The Arrow #129

Hello everyone.

Greetings from Montecito.

Where it has been sunny for the last three days, but overcast and chilly today. And this is all while Texas is suffering a brutal heatwave. I suppose it’s better right now to be here than there. I’ll be back there soon enough. And will doubtless be wishing I were back where it is cold and foggy.

I had my birthday a few days ago and finally got some personal benefit from the DEI movement. My birthday is now a national holiday: Juneteenth! If I ever become a federal employee, I’ll always have my birthday off.

An Update on the Thin So Fast Saga

The Vitales and Medifast

A reader sent me a pdf of the full article I was missing from the Baltimore Sun. I was wrong. It wasn’t from an obituary of Dr. Vitale. It was instead an article detailing all the many lawsuits the Vitale family were dealing with that drove their Medifast company into bankruptcy. The title of the article says it all. “Slimming Down Medifast marketer plagued by suits, plunging sales.” The first line of the piece summarizes what happened to the Vitale family and their company Jason Pharmaceuticals, the maker of Medifast:

Jason Pharmaceuticals Inc. grew fat when Oprah got thin, and thin when Oprah got fat again.

For those of you interested, I’ve saved it in my Dropbox. (Link here.)

Dr. Vitale lived almost another 20 years before dying in 2020 during the Covid pandemic. I don’t know if he died from Covid or some other cause, but he lived to be almost 93. Based on the commentary on his funeral site, he was a really nice guy. I thought so, too, for a while. But I suppose even nice guys can have terrible tempers. The Baltimore Sun article mentions his temper as a driving force behind one of the many lawsuits the family faced.

Dr. Vitale sold the family business to his kids “a few years” before the Sun article, which was published in 1993.

Since then, the Vitale kids sold the business to another entity that does business as Medifast and is publicly traded on the NY Stock Exchange. They still use the same Medifast trademark and operate using the multilevel marketing model. From their public financial information, Medifast is now an almost $2B company.

Before we leave the Vitale-Medifast-Thin So Fast story, I want to go back to the Sun article and clear up a few medical misconceptions.

Before even getting to those, there is another point of interest. In last week’s Arrow I put up a photo of my Medifast certificate. And I mentioned what a Mickey Mouse kind of deal it was. According to the article

In a well-publicized 1990 hearing before a subcommittee of the ++ House Committee on Small Business, congressmen grilled diet industry executives about the safety risks effectiveness of their plans and about allegedly misleading advertising.

Dr. Vitale was sharply questioned by Chairman Ron Wyden, D-Ore., about Jason's system for certifying physician associates.[sic] turned out that the only required training was a "self-directed" course of study -- essentially a three-part manual doctors were supposed to read before administering the program. (My emphasis)

Okay, let’s get to the medical issues.

Low-fat diets and gallstones

First, the article states

Meanwhile, the public began to learn about a rush of product-liability lawsuits brought by users of such "very low calorie diets." Most of them concerned the Nutri/System plan, which was sued by numerous patients who claimed they developed gallstones after rapid weight loss. The bad publicity spilled over to all weight-loss programs. (My emphasis)

The gallstone issue was one I was aware of. And it was why I decided to add one full meal to the Medifast regimen I used. It was also why I insisted on one protein meal in Thin So Fast. I knew what would happen on an all-protein-powder very-low-fat diet.

I wrote a long blog post about this gallstone phenomenon a few years ago, but I’ll give you the short version here.

One of the roles of the bile that is released from the gall bladder after a fatty meal is to break down or emulsify the fat coming into the small intestine from the stomach so that it can more easily be absorbed. Bile has a high cholesterol content.

When the fat hits the small intestine, it stimulates the release of cholecystokinin (CCK), which is an important hormone with a multitude of functions, one of which is to stimulate the gallbladder to squirt out bile to help with the digestion of fat.

(Another function is to reduce hunger, which is why it’s difficult to overeat fat. You get full fast. But, interestingly, this fullness function can be over ridden by refined carbohydrates, especially sugar. It would be tough to overeat butter. But add a little sugar to it, and you have frosting. Which is not difficult at all to overeat. And which is why dessert is always served last. You may be so full that you couldn’t contemplate another bite of meat, but then the dessert cart comes by and …)

When fat comes down the pipe, CCK speaks to the gallbladder, which squirts out its bile.

But what if there is no fat coming down the pipe? You’re on a Medifast diet made up of five packets of protein powder, a little sugar, and almost no fat, all mixed together with a diet soft drink. What happens then?

Since no fat is coming down the chute, there is no stimulation of the gall bladder. The galbladder just sits there full of its high-cholesterol bile. As time goes on, the cholesterol precipitates out of the liquid bile and begins to form little cholesterol stones (the most common kind of gallstones). You’re not bothered by it because the stones stay in the gallbladder.

But then.

Ah yes. Then you decide to go out and celebrate all the weight you’ve lost on Medifast, Optifast, or Nutrisystem or whatever other very low-fat program you’ve been following. You chow down on a big, juicy steak. And when it hits your duodenum (the upper part of your small intestine), CCK heads to the gallbladder to stimulate the release of bile. Your gallbladder responds and squeezes out the bile along with one of these little cholesterol stones, which end up getting stuck in the duct that runs from the gallbladder to the small intestine.

Ducts don’t like to have stones in them. Doesn’t matter if is a ureter that has a kidney stone or the duct running from your gallbladder. Or a baby in a birth canal. It hurts like hell.

You go to the ER, where the doc does a scan and determines you’ve got a gallstone in a critical duct. So it’s off to the surgery suite with you.

Since having trained as a surgeon (Vitale trained as a dermatologist—what do dermatologists know about the gallbladder?), I understood all this, so decided to make sure my patients got a fatty meal once per day to prevent gallstones.

MD and I did one drug study in our practice. We were the largest center in the world in a phase 3 study of the weight-loss drug orlistat. Hoffman LaRoche owned the patent on orlistat at the time and wanted to see if it would work as a maintenance drug for those people who had already lost weight.

Here’s how the study worked.

Subjects were recruited and ALL were started on low-fat diets, the supposedly ‘best diets’ for weight loss as determined by the “experts” in 1993. As part of our study, we had to hire a dietitian to manage these patients and instruct them in how to follow a low-fat diet and monitor them for the next six months. After these patients lost weight, they were then randomized into four different groups. One a placebo group and three groups that got three different doses of orlistat.

At the start of the study, these subjects got all kinds of lab work, an EKG, a body composition measurement, and a gallbladder ultrasound to look for the presence of gallstones. If stones were present, these subjects were rejected from the study. After the six-month weight loss period, the subjects were all given gallbladder ultrasounds again to check for stones. None of these subjects had gallstones going in, but after six months on a low-fat food diet (not powders), 15 percent of them were found to have developed gallstones. These folks could not continue the study. So 15 percent developed gallstones in six months on a low-fat diet!

As an aside that has nothing to do with gallstones, you wouldn’t believe how difficult it was to get patients to lose weight on a low-fat diet. In order to qualify for the final stage of the study, which was when these subjects finally got to go on the drug, the subjects had to lose four percent of their body weight in the six-month weight loss phase. Most of them weighed about 200 pounds going in, so that meant they had to lose eight pounds over six months. You wouldn’t believe how many people couldn’t hit that mark on a low fat diet.

In six months!

Our own patients on low-carb diets did that easily in a month or so. If I hadn’t been a believer in the efficacy of the low-carb diet before, I certainly would have been after evaluating patients on this study. (Which, interestingly, is exactly what happened with our hired dietitian. She was a low-fat fanatic before getting involved with us in this study. Because she did have a functioning brain and believed her own eyes, her mind changed quickly.)

The take home message is that if you follow a low-fat diet for any length of time, don’t be surprised if you develop gallstones.

Low-cal, high-protein diets and diabetes

The Baltimore Sun article above mentioned one of the half dozen or so product liability lawsuits filed against Jason Pharmaceuticals.

One of the most serious cases involves Eulas White, a 54-year-old Texas man who weighed about 370 pounds when he started the Medifast regimen in September 1989 at the urging of his physician. Mr. White, a diabetic, said his doctor took him off his diabetes medication when he began the program, under which he consumed 445 calories a day.

Without that medication, Mr. White said, he developed leg ulcers that led to gangrene. He said he was rushed to a Dallas hospital, where doctors amputated his right leg 5 inches below the knee. He is suing the doctor and Jason.

Since the article was published in 1993 and the plaintiff started the Medifast program in 1989, it’s difficult to know how long the guy was on Medifast. And we don’t know when the lawsuit was filed. I’m sure lawyers have a way to search the records. I tried googling, but couldn’t find squat. In fact, I couldn’t even find a person named Eulas White. A lot of people named Eula, all of whom were female, but not a Eulas. If any of you lawyers out there can track this case down for me, I would love to see it.

Here is the situation as I have reconstructed it.

This 370 pound diabetic man came in seeking treatment. As the article states, the doctor following him took him off his diabetes medication. I don’t know if he was on multiple medications or just a single medication. But if this patient presented to me, I would have done the same thing. If not immediately, then soon.

Here’s why.

The guy obviously had type 2 diabetes. How do I know? Because 370 pound people with type 1 diabetes are rare. If he had type 1 diabetes and weighed 370 pounds, he was on way, way too much insulin. And they were covering that excess insulin with carbs.

His type 2 diabetes was probably a function of his obesity. So, if his doctor solves his obesity issue, the type 2 diabetes will doubtless go away. As long as he maintains his newer, thinner weight.

The protein-sparing modified fast (PSMF), which is the generic name for Optifast and Medifast type diets, typically brings about a reduction in both blood pressure (if elevated) and blood sugar (if elevated) extremely quickly. How quickly? It can be in just a couple of days in some cases.

If people start a PSMF while on certain types of blood pressure medicines (diuretics, in particular), they can drop their BP in a hurry. They can get dizzy when they stand up and can even pass out. The same with blood sugar medicines.

If you, as a doctor, put someone on a whole food low-fat or low-calorie diet, it will take a while for either blood pressure or blood sugar to come down. (If they ever do.) So you have time to wean the patients off of their meds as they lose weight. This is not the case with the PSMF. It works very quickly.

I learned from bitter experience to take my PSMF patients off of their blood pressure and blood sugar meds the day they started their new diet. Almost all of them reduced their blood pressures and blood sugars quickly and were able to stay off these meds. The few who were not able to do so, I added meds back in until their BPs and/or BSs were stable. Then watched them like a hawk to make sure they still needed the meds as their weight loss progressed, ready to taper as needed.

What I suspect happened to the unlucky Mr. White is that he followed the PSMF for a bit, then tired of it. But he never went back on his meds. And he never went back to his doctor.

Leg ulcers and gangrene don’t develop overnight. My guess is that some time passed, and he developed the problems, which had nothing to do with the PSMF. He ended up looking for someone other than himself to blame, and found an attorney who would sue the doc and Jason.

That is all total speculation on my part, but makes sense from the timeline of the article. Which is why I would love to see the details on the lawsuit and the outcome if someone who knows how to get it can send it to me. My bet is that there was a settlement as neither the lawyers representing the doctor nor the ones representing Jason wanted to try to explain all this to a jury. Especially not when the plaintiff had his leg amputated. Juries are sympathetic.

Speaking of which…

A few weeks ago I got paired up in a golf round with a big time defense attorney from Atlanta. Once he found out I was a doctor, he quickly let it be known that he defended doctors instead of suing them.

He told me that he defended a lot of docs and other people who had been sued, but he said he only had to go to trial about once a year, because all the insurance companies ended up settling. Juries, he said, ended up coming up with such monstrous awards that no insurance company wants to take the risk of going to trial.

More On Vaccines

Rochelle Walensky Gets Caught Lying…Definitively

Which is like saying Donald Trump gets caught being brash. I don’t know what we’re going to have to do to clean up our government agencies. I can understand our defense department and our intelligence agencies (sort of) keeping secrets from our enemies. But what about the agencies that are supposedly in place to provide services and protect we the people? Why would they keep secrets? And keep the truth from us?

One reason might be that they are stupid and don’t realize the truth. But given the educational levels, the pedigrees, and the inside information these folks have, it beggars belief that they don’t know the truth.

Take Rochelle Walensky for example. In last week’s Arrow, I posted a video of her absolutely lying through her teeth about the mRNA Covid vaccines. I suppose folks who haven’t been keeping up with all the vaccine news might think she was telling the truth. Or at least the truth as she understood it at the time she said it publicly.

But now, thanks to the results of FOIA request, we know differently. The Washington Examiner broke a story a couple of days ago about emails obtained through the Freedom of Information Act that prove Walensky knew all along that the vaccines had serious issues

Emails obtained through a Freedom of Information Act request show that CDC Director Rochelle Walensky and former NIH Director Francis Collins were aware of, and discussed, “breakthrough cases” of COVID in January 2021 — right when the vaccines became widely available. In her email, Walensky says that “clearly,” it is an “important area of study,” links to a study raising the issue, and assures the person she is sending it to that Dr. Anthony Fauci is looped into these conversations.

However, in public, Walensky was saying something quite different. Two months after discussing this data, she said vaccinated people “don’t carry the virus” and “don’t get sick.” In a congressional hearing, after it became clear people were able to get infected with COVID even after receiving the vaccine, she defended her original statements by claiming it was true at the time she said it — namely, for the strands we were dealing with in early 2021.

We now know that was not true and that Walensky herself knew it was not true. [My emphasis]

Here is a copy of the redacted email.

Note the date, which I have underlined in red. January 30, 2021. That is ten days after Biden’s inauguration when the vaccine roll out was just getting ramped. Walensky knew early on that there was a problem. Had the article shown above been written by anyone other that Paul Offit, a true believer in all vaccines for all causes, she might not have worried so much. But since Offit is part of the connected, credentialed class, it got her attention. Not only that, she makes it clear that Francis Collins, who famously called Sunetra Gupta and Martin Kulldorff “fringe epidemiologists,” and Anthony Fauci, “Tony” in the email above, knew as well.

If there are issues with the vaccines, as reported in the paper, why hide them from the American people, whom you are being paid to protect? And by whom you are paid to provide accurate information.

As Swedish epidemiologist Johan Giesecke famously said, “People are not stupid.” Give them the facts, and they’ll do what’s best.

These people—Walensky, Fauci, and Collins—were so hell bent on getting everyone vaccinated that they ignored information that might stand in the way of letting that happen. Even at the expense of their fellow Americans, many of whom are now dead as a consequence.

Some of you may think it was a lie that saved millions of lives, so therefore it was justified. The idea that millions of lives were saved is anecdotal, not scientific. I know you’ve heard it a thousand times from all those who promoted the vaccines, but it is still anecdotal. The only actual data we have—thanks to how the study was done—comparing vaccines to placebo shows that the same number of subjects died who got the placebo as did those who got the vaccine. In other words, the vaccine did not prevent deaths from Covid. At least not in the total study group of ~44,000 subjects.

That’s it. Those are the only data we have from randomized, controlled trials. No difference in deaths between those who got the vaccine and those who didn’t. Actually, there were more deaths in the group who got the vaccine, but the numbers didn’t reach statistical significance. In other words, the P wasn’t wee enough. If you believe in those kinds of things.

But what about all the stories of people dying like flies. Corpses stacked like cordwood. Doctors and nurses overloaded with Covid patients and working tirelessly to save them. The more these stories are delved into, the more they turn out to be false. In New York, for example, which was one of the hardest hit cities in America, the USS Comfort, a ship used to assist in situations like this, ended up with about ten beds out of its over 1200 used for Covid overflow. Same with the Javits Center. It was revamped to deal with Covid patients, and was pretty much vacant.

It seems almost impossible that we could be lied to this overtly. Well, if you wonder about that, scroll back up and take a look at Walensky’s congressional testimony then look at her email. That should tell you a lot.

But wait, how about how the study was done? Above it says “thanks to how the study was done.” That implies that the study was screwed up somehow. Maybe that’s why the data is wrong.

Nope. But here’s how the study was screwed up. And it was genius on the part of Pfizer, I’ll have to admit. The volunteers for the vaccine all wanted the vaccine, because at that time, everyone was scared shitless of Covid. Remember, there was no vaccine available then. And thanks to the halo effect of vaccines (which is now mercifully becoming undone) subjects leapt for the chance to get vaccinated. And they all wanted the real stuff, not the placebo.

Pfizer told them that the shots they would be getting would be either the real mRNA vaccine or a placebo, but after the study period was over, all those who got the placebo would be given the real vaccine as a consolation prize. By doing so, there is no placebo group to use to compare over the long term what happens. The only data we have show that as many people died who got the vaccine as those who didn’t.

I’m sure that out of the ~22,000 people who got the placebo, not all of them took Pfizer up on its offer of free vaccines. And I’m sure a portion of those who didn’t take the offer did not take the vaccines when they were rolled out in late 2020/early 2021. It would be nice if a) there were enough of those people to provide a decent data sample, and b) Pfizer would track them down to see how they fared as compared to those who were vaccinated.

But, for obvious reasons, Pfizer has no intention of doing that.

More’s the pity

Childhood Vaccination Rates Falling

I don’t know if this is good news or not, but it could be valuable news. Trial Site News just published an article headlined “Childhood Vaccination Rates Declining Across Parts of America.” The author discussed how vaccinations for childhood diseases were on the fall throughout the US. It included a link to CDC statistics confirming the drop off.

State and local school vaccination requirements protect students and communities against vaccine-preventable diseases . This report summarizes data collected by state and local immunization programs on vaccination coverage and exemptions to vaccination among children in kindergarten in 49 states and the District of Columbia and provisional enrollment or grace period status for kindergartners in 27 states for the 2021–22 school year. Nationwide, vaccination coverage with 2 doses of measles, mumps and rubella vaccine (MMR) was 93.0%; with the state-required number of diphtheria, tetanus, and acellular pertussis vaccine (DTaP) doses was 92.7%; with poliovirus vaccine (polio) was 93.1%; and with the state-required number of varicella vaccine doses was 92.8%. Compared with the 2020–21 school year, vaccination coverage decreased 0.8–0.9 percentage points for all vaccines. Although 2.6% of kindergartners had an exemption for at least one vaccine, an additional 4.4% who did not have an exemption were not up to date with MMR. Although there has been a nearly complete return to in-person learning after COVID-19 pandemic-associated disruptions, immunization programs continued to report COVID-19–related impacts on vaccination assessment and coverage. Follow-up with undervaccinated students and catch-up campaigns remain important for increasing vaccination coverage to prepandemic levels to protect children and communities from vaccine-preventable diseases.

You might be surprised to learn that I think this is a good thing.

Why?

As I’ve written in previous editions of The Arrow, I’m working my way through two excellent books: Dissolving Illusions: Disease, Vaccines, and The Forgotten History and Turtles All the Way Down: Vaccine Science and Myth. The first one describes in gruesome detail the squalor in which most people lived until relatively recently. The books also delves into the early history of vaccinations. I haven’t finished it yet, so I can’t comment on it in its entirety. But what I found surprising was the history of the smallpox vaccine. Throughout my schooling, I was taught about how Edward Jenner scraped pus from a cowpox pustule on a milking maid and injected it into a little boy. Jenner then infected the boy with material from an actual case of smallpox. The boy didn’t get smallpox, and that was the beginning of the story on the miracle of vaccines.

As I’ve learned from this book, that is far from the actual and accurate history. Probably more people died from smallpox as a result of the vaccine than died of smallpox without it. Yet, just like today, many localities mandated that citizens be vaccinated.

Which I always thought was a good thing until the Covid panic-demic (I just coined that phrase on the fly—so please don’t tell me you’ve seen it somewhere else), which vaccinated me against the halo effect of vaccines. If vaccines are truly safe and effective—let’s back up and just say effective—so if vaccines are effective, why does it matter if everyone is vaccinated? If they’re effective, then the vaccinated won’t get whatever is being vaccinated against. They have nothing to fear from the unvaccinated. If vaccines are effective, the only people who are at risk are the unvaccinated. So if they choose to not get vaccinated, they suffer the consequences. If the vaccines are not effective, then what difference does it make whether anyone is vaccinated or not?

The whole idea of vaccination brings out the autocrat in many people.

The second book above goes into the dodgy way vaccines are tested. Until I read the book, I did not know vaccines were not tested against placebo, but against other vaccines. Since all vaccines cause side effects—they are designed to cause side effects in that they do harm to stimulate an immune response—comparing any vaccine against another vaccine instead of against a placebo does not give an accurate representation of the amount of harm caused.

Getting back to the CDC report cited above, it looks like the childhood vaccination rate has fallen by about one percent. Since the population of children under five years old in the US is ~18.8 million, a one percent drop in vaccinations would total 188,000 kids. According to the CDC report, the percentage of children receiving childhood vaccinations is ~93 percent. Which means the total number of unvaccinated children under five years old would be ~1,316,000 kids. Which is a lot of kids.

You’ve got to figure that this number includes kids who have had a vaccine here and there, but not the entire panoply of childhood vaccines. I suspect most of these kids fall into two categories. One would be the very rural, very poor, whose kids don’t go to school, where vaccines are mandated. Or the very poor inner city kids. Or the home schooled, which would be a separate category. Most home schooled kids do not come from destitute families.

I think it would be a terrific idea for a study on the long-term effects of vaccination. Track down a bunch of people who got no childhood vaccines, who are now adults and compare them to an age, sex, and income matched group who did get all the vaccines. Since there are bound to be millions of people out there who have never been vaccinated, I doubt it would take a lot of effort to track them down. Such a study would provide excellent data on the health difference—if any—between the vaxxed and the unvaxxed. The researchers could also look at death rates between the vaxxed and the unvaxxed at various years of life to see if the vaxxed or the unvaxxed died at different rates. And they could even determine the cause of death. The data would be invaluable.

But who would pay for it?

The NIH? Hah. If the data were to show those vaxxed to be healthier and to have greater longevity, the NIH would say, We knew that all along, so we just wasted millions of dollars. If the converse were found, the NIH would be in real trouble with Big Pharma, which holds it captive. It’s a no-win situation with the NIH, so it will require private funding to undertake such a study.

Were it done, it would be one of the most important studies ever published. Hundreds of millions of dollars have been spent to “prove” cholesterol causes heart disease. And those looking have come up empty. Why not spend a few tens of the millions to establish or refute the effectiveness of vaccines?

There Is a Move Afoot to Trash the BMI

As long as I can remember, the body mass index (BMI) has been the single unit used to define obesity. The BMI is calculated by dividing the body mass by the square of the body height, and is expressed in units of kg/m2, resulting from mass in kilograms and height in meters. Most people determine it by finding the intersecting lines for weight and height on a chart such as the one below:

Those of us in the weight-loss field have bitched about this method of determining obesity for years. It works for average people, but it doesn’t work at all for non-average people. Take me, for example. When I was 17 years old, I was 6’2” and weighed 150 lb. I was on the verge of being underweight. The famous baseball player Ted Williams weighed about 150 when he came up to the Majors and was 6’3”. He would be deemed underweight, yet he routinely pounded homers into the upper deck of right field, so he certainly wasn’t puny. Virtually all the football players in the NFL would be considered obese, when instead most are lean and very muscular.

A much better way to assess fitness is the waist-to-hip ratio, but it hasn’t really caught on. To calculate the BMI, you have to weigh the subject and measure his height. So, two calculations. Same with the waist-to-hip ratio, which is a vastly more meaningful calculation because it actually tells you how obese a person is. Or, at the very least, it gives you a much more accurate picture than the BMI.

A typical sleek running back in the NFL would come out with a much different waist-to-hip ratio than an obese man with the same BMI.

Of course there are other methods of determining the level of obesity. There is underwater weighing, DEXA scans, and bio-impedence analyzers. But for simplicity, nothing beats the waist-to-hip ratio.

Now, all of a sudden, I’m seeing articles in the medical press bashing the BMI. Why now? Why not years ago when everyone who works in the field starting bitching about the inaccuracy of the BMI?

Before we had the BMI and long before DEXA scans and all the rest, we used the insurance height and weight tables. They were different for men and women, whereas the BMI is used for both sexes. The insurance tables were calculated by actuaries, who looked at the data on death and disease and from it drew an idea of what was a healthful weight as a function of height.

Then the BMI came along. Who figured it out?

It started with a Belgian named Lambert Quetelet in the late 1880s, who was looking for the statistics defining the average man. He stumbled onto what we call the BMI, which people of his time called the Quetelet Index.

It was superseded by the insurance company-generated ideal or desired height to weight tables, which were used for years. Then came the BMI, which was the new term for the Quetelet Index. Who came up with the term BMI? You will be surprised. I was.

I read an article a few days ago in Statnews, a subscription publication for those in the healthcare industry. You can read the article, which I’ll excerpt below, but I was surprised when I watched the embedded video.

Here is is. And it is queued to the appropriate point. See if you’re as surprised as I was.

Our old buddy Ancel Keys was behind it. Who knew? I certainly didn’t. The whiney voice of the narrator of this video almost drove me over the edge, but the information was worthwhile.

So, why is the BMI under fire all of a sudden? It’s been around since the 1950s. And people in the industry have been complaining about it since. So why now?

These paragraphs from the article will give you a clue. It has to do with the cause celeb du jour.

A high BMI has also been cited as a reason to deny gender-affirming surgery for some patients.

Loren Schechter, a plastic surgeon at Rush University, said that he personally stopped using a BMI cutoff to assess genital surgery eligibility years ago, and now considers a combination of factors including comorbidities and body composition.

“I think the trend is moving away from BMI, but these entrenched issues don’t fade away easily,” he said. “Unfortunately, oftentimes you need a lot of literature and experience to do away with some of these things that have been ingrained in the system for a while.”

Gender affirming care. I’ve always marveled at the way people can come up with terminology to define certain beliefs. Gender affirming. Who would deny gender affirming? It sounds so positive. How about gender altering? Doesn’t have the same ring, does it? But it means the same thing.

So, now we’re getting a hint at what might be motivating the change. If only the powers that be could figure out how it could be racist, it would be changed immediately.

Wait. This just in. From the Daily Mail…

The American Medical Association, the largest organization of doctors in the US, said the metric has been used for ‘racist exclusion’ and fails to consider differences in body composition that vary based on race and sex.

Body mass index (BMI), devised by a white man considering white bodies, is measured by dividing a person's weight in kilograms or pounds by the square of height in meters or feet, and it has been deeply ingrained in the medical system as a way to measure population health more broadly.

The AMA Council on Science and Public Health said: ‘Our AMA recognizes: the issues with using body mass index (BMI) as a measurement because: (a) of the eugenics behind the history of BMI, (b) of the use of BMI for racist exclusion, and (c) BMI cutoffs are based on the imagined ideal Caucasian and does not consider a person’s gender or ethnicity.’

BMI was not devised by a doctor or other type of healthcare professional, but rather by a Belgian mathematician named Lambert Adolphe Jacques Quetelet, who sought to measure the height and weight of the ‘average’ man based on a sample of white, European men.

While BMI can be a useful tool for researchers to gain a macro-level view of a population’s overall health, the AMA argues it cannot predict the risk of disease on an individual level, particularly across different racial and ethnic groups. [Link in the original to the multipage AMA report]

I’m not sure I would call the BMI a racist measurement, but it was calculated based on measurements of white Europeans. Most NFL players are black and most would be considered obese by the BMI.

Most white people are considered to begin developing risk for type 2 diabetes at a BMI of 25, whereas it is 20 for Asian folks. So there are indeed racial differences.

Why did it take so long to figure out the BMI sucks?

This is at least one good thing to come out of the current zeitgeist of blaming everything on racism.

Speaking of which…

New Tucker Twitter Monologue

It’s hard for me to believe, but I just watched the latest Tucker piece that dropped on Twitter.

https://twitter.com/TuckerCarlson/status/1672014260480901120?s=20

In it he goes over all the stuff I just wrote in the above two sections. Bizarre.

It’s mainly about RFK, Jr., but he discusses some of what I wrote above about vaccines and the idea that the BMI is racist.

Weird.

You know you should, so…

The Taurine Study

Well, all I can say is that I hoped for better.

I read the study I mentioned last week in great detail, and it turned out to be a major disappointment.

Let me tell you why.

Before we get into it, here are the links for the study, the Wall Street Journal and the New York Times articles about it.

Before we get into the nuts and bolts of the study, let me explain to you how these types of studies get the PR they do. There are over 8 million papers published each year in the academic literature. So how do the few out of this mass end up getting written up in the Wall Street Journal and the New York Times. MD and I along with Loren Cordain published a paper in an academic journal called Comparative Biochemistry and Physiology 20 years ago. There were a lot fewer than 8 million papers published per year back then, but ours didn’t get picked up by any major newspapers.

Ours even had a better title: “Hyperinsulinemic diseases of civilization: more than just Syndrome X.” That’s a lot sexier than “Taurine deficiency as a driver of aging,” which is the title of the paper under discussion. How come ours wasn’t in any of the major papers?

Partially it’s a matter of the prestige of the journal. Science is the most prestigious scientific journal published in the US. Comparative Biochemistry and Physiology is way down the list of prestige as compared to Science. And partially it is the institution where the study was done. From looking at the author list, most of the researchers worked in India, but the corresponding author was from the Columbia University College of Medicine, which is right there in NYC. Not far from the WSJ and the NYT. The work certainly wasn’t done at Colorado State University in Fort Collins, CO where ours was.

The topic has to be catchy. Something people want to read. At the time our paper was published, no one much knew what hyperinsulinemia even was. But everyone wants to know how to stay young longer. And to postpone a visit from the Grim Reaper.

Finally, both Science and Columbia do PR, which Colorado State doesn’t do.

And that’s why some papers get all kinds of press coverage, while the rest of the 8 million don’t.

The title of the paper I’m going to discuss is kind of misleading in a subtle way. “Taurine deficiency as a driver of aging.” Makes it sound like taurine deficiency is a driver of aging. In my view, it should more accurately be written as Taurine deficiency as a driver of aging? The missing question mark in the original makes all the difference.

At least some of the authors of the study have been wondering about taurine and aging for a number of years. It has been shown that taurine levels are lower in elderly people than they are in younger people in the bloom of youthful good health. So it’s a reasonable question to ask.

But the real question is are lower taurine levels a consequence of aging or are they a driver of aging? Which is why I think the original title should have the question mark.

If they are a consequence of aging, it might not do a lot of good to increase them. It would be like dyeing gray hair. It might make the labwork look better and more youthful, but it probably wouldn’t have an effect on the aging process. If, on the other hand, lower taurine was a driver of aging, then increasing its levels might slow aging.

Which is what the authors wanted to study.

Taurine isn’t the first substance people have looked at to forestall aging. Researchers have been studying testosterone for decades. It’s pretty well known that testosterone will stimulate muscle growth in elderly males, but—at least as far as I know—it doesn’t really extend age. (A caveat here: I am not up to date on all the latest testosterone studies, so there may be recent evidence that it does forestall aging. Back in the day when I did look at the data, the consensus was that testosterone wouldn’t make you live any longer, but it would provide you with a more beautiful corpse when you died.)

Here is how studies like this one should be done.

First, someone makes an observation. In this case, older people have lower taurine levels than do younger people and the converse.

The next step is to come up with a hypothesis that says increasing taurine will prolong life.

Then you test that hypothesis.

Of course, you can’t start giving humans taurine to see if they live longer. It would take way too long. Plus you don’t want to experiment on humans until you’ve done animal studies.

Which is exactly what these authors did.

They looked at yeast, worms, mice, and monkeys.

The yeast were a dud. Taurine didn’t do squat to help yeast live longer.

But they hit pay dirt with the worms, the mice, and the monkeys.

This nice graphic shows what they found.

You can see that the mice lived longer as did the worms. The monkeys aren’t included, because there wasn’t enough time—monkeys live a lot longer than worms and mice—to determine longevity. We’ll discuss what happened to monkeys in a bit.

Not only did the mice live longer to the tune of about 12 percent for female mice and 10 percent for males, they had better health in many different systems. I’ll have to hand it to the researchers; they left no systems unstudied. You can see from the graphic above in the parts showing health span and effects on aging hallmarks which systems they evaluated. And virtually all of them showed improvement.

How much taurine did it take to bring about these fabulous changes?

A lot, as it turns out.

They calculated the amount required to get maximal changes in several parameters, and that amount ended up being 1000mg (or 1 gram) per kg of mouse. Mice don’t weigh all that much, but if you look at it in human terms, it calculates to 70 g of taurine for a 70 kg (~150 lb) person. That’s a lot.

An egg weighs about 70 g. What else weighs ~70 g? Google provides the answer. 30 pennies. 17 dice. 40 playing cards. In just volume, that’s a lot of pure taurine to be taking each day. Every day. But that’s equivalent to what the mice took.

They tested the mice with dosages of 1000 mg per kg and 500 mg per kg. There was a fall off in effect when the dose dropped by half. How did they come up with the 1000 mg dose? They looked at blood levels in young mice and checked to see how much taurine they had to give the older mice (the study started with mice at 14 months of age, which is old for a mouse) to get their level up to the level of young mice.

I wondered how they got the mice to eat the stuff. I had to go to the methods section, which isn’t included in the published study. You’ll have to scroll to the bottom of the study and click the download button underneath where it says Supplementary Materials.

The mice were gavage-fed. Here’s how it worked.

A feeding needle appropriate for the age of the mouse was used. A curved gavage needle was used to reduce the likelihood of trauma in the upper gastrointestinal tract. During the procedure, mouse was held firmly, pulling up the loose skin so that it could not move its head. The head was held in vertical 40 alignment with the esophagus. Needle tip was inserted behind the incisors and directed toward the back of the throat. During the procedure, the color of the mucous membranes was closely monitored. Vehicle or taurine solution was injected slowly, and when injection was completed, the needle was pulled out. For consistency, rigor, and reproducibility, mice were always gavaged at the same time of the day (10:00 am)…

I’m sure the mice looked forward to feeding time.

The mice were kept on this schedule from the time they started until they died. Every single day. At 10 am. In looking through the methods of the study, I noticed that the people tending the mice would sometimes dispatch them a little early instead of letting them die on their own. If the mice looked to the keepers as if they were at death’s door, the keepers would finish them off. If the keepers didn’t know which mice were in what group, it probably all evens out. If they did know which was in what group, however, then…

The monkeys got a lesser dose of taurine than did the mice. The monkeys ended up with 250 mg per kg, which is a quarter of the dose the mice got, which in 70 kg human terms would still be almost 20 g, which is a lot. Especially when you consider that the taurine content of a big steak is about 300 mg, and steak is a great source of taurine.

The researchers tricked the monkeys into eating the stuff by wrapping it in banana. And they waited till the monkeys had eaten it all to ensure they had their proper dose. I couldn’t find anywhere how the research team came up with the 250 mg per kg dose for the monkeys.

What I did discover, however, is that the fact checkers for the NY Times must have been off the day the article was published about this study. It says

The mice and monkeys in the new study were given a dose equivalent to about three to six grams a day for humans — a level deemed safe by European regulators, but still on the higher end of the spectrum.

They are way, way off.

The health changes in the monkeys were pretty remarkable. The rhesus monkeys studied were around 15 years old, which is equivalent to 45-50 years old in human years. In a few hours after the dosage of taurine, the blood levels of those so dosed were about twice that of controls.

Monkeys that received taurine gained 0.75 kg less body weight, and their fat percentage tended to be lower compared with that of controls. In-life dual-energy x-ray absorptiometry (DEXA) analysis after 6 months of taurine treatment showed that taurine increased bone density and content in the lumbar spine (L1 to L4) and legs, but not in the head, in taurine-treated monkeys compared with control monkeys…

The levels of bone forming hormones went up in the monkeys on taurine, while the hormones responsible for bone resorption went down. Which, of course, explains the stronger bones.

Taurine treatment reduced fasting blood glucose concentrations by 19%. Taurine also reduced the serum concentrations of liver damage markers AST and alanine transaminase (ALT) by ~36 and 20%, respectively. Numbers of WBCs, monocytes, and granulocytes, which increase with age, were decreased by ~50% in taurine-treated monkeys compared with control monkeys…

Markers of metabolic health improved substantially.

The study lasted only six months and for some reason inexplicable to me, the researchers used only female monkeys for that part of the study, and to keep from having any menstrual problems confound the findings, they surgically removed their ovaries. Why not just use male monkeys?

So, our researchers have their hypothesis that consuming taurine extends life. In the case of mice it certainly appears to do so. In female monkeys with their ovaries removed, it appears to improve health over six months. Lifespan wasn’t determined.

Okay, so what about humans. Does it work for us?

When they get to the end of the paper, as far as humans are concerned, it’s pretty thin gruel. They mention a couple of studies showing that taurine levels increase after intense endurance exercise in healthy men and after 24 weeks of exercise (no method described) in obese individuals. They also mention one study in which humans were actually dosed with taurine. It was done in China, which makes it suspect in my view. (The issue with studies done in China is a story for another day, but suffice it to say, due to the incentives involved, they can’t always be believed.)

The Chinese study showed that humans dosed with up to 6 g of taurine per day had minimal improvements in cholesterol and triglyceride levels, but no reduction in body weight, BMI, or glucose levels.

And that’s about it. So, no real data on humans in this study.

But that doesn’t keep the authors from implying there is such data.

Here are two little sections I clipped out to show you what I mean and why these studies need to be taken with a grain of salt.

…together with our supplementation studies in 15-year-old monkeys, the results presented in this work suggest that an increase in taurine concentrations or its actions may have the potential to suppress the decline in biological functions that occurs during human aging.

And my favorite

Blood cell parameters like hemoglobin, platelets, and WBC count correlated positively with the three taurine metabolites. Association does not establish causation, but these results are consistent with taurine deficiency contributing to human aging. [My emphasis]

This brings to mind a paper I read critiquing another paper during the panic-demic. Here is the crux of the criticism.

…Williamson et al. responded by cautioning against “interpreting… (the) estimates as causal effects,” but neglected to clarify what, if anything, the reported estimates actually estimate or how the results should instead be interpreted. They also drew clear inferences about the contribution of pre-existing conditions and deprivation to the higher risk of death in Black and minority ethnic people. What we will call Schrodinger’s inferences like this—where the authors caution against causal interpretations while themselves offering causal interpretations—should be avoided by using clear language and appropriate methods, else confusion is inevitable. [My emphasis]

This is exactly what the authors of the taurine study did in the last bolded paragraph I posted from their paper.

Okay, so don’t spend your life savings investing in a taurine factory any time soon.

Videos of the Week

For your viewing enjoyment, there are three this week.

The first is an absolutely amazing piece of camera work showing a bald eagle eating on the fly. I don’t know how they got this footage, but it’s astounding. It is a YouTube short, which apparently won’t embed. You can watch it here. You won’t be disappointed.

As I mentioned a few weeks ago, I’ve become obsessed with the New Zealand singer/songwriter Delaney Davidson. One of his first early hits that got him noticed was a song titled Little Heart. I posted a video of it a while back, which, admittedly, is a weird video. But I love the tune. Here is is again for those who haven’t seen it. Or who want to see it again. I’ve watched it 50 times trying to pick up the quirky guitar riffs.

Here is another version that I actually like better. This one he does with Marlon Williams as the lead singer. Delaney is the backup singer and lead guitar.

Marlon Williams came from the same town in New Zealand—Littleton—that Delaney came from. They did three albums together, and since then Marlon has traveled the world performing. Williams was performing at the Troubadour in Los Angeles several years ago at a night when Bradly Cooper happened to be in the audience. Cooper asked Williams if he would be in Cooper’s movie A Star Is Born. Williams who had never acted, agreed. So, if he looks familiar to you, that’s probably where you’ve seen him. He has now become a noted actor as well as a musician. And his rendition above of Little Heart is terrific.

Okay, that’s about it for today. Got some good stuff cooking up for next week. We’ll go over the Randle cycle and another low-carb paper dissection.

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

Thanks for reading all the way to the end. This post is public, so feel free to share it as you like.

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