The Personal Fat Threshold Concept

Hey Kids!

It’s been ages since I’ve posted what I would call a “real” blog post. Something meaty and educational. Something you can really sink your teeth into. The last one was way back in August, when I wrote about whether protein is bad for the kidneys. (Hint: it’s not.) I’ve posted a few things since then, but nothing all that substantial. I’m glad to say today’s post makes up for lost time, because it is LONG. So grab yourself a cup of coffee or tea (or...*gag*...broth, if you must), put your phone on silent, and dig in.

I’m excited to share this with you. So excited, in fact, that I’ve been procrastinating on writing this for no less than 6 months. In looking at the folder of blog post drafts on my computer, I started jotting down notes for this in July 2018. The reason I kept putting it off is that I knew this was going to be a LONG post—massively long, even for me. But then I gave a talk on this topic at a keto event in Canada in December, so I finally had to organize my thoughts and put them together coherently. Once that was done, I figured it would be easier to get this written, since I could just flesh out the details of what was on the slides. Don’t kid yourselves, though. This still took four days to write and edit. (It’s much faster to talk and show images on slides than it is to type everything out in detail in a blog post!) Nevertheless, I’ve wanted to write this for a long time, so here we finally are. And the benefits a blog post has over a talk is that you can read this at your leisure, click on whatever links you’d like to explore further, and go as deeply down any of those rabbit holes as your heart desires. And to any of you who are happy at such a long post and who prefer reading to watching videos, I’m with you. I started my YouTube channel to bring my message of Keto Without the Crazy™ to a wider audience, but I, myself, prefer reading.    

One of the things I love most about writing my blog is sharing with you, my beloved readers, the fascinating and important things I learn as I deepen my understanding of human metabolism and physiology. The reason they call it “commencement” when you graduate with a degree in something is that it’s the start of your education, rather than the end of it. This has certainly proven true for me since getting my M.S. in nutrition.

One of the most intriguing things I’ve come across recently is the concept of the personal fat threshold. I don’t know who first coined this term, but it appears to have been Roy Taylor and Rury Holman, in their 2015 paper, Normal weight individuals who develop type 2 diabetes: the personal fat threshold. Other researchers wrote about the concept long before this paper, but I think Taylor & Holman were the first to use the phrase personal fat threshold. (Their paper is the first place I ever saw it in print, anyway. A researcher named Keith Frayn wrote some outstanding papers on the same topic years before without using the term. I cite his work liberally throughout this post. If you’d like to read the full text of any of the key papers I cite here, feel free to email me and I’ll send you a copy.)

Preamble

Overweight and obese people are the last acceptable targets, right? It’s no longer politically correct to comment on or make fun of someone’s race, religion, color, or sexual orientation. But it’s always open season on fat folks, right? Making fun of them never goes out of style. We make assumptions about people based solely on the size of their bodies, as if, by knowing nothing else about someone except the size and shape of their body, we can know exactly what they eat, how much they eat, whether they exercise, and if so, how often and how hard. That’s one hell of a crystal ball some people think they have, huh?  

In my opinion, the unfortunate results of this manifest in many ways. Here are just a few examples:

• Moral judgments against larger individuals: they’re lazy, greedy slobs. They should just eat less and exercise more, and if they don’t do that, then it’s their own fault they’re overweight and are dealing with whatever illnesses might come along with that.
• Bias in the workplace: bias against hiring or promoting heavier people, even if they’re the most qualified person for a particular job.
• Weight stigma in healthcare: doctors who are ignorant about the finer points of metabolism and weight regulation can make it a harrowing experience for an overweight person to have a medical visit. Some doctors express explicit anti-fat bias that might make overweight patients reluctant to take care of even minor, routine medical issues. People who are scared to see a doctor for fear of being insulted and ridiculed might ignore problems that are fairly benign or easy to treat in the early stage, but, when left unaddressed, can progress to something far more serious. People with serious medical problems are often written off, their concerns ignored or dismissed, and everything—everything—attributed to their weight. A serious medical problem might be ignored—something that, in a thinner person, would have been taken more seriously at the outset, since there would have been no excess body fat to misattribute the problem to. Broke your arm playing tennis? You should lose weight. Ingrown toenail caused an infection? It’s because you’re obese. Burned your hand serving hot soup to the homeless? Lose some weight. (This essay is highly recommended for a truly sad, disturbing, and eye-opening look at these issues.)

As someone who’s battled weight for most of her life, from Weight Watchers, to the cabbage soup diet, to running marathons, to abusing ipecac syrup, and self-flagellating with exercise, I’m tired of this. Sickened by it, in fact. I’ve written before about the fallacy of believing that obesity is the main causal factor in T2D, metabolic syndrome, CVD, hypertension, and all the other nefarious stuff most people think is “associated with” excess weight. I am absolutely done with uninformed people’s kneejerk assumptions about a causal relationship between body size and metabolic disease. This is more than a blog post to me. It is deeply personal.

The personal fat threshold concept offers a new and very intriguing way to look at things. To be clear, as far as I know, this is a hypothesis, or maybe it’s a theory. I don’t know if it’s been proven for certain, but it certainly seems solid to me. I’ll call it a “concept” just to play it safe.       

Introduction

Which person is healthier?
We don't know.
We can speculate, but the truth is, we can't know for sure
just by looking at the size and shape of someone's body.
REPEAT: We can't know for sure just by looking at them.

Any paradigm that attempts to explain the etiology of type 2 diabetes, obesity, and any of the conditions driven by metabolic syndrome (chronically high insulin, a.k.a. hyperinsulinemia) should account for at least 5 things, each of which I will explore in detail:

1.     Why all of the metabolic “diseases of civilization” (e.g., hypertension, T2 diabetes, cardiovascular disease, gout, non-alcoholic fatty liver disease [NAFLD], Alzheimer’s, PCOS, etc.) can occur in people at any body weight—not just those who are overweight or obese, but also in people at what we would consider a “normal” or “healthy” weight. (Who the heck came up with these terms, anyway? What is a “normal” body weight? And after reading this post, you’ll appreciate that a person’s weight gives you zero information about their health, so there’s really no such thing as a “healthy weight.”)

2.     Why being overweight appears to be protective against some of these cardiometabolic diseases. Contrary to what ivory tower researchers and mainstream medical and public health professionals would assume, some people who are overweight have lower rates of T2 diabetes and CVD, and better survival in metastatic cancer. (They call this “the obesity paradox,” but after reading this post, you’ll understand that this not paradoxical at all, but rather, makes perfect sense when viewed through the lens of the personal fat threshold.)

3.     Why people who undergo bariatric surgery, adopt a fasting practice, or implement a low-carb or ketogenic diet experience rapid and dramatic improvements in things like T2 diabetes, hypertension, NAFLD, and other metabolic dysregulations long before they’ve lost any substantial amount of weight. If obesity were the cause of these issues, we would see little to no improvement until these people had lost a great deal of weight, but we do see improvements. Quickly and powerfully.

4.     Why people with the condition lipodystrophy often exhibit a slew of metabolic and hormonal abnormalities and adverse health consequences. Lipodystrophy is a disorder in which people have limited capacity to store body fat. These people are sometimes emaciated, yet they have high rates of T2 diabetes, CVD, PCOS, NAFLD, kidney failure, and other metabolic sequelae we typically associate with, or worse—attribute to—being overweight or obese. How can these people, with a constitutional inability to store body fat, have the same conditions we typically see in heavier folks?

5.     Why high carb, low fat diets do actually work in some people. (It’s true!) If you’re a fan of my blog, then it’s likely that the low fat approach didn’t work for you, but we can’t deny that there are, in fact, some people out there who do get good results from low fat diets. Let's understand why.

Any theory that satisfactorily explains obesity and cardiometabolic disease must—must—account for all of the above. From my own personal interest, I cannot stress enough that all of these issues—type 2 diabetes, hypertension, cardiovascular disease, PCOS, gout, erectile dysfunction, fatty liver, dyslipidemia, and more—are observed in people all across the body weight spectrum: obese people, “normal” weight people, and thin people. We cannot say obesity is the cause of any of these conditions when they occur in plenty of people who aren’t obese. 

The personal fat threshold concept explains all of the above very elegantly.

The Personal Fat Threshold

The personal fat threshold (PFT) concept holds that each person has a unique and individual, genetically determined capacity to store body fat—specifically, to store subcutaneous adipose. Subcutaneous means “under the skin.” Adipose means “fat.” So, subcutaneous fat is the fat we love to hate under the skin on our hips, thighs, backsides, upper arms, chin, etc. However, the thing to know is, this is where fat is supposed to be stored. This is what adipose tissue is for: to hold fat. In the modern beauty aesthetic of the 20^th and 21^st centuries, we might not like the way this kind of fat looks, but metabolically speaking, health-wise, this fat is mostly benign.

Contrast this with two other types of fat: fat stored in muscle tissue, and fat stored in and around the abdominal organs. 

Fat stored in the muscles is called intramuscular lipid, or intramyocellular lipid (IMCL). (“Myo” means muscle; a myocyte is a muscle cell.) There’s normally a very small amount of adipose interspersed within muscle tissue, and that’s normal. But IMCL is when lipid droplets (that is, fat) gets inside muscle cells, where it’s not supposed to be. This is, to use the technical term, no bueno.

Fat stored in and around the abdominal organs is called visceral fat. (Those organs, and your entrails and such, are called “viscera,” hence, the term visceral fat.) When fat accumulates in and around these organs—particularly your blood sugar regulating organs, that is, your liver and pancreas—this is really, really NO BUENO. This fat is more metabolically harmful than the subcutaneous fat, the fat we can see. It’s the fat we can’t see—the intramuscular and even more so the intra-organ fat—that’s a problem. 

Fat is not supposed to be stored inside your muscle cells, nor in and around your internal organs. So what’s it doing there?

The personal fat threshold concept posits that once your subcutaneous adipose storage capacity is at its maximum—once you have reached your own personal fat threshold—your body has no choice but to store fat somewhere else. It doesn’t want to put it in your muscle cells, or in your liver and pancreas, but it has nowhere else to put it, because you are at your personal fat threshold.

It doesn’t take much insulin to put fat in subcutaneous adipose tissue, because that’s where it’s supposed to be. It takes a lot more insulin to shove fat into places it’s not supposed to be, so the PFT posits that this is when insulin rises. Insulin has to rise in order to force that excess energy into places the body really doesn’t want it to be.

Image courtesy of Ted Naiman, MD

As you can see in this image from Ted Naiman, MD, basal insulin (in green) is keeping normal fat storage in your subcutaneous adipose tissue. No problem. This is what happens in a healthy person. (Basal insulin is the insulin your body keeps parked in the bloodstream even when you’re not eating. Except for type 1 diabetics, we all always have at least a little bit of this, and that’s fine. We're supposed to have a little bit. Just because too much insulin is a bad thing doesn't mean none is a good thing.) However, when the fat tissue is full, we need more insulin to keep storing incoming energy elsewhere. This is hyperinsulinemia (in yellow). Once everything is maxed out—your subcutaneous adipose is full, your muscle cells are full, your liver and pancreas are full—now you have type 2 diabetes. Your blood sugar is high because either you're pumping out a ton of insulin but it's still not enough to sock away excess incoming energy, or your pancreas isn't able to keep up with the demand for insulin and you don't pump out all that much. (This is the red arrow spilling out above the yellow toward the right.) Either way, at this point, you have high blood sugar, and BAM, T2D diagnosis. Keep in mind, though, as I wrote about a while back, the high insulin can go on (and go undetected) for years before the blood sugar starts to rise. 

The thing to know here is, everyone has a different personal fat threshold. This is why some people can store energy to the tune of becoming 400, 500, 700 pounds, and other people can eat and eat and eat and eat, and not accumulate a huge amount of body mass. HOWEVER—and I’ve written about this before—not being obese does not mean those people are healthy.  

I Don’t Like the Phrase “Insulin Resistance”

I’m glad Dr. Naiman used the word hyperinsulinemia in the image above, rather than insulin resistance. I really don’t like this phrase anymore. I never really liked it, but I guess I used it because everyone else was using it, and it was convenient. (Kind of like how I sometimes say “PIN number,” even though that is ridiculous and we should just say “PIN.” I say it that way because everyone else does, to the point that saying it the correct way sounds weird.) As it happens, Dr. Jason Fung doesn’t like “insulin resistance” either, and he explained why on this episode of the Low Carb MD podcast. (Also available on iTunes.) I largely agree with him—it’s too vague. What does it even mean? Insulin resistance? Resistant how? If you’re gaining body fat, you are insulin sensitive. If you are not able to lose body fat, you are insulin sensitive. Your adipose cells are doing exactly what they’re supposed to do in the presence of insulin: take up and sequester fat. If your liver has a ton of glycogen in it, you’re insulin sensitive. If you have high blood pressure, high triglycerides, and high uric acid, you are insulin sensitive. That’s what insulin does.

I much prefer the word “hyperinsulinemia.” The word itself tells you exactly what it means:

hyper: high

insulin: insulin

-emia: in the blood

Hyperinsulinemia means too much insulin in the blood. Even more than hyperinsulinemia, I prefer the phrase chronic hyperinsulinemia. A big rise in insulin once in a while when you fall face-first into a pint of ice cream or a bag of cookies is not the same thing as elevated insulin all day, every day, from a constant onslaught of carbohydrate from the time you wake up until the time you go to sleep.

Also, the phrase chronic hyperinsulinemia hints at its own solution. You have too much insulin in your blood, too often? BRING INSULIN LEVELS DOWN. “Insulin resistance,” on the other hand, is like, what? What does that even mean, and what do we do about it? How do we restore sensitivity to insulin? Maybe we should give more insulin in order to overcome this “resistance.” So you can see this is not helpful.

If you know you have chronically high insulin, though, and that this is driving most of the health problems you’re dealing with, the answer becomes obvious: take steps—and there are many different ones that are effective—to lower insulin.

But there’s an even bigger reason I dislike the term “insulin resistance” than just its vagueness. I actually don’t think most cells are “resistant” to insulin at all. Here’s an analogy:

Let’s examine this suitcase. The straps look to be in working order, right? The buckles look okay; everything looks like it’s in good repair. There’s nothing wrong with this suitcase. So what’s the problem, then? Why is clothing spilling out onto the bed? The suitcase isn’t broken. It’s not “resistant” to more clothing, it’s just full. There’s no more room for anything to go in.

Your subcutaneous adipose is like this suitcase: are your fat cells resistant to insulin, or are they just full? Your pancreas can pump out as much insulin as it wants, more and more and more, but if your fat cells are full, there’s nothing they can do about it. They’re not resistant to it; there’s just no more room, so they can’t take up any additional energy.

“The net effect is as though adipocytes are full up and resisting further fat storage. Thus, in the postprandial period especially, there is an excess flux of circulating lipid metabolites that would normally have been absorbed by adipose tissue. This situation leads to fat deposition in other tissues. Accumulation of triacylglycerol in skeletal muscles and in liver is associated with insulin resistance.” (Source: Frayn, KN. Adipose tissue and the insulin resistance syndrome.)

It’s the same with muscle cells and your liver, with regard to glycogen: once the glycogen storage capacity is full, it’s full. Ain’t no more room at the inn. Your liver and muscle cells aren’t “resistant” to insulin; they just can’t store any more glucose because they’re already at max capacity.

Dr. Fung uses the analogy of the Tokyo “subway pushers” shoving commuters into already crammed-full train cars, although he describes it in relation to putting more glucose, rather than fat, into cells. The principle is the same. (Dr. Fung’s book, The Diabetes Code is absolutely excellent. Read it soonest.)

Here’s what we’re talking about, in more formal language:

“The adipose tissue expandability hypothesis can be stated as follows; adipose tissue has a defined limit of expansion for any given individual. As an individual gains weight a point will eventually be reached when their adipose tissue can no longer store more lipid. Once adipose tissue storage capacity is exceeded then net lipid flux to non-adipose organs will increase and lipids will begin to be deposited ectopically. Ectopic lipid accumulation in cells such as myocytes hepatocytes and beta cells then causes toxic effects such as insulin resistance and apoptosis. Adipose tissue mass by itself is unlikely to be the driving factor linking obesity to diabetes. If there was a simple and direct correlation between adipose tissue mass and insulin sensitivity, all individuals would become diabetic at the same adipose tissue mass. However, on an individual level this is not true, some relatively lean individuals become insulin resistant whereas some very obese individuals do not.” (Source: Virtue S, Vidal-Puig A. Adipose tissue expandability, lipotoxicity and the Metabolic Syndrome--an allostatic perspective.)

With all this in mind, let’s take a closer look at the PFT in action, as we address the 5 points above.

  1. Metabolic Dysregulation and Hyperinsulinemic Conditions Occur in People of All Body Weights

If obesity was the cause of T2D, CVD, hypertension, gout, NAFLD, and all the other nefarious cardiometabolic problems being overweight typically takes the blame for, then two things would be true:

1. We would rarely to never see these conditions develop in people at a "normal" weight.
2. Every single person who is overweight or obese would have one or more of these conditions.

Neither of these is true. There are plenty of people at a “normal” weight who have raging T2D, who die from heart attacks, who have severe atherosclerosis and other forms of CVD, who have fatty livers, PCOS, etc. (As many as 50% of women with PCOS are not “overweight.”)

As I explained, fat stored in subcutaneous adipose is mostly benign. Fat stored in and around the organs that regulate blood sugar, however, is not benign at all. The body needing to store excess energy in these places it’s not supposed to be stored is why insulin starts rising, and the elevated insulin brings along with it higher blood pressure, kidney damage, gout attacks, problems with the eyes, an enlarged prostate gland, erectile dysfunction and more.   

And remember, people can have a buildup of intra-organ fat at any body weight. You can be at a “normal” body weight and have a massively fatty liver or pancreas, and you can be quite obese, yet not have fat building up in those critical organs. It all depends on your personal fat threshold, and whether you’ve reached it or exceeded it.

This is why there are currently exploding rates of T2D in China and India, two nations not especially known for obesity. As of 2013, nearly half of Chinese adults (47%) were diabetic or pre-diabetic, and a 2016 article in the Times of India called India “the diabetes capital of the world.” Except maybe for sumo wrestlers, East Asians and South Asians simply don’t have the genetic constitutions to become 400 pounds or more the way we now see somewhat regularly in North America. They have much lower personal fat thresholds. But because they have low personal fat thresholds, they can’t become that large, and since their subcutaneous adipose can’t keep expanding, their bodies have to store excess energy in the liver and pancreas at a lower total body weight. So they experience all the same metabolic complications even though they’re not obese.

There are overweight and obese Indian and Chinese people, but it’s uncommon. What is not uncommon, though, is raging T2D. These people experience hyperinsulinemia and T2D at much lower body weights than we do. They’re not obese on the outside, but on the inside, their pancreas is engorged with fat. Their liver is engorged with fat. Hence, they have hyperinsulinemia, T2D and related comorbidities even though they have a “normal” BMI. 

This brings us to the concept of body mass index…

2. The Obesity Paradox:

Why BMI is (Mostly) Useless

In case you didn’t know, the body mass index (BMI) is a mathematical relationship between two things: your height and your weight. (Specifically, it’s your weight in kilograms divided by your height in square meters. How they decided this was indicative of anything is beyond me, but I digress.) Note that BMI takes into account only your height and the force of Earth’s gravity upon your physical body (that is, your weight). It says nothing—nothing—about your body composition. It does not take into account how much water your body contains, nor how much of your weight is muscle, organs, and bones, versus how much of it is fat. It also says nothing about where any of this fat is stored. Is it safely tucked away on your rear end, or is it wreaking havoc in your pancreas?

Since BMI takes into account only height and weight, this is why there are professional athletes who are “obese” based on BMI, and people at a “normal” weight who are actually quite fat. The latter have a high body fat percentage and low muscle mass. These are the folks who are “thin,” but who couldn’t bang out 5 pushups if they had to. You’ve probably heard these people called “TOFI, for thin outside, fat inside. Some people also use the phrase “skinny fat.” The medical literature refers to them more formally as “metabolically obese normal weight” or the “normal weight obese.”

On the flipside, we have the “metabolically healthy obese” – the folks who are very large, and whom you might expect to have all sorts of terrible health problems, but they’re actually pretty healthy. As one paper stated, “…despite a high body fat mass, low visceral fat accumulation is a major feature of the metabolically healthy profile observed in some obese individuals.” 

NORMAL WEIGHT OBESITY	METABOLICALLY HEALTHY OBESITY
“Normal” BMI but overfat; a.k.a. TOFI; “skinny fat”	Overweight or obese by BMI
More fat stored in liver, pancreas, skeletal muscle	More fat stored in subcutaneous adipose tissue
Increased risk for cardiometabolic disease	Decreased risk for cardiometabolic disease: The obesity “paradox”

I’ve heard some of the low carb & keto MDs say something like, “Obesity is the price you pay for not becoming diabetic.” In other words, being able to store more fat in subcutaneous adipose “protects” you from the gnarly health problems that occur when you can’t store that fat in your adipose tissue and it ends up in your liver and pancreas instead.

So T2D, CVD, and all those other undesirable things don’t happen because you’re fat; they happen because you can’t get fat ENOUGH: “When adipose tissue cannot expand further to store excess nutrients then lipid accumulates in other tissues.” (Source.)

“In our opinion, the principal allostatic load that leads to insulin resistance in the context of obesity is a failure in adipose tissue expansion. This in turn causes increased lipid flux to non-adipose organs and leads to pathogenic accumulation of toxic lipids in non-adipocyte cell types, which then causes insulin resistance.” (Source)

If you could keep getting fatter and fatter—in your arms, your legs, your hips, your tush—you’d actually be okay. I mean, you might have limited mobility and you might be in pain from the stress & strain on your joints, but you wouldn’t have the kinds of metabolic problems we see in much thinner people with a buildup of fat in and around the blood sugar regulating organs.

Before moving on, let me say that we shouldn’t dismiss BMI altogether. On a population level, BMI is informative. As a general observation, has the American population gotten much heavier? Yes. On the whole, have people in most of the industrialized world gotten heavier? Yes. So it’s not useless. It’s good for identifying trends over time, and across large groups of people. But we must be aware that it tells us nothing about individual people.  

BMI: Not helpful. Two people can have the same BMI but be in completely different states of health.

3. Last in, First Out: Why T2D and Other Hyperinsulinemic Conditions Improve Before People Lose a Lot of Weight

The third thing any satisfactory explanation of obesity, T2D, and other cardiometabolic and hyperinsulinemic issues must account for is why people who undergo bariatric surgery, adopt a fasting practice, or implement a low-carb or ketogenic diet experience rapid and dramatic improvements in their conditions long before they’ve lost a substantial amount of weight. As I said, if obesity were the cause of these issues, we wouldn’t see much, if any, improvement until these people had lost a great deal of weight. But we do see improvements. All the time. People with type 2 diabetes can have such rapid improvements in blood sugar, in fact, that Dr. Eric Westman cautions other doctors that insulin injections sometimes have to be discontinued on the first day that a T2 diabetic adopts a ketogenic diet. The first day! Those people haven’t lost 50 pounds in one day, but damn if their blood sugar isn’t already almost normal. Blood pressure also tends to normalize quickly on a low carb or ketogenic diet, although sometimes it can take weeks to months, rather than days or weeks, like with blood sugar. Again, these improvements occur long before significant amounts of weight are lost, so how can we say that obesity is causing them?

We can say that excess fat is causing them, but it’s not about the total amount of fat. It’s about where the fat is stored. Stored in your arms, your double chin, or your thighs? No problem! Stored in your liver and pancreas? Uh-oh…

The reason some of the metabolic issues improve so quickly is that the liver fat and pancreatic fat are the first to go. Last in, first out. Because it’s the most harmful, and it’s the last place the body wanted to have to cram triglycerides—and it only did so because your personal fat threshold was already at max capacity and there was nowhere else for that excess energy to go—it’s the first place your body is going release fat from, to get it out of there as soon as possible. 

This is probably why people who go on a low carb or ketogenic diet and find their blood sugar and insulin levels dramatically improved still sometimes struggle to get rid of excess body fat. Depending on someone’s starting weight, a person could still be looking to lose a hundred or two hundred pounds, yet they’re no longer diabetic. They might be off many of their meds. Because it’s not about the total body weight.

Even though these people might not be satisfied with their physical appearance, their metabolic health is much improved from where they were before low carb. The most dangerous fat is gone, and getting rid of the subcutaneous fat is less of a priority for the body, because the fat there is relatively safe. These folks have more fat stored there than they wish they did, but because it’s stored where it’s supposed to be stored, the body isn’t in as big a hurry to get rid of it. They might even have to take extra measures to force their body to give up those last bits of excess fat, such as fasting, resistance training (to build muscle that will require fuel just to exist), or learning to relax and get more sleep, if they’re a chronically under-sleeping stressball.  

The point here: if you’re in the early stages of a low carb or ketogenic diet, or you’ve started a fasting regimen, you might not look like a supermodel, but you are MUCH HEALTHIER than you were before. Don’t make yourself crazy over the weight that won’t budge just yet. Celebrate how far you’ve come. That’s what keto is about: getting your life back, more than fitting into smaller jeans.

Dr. Fung calls bariatric surgery “surgically enforced fasting.” The neat thing is, being that adopting a ketogenic diet or doing some fasting (even if not on a low carb or keto diet) yields similar metabolic results to the surgery, you could do keto or implement some fasting and get fabulous results without having your stomach and/or intestines ripped to shreds and increasing your risk for deficiencies of B vitamins, iron, zinc, bone loss, alcoholism, self-harm and suicide. Instead, you could increase your risk for enjoying a nice fatty steak or some brussels sprouts roasted with bacon. Oh, the hardship! How will you ever survive such a restrictive diet?

4. Lipodystrophy 

Moving on to the fourth point any satisfactory explanation of all this “stuff” has to account for, we have lipodystrophy. As I mentioned, lipodystrophy is a disorder in which people have limited capacity to store body fat. These people cannot and do not become obese. If, like me, you’ve battled weight for much of your life, this probably sounds pretty darn great. A biological inability to get fat? Where do I sign?

Nah, man, think again. This is a very gnarly, very nasty condition, and you do not want to have it.

People with lipodystrophy have limited ability to store subcutaneous fat—the kind you want to have. But they are champions at packing fat into their liver and pancreas, precisely where you don’t want it. For this reason, people with lipodystrophy have high rates of all the cardiometabolic conditions we normally “associate” with obesity even though they’re not overweight. Lipodystrophy is probably the most extreme example of “TOFI.”

To be clear, though, there are many different types of lipodystrophy. It is not a homogeneous, single entity. You can have generalized lipodystrophy, which affects the whole body, or some people have a localized or partial form that affects only certain areas of the body—some parts of a person’s body will be almost emaciated while other parts are much bigger. Some lipodystrophies are congenital, meaning people are born with them, and others are acquired later in life. (You can look through severa limages of various lipodystrophies here. If you do, you will notice that in several of the images, the patients are practically emaciated on their arms and legs, but they have protruding bellies, because they have enlarged livers and are storing most of their fat—the little fat they can store—in the abdominal area.)  

Original caption: Consequences of Lipodystrophy: The figure summarizes metabolic derangements and end-organ complications in patients with lipodystrophy (Left: MRI showing near total lack of adipose tissue; Right top: Liver biopsy shows hepatic steatosis in lipodystrophy (Hematoxylin and eosin staining; magnification 100X), Right bottom: CT of abdomen obtained during an episode of acute pancreatitis in lipodystrophy; Middle top: Diabetic foot ulcer in a patient with generalized lipodystrophy; Middle bottom: Renal biopsy specimens (Left: Electron microscopy image reveals lipid vacuoles which suggest ectopic lipid accumulation; Right: Light microscopy image documents chronic kidney disease in lipodystrophy (Hematoxylin and eosin staining; magnification 40X) 

Source: Akinci B, Sahinoz M, Oral E. Lipodystrophy Syndromes: Presentation and Treatment. In: Endotext.

From Keith Frayn, whom I mentioned earlier:

“…the normal role of adipose tissue is to buffer the daily influx of dietary fat entering the circulation. If adipose tissue is overloaded, as in obesity, this buffering capacity is lost and other tissues are exposed to an excessive influx of fatty acids. If there is a deficiency of adipose tissue, as in lipodystrophy, then again this normal buffering action of adipose tissue is deficient (or absent) and other tissues are again exposed to an excessive flux of fatty acids. The result is accumulation of fatty acids in the form of TG in other tissues and interference with insulin-mediated glucose disposal (or glucose-stimulated insulin secretion, in the case of the β-cell).”

(Source)

You understand how this works, right? The reason lipodystrophy patients have many of the cardiometabolic complications we associate with obesity is because of where they store their fat. Having lipodystrophy—very little subcutaneous adipose storage—is kind of the same as someone with a lot of storage but who has exceeded their personal fat threshold. Here’s an image that depicts this in action, once again from the great work of K. Frayn:

Source: Frayn KN. Adipose tissue and the insulin resistance syndrome. Proc Nutr Soc. 2001 Aug;60(3):375-80.

5. Low Fat Diets Do Work for Some People (*Gasp!*)

The fifth thing any satisfactory explanation of obesity, T2 diabetes and metabolic syndrome has to account for—especially for me and my low-carb & keto loving audience—is why high carb, low fat diets are effective for some people. No, really, they are. And we can’t deny that. What we should do, is understand why. A low fat diet didn’t work for me, and I’ll assume it didn’t work for you, or you probably wouldn’t be reading this blog. But that doesn’t mean low fat doesn’t work for anyone. So what gives? Who are these weirdos who can eat cereal, fruit, pasta, rice, and bread, and not wreck themselves?

The first thing to know is, most stored body fat originates as dietary fat. We in the low carb world like to think it’s from carbs, from de-novo lipogenesis (DNL, the process by which glucose is converted into fat), but the truth is, most of it is dietary fat. (Only about 10% comes from DNL.) But the second thing to know, and probably more important, is that “carbs displace fat oxidation.” (Another gem from Dr. Naiman.) In plain English, this means that when you’re burning carbs, you’re not burning fat.

The availability of glucose is the prime determinant of which fuel source predominates: glucose or fat. When both are present together in the diet, the glucose will be burned/oxidized first, leaving the fats to be stored. In a very low fat diet, the glucose is oxidized, but there is very little fat to be stored. So if there isn’t a lot of fat coming in from the diet, you eat carbs, burn carbs, eat carbs, burn carbs, and it’s no problem.

Conversely, if you’re on a very low carb diet, and there isn’t a lot of carbohydrate coming in, you eat fat, burn fat, eat fat, burn fat, and it’s also no problem.

The problem is when we eat both, together. Think bagel with butter. Pasta with cream sauce. Macaroni & cheese. Potato chips with sour cream dip. When you eat carbs + fat, you burn the carbs and store the fat. You have to. You will always burn carbs first. (Why? Because we have a limited storage capacity for glucose. We don’t store all that much glycogen. But we have a much, much larger storage capacity for fat—almost unlimited, in fact, especially if you have a high personal fat threshold. Since we can’t store much glucose but we can store plenty of fat, we burn glucose first and store the fat away for use some other time.) Now, if your total energy intake is low enough, or you don’t hyper-secrete insulin when you consume carbohydrates, it’s possible to eat both together and not become obese. For example, French people who eat a buttery croissant, or fatty pâté with a baguette. I would argue they are not gorging at meals, nor snacking around the clock.

I would also posit that many of us probably could do all right on a low fat diet, and if we think we failed at it in the past, we probably didn’t eat low enough fat. We keto and low carb fans like to say that the reason so many studies on “low carb” diets have unimpressive outcomes is because they’re not actually low carb diets. Some of these “low carb” studies have people consuming upward of 30-40% of their calories from carbohydrate. That might be low-ER than the standard American diet, but most of us wouldn’t call that truly low carb.

So what about a low fat diet, then? If we were still eating 20-30% fat, could we consider that truly low fat? Maybe if we had gotten down to, say, 10% fat, we would have had better results. But if we weren’t that low—and honestly, most of us probably weren’t (truth be told, I know I wasn’t)—then we were locked into burning the carbs and storing the fat, however little of it might have been coming in. Burn carbs, store a little fat, burn carbs, store a little fat … All that “little fat” storage would have added up to a substantial amount of weight over years, over decades, of not quite being low enough in dietary fat while simultaneously having a very high carbohydrate intake.

And even if we weren’t getting fatter—i.e., we weren’t gaining weight—we wouldn’t be losing any. The incoming carbs (and resultant insulin rise) would have been enough to keep us in carb burning mode and keep the fat locked away in our fat cells. (Insulin is directly inhibitory to burning fat. More on this in an upcoming post about insulin that will blow your mind. It will also be insanely long. Hey, I’m making up for lost time!)

Me, Pittsburgh marathon, 2001.
Thanks for NOTHING, carb loading!!

This is why it didn’t even work for those of us who combined a so-called “low fat” diet with tons of exercise. If you exercise a lot on a high carb, low-ISH fat diet, then you eat carbs, burn carbs, store fat; eat carbs, burn carbs; store fat. You are literally and figuratively on the treadmill to nowhere. Even worse, you refuel with a granola bar, an energy bar, whole grain cereal, pasta… You’re desperate to lose weight, and you think you’re doing the right thing by avoiding high fat foods. But you’re actually keeping yourself locked into carb burning mode. Eat carbs, burn carbs, refuel with carbs. When does burning fat ever enter the picture? It doesn’t! If only I knew any of this when I ran not one, but two marathons, thinking there was no way I could train for a marathon and not lose weight. (Ell-oh-ell. Joke was on me, and I have the chubby finish line photos to prove it!) 

So, not to be a heretic or anything, but I think low fat diets can work, provided that they are really, really low fat. Like, really low fat. The thing is, I think that kind of diet would be much more difficult to stick to over the long term than one where you can eat bacon, ribeye steaks, blue cheese, macadamia nuts, guacamole, pork rinds, fatty pork chops, and all manner of other extremely delicious, fatty foods. One study’s authors noted that appetite suppression on low carb diets is due to a relatively higher protein content, the state of ketosis, satiety signals from fat, and, most tellingly, “the absence of hunger-promoting carbohydrate components like sucrose and/or fructose.”        

I also think you have a greater risk for nutrient deficiencies on an ultra-low-fat diet than on a low carb diet, particularly with regard to essential fatty acids and fat-soluble vitamins. But for the folks out there who prefer grape juice, rice cakes, plain white rice, pineapple, corn flakes, and plain potatoes (or maybe with fat-free sour cream), I can see how someone can eat this way and not become obese nor have any hint of metabolic syndrome. (I kinda suspect fruit juice probably still isn’t the best thing for anyone to drink, but whatever.)

So yeah, most stored body fat comes from dietary fat, but the reason we store it is because of the carbs we eat along with it: “From an allostatic perspective, ectopic lipid accumulation in non-adipose organs may actually be a mechanism to cope with the lipid overload.” (Source.) English translation: fat being stored in non-fat tissue is the body’s way of dealing with all the fat coming in. If one eats carbs without the fat coming in, the body doesn’t have to deal with it.

With that in mind:

“Removing toxic lipids from circulation directly prevents their accumulation in non-adipose organs.” (Source) And how do we remove lipids from circulation? We can fast and burn them. We can go on a low carb diet and burn them. Or we can follow a super-low-fat diet and not eat them in the first place. I know which one I prefer.

What About People Gaining Weight on Keto?

One more elephant in the room to address. If you’ve spent a while in the keto community, you know that keto fat loss isn’t magic for everyone. Some people lose fat very, very slowly. Some people even gain fat. What gives? I thought if I was eating really low carb, I’d be burning fat. In fact, Amy, you just said that exact thing a minute ago. I can eat all the fat I want as long as I don’t eat carbs, right? If carbs displace fat oxidation and I’m hardly eating any carbs, then I have to be oxidizing fat, right?

Yes, but…

First, know that it is entirely possible to gain fat on keto if you are eating a ridiculous amount of fat. Being in ketosis means only that you are burning fat. It doesn’t tell you whether you’re burning your stored body fat or the butter, heavy cream, walnuts, and fat bombs you snack on all day. Low thyroid function can also be a huge roadblock to fat loss, but assuming you don’t have a thyroid problem, you might just be eating too much fat.

This is especially a problem if you think you’re very low carb but you’re eating just enough carbs to tip you into carb burning, and thus having to store the copious amounts of fat you’re taking in. I have made this mistake more times than I care to admit—letting “carb creep” get the best of me while still consuming ad libitum fat as if I was on a truly ketogenic diet. This was a recipe for fast and furious fat gain.

To be clear, this is really an individual thing. Some people can do super-high-fat keto and still lose weight, but some of us have to use a lighter hand with the added fats and oils. Here’s what Dr. Naiman said on an outstanding episode of the Human Performance Outliers Podcast:

“In my clinical practice, on a regular basis, I see people on strict ketogenic diets who are completely stalled out. Like, they eat absolutely no carbs and they’re way fatter than they want to be. I see diabetics whose blood sugar stops going down. I see people who their waist circumference stops going down. I’ve seen people gain 50, 60 pounds on a strict ketogenic diet. I’m talking food logs, and ketone readings, and the fact is, as soon as you restrict carbs, you become fat-adapted. You become very good at burning fat. That’s great. But if the amount of fat you eat every day exceeds the amount of fat you burn, you are literally gonna gain weight and your blood sugar’s gonna go up if you’ve exceeded your personal fat threshold. I’ve had diabetics come in and their A1c has gone up several percentages on a strict ketogenic diet. I know that it’s possible to eat too much fat, and personally I think it’s because their protein-to-fat ratio is too low, so they’re overeating fat.”

Think this might be happening to you? Check out my blog post on how to cut fat on keto and why you might want to, and maybe watch this video on things that can stall fat loss on keto. (I also did a brief follow-up part 2 video to explain things better.)

Again, this is not to scare anyone away from eating fat. Even if you’re trying to lose weight, keto is still a high fat diet, but just remember that you want some of that fat to come from your body, instead of all from your food. (And yes, there is a lot of food addiction, emotional eating, and self-sabotage among those of us who struggle with weight. I deal with this myself, even now. I gave a very candid talk about it a few weeks ago. I’ll update this post with a link to the video when it’s up.)

(Fat Cell) Size Matters

At the risk of bringing another nuance into this, personal fat threshold isn’t only about the storage capacity of your subcutaneous adipose tissue. It’s also about the size of your individual fat cells. Research indicates that having smaller fat cells is preferable to having larger fat cells. Not because they can hold less fat, but because of the nature of smaller cells, themselves.

You can hold the same total amount of fat in a large number of small fat cells as you can in a small number of large fat cells. The former appears to be better, metabolic health-wise. Unfortunately, as far as I know, this is genetically determined and there’s nothing much we can do to change this. (Certain diabetes drugs can influence this, though. I’ll get to that in a minute.)

Image courtesy of Ted Naiman, MD. (Watch his talk on insulin resistance: phenomenal stuff.)

You can see in the image above that the small adipocytes (on the left) have multiple individual lipid droplets inside them. The cell cytoskeleton/scaffolding is intact and has no problem helping the insulin-sensitive glucose transporter (GLUT4) move to the surface of the cell. The large adipocyte, however (on the right), has a single very large lipid droplet. The cell is engorged, which limits the mobility of the actin filaments, so the glucose transporter has a harder time getting into the correct position at the cell surface. If the glucose transporter is not oriented correctly, guess what: glucose can’t get in. If glucose can’t get in, blood sugar will remain elevated. If blood sugar remains elevated, the pancreas will probably pump out more insulin (if it can).

In order to understand the next point, you have to understand the difference between hypertrophy and hyperplasia. Cell hypertrophy is when cells get larger: individual cells expand in size. Hyperplasia is when cells increase in number—there are more cells. As I mentioned, for the same total amount of fat mass, you can have a few fat cells that are very large, or you can have lots of small cells. The total amount of fat stored might be the same, but the metabolic consequences appear to be different:

 

Source: Source: Laforest et al., 2015. Adipocyte size as a determinant of metabolic disease and 

adipose tissue dysfunction. Crit Rev Clin Lab Sci. 2015;52(6):301-13.

Here’s the caption from the paper: “Obesity is a multifactorial disease characterized by expansion of adipose tissue occurring through adipocyte hypertrophy (enlargement of pre-existing cells) or adipocyte hyperplasia (generation of new cells through adipogenesis). Limited expandability of adipose tissue through hyperplasia leads to increases in fat cell size (adipocyte hypertrophy), which represents a critical marker of central adiposity, adipose tissue dysfunction and concomitant metabolic disease risk.”

So even beyond the concept of a personal fat threshold, there’s this fat cell size issue. When you can’t make more fat cells but you have excess energy coming in, the fat cells you already have need to get bigger. And when they do, this appears to be bad juju for all the gnarly metabolic outcomes most of us want to avoid.

Frayn and his co-author on this paper agree: “It may well be that a large, fat-filled adipocyte is metabolically less ‘flexible’, or dynamic in its responses, than a smaller adipocyte with more storage capacity to spare.”

I’ve mentioned that it’s the intra-organ fat that seems worst for cardiometabolic health. But to take things a step further, there’s some indication that subcutaneous adipose can be harmful if your subcutaneous fat cells are small in number but large in size—that is, when your subcutaneous fat has expanded via hypertrophy rather than hyperplasia:  

“We propose that excess visceral adipose tissue accumulation and SC [subcutaneous] fat cell hypertrophy may represent markers of a common phenomenon: limited hyperplastic capacity of adipose tissues, which in turn associated with the presence of numerous cardiometabolic alterations.” (Source) In the interest of full disclosure, though, the next sentence reads: “However, we also emphasize that available studies are far from unanimous, in particular when addressing the relationship between FCS [fat cell size] and parameters of adipose tissue function.”

If I had to take a position on this, I would say you’re probably still better off having more subcutaneous fat than visceral and intra-organ fat, even if your subcutaneous fat cells are small in number but large in size. And since there’s not much any of us can do about our fat cell size anyway, the best thing to do, regardless of the size of your fat cells, is stay below your personal fat threshold. How do you know what that is? Well, if you have no signs or symptoms of hyperinsulinemia, you’re probably okay.

Adipocyte hyperplasia explains why the class of diabetes drugs called thiazolidinediones or TZDs (also called glitazones) makes people gain weight while improving blood sugar. These drugs cause the body to make more (but smaller) fat cells. Since they basically build new subcutaneous fat tissue, they increase someone’s personal fat threshold. Their adipose tissue can now hold more fat, so it doesn’t have to be shoved into the liver or pancreas. So someone gains body fat, but their blood sugar and perhaps insulin levels improve slightly. (It’s true: becoming obese is a tradeoff for not having T2 diabetes, or, if you already have it, then gaining weight is the tradeoff you make for your blood sugar not being even worse.)

As the brilliant Frayn put it: “The TZDs also lead to weight gain whilst improving sensitivity to insulin, apparently a paradox but clearly explained under this hypothesis.”

EXACTLY: None of this is “paradoxical” when you understand that it’s not total weight or even total fat mass that drives T2D or chronic hyperinsulinemia, but rather, where the fat is stored, and possibly the size of the fat cells.

Implications for Treatment of T2 Diabetes and Metabolic Syndrome

If you’re thinking that, based on what you’ve just read, treating diabetes solely by addressing blood sugar is darn near useless and might even be counterproductive, you are correct!

“In our opinion, this suggests that therapeutic strategies for diabetes that only target hyperglycaemia are not actually targeting the main underlying pathogenic factors leading to both diabetes and cardiovascular disease (factors including insulin resistance, defective lipid homeostasis and inflammation).” (Source)

“However, it is doubtful if there is limitless capacity to expand beta cell mass and furthermore targeting beta cells will not alleviate the underlying allostatic load of failed adipose tissue function and lipotoxicity induced insulin resistance. From an allostatic perspective, treatments that exclusively target the beta cell are perhaps less suitable than those that try to treat the underlying causes that create the demand for insulin.”

Um, ya think??!!

This is why type 2 diabetics who get put on insulin never, ever get any better. They get worse and worse; they lose feet, they lose legs, they go blind, their kidneys fail, they have heart attacks and strokes, increased risk for Alzheimer’s, and then they die. On the other hand, if you get below your personal fat threshold by implementing strategies that can keep fat from building up inside your critical organs, or to get rid of the fat that’s already there—a low carb or very low fat diet, fasting, massive amounts of exercise—then you have a shot at dramatically improving your metabolic health and hopefully reversing some of the damage that occurred while you were chronically hyperinsulinemic. 

Coming Up

I’ll have a post coming up soon that goes into a bit more detail regarding the buildup of fat in the pancreas, specifically, and the implications for diabetes, metabolic syndrome, and their treatment. (The phrase above, “lipotoxocity induced insulin resistance,” plays a big role.) It’s fascinating stuff. Insulin is so, so much more than just a “blood sugar hormone.” And diabetes isn’t solely about carbohydrates. (What? Did she really just say that? Yes. Yes, I did. All will be explained soon!)

If you’re new here and you haven’t already read my series on insulin, you’ll probably want to do that at some point, but the post I have coming up will make sense even you haven’t read that.

I gave a talk on the personal fat threshold a few weeks ago. I’ll post a link to the video when it’s available. (Honestly, though, this post is far more detailed!) In the meantime, here’s a shorter version I did for Adapt Your Life. (Just one word of caution: I misspoke at ~22:05 when I said the liver & pancreatic fat is "first in, last out." Obviously, I meant to say "last in, first out.")

P.S. If you enjoyed this post and found it educational, please consider supporting my writing through a contribution via PayPal. (I don’t have a Patreon account at this time.) You can send from www.paypal.com to my email address: tuitnutrition@gmail.com. Any and all amounts are welcome and much appreciated. Consider sending just $2 or $3 – buy my next bag of pork rinds or cup of coffee and keep me well caffeinated and fed with low carb foods while I write more posts!  :)

Disclaimer: Amy Berger, MS, CNS, NTP, is not a physician and Tuit Nutrition, LLC, is not a medical practice. The information contained on this site is not intended to diagnose, treat, cure, or prevent any medical condition and is not to be used as a substitute for the care and guidance of a physician. Links in this post and all others may direct you to amazon.com, where I will receive a small amount of the purchase price of any items you buy through my affiliate links.