The Effects of Omega-3 and Vitamin E Co-supplementation on Carotid Intima-media Thickness and Inflammatory Factors in Patients with Polycystic Ovary Syndrome.

OBJECTIVES: We sought to evaluate the effects of omega-3 and vitamin E co-supplementation on carotid intima-media thickness (CIMT) and inflammatory factors in patients with polycystic ovary syndrome (PCOS). METHODS: This randomized, double-blind, placebo-controlled trial was done among 60 women with PCOS. Participants were randomly assigned into two groups (n = 30 each group) and assigned to take either 1000 mg omega-3 plus 400 IU vitamin E supplements or a placebo for 12 weeks. RESULTS: Compared with placebo, omega-3 and vitamin E co-supplementation led to significant decreases in maximum levels of left CIMT (-0.006±0.006 vs. +0.002±0.007 mm, p < 0.001), mean levels of left CIMT (-0.005±0.006 vs. +0.002±0.010 mm, p = 0.010), maximum levels of right CIMT (-0.006±0.010 vs. +0.006±0.010 mm, p = 0.010), and mean levels of right CIMT (-0.005±0.005 vs. +0.001±0.010 mm, p = 0.020). Change in high-sensitivity C-reactive protein (hs-CRP) (-390.6±942.9 vs. +237.0±754.3 ng/mL, p = 0.006) was significantly different between the supplemented patients and placebo group. We did not observe any significant effect in plasma nitric oxide (NO) values following supplementation with omega-3 plus vitamin E compared with the placebo. CONCLUSIONS: Co-supplementation with omega-3 and vitamin E for 12 weeks among patients with PCOS had beneficial effects on CIMT and serum hs-CRP values, but unchanged NO values.

The effects of vitamin D and omega-3 fatty acid co-supplementation on glycemic control and lipid concentrations in patients with gestational diabetes.

OBJECTIVE: This study was performed to evaluate the effects of vitamin D and omega-3 fatty acids co-supplementation on glucose metabolism and lipid concentrations in gestational diabetes (GDM) patients. METHODS: This randomized double-blind placebo-controlled clinical trial was done among 140 GDM patients. Participants were randomly divided into 4 groups to receive: (1) 1000 mg omega-3 fatty acids containing 360 mg eicosapentaenoic acid and 240 mg docosahexaenoic acid (DHA) twice a day + vitamin D placebo (n = 35); (2) 50,000 IU vitamin D every 2 weeks + omega-3 fatty acids placebo (n = 35); (3) 50,000 IU vitamin D every 2 weeks + 1000 mg omega-3 fatty acids twice a day (n = 35), and (4) vitamin D placebo + omega-3 fatty acids placebo (n = 35) for 6 weeks. RESULTS: After 6 weeks of intervention, patients who received combined vitamin D and omega-3 fatty acids supplements compared with vitamin D, omega-3 fatty acids, and placebo had significantly decreased fasting plasma glucose (-7.3 ± 7.8, -6.9 ± 6.6, -4.0 ± 2.5, and +1.0 ± 11.4 mg/dL, respectively, P < .001), serum insulin levels (-1.9 ± 1.9, -1.3 ± 6.3, -0.4 ± 6.3, and +2.6 ± 6.5 µIU/mL, respectively, P = .005), homeostatic model of assessment for insulin resistance (-0.7 ± 0.6, -0.5 ± 1.4, -0.2 ± 1.5, and +0.6 ± 1.5, respectively, P < .001) and increased quantitative insulin sensitivity check index (+0.01 ± 0.01, +0.008 ± 0.02, +0.002 ± 0.02, and -0.005 ± 0.02, respectively, P = .001). In addition, changes in serum triglycerides (-8.2 ± 41.0, +7.6 ± 31.5, +3.6 ± 29.9, and +20.1 ± 29.6 mg/dL, respectively, P = .006) and very low-density lipoprotein cholesterol (-1.6 ± 8.2, +1.5 ± 6.3, +0.8 ± 6.0, and +4.0 ± 5.9 mg/dL, respectively, P = .006) in the vitamin D plus omega-3 fatty acids group were significantly different from the changes in these indicators in the vitamin D, omega-3 fatty acids, and placebo groups. CONCLUSION: Overall, vitamin D and omega-3 fatty acids co-supplementation for 6 weeks among GDM patients had beneficial effects on fasting plasma glucose, serum insulin levels, homeostatic model of assessment for insulin resistance, quantitative insulin sensitivity check index, serum triglycerides, and very low-density lipoprotein cholesterol levels.

The Effects of Omega-3 Fatty Acids and Vitamin E Co-Supplementation on Indices of Insulin Resistance and Hormonal Parameters in Patients with Polycystic Ovary Syndrome: A Randomized, Double-Blind, Placebo-Controlled Trial.

This study was conducted to determine the effects of omega-3 fatty acids and vitamin E co-supplementation on indices of insulin resistance and hormonal parameters in women with polycystic ovary syndrome (PCOS). This randomized double-blind, placebo-controlled trial was done on 68 women diagnosed with PCOS according to the Rotterdam criteria aged 18-40 years old. Participants were randomly assigned into 2 groups to receive either 1 000 mg omega-3 fatty acids from flaxseed oil containing 400 mg α-Linolenic acid plus 400 IU vitamin E supplements (n=34) or placebo (n=34) for 12 weeks. Hormonal parameters were quantified at the beginning of the study and after 12-week intervention. After 12 weeks of intervention, compared to the placebo, omega-3 fatty acids and vitamin E co-supplementation resulted in a significant decrease in insulin (-1.0±3.5 vs. +2.7±6.6 µIU/mL, P=0.004), homeostasis model of assessment-estimated insulin resistance (-0.2±0.8 vs. +0.6±1.5, P=0.005), homeostasis model of assessment-estimated B cell function (-4.3±14.3 vs. +10.5±24.5, P=0.004) and a significant increase in quantitative insulin sensitivity check index (+0.006±0.02 vs. -0.01±0.04, P=0.008). Supplementation with omega-3 fatty acids plus vitamin E led to significant reductions in serum total testosterone (-0.5±0.7 vs. -0.1±0.5 ng/mL, P=0.008) and free testosterone (-1.2±2.1 vs. -0.2±1.7, P=0.04) compared to the placebo group. We did not observe any significant effect of omega-3 fatty acids and vitamin E co-supplementation on fasting plasma glucose and other hormonal profiles. Omega-3 fatty acids and vitamin E co-supplementation for 12 weeks in PCOS women significantly improved indices of insulin resistance, total and free testosterone.

The effects of omega-3 fatty acids and vitamin E co-supplementation on gene expression of lipoprotein(a) and oxidized low-density lipoprotein, lipid profiles and biomarkers of oxidative stress in patients with polycystic ovary syndrome.

This study was conducted to determine the effects of omega-3 fatty acids and vitamin E co-supplementation on gene expression of lipoprotein(a) (Lp[a]) and oxidized low-density lipoprotein (Ox-LDL), lipid profiles and biomarkers of oxidative stress in women with polycystic ovary syndrome (PCOS). This randomized double-blind, placebo-controlled trial was done on 68 women diagnosed with PCOS according to the Rotterdam criteria aged 18-40 years old. Participants were randomly assigned into two groups to receive either 1000 mg omega-3 fatty acids from flaxseed oil containing 400 mg α-Linolenic acid plus 400 IU vitamin E supplements (n = 34) or placebo (n = 34) for 12 weeks. Lp(a) and Ox-LDL mRNA levels were quantified in peripheral blood mononuclear cells of PCOS women with RT-PCR method. Lipid profiles and biomarkers of oxidative stress were quantified at the beginning of the study and after 12-week intervention. Quantitative results of RT-PCR demonstrated that compared with the placebo, omega-3 fatty acids and vitamin E co-supplementation downregulated expressed levels of Lp(a) mRNA (P < 0.001) and Ox-LDL mRNA (P < 0.001) in peripheral blood mononuclear cells of women with PCOS. In addition, compared to the placebo group, omega-3 fatty acids and vitamin E co-supplementation resulted in a significant decrease in serum triglycerides (-22.1 ± 22.3 vs. +7.7 ± 23.6 mg/dL, P < 0.001), VLDL- (-4.4 ± 4.5 vs. +1.5 ± 4.7 mg/dL, P < 0.001), total- (-20.3 ± 16.6 vs. +12.2 ± 26.1 mg/dL, P < 0.001), LDL- (-16.7 ± 15.3 vs. +11.9 ± 26.1 mg/dL, P < 0.001) and total-/HDL-cholesterol (-0.5 ± 0.6 vs. +0.4 ± 0.8, P < 0.001). There were a significant increase in plasma total antioxidant capacity (+89.4 ± 108.9 vs. +5.9 ± 116.2 mmol/L, P = 0.003) and a significant decrease in malondialdehyde levels (-0.3 ± 0.4 vs. -0.008 ± 0.6 µmol/L, P = 0.01) by combined omega-3 fatty acids and vitamin E intake compared with the placebo group. Overall, omega-3 fatty acids and vitamin E co-supplementation for 12 weeks in PCOS women significantly improved gene expression of Lp(a) and Ox-LDL, lipid profiles and biomarkers of oxidative stress.

Oral carnitine supplementation reduces body weight and insulin resistance in women with polycystic ovary syndrome: a randomized, double-blind, placebo-controlled trial.

OBJECTIVE: Limited data are available for evaluating the effects of oral carnitine supplementation on weight loss and metabolic profiles of women with polycystic ovary syndrome (PCOS). This study was designed to determine the effects of oral carnitine supplementation on weight loss, and glycaemic and lipid profiles in women with PCOS. DESIGN, PATIENTS AND MEASUREMENTS: In a prospective, randomized, double-blind, placebo-controlled trial, 60 overweight patients diagnosed with PCOS were randomized to receive either 250 mg carnitine supplements (n = 30) or placebo (n = 30) for 12 weeks. Fasting blood samples were obtained at the beginning and the end of the study to quantify parameters of glucose homoeostasis and lipid concentrations. RESULTS: At the end of the 12 weeks, taking carnitine supplements resulted in a significant reduction in weight (-2·7 ± 1·5 vs +0·1 ± 1·8 kg, P < 0·001), BMI (-1·1 ± 0·6 vs +0·1 ± 0·7 kg/m(2) , P < 0·001), waist circumference (WC) (-2·0 ± 1·3 vs -0·3 ± 2·0 cm, P < 0·001) and hip circumference (HC) (-2·5 ± 1·5 vs -0·3 ± 1·8 cm, P < 0·001) compared with placebo. In addition, compared with placebo, carnitine administration in women with PCOS led to a significant reduction in fasting plasma glucose (-0·38 ± 0·36 vs +0·11 ± 0·97 mmol/l, P = 0·01), serum insulin levels (-14·39 ± 25·80 vs +3·01 ± 37·25 pmol/l, P = 0·04), homoeostasis model of assessment-insulin resistance (-0·61 ± 1·03 vs +0·11 ± 1·43, P = 0·04) and dehydroepiandrosterone sulphate (-3·64 ± 7·00 vs -0·59 ± 3·20 µmol/l, P = 0·03). CONCLUSIONS: Overall, 12 weeks of carnitine administration in PCOS women resulted in reductions in weight, BMI, WC and HC, and beneficial effects on glycaemic control; however, it did not affect lipid profiles or free testosterone.