Every cell in your body has chemical (metabolic) reactions occurring that either consume or release energy. These reactions are divided into two classes: Anabolic and catabolic; the former class of reactions utilize free energy to manufacture cellular constituents while the latter class of reactions release energy by breaking down complex molecules (such as glucose).
Myriad factors determine the rate and frequency at which anabolic and catabolic reactions take place. These factors include things like endocrine signaling, muscular contraction, energy balance, immune function, etc.
With a better grasp of the aforementioned reactions, let’s take a look at how insulin modulates them (and ultimately impacts body composition).
Insulin is a peptide hormone manufactured by the pancreas that primarily works to lower blood sugar levels by increasing activity of glucose transport proteins (GLUTs). It is a potent anabolic (storage) hormone that induces protein synthesis throughout the whole body when dietary amino acids are replete.[1] Moreover, when insulin levels are elevated with limited amino acids available, protein synthesis does not increase (however protein breakdown decreases).[2]
Don’t misconstrue the previous points to mean “more insulin is better,” because there appears to be a ‘cap’ to its effects on muscle protein synthesis.[3] With that in mind, let’s take a look at why insulin’s anabolic effects can be harmful.
If your main goal is to lose fat and keep it off, it stands to reason that combining large amounts of fat and sugar together into a meal is not the greatest idea. Reason being is that most sugars, especially processed sugars like high-fructose corn syrup, cause insulin levels to increase significantly and more rapidly than complex carbohydrates and fiber from whole grains.
Thus, when you combine rapid surges in insulin secretion from sugar with large amounts of fat from food, your body has an excessive amount of triglycerides and sugar available to store in adipose/fat tissue. Essentially, large amount of dietary fat and sugar are the perfect cocktail for fat gain in the body.
Thus, carbs as a whole tend to get a bad rap because many obese individuals eat a diet loaded with simple sugars while remaining highly sedentary. Intuitively, people assume that eliminating carbs altogether will solve everything. However, it just won’t remain a practical long-term lifestyle to avoid carbohydrates, and by keeping them at a level to support energy and mood (among a host of other benefits) while maintaining a fat-loss regimen will only be a positive factor. Therefore, knowing your genetic tendencies and body type is key for formulating a proper diet.
Make no mistake that this has all been strongly validated by scientific research, as studies show a tight correlation between insulin levels and fat gain.[4] Moreover, insulin resistance is also correlated with fat gain.[5] This makes sense physiologically since insulin resistance is when cells become ‘numb’ to the primary effects of insulin (which is to remove sugar from the blood).
Unfortunately, what this means is that beta cells in the pancreas keep secreting insulin because blood sugar levels don’t drop as they normally would, resulting in a state where excessive amounts of insulin are circulating in the blood. Eventually, this manifests into full on diabetes and your body no longer handles carbohydrates the way it should.
So what are the consequences of insulin resistance? Take a look at the chart below and you’ll get a better grasp of why it’s not a good problem to have:
Being highly insulin sensitive, on the other hand, means your cells respond efficiently to insulin’s signaling. Essentially, your body is better at putting carbohydrates to proper use and you’re less likely to store them as adipose tissue (body fat).
We all have that one friend who can eat seemingly endless amounts of junk food like donuts and pizza without gaining an ounce of fat. Are they just a genetic anomaly amongst the rest of us? Well, yes and no.
Such individuals can get away with eating so much because they have very fast metabolic rates and high sensitivity to insulin; basically, they are the physiological inverse of obese individuals.
There are three basic somatotypes (body shapes/structures) in humans: ectomorph, endomorph and mesomorph. Ectomorphs are generally skinny, fairly lean, highly insulin sensitive and have a hard time gaining muscle, or any weight at all (these are the individuals we just alluded to).
Endomorphs generally have a pear-shaped body structure and tend to put on fat easier than the other somatotypes due to lower insulin sensitivity and metabolic rate. And lastly, mesomorphs are a sort of sweet-spot between ectomorphs and endomorphs; they are naturally broad-shouldered and muscular, and tend to put on a good amount of weight (mostly muscle) with diligent exercise and proper dieting.
While it is a bummer to think that some of us can just look at a donut and gain weight, there is something we can learn from our slim, ectomorphic counterparts: Genetics do matter, and you need to feed your body accordingly.
For endomorphs, this generally means less carbohydrates and more protein (no matter what the goal is). Ectomorphs and mesomorphs typically need more carbohydrates to support muscle growth, and don’t need to restrict carbs as much to lose body fat. Remember, some sugar in your diet is fine and won’t in and of itself magically make you gain weight. Just be smart about your intake. Ultimately, your body type and genetic makeup are what determine how you can diet effectively, along with lifestyle.
[1] Sakurai, Y., Aarsland, A., Herndon, D. N., Chinkes, D. L., Pierre, E., Nguyen, T. T., ... & Wolfe, R. R. (1995). Stimulation of muscle protein synthesis by long-term insulin infusion in severely burned patients. Annals of surgery, 222(3), 283.
[2] Gelfand, R. A., & Barrett, E. J. (1987). Effect of physiologic hyperinsulinemia on skeletal muscle protein synthesis and breakdown in man. Journal of Clinical Investigation, 80(1), 1.
[3] Garlick, P. J., & Grant, I. (1988). Amino acid infusion increases the sensitivity of muscle protein synthesis in vivo to insulin. Effect of branched-chain amino acids. Biochemical Journal, 254(2), 579-584.
[4] Ward, K. D., Sparrow, D., Vokonas, P. S., Willett, W. C., Landsberg, L., & Weiss, S. T. (1994). The relationships of abdominal obesity, hyperinsulinemia and saturated fat intake to serum lipid levels: the Normative Aging Study. International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity, 18(3), 137-144.
[5] DeFronzo, R. A., & Ferrannini, E. (1991). Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. Diabetes care, 14(3), 173-194.
