As we get ready for NYNY2016, I’d like to share some of the science behind your body’s use of hormones.
The 411 on Insulin – the transport hormone
If you really want to geek out on Insulin, google it. This article is written for the lay person and aims to shed some light on some pretty deep topics. So I am really only going to give you information on what I think is relevant and pertinent to you and weight loss.
When you consume protein and/or carbs (mostly carbs, it takes a relatively high amount of protein to get an insulin release) you get an insulin release. The amount of insulin released is directly related to the glucose load in the blood stream. Insulin’s job is to pull glucose out of the blood stream and shuttle it into cells. Ideally we want that glucose to go to muscles and working tissue. Your body just wants it out of the blood stream as high levels of circulating glucose can cause a lot of systemic damage, like diabetes.
If insulin can’t push glucose into the muscle cells, it will push it into any cell that it can. Every cell in your body runs off of glucose so your body can always put glucose some where, unless you’re insulin resistant – that’s another story.
Insulin production also signals a slew of other hormones to either be produced or stopped from being produced. For instance, insulin production causes Leptin to stop being produced.
The 411 on Leptin – the “I’m full/satiety” hormone.
Everyone, for the most part has heard of insulin, but few people have heard of the hormone Leptin. Leptin essentially tells your brain that you are full and don’t need any more calories. Rise in insulin = (generally) increase in Leptin, “I’m Full!” Leptin is opposed by Ghrelin (the feed me hormone). When Leptin goes up, Ghrelin goes down and vice versa.
Some interesting side notes:
- Leptin is produced from fat cells (adipose tissue).
- You would think the more fat cells you have, the more Leptin you produce, which is correct. But, obese individuals can actually become Leptin resistant – which is one of the reasons why they can put away so many calories and claim that they are always hungry.
- As body fat % declines, Leptin levels rise! That’s right, your body is fighting you from losing fat by telling you to eat more food! Crazy shit, I know.
The 411 on Ghrelin – the “I’m Hungry” hormone.
Ghrelin is opposed to Leptin, as Leptin levels rise, Ghrelin levels should go down. Ghrelin is essentially controlled by the volume of food in your stomach and how much your stomach stretches. Less volume = less stretch = more ghrelin. Your stomach is roughly the size of a softball when it’s totally empty but can expand to the size of a large cantaloupe (roughly). So, if you chow down on some food your stomach will signal Ghrelin to stop being produced.
Fructose’s effect on Insulin
There is no effect, fructose does not raise insulin levels. Why? For the sake of this article it’s not important. All you need to know is that fructose doesn’t cause an insulin release.
And because fructose doesn’t cause an insulin release, there is no subsequent Leptin release, which means, as far as some aspects of your body are concerned…you still need calories and you’re still hungry!
Ever wonder why someone can throw down a huge calorie load from McDonalds a large coke, a big mac, large fries and still be hungry a few hours later? That’s roughly a days worth of calories for most people in one meal!
Initially they are satiated for the sole reason that Ghrelin (hunger hormone) is essentially controlled by stretch receptors in your stomach. Lots of food volume means lower production of Ghrelin, low food volume in your stomach, means higher production of Ghrelin. Makes sense when you think about it, nothing in your stomach = hunger hormone to be produced.
Leptin is normally produced as insulin levels rise. But! In this case, insulin doesn’t rise, so no increase in Leptin. So, this is what your body thinks “WTF IS GOING ON HERE?! I just ate something, my stomach is full, but I am still hungry?!”
For you overachievers, here is a great geeky post from the American Journal of Clinical Nutrition –http://ajcn.nutrition.org/content/76/5/911.full
“Both plasma insulin and leptin act in the central nervous system in the long-term regulation of energy homeostasis. Because fructose does not stimulate insulin secretion from pancreatic β cells (this statement can also be found in the book Ross et al. “Modern nutrition in health and disease”, page 43, left column, bottom of the paragraph continued from page 42) the consumption of foods and beverages containing fructose produces smaller postprandial insulin excursions than does consumption of glucose-containing carbohydrate. Because leptin production is regulated by insulin responses to meals, fructose consumption also reduces circulating leptin concentrations. The combined effects of lowered circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the likelihood of weight gain and its associated metabolic sequelae.”
KDR = KNOWLEDGE DRIVEN RESULTS.
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