The Arrow #113
Greetings from Montecito.
My weather luck has been holding. Wherever I happen to be, the weather sucks. Below is a photo of the hills above Montecito. It’s unusual to see snow and palm trees in the same photo, but it’s been really cold here (for Montecito), and we had a dusting of snow high on the hills above town.
It’s an unusual sight. Nice and sunny and looks warm. But it’s not. It is cold.
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Masks Again and Some Hilarity
I meant to post this last week, but ran out of time. Barely got last week’s Arrow off before midnight, so I could at least say it went out on Thursday. My apologies to those who were waiting on it.
The section of my post was going to be titled I Scooped the NY Times. A couple of days after the Arrow from two weeks ago in which I wrote about Maryanne Demasi’s interview with Tom Jefferson, the lead author of the Cochrane Report on masks, Brett Stephens of the NY Times wrote about it too.
And just like I did, Stephens basically wrote that the Cochrane Report more or less laid to rest the nonsense about masks being protective against Covid. If you read his piece (free link here), you’ll see he pretty much said the same thing I did. Not that he was copying me, but the report is pretty clear as was Jefferson’s commentary on it, so anyone who was honest about it would report it the same way Stephens and I did.
The fun part of the Stephens piece was not the article itself, but the thousands of comments on it. They were beyond fun to read, because many of them were so shrill. They typify precisely what you would expect out of a dyed-in-the-wool NY Times reader. The kind of readers who do not want to read anything that disagrees with their world view. The kind of readers who raised such a fuss when one of the editors dared to publish an opinion piece by a conservative US Senator that the NY Times fired the editor to staunch the flow of people unsubscribing.
I didn’t read all 3,700 or so comments (as of this moment), but I did read enough to get the flavor of them.
Here is one of my favorites from a true non-thinker:
Doug disagrees with the Stephens piece, but he just doesn’t know why? He is unable to read and understand the underlying Cochrane Report and/or the Demasi interview with its lead author. He is wallowing in cognitive dissonance and is looking for someone to save him. Please, please, please someone, anyone, write an article refuting all this, so I’ll have some peace.
What a piece of work. Sadly, far too many people are like Doug, whose confirmation bias runs high. He knows in his heart of hearts that masks are good. All he needs now is for someone tell him he’s right.
Sorry Doug. You’re screwed.
Here is another one pretty typical of the lot.
Poor Rachel. She doesn’t realize she’s an idiot with (it’s fair to say) pretty sketchy command of standard English spelling and usage. Nor does she realize what a Cochrane Report is. It is exactly what she’s begging for: a balanced view on the subject. As we’ve discussed in this newsletter, a Cochrane Report is not a paper by a single author or a handful of authors. Those putting together any particular Cochrane Report gather all the pertinent studies on a given subject and weight them on the strength of the evidence and come up with a summary of what the evidence shows, or doesn’t show.
In this case, the balance of the evidence showed there was no real evidence that masks work to prevent Covid.
I want to come back to this concept in a moment, but first let’s look at one more comment. There were many, many of these comments in the couple of hundred or so I read.
Do you think anyone writing these comments took the time to stop and think about what surgical masks are for? Or if they even work? Or do they just assume since everyone wears them while in the operating room that they must work.
When I was in my residency (a surgical residency at that) I got in trouble because of an encounter I had with a non-thinking surgical nurse. I can’t even remember now what the case was that we had just finished, but it was some kind of abdominal case in which there as a huge intra-abdominal abscess. When we opened the abscess, pus spewed out all over everything. The entire OR became unsterile and had to be re-sterilized before being used again. There were two of us docs working on the case and when the case was over and the patient moved, we took off our masks. The head surgical nurse went ballistic. You can’t take off your masks in the operating room, she screamed. We looked at her as if she were the fool she obviously was. There was frigging pus all over the place, so how could we possibly make it worse by going maskless? Moreover, the whole space was about to be completely cleaned and sterilized again.
We basically told her she was full of shit. And refused to put our masks on. She was one of those people who blindly follow rules without a real understanding of what the rules are for. She was also in charge of running the OR. A bad combination.
She reported us to the surgical faculty of the med center, and both of us got called on the carpet. The head of the surgery department knew the woman was an idiot, but he needed to keep the peace. He went easy on us, but demanded we apologize to her. So we did. As you might imagine, I had to bite my tongue to keep it to a simple apology.
Surgical masks prevent droplet spread. If you’re doing a case and speak, which you do throughout the case, you can transmit droplets. Or if you cough. When you have someone’s abdomen open, it is like a giant petrie dish. It’s a great environment for bacterial growth, so you don’t want to contaminate it with anything. And masks prevent blood or pus or other bodily fluids, some of which can be under pressure, from squirting up into the surgeon’s mouth or nose. It’s kind of a two way street.
But, there has always been controversy over whether or not surgical masks are worth the bother or if they are simply theater.
Eugyppias wrote a nice post on that recently. He’s looked into it much more deeply than I, and there has been vastly more work done on the subject than I would have imagined:
This Twitter user has gathered almost all of the available scientific literature on masking into this massive directory of 462 files on archive.org. Of that research, I want to draw your attention in particular to this 2015 review of the literature on surgical masking, and – because it is one of the best individual studies on the question– this 1991 Swedish paper by T.G. Tunevall, who designed his partially randomised trial to investigate an earlier finding that face masks might actually increase the rate of postoperative infections. Across 3,000 operations, Tunevall failed to find any statistically significant difference in patient outcomes, whether surgical teams wore masks or not.
Surgeons began experimenting with masks as the study of bacteria matured at the turn of the twentieth century, and scientists realised that particles expelled from the mouth were full of culturable pathogens. Bacteria in wounds is obviously bad, and masks seem a plausible way of preventing bacterial contamination. As with community masking, the theory is there; it just doesn’t pan out in practice. This shouldn’t be surprising, because almost all proposed medical interventions fail, despite the fact that there’s a theory behind every single one of them.
I love the last line.
“…almost all proposed medical interventions fail, despite the fact that there’s a theory behind every single one of them.”
Ain’t it the truth?
Getting back to the Cochrane Report on masks and the fact that it showed no real evidence that masks work, there is an old adage in research that says if there is a causal factor, the more you study it, the stronger the effect becomes. Conversely, if there isn’t, the more you study it, the weaker the effect becomes.
In other words, if your hypothesis is that A causes B, and, if in reality, A really does cause B, the more research you do, the stronger the evidence becomes that A causes B. If, on the other hand, A does not cause B, but your hypothesis is that A causes B, the more research you do, the weaker the evidence becomes that A causes B.
That’s what we’re seeing with this Cochrane Report. There are all the studies in which people are trying to show that masks prevent the spread of Covid, but as the mass of them stacks up, the evidence becomes more inconclusive. Which means idiots such as those commenters in the NY Times article seek refuge in the fact that the studies are inconclusive.
They say, these studies don’t really prove that masks don’t stop the spread, and if they keep on doing these studies, they are bound to come up with one that does show masks stop the spread.
Sorry, but when they’ve done this many inconclusive studies—and most of them by people wanting to show masks are effective—the evidence is going to do nothing but get weaker.
Let me give you another example.
This time the subject is saturated fat.
Here is a Cochrane Report from 2020 on saturated fat and risk for heart disease.
If you read the report, and I encourage you to, you will find the Cochrane authors concluded that there was weak evidence linking consumption of saturated fat to heart disease.
The report abounds in weasel words. Take a look at the Main Results section about the findings of the various studies they evaluated. My bold emphasis.
Meta‐regression suggested that greater reductions in saturated fat (reflected in greater reductions in serum cholesterol) resulted in greater reductions in risk of CVD events, explaining most heterogeneity between trials. The number needed to treat for an additional beneficial outcome (NNTB) was 56 in primary prevention trials, so 56 people need to reduce their saturated fat intake for ~four years for one person to avoid experiencing a CVD event. In secondary prevention trials, the NNTB was 53. Subgrouping did not suggest significant differences between replacement of saturated fat calories with polyunsaturated fat or carbohydrate, and data on replacement with monounsaturated fat and protein was very limited.
We found little or no effect of reducing saturated fat on all‐cause mortality (RR 0.96; 95% CI 0.90 to 1.03; 11 trials, 55,858 participants) or cardiovascular mortality (RR 0.95; 95% CI 0.80 to 1.12, 10 trials, 53,421 participants), both with GRADE moderate‐quality evidence.
There was little or no effect of reducing saturated fats on non‐fatal myocardial infarction (RR 0.97, 95% CI 0.87 to 1.07) or CHD mortality (RR 0.97, 95% CI 0.82 to 1.16, both low‐quality evidence), but effects on total (fatal or non‐fatal) myocardial infarction, stroke and CHD events (fatal or non‐fatal) were all unclear as the evidence was of very low quality. There was little or no effect on cancer mortality, cancer diagnoses, diabetes diagnosis, HDL cholesterol, serum triglycerides or blood pressure, and small reductions in weight, serum total cholesterol, LDL cholesterol and BMI. There was no evidence of harmful effects of reducing saturated fat intakes.
See what I mean. This is the weakest evidence imaginable. And I can guarantee you the more times saturated fat vs heart disease is studied, the weaker and weaker this evidence will become—though it’s difficult to see how it could get a lot weaker than this.
The American College of Cardiology (ACC) has long advocated a reduction in dietary saturated fat due to its propensity to cause elevated LDL in some subjects. But even the ACC has now published a position paper in their house journal absolving saturated fats. Had I not read it with my own eyes, I never would have believed the ACC would have published such a thing given their decades-long antipathy, if not outright hostility, toward saturated fat.
The Quality of Dietary Protein
I just came across an article about protein quality in a medical news service I subscribe to. It was just published yesterday, but it’s already way out of date.
The article discusses how deficient plant-based milks are in protein quality. It starts out
New guidelines released by the Food and Drug Administration can help consumers better understand nutritional difference between plant-based and dairy milks, according to a food science expert.
Some people believe plant-based and dairy milks are nutritionally similar, but that is not the case, says Melissa Wright, director of the Food Producer Technical Assistant Network at Virginia Tech.
Melissa Wright is right as rain, but as the article goes on, it becomes apparent that she is relying on old data. Plant-based “milks” are much worse than she claims.
She goes on
“It’s important for consumers to educate themselves about what food labels tell us about what we are putting into our bodies. The largest nutritional differences are with protein and carbohydrates,” says Wright. “While plant-based beverages might contain as much protein as dairy milk, the key piece of information that consumers don’t always know is that not all protein is equal when it comes to human digestion.” [My bold for emphasis]
She is absolutely correct. It’s not the total amount of protein that is important, it’s the amino acid make up of that protein. In terms of human health, the total amount of protein is limited by the least available essential amino acid. In plant foods, that is usually lysine.
Wright explains that all sources of protein have a PDCAAS, or protein digestibility-corrected amino acid score. This method evaluates the quality of a protein based on the amino acid requirements for humans and their ability to digest it.
She’s a little behind the times here. And a little mistaken. Let me digress and tell you why.
First, she keeps saying that there is a difference in ability to digest the protein. That isn’t exactly correct. All these proteins digest the same. The issue is availability. We can best use proteins that have the correct essential amino acid composition that matches with the protein structures we’re using the dietary protein to repair or replace. Even if we take in a massive amount of the protein and it has a deficiency of just one single essential amino acid, we can use it only to the extent of the availability of that one deficient amino acid.
The RDA of protein was determined way back in 1943 using nitrogen balance studies on military recruits. Without getting into all the reasons, let me assure you that nitrogen balance studies are notoriously inaccurate, yet we’ve been using the RDA calculated by them since 1943.
Since that time, there have been a series of attempts to come up with a better way to determine adequate protein intake without a lot of success.
In 1991 (almost 50 years after the RDA) The Food and Agricultural Organization of the United Nations/World Health Organizations (FAO/WHO) and the US FDA proposed a more accurate way of determining protein quality. It is called the Protein Digestibility-Corrected Amino Acid Score (PDCAAS). It’s referred to in the biz and pronounced PD Cass. As in Pee Dee Cass.
This was a huge step in the right direction, but was kind of screwed up by our old friend saturated fat. When the folks who developed the PDCAAS looked at the highest quality proteins, they discovered, to no one’s surprise, that the highest quality proteins came from foods of animal origin: meat, eggs, and dairy. Based on their methodology, any protein source hitting or exceeding 100 percent of the protein required of a growing child was listed as 1.0. Even if the protein source clocked in at greater than 100 percent, it was truncated to 1.0. I’ve heard some folks explain this as due to all these quality protein sources being rich in saturated fat. Those coming up with the PDCAAS didn’t want to encourage overconsumption of a food humans have thrived on for millennia, but that was then thought to increase the risk for heart disease.
In 2013, the same FAO came up with a vastly better protein scoring system: the Digestible Indispensable Amino Acid Score (DIAAS). Pronounced DI AS, as in Dye as.
Problem with this scoring system is that it hasn’t tested the huge number of foods to get scores as has PDCASS.
But it’s vastly better. The PDCASS was developed using samples from the end of the digestive process in mouse feces. DIASS, on the other hand, used sample from the end of the ileum (the point at which all protein should have been absorbed) in pigs, which are much more like humans digestive-tract-wise than mice.
And the protein quality wasn’t truncated at 1.0.
So, Melissa Wright is a little behind the times in using the PDCASS. Whatever that scoring system shows, the DIAAS is better.
Here is a comparison of the two:
The red line I’ve drawn shows the breakpoint between high-quality protein providing all the essential amino acids in the correct amounts and not-so-high quality protein.
Here is another chart showing the same thing from a paper by Robert Wolf. Wolf is one of the world’s leading researchers on protein, so I would tend to trust his figures more.
One of the things you’ll discover when you learn about protein is that when plant protein is processed, it loses a lot of its protein quality. But animal protein does just the opposite. If it is processed into, say, salami, it increases its protein availability a bit.
As you can see from the chart above, wheat is a crappy protein source. When it is processed into breakfast cereal, it becomes even crappier. And when well-meaning moms top it off with oat milk or almond milk or soy milk, it is dreadfully protein inadequate. How many growing kids do you think start off their day like that? I would think a pretty substantial number do.
Covid Myths Debunked…You Were Right!
A reader sent me this article from the New York Post titled “10 myths told by COVID experts — and now debunked” with a note saying “You were right.”
The 10 myths in order:
Natural immunity offers little protection compared to vaccinated immunity
Masks prevent COVID transmission
School closures reduce COVID transmission
Myocarditis from the vaccine is less common than from the infection
Young people benefit from a vaccine booster
Vaccine mandates increased vaccination rates
COVID originating from the Wuhan lab is a conspiracy theory
It was important to get the second vaccine dose 3-4 weeks after the first dose
Data on the bivalent vaccine is ‘crystal clear’
One in five people get long COVID
After looking this list over, I think I can claim credit for 1, 2, 3, 4, 5, & 7.
I would have assumed the vaccine mandates would increase vaccination rates. I’m not sure I ever commented on #8, though if asked, I would have said, Don’t get the second one. I don’t think I ever mentioned number 9. I’m pretty sure I did mention long Covid obliquely, but I never put a number on it. I just said based on my experience both personally and as a physician, people can have longer than normal recovery times from almost any virus.
Since I got as many of these right as I did, is that a tribute to my genius?
Absolutely not. It’s a tribute to my ability to disbelieve most of what I get from the press and especially from the government. And to my long experience as a practicing physician.
Let’s take #1, for example. There has been no vaccine ever made that provides better immunity than having the disease. If you get the measles—as I did—you are pretty much protected for life from getting them again. If you take the measles vaccine, which is one of the better vaccines out there, you have about 95 percent protection. Vaccinated people do get the measles, as the college campus measles outbreaks a few years back proved. Those who have had them, don’t.
So why would the Covid vaccine be any different? That one was easy.
#2 I figured out from the Danish study that I wrote about here many times. In that study, during the early days of Covid, when people were coming down with it right and left, half of the subjects wore masks while the other half didn’t. There was no difference in the rate of contracting Covid whether you were masked or not. This study was done before politicization of the pandemic had set in.
Plus, I knew masks weren’t effective against aerosols. Sars-CoV-2 is an aerosol. So that one was a no brainer.
#3. In Sweden schools stayed open. Students were fine, and, more importantly, teachers contracted Covid less frequently than non-teachers.
#4 I’ve been a doc for a long time, and it just isn’t that common to see patients who have developed myocarditis. Once the vaccinations started, cases began to pop up everywhere, especially in kids, in whom you don’t usually see it and who hadn’t been profoundly impacted by the actual disease as a group.
#5 After I learned that, unlike with influenza, healthy kids didn’t really have a problem with Covid, I figured why vaccinate them. They would then assume the risks from vaccination without any benefit on the other side. A no brainer.
#7 I had no clue as to whether Sars-CoV-2 came from a lab or from nature. But then I read the two terrific pieces by Nicholas Wade in Bulletin of the Atomic Scientists and Medium, I became persuaded that the lab leak hypothesis was more likely true than the it-emerged-from-nature hypothesis.
The reason I found these articles so persuasive is that I had just read a brand new immunology textbook I was inspired to purchase by the idiocy of the #1 myth above. The one Fauci and the rest were babbling on about saying the vaccines provided better protection than natural immunity. Had the info in that textbook not been so fresh in my mind, I might not have seen so clearly how the evidence presented in those two articles was accurate.
So it wasn’t brilliance. It was just a healthy skepticism. A wide reading of the information out there. And the fresh reading of a textbook on immunology.
One of the myths that wasn’t listed in the top ten that I think I debunked somewhere along the way, or at least should have if I didn’t, was the idea that the mRNA vaccine stayed in the shoulder. As it turns out, it goes all over the place. But anyone who has any medical schooling at all should have known that.
When I used to work in the ER years ago, we gave 4.8 million units of penicillin—2.4 in each hip—to patients who tested positive for gonorrhea, i.e., the clap. In males, gonorrhea infects the urethra (the tube for urine passage between the bladder and the outside) and can get into the prostate, causing prostatitis. In females, it infects the cervix (the mouth of the womb) and can get into the pelvic organs, which is called pelvic inflammatory disease (PID). The penicillin shots we gave went into the patients’ butts, not into their urethras or cervices (or cervixes if you like). But we knew the penicillin would make its way to those structures and wipe out the bad bugs.
Same with strep throat. We would give kids shots of penicillin in their rears, if we had any doubts the parents would get a prescription filled. We didn’t squirt the penicillin in their throats. We just knew it would get there from their rear ends.
It’s the same with all injections. Other than injecting a joint, it’s difficult to think of an injection you give at the site of the infection.
Cells are awash in fluid called interstitial fluid, i.e., the fluid between cells. When you inject into the muscle of the shoulder or the hip, you are injecting into this interstitial fluid. I doubt that much, if any, of the medicine goes into the muscle cells. Most, I’m sure, ends up in the interstitial fluid, which is basically in equilibrium with the blood. Blood vessels have little pores in them through which flow various nutrients and waste products going to and from the cells. They go from the blood to the interstitial fluid to the cells and go back the same way in reverse, from the cells to the interstitial fluid to the blood. Which is why if you inject someone’s butt for strep throat, the medication gets from butt to throat fairly quickly.
Why would anyone think the mRNA vaccines would stay put in the shoulder when that doesn’t happen with any other injection?
Don’t Believe Everything You See
Okay. After telling you how I was not taken in by the myths above, here is one I bought hook, line, and sinker. You may have, too.
How could you not believe it? You saw it with your own eyes.
I’m talking about the Central Park Karen.
Remember her? She was the one walking her dog without a leash in a remote part of Central Park in New York. While doing so, she came upon an African American man who was out birdwatching. He asked her to put her dog on a leash, and she began acting weird and telling him she was going to call the police as she felt threatened by him. He said go ahead and call them. Meanwhile, he was recording the whole interaction. She gets the police on her cellphone and tells them in increasingly hysterical fashion that an African American man is threatening her in Central Park.
I’m sure most of you saw the video.
And I’m sure most of you had the same reaction I did when the media jumped all over it. She got fired from her job, her dog got taken away from her, and she was totally humiliated.
Good enough for her, I said. I suspect many of you felt the same way.
But we were all victims of the attribution bias.
The attribution bias is when we attribute personality defects to others for behaviors we are able to explain away in ourselves by having good reasons to act the way we did.
For instance, let’s say you are short with a co-worker, because you have a splitting headache and feel as if you are coming down with something. If someone asks you about it a few days later, you say, Oh, I had a terrible headache and thought I was getting sick. Which is your excuse. It wasn’t that you are a bad person; you were just in pain.
But if that co-worker is short with you, you probably don’t say to yourself, Oh, he probably just doesn’t feel good. He might have a headache. Instead you say to yourself, What a prick he is.
You have an excuse for your bad behavior. But bad behavior in others is a defect in their personalities. That is the attribution bias.
And the attribution bias was writ large in me in the Central Park Karen affair.
Bari Weiss, who writes and employs other writers, is a Substack favorite of mine. She shared an interview with the Central Park Karen, who now lives anonymously in another country. She’s suffered mightily since the events in the video we all saw transpired. Death threats, abuse threats, threats to her parents, the whole gamut of what people with a shield of anonymity can inflict on others.
When you listen to her interview and understand what was really going on at the time—not just what the birdwatchers video showed—and the history the videoing guy has—as sussed out by the interviewer, who is himself an African American—you come away with a totally different perspective. At least I did.
And I was ashamed of myself for getting sucked into the whole thing just as the media wanted me to.
It has been a lesson to me to be careful of taking things at face value, even things I see on video.
More on Simaglutide
One of my favorite bloggers on the internet is Peter Dobromylskyj, who writes the Hyperlipid blog.
I always read everything he writes, but over the past month I’ve had so much going on that I’ve given it short shrift. I had a little time last night while MD was at her chorus rehearsal that I started catching up.
A month or so ago—that’s how far I am behind—he wrote a post on simaglutide, the generic name of Ozempic and Wegovy, the two expensive, injectable weight loss drugs sweeping through Hollywood and those groups well heeled enough to fork over $1,000+ per month for them.
As usual, Peter has dug deeply into the literature to snuffle out the mechanisms involved in how these drugs work. And, in the process, came across the potential for some pretty serious long term problems.
I encourage you to read his entire post. I’m going to hit a few highlights here, so you can see the issues involved.
Here is one of the findings he pulled from the literature:
So the GLP-1 agonists stimulate adipose hyperplasia meaning you develop lots of small adipocytes which are much better able to act as a sump for calories. There appears to be a shift of fatty acids out of pre-existing hypertrophied adipocytes, and out of ectopic fat deposition sites too, and in to these spanking new baby adipocytes.
What does this mean?
In physiology in general things have an easier time returning to a normal state than they do an abnormal state. It’s long been thought that children and adults develop obesity differently. Children develop obesity by increasing the number of normal-sized fat cells, while adults develop obesity by increasing the size of the fat cells they already have. It is easier to help the enlarged fat cells that obese adults possess return to normal size via diet than it is for normal sized fat cells in obese children to reduce to below normal size. That’s why people who have been obese since childhood have a more difficult time losing than do people with the same degree of obesity developed in adulthood.
In one case, the enlarged cells are returning to a more normal size while in the other the many small cells have to lose fat to become lower than normal in size.
He goes on to show how some of the literature shows that GLP-1 agonists work by increasing uncoupling.
Uncoupling is kind of a complex process, so I’ll try to simplify it. There are a couple of ways your body generates energy. One way is by breaking down glucose in the cytoplasm of the cells. That way provides a bit of energy, but the vast majority of the energy (read: ATP) your body produces happens inside the mitochondria in a coupled process. As the energy from fat and/or glucose breakdown is fed into the various complexes in the mitochondria, they end up creating an electro-chemical gradient across the membrane. More protons are on one side of the membrane than on the other.
This differential in electro-chemical pressure ends up driving many little turbines in the membrane to basically turn and churn out ATP.
If you generate a big electro-chemical imbalance, you crank out ATP like crazy. But if a drug or whatever releases the protons across the membrane to make the sides more equal in electro-chemical energy, that’s called uncoupling. If you uncouple ATP production from the process of storing energy across the gradient, then you dissipate the energy you would have used to make ATP. Since you still need the ATP, your mitochondria have to keep chugging. And if you’re uncoupling while that’s going on, you dissipate a lot of energy that would otherwise have been used to generate ATP. And usually lose weight in the process.
Peter also discusses briefly a paper showing perhaps GLP-1 agonists may cause breast cancer. He comments that the producers of these drugs have taken it seriously enough to try to hide it in a meta-analysis.
And finally he predicts that ultimately the drugs will be withdrawn.
So what will happen to folks with years of adipocyte hyperplasia, where individual cell hypertrophy has been suppressed? Their very numerous small adipocytes will, without their uncoupling drug, become enormous. People will become hungry as they develop hypertophy of all of those lovely tiny insulin sensitive adipocytes. Oops. It's gonna be bad, but that's years down the road.
That will be bad for those today who are going for these drugs whole hog. There may be a real reckoning at some point.
As I’ve said since I’ve been writing about them, they are better off avoided. I don’t have any idea if that same effect is true for the poor man’s version — the Yacon Syrup — but as they said in Ancient Rome: caveat emptor.
Video of the Week
I love this video of Tucker Carlson on Tulsi Gabbard’s podcast. It’s fun to watch him go ballistic over someone calling him an agent of Russia. Also funny how that is the worst insult you can sling at someone today… other than racist.
Okay, that’s about it for today. My schedule has been brutal the past month, but as of tomorrow it slacks off. MD and I are going to be all in on Protein Power 2.0. Our plan is to have it available toward the end of the year. We have pretty much cleared everything from our agenda except that book. And The Arrow. And the third installment on her Caddo Bend novel series, which is coming along.
I’ll be back next Thursday. Keep in good cheer, and I’ll see you then.