“I read that sugar feeds cancer.”

This is one of the most common statements I hear from my patients.

In fairness, this statement brings the fear of saying goodbye to carbohydrates and some of their favorite treats.

If you look back at one of my previous posts, 5 Cancer Fighting Foods to Avoid, you may be shocked to see sugar is not one of the top five foods. So, if I haven’t listed in the top 5 does that mean sugar feeds cancer?

The answer is yes. BUT —  it also feeds all of our healthy cells! Hence, why didn’t make it on the top five foods to avoid. Let me explain.

Any time we eat carbohydrates our body turns it into sugar, or glucose. There are many types of sugar (e.g. maltose, sucrose, etc.) but for simplicity purposes, let’s use the words sugar and glucose interchangeably.

Glucose = Sugar

Glucose is the primary fuel source for EVERY cell in our body. Our muscles prefer it. Our heart prefers it. Even our brain prefers it. It is so important to our body’s functions, our body can make glucose from fat and muscle if it doesn’t have enough. (This is a process called gluconeogenesis for my science nerds out there.)

So, would cancer die without sugar? Yes.

But, what would happen to our healthy cells? They too would die or be unable to THRIVE and fight against cancer.

Another way to look at it is, would cancer die without oxygen? Absolutely.

But, so would we.

Research shows it is actually sugar’s relationship to insulin or more precisely insulin resistance, and the result of high insulin levels which influences cancer growth the most–along with the risk for other types of chronic disease. (1)

What causes high levels of insulin and insulin resistance? Surprisingly enough, sugar nor a carbohydrate-rich diet causes insulin resistance. Rather, a diet high in fat and animal products (which are naturally high in or higher in fat) (2).

Simply put, fat and the toxic breakdown of it within our cells causes insulin to not work correctly. When insulin does not work correctly, glucose cannot enter the cell causing it to stay within the bloodstream resulting in high blood sugars. This is insulin resistance.

Instead of focusing on a low-carbohydrate, high-fat diet — which is so popular these days — evidence strongly supports a diet focused on carbohydrate-rich, whole plant foods as a cornerstone for preventing and fighting cancer.

Although research supports a high carbohydrate diet, it DOES NOT support carbohydrates sourced from added sugar or refined carbohydrates. These foods are deficient in essential nutrients and phytochemicals that are important to human function and preventing disease.  

Carbohydrates from whole grains, fruits, vegetables, and legumes are associated with longer life and reduced risk of cancer and chronic disease (3), whereas the processed and refined foods (common carbohydrates in the standard American diet) do not.

Let me sum this up.

It is not sugar itself (or, glucose) that increases the risk and progression of cancer, but rather its relationship with high insulin levels and insulin resistance — commonly caused by a high fat diet.

Understanding the relationship between blood sugar, insulin, insulin resistance, and fat can be difficult to understand. So if you are still a little confused, Dr. Greger from NutritionFacts.org, as always, does an unbelievable job presenting the most available research regarding this confusing topic in his 5-minute video you can view below.

References:

1. Arcidacono, B., Iritano, S., Nocera, A., Possidente, K., Nevolo, M., Ventura, V., . . . Brunetti, A. (2012). Insulin Resistance and Cancer Risk: An Overview of the Pathogenetic Mechanisms. Journal of Diabetes Research, 2012. Retrieved January 11, 2019, from https://www.hindawi.com/journals/jdr/2012/789174/.

2. Greger, M., MD, FACLM. (2017, January 6). Retrieved January 08, 2019, from https://nutritionfacts.org/video/what-causes-insulin-resistance/.

3. Sahyoun NR, Jacques PF, Zhang XL, et al. Whole-grain intake is inversely associated with metabolic syndrome and mortality in older adults. Am J Clin Nutr. 2006 Jan; 83(1):124-31.