Limits...
Consequences of essential fatty acids.

Lands B - Nutrients (2012)

Bottom Line: Both n-3 and n-6 nutrients have beneficial actions, but many common health disorders are undesired consequences of excessive actions of tissue n-6 HUFA which are preventable.That action may prevent the unintended consequences that come from eating imbalanced diets which support excessive chronic actions of n-6 mediators that harm human health.The consequences from preventing n-3 and n-6 nutrient imbalances on a nationwide scale may be very large, and they need careful evaluation and implementation to avoid further harmful consequences for the national economy.

View Article: PubMed Central - PubMed

Affiliation: wlands@mail.nih.gov

ABSTRACT
Essential fatty acids (EFA) are nutrients that form an amazingly large array of bioactive mediators that act on a large family of selective receptors. Nearly every cell and tissue in the human body expresses at least one of these receptors, allowing EFA-based signaling to influence nearly every aspect of human physiology. In this way, the health consequences of specific gene-environment interactions with these nutrients are more extensive than often recognized. The metabolic transformations have similar competitive dynamics for the n-3 and n-6 homologs when converting dietary EFA from the external environment of foods into the highly unsaturated fatty acid (HUFA) esters that accumulate in the internal environment of cells and tissues. In contrast, the formation and action of bioactive mediators during tissue responses to stimuli tend to selectively create more intense consequences for n-6 than n-3 homologs. Both n-3 and n-6 nutrients have beneficial actions, but many common health disorders are undesired consequences of excessive actions of tissue n-6 HUFA which are preventable. This review considers the possibility of preventing imbalances in dietary n-3 and n-6 nutrients with informed voluntary food choices. That action may prevent the unintended consequences that come from eating imbalanced diets which support excessive chronic actions of n-6 mediators that harm human health. The consequences from preventing n-3 and n-6 nutrient imbalances on a nationwide scale may be very large, and they need careful evaluation and implementation to avoid further harmful consequences for the national economy.

Show MeSH

Related in: MedlinePlus

Selective events for n-3 and n-6 homologs during prostaglandin formation and action. The number beside each event shows the efficacy of the n-3 homolog relative to the n-6 homolog. Abbreviations for the enzymes and receptors are: cPLA2, cytosolic phospholipase A2; sPLA2, soluble phospholipase A2; COX-1, cyclooxygenase-1; COX-2, cyclooxygenase-2; L-PGDS, lipocalin prostaglandin D synthase; H-PGDS, hematopoietic prostaglandin D synthase; m-PGES-1, microsomal prostaglandin E synthase-1; PGFS, prostaglandin F synthase; PGIS, prostaglandin I synthase; TXAS, thromboxane synthase; DP, prostaglandin D receptors (1–2); EP, prostaglandin E receptors (1–4); IP, prostaglandin I receptor; TP, thromboxane receptor. The figure is modified from that published by Wada et al. [15].
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC3475243&req=5

nutrients-04-01338-f002: Selective events for n-3 and n-6 homologs during prostaglandin formation and action. The number beside each event shows the efficacy of the n-3 homolog relative to the n-6 homolog. Abbreviations for the enzymes and receptors are: cPLA2, cytosolic phospholipase A2; sPLA2, soluble phospholipase A2; COX-1, cyclooxygenase-1; COX-2, cyclooxygenase-2; L-PGDS, lipocalin prostaglandin D synthase; H-PGDS, hematopoietic prostaglandin D synthase; m-PGES-1, microsomal prostaglandin E synthase-1; PGFS, prostaglandin F synthase; PGIS, prostaglandin I synthase; TXAS, thromboxane synthase; DP, prostaglandin D receptors (1–2); EP, prostaglandin E receptors (1–4); IP, prostaglandin I receptor; TP, thromboxane receptor. The figure is modified from that published by Wada et al. [15].

Mentions: In contrast to the events in Figure 1, the gene-defined selective processes in Figure 2 tend to provide more vigorous and intense actions with n-6 than n-3 homologs [15]. Although the overall set of events in Figure 2 is often called the “arachidonic acid cascade”, eicosapentaenoic acid produces a corresponding set of n-3 homologs (noted in parentheses). The n-6-mediated actions in inflammatory and thrombotic events support a multi-billion dollar market in aspirin-like non-steroidal anti-inflammatory drugs that inhibit COX-1 and COX-2 and moderate unwanted EFA-derived consequences. However, to slow excessive signaling by n-6 mediators, we may choose either to lower tissue proportions of n-6 in HUFA with competing n-3 HUFA or to design more effective drugs. The wide range of consequences that EFA-based signals have on human health and behavior is illustrated by a few examples in the following section.


Consequences of essential fatty acids.

Lands B - Nutrients (2012)

Selective events for n-3 and n-6 homologs during prostaglandin formation and action. The number beside each event shows the efficacy of the n-3 homolog relative to the n-6 homolog. Abbreviations for the enzymes and receptors are: cPLA2, cytosolic phospholipase A2; sPLA2, soluble phospholipase A2; COX-1, cyclooxygenase-1; COX-2, cyclooxygenase-2; L-PGDS, lipocalin prostaglandin D synthase; H-PGDS, hematopoietic prostaglandin D synthase; m-PGES-1, microsomal prostaglandin E synthase-1; PGFS, prostaglandin F synthase; PGIS, prostaglandin I synthase; TXAS, thromboxane synthase; DP, prostaglandin D receptors (1–2); EP, prostaglandin E receptors (1–4); IP, prostaglandin I receptor; TP, thromboxane receptor. The figure is modified from that published by Wada et al. [15].
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3475243&req=5

nutrients-04-01338-f002: Selective events for n-3 and n-6 homologs during prostaglandin formation and action. The number beside each event shows the efficacy of the n-3 homolog relative to the n-6 homolog. Abbreviations for the enzymes and receptors are: cPLA2, cytosolic phospholipase A2; sPLA2, soluble phospholipase A2; COX-1, cyclooxygenase-1; COX-2, cyclooxygenase-2; L-PGDS, lipocalin prostaglandin D synthase; H-PGDS, hematopoietic prostaglandin D synthase; m-PGES-1, microsomal prostaglandin E synthase-1; PGFS, prostaglandin F synthase; PGIS, prostaglandin I synthase; TXAS, thromboxane synthase; DP, prostaglandin D receptors (1–2); EP, prostaglandin E receptors (1–4); IP, prostaglandin I receptor; TP, thromboxane receptor. The figure is modified from that published by Wada et al. [15].
Mentions: In contrast to the events in Figure 1, the gene-defined selective processes in Figure 2 tend to provide more vigorous and intense actions with n-6 than n-3 homologs [15]. Although the overall set of events in Figure 2 is often called the “arachidonic acid cascade”, eicosapentaenoic acid produces a corresponding set of n-3 homologs (noted in parentheses). The n-6-mediated actions in inflammatory and thrombotic events support a multi-billion dollar market in aspirin-like non-steroidal anti-inflammatory drugs that inhibit COX-1 and COX-2 and moderate unwanted EFA-derived consequences. However, to slow excessive signaling by n-6 mediators, we may choose either to lower tissue proportions of n-6 in HUFA with competing n-3 HUFA or to design more effective drugs. The wide range of consequences that EFA-based signals have on human health and behavior is illustrated by a few examples in the following section.

Bottom Line: Both n-3 and n-6 nutrients have beneficial actions, but many common health disorders are undesired consequences of excessive actions of tissue n-6 HUFA which are preventable.That action may prevent the unintended consequences that come from eating imbalanced diets which support excessive chronic actions of n-6 mediators that harm human health.The consequences from preventing n-3 and n-6 nutrient imbalances on a nationwide scale may be very large, and they need careful evaluation and implementation to avoid further harmful consequences for the national economy.

View Article: PubMed Central - PubMed

Affiliation: wlands@mail.nih.gov

ABSTRACT
Essential fatty acids (EFA) are nutrients that form an amazingly large array of bioactive mediators that act on a large family of selective receptors. Nearly every cell and tissue in the human body expresses at least one of these receptors, allowing EFA-based signaling to influence nearly every aspect of human physiology. In this way, the health consequences of specific gene-environment interactions with these nutrients are more extensive than often recognized. The metabolic transformations have similar competitive dynamics for the n-3 and n-6 homologs when converting dietary EFA from the external environment of foods into the highly unsaturated fatty acid (HUFA) esters that accumulate in the internal environment of cells and tissues. In contrast, the formation and action of bioactive mediators during tissue responses to stimuli tend to selectively create more intense consequences for n-6 than n-3 homologs. Both n-3 and n-6 nutrients have beneficial actions, but many common health disorders are undesired consequences of excessive actions of tissue n-6 HUFA which are preventable. This review considers the possibility of preventing imbalances in dietary n-3 and n-6 nutrients with informed voluntary food choices. That action may prevent the unintended consequences that come from eating imbalanced diets which support excessive chronic actions of n-6 mediators that harm human health. The consequences from preventing n-3 and n-6 nutrient imbalances on a nationwide scale may be very large, and they need careful evaluation and implementation to avoid further harmful consequences for the national economy.

Show MeSH
Related in: MedlinePlus