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Hello everyone.

Greetings from Montecito.

Where it has been on the cool side. Left Dallas to escape the unseasonably late hot weather, looking forward to some cooler weather here on the west coast, but it’s been a bit too cool.

Had an interesting flight in from Dallas. As we were coming in to land at the Santa Barbara airport, I thought the pilot was coming in a little too high. I’ve probably landed in SBA vastly more times than he has over the last 20 plus years, so I know what it looks like. He ended up blowing the runway approach, and we had to go back around. In all the years I’ve been flying, I’ve had that happen only once. And that time, the pilot announced it before we did it.

This time no announcement, no nothing. Just increased power and up we went. Five miles or so out over the ocean, then back in for another try. Which was successful, though he came in a little low and had to goose the throttle.

No pilots out in front, as they usually are, seeing the passengers off. Cockpit door was shut. I suspect a lot of report writing and ass covering was taking place.

Other than that, a perfectly lovely flight, during which I got a lot done. I made a good start at dealing with the hundreds and hundreds of tabs I have up on my browser.

I got my wish on the election a couple of nights ago: it didn’t linger, which is what I feared the most. Last week I wrote that all I wanted was for it to be over, and it is.

And all I can say is I sure hope restaurants start ditching their seed oils and loading up on beef tallow now. When they do, it will be a great boon to health.

Usually right about now, I head into the comments and poll responses. I will get to those, but first I want to unburden myself of a few things I’ve had hanging around in tabs on my browser for a while.

Working at Home vs Working at the Office

I don’t know how many of you are following the big brouhaha between Amazon and it’s employees who have been working from home since Covid. The head honchos at Amazon decided these employees need to RTO (return to the office). The home-working employees are pushing back.

First off, I’m glad it’s Amazon that’s getting hammered with this (though, I’m sure many other businesses are getting hammered, too), because they were one of the Big Tech players that tried to censor things during Covid.

I know why Amazon wants the employees back in the office. They are more productive there. The employees disagree, but, in my view, the employees are full of it. I’ve worked from home, and I can tell you, I was significantly less productive than I would have been at an office. I’ve hired many, many employees who worked at home. And their productivity declined. I’ve had a couple of employees who worked great from home, but most don’t. There is a definite decline in productivity, especially for some people.

Employees love to work at home for the same reason businesses would rather have them in the office: it’s much easier to screw off at home than at an office. Plus, there are other situations. I suspect many parents who began working at home were paying for child care while they were at the office. Once working from home, they let the kid(s) stay home, too. Saved the parents a lot of money. All they had to do was keep them quiet during Zoom calls.

Plus, if you’re home and your friend sends you a ten-minute funny video, you probably stop what you’re doing and watch it. No one is looking over your shoulder. The temptation to not keep your nose to the grind stone is hard to overcome.

All this got me thinking about ways this could turn out as a win-win.

Having run multiple businesses, I know the cost of leasing office space is a substantial part of your monthly outlay. So maybe getting rid of the lease payments for office space for, say, ten people might well be worth the loss in productivity by having them work from home.

It would be a win-win.

Your (i.e., the business owner’s) lease expenses would go down (maybe by even more than the loss of productivity is costing you), which would be your compensation for the reduction in productivity from the employees. The employees could save on child care expenses, gas to drive to work, buying appropriate office clothing, etc., plus they could sleep in later to avoid the commute and be home earlier at day’s end. So they would win on the deal, too.

Just a thought. You can let me know what you think of the idea in the comments and via the poll.

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We’ve Eaten Carbs for 800,00 Years

The dopes at Medscape are obviously unaware of the long nutritional history of humans and proto humans. Below is the lede to a recent article.

What brought this on?

Humans do indeed sport multiple genes that code for amylase. Amylase breaks down complex carbs to simple carbs, allowing for better digestion. There are amylase enzyme in both the mouth (the salivary glands, actually) and the pancreas. You can see how the amylases in your mouth work if you chew something carby, but not sweet. Say, a saltine cracker. If you bite off a piece and start to chew it, you will notice it becomes sweet. That’s your salivary amylase breaking down the carb in the cracker and turning it into a simple sugar.

The article makes much of this discovery because agriculture didn’t come on the scene until ~10,000 years ago (no one is certain of an actual date, but probably about the thousand years ago give or take a few thousand).

They are basically making the point that since the amylase gene was around 800,000 years ago, we must have eaten carbs then. Which means, by their reasoning, that we didn’t just start ~10,000 years ago, that we obviously have a long history of eating carbs, so should therefore be adapted to them.

Uh, the human body doesn’t need any carbs at all to function A-okay. If you disagree, name me a single carb-deficiency disease.

The Medscape writer is trying to make the case without coming right out and saying it that the ancestral diet is bunk. Especially if you think the ancestral diet is primarily a meat-based diet. And they have the amylase to prove it.

What has escaped their notice is that before the first real hominid line—Australopithecus afarensis (the famous Lucy)—the predecessor was probably a vegetarian. Lucy and her kin ate a bit of meat, but probably not a lot. But those before her ate mainly plants.

Lucy is ~3-3.5M years old. After she and her kin began to eat a little meat, meat consumption increased as her progeny continued to evolve. As they did so, they got bigger heads (brains) and smaller GI tracts, as meat was both more nutrient dense than plants and much easier to digest. So, more food for the brain, less work for the gut.

My bet would be that Lucy’s predecessors probably had more genes for amylase than we do now. As we spent the next three million years eating more and more meat, we probably got rid of a few amylase genes, as they weren’t necessary.

So, to my way of thinking, it should be no surprise to find genes for amylase existing 800,000 years ago. In fact, I would be surprised if we didn’t find genes coding for amylase. I don’t think these findings tells us that because we have the gene(s) for amylase, that we should forgo meat and go face down in carbs.

Big Pharma and GLP-1 ra’s Reverse the Paradigm

For years all the chronic diseases that afflict so many people were blamed on obesity. People appeared to be in pretty good health, then they started gaining weight. As they became more and more overweight, they began to develop high blood pressure, lipid problems, type 2 diabetes (T2DM), and all the rest of what people refer to as the diseases of civilization. These chronic diseases all seemed to trail in the wake of obesity.

Anything done to help decrease the excess weight—dieting, primarily—would also get rid of the rest of the problems, or reduce their severity at the very least. As a consequence, it is easy to see how in the minds of most obesity became the driving force behind all the other issues.

Then the paradigm began to change. A few doctors and researchers noticed that the old way of thinking might be outmoded. Rosalyn Yalow and Solomon Berson had figured out how to measure insulin in the late 1950s (Yalow received the Nobel prize for it in 1977; Berson had died by then). Once researchers started testing with these new techniques, they discovered that most of the obese, many people with high blood pressure and lipid disorders, and virtually everyone with T2DM had elevated insulin levels (hyperinsulinemia).

Prior to that, others had determined there was insulin resistance because they had to give much larger doses of insulin to people with T2DM than they did to those with type 1. They intuited that those with T2DM had insulin resistance, but it wasn’t until the techniques developed by Yalow and Berson were put into wide use that they knew for sure.

By the 1980s people were speculating that maybe elevated insulin levels were the problem driving all the other problems. They were beginning to look askance at the paradigm shown below that had been in place for decades.

Gradually, the paradigm began to switch to be one in which hyperinsulinemia was the driving force in the development of all these disorders, including obesity. In other words, obesity didn’t drive all these other chronic diseases, hyperinsulinemia did. And it drove obesity as well. The new, more accurate, paradigm is shown below.

This new paradigm is what I wrote about in Thin So Fast back in the late ‘80s and that MD and I wrote about in Protein Power back in the ‘90s.

Although this paradigm is vastly more accurate than the previous one, there is one problem with it. At least in the view of Big Pharma. And that problem is that hyperinsulinemia can’t be treated with a drug. It can be treated only with diet.

What kind of diet?

A low-carb diet works best. Carbs make insulin go up. Removing the carbs lets insulin come down. But even low-calorie diets can reduce insulin levels simply because cutting calories usually also cuts carbs. A terrific study by Golay et al showed this nicely way back in the mid-1990s. Unfortunately, this study was published right after Protein Power came out, so we didn’t get the chance to include it.

In the Golay study, 43 subjects were randomized into two groups, both of which went on 1,000 kcal/day diets. One group reduced carbs to 15 percent of calories, while the other group received 45 percent of their calories as carbs. These two groups staying in a metabolic ward and had their food served to them for six weeks.

At the end of the six weeks, the 15 percent carb group lost a little more weight, but not enough to hit statistical significance, whatever that means. (A continuation of this study published later showed the lower-carb group to ultimately lose more weight.) Despite the lack of a big difference in weight loss, the lower-carb group reduced their insulin levels by almost half, while those on the higher-carb diet reduced their insulin levels by just a touch over 8 percent.

But those on the higher carb diet didn’t really consume the amount of carbs you would think simply because overall caloric intake was so limited. Those on the higher-carb diet averaged about 115 grams per day, which isn’t all that high.

Here is the chart showing the intake of the two groups of subjects.

As you can see, none of the subjects ate a lot of anything. I don’t like these kinds of studies for evaluating weight loss, because the caloric content is so low. If you cut the calories enough, both groups are going to use every calorie that comes in, and you won’t see a big weight loss difference.

If you do overfeeding studies, then you can learn something about the make up of the calories, and what happens to weight gain. Which is the problem. Obesity is a problem with excess weight, so why do we continuously study it with calorically-restricted diets?

But this study does show the power of cutting carbs to reduce insulin levels.

No drug will do this. As far as I know, the only way you can reduce insulin levels is by reducing carbohydrate intake.

I found one of the sheets I used to go over with all my patients explaining how insulin drove most of the problems they were experiencing.

It was hand drawn, run off on the copy machine, and pretty effective at teaching what was going on and why it was essential to reduce the carbs.

As I wrote above, we have no drugs to lower insulin levels. But now we do have drugs to reduce obesity. The drugs involve a sort of drug-induced starvation. So, with the reduction in food intake these drugs bring about, those taking them reduce their intake of calories and carbs. Just like the people in the above study did. So they will lower their insulin some. Not as much as they would have had they gone, say, keto, but some.

As a result, their blood sugar levels will fall, their high blood pressure may be reduced (should they have HBP to begin with), and their lipids will probably improve.

Because of all this, and especially because it is done with drugs, some are starting to re-imagine the paradigm shown above back to what it formerly was: obesity drives everything.

Don’t believe me that medicine can be this screwed up? Think again.

Below is the opening paragraph of an opinion piece written by Dr. Leana Wen recently. Remember Dr. Wen? She was the Covid vaccine, mask, lockdown zealot who was ubiquitous on all the mainstream cable shows a few years ago.

Says she

Jesus wept.

Just what Big Pharma wants to hear. You don’t have to worry about using diet to treat any of this stuff, just take the shots. Obesity first, it’s now called. How appropriate.

She continues

So, with “obesity first,” we’re back where we started before we understood what drove all these issues. Back to the future, I guess.

One last small thing, then we can get on with it.

They Always Look for a Drug

Here is the headline of an article I just came across: “Scientists identify immune molecule that keeps metabolism in tune and on time.”

The article is about the identification of a molecule that supposedly has an impact on metabolism. These articles come out all the time, and almost always end up not amounting to much. But that’s okay. That’s how research works.

This article has something in common with almost every similar article so written. Take a look at the last sentence in the 2nd paragraph.

No one who writes these articles ever mentions that maybe the finding in question can help people change their diets to deal with metabolic issues, which, after all, are a function of diet. It’s always drugs. I’ve got at least a half dozen of similar articles up in my tabs. All of them focus on drug development for issues that may well be amenable to the right dietary changes.

I know drugs are where the money is, but it would be nice if just occasionally the authors of these kinds of articles would at least mention diet.

Comments, Poll Responses, and Emails

Metabolic Flexibility and the Lumen

Here’s a response from last week’s poll.

My short answer is that I disagree with the Luman folks on this one.

I think the Lumen is a great device, but I think we ought to strive to be in fat burning mode most of the time. I wouldn’t pay a lot of attention to their instructions on diet as a function of interpretation of what the device says.

Theoretically, metabolic flexibility means being able to oxidize whatever fuel you’re presented with. You are metabolically flexible if you can eat carbs and dispose of them. Same for fat. Kids have great metabolic flexibility. They can pretty much eat anything they want and suffer no consequences. Which is kind of the definition of metabolic flexibility.

This ability declines with age as we’re confronted with insulin resistance and the consequent glucose intolerance.

If we reduce carbs a lot, as we would do with a low-carb/ketogenic diet, we end up being less metabolically flexible (sort of) than we were before we started the diet.

If you take a glucose tolerance test while you’re on a standard American diet, it will show you whatever it shows you, given your baseline glucose disposal ability. (Glucose disposal means the ability to drive glucose from the blood into the cells.)

If your ability to dispose of the glucose you drink for a glucose tolerance test is perfect, then great for you. But I can guarantee you that if you go on a low-carb/ketogenic diet for, say, two weeks, then take a glucose tolerance test, it will come out telling you you are glucose intolerant.

So the low-carb/ketogenic diet makes you glucose intolerant? In a word, yes. But it’s a good glucose intolerance.

Let me explain.

Your metabolism changes to meet the challenges it is confronted with when you eat different foods. Just like everything else, your various metabolic pathways are catalyzed by various enzymes. These enzymes are all coded for in your DNA, but they aren’t actually produced unless you need them. You’ve got God only knows how many enzymes coded for that you seldom or even ever need, but the coding for them is there. If you do need them, they’re there, but they don’t materialize immediately. The pattern to make them is there in the DNA. But when needed you still have to build them.

People who eat mixed meals—a lot of carb and a lot of fat—have circulating enzymes at the ready to deal with the incoming carbs and fats. They are able to dispose of them as best they can given any insulin resistance they may have. If you’ve got a bit of insulin resistance, it will show up as a higher rise in blood sugar on an oral glucose tolerance test and a tail that takes longer to go down. So, overall, the glucose hangs around in your blood longer.

When you consume a diet that is high in fat and protein and low in carbohydrate, your enzymes for dealing with carbohydrates go away, or better put, quit being produced. And you don’t regenerate them as long as you don’t eat carbs. If you’ve been on such a diet for a while and go in for a glucose tolerance test, you’ll probably end up with the test fingering you as glucose intolerant, or maybe even slightly diabetic.

This does not mean you are glucose intolerant or diabetic. It just means you are fat adapted and don’t have the enzymes circulating around that catalyze the rapid metabolism of carbs. When the glucose you drink for the test hits your GI tract, it sends a message and the process begins to make the enzymes that deal with the carbs, but it doesn’t happen instantly. Thus the test showing glucose intolerance.

This is why it is always recommended that you eat carbs the day or two before your glucose tolerance test. You’ll have the enzymes you need in place to grease the skids of glucose metabolism.

There is nothing wrong with being fat adapted. In my view, it is the best way to be. But if you are fat adapted, you’ll be burning fat all the time when you blow into your Lumen. And you’ll test glucose intolerant if you chug a bunch of carb to do a glucose tolerance test.

I would be happy as a clam if my Lumen always showed heavy fat burning. Which it is more and more as I continue to use it. Except when I go to muscle failure. Then I expect to see a lot of carb burn.

We’ve discussed before how your optimal steady state is burning fat aerobically, which means burning fat and carbs in the presence of oxygen. If you do intensive exercise that takes you to failure or close to it, you go anaerobic, which means burning carbs (glucose) only. Fat can’t burn unless it has plenty of oxygen. Glucose can also burn with oxygen, but it is the only thing that can burn if there is no oxygen. It burns, but it doesn’t provide nearly the energy as it does burning with oxygen. So when you go anaerobic in your workout, you can’t go for long.

You may be asking yourself, Why would I ever want to go anaerobic if it’s so inefficient?

That’s good question. The answer is that that is how you improve your conditioning.

Every time you go anaerobic, you add a little increment onto how long you can go before you go to failure. The longer you can go with intense exercise before you go anaerobic, the better shape you are in.

One of the reasons high-intensity-interval training (HIIT) burns so much fat is that it takes you right to the verge of anaerobic, but doesn’t really get you into anaerobic glucose burning. MD does all kinds of training in her weekly workouts following the MPC protocols. When she does HIIT, she shows massive fat burning on her Lumen right after her workout.

If she does other types of heavy weight training that send her anaerobic, she blows high carb burning on her Lumen. Which means she is improving her conditioning. If she were wearing a CGM during these anaerobic bouts, she’d probably see a major rise in blood glucose, which is what she’d be burning.

Way back in the late 1990s, I corresponded with a doc who did research at the naval training facility in San Diego. He told me that his studies on enlisted naval subjects showed that those who were on low-carb diets could perform well as long as they didn’t really work out hard. On endurance types of exercise, they were superb.

But on anything requiring them to go anaerobic, they quickly played out. But if they were given a glucose drink, they could keep going.

He sent me a bunch of naval publications on these studies that weren’t published in the scientific literature. I’ve got the things, but they are in storage right now. But I read them and remember them well.

When I’m finally able to get all that stuff out of storage and recreate my library, I’ll scan these and make them available.

The take home message from all this is that you don’t need to eat a bunch of carbs just to make your Lumen show you’re burning carbs, so it can deem you metabolically flexible. If you’re fat adapted, you’ll be plenty metabolically flexible. It just won’t happen instantaneously. It’ll take a bit longer than a glucose tolerance test lasts, but not much.

The other take home message is that if you want to burn a lot of fat, do high-intensity interval training and take it to the point right before failure. You’ll burn maximal fat. You will also improve your conditioning.

But if you want to improve your conditioning quickly, go to failure. That’s what I do during my band workouts. It is not fun. But it definitely increases the time before you go anaerobic and then fail.

If you decide to spring for a Lumen, I would suggest you ignore their literature about how to increase your metabolic flexibility. If you follow the steps above (irrespective of whether or not you have a Lumen), you will be fine. Try to keep in fat burning mode as much as possible. Look for what gets you out of fat burning mode (for me, it is drinking booze at night), and try to avoid whatever that is. Take yourself to failure if you want to maximally improve your conditioning.

Lactose in the Danish Study

Last week I discussed a study from Denmark showing what happened to 8-year-old boys who went on diets containing either meat protein or protein from skim milk. The boys in both groups ended up consuming about half again as much as they did on their regular diets, but those who consumed their protein as skim milk saw a major increase in both their fasting insulin levels and their insulin resistance. The authors thought it might be the branched-chain amino acids in the whey (skim milk) that caused this increase, but they found equal levels of BCAA in both groups.

A reader pointed out in the comments that there is considerable lactose (milk sugar) in skim milk, and that the additional added carb might be the cause of the rise in insulin.

I don’t know what happened to my reply to this comment. I went back to reread it when one of the poll respondents wrote this:

Of course, I went back to reread what I had written to the original commenter, and it was kind of incoherent. I think the platform deleted something, or I deleted something. I can’t go in and edit my response like I could on Substack, so instead of screwing around with it, I’ll just do it here.

I assumed the study authors corrected for the extra lactose in the skim milk. In going through the study again, I couldn’t find anything in the methods section describing how they added specific carbs to the meat group to match up with the carbs from the lactose in the milk group. But they must have done so, because here is the chart showing the macronutrient breakdown.

As you can see, the carbohydrate intake in both groups was similar. This study is now almost 20 years old. If it were newer, I would reach out to the authors and ask how they did it, but I doubt if these folks are even still at their posts. I don’t think they would overlook something as basic as evening up the carbs, especially if insulin levels and insulin resistance are two of the parameters they are planning on measuring.

For the Post- and Peri-Menopausal Among Us

Since I wrote that MD had her own methods of dealing with menopause, I’ve had many, many requests asking how she manages her own issues. I’ve asked her to detail for me what she’s done over the years, so I could pass it along. Instead of telling me and risking my screwing it up in the retelling, she said she would just describe it herself.

I’m not going to put her words up in quotes. What follows are her words. Take it away.

I spent most of my life never really having to worry about my weight. In my teens I was athletic and strong, but still lean and muscular. Despite that, I was convinced I was overweight and pudgy, as most all teenage girls are. But I was a perfectly healthy weight. I did put on some pounds when I began taking the birth control pill in my 20s but lost it all when I stopped taking them and opted for an IUD instead. And my weight remained appropriate and stable until I hit about age 51 and peri-menopause began in earnest. These gains show the power of hormone changes to pack on pounds at both ends of the reproductive spectrum.

Girls naturally fatten a bit as they go through puberty, under the influence of estrogen, putting on some padding in all the hormonally-directed places usually designated for women; that’s a normal state of events. Just as boys, under the influence of their gender-specific hormonal direction at puberty build bigger, longer, stronger bones and put muscles on them. Well, that is if they’re fed a decent diet and encouraged to go outside and play at will rather than parking themselves in front of a video console.

But something definitely happens at menopause (and andropause in men, for that matter) that shifts the landscape seismically. And fat begins to accumulate, and suddenly nothing works as it did before to get it off. Again, this is hormonally driven, or perhaps better cast as ‘lack of hormonally driven.’

In women, the first hormone that begins to dwindle is usually progesterone (which causes sleep disruption as a main symptom), and its falling level causes a relative abundance of estrogen, or at least an exaggeration of estrogen’s effect, which is, as you recall from puberty, a tendency to fatten. When estrogen levels then also begin to fall, the hot flashes and brain fog and mood swings set in. Accompanied by the development of a sort of menopausal insulin resistance, if it weren’t already there, or a worsening of it, if it were.

So you find yourself relentlessly gaining fat. And we know too much estrogen makes you fat. But now not enough estrogen makes you fat, too? So which is it? It’s truly the devil’s knot of a tangled up no-win situation to try to figure it out from symptoms alone.

If you’re still struggling with your weight (and following a thoughtfully-structured, whole food, low-carb or keto or carnivore diet), not drinking much alcohol, and getting regular cardio and resistance exercise, you need to test your hormones.

The only way to know how to address the situation properly is to test to find out what your hormone levels actually are. And not just the follicle stimulating hormone (FSH) that’s usually the go-to test most GYN or family docs will use to determine whether someone is in menopause. Yep, they’ll say, it’s elevated; you’re in menopause. Congratulations! And then do precisely nothing to help.

At a minimum, you need to get all the reproductive hormones: estrogens 1, 2, and 3 (estriol, estrone, and estradiol), testosterone (yes, even in women), DHEA, and progesterone. And FSH. The specific recommendation would depend on your symptoms, yes, but in light of what the testing shows. For most women, it’s going to be some strength of transdermal estradiol (the E3 patch) plus some strength of progesterone (note: not progestin, the synthetic, progesterone) in either oral micronized form or bio-identical topical cream. Occasionally a bit of DHEA or testosterone, too. There’s a lot of ‘hunt and peck’ to figuring out the dose and form, the ‘recipe’ if you will, that works best for any particular person. Then you have to stay on it a while and let it reach a stable place (months) and check the hormone levels again and see where you are. And adjust and repeat. And adjust…

After years of experimenting with different ‘recipes’ I finally settled on a 0.025mg estradiol patch twice a week, 60mg progesterone cream (compounded) nightly, and DHEA 25 mg orally daily. But your mileage will surely vary. One of the GYNs to the stars in Hollywood uses the basic maxim: use the lowest dose of estrogen that relieves symptoms (hot flashes, sweats, mood swings, etc) and push the progesterone level as high as tolerated.

How would you know if you were at or beyond tolerance? Too much progesterone can cause acne, weight gain, anxiety, water retention, bloating, increased appetite, muscle and joint pains, insomnia. When you read through that list, it’s easy to see how similar it is to issues from too much or too little estrogen. And consequently how tough it would be from symptoms alone to tell if you have too much estrogen, too much progesterone, or too little of them. Truly, without testing you’re walking in the wilderness, in the dark, barefooted.

But I do think the progesterone part of the equation is what is often missed. If you are a woman with a uterus (haven’t had a hysterectomy) and you’re deemed in menopause (no period for 12 months and an elevated FSH) and have symptoms, you’re given estrogen of some sort and a standard dose of 50 mg progesterone (orally) and told to go forth. Women who no longer have their uterus don’t usually get any progesterone at all.

I remember about ten or fifteen years ago (early in my journey) going for a consultation with a nurse practitioner recommended to me by a friend as a ‘wizard in hormone therapy’, hoping to get her to help me sort it all out. (I promise it’s even a wilderness for a physician!) She tested my blood and examined me and prescribed some dose or other of estrogen and 50 mg oral progesterone. In our discussion, I realized this wizard seemed to be utterly unfamiliar with progesterone’s having anything whatever to do with anything other than protecting the uterus from estrogen’s unopposed effect (and raising the risk for cancer). When I asked what my progesterone levels were, she responded that she didn’t pay any attention to progesterone. It didn’t have anything to do with the problem. And then why the prescription for the 50 mg of progesterone, I asked? Because they tell me I have to give it to you if I put you on estrogen and you have a uterus.’ Oy! First and last visit.

Progesterone has many important roles physiologically. It’s a better bone builder than estrogen. In fact, estrogen only exerts an inhibitory effect on the osteoclasts (the cells that remove old/damaged bone) and helps to prevent more bone loss. Progesterone actually encourages the osteoblasts (the cells that lay down new bone) to build more bone. It’s protective of both the uterus and the breasts against cancer (and even without a uterus, most women do still have breasts to protect.) It stimulates the limbic system to improve mood. It enhances sleep. It improves memory and fat burning. A long, long list of beneficial effects.

The point is that the hormone system is just that – a system – and for it to work, it needs to be balanced. You want a physiological balance among all these hormones. Not too much, not too little, just right. What’s just right for you won’t necessarily be just right for someone else. And though it can be a long and twisting road of testing and adjusting and testing again to figure it out, usually, when you get there, things fall into a better place.

Odds and Ends

• Nearly 200 years after composer’s death, the curator at the Morgan Library and Museum in NY unearths a lost Chopin waltz. I would love to hear it played.

• A simulation by US theoretical physicists has provided the first fully microscopic characterization of the moment an atom splits in two.

• Short video on X of a polar bear just hanging out and having fun. As much fun as could be had in freezing cold water, I suppose.

• From insects to elephants, alcohol consumption is widespread in the natural world. I always wondered why we ever evolved alcohol dehydrogenase (one of the enzymes that detoxify booze). I guess because alcohol has been around forever.

• Archaeologists discover 4,000-year-old Bronze Age settlement hidden in Saudi Arabian oasis.

• Apparently the creation of Blue Zone certified clinicians is in the offing. If it comes to pass, God help us all.

• An amateur brewer in Utah gathered rare figs and a strain of yeast from 850 B.C. to make a sour, fruity beer inspired by ancient Egyptian recipes.

• Doctors seek additional training in wake of the obesity boom. More likely is that they want to get in on the gravy train that is the GLP-1 receptor agonist boom.

• Researchers explore the reasons behind the quintessential canine question: Why do dogs wag their tails?

• The Serengeti Plain: Fallacies that maybe aren’t fallacies after all.

• Great site for looking up and playing old and rare movies, many of which I had never heard of. But a lot I had.

• The red ruby slippers worn by Dorothy in the film The Wizard of Oz are up for auction. Right now the bid stands at a cool million. You could still have them.

• Strange conglomeration of bones from people whose lives spanned a period of 2,500 years make up a single Roman skeleton in Belgium. The mystery is, why?

• A 17 yo female footballer with suspected autism has been hit with a six-match ban after asking a “bearded” transgender opponent: “Are you a man?”

• A crazy idea for treating lupus and other autoimmune disorders may be validated in the future. I would wait for a little more evidence before going this route. So many of these kinds of things have started out looking good, then blown up.

• Tourists visiting the picturesque and upscale Lake Como in Italy can now take home a unique souvenir—canned air—for a mere $11. Lake Como is wonderful. MD and I were in a boat wreck on the lake once. I still love it, but wouldn’t fork over $11 for a can of air.

• German coalition government collapses as Scholz sacks his finance minister.

• Raccoons are everywhere these days. First Fred, who was executed by the State of New York. Now this one that plunged through an overhead vent a LaGuardia airport.

• New study finds Arctic warming, declining sea ice may be a ‘benefit’ to the very animals it was supposed to harm: polar bears and ringed seals.

• Scientists have a new theory. as to why Neanderthals and humans buried their dead. Who knows it it’s true or not. It is science, so it needs to be validated.

Newsletter Recommendations

Video of the Week

The VOTW this week was a last minute selection. Since I started on great violinists who inspired me as I was learning to play, I was going to put up one of my favorite pieces—Liebesfreud—by Fritz Kreisler, who was a Viennese violinist born in the late 1800s. I even found a recording of him playing it, so I knew exactly what the guy who wrote it wanted it to sound like. It’s a piece I actually worked on myself. I badgered my instructor to teach me to play up in the positions way before I was skilled enough to do so, just because I loved the piece so much. But instead of Liebesfreud this week, I decided on a different video.

A friend sent me this hilarious skit from a recent Saturday Night Live show. I must have forwarded it to 50 people. I’ve watched it myself at least ten times. It has political overtones, but is really, really funny. Everyone plays their parts to perfection. Even the mystery guest, who is perfect. Enjoy!

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

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

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

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