The Arrow #133

Hello friends.

Greetings from Montecito.

Looks like I’m finally cured of RSV. But MD came down with a light case of it. She wasn’t nearly as sick as I was, however. In fact, she’s as good as well already. I guess it’s the difference in prior exposure. When we both got Covid, she was much sicker than I, so I must have been exposed to a coronavirus somewhere along the way that was closer to SARS-CoV-2 than whatever her previous exposure was. Anyway, we are both recovered and good as new. Thank God. And thanks to all the well wishers for a speedy recovery.

At least we didn’t die, which brings me to

Excess Deaths in the US

Before coming to any conclusions, I try to read as much as I can on both sides of a given issue. There has been a ton of information published over the last few months about an increase in excess deaths in countries all over the world. I’ve been waiting to see data from the United States before really diving into the situation.

I came across this graphic (which you can download from this Dropbox link) showing an increase in excess deaths in the US in late 2022, but I haven’t seen anything from the CDC. If you download the graph, the links are live.

As you can see, the US is right in the middle just below the line. If the CDC were doing the job for which it is funded instead of gaslighting us, it would be providing this data.

I did ultimately find it by reading the Substack of Your Local Epidemiologist (YLE), which is written by a person Nassim Taleb would call an IYI (intellectual yet idiot). I prefer the term pinhead, but that’s just me. (I’m sure she and her children got every Covid jab that was available.) YLE posted the latest CDC data on excess deaths in the US.

In reference to the above graphic, YLE writes

Since late January 2023, excess deaths have reached pre-pandemic levels. This has been a massive reprieve.

You can always count on YLE to write whatever the mainstream wants you to believe. Which is why I read her every post.

Looking at the data above, ignore everything to the right of the vertical red line I added. The CDC is notoriously laggard in getting its data gathered, compiled, and published. It usually runs at least six months behind, so everything beyond the vertical red line is extrapolated. It’s not real data. Which YLE should know, but chose to ignore to keep in step with the mainstream narrative.

Looking at everything to the left of my vertical red line, it appears to me that excess deaths have not leveled out. Nor have they decreased as much as the extrapolated data past the vertical line would imply.

Had Covid been a typical serious viral illness (like, say, a bad flu year), you would see patterns in excess deaths that look like what you see in the years before 2020 in the CDC graphic above. A sort of sinusoidal pattern.

Why is this?

Let’s take a look.

(As an aside, I bought an Apple pencil to use on my iPad. And I downloaded Autodesk Sketchbook, a program that lets one do all kinds of artistic renderings on the iPad. Problem is, it is complicated and there is a learning curve. I’ve been wanting to do something like this for years, so that I could create various kinds of graphics to help illustrate concepts without having to do it with words. The graphs below are my first pitiful, crude efforts. It will get better. It is difficult to do, and I can tell you for a fact that I am a pretty good artist using a graphite pencil, charcoal, watercolor, pastel, oil, and even clay. But this digital stuff will take me some time to master.)

Here is what an excess death graphic would look like if there were no diseases and everyone just died of old age.

You would see a little variation, but not a lot. Nothing would be killing people off, so they would simply succumb to the non-contagious diseases of aging (heart disease, diabetes, etc.)

When you throw infectious diseases in the mix, you get a different picture.

Let’s take Covid, for example. It killed mainly older people who were already weakened by a host of other non-infectious co-morbidities. Had these people not gotten Covid (and had they not fallen into the hands of the government-approved treatment by ventilator) they would have continued to die on schedule as shown in the graphic above. A gentle wave of a little less, a little more, but about the same number of them every year.

But they didn’t. Covid (and the early treatment by ventilator) took out all the folks who were already going to die on schedule plus a whole lot more who would have lived a year or two or three longer before succumbing to their non-infectious disease.

When all those people died a few years prematurely, they were removed from the population that would have died a few years later. This would mean that there would be a decrease in excess deaths following the year(s) in which there was an increase in excess deaths. The typical pattern is shown below.

You see this pattern repeated in the CDC data in the years prior to Covid. Once Covid arrived, the pattern changed. And since, as it has turned out, Covid shouldn’t have been much, if any, worse than a bad flu year, something else is afoot. What could that be? What was different about Covid than any other disease in our lifetime? And what was the remedy? I’ll leave it to you to puzzle out. All I can say is that there should be a huge drop in excess deaths, and there hasn’t been.

This fallacy is also promoted by The NY Times. A few days ago David Leonhardt— who for a NY Times writer is a pretty reasonable fellow — wrote an article titled “A New Covid Milestone.” The subtitle of his piece reads “In a sign that the pandemic really is over, the total number of Americans dying each day is no longer historically abnormal.”

He goes on

The United States has reached a milestone in the long struggle against Covid: The total number of Americans dying each day — from any cause — is no longer historically abnormal.

Excess deaths, as this number is known, has been an important measure of Covid’s true toll because it does not depend on the murky attribution of deaths to a specific cause. Even if Covid is being underdiagnosed, the excess-deaths statistic can capture its effects. The statistic also captures Covid’s indirect effects, like the surge of vehicle crashes, gun deaths and deaths from missed medical treatments during the pandemic. [Links in the original]

The article goes on with all the mainstream, Big Pharma-driven blather about how successful the vaccines have been in staving off deaths, despite the fact that there have been more Covid deaths since the vaccines came on the market than there were before. But we can’t let a fact like that stand in the way of The Narrative.

And the piece repeats the nonsense that “the total number of Americans dying each day…is no longer historically abnormal.” That simply isn’t true.

As I showed in my primitive graphics above, given the massive increase in deaths above the excess deaths line, there should be a similar decrease in excess deaths soon after. If we’ve just gotten back to the excess deaths line where excess deaths are “no longer historically abnormal,” it means there are still a shitload of excess deaths. Why? That ought to be the question journalists should be wrestling with. Not just trying to calm us by saying, we’re all safe now. The pandemic is over.

On another note, deep within the Leonhardt article there is this paragraph:

The official number [total Covid deaths] is probably an exaggeration because it includes some people who had virus when they died even though it was not the underlying cause of death. Other C.D.C. data suggests that almost one-third of official recent Covid deaths have fallen into this category. A study published in the journal Clinical Infectious Diseases came to similar conclusions. [Links in the original] [My bold for emphasis]

This is what many of us said from the start: there is a big difference between dying from Covid and dying with Covid. And we were pooh poohed for it.

Now, just like it did with the Hunter Biden laptop, the NYT admits the truth, but buries it deep within an article instead of headlining it.

Pretty damn sleazy if you ask me.

More Big Pharma Treachery

Or, I guess I should just say more Big Pharma business as usual.

I wrote a year or so ago about using IV colchicine to deal with frozen shoulders and other inflammatory problems. It works like a charm, but most docs don’t even know about it. I found out because it worked on me.

Colchicine is a drug most commonly used for gout. It comes from the plant autumn crocus (Colchicum autumnale) and has been used as an anti-inflammatory since 1500 BC. It was written about in the Ebers Papyrus, an ancient Egyptian medical text. Benjamin Franklin, who suffered from gout, brought the plant to America, so he could have some relief.

Colchicine was being used as a drug long, long before the FDA came into being. There were many similar drugs that had been around forever and the FDA, unlike with any new drugs, simply approved them without any clinical testing. Consequently, colchicine, aspirin, and a host of other old, yet effective, drugs have always been dirt cheap.

But, in the case of colchicine, not any longer.

I was catching up in my backlog of Medscape articles last week and came across one titled “FDA OKs Low-Dose Colchicine for Broad CV Indication.” According to the article

The US Food and Drug Administration has approved the anti-inflammatory drug colchicine 0.5 mg tablets (Lodoco) as the first specific anti-inflammatory drug demonstrated to reduce the risk for myocardial infarction (MI), stroke, coronary revascularization, and cardiovascular death in adult patients with established atherosclerotic disease or with multiple risk factors for cardiovascular disease.

The article went on to report

Data supporting the approval has come from two major randomized trials, LoDoCo-2 and COLCOT.

In the LoDoCo-2 trial, the anti-inflammatory drug cut the risk of cardiovascular events by one third when added to standard prevention therapies in patients with chronic coronary disease. And in the COLCOT study, use of colchicine reduced cardiovascular events by 23% compared with placebo in patients with a recent MI.

Wow, I thought, what company went through all the brain damage, not to mention the millions and millions of dollars, to get a generic drug approved. And with two studies, to boot.

Colchicine costs pennies per dose, so how were they ever going to recover their investment?

I should have known something was rotten in the state of Pharma.

It was of course a hand-in-hand deal between a drug company and the FDA.

I got tipped off by another Medscape article I found while looking for more info. This one titled Low-Dose Colchicine Approved for CVD: Now What? takes a more jaundiced look at what happened.

Did you know that colchicine has been used for hundreds of years? It’s so old that it was never approved by the US Food and Drug Administration (FDA) for a formal indication. That led to a regulatory mess around 2010 in which a single drug company decided to test colchicine formally in a trial, a very small and inexpensive trial, and it garnered formal approval of branded Colcrys for gout. That led to a 3-year term of marketing exclusivity, prohibition of generic sales, and a 50-fold increase in price.

Oral colchicine remains expensive today.

Biologically, colchicine has broad anti-inflammatory effects, and we all know that atherosclerotic disease is at least partially an inflammatory disease.

Recently FDA has approved lower-dose 0.5 mg daily of colchicine as the first anti-inflammatory drug demonstrated to reduce the risk of MI, stroke, coronary revascularization, and CV death in patients with either known heart disease or high risk for CV disease.

The author of the piece goes on to say he hopes colchicine doesn’t replace statins as the mainline therapy for those with heart disease. Heaven forfend!

But the fact that colchicine works is an indictment against statins and the purpose for which they were designed. There are all kinds of competing theories as to what causes heart disease. One group—the statinators of the world—believe that LDL-cholesterol is the driving force behind the development of coronary arterial plaque. Another group believes that inflammation drives the process. This evidence is strong enough that even many statinators say that statins work in part by acting as anti-inflammatory agents.

As far as I know—and I haven’t made it my life’s work to dig up all the papers on colchicine and LDL—colchicine does not lower LDL, so whatever benefit it has on preventing heart disease isn’t secondary to LDL lowering.

Getting back to our colchicine story, what happened was that after centuries of use as an anti-inflammatory for gout, a pharmaceutical company decides to do an actual study—a small, inexpensive one as reported above—to confirm colchicine really does work to reduce inflammation in gout.

According to Wikipedia

On 30 July 2009, the FDA approved colchicine as a monotherapy for the treatment of three different indications (familial Mediterranean fever, acute gout flares, and for the prophylaxis of gout flares, and gave URL Pharma a three-year marketing exclusivity agreement in exchange for URL Pharma doing 17 new studies and investing $100 million into the product, of which $45 million went to the FDA for the application fee. [my bold emphasis]

What happened then?

The price of colchicine went from about 9 cents per pill to almost $5 per pill.

That’s your government at work.

Now what with the two new studies that just came out showing colchicine helps prevent cardiovascular disease, the patents will not run out until 2029. By then, I suspect, there will be some other Mickey Mouse study showing the effectiveness of colchicine for some other malady, and the patent will be extended. And the price of colchicine will go up, up, up.

After this fiasco in 2010, the New England Journal of Medicine had some hot words for what had happened.

The colchicine case demonstrates some important limitations of our current system for rewarding innovation in the pharmaceutical market. Incentive programs like those enacted by the Waxman–Hatch Act and the Orphan Drug Act offer market exclusivity to encourage drug research, but these rewards are not calibrated to the quality or value of the information produced. Although the goals underlying the development of Colcrys were sound— few would argue against the need to comply with FDA requirements and the need to ensure the safety and efficacy of all prescription drugs — and the manufacturer seems to have followed FDA guidance, the reward appears to be out of proportion to the level of investment. More important, there is no evidence of any meaningful improvement to the public health. We believe that when creating and implementing incentives for private investment in drug research, policymakers should seek to avoid policies that can lead to such outcomes. An alternative solution, probably much less expensive, would be for the FDA or the National Institutes of Health to fund trials that address outstanding questions related to widely available drugs such as colchicine.

In addition, it is important to remember that the financial burden of market-exclusivity incentives in the United States falls primarily on the patients who are given prescriptions for the drug, or their insurers. Consequently, it seems reasonable to expect that costly new drugs or increases in drug prices would be accompanied by a substantial benefit in disease management to be enjoyed by these patients. This standard is not met by Colcrys [the trade name for colchicine]; in this instance, the public may bear considerable costs for a poorly executed administrative goal.

If you have any interest in reading more about this travesty, read the NEJM article in its entirety. It is pretty obvious this is where Wikipedia got most of its information.

So, there you have it. Big Pharma working hand in glove with the FDA to screw American citizens. Take a drug that’s been around for millennia, and that works, do a short (one week, in this case) study on it, get the FDA to give you a monopoly to prevent the generic sales, and pocket your millions. The only loser is us.

While we’re on the subject of Big Pharma and Big Gov’t…

This popped up on my daily email from Readwise a couple of days ago.

Which leads me to this…

What Is A Placebo?

As I’ve mentioned several times in discussing the book Turtles All the Way Down, vaccines are not tested against a true placebo, which is an inert substance that should not cause any health issues. Sterile saline (salt water), for example.

Vaccines, as it turns out, are tested not against inert placebos, but against earlier versions of the same vaccine. Or even other vaccines. Or against a “placebo” that is the same as the vaccine, but without the active viral ingredient. In other words, just maybe the adjuvant (a substance that helps make the vaccine more potent). There is a massive halo effect around vaccines. The manufacturers have persuaded us all that vaccines are truly God’s gift to the world, and that to test a vaccine against a true placebo would be unethical. Why? Because a vaccine would be denied to the control group of subjects. Therefore the control gets the previous version of the vaccine. Wouldn’t be ethical to allow them to go unvaccinated, now would it?

Vaccines have a strange history, which I will touch on briefly.

Prior to 1986, vaccines were the redheaded step children of the pharmaceutical industry. They were products made almost under protest by the drug companies because they were so unprofitable. Plus, they were magnets for lawsuits due to the many adverse events associated with them.

Even though there were only about five vaccines available for kids to take, the big worry was that the pharmaceutical companies would quit making them. Then what?

Congress passed a bill, and Reagan signed it into law, which gave Big Pharma (which wasn’t nearly as big then as it is now) immunity against vaccine lawsuits.

Once this happened, the door opened for the manufacture of more and more vaccines until now there are some 80 or so of them out there, many of which children have to get before they can attend school.

Now, instead of vestigial products worth very little, they became cash cows for Big Pharma.

I always assumed that these vaccines were tested against true placebos, but, as I learned, they are not.

But I figured other drugs were. All the testing for drugs are supposed to be placebo-controlled. All the papers on drug testing say the trials were placebo-controlled.

Sadly, such is not the case.

As I learned from a recent Substack by my friend Dr. Maryanne Demasi, drug companies come up with their own proprietary “placebos”.

Drug companies will often manufacture their own placebo for use in clinical trials. The technical data and analytical methods used for the placebo are detailed in the certificate of analysis (CoA), which is part of the dossier submitted to the relevant drug regulator as part of a licensing application.

…the exact formulation of a placebo is rarely disclosed in the peer-reviewed publication of a clinical trial. Further, medical journals do not require authors, nor drug manufacturers, to disclose the contents of a placebo or publish the CoA. Placebos may contain excipients such as chemicals, dyes, or allergens, which might unintentionally cause side effects, raising concerns about the reliability of trial data and the transparency of important information.

If I didn’t know this—and I read way more studies than the average bear—then I suspect it will be news to a lot of people.

Dr. Demasi was intrigued by the fact that in the Jupiter Study (a famous study done of the statin drug Crestor (rosuvastatin), there were more complaints of muscle pain in the placebo group than in the study group. One of the main complaints of patients taking statins of any kind is muscle pain, so how could the placebo possible end up giving more people muscle pain than an actual statin? (I wrote about this study years ago when it first came out and wondered about this same thing. I called it fishy at the time. If you go to the link to my post, be forewarned. This is an old post I haven’t updated yet, so many of the links likely won’t work, and it doesn’t have a featured image.)

Dr. Demasi began trying to figure out what was in the placebo that might have caused the muscle pains. Clearly, it wasn’t an inert placebo. She contacted the lead author, who didn’t respond. She then began contacting all the regulatory agencies in the US, Europe, and Australia that had approved the drug. If they got back to her at all, they told her they couldn’t give out the information in the CoA, and that the only way she could get it was to contact AstraZeneca, the maker of Crestor, directly and try to pry it out of them.

So she tried.

After multiple emails and lengthy delays, we finally obtained a response from AstraZeneca stating that we could ‘apply’ for access to the information but that we could not share the data with any third parties without restrictions. The company stipulated in its conditions that we could not publish the CoA in the peer reviewed literature and that any analysis of the CoA by us, would have to be “pre-reviewed” by the drug company since they were owners of the information.

We refused to abide by AstraZeneca’s conditions of access. This type of oversight, whereby research needs to be vetted by drug companies or where researchers are required sign confidentiality agreements, can stifle open science.

So there you have it friends and neighbors. Big Pharma can make their own placebos to compare against drugs they are trying to get approved just like they do with vaccines.

Doesn’t give me a whole lot of comfort.

I encourage you to read Dr. Demasi’s short Substack post to see just how much effort she put into this project and how she was rebuffed at every step. And I suggest you subscribe. I read everything she publishes.

What's in the placebo?

Climate Follies, The Lake Tulare Edition

In the late 1800s/early 1900s there was a huge lake in the heart of the San Joaquin Valley. Called Lake Tulare, it was the largest fresh water lake west of the Mississippi River. The banks of Lake Tulare were the home of the Tachi Yokut tribe in central California. I would use the term indigenous people to describe the Tachi Yokut, but since the entire history of the planet is one of various tribes, clans, hordes, whatever conquering others, who knows who the real indigenous people living around Lake Tulare were. Could be the Tachi Yokut, but probably not. At any rate, they were there as long as the current history of the area has been known. And the lake was its cultural and spiritual center.

Unfortunately for the Tachi Yokut, white settlers in the San Joaquin Valley began diverting the water that normally spilled into and maintained Lake Tulare into agricultural land nearby. Over time, the lake diminished in size and the ground it formerly occupied was converted to agricultural purposes. Ultimately, Lake Tulare disappeared, and its entire area was turned to agricultural use.

Which did not set well with the Tachi Yokut, but they had little say in the matter.

The spring of 2023 saw Lake Tulare re-appear. After years of drought in the area and deafening cries of climate change is destroying the earth, Mother Nature opened up the heavens and it rained, rained, rained.

As the former Lake Tulare became the current Lake Tulare, farmers rushed to move equipment and what structures they could. Now pistachio trees, cotton plants, and a multitude of other crops and buildings are covered in water.

Now, just in case you’re thinking Lake Tulare is a good sized pond, let me tell you that it is about the same size as Lake Tahoe, which is 22 miles long and 12 miles wide. It is a big lake. While not nearly as deep as Lake Tahoe, which is about 1,600 feet deep at its deepest, even at 30 feet deep Lake Tulare covers a bit over 13,000 acres, which is a massive amount of area.

You can click here to see images of this now vast lake.

Here is a time-lapse series of satellite photos showing what has happened over just the space of about a month of heavy rains and run off from record snowfall in the mountains.

The prediction is that Lake Tulare isn’t going anywhere anytime soon. Even if it doesn’t rain, runoff from the massive snow pack in the Sierra’s will be enough to keep it filled for a couple of years.

I doubt any of the climate models predicted this. I suspect they all predicted more and more drought. I would bet most of the Big Ag outfits running the various operations in what is now the bottom of Lake Tulare had been figuring ways to cope with the predicted worsening drought and making plans to somehow get water to the area.

Surprise! Surprise?

Doomberg is one of my favorite Substacks, and its writers did a bang up job on the reappearance of Lake Tulare.

Here we have an example of nature undoing artificially altered ecosystems, restoring the region to its pre-industrial form more closely. This development would seem to align with the stated objectives of progressive environmentalists. For those displaced by the floods, the affair has undoubtedly been a tragedy—difficult tradeoffs are inevitable under all climate scenarios. As noted by ecologist-turned-climate-skeptic Jim Steele, much of the traditional media has been putting a rather more negative spin on this unexpected turn of events. A recent NBC News article ominously titled “Climate in Crisis: Tulare Lake Reforms Causing Flooding” unironically claims “area people have worked for a century to make California’s Tulare Basin into a food grower's paradise,” and the reappearance of the lake is “another example weather whiplash due to the influence of climate change which can make extremes more intense and more frequent.”

Whiplash, indeed.

You can read the entire post about Lake Tulare below. There is a lot of material about the Colorado River Basin and the flooding that’s behind the paywall, but the info on Lake Tulare is available to all subscribers, paid or free. It’s a great read.

Wet Blanket

Muscle Loss on Low-Carb or Ketogenic Diet?

I got the following email from a reader.

Doc,

People lose lean muscle mass on weight loss drugs but don’t they lose lean muscle mass on a low carb or ketogenic diet too?

It’s a bit unclear to me in general what the issue is with lean muscle mass and these drugs - do they make adding lean muscle mass harder after people come off them? Harder than if they lost the same lean muscle mass with a low carb diet.

Whenever I get emails like this one, I always figure they represent a lot of other people who have the same question. So, if you are one of these other people, here is your answer.

Ozempic, Wegovy, Mounjaro and others coming down the pike repress hunger via a couple of pathways. And they prevent cravings. So much so, in fact, that they are being evaluated for use in breaking of various addictions.

When people are not hungry, they tend not to eat. Or at least tend not to eat as much.

As I’ve written over and over in these pages, after the age of thirty-ish muscle mass becomes a precious commodity. It no longer just stays there or grows almost no matter what you do or what you eat. It starts to slowly go away.

The maintenance of muscle mass switches from hormonally (insulin, growth hormone, IGF-1, etc.) driven to primarily driven by the mTOR system, which requires sufficient dietary protein and resistance exercise together to maintain and/or grow muscle mass.

The amount of dietary protein required to trigger mTOR is fairly substantial. About 30-40 grams of animal protein at least twice per day, preferably early in the day and at midday. If you’re trying to get your protein from plants, it will take about twice that much.

To make use of this protein optimally, you have to do resistance exercise. If you keep the protein intake up and don’t do the resistance exercise, about the best you can hope for is that your muscle mass won’t dissolve as quickly.

If you take one of the weight-loss drugs mentioned above, which substantially reduces your hunger, you end up not eating very much. And, knowing how this all works, as I do, most of what you eat will be carb-based. I doubt a lot of people on Wegovy chow down on a big steak and salad. Probably some do, but I would bet most don’t.

If you think about it, fat and carb don’t come packaged together in nature. There are avocados, which contain a lot of fat, but very little carb. And there are a host of other plants that are full of carb—grapes, for example—but contain almost no fat. Meat is full of fat, but has virtually no carbs. About the only thing that has some carbs and fat is full-fat milk, which is basically designed by nature for rapidly growing babies. Granted, we adults drink it, but it wasn’t designed for us.

Fat and protein are usually found together. Meat is the prime example. Fat and protein are satiating. When you’re not really very hungry fat and protein don’t appeal.

So, I suspect most people on the new weight-loss drugs unconsciously eat as per the oft-repeated and ignorant quote from Michael Pollan:

“Eat food. Not too much. Mostly plants.”

If you do that, you don’t get enough protein, and you put your muscle mass at risk.

Which is why there is the syndrome called Ozempic face. Your body is in many cases a lot smarter than your brain. At least where your survival is concerned. If you don’t get enough protein and are wasting body mass, your body at least kind of directs where that muscle mass comes from. It’s going to spare your survival muscles and waste your muscles upon which you don’t depend as much. As in your facial muscles. Your face hangs on the structure of the muscles over your skull. If you lose those muscles due to lack of protein intake, you get Ozempic face and have to use fillers to keep from looking haggard.

Now, why doesn’t this happen with a low-carb diet or a ketogenic diet. Well, it can…if you don’t eat enough. But since you’re restricting carbs on either one of these diets, you’re loading up on fat and protein. Unlike fat and carbs, fat and protein are almost alway found together in nature. So unless you’re just eating all fat, you should be getting a substantial dose of protein along with it.

At the very least keeping your protein intake up will minimize the muscle mass loss that comes with aging. Doing resistance exercise along with the protein, will really limit the loss and may even add muscle mass.

Just about the worst thing that can happen to you is to be hospitalized. I just had lunch today with a friend I play golf with from time to time. He’s in his mid-70s and has been a good athlete most of his life. He’s a steady golfer who is able to really bear down during tournaments and usually comes out a winner.

He is about two months out from a two-week hospital stay during which he underwent two serious operations.

He lost over 20 pounds—and he wasn’t overweight to begin with—and has had to purchase new clothes because the ones he had fall off of him. Looking at him, I would suspect most of the 20 pounds he lost was muscle. It will take him a long time—if ever—to regain the muscle he lost during two weeks of hospitalization.

The hospital food didn’t help, I’m sure. It is atrocious. And it almost has to be.

I’m sure most readers are aware of the nutritional guidelines and how sorry they are nutritionally. If not, read Nine Teicholz’s book and her Substack.

What most people don’t know is that though the nutritional guidelines are just that—guidelines—they are really more. There was a law passed years ago that says any entity that receives government funding or food has to comply with whatever the current nutritional guidelines are. This includes schools, prisons, the military, etc. Since hospitals get federal money in the form of Medicare and Medicaid, they have to comply as well. Which is why hospital food is so lousy. It’s a system where ketchup counts as a vegetable and Jell-O counts as ‘protein’ even though it’s just gelatin.

Eat protein. Do resistance exercise. And stay out of the hospital. If you have to go in, have someone smuggle you in some protein.

Low Carb USA - San Diego

I keep forgetting how close this meeting is. Just a little less than a month away. I’ll be speaking, and MD will be there with me. If you decide to attend, track us down and say Hi. I met a lot of Arrow subscribers in Boca Raton last January.

Hot Flashes and the Ketogenic Diet

Okay, I suspect only half the readers here are going to be subject to hot flashes, but those who aren’t subject to them themselves may be married to someone who is. So, I figured this might be helpful to all.

The hot flash, or flushing as some call it, comes about with the advent of menopause due to a drop in estrogen. No one really knows for absolute certain why, but there is a theory that makes perfect sense to me.

Before we get into the theory, we need to review how glucose gets into the various tissues. Insulin may jump to your mind, but you might be surprised to learn that glucose can get into the cells of the body by simple diffusion along a concentration gradient. In other words, if there is a lot of glucose in the blood and not much in the cells, the glucose will simply flow into the cells much like water running downhill.

But what about insulin?

Well, insulin works to reduce blood sugar by stimulating glucose transporters called GLUT-4 (rhymes with newt) to come to the surface of the cells, grab a glucose molecule from the blood and carry it to the interior of the cell where it is released. Most people believe insulin runs around driving sugar into the muscles because it’s too high in the blood, but insulin’s real job is to prevent the liver from making too much sugar in the first place. Mice, which have been studied extensively, operate just fine without insulin as long as their glucagon is blocked. No glucagon, no stimulus for the liver to crank out sugar. Mice are fine with just the diffusion of glucose into the muscle cells, so long as glucagon is out of the mix.

There are a number of different glucose transporters (GLUTs) in different tissues. The brain is different. Unlike with the muscles, glucose can’t simply diffuse across the blood-brain barrier. It has to be transported into the brain by GLUT-1. All the GLUTs are protein structures, and like all proteins are coded for in the DNA. If there is a mutation that takes place in the coding for GLUT-1, there are usually serious consequences.

Here is a short video about a young boy whose GLUT-1 doesn’t work. It’s in Italian, but there is an English translation, so you can get the picture.

GLUT-1 doesn’t work as well in females heading into menopause, because estrogen drops. Young pre-pubertal girls who haven’t started producing estrogen don’t have a problem. But after they’ve reached puberty and have been producing estrogen in large amounts for many years, the GLUT-1s become dependent on the estrogen to work properly. In fact, some studies say the removal of estrogen reduces GLUT-1 by up to 40 percent.

When estrogen is withdrawn, as it is in menopause, the reduced number of GLUT-1 can’t get glucose into the brain as well as it did when it worked in conjunction with estrogen. It can still transport some in, just not as much as it did with estrogen around.

When blood sugar falls a bit, the sluggish GLUT-1s can’t keep up with the brain’s need for glucose, so the brain sends out an alarm call for more glucose. It does this by stimulating the release of norepinephrine. The norepinephrine nudges the liver to make more sugar and release it into the blood. The norepinephrine runs body temperature up and causes the symptoms associated with hot flashes.

Not only does the lack of glucose in the brain as a function of the decrease in numbers of GLUT-1 cause the hot flashes, it can cause brain fog as well. A brain short of nutrients doesn’t think as well as one fully supplied.

How can we fix it?

Ketones.

Ketones diffuse easily across the blood brain barrier and provide excellent nutrition for the brain, making it not so dependent upon glucose as its only fuel. (Fats can’t cross the blood brain barrier and there aren’t any transporters for fat, so they can’t be used as fuels for the brain.)

The kid in the Italian video above has a genetic abnormality that prevents him from making GLUT-1. He does fine on a ketogenic diet.

A GLUT-1 deficiency typically leads to seizures due to a lack of glucose getting to the brain, which is one of the reasons the ketogenic diet was developed to prevent seizures.

If you, or someone you love, or someone you have to live with is going through menopause, I would recommend a ketogenic diet.

If any of you have pertinent experience with the ketogenic diet while going through menopause, I would love to hear from you.

Odds and Ends

From the ‘most scientific articles are false’ department, another one bites the dust.

The president of Stanford University resigns because of manipulated research findings. And papers that have to be retracted. Don’t believe everything you read in even the most prestigious journals.

Last week I wrote that I was going to discuss Mendelian randomization this week. I’ve run out of time and words, and I still have a bit of reading to do. All I can say now is that I don’t think it is all it is cracked up to be. Works in certain specific situations, but those are rare. I think it is often used when randomized controlled trials don’t give the answer many people are looking for.

I will give a more comprehensive explanation next Thursday. I promise.

Video of the Week

Today’s VOTW is the opening remarks of Robert F. Kennedy Jr. at a congressional hearing. As I’ve written many times, I have issues with RFK, Jr, but I’m in agreement with virtually everything he has to say here. Like RFK, Jr (or at least like RFK, Jr opines) I am a total 1st Amendment kind of person. If we don’t have a 1st Amendment, we don’t have the country we’ve had for going on almost 250 years. He makes many important points that we all should heed about what many people call the industrial censorship complex.

Click on graphic for video or click below:

https://twitter.com/alx/status/1682031762912997387?s=20

The saddest thing about this hearing—if you watch the whole thing—is the Democrat attack on him. Twenty years ago, the Democrats would have been defending him.

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

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