Insulin: the very name of this hormone seems to strike the most fear in the hearts of…anyone, really. Not just those seeking to lose weight. But how many of us really understand what it does (both the good and the bad), and how it can make fat-loss attempts harder?
PS: To be perfectly honest, this is pushing the limits of my comfort zone and what I feel equipped to talk about with any semblance of authority, and as such I’m not going to be dealing with (either type of) diabetes in this article, since that’s well and clearly outside of my wheelhouse of nonexistent expertise. As with any content, but particularly with reference to medical-ish territory I cautiously wade into, usual disclaimers apply.
What is insulin?
Let’s start from the very beginning. Insulin is an anabolic hormone and is produced by islets of Langerhans, aka beta cells (β-cells), in the pancreas.
The function of insulin that most of us are probably familiar with is to regulate blood glucose levels by stimulating the uptake of blood glucose into cells (one of the results of this is the process by which carbohydrates are converted into fat). But that’s not all insulin does, and insulin isn’t an inherently bad thing by any means.
A super simplified description of how insulin works is: you eat carbohydrates which get broken down, blood glucose levels increase, which signals the pancreas to ramp up production and secretion of insulin, so it can help shuttle blood glucose out of the bloodstream and into various cells in your body.
What does insulin do?
The key thing to note about insulin is that it’s anabolic, which is to say it relates to constructive metabolism, i.e. the synthesis of complex molecules from simpler ones (usually for energy storage needs). Yes, one aspect of that is its role in fat production and storage, but always bear in mind the First Law of Thermodynamics, i.e. if you are not consuming a surplus of energy relative to your body’s expenditure, you can’t grow fat out of thin air.
Alongside increased fat synthesis and decreased lipolysis (breakdown of fats into fatty acids), insulin is also responsible for synthesis of glycogen (the awesome little energy bars your muscles use), decreases in proteolysis (breakdown of proteins and peptides into amino acids) and autophagy (catabolising the body’s own tissues as a metabolic process), and increases in amino acid uptake. It has a positive effect on cognitive processes, plays a role in regulation of blood pressure (via its effects on arterial muscle tone), and even plays a role in promoting serotonin uptake! (That last nugget is my favourite bit of insulin-related trivia.)
Insulin resistance
For all intents and purposes, it seems like insulin’s the real MVP here — how did it go from there to becoming persona non grata in the health/fitness world? The real issue isn’t with insulin itself, but with insulin sensitivity, or the lack thereof, i.e. insulin resistance (IR).
The worst part about IR, to me, is the chicken-and-egg negative cycle of how it’s a system that compounds itself: every time a cell is exposed to insulin, its production of glucose transporter type 4 (GLUT4) reduces, which is to say that insulin causes (a kind of) insulin resistance. However, in the presence of higher levels of insulin, this down-regulation is thrown into a (bad) positive-feedback loop, further increasing the need for higher insulin levels.
Insulin also prevents lipolysis of stored fat — with IR, lipolysis is elevated, which means there’s also a higher incidence of free fatty acids in the bloodstream, which increases hepatic glucogenolysis (breakdown of liver glycogen to produce more blood glucose), prevents insulin-dependent glucose uptake, and contributes to further IR.
Introducing Ash, and understanding IR
NB: This is an incredibly reductive and simplistic description of some of the physiological effects IR can have on a person (the insulin/glucose/carbohydrate units and ratios are more or less made up) but just roll with it so I can illustrate how things work. Ash, in case it needs to be said, is fictional.
Ash is a middle-aged person with a growing belly, who works long hours at a desk job in a first-world city, and doesn’t really relish the thought of being a gym rat (especially not alongside all those super-ripped bodybuilders who don’t seem to do anything but work out and oil their beautiful muscles). Ash hasn’t been to the gym or hit their daily step goal in 3 weeks, and has just eaten a delicious pastry for breakfast. Because of their sedentary lifestyle, Ash’s muscles are more or less always at capacity for glycogen storage (we deplete glycogen stores when we exercise/use our muscles, or when we run out of food). Ash sounds familiar to a lot of you, don’t they?
Now, let’s imagine that one pastry contained 10 units of simple carbohydrates, which have now resulted in 10 units of blood glucose circulating around Ash’s system. This is 10 units more than their resting blood glucose levels, so Ash’s brain notes this elevated blood glucose level, and tells the β-cells in their pancreas to release 10 units of insulin to shuttle this extra blood glucose into cells. Each unit of insulin picks up a unit of glucose and goes knocking on cell doors, asking GLUT4 to help a buddy out and let one of their refugees in. Let’s say, after canvassing the entire neighbourhood, Team Insulin managed to find homes for 5 units of blood glucose. Now all muscles are at Full Tank with regards to their glycogen storage capacity, but there’s still 5 units of blood glucose floating around. Ash’s brain has been busy with a bunch of other processes, and doesn’t realise what’s going on, but notes that there’s still an elevated blood glucose level, and therefore signals the β-cells to release an additional 5 units of insulin. Now, Ash has got 5 units of glucose and 10 units of insulin floating around with nowhere to go.
When Ash’s blood insulin levels are elevated, this actually sends a signal to their brain that what they need is more carbs. At the same time, Ash is feeling fatigued, lethargic, irritable, and sleepy. All of which tend to result in a higher level of internal disinhibition, so even though Ash probably knows at some level that the last thing they need is a doughnut, they walk past the pantry at work and see a box of Krispy Kremes, and end up grabbing one. Let’s assume this doughnut contributes another 10 units of glucose circulating around Ash’s system — so if we’re keeping count, we’ve now got 15 units of blood glucose, 10 units of blood insulin, all still with nowhere to go. What happens next? You’ve guessed it: brain tells β-cells to release another 5 units of insulin; wash, rinse, repeat.
Maybe, if Ash is lucky, someone’s told them to go for a jog, or they manage to eke out a little time and energy to hit the gym that night after work (and boy what a SLOG of a workout that was — poorly moderated blood insulin and glucose levels contribute to those feelings of fatigue, irritability, and lethargy). In which case, they’ve made a little ‘space’ in their muscles which could theoretically receive a little more of that blood glucose into the muscle glycogen holding tanks, but we’ve still got a system-wide case of Door Bitch mode happening with all the GLUT4, compounded by the repeated exposure to the little insulin soldiers constantly banging on all those doors.
And, as I’m sure all of you have probably experienced personally by now, the sheer brute force of willpower and stubbornness is painfully finite, even in the most pig-headed of individuals, so even though Ash probably knows, at least at an intellectual level, that exercise will help, they’re too goddamn exhausted and tired of being told to move more when it feels as though every fibre of their body is screaming at them to rest and eat some more damn carbs.
So how now, brown cow?
It’s not all doom and gloom though. And while the last thing someone like Ash may want to hear is that weight loss and regular exercise will get them the most bang for their buck, hopefully understanding why they feel the way they do can help them to understand how it will help, and therefore give them that little extra fuel to push through the initial grind (hollaback to my previous issue on Acceptance Based Therapy).
One study estimates that each 500-calorie increase in energy expenditure per week reduces the risk of type 2 diabetes by 6% — that’s a mere 71 cals/day, so it’s not as if you need to force yourself into the gym for 2 hours thrice a week, it’s simply a matter of getting an extra 30 minutes or so of walking into your day. And if you do have time for some dedicated exercise on top of hitting your step goal, another study found that women who engaged in “vigorous exercise” had reduced their risk of type 2 diabetes by a whopping 33%.
And while I’m not a huge fan of recommending low-carb diets for the average person as a blanket fat-loss intervention, this is one instance in which it does make a lot of sense, whether or not that’s your preferred style of eating, at least in the short term.
Another intervention that can ameliorate some IR and type 2—related effects is supplementing with fish oils, and while supplementing with vitamin D hasn’t been shown to reduce IR, vitamin D deficiencies are associated with IR and β-cell dysfunction, so it may be worth getting checked out to ensure that you aren’t deficient.
That said, none of this negates how hard it can feel, or how hard it may be, to do what you have to do, but if there’s a chance this helps you feel a little less impotent, or at least that you can take comfort in how it’s not simply some lack of willpower that may be making you feel the way you do, then…I hope there’s some comfort to be derived from that.