The Arrow #164

Hello friends.

Greetings from Montecito.

Where it rained for the first two days we were here. It wouldn’t be The Arrow if you didn’t have to read about an Eades travel nightmare. We left our house in Dallas in plenty of time to get to the airport. Got there early, whizzed through check in and TSA. I told MD something is going to happen—it’s all gone way too smoothly.

Sure enough, we get to the gate for our flight to Santa Barbara, and it says Los Angeles. I figured we were there early enough that they just hadn’t changed the sign yet. But no. A few minutes after we get there, a woman comes on and makes an announcement that our plane is going to LAX instead of the airport in Santa Barbara (SBA), because the airport in Santa Barbara is closed due to flooding. As it turns out, there had been a humongous rain the night before that flooded a lot of areas, including around the airport.

So just as everyone is trying to figure out what to do. The same woman comes back on and tells us all there will be ground transportation provided for us from LAX to SBA. Which at least solved that problem.

For about ten minutes.

Then the same woman comes back on and says, Correction: There will not be ground transportation provided to SBA.

I spring into action and rent a car for the hour and a half drive home. So, problem solved.

We get on the plane in sunny Dallas and fly uneventfully to Los Angeles. As we were descending into LAX, the rain starts to pound. The landing was smooth as silk, but it was pouring rain. Of all the countless times I’ve flown into and out of LAX, this was the first landing during a deluge. As they say in the song: ‘It never rains in California, but girl, don’t they warn ya’? It pours, man it pours!’

We get off, head to the baggage claim, and wait. And wait. And wait. And wait. Almost an hour after we’ve been waiting, someone announces that our baggage had been delayed because no one in baggage handling was expecting this flight from Dallas to come in. Which I had already figured out and mentioned to MD.

But someone knew our flight was coming in. We had a gate waiting for us. Why did this person not notify the baggage handling people? Seems like a reasonable thing to do.

And while I’m on a roll, why is it when an announcement has to be made over shitty speakers while all kinds of other noise is going on a non-native English speaker is chosen for the task when there are a dozen native American English speakers standing around? I mean, I applaud people from other places who have learned a difficult language like English. I salute them. I enjoy hearing them speak one on one. Truly. They speak English far better than I speak whatever native language they speak. But when clear communication over a squawky speaker is the object, clear unaccented words in whatever the language of the country is work best.

We finally get our bags and bolt for the rental shuttle, which is always an adventure in LAX. We get dropped off at Hertz, and the only seamless part of the trip starts. Our name is on a board, an attendant points out a half dozen cars we can take our pick of, and we get in, exit the airport, and head to Montecito. In the driving rain.

I had chosen an electric vehicle, because it was the cheapest option and I figured there would be no gasoline charge. And there wasn’t. But they expected the car to be returned charged. Which I figured would be a helluva lot cheaper than $6 per gallon gas in Cali.

Got home without a hitch. Unloaded all our stuff, then took the car back. MD followed me. Before we left, we discovered the charging port was different than the Tesla charging port and the car had no adapter, so we had to find a place to charge it. Which we did, but because it was not a Tesla supercharging station, it took forever. As in almost an hour.

Finally, MD followed me to the airport. I parked the car and ran inside to the Hertz counter. The guy says, Have you got the key? I give it to him. He says That’s it. You’re good to go.

The entire Hertz experience was wonderful. If only American Airlines would have been the same.

I have Hertz Gold as part of my credit card package, so I don’t know if people just signing up for a car online with Hertz would have the same experience.

Okay, on to something other than my perpetual grousing about travel woes.

A lot of good stuff today.

Before we get into all the nutritional scientific nitty gritty, I want to tell you about a heartwarming article in Retraction Watch.

Karma Is So Sweet

Retraction Watch reported on a ruling by a three judge panel in the District of Columbia Court of Appeals that slapped a Stanford professor down hard.

Here’s the deal.

This Stanford professor who studies renewable energy wrote an article in 2015 in the prestigious Proceedings of the National Academy of Sciences (PNAS). I read the article, but it really doesn’t matter what it said in terms of what happened. In 2017 another professor from somewhere wrote an article (also PNAS) taking the author of the 2015 to task on the merits.

The author of the first article, one Mark Jacobson, got pissed because the guy in the 2017 PNAS article disagreed with him.

These kind of journal catfights happen all the time. And they can be vicious. Which brings to mind my favorite Henry Kissinger quote: “Academic politics are so vicious precisely because the stakes are so small."

It’s a case of two eggheads arguing over who is right and who isn’t.

It’s traditional to fight these battles in the pages of the academic journals in verbiage that barely conceals the hatred.

But in this case, Jacobson was apparently butthurt by the attack. Instead of answering back in the journal and hashing the differences out in a format where other scientists in the field could observe (and maybe even add their two cents’ worth in) Jacobson decides to file a lawsuit for $10M against both the author of the paper and the journal for defamation.

Lawfare, the use of the legal system to financially cripple a political (or in this case, an academic) opponent is vile. At least in my opinion. I don’t know if that was the motivation here or not, but it certainly ran up legal bills for the defendants in this lawsuit. Ran them up to circa $420,000, in fact.

So Jacobson forces the defendants to fork over massive legal fees in preparation for trial. Then, at the last minute, he drops the case—I have no idea what his motivation was, but the panel of judges did—but makes clear to the defendants that he might refile it at any time while he continues to get them to back off on what they said about his article.

He apparently ran up $70,000 in legal fees himself, or at least that’s what Stanford reimbursed him to protect his reputation, which is part of his job.

When the ruling came down that he owed the defendants ~$420,000, Jacobson decided to appeal. “Jacobson is confident that he will win his appeal, he told Retraction Watch.”

He figured he would win, I’m assuming, because the anti-SLAPP laws are

“designed to provide for early dismissal of meritless lawsuits filed against people for the exercise of First Amendment rights.” Jacobson tried to argue that, by dropping the suit, he was no longer liable for legal fees because the statute requires that defendants “prevail.” [Links in original]

The three judge panel disagreed. Said they

under Jacobson’s preferred approach, a plaintiff could engage in harassing and meritless litigation up until the point at which they sense the court might dismiss the case, and then voluntarily dismiss the suit themselves, all the while keeping the threat of refiling hanging over the defendants’ heads and running up their legal bills.

The specter of repeat litigation by Jacobson is not farfetched.  In his briefing to this court, Jacobson continues to take issue with “the refusal of Dr. Clack and NAS to correct the false facts to this day, in reckless disregard for the truth.”  Much of his brief rehashes his claims that NAS and Clack defamed him and he persists in condemning Clack’s article.  In arguing that NAS and Clack have not “prevailed,” Jacobson repeatedly asserts that he retains the ability to refile his defamation suit, “keeping the defendant[s] at risk.” 

And they ran the total up to over $500,000.

Now Jacobson is deciding whether to appeal to the full court.

If he does, it will cost more, and I suspect end up with the same outcome.

The judges weren’t fooled. In commentary on the case, they wrote:

What animates Jacobson’s $10 million defamation suit is nothing more than his indignation at an article critical of his work. Such criticism comes with the territory of academic debate.

Sweet.

One more pre-science section.

One of my favorite Substacks to follow is The Honest Broker by Ted Gioia. It has nothing to do with medicine or diet. He writes mainly about music (jazz, primarily), but is an astute interpreter of cultural trends, and his latest is kind of harrowing. It’s incredible what we’ve come to as a society. If politics is downstream from culture, I have no idea what we’re headed for. You can read it in full below. If you do, you’ll be as worried as I am. What comes next after where we find ourselves now?

Excess Deaths in the United States

I’m a paid subscriber to God only knows how many Substacks and newsletters on other platforms. I try to keep up with all the important Covid info, so I can pass it along in The Arrow.

Most of the authors of these newsletters are rabid anti-Covid-vaxxers, and some are total anti-vaxxers. Consequently, their posts are always filled with stories of young people who have died. Most of them imply that everyone who died a premature death is a victim of the Covid vaccine. Since not everyone who dies young died as a consequence of getting the Covid jab, I’m always a bit skeptical of these reports of causality.

Before the entire Covid pandemic was even heard of, I personally knew of two young women who died suddenly. Since there was no Covid vaccine (nor Covid, for that matter) around back then, these two young women definitely did not die as a consequence of getting the mRNA Covid vaccine. Young people do die suddenly from causes other than the vaccine.

I’ve been having cognitive dissonance reading about all these supposed Covid-vaccine-related deaths when I know only one person in the large group of people in my friends and family who has died suddenly. He was 49 and may well have been a victim of the Covid jab. Based on his politics, which he wore on his sleeve, I’m sure he was vaccinated, but I don’t know that that was what took him down.

I keep seeing these polls published in many of the Substacks I read saying that 20%, 30%, even 40% of respondents say they know someone personally who died from the Covid vaccine. Up until the guy I know, who died a few weeks ago, I didn’t know anyone personally who died suddenly due to anything. So, based on the universe of people I know personally (the vast majority of whom took the vax) only one person has died suddenly a few weeks ago.

Granted, this is my circle of friends and acquaintances, which may be different in makeup than anyone else’s, but I kind of doubt it.

The CDC, the agency that should be on top of this and providing the real figures, has abdicated. Same in the UK. Their governing body for this sort of thing has changed the way they do it, so all the Substackers are saying the excess deaths are skyrocketing, but the government won’t release the correct stats, because it will make those running the government during the lockdowns and vaccine mandates look bad.

Given all this uncertainty, I haven’t wanted to opine on the excess deaths. I would much prefer to have some kind of decent evidence before I jump into the fray and post some statistic that will later be shown to be totally false.

A couple of days ago I came across a paper published in the Journal of the American Medical Association (JAMA) looking at the issue of excess deaths that, although more than a bit deceptive, gave me the figures I have been looking for.

Based on the data presented, there are without doubt many excess deaths since the end of the pandemic. Are these deaths due to the mRNA vaccines or the lockdowns and other idiocy promulgated by our government or from a combination of both? The data don’t say, but with a little critical thinking, it’s easy to see there are plenty of excess deaths.

The article doesn’t say there have been a lot of excess deaths, but instead says the very opposite. But I’m going to show you how the authors are incorrect either by failure to think or by intention. Given that the AMA has kind of been captured by the various governmental agencies—the CDC, for example—I suspect the deception was intentional.

Let’s take a look.

The authors used statistics from the National Center for Health Statistics (NCHS), which, I’ll have to admit, I didn’t even know existed. I had been searching in the CDC data and ending up frustrated and empty handed.

Here is what they looked at:

We calculated annualized age-standardized death rates (ASDRs) across 5.25 years from March 1, 2018, to May 31, 2023, by sex, race and ethnicity (as defined by death certifiers and NCHS), metropolitan status, and region. We estimated and compared mortality rate ratios across 4 summary periods: before the pandemic (combining 2018 and 2019 due to stable mortality rates), the pandemic’s first year (largely before the vaccine), the pandemic’s second year (after widespread vaccine availability), and the postacute period (largely after the first Omicron wave)

Here are the graphics showing what they found.

SOURCE in case you want to blow it up to see it better

If you look at the graphics, they track pretty much with what the paper says.

Mortality increased during both acute pandemic years before returning to near-prepandemic levels for most groups. The mortality increase was not equal across groups; it was largest for men, all minoritized racial and ethnic groups, nonmetropolitan areas, and the South. [My bold]

And this from the Discussion section:

There has been a public debate about whether the US has “returned to normal” after the pandemic. Our study suggests that this has largely been the case with respect to disparities by gender, race and ethnicity, and region. Although mortality remains somewhat higher than before the pandemic, this additional mortality is largely proportional to 2018-2019 mortality with respect to major demographic comparisons. This continuity suggests that these disparities are persistent; even a pandemic-level mortality shock does not permanently alter them. [My bold]

We don’t really need any numbers to work our way through this data to see the real story. Looking at the bolded text in the two quotes above along with the graphics gives us all the info we need to reason out what’s going on.

Because there are seasonal respiratory infections that occur every few years or so, the total death curves are not level. They fluctuate with the severity of the disease that comes through, which is usually the flu. There are bad years and not so bad years, and they both follow the same pattern.

The excess deaths line is an arbitrary figure determined by someone somewhere using some sort of equation. We don’t really need to know what it is, we just need to be able to compare the annual deaths to this excess deaths line, which changes kind of slowly. Again, depending upon the equation involved.

Let’s look at an example. If the flu (which is the usual culprit killing people off) never varied in its severity, the annual death rate would pretty much follow, but stay below the excess death line. But the flu isn’t the same in degree of virulence. In some years it kills a lot of people, while in other years it doesn’t.

When flu season arrives each year, there are a number of people out there with different degrees of vulnerability. If the flu is mild, only the really vulnerable end up dying from it. Conversely, if the flu is a bad one in a particular year, a whole lot of people die from it.

Here is the crux of the situation.

If a few years go by in which the flu is mild, a lot of vulnerable people don’t die. They in essence stack up awaiting a bad flu year. When the bad flu year comes along, it kills almost all of the vulnerable people.

Which means that there are few vulnerable people left for the next flu season to kill off. Consequently, the next year’s flu doesn’t make much of a mark. It takes a few years for the really vulnerable people to stack up. And the cycle repeats.

Here is the male/female data from the graphic above. I could have used any of them to prove the same point, it’s just that this one is less busy. Pay attention to the area I circled.

I’m going to put up some graphics I created to show what’s going on, and why I believe the excess deaths are pretty high.

Here is what total deaths vs the excess death line typically look like.

As you can see, total deaths (in blue) vacillate around the excess deaths line. In years following a bad flu season when total deaths were higher than normal, the total death curve drops below the excess deaths line. The total deaths in the years when the flu is brutal usually jump above the excess deaths line followed by dropping below it the next year. Again, because there are so many fewer vulnerable people around for the flu to do in.

Here is what you would find during a really bad flu season (enlarged).

Now if you scroll back up and look at the graphic from the JAMA paper, you’ll see that it doesn’t look anything like the curve above. God knows Covid killed a lot of people one way or another. So when Covid finally got rid of all the vulnerable people—who were the ones who mainly died: the elderly with co-morbidities for the most part—you would expect to see a huge drop off in deaths in the year after. Especially since the flu has been pretty mild.

But that’s not what the graphic from the paper shows. The graphic from the paper representing the actual data looks like this:

The total deaths shown on the graphic from the JAMA paper look like the solid blue line on the above graphic. The deaths went up then slowly came down approaching—but still above—the excess deaths line. The line should have followed the dotted line instead. But it didn’t.

So the reality is the total deaths are excessive. By an amount represented by the difference between the dotted blue line and the solid one. Which appears to be a pretty large number.

But according to the JAMA paper

Although mortality remains somewhat higher than before the pandemic, this additional mortality is largely proportional to 2018-2019 mortality with respect to major demographic comparisons.

So they’ve kept the excess deaths line what it was in 2018-2019 and are trying to make the case that the excess deaths have just about gotten back to normal. Which, based on my analysis is way, way off the mark.

They write in reassuring tones

Mortality increased during both acute pandemic years before returning to near-prepandemic levels for most groups.

Oh, okay, wow, it’s over at last. Deaths are back to normal.

As I’ve shown, that’s not quite the case. Something is still out there killing people. The vulnerable are no longer with us. So who is dying now?

And why?

That’s the big unanswered question.

I suspect the authors and JAMA are gaslighting us at the behest of their overlords in the CDC and other alphabet agencies.

If anyone has an answer or if anyone disagrees with my analysis, let me know in the comments.

Just so you’ll know how flimflammed and gaslighted we were about the vaccines, here is a little video summary. Shows how our overlords and corporate media can’t be trusted. Great music, too.

Okay, it’s now time for my piteous whine for paid subscribers. But I’m not going to do it. Instead I would like to thank those of you who have signed up as paid subscribers from the bottom of my heart. I really, really appreciate it. So does MD. We both thank all of you who have contributed and those who might in future very, very much!

Dementia in the Ancients

An article I came across last week grabbed my attention. It was titled Dementia was rare in ancient Greece, analysis shows and was a write up about a study published in the Journal of Alzheimer's Disease.

This is just the kind of study that rings all my chimes. I wrote Caleb Finch asking for a copy. He responded that he wouldn’t have a copy for a few days, but he would send it when he did.

I received it a couple of days later and pored over it. Here is what kicked off their research.

We explore the possibility that the modern high prevalence of Alzheimer’s disease and related dementias (ADRD) are diseases of modern environments and lifestyles that were uncommon in the ancient Greco-Roman world. The prevalence of ADRD increases after age 65 in most modern populations. The Alzheimer’s Association estimated lifetime risk at age 65 in 2022 of 11.6% for men and 21.1% for women. In several populations, the prevalence of ADRD increases exponentially with age after 60.

A challenge to assumptions that high prevalence of ARDA is normative is given by the Tsimane, indigenous Ameriandians of Amazonian Bolivia; with high, life-long mortality from accidents and infections. After age 60, mild cognitive impairment (MCI) was increased, but clinical grade advanced AD was not found up to the oldest age of 93.

The authors reckoned that the ancient Greeks and Romans were in the same situation as the Tsimane: Their main risks were accidents (trauma) and infections. And they figured the ancients consumed a diet much different than the one modern man consumes (as do the Tsimane), so they wondered if the change in diet might have anything to do with the rates of dementia today.

They plunged into the ancient writings to see if they could come up with any descriptions of ADRD or MCI in those times.

Our analysis sought primary texts to appraise the awareness and scope of mental decline during aging in ancient Greece and Rome.

We focus on ancient Greece and Rome because some other ancient literatures have few known references to memory loss in old age.

They go on in their Methods section to write

Four decades ago, the historian M.I. Finley observed “I can find hardly any reference specific to mental illness in old age . . . .I do not conclude from this silence that senile dementia was non-existent in antiquity, but I know of no way to penetrate the almost total silence.” Consistent with Finley’s observation, we found few primary citations of a connection between the aging process and memory loss in Greek and Roman medical texts. Nor was memory loss mentioned in authoritative summaries of ancient medicine…

Our study carefully researched standard editions of Greek and Latin texts, primarily, but not only, ancient medical and philosophical texts that discussed the human life cycle from the 8th century BCE into the 3rd century CE. There are no statistical data for the incidence of mental illness; moreover, technical terms matching contemporary terminology for mental disorders are lacking for antiquity. Therefore, we searched for passages providing detailed descriptions of the physical, medical, and mental characteristics of the elderly.

What they came up with in their search ended up being pretty thin gruel. But the absence of evidence doesn’t mean the condition didn’t exist. Anyone who has taken care of a person with ADRD is changed by the experience.

Given the vast amount of written material from the Greeks and Romans, it would be difficult for me to believe they wouldn’t have written about severe dementia if it were a common finding.

After citing a few quotes from the ancient Greek literature, the authors write

The duration of premorbid collapse of body and mind must have been much shorter than the prolonged agonal phase enabled by modern medical technology.

These few references suggest that ancient Greeks recognized that aging commonly brought memory issues we would recognize as MCI. The cognitive losses as described may approach early- or mid-stage AD, but not chronic progressive ADRD-like symptoms with major loss of memory loss, speech, and reasoning.

Moving on to the Roman literature, they come across enough evidence to make them believe there may have been a bit more dementia in Rome than in Greece.

Centuries after Aristotle, in the Roman Era, we found four statements of severe memory loss, suggesting the gradual emergence of more advanced dementia. Baseline age expectations for elite Roman men resembled the prior Greek elites. The Roman requirement for military service ended at age 46; health permitting, former officers were expected to continue political and administrative activity into later ages. Mental decline was recognized but was considered exceptional. As Cicero noted in De Senectute (44 BCE) and the earliest surviving book on this topic, but extreme memory loss was not generally expected:

“Elderly silliness [senilis stultitia], which is usually called dotage [deliratio], is characteristic of irresponsible old men [senum levium], but not of all old men.” [Italics in the original]

And as they point out later, Cicero did not include any sort of severe memory loss or anything similar to dementia in his list of the four evils of old age: “the end of an active life, physical weakness, the cessation of pleasures, and nearness of death.”

I suspect that Cicero, who was around a multitude of people over his lifetime, would have noted severe dementia had it been common.

In the 2nd century AD, the satirist Juvenal in his list of the evils of aging:

“Greater than all the damage to limbs is dementia, which does not know the names of slaves or the face of the friend with whom it dined the previous night or those whom it engendered and brought up.” [Italics in the original]

He even uses the term “dementia,” which according to the authors of the paper meant literally “out of mindedness.”

And it was mentioned in Roman law during trials about responsibility of fulfilling duties.

The authors summarize:

In sum, we identified Greco-Roman texts that describe memory loss and some form of dementia in the elderly from the 6th BCE to the 2nd CE. The equivalent of MCI was not uncommon in later years, possibly after age 70, like today. Severe cognitive dysfunction was less noted. The few ancient sources we found make clear that some dementias of aging arose in pre-modern times. We cannot know which pathologies were involved. Age-related neurodegeneration extends beyond ‘classical’ neurofibrillary degeneration and amyloid plaques to include vascular amyloid, microbleeds, and aggregates of alpha-synuclein (Lewy bodies) and TDP-43.

They go on to discuss how dementia was more common in Roman times than in that of the ancient Greeks, and they raise the possibility that it could be a function of lead poisoning the Romans from lead water pipes and eating and drinking vessels, etc.

Based on the paucity of written descriptions of severe dementia, the authors suppose (and I agree) that the rates of ADRD and MCI today vastly exceed the rates in the ancient Greeks and Romans. If this is true, then the question becomes What has caused the difference?

Since Alzheimer’s is often called diabetes of the brain or type 3 diabetes, the vast increase seen today may have something to do with a change in diet. When I was a kid in the Ozark mountains in the 1950s, I was around a lot of old people. We had a big family and big family get togethers from time to time, and I remember only one very old relative—a great grandmother—who had dementia.

Of course, my own personal experience means nothing in terms of a scientific finding, but I’m just saying. If that same group of relatives got together today, given today’s stats, a bunch of them would have type 2 diabetes. And no one in the group had it back then.

We know that type 2 diabetes is a function of diet in that it can usually be reversed and controlled by switching to a low-carb/ketogenic diet. Which implies eating the opposite diet may bring it on.

And remember, sugar has only been around for about 1,200 years, so it wasn’t available to the Greeks or Romans of old.

Protein and Atherosclerosis

I received about 80,000 emails over the past few days from people asking about a new study positing that too much protein drives heart disease. And that so-called high-protein diets are bad. (The 80,000 is only a mild exaggeration.)

Before we get into the details of the study, let me tell you a little about how the PR for these things works. I have no idea how many medical/scientific studies come out each day, but I would bet it’s in the thousands. Of those thousands that come out on any given day, how does one like this one get selected from the great amorphous herd and make it into the corporate media?

Well, it usually starts with some kind of press release. Here is the press release for this particular paper.

When scientists write papers, they are usually pretty circumspect about what they commit to paper for a couple of reasons. First, the paper is going to be reviewed by their peers, who usually know the science involved. The authors don’t want to be taken to task for exaggerating. Second, if their reach exceeds their grasp and the peer reviewers don’t catch it, other scientists reading the paper will. So circumspection is usually the order of the day.

But none of these restrictions apply to the press release. They can—and often do—say almost anything in the hope of getting the paper picked up by some national media outlet.

Lazy journalists sit around waiting for these things to hit the wire. And anything remotely discouraging of eating meat or following a low-carb/ketogenic diet is catnip to them. (OMG, this diet is destroying the planet!) They don’t bother to read the paper, which in this case they couldn’t (I’ll explain below), but instead basically just rewrite the press release in their own words. Or, worse, just copy and paste sections of the press release. Some of the more industrious journalists may go so far as to call the authors, primarily to get a quote.

Very, very few actually dig into the study to see what it really says or means.

Then the headlines become more and more strident. The New York Post writer headlines her article You might be eating an artery-damaging amount of protein, new study warns.

I had found this article before I read about it in the news or started getting emails. I found it in my daily troll through the medical literature. I wrote to the corresponding author, who replied that she didn’t have a copy of the formatted article, so she sent me the manuscript copy. Unformatted manuscript copies are a pain. When formatted into journal form, typical articles are anywhere from 5-6 pages up to maybe 20, if it’s a big paper. The unformatted manuscript copy I received was 61 pages long. And with the lack of formatting, these long manuscripts are a pain to read.

If I got the unformatted copy, then any of these journalists writing about the paper got the same thing. Which really makes me even more suspicious that they didn’t go through all 61 pages.

Okay, so you now know how all this works.

But what does the paper say?

First, let’s look at the press release. Here are some quotes:

University of Pittsburgh School of Medicine researchers discovered a molecular mechanism by which excessive dietary protein could increase atherosclerosis risk.

The study, which combined small human trials with experiments in mice and cells in a Petri dish, showed that consuming over 22% of dietary calories from protein can lead to increased activation of immune cells that play a role in atherosclerotic plaque formation, driving the disease risk. Furthermore, the scientists showed that one amino acid – leucine – seems to have a disproportionate role in driving the pathological pathways linked to atherosclerosis, or stiff, hardened arteries.

“Our study shows that dialing up your protein intake in pursuit of better metabolic health is not a panacea. You could be doing real damage to your arteries,” said senior and co-corresponding author Babak Razani, M.D., Ph.D., professor of cardiology at Pitt.

Their work showed that consuming more than 22% of daily dietary calories through protein can negatively affect macrophages that are responsible for clearing out cellular debris, leading to the accumulation of a “graveyard” of those cells inside the vessel walls and worsening of atherosclerotic plaques overtime. Interestingly, the analysis of circulating amino acids showed that leucine – an amino acid enriched in animal-derived foods like beef, eggs and milk – is primarily responsible for abnormal macrophage activation and atherosclerosis risk, suggesting a potential avenue for further research on personalized diet modification, or “precision nutrition.”

“Perhaps blindly increasing protein load is wrong,” Razani said. “Instead, it’s important to look at the diet as a whole and suggest balanced meals that won’t inadvertently exacerbate cardiovascular conditions, especially in people at risk of heart disease and vessel disorders.”

Razani also notes that these findings suggest differences in leucine levels between diets enriched in plant and animal protein might explain the differences in their effect on cardiovascular and metabolic health. “The potential for this type of mechanistic research to inform future dietary guidelines is quite exciting,” he said.

Jesus wept.

All the bold in the above quotes are mine. They are for emphasis.

The lead author is a cardiologist, and I’ll bet you anything he is a plant-based dieter. He says in the press release that a quarter of people in the US consume more than the 22 percent of protein they estimate is the upper limit before the damage starts. And, of course, those vile protein eaters chow down mainly on animal sources of protein.

Okay, now that you’ve seen the press release, let’s look at the actual paper.

Let’s go through the abstract.

The first few lines are pretty innocuous.

High protein intake is common in Western societies and is often promoted as part of a healthy lifestyle. However, amino acid-mediated mammalian target of rapamycin (mTOR) signaling in macrophages has been implicated in the pathogenesis of ischemic cardiovascular disease. In a macrophages has been implicated in the pathogenesis of ischemic cardiovascular disease. In a series of clinical studies on male and female participants (NCT03946774 and NCT03994367) that involved graded amounts of protein ingestion together with detailed plasma amino acid analysis and human monocyte/macrophage experiments, we identify leucine as the key activator of mTOR signaling in macrophages. [My bold]

Okay, so everyone who knows anything about mTOR knows leucine is a key activator. Leucine is a key activator for muscle protein synthesis (MPS), which I’ve gone over in these pages ad infinitum.

We describe a threshold effect of high protein intake and circulating leucine on monocyte/macrophage wherein only protein in excess of ~25 grams/meal induces mTOR activation and functional effects.

Nothing new here. I’ve written countless times that it takes at least 25 grams of animal protein per meal to provide the necessary 2.5-3 g of leucine to promote muscle protein synthesis.

By designing specific diets modified in protein and leucine content representative of intake in the general population, we confirm this threshold effect in mouse models and find ingestion of protein in excess of ~22% of dietary energy requirements drives atherosclerosis in male mice.[My bold]

So they confirm what every other protein researcher has found. There is a threshold effect in protein consumption required to trigger mTOR to do its thing.

They basically took a look at what humans ate in a couple of studies, then designed a bunch of different diets for mice—mice, I might add, that are prone to develop atherosclerosis—to see what effect they had. They discovered that protein intake in excess of ~22 percent of calories triggered the changes in macrophages that contributed to atherosclerosis. In mice prone to atherosclerosis.

These data demonstrate a mechanistic basis for the adverse impact of excessive dietary protein on cardiovascular risk.

On mice prone to atherosclerosis. That’s it. That’s the study. Now go back and read the press release and the New York Post article just to see how shrill and over the top they are.

You may ask how I know the mice used are prone to atherosclerosis? According to the paper “all mice used in this study were on C57BL/6J background and ordered from Jackson Lab. If you go to the Jackson Lab website, you’ll find the following:

C57BL/6J mice are resistant to audiogenic seizures, have a relatively low bone density, and develop age related hearing loss. They are also susceptible to diet-induced obesity, type 2 diabetes, and atherosclerosis. [My bold]

Now that we know what a bunch of BS this all is, let me tell you how the whole protein synthesis process works.

First, let’s start with this graphic.

AMPK (5' AMP-activated protein kinase) is a signaling protein that has a multitude of effects as you can see from the picture above. I’ve circled its effect on mTOR, which shows that AMPK inhibits the action of mTOR.

As we’ve discussed many times, mTOR (also a signaling protein) promotes the synthesis of new muscle. As we’ve also discussed, up to about age 30 or so, insulin and other metabolic, reproductive, and growth hormones stimulate mTOR to make new muscle tissue. After circa age 30, mTOR is stimulated instead by leucine, one of the essential amino acids.

As numerous studies, including the one under discussion, have shown, it takes 2.5 to 3 grams of leucine to stimulate mTOR enough to drive muscle synthesis. In another paper we discussed, it appears—especially in older people—that the more leucine, the more muscle synthesis.

You can get 2.5 to 3 grams of leucine in about 4 or so ounces of animal protein.

The study under discussion confirmed all this as have dozens of other studies.

AMPK is upstream to mTOR, so if AMPK is active, mTOR is inhibited. So how do we get mTOR to work if we have all the leucine we need, but AMPK is inhibiting it?

To understand, let’s first look at AMPK. As I wrote above, it is a fuel sensing protein that controls a multitude of downstream actions, one of which is mTOR.

AMPK is activated when fuel levels are low. If we are exercising, if we don’t have enough ATP and have a buildup of one of its precursors AMP, if we are fasting, all these are situations in which AMPK is activated.

Here are a number of actions of AMPK when it is activated:

  • Increases glucose uptake: We want to get glucose out of the blood and into the cells to burn.

  • Increases glycolysis: We need to break down glycogen (stored sugar) to get the glucose to burn.

  • Increases fatty acid oxidation: An obvious one. We want to start burning fat to replenish the depleted energy stores.

  • Increases mitochondrial biogenesis: we want to make more mitochondria to burn fat and generate as much ATP as possible.

  • Inhibits gluconeogenesis: We don’t want to spend energy making more sugar – we want to burn it.

  • Inhibits glycogen synthesis: Same thing – we don’t want to store sugar, we want to burn it.

  • Inhibits fatty acid and cholesterol synthesis: We don’t want to spend energy making fat and cholesterol.

  • Inhibits insulin secretion: We want insulin to be low, so that we can move stored fat and sugar to where it needs to be burned.

And it inhibits muscle synthesis. Why would we want to be building muscle if we were starving? We would be breaking it down to convert it to glucose.

Now here is where it gets interesting.

How can we keep AMPK activated and do all the things listed above while at the same time making new muscle?

Remember, fasting is an activator of AMPK. A low-carb diet replicates the fasting response and activates AMPK. And a low-carb diet usually contains a fair amount of protein, typically animal protein. The very kind that is full of leucine, the trigger for mTOR.

So, we have this paradoxical situation where the overall diet—the low-carb diet—activates AMPK, which is great for everything except increasing muscle synthesis. Activated AMPK blocks mTOR.

But it’s obvious people can build muscle while on low-carb diets, so something isn’t computing.

It never used to compute for me, either, until I came across a great paper several years ago that made everything clear and resolved the paradox.

The paper, The Role of AMPK and mTOR in Nutrient Sensing in Pancreatic β-Cells, is highly technical. It describes a series of experiments teasing out what inactivates AMPK to allow mTOR to do its muscle-synthesis work when leucine is present.

What makes this magic happen?

As it turns out, amino acids themselves—especially glutamine (the most abundant amino acid in meat) and leucine—inhibit the activation of AMPK.

All the papers—at least all the ones I’ve seen—recommend that to build muscle, one should consume adequate amounts of protein a couple of times per day. By adequate, they mean enough to provide 2.5-3 grams of leucine.

In doing so, the glutamine and leucine deactivate AMPK temporarily allowing the leucine to do its work stimulating mTOR without the AMPK inhibiting it. Once the mTOR has done its job and set the muscle synthesis pathway to work, the AMPK reactivates and begins to once again inhibit mTOR.

Which solves the situation of mTOR being active all the time, which could end up driving the growth of cancer.

Ain’t nature grand?

Now what will deactivate AMPK is high blood sugar, which is probably why people with type 2 diabetes and/or obesity tend to have a greater incidence of cancer.

Also, it’s probably not all that wise to eat constantly throughout the day, since that, too, will deactivate AMPK. Is it any wonder the obesity stats are what they are? These days everyone seems to eat all day long every day. Their poor AMPK never gets to activate, except maybe for a bit at night.

The more your AMPK stays activated, the better off you are.

And don’t worry about exceeding the 22 percent protein limit as described by the study that kicked all of this off. The AMPK-mTOR system will take care of itself if you’re following a low-carb diet.

Odds and Ends

Video of the Day

Haven’t put one of these up in ages. Just came across this one and have to put it up. It shows Paris in the Belle Epoque era. Notice how thin everyone was back then. Their AMPK was active most of the day.

Okay, time for the poll. I’m running late again and don’t have time to come up with something clever, so it’s stars once again.

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

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