The Arrow #177

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Hello everyone.

Greetings from Montecito.

A lot of traveling since the last missive. MD and I drove to Little Rock last Friday to celebrate the graduation of our grandson from high school. The Saturday before we’d had one grandson graduating from college, then not quite a week later another one getting out of high school.

Ben graduated from Catholic High School for Boys in Little Rock, a local college prep school famous for its difficult curriculum and its dress and hair standards. We are not Catholic, but all three of our sons graduated from Catholic High. And now one from the next generation.

It rained on us between Fayetteville and Little Rock, but despite looking overcast it did not rain on the ceremony. Here is the class with the threatening sky overhead.

And here is Ben looking full of himself. He’s the one on the end with the big smile looking directly at the camera.

Ben is in the midst of deciding whether to major in philosophy (he was the president of the philosophy club at Catholic High) or go the aviation route. He was all set to go the philosophy route, then his father arranged for him to take an introductory flight just to see what it was like. Ben took the plane off, flew it around, and landed it. Given how Ben handled the plane, the instructor who was the actual pilot in command, thought he (Ben) had been flying for a while, and was stunned to learn it was his first time. He’s a natural.

Since I love aviation so much, I encouraged all our sons to go into it, but none took me up on it. Until now. Ben’s father—our youngest—just got accepted into an incredibly competitive accelerated program for airline pilots. So, maybe all my haranguing over the years may pay off twice. A son and maybe even a grandson up in the air.

Okay, I’ve got another personal story to relate, so if you don’t want to read the personal stuff, skip on down.

Ricki Lake (Yes, that Ricki Lake), MD, and Me

A couple of days ago I read Nina and Gary’s most recent Unsettled Science Substack, which included a segment on Ricki Lake and her recent weight loss. It also included a link to the video below. Give it a quick watch. It’s short.

Nina and Gary discuss (behind a paywall) how Ricki lost her weight, which was not by using Ozempic. Her doctor told her that since she was peri-menopausal (she’s 57), she had no hope of losing weight without a little help from her GLP-1 agonist friends. She declined her doc’s offer to give her the Rx for Ozempic and instead did it on her own by a combination of a ketogenic diet and intermittent fasting. She looks a lot better than she did the last (only) time I ever saw her in the flesh.

Back in the late 1990s, much to our later chagrin, MD and I made an appearance on the Ricki Lake Show.

Here’s how it happened.

I was at some kind of clinic-related business meeting when I get a call from MD. She tells me the producer of the Ricki Lake Show just called and asked if we would be on the show the next day as nutritional and obesity medicine experts. She was calling to ask me if I had any scheduling conflicts, and if not, did I want to be on the show.

Other than the fact that it was a popular show on a major national network, neither MD nor I knew anything about it (or about Ricki Lake, for that matter), so I thought, Why not? Protein Power hadn’t been out long, so I figured we would get some good book promo from it. MD calls them back and says we’re a go.

I get home later that night and find out there will be tickets waiting for us at 6 AM the next day at the Little Rock airport. Our youngest kid comes home—the only one still at home at that time—and we tell him we’re going to be gone for a couple of days, so he’ll have to fend for himself. We tell him we’re headed to New York to be on the Ricki Lake Show.

He says, “You’re going to be on the Ricki Lake Show?!?”

I say, “Yep.”

He’s says, “Oh my God, I can’t believe it. You’re going to be on the Ricki Lake Show?!?!”

I’m starting to get a sinking feeling in the pit of my stomach.

I say, “Yes, it’s a national show. We should sell a lot of books.”

“Oh, my God. You’re going to be on the Ricki Lake Show. I can’t believe it. Have you ever seen the Ricki Lake Show?”

Now, I’m really stressing. “No, I haven’t ever seen it, but it’s a national show. As the old saying goes, there’s no such thing as bad publicity.”

“You’ve got to watch the show. It’s on tonight,” he says.

So, we do.

After watching it, I could have torn my tongue out for giving the okay to go.

The episode we watched that night was titled “You took my virginity and then you took off.” It featured women who had had intimate experiences with men who had seduced them and then disappeared.

As I recall, the first woman told her tale and talked about how much she loved this guy and how she would never have given herself to him had she not thought he was going to be around for the long haul.

Meanwhile, unbelievable as this sounds, the guy who was the source of her misery is sitting in an isolation booth—where he can’t hear or see what’s going on—while she’s blubbering out her tale of woe.

(All I could think of as I watched with mounting horror as all this developed was that the poor bastard in the iso booth (as they called it) got the same kind of call that MD got. They must have told him he was going to be in the iso booth on the Ricki Lake Show, and he agreed. I mean nothing good could possibly come of that, and this guy agreed. Yeesh.)

The guy wanders out, sees the woman he’s deflowered, and looks kind of sheepish. They have a confrontation mediated by Ricki herself. And I’m about to go mad thinking I’ve agreed to be on this very set the next afternoon.

A car picks us up at La Guardia the next day and drives us to the studio. When we get there, Ricki is filming another episode. (They film a bunch of them one after another). Someone tells us to go get changed in the restroom, which we do. I put on my suit, and MD gussies herself up for the nightmare that awaits us.

We then are taken to the makeup chair. As the makeup girl is applying my makeup, she says, “You must be one of the experts.”

I nod yes and ask her how she knows.

She says, “It’s pretty easy to tell the experts from the guests on this show.”

Which did nothing to minimize my angst about the whole affair.

We are ushered into the green room, where we can watch what’s going on in the studio, and we get our first idea of what we’re in for when they do the promo for our upcoming segment. It is titled “I’m 500 pounds and gaining. Help me, Ricki, you are my last hope.” Ugh.

Finally, the filming starts.

As the show proceeded one hugely overweight person after another came out telling his or her story, all of which were heartbreaking. In some cases there was input from a loved one or concerned friend either on tape, live in the studio, or in the iso-booth. Ricki worked them all into an emotional frenzy, then cut to a commercial, with whichever person she was interviewing in tears. All described the hopelessness they felt over their situations, and Ricki would go to break saying that help was coming and that she would solve their problems by the end of the show.

We watched aghast. We thought that perhaps Ricki was planning on offering us as the solution. We had cared for many thousands of overweight patients, and we knew that there were no simple solutions for people weighing in excess of 500 pounds. One of the subjects was only present on tape because the woman weighed almost 1500 pounds and couldn’t get out of bed to come to New York. It takes long-term medical management along with a lot of commitment and self-discipline on the part of the patient. And even with that, it’s enormously difficult..

After all these people had been trotted out and made to cry for the TV cameras, it was time for us. There was a commercial break and they brought us out and seated us along with all the morbidly obese people on the set.

Then Ricki identifies us as experts in the treatment of obesity and asks MD how these people got to weight 500-600 pounds. MD answered that it wasn’t simply because they ate too much and didn’t exercise enough. It was because they had serious medical issues, metabolic issues, that needed to be addressed by a competent physician who knew how to treat such cases.

Ricki then turns to me and asks what kind of serious medical problems these people might have. I run through the list and reiterate that these folks had serious medical and metabolic issues and needed to be under the care of an experienced doctor who understood these issues and knew how to deal with them.

Ricki then chirps out something along the lines of “That’s excellent advice. You all have doctors, right?”

All the guests nod in the affirmative.

She says, “That’s great. When we come back, these people will get the help they’ve been waiting for.”

We break for a commercial. When everything starts up again, Ricki tells all these folks, “Okay, now you’re going to get the help you’ve been waiting for.”

She introduces some guy whose name I can’t remember, who she says is going to solve the problem of all these hugely overweight people.

I’ve got to admit that I was curious to see what the solution she had come up with was.

The guy comes out with large gift bags for each guest. And we learn he is the president of the New York chapter of Weight Watchers. He gave all these poor people a lifetime membership in Weight Watchers. That was Ricki’s solution to their problems.

Both MD and I were stunned. And embarrassed to have been a part of this travesty.

We were all shuffled offstage to make room for the next episode of the Ricky Lake Show.

After the fiasco was over, we—MD and I and all the overweight people—were each given a crisp fifty dollar bill and sent via car to our various flea-bag hotels. The overweight people were crushed. They realized their misfortune; their medical challenges had been exploited for entertainment purposes.

MD and I felt terrible for them. Before we all left, we spent a bit of time with each of them and gave them our cards. We told them to call us, and we would help anyway we could. (None of them ever did.) And we all went our separate ways.

The entire experience was awful.

I’m glad Ricki is living large in Malibu with a private chef to prepare her keto dinners. I hope she realizes she got there on the backs of people like the ones we were on her show with. And I pray she at least pauses from time to time to consider the disservice she did to them.

The funny and dispiriting part of this whole thing is that I realized just how many people watch this kind of TV.

MD and I have been on virtually every daytime TV show known to man. We’ve been on all the major shows over the years. We’ve been on countless shows on all the major networks and all the cable networks. And, occasionally, we’ll hear from people who say, Hey, I saw you on such and such show last night.

We’ve had more people tell us they saw us on the Ricky Lake show than any other show we’ve ever been on.

I would call a pharmacy to call in a prescription for a patient, and the pharmacist would say (and they all start off the same way) Hey, I was channel surfing the other night, and there you were on the Ricki Lake show.

Bear in mind, these pharmacists had never seen us in the flesh. We were nothing but disembodied voices to them, some doc calling in a script. How did they know what we looked like, so they would stop channel surfing because they saw us?

Made me realize how many people watch this kind of trash. It really was a bummer.

News You Can Use

I’m going to pass along to you something I stumbled into that is absolutely stunning. Many of you, I’m sure, already know about what I’m going to tell you. But many don’t, and it is to those I’m aiming this section.

I’m kind of a tech Luddite and typically don’t understand the full capability of all the tools I have available to me. In this case, an iPhone. And not a top of the line, brand new one, but an iPhone 13 Pro I’ve had for a few years. (MD and I drive our cars till the wheels fall off of them and do the same with smart phones, tablets, and computers.)

I have thousands of photos stored in my iPhone that I took using my current iPhone and past iPhones. When I’m at medical conferences, I take photos of particular slides that interest me or that I want to pull data from later. Maybe it’s a literature citation or photo I like or whatever.

I couldn’t remember the conference where I saw the slide I was looking for or when it was exactly. I knew it was a few years back, so I began scrolling through photo after photo after photo. It was a mind numbing chore, and I never did find the photo I was looking for. Then I remembered hearing somewhere that the iPhone (and I’m assuming other smart phones) index writing that appears in photos.

So, I gave it a try.

And I was astounded at the results.

Unfortunately, I did not find the slide I was looking for, but I will when I have more time to search various words. I thought the slide in question had the word “aging” in it, so I searched for “aging.” When I did so, my iPhone converted the lower cased aging to upper case aging with the weird symbol to the left of it as shown below:

I click SEARCH at the bottom of the screen and I’m presented with six photos and a notice that says there are 20 photos in all. So I click and here are all 20 photos.

I enlarged all of them that looked like slides from a presentation, but none of them were what I was looking for. But as I enlarged each of the photos with my fingers, a little yellow dot appeared. Below is the lower right photo of my desktop computer from the array above blown up a bit so you can see the yellow dot that appeared.

As you can see, my desktop at the time was clotted with a ton of pdf files, which is pretty typical. I don’t know why I took the photo, but I did. The little yellow dot that is blown up here is over a pdf icon. When I blow it up, I get this.

It’s insane. The iPhone is able to pick up this tiny word in a photo and index it for search. It’s just incredible.

I was so gobsmacked at discovering this that I wasted a couple of hours searching for all kinds of stuff. I came up with book after book (along with a lot of other stuff) indexed by various words, usually the title. Or even the subtitle.

But it doesn’t work perfectly. For example, I had a photo of one of my bookshelves in Dallas. I focused on one of the shelves and searched to see if it would pick up the author of one of the books.

I first searched for “Semmelweis,” the title of the thin black book on the top of this stack. No go. Nothing found. Then I searched for “Anthony Powell,” and, again, nothing. Then I searched for Anthony, and Bingo! it came up.

Then I tried “Powell” to see if that would pick it up. It did not pick it up in the bookshelf in Dallas, but it did pick it up from a photo of my nightstand at our former house, where it was housed at that time. I’ve got to put up this entire photo, because I didn’t remember how stacked my nightstand was at the time. MD bitched about it often and mightily, however. It hasn’t come close to those proportions since we moved. [The bride begs to differ.]

And when enlarged, you can see that the yellow spot was on Powell.

One more, then I’ll quit. I just can’t believe this is really possible. On the bookshelf in Dallas I have a biography of Hitler, with his name in big black letters on the spine. So I decided to do a search for Hitler to see what turned up. And I get a bunch of photos, one of which is the one below.

This was taken on my birthday in Rome about nine years ago when MD was on a singing tour over there. There was a birthday dinner for me, and some of the people with us had actually brought hardcover books over to gift to me. I was speechless. Anyway, here are three of them. I think I got about six or seven total, but I could hold only three at a time for photos.

As you can see, the little yellow dot is on The Nazi Hunters. When I blew it up, I found this:

The author of this book was also the author of a book titled Hitlerland, which I have never read. But the program picked the word “Hitler” out of a longer word. It’s absolutely beyond belief. For me, at least. As I’ve shown, it doesn’t work perfectly, but it works really well.

I’m planning to snap photos of all my bookshelves in both places, so instead of searching for books by standing and looking at them one by one where they sit on the shelves (I don’t have them in order), I can simply search my photos to discover a) if I have the book at a particular domicile, and b) which shelf it’s on.

It will save me massive amounts of time. My hope is that this description of these capabilities may save you a lot of time, too.

As I wrote earlier, many of you probably already know about this, but to me, it was a real revelation.

One last note, I tried it on the Photos app on my MacBook Pro laptop, and it didn’t work anywhere near as well as it did on the iPhone.

When I saw this tweet a couple of weeks ago, I didn’t really believe it. After what I’ve seen from my own iPhone, I do believe it now.

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

Low-Carb, Low-Fat, and Diet Fatigue

The authors (and anyone else who has ever dieted or taken care of overweight patients) are aware that people starting a new diet typically lose a lot right at the start, but over time the rate of weight loss falls off. There are a few reasons for this phenomenon.

First, as we lose, our bodies more or less try to fight back. Our bodies are protecting against weight loss. They are trying to achieve homeostasis. When we lower our calories, we don’t move as much. Our NEAT (non-exercise activity thermogenesis) drops off. We tend to sleep a bit more. We do all kinds of things unconsciously to conserve energy.

Second, as we get smaller, we don’t need as much intake to fuel our smaller bodies, so if we continue eating the same amount, it makes sense that we incrementally lose less and less over time.

Third, we just get tired of being on a diet. We live in a food-rich world. Food of all kinds is all around us all the time. Virtually every diet study ever performed shows people losing less later in the diet than at the first. Diet fatigue sets in.

The authors of this study randomized 61 subjects into two groups (this was not a huge study), one of which started on a low-carb diet while the other went low fat. Both diets contained about the same number of calories. The subjects were asked to follow their assigned diet for six months, being monitored at a 3-month and 6-month interval.

Then the plan was to switch to the other diet.

Those who started the low-carb diet would switch to a low-fat diet for the final six months of the study, while those originally on the low-fat diet would jump to low-carb.

One of the purposes of the study was to see if doing a complete 180 on diet would somehow overcome diet fatigue and give the faltering weight loss a pop.

Alas, it really didn’t. At least not to any major extent. But we can learn something about the differences in effectiveness of the two diets from what happened both before and after the switch.

This chart basically tells the tale, but before we get to it, let’s take a look at the diet composition and number of calories involved.

The graphic above shows the “habitual” diet of the subjects before randomization on the left. Those starting with the low-fat diet are in the middle, and those starting low-carb on the right. As you can see, the diets really were low-fat and low-carb. When I first started reading this study, I was afraid the low-carb diet would be something like 130 g of carb, which isn’t by a stretch ‘low’. But if you calculate based on calories, the low-carbers were consuming about 44 g of carb during the first three months. It jumped a bit to about 73 g of carbs in the second three months, which is still fairly low.

You can see that those on the low-fat, high-carb diet kept their carbs about the same for both the first and second three-month periods, whereas there was a bit of carb creep among the low-carbers.

Here’s what happened when they switched.

It’s a little difficult to understand. I had to read the description a couple of times before I figured it out. But here’s what the chart above shows.

Those in the kind of dark grey are the subjects who started on the low-fat diet and switched to low-carb. Those in orange started on low-carb and switched to low-fat.

As you can see, those on the low-carb diet lost more weight at both the 3-month and the 6-month check in periods, which accords with the majority of studies out there. Low-carb almost always wins. In this case, it would probably have won even more had the dieters in that arm not had carb creep.

But look what happened at the switch over point. During the first three months on the low-carb diet, the former low-fatters lost more weight by switching to low-carb than the low-carbers did switching to low-fat. In fact, the former low-fatters lost more during the third 3-month period on the low-carb diet than they did on the second 3-month period on low-fat.

But the weight loss of the former low-carbers came to a screeching halt during the third 3-month period after switching to low-fat, high-carb.

What this tells us is that if we’re trying to lose weight over the long run, carbs are not our friends. And keeping carbs lower is beneficial to better weight loss.

Which is not the same conclusion the authors of the study drew. What they came away thinking is that switching diets at the 6-month mark, the time at which dietary fatigue usually begins to set it, doesn’t really bump weight loss back to where it was at the start of the process. Which, in a way, is a kind of valid read. Here is how they put it.

After switching diets at 6 months, weight modestly decreased until 9 months, but at a rate slower than the initial 3 months and slower than the rate from 3 to 6 months. This suggests that the weight loss plateau typically seen at 6 months is physiological and cannot be overcome by simply switching to a different weight-loss diet.

And they included a graphic of overall weight loss in both groups combined to prove their point.

This graphic is of both groups combined, which does show no difference in switching from one diet to the other at six months.

But, as we saw in the graphics above this one, switching to the low-carb diet brought about more weight loss in the low-fatters than they experienced in the previous three months on a low fat structure. But that is all hidden in the graphic showing both groups combined.

They do mention the difference in the body of the study.

One notable subgroup is that between 6 and 9 months, participants who switched from LF to LC maintained an average percent weight change of − 2% while participants who switched from LC to LF experienced a nearly 0% average percent weight change.

But not in the conclusions, which lead anyone just reading the abstract—which, sadly, is what the vast majority of people read—to believe there was no difference after the switchover.

But, then, the lead author of this paper is Chris Gardner, who is a vegetarian and never misses an opportunity to take a swipe at the low-carb diet.

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Too Good to be True? You Make the Call

A few days ago Nick Norwitz posted a video on YouTube about an amazing new study in the prestigious journal Nature Aging describing how blood transfusions from younger people can make us all younger. It’s pretty phenomenal stuff. Watch the video, then I’ll give you my take.

Here is a link to the paper titled “Small extracellular vesicles from young plasma reverse age-related functional declines by improving mitochondrial energy metabolism” so you can read it yourself. The paper is loaded with nice scientific looking charts and graphics of one kind or another. It tells us basically that all we have to do is get small extracellular vesicles (sEVs) transfused into us from younger people—or if we’re a mouse, from younger mice—and the aging process will be reversed to some extent.

It all sounds great, but in my view it is absolute and total bullshit.

Why do I say this?

For a couple of reasons.

First, the more spectacular the results you see in a study, the more likely it is that it can’t be reproduced.

Remember just a few years ago, a researcher claimed to have discovered a room-temperature superconductor, which would have been a spectacular achievement. But the results couldn’t be replicated by other labs. As it turned out, the author had fabricated data. The paper was retracted and the author canned.

A few years before that there were two papers published (in Nature, I think) in which the author claimed to have discovered a simple way to reprogram mature cells into pluripotent stem cells called STAP (stimulus-triggered acquisition of pluripotency) cells. Again, a number of other researchers could never replicate the results. Ultimately investigators discovered data fiddling, mislabeled samples, and God knows what else. Both papers were retracted. And the researcher’s supervisor killed himself.

There are many more such cases. Generally, the more over the top the claims, the higher the likelihood of data manipulation, sloppy lab work, and out and out fraud. (Perhaps particularly so if there is some magic pill or procedure involved and a company ready with the purported technology to provide it.)

The second reason I have for disbelieving this study is that it was done in China.

Chinese academics are rewarded for getting papers published in major journals. Their careers get a whopping boost, and the government even rewards them financially. Not too long ago, I discussed an article in which more than half of Chinese researchers admitted to fudging data. If it’s more than half, then any study coming out of China has a greater chance of being wrong than on the up and up.

Couple that with the notion that the more spectacular the results, the more likely they are incorrect or not replicable, and you’ve got an almost dead-lock cinch that this study isn’t worth the paper it is written on.

In my view, Nick should have gone with his first instinct and said it was BS. I predict that’s exactly how it will turn out. If it turns out to be replicable and the real thing, I’ll eat my words.

And I’ll be deliriously happy to get a few small extracellular vesicles transfused from my kids and grandkids. Robbie, I’m thinking of you. (He’s the youngest). But I’m not holding my breath.

They’re Finally Getting the Message on GLP-1 Agonists

I recently had a bit of time to catch up on my backlog of physician newsletters about a host of subjects. One in particular gladdened my heart…sort of. At least it let me know that more and more docs are realizing that loss of lean body mass is a problem with all the GLP-1 agonists drugs such as Ozempic, Wegovy, and others.

But since these newsletters, which are free to physicians, are paid for by the pharmaceutical industry, they’ve got to be a little bit careful not to bite the hand that feeds them. Consequently, they focus on the lean body mass loss that generally comes with overall weight loss in general.

The title of the one I read was “Tackling Lean Mass Loss When Weight Loss is Successful,” which does not mention GLP-1 agonists, but I’m sure every doc who sees it knows what it’s about.

I don’t know if this is behind a paywall or not, so I’ll quote from it liberally.

It starts out with

In addition to the established gastrointestinal side effects common with the highly effective anti-obesity drugs, there is growing discussion around their potential to contribute to the loss of lean mass, necessary to keep the metabolic engine running full-steam.

And although measures should be recommended to prevent those effects, experts also want to remind clinicians that the loss of lean mass is indeed expected with most weight loss interventions — when they’re successful.

“The bottom line is if you’re successful with weight loss, it’s a normal process that you’re going to lose some lean mass,” Angela Fitch, MD, associate director of the Massachusetts General Hospital Weight Center in Boston, said during a presentation on the issue at Obesity Medicine 2024.

“It’s what we would expect to see if you successfully lost weight with bariatric surgery or with an intense lifestyle intervention,” said Dr. Fitch, past president of the Obesity Medicine Association.

The difference is, there haven’t been nearly as many people being successful with weight loss with those other interventions,” she noted. “But with the popularity of the glucagon-like peptide 1 (GLP-1) medications, people are hearing this for the first time and saying, ‘Oh my gosh, 30% of the weight loss is muscle mass — that’s horrible.’ “[My bold]

Okay, let’s deconstruct this a bit. Yes, there is usually a loss of lean body mass along with any substantial overall weight loss. Part of this loss arises from the fact that if there is a, say, 40 pound weight loss, the person losing that 40 pounds doesn’t need as much muscle as he/she did when carrying the extra 40 pounds. There have been a couple of studies I’ve read over the years in which subjects dieting wore vests 24 hours a day with weights representing their lost weight. In other words, if one of these subjects lost three pounds in a week, the researchers would put three pounds of weight in the vest the subject wore during waking hours.

As the weight dropped off from the diet, it was added to the vest. In these cases, the subjects lost very little lean mass, because, thanks to their ever heavier vests, they were toting around the same weight as they were when they started the diet.

So it’s normal to lose some lean mass with a significant weight loss, but you don’t want to lose too much.

In the above quote, Dr. Finch pimps for the new GLP-1 agonists by basically saying at no time in the past with other interventions have people lost as much weight in such a short period of time as they have with GLP-1 agonists. Her statement is kind of an infomercial for these drugs.

She first throws out the idea that a 30 percent loss in lean body mass is a bad thing, but then goes on to say

An underlying goal in the treatment of obesity is the reduction of fat mass, and significant fat mass reduction can provide benefits exceeding the drawbacks resulting from lean mass loss, which have been reported in clinical trials of the GLP-1s semaglutide and the dual glucose-dependent insulinotropic polypeptide tirzepatide to range from about 25% to 40%, respectively, of weight loss.

“Excess adiposity is what makes us sick — not our weight,” Dr. Fitch underscored. “The amount of fat that people are losing [with anti-obesity medications] is far more beneficial than maybe the potential that they’ve lost a little bit of lean mass,” she said.

She cited research suggesting that significant weight loss from bariatric surgery is linked to increases in life expectancy, cardiovascular risk reduction, cancer risk reduction, and a wide array of other positive effects — despite the loss of lean mass that occurs with the weight loss. [My bold]

Where do I start? I’m not so sure “significant fat mass reduction can provide benefits exceeding the drawbacks resulting from lean mass loss.” Fat mass reduction can provide more benefits if the lean mass loss is limited to what I mentioned above, that which comes about because you have less weight to carry around. If you lose more than that, then the benefit is not that clear cut.

“Excess adiposity is what makes us sick,” she says, but adequate lean body mass is what makes us able to fend off frailty and makes us live longer.

She mentions the studies showing that significant weight loss from bariatric surgery is linked to increased life expectancy, but people who undergo bariatric surgery are generally morbidly obese. Many people taking GLP-1 agonists are not that overweight. Big difference.

“It can be very hard to be in an energy deficit (due to a weight loss regimen) and gain muscle mass,” she said. “When athletes are trying to gain muscle mass, they’re increasing their intake to do so. It doesn’t come naturally in today’s world.”

Nevertheless, patients can be reassured that the losses can be reversed with some effort, Dr. Fitch noted. [My bold]

If patients are over 30 (and the older, the more difficult it is) the losses can’t be reversed with some effort. It takes a lot of effort. Dr. Finch is minimizing the amount of effort required.

Dr. Finch goes on

Efforts at staving off lean mass loss are particularly important in older patients, who are already most vulnerable to experiencing it naturally with age, even if not on a weight loss regimen.

But Dr. Fitch offered that age does not necessarily have to be a barrier in tackling those effects.

She described two cases of treating patients in their mid-70s, a male and female, with GLP-1s for obesity. Not only were they able to achieve substantial reductions in body mass index over nearly a year on treatment, but they were also able to avoid skeletal muscle mass loss during a period when it would have likely naturally occurred.

She noted the need to augment strength training with protein intake to help build muscle, citing recommendations including consumption of 1.4-2.0 g of protein per kg of body weight for building muscle and maintaining muscle mass. [My bold]

We’re at the crux of the matter here. It requires a huge intake of protein and strength training to maintain (let alone build) lean body mass. I think it takes 1.8-2.0+ g of protein per kg along with the strength training to maintain lean body mass.

The next thing she says strikes at the heart of the problem.

Importantly, “make sure patients aren’t too appetite suppressed so they can keep up with their nutrition,” Dr. Fitch said.

The way GLP-1 agonists work is by slowing gastric emptying and thereby reducing appetite. You eat less, so you lose weight. You’re not hungry, so you don’t have much desire to eat much. Therefore you don’t.

Think about this.

Remember a time you were at a restaurant and you had eaten till you couldn’t eat another bite. You are stuffed. One of your dining companions says, Oh, you’ve got to try just one little bite of my ribeye. It’s delicious. You can’t even imaging taking a bit of the ribeye. In fact, it almost nauseates you to contemplate it, so you kindly refuse.


Then the dessert cart comes around. Suddenly, you’re not so stuffed. Hmmm. A little ice cream, maybe. Or perhaps a piece of that carrot cake. Or a crème brûlée. Why not?

Carbs shut off the hunger center. You know you have some room for carbs, so you order dessert.

Don’t tell me this has never happened to you. If it hasn’t, you’re one in a million. It’s happened to me countless times.

The point is, when you’re not particularly hungry, protein doesn’t appeal to you at all. You’ll do carbs, right enough, but not really protein.

And if you’re on a GLP-1 agonist drug, you need protein most of all. But the drug quells your appetite for it. It’s hard to push the protein under those circumstances. Which leads to a loss of lean body mass.

The drug companies go to great lengths to hide the loss of lean body mass in their studies.

Take a look at the first study of GLP-1 agonists published in the New England Journal of Medicine in 2021 under the title “Once-Weekly Semaglutide in Adults with Overweight or Obesity.”

If you read through this study looking for anything on the loss of lean body mass, you really can’t find it. What you can find is the following:


In the DXA subpopulation (140 participants), total fat mass and regional visceral fat mass were reduced from baseline with semaglutide (Table S5). Although total lean body mass decreased in absolute terms (kg), the proportion of lean body mass relative to total body mass increased with semaglutide. [My bold]

What you read is that a subpopulation of patients in this study were evaluated by a DEXA scan to determine how much lean vs fat mass was lost.

You have to go to another document to find out anything about this. When you go to the other document, it is in pdf format and is 39 pages long. If you persevere, as I did, you ultimately come to page 24, which has this chart on it.

It doesn’t tell you how these particular 140 subjects were selected to undergo a DEXA scan. Were they the ones who lost the most weight, or the least, or an average amount? Not disclosed.

If you add all the weight lost (8.36 k of fat and 5.26 k of lean) you get a total weight loss of 13.62 k (~30 pounds). If you divide the weight of lean loss by the total loss (5.26/13.62) you discover that almost 39 percent of the 30 pound weight loss is lean body mass.

If you go back to the study quote from above, you see that the last sentence says

Although total lean body mass decreased in absolute terms (kg), the proportion of lean body mass relative to total body mass increased with semaglutide.

Which is totally fatuous. They’re saying, Sure, these subjects lost some lean body mass, but they lost less lean body mass than they did fat mass with the drug, so that’s a good thing. (In other words, they lost less than half of their weight as lean mass, and that’s supposed to be a victory?)

Let me leave you with this question.

Which do you think will be the easier to regain once these folks go off the drug? Which they ultimately will. The 8.36 k of fat they lost? Or the 5.26 k of lean mass they lost?

I can predict with almost certainty that there will be many unintended consequences with these drugs. And I’m not just talking Ozempic face and Wegovy butt. Every week I come across another problem people have experienced with these drugs, so buyer beware.

Don’t fall for the the soft promoters of them like our Dr. Fitch, who consider maintaining lean body mass as being easy. Our Dr. Fitch is a pusher.

Here are her pusher credentials.

Dr. Fitch disclosed ties to Eli Lilly, Novo Nordisk, Currax, Vivus, SideKick Health, Jenny Craig, Carmot, and Seca. Dr. Kushner is on the advisory boards of Novo Nordisk, Weight Watchers, Lilly, Boehringer Ingelheim, and Altimmune.

‘Nuff said.

Fauci’s Wing Man Blows Up

I watched a bit of the slow-rolling disaster that was David Morens’ testimony to congress about his emails the committee had come across. I intended to write about it in some detail, but others have beaten me to the punch, so I’ll let them step in.

Morens (whose name would be more appropriate were the “e” replaced with an “o,”) was trying to clean up after a slew of emails implicating a bunch of people—including Fauci—in a lot of wrong doing. Congress wasn’t buying it.

Here is just one example.

I mean how stupid do you have to be to do that? It beggars belief.

You can read more if you’re interested in this post by The Bad Cat, one of my favorite Substack writers.

Your government hard at work making life better for its citizens.

Why We Fear Saturated Fat and LDL Cholesterol

A week or so ago, someone posted a new paper on the academic low-carb email list I follow titled “The Lipid–Heart Hypothesis and the Keys Equation Defined the Dietary Guidelines but Ignored the Impact of Trans-Fat and High Linoleic Acid Consumption.” (Full text)

The paper does a masterful job at describing just how the widespread fear of saturated fat, cholesterol, and LDL cholesterol came to be. As we all know, much of it was driven by Ancel Keys, but this paper delves into where Keys, who was a smart guy, made multiple mistakes in his analysis.

One of the biggest was to combine partially-hydrogenated (trans) fats in with saturated fats in his various analyses. At the time, it wasn’t known how harmful to health these fats actually were, so many of the issues attributed to saturated fats may well have been caused by trans fats. I was not aware of all of this, so it made for fascinating reading for me.

The authors point out one of the issues I’ve discussed in various talks and in writings on my blog. When the fear of saturated fat was at its zenith, and people were avoiding it whenever possible, the rates of heart disease began to fall. Which seemingly gave credence to the notion that a reduction in saturated fat had something to do with lesser rates of heart disease. What most people fail to mention is that during this same period, smoking rates also fell off fairly rapidly.

There is no doubt in the minds of any researchers in the field that smoking is a major known risk factor for heart disease just as it is for lung cancer. As this paper shows, the rates of heart disease fell as more and more smokers quit. Or didn’t take up smoking in the first place.

I’ve used much the same statistics to argue that statins aren’t all they’re cracked up to be. Statins came into use in the late 1980s/early 1990s when the reduction in rates of heart disease due to the fall off of smoking was starting to take effect. By the time statins were in widespread use, the rates of heart disease began to fall off minimally and sort of stabilize, despite more and more people continuing to quit smoking. If statins are the wonder drugs most cardiologists think they are, the rates of heart disease should have tumbled farther and faster. Which they haven’t.

Another thing I did know about, but still enjoyed reading in this paper was a summary of the papers done back in the days when Keys was active and could make or break a person’s career who dared to show saturated fats to be not problematic. When the data came in on these papers, the authors refused to publish. Due to a variety of circumstances, some of these papers found the light of day over the past few years.

In numerous studies, some of which were not published at the time they were done, the subjects who replaced saturated fat with corn oil and other PUFAs died at greater rates than those who stuck with saturated fat. These were some of the studies the authors decided not to publish.

The paper delves into the health problems caused by PUFAs and discusses the health benefits of coconut oil, which is highly saturated.

The article isn’t laced with scientific terminology, so it isn’t a daunting read. If you’re interested at all in this subject matter, pull down the full text above and give it a read. You’ll be glad you did.

Odds and Ends

Newsletter Recommendations

I’ve got a good one for you this week. Since I often focus (as in today) on lean body mass and building it and recommend books from time to time, imagine my surprise when I came across a newsletter titled Books and Biceps. Who wouldn’t want to read about meatheads who read? It’s really a fun newsletter with tips on strength training AND book recommendations. And not just books on body building.

And, as always, I’ve got to recommend my bride’s Substack OutlanderMD, which explains 18th century medicine and how they got it wrong (or right) in the long running Outlander series.

Video of the Week

This week’s video is of a wonderful piece of Renaissance music. It’s a song by John Dowland (1563-1626), published in The First Booke of Songes or Ayres in 1597. The song is called Come againe. It may not be everyone’s cup of tea, but its simple rhythm and melody captivated me. And MD.

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

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And don’t forget my newest affiliate sponsor Jaquish Biomedical. Highly recommended to increase your lean body mass.


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