The Arrow #176

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Hello friends.

Greetings from Fayetteville, Arkansas.

We’re up here for the graduation of our grandson, Will. And here is the happy graduate. Happy to be out of school, that’s for sure. But not all that happy to give up the college experience. Many purveyors of various alcoholic beverages will lament his absence.

Aside from all the other festivities, I was able to visit one of my favorite steak houses in the world: Doe’s Eat Place. It is incomparable. Here is my steak last night. It was a T-bone, which is sold by the pound, not by the ounce. The smallest, which is what I ordered, is the one-and-a-half pound version. Here it is with all the trimmings.

it doesn’t look as big in this photo as it did in the flesh, but it was a whopper. Perfectly cooked and seasoned. I couldn’t eat it all, so I had the rest of it for lunch today.

One last thing before we move on. Marvel at how I haven’t whined about the platform. Everything seems to be working as it should. All appendages crossed.

Okay, off to the important stuff.

Physiological Insulin Resistance & Low-Carb Diets?

One of the questions I get asked over and over from people on low-carb diets is about increased blood glucose levels. Everyone thinks low-carb diets should lower glucose levels, not elevated them. And those who find their glucose levels going up often become concerned.

For example, here is an inquiry that came through as a poll response. This is pretty typical.

BTW, KETO for 4 months, averaging 36g carbs/day, yet fasting panel showed 105mg/dl glucose???? How is that possible? And on a different day, 4 hrs after 12g net carbs, 70g fat, and 53g protein (asparagus & ham quiche), it was 117. Thanks in advance for answering that.”

What can be happening here? A low-carb diet is by definition low in sugar and other carbs, so how can following such a diet make blood sugar go up?

If you start reading on the subject, you’ll find many low-carb aficionados say it is a function of physiological insulin resistance. But is that really the case? Low-carb diets are known to improve insulin resistance, so how could such a diet both improve insulin resistance and cause it?

The insulin resistance that develops when we become overweight and perhaps glucose intolerant is called pathological insulin resistance. Pathological implies a disease process, which this type of insulin resistance certainly is.

The “physiological” of physiological insulin resistance is defined as a normal process. In other words, physiological insulin resistance would be defined as something that happens in the normal course of life. But there are only two times in life that true physiological insulin resistance takes place: During pregnancy and during puberty. It occurs during both pregnancy and puberty due to hormonal changes helping to facilitate important biological processes during these particular life stages.

Physiological insulin resistance during pregnancy is probably the most studied case. It takes place to basically increase maternal glucose so more can be shunted to the growing fetus. There are probably other reasons as well, but pregnancy is not my area of expertise.

Puberty is another area of medicine in which I’m not all that well versed even though, unlike pregnancy, I did personally experience it. And have the psychic scars to prove it. Physiological insulin resistance in puberty occurs in an effort to increase the nutrients required for the puberty-induced growth spurt.

As far as I know, these two situations are the only instances of true physiological insulin resistance.

When people with pathological insulin resistance go on low-carb diets, their insulin levels almost always go down. Their insulin resistance improves. So they don’t really have physiological insulin resistance, rather they experience improvement or the cessation of pathological insulin resistance. They become less insulin resistant and more insulin sensitive. And it happens fairly quickly.

So, if people are more insulin sensitive after being on a low-carb diet for a bit, why would their blood sugar levels increase?

It’s complicated, so in an effort to stay out of the deep weeds, I’m going to more or less broad brush what’s going on. Just to give you a taste of how complicated it is, take a look at the two graphics below. We’ve all seen the simplified version of what an insulin receptor looks like. Here is a more complex picture.

The above shows all the known components of the insulin receptor. Now let’s take a look at the various actions of the insulin receptor.

I have circled in red the action of the insulin receptor we’ll be discussing, i.e., its recruitment of the GLUT-4 glucose transporter.

Most people think that the only way glucose can get into the cells is by way of insulin stimulation. This is not true. Glucose can passively enter the cells based on its concentration in the blood. Mice that have had their beta cells (the cells that make and release insulin) destroyed can still function just fine as long as their glucagon production can be suppressed.

I have a nice video that I’m unable to embed here of such mice scampering about with normal glucose levels. In the same video there are other mice with destroyed beta cells yet with normal glucagon, and these mice are extremely ill. The ‘healthy’ ones without glucagon or insulin are able to use glucose just fine. (One of my complaints about this platform is its inability to let me embed MP4 videos.)

Although glucose can get into the cells on its own, to really drive it in there quickly requires some insulin. Insulin, acting through its receptor, brings GLUT-4 to the surface of the cell and transports the glucose out of the blood into the interior of the cell. Here is a short video (~1 minute) showing how this works. (Sorry in advance for what sounds like baby talk by the narrator—it was just the shortest comprehensive video I could find.)

Now let’s think about what happens during a ketogenic or low-carbohydrate diet.

There are really two fuels for the cells: fat and carbohydrate. Protein can be used as a fuel, but the body would prefer to burn the other two first, saving the protein as a raw material for structural components.

If you eat a lot of carbs, everything works as expected. The carbs are broken down into glucose and absorbed into the blood. Blood sugar goes up triggering insulin release from the beta cells in the pancreas. Insulin then goes up and recruits GLUT-4 (as shown above), which transports the excess blood sugar into the cells.

It works differently when fat is the primary fuel, as it typically is in the low-carb diet. The dietary fat goes into the muscle, where it can be burned for energy. The liver generates some ketones as well, which can also be burned for energy and act as a substitute for glucose in the brain and other tissues.

The ketones and the fat tend to block insulin’s recruitment of GLUT-4, so there isn’t a rapid transfer of glucose into the cells. Here is a graphic from a paper showing this nicely.

The above graphic is from a journal article* about how ketones and palmitic acid (a saturated fat) block the action of insulin in terms of recruiting GLUT-4. The red columns show how much insulin generates GLUT-4 under various conditions.

On the far left LP stands for low palmitic acid in the cells. As you can see, insulin is able to stimulate a lot of GLUT-4 transporters as compared to basil (the situation with normal circulating insulin). The middle labeled HP (high palmitic acid) shows virtually no difference in GLUT-4 recruitment than under basal conditions. The right labeled 3HB (3-beta-hydroxybutyrate; a ketone) shows the same thing.

What this means is that elevated fat and/or ketones in the muscle more or less blocks insulin from bringing GLUT-4 to the cell surface where it can grab glucose and transport it into the cells.

It’s not really insulin resistance as much as it is insulin interference. But the important thing is that it doesn’t raise insulin levels. People on low-carb diets almost always see an improvement in both insulin sensitivity and insulin levels. And, surprisingly enough given the sometimes elevated blood glucose levels, they see lowered HgbA1c levels.

Pathological insulin resistance usually manifests in just the opposite: Higher HgbA1c and high insulin levels.

The only time people on low-carb diets run into issues with this normal situation is if they take a glucose tolerance test. When they do so, glucose levels often shoot into the diabetic range, causing consternation to both patient and physician.

And this is the reason people following low-carb diets are told to load up on carbs for two or three days before taking a glucose tolerance test.

If you are on a low-carb diet and are worried about the elevated blood glucose you might find when you test yourself, I suggest you get a HgbIAc test and/or a fasting insulin. The results should rid you of any anxiety you may have.

*This journal article is about heart muscle cells not regular muscle cells. And it takes a negative view of fat and ketones blocking insulin from recruiting GLUT-4. There are other articles out there with a different viewpoint, but this one had the graphic I liked best.

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

Canceled for Teaching Critical Thinking

I find the short video below absolutely stunning for two reasons. First, given the sorry state of education these days, I’m surprised that there exists a teacher who would engage in a Socratic dialogue with a student. And second, I’m flabbergasted that such a teacher would be fired for doing so. It is breathtaking. I would have killed to have had a teacher like this when I was i high school. (I came across this guy on Elon Musk’s Twitter feed.)

This guy should get every teaching award available, but instead he got canned from his job. Some more enlightened school will be lucky to have him.

Here’s what he has to say about it.

I find this absolutely incredible. This is just the kind of guy we need teaching students. Although I don’t know for sure, my guess is that this guy got canned not for teaching critical thinking, but for the particular subject matter he taught critical thinking about in this video. That’s what comes from DEI and wokeness, both of which should be banished. In my view, at least.

I just found this, but I’ve been unable to find anything out about this guy. I’m as terrible in searching social media, Reddit, and the like as I am good at searching the scientific literature. If anyone knows anything about this person, enlighten us all in the comments. I, for one, am really curious.

AI Now. Not in the Future, but Right Now

The video below is mind blowing. At least it blew my simple mind. I had no idea artificial intelligence has come this far. If this video isn’t some hyped up version of fake AI that really doesn’t exist, then I am worried. If it is a true representation of the state of the art, then we, my friends, are in trouble.

If we call customer service, we’ll never know if we’re talking to a human or to an AI bot (or whatever the proper terminology is). Same for government agencies, poison control centers, and God knows what else.

Just give this video a watch. It’s almost 30 minutes long, but the last five or six minutes are an ad for the service. All you have to do is watch about ten minutes to get the idea as to what our future holds. Assuming, of course, that this works as advertised.

This is apparently available to us all today for a fee. I kind of wish I could pay to make it go away.

Let me know what you think in the comments. Am I overreacting?

What Nutrition & Climate Science Have In Common

Gary Taubes wrote a terrific Substack piece a couple of days ago I would like to share with you. The article, titled “The scientist activist problem,” has the subtitle “What nutrition and climate science have in common,” which I co-opted for my title of this section.

In this article, Gary tells how on a trip back from a lecture he had given he grabbed a novel to read on the flight home. The novel happened to be Michael Crichton’s techno-thriller State of Fear, which I read myself years ago. The book, which is excellent, is Crichton’s novelization of what he saw as the perversion of science in the furtherance of a faulty theory. In this case climate change and its forerunner global warming.*

In reading the book, it dawns on Gary that he, himself, had been experiencing the same situation in current nutritional science that he was reading about in Crichton’s book.

In both fields, researchers come to conclusions very early in the game about the likely causes of a potentially critical issue of public health – a warming climate in one case, diet-induced heart disease in the other. In both fields, these preconceptions evolve into a consensus narrative despite the absence of experiments rigorously testing their validity. In both, this compelling narrative of cause and effect disseminates through the field, adopted by other researchers and institutions, and evolves into the only politically acceptable conclusion of all research. These narratives, after all, inform our understanding of what must be done to save humans lives; they become impossible to challenge, resistant to all contrary evidence. In short, the existence of an initial preconception about a “right answer” to these critical questions, biases all the science (and policy) that follows.

Gary discusses and links to an article written in NPJ Climate Action by a climate scientist titled “The importance of distinguishing climate science from climate activism”.

The article, which is well worth reading, discusses how many climate scientists have become climate activists, which brings their scientific credibility into question. Gary suggests reading the article and every time the author “uses the word climate, replace it with nutrition, and you will have the exact issue we confront in our field.”

It’s an enlightening exercise. You should try it. Doing so shows what we’re up against.

As I wrote above, Crichton’s State of Fear is an excellent read, but if you don’t want to read or don’t have time to read a great edge-of-your-seat thriller, then give his famous Caltech lecture a go.

On September 17, 2003, Michael Crichton delivered what I think is a splendid lecture at the California Technology Institute. Titled “Aliens Cause Global Warming,” the wide ranging talk includes a few paragraphs that are gold.

It was a time of widespread fear and uncertainty, but even as a child I believed that science represented the best and greatest hope for mankind. Even to a child, the contrast was clear between the world of politics—a world of hate and danger, of irrational beliefs and fears, of mass manipulation and disgraceful blots on human history. In contrast, science held different values— international in scope, forging friendships and working relationships across national boundaries and political systems, encouraging a dispassionate habit of thought, and ultimately leading to fresh knowledge and technology that would benefit all mankind. The world might not be a very good place, but science would make it better. And it did. In my lifetime, science has largely fulfilled its promise. Science has been the great intellectual adventure of our age, and a great hope for our troubled and restless world. But I did not expect science merely to extend lifespan, feed the hungry, cure disease, and shrink the world with jets and cell phones. I also expected science to banish the evils of human thought—prejudice and superstition, irrational beliefs and false fears. I expected science to be, in Carl Sagan’s memorable phrase, “a candle in a demon haunted world.” And here, I am not so pleased with the impact of science. Rather than serving as a cleansing force, science has in some instances been seduced by the more ancient lures of politics and publicity. Some of the demons that haunt our world in recent years are invented by scientists. The world has not benefited from permitting these demons to escape free. [My bold]

We have all too recently seen how “science…has been seduced by the more ancient lures of politics ad publicity” in the whole Covid-19 pseudo-pandemic exercise. The Science, indeed. Remember how Fauci, Walensky, Birx, et al kept referring to the “scientific consensus”?

Here is what Crichton says about scientific consensus in his talk. (And remember Crichton was a graduate from Harvard Medical School, so he’s not just a scientific amateur.)

I want to pause here and talk about this notion of consensus, and the rise of what has been called consensus science. I regard consensus science as an extremely pernicious development that ought to be stopped cold in its tracks. Historically, the claim of consensus has been the first refuge of scoundrels; it is a way to avoid debate by claiming that the matter is already settled.

Whenever you hear the consensus of scientists agrees on something or other, reach for your wallet, because you’re being had.

Let’s be clear: the work of science has nothing whatever to do with consensus. Consensus is the business of politics. Science, on the contrary, requires only one investigator who happens to be right, which means that he or she has results that are verifiable by reference to the real world. In science consensus is irrelevant. What is relevant is reproducible results. The greatest scientists in history are great precisely because they broke with the consensus.

There is no such thing as consensus science. If it’s consensus, it isn’t science. If it’s science, it isn’t consensus. Period. [My bold]

Truer words were never spoken.

I encourage you to read Gary’s Substack in conjunction with Crichton’s talk. I’ve searched the internet and can’t find Crichton’s talk in its entirety in a link. I’ve found only excerpts. You can find the whole thing in pdf at this link. If I were you, I would download it, because I have no idea how long it will be available in full.

*Funny. When I went to Amazon to get the link for State of Fear, I simply entered Michael Crichton in the search window. Up popped the search term: “Michael Crichton books,” which I clicked. There was an entire listing of all his books…except State of Fear. I had to search for it specifically. It’s just Amazon demonstrating its woke bonafides, I guess.

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Covidistas Starting to Twist in the Wind

We’re finally getting some statements from those who made our lives miserable during the faux Covid pandemic. Some of the statements are under oath, and the makers of the statements are forced to be truthful or lie. Some of the statements are not under oath, but in a public forum. Those statements aren’t always as truthful. Let’s take a look at a couple.

First, that idiot Deborah Birx. I don’t know the woman, but I’m going by what I read from Scott Atlas and what I heard from Jay Bhattacharya. The woman is a dolt. I haven’t read her book, but according to those who have, she admitted to flimflamming Trump during the Covid days. Anyway, I have nothing but disgust for her.

Here she is in an interview with Chris Cuomo, who, himself, was vaccine injured and since being canned from CNN has become red pilled on the issue. She babbles on idiotically but with great conviction (her ability to do this is probably her only asset). If you don’t want to watch the whole thing, go to ~2:45.

She is calling for transparency and a 9/11 type commission to look into the whole fiasco. I suspect were such a commission formed, she would be one of its first victims.

Anyway, Cuomo asks her about the vaccine effectiveness at around the 2:45 mark. Here is what she says about them.

They were very effective for what they were supposed to be used for, which was to prevent severe disease and hospitalization and death. And that’s what the vaccines were studied for in this country. And that’s what they did.

That may be what they were studied for, but that’s not what the studies showed. The published Pfizer study is the only double-blind, placebo-controlled study of these vaccines I’ve seen. And in this study, more people died in the vaccine arm of the study than the placebo arm. The difference did not reach statistical significance, but there is no way on earth it can be spun that the study showed the vaccines “prevent[ed] death,” as Dr. Birx stated.

Also, the study didn’t test hospitalizations or seriousness of disease. It looked at how many people tested positive for Covid in the vaccine group versus in the placebo group seven days after the last of two injections. There were 162 positive cases in the placebo group and only 8 cases in the vaccine group. There were around 20,000 subjects in each group, so the absolute infection rate in the vaccine group was 0.0004 (8/20,000) and in the placebo group 0.081 (162/20,000), which is hardly a major difference. It ended up being 0.04 percent vs 0.8 percent. That’s four one hundredths of a percent in the vaccine group against 8 one hundredths of a percent in the placebo group. I’m not even sure those differences were statistically significant. (I made an error on this in the original post. It should be 0.8 percent as written above instead of the 0.08 percent as I originally wrote.)

But the powers that be sold the vaccines based on their relative risk, not their absolute risk. They divided 8 by 162 and came up with 0.049, which they rounded up to 0.05, and they said the vaccines were 95 percent effective. I pointed this out when it happened. It’s sleight of hand nonsense.

Then, based on this flimsiest of evidence, the grand push began to have everyone vaccinated. And that included the mandates, which were later shown to be unconstitutional.

So, it was all bullshit from the get go. And it made a fortune for the drug companies involved.

How would you like it if the government came to you and said, Hey, we want you to develop a vaccine for us, and we’re going to pay for you to do it. And not only that, once you’ve got it developed (at our expense), we’re going to pay you for each dose. And what’s more, we’re going to force everyone to take it to be able to travel or go to restaurants or whatever. And, finally, we going to indemnify against any lawsuits if the vaccine turns out to be problematic.

Would you take that deal? Anyone would. And the drug companies certainly would. And did.

How about the rest of what BIrx said on the Cuomo show? She said Long Covid is a much worse problem than any supposed vaccine injury. And that many more people have long covid than have vaccine injuries.

Let’s deconstruct this a bit.

If you remember the Cleveland Clinic data I posted a couple of years ago showing the more vaccines employees got, the greater the number of Covid cases.

It was a nice dose-response curve showing the more vaccines the greater the chance of getting Covid.

According to a Pew Research Center analysis the vast majority of Americans were vaccinated with at least one jab. And if more jabs—including just one—end up with more people getting Covid (as the Cleveland Clinic data shows), then it stands to reason that a whole helluva lot more people with Long Covid were vaccinated than non-vaccinated. So maybe Long Covid is a vaccine injury.

Okay, enough on the loathsome Deborah Birx and her idiocy. Let’s look at what Francis Collins revealed in under-oath testimony.

As I’m sure you’ll recall, Francis Collins was the head of the National Institutes of Health (NIH), who famously wrote Fauci in an email about Bhattacharya, Gupta, and Kuldorff being “fringe epidemiologists.” As far as I can tell, Collins went along with the entire scare-mongering plot.

Now that it has kind of blown up, and he is called to task for his part of it, the truth comes out.

He practically swore on a stack of bibles—good Christian gentleman that he is—that there was no lab leak. That was all a conspiracy theory. Now when he’s asked about it under oath, he tells a different story.

Majority Counsel: “All it’s calling for is a “yes” or “no.” Is the possibility of a lab leak a conspiracy theory?”

Dr. Collins: “You have to define what you mean by a lab leak.”

Majority Counsel: “Putting aside de novo, the possibility of a laboratory or research-related accident, a researcher doing something in a lab, getting infected with a virus, and then sparking the pandemic. Is that scenario a conspiracy theory”?

Dr. Collins: “Not at this point.”

Majority Counsel: “We have talked about this an awful lot, I think I know the answer to the question, but I want to ask it. Is the origin of COVID-19 still unsettled science?”

Dr. Collins: “Yes.”

A little switcheroo in attitude I would say. He was so certain before. Remember what Michael Crichton wrote about science.

Here, according to a report from the congressional subcommittee, is how Dr. Collins ended up in the meeting where Fauci got everyone on the same page about there being no lab leak:

Dr. Collins claims that Dr. Fauci invited him to participate in the infamous February 1, 2020 phone call that allegedly “prompted” the public narrative that COVID-19 originated from nature and that vilified the lab leak hypothesis. This testimony directly contradicts earlier statements made by Dr. Fauci.

Majority Counsel: “How were you made aware of this call?”

Dr. Collins: “I was, I think – again, it’s four years ago – initially informed by Dr. Fauci that the call was happening. And then, I think I got this email forwarded about what the agenda was going to be from Dr. Farrar, who was clearly the person organizing the call.”

Majority Counsel: “Did Dr. Fauci ask you to join the call?”

Dr. Collins: “Yes.”

Finally, here is Collins testimony in which he admits that there was no data demonstrating any evidence that six feet of “social distancing” did squat to prevent the transmission of Covid.

Majority Counsel: “Moving on to social distancing and the various regulations surrounding that. On March 22, 2020, the CDC issued guidance describing social distancing to include remaining out congregant settings [sic], avoiding mass gatherings, and maintaining a distance of approximately six feet from others when possible. We asked Dr. Fauci where the six feet came from and he said it kind of just appeared, is the quote. Do you recall science or evidence that supported the six-feet distance?”

Dr. Collins: “I do not.”

Majority Counsel: “Is that I do not recall or I do not see any evidence supporting six feet?”

Dr. Collins: “I did not see evidence, but I’m not sure I would have been shown evidence at that point.”

Majority Counsel: “Since then, it has been an awfully large topic. Have you seen any evidence since then supporting six feet?”

Dr. Collins: “No.”

But he was so certain before. The take home message is to never listen to an entrenched bureaucrat.

The Metabolic Basis of Frailty

I came across what I thought would be a great article in Cell Metabolism, one of my favorite scientific journals. It was behind a paywall, so I fired off an email to the author asking for a copy. Which she duly sent my way.

The title “The intersection of frailty and metabolism” really excited me, but the article itself was a bit of a disappointment.

Everyone in academia wants to get published. And the more publications on one’s CV, the better for promotional and tenure purposes. Publish or perish, as the saying goes.

There are a number of ways to get published. The most important and most difficult is to do original work to sort out some sort of issue. Usually these papers involve randomized, controlled trials that generate valuable data. Unfortunately, there are fewer of these studies published than anything else.

Then you’ve got the observational studies that are next to worthless. They don’t even try to prove causality, though causality is implied in most of them. They are the ones filled with weasel words: linked, associated with, may be, etc.

And then there are the summary-of-work-done papers. The authors of these papers go through the medical literature and find all the work that has been done on a particular subject and summarize it. The paper in question is one of those. It summarizes a ton of papers on frailty and metabolism and the intersection of the two.

We don’t learn anything original in the paper, but it did introduce me to a number of papers I wasn’t aware of. But pretty much all of them said the same thing: dietary protein is essential for preventing frailty. Resistance exercise is extremely helpful.

I did learn a bit that I didn’t already know. For example, I was unaware there was a frailty index. In fact, there are two. These are different ways of being able to put a number to the degree of frailty. These are called frailty assessment instruments.

The first one—in my opinion, at least—is pretty much worthless. It’s called the Frailty phenotype tool and is shown below:

According to this model, a person who shows at least three of these characteristics can be considered frail.

Well, on any given day, I could have all of them except possibly weight loss. and maybe weakness. And I don’t consider myself frail at all. On most days, I don’t experience any of these issues, so I guess they’re talking about most of the time. In my view, this isn’t a very good tool.

The frailty index, on the other hand, I think is pretty good. It takes into account a lot more issues, so is much more comprehensive.

Okay, thank God, based on this one I’m definitely not frail. Which is, I suppose, why I like it more. But other than the gait/posture disorders and poor mobility, it doesn’t really get into what most people think of as frail. The way frailty is determined in this index is by listing all the issues one has, then dividing that by the total number of issues possible in the index (13), which will give a number between 1 and 0. The closer to 1, the greater the frailty.

In my case (if you’re counting cataracts—that and a bit of a hearing deficit, which I’ve had for years thank to a lot of shooting without ear protection in my youth), I have two, so 2/13 = 0.15, which puts me closer to zero than 1. Thank God.

Seems like there could be a better screening tool. Maybe something like How far can you hit a golf ball with a driver? [Or, the bride chimes in: how many burpees can you do?]

Anyway, these are tools used to diagnose frailty. I’m more of the same opinion as the Supreme Court justice years ago who famously said about pornography: “You’ll know if if you see it.”

We all pretty much know if we or others are frail. It’s really pretty easy to tell.

But people who write papers and people who make diagnoses love to have numbers to connect with a disorder, so this is perfect for them.

So what does the paper say about frailty and metabolism?

Overall, most studies have shown a clear association between under-nutrition and frailty. This idea was highlighted in Fried’s original paper describing the frailty phenotype. The authors proposed a ‘‘cycle of frailty,’’ whereby poor nutrition leads to weight loss (specifically muscle loss and sarcopenia), which reduces physical activity and reduces muscle mass further, leading to reduced function and poor nutrition, which in turn ex- acerbates these issues. Although it remains unclear which of these factors comes first and where the cycle starts, evidence for this relationship between nutrient intake and frailty has been consolidated since 2001 in large-scale studies in the community- and institution-based older cohorts from a variety of regions. Studies have shown that specific dietary factors drive this relationship, with low protein, vitamins C, D, E, and calcium intake all especially associated with increased risk of frailty. [My bold]

All of these requirements can be met with a diet high in foods of animal origin. Even calcium if dairy is included. Fresh meat will provide even vitamin C or an anti-scorbutic analog of it. Throw in a few non-starchy veggies, and you’ve got it covered.

But you don’t want to eat everything that is not red hot or nailed down, because obesity is also a risk factor for frailty.

overnutrition and obesity are also associated with an increased risk of frailty. This increased risk has been shown to be associated with high body fat mass rather than necessarily high body mass index or body weight. It is clear that in both groups (those who are underweight and those with high body fat mass), there is a consistent association between low skeletal muscle mass and frailty risk.

As we’ve discussed over and over and over in these pages, muscle mass is the key. If you look like a body builder, your BMI may be high, but you definitely won’t be frail.

Several clinical studies suggest that the consequences of metabolic and nutrition-related complications seem to be different in those who are frail vs. those who are not. Wei et al. showed that poor nutrition without frailty was not associated with poor outcomes, but poor nutrition in those who are frail significantly increased the incidence of poor outcomes including mortality. Metabolic rate, when corrected for lean mass, is stable up to age 65 years but declines thereafter in older individuals. Recent work has shown a specific relationship between a high resting metabolic rate and a lower risk of disability and other adverse outcomes, but only in those who are frail. This indicates that metabolic factors become more important or consequential in the context of frailty, and careful consideration must be given to optimal dietary interventions for this population.

If you are one of the lucky few in whom a crappy diet doesn’t seem to impact your degree of frailty, then good for you. But my prediction is that it will ultimately catch up with you.

Here is a graphic from the article showing all the factors mentioned that add up to frailty.

Here is the same graphic showing all the issues improved with a low-carbohydrate diet. I put a red rectangle around each one improved with a low-carb diet. I’ll go through each of them.

Let’s go through them starting at the upper left and moving clockwise. Undernutrition should be pretty obvious. If you are on a good quality low-carb diet, you don’t have to worry about undernutrition. If you are eating meat, your undernutrition problems should be non-existant.

Glucose insulin signaling virtually always improves. We discussed that in the first section of today’s Arrow.

You don’t have to concern yourself with low-amino acids as long as you are consuming meat in your diet.

It is well established that beta-hydroxybutyrate, the primary ketone body in sustained ketosis, inhibits the inflammasome. Anything that inhibits the inflammasome reduces inflammation.

People who avoid meat can become deficient in tryptophan. Eat plenty of meat on your low-carb diet, and you will be fine tryptophan-wise.

A good low-carb diet should provide you with plenty of protein. Enough to trigger mTOR and increase muscle protein synthesis. If you have inadequate protein, especially leucine, you can have issues. But you get sufficient amounts if you eat plenty of meat on a low-carb diet.

Ditto for muscle mass. Adequate protein intake provides the raw material for muscle protein synthesis.

And, finally, obesity. There is no way to lose fat faster than on a low-carb diet. The folks at the Public Health Collaboration have shown that.

This paper is pretty easy to read. It doesn’t have a lot of technical jargon cluttering it. It’s behind a paywall, but I’ve put a copy in my Dropbox you can download if you want to read it.

Basically, it confirms what we’ve discussed in past issues of The Arrow. You’ve got to eat plenty of quality protein (animal protein) and do resistance training to prevent or reverse frailty. You can see this over and over as you read the studies this paper summarizes.

But you’ll do yourself a lot more good if you just go and do a resistance band workout than if you spend time reading the paper.

Newsletter Recommendations

I’ve been involved in the graduation festivities here in Fayetteville and haven’t had the chance to track down any new and exciting newsletters.

But, as always, there is my lovely bride’s Substack newsletter Outlander MD, which offers an examination of the many medical interludes of STARZ Outlander as seen through the eyes of a physician and scientist--and true Outlander fan. She goes into where they hit the mark and where they miss. And why. An enjoyable diversion for anyone who loves Outlander and great relief during the Droughtlander. FREE but subscription supported.

Odds and Ends

Video of the Week

Last weeks VOTW was of an old guy doing a mega box jump. This week we’ll see another old guy—even older than last week’s old guy—perform like he did when he was 30 years younger. This is really pretty amazing.

You can tell by they bright red, unmade up face on the left just how strenuous this is. The version on the right was not all that long before he died, so this is really a feat to behold.

I always will have a soft spot in my heart for Pavarotti, because when MD and I bought our first little house, we did all the renovations ourself mostly to the tune of Pavarotti’s album of Italian Street Songs. Whenever I hear one of them, I always think back to those days. It was a vinyl LP record, so I’m sure it’s out of print now. I couldn’t find it on Amazon.

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

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

Please help me out by clicking the Like button, assuming, of course, that you like it.

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

Thanks for reading all the way to the end. Really, thanks. If you got something out of it, please consider becoming a paid subscriber if you aren’t yet. I would really appreciate it.

Finally, don’t forget to take a look at what our kind sponsors have to offer. Dry Farm WinesHLTH CodePrecision Health Reports, and The Morning Brew (free)

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


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