I want to repeat this crucial point:
Hormones control every single activity in our bodies, including our metabolism of fat.
But for now we continue with the superstar – Insulin! I keep repeating that there are many players in this game, and I will introduce them in due course, but by far the most common cause of metabolic breakdown today is insulin dis-regulation.
In my last post I flirted with the idea that from our evolutionary perspective, it was important to make sure that we never end up with a low blood glucose (BG) level because that would kill us. We examined the chart below, and saw that we have a triple redundancy to make sure of that. Back in the day, getting BG up at the appropriate time was lifesaving. Today, however, keeping BG (and insulin) up all the time is quite literally killing us.
Insulin is not toxic. It is a damn handy hormone to have—when your body responds to it properly.
Well, let’s look at the chart again from the perspective of ‘fatty acid’. Three of these hormones—glucagon, epinephrine, and cortisol—all “stimulate fatty acid release from adipose tissue.” You know what that means, right? That’s lipolysis—the breaking down of fat—stored body fat! But now look at insulin. It is the only one—the only one—of these four hormones that “stimulates fatty acid synthesis & storage after a high-carbohydrate meal.” And you know what that means, right? The storing of fat on the body. Indeed, THIS may be the primary role of insulin: inhibition of lipolysis. (Or, anti-catabolism, in general — the building up, rather than the breaking down, of tissue. An anabolic role).
With 3 hormones initiating fat breakdown and just 1, teensy weensy 1, initiating fat storage, why are we becoming a fat world ?!!
For arguments sake, even if we consider that lowering blood glucose is the primary function of insulin ( and not building up of fat tissue), then the method by which this is accomplished sheds a lot of light on what insulin does and explains the rest of insulin’s effects more satisfactorily.
In tackling the role of insulin on the accumulation of adipose tissue, first we need to explore just a few more things about insulin’s biochemical & physiological roles. After that, we’ll see how it all plays out in the real world—that is, in our body.
Think about what happens when you eat a meal. The sugar (glucose) is released and taken into your body through the digestion process, during which it enters your bloodstream. Your body responds to the glucose in your blood by secreting insulin from your pancreas into your bloodstream. Insulin escorts the glucose out of the bloodstream and into the cells. That’s what we vaguely know, right? Let’s see how this happens.
How insulin does this is another story. Insulin doesn’t actually escort glucose out of the bloodstream and into cells. What insulin does is act more like a signaling agent: insulin binds to a receptor on the surface of the cell membrane, and in response to the binding of insulin, glucose transporters (GLUTs) are moved (or “translocated”) from inside the cell to span the cell membrane. It’s the GLUTs that actually suck the glucose into the cell. And, just so we know the full story here, some GLUTs require insulin to stimulate their translocation; others don’t. So insulin is not the only way glucose can get into cells (physical activity is a great way to induce “non-insulin mediated glucose uptake.”)
Insulin: A must for Fat tissue
So, insulin’s action enables GLUT’s to move the glucose from the bloodstream into the cell, thus lowering our blood-glucose levels. What else does insulin do? Well, whereas cortisol, epinephrine, and glucagon are catabolic, insulin is anabolic. The first three break things down; insulin builds things up. What does it build up? At the very least, it stimulates the buildup of glycogen; the synthesis of structural & skeletal protein; and the synthesis of fatty acids via the conversion of glucose into triglycerides. (See, insulin is a hormone, not an enzyme. Again, as a hormone, it’s more of a signaling agent than something that actually does anything, itself. Insulin stimulates or inhibits various biochemical processes by affecting enzymes, which in turn, actually make things happen at the cellular level. So when we say that ‘ insulin does x, y, and z’ it actually means that ‘insulin signals other players to do x, y and z’)
Two of the enzymes insulin affects are hormone sensitive lipase (HSL) and lipoprotein lipase (LPL).
When we look at an untreated type-1 diabetics, it is easy to figure out that (barring any other hormonal complication) it is near impossible to accumulate body fat in the absence of insulin. On the other end, we need only to look at an insulin-dependent type-2 diabetic with poorly managed blood glucose to understand that sustained, elevated insulin levels make it near impossible not to accumulate excess body fat.
The reason is partly this: Insulin stimulates an enzyme that lets fat get into adipose cells, and it inhibits an enzyme that allows fat to get out of adipose cells. Talk about a double-whammy. Insulin is like a prison guard, who helps lock triglycerides into fat cells, and then stands there in order to make sure they never get back out. What the …..!
This requires a bit of explanation. Triglycerides—that is, three fatty acid molecules connected to a glycerol backbone—are too large to enter and leave cells freely. Many of you must remember this molecule if you have ever done a blood panel test!! They can’t cross the cell membrane. Therefore, in order for triglycerides to get into the cell, they have to be broken down into individual fatty acids. The primary enzyme that does this is called lipoprotein lipase. Once inside the cell, the fatty acids reassemble themselves into triglycerides (or TGLs, for short). So you see the problem now? If TGLs are too large to cross the cell membrane and get inside, then we probably need some other enzyme to break them back down into individual fatty acids before they can be released back out of the adipose cells. After all, that’s what we want, right? Fatty acids to be released from adipose tissue so they can be used as fuel somewhere else, such as in cardiac muscle or skeletal muscle cells—that is, we want to burn fat.
Well, the enzyme that breaks TGLs back down into fatty acids inside the cells is hormone-sensitive lipase (HSL), and, as I mentioned earlier, insulin inhibits the action of this enzyme (there are lots of other things that might influence HSL, but insulin is a biggie). Basically you want this enzyme to be rocking!!
So, you can clearly see how insulin affects both the storage and mobilization of fatty acids. Leaving other potential influencing mechanisms aside for now, you can also see why, in chronically hyperinsulinemic people (people with elevated levels of insulin and inhibited HSL action), it is near impossible to lose body fat. The prison guard is always at the gate, never giving the inmates a chance to escape. And you can see why lowering insulin levels—be that through a low-carbohydrate intake, a moderated protein intake, fasting, physical activity, pharmaceutical drugs, nutritional supplements, or some combination of all of these—can result in fatty acids finally being able to leave the adipose cells.
FEAST – FEAST – FEAST – FEAST
Going back to the graph above, if we eat 6 times a day, big meals or small meals, insulin will be elevated to move the excess energy (glucose from carbs) to the cells that need it. If the cells say, “sorry Insulin, I am full, not opening the gates”, then insulin moves to other cells and knocks. When our system as a whole is overloaded with energy (as is the likely case when we eat constantly and our muscles and liver can store only a limited amount) and nobody opens the gates, insulin has no option but the move the excess glucose into the fat cells for storage. Besides, a constant state of feeding (insulin influx) means that the prison guard is always at the gate giving the inmates (fats) no chance to escape. A classic double-whammy!!
Bottom line: As long as insulin levels are high (area under the green curve), it will be extremely difficult to lose body fat.
Insulin, in and of itself, is a good and necessary thing. It promotes the storage of nutrients after all. In our natural, primal state, this was an essential process. Even in our modern lives, this storage process is still vital. (We just have a nasty habit of flooding the system with energy these days.)
“Insulin is vital for lipogenesis. Its role as a lipogenic hormone is underplayed, but we know that without insulin, you can’t get fat.”
–Dr. Roger Unger
Just picture the modified graph below. This is what our ancestors did, this is what we did growing up, until Big Food with the help of accommodating nutritionists and professionals advised us otherwise.
FEAST – FAMINE – FEAST – FAMINE
This was the natural cycle of meals when I was growing up in the 70’s and 80’s. Snacking was taboo. It was during the ‘blue’ periods between meals that we burned our fat reserves. It was during this period that insulin was low and the enzyme HSL was rocking to unlock the fat stores to supply us with endless energy hitting balls until the street lights came on and it was time to go home. Our moms didn’t obsess about us being hungry. This was a normal daily cycle and obesity was rare.
‘Get back to where you once belonged’ …..John Lennon/Paul McCartney
This is the starting point. First and foremost, we have to make sure that we do not put any edible stuff in our mouths in-between meals (yes, chewing gum does count). May not be the end game for everybody though, but a great starting point.
As a second step, we will talk about lifestyle based adjustments and of course, most importantly, what you put inside your mouth.
In the modern world, when we use our cars to drive around the block to the supermarket, or worse, when we can shop online and get things delivered to our doorstep, when we have smart homes to WhatsApp our loved ones in the other room, even this kind of traditional meal times may lead to excess energy. Excess energy will lead to sustained high levels of insulin (hyperinsulinemia) and lipolysis (inhibit fat burning).
Our ancestors, even our parents a couple of decades ago, used to work much much harder, walk much more, move much more than we do today. I feel, this feeding pattern is fine for growing kids, professional sportsmen, and high physical activity individuals, but NOT for ‘the new normal’ modern sedentary lifestyle.
For sedentary folks, folks sitting behind computers all day, you really need to modify the eating window according to your comfort zone. There is no such thing as the best way or the only way prescribed in some fancy article or by some high profile nutritionist of big star ‘celebs’!! As you can see, your breakfast is the first meal that stops your fat burning. But then again, it is not for everybody to skip it either. I never have breakfast, but that’s me. Believe me guys, if you’ve understood even a little bit of what you have read so far, you need to FIRST induce low levels of circulating insulin at some point in the day to even access your fat stores. There are many ways to achieve it and I will give you a few alternatives in the coming posts.
You can turn from a sugar-junkie to a fat burner in many different ways AS LONG AS you understand the actions of the hormones (mainly insulin) and as long as you understand your energy requirement for your lifestyle.