to build muscle you need protein and you need resistance exercise. I eat plenty of protein, and I do resistance exercise three times per week.

Since MD and I were going to the meeting in Scottsdale, AZ on Friday a couple of weeks ago and not coming back till Monday, I decided to forgo my weight lifting for a couple of sessions. Then, after thinking about it, I decided to forgo it for two weeks just to see what would happen.

I kept my protein intake high and continued with the rest of my daily routine. I walked 6-7 miles a couple of times a week and spent at least a half hour each day at the driving range.

And this Monday, I decided to see how I would do. How much weight and how many reps could I go before failing?

It was a disaster. I had to go down on the weight AND down on the reps. I learned that just a hefty protein intake isn’t enough to keep muscles strong. I didn’t do any water-weighing or anything, so I don’t know what my actual lean body mass was before and after I decided to forgo my regimen for a week.

But I can sure tell you that my strength had diminished. So, I suspect I lost a bit of muscle mass despite eating plenty of animal protein.

Were I 20 years old, I doubt this would have happened.

The take away here is that you can’t eat your way to a large muscle mass. Certainly not with any age on you. You need the protein (leucine, specifically) to stimulate mTOR, but you’ve also got to stress the muscles. As I’ve learned, it takes both.

Unfortunately, it’s a lot easier to simply eat a lot of protein than it is to take your muscles to failure, but, as I’ve discovered, that alone doesn’t work. And it doesn’t take long to see a difference.

I toyed with the idea of eating very little protein while working out at my normal pace, just to see what would happen. But I abandoned that idea after about five seconds. I don’t want to take the chance that I’ll lose even more muscle. Of the two muscle building activities, eating is vastly more fun than taking your muscles to failure. So why abandon the fun part and keep the hellish part?

Even in the name of science. That’s what we have subjects for.

So, a word to the wise. Don’t be like Mike. Keep up your resistance training.

Sarcopenia and Increased All-Cause Mortality

Just a couple of days ago a study appeared in the Journal of the American Medical Association (JAMA) titled Sarcopenia and Sarcopenic Obesity and Mortality Among Older People showing an association between sarcopenia and early death.

Sarcopenia is usually defined as a loss of muscle mass with aging, but can be due to a loss from other causes. The study focused on the loss of muscle mass with age. Here is a graphic that clearly demonstrates sarcopenia.

Sometimes sarcopenia isn’t this obvious, especially when the victim of it is obese. The extra layers of fat hide it, but it is there nevertheless. And sometimes referred to as sarcobesity.

The JAMA study goes to great length to show there is an association between sarcopenia and an increase in all-cause mortality. The word “association” is the tip-off that this is an observational study. And we know observational studies can’t really prove causation. But sometimes that’s the only evidence we can obtain, so we just have to go with it.

It would be impossible to do a randomized, controlled trial on sarcopenia and early death. You would have to randomize young people without sarcopenia into two groups. Then underfeed one group protein and prevent them from exercising while encouraging the other group to eat protein and do resistance training. And you would have the two groups keep at it for years and years until the low-protein, no-exercise group became sarcopenic. Then you would have to wait around to see if those who developed sarcopenia died earlier than those who didn’t.

Such a study would be impractical, not to mention highly unethical. Plus, who in their right mind would sign up for it?

So we’re left with what we can glean from the observational information at hand.

The authors describe the prevalence of sarcopenia here (edited for clarity).

And described the study goals (again, edited for clarity).

The subjects in this study were almost 6,000 subjects who were part of a larger investigation called the Rotterdam Study. Mainly of northern European heritage, the subjects were an average age of 69.5 years and average BMI of 27.5.

To determine sarcopenia, the researchers measured the handgrip strength (measured on the non-dominant hand) of the subjects as well as their appendicular skeletal muscle mass. To evaluate the latter, DXA scans measured the lean mass of a variety of areas in the subjects’ bodies. The sum of the lean mass of the upper and lower limbs is referred to as appendicular lean mass (ALM). Appendicular skeletal muscle mass is the ALM divided by the height of the subjects’ squared.

The handgrip strength is obviously a measure of muscle function while the appendicular skeletal muscle mass is a measure of muscle volume.

After taking these measurements and running them through various statistical manipulations (which always raises my index of suspicion), the researchers determined that 2.2 percent of the subjects had sarcopenia (I would have bet good money that the figure would have been higher) and that 5 percent had sarcopenic obesity.

After ten years, a number of these subjects had died. And, again, after a statistical analysis, the authors of the study determined that those with sarcopenia had a significantly higher risk of dying earlier with a hazard ratio of ~2. Which is pretty high.

So, again, don’t be like Mike and blow off your resistance exercise and lose your muscle mass. It’s difficult to get back. And there are consequences.

Campbell’s Law and the Handgrip Test

Donald T. Campbell was a psychologist and social scientist who taught at a number of prestigious universities and died in 1996.

The law he came up with, now named after him, states

A good example of this is the SAT, the achievement test used to determine suitability for admittance to select colleges and universities.

Those in the know determined that kids with high scores on the SAT did better in college than those with lower scores, so the test became a selector as to who got in and who didn’t.

In essence, the SAT was a crude measure of overall intelligence, at least the kind of intelligence that allowed someone to do well in a college setting. Once scoring well on the SAT became an important qualifier as to who gets into prestigious centers of higher learning, it began to be gamed.

All kinds of courses blossomed guaranteeing higher SAT scores if the parents would fork over loads of cash for their kids to take them. The companies running these courses got hold of past SAT exams and deconstructed them to learn how they were designed and created their courses around beating the test. Once that happened, it became not a crude measure of raw intelligence, but more of a measure of who could game it.

I inadvertently gamed it myself. Not the SAT. The SAT wasn’t around back in the olden days. But its precursors were the various so-called achievement tests given annually at schools all over the United States.

When I was in second grade, I developed a love for reading that is with me to this day. Because I’ve done it so much, reading is effortless for me. It’s total enjoyment. It is a part of me. If I go somewhere and have to wait, I suffer minor anxiety if I don’t have something to read. When I go to MD’s concerts, I always have to go early to take her, so I sit in my seat in the empty chorus hall and read.

When I was a kid I read all the time. Because of that, you may find it strange that I was a mediocre student at best. Which was because I read what I wanted to read, not what my teachers wanted me to read.

So, I would drift along in the middle of the class (or sometimes sub-middle) grade-wise, and then would come the annual achievement test. I would always blow the top out of each one, which would end up generating the annual parent-teacher conference.

Which would go like this.

Teacher: Michael is not working up to his potential. His achievement test scores are very, very high, yet his grades are terrible. Or mediocre. Or C-level. He should be getting straight As.

My Parents: Would nod and say, We know, he’s a smart kid.

Teacher: When we see kids like Michael, we usually find out they’re watching way too much television. Maybe you should restrict Michael’s television watching.

My Parents: Michael doesn’t watch TV. (And Michael didn’t. I had a show or two each week I liked to watch, but that was about it.)

Teacher: What does he do with his time, then?

My Parents: He reads.

Teacher: Stunned silence. Then, Well, what does he read?

My Parents: Anything he can get his hands on.

I just counted up, and I went to 12 different schools from 1st through 6th grade, and 5 different schools from 7th through 12th grade. Two years was the most I ever spent in one school and those were 7th and 8th grade and 11th and 12th grade. My family moved a lot, so I was the new kid in school many, many times.

Because of all this moving around, the teachers were almost always new to me when these achievement test scores came in, so it was always their first rodeo. With me at any rate.

So, reading a lot is a hack for the SAT and other such tests. I have a friend who was on the admissions committee at Yale. He told me that Yale relied on the verbal part of the SAT more than the math part even for students up for admission as math majors. They had discovered over time and many, many students that high verbal scores correlated with success better than high math scores even for those going into math.

So if you want to help your kid or grandkid get into a good college or university, teach them to love to read.

My issue was that I had the scores, I just didn’t have the grades. Which more or less identified me as being lazy. Which was probably on point to a certain extent.

The one time I ran afoul of test scores was when I decided I wanted to go to medical school and had to take the MCAT (the SAT on steroids for med school). By this time, I had been through engineering school, so I had the math part down. I figured with all my reading, I would blow through the verbal part without a hitch just like I always had. Imagine my surprise when I was middle of the road in the verbal on my practice test. I couldn’t believe it, so I took another. Same score.

Whisky. Tango. Foxtrot!

I was both devastated and pissed. If anyone who reads as much as I can get only a middling score on this test, then the test is screwed up. Or so I thought. At the time I was taking organic chemistry and a couple of other classes I needed as prerequisites for med school as a part time student at the University of California at San Diego. I saw a notice that there was going to be an MCAT review course given on such or such night, so I signed up. At the course, I got another couple of practice tests to work through, and the instructor told us that it was essential we improve our vocabularies. Which I thought was so much BS. I figured I had a better vocabulary than he did, but I didn’t say so.

I went out and bought a box of 1,000 vocabulary flash cards and went through them. I knew around 800 of the words, but did not know the other 200. Again, I figured this is BS, but I’ll learn them just to be able to do well on this test.

Every day I grabbed 10-15 words from the 200 I didn’t know and carried them with me and reviewed them throughout the day, quizzing myself at any opportunity. And I was really angry, because I thought no one uses these words. Anyone who has read as much as I have would have known these had they been in common use. This is just a one and done exercise, so I can get into medical school. A real pisser.

So, I learned the 200 words I didn’t know and figured I would never see again. And guess what? I saw them all the time. Once I knew them, I encountered them everywhere in my reading. It finally dawned on me that I had seen them—doubtless many times before—but just sort of figured them out from the context. But never remembered them.

Now, every time I come across a word I don’t know in my reading, I always underline it and look it up. There are fewer and fewer, but I still find them. And I always look them up. If I’m reading a physical book (versus a Kindle), I even write them in the back of the book and list the page they are underlined on.

Oh, and I did get into medical school.

Sorry for the digression. What made me think of Campbell’s law was the reference to the handgrip strength in the article above. I came across a piece in Medium by a young man who had read a similar study showing handgrip was correlated with longevity. So he set out to improve his handgrip strength.

In general, people who have good handgrip strength have pretty good overall muscle mass. Handgrip strength is easily measured and is used as a proxy for overall strength and muscle mass. And as the above study showed, along with a number of others, more muscle mass, i.e., less sarcopenia, leads to a longer life. But will simply making your grip stronger by squeezing a grip builder save you from sarcopenia, and thus make you live longer?

I would say it is highly doubtful.

Same with many other tests in medicine.

Take triglycerides, for example.

If you’ve got high fasting triglyceride levels, it’s a sign you’ve got a metabolic problem. No two ways about it.

How do most doctors want to treat high triglycerides? By giving a drug to bring them down. That’s Campbell’s law in action. Just game the system—don’t try to fix the metabolism.

Same with LDL-cholesterol levels. As David Diamond demonstrated in a wonderful talk that hasn’t yet been released, a high LDL along with low HDL and high triglycerides is a sign of a screwed up metabolism. So what do docs do? We gotta get that LDL down. Take this statin or this PCSK9 inhibitor.

Campbell’s law writ large.

How about type 2 diabetes? Same thing. Gotta get that blood sugar down. Take this pill.

All the pill does is artificially lower the blood sugar. It doesn’t treat the real metabolic problem, which can usually be treated with the proper diet.

When you are addressing a health issue, always think Campbell’s law (which I doubt 1 out of 5,000 doctors is even aware of) and make sure you’re not just learning a lot of vocabulary words to beat the SAT. Try to get to the underlying problem and solve it.

Magnesium for All

If I were asked what one supplement I would recommend for everyone, it would be magnesium.

Why?

Because it’s involved in many, many processes in the body (over 300 of them), and because most people don’t get enough of it.

I was reminded of it by a new study that just came out. The study is out of China, so normally I wouldn’t give it the time of day. But it merely confirmed what I already knew, so I’ll present it.

Now, lest you think I’m being too hard on our neighbors in Asia, take a look at another study published in the British Medical Journal. Granted, the study was also done in China, but the results speak for themselves. The study showed that over half the enrollees in the study had committed some sort of research fraud at one time or another. I think a little over half is way short of the mark. I think it’s higher than that, given the reward for getting published in a US journal.

But at even half, that means you can’t depend on any study. You don’t know which half the study came from. The half that committed fraud or research misconduct, as they call it in the paper, or the half that did it correctly.

Might as well flip a coin.

In the case of the magnesium study titled Magnesium Depletion Score and Metabolic Syndrome in US Adults: Analysis of NHANES 2003 to 2018 it pretty much conforms to what I’ve read in countless other studies. If this were something new, I wouldn’t trust it as far as I could throw it.

This paper discusses magnesium levels as related to the metabolic syndrome. The reason I even looked at the study is because years ago there was a school of thought that the entire metabolic syndrome might be a reflection of a magnesium deficiency.

And it may well play a large role.

Here is what the authors had to say about the importance of magnesium. And it is all true.

I had an interesting experience with magnesium once when I was working in one of our primary care clinics. As per usual, when I came out of an exam room, I always asked my nurse who was next on my hit parade. In this case, she told me the guy who was next was in for a physical exam for a new job and that his blood pressure was sky high. I don’t remember the exact numbers, but it was something in the 180/120 level, which is pretty high.

I walked into the room, introduced myself, and asked the guy, who was in his late 30s/early 40s, what he needed.

He told me he had just had a job offer to be a truck driver. And that he was going to be paid almost $12,000 per year. He said he had never made anywhere close to that amount of money in his life, and that he just had to pass this physical to get this job.

I figured he had a bad case of white coat hypertension. I examined him and everything looked fine. I used an ophthalmoscope to look into the backs of his eyes, and his retinas looked fine (often one of the signs of chronic high blood pressure are retinal changes). I asked him if he had seen other doctors. He said yes. I asked if anyone had ever told him he had high blood pressure. He said no. He said he had even checked it himself at a pharmacy a year or so before, and it was normal.

I asked him a bunch of other questions trying to ferret out if he really had hypertension, or if it was just being in the clinic with so much on the line. I really felt sorry for the guy.

I took his BP again myself, and it was still up. But I was pretty certain it was situational as his pulse was racing.

So, I told him not to worry about it. That we would get it fixed. I didn’t want him to lose out on this job. I pulled out the extension on the exam table, so he could lay down flat. I told him I would send the nurse in to give him something to relax him and that he should just lie there and think pleasant thoughts.

I told the nurse to give him two magnesium capsules, then turn out the light, and let him relax for a while.

I sent her back in an hour or so later, and the guy’s BP was still up a bit, but not out of the normal range. She recorded it, and I passed him on his physical.

Magnesium is a wonderful supplement.

In this Chinese study, the authors looked at the NHANES data from 2013 through 2018 to determine how many of the 15,565 subjects were diagnosed with the metabolic syndrome. For your reference, subjects were diagnosed with the metabolic syndrome…

Which is the standard diagnostic criteria for metabolic syndrome.

They then cross referenced those subjects diagnosed with metabolic syndrome with those who had undergone a magnesium depletion score (MDS), which is defined as

Which is basically a determination of how much magnesium is lost through the kidneys in the urine. And is a proxy for magnesium levels in the body.

I’m not all that familiar with the MDS, but it turned out that MDS was associated with increased odds of metabolic syndrome. Which I do believe based on my own clinical experience.

According to the authors “each unit increase in MDS was associated with approximately a 30% higher risk for MetS, even after adjusting for confounding factors…” Which I’m also willing to believe, especially since it was in a dose-response relationship, which does make the data a little stronger.

I would encourage everyone to take magnesium, because the likelihood of a deficiency is probable. It’s inexpensive, and even if you aren’t deficient, it won’t hurt you. I take one capsule every night at bedtime, because it helps me sleep.

The problem with magnesium is in figuring out how much you’re getting. The labeling is totally screwed up. Some magnesium comes as the elemental variety and some comes as a chelate. And the doses are all over the place.

When we were in practice, we used Thorne magnesium, which, at that time, was sold only to healthcare practitioners. We tried multiple brands, and the Thorne brand was the one that seemed to work the best and had the fewest complaints from patients about side effects. Diarrhea is probably the most common side effect—to wit, the milk of magnesia effect—so beware. It doesn’t happen often with the Thorne, unless you overdo it. The bottle says 1-3 per day. Go for the 1. Preferably at bedtime.

The link above is to my Amazon affiliate account, which means I get a small commission (with great emphasis on the word small) from Amazon with each unit sold. In case you skeptical readers out there might be thinking this whole section is just one long written infomercial for Thorne magnesium, think again.

My commission on this product will be about 18 cents. The most I’ve ever sold of any product on Amazon through The Arrow is about 20 units. And that’s the most. If 50 people buy the Thorne magnesium—which would be a first, by a long shot—I would trouser a whopping six dollars. You couldn’t pay me to write this section for 6 bucks, so I promise I’m not out to fleece you.

You can get magnesium everywhere, maybe even Thorne magnesium. It might be sold at Whole Foods. I don’t know. If you do purchase it somewhere else, don’t lose any sleep over denying me my much-needed 18 cents.

Okay, on to one last study. Maybe the one you’ve all been waiting for.

Ketogenic Diet Works As Well As Ozempic to Maintain Lost Weight

This study comes from Virta Health, the telemedicine company that has successfully treated countless patients with type 2 diabetes and/or obesity.

Like the magnesium study, this one is not a randomized, controlled trial, but it never could be. When you’re comparing a diet to getting shots, how are you going to randomize it? Unless you give placebo shots and provide liquid meals, you could never do it.

The study, which carries the unwieldy title Impact of Glucagon-Like Peptide 1 Agonist Deprescription in Type 2 Diabetes in a Real-World Setting: A Propensity Score Matched Cohort Study was done by the folks at Virta Health, many of whom I know. And they are all world-class researchers for whom I can vouch unabashedly.

As I’ve commented in these pages over and over and over, all of these weight loss drugs are a Faustian bargain. Sure, you’ll lose weight like crazy when you are on the shots, but what about when you go off. And your appetite returns. According to the studies, so does the lost weight.

And even worse, since you aren’t hungry while on the shots, you do lose weight, but it’s the wrong kind of weight. Almost half of it is lean body mass—muscle mass that you’ll play hell ever getting back. So when you regain, you end up fatter percent-composition-wise than you were to start. And have an even more difficult time losing next time around.

With that in mind, here is how the authors of this study set it up. They matched type 2 diabetic patients in their own clinic who had been de-prescribed from GLP-1 agonist shots because they had lost weight and reduced their HgbA1c levels with similar patients who remained on the GLP-1 agonist shots.

The patients in the clinic reverted to a carbohydrate-restricted nutritional regimen (CRNR) described as follows:

So they compared their clinic patients who stopped the GLP-1 shots to a similar cohort of patients who continued the GLP-1 shots.

The data tells the tale. Over the 12 months the test was run, you can see that there is no difference in outcome. The CRNR worked just as well as the shots to maintain reduced HgbA1c and weight.

Here is the graphic for the HgbAic

And here is the graphic for weight maintenance

For those who can’t see this illustration, here is a link to the graphic in the study.

In case you’ve forgotten, here is what the graph looks like for those who go off of a GLP-1 agonist.

As you can see to the right of the vertical dotted line, the weight loss goes screaming upward when folks go off the shots and back on to their regular diet. (The upper grey line is the weight curve for the placebo group who never got the shots.)

You can easily see that the carbohydrate-restricted nutritional regimen did as well as the shots in maintaining the lost weight. If I could hazard a guess, I suspect it would have done as well in the weight loss phase, too. But they didn’t test that.

I also suspect that were body compositions looked at, those in the CRNR would find themselves with more lean body mass than those who remained on the shots.

Again, for those who can’t see the graphic above, here is a link to the study where you can find it.

This study is pretty impressive, if you ask me.

Moving on to more Virta Health news…

Sarah Hallberg’s Book Is Available

For those of you who don’t know, Sarah Hallberg was a tiny human dynamo, who was one of the driving forces behind Virta Health. She was the first medical director and helped set many of the protocols. I knew her, and I, like everyone who knew her, was devastated when she was diagnosed with terminal lung cancer. She had never smoked.

In the last months of her life she completed a book on managing diabetes, which has just been released, posthumously. I grabbed a copy of her book a couple of days ago and started reading it. It is about how she managed people on low-carb diets, but so far, I haven’t made it past the words below:

As I sit and peck away at Protein Power 2.0, I can’t imagine the wrenching angst and sorrow I would feel if I had to type that last sentence.

I urge you to purchase her book to help her family. Sarah was way, way too young, and way, way too good a person to have this happen. RIP.

Odds and Ends

• Stop your car from spying on you. Modern cars are smartphones on wheels, but with less protection for your data.

• FDA study shows higher risk for seizure in toddlers after receiving Covid vaccine.

• For global elites, countries are merely exotic names for trade zones and labor camps, and citizenship has about as much ethical or emotional significance as a gym membership. Most Americans feel otherwise.

• Great photo of a bobcat nailing a Blue Heron in mid-flight. Must have been a huge surprise for the Heron. I know how high a bobcat can jump. A friend raised one from a kitten, and it could leap straight up and grab a paper from his hand held over his head. Pretty impressive to see in person.

• Hilarious. The roof on Google’s spectacular new building blocks wifi. Looks like the brainiacs there outsmarted themselves.

• Study suggests statins could help fight gum disease. The word “suggests” tells you it’s an observational study, which is meaningless. Next thing you know, we’ll be seeing studies showing statins help with gender transition.

• Great article including a video of beavers being parachuted into remote areas in Idaho in 1948. Love the so-called Mid-Atlantic accent of the narrator, which was common then and almost never heard now.

• What’s a Mid-Atlantic accent (sometimes called a transatlantic accent)? It’s a made up accent used by many actors and announcers up till the 1950s. And taught in some Northeastern centers of higher learning. Learn its fascinating history here. (Video)

• Five arrested in South Texas for allegedly trafficking military grade weapons to Mexican drug cartel.

• How China ended up financing the Houthis’ Red Sea attacks.

• Colorful paintings of daily life uncovered in 4,300-year-old Egyptian tomb.

• TikTok’s troubles just got worse: The FTC could sue them, too. Why not? The FTC is suing all the Big Tech companies. And pretty much losing across the board.

• Dust storms can spread bacteria and fungi around the world. And if they can spread bacteria and fungi, they sure as heck can spread viruses, too.

• Novo Nordisk sells its diabetes/weight loss drug Ozempic for ~$1,000 per month. A new study found it could be produced for less than $5/month. A nice gig if you can get it.

• I don’t particularly like the taste of hot-dog-flavored hot dogs. Why would I ever buy hot-dog-flavored water? Especially if I had to go into a 7-11 to get it.

• Construction site discovered in Pompeii. Reveals ancient building techniques.

• A $15 toll to drive into part of Manhattan has been approved. That’s a first for U.S. cities. I would pay more than $15 to avoid driving in Manhattan.

• Apparently reindeer undertake some kind of a circling maneuver called a reindeer cyclone when threatened. Who knew? I certainly didn’t.

A bunch of you signed up for Alex’s & Books Newsletter. It’s a great weekly newsletter if you want to get reviews of non-fiction books and reading tips. You can sign up here, and best of all, it’s free.

Here’s another one, if you’re into quick takes on health. It’s called Sunday Coffee and comes out, strangely enough, on Sundays. I don’t always agree with everything, but I always read it. Short, sweet, and free.

Okay, time for the video of the week!

Video of the Week

This one is short and sweet, but I can’t imagine the effort that went into it. It’s only three minutes long. At first, you’ll witness your own insignificance, then realize how you are a universe unto yourself. Crazy good.

Okay, that’s about it for this week. I meant to deal with another Dr. Mercola post, two of them in fact, but I had a computer disaster and lost them. I’ll get them back, and we can go over them next week.

It’s poll time. Let me know how I did this week.

Thanks for hanging in there throughout the whole changeover process. And, remember, it might look a little different over the next few weeks as I get more familiar with the platform and figure out how to tweak it.

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

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