The Impact of Supplementation with Omega-3 Long-Chain Polyunsaturated Fatty Acids on the prevalence of Metabolic Syndrome in Obese Adolescents
The FASEB Journal, April 2016, vol. 30 no. 1 Supplement
Patricia Inda-Icaza1, Mardia Lopez-Alarcon2, Maria de Lourdes Barbosa-Cortez2, Concepcion Marquez2, Andrea Armenta-Alvarez2, Maria Teresa Bram-Falcon2 and Marielle Mayorga-Ochoa2
1Health Science, Universidad Anahuac, Huixquilucan, Mexico
2Unit of Research in Medical Nutrition, Mexican Institute of Social Security, Mexico City, Mexico
- Overview Metabolic Syndrome and vitamin D
- Overview Obesity and Vitamin D
- Overview: Omega-3 many benefits include helping vitamin D
The items in Obesity and Omega-3 are listed here:
- Severe Non-Alcoholic fatty liver disease treated by Omega-3 – RCT April 2018
- How Omega-3 fights metabolic syndrome and weight (behind paywall) – Feb 2018
- Fatty liver disease in children nicely treated by combination of Vitamin D and Omega-3 – RCT Dec 2016
- Obese youths 2X less likely to develop Metabolic Syndrome if take Onega-3 – RCT April 2016
- Omega-3 in infancy reduces Obesity following antibiotic (confirmed in rats, suspected in humans) – Feb 2016
- Huge increases in Omega-6 to Omega-3 ratio increase risk of obesity, etc. – March 2016
- Overweight women on caloric restriction diet got 3X benefits from 8 weeks of Omega-3 – RCT Dec 2015
- Hypothesis – Omega-6 to Omega-3 ratio increases obesity – Nov 2015
- Omega-3 reduced vitamin D3 inflamation for obese – RCT Jan 2013
- Reasons for low response by vitamin D level in the blood
Objective To demonstrate the impact of supplementation with n-3 long chain polyunsaturated fatty acids (n-3 LCPUFA) on the prevalence of metabolic syndrome (MS) of obese adolescents.
Material and methods In a randomized clinical design, obese individuals were selected and randomly assigned to receive 1.2 g n-3 LCPUFA daily during 3 months together with a hypocaloric diet (O3), or 1.0 g sunflower oil and a similar diet as placebo (P). Dietary information, using the multiple pass 24h-recall questionnaire, blood pressure and anthropometry were monthly registered. Peripheral blood samples were obtained at inclusion and at the end of follow-up to determine fasting glucose, triglycerides (TAG) and HDL-cholesterol (HDL-C) by colorimetric methods. To diagnose MS we used the IDF cutoff points for central obesity, glucose and HDL-C. However, we used the criteria of the American Academy of Pediatrics to detect hypertension, and for hipertriglyceridemia a cutoff point of 110 mg/dL was considered. Non-parametric statistics, Chi2 test and logistic regression models were used for analysis.
Results From 354 individuals, 105 and 111 completed the study for the O3 and P groups respectively. Adherence to treatments and changes in anthropometric and biochemical parameters after supplementation were comparable between groups. At baseline, 69 (31%) individuals from the complete sample met the criteria for MS; the frequency was similar in both groups (30.91% vs. 30.97%, p = 0.992) for O3 and P respectively. Likewise, at the end of the study, 63 individuals presented MS and the frequency was comparable between groups (26.36% vs. 32.14%, p = 0.344). Nevertheless, a detailed analysis exhibited that from the 69 individuals with MS at baseline, 30 remitted at the end of the study, but 26 who did not have the syndrome at baseline, acquired it at the end. While the frequency of remission was comparable between groups (12.2% vs. 14.3%, p = 0.734), the frequency of individuals who acquired the syndrome tended to be smaller in the O3 than in the P group (8.18% vs. 15.18%, p=0.10). Adjusting by basal body mass index z-score; Tanner status; and dietary energy, calcium, magnesium and n-3 fatty acids intake, the supplementation with n-3 LCPUFA protected against the risk to present MS at the end of the follow-up (OR = 0.58, IC95 = 0.29, 1.11).
Conclusions The results of the study provide evidence that LCPUFA n-3 supplementation to obese adolescents protects against the risk to acquire MS.
The study was funded by the Mexican Institute of Social Security, funding # FIS/IMSS/PROT/PRIO/11/014
Footnotes: This abstract is from the Experimental Biology 2016 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.