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Nutrition research on abdominal obesity shows nurture modifies nature

UCD Conway researchers and their collaborators in France, the United States and Ireland have shown how genetic predisposition and specific environmental factors such as dietary fat intake interact to influence our risk of chronic disease. The results of the study involving over seventeen hundred French men and women are published in the current issue of the Journal of Nutrition and the December issue of the American Journal of Clinical Nutrition.

Scientists use the term metabolic syndrome to describe a cluster of health abnormalities such as abdominal obesity, abnormal blood lipid levels, hyperglycaemia and hypertension that can predispose a person to type 2 diabetes, stroke and heart disease. Although it is thought that metabolic syndrome stems from the interplay of both environmental and genetic factors, this group believe that metabolic stressors (high-fat diet, obesity, etc.) and low-grade, chronic inflammation may play a prominent role.

Led by Conway Fellow, Professor Helen Roche and senior postdoctoral scientist Dr Catherine Phillips, the researchers looked in particular at two proteins released during the early stages of the inflammatory process called signal transducer and activator of transcription 3 (STAT3) and complement component 3 (C3). Different alterations (polymorphisms) of these proteins have been previously identified in humans and occur as a result of changes to the genes encoding STAT3 and C3.

Data relating to STAT3 and C3 genetic polymorphisms, dietary fat intake, plasma fatty acid composition and risk of developing the metabolic syndrome collected over a 7.5 year period indicated that having any of the five STAT3 alterations studied was not, by itself, related to risk for developing metabolic syndrome. However, having any one of them doubled a person’s risk of abdominal obesity, the key risk factor for the metabolic syndrome.

Increasing dietary saturated fat intake exacerbated abdominal obesity, but only in individuals with more than one genetic risk factor. For example, those people consuming the greatest amount of saturated fat with more than two STAT3 protein polymorphisms were 3.3 times more likely to have abdominal obesity compared to those consuming similar amounts of saturated fats but having one or no polymorphism.

In addition, this analysis also confirmed for the first time that certain polymorphisms in the C3 gene were associated with decreased metabolic syndrome risk, in part due to reduced risk of hypertriglyceridaemia and lower C3 levels. Furthermore, this data suggests that these beneficial effects were even more pronounced in people consuming a diet high in polyunsaturated fat, in particular omega-3 fatty acids such as those found in oily fish.

Commenting on the findings, Professor Roche says, “Further research concerning how saturated fats can amplify the negative effects of genetic background and how omega-3 polyunsaturated fatty acids can ameliorate the protective effects of genetic background might lead to personalised or targeted strategies for prevention and treatment of conditions such as abdominal obesity, the metabolic syndrome & diabetes”.

The research is supported by the European Commission, Framework Programme 6 (LIPGENE).

References
Phillips CM, Goumidi L, Bertrais S, Field MR, Peloso GM, Shen J, McManus R, Hercberg S, Lairon D, Planells R, Roche HM. Dietary saturated fat modulates the association between STAT3 polymorphisms and abdominal obesity in adults. Journal of Nutrition 139:2072-2078, 2009.

Catherine M Phillips, Louisa Goumidi, Sandrine Bertrais, Jane F Ferguson, Martyn R Field, Enda D Kelly, Gina M Peloso, L Adrienne Cupples, Jian Shen, Jose M Ordovas, Ross McManus, Serge Hercberg, Henri Portugal, Denis Lairon, Richard Planells, and Helen M Roche. Complement component 3 polymorphisms interact with polyunsaturated fatty acids to modulate risk of metabolic syndrome. American Journal of Clinical Nutrition 90:6, 2009