1. What happens when we eat carbohydrates?
2. What happens when we consume too many carbohydrates or refined carbohydrates?
3. What happens when we consume too many carbohydrates (in-depth version)?
4. Studies on insulin resistance and vessel damage
5. Can't I just take medication?
6. Glycemic Index & Glycemic Index
7.Why does the glycemic load matter?
8. Glycemic Load examples and takeaways
9. My carbohydrate choices
10. Conclusions
What happens when we eat carbohydrates?
When you eat a meal containing carbohydrates, your body breaks them down into a sugar molecule called glucose and are absorbed into your blood stream just like most things that you eat. Now you have glucose circulating through your blood stream and the body needs to do something with this.
Having high levels of glucose in your blood stream for a long time is a very bad thing! This is why type II diabetics are put on insulin or medications that help them lower glucose. We need to get glucose down to prevent things like diabetic nephropathy (small vessel damage in the kidneys), diabetic neuropathy (damage to nerves in the feet), and diabetic retinopathy (damage to the retina in the eye). You might be thinking to yourself that you are not a diabetic but all of this still applies to you.
When we get enough glucose swimming around in the blood, your pancreas, an organ located in the center of your abdomen, gets happy and secretes a substance called insulin. This is the stuff that type I diabetics cannot make, so they have to receive this through an insulin pump. Insulin is necessary so that your muscles and fat cells can snatch the glucose out of the blood stream and put it away in storage until it is needed (1). This is how it is supposed to work! Now, let's look at how the body deals when we get too much glucose in the blood stream over a long period of time.
What happens when we consume too many carbohydrates or refined carbohydrates?
Now that you know how it is supposed to happen, here's what happens when we overdo it with carbohydrates. When we constantly bombard ourselves with processed and refined carbohydrates, our body gets worse and worse at snatching the extra glucose out of our blood stream. Sciency people like to call this 'insulin resistance' which is the precursor to Type II diabetes.
Now, because we aren't able to get this excess glucose out of our blood stream, our bodies send out more insulin to get the job done. The result is elevated levels of insulin in our blood stream! We've already talked about the damaging effects of too much glucose in the blood stream above, but what about too much insulin?
When we have too much insulin in the presence of elevated blood sugar, it leads to the development of fatty plaques in the arteries. This is where atherosclerosis and vascular diseases like coronary artery disease come into play (2).
That's the simple version of things. In the next section, I am going to explain this process that I just described in much more detail. It gets a little nitty gritty, but for those of you who are interested, have at it!
What happens when we consume too many carbohydrates (in-depth version)?
Glucose is monitored by the beta-cells of the islets of Langerhan. This is just fancy for saying that there are cells in the pancreas that measure the glucose in the blood and secrete insulin when we need it. When the glucose concentration begins to elevate after we've eaten carbohydrates, the beta-cells take in the glucose through transporters like GLUT2 (Glucose Transporter 2) and break it down (metabolize it) to form ATP which is the cellular currency of energy. As a result, ADP gets converted to ATP, so there is more ATP and less ADP. Because there is an increased concentration of ATP in relation to ADP within the beta-cells, this concentration gradient causes K-ATP channels to close and voltage-gated calcium channels to open on the surface of the beta-cells. All this means is that this allows Ca2+ (calcium ions) to flow into the cell and increases the Ca2+ concentration inside the pancreatic beta-cell. The influx of Ca2+ causes the exocytosis (release of) insulin from within the beta-cell into the circulatory system. There is generally a repolarization (recharging) period of the beta-cells which is why it is common to see a bi-phasic or pulsatile release of insulin (1). Okay, so that's step one, insulin is out and ready for action!
Let's look at what would normally happen when insulin is released. First, insulin binds to the insulin receptors on the blood vessel walls (endothelial lining) which results in the activation of two different molecules: (1) insulin receptor substrate (IRS) and (2) Shc.
1. IRS activates the eNOS (endothelial nitric oxide) pathway which produces nitric oxide. Sources refer to this the anti-atherogenic arm of the insulin pathway, meaning it prevents fatty plaques from developing in the arteries.
2. Sch activates another pathway called the MAPK pathway that increases endothelian-1 (ET-1) expression. This is the atherogenic arm of the insulin pathway, that leads to the development of fatty plaques in the arteries.
So here we have two different pathways that respond to the presence of insulin. One pathway prevents the accumulation of fatty plaques, and the other promotes it. When all is well and good, these two pathways can dance in harmony and vascular health is the result.
Let's say we eat lots of refined carbohydrates that are described in the Part 1 blog post and really spike our blood sugar. This requires a great insulin response to deal with the excess sugar that was eaten. Do this over a long period of time and you can become insulin-resistant. When someone becomes insulin resistant, they are unable to use this first pathway that we talked about (the eNOS) pathway. The result is that they cannot produce nitric oxide or vasodilate their vessels as well. Remember this is the pathway that prevents fatty plaques from developing in the arteries. However, the second MAPK pathway that produces ET-1 is preserved which promotes the cellular division of cells in the vascular lining and leads to the development of fatty plaques in the arteries. This is believed to be the cause of the vascular effects associated with insulin resistance (2).
Studies on insulin resistance and vessel damage
A study was performed using human umbilical vein endothelial cells where they exposed the cells to high concentrations of glucose and then to physiological levels (levels that would normally be found in the body) of insulin. It turns out that the cells were not able to activate the eNOS pathway to prevent the fatty plaques from developing in the arteries. However, the cells were still able to utilize the MAPK pathway that leads to the development of fatty plaques and this pathway was actually upregulated!
Break this down for me you say? Okay, here it goes. We eat too much ice cream. Our blood sugar spikes. We do this for years. Our cells stop taking up all of the glucose. We secrete more insulin to push the extra glucose into our cells. Insulin rises. We become insulin resistant and diabetic. We damage our blood vessel linings because the high amount of insulin only promotes the pathway that causes fatty plaques to develop. We have atherosclerosis (clogged arteries), coronary artery disease (heart disease), diabetes, and damaged kidneys, eyes, and nerves.
Can't I just take medication?
This next point applies to all people, including diabetics: just that your pancreas works or that you take enough insulin to get your glucose number down does not mean that you are doing your body a favor by feeding it high concentrations of carbohydrates (sugar)! Remember, it's not just about getting your glucose number down. It's also about how much insulin you have in your system and too much insulin/impaired insulin signaling contributes to the vessel damage that we just talked about. You can't medicate yourself around consuming excess carbohydrate, even if your glucometer gives you a good value (2).
Glycemic Index & Glycemic Load
In order to understand the foods that contribute to glucose and insulin spikes and the processes that contribute to vessel disease that we discussed above, we need to cover a few definitions. The first being "glycemic index." Glycemic index is measured by the amount that a food raises your blood sugar over the first two hours after consuming it. High glycemic index foods raise your blood sugar the most, while low glycemic index foods do not raise it as aggressively (3).
The second definition to cover is glycemic load. Glycemic load is calculated by multiplying the amount of available carbohydrates in a single serving of a food by the glycemic index of the given food. Don't be confused by that definition. Glycemic load is just a better way of understanding the overall effect that eating a normal portion of a food has on your body's glucose response, rather than comparing equal amounts of different food. A better way of putting this is to compare a teaspoon of honey to a large carrot. The honey can certainly raise your blood sugar more than a carrot can if you were to eat the same amount of honey as you were to eat carrot, but because we are only talking about one teaspoon of honey as opposed to a whole carrot, the carrot is going to have a greater overall effect on your blood glucose response because a normal portion of carrots is much bigger than a normal portion of honey. This overall response is what we consider the glycemic load.
Why does the glycemic load matter?
The higher the glycemic load, the greater the elevation of blood glucose and the greater demand on insulin to respond to this elevation of glucose. The lower the glycemic load, the lower the glucose and insulin effect from the food (3).
Why is this important? Diets with a high glycemic are independently associated with an increased risk of type 2 diabetes, cardiovascular disease, and cancers (3).
Glycemic Load examples and takeaways
Chocolate cake: 20
Vanilla cake: 24
Strawberry cupcake: 19
Pancakes: 39
Coke: 16
Apple juice: 13
Gatorade: 12
Bagel: 25
Wheat bread: 10
White bread: 10
Cornflakes: 18
Froot Loops: 18
White Rice: 23
Wheat Crackers: 10
Ice cream: 8
Full-fat Milk: 3
Apple: 6
Banana: 12
Cherries: 3
Peach: 5
Pineapple: 7
Chickpeas: 8
Kidney Beans: 7
Lentils: 5
Linguine: 22
Macaroni: 23
Spaghetti: 21
Cashews: 3
Peanuts: 1
Agave: 1
Fructose: 2
Glucose: 10
Honey: 10
Corn: 9
Beets: 5
Carrots: 3
Potato: 26
Sweet Potato: 17
As you can see based on the values above that items like linguine, macaroni, and spaghetti have relatively high glycemic loads compared to fruits like an apple or cherries. Wait a minute, spaghetti has a higher glycemic load than honey! And Glucose! And Fructose! Let's look at glucose and spaghetti and remember what I told you earlier.
Glucose actually has a glycemic index of 99 +/- 3 (not on the chart). Spaghetti has a glycemic index of 44 +/- 3. Glucose can spike your blood sugar twice as well as spaghetti, but the average serving of glucose is only 10 grams, where the average serving of spaghetti is 180 grams! That's why the total glucose burden (the glycemic load) is more from the spaghetti than the glucose. This does not make glucose a healthier food by any means. Glycemic load is just a tool that helps quantify the overall effect that a normal serving of a food has on an average person's blood sugar.
As you can see from these relative glycemic loads, that grains, dessert items, and pastas generally incur the greatest glycemic load. In general, it is a good rule of thumb to eliminate pastas, breads, dessert items, and anything that gets your sweet tooth excited for glycemic reasons. This is not even taking into consideration the other harmful effects that these foods may confer such as their lectin concentration, refined and highly processed nature, genetic modification, and preservatives and additives that may be present in these foods.
If you observe the recipes that I use with my clients (whether you are a current client or if you view the monthly menu on my site), all of the recipes that I use are aimed to be relatively low in glycemic index and glycemic load to lessen the glucose and insulin responses that are associated with insulin resistance, Type II Diabetes, and atherosclerosis.
My carbohydrate choices
Roots and tubers as great carbohydrate sources including but not limited to sweet potato, parsnip, beets, potato, and carrots! Other produce that contains some carbohydrate, though not as high as a concentration include broccoli, brussels sprouts, cabbage, sugar peas, tomatoes, and onions. Seasonal fruits, especially berries (blueberries, raspberries, strawberries, and blackberries) are a great source in moderation and are packed with antioxidants and nutrients as well. Other grain free sources like cassava flour based tortillas or cassava chips are also on my menu.
Conclusion
When we eat carbohydrates, we digest these and as a result our blood glucose rises. To compensate for the rise in blood glucose, our body wants to store away the excess glucose by secreting insulin from the pancreas. Insulin normally promotes two pathways, the eNOS pathway that prevents fatty deposits from forming in the vessels, and the MAPK pathway that promotes fatty deposits forming in the vessels. Under normal conditions, these pathways are at an equilibrium. When we eat refined carbohydrates or excess carbohydrates, we elevate our blood glucose more frequently and demand our pancreas to produce higher amounts of insulin. Over time, insulin signaling becomes worse and we call this insulin resistance, the precursor to type 2 diabetes. In addition, the insulin signaling with the eNOS pathway is decreased, while the MAPK pathway that promotes fatty deposits to form remains, leading to the formation of fatty plaques in the blood vessels. Glycemic index and glycemic load are valuable tools to monitor how much of an effect a specific food has on raising your glucose and therefore how great of an insulin response is required. Substituting higher glycemic foods like grains, desserts, and sweets for lower glycemic foods like beets, carrots, or sweet potatoes is likely beneficial for many people, as diets with higher glycemic loads are associated with insulin resistance, type 2 diabetes, and atherosclerosis (fatty deposits in blood vessels). I hope that this was a sweet, sweet read (pun intended, lol)!
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