Introducing the Power of IGF-1
IGF-1 stands for “insulin-like growth factor.” It’s called “insulin-like” because its molecular structure is very similar to insulin, so much so that insulin and IGF-1 actually compete for the same receptors on the cell membrane.1
You can think of both insulin and IGF-1 as fuel nozzles that are used to feed your cells. But the differences in the way they do it is critical to fat loss and critical to your health.
When you are a sugar burner, the primary pump delivering fuel for your cells is insulin. And this is a problem because insulin is the fat-making hormone, delivering fat-making messages that we’d prefer our cells not hear.
What’s more, insulin is darn good at its job—the more insulin you’ve got circulating in your bloodstream, the fatter you get.
IGF-1, on the other hand, is a fat-burning hormone. It therefore stands to reason that when you’re a fat-burner, your cells are “listening” to IGF-1.
Which is exactly what you want.
Whenever you eat food, your blood sugar goes up. In response to this increase in blood sugar, the pancreas releases insulin into the bloodstream. Insulin’s job is to act as a sugar wrangler, gathering all that excess sugar up and delivering it to your cells where it can be “burned” for energy.
When you eat the standard American diet full of high-carb foods (including those you’ve been told are good for you like “low-fat” cereals, pasta, rice, potatoes and bread), your blood sugar rises a lot—and the pancreas has a heck of a time keeping up with the demand for insulin.
The problem is compounded because the muscle cells—which are supposed to welcome all this sugar in—are pretty much on vacation, at least if you’re living a sedentary life and they eventually stop paying attention when insulin comes knocking on their door. They become resistant to its effects—a condition known, not surprisingly, as insulin resistance.
Now you’ve got high-blood sugar, which is bad enough, and you’ve also got high levels of insulin. The insulin keeps knocking on the doors of the muscle cells but the muscle cells aren’t having it.
Eventually, insulin turns to the fat cells, which are quite happy to have the sugar payload. When the fat cells can’t take any more, they too become resistant to insulin. Now you’re on your way to full-blown diabetes, obesity and all the rest of the stuff that comes with insulin resistance.
Not a pretty picture.
Changing Your Fuel Pump
Theoretically, insulin should only be elevated for a short time, a few times a day, right after you’ve eaten. Which is a good thing. The rest of the time, your cells should be getting their fuel primarily from the IGF-1 fuel pump.
Why is this important? Pull up a chair.
IGF-1 feeds the cells much like insulin does, but it also sends a number of important signals to the body at the same time. One of those signals is to rebuild and repair your most metabolically active tissue—your M.A.T.—which includes your organs, glands, bones and nerves.
And what does IGF-1 use to feed all those cells? Your fat. That’s why it also sends a signal that tells your fat cells to open up and release all of the stored fat inside. as opposed to filling them up the way insulin does. IFG-1 breaks into the fat storage banks, releasing fat from the fat cells so that it can be used to feed the rest of your body.
Think about it. When you have enough IGF-1 around you burn fat naturally, your heart, brain, bones, and nerves are strengthened, and aging is slowed down. Indeed research has shown that heart disease risk increases by 38% for every 40 ng/ml decrease in IGF-1 levels;2 and those with the lowest levels of IGF-1 have a 51% greater risk of Alzheimer’s3 and a 23% increased chance of hip and spine fractures.4 (People spend a lot of money at anti-aging clinics to be treated with expensive drugs which, among other things, raise their IGF-1 levels to youthful levels.)
Needless to say, you want IGF-1 to be your primary fuel pump, and you want insulin to hang around just long enough to take care of excess blood sugar, do a couple of other housecleaning chores and then get the heck out of the way so IGF-1 can go back to work keeping your metabolic machinery in good working order.
Unfortunately, when you’ve got too much fat on your butt, thighs and belly, that’s not what happens.
Now here’s where it gets interesting. Because insulin and IGF-1 are so molecularly similar, they can—and frequently do—compete for the same receptors on your cells.5
A Competition for Cellular Attention
Imagine the receptors on the cells as parking spaces, and insulin and IGF-1 as cars. The drivers of the insulin cars are way more aggressive, and when they’re around, they grab all the parking spaces, leaving IGF-1 to cruise around with nowhere to land.
Remember, IGF-1’s metabolic message is to build, repair and spare muscle, protein, bone, your brain and nerves, organs, glands, and connective tissue, and to burn fat. Obviously, we want to increase IGF-1 activity while reducing insulin levels. That way the fat-burner signal is much stronger—and much longer—than the fat-maker signal.
Makes sense, right?
But when you’ve got a ton of aggressive insulin cars driving around in your bloodstream and vying for the parking spaces on your cells, guess which message gets into the cell?
Yup. The message that gets through loud and clear is, unfortunately, “Store fat! And shut the doors to the fat cells so nothing escapes!”
Now don’t get me wrong, insulin does a number of really good things in the body—like, for example, getting amino acids (protein) into the muscle cells and increasing the uptake of potassium.
Insulin’s not a “bad” hormone. In fact, we’re going to make judicious and strategic use of insulin by driving it up at specific times in specific ways that will actually help you burn fat.
But for the most part, it’s critical that insulin passes the “Goldilocks” test—not too much, not too little.
Aside from a few strategic insulin spikes, we want to reduce our insulin levels so that IGF-1 can grab those parking spots and send its muscle-sparing, fat-burning messages to the cells.
And that’s where a lot of diet programs simply stop. They bring down insulin levels—which you can easily do with a low-carb diet—and call it a day. What makes The Metabolic Factor unique is that it focuses not only on driving insulin down, but driving IGF-1 up. And it takes into account your entire hormonal symphony, which is where the real action is when it comes to fat burning.
1 Yongmei, Y. et al. “Reciprocal Interactions of Insulin and Insulin-Like Growth Factor 1 in Receptor-Mediated Transport across the Blood-Brain Barrier.” Endocrinology. 2006. 147(6).
2 Laughlin, G., Barrett-Connor, E., Cirqui, M. and D. Kritz-Silverstein. The Prospective Association of Serum Insulin-Like Growth Factor I (IGF-I) and IGF-Binding Protein-1 Levels with All Cause and Cardiovascular Disease Mortality in Older Adults: The Rancho Bernardo Study. The Journal of Clinical Endocrinology & Metabolism. 2003. DOI: http://dx.doi.org/10.1210/jc.2003-030967
3 Westwood, Andrew J., et al. “Insulin-like growth factor-1 and risk of Alzheimer dementia and brain atrophy.” Neurology. 2014. 82(18): 1613-1619.
4 Ohlsson, Claes, et al. “Older men with low serum IGF‐1 have an increased risk of incident fractures: The MrOS Sweden study.” Journal of bone and mineral research. 2011. (26)4: 865-872.