The Arrow #199

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Hello friends.

Greetings from Dallas, where it has once again turned hot. Unseasonably hot since it’s almost at the end of October.

Before I kick off this issue of The Arrow, I want to post a few poll responses that don’t really fit into the category of poll responses about nutritional issues. Here we go.

Yes, we're all painfully familiar with the trials and tribulations of air travel these days. No need to rant about it.

All round interest, good content on nutrition and health which is why we are all here in the first place, don’t forget that. Airport details are the rubbish part and of no interest or us - sorry Keep up the good work. [My bold]

Lot's of words, not much health substance.

Something most of you probably don’t know about me is that I suffer (and always have) from AHDH to some degree. One of my main symptoms is approach avoidance. I hate to get started on anything that approximates work. The Arrow falls into that category. Don’t get me wrong; I really enjoy writing it, and I particularly enjoy the research required to write the newsletter. I’m animated by an intense curiosity about many things, including why I’m not curious about certain other things. Digging into the research I don’t even consider work—that’s more fun than work for me—it scratches a severe itch. But writing about it takes time and thought and effort—which is sort of work.

I do research constantly, and I think about it all the time. Right now I have four medical textbooks I’ve been consulting on the floor beside my chair and about a dozen papers on my computer desktop. I save the contents of my desktop to a file in my documents folder about every two weeks. I just checked the last save, which was on Oct 20, and there were 47 papers saved. Which, again, I don’t consider reading all these papers as work. And you’ve seen all the tabs I keep open—all out of curiosity about a million things.

But getting started writing is a hurdle I have to overcome every week. I’ve done it for 199 weeks in a row now, but it hasn’t always been easy. One thing that does make it easier is to have a rant or something I want to get off of my chest. So when I get screwed around by the airlines, I get pissed off. And being pissed off makes it much easier for me to start The Arrow. It lets me vent my spleen, and I’m much more amenable to sitting down and getting going than had I not had something to bitch about. I know everyone knows flying, dealing with airports, TSA, and security sucks. I’m not whining because I think I’m the only one who suffers these indignities.

But it does get me writing. And once I start, I’m in the groove and off and running.

I’m not being overly sensitive because of three poll responses. I have about twelve thousand subscribers right now, and I know if three people whine about something that means that probably a hundred (or more) times that number feel the same way.

So, all I’m asking is that you help a brother out. Indulge my little fits of pique at the start since you now know their purpose. Today this particular one fit the bill. So, many thanks to those three respondents for giving me something to get me going on #199.

One another note…

MD and I experienced voter suppression on Monday, the first day of early voting in Texas. We had to present our drivers licenses to be allowed to participate. It wasn’t nearly as bad as flying suppression where we have to not only show some form of picture ID, but also have to stand in a long line to wait to go through a metal detector. Sometimes we even have to take off our shoes. We didn’t have to do anything other than provide ID and make sure our signatures matched to vote. But still it was onerous, and I can’t imagine how many people were put off by having to actually show an ID to be allowed to vote.

The worst part of the voter suppression we experienced was the incompetence of the poll workers. There was a huge line to vote, which I should have expected, but didn’t. The folks working there definitely did not have their acts completely together. But I’m hoping they improve with experience. Where do they find these people?

MD and I usually vote on election day, but we are going to be out of state on election day this year, so we voted early for maybe the first time. And the lines were as long as they are on election day.

Comments, Poll Responses, & Emails

The Shittification of everything

I threw this word off in writing about my misadventures with the airlines and got the following response in one of the comments.

"the shittification of everything".... absolute genius.

My quote of the week.

Thank you.

I wish I could take complete credit for the word, but it is my neologistic change of a word coined by Cory Doctorow: Enshittification. Which he applied to the changes in Big Tech applications. I remember his first writing it, but I couldn’t remember exactly where I saw it. Wikipedia to the rescue. According to Cory, enshittification happens thusly:

Here is how platforms die: first, they are good to their users; then they abuse their users to make things better for their business customers; finally, they abuse those business customers to claw back all the value for themselves. Then, they die. I call this enshittification, and it is a seemingly inevitable consequence arising from the combination of the ease of changing how a platform allocates value, combined with the nature of a "two-sided market", where a platform sits between buyers and sellers, hold each hostage to the other, raking off an ever-larger share of the value that passes between them.

Wikipedia goes on to describe an editorial of his in the Financial Times this year in which he writes:

'enshittification' is coming for absolutely everything" with "enshittificatory" platforms leaving humanity in an "enshittocene.

Which is quite clever. I was surprised I hadn’t seen it there as I am a long-time subscriber to the Financial Times. I wordnapped “enshittification,” which was applied to tech platforms and converted it to shittification, which, by my definition, means what has happened all around us. Nothing works. Customer service sucks everywhere. Things break. You try to call a company for help and can’t get a human on the phone. You spend 20 minutes on a text chat, when you could have solved the problem with a three minute call. How-to videos leave you hanging, because the platform they are explaining how to use has changed a step. And on, and on, and on.

In Jeff Childers column today, he reported on a story in the New Statesman that contained this long paragraph:

It may be difficult for Europeans to understand how dysfunctional much of America has become. Nothing works. Bathrooms in bus stations and fast-food joints have often been closed for months. Public facilities are invariably old. Streets are spectacularly dirty. Service workers may go on small, local strikes no one hears about. Supermarket shelves may be empty because of shoplifters. In Erie, Pennsylvania, two days before the Warren campaign event, I took a train in the middle of the night. Outside the station, the homeless begged to enter the waiting room, only to be denied by the station master, who promptly fell asleep on the floor. I was told that many people try to jump on moving freight trains as they have no money for tickets. Once the station master woke up from his drunken slumber, he told me a “bum” had been run over by a moving train while sleeping on the tracks just a few days before. Now he worries because no one is checking the tracks every night.

The perfect description of the shittification of everything.

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Vaccines

I had a number of inquiries on my stance on vaccines last week. (For those of you just joining the conversation, I wrote that I’m against them all.) Most of those who wrote are probably subscribers who haven’t been with me from the start almost four years ago when we were in the depth of the Covid debacle. Those who have been readers since then have watched my stance on vaccines evolve, so probably weren’t so surprised.

To recap, when I was in medical school, we were never taught anything about how vaccines were developed or tested, only that they were good. Of course, when I was in medical school, there were only a small handful of vaccines available, not the 80 or so that little kids get today.

Even when I began to question the efficacy of vaccines, I didn’t include the smallpox vaccine or the polio vaccine. I figured those were absolutely worthwhile. The smallpox vaccine hasn’t been given for a long time, but I figured it was still a great thing and had saved countless lives.

Then I read the two books that are my go-to books on vaccination: Dissolving Illusions and Turtles All the Way Down. And that’s not to mention the writings of Aiden Cockburn. Years ago I met Eve Cockburn (pdf file), who, along with her husband Aiden, was the organizer of the Paleopathology Association, of which MD and I were members for years. (Reminds me, we need to re-up.) She got me interested in her husband’s work, which showed that infectious diseases evolved to become less virulent and more infective as a survival strategy.

Infectious agents, like all of us, want to reproduce and thrive and do so by evolving. If an infectious agent kills its host, the bug dies as well. But if an infectious agent barely makes its host sick, then the host goes out and about spreading the infectious agent. The infectious agent’s job isn’t to kill the host, but to survive and reproduce, which it does by attenuating and becoming more infectious.

We saw this with the Omicron strain of Covid, which came about after my having written the description above in one of the early issues of The Arrow. The Omicron variant infected just about everyone, including MD and me, both of whom hadn’t gotten Covid despite much traveling and being out and about. We both got sick for a couple of days, and that was that. It was vastly milder than the original strain and much more infective.

As you might have noticed in the graphic I put up last week from Dissolving Illusions, the dramatic decrease in the rates of death from all the killer diseases long before any vaccines became available. Here is the graphic again.

You can see that all of these diseases that killed millions of people were basically non-deadly long before vaccines became available. The greatest killer of all in the 19th century was scarlet fever, and we’ve never had a vaccine for that. And now no one dies from scarlet fever.

Also, you can see that deaths from smallpox pretty much died out before the 20th century. I ended up getting the smallpox vaccine twice (both times unnecessarily), once when I was a child and again when I was 20 and went to Europe for the first time.

If you read the meticulously researched Dissoving Illusions, you will discover that probably as many people died from the smallpox vaccine as from smallpox. I read a number of the many, many citations, which confirmed what the authors wrote. I did not read all of them, but I read enough to satisfy me that they had done a thorough job.

In case you don’t remember the story of how the smallpox vaccine came to be, I’ll briefly tell the history.

It had been noticed for years that milkmaids who developed cowpox, a viral infection that caused blistering of the hands and glandular swelling in those who worked closely with infected cows, seldom came down with smallpox. Over the years, a number of scientists had noticed this phenomenon, but in 1796, physician Edward Jenner took the pus from the blisters of one of his milkmaids and injected the contents into the skin of the eight-year-old son of his gardener. The kid came down with a mild illness, from which he quickly recovered. Jenner then injected him with material from the scabs of a person with smallpox. The kid—James Phipps, the real hero of this story—did not develop smallpox. Thus the smallpox vaccine was developed.

Bear in mind that this was 1796, almost a hundred years before Robert Koch and the germ theory of infection. Imagine the conditions involved in preparing this vaccine. No thoughts of sterility whatsoever. Just grab pus from some lesions and stick them into peoples’ skin. What could go wrong?

Well, plenty went wrong. You can read all about it if you so desire.

The smallpox vaccine was not the panacea it is presented to be today. If you read Dissolving Illusions and the supportive data in the citations, you will learn that there was as much fighting about the smallpox vaccine as there was about the Covid vaccine. In many cases, people were required to vaccinate their children. Often the children died. Think about it. They were injecting pus into kids. And at that time there were no antibiotics. And kids died.

Reading about the conditions under which these vaccines were made is sickening. It would be impossible now to compare the deaths saved from the smallpox vaccine to deaths occasioned by the vaccine itself.

By the time an actual sterile vaccine could be made that contained a strain of the smallpox virus and nothing else, deaths from smallpox were a thing of the past as you can see from the above graphic.

Because of all the heroic tales of Jenner and all the lives allegedly saved as a consequence of his vaccine, it is firmly entrenched in the minds of the majority of people who don’t know the real history that Jenner saved more lives than any man in history. If you read the real history, you know better. But most have never read the real history.

Last night I finally got around to watching the long interview Tucker Carlson did with Elon Musk. Both of these guys are smart, but Musk is off-the-charts smart. The issue of vaccines came up at 33:40 in the discussion. Both of them basically were on the same page on how the smallpox and polio vaccines saved so many lives and so much crippling, which made it obvious to me that neither of them had ever read a detailed history of either of these vaccines. (On another note, if you’re interested at all in what might happen if AI goes wild, watch the last third or maybe quarter of the interview. Musk lays out the scenario, which I had never considered. Probably because I don’t know squat about AI, while he knows a lot about it.)

If you want to read an excellent book on polio and the polio vaccine, read The Moth in the Iron Lung, another great read that I ought to add to the two above.

One of the things—I can’t remember if it was Tucker or Elon who made mention—was how you still see elderly people walking around who did not take the polio vaccine and who have been crippled for life as a consequence. In my life, I have personally met two people who have been crippled by polio, and both of them got it from the vaccine. A not uncommon occurrence with the early vaccines.

I, myself, was in one of the first groups to be vaccinated. I showed up for school one day in the 2nd grade and we were all shuffled off to the gymnasium, where we all got the polio vaccine without so much as a by your leave. Imagine what would happen today if that were to occur in a public (or private) school without parental permission. My parents knew nothing about it, but my mother was delighted when I came home and told her. Fortunately, I did not come down with polio.

Speaking of which, the polio vaccine is just about the only current vaccine I don’t have a problem with. It is an oral vaccine, so it is given the same way polio is transmitted: orally.

The second book on my list above, Turtles All the Way Down, written by a number of Israeli researchers, details the lack of careful study in the development of vaccines. None of the vaccines in use today has been tested against placebo, which seems outrageous. I didn’t believe it as I began to read, but when I checked the citations, there it was.

Cohort studies that have been done show that kids who have never been vaccinated have fewer doctor and ER visits and miss fewer days of school than kids that have been vaccinated. But these are not randomized controlled trials. Many people have asked the regulatory agencies (which have all been captured by Big Pharma) to demand RCTs, but their response is that it would be unethical to deny a control group the vaccine. Instead, the new version of the vaccine is tested against an older version. If those getting the older version have X number of adverse effects and those taking the new version don’t have a significantly greater number than X, then the vaccine is approved.

I don’t know if Maryanne Demasi, who is a friend of mine, was inspired by what I wrote last week about Stanley Plotkin, or if she had been working on it all before I mentioned it, but she has a great Substack article that came out yesterday in which she reports on her interview with the good doctor. It is well worth reading.

Okay, I’ve gone on long enough about this. I’m sure you get the picture. The idea that vaccines are not the be-all and end-all everyone—including Elon and Tucker—think they are took me a long time to come to. But I’m there now. And till some new data persuades me, I’m there to stay.

If they ever test these vaccines against placebo and they turn out not to cause problems, then I may change my mind.

The Lumen

I’ve received a number of poll responses and emails from people who have tried the Lumen and are confused by the results.

When I wrote about the Lumen last week, I hadn’t had much experience with it. Now both MD and I have had over a week’s experience with it, and I can tell you, it is an amazing tool. It just requires a little understanding to figure out what’s going on. Which understanding we are gaining day by day.

I think it is more valuable than a continuous glucose monitor (CGM). CGMs are nice for telling you what foods shoot your blood sugar up and keep it there. For MD and me, the food that did that the worst was oatmeal made with steel-cut oats and consumed with a bit of half-and-half. It sent both of our blood sugar levels way up and they stayed up for a full two hours.

So, CGMs are good for discovering those kinds of facts, but they can also be deceptive. For instance, consuming a fair number of French fries did not run my blood sugar up at all. I tried it multiple times, all with the same result. Barely a blip in my blood sugar levels. Same with ice cream. I tried it as a dessert and then tried it again after fasting all night and half of the next day. No significant rise.

Fat by itself is not supposed to drive up blood sugar or insulin very much, if at all. But fat with sugar should drive up blood sugar. The fact that it doesn’t tells me that it drives insulin way up, which I’ve confirmed by reading papers on studies of the effect.

I’ve read accounts online of people saying this or that brand of ice cream doesn’t raise their blood sugars as shown by CGM. The implication is that somehow combining fat with sugar modulates the blood sugar rise. And indeed it does…because it raises insulin levels. I would rather have a short rise in blood sugar than I would a longer, more profound, rise in insulin.

The lumen measures how much fat one is actually burning by looking at the oxygen in vs CO2 out. If you look at a picture of a glucose molecule, you’ll notice that for each carbon there is also an oxygen. If you look at a long-chain fat—which is mainly the kind of fat we eat—you’ll see many carbon atoms (16,18,20, 22), but only two oxygens.

In research labs fat vs carb burning is calculated by what’s called the respiratory quotient, or the RQ. Anyone burning pure carbs will have an RQ of 1, i.e., basically the same amount of oxygen going out as coming in. If one is burning fat only, then the RQ is ~0.7. Anywhere in between those two numbers means a mixture of fat and glucose, and the relative amounts can be calculated.

The equation is: RQ = volume of CO2 produced/volume of O2 consumed

If you eat nothing but fat, you produce 70% of the CO2 you would produce consuming pure carb.

This fact has not been lost on pulmonary doctors, who, for years, have put their patients with impaired lung capacity on low-carb diets. The job of the lungs is to bring in oxygen and get rid of carbon dioxide. If you have an issue with your lungs, it is much easier to get rid of only 70 percent of the CO2 you would have to get rid of were you on a high-carb diet.

I’ve always wondered why a device that measures RQ wasn’t available for public use. I figured the technology required would be too expensive to make such a device practical, but Lumen seems to have solved that problem. If that was the problem.

I can tell you a couple of things based on MD’s and my use of the product for a bit over a week now.

First and foremost, no matter what it says in the old Drinking Man’s Diet book, drinking impairs fat burning.

In one of our first experiments, MD and I had a drink at ~5 PM, then we had a very low-carb dinner (maybe 15 g of carb total), then we watched something on TV and had two more small drinks as we did so. I had Jameson Irish Whiskey straight up and she had her favorite Scotch likewise. We sipped these drinks slowly over maybe two hours.

Next morning, we were both burning 95 percent glucose and 5 percent fat.

The next day we followed the same dietary regimen and had a drink at ~5 PM. We did not have the other drinks spread over two hours as we did the night before. The next morning we were both burning 65 percent fat and 35 percent carb. We fiddled with this over the past few days enough for me to know that alcohol definitely inhibits fat burning. Now I’ve just got to trace out the various pathways to figure out why. Which I have not done yet.

Reminds me of a conversation MD overheard in the women’s locker room of a golf club we used to belong to. I’ve written about this before, but it bears repeating.

Woman #1 after running into woman #2: “Wow, you look great! You’ve lost a lot of weight. What kind of diet are you on?”

Woman #2: “I’m not really on a diet. I just cut back a lot on my wine drinking.”

Woman #1: “Well, that’s just too extreme!”

Early on when we first got the Lumen, MD did a brutal workout and ended up burning 85 percent carb and only 15 percent fat. Which was expected as this was a heavy duty workout that assuredly went anaerobic. Yesterday, she did another brutal workout, but was mainly aerobic. She ended up burning 95 percent fat and only 5 percent carbs. Shows the difference between aerobic and anaerobic workouts. Doesn’t mean aerobic is better. It just means that you’ll be burning carbs while anaerobic because that’s the only way you can get energy to burn.

I would rather read 95 percent carb after a workout than 95 percent fat. The former would tell me I went anaerobic, which is nice to know. Lets you know you really did a serious workout.

Even though you’re not fat burning during the latter stages and right after, it tells you you have really gone to or approached failure, which is what the muscles need to grow.

I did a band workout a couple of days ago during which I set a number of personal records. I was absolutely thrashed after and fell into a pile while I recovered. Then, like the moron I sometimes am, I got distracted by something and completely forgot to blow in the Lumen till a couple of hours later, when I blew 75 percent fat and 25 percent carb. I wanted to see what it was right after, but didn’t do it.

I did discover another weird thing, which I don’t know if true or not.

Last night I didn’t sleep for crap. I somehow had a half-awake dream that I had started writing a section in The Arrow about a medical paper. In this half-awake, half-asleep dream, I discovered the paper was truly worthless and was awful, but I had spent a lot of time writing about it. I kept tossing and turning and waking up thinking about it. I had a miserable night and instead of popping awake at my normal 6 AM (the time I normally spontaneously awake), I slept fitfully until almost 8:30. The minute I was truly awake, I realized I hadn’t written anything about the paper that had haunted my sleep. In fact, the paper didn’t even exist. But it had kept me disturbed throughout the night.

I blew into the Lumen first thing, and it came up 85 percent carb and 15 percent fat. Which I found strange, since all the other mornings except for the one with the late booze the night before I had been burning mainly fat.

I clicked on the EXPLAIN MY RESULTS link and was asked first how many carbs I had eaten the day before. Maybe 25. It asked how many at the evening meal. Maybe 5, if that. It then asked about alcohol. I said one drink at about 5 PM. Then it asked about my night’s sleep. It gave me four choices, with one asking if I slept poorly, which is the one I clicked. It then said that poor sleep causes a rise on cortisol, which causes a rise in blood sugar. The latter is definitely true. But I don’t know about the former. It never occurred to me that a wretched night’s sleep might stimulate cortisol, but it does make sense in a way.

I’ll report more as I get a better handle on what’s happening metabolically in various circumstances.

Gnawing Hunger

I had a bunch of poll responses from people who said they did have gnawing hunger despite my insistence that people couldn’t have gnawing hunger a couple of hours after eating. Here is a comment that quotes what I said, then followed with her own experience.

"If you just ate two hours before, you can’t be in the grip of the kind of gnawing hunger that can’t be overcome." [She is quoting what I had written.]

 

But when doing a very low fat diet years ago that description is exactly how I felt all day -- eat something, then an hour or so later have a "gnawing hunger that can't be overcome". Willpower would only give me maybe another hour before I'd give in (~2 hours after previously eating). I had multiple people tell me that was just me being "weak" --but once I stopped eating very low fat, even though I then went back to my 'traditional dieting' (i.e. low calorie), that gnawing hunger went away, so it wasn't at all willpower or being weak but some kind of reaction to the diet itself.

My reply to her comment was

I understand your point. But I've got to ask you a question. If at the moment the final hour of holding off hunger expired you had a knock on your door and you opened it to find one of your absolute best friends you hadn't seen for years standing there, would you have slammed the door and made a run for the fridge? Or would you have let the friend in and completely forgotten about your hunger? For a while at least. If the latter, then it wasn't gnawing hunger that couldn't be overcome.

My answer was in accordance to Dr. Glasser’s control theory as I discussed a few weeks ago. As I quoted about Dr. Glasser’s theory in a chapter in the first book I wrote

Dr. Glasser says, basically, that there are four components to any behavior: the doing component, the feeling component, the thinking component, and the physiological component. Of the four, we have complete control only over the doing component, and partial control over the thinking component--over the other two, we have no control whatsoever.

If we haven't eaten for a time and we see or smell food that appeals to us, we feel hungry-the feeling component. We can't help it that we feel hungry, it's beyond our control. Our mouths water and our stomachs growl-the physiological component. We can't keep our salivary glands from working, and we can't do thing about our intestinal muscles that are becoming active. We have no control over these physiological processes. We look at the food and smell the aroma, and we imagine how good it will taste ―the thinking component. As long as we are hungry and in the presence of this wonderful food, we will probably think about it. We can, however, force ourselves to think of other things, but more than likely, our thoughts will occasionally revert back to the food. We can partially control our thinking-the stronger-willed of us more than others. We sit down and eat the food-the doing component. This act, we can completely control. We can eat or not, as we please. Unlike the workings of our salivary glands, or our feelings of hunger, we have total, 100-percent control over whether or not we eat.

The interesting thing about all this is that although many of us allow the uncontrollable components of behavior to direct the controllable component, it can work in the reverse direction. If we take charge of the doing component, over which we have total control, the other involuntary components will fall into step. In our example above, if we walk away from the food and involve ourselves in a different activity, one unrelated to food or eating, slowly our feelings, physiology, and thinking will change and adapt themselves to our new activity. We have controlled what we can and as a result, have ended up controlling indirectly those components that we can't control directly.

My point in my reply to the commenter above is that if you sit around and ruminate on how hungry you are, your feelings of gnawing hunger are going to do nothing but get worse. If you take some kind of action, you’ll overcome these feelings. Unless, of course, you do have true gnawing hunger because you’ve been starved.

If you’re interested in true starvation and what it really means and feels like, grab a copy of the book The Great Starvation Experiment about how Ancel Keys kept 36 conscientious objectors under lock and key under the football stadium at the University of Wisconsin during the waning days of WWII. It was the greatest starvation experiment in history and couldn’t be repeated now.

At the time, the War Department realized WWII was drawing to an end, and that the Allies were going to triumph. The people in charge thought there would be widespread starvation in Europe after, so they sought a plan to deal with it. They contracted with Keys, who had created the K-rations (The K stood for Keys) to figure out what would happen if the European population consumed a diet composed of what Keys thought would be available to them.

He recruited young, healthy men and fed them a diet of mainly carbs along with a bit of protein and fat. The exact breakdown of their daily diet was protein 100 gm, fat 30 gm, and carbohydrate 225 gm. If you express these intakes as percentages, you come up with 25.5% protein, 17.2% fat and 57.3% carbohydrate. The average energy intake was 1570 calories per day.

Now you might be thinking, Hey, those aren’t starvation rations. I’ve done diets like that and haven’t starved. Well, you would be wrong. You may have done a diet like that for a few weeks or a couple of months and lived off your own adipose stores.

These young men were accepted into the study because they were normal weight, not obese. They were chosen to be representative of the Europeans who were already in bad shape from the privations of a war that had been going on for them for six years.

These young men were kept on this diet for 24 weeks. And the results were grim.

Here is a photo of one of them at the start and toward the end of the study:

These men truly starved on these rations. There are many more such pictures in the book, so I’m not just cherry picking this one.

As the study progressed the subjects not only lost a considerable percentage of their body weights, but suffered other problems as well. As the time wore on the men thought ceaselessly about food, they became lethargic, they were cold all the time, they became depressed, they developed bleeding disorders, their ankles became edematous, and some developed more serious psychological disorders.

In fact, the man in the photo above suffered such psychological turmoil from the semi-starvation that he chopped off several fingers of his left hand a month or so after the bottom picture was taken.

This is true gnawing hunger. Had an old friend appeared to one of these guys, I doubt he would have immediately forgotten about their hunger. It was all consuming.

Keys wrote a book about this study laying out all the details available in two volumes. I have both, and they don’t make for easy reading. Not just because of the technical detail, but for the descriptions of what these men went through while eating almost 1,600 calories per day.

Keys’s starvation studies aside, enough people have written me about how they have experienced what they consider a hunger that must be appeased that there must be something to it.

So, I decided to dig deeper.

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Causes of Hunger

Whenever I start thinking about what causes hunger, I always default to the huge increase in seed oils we have included in our diet since the obesity epidemic kicked off in the late 1970s/early1980s. A few years ago, I gave a talk on one hypothesis as to how this might influence obesity, but there are other hypotheses kicking around out there.

Here is a chart from the above talk showing the vast increase in seed oils over the past decades.

The big chart shows the overall increase in seed or vegetable oils, which pretty much mimics all the charts showing the growth of obesity. The little chart in the upper left shows the breakdown of the makeup of these seed oils, with soybean oil vastly outpacing the others.

Here is a chart showing the fatty acid composition of various fats and oils used for cooking.

This is just one of many such charts you can find online. It shows in general the fatty acid composition of the various oils, but bear in mind that thanks to various breeding processes, these plant oils can have amounts of specific fatty acids that vary from what is shown on this chart.

In my talk linked above I mainly discussed the omega-6 fat linoleic acid. I didn’t spend any time talking about omega-3 fats. If you look at the chart above—with the exception of flaxseed oil (linseed oil) there is very little omega-3 fat in the commonly used oils. The most commonly used oil, soybean oil, contains a bit more than most, but still not much as compared to omega-6.

If you look at the change in the type of meats we’ve been eating over the past 50-60 years, you’ll find that we—as a country—have vastly increased our consumption of poultry and slightly increased our consumption of pork. Beef and fish consumption has fallen off a bit.

Both pork and poultry contain substantially more omega-6 fat than beef. All in all, with the vast increase in seed oils in the diet in combination with the increased poultry and pork consumption, we, as a nation, are gobbling down way, way more omega-6 fats than we have any time in history.

And obesity is at epidemic proportions.

But just because the two have risen in lock step doesn’t mean one has caused the other. But it doesn’t mean one hasn’t caused the other either.

If there is no correlation, there is probably no causation. If you look at the big drop off in beef consumption, then listen to people say the epidemic of type 2 diabetes is driven by red meat consumption, you can pretty much figure that is bogus.

But when omega-6 consumption has skyrocketed right in step with the increase in obesity, then it’s reasonable to speculate that it might be causal.

Having said all this, I haven’t really looked into the idea of omega-6 being a driving force for obesity except for the hypothesis I outlined in the talk linked above. But since so many people are complaining about gnawing hunger, I figured I would look a little deeper.

In doing so, I solved a major problem of my own. And came across a couple of other ideas along the way.

I’ve heard of endocannabinoids being involved somehow with seed oils, but I never paid a lot of attention to it. And I didn’t even know if there was any truth to it. So I took a look. I did so because I was in college during the hippie years, so I knew all about the munchies after smoking weed.

I discovered that THC, the active ingredient in marijuana, activates certain pathways in the body. Since pathways don’t get activated unless there is some sort of receptor involved, then it makes sense we, and rats, have receptors for THC. If we have receptors for it, then we must somehow make it ourselves, i.e., endogenous THC or endocannabinoids.

And indeed we do.

We make two that I could find. And both are made from omega-6 fats. There is some controversy over which of the two cause the munchies, or if only one causes the munchies. But they clearly do cause an increase in food consumption and are found in greater concentrations in obese people than in thin ones.

I haven’t read a lot of papers on these, but I’ve skimmed through PubMed enough to get a rough picture. I’m sure my friend Tucker Goodrich, who I suspect is all over this, will inundate me with papers when he reads this.

I kind of stumbled onto the endocannabinoid bit accidentally as I was searching for papers on omega-6 consumption and disease, of which there are plenty. Since most of the people who wrote me about severe hunger were female, I looked to see if I could find anything specific to females, and indeed I did.

I came across what I think is a pretty great paper, though I haven’t heard back from the author. I requested the full text, but haven’t gotten it yet. The abstract pretty much tells the tale, though. Its final conclusion after feeding pre-menopausal females various combinations of O-6/O-3 fats was that

Lowering dietary LA did not result in the expected changes in fatty acids associated with the LA-ARA inflammatory axis in women with overweight and obesity.

LA is linoleic acid, an 18-carbon omega-6 fat, which is the most commonly consumed polyunsaturated fat (PUFA) in America (if not the world).

Many people try to avoid LA as much as possible, but this study shows that just getting rid of the omega-6 LA doesn’t do the job in terms of reducing the bad endocannabinoids it produces.

This is what I’ve been trying to do for years myself. I avoid LA like the plague. I know I’m not a premenopausal female, but I figure if it would work for them, it would work for me. And if it didn’t, I guess that explains why it didn’t work for me. More about which in a bit.

The absolute best part of this study was that it led me to a terrific study. These days PubMed includes a section titled Similar Articles following the study you’re reading. And right there at the head of the list was the study that did me right.

Titled “Dietary linoleic acid elevates endogenous 2-AG and anandamide and induces obesity” the study gave me some direction. The study introduction starts with

Excessive endocannabinoid system activity is likely to have a causal role in obesity acting through multiple organ systems, but has not as yet been linked to the worldwide epidemic of obesity. The endocannabinoid system includes the two endogenous ligands 2-arachidonoylglycerol (2-AG) and N-arachidonoylethanolamine (anadamide or AEA) and two cannabinoid receptors (CB1 and CB2). Central CB1 receptor activation by increased endocannabinoid levels or exogenous agonists induces hyperphagia along with increased lipogenesis and peripheral adiposity.

Okay. Let’s translate. 2-AG and AEA are the endocannabinoids we’ve been discussing. They call them cannabinoids, so we’ll stick with that. The endo on the front means they are made in the body, not taken from the outside. The CB1 and CB2 are the cannabinoid receptors, which once activated by the cannabinoids drive hyperphagia, which means overeating. Or perhaps gnawing hunger leading to overeating.

Here is the important paragraph:

Endocannabinoids are endogenous lipid mediators made from essential fatty acids available only from dietary sources. The two best characterized endocannabinoids, 2-AG and AEA, are both metabolic derivatives of a single fatty acid precursor, the ω-6 arachidonic acid (AA, 20:4n-6) in phospholipids (AA-PL). Since humans cannot synthesize AA de novo, tissue PL concentrations are dependent upon the competition between dietary intakes of ω-6 and ω-3 fats: (i) linoleic acid (LA, 18:2n-6, the precursor to AA), (ii) preformed dietary AA, (iii) α-LA (18:3n-3, the precursor to eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n-3), and (iv) preformed dietary EPA and DHA. Endocannabinoids are formed enzymatically on demand from the pool of ω-6 membrane PL-fatty acid precursors. During the 20th century, elevations in AA-PL have been estimated from the dramatic increase in dietary LA resulting from a >1,000-fold increase in the estimated per capita consumption of soybean oil from 0.006 to 7.38% of energy. Here, we modeled these ecological dietary changes in mice to determine if increasing LA as a controlled dietary variable could elevate AA-PL composition, increase endocannabinoid levels, and induce metabolic and phenotypic changes consistent with obesity.

Okay, here we go. Look at the sentences I bolded.

The 2-AG and the AEA (the cannabinoids) are made from the omega-6 arachidonic acid (AA), which is found in the membranes of all the cells (the phospholipids). Humans cannot synthesize AA out of nothing. AA must be made from precursor omega-6 fats. The more omega-6 fats in the cell membranes, the more AA that can be made. Thanks to the 1,000 fold increase in the intake of omega-6 fats (primarily from soybean oil), our cell membranes contain greatly elevated levels of AA.

The researchers fed mice a variety of combinations of omega-6 and omega-3 fats along with and without saturated fat, then measured what happened to their cannabinoids. And their levels of obesity.

As it turned out, the amount of LA (the omega-6 linoleic acid) determined the levels of the endocannabinoids. And it “increased food intake, body weight, and adiposity” regardless of the amount of fat in the diet.

Adding 18-carbon omega-3 fat, reversed the process, despite the high saturated fat content of the diet. In fact, the highest omega-3 fat diet along with the lowest omega-6 diet AND the highest saturated fat diet produced the skinniest mice.

There are some grisly photos in the full text of the article linked above that show just how much fat accumulated in the high O-6, low O-3 diet fed mice. Not a pretty sight.

So, the 18-carbon O-6 (linoleic acid) intake (not the total fat intake) determined the level of cannabinoids, whereas the level of O-3 (linolenic acid) appeared to be the controlling factor. If you consume O-6 along with plenty of O-3, you do okay. If you consume a lot of O-6 and little O-3, you’re in trouble. If you avoid O-6 as much as possible and up your O-3, your golden.

At least if you are a mouse.

Now I didn’t say above, but the amounts of O-6 and O-3 they used in this study mimicked those in the human diet prior to the start of the obesity epidemic and after it was full-blown, when O-6 intake had increased 1,000 fold.

Okay, you’re probably saying to yourself, yeah, but so what. This is a mouse study. Which is exactly what I said myself. But, I thought, what can it hurt to give it a try?

MD and I went out and bought a bunch of tins of sardines packed in water. We avoided the olive oil ones, because they a) are probably not packed in real olive oil, and b) even if they are, there is a fair amount of linoleic acid in olive oil. We also purchased a bottle of 365 flaxseed oil from Whole Foods, which actually makes a pretty good oil for an oil and vinegar salad dressing.

As you are aware from the first few paragraphs of this Arrow, I am totally okay whining about all the injustices heaped on me by the airlines and anyone else who makes my life inconvenient. But I don’t like to whine about my own health issues.

But this is pretty phenomenal.

I have had a couple of problems I’ve been battling. One is a terrible itch on my back and the cheeks of my rear end. I’ve written it off to the dry skin of old age. MD keeps telling me to put some kind of skin conditioner on my back and butt, but I just don’t want to oil myself up. So I don’t. I also have mild back pain, probably from golf and doing dead lifts with the bands. My back is ancient and has suffered a lot of abuse over my fairly active life.

MD and I started the sardines once a day and the flaxseed oil salad dressing with every meal, and my itching vanished within a week. I kid you not. And my back pain is all but gone.

So, in the words of the famous Monkee’s song, “now I’m a believer. Not a trace of doubt it my mind.”

Just adding that bit of omega-3 to my diet has paid huge dividends. It has rid me of two problems that aggravated the crap out of me.

Unlike the people who have written me about gnawing hunger, I don’t ever have gnawing hunger. I can go forever, it seems, and never get hungry, so I guess I don’t have a lot of sympathy for those who do. But what I’m saying is that I don’t know if the increase in omega-3 fats decreased my hunger or not, because hunger isn’t my issue. I do know it got rid of my chronic itch and my back pain and did so quickly.

This is just one component of the advantages of omega-3 fats. I’ll explore some others in future issues of The Arrow.

Odds and Ends

Newsletter Recommendations

Video of the Week

The video of the week this week is a little different. I’ve had a run of music videos, but this is sort of music, but not music in the traditional sense. The kid in this video is autistic, and he has developed an ability to accurately mimic various bird calls using just his voice. In reading about him, I discovered he defeated an online app for identifying bird calls. He used his mouth, and the app thought they were real bird calls. It’s phenomenal what he has been able to do, and he’s just a little kid. He brought up the idea that maybe he should do his bird calls at a talent show at school. His parents had doubts, because they feared the kids would ridicule him. But he wanted to do it anyway. So, here he is. Watch and be amazed.

@diabetic4one

This is Samuel’s bird call performance at his schools talent show. He loved every minute of this #autism #birder #fypage #talent #agt

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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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