The Arrow #154

Hello everyone.

Greetings from Montecito.

We are back here to celebrate Christmas with the Santa Barbara branch of the fam and suck up a little California sunshine.

Before we get into all of today’s topics, I want to take some time to address a couple of questions I got via email.

What Is Processed Food?

I got a question based on what I wrote last week about processed foods. In discussing a couple of yogurts, I wrote

The Fage yogurt is pretty pure. The Chobani contains some processed soy products in it, which, if these stimulate an incretin response, might qualify it as processed. [My bold]

The reader asked how the Chobani would not be processed if it contained “processed soy”?

It’s a good question that I should have spent more time explaining.

There is no formal definition of a processed food. At least not one that I know of.

The lady writing the Wall Street Journal article on processed foods, which was the topic of last week’s discussion, defines them as foods containing a lot of substances that wouldn’t be found in the food in nature.

WebMD has a broad definition.

Processed foods refer to any food that’s changed from its natural state. This can include food that was simply cut, washed, heated, pasteurized, canned, cooked, frozen, dried, dehydrated, mixed, or packaged. It also can include food that has added preservatives, nutrients, flavors, salts, sugars, or fats.

By their definition, adding a little salt to a raw tomato you’re eating converts it to a processed food, which is nonsense.

The Heart & Stroke group from Canada defines them thus:

Unprocessed or minimally processed foods: Think vegetables, grains, legumes, fruits, nuts, meats, seafood, herbs, spices, garlic, eggs and milk. Make these real, whole foods the basis of your diet.

Processed foods: When ingredients such as oil, sugar or salt are added to foods and they are packaged, the result is processed foods. Examples are simple bread, cheese, tofu, and canned tuna or beans. These foods have been altered, but not in a way that’s detrimental to health. They are convenient and help you build nutritious meals. See? Not everything in a package is bad for you!

Ultra-processed foods: Here’s the category where almost 50% of our calories come from – and where we should cut back. These foods go through multiple processes (extrusion, molding, milling, etc.), contain many added ingredients and are highly manipulated. Examples are soft drinks, chips, chocolate, candy, ice-cream, sweetened breakfast cereals, packaged soups, chicken nuggets, hotdogs, fries and more.

Which is also insane. You can’t eat grains unprocessed, or even minimally processed. Go out and try it if you don’t believe me. If you eat a hot dog, it’s like eating meat, which is listed as ultra-processed.

If you Google processed or ultra-processed foods, you’ll find countless definitions. So since everyone out there seems to have their own definition, I might as well get into the act and come up with my own.

I define processed or ultra-processed foods as any alteration of the food that changes its incretin effect. Remember, the incretin effect is what happens to GIP and insulin after the food is consumed. I posted a short video of the incretin effect a couple of weeks ago.

If we eat an apple—an unprocessed food—we have a particular incretin response. If we purée the same apple, we will have altered its structural integrity, and we will experience a greater incretin response than we provoked when we ate the whole apple. If we purée the apple and add a little antioxidant chemical to it as a preservative, we’ll still get the same incretin response. The purée isn’t more processed just because we added the antioxidant.

Now if we push the apple purée through a fine strainer, and end up with apple juice, we will have processed it a little more, and the incretin response will again be more pronounced.

If we eat the apple whole with a little salt sprinkled on it (try it; it isn’t bad), then we still, by my definition, are eating a non-processed food. The incretin response won’t change with a little salt added.

The “processed soy” protein added to the Chobani yogurt mentioned above does not really change the incretin response to the yogurt, so I don’t consider it a processed food.

Think structural integrity of the food in question, and the incretin response to it. If the change alters the incretin response, then the food is processed. In my world at any rate.

Visceral Versus Subcutaneous Fat

Got the following question from a reader:

I’ve been low carb for quite some time and still overweight. However, the vast majority of the fat, I believe, is subcutaneous and not visceral. Why is subcutaneous fat so hard to lose?

Where do I start?

This is a pretty common question. The answer is sort of a good news/bad news one.

Subcutaneous fat is more difficult to lose than visceral fat, but it is also less dangerous than visceral fat. Which, I’m sure, is small solace to those struggling to lose it.

The volume and distribution of subcutaneous fat for storage is pretty much genetically determined. Visceral fat, not so much.

We, as humans, are designed to store fat away. We eat more than we need for our immediate energy needs, and the surplus is stored and released as needed throughout the day. Under normal circumstances, this extra energy will be stored as subcutaneous fat. That’s the body’s natural fat storage depot.

You can think of subcutaneous fat as the body’s equivalent of closets, cabinets, attics, and garages. If you are a packrat, as I am, you store all kinds of stuff you don’t immediately need in closets, attics, etc. As long as there is space in those storage areas, the rest of your house looks nice, clean, and ordered.

But if you keep on cramming items into those storage areas, ultimately you will run out of storage space. And you will begin to pile stacks of National Geographics in your living room.

The same thing happens with subcutaneous fat. You can overeat, and as long as your genetically determined subcutaneous fat depots can keep storing, you will continue to put fat there. Once your subcutaneous space is full, then you start packing fat into your viscera. Which is not a good thing.

Organs and viscera are not intended for fat storage. They will accept the excess fat, but they won’t like it. In fact, they’ll view it as a foreign body, much as if you had jabbed a splinter into your viscera.

The graphic above shows the inflammatory response to a foreign body, in this case, a splinter. Although there is no bacteria involved when fat ends up in the viscera, the inflammatory response is the same. Macrophages will rush to the area to try to clean up the fat that isn’t supposed to be there just like they would if you had a splinter. Once they arrive, the macrophages begin sending out help signals and other macrophages rush in to help. As a result, in many cases the visceral fat is composed of 50-60 percent macrophages. All sending out distress signals and generating a huge immune response.

(Slide from a talk I gave a few years ago on this topic)

Which is why visceral fat is so inflammatory and is a risk factor for heart disease and a host of other disorders.

But the good news is that since visceral fat is fat in places it shouldn’t be, the body gets rid of it first. When you start losing weight, it is the first to go.

Not so with subcutaneous fat, because it is where stored calories are supposed to be. So there is no mad rush to get rid of it. People who have a lot of subcutaneous fat have to work a little harder to shed themselves of it.

Going back to our closet/attic analogy, if you’ve got a bunch of stuff scattered about your house, and someone calls to tell you they’re dropping by, you can dash through the house and clean it up pretty quickly. Not the same when you decide to clean out your jam-packed attic. That typically is a much longer process.

It’s the same with subcutaneous fat.

Generally, people spontaneously eat less on a low-carbohydrate diet. And the diet is more thermodynamically active. In other words, it requires more energy than does a low-fat, high-carb diet to simply deal with the incoming macronutrients. As a consequence, most people lose nicely on a low-carb diet without being hungry.

But some people can overdo it and continue to maintain excess subcutaneous fat stores even on a sound low-carb diet. These people need to be more diligent and really make sure they hew to the diet. In our experience, the three things they have to watch are nuts, nut butters, and cheese. These three foods don’t contain many carbs, but are laden with calories. So people can stay within their carb limits, while at the same time consuming a ton of fat calories. In some cases, plenty enough to meet all their energy needs and thus maintain their weight.

[The bride begs I not forget about alcohol, which can be zero carbs, but lots of calories that have no place to be stored in the body and must therefore be burned before any other calories are burned.]

A low-carb diet reduces insulin levels, which opens the way for the fat to escape from the fat cells. But if there are enough fat calories coming in (or more) to fuel all the body’s requirements, then there is no need for the subcutaneous fat cells to release their contents to make up a deficit, because there is no deficit.

So, if you are struggling to lose subcutaneous fat, you need to watch the three [four?] foods mentioned above and strictly adhere to your whole food low carb diet. And you need to assiduously avoid vegetable oils (for reasons we’ll discuss another time). The other tip would be to crank up your output, with regular pretty high intensity physical activity. I know that’s not what you want to hear, but it is the reality.

Once you’ve shed the excess subcutaneous fat, then you don’t really care if you don’t lose more fat from the fat cells, so you don’t have to worry about it. You just have to fight through to get to that point. Then, as long as you control your insulin, you should be fine.

Below is a graphic from one of my talks showing the difference between visceral and subcutaneous fat via full body scan and cross-sectional areas.

Paleopathology in Australia

My talk in Sydney just went public for those who care about such things. Feel free to comment on the YouTube. Give Low Carb Down Under some clicks. Enjoy.

Next week, I’ll post MD’s talk, so you’ll have something to look forward to.

Excess Deaths in Young Vaccinated Athletes?

It seems as if every time I turn around, I’m seeing a report of the sudden death of a young athlete. Now comes a paper from a sports medicine doc from the University of Washington showing a decline in the number of cardiovascular deaths of NCAA athletes over the past 20 years.

Which, on the surface, seems strange since most of the deaths I see reported sound like cardiovascular deaths. And most appear to be attributed to myocarditis, which is a known risk factor of the Covid-19 mRNA vaccines.

I learned about this paper from an alert by the Journal of the American Medical Association (JAMA), which sends me periodic notices of articles of interest published in other journals. Here is JAMA’s summary.

The rate of sudden cardiac death (SCD) in the US among National Collegiate Athletic Association athletes declined from mid-2002 through mid-2022, a recent study involving 143 SCD cases found, while deaths related to noncardiovascular causes remained stable over the period.

The SCD incidence tended to be higher among certain groups of athletes, particularly Division I male basketball players. Overall, male or Black athletes were more likely to have experienced SCD than female or White athletes, respectively. About half of the deaths were related to exertion, and none were attributed to COVID-19 myocarditis.

“Continued efforts are needed to improve cardiovascular screening, risk stratification, emergency action plans, availability of automated external defibrillators, and training in cardiopulmonary resuscitation,” the researchers wrote in Circulation. [Link in the original][My bold]

The study is behind a paywall, so I reached out to the lead author to see if I could get a copy. She sent me a pdf almost immediately (my Dropbox link here).

I gave the paper a quick read. The data analysis ended on June 30, 2022, which was about a year after the major push for vaccines really kicked in. So, of course, I wondered what had happened since and wondered if there was any additional information.

Since the author of the article had responded so quickly, I thought she might still be at her desk, so I emailed and asked her. She promptly emailed me back with the following:

There is much more media attention to it but we have not noticed an increase. In fact the rate of SCD has gone down. We are going to try and look at the overall rate of sudden cardiac arrest (SCA) and SCD which we believe will be stable. We think the decrease in SCD is likely because of improved resuscitation and perhaps better screening. They have seen similar trends in Europe with a decrease in SCD and no increase in cardiovascular death due to myocarditis since the beginning of the pandemic.   

At this point it seems the COVID-19 is a much milder illness, especially in our young athletes now that they have developed some immunity whether that be naturally (due to infection) or acquired (from vaccination). It has essentially been a non-issue for the past year or more. 

Since reading this paper and her response to my inquiry, I’ve been trying to reconcile all this with the media reports I’ve been reading, which make it seem that young athletes are dying like flies.

I follow only two professional sports even semi closely: the NFL and MLB. Each of the NFL teams has a roster of 55 players, which makes 1760 in total. Each of the 30 MLB teams has an expanded roster of 40 players totaling 1200 for baseball.

Of these two sports totaling 2960 professional athletes, as far as I can recall, there hasn’t been a case of sudden cardiac death. The Buffalo Bill’s safety Darmar Hamlin came close on a Monday night football game, but he was resuscitated on the field and has lived to play again.

So, that’s one close call out of ~3,000 professional athletes over about a ten month span, which takes in MLB spring training until now.

All of our three sons are college football fanatics, and if a player had died suddenly in college football, I’m sure I would have heard about it.

But according to the Circulation article, a few NCAA athletes did die. But the deaths are all listed in deaths per athlete years, which I can’t use to compare to the NFL and MLB stats I used above. Of all the NCAA deaths during the study period (there were 1,102), there were only 143 deemed to be sudden cardiac deaths. Based on autopsy findings, only 8 of those were due to myocarditis. And only 1 of these 8 occurred during the Covid years. This one Covid-era death was not attributed to either Covid or the vaccine.

Now that I’ve thought about it after reading this paper, most of the deaths I’ve read about have been in high school athletes. There are vastly more high school athletes than there are NCAA athletes, and these high schoolers don’t get very thorough physicals before they are allowed to compete. I don’t think any of them get EKGs or chest x-rays. I’ve done a bunch of such screenings myself in years gone by, and they involved listening to the heart and lungs, checking for hernias, looking in ears, noses, and throats, and, in general, just looking the kids over.

It’s not like that in the pros—those folks go through mega physicals because of the money involved. College screening is somewhere in between.

Again, because of the money involved, pro teams have skilled physicians at hand always along with plenty of resuscitation equipment. Not so in high school. Had Damar Hamlin gone down in a high school football game, it is unlikely he would be with us today.

If we use the stats I generated for SCD (or near SCD) in pro athletes as being 1/3000, then you might expect SCD in maybe 1/2500 high school athletes. (I’m cranking down the denominator number a bit because the high schoolers aren’t nearly as well screened as the pros.)

According to NCSA, there are approximately 8M high school athletes. So, in any given year, you would expect 3,200 SCD, based on 1/2500. I suspect that figure is way too high. But even if it were 1/100th of that, it would still mean 32 kids die each year in high school sports, which is about three per month. I suspect it is more than that.

Since these days, most of those kids would be vaccinated, the vaccination might get blamed. Especially since it has been shown to cause myocarditis in young males.

Reading these figures and performing the above calculations have not made me run out and get vaccinated or encourage my family to get vaccinated. I still think the Covid vaccines are a disaster and would not take one on a dare. But now I’m less inclined to think of every sudden death of a kid as vaccine induced. Though I do believe many are.

The risk-reward ratio is simply too high to take a vaccine with the potential for adverse effects for God only knows how long against not much benefit for a disease that isn’t much of anything. We’re not talking polio or smallpox here. We’re talking a disease that is not much worse than the common cold, especially since it has mutated to a much more benign version.

But even with the original version, it appears the majority of deaths were caused by improper treatment.

I’m still convinced the vaccines are an issue over the long run. The insurance industry has reported an enormous increase in excess deaths in the United States that can’t be attributed to Covid. If these deaths were caused by lack of care or follow up care during the idiotic lockdowns, then one might expect an increase in deaths due to chronic disease, which would be more predominant in the elderly. But the deaths have increased in a younger population.

According to The Hill, certainly not a bastion of right wing thinking, a new report from the Society of Actuaries tells the tale.

Mortality was 26 percent higher among insured 35-to-44-year-olds, and 19 percent higher for 25-to-34-year-olds, continuing a death spike that peaked in the third quarter of 2021 at a staggering 101 percent and 79 percent above normal, respectively.

Let’s look a little bit more at the vaccines and the lab leak theory. If you have lost interest in all this, skip on down to the sections after.

Kadlek Spills His Guts on Fauci and the Lab Leak

For those of you who don’t know who Robert Kadlek is, he is a physician and was the Assistant Secretary of Health and Human Services (Preparedness and Response) from August 2017 till January 2021. He was also responsible for the creation of the Covid-19 development program called Operation Warp Speed. During the Covid crisis, Kadlek was essentially Fauci’s boss.

As pretty much everyone now knows, Fauci wrangled a bunch of serious scientists, all of whom were of the opinion that the odds were high SARS-CoV-2 was a consequence of a lab leak in Wuhan, into jointly publishing an article Fauci pushed through The Lancet saying the virus was of zoonotic (ie, animal) origin. The paper became infamously known as the “proximal origins” paper.

Along the way, Fauci made a handful of trips to the CIA, where a number of agents assigned to study the situation, and who, apparently, believed the lab leak origins to be the most probable were bribed to say the opposite.

The speculation has been that Fauci did all this to cover his tail since he had funded the Wuhan lab. Had this disaster been a consequence of a leak from a lab he had funded to do gain-of-function research, which had been outlawed, he would have been in a pickle.

Here is an interview with both the former head of MI-6, the UK equivalent of the CIA, and Robert Kadlek on what happened. Kadlek apparently decided to spill the beans to an astute Australian journalist instead of one from the US. This is from Australian Sky TV.

The entire video is only about 5 minutes long, and is well worth watching in its entirety. The part where Fauci lies through his teeth about the proximal origins paper starts at 1:17. Kadlek’s interview follows.

If you want to read more about the proximal origins paper and how it all came together, you can find an exhaustive timeline here. For those who are interested, it really shows in explicit detail what went on and how these scientists changed their tune at Fauci’s request.

Okay, one more bit on the vaccines because I promised last week…

Frameshifting in the mRNA Vaccines

As we all know by now, the mRNA vaccines “work” by hijacking our own protein synthesis machinery into producing the spike protein. If things go according to plan, the self-produced spike protein will then stimulate an immune response that will in turn protect against the spike protein on the Covid virus.

During the development phase of the vaccine, scientists were having problems getting the actual mRNA (the template for the production of the spike protein) to stay around long enough to drive the production of enough spike protein to stimulate a response. The cells were immediately degrading the mRNA, which is what the cells do when mRNA has done its job. Since it’s not natural to make spike protein in a human cell, the cell simply gets rid of the mRNA.

In an effort to keep the spike protein mRNA around long enough to produce some actual spike protein, the scientists substituted one nucleotide for another in the mRNA chain. That seemed to do the trick. The mRNA stayed around long enough to make the spike protein. Problem is, it may have stayed around too long. Usually mRNA gets degraded as soon as it does its job. This one with the substituted nucleotide stayed around a lot longer.

Also, they used humanized codons. Codons are the genetic symbols that tell the protein assembly machinery to put a certain amino acid in place. A number of codons can code for the same amino acid. There are human codons and there are viral codons that are different, but code for the same amino acid. Since the developers of the mRNA vaccines used humanized codons instead of viral codons, no one knows if the spike proteins are exactly the same because the proteins might be folded a bit differently.

The Nature paper we discussed last week showed that these different or ‘frameshifted’ proteins show up in about a quarter of people. No one knows what the significance is or will be.

Here is a fascinating interview from a year or so ago—long before the Nature paper was published—with Kevin McKernan, who was the former research and development lead on the Human Genome Project. He is also the scientist who recently discovered DNA (versus mRNA) and the simian virus SV40 as well in some batches of the mRNA vaccine. Those of you who can remember back to the 1950s might recall that some of the vaccines were contaminated with SV40, which is an infectious pathogen thought to cause a number of different cancers.

The information in this short (~11 mins) clip is fairly dense and technical, but not beyond the understanding of readers of this newsletter. While watching, remember that McKernan predicted all this more than a year before the Nature paper came out confirming it.

Vegetarian vs Omnivore Diets. Which Is Better?

I’m sure readers of The Arrow know the answer to this question, but many others don’t. The vegetarian diet has this halo effect about it that has many people believing it to be superior in terms of being healthful, but such is not the case.

I subscribe to a host of newsletters for physicians of all different stripes. I’ve gotten a least a half dozen of them mentioning a new twin study out comparing the vegetarian diet to the omnivore diet. The implication is that the vegetarian diet is better. Here is an example from one of the many emails I received.

My plan was to dig in to this paper and discuss it in detail. But, this week two of my friends beat me to it, so there is no need for me to re-invent the wheel. Zoë Harcombe went over the results in detail in her weekly missive that comes out on Mondays (you should subscribe). And Nina Teicholz came out with hers on Substack a couple of days ago.

In brief, here is what happened. The researchers placed 22 pairs of identical twins on either vegetarian or omnivorous diets for 8 weeks. At the end of the trial, those subjects on the vegetarian diet experienced a drop in LDL-cholesterol levels, a fall in fasting insulin, and greater weight loss.

As the authors of the study wrote in their conclusion

In this randomized clinical trial, we observed cardiometabolic advantages for the healthy vegan vs the healthy omnivorous diet among healthy, adult identical twins. Clinicians may consider recommending plant-based diets to reduce cardiometabolic risk factors, as well as aligning with environmental benefits. [My bold]

Usually the conclusions are a little more specific. In fact, they usually include the statistics for the various “cardiometabolic” parameters measured. In this case, they were pretty vague.

Both Zoë and Nina noted that the decrease in LDL levels comes about as a consequence of increased plant sterols in the vegetarians.

Zoë writes

The write-up of the study on Stanford’s web site headlined “Twin research indicates that a vegan diet improves cardiovascular health” (Ref 12). Oh no it doesn’t. It proved that higher intake of plant sterols lowers cholesterol. However, original research that I have done has shown that consuming plant sterols is worse for cardiovascular health (and worse for cancer) (Ref 13).

---

Ref 13: Harcombe & Baker. Plant sterols lower cholesterol, but increase risk for coronary heart disease. Journal of Biological Sciences. 2014.
https://thescipub.com/abstract/ojbsci.2014.167.169 [Link in the original]

Nina mentions the plant sterols as well.

This result is not surprising, as all plant-based diets lower the “bad” LDL-cholesterol, largely because plant sterols replace some of the body’s natural cholesterol in the cell walls. (The saturated fat from meat and dairy in the omnivore diet could have been expected to cause LDL-C to rise compared to the vegan diet, but in this study, both groups reported eating less saturated fat than they had at the start of the study.¹) [Links in the original]

Zoë shows the animal protein differential between the two groups.

As you can see from the data in the middle and on the right, the omnivores—as would be expected—consumed vastly more animal protein than did those on the vegetarian diet. In a different graphic in her post, Zoë also shows those on the vegetarian diet consumed less protein overall (plant plus animal) than did those on the omnivorous diet.

Since it takes significantly more plant protein to provide adequate quantities to support muscle protein synthesis, i.e., maintenance of muscle mass, and since those on the vegetarian diet consumed less total protein than those on the omnivorous diet, those in the vegetarian arm were protein deficient. And would be more so over time and end up with a serious loss of lean body mass as a consequence. So weight loss, but at a severe cost to lean body mass.

One other interesting finding was that were no statistically significant differences in TMAO, a substance produced during the digestion and metabolism of meat and thought by many to be a risk factor for cardiovascular and early death, between the two groups.

The data from the study show that those on the vegetarian diet had lower fasting insulin levels along with a greater weight loss. Which would seem to show a definite improvement in those parameters, which are significantly related to cardiovascular risk.

But not so fast…

And, as Nina explains

Gardner also found that the twins randomized to a vegan diet had better fasting insulin (2.9 μIU/mL less) and lost 4.2 pounds more than their omnivore counterparts at the end of the study. Why these variances emerged, we can’t really know, and Gardner does not speculate in his paper. One possible explanation is that the vegans recorded eating less sugar than did the omnivores as well as about 180 fewer calories per day. Subjects were not told to try to lose weight, but perhaps the vegan twins ate less, because they had lower “diet satisfaction” as reported on a five-question survey, compared to the omnivore twins?²

A major problem with these two outcomes—weight and fasting insulin--is that neither was listed as an “endpoint” in the original protocol for the trial, submitted to the clinical-trial registry at the National Institutes of Health. If a researcher changes the outcome measures after the study is concluded, as Gardner seemingly did here, there’s a good possibility that this choice reflects cherry picking, meaning the selection of measurements that look good for one’s preferred outcome, while disregarding (or burying in the rarely-read supplemental materials) those that don’t look so good. The whole point of submitting a protocol in advance is to prevent such post-hoc selection of data. [Links in the original] [My bold]

What I have put in bold in the paragraph quoted above is extremely important.

It used to be that researchers could just do a study like this, wait for the results, then put everything that ended up being statistically significant in their conclusion, which is called p-hacking. Not so much any longer. Now you have to list what you’re looking for before you do the study. I suspect Gardner et al didn’t expect to find a lower insulin level or an increased weight loss, so they didn’t put those in the protocol.

I recommend you read Nina’s entire Stack, which is primarily about the ideological biases of both the lead researcher and the funders of this study.

Stanford’s Vegan Twin Study: Science or PR Stunt?

Okay, now it’s time for my piteous plea for you to become a paid subscriber. The Arrow costs a measly 20 cents per day (19.78022 cents, to be exact, and that’s if you sign up monthly). If you sign up for an annual subscription, it’s only 16.438356 cents per day. A bargain to be sure. That’s about the cost of a big spoonful of some awful sugar-coated cereal. And The Arrow won’t raise your insulin. Click below and sign up.

Is There a Rebound With Zepbound?

What the heck is Zepbound? you may be asking. Well, Zepbound is the same drug as Mounjaro, the diabetes drug that has been used off-label for weight loss. Now that Eli Lilly has gotten approval for the drug, they’re using the name Zepbound for the weight-loss version and continuing with Mounjaro as the diabetes drug.

As an aside, before I go further, it’s interesting how drugs are named. The drug in question here is called generically tirzepatide, which is a combination of a GLP-1 agonist and a GIP agonist. I’m surprised the FDA, the agency that regulates drug naming, let them get by with the Zep part of Zepbound, since it repeats part of the generic name. The FDA, for its own reasons, doesn’t cotton to any drug names that even give a hint as to what the drug does. So there can be no drug names that in any way tell what the drug has been approved for. For example, if you tried to name a drug for erectile dysfunction something like Turgine or Bonupia, they would shoot you down. Instead, you would have to go with Viagra or Cialis, neither of which tells you anything about what the drug does.

Seems like a stupid regulation to me, but, in my view, the vast majority of regulations are stupid. In the case of drug names, you’ve probably got a group of people at the FDA with combined salaries of over a million dollars a year scrutinizing potential drug names to make sure one doesn’t imply a function. Or maybe now they let AI do it.

As you probably know, there has been a huge push to get these very expensive injectable weight-loss drugs approved for insurance payment. The drug companies would love it, as would those who want to have their weekly injections subsidized. The insurance companies are fighting back, saying that obesity is a lifestyle disease. In other words, it could be eliminated by lifestyle changes. The insurance company position is that they don’t want to pay for people who choose to overeat.

As we all know, it is more complex than that, but given the prevalence of obesity, it could send premiums through the roof for every insurance holder if every overweight person were able to get these drugs for next to nothing.

Not only does Big Pharma want to get these drugs paid for by insurance for weight loss, they are also working to get them paid for weight maintenance, which would really be a budget buster. They say obesity is a chronic disease just like diabetes or high blood pressure. [And that’s true enough.] No one in their right mind would take a pill for high blood pressure or high blood sugar, then as soon as the BP or blood sugar went down, stop taking the pill and say they were cured. So if a drug is successful in helping people lose weight, then why not keep them on it to keep the weight low.

Which is exactly the reason behind the funding of the latest tirzepatide study by Eli Lilly titled Continued Treatment With Tirzepatide for Maintenance of Weight Reduction in Adults With Obesity.

Here is the setup.

Researchers put 783 subjects on tirzepatide for 36 weeks. At that point, 670 subjects were randomized to either continue to get injections of tirzepatide or injections of a placebo. The randomization was blinded, so neither the subjects nor the researchers knew who got what.

Here we can graphically see what happened.

As it is plain to see, those who went on placebo ended up gaining back their lost weight.

But let’s look a little closer to see what else we can glean from the graphic.

It’s pretty obvious that the weight loss is bottoming out with the tirzepatide starting not long after the 36-week randomization. Subjects on the full-tirzepatide regimen lost a little weight between week 36 and week 52, but not a lot. At week 64, they hit bottom and didn’t budge over the next 24 weeks.

It looks to me like the curve is starting to go back up, which would mean that despite the weekly injections of tirzepatide a bit of weight was starting to come back on. It’s difficult to tell by just eyeballing the curve, but at the very least weight loss had stalled.

Here is another graphic from the study that is even more telling.

The waist circumference followed the same trajectory in the placebo group as it did with weight loss. Since waist circumference is kind of a proxy for visceral fat, this tells us that the visceral fat was piling back on. Which is not good juju.

It tells us that tirzepatide gets rid of mainly visceral fat, which is the easiest fat to lose. But it’s also the most dangerous fat, so that’s good.

But if you look closer at the stats, you’ll notice that the weight loss with tirzepatide bottoms out while the subjects are still considered obese. According to the CDC, the following categorizations apply in terms of BMI.

• If your BMI is less than 18.5, it falls within the underweight range.

• If your BMI is 18.5 to <25, it falls within the healthy weight range.

• If your BMI is 25.0 to <30, it falls within the overweight range.

• If your BMI is 30.0 or higher, it falls within the obesity range.

Here are the study stats on changes in BMI over the course of the first 36 weeks.

As you can see, the BMI doesn’t drop below the threshold for obesity after 36 weeks, which pretty much means most of the weight lost was probably from visceral fat, the easiest fat to lose.

But also, as those randomized to placebo discovered, the easiest to gain back.

Looking back at the top chart—the one showing total weight loss—demonstrates that at a little over a year’s time on the real tirzepatide the folks considered obese are still obese, though a little less so. And then weight loss levels out and stays the same for the next year. I’m not sure had they not been on a study that these people would have kept up with the weekly injections once the weight loss stopped, especially in view of the side effect profile of these drugs. And the cost.

Going back to this study, they started off with 783 subjects, but after 36 weeks (~9 months) 113 had dropped out. One assumes these were people eager to lose weight and get free drugs to do so, yet almost 15 percent of them dropped out.

My view of all this is that ultimately despite being on the drugs, most people will gain their weight back. The studies don’t show this, but the studies are all stopped after the weight loss has bottomed out and appears to be moving in the wrong direction.

I would avoid them.

But MD and I did have dinner a few weeks ago during which we met a lady whose son was doing great on Wegovy. She told us he had been overweight since his teens and had never been interested in losing weight. Once these drugs came along, he went after it with a vengeance. She said he looked so much better she couldn’t believe it.

I, of course, told her he needed to really make an effort to eat a lot of protein so he wouldn’t lose his lean body mass. She told me he was. That he had discovered the ketogenic diet, and he was loading up on protein. And working out with resistance. Under those circumstances, the weight loss shots might be okay.

But then why even take the shots? The ketogenic diet and resistance work will do it alone.

Okay, let’s hit the video.

Video of the Week

This one blew me away. I don’t know how many of you know the Texas singer/songwriter Jerry Jeff Walker (RIP), but he’s known for a sort of Texas brand of song. One of his biggest hits was Up Against the Well Redneck Mother, which he didn’t write, but did make famous. At least among those of us who loved him and that song. Our kids grew up listening to that song.

I had no idea he had written the song below. I always thought Bob Dylan had written it. He (Bob) is the one who made it famous. But, no, it was none other than Jerry Jeff Walker.

Who knew?

Okay, that’s about it for this week.

Oh, wait, I forgot the poll.

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

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