IngredientsThe synthesis of oleoylethanolamide (OEA) is mediated by two concerted reactions: the first is the N-acylation of phosphatidylethanolamine (PE) from the phospholipid bilayer of the cell membrane, mediated by an N-acyltransferase (NAT), to form N-oleoylphosphatidylethanolamine (NOPE); the second is the phospholipase D (PLD)-mediated hydrolysis of NOPE.
N-Oleoyl-phosphatidylethanolamine (commonly abbreviated NOPE, and also rendered in the scientific literature as N-oleyl-phosphatidylethanolamine or oleoyl-phosphatidylethanolamine) is the direct biosynthetic precursor to the lipid mediator oleoylethanolamide (OEA). It belongs to the broader family of N-acylphosphatidylethanolamines (NAPEs) — a class of bioactive phospholipids in which a fatty-acid residue is covalently attached to the nitrogen of a phosphatidylethanolamine (PE) backbone.
Phosphatidylethanolamine consists of a glycerol backbone linked to two fatty acid chains and a phosphate group conjugated with ethanolamine. This configuration gives PE a cone-shaped molecular geometry, unlike the cylindrical shape of phosphatidylcholine (PC). In NOPE, the distinguishing feature is an oleic acid (18:1, cis-Δ9) moiety attached to the free amine group of the ethanolamine head of PE, making it an N-acylated derivative of PE rather than a conventional diacyl phospholipid.
This hygroscopic phospholipid, also called cephalin, is an important constituent of biomembranes and lipoproteins. The parent class, phosphatidylethanolamine, is the second most abundant phospholipid in animals, plants and yeast and the major lipid in bacteria. Phosphatidylethanolamine (PE) is a type of phospholipid that is primarily located in the internal leaflet of biological cell membranes and is particularly abundant in mitochondria.
Freshly prepared phosphatidylethanolamines are white solids that turn yellow and brown on exposure to air. They typically sinter between 80 and 90°C and melt in the neighborhood of 175°C. Solutions of phosphatidylethanolamine slowly decompose at room temperature (roughly 0.3–0.5% per day); hence, solutions should always be freshly prepared and kept cold prior to use. It is labile in alkaline conditions.
N-acylphosphatidylethanolamines are known compounds, the occurrence in nature of which was investigated in depth by J. L. Newman in Chem. Phys. Lipids 42 (1986) pp 249 ff. This type of product was found in micro-organisms, plants, tissue of vertebrates like the myocardium or the epidermis, as well as in amoebae and plant seedlings.
N-oleoyl-phosphatidylethanolamine is a phospholipid present in foods such as soja, egg, chocolate, etc. Phospholipids (PL) are crucial lipid components of biological membranes and, whilst present in the diet in much smaller gram amounts than triglycerides, are found typically in items including eggs, dairy, liver and oils such as soybean.
Soybeans, flaxseed, sunflower, wheat germ, egg yolk, milk, and canola seed all contain natural phospholipids, such as phosphatidylcholine, phosphatidylglycerol, phosphatidylserine, and phosphatidylethanolamine.
Soybeans are one of the richest plant sources of PE, commonly extracted as part of soy lecithin. Plant-derived PE is often used in liposomal encapsulation, nutraceutical products, and functional foods.
Within the body, NOPE is generated enzymatically in the intestinal mucosa. Intestinal mucosal cells internalize oleic acid released during fat digestion, through a mechanism that requires the membrane glycoprotein CD36; they then use the newly absorbed fatty acid as substrate for the biosynthesis of NOPE, a member of the N-acylphosphatidylethanolamine (NAPE) family of membrane phospholipids, and finally cleave NOPE to generate OEA.
The long evolutionary history of feeding-dependent OEA mobilization — and thus of NOPE biosynthesis — is indicated by its occurrence in the upper gut of mammals (mice and rats), reptiles (Burmese pythons, Python molurus), and fish (goldfish, Carassius auratus).
Oleoyl-phosphatidylethanolamine (OPE) is a phospholipid derived from phosphatidylethanolamine with an oleic acid moiety. While its direct historical use in traditional remedies is not widely documented, its parent compounds and related phospholipids have been integral to medicinal and nutritional practices for centuries.
Phospholipids, such as those found in lecithin-rich herbal and animal extracts, have been utilized in various cultures for their health-promoting properties, particularly in supporting cognitive function, liver health, and cellular vitality.
No documented tradition of the isolated compound NOPE exists as a discrete ingredient in pre-modern pharmacopoeias or ethnobotanical records. NOPE's profile as a dietary supplement ingredient is an entirely modern development, emerging from late twentieth- and early twenty-first-century biochemical research into the endogenous lipid-mediator system. Its scientific investigation as a supplement ingredient began substantively only after the identification of OEA's satiety-promoting properties in animal models in the early 2000s. The foods in which NOPE naturally occurs — eggs, soy, and chocolate, among others — do, however, have extensive traditional nutritional and medicinal histories across many cultures.
NOPE is not regarded as a pharmacologically active molecule in its intact form. Its significance arises from its role as the obligate biosynthetic precursor to oleoylethanolamide (OEA), a small bioactive lipid. The two-step biosynthetic cascade is well characterized in the scientific literature:
This produces an N-acylphosphatidylethanolamine, which is then split (hydrolyzed) by N-acyl phosphatidylethanolamine-specific phospholipase D (NAPE-PLD) into phosphatidic acid and OEA. The biosynthesis of OEA and other bioactive lipid amides is modulated by bile acids.
Duodenal infusion of fat stimulates OEA mobilization in the proximal small intestine, whereas infusion of protein or carbohydrate does not. OEA production utilizes dietary oleic acid as a substrate and is disrupted in mutant mice lacking the membrane fatty-acid transporter CD36.
OEA itself — the active metabolite of NOPE — has been extensively characterized. Oleoylethanolamide (OEA) is an endogenous peroxisome proliferator-activated receptor alpha (PPAR-α) agonist. It is a naturally occurring ethanolamide lipid that regulates feeding and body weight in vertebrates ranging from mice to pythons. OEA is a shorter, monounsaturated analogue of the endocannabinoid anandamide, but unlike anandamide it acts independently of the cannabinoid pathway, regulating PPAR-α activity to stimulate lipolysis.
Importantly, recent evidence suggests that NAPEs including NOPE may exert some appetite-relevant signaling independently of their conversion to NAEs. NAPEs have been considered for a long time simply as phospholipid precursors of lipid mediator NAEs, but an increasing body of evidence suggests a role in many physiological processes including the regulation of feeding behavior. Several observations demonstrated that among NAEs, oleoylethanolamide (OEA) acts as a satiety signal, generated in the intestine upon the ingestion of fat, and signals to the central nervous system. At this level, different neuronal pathways — including oxytocinergic, noradrenergic, and histaminergic neurons — seem to mediate its hypophagic action.
PE is known to be metabolized endogenously into a range of ethanolamides of long-chain fatty acids, collectively termed the N-acylethanolamines (NAEs), which include N-arachidonoylethanolamine (anandamide) and its analogue oleoylethanolamide (OEA). OEA is a lipid which has become prominent as an established inhibitor of food intake in animal models and which appears to regulate feeding through activation of the nuclear receptor peroxisome-proliferator-activated receptor-α (PPAR-α).
Among the several endogenous ligands proposed for PPARα, N-oleoylethanolamine (also known as oleoylethanolamide or OEA) activates with high-potency PPARα-driven transactivation in a heterologous expression system with a half-maximal concentration (EC₅₀) of 120 nM.
Synthetic PPAR-α agonists, but not agonists of PPAR-δ and PPAR-γ, produce a hypophagic response that is behaviorally indistinguishable from that elicited by OEA, and this response is absent in mutant mice lacking PPAR-α. A parsimonious interpretation of these results is that OEA regulates food intake in rodents by selectively activating intestinal PPAR-α.
Notably, OEA can also activate the G protein-coupled receptor GPR119 and the vanilloid receptor channel TRPV1, albeit at micromolar concentrations. However, the contribution of these receptors to the satiety-inducing effects of OEA is still undefined.
Evidence indicates that OEA operates as a local messenger within the gut and promotes satiety by recruiting afferent fibers of the vagus nerve. The lipid messenger OEA mediates fat-induced satiety by engaging sensory fibers of the vagus nerve that project centrally, and depletion of brain histamine blunts OEA-induced hypophagia in mice.
The OEA precursor, N-oleoyl-phosphatidylethanolamine (NOPE), and other N-acylated PE derivatives are also generated by the arrival of fat-containing chyme in the upper gut and may exert effects that are functionally similar but mechanistically distinct from those of OEA.
Targeted disruption of CD36 or PPAR-α abrogates the satiety response induced by fat. The results suggest that activation of small-intestinal OEA mobilization, enabled by CD36-mediated uptake of dietary oleic acid, serves as a molecular sensor linking fat ingestion to satiety.
The effects of OEA are mediated primarily by the activation of the peroxisome proliferator-activated receptor-α (PPAR-α). PPAR-α is a nuclear transcription factor that governs the expression of genes regulating fatty acid oxidation, lipid transport, and lipoprotein metabolism. The peroxisome proliferator-activated receptor α (PPARα) is a nuclear receptor involved in the control of lipid metabolism. The large multifunctional ligand-binding pocket of PPARα allows it to recognize a number of structurally heterogeneous molecules, both synthetic and natural.
A growing body of evidence indicates that oleoylethanolamide (OEA), a bioactive lipid mediator, has anti-inflammatory and antioxidant properties.
It was found, as a surprise especially in respect with the contrasting results of investigations of related products, that N-acylphosphatidylethanolamines can protect unsaturated fatty acids in free as well as bound form against oxidative decomposition. This product group provides several advantages in comparison with previously used antioxidants: these compounds are present in humans, animal, and plant organisms and are toxicologically safe.
In macrophage cell culture, an OEA-based dietary supplement (OEA-DS) reduced the intensity of cellular inflammatory reactions, accompanied by a decrease in markers of cellular inflammation and proliferation such as CD68, Iba-1, and Ki67 in spleen tissue, and stabilized the level of proinflammatory cytokines (IL-1β, IL-6, TNFα). In macrophage cell culture (RAW264.7), OEA-DS also suppressed the production of reactive oxygen species and nitrites in LPS-induced inflammation.
Similarly to NAEs, NAPE levels are regulated by the fed state; this finding was initially interpreted as fluctuations in NAE precursors. However, the observation that exogenously administered NAPEs are able to inhibit food intake, not only in normal rats and mice but also in mice lacking the enzyme that converts NAPEs into NAEs, supported the hypothesis of a role for NAPE in the regulation of feeding behavior. Indirect observations suggest that the hypophagic action of NAPEs might involve central mechanisms, although the molecular target remains unknown.
Epigallocatechin-3-gallate (EGCG) and oleoylethanolamide, together with its phospholipid precursor N-oleoyl-phosphatidylethanolamine (NOPE), are nutritional compounds that might improve the oxidative stress status of obese people. Unfortunately, the bioavailability of these compounds is low; however, the coadministration of NOPE with EGCG has been shown to ameliorate both the plasma availability of EGCG and the intestinal levels of NOPE in rats.
Produced primarily in the small intestine upon the absorption of dietary fat, OEA was demonstrated to act as a satiety signal in rodents by prolonging the interval between meals.
OEA decreases food intake by as much as 40–70% when introduced both by intra-peritoneal injection and orally into long-term fasted animals. Hence OEA has become a possible therapeutic target for modification of food intake and subsequent weight loss in humans. Effects of OEA are rapid, with significant changes in food intake observed 60 minutes post-dose and maintained over a period of 12 hours.
An early rat study published in Gazzetta Medica Italiana (2005) directly examined NOPE as a dietary supplement. Treatment for 8 weeks with a diet rich in saturated fats and cholesterol, compared to a standard diet, induced a dramatic increase in body weight and fat content of rats, with a decrease in protein mass and hydration state of tissues. There was also a significant increase in blood levels of triglycerides, total cholesterol, and glucose. The phospholipid was able to reduce food intake in the rats, probably through a mechanism that augments the endogenous level in the gut of its N-oleoylethanolamine derivative, a lipid mediator involved in the peripheral regulation of feeding.
In a previous study it was demonstrated that an oily dispersion of EGCG complexed with NOPE was more active than NOPE alone or EGCG alone in: (1) reducing food intake, (2) ameliorating in vivo plasma availability of EGCG, and (3) increasing the intestinal levels of NOPE, and consequently of NOE, in a group of diet-induced obese rats.
The most substantial clinical evidence for NOPE in weight management comes from a randomized, double-blind, placebo-controlled trial published in the British Journal of Nutrition (2008). The main aim of this study was to evaluate the efficacy of 2 months of administration of an oily NOPE-EGCG complex (85 mg NOPE and 50 mg EGCG per capsule) and its effect on compliance with diet in healthy, overweight people. Secondary endpoints were body composition, metabolic parameters, sensation of appetite, depressive symptoms, and severity of binge eating. Using a parallel-arm, double-blind, placebo-controlled design, 138 healthy, overweight women (106) and men (32) were randomly assigned to one of two groups: the treatment group (71 patients) taking two capsules per day of an oral supplement, or the placebo group (67 patients).
Key findings from this trial: Dropout was 6% in the NOPE-EGCG group and 27% in the placebo group (P < 0.001). The treatment induced a significant weight reduction in both groups (−3.28 kg and −2.67 kg in NOPE-EGCG and placebo, respectively); the weight changes were not significantly different between the groups. NOPE-EGCG treatment improved insulin resistance (P < 0.001), the sensation of fullness (P < 0.05), depressive symptoms (P < 0.004), and severity of binge eating (P < 0.0001).
The main finding of the present study was that administration of the NOPE–EGCG complex significantly improved compliance with diet in a group of healthy, overweight or obese subjects, as demonstrated by the patient dropout rate. This is a meaningful finding, in that both groups lost weight under caloric restriction but the supplement group was substantially more adherent to the dietary regimen — suggesting the primary benefit was one of appetite and mood rather than direct metabolic action on fat catabolism.
A second double-blind, randomized controlled trial published in Lipids in Health and Disease (2012) tested a slightly different dose. A dietary supplement containing a blend of 170 mg of N-oleyl-phosphatidylethanolamine (NOPE) and 100 mg of epigallocatechin-3-gallate (EGCG) had been shown to improve compliance to low-caloric diets. Considering the cost of dietary ingredients, many manufacturers attempt to determine the lowest efficacious dose. The purpose of this study was to evaluate the efficacy of 8-weeks of supplementation with a daily intake of 120 mg of NOPE and 105 mg of EGCG in conjunction with a low-caloric diet and regular, moderate exercise on dietary compliance in healthy, overweight adults.
Fifty healthy, overweight (BMI > 25 kg/m²) men (15) and women (35) were recruited for a double-blind, placebo-controlled study. Each volunteer was randomly assigned to either the supplement (n = 25) or placebo group (n = 25).
The conclusions of the 2012 trial were more modest: supplementing with a combination of 120 mg of NOPE and 105 mg of EGCG does appear to enhance compliance to a low-caloric diet and improve mood for 4 weeks, but loses its effectiveness by week 8. The results of this study suggest that a daily intake of 120 mg NOPE and 105 mg of EGCG for 4 weeks can enhance compliance to a low-caloric diet, total mood score, and feelings of fatigue and confusion, but does not alter body mass or body fat to any greater magnitude than placebo.
A separate trial — also a randomized crossover design — published by Lithander et al. (2008) in Lipids in Health and Disease assessed PE-containing lipids (not NOPE-specific) in 18 male participants. This was a 4-treatment intervention where 18 male participants were given a high-fat test breakfast containing (i) high-phospholipid, high-PE lipid, (ii) high-phospholipid, medium-PE lipid, (iii) no-phospholipid, no-PE control lipid, or (iv) water control, in a randomized crossover. Visual analogue scales (VAS) were used to assess post-ingestive hunger and satiety, and energy intake (EI) was measured at an ad libitum lunch meal after 3.5 hours. When compared with the water control, the 3 lipid treatments resulted in lower levels of hunger and thoughts of food, greater fullness and satisfaction (all, treatment×time interaction, P < 0.001), and a lower EI (P < 0.05). However, there were no differences between the PE-containing and non-PE lipid conditions, weakening direct attribution of any effect to PE or NOPE specifically.
The clinical evidence for NOPE in weight management is preliminary to moderate. The two most relevant human RCTs involved a NOPE-EGCG combination, making it impossible to isolate NOPE's contribution from EGCG's effects. Sample sizes were small (50–138 participants). The most robustly replicated finding across studies is improved dietary compliance and subjective fullness — not a direct pharmacological reduction in body mass. Weight loss outcomes did not differ from placebo in either primary trial. Larger, adequately powered, NOPE-only RCTs in humans are absent from the published literature.
Oxidative stress and lipid peroxidation are considered key factors linking obesity with its associated complications. Epigallocatechin-3-gallate (EGCG) and oleoylethanolamide, together with its phospholipid precursor N-oleoyl-phosphatidylethanolamine (NOPE), are nutritional compounds that might improve the oxidative stress status of obese people.
A human RCT published in the Journal of Medicinal Food (2020) investigated this further. This double-blind, placebo-controlled study investigated the effects of 2 months' supplementation with EGCG complexed with NOPE, combined with moderate energy restriction, on plasma oxidative status of overweight and class I obese subjects. A total of 138 subjects (BMI: 25–35 kg/m²) were recruited and randomized into two groups: the first (n = 67) received placebo capsules and the second (n = 71) received capsules of an oily dispersion. In total 116 subjects (27 M/89 F) completed the supplementation period, 49 in the placebo group and 67 in the treated group. Treatment induced a similar significant weight reduction in the two groups.
In animal models, the levels of malonyldialdehyde (an index of lipoperoxide content) in plasma and liver had increased with the obesity-producing diet. There was also a decrease of reduced glutathione, ATP, and membrane "fluidity" in the liver. These adverse changes were shown to be attenuated when NOPE was added to the diet in the animal experiment.
In a clinical trial focused specifically on OEA (the active metabolite), a randomized controlled trial was conducted on 60 obese patients with NAFLD. The patients were treated with OEA (250 mg/day) or placebo along with a low-calorie diet for 12 weeks; inflammatory markers and oxidative stress and antioxidant parameters were evaluated pre- and post-intervention. OEA supplementation could improve some oxidative stress/antioxidant biomarkers without any significant effect on inflammation in NAFLD patients. Further clinical trials with longer follow-up periods are demanded to verify the beneficial effects of OEA in these patients.
Evidence for antioxidant activity is preclinical (animal/in vitro) to preliminary human. The key human data involve the combined NOPE+EGCG formula, not NOPE alone. Mechanistic plausibility is high given PPAR-α's role in regulating oxidative stress pathways, but further human trials isolating NOPE's specific antioxidant contribution are lacking.
Obesity was induced by a 2-month high-fat, high-cholesterol diet, resulting in significant morphological changes in liver tissues and elevated cholesterol levels in the animals' blood serum. Elevated levels of proinflammatory cytokines, oxidative stress, and hepatocyte apoptosis were also observed in the liver tissue. The aim of a key study was to examine the mechanisms through which an OEA-based dietary supplement (OEA-DS) exerts a comprehensive influence on multiple aspects of the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD), thereby demonstrating a robust hepatoprotective effect.
Liver tissues and blood serum were analyzed for cholesterol levels, inflammatory markers (CD68, Iba-1, CD163, IL-1β, IL-6, TNFα), apoptotic markers (Bad, Bax, Bcl-2), nuclear receptors (PPAR-α, PPAR-γ, AdipoR1), and enzymes involved in lipolysis (Acox1, Cpt1a) and cholesterol metabolism (Ldlr, Furin, Pcsk9).
Regarding hepatic lipid metabolism specifically, oleoylethanolamide (OEA) is a naturally occurring bioactive lipid belonging to the family of N-acylethanolamides that has received great attention in the last two decades for its biological properties. Diet-derived oleic acid promotes OEA formation in the small intestine of different species including rats and mice; the membrane protein CD36, a multiligand class B scavenger receptor located on cell-surface lipid rafts, plays a pivotal role in OEA biosynthesis by acting as a biosensor for food-derived oleic acid and facilitating OEA mobilization.
Oleoylethanolamide (OEA) is an endogenous lipid messenger with multiple bioactivities and has therapeutic effects on various liver diseases.
This evidence base consists almost entirely of animal studies. No dedicated human clinical trial has evaluated NOPE specifically for liver health as a primary endpoint. Evidence for OEA (NOPE's active metabolite) in NAFLD/MASLD is limited to one small human RCT (n = 60) showing modest antioxidant improvements without significant anti-inflammatory effects. This area requires considerably more clinical investigation.
The 2008 British Journal of Nutrition trial also evaluated metabolic outcomes. NOPE-EGCG treatment improved insulin resistance (P < 0.001), the sensation of feelings of fullness (P < 0.05), depressive symptoms (P < 0.004), and severity of binge eating (P < 0.0001).
The improvement in insulin resistance is notable but must be interpreted cautiously because (a) the active preparation contained both NOPE and EGCG (which independently has been investigated for insulin signaling effects), and (b) both groups lost weight under caloric restriction, which independently improves insulin sensitivity.
Evidence is weak to preliminary in humans. One relatively small RCT reports a statistically significant improvement in insulin resistance with NOPE+EGCG, but the confounding effects of EGCG and caloric restriction cannot be separated. No dedicated NOPE-only human trial for metabolic parameters is available in the published literature.
In the primary 2008 RCT, NOPE-EGCG treatment improved depressive symptoms (P < 0.004) and severity of binge eating (P < 0.0001) compared to placebo.
These mood-related findings were partially replicated in the 2012 trial: a daily intake of 120 mg NOPE and 105 mg of EGCG for 4 weeks can enhance compliance to a low-caloric diet, total mood score, and feelings of fatigue and confusion. However, this effect was not sustained: supplementing with a combination of 120 mg of NOPE and 105 mg of EGCG does appear to enhance compliance to a low-caloric diet and improve mood for 4 weeks, but loses its effectiveness by week 8.
Evidence for mood and binge-eating improvements is preliminary. Results across the two available RCTs are inconsistent — the larger trial detected significant improvement while the smaller trial found only short-term (4-week) benefit. The active supplement in both studies was the NOPE+EGCG combination, precluding attribution to either component individually. EGCG has independent evidence in mood modulation that complicates attribution.
A hypercaloric diet high in carbohydrates and cholesterol led to the development of systemic inflammation, accompanied by organ morphological changes and increased production of proinflammatory cytokines. In parallel, the use of OEA-DS reduced the intensity of cellular inflammatory reactions, accompanied by a decrease in markers of cellular inflammation and proliferation, such as CD68, Iba-1, and Ki67 in the spleen tissue, and stabilized the level of proinflammatory cytokines (IL-1β, IL-6, TNFα) both in animals and in cell culture.
This is predominantly preclinical evidence. The one human RCT using OEA directly in NAFLD patients found OEA supplementation could improve some oxidative stress/antioxidant biomarkers without any significant effect on inflammation in NAFLD patients.
Evidence for anti-inflammatory activity is primarily animal and in vitro, with limited and mixed results from available human data. The discordance between preclinical anti-inflammatory signals and the null finding in inflammation markers in the one relevant human RCT underscores that translation to humans has not been established.
All dosages listed below are as reported in the cited peer-reviewed literature and do not represent recommendations.
All human trials of NOPE for which peer-reviewed data are available have used NOPE in combination with EGCG. No published human trial has examined NOPE as a single ingredient in isolation.
N-acylphosphatidylethanolamines can protect unsaturated fatty acids against oxidative decomposition. These compounds are present in humans, animal, and plant organisms and are toxicologically safe. This assertion about toxicological safety is based on NOPE's status as an endogenous compound and a normal dietary constituent.
Epigallocatechin-3-gallate (EGCG) and oleoylethanolamide, together with its phospholipid precursor N-oleoyl-phosphatidylethanolamine (NOPE), are nutritional compounds. In the human trials reported in the literature, no significant adverse events specifically attributable to NOPE were reported in the published results.
The bioavailability of these compounds is low; however, the co-administration of NOPE with EGCG has been shown to ameliorate both the plasma availability of EGCG and the intestinal levels of NOPE in rats.
Regarding the active metabolite OEA: the extreme insolubility of OEA has become a major obstacle to its application. Plus the fact that OEA could be enzymatically hydrolyzed and rapidly deactivated, OEA could not be used in the clinic in its current form. This bioavailability limitation applies to OEA as a direct supplement and is one reason NOPE (as its phospholipid precursor) has been investigated — it serves as a more lipid-compatible source from which OEA can be generated in situ in the intestine.
Solutions of phosphatidylethanolamine slowly decompose at room temperature (roughly 0.3–0.5% per day); hence, solutions should always be freshly prepared and kept cold prior to use. It is labile in alkaline conditions.
Alterations of the anorexiant NAE pathways might contribute to hyperphagia and to the development of obesity. Observations suggest that the mechanism of endogenous OEA mobilization is altered in animals rendered obese by exposure to a high-fat diet or in animals fed a high-sucrose, low-fat diet, in which OEA and LEA mobilizations from the intestine do not respond to the intraduodenal infusion of lipids. This may have implications for efficacy of supplemental NOPE in already obese individuals, as the biosynthetic and signaling pathways may be compromised.
Formally designated safety studies (preclinical toxicology with regulatory-grade design, maximum tolerated dose studies, or genotoxicity panels) on NOPE as an isolated supplement ingredient are not available in the published open-access literature reviewed here. The existing human trial data (n = 50–138, duration up to 8 weeks) do not provide an adequate basis to characterize the safety profile at doses other than those tested, in populations other than healthy overweight adults, or over durations longer than 8 weeks. Further clinical trials with longer follow-up periods are demanded to verify beneficial effects.
Health conditions that Oleoyl-phosphatidylethanolamine may help support.
Body systems that Oleoyl-phosphatidylethanolamine may help support.
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