Foods fried in vegetable oil are popular worldwide, but research about the health effects of this cooking technique has been largely inconclusive and focused on healthy people.
For the first time, UMass Amherst food scientists set out to examine the impact of frying oil consumption on inflammatory bowel disease (IBD) and colon cancer, using animal models.
In their paper published Aug. 23 in Cancer Prevention Research, lead author and Ph.D. student Jianan Zhang, associate professor Guodong Zhang, and professor and department head Eric Decker showed that feeding frying oil to mice exaggerated colonic inflammation, enhanced tumor growth and worsened gut leakage, spreading bacteria or toxic bacterial products into the bloodstream.
“People with colonic inflammation or colon cancer should be aware of this research,” says Jianan Zhang.
Guodong Zhang, whose food science lab focuses on the discovery of new cellular targets in the treatment of colon cancer and how to reduce the risks of IBD, stresses that “it’s not our message that frying oil can cause cancer.”
Rather, the new research suggests that eating fried foods may exacerbate and advance conditions of the colon.
“In the United States, many people have these diseases, but many of them may still eat fast food and fried food,” says Guodong Zhang.
“If somebody has IBD or colon cancer and they eat this kind of food, there is a chance it will make the diseases more aggressive.”
For their experiments, the researchers used a real-world sample of canola oil, in which falafel had been cooked at 325 F in a standard commercial fryer at an eatery in Amherst, Massachusetts.
“Canola oil is used widely in America for frying,” Jianan Zhang says.
Decker, an expert in lipid chemistry performed the analysis of the oil, which undergoes an array of chemical reactions during the frying process.
He characterized the fatty acid profiles, the level of free fatty acids and the status of oxidation.
A combination of the frying oil and fresh oil was added to the powder diet of one group of mice.
The control group was fed the powder diet with only fresh oil mixed in. “We tried to mimic the human being’s diet,” Guodong Zhang says.
Supported by grants from the U.S. Department of Agriculture, the researchers looked at the effects of the diets on colonic inflammation, colon tumor growth and gut leakage, finding that the frying oil diet worsened all the conditions. “The tumors doubled in size from the control group to the study group,” Guodong Zhang says.
To test their hypothesis that the oxidation of polyunsaturated fatty acids, which occurs when the oil is heated, is instrumental in the inflammatory effects, the researchers isolated polar compounds from the frying oil and fed them to the mice.
The results were “very similar” to those from the experiment in which the mice were fed frying oil, suggesting that the polar compounds mediated the inflammatory effects.
While more research is needed, the researchers hope a better understanding of the health impacts of frying oil will lead to dietary guidelines and public health policies.
“For individuals with or prone to inflammatory bowel disease,” Guodong Zhang says, “it’s probably a good idea to eat less fried food.”
Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory disease of the gastrointestinal tract. Although the precise etiology of IBD remains incompletely understood, accumulating evidence suggests that various environmental factors, including dietary nutrients, contribute to its pathogenesis. Dietary nutrients are known to have an impact on host physiology and diseases.
The interactions between dietary nutrients and intestinal immunity are complex. Dietary nutrients directly regulate the immuno-modulatory function of gut-resident immune cells. Likewise, dietary nutrients shape the composition of the gut microbiota.
Therefore, a well-balanced diet is crucial for good health.
In contrast, the relationships among dietary nutrients, host immunity and/or the gut microbiota may be perturbed in the context of IBD. Genetic predispositions and gut dysbiosis may affect the utilization of dietary nutrients.
Moreover, the metabolism of nutrients in host cells and the gut microbiota may be altered by intestinal inflammation, thereby increasing or decreasing the demand for certain nutrients necessary for the maintenance of immune and microbial homeostasis.
Herein, we review the current knowledge of the role dietary nutrients play in the development and the treatment of IBD, focusing on the interplay among dietary nutrients, the gut microbiota and host immune cells. We also discuss alterations in the nutritional metabolism of the gut microbiota and host c
ells in IBD that can influence the outcome of nutritional intervention. A better understanding of the diet-host-microbiota interactions may lead to new therapeutic approaches for the treatment of IBD.
Monounsaturated Fatty Acids (MUFAs)
MUFAs are classified as fatty acids containing a single double bond. Oleic acid, the most common omega-9 MUFA, is found in various vegetable oils, such as olive oil and canola oil.
The levels of MUFAs, including oleic acid, are significantly reduced in IBD patients compared to control subjects, both systemically (blood) and locally (intestinal mucosa) (139, 140).
Epidemiologically, the Mediterranean diet containing high levels of MUFAs, especially oleic acid, is well-recognized for its beneficial effects on metabolic syndrome and cardiovascular health (141).
The effects of MUFAs on IBD remain unresolved.
There are conflicting reports regarding the therapeutic potential of MUFAs in IBD.
A large prospective cohort study has demonstrated that dietary oleic acid intake is inversely associated with UC development (142).
In contrast, other studies have shown that a high intake of MUFAs increases the risk for the development of UC and CD. Several animal studies have consistently demonstrated that supplementation of oleic acid or olive oil attenuates intestinal inflammation in DSS-induced colitis (135, 143).
More information:Cancer Prevention Research (2019). DOI: 10.1158/1940-6207.CAPR-19-0226 , https://cancerpreventionresearch.aacrjournals.org/user/login?destination=/content/early/2019/08/21/1940-6207.CAPR-19-0226
Journal information: Cancer Prevention Research
Provided by University of Massachusetts Amherst
