Hello everyone.

Greetings from Shreveport, LA. MD and I drove over a couple of days ago to visit some doctor friends. We’re heading back to Dallas this afternoon, where I will finish this newsletter. So, I guess we’ll actually be in Dallas when it goes out.

I got a number of emails and comments on last week’s Arrow from folks complaining that it was truncated. I don’t think it had anything to do with The Arrow, but it did have something to do with the various email platforms in use. Some of these platforms (Gmail, for one) will truncate the email version if it is too long, based on their internal settings.

Last week’s Arrow pushed the limit on the number of characters I can use in my own platform. As I mentioned, I had to go back and rejigger and delete some previous text, so I could finish what I was writing. I’m sure I exceeded the length or character limit for a bunch of email programs.

If you look at the upper right corner of the email version, you will see a link that says Read Online. I’ve got it circled in red below. Simply click on that, and you’ll be taken to the web version.

If you want to go back and read the truncated part of last week’s Arrow, click here, and you will be taken to the online version.

I have no idea why some email providers limit the length and others don’t. I had MD check hers—she is a faithful subscriber—and, sure enough, hers was truncated. That’s Gmail for you. She has used it forever. We both got Gmail accounts back when you had to be referred from someone who already had an account. We got referred from a Google exec probably 20 or more years ago when we met him at a Renaissance Weekend (do they still do those?).

I got an address just to get one, but I didn’t like it. I thought the ads that popped referencing things you had written in the email were creepy. Plus I had another email provider I really liked. MD hated the email provider she had, but she fought transferring to Gmail, which she finally did and has used it since as her personal email. She is strange in that she has to “make friends” with something new like that before she will use it. Once she does make friends, she never wants to give it up. (Which is probably why she hasn’t abandoned me yet.) I’ve tried to wean her off Gmail, but nothing doing.

Speaking of emails…

What with all the travel thrown in, this has been a brutally busy week. Consequently, I am terribly behind on emails from readers. I’ll try to catch up this weekend.

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Ex-NY Times Reporter Gets Darwinism All Wrong

I’ve always kind of had a soft spot in my heart for the former NY Times reporter Donald McNeil, Jr. since his being unceremoniously dumped by the paper where he had worked for 45 years. But some of his latest writing on Medium are changing my mind.

He had been on the science beat at the Times for years, writing mostly about epidemics, pandemics and vaccines all over the world. He was obviously absolutely all in on vaccines of every kind, but I didn’t hold that against him. I was the same way back when he was writing all those pieces. Ignorance is bliss.

Gary Taubes has been writing a Substack series on the job of scientific journalism, which is to understand the science and report it accurately to the lay reader. Gary points out that the scientists know much more about the science than do the journalists writing about it, but all good scientific journalists should be able to read a study and know if it was done well or done poorly. And not simply parrot whatever the authors who wrote it want people to believe about it.

At that McNeil fell down, at least in my estimation. He is a big believer in every vaccine that comes down the pike. Were he a good scientific journalist, he would have delved into the methods followed in the vaccine studies and realized there were no placebos involved. That all the vaccines were tested against previous versions of the vaccine under consideration or of even non-related vaccines. But not against placebo. Which is the only way any drug or vaccine can be shown to be more beneficial than harmful.

His job should have been looking into how the vaccines were tested.

I won’t go into his downfall. He’s written about it extensively (linked below), so I have nothing to add other than my opinion that the Times erred in getting rid of him. He was being accused of racism, so he emailed Nikole Hannah-Jones, the woman at the Times who created the 1619 Project. Since he was being accused of racism, McNeal wanted to discuss his situation with her. He reached out to her to meet him in person.

Before she could get back to him, his situation re his bosses had deteriorated to the point that he had hired an attorney, who, of course, told him not to speak to anyone.

When she did get back to him, he emailed her and told her he wouldn’t be able to meet about what he wanted to meet her about, but that he would love to get together after the whole brouhaha had passed.

This is the Covid vaccine he’s talking about because this all went down in February, 2021 when the vaccine roll out really began. You can see where his head is vaccine-wise.

I think he got screwed in the whole thing, but if you live by the Woke, you die by the Woke. If you want to read his story, he wrote it shortly after the whole affair was over and it was much on his mind. The first part is here, and he has a link to get to the second part and on down the line. It’s worth reading just to see how treacherous some people can be. Especially Woke people.

Since I felt bad for him over all of this, I’ve kind of kept up with his Medium writings, though not as much lately.

A few months ago, he came up with one that really got my attention titled “Whatever RFK Jr. Does, Darwinism Will Undo.” It’s been hanging around in my live tabs, because I’ve meant to write on it since he wrote it, but something else kept displacing it every week. Near the beginning of this article, he mentions that he had written another article a month earlier that he had decided not to publish. He then basically said to hell with it, I’m gonna publish anyway. This article is titled “I’m Waiting For One Photogenic Child To Die of Measles” with the subtitle being “A Single Adorable Victim Will Remind Anti-Vaxxer Parents What Is Really At Stake.”

The first article came replete with a photo from the CDC of a kid with measles, which looks absolutely ghastly to people who have never seen anyone with measles.

For those of you who have been reading me for a while, you’ve seen the many charts I’ve posted showing how deaths from measles had dropped to almost zero before the measles vaccine came into use. (You can search back over the last few issues of the Arrow to find these charts if you haven’t seen them.)

As I’ve written dozens of times, I lived through the measles as did every kid I knew. Measles is a highly contagious virus, but it isn’t really deadly any longer because of Darwinism, sanitation, and better nutrition. Had the measles vaccine not been developed 62 years ago, measles would probably be much like the common cold today in terms of severity.

Viral diseases attenuate over time, which is why I mentioned the word Darwinism above. Viruses, like all of us, want to be able to reproduce and thrive. In order to do so, they mutate in a way that makes them less virulent. It’s called attenuation. Why do they do this? Because it is a survival strategy for them.

If a virus is deadly, it kills its host. And dies with the host. When the host dies, so does the virus. If the virus mutates in a less virulent direction, the disease it causes is less severe and the host survives to pass along the virus to others. If the virus mutates to such a point in which it makes the host barely ill, the host will go to work, school, wherever and spread the virus.

The other part of the mutation strategy is to make the virus more infectious. If the virus mutates to the point where it barely causes sickness and is highly transmissible, that is true viral Nirvana. That is what viruses live for.

Given how quickly measles deaths decreased up until 1963, at the point when the vaccine came into use, imagine how much it would have attenuated over the next 62 years. A measles infection would probably be almost unnoticeable today. Add to the attenuation the better sanitation and improved nutrition (though that is questionable over the past few decades), and measles would probably be a nothing disease by now.

Would a few children have died over the course of the last 62 years? Of course they would have. But how many would have been saved by not getting the vaccine, which doubtless killed some kids. That’s the unknown, and it’s unknown because—as with all vaccines—there were no placebo-controlled trials.

The vaccine situation reminds me of the philosophical enigma the ethicists love to bat around called the Trolley problem. Here’s how it is laid out.

There is an out of control trolley barreling down the track, headed straight for five people who don’t see it coming. If no one intervenes, the trolley will kill the five people. But you, who see the trolley screaming ahead are right beside a switch. If you throw the switch, the trolley will divert on to another track that has just one person standing on it. If you throw the switch, you will end up killing one person who was not in harm’s way before you diverted the trolley. If you let the trolley continue down its path, five people will die, if you don’t play a role in the whole affair. What do you do?

Do you personally kill one person to save five who would have otherwise died? Or do you let nature take its course and kill five, but your hands are clean of murder?

This is precisely the position we are in with vaccines. Except that the trolley is flying down the track, but we don’t know which track the five people are on or which the one person is on. We could be killing the five while letting the one live. Or it could be just the opposite. Problem is, we don’t know without a placebo-controlled trial.

We know that measles has pretty much been eliminated. But we don’t know if that’s a good thing or a bad thing. Perhaps a measles infection primes our immune system in a certain way that provides immunity against other problems. We’re clueless.

There are a handful of studies out there done by physicians who looked at patients in their own practices and followed up on later diseases in those who were vaccinated and those who weren’t. In every one of these studies, those kids who didn’t get the vaccines had fewer office visits, fewer trips to the ER, and fewer serious diseases (and even less ADHD) than kids who were vaccinated.

But those are not randomized-placebo-controlled trials. The subjects aren’t randomized. Perhaps parents who choose not to get their kids vaccinated keep cleaner homes, and provide more nutritious meals, and are nicer to their kids. We don’t know, because these studies aren’t randomized.

We know all drugs have side effects, including vaccines. Drugs other than vaccines have to go through extensive placebo-controlled trials monitored by the FDA to ensure that the drugs do more good than harm. But that doesn’t apply to vaccines, because they aren’t tested against placebo. We know only that they are no more harmful than the vaccine they were tested against, but we don’t know whether they are more harmful than not getting the vaccine at all.

This is the kind of serious journalism Donald McNeil should have been doing. Instead he has become a shill for the vaccine manufacturers, which isn’t a journalistic endeavor at all. And he has the balls to be pissed off and invoke Darwin when people are skeptical about the vaccines, because they haven’t been thoroughly tested. We don’t know which track the train is headed down, so we can’t make intelligent decisions.

Unfortunately, a child died in Texas from the measles over the past few days. I’ve tried to find the details, but I haven’t had any luck. I did go to the Texas Department of State Health Services (DSHS), to see if I could find any details, but no luck.

The report I did find said “the school-aged child who was not vaccinated was hospitalized in Lubbock last week and tested positive for measles.”

We don’t know the cause of the hospitalization. Was the kid immunosuppressed? Did he/she have other serious problems? Was the hospital admission for something else, and they tested for measles? We don’t know, but given what I know about the measles, I doubt this was a healthy kid who caught the regular measles.

The report from the DSHS was totally bogus.

The total ignorance about measles stuns me until I remind myself that most of the people alive today have never actually seen a case of the measles. You would have to be in your late sixties to have seen measles in its prime. When I was a kid, every kid got the measles. It was no big deal. You didn’t even go to the doctor. All you got was two weeks off school until the spots went away. The paragraph above is totally false, at least as it was for the measles 62+ years ago.

The idea that one in five people would require hospitalization is ludicrous. My family moved around a lot. I went to 12 different elementary schools, so I saw a lot of measles. No one that I knew ever went to the hospital. I never heard of anyone getting pneumonia from the measles. You ran a fever for the first few days and felt kind of punk, but nothing even approaching how bad you would feel with the real flu.

Once you got past the first couple of days, you were golden. You still had the rash, and you felt normal, but you couldn’t go back to school.

Now I’m not saying no one ever died of the measles, because I’m sure some kids did. Nor am I saying there was never a case of pneumonia caused by the measles, because there probably were a few. But nothing even in the ballpark to what the DSHS paragraph quoted above said. Unless, of course, they are getting their stats from undeveloped countries where kids are still undernourished and living in squalor.

Once you got the measles, you were immune for life, which is not the case with the vaccine. It can fade, requiring you to continuously get revaccinated.

Now, one of the things that I don’t know about the current outbreak of measles is how the virus might have mutated thanks to the vaccines. It’s possible that the vaccines have driven the mutation in a more virulent direction. That, as I say, I don’t know.

But having lived through the measles along with four siblings and God only knows how many friends and schoolmates, I can tell you it just isn’t that bad. [The Bride agrees re her siblings and school.]

And since we’ve never had placebo-controlled studies, we’re all dealing with the Trolley problem. Given his exalted perch at the NY Times, if Donald McNeil would have done his job journalistically, perhaps it would have driven the drug companies and the regulators into performing the proper studies. Instead, he opted to shill for the vaccine manufacturers.

I’m going to keep my ear to the ground about the kid from Texas to see if I can learn anything more. If I do, I’ll report back on it.

Is Lard Making a Comback?

In an effort to keep up with British politics, which fascinates me, I read The Spectator regularly. Imagine my surprise when last Sunday I came across an article about lard. An article about lard, no less. It is headlined In Defence of Lard: It’s Time to Look Beyond Butter. (Link here; Archive here if the link doesn’t work.)

At the top was a giant picture of the stuff itself.

It’s a short article. Here are some highlights.

What they didn’t mention in the article is that there are two types of lard. There is regular old lard, which is just the fat from the hog rendered into lard that same way beef tallow is come by. Then there is leaf lard, which is more delicate and doesn’t have much of a taste. Leaf lard is the one used for baking.

If you are faint of heart, you should probably skip on down beyond the photos.

Here is yours truly starting the butchering process after the hog has been scalded and had the hair shaved off with a knife.

The regular lard comes from fatty parts of the hog that are sliced off of the meat. These chunks are rendered until they resolve into a yellowish liquid. You pour it into jars and let it cool, and when it does, it turns pure white. The bits of meat left in the bottom of the rendering pan are called cracklings, and they are delicious to eat.

Leaf lard comes from the fat inside the abdominal wall of the hog. Below you can see the slick white rolls of fat before it is removed.

The leaf lard is removed by tearing it away with a set of hands. The photo below shows MD removing the leaf lard.

You render the leaf lard the same way as the regular lard, but it sets up even whiter—if that is possible—than the regular lard.

You probably now know more about lard than you ever wanted to know, but it is a great product. Problem is, it hasn’t reached the mainstream in the US as it apparently has in the UK. Which is a shame. Given the price of butter, lard at a quarter of that would be nice.

I have found it at Hispanic grocery stores, but never at the regular grocery stores.

I hope a lard revival is in the future in the US, because it is great stuff.

More On My Ketogenic Quest

I’m pretty sure I’m closing in on why my blood sugar is what it is. I’ve gotten a bunch of emails and comments telling me that I am insulin resistant as a consequence of eating all the fat I’ve been eating. And that my protein is turning to glucose via gluconeogenesis, and that my glucose is then elevated because of the insulin resistance. A few people have termed it physiological insulin resistance, which is what a lot of people call it. But it’s not.

The definition of insulin resistance is a state of reduced responsiveness to normal circulating levels of insulin. In other words, normal levels of insulin don’t get the job done of moving glucose out of the blood and into the cells—mainly muscle, fat, and liver cells. When the glucose isn’t moved from the blood, the elevated blood levels keep putting in the call for more insulin. The pancreatic beta cells release more insulin, which helps a bit, but not completely. The call for more insulin goads the pancreas to secreting even more. The increased insulin levels further impair the insulin receptors, and glucose levels go up. It ultimately reaches the point at which both insulin and glucose levels are greater than normal. A state best avoided.

That is insulin resistance. Elevated insulin, elevated glucose. You need to have both for a diagnosis of insulin resistance.

What I and other ketogenic diet followers have experienced is elevated glucose levels in the face of low insulin levels. Our insulin is working fine, and our levels are normal to low. This is not insulin resistance.

In delving into all this, I went back and read some old papers on early man’s carnivore diet and how it caused ‘physiological insulin resistance’ in an effort to provide glucose for the brain and other glucose-dependent cells.

The most recent of these papers titled “The Carnivore Connection Hypothesis: Revisited” was published in 2011. Two of the same authors had published two other papers on this same subject years before, so this one was an update.

Here is how the paper starts.

Based on readings I’ve done since 2011 (the pub date of the paper in question), it appears that meat eating predated Homo habilis, and extended back to Australopithecus. But that doesn’t really affect our story.

The authors continue.

This is not so. For a diagnosis of insulin resistance—even an historical one—requires elevated insulin levels. I seriously doubt our ancient progenitors were insulin resistant. I would bet they had low insulin levels.

The very next sentence after the one above is the kind of thing I hate to find in the scientific literature, because it just confirms to me that I always have to look up the reference to see if it truly corroborates the point the author is making.

In a well written scientific paper, you construct your case statement by statement, with each one building on the one before it. Each of these statements is usually referenced to a paper or papers that substantiate the claim made.

Careful readers of the literature go back and check these references to ensure they really corroborate the statement in the paper being studied.

All too sadly, often they don’t. The very next sentence in the paper is a case in point.

Here is the important part: “a low-carbohydrate, high-protein diet increases insulin resistance,…”

I knew this couldn’t be true, so I pulled the referenced paper, which was titled “Effect of long-term dietary protein intake on glucose metabolism in humans” and was published in 2000.

If you read this paper carefully, you’ll find that it does not support the statement above in the referring paper. Let’s take a look.

The authors don’t go into any detail on how and where they recruited the subjects, but apparently they asked a group of potential subjects to record all their food for seven days. Then they went through the surveys and harvested all those who were either consuming ~1.9 g of protein per kg body weight (those would be the high-protein subjects) and those who consumed ~0.8 g protein per kg body weight or below (the low-protein subjects).

(As an aside, in the graphic down below, you’ll see the term “probands” at the top. I went through the paper trying to figure out what a proband was. It was mentioned just a couple of times, but without definition. I assumed from the context that it meant subject of a study, but I didn’t know for sure as I had never encountered the word. I looked it up, and sure enough, it means the subject of an experiment. I’ve probably read more scientific studies than 99.9 percent of people alive, and I’ve never seen or heard the word used before this. This is a study from Germany, so they may have just looked it up in an English/German dictionary and figured it was how we say “subject.”)

Once they got their two groups of probands (last time, I promise), nine in each group, which were matched for age, sex, and calorie intake, the researchers began evaluating them for insulin secretion, glycogen turnover, and gluconeogenesis.

Without getting into all the technicalities involved in determining the outcome, here is what the researchers found as described in their conclusion.

Maybe the folks who wrote the original paper and referenced this one just looked at the abstract and thought, well, there you go, high-protein diets stimulate insulin release and gluconeogenesis.

That is what the data from the study show, but you’ve got to look a little deeper into these things, especially if, like me, you don’t believe a word of it.

How on earth did they come up with this finding?

If you simply look at the graphic showing the diets of the two groups of subjects, it easy to see how. Take a close look to see if you can spot the problem before skipping on down.

Did you see it? l’ve identified it in the same graphic shown below with the red line.

This study was looking at what happens with a more or less standard diet that contains a lot of protein. Whenever you’ve got four variables—as you do in this study: protein, fat, carbohydrate, and calories—you can’t change one without impacting the others.

Those on the high-protein diet were also consuming 2.31 g of carb per kg. If you use the standard 70 kg person, that calculates to ~162 g of carbohydrate, which is far from a low-carb diet in anyone’s estimation. If you take me, for example, at ~86kg, I would be eating almost 200 g of carbohydrate.

If we go back to the original paper citing this reference, the line referenced says “Long-term consumption of a low-carbohydrate, high-protein diet increases insulin resistance,…”

The paper they cited definitely did not corroborate.

Just for grins, I looked at the next paper they cited for the completion of the above sentence. Here is the complete sentence with the references.

Reference #20 is the one we just discussed above, the one showing what happens with a high-protein, high-carb diet. The next reference, #21, is to an article titled “Effect of dietary protein on in vivo insulin action and liver glycogen repletion” published in 1989. It’s behind a paywall, but as it turns out, I have a copy I must have gotten long ago, but don’t really remember it now.

Unfortunately, this is a rat study, not a human study, so we have to be careful what conclusions we draw from it. But there is one graphic that, in my view, at least, tells what’s going on in humans on high-protein, low-carb diets.

The above represents a ratty glucose tolerance test. And it shows pretty much what would happen during a human glucose tolerance test. The broken lines represent the rats on a high-carb, low-protein diet, while the solid black lines shows the outcome for the rats with a high protein intake.

I went back and looked at the macronutrients, and, as I mentioned above, when you increase one, you have to decrease another to keep the calories the same. Both the high-protein, low-carb rats and the low-protein, high-carb rats consumed exactly the same amount of fat, but the low-protein, high-carb rodents got over three times as much carb as did the high-protein, low-carb ones.

If you look at the upper part of the graph above, representing the glucose tolerance curve, you can see exactly what is happening to me. The red circle shows a higher pre-test blood sugar level in the high-protein, low-carb rats, whereas the high-carb rats have lower starting blood glucose level.

But after consuming the glucose, the rats on the low-protein, high-glucose food find their blood glucose skyrocketing, while those on the high-protein, low-glucose regimen don’t see theirs go up a lot.

The bottom section looks at what happens to insulin during the test. Both groups start out the same, but those higher-carb rats find their insulin levels going up way more than the low-carb rats. You’ve got lower insulin levels lowering glucose levels even more. That is a sign of vastly better insulin sensitivity, not insulin resistance.

So, this second paper doesn’t confirm what it was supposed to confirm either.

Reading these studies made me go back and reread one of my all-time favorite papers written by a couple of British anesthesiologists.

Titled “Insulin: understanding its action in health and disease” is a masterpiece. It outs a bit of dogma that infected the medical profession for years, and still does.

Eight years before Banting and Best discovered insulin in 1921, Sir Edward Schafer, who was Professor of Physiology in Edinburgh, gave a series of lectures in California during which he predicted a substance he called insuline that turned out to act exactly as insulin acts, though it took years before these actions were all realized. He published a book on the material in these lectures titled The Endocrine Organs. I was so taken with this paper and its description of the book that I tracked down a copy and purchased it. Unfortunately, it is now boxed away with the rest of my library awaiting a new house if all the real estate nonsense and high interest rates come to an end. Otherwise I would show you a photo of it

I cut off the last part of the sentence, because I want you to take the test given to a group of British anesthesiologists in a basic science study section and repeated on countless graduate and undergraduate students. Almost no one gets the correct answer.

Question: is the fasting hyperglycemia of diabetes due to overproduction of glucose by the liver or underutilization of glucose by peripheral tissues?

What is your answer? Why is blood sugar elevated in those with diabetes? A) The liver pumping out too much glucose. Or B) Are the cells unable to take the glucose in because of lack of insulin to drive it into the cells?

If you are like the vast majority of doctors and others to whom the question was asked, you’ll answer B. The cells are unable to take up the glucose.

The real answer is that the liver is pumping out way too much glucose.

What Professor Schaefer figured out—even though insulin had not yet been discovered—was that it had two functions. One was excitatory and the other inhibitory. And of the two, the inhibitory was by far the stronger.

If the liver is left to its own devices it will pump out sugar like crazy under the stimulus of glucagon, insulin’s counter-regulatory hormone. But if insulin is acting properly in the right amounts, it inhibits glucagon’s actions and the liver quits pumping out glucose.

Insulin’s excitatory actions should drive excess sugar into the cells, but since that is a weak action, insulin doesn’t do a lot in terms of driving glucose into the muscle and/or fat cells. Insulin enters the cells via GLUT-4 transporters, which are on the surface of the cell and pull the glucose in. Insulin doesn’t play much of a role in this process unless levels are really high. Then it will move some glucose into the cells. But mainly the sugar gets in without a lot of help from insulin.

Insulin’s main job is to shut off the sugar pump in the liver, and it does so by tamping down glucagon.

The liver produces glucose from protein (the glucogenic amino acids) and from the glycerol backbone of triglyceride molecules that are broken down from fat to head for the Kreb’s Cycle.

So where would this leave us in my situation and that of all the others who have been on ketogenic diets and experienced a rise in blood sugar levels? Not a massive rise, but a jump from the normal 70-80 mg/dl up to 90-100+.

If we are eating almost no carbs, we are not running up our insulin levels. The insulin levels go high enough to prevent the liver from pouring out glucose. An inhibitory action. But it doesn’t get high enough to drive glucose into the cells. An excitatory action, which is insulin’s weakness. But low insulin levels don’t really inhibit lipolysis, so fat is pouring out of the fat cells and gets burned or taken up by the muscle cells.

Increased fat in the muscle makes it more difficult to drive glucose in. If we’re consuming a lot of protein with our ketogenic diet, we’ll be converting some of it to sugar simply because it has nowhere else to go. The muscles take some of it up, but they can only make so much new muscle, and if they’re overwhelmed with protein, it ends up getting picked up by the liver and converted to sugar or even fat, which is cycled back out if insulin is low.

So under this scenario, what you would expect to see in terms of glucose and insulin levels in a blood test?

I would expect to see blood glucose running a little higher than normal and a low insulin level. And even though blood glucose may be a little high, I would expect a low HgbA1c, because there would not be wide fluctuations in the glucose level. Look again at the glucose levels from the rat study discussed above.

The fasting glucose is a little high, but the levels never get as high as those on the rats with the high-carb diet. Same with insulin.

Along with a fasting blood glucose that is a little high, you would probably see a low to normal insulin level. And if you were seriously on a ketogenic diet as I have been, you would expect to see a low HgbA1c since glucose levels have not been going up and down like a rollercoaster.

While MD and I were visiting my doctor friend, I had him send off some labs for me.

Here they are:

• Fasting glucose: 99 mg/dl

• Fasting insulin: 6.4 uIU/ml

• HgbA1c: 4.8

When I calculated my HOMA, a measurement of insulin resistance, it came out to be 1.56. Anything below 2.0 is in the not-insulin-resistant territory. So I definitely do not have insulin resistance.

I’m about to run out of words again today, so I better cut this off. I may pick it up a bit next week. I’ll continue noodling on it all, but I feel much better about things now that I’ve had some labs done, which results comport with my thinking.

Odds and Ends

• Study finds evidence linking the intake of small fish, eaten whole, with a reduced risk of all-cause and cancer mortality in Japanese women. I don’t doubt it.

• The tree of Old World languages. Very cool thing to contemplate.

• Incredible X(Twitter) thread on how productive AI can be if the right prompts are used. And how proper prompting can generate 65-100 page reports filled with good info.

• Another X(Twitter) thread showing how you can’t really trust the results you get even if you use a great prompt.

• How dirt paths and hashtags reveal a population's desires. I’ve known about these conceptually for a long time, but I never knew they were called desire lines.

• If you want to know more about how AI works, read this article by Stephen Wolfram. It’s the best detailed description I’ve read yet, but it gets way into the weeds.

• The ancients used asphalt (bitumen) for countless purposes. As sealants, adhesives, mortar, incense, pigment, and on and on. And all along, I thought it was a relatively modern thing.

• Alan Turing, one of the early pioneers of computer science and the man who cracked the Nazi’s Enigma Code was also an accomplished runner, who almost qualified for the Olympics.

• It's so cold in Minnesota, satellites think the Midwest is a cloud. Which is one of the many reasons (mosquitos) I don’t live there.

• Research discovers that ancient seafarers of Asia built sophisticated boats 40,000 years ago.

• What if farming was not the catalyst to build civilization as we once thought. Perhaps it was born of necessity when traditional hunting and gathering became untenable. There are plenty of examples of reversions to hunting when farming didn’t work out.

• Analysis of an archeological site in Sweden found pretty severe dental disease to be rampant in 10th-12th century Vikings. At least at that site.

• Revealing story about how one man greatly reduced his medical bills.

• Cells seem to “figure out” solutions to new problems, sometimes in ways scientists can’t yet explain. What if science could harness this healing ability to repair, or even regenerate tissues and organs.

• Cannibalism was surprisingly common in medieval Europe.

• Universities failed us during the Covid pandemic. By not having honest debates about the NIH funding, universities are falling short once again.

• Patrizia Cavazzoni, former head of FDA’s drug center, joins Pfizer as chief medical officer. This is the problem. May be regulatory capture in spades. Was she working for Pfizer while at the FDA and is now being rewarded? That’s how those things usually go. I just discovered she worked for Pfizer before joining the FDA. Hmmm.

• Here’s another. Former Energy Secretary Jennifer Granholm gave California utilities $600M, now she'll sit on their boards. Is this a reward?

• I put the Patrizia Cavazzoni entry above a couple of days ago. I didn’t really do a deep dive on her record, but Alex Berenson did. And it’s worse than you might imagine. The very definition of the revolving door. You can see why things never change.

Newsletter Recommendations

Video of the Week

Today’s VOTW is an old, old one. From way back when I was in college. There was a TV show then that, as I recall, was the most popular show on the tube for a few years running. It was Rowan and Martin’s Laugh In. I was never much of a TV watcher as a kid, but I figured out a way to always catch Laugh In. It was all anyone talked about the next day.

One night I was watching it and they brought on this singer named Tiny Tim. It was without doubt the weirdest thing I had ever seen. So weird it was kind of creepy. But Tiny Tim’s appearance on Laugh In launched a huge career for him for a few years. He was on every show on TV. He even got married on the Johnny Carson show.

Talk about a rocket ride. Miss Vicki ditched him. And he died young. A tragic story, really.

But you just never know what will tickle the public’s fancy and rocket someone to stardom. I would never have believed it would happen to Tiny Tim, aka Herbert Butros Khaury (1932-1996).

Time for the poll, so you can grade my performance this week.

That’s about it for this week. Keep in good cheer, and I’ll be back next Thursday.

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This newsletter is for informational and educational purposes only. It is not, nor is it intended to be, a substitute for professional medical advice, diagnosis, or treatment and should never be relied upon for specific medical advice.

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