Lipid-lowering drugs and essential omega-6 and omega-3 fatty acids in patients with coronary heart disease

Lorgeril, Michel de; Salen, Patricia; Guiraud, Annabelle; Zeghichi, Sabrina; Boucher, François; Leiris, Joël de

doi:10.1016/j.numecd.2004.09.001

Cited by 31 publications

(20 citation statements)

References 32 publications

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“…For example, PPARa activators, such as the cholesterol-lowering drugs fibrates, have been shown to upregulate hepatic D6 desaturase expression and activity (29). However, we have shown in a randomized trial in patients that fenofibrate actually decreases rather than increases EPA and DHA levels (30). At the same time, fenofibrate significantly increases arachidonic acid levels, which was not the case with ACN in the present study.…”

Section: Discussioncontrasting

confidence: 64%

Dietary Flavonoids Increase Plasma Very Long-Chain (n-3) Fatty Acids in Rats,

Toufektsian¹,

Salen²,

Laporte³

et al. 2011

The Journal of Nutrition

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Flavonoids probably contribute to the health benefits associated with the consumption of fruit and vegetables. However, the mechanisms by which they exert their effects are not fully elucidated. PUFA of the (n-3) series also have health benefits. Epidemiological and clinical studies have suggested that wine flavonoids may interact with the metabolism of (n-3) PUFA and increase their blood and cell levels. The present studies in rats were designed to assess whether flavonoids actually increase plasma levels of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), the main very long-chain (n-3) PUFA. Rats were fed a corn-derived anthocyanin (ACN)-rich (ACN-rich) or ACN-free diet with constant intakes of plant and marine (n-3) PUFA for 8 wk (Expt. 1). Plasma fatty acids were measured by GC. The ACN-rich diet contained ~0.24 ± 0.01 mg of ACN/g pellets. There were no significant differences between groups in the main saturated, monounsaturated, and (n-6) fatty acids. In contrast, plasma EPA and DHA were greater in the ACN-rich diet group than in the ACN-free diet group (P < 0.05). We obtained similar results in 2 subsequent experiments in which rats were administered palm oil (80 μL/d) and consumed the ACN-rich or ACN-free diet (Expt. 2) or were supplemented with fish oil (60 mg/d, providing 35 mg DHA and 12 mg EPA) and consumed the ACN-rich or ACN-free diet (Expt. 3). In both experiments, plasma EPA and DHA were significantly greater in the ACN-rich diet group. These studies demonstrate that the consumption of flavonoids increases plasma very long-chain (n-3) PUFA levels. These data confirm previous clinical and epidemiological studies and provide new insights into the health benefits of flavonoids.

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Section: Discussioncontrasting

confidence: 64%

Dietary Flavonoids Increase Plasma Very Long-Chain (n-3) Fatty Acids in Rats,

Toufektsian¹,

Salen²,

Laporte³

et al. 2011

The Journal of Nutrition

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“…Numerous studies in a variety of experimental models show that linoleic acid and ␣-linolenic acid are the most easily ␤-oxidized of the common dietary fatty acids (for review, see Cunnane et al, 2003), and both these fatty acids decreased after bezafibrate (20 and 24%, respectively; Table 2). De Lorgeril's team observed the same effect after 12 weeks on fenofibrate (de Lorgeril et al, 2005).…”

Section: Discussionmentioning

confidence: 72%

Bezafibrate Mildly Stimulates Ketogenesis and Fatty Acid Metabolism in Hypertriglyceridemic Subjects

Tremblay‐Mercier¹,

Tessier²,

Plourde³

et al. 2010

J Pharmacol Exp Ther

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Our objective was to determine whether bezafibrate, a hypotriglyceridemic drug and peroxisome proliferatoractivated receptor (PPAR)-␣ agonist, is ketogenic and increases fatty acid oxidation in humans. We measured fatty acid metabolism and ketone levels in 13 mildly hypertriglycemic adults (67 Ϯ 11 years old) during 2 metabolic study days lasting 6 h, 1 day before and 1 day after bezafibrate (400 mg of bezafibrate per day for 12 weeks). ␤-Hydroxybutyrate, triglycerides, free fatty acids, fatty acid profiles, insulin, and glucose were measured in plasma, and fatty acid ␤-oxidation was measured in breath after an oral 50-mg dose of the fatty acid tracer [U-13 C]linoleic acid. As expected, 12weeks on bezafibrate decreased plasma triglycerides by 35%. Bezafibrate tended to raise postprandial ␤-hydroxybutyrate, an effect that was significant after normalization to the fasting baseline values (p ϭ 0.03). ␤-Oxidation of [U-13 C]linoleic acid increased by 30% (p ϭ 0.03) after treatment. On the metabolic study day after bezafibrate treatment, postprandial insulin decreased by 26% (p ϭ 0.01), and glucose concentrations were lower 2 to 5 h postprandially. Thus, in hypertriglyceridemic individuals, bezafibrate is mildly ketogenic and significantly changes fatty acid metabolism, effects that may be linked to PPAR␣ stimulation and to moderately improved glucose metabolism.As the population ages, the prevalence of cognitive impairment in the elderly, particularly Alzheimer's disease (AD), is increasing markedly. Glucose is the brain's main energy substrate, providing energy to make ATP to maintain ion gradients, synaptic transmission, protein synthesis (for review, see Hoyer, 1996), and fatty acid turnover in membranes phospholipids (Rapoport et al., 2001). A decline in cerebral glucose metabolism is widely reported in AD (Foster et al., 1984;Blennow et al., 2006;Mosconi et al., 2007). This deterioration in brain fuel supply is progressive, correlates broadly with dementia severity, and may appear during normal aging at which time there can be an approximately 6% reduction in glucose uptake per decade (Petit-Taboué et al., 1998). Reduced brain glucose metabolism can arise before the clinical symptoms of AD (Reiman et al., 2004) and may contribute to neurodegenerative processes leading to AD (Liu 2004(Liu , 2008. As such, an alternative brain fuel to glucose may be therapeutically useful in AD.Physiologically, ketone bodies [or ketones; ␤-hydroxybutyrate (␤-OHB), acetoacetate, and acetone] are the main alternative energy substrate to glucose for brain metabolism and are especially important during periods of glucose deprivation. Ketones can supply up to two thirds of the energy requirement of the brain during starvation (Owen et al., 1967). Mildly increasing ketone synthesis has been proposed as a possible therapeutic approach to correct or bypass brain

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“…In the same line of reasoning, it is important to recall that the most frequently prescribed cholesterol-lowering drugs (including statins) increase the blood concentration of arachidonic acid, the main omega-6 PUFA in cell membranes [31]. Also, studies have suggested that low cholesterol and/or cholesterol-lowering are associated with an increased risk of cancers [32].…”

Section: Dietary Fat and Cancermentioning

confidence: 99%

New insights into the health effects of dietary saturated and omega-6 and omega-3 polyunsaturated fatty acids

Lorgeril

Salen

2012

BMC Med

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109

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Cardiovascular diseases and cancers are leading causes of morbidity and mortality. Reducing dietary saturated fat and replacing it with polyunsaturated fat is still the main dietary strategy to prevent cardiovascular diseases, although major flaws have been reported in the analyses supporting this approach. Recent studies introducing the concept of myocardial preconditioning have opened new avenues to understand the complex interplay between the various lipids and the risk of cardiovascular diseases. The optimal dietary fat profile includes a low intake of both saturated and omega-6 fatty acids and a moderate intake of omega-3 fatty acids. This profile is quite similar to the Mediterranean diet. On the other hand, recent studies have found a positive association between omega-6 and breast cancer risk. In contrast, omega-3 fatty acids do have anticancer properties. It has been shown that certain (Mediterranean) polyphenols significantly increase the endogenous synthesis of omega-3 whereas high intake of omega-6 decreases it. Finally, epidemiological studies suggest that a high omega-3 to omega-6 ratio may be the optimal strategy to decrease breast cancer risk. Thus, the present high intake of omega-6 in many countries is definitely not the optimal strategy to prevent cardiovascular disease and cancers. A moderate intake of plant and marine omega-3 in the context of the traditional Mediterranean diet (low in saturated and omega-6 fatty acids but high in plant monounsaturated fat) appears to be the best approach to reduce the risk of both cardiovascular diseases and cancers, in particular breast cancer.

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Lipid-lowering drugs and essential omega-6 and omega-3 fatty acids in patients with coronary heart disease

Cited by 31 publications

References 32 publications

Dietary Flavonoids Increase Plasma Very Long-Chain (n-3) Fatty Acids in Rats,

Dietary Flavonoids Increase Plasma Very Long-Chain (n-3) Fatty Acids in Rats,

Bezafibrate Mildly Stimulates Ketogenesis and Fatty Acid Metabolism in Hypertriglyceridemic Subjects

New insights into the health effects of dietary saturated and omega-6 and omega-3 polyunsaturated fatty acids

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