Sugar-laden Western diet promotes breast cancer tumours
The study is the first to investigate the direct effect of sugar consumption on the development of breast cancer using breast cancer animal models. It also attempts to identify the exact mechanisms sugar is acting upon.
Given that the per capita consumption of sugar in the U.S. has increased to over 45 kilograms (100 lbs.) per year, recognising the causes and risks for breast cancer has become a significant public health issue. The increase in consumption of sugar-sweetened beverages has been identified as a significant contributor to an epidemic of obesity, heart disease and cancer worldwide.
The study used multiple mouse models to investigate dietary sugar’s role on mammary gland tumour development along with mechanisms that may be involved. Researchers found that sugar increased expression of the enzyme 12-lipoxygenase (12-LOX) and its arachidonate metabolite.
The researchers determined that fructose derived from sucrose played a key role in aiding lung metastasis and 12-HETE production in breast tumours, concluding that dietary sugar promoting 12-LOX signalling to increase risks of breast cancer development and metastasis.
The weakness for sweetness
The role of sugar in the Western diet has been subject of multiple studies investigating how an excess can wreak havoc on the human body not only in adults but also in offspring.
A recent study found a maternal diet high in salt and fructose had lasting effects on offspring in animals. It was discovered that the mothers’ diet affected their
offspring’s cardiovascular function, with sugar having a greater effect on female offspring.
In addition, new research in school children suggested lowering the consumption of sugar sweetened beverages (SSBs) by at least one serving per week could help improve markers of cholesterol.
Previous studies have pinpointed the role of sugar, especially glucose, in energy-based metabolic pathways in cancer development. It has been well-documented that increased glucose flux and metabolism promotes several hallmarks of cancer such as excessive proliferation, anti-apoptotic signalling, cell cycle progression and angiogenesis.
Study details
This study, carried out at the University of Texas MD Anderson Cancer Center, set out to determine whether the inflammatory cascade was an alternative route of studying sugar-driven carcinogenesis.
Four different studies were undertaken in which mice were randomised to different diet groups and fed one of four diets. At six months of age, 30% of mice on a starch-control diet had measurable tumours, whereas 50-58% of the mice on sucrose-enriched diets had developed mammary tumours.
The study also showed that numbers of lung metastases were significantly higher in mice on a sucrose- or a fructose-enriched diet, versus mice on a starch-control diet.
“We determined that fructose derived from the sucrose was responsible for facilitating lung metastasis and 12-HETE production in breast tumours,” the study stated. “Overall, our data suggested that dietary sugar induces 12-LOX signalling to increase risks of breast cancer development and metastasis.”
"This study suggests that dietary sucrose or fructose induced 12-LOX and 12-HETE production in breast tumour cells in vivo," said co-author Dr Lorenzo Cohen, professor of Palliative, Rehabilitation, and Integrative Medicine. "This indicates a possible signalling pathway responsible for sugar-promoted tumour growth in mice. How dietary sucrose and fructose induces 12-HETE and whether it has a direct or indirect effect remains in question."
The study concluded that the mechanism by which dietary sucrose or fructose affected breast tumour growth and metastasis, especially through the 12-LOX pathways, warranted further investigation.
Source: Cancer Research
Published: January 1, 2016 76:24-29; doi: 10.1158/0008-5472.CAN-14-3432
Title: “A Sucrose-Enriched Diet Promotes Tumorigenesis in Mammary Gland in Part through the 12-Lipoxygenase Pathway”
Authors: Yan Jiang, Yong Pan, Patrea R. Rhea, Lin Tan, Mihai Gagea, Lorenzo Cohen, Susan M. Fischer, and Peiying Yang
