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Does Sugar Feed Cancer?

Does Sugar Feed Cancer?

The SIO Research Committee is pleased to offer this first installment in a new blog series known as “Myths of Cancer”. In this series we will address some of the most common myths and misperceptions that arise around cancer risk and treatment related to diet and natural health products, as well as other complementary therapies such as yoga, acupuncture and meditation. If you have a question you’d like us to address or comments about this post, please send your suggestions to:

We hope you enjoy the series!
Linda Carlson and Eugene Ahn, Research Co-Chairs.

Co-written by Eugene Ahn, MD and Kristen Trukova, MS, RD, LDN, CNSC, CSO
© 2016 Rising Tide

Eugene Ahn, MD is the medical director of clinical research and medical oncologist at Cancer Treatment Centers of America® (CTCA) at Midwestern Regional Medical Center (Midwestern), and Kristen Trukova, MS, RD, LDN, CNSC, CSO is a clinical oncology dietitian at CTCA® at Midwestern. They are both SIO members and have a passion for education and keeping their communities up to speed on the latest in scientific research. Disclaimer: The opinions expressed here are the authors’ own, and not necessarily those of the Society of Integrative Oncology or Cancer Treatment Centers of America. The SIO and CTCA supports open dialogue between health care practitioners and patients to make sure patients can make informed decisions. As always, your comments and feedback are welcome.

There are so many questions we get from patients in our clinics that are provocative but lack simple answers, and today we tackle one of the most common questions: “Does sugar feed cancer?” To condense the topic into a blog entry, we will not address specifically a ketogenic diet (low carbohydrate and protein, high fat, caloric restriction and fasting diet), but will save that for another blog, so stay tuned!

Quick Answer Box

It’s complicated. But one should feel comfortable taking in sugars through fruits and vegetables due to their higher nutritional value and content that goes with the sugars. Some cancers might become more resistant to treatment with high sugar intake, but the science of predicting which cancers would benefit from a low sugar diet is too early in its infancy to make any general recommendations.

Let’s take a closer look at the science behind this question with the goal of determining a reasonable dietary change to impact both cancer risk and potentially cancer outcomes. One of the best principles in discerning the truth of information available on the internet is being mindful of our desire to over-simplify the complex. Answers given on the internet on this topic tend to make two erroneous assumptions 1) all cancers have the same biology and sensitivity to manipulation of sugar intake, and 2) because diet or excessive sugar consumption may increase risk of cancer, sugar cessation is an adequate treatment for cancer alone.

First, the answer to the question “does sugar feed cancer?” is yes, but it’s important to recognize that all of the cells in our bodies use glucose (blood sugar) for energy. In fact, the brain can only use glucose for energy. Even in a diet that contains absolutely no sugars or carbohydrates, our bodies have processes to convert some of the calories we consume from protein and fat into blood sugar so your brain and other tissues can function (thank goodness).

However, there is scientific evidence that high sugar intake is at least indirectly responsible for increased cancer risk. For example, research has shown that diets excessive in sugary beverages increase the risk of many cancer types ( These studies point to excessive caloric intake from sugar that promotes weight gain and obesity (a known risk factor for several cancers) and secondarily increases insulin and other growth hormones in the body (which as we will learn later, is one of the proposed mechanisms by which high sugar intake could worsen cancer outcomes). What we know sugar does not do is directly damage DNA or cause cancer, but the secondary effects of excessive sugar intake – obesity and increased insulin and insulin-like growth factors – might create an environment where cancer evolution is more likely to occur.

Given that several cancers express the insulin growth factor family of receptors on its surface, it is biochemically plausible that reducing sugar intake and thereby reducing insulin and insulin growth factor levels could help improve cancer outcomes in cancers that gain survival/growth benefits through that signaling pathway. However, this has not been proven yet in rigorous, well-designed randomized clinical trials. The best evidence we have to support this concept comes from animal models. To highlight one study among several, mice implanted with prostate cancer cells that became palpable were randomized to high carbohydrate, high fat meals or low carbohydrate, high fat meals. The investigators found that the mice fed high carbohydrate meals had statistically significant higher insulin and IGF-1 (Insulin Growth Factor-1) levels and body weight as well as nearly two times greater prostate cancer cell growth (Venkateswaran V, 2007).

Evidence is less strong for human studies, but in a retrospective study, investigators found that consumption of sugary beverages correlated to shorter survival with cancers of the upper aero

-digestive tract (Miles FL, 2016). Also, individuals with Laron syndrome (mutations in the growth hormone receptor that lead to severe congenital IGF-1 deficiency, with decreased insulin/IGF-1 signaling) have reduced cancer risk.

The next question you might be asking is, why are these studies focusing on insulin levels and IGF-1 levels and not blood glucose? First, the blood glucose of these mice would likely have been normal. Our bodies have an intricate biochemical system to make sure blood glucose levels stay within a tight range (when out of balance, diabetes ensues) and insulin is a key regulator of this. But the current paradigm of understanding the harmful effects of high glucose intake is rooted in the concept of secondary hyper-insulinemia required to cope with such a lifestyle and the effects insulin, IGF-1 can have on both cancer growth and resistance to conventional treatment such as chemotherapy or hormone therapy.

For the most current understanding of how insulin, IGF1 affect cellular function, see Figure 1.

Sugar figure 1

Djiogue et al 2013 “Insulin resistance and cancer: the role of insulin and IGFs” Endocr Relat Cancer Feb 1 2013 R1-R17

The main point of showing this figure is to demonstrate the futility of making general statements like “sugar feeds cancer”, “insulin feeds cancer” or even “IGF1 feeds cancer”. The figure shows that there are several receptors that can bind insulin or IGF1. How a cancer cell reacts to insulin or IGF1 depends on the context of which, if any, of those receptors lies on its surface. For example, insulin could just simply mediate sugar metabolism (through Insulin Receptor B), or it could deliver proliferation signals through an Insulin Receptor A, IGFR-1 or a hybrid of these two receptors, and speed up cancer growth or make the cancer cells more resistant to conventional cancer treatment. Lastly, if the cell does not have Insulin Receptor A or IGFR-1 on its surface, no effects might be seen.

A closer look at the clinical relevance of the IGF signaling pathways

To avoid confusion, sugar does not specifically drive increased IGF-1 production, but the secondarily increased insulin does suppress production of insulin growth factor binding proteins, which makes IGF-1 more available to both normal and cancer cells (M, 2012). Also, drugs that have been studied in human clinical trials that target and block the IGF1R receptor have been disappointing and benefit has mainly been seen in the subset of patients who have high circulating IGF1 levels. One of the common explanations given for the disappointing results is the degree of “cross-talk” and “redundancy” between the different receptors and signaling pathways, where blocking IGF1R only inhibits one route of several by which cells are given growth stimuli. Additionally, the recent published preclinical study has demonstrated that sucrose and fructose overconsumption in mice greatly accelerates the onset and progression of breast tumors in three different mouse or human breast tumor models through modulation of inflammatory pathways, independent of weight change or blood sugar (Jiang Y, Cancer Research, 2016).

So what should I do about sugars?

Although not reviewed here, there are many long-term benefits of reducing sugar intake such as weight control. Several studies have shown women who gain weight after breast cancer diagnosis trend towards worse cancer specific outcomes and clear improvement in all-cause mortality (Playdon MC, 2015). The best anyone can say with the current science is that limiting sugar intake for someone dealing with cancer diagnosis will improve overall health and weight, and reduce side effects of cancer treatment (sugar intake can worsen hot flashes from anti-hormonal treatment). It might also enhance the benefits of conventional treatment (surgery, chemotherapy and radiation) and reduce risk of future cancer diagnoses. And for a subset of the cancers diagnosed, there might be a benefit in reducing sugar intake and secondary insulin and IGF1 availability as well as reducing inflammation on actual cancer outcomes, but the data is limited to animal studies and specific cancer cell lines.

So if one were inclined, the 2015 Dietary Guidelines for Americans encourage a limit of only 10 percent of calories per day from added sugars. For the average person, this means only 200 calories (50gm) from added sugars out of 2000 calories total should be consumed. This is a tough order. For example, a 12oz. can of soda or a single serving size of your favorite sweetened yogurt likely contains up to 40 gm of added sugars. One teaspoon of sugar is equal to four grams of sugar. Thus, sugary beverages which include soda, fruit juices, sports drinks, energy drinks and specialty sweetened coffees should be consumed only occasionally. Are these guidelines effective enough to harness a potential anti-cancer effect? We do not know. But, if your baseline sugar intake is greater than 50gm/day currently, chances are your overall health will eventually be compromised.

But thinking further, what does this mean for brown sugar, raw sugar, honey, molasses, maple syrup and jam? Beyond sweeteners, what about foods that contain natural sugars, as in fruits and plain yogurt, as well as added sugars, which include just about everything you can think of from ketchup to bread? What about carbohydrates, like starches, fruits and milks, which are broken down into sugars? What is left to eat?

Keep in mind that a plant-based diet has been found to be cancer protective. Choosing whole grains, vegetables, beans and fruits in the right portion provides important phytochemicals, antioxidants, electrolytes and fiber in addition to the carbohydrates. One key to success is to avoid “empty calories” such as soda, refined grains and highly processed foods, where very little nutritional value is being provided outside of the calories. And take the time to read the sugar content on the food labels. Find the cereals and yogurts with the least sugar possible. Eat your fruit to get more fiber/pulp in lieu of juices. And be aware that too much portions of a healthy food can still make it unhealthy from a caloric standpoint.

Finally, malnutrition and severe weight loss, especially muscle weight, is very common during cancer treatment. Adequate nutrition is critical. It has been shown that weight loss and malnutrition during cancer treatment decreases tolerability of cancer therapy and is associated with worse outcomes (Barret M, 2011). Any dietary change that results in a lower caloric intake should be reviewed by your health care provider, and other foods might be required to meet nutritional needs. Making weight loss the only end point for your dietary and lifestyle choices could lead to harmful outcomes, so please seek guidance from an available dietitian.v

Eugene Ahn

Breast medical oncologist and integrative oncologist at City of Hope Chicago SIO VP Communications Associate Professor City of Hope Director of Clinical Research at COH Chicago/Atlanta/Phoenix