Excessive dietary linoleic acid promotes plasma accumulation of pronociceptive fatty acyl lipid mediators

Birkic, Nada; Azar, Toni; Maddipati, Krishna Rao; Minic, Zeljka; Reynolds, Christian A.

doi:10.1038/s41598-022-21823-y

Cited by 4 publications

(1 citation statement)

References 39 publications

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“…Chronically elevated levels of AA can contribute to a state of chronic inflammation and have been associated with autoimmunity [ 55 ]. This has led to some popular debate regarding the influence of LA intake on AA levels, with some recent papers suggesting that an excessive LA intake can lead to the accumulation of AA-derived pronociceptive lipid mediators and a reduction in antinociceptive lipid mediators obtained from omega-3 fatty acids [ 56 , 57 ]. However, a systematic review found that LA intake was not associated with tissue concentrations of AA in human beings [ 58 ].…”

Section: Pathophysiological Mechanism Of Elevated La Levelsmentioning

confidence: 99%

Linoleic Acid: A Narrative Review of the Effects of Increased Intake in the Standard American Diet and Associations with Chronic Disease

Mercola

D’Adamo

2023

Nutrients

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The intake of linoleic acid (LA) has increased dramatically in the standard American diet. LA is generally promoted as supporting human health, but there exists controversy regarding whether the amount of LA currently consumed in the standard American diet supports human health. The goal of this narrative review is to explore the mechanisms that underlie the hypothesis that excessive LA intake may harm human health. While LA is considered to be an essential fatty acid and support health when consumed in modest amounts, an excessive intake of LA leads to the formation of oxidized linoleic acid metabolites (OXLAMs), impairments in mitochondrial function through suboptimal cardiolipin composition, and likely contributes to many chronic diseases that became an epidemic in the 20th century, and whose prevalence continues to increase. The standard American diet comprises 14 to 25 times more omega-6 fatty acids than omega-3 fatty acids, with the majority of omega-6 intake coming from LA. As LA consumption increases, the potential for OXLAM formation also increases. OXLAMs have been associated with various illnesses, including cardiovascular disease, cancer, and Alzheimer’s disease, among others. Lowering dietary LA intake can help reduce the production and accumulation of OXLAMs implicated in chronic diseases. While there are other problematic components in the standard American diet, the half-life of LA is approximately two years, which means the damage can be far more persistent than other dietary factors, and the impact of reducing excessive LA intake takes time. Therefore, additional research-evaluating approaches to reduce OXLAM formation and cardiolipin derangements following LA consumption are warranted.

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