ITIS -- It's the Insulin, Stupid (pt 5/8)

In part 3 of this series, we covered the role of insulin as a counter-regulatory force that keeps catabolic glucagon in check. (Reminder: in the absence of insulin, glucagon run amok will cause the body to waste away by catabolizing its own muscle and fat tissue for fuel). And in part 4, I mentioned that lowering blood glucose (BG) is probably not insulin’s primary function, but rather, one of the ways by which insulin helps keep BG in check gives us a clue as to one of its more important functions: it is anti-catabolic. While several other hormones break tissue down in order to provide glucose and fatty acids to fuel the body, insulin builds tissue up.

That’s right. Insulin is an anabolic hormone. It stimulates tissue growth, be it of muscle or adipose. (If the phrase “stimulates tissue growth” reminds you of cancer, hang onto that thought. I’ll be addressing insulin eventually in the cancer series.) If a lack or insufficiency of insulin causes type 1 diabetics to waste away due to catabolizing muscle and fat, then that tells us that insulin helps build up muscle and fat. (Or, at the very least, insulin hinders its breakdown.) Veteran bodybuilders can tell you that insulin spikes (properly timed) can help build muscle mass, and veteran low-carbers can tell you that insulin spikes can help build fat mass. Remember: insulin isn’t “toxic.” It’s all about context. Since we’re focusing on obesity here, we’ll leave muscle out of the discussion and focus on fat.

If you want to burn fat, it is counterproductive to regularly consume sugar- and starch-dense carbohydrates, which, via insulin, send your body 
the message to NOT burn fat.

By orchestrating the body’s conversion of excess carbohydrate into fat, and its subsequent deposition & storage in adipose tissue, the anabolic effect of insulin becomes obvious. It becomes obvious on our thighs, hips, bellies, upper arms, chins, and also in and around our organs. As I wrote about in detail back in the fuel partitioning series, remember: the human body has only a small capacity to store glucose & glycogen, but we can store a darn near unlimited amount of fat.  

Insulin is not the only thing that causes us to store fat, but it’s surely one of the most powerful forces that does so. As a general principle, when insulin levels are high, the body will have a mostly glucose-based metabolism, and when insulin levels are low, the metabolism will shift to running mostly on fat and possibly some ketones. So, as a general rule, if we want to be mobilizing and oxidizing (“burning”) fat, we need to keep insulin levels low. Maybe not all the time, but certainly they need to be low more often and for longer periods of time than they’re high. (Anyone who’s had success on Kiefer’s CarbNite or Carb Backloading programs can attest that insulin spikes can be very helpful for body composition, in the correct context.) The concept many of us are familiar with here is, we can be sugar-burners, or we can be fat-burners.

HOWEVER: As is my habit, in the interest of being physiologically accurate, let me take a moment here to remind everyone that being a sugar- or fat-burner is not a binary thing. It’s not a yes/no, on/off scenario. It is not the case that the human body—every single cell in every single organ, tissue, and system—is either fueled by glucose OR fueled by fat. Different parts of the body are running on different fuels concurrently, and the proportions of different fuel types that are used can change, based on the type of activity a tissue is engaged in. I laid out the details in this post from the fuel partitioning series, but here are two quick examples:  1) Red blood cells have no mitochondria. Therefore, they must use glucose exclusively. They can’t use fats or ketones. They literally do not have the physiological means. 2) Depending on the intensity of physical exercise and an individual's level of conditioning, muscle cells can use predominantly glucose or predominantly fatty acids.

Okay. That was just to remind us that, when we’re talking about elevated insulin being anti-lipolytic, it’s not that using fat is 100% shut off, and when insulin is low, using glucose is 100% shut off. The body is a hybrid engine that can and does run on a variety of fuels concurrently. 

How This Plays Out in the Body

Just as elevated insulin is not the only thing that causes the body to store fat, dietary carbohydrate is not the only thing that elevates insulin. But since it is surely one of the most powerful forces that does so, let’s take a look at how consuming carbohydrates affects insulin. (Starchy and sugary carbs, that is. I’m not talking about asparagus and eggplant here, if ya know what I mean.)

Keeping in mind that “three square meals a day” is a construct of the modern world, and that our dietary ancestors likely had no concept of breakfast, lunch, and dinner, let’s see how a few different eating scenarios affect insulin. I am pretty much the worst artist in the world, so please forgive the crudeness of the following graphs. (There’s a reason I stick to writing!) They are not to any exact scale at all; I’m simply using them to illustrate a point.

Obviously, the shape of the graphs will differ from person to person, depending on individual insulin sensitivity. We all know people who are freakishly insulin sensitive, right? They just don’t seem to need a whole lot of it, almost no matter what they eat. For the rest of us, who weren’t born so lucky, it seems like we can spike our insulin by just looking at a cupcake. So, yes, individual differences will mean that not everyone’s insulin rises to the same degree upon ingestion of exactly the same foods. (The rise in insulin levels might also depend on one's physiological state at the time of the meal -- is it right after a workout? After a fast?) These are crude illustrations to help demonstrate a general idea.

The thing to focus on here is area under the curve (AUC): the total amount and duration of insulin excursions from baseline. To be honest with you, I don’t know which is worse, physiologically, for the body: having a very high insulin level for a short period of time, or a moderately high-ish level for a much longer amount of time. (I have my theories, but I’m not ready to share them with the world. Kiefer definitely has his theories, and, based on the success he’s had with clients, I’d have to guess that, for body composition purposes, it’s far better to have isolated large, but quick, spikes, at the proper time, than it is to have only slightly elevated insulin, but have it for many hours a day, every day.)

Okay, on to my terrible artwork!

This is your basic three meals a day. Assuming a mixed diet of protein, fat, and carbohydrate, we’ve got three times where insulin rises and then falls. You'll notice insulin tends to take longer to come back to baseline than it does to hit its peak when it's rising. Again, individual variation is a factor here, but this is how it generally works. If this person has decent insulin sensitivity, and insulin doesn’t remain elevated for several hours after eating, then they’re back to baseline by the time they start their next meal. Even though there are several hours throughout the day where insulin is elevated, there are also pockets of time during which it's back to baseline and lipolysis is free to proceed. Not really any issues here, except wondering if it’s wise to have this happen three times a day, every day, for your entire life.

This next scenario looks at three meals a day, plus snacks—as many nutritionists and dietitians recommend, for the purpose of “keeping blood sugar up.” (Seriously…) Even in someone with decent insulin sensitivity, if they’re reaching for a snack two hours after a meal, their insulin levels are probably still elevated from that meal. Maybe not as high as they were just one hour after the meal, but they haven’t come back to baseline yet, and here we are, raising them up again. 

If you find yourself needing to snack not long after a meal, either your meal wasn’t large enough, or its composition of protein, fat, and carbohydrate wasn’t a good match for your individual metabolic constitution. (And, of course, sometimes we find ourselves snacking for emotional reasons. Hey, we’re human; no shame in that. But let’s acknowledge that that has nothing to do with actual physiological hunger.) Regardless, this is not a place you want to be. The insulin area under the curve is massive. There is almost no point during which there is any significant mobilization of fat. This person is a sugar-burner all the way, and they are also probably fatigued and riddled with brain fog. (You would be, too, if you had no access to the lovely, long-and steady-burning fuel that is fat.) They probably also lack metabolic flexibility, since their cells are not accustomed to needing to use fatty acids for fuel, so their cellular energy factories (mitochondria) are not up to the task of easily switching between glucose and fat. This might be why these people get hypoglycemic, which results in their perceived need to be constantly snacking & grazing.

Bottom line: You can see why the conventional advice to be eating all day long is absolutely disastrous—particularly when conventional advice also advises these constant snacks & grazes to consist of fat-free or low-fat carbohydrates: rice cakes; granola bars; whole grain crackers; fruit juice; un-buttered popcorn; applesauce; etc. So what if they're low-calorie? This is a roadmap for chronic elevation of insulin. And it’s exactly why the low-fat & low-calorie diet recommendations backfired so stunningly for so many of us.

Keep in mind, too, that the hypothetical people in the graph above are not already insulin resistant. If they were already T2 diabetic or insulin resistant, there’s a good chance they would start their day with insulin already elevated, before they even eat breakfast. In the insulin-spiking onslaught that is low-fat & low-calorie nutritional dogma, these folks don’t stand a chance. They are f_ck_d from the moment they wake up. (Assuming they have a conventional breakfast, that is. They could turn things around in short order by having a nice LCHF meal, or skipping breakfast altogether.)

(By the way: this is probably the single best explanation of “metabolic flexibility” that I know of. More than worth your time if you’re interested in this. I’ll be talking more about this in a future post about why some people struggle to lose fat even on a low-carb diet.)


Now let’s look at a scenario with less frequent eating. This shows two meals a day. People who do intermittent fasting on a 16:8 schedule might have patterns like this. (16:8 meaning, they consume food only during 8 hours of the day, and don’t eat for the other 16 hours. Strategies run the gamut, but most people who do this eat 2 large-ish meals.)

Even with two big insulin spikes per day, this person spends a significant amount of time in the low insulin zone. The total insulin AUC is smaller; they spend more of their time in fat-mobilizing mode than in fat-storing mode. And this graph assumes the two meals are typical combinations of fat, protein, and starchy carbs. Imagine how much lower the AUC for insulin would be if these were two low-carb meals per day. The meals would probably be relatively high in protein, so there would still be rises in insulin, but lower ones than I’m showing here with my piss-poor attempts at illustrating this. Nevertheless, even with starch-containing meals, if someone only eats twice a day, with no snacks, you can see how the total AUC for insulin would still be lower than someone eating the same way three times a day.

And, finally, let’s look at the presumptive graph of someone with good insulin sensitivity who sticks to a low-carb diet:

The AUC for insulin is very low. At breakfast, insulin barely budges. Bacon & eggs, perhaps? Fatty sausage with sautéed greens and a cup of coffee with heavy cream or coconut oil? Very little insulin action!

Just for kicks, let’s think about what the graph might look like for a low-carber who, for whatever reasons, chooses to snack a few times throughout the day. Assuming they stick to low-carb snacks (for example: hard-boiled eggs; a spoonful of almond butter; nuts; cold bacon; cheese; salami & pepperoni; olives, raw vegetables.), insulin might rise a little bit each time, but overall, the total AUC for insulin would still be small, and this person would spend the majority of their time in fat-mobilizing territory. Fasting is all well and good, but there really is a lot to be said for individual variation. From my own personal experience, a while back, I was maintaining my very best body composition ever while eating low-carb (but not ketogenic) and having snacks – low-carb snacks that would not induce large insulin excursions. 

Disclaimer: I’m trying to be kinder to myself these days and embrace some of the body positivity and "health at every size" messages out there. I have some terrible, terrible body image demons that will likely never go away completely, and they regularly interfere with my enjoyment of life. So, to be clear, I’m not saying that chronically elevated insulin is bad because it makes some people accumulate body fat. If you like yourself (and/or your partner[s]) a little rounder, no problemo! It takes all kinds of people to make the world go ‘round, and being “thin” certainly shouldn’t be anyone’s end-all be-all goal in life. But if you happen to desire losing some body fat, and your personal aesthetic preference is for you to have a trimmer body, then yes, you will want to avoid marinating your cells in a constant bath of insulin.

And, before we get the wrong idea here, let’s say it together: being “thin” doesn’t automatically translate to being healthy. I have deliberately used the word “thin” here rather than lean, because they are not the same thing. Someone who is “thin” is not necessarily lean, and what shows on the outside often does not represent what’s going on inside. Chronic hyperinsulinemia doesn’t always result in the accumulation of adipose tissue. As we discussed in part 2, sometimes, it results in dementia, or infertility, or hypertension, or tinnitus, or heart disease, or kidney failure—regardless of body weight.

So, then, why do some people gain weight, and others don’t? And what about what I’ve said in the past about body fat accumulation possibly being protective? What is this crazy talk?

Find out next time...

In the meantime, I’ll leave you with another fabulous (and instructive!) image created by Ted Naiman, MD, who is a far more skilled artist than I am.

Continue on to part 6 of this series.

Remember: Amy Berger, M.S., 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.