Greetings everyone.

Sorry I’m a little late on this edition of The Arrow, but MD and I took a brief vacation. Really the first one since I recovered from my cancer diagnosis. We visited friends in Boulder, Colorado (our old stomping grounds), who took very good care of us. The last time we were there for a visit about a year ago, I wasn’t much of a good guest. This time, we actually had fun.

Okay, on with the show.

In my never ending efforts to clean up my computer files and tabs, I was wrestling a bunch of pdf versions of papers into some semblance of organization. As inevitably happens whenever I try to do this, I end up starting to read some of the papers instead of simply filing them away.

During this most recent process, I came across a paper I had saved, but hadn’t really read. I couldn’t remember when, or why, I downloaded it. I started to give it a quick once over, but became absorbed with it.

The paper, published in 2011, titled “Using the Edmonton obesity staging system [EOSS]to predict mortality in a population-representative cohort of people with overweight and obesity” (despite its mind-numbing title) seized my attention as I skimmed through it. I have no idea why I downloaded it in the first place. Which isn’t unusual. When I’m in a paper-downloading frenzy, I find a paper, go through several steps to find the pdf (if it isn’t immediately available), and suck it down. Give it a quick skim then move on to the next. Often I look at the list of citations. If I find something that grabs my attention, I try to find that one and download it. At the end of this feverish endeavor, I’ll have 20 or 30 papers clogging my desktop.

I have my own way of categorizing these papers, so I can find them quickly as needed. I shove them all in a file and end up putting that file into my big Scientific Papers file. Then, when I have some time to kill, I’ll go through a couple of these files and stick the papers into my Zotero program that ends up pulling all the meta data from them, making them even easier to find if needed.

When I skimmed through the 2011 paper above, I was stunned.

At first, at least.

It’s about a method – EOSS – of determining the degree of obesity in an individual that involves only the disease process the individual in question may have. It doesn’t involve any weighing or measuring or even looking at a person to determine whether said person appears to be obese or not.

Or so I thought. Then I read it a little more carefully and realized the subjects being compartmentalized as a function of their metabolic disease status had already been fingered as being obese or overweight by their BMI calculations

As I’ve discussed many times in these pages, BMI is kind of valuable on a population basis, but is a notoriously inaccurate statistic on an individual basis.

Here is how the EOSS defines obesity:

Now remember, these subjects have already been identified as being obese before they were put into the various categories.

Those defined as zero are obese to some degree as defined by BMI, but have none of the issues the others have.

There are indeed healthy obese people, which we will discuss in due course. There is a reason these folks are in good shape healthwise despite carrying excess weight. In some cases even, a lot of excess weight.

By the same token, there are subjects who are normal weight (or below), who have all the issues normally associated with obesity: elevated triglycerides, blood sugar issues, hypertension, etc. Back in the day we diagnosed these folks as metabolically obese normal weight (MONW). I wondered if this term had been superseded by a different term in this day and age of wokeness (because ‘normal’ is an oppressive societal construct, right?).

I checked with my good buddy Perplexity, who assured me that the term had not changed. It is still in use. Some folks have tried to get it changed, but apparently not too successfully.

Reading this paper got me curious.

I searched to see if there was a more recent method of categorizing the health status of overweight people. And indeed there was.

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In 2025 The Lancet Diabetes & Endocrinology published a paper titled “Definition and diagnostic criteria of clinical obesity.” It was put together by a committee. A large committee, to be exact. And you probably know from bitter experience the kind of output that comes from a committee.

Here is the list of the members of the committee, all of whom are recognized as authors on the paper.

Below is another list that you might find shocking. But you shouldn’t. This is the way publishing by committee works.

What you see below is just the partial list of the so-called Declaration of Interests of the authors involved. These are the ways they are getting paid that could possibly lead to conflicts of interest. And when I say a partial list, it is a small part of the total. I measured it as best I could, and what’s shown below represents about one sixth of the total. If you don’t believe me, click the link to the paper above and scroll to the bottom.

As you might imagine from a paper created by a committee of over 55 people (yes, I counted them), much like its title, this Lancet article is long and dreary. I can tell you it doesn’t add much to the subject of obesity and its treatment. Nor does it categorize obesity into neat packages of five based on underlying disease as the EOSS does.

It does recognize a fact that most of us have been familiar with forever – that BMI sucks as a measurement of obesity. They use this clever graphic to demonstrate.

The authors spent most of their verbiage on describing all, and I mean all, of the diseases associated with obesity. A lot of these issues prevail in those who aren’t obese, but if they do occur in those who are overweight, it puts them in a different category. They produced a graphic showing all these disorders, so you don’t have to do as I did and slog through them all.

In the end, the brilliant summary by all these obesity-treating luminaries divides the obese into two categories – the clinically obese (those who have one or more of the issues shown above along with their excess body fat), and those who don’t, whom they label as pre-clinically obese. Implying, of course, that clinical obesity lies in wait for them at some future point.

Okay, all of the above is but a prelude to the real topic of this essay, which is about the difference between subcutaneous fat and visceral fat. Neither of which any of the illustrious authors of the papers discussed above dwelt on. Which, in my view at least, is the most important issue in obesity diagnosis and treatment.

When I first forced myself to read through the articles linked above, I found no mention of visceral fat. I was stunned. With all these luminaries involved, how could they not mention visceral fat? I didn’t trust myself. I figured I had just missed it.

So, I asked my good buddy Perplexity to read through the papers to see if he/she/it could find a mention. Indeed he/she/it did.

I first asked Perplexity to search for the term “visceral obesity.” It came back negative. Then I asked about “visceral fat.” It did find that (and I had missed it). Here’s what it came up with.

Perplexity helpfully reminded me that there was another term for “visceral fat,” which is “visceral adiposity.” It listed the four times that term was used.

I must have been brain dead from trawling through all the mad gibberish in these papers to have missed these, but I did.

These are minor points made by these authors. In my view, visceral obesity is the most salient health factor of those carrying extra weight.

Let’s dig in and go where the experts obviously feared to tread.

Visceral Fat

First, how do we tell if someone is obese or overweight?

As Yogi Berra purportedly said, “You can see a lot just by looking.” Most of us can glance at a particular individual and tell if that person is overweight or obese. In 1964, Supreme Court Justice Potter Stewart famously said about hardcore pornograpy that he could not precisely define it, but “I know it when I see it.” Most of us feel the same way about obesity.

The two papers discussed above took a total of 50 pages (literally) to attempt to define it, but I suspect most of us could tell with a quick look.

It’s a little more difficult to recognize it in ourselves than it is to see it in others. Most of us who are or have been obese know we are (or were), but we don’t know to what degree.

(Twenty some years ago, I was dragged into a lawsuit in Denver. The famous attorney I ended up working with (RIP), who was absolutely brilliant, asked me how long I thought it would take for him to lose his “excess 30 pounds.” The guy was at least 100 pounds overweight, but he thought he was only 30 pounds over the limit. And he was a bright guy.)

In my view, the difference between healthy obese or overweight people and those who are unhealthy is the amount of fat carried as visceral fat.

There are people who carry a lot of excess weight, but are remarkably free of metabolic disease. And there are thin folks who have metabolic syndrome and a host of other health issues usually attributed to obesity, the folks who would be considered MONW (medically obese, normal weight). Their health issues are a function of their level of visceral fat.

We humans basically carry two kinds of fat: subcutaneous fat and visceral fat.

Subcutaneous fat, the fat under our skin, but outside our body cavities is normal fat. It’s not unhealthy. Different individuals carry it in different places. Some in the butt, some in the legs, some on the back, some in the neck, some in the belly (under the skin), and some carry it in all these places. It’s there for a variety of issues — to store calories for later use, to insulate us from cold, to pad bony prominences, etc.

The places subcutaneous fat is stored is (in my view, at least) genetically determined. If you have a lot of subcutaneous fat, you probably have it in the same places your parents and close relatives do.

An abundance of subcutaneous fat may be unsightly, but it doesn’t really cause any health issues. It’s where excess fat was designed by nature to be stored.

But in most people, these storage depots are finite. They differ from person to person. Some folks have enormous storage depots for subcutaneous fat, and they can be huge and healthy.

Think of the subcutaneous storage depots in your body as the attic, closets, cabinets, basements, and garage of a house. Let’s say you’re a hoarder. You compulsively buy all kinds of stuff, but at the same time, you want a tidy house. You hide away all your purchases in closets, the attic, the basement, etc. and keep your house spic and span. If you keep hoarding, you will ultimately fill up all your storage sites and the stuff you keep buying will spill into your living space and junk up your formerly pristine house.

This is what happens with visceral fat.

If you continue to store fat, the genetically prescribed storage depots under the skin at some point get full, and fat starts to spill over into your internal abdominal area, the viscera. It becomes visceral fat and begins to surround your internal organs and can ultimately invade them.

Visceral fat is no bueno.

Just as some hoarders have larger houses with more storage for junk purchases than other hoarders, some people have larger subcutaneous fat-storage depots than others. These folks can store more subcutaneous fat before it spills over into the viscera. They can stay healthy much longer than those who don’t have the large subcutaneous fat storage depots.

Visceral fat both increases insulin resistance and is driven by insulin resistance.

Before we get into how all this happens, let me discuss one of my favorite proteins that I’ve written about before – hypoxia-inducible factor-1α (HIF‑1α). HIF-1α is a constitutive protein, which means it is being made constantly by all the cells in the body. It hangs around for about five minutes, then is degraded and destroyed.

Stop and think about this for a second. Our bodies continuously make a protein, then degrade it after five minutes, then make it again? And again. Over and over for our entire lives. Seems on its face like a real waste of energy.

Imagine if you had a huge factory that produced some kind of product. There was one tool that had to be available to make that one product, and if the tool broke, your entire factory would shut down and be difficult to reopen.

In order to have this tool immediately available to prevent disaster, you have a machine in the factory that constantly makes this tool. The tool is unstable, so it deforms and is unusable after about five minutes. So you not only have to continuously make the tool, you also have to destroy what you just made five minutes ago. You have a machine that makes the tool and a machine that destroys the unused tool after five minutes. The machines run on electricity. Imagine how much power it takes to run these two machines for no other reason than you need the tool they make and destroy in case you need it to keep your factory running. It’s an expensive process, but necessary for the continuous operation of your factory.

That’s what producing HIF‑1α is to the body. An enormously energetically-expensive process continuously being recycled to prevent disaster.

What disaster?

Low oxygen levels in the cells, which could ultimately kill them. Sometimes quickly.

When cellular oxygen is low, the HIF‑1α that is typically destroyed instead heads to the nucleus where it stimulates the production of all kinds of processes to save the cell from dying due to lack of oxygen.

HIF‑1α was doubtlessly evolved to protect against infection, which reduces oxygen levels in the cells under attack. The genes triggered by HIF‑1α orchestrate an entire response to the lack of oxygen including stimulating glycolysis, which produces energy (ATP) without requiring oxygen. Under conditions of low oxygen, HIF‑1α races to the cell nucleus to fire off the genes that make proteins to drive growth and inflammation. These genes signal to increase the vascularity, to improve blood flow, to up oxygen levels, and also signal macrophages, the cellular garbage trucks, to flood the scene and start gobbling the invaders.

Now that we know what HIF‑1α is and does, let’s look at what happens when the visceral fat begins to accumulate.

It takes a while, but with enough time and excess (or wrong) food consumption, the visceral fat mass begins to expand. Over time it expands faster and faster. Ultimately, it can outgrow its blood supply. Yep, the fat cells can grow faster than the vascularity that provides them with sustenance.

When that happens, these overgrown fat cells struggle for oxygen.

When fat cell oxygen levels fall they develop hypoxia (low oxygen levels). Their hypoxia activates HIF‑1α (remember, the full name is hypoxia-inducible factor-1a). Then the fun begins.

When the visceral fat cells outgrow their vascular supply, HIF‑1α kicks into action and does all the things it does. Although HIF‑1α does work to increase vascularity, it also increases all the inflammatory processes mentioned above. It signals for macrophages to come a-runnin’. As a consequence, visceral fat often has as many or more macrophages as it does fat cells.

Ponder on that for a bit.

If you're carrying around a load of visceral fat, half or more of it is composed of macrophages.

These macrophages release inflammatory cytokines and messages calling for even more macrophages to join the fight. Even though visceral fat is not attacking the body, it is in a place where it doesn’t belong. So the immune system more or less treats it like a foreign invader.

Think of it as having a big splinter in the middle of your belly. If you pull a splinter from your finger, it usually comes with a quantity of pus, which is nothing but macrophages attacking the splinter from within. Distasteful as it sounds, that’s basically what’s going on in your abdomen if you’ve got a lot of visceral fat in there.

I’ve just touched on the basics of what happens when the fat cells become hypoxic. The graphic below from a 2024 paper by Engin demonstrates what a veritable Mad Hatter’s tea party of disturbance takes place.

I’ve put a black box around the HIF‑1α activity and the processes it drives, which are plentiful.

Ultimately, hypoxic visceral fat can lead to fibrosis and many other bad effects, including insulin resistance. And insulin resistance, in its turn, leads to more visceral fat. So the whole process becomes a vicious cycle.

But, sadly, it doesn’t stop there. It gets even worse.

The inner organs can become infiltrated with fat, which reduces their effectiveness. The liver, for example, goes from being a normal liver to being a fatty liver. With disastrous consequences if the process continues.

Plus, there is a spill over effect onto muscle. The viscera fat cell inflammation leads to fatty infiltration into skeletal muscle, which results in an overall decrease in strength and functionality. Fat accumulates within and between muscle cells. This intramuscular fatty infiltration induces mitochondrial dysfunction, lipotoxicity, and insulin resistance. Along with which come all the issues of inflammation in the muscle tissue.

All the inflammatory secretions can end up causing another vicious cycle within the muscle tissue which leads to sarcopenia, the wasting of muscle.

This end process results in a big belly and kind of wasted limbs as those with visceral fat age. It’s a combination of muscle loss (sarcopenia) and visceral fat. It’s now sometimes called sarcobesity.

The graphic below is from a slide I made for a presentation on inflammation I gave in Chicago years and years ago. Sadly, there is no video, or I would post it. You can see the typical elderly male with a big belly and small limbs. By and large women typically have more subcutaneous fat on their arms and legs than do men, so they don’t always present with this apple belly and stick arms and legs body habitus. But take my word for it, the sarcobesity is there.

Given what you now know about visceral fat, don’t you find it unfathomable that the two big, influential papers I described at the start of this essay — 50 pages in total — didn’t make more of an issue about it?

I certainly do.

Everything I wrote above came not from my feverish imagination, but from solid science. Yet the two papers barely mentioned it. Weird.

Now that you understand the dangers of visceral fat, wouldn’t you like to know how to measure it? To see if you, yourself, are suffering from a surfeit of the stuff?

You can absolutely measure it. You can do it expensively and very accurately. Or you can do it for nothing and still get a pretty accurate determination.

The absolute best way to determine the extent of any visceral fat you may have is by either an abdominal CT scan or an abdominal MRI. Authorities differ, but I suspect the abdominal CT scan is the more accurate. But there is no ionizing radiation from the MRI.

These tests can run anywhere from ~$300 all the way to ~$4,000 if you get them at a hospital outpatient service.

The next best way to determine your visceral fat level is by DXA with VAT (visceral adipose tissue) software. This process, often called DEXA, is much less expensive. It can usually be found for a hundred bucks or so. It is cheaper, but less accurate than the above two methods.

If you do decide to go for the MRI, be sure to ask the facility something along the lines of, “Do you offer a non-contrast abdominal body-composition MRI with quantified visceral adipose-tissue area or volume—not simply a diagnostic abdomen MRI?” Do not go for a diagnostic abdomen MRI. It won’t give you the info you're seeking.

There are other ways you can do it at home for free that are not nearly as accurate as the above..

The first is the least accurate, but it’s easy to do and doesn’t cost a dime. Other than the cost of a tape measure if you don’t already have one.

You can measure your waist and your hips, divide the two measurements and get a reasonable estimate of your visceral fat. The result is your waist-to-hip ratio (WHR). (add to the above sentence)

Caveat: it’s a reasonable approximation, but not nearly as accurate as the methods discussed above.

The WHR had been debated for ages as a better measurement of obesity than the BMI, and in my opinion it is better.

But there is another measure that is much more accurate than the WHR. It is the waist-to-height ratio (WHtR).

The flaw in the WHR is that both the waist and the hips can change with weight loss or gain. Neither is an unchangeable standard. If you lose weight, you’ll doubtlessly get rid of some visceral fat, but both your hips and your abdomen will get smaller. You may have the same WHR despite losing ten pounds.

The WHtR ratio has proven to be more accurate, because if you lose ten pounds, your waist circumference will change, but your height won’t. By retaking your waist circumference (if done properly), you will find an improvement in your WHtR that you might not find in your WHR.

What is a ‘normal’ WHtR?

Most papers consider a WHtR of 0.5 (meaning your waist measures at least half your height) or higher as a standard screening threshold that indicates abdominal obesity. It’s not really diagnostic for visceral fat, but, in my view, it sort of is. Not as accurate as an MRI or CT, of course, but you can get a general idea.

It becomes more useful if your weight changes. If your weight drops, then your WHtR will drop along with it. If your first measurement was above 0.5, and your next one drops to 0.45, you’ll know you're making progress in ridding yourself of visceral fat.

From the literature, the breakdowns are as follows:

• 0.40–0.49 No increased risk from central fat

• 0.50–0.59 Increased central adiposity Increased health risk

• ≥0.60 High central adiposity Further increased risk

I want to repeat myself on this point. These calculations are not nearly as accurate as the other imaging methods above. But they do provide readily accessible waypoints you can measure over time to see how you are progressing.

I suspect that most who come in somewhere in the high 0.5s and above already have some of the issues driven by visceral fat: high triglycerides, high blood pressure, blood sugar disturbances, etc. These should begin to resolve as your WHtR decreases.

In order for these measurements to approach any kind of recurring accuracy, it is imperative that they be done correctly. I started to write out the steps for making the measurements properly, but about half way through I decided to let Perplexity do it instead. He/she/it did a much better job of it than I was doing.

The steps above are for measuring your waist only. You also need to measure your height. And do so precisely.

I suspect most people think they know what their height is. But height changes with age. Don’t just take your height for granted. Measure it with the same tape you use for your waist. You don’t have to measure your height each time you check your WHtR, it won’t change from month to month. But do get an accurate measure to start.

Below is a graphic showing how to accurately measure your waist for purposes of the WHtR calculations.

Okay, now for the good part.

How do we get rid of visceral fat?

The great news is that it is much easier to get rid of visceral fat than you might think given the threat to health it poses.

In terms of fat loss, it’s last in, first out. When you start storing excess fat, you first store it subcutaneously. That’s where excess fat is stored without affecting your health. As those stores fill up, the fat begins moving into the viscera, bringing with it all the issues discussed above.

When you get rid of fat, the visceral fat goes first. The body doesn’t want it, so it gets rid of it ASAP.

But that doesn’t just happen. You have to change your way of eating (and moving, though of the two eating is more important) to make it happen.

In my view, the very best way to do it on the eating front is with a whole food, low-carb ketogenic diet. That does it faster than anything else I’ve ever come across, except perhaps carnivore, which in fairness is just a very low carb, very ketogenic diet.

Other diets will work, they just don’t work as well. I’ll write soon about a brand new paper showing the rapid changes brought about by a low-carb diet versus other diets. But any diet will do as long as you stick to it and are losing weight.

I would not recommend a total plant-based diet, because you will need plenty of high-quality protein to preserve and build your muscle mass. You can get plenty of protein on a plant-based diet, but it isn’t complete protein unless you go through the pain in the rear of balancing your amino acids to ensure you’re getting all the amino acids in the right proportions to build or even maintain your muscle mass. Unlike with plants, you don’t have to worry about what kind of meat you consume. They all contain the right mix of amino acids. And it’s hard to get enough complete protein from plants without more carbs than you likely want.

If you cut the carbs, increase the protein, and don’t worry too much about the fat, you’ll see your WHtR getting smaller right along with your belly. Once you get rid of your visceral fat, you’ll start losing subcutaneous fat, but it is a slower loss than the visceral fat. Remember, the body wants to ditch visceral fat. All you have to do is help it out.

But what about exercise?

Most of the heavy lifting here is done by diet, but exercise does help. You’ve probably heard the old saying You can’t outrun a bad diet. It is true. You can’t.

As I’ve mentioned previously, I’ve been working out hard at a facility designed to improve strength and mobility. I’ve been there multiple times per week for about nine months. What I’ve noticed is that everyone is getting stronger, but no one seems to be losing any weight. At least as judged by my eye looking at their waists.

If you couple a good diet with exercise, then you’ll really see your belly shrink. Resistance training and high intensity interval training (HIIT) will reduce you waist size more quickly than either alone. But if I were forced to do only one, I would choose diet.

Okay, that’a about it. Let me know what you think in the poll and comments. Now that I’ve had my vacation, I should be back soon.

Odds and Ends

• MD and I have always been deeply interested in all things ancient Egyptian (as evidenced by the Egyptian chapter in Protein Power, the rabbit hole of which I traveled that almost threatened to derail the whole book. Once in Berlin we visited the museum housing the gloriously beautiful bust of Queen Nefertiti. Now some archeologists say they think they've maybe found her tomb, hidden inside the unusual tomb of another famous pharaoh. Catnip to me.

• Among my grammatical pet peeves, this one ranks high. But I'm not so opposed to 'a more perfect union'. 

• I love etymology; I'm always curious about how a word came to be. So I clicked to find out why we call a rotating tray a Lazy Susan? Who was Susan anyway?

• Yet another batch of collective nouns for animals going beyond the typical unkindness of ravens or murder of crows. Some I knew; others I didn't.

• The missing town of Lutetia (ancient Paris) sacked by Julius Caesar in 52BC found under hospital courtyard on Ìle de Cité. Next trip to Paris, if it’s viewable by normal folk, this is a must see for us!

• The oldest Natural Science and History Museum in the Western Hemisphere (in Philadelphia, PA) has announced its closure, but you can take a virtual tour of their collection that houses 19 million specimens, including 200 plants collected by Lewis and Clark, if you're of a mind. Another Covid era casualty I think and because people no longer like to roam among the actual artifacts of times past preferring the 2-D comfort of their phone screen. The Bride actually became my bride in just such a place almost 46 years ago. We held our wedding and brunch reception in the Aesthetic Club Room of the Arkansas Museum of Science and Natural History, so these museums hold a special place in our hearts. 

• There are a surprising number of shipwrecks in the oceans. And less than 1% of them have been explored. Reading this article made me want to don my SCUBA gear and go find one.

• As a kid, I used to thumb through the Sears catalog regularly, especially the Sears Home and Ranch catalog, with my younger brothers, picking out all the things we'd need to equip our dream ranch. So this article about the most unusual page in the Sears catalog brought a wave of nostalgia. Maybe it will for you as well.

• MD and I have been to every US state but three. So I was surprised that of these 10 US tourist sites even Americans should visit, we've visited only half. Sounds like we need to get busy!

• A new, anatomically bizarre dinosaur found in China. Bizarre for several reasons, including sporting talons longer than Edward Scissorhands and yet stubby teeth like an herbivore. Whatever would it need those claws for? Maybe digging?

• A recent archeological find proves the point that mankind has been searching for the elusive peaceful world for many millennia, even though treaties get made and broken regularly along the way. Don't suppose we should expect the here and now to be so different.

Newsletter Recommendations

Be sure to take a look at MD’s OutlanderMD Substack this coming Sunday. She is covering electroconvulsive therapy, i.e., shock treatment. I make a cameo appearance.

Video of the Week

This VOTW is a little different, but fascinating to watch. For me, at least.

It shows graphically the rise and fall of the Roman empire, which started ~400 BC and ended during the Middle Ages. If you would prefer to read about it instead of watching a five minute video, I would suggest Edward Gibbon’s The The History of the Decline and Fall of the Roman Empire. But it only addresses the decline. For the most part, it is totally inaccurate, but Gibbon was a terrific writer. Back then most writers wrote long, clunky sentences, at least by today’s standards. Gibbon’s were also long, but not clunky. His writing flows in comparison to most writers back then. Whenever I jump in to anywhere in his magnum opus, I’m amazed at his writing. I find it difficult to quit reading.

Anyway, if you don’t want to read Gibbon, watch the video below. And marvel at how a tiny civilization grew, took over the Western world, then let it slip from its fingers.

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

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

Please help me out by clicking the Like button, assuming, of course, that you like it.

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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