The Heart of the Matter (Part II)

The purpose of this post is to explain in relatively simple terms how excessive carbohydrate consumption increases triglyceride (fat) and blood pressure levels (aka the risk factors for developing heart disease). I will preface this by making clear that this is a complex process that I will not pretend to understand in its entirety; however, there are some basic concepts behind the process of arterial plaque formation that I’m aiming to outline.

For the sake of clarity, I will start off with an obvious but crucial fact: all carbohydrates we consume (e.g. candy, white flour, whole wheat bread, oatmeal, pasta, legumes, high sugar fruits, agave nectar, evaporated cane juice, quinoa, etc)  are broken down into sugar, or glucose.

Complex carbohydrates take longer to break down, so they cause a more gradual (and consequently less damaging) spike in our blood sugar; unfortunately, in the end, they all become blood sugar which triggers the need for insulin, a hormone secreted by the pancreas that manages our blood sugar levels. This leads into a discussion of the variables in developing heart disease: 

1. Insulin Resistance:  When you ingest sugar, blood sugar rises, and the pancreas releases the amount of insulin needed to take the excess glucose and store it in the liver and muscles as glycogen. This is certainly useful for having energy reserves stored for later if need be.

But if your  glycogen reserves are already filled up (depending your activeness and the amount of sugar you ate), then there is no room for that excess glucose in the liver or muscles. This begins the process of insulin resistance: the pancreas needs to pump out more insulin to get the same effect, the excess glucose and insulin remain in the blood stream for longer, and and the sugar is eventually stored in fat cells.

2. Glycation: Glucose should not be present in the bloodstream for longer than necessary; the longer it floats in the bloodstream, the higher the risk of glycation. Glycation occurs when a sugar molecule like glucose or fructose  binds to a protein  or fat molecule without the protective help of an enzyme. Without an enzyme to moderate the reaction that protein or fat molecule gets damaged.

More importantly, this reaction leads to advanced glycated end-products (AGEs). AGEs can degrade any cell in the body, and the accumulation of their destruction signals an inflammatory response.

3.Inflammation: Generally speaking, inflammation is defined as the immune system’s response to damaged cells, foreign invaders, toxins, etc. If you hurt your leg, it might swell and bruise. While it hurts, this is the immune system initiating the healing process. This is an example of a straightforward case of acute inflammation.

Chronic, low-level inflammation, on the other hand, keeps your body in a state of alarm: the immune system is waging a constant battle that is neither significantly traumatic nor ignorable. This battle often requires the expenditure of cytokines and various types of  infection-fighting white blood cells like monocytes and macrophages. The longer the inflammation goes on, the higher the risk of tissue damage.  In short, regular, excessive carb/sugar consumption leads to chronic AGEs which lead to chronic inflammation.

Below is an image of a glucose molecule binding to a protein molecule to produce an AGE that triggers an immune response from a macrophage:

Luckily, there are ways to quantify inflammation and blood glucose levels. Inflammation is often measured via a white blood cell count (WBC) and C-Reactive Protein (CRP) level. A 1-h plasma glucose test measures short-term (one hour to be exact) blood sugar levels, and Hemoglobin A1c (HbA1c) measures long-term blood glucose levels. Knowing this, let’s tie the evidence together:

  • There is a link between inflammation and insulin resistance: this study establishes a connection between insulin resistance and inflammation, again, in nondiabetic people. Inflammatory markers like CRP and white blood cell counters were associated with insulin resistance, and CRP levels were positively correlated to weight.
  • High blood sugar levels have been studied as a risk factor for heart disease. Another study also finds a connection between HbA1c levels (long-term blood glucose) and heart disease.
  • AGEs are correlated to to inflammation and atherosclerosis in diabetics.
  • Chronic inflammation is also strongly correlated to heart disease. One study observed a higher incidence of aortic inflammation with people who have inflammatory rheumatic disease than those with no inflammatory diseases.

So if atherosclerosis isn’t the mere accumulation of dietary fat and cholesterol, then how does it form?

To be continued….


2 responses to this post.

  1. Posted by MTD on January 18, 2011 at 2:49 pm

    Very impressed with the overview provided in part II. You touch upon a lot of key players in the development of atherosclerotic plaques. In addition, there is a lot of ongoing research to further characterize the roles of insulin resistance, inflammation, cytokines, etc…


  2. Thank you! The more information I find, the more fascinating the whole topic becomes.


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