May 14, 2016

How might sugar fuel cancer growth?

Foods with a high glycaemic index (GI) or meals with a high glycaemic load increase cancer risk via two pathways – directly influencing biochemical pathways that promote cancer development and growth; indirectly by contributing to the development of diseases that then have an influence on cancer.

Indirect mechanisms sugar and refined carbohydrates and risk cancer

Epidemiologic studies have independently linked foods with a high GI with a significant risk of obesity, diabetes, dental caries and depression, which, in turn, contribute to the risk of subsequent cancer and poorer outcomes after cancer treatments. The mechanisms of how these are linked to cancer are now described:


Several studies have linked consumption of high sugar diets with obesity [Te Morenga]. Sugary drinks particularly pack on the pounds because energy in liquid form is less satiating (signaling to body to stop eating when you have had enough calories) than when derived from solid foods, resulting in higher consumption than necessary [Di Meglio]. Sugary drinks or meals also trigger a damaging yo-yoing effect on blood glucose and insulin levels – the body responds to an initial “addictive” sugar rush by rapidly increasing insulin levels that metabolises the excess sugar into energy storage, such as glycogen in the liver. As sugar has only been around in the human diet for the last 150 years, our body thinks that this level of sugar hitting the blood stream must be associated with a very large meal of complex fats and carbohydrate so it over produces insulin that then causes sugar levels to drop (hypoglycaemia), stimulating hunger, fatigue and lightheadedness. The natural reaction to this is to consume another high calorific sugary snack or drink, which gives instance relieve but triggers the process starts all over again.

Fortunately, it’s never too late to cut out sugar, a meta-analysis of 68 studies showed that individuals who embarked on diet plans which reduced sugar intake instead of more slow release energy sources lead to a significant decrease in body weight [Te Morenga]. Obesity, especially in postmenopausal women, increases levels of oestrogen, insulin-like growth factor (IGF) and other hormones, such as leptin, all of which in laboratory experiments increase proliferation and markers of aggressiveness and spread of cancer cells [Surmacz, Calle]. No surprise then that numerous studies have linked obesity with a greater risk of cancer but also a greater risk of relapse and worse overall survival after successful cancer treatments [Palmqvist, Meyerhardt, Freedland].

Diabetes and glucose intolerance

Independent from the risk from obesity, high excess sugar intake directly increases the risk of diabetes by overloading the insulin pathways [Basu]. Individuals with type 2 diabetes (coming on later in life) have higher serum insulin levels as the pancreas produces more to try and overcome insulin resistance within the normal cells. Unfortunately, cancer cells have insulin receptors which if stimulated cause them to grow faster and be more aggressive. It is not a surprise, therefore, that numerous studies have shown that the risk of developing a range of solid tumours is increased with type 2 diabetes [Giovannucci]. Even without a formal diagnosis of diabetes, elevated blood glucose (glucose intolerance) has been shown to be a risk for cancer. Researchers, funded by the WCRF, measured blood sugar levels in over half a million people from Norway, Austria, and Sweden and found that those with excess blood sugar, particularly overweight women were more likely both to develop a range of cancers and to die from it [Stocks].


An analyses on data from 3486 participants within the Whitehall II prospective cohort reported that those with a high consumption of sugary drinks, sweetened desserts, chocolates, processed meat and fried foods had a 58% increased odds of depression [Akbaraly]. Distressing in itself, depression is also linked to increased risk of serious cancer as reported in a study, which followed 41,275 men with prostate cancer from California. They identified 1,894 men with an associated depressive illness and these were 20–80% more likely to die specifically of prostate cancer compared to those with normal mental health [Prasad].


A study, published in the prestigious Journal of the American Medical Association (JAMA), involved 6110 Americans. After several years, those who eat more than 10% of their daily calories as sugar had raised triglyceride levels and low HDL (good) cholesterol levels [Welsh]. Although this lipid pattern is a clear risk for cardiovascular disease it is also known that a higher proportion of LDL (bad cholesterol) compared to the other serum fats is also an increased risk factor for prostate and breast cancer independent of other lifestyle habits [Kitahara].

Dental caries

Everyone knows that sugar consumption is a major cause of tooth decay, especially the consumption of boiled sweets, toffies and sugary drinks [Burt]. What is less well known is that dental caries may also be an increased factor for bowel cancer. Two studies, between them looked at more than 100 samples of healthy and cancerous bowel tissue – one from Canada and another from Boston USA and published in the journal Genome. They both found that DNA codes from bacteria, commonly found in dental caries (Fusobacterium) was present in the bowel cancer genes but not normal genes – this raises a strong suspicion that the bacterial DNA traveling through the body interacts with and gets absorbed into gut cells causing them to become cancerous [Kostic].

Direct mechanisms sugar and refined carbohydrates can risk cancer


There are several laboratory studies, which show that high GI foods promote cancer growth directly but the one that was most convincing involved a group of mice with implanted breast cancers. Half were fed sucrose with their usual meal at comparable levels of Western diets and the other half a normal diet. The western diet led to increased tumour growth and metastasis to the lung and liver, when compared with mice fed a non-sugar starch diet [Yang 2015]. This effect was ascribed in part to increased expression of inflammatory markers including 12-lipoxygenase (12-LOX) and its arachidonate metabolites [Yang 2015].

Insulin-like growth factor (IGF)

The section above explained how sugar increases the risk of obesity, which is associated with higher levels of several hormones, which can trigger cancer. Many of these biological changes can also be generated directly, not necessarily with associated obesity. High sugar and insulin levels also lead to direct overproduction of IGF. After binding to its receptor tyrosine kinase, IGF activates several signaling pathways, leading to the inhibition of apoptosis, the promotion of cell growth and angiogenesis [Yu, Frierer]. Higher levels of IGF-1 in humans would therefore be expected to increase tumour growth, and has been reported to be associated with a greater cancer risk [Ryan, Ma]. To substantiate this, two very large international studies involving people with treated bowel cancer both reported those who eat higher GL diets had higher average IGF levels and an increased relapse rate after primary surgery and chemotherapy [Palmqvist, Meyerhardt].

Genetic damage

Studies have found suggested that high sugar levels can result in the formation of oxidative metabolites which increase intracellular free radicals [Bucala]. Certainly markers of single strand DNA breaks have been reported in the presence of hyperglycaemia [Lorenzi]. Other laboratory experiments using Vitamin B6 deficient flies reported that feeding them with pure sugar led to significantly higher direct DNA damage and chromosome instability [Marzio].

Akbaraly T et al Dietary pattern and depressive symptoms in middle age. The British Journal of Psychiatry 2009, 195 (5) 408-413.
Basu S et al , The Relationship of Sugar to Population-Level Diabetes Prevalence: An Econometric Analysis of Repeated Cross-Sectional Data Plos 2013. DOI: 10.1371/journal.pone.0057873
Bucala R et al modification of DNA by reducing sugars: a possible mechanism of nucleic acid aging, age-related dysfunction in gene expression. 1984, Proc Natl Acad Sci USA 81;105-109.
Calle EE and Kaaks R. Obesity, hormones and cancer; epidemiological evidence and proposed mechanism. Nature Reviews Cancer 2004, 4, 579-591.
DiMeglio DP, Mattes RD. Liquid versus solid carbohydrate: effects on food intake and body weight. Int J Obes Relat Metab Disord 2000;24:794-800.
Freedland SJ, Aronson WJ, Kane CJ et al Impact of obesity on biochemical control after radical prostatectomy for clinically localised prostate cancer:. JCO 2011; 22(3) 446-53
Freier S, Weiss O, Eran M, et al.; Expression of the insulin-like growth factors and their receptors in adenocarcinoma of the colon. Gut 1999; 44: 704-708.
Giovannucci E et al Diabetes and cancer: a consensus report. Diabetes Care 2010: 33(7): 1674-85 doi: 10.2337/dc10-0666.
Kitahara c et al Total Cholesterol and Cancer Risk in a Large Prospective Study. 2011 J Clin Oncol 29:1592-98.
Kostic A et al. Genomic analysis identifies association of Fusobacterium with colorectal carcinoma18, 2011, doi: 10.1101/gr.126573.111
Lorenzi M High glucose induces DNA damage in cultured human endothelial cells. 1986. L clin Invest 77(1) 322-25.
Ma J, Pollak M, Giovannucci E et al. Prospective study of colorectal cancer risk in men and plasma levels of Insulin like growth factor (IGF)-1 and IGF binding protein-3. J Natl Cancer Inst. 1999 7; 91 (7): 620-5.
Marzio A et al Sugar and Chromosome Stability: Clastogenic Effects of Sugars in Vitamin B6-Deficient Cells PLoS Genet. 2014; 10(3): e1004199.
Meyerhardt JA, Sato K, Niedzwiecki D. Dietary glycemic load and cancer recurrence and survival in patients with stage III colon cancer: findings from CALGB 89803. J Natl Cancer Inst. 2012 21;104(22):1702-11.
Palmqvist R, Halmans G, Rinaldi S, et al. Plasma insulin-like growth factor, insulin-like growth factor binding protein, and colorectal cancer: a prospective study in northern Sweden. Gut 2002; 50: 642-6.
Ryan CJ, Hagg CM, Simko J, Nonaka DF, Chan JM, Weinberg V, et al. Expression of insulin-like growth factor-1 receptor in local and metastatic prostate cancer. Urol Oncol 2007;25:134-40.
Stocks T et al Blood Glucose and Risk of Incident and Fatal Cancer in the Metabolic Syndrome and Cancer Project (Me-Can): Analysis of Six Prospective Cohorts. Plos 2010 DOI: 10.1371/journal.pmed.1000201
Surmacz E; Obesity hormone leptin; a new target for breast cancer? Breast Cancer Res 2007; 9(1): 301.
Te Morenga L et al Dietary sugars and body weight: systematic review and meta-analyses of randomised controlled trials and cohort studies BMJ 2013;346:e7492
Welsh J et al Caloric sweetener consumption and dyslipidemia among US adults.2010 JAMA 21; 303(15),pp1490-7.
Yang J et al A Sucrose-Enriched Diet Promotes Tumorigenesis in Mammary Gland in Part through the 12-Lipoxygenase (inflammatory) pathway. 2015 Cancer Res; 76(1); 24-29.
Yu H, Rohan T. Role of the insulin-like growth factor family in cancer development and progression. J Natl Cancer Inst 2000; 92: 1472-89.


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