Omega-3s and infants

Cardiovascular
Omega-3 start give beneficial effects already after 3 months.

Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto. Miocardico (GISSI)-Prevenzione. Marchioli Roberto; Barzi Federica; Bomba Elena; Chieffo Carmine; Di Gregorio Domenico; Di Mascio Rocco; Franzosi Maria Grazia; Geraci Enrico; Levantesi Giacomo; Maggioni Aldo Pietro; Mantini Loredana; Marfisi Rosa Maria; Mastrogiuseppe G; Mininni Nicola; Nicolosi Gian Luigi; Santini Massimo; Schweiger Carlo; Tavazzi Luigi; Tognoni Gianni; Tucci Corrado; Valagussa Franco
Department of Clinical Pharmacology and Epidemiology, Consorzio Mario Negri Sud, Santa Maria Imbaro, Chieti, Italy. marchioli@negrisud.it Circulation; 105 (16) p1897-903
Apr 23 2002

BACKGROUND: Our purpose was to assess the time course of the benefit of n-3 polyunsaturated fatty acids (PUFAs) on mortality documented by the GISSI-Prevenzione trial in patients surviving a recent (<3 months) myocardial infarction.

METHODS AND RESULTS: In this study, 11 323 patients were randomly assigned to supplements of n-3 PUFAs, vitamin E (300 mg/d), both, or no treatment (control) on top of optimal pharmacological treatment and lifestyle advice. Intention-to-treat analysis adjusted for interaction between treatments was carried out. Early efficacy of n-3 PUFA treatment for total, cardiovascular, cardiac, coronary, and sudden death; nonfatal myocardial infarction; total coronary heart disease; and cerebrovascular events was assessed by right-censoring follow-up data 12 times from the first month after randomization up to 12 months. Survival curves for n-3 PUFA treatment diverged early after randomization, and total mortality was significantly lowered after 3 months of treatment (relative risk [RR] 0.59; 95% CI 0.36 to 0.97; P=0.037). The reduction in risk of sudden death was specifically relevant and statistically significant already at 4 months (RR 0.47; 95% CI 0.219 to 0.995; P=0.048). A similarly significant, although delayed, pattern after 6 to 8 months of treatment was observed for cardiovascular, cardiac, and coronary deaths.

CONCLUSIONS: The early effect of low-dose (1 g/d) n-3 PUFAs on total mortality and sudden death supports the hypothesis of an antiarrhythmic effect of this drug. Such a result is consistent with the wealth of evidence coming from laboratory experiments on isolated myocytes, animal models, and epidemiological and clinical studies.

Infants
Docosahexaenoic acid and arachidonic acid in infant development.

Carlson S E; Departments of Dietetics and Nutrition (School of Allied Health) and Pediatrics (School of Medicine), University of Kansas Medical Center, Kansas City, KS, USA; Seminars in neonatology : SN; 6 (5) p437-49.

Docosahaxaenoic acid and arachidonic acid are highly concentrated in the central nervous system. The amount of these fatty acids in the central nervous system increases dramatically during the last intrauterine trimester and the first year of life. A central question of research conducted during the past 20 years is if the essential fatty acid precursor of docosahexaenoic acid is sufficient to achieve optimal DHA accumulation in the central nervous system and, therefore, infant development. The important role of non-human primate studies in characterising the behavioral effects of n-3 essential fatty acid deficiency and subsequent low brain DHA accumulation, the difference between essential fatty acid deficiencies and conditional deficiencies of docosahexaenoic acid and arachidonic acid, and the evidence that human infants have a conditionally essential need for docosahexaenoic acid and, perhaps, for arachidonic acid are summarised. The current suggestive evidence for several possible mechanisms underlying behavioral effects are also provided.
Copyright 2002 Elsevier Science

Obesity
Factorial study of the effects of atorvastatin and fish oil on dyslipidaemia in visceral obesity.

Chan D C; Watts G F; Mori T A; Barrett P H R; Beilin L J; Redgrave T G; Departments of Medicine and Physiology, University of Western Australia, Western Australian Institute for Medical Research, Royal Perth Hospital, Perth, Western Australia. European journal of clinical investigation; 32 (6) p429-36

BACKGROUND: Dyslipidaemia may account for increased risk of cardiovascular disease in central obesity. Pharmacotherapy is often indicated in these patients, but the optimal approach remains unclear. We investigated the effects of atorvastatin and fish oil on plasma lipid and lipoprotein levels, including remnant-like particle-cholesterol and apolipoprotein C-III, in dyslipidaemic men with visceral obesity. METHODS: We carried out a 6-week randomized, placebo-controlled, 2 x 2 factorial intervention study of atorvastatin (40 mg day-1) and fish oil (4 g day-1) on plasma lipids and lipoproteins in 52 obese men (age 53 1 years, BMI 33.7 0.55 kg m-2) with dyslipidaemia and insulin resistance. Treatment effects were analysed by general linear modelling.

RESULTS: Atorvastatin had significant main effects in decreasing triglycerides (-0.38 0.02 mmol L-1, P = 0.002), total cholesterol (-1.89 0.17 mmol L-1, P = 0.001), LDL-cholesterol (-1.78 0.14 mmol L-1, P = 0.001), remnant-like particle-cholesterol (-0.08 0.04 mmol L-1, P = 0.035), apolipoprotein B (-49 4 mg dL-1, P = 0.001), apolipoprotein C-III (-12.6 6.1 mg L-1, P = 0.044) and in increasing HDL-cholesterol (+0.10 0.04 mmol L-1, P = 0.007). Fish oil had significant main effects in decreasing triglycerides (-0.38 0.11 mmol L-1, P = 0.002) and in increasing HDL-cholesterol (+0.07 0.04 mmol L-1, P = 0.041). There were no significant changes in weight or insulin resistance during the study.

CONCLUSIONS: Atorvastatin and fish oil have independent and additive effects in correcting dyslipidaemia in viscerally obese men. Improvement in abnormalities in remnant lipoproteins may occur only with use of atorvastatin. Combination treatment with statin and fish oil may, however, offer an optimal therapeutic approach for globally correcting dyslipidaemia in obesity.

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