The Arrow #132

Hello everyone.

Greetings from Montecito.

Believe it or not, I’m still in the throes of the upper respiratory infection I had. Maybe I’ve got Long RSV. :) It’s mostly gone, but it’s got a long tail. Each day I wake up and think okay, it’s over. But it is still hanging on, though less and less with each passing day. It’s not that I feel bad, I just don’t feel my normal peppy self. But, this, too, shall pass.

Ontological Shock

One of the commenters to last weeks Arrow wrote

There's none so blind as those who will not see. I picked up the term 'Ontological Shock' from Robert Malone. After my ontological shock from the last three years nothing surprises me now.

I had seen the term “ontological shock” a time or two, and had kind of figured it out from context. After the above comment, I looked it up. When you search for something in the Brave Search, you get a summarizer. Here’s what it had to say about ontological shock

Ontological shock is a philosophical term that refers to the state of being forced to question one's worldview when one's fundamental understanding of reality, existence, or the nature of being is disrupted or challenged. It is a profound disorientation that occurs when one encounters a concept, experience, or idea that fundamentally contradicts their established beliefs, assumptions, or worldview. Ontological shock often leads to a period of reflection, reevaluation, and potentially a shift in one's fundamental understanding or perspective on life and existence. It can also refer to changing one's thoughts and views of everything that they believe in, thinking in a completely different way of all things. [Emphasis in original]

If the last three years haven’t caused an ontological shock, then I don’t know what it will take.

When confronted with ontological shock, one is thrown into cognitive dissonance. Cognitive dissonance is an uncomfortable state of being. When you’re in it, you cast about for some way to get out of it. As I’ve mentioned before, partisan politicians are always at hand to provide an escape. If you choose not to accept the easy escape they offer, then it requires a lot of thought and reflection—and sometimes an entire change of worldview—to come to terms with it.

In my own case, it started with what I was hearing about SARS-CoV-2. Long before anyone could imagine a vaccine being available, there were all sorts of tales going around as to how the virus affected people. When I heard all this, it was sort of an ontological shock to me, because it so went against everything I had learned about virology and immunology in medical school. And against everything I had seen in many years of clinical practice.

Since it had been a long time since I was in medical school, my first thought was that perhaps virology and immunology had changed markedly since I last studied it. I looked for the latest edition of a famous immunology review guide and found the edition that had just been published a year earlier. I bought it and read it from cover to cover. From what I could tell, virology and immunology were pretty much the same in 2019 (the edition of the book) as they were years before when I studied it. There were a few updates, of course, but nothing really major.

After reading that book, I realized we were being gaslit about the whole pandemic, which was just getting rolling as I finished the book. For the life of me, I couldn’t figure out why the CDC, FDA, and NIH would be out-and-out lying about the situation, but they clearly were.

I happened upon an interview with Knut Wittkowski, who is a biostatistician and epidemiologist and head of Department of Biostatistics, Epidemiology, and Research Design at The Rockefeller University for 20 years. Prior to that, he had worked for 15 years with Klaus Dietz, a leading epidemiologist in Germany. In the interview, Wittkowski explained that Covid-19 was relatively dangerous for older people, especially those with multiple co-morbidities. Which we all know now, but he was saying this back in 2020, early on in the pandemic. He also pointed out that young people, children in particular, had mild symptoms, if any.

He said closing schools was the worst thing that could happen. If the schools stayed open, the children would all become infected with SARS-CoV-2, experience minimal symptoms, and hasten herd immunity, which effectively would put a halt to Covid.

It all made sense to me, because that was what I had learned in medical school, and what the new immunology review book told me.

Then I stumbled onto a talk by Stanford professor Michael Levitt, who was a Nobel laureate. He showed that infectious diseases follow a Gomperz function and that SARS-CoV-2 was no different. He created a handful of short videos on the Gomperz function and showed how Covid followed the Gomperz curve. The Gomperz function is basically the math showing how herd immunity comes about.

When I started writing The Arrow in early January 2021, I tried to find the Wittowski interview, which had been on YouTube. It had already been canceled. I watched an interview with Michael Levitt in which he expressed his disbelief in how he had been treated by his colleagues at Stanford after explaining what was happening with Covid on Fox News. Which, he said, was the only network that asked him to come on.

Wittkowski left Rockefeller University and his talks on Covid so went against “the narrative” of the medico-pharmaco-industrial complex, which was amplified by the corporate media, that Rockefeller University felt the need to pile on in a press release denigrating Wittkowski’s time there.

I was confronted with making a choice. Did I go along with what I felt in my bones was right? What my medical education had taught me about immunology, which had been confirmed by the immunology review text? Or did I go along with the CDC, FDA, and NIH, institution that theretofore I had never really questioned?

I ultimately went with my gut. And after considerable study, I’m glad I did. The scales fell from my eyes about the medico-pharmaco-industrial complex, and I’ll never view government- and industry-based “science” the same way again.

Based on my exhaustive reading, I decided not to get the Covid vaccine. After discussion with the rest of our immediate family, they all decided against the vaccine as well. So, we’re all happily fully unvaccinated.

I’m sure every reader of this newsletter was confronted with ontological shock during the pandemic, or panic-demic, as I like to call it. It’s not fun, but it does shake up your world view. In my case, I think much for the better.

Those of you who have been readers over the past two plus years have seen my thinking evolve. It’s been a journey. I’m truly thankful for the ontological shock I experienced, which shook me out of a number of incorrect beliefs I had harbored for years.

The fact is, I should have known. I had the medical version of Gell-Mann Amnesia. I knew how screwed up nutritional medicine was, yet I continued to believe that all the other specialties weren’t. Bad mistake. Now I question everything. And you should, too.

The Science and the Experts

I’ll just put this up without commentary.

Anthony Fauci

“Attacks on me, quite frankly, are attacks on science.”

Richard Feynman

“Science is the belief in the ignorance of experts.”

Good Question, Matt; I’ve Often Asked It Myself

Every day, it seems, one or more reports surface showing how the federal government is leaning on private companies to censor in ways the government itself can’t. Matt Taibbi’s post says it well. Here it is in its entirety.

Where Have All The Liberals Gone?

Why Do Low-Carb Diets Improve Lipids?

Diet trials are difficult to do, mainly because there are so many variables. When you eat food, you’re eating a combination of fats, protein, and carbohydrates. And there is another variable thrown in just to make it even more problematic: calories (kcal).

If you’re doing a study to try to determine which of these four variables brings about a change in, say, weight, it’s difficult to get a clean answer.

Here’s why.

Let’s say you start out with two groups of overweight people on two different diets, both containing the same number of kcal. You put one group on an 1,800 kcal diet composed of 20 percent carbohydrate, 20 percent protein, and 60 percent fat (20/20/60). The other groups goes on an 1,800 kcal diet made up of 50 percent carbohydrate, 20 percent protein, and 30 percent fat (50/20/30).

You keep both groups on this diet for six months. At the end of the study, you find that the group on the lower carbohydrate diet lost an average of 8 pounds more than those on the higher carbohydrate diet (a common finding in studies like these).

What conclusions might you draw from this study? Well, you could say restricting carbohydrates makes people lose weight. You could say that, but you could also say increasing fat makes people lose weight. You not only decreased the carbohydrate intake in the first group; you also increased fat intake. So, maybe it is the fat increase that did all the work. Or, you could even say that the combination of cutting carbs and adding fat did the trick.

It’s difficult to tease out what the real driving force is.

Okay, you say, we can sort this out. Let’s redo the experiment.

We take another group of similarly overweight people and put them on a diet of 20 percent carbs, 20 percent protein, and only 30 percent fat (20/20/30). But wait…that doesn’t add up to 100 percent. The only way we can cut the fat by half and keep the kcal the same is to increase the carbs and/or protein. If we keep the carbs the same and cut the fat, then we have to go way up on the protein.

If we do that, whatever we end up finding after the six month study is over could well be due to the increase in protein, not the carb restriction or the decrease in fat.

Okay, you say, let’s figure out how many grams of carb, protein, and fat were in the original study, and then we’ll simply cut the fat by half in our new study.

The first diet, the 20/20/60 1,800 kcal one, contained 90 grams of carbohydrate, 90 grams of protein, and 120 grams of fat. So, let’s cut the fat by 60 grams and see what happens.

When you cut the fat by 60 grams while keeping the carbs and protein the same, you reduce the total calories in the diet by 540 kcal. As a consequence, any changes in weight loss can be attributed to the reduction in kcal.

See what I mean? Given these four variables, changing one always changes one or more of the others. It’s impossible to change one without changing another, so it’s impossible to know with certainty which change brings about the result you’re evaluating, which, in the case of our imaginary study, was weight loss over six months. Is it carbs, fat, or calories? You can’t conclusively say from the data.

Fat? Carb? Protein? Calories?

There are a lot of papers out there comparing low-carb, higher-fat diets to lower-fat, high-carb diets where calories are not controlled. These studies are designed to see what happens when dieters simply follow one or the other diets, much the way they would if they had purchased a diet book. Sort of “real world” experience trials.

When people write books promoting low-fat diets, they usually tell readers to keep fat to some minimal level percentage-wise. Eat all you want, but don’t exceed, say, 20 percent fat. Those who write low-carb books typically set the carb levels in grams per day or grams per meal.

If you’ve tried both of these approaches, you’ve probably discovered that you can eat a whole lot of food and still keep the fat percentage low. A bagel has very little fat. Slop some jelly on it—zero fat—and eat away. Maybe even the thinnest sheen of butter, and you’re still under the fat limit. There is almost no shut off switch for carb consumption. Which is why, when you are absolutely stuffed with a meal, there is always room for dessert. It’s really easy to overeat carbs.

It’s not the same with fat. If you cut the carbs from your diet, it’s difficult to overeat fat. It can be done, but it’s not easy. No one sits down and eats a stick of butter. But a lot of people love frosting, which is butter mixed with sugar. Throw the carb in the picture, and it allows you to override the normal fullness you would get from the fat alone.

Typically, when people remove a lot of carbohydrates, especially processed carbohydrates, from their diet, they eat less. Both fat and protein—the only macronutrients left when you cut the carbs—are satiating. Consequently, when people go on low-carb diets, they almost always voluntarily reduce their caloric intake.

Which makes these free-living studies difficult to interpret.

In the vast majority of cases, these studies end up with the group following the low-carb diet losing the most weight. When these studies started being published in the early 2000s, people said, Oh, sure, you can lose weight on low-carb diets, but you’re clogging your arteries with all that fat while you’re doing it. You’ll lose the weight, but you’ll die with heart disease.

As a consequence, people doing these studies started looking at what happens to lipid levels when subjects go on low-carb diets. Surprisingly—to the naysayers, at least—most people on low-carb diets reduced their LDL levels, and virtually all of them reduced their triglyceride levels.

You would think this would shut the critics up, but it didn’t. Their next response was, Oh, well, these are all short term studies. Let’s see what happens after ten years of it. Which can’t really be argued against, because no one will foot the bill for a ten-year study. Of course, I always counter with, Well, the entire country has been on one, long, multiple-decade study, the hypothesis of which is the low-fat diet will make us thinner and healthier. Every government agency has promoted the low-fat diet, and Americans listened. When the new low-fat nutritional guidelines came out in ~1980, the American diet was about 47 percent fat. Over time it dropped into the low 30 percent level. How has that worked out for us? Obesity is at an all time high, and diabetes is at epidemic proportions.

Going back to our two studies of low-fat versus low-carb… As I mentioned above, when you cut the fat, it’s easy to overeat carbs. But when you cut the carbs, it’s more difficult to overeat fat. Consequently, most of these free-living studies showing the low-carb diet to be superior to the low-fat diet in terms of weight loss also showed that the low-carb dieters consumed fewer calories.

Once this was noted, the naysayers said, Oh, well, no wonder the low-carb dieters lost more weight; they were simply eating fewer calories. And no wonder their lipids improved. It had nothing to do with the carb restriction—it all came about because the low-carb dieters lost more weight.

Thus, the setup for the study I’ll discuss today.

But before I do, just to set the table, let me go into a little physiology and biochemistry. Everyone’s two favorite subjects.

I’ll try to make it as simple as possible.

Ignoring protein, let’s take a look at what happens digestively when we eat carbs and when we eat fat.

Carbs are broken down into their constituent sugars, mainly glucose, and absorbed into the cells lining the GI tract. They leave those cells on the other side of the intestinal lining and enter the blood stream. All of the blood from the digestive tract leaves by way of the portal vein, a large blood vessel that goes directly to the liver. The liver takes the sugars from this incoming blood and deals with them.

Fats are handled differently.

There are basically two types of fat: long-chain fatty acids (LCFA) and short and medium chain fatty acids, also called medium-chain triglycerides (MCT). In discussing fats in the bloodstream, it must be noted that blood (which is water-like) and fats don’t mix. In order for fats to be moved along in the bloodstream, they have to be attached to a protein that makes them soluble (able to dissolve) in the blood.

When LCFA come down the digestive tract they are broken down somewhat and absorbed into the cells lining the small intestine. They are then combined with a protein called Apolipoprotein B48 (Apo B48), which makes them soluble in the blood. But instead of being dumped into the portal vein like the sugars are, the Apo B48-LCFA complexes, which are called chylomicrons, get shunted into the lymphatic system, a circulatory system separate from the one that carries blood.

Just like smaller blood vessels dump into larger blood vessels, which in turn dump into even larger ones, the lymphatic system does the same. All the lymphatics coalesce into a large lymphatic vessel that ultimately dumps its contents into the left subclavian vein via the thoracic duct.

Here is a short, short video on the thoracic duct for anyone interested in learning more. Just watching it gives me hives. It is just like a medical school lecture. and all of this stuff would be fair game for a test.

When the chylomicrons are dumped into the subclavian vein, they are then transported throughout the body dumping the fatty acids inside wherever they are needed. As the LCFA contents get offloaded to the tissues, the chylomicrons decrease in size until they become what are called chylomicron remnants, which the liver then pulls out of circulation and disassembles.

The GI tract handles the MCT differently. Instead of packaging them in chylomicrons and dumping them into the lymphatic system, the MCT are sent directly to the liver just as are sugars. The MCT get to the liver and can get directly into the mitochondria, where they are converted to ketone bodies and sent out to the tissues. The process with LCFA after they are dumped from the chylomicrons works much more slowly. The LCFA have to first catch a ride on the carnitine shuttle to get into the mitochondria where they undergo beta oxidation. The MCT bypass all that and can be converted to energy quickly.

The Magic of Medium Chains

Due to this difference, there has been a lot of study of MCT. These fats, which are found in large amounts in butter and coconut oil, have been shown to hasten weight loss, improve athletic performance, depress appetite, hasten ketogenesis, and a host of other positive benefits. The only downside is that some people get nauseated if they consume a lot of it.

(As an aside, in my opinion, the best way to take in MCT oil—other than butter, which I love, and coconut oil—is to take it in micro-encapsulated form. It’s like a fine powder that can be used in sauces, soups, bouillons, smoothies, shakes, yogurt, hot chocolate (low-carb, of course) and a host of other things. It is tasteless and mixes easily. I even use it in my coffee. It turns my black coffee kind of beige, but there is minimal, if any, flavor change. I’m not sure if the minimal flavor change I seem to notice is because I can see the change in color. I guess I need to do a blind tasting. There are a bunch of brands out there. I like this one because it’s cheap and mixes easily. YMMV.)

Here is a graphic summarizing how the different fats are absorbed.

As you can see, you can get quick, sugar-like energy with MCT without all the negative effects of sugar.

Now let’s take a look at what happens with LCFA when they get to the liver, or are made there.

The liver stores about 100 grams of glucose as glycogen. The muscles store another 400 or so grams. The totality of the stored glycogen represents about 2,000 kcal, which is about a day’s worth of energy.

If your glycogen stores are filled and you eat a meal containing 150 grams of carbohydrate, you don’t really have any place to put it. Glycogen storage is limited—fat storage is not. So it would makes physiological sense for your liver to convert the incoming 150 g of sugar into fat. Which is exactly what it does.

The liver converts the excess carbohydrate to palmitic acid, a 16-carbon saturated fat. The liver then packages this fat along with cholesterol and Apolipoprotein B100 (Apo B100) into a particle called VLDL, which stands for very low density lipoprotein. The liver then releases the VLDL, which is soluble and travels through the blood stream to the various tissues, where it offloads the fats (packaged as triglycerides). Since fats are light—they float on water—and the VLDL is full of them, it is very low density. Thus its name. As the fat is offloaded, the particle becomes more dense and ultimately reaches the point at which it becomes a low-density lipoprotein, aka LDL.

Now it shouldn’t take a genius to understand that if the liver doesn’t make and release a lot of VLDL, there won’t end up being a lot of LDL.

And it should be obvious that if there isn’t a lot of sugar coming in, the liver won’t need to convert it to fat. Consequently, there won’t be a lot of VLDL made, and so little conversion to LDL.

Which explains perfectly well why people who go on low-carb diets typically see their LDL levels fall. It’s what we saw in our practice year after year.

One more thing before we get to the paper.

When you get your triglycerides checked, the lab takes your blood and measures all the fat in it. It’s in both the chylomicrons, which, if you’re fasting, should be pretty low in fat, and in your VLDL and LDL.

Total cholesterol is the total amount of cholesterol measured in the blood. It is a sum of all the cholesterol contained in VLDL, IDL (intermediate density lipoprotein—kind of a halfway point between VLDL and LDL), LDL, and HDL.

LDL cholesterol is the amount of cholesterol in the LDL particles. LDL is typically calculated, so it’s not always accurate. Especially if triglycerides are very low or very high.

Now that we’ve got all the various pathways and terminology out of the way, we can look at the 2006 paper by Krauss et al titled “Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia.”

And Now to the Study…

Here is the objective of this study:

The objective was to study the effects of moderate carbohydrate restriction on atherogenic dyslipidemia before and after weight loss and in conjunction with a low or high dietary saturated fat intake.

Here is how they begin the introduction:

Excess body weight can result in changes in plasma lipids and lipoproteins that increase the risk of atherosclerotic cardiovascular disease (CVD), ie, increases in triacylglycerols [a fancy, allegedly more accurate way to say triglycerides] and small, dense LDL particles, with variable increases in total LDL cholesterol, and decreases in HDL cholesterol. Atherogenic dyslipidemia associated with excess adiposity is highly correlated with reduced insulin sensitivity and is a major feature of the metabolic syndrome.

Dietary carbohydrates, especially simple sugars, can also promote atherogenic dyslipidemia, in large part because of effects on the metabolism of plasma triacylglycerol-rich lipoproteins. High-carbohydrate, low-fat diets have been shown to induce increased concentrations of small, dense LDL and expression of the small, dense LDL particle phenotype (LDL subclass pattern B) in a high proportion of healthy men.

Basically what these two paragraphs say is that obesity increases the risk of cardiovascular disease because obesity is usually associated with elevated triglycerides along with elevated LDL and low HDL. A lot of carbohydrate in the diet can bring about the same findings: high triglycerides and LDL along with low HDL.

The goal of the researchers is to tease out which of these situations—obesity or a high-carb diet—is the main driving force underlying the high triglycerides and LDL and the low HDL.

They wanted to lay to rest the arguments against low-carb that I discussed at the beginning of this very long section. Is it the carb restriction or is it the weight loss that does the trick?

Here’s how they set up the study.

They recruited 178 overweight males who had an average BMI of 29.2 and elevated, but not too elevated, LDL, triglycerides, and blood pressure. None were on lipid-lowering medications.

These men went on a one-week basal stabilization diet composed of 54 percent carbohydrate, 16 percent protein, and 30 percent fat diet (54/16/30). After one week, the men were randomized into four groups.

Group 1 These men remained on the basal diet of 54/16/30

Group 2 This diet had carbs restricted to 39 percent of kcal 39/29/31

Group 3 Carbs restricted to 26 percent of kcal 26/29/46 but with only 7-9% of energy as saturated fat

Group 4 Carbs restricted to 26 percent of kcal 26/29/46, but 15 percent of energy as saturated fat

Based on what they wrote in the early part of the paper, I’m pretty sure the researchers knew the lower-carb diets would bring about the greatest changes, so they used two different saturated fat percentages in those diets to see if that made a difference.

Once randomized, the subjects in these groups stayed on these diets, which contained enough calories to maintain the starting weights of the subjects for four weeks.

After four weeks, the researchers cut the diets by 1000 kcal, but kept the ratios of carbs, protein, and fat the same as before. The subjects remained on this lower kcal regimen for the next five weeks.

Then after this five-week period of weight loss, the researchers adjusted the kcal intake of the subjects to maintenance level for the final four weeks.

The total study duration was 13 weeks. Here it is in graphical form from the paper.

You can’t really tell a lot from this graphic. In fact, the entire article is put together in what I would call a really shitty way (that’s the technical term) for explaining what the researchers did and the data they generated.

Not only does it demand a lot of work just to read through what is really a valuable paper, it requires a bit of guessing. The authors do not provide the data required to basically double check their findings.

For example, they start off with the 178 men with average BMIs of 29.2. They don’t provide an average age. And they don’t tell you what their activity level is—they simply tell you that they told the subjects not to change their activity level during the course of the study. They don’t tell you what the kcal were for any phase of the study—they simply tell you they reduced the subjects’ intake by 1,000 kcal per day starting on week 5.

They did provide average weights for the subjects in each group. Using those weights, I was able to reverse engineer the BMI to determine the average height to be about 5 ft 10 inches. I guessed that the average age would be 50 and the activity level would be moderate. Then I used one of the many online kcal calculators based on the Harris-Benedict equation to determine the kcals needed to maintain their starting weight. It came out to be 2,783 kcal, which I rounded up to 2,800 just to make life easier on myself.

It would have been so easy to have included this data, but, for some reason, they chose not to.

If we assume the first week at 54/16/30 represents 2,800 kcal, then we can figure out how many grams of carb, fat, and protein we’re talking about. Just because I’m a helluva guy, I went ahead and did this on Excel, so you can see it below.

Now that we have this before us to refer back to, we can make sense out of some of the findings that might be in a bit of conflict with what the authors came up with.

In the first phase of the study after randomization, the subjects on the same kcal intake but with varying carb/protein/fat combinations had some significant changes. Remember, this was the part of the study where weight remained stable for four weeks, so no weight loss was to occur to confound the data. In other words, this was the part of the study that showed the macronutrient combination to be responsible for any changes in lipids as the weight of the subjects remained stable.

Here’s what they found.

In the initial Δdiet, stable-weight phase of the study, the 26%-carbohydrate, low-saturated-fat diet resulted in reductions from baseline in total cholesterol, triacylglycerol, apo B, and total:HDL cholesterol that were greater than the changes observed in the group remaining on the 54%-carbohydrate diet. However, the difference in the change in LDL cholesterol between the 26%-carbohydrate diet and the control diet was not significant by post hoc analysis (P = 0.13). [My bold for emphasis]

Uh oh, the LDL change was no longer significant after post hoc analysis?!?! What does that mean?

The next couple of sentences explain.

Despite our effort to maintain constant weight, the 26%-carbohydrate, low-saturated-fat diet group lost more weight than did the 54%-carbohydrate group during the stable-weight period. There was also a trend for a greater reduction in percentage body fat with the lower-carbohydrate diets.

Ah, the researchers had difficulty getting the lowest-carb subjects to keep their weight stable. In other words, these subjects lost weight despite the efforts of the researchers to fiddle with their total caloric intake while keeping their macronutrient ratios the same. In terms of weight-loss efficacy, that speaks volumes for the low-carb diet, but it must have had the researchers pulling their hair out.

Once they took into account the difference in weight loss between the lowest carb group and the highest (post hoc analysis), then recalculated the LDL, it turned out it wasn’t significantly different in terms of wee p than that of the 54 percent carb diet.

But, still, total cholesterol, triglycerides, Apo B, and the HDL to cholesterol ratio all improved with just a reduction in carbohydrate intake.

I would bet they didn’t have to horsewhip those on the higher carb diet to eat more to maintain their weight. Just saying.

So, what happened after the five weeks of 1,000 kcal reduction weight-loss segment of the study.

You might be surprised. I was until I thought about it for a bit.

In contrast with the findings during the initial Δdiet, stable-weight phase, weight loss and stabilization led to reductions in each of these variables that were significantly greater with the 54%-carbohydrate diet than with the 26%-carbohydrate, low-saturated-fat diet.

Whoa! So all these variables—total cholesterol, LDL, and all the rest—went down more when the dieters restricted their diets by 1,000 kcal while maintaining the same macronutrient ratios?

I’ll tell you first what the researchers made of it. Then I’ll tell you what I made of it. You can then decide who you think is correct. Hint: I vote for me.

Here’s what they say:

We found that, with weight loss, there were reductions in major lipid and lipoprotein indicators of CVD risk (LDL cholesterol, triacylglycerol, apo B, total:HDL cholesterol, and small, dense LDL), and that these reductions were much greater with the higher- than with the lower-carbohydrate diet.

Here is the word salad they’ve come up with to explain these findings, and once I read it again, I can see they’re nibbling around the edges, but they fail to make the real connection.

…the absolute reduction in carbohydrate intake after weight loss in the subjects who consumed the 54%-carbohydrate diet was much less than that achieved in the subjects who consumed the 26%-carbohydrate diet during the Δdiet, stable-weight phase. Hence, although this difference in carbohydrate intake could have contributed to some extent to the differences in lipoprotein changes after weight loss with the higher versus lower carbohydrate diets, the results indicate that there is an interaction between the effects of carbohydrate intake and weight loss on these lipoprotein measurements. It is possible that this finding reflects a convergence of the effects of adiposity and carbohydrate intake on common pathways that affect these lipoprotein measures, such that reductions of either can achieve similar results. However, at least under the conditions studied here, the effects are not additive—a result that is consistent with earlier observations. [My bold for emphasis]

Unless they know something I don’t, which is possible since they have the actual data, and I’m going on data I calculated based on what little they provided, I think they are off base here.

Let me explain.

We know from the first phase of the study—the weight maintenance phase—where the macros varied considerably while the intake and body weight remained the same (sort of), that the reduction in carbohydrate made a significant difference in all the parameters they measured. Even the LDL, but then they recalculated based on the bit of extra weight loss in the low-carb group. (I say bit, but they don’t tell us what it really is—a true aggravation.) Even then the LDL was lower, but didn’t reach a wee enough p to reach what they considered significance.

Based on the above, we know that restricting carbs brings about good things lipid-wise. So why wouldn’t restricting more carbs do the same? I think restricting more carbs would do the same.

So, let’s look at the Excel sheet I created and posted above.

I’ll even add it here, so you don’t have to scroll back.

Take a look at the carb content of the starting 54/16/30 diet. The subjects on that arm of the study were consuming 378 g during the maintenance phase. A whopping amount since a cup of pure sugar is 200 g of carbohydrate, so these folks were consuming almost two cups of sugar per day.

Those on the lowest carb content diet during the weight maintenance phase were eating 182 g of carb per day, which is 196 g less than those in the highest-carb arm of the study. So, the reduction of that much carb makes a big difference.

Now if we look at what happened during the 1,000 kcal reduction part of the study, we can see that the highest-carb group dropped their carbs from 378 g to 243 g, which means a 135 g drop (378-243). The subjects on the lowest carb maintenance diet dropped their carbs from 182 g to 117 g. So they reduced carbs by only 65 g (182-117).

The subjects in the highest carb group dropped their carbs by a bit more than twice what those in the lowest carb group did (135 g versus 65 g).

Now, if carbs truly do drive triglycerides, LDL, and all the rest in the wrong direction, and cutting carbs rights the ship, why wouldn’t we expect the group that cut the most carbs have the better results?

If anyone has a counter argument, post it in the comments or send it my way.

A couple of things just to tie up some loose ends. First, virtually every parameter tested got better on the lower carb diet. I didn’t really get into particle size, HDL, and all that, but everything improved. The study is linked above, so you can read about any lipid specifics you might have a particular interest in.

Second, what about the difference between the low-carb, low-saturated fat diet and the low-carb, high-saturated fat diet?

Here’s what the authors have to say.

With the 26%-carbohydrate diet, lipoprotein changes with the higher saturated fat intakes were not significantly different from those with the lower saturated fat intakes, except for LDL cholesterol, which decreased less with the higher saturated fat intake because of an increase in mass of large LDL. [My bold for emphasis]

There you have it. Saturated fat—at least in this study—didn’t do anything except make the LDL particles larger and more buoyant, which is correlated with a lowering of heart disease risk.

One final item that isn’t part of the study.

If we look at the grams of macronutrients I calculated in the Excel spreadsheet, we find something interesting.

The daily intake in the highest carb arm was 583 g whereas that in the low-carb arm was 528g. Which is a difference of 55 g per day. Multiply this by 28 days (the 4 weeks of that part of the study) and you’ll find those on the highest carb diet took in 1540 more grams of food than did those on the lowest carb diet. 1540 grams converts to about 3.4 pounds. Remember, both of these diets contained the same kcal content—just a different array of macronutrients. It’s no wonder the researchers had such difficulty keeping the low-carb arm from losing weight.

If you have no idea what I’m talking about here, you must be a new reader. Check out this section of a previous Arrow, and all will be clear.

Video of the Week

Okay, this isn’t a pleasant or fun video of the week. It’s just here to show the changes that have taken place in the two major political parties over the past 20-25 years or so.

Florida GOP congressman Matt Gaetz puts my teeth on edge, but here he is going after Christopher Wray, the director of the FBI. What I find absolutely amazing is that a couple of decades ago, it would have been a Democratic congressman going after the FBI. It’s a stunning turn around…at least to me.

In 1974 the Church committee led by Democrat Frank Church flayed the CIA for many of these same issues. The result was the FISA court, which was supposed to make the FBI, CIA, and other law enforcement and intelligence agencies provide proof to a judge that something nefarious might be going on before they would issue a warrant for spying on said person. Through 2017 there have been 41,222 FISA warrants applied for, and only 85 were rejected. God only knows what the totals are now.

Section 702 of the FISA act allows government officials to surveil US citizens without their knowledge or approval. The law was set up for US intelligence and law enforcement agencies to surveil people from foreign countries who are thought to be possibly dangerous to the US. Part of the act says that if while one of these people is under surveillance and the name of a US citizen comes up, then that US citizen can be looked at.

The FBI has just been found to be in egregious violation of this act. According to the Washington Post, there have been hundreds of thousands of misuses of this law. In June, 2020, during the BLM riots after the death of George Floyd, the FBI searched digital data using 702 on 133 suspects who were arrested.

It’s even more amazing what happened after Jan 6, 2021.

After the Jan. 6, 2021, riot at the U.S. Capitol, an FBI employee ran batches of inquiries that amounted to 23,132 separate queries of presumed Americans “to find evidence of possible foreign influence, although the analyst conducting the queries had no indications of foreign influence related to the query term used,” Contreras found. There, too, Justice Department officials concluded that there was no specific factual basis to think the searches would turn up foreign intelligence information or evidence of a crime.

The FISA act is set to expire at the end of this year unless congress renews it. I’m hoping they don’t. I’ll be interested to see how Oregon senator Ron Wyden, an old time pro-freedom of speech Democrat will vote.

I hope he puts his money where is mouth is.

Sen. Ron Wyden (D-Ore.), a longtime critic of what he says is dangerous overreach by U.S. intelligence officials, decried what he called the “shocking abuses of FISA Section 702.” He said that the abuses have been going on for years and that officials are still withholding key details from the public.

“There is important, secret information about how the government has interpreted Section 702 that Congress and the American people need to see before the law is renewed,” Wyden said in a written statement.

Since he is a senator, his vote could throw it one way or another. I’m wondering if his long-time fight for civil liberties will overcome his trend of voting with the pack.

As a civil libertarian, I’m keeping my fingers crossed.

Okay, that’s about it for today. Keep in good cheer, and I’ll be back next Thursday. Hope to be able to dig into Mendelian randomization along with a host of other interesting tidbits.

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