Eat Like a Flintstone (Part 2)

Insulin has an especially dramatic influence on enzymes called lipases. Lipases are like little Pac Men who run around your body, releasing body fat from its cushy containers so it can be shuttled into muscle cells to get burned off (yeah!). When insulin levels are high, it hits the “off” switch on lipases, putting them into a holding pattern until further notice. In fact, the most prominent lipase involved in fat burning is called Hormone Sensitive Lipase or HSL for short.[1] HSL is the premiere key holder that unlocks those fat storage containers which make you leaner. Unfortunately, the more insulin that’s present, the less HSL is available to release fat for energy and the end result is you become fatter (not so yeah).

As insulin is blocking fat burning it’s also creating an internal environment that is ripe for fat storage. It accomplishes this act through the aid of another lipase enzyme—this one’s called Lipoprotein lipase or LPL for short and it is so effective at bloating fat cells that some obesity researchers even call it ‘the Gatekeeper of Fat Storage’. It’s next to impossible for the body to store fat without a certain amount of insulin floating around. As you can see, insulin is something we need, but we don’t want too much of it. Otherwise, we end up with a body that acts as a 24/7 fat-storing factory (as too many people already experience)!

Controlling Insulin

Almost any food—including the mere thought of food—can cause insulin release, but carbohydrates are the primary driver to a flood of insulin. High-carb foods—especially the highly processed and refined variety—cause glucose levels in your blood to shoot way up.[2] However, the body doesn’t work very well when glucose gets too high, so it sends out a stream of insulin to control the rising tide of glucose. Gobs of insulin will definitely drive glucose down, but it will also turn the vast majority of that glucose into newly formed fat.

On the other hand, when insulin levels are under control, the body swiftly transitions into fat burning mode. Normal insulin levels cause lipases to spring into action. Also, a hormone often viewed as insulin’s opposite, glucagon, starts to rise. Glucagon travels around the body, ordering fat cells to relax and let go of the fat they’re clinging to.

It’s accurate to view eating and lifestyle as a hormonal event. In a primitive dietary world made up of fresh—and local—produce (including roots, shoots, seeds and nuts) and wild game meat, our hormones were never a problem – in other words there weren’t many, if any, obese cavemen or ladies . If a caveman was lucky enough to stumble upon a beehive filled with honey or a bush sprouting plump berries, insulin was there to process the carbohydrates properly. But for the most part, the diet that our pancreas was designed for, only called insulin into action on a part-time basis. Our modern-day fast food/processed/high glycemic diets forces our pancreas to work double or triple shifts! Our body was simply not designed to metabolize all these carbs. The real kicker is that, because of our ravenous appetite for insulin-stimulating processed foods, the weight we’ve been accumulating over the last few decades is pure, unadulterated fat, which isn’t just unsightly but brings with it a whole host of health issues to boot![3]

In Abundant Health,
Brad King, MS, MFS
TransformingHealthing.com

[1] Magré, J., et al. (1998) Human hormone-sensitive lipase: genetic mapping, identification of a new dinucleotide repeat, and association with obesity and NIDDM. Diabetes. 47:284-286

[2] Ludwig, D. S. (2000) Dietary glycemic index and obesity. J. Nutr. 130:280S-283S.

[3] Due A, Larsen TM, Mu H, Hermansen K, Stender S, Astrup A: Comparison of 3 ad libitum diets for weight-loss maintenance, risk of cardiovascular disease, and diabetes: a 6-mo randomized, controlled trial. Am J Clin Nutr 2008, 88(5):1232-1241

 

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