IngredientsLysophosphatidylcholine (abbreviated LPC; also historically called lysolecithin) is a class of bioactive glycerophospholipids defined by the presence of a single fatty-acid acyl chain attached to a glycerol backbone that also carries a phosphocholine head group. A lysophospholipid is a glycerophospholipid having a single fatty acid acyl chain bound to the glycerol by an ester bond. The "lyso-" prefix reflects the removal of one of the two fatty acids normally present in the parent phosphatidylcholine (PC) molecule, which introduces a free hydroxyl group in its place. The lysophospholipid is obtained by the removal of one fatty acid unit per molecule from a phospholipid and the introduction of a hydroxyl group in place thereof.
Lysophosphatidylcholine is a hydrolyzed phospholipid that is generated from the action of either phospholipase PLA1 or PLA2. There are two types of LPC: 1-LPC (where the omega-3 fatty acid at the sn-2 position is acylated) and 2-LPC (where the omega-3 fatty acid at the sn-1 position is acylated). The nature of the fatty acid esterified at the remaining position determines the specific molecular species. Common naturally occurring species include palmitoyl-LPC (16:0), stearoyl-LPC (18:0), oleoyl-LPC (18:1), linoleoyl-LPC (18:2), arachidonoyl-LPC (20:4), eicosapentaenoyl-LPC (LPC-EPA, 20:5), and docosahexaenoyl-LPC (LPC-DHA, 22:6).
In contrast to phospholipids, LPCs are "cone-shaped", with a polar "head" and a non-polar "tail" and therefore possess detergent-like properties. The geometry of the LPC structure is also determined by the degree of saturation of the acyl chain. Combined, the saturation and length of the acyl chain is detrimental to its biophysical properties as well as its activity.
Lysophospholipids are very widespread in nature, in both animals and plants, although they typically represent only a small fraction of the lipid components of cells. The existence of a polar part and of a lipophile in the molecule imparts particular properties to lysophospholipids and their presence modulates the rigidity and stability of the structures of the cell walls as well as that of artificial model membranes.
Formerly known as lysolecithins, elevated plasma levels of lysophosphatidylcholines (LPCs) were discovered in the 1950s in certain pathological conditions and were identified as a metabolic product of snake venom. As endogenous molecules, LPCs occur constitutively in human plasma at significant concentrations. Human blood of healthy donors contains about 100–500 μM LPC. In hyperlipidemic patients, its concentration can increase up to 1 mM.
The major dietary and exogenous sources of LPC include:
In nature, LPs (lysophospholipids) are present within the lipid matrix and are mostly available as lecithin (a complex mixture of phospholipids and glycolipids).
LPC products are prepared by the enzymatic action of phospholipase A2 on the respective tissue or diacyl L-α-phosphatidylcholine. Lysophospholipids have been produced generally by causing an enzyme to act on natural phospholipids or phospholipid-containing substances derived from organisms or by subjecting these to alkali hydrolysis. Large quantities of lysophospholipids are also used as emulsifiers in the food industry.
LPC does not have a documented history of use as a named, isolated constituent in any classical herbal or pharmacopeial tradition — it is an endogenous mammalian lipid metabolite and a component of complex mixtures such as lecithin, rather than a botanical drug with its own historical monograph. The broader compound class from which it derives, lecithin, was first isolated from egg yolk by the French chemist Théodore Gobley in 1845. The term "lysolecithin" entered the biochemical literature in the early 20th century when researchers identified it as a product of phospholipase hydrolysis of lecithin, including from snake venoms. Elevated plasma levels of lysophosphatidylcholines (LPCs) were discovered in the 1950s in certain pathological conditions.
The broader lecithin-rich food sources from which LPC derives — eggs, brain and organ meats, fish roe, soybeans — have been consumed in traditional diets across East Asia (particularly in Chinese and Japanese cuisine, where tofu, edamame, and fish roe are staples), in European peasant cooking (where eggs and offal were dietary cornerstones), and in coastal cultures globally. However, no traditional system specifically ascribed physiological effects to LPC as an isolated constituent. The modern scientific investigation of LPC as a distinct bioactive entity began substantially in the 1990s and accelerated rapidly with the advent of mass spectrometry-based lipidomics in the 2000s.
In addition to the structural function, lyso-PCs act as regulators of various enzyme activities, and can be used as biological markers to indicate pathological states. The use of lysophospholipids as ingredients in pharmacological formulations is widely documented; for example, lyso-PC has been studied as an ingredient of nasal formulations and oral formulations.
LPC is not a single compound but a family of molecular species differentiated by the length and degree of unsaturation of their acyl chain. In human plasma, the dominant species by abundance are LPC 16:0 (palmitoyl), LPC 18:0 (stearoyl), LPC 18:1 (oleoyl), and LPC 18:2 (linoleoyl), with polyunsaturated variants such as LPC 20:4 (arachidonoyl), LPC 20:5 (EPA), and LPC 22:6 (DHA) present in smaller amounts but of high biological interest.
Plasma LPCs are bioactive lipid metabolites of phosphatidylcholine, which are mainly produced by the action of secretory phospholipases A2 (sPLA2) after removal of a fatty acid. LPCs are also produced by the action of HDL-associated lecithin-cholesterol acyltransferase in the reverse cholesterol pathway. LPC is a bioactive phospholipid generated primarily by the action of phospholipase A2 (PLA2) enzymes on plasma membrane- and lipoprotein-phosphatidylcholine containing saturated fatty acid at the sn-1 and mostly unsaturated FA at the sn-2 position. LPC can also be produced as a by-product by lecithin cholesterol acyltransferase (LCAT) in high-density lipoprotein (HDL) as well as from oxidation of low-density lipoprotein (LDL) and by endothelial lipase (EL).
Lipoprotein-associated phospholipase A2 (Lp-PLA2, also known as PAF-AH) is a specific pathway of LPC generation in the context of cardiovascular disease: it catalyzes the breakdown of oxidized phospholipids within oxLDL, especially oxidized phosphatidylcholines, producing two signaling molecules: LysoPC and oxidized non-esterified fatty acids.
The family of sPLA2 enzymes contains 10 catalytically active isoforms (IB, IIA, IIC, IID, IIE, IIF, III, V, X), which are differentially expressed in tissues and exhibit unique substrate selectivity.
LPC plays a biological role by binding to G protein-coupled receptors and Toll-like receptors. Lysophosphatidylcholine has been found to serve in cell signalling, and possible receptors (coupled to G proteins) have been identified, i.e., GPR119, GPR40, GPR55 and G2A (GPR132), with the last probably most important, in addition to Toll-like receptors and ion channels.
Importantly, LPC can bind to G protein-coupled receptors (GPCRs) and Toll-like receptors (TLRs), activate transcription factors, stabilize mRNA and then increase the expression of target genes through Ca²⁺-mediated second messenger or directly inducing downstream inflammatory signalling pathways, which could increase the release of inflammatory factors, or induce the expression of adhesion molecules.
LPC can induce the migration of lymphocytes and macrophages, increase the production of pro-inflammatory cytokines, induce oxidative stress, and promote apoptosis, which can aggregate inflammation and promote the development of diseases.
Exogenous LPC induces pro-inflammatory effects such as upregulated gene expression for smooth muscle/fibroblast-directed growth factors and adhesion molecules in endothelial cells, increased release of interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) from adipocytes, enhanced secretion of interferon-γ from peripheral blood mononuclear leucocytes, and increased activation of B cells and macrophages. However, LPC enhances the Foxp3 expression and suppressive function of naturally occurring regulatory T cells (nTregs); these actions are believed to be mediated through G2A signaling.
This dual role is a central theme in LPC research. Lysophosphatidylcholines are widely regarded as potent pro-inflammatory and deleterious mediators, but an increasing number of more recent studies show multiple beneficial properties under various pathological conditions. Many of the discrepancies in the published studies are due to the investigation of different species or mixtures of lysophosphatidylcholines and the use of supra-physiological concentrations in the absence of serum or other carrier proteins.
There are many mechanisms by which LPC induces apoptosis, such as caspase activation, calcium influx, the release of cytochrome C, and the mitochondrial pathway. LPC increases ROS generation and enhances oxidative stress.
Lysophosphatidylcholine is the precursor of the lipid mediator lysophosphatidic acid via the action of the enzyme autotaxin in plasma, and this may be the true source of some of the effects on cell migration and survival ascribed to the former. LPC and lysophosphatidic acid (LPA), the most prominent lysoglycerophospholipids, are emerging as a novel class of inflammatory lipids, joining thromboxanes, leukotrienes and prostaglandins with which they share metabolic pathways and regulatory mechanisms. Enzymes that participate in LPC and LPA metabolism, such as the phospholipase A2 superfamily (PLA2) and autotaxin (ATX, ENPP2), play central roles in regulating LPC and LPA levels and consequently their actions.
Recent studies show that PUFAs such as DHA (22:6) are transported across the blood–brain barrier (BBB) in the form of lysophosphatidylcholine (LPC) via a specific LPC receptor at the BBB known as the sodium-dependent LPC symporter 1 (MFSD2A). Mfsd2a transports long-chain unsaturated fatty-acids, including DHA and α-linolenic acid (ALA), that are attached to the zwitterionic lysophosphatidylcholine (LPC) headgroup. These activities appear to be facilitated by the acute function of a major facilitator superfamily domain-containing protein 2 (Mfsd2a), expressed in BBB endothelium, as a chief transporter for LPC-DHA uptake to the brain.
The 2-LPC type is more highly bioavailable to the brain than the 1-LPC type.
LPC(16:0) and LPC(18:1), which represent approximately 60% of total plasma LPC, can act as lipid signaling molecules, activate PPARδ-dependent gene expression and reduce fatty acid-induced inflammation in human myotubes. Thus, data suggest that the reduced plasma LPC levels reported in obese and insulin resistant subjects can contribute to the development of the metabolic syndrome, while high LPC levels might be protective.
Although 18:2 LPC was inactive, 16:0, 18:1, and 20:4 LPC induced PGI2 (prostacyclin) production in human aortic endothelial cells by 1.4-, 3-, and 8.3-fold, respectively. LPC-elicited 6-keto PGF1α formation depended on both cyclooxygenase (COX)-1 and COX-2 and on the activity of cytosolic phospholipase type IVA (cPLA2).
Blood-Brain Barrier Transport and DHA Delivery (Preclinical)
The most robustly mechanistically supported area of LPC research concerns its role as the physiologically preferred carrier form for delivering long-chain polyunsaturated fatty acids, particularly DHA, across the BBB. The major pathway by which omega-3 fatty acids are taken up by the brain is through their natural conjugation to LPC and transport into brain by Mfsd2a. Triglycerides containing omega-3 fatty acids and non-conjugated fatty acids are not transported by this major pathway and thus are taken up primarily by the liver and other organs. Moreover, Mfsd2a deficient mice exhibit small brains and neurological deficits, and are deficient in brain DHA. Brain uptake of LPC-fatty acids such as LPC-DHA and other common LPC-fatty acids are essential for normal brain growth and function.
Animal studies have provided quantitative evidence of differential brain uptake. In a rat model, LPC-DHA was found to be preferentially taken up by the brain at a level of 4.5% of the injected radiolabelled LPC-DHA, compared to free DHA that was taken up at only 0.3–0.4% of radiolabelled non-esterified DHA. Another study showed that oral gavage with DHA esterified in LPC resulted in higher enrichment of DHA in several regions of the brain, than gavage with DHA esterified in phosphatidylcholine (PC). In that study, levels of DHA were twice as high in the hippocampus, the striatum, and amygdala of rats given LPC-DHA compared to those not given DHA in any form.
For EPA specifically, the brain contains negligible amounts of EPA, and dietary supplements fail to increase it appreciably. The hypothesis was tested that this failure is due to absorption of EPA as triacylglycerol, whereas the transporter at the blood-brain barrier requires EPA as lysophosphatidylcholine (LPC). A comparison of tissue uptake was made in normal mice gavaged with equal amounts (3.3 μmol/day) of either LPC-EPA or free EPA (surrogate for current supplements) for 15 days.
Dietary lysophosphatidylcholine (LPC)-DHA significantly increases brain DHA, which results in increase of brain BDNF. Since there is bidirectional transport of BDNF through the BBB, plasma BDNF was tested as a potential biomarker for brain DHA enrichment.
ApoE Genotype Dependency (Preclinical)
A study showed that oral supplementation with lysophosphatidylcholine (LPC)-bound omega-3 fatty acids increases cortical eicosapentaenoic acid (EPA, C20:5n-3) but not docosahexaenoic acid (DHA, C22:6n-3) in an apolipoprotein E (APOE)- and duration-dependent manner. This finding has implications for the use of LPC-omega-3 supplementation in APOE ε4 carriers, who face elevated Alzheimer's disease risk, but direct human clinical trials are needed.
Evidence Strength: The mechanistic evidence for LPC as a BBB transporter for DHA and EPA is well-established through multiple animal and molecular biology studies, including cryo-EM structural characterization of the Mfsd2a transporter. LPC-bound forms of DHA/EPA may allow for enhanced brain uptake and utilization. Clinical trials are needed to confirm neuroprotection and the safety profile. At the time of this writing, the human clinical evidence for LPC-omega-3 supplementation improving cognitive outcomes remains preliminary and lacking from large randomized controlled trials.
Multiple human observational and lipidomic studies have examined LPC species in the context of Alzheimer's disease (AD). To explore the lipidomic biomarkers associated with cognition function and neuropathological changes in AD, non-targeted mass spectrometry was utilized on 316 post-mortem brains from participants in the Religious Orders Study (ROS) or Rush Memory and Aging Project (MAP) cohorts classified as control, asymptomatic AD (AAD), or symptomatic AD (SAD). Lysophosphatidylethanolamine (LPE) and lysophosphatidylcholine (LPC) species are significantly lower in SAD than controls or AAD.
Plasma metabolites were measured in 1,068 participants of Caribbean Hispanic ancestry (250 patients with AD and 818 healthy controls) across 2 cohorts and analyzed for their relationship with clinical AD, biomarker-supported AD and plasma biomarkers. Through several dimensionality reduction approaches, researchers identified an APOE-ε4 dependent relationship between lysophosphatidylcholines (lysoPCs) carrying polyunsaturated fatty acids and biomarker-supported AD.
In some studies, the LPC:PC ratio decreased either in plasma or cerebrospinal fluid from patients with Alzheimer's disease. However, findings from recent clinical lipidomics studies have been controversial and somewhat confusing. For example, plasma LPCs showed an inverse relationship with cardiovascular diseases in some analyses.
Evidence Strength: The association of altered LPC species with AD biomarkers and post-mortem brain pathology is supported by multiple human observational studies and lipidomic analyses. However, all findings are associational — causality has not been established, and no controlled human trials of LPC supplementation for AD prevention or treatment have been completed.
The role of LPC in atherosclerosis is well-studied but remains genuinely dual in nature. LPC is the main component of oxidatively damaged low-density lipoprotein (oxLDL). The effects of LPC on endothelial cells, vascular smooth muscle cells and arteries play a vital role in the progression of atherosclerosis and other cardiovascular diseases.
To determine whether the level of lysophosphatidylcholine (lysoPC) generated by lipoprotein-associated phospholipase A2 (Lp-PLA2) is associated with severity of inflammation in human atherosclerotic plaques: Lp-PLA2 hydrolyzes low-density lipoprotein–oxidized phospholipids generating lysoPCs. According to in vitro studies, lysoPCs are proinflammatory but the association between their generation and plaque inflammation remains unknown. Inflammatory activity in carotid plaques (162 patients) was determined immunohistochemically and by analyzing cytokines in homogenates. LysoPCs were quantified using mass spectrometry and Lp-PLA2 and the lysoPC metabolite lysophosphatidic acid (LPA) by ELISA. There was a strong correlation among lysoPC 16:0, 18:0, 18:1, LPA, and Lp-PLA2 in plaques.
Lipid moieties such as lysophosphatidylcholine (LPC) and ceramide (CER) contribute to atherogenic events. LPC and CER both cause endothelial mitochondrial dysfunction, leading to fatty acid and triglyceride (TG) accumulation. In addition, they cause immune cells to differentiate into proinflammatory phenotypes.
Conversely, anti-atherogenic properties have also been documented. An increasing number of more recent studies show multiple beneficial properties under various pathological conditions. In clinical lipidomic studies, plasma LPCs showed an inverse relationship with cardiovascular diseases. In cardiovascular disease, certain phospholipases A2 generating LPC from cell membrane or lipoprotein derived PC have been evaluated as biomarkers of cardiovascular risk. This includes the family of secretory phospholipases A2 (sPLA2) of which elevated levels and certain polymorphisms of GIIA sPLA2 predict cardiovascular events. Similar results were described for lipoprotein phospholipase A2 (LpPLA2), indicating higher risk for coronary heart disease and ischemic stroke in individuals with higher LpPLA2 activity or concentration.
Evidence Strength: The association between LPC (particularly saturated species generated from oxLDL) and atherosclerotic plaque inflammation has been demonstrated in human tissue studies. Epidemiological lipidomics data on circulating LPC and cardiovascular risk are mixed and sometimes contradictory, depending on the LPC species measured, the analytical method, and whether LPC is derived from beneficial (e.g., HDL-LCAT activity) or deleterious (e.g., oxLDL) pathways. No intervention trials using exogenous LPC supplementation to reduce cardiovascular risk have been reported.
Reduced circulating LPC in sepsis has been documented across multiple clinical studies. Researchers evaluated serum lysophosphatidylcholine (LPC) 16:0 as a biomarker of sepsis using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). Patients admitted to an intensive care unit were prospectively enrolled. Of 127 patients, 14 had non-infectious SIRS, 41 had sepsis, and 72 had septic shock. The mean serum LPC 16:0 concentration (µmol/L) in non-infectious SIRS was significantly higher than in patients with sepsis and septic shock (101.1 vs. 48.92, p < 0.05; 101.1 vs. 25.88, p < 0.001, respectively).
The mean serum LPC concentrations were 43.49 ± 33.09 µmol/L in sepsis patients and lower than those of 21 healthy controls (234.68 ± 30.33 µmol/L, P < 0.001). Previous studies showed that LPC was significantly decreased in sepsis patients and might be an important biomarker to predict sepsis-related mortality.
In sepsis patients, absolute concentrations of total LPC as well as of major LPC species were found significantly decreased compared to healthy controls.
Evidence Strength: Multiple prospective and cross-sectional clinical studies in ICU populations have consistently documented that serum LPC is significantly depressed in sepsis, with deeper reductions correlating with greater severity. The biomarker utility of LPC 16:0 for diagnosing sepsis is supported by human clinical data. These are observational findings; no trials have tested LPC supplementation as a therapeutic intervention in sepsis.
Metabolomics studies of human plasma demonstrate a correlation of lower plasma lysophosphatidylcholines (LPC) concentrations with insulin resistance, obesity, and inflammation.
In a quantitative plasma lipid profiling study of obese subjects before and after 3-month weight loss, as well as in a control group, the comparison of obese subjects with control subjects before weight loss revealed significantly lower lysophosphatidylcholine (LPC) concentrations in obesity.
Data from a human cohort showed a reduction in a number of LPC species in obese and obese individuals with T2DM. Interestingly, no differences were found between the obese otherwise healthy individuals and the obese T2DM patients. Irrespective of species, lipidomic profiling revealed a generalized decrease in circulating LPC species in states of obesity. Moreover, data indicate that diet and adiposity, rather than insulin resistance or diabetes per se, play an important role in altering the plasma LPC profile.
Total LPC as well as a number of LPC species not only correlate negatively with BMI but also with CRP, possibly indicating a role of LPC as a marker of inflammation in obesity.
The "lysophosphatidylcholines to phosphatidylcholines" and "cholesteryl ester to free cholesterol" ratios were reduced in metabolic syndrome, pointing to a lower activity of lecithin cholesterol acyltransferase (LCAT); LCAT activity was positively correlated with high-density lipoprotein cholesterol (HDL-C) and negatively correlated with body mass index (BMI) and insulin resistance.
Evidence Strength: Multiple independent human lipidomic studies — using ESI-MS/MS and related platforms — have consistently shown an inverse association between plasma LPC species and obesity/insulin resistance. This is an area of robust biomarker evidence. However, the evidence is exclusively observational/associational. Whether LPC reduction contributes causally to metabolic syndrome or simply reflects it is not yet established, and no human trials of supplemental LPC for metabolic outcomes have been reported.
For decades, lysophosphatidylcholine (LPC, lysolecithin) has been used to induce demyelination, without a clear understanding of its mechanisms. LPC is an endogenous lysophospholipid so it may cause demyelination in certain diseases. Research investigated whether known receptor systems, inflammation or nonspecific lipid disruption mediates LPC-demyelination in mice. LPC integrates into cellular membranes causing cell death and demyelination due to its lipid-disrupting properties.
LPC exerts toxicity through disruption to lipids within the myelin sheath, increasing membrane permeability, compromising myelin integrity, leading to eventual breakdown and loss of oligodendrocytes. As such, LPC is considered directly toxic to mature, myelin-producing oligodendrocytes as opposed to non-myelinating cells of the oligodendroglial lineage.
Evidence Strength: This application is confined to preclinical experimental research and is not a health-promoting use of LPC supplementation. Rather, it establishes that locally elevated, non-physiological concentrations of LPC applied directly to nervous tissue are demyelinating — a finding relevant to understanding pathological conditions but not to oral supplementation.
At the maternal plasma/placental interface, phosphatidylcholine is taken up and hydrolyzed to sn-2-lysophosphatidylcholine, presumably by the endothelial lipase, to facilitate transfer of polyunsaturated fatty acids across the basal membrane into the foetal circulation with the aid of the LPC transporter. It may also be a source of choline for the developing foetus.
Defects in Mfsd2a are linked to ailments from behavioral and motor dysfunctions to microcephaly. This indicates the physiological importance of the LPC transport system for normal brain development, though research in this area remains predominantly preclinical.
LPC does not have an established recommended dietary allowance (RDA), tolerable upper intake level (UL), or pharmacopeial monograph with defined dosing. The following dosages appear in the peer-reviewed scientific literature:
LPC-enriched supplements are commercially available primarily as LPC-DHA and LPC-EPA preparations derived from marine sources. A clinical study in premenopausal women (n=11) found that the alterations to the plasma lipidome differed following supplementation with krill oil and fish oil, which differ in the molecular form composition of omega-3 PUFAs. Krill oil led to greater changes in levels of phosphatidylcholine-bound omega-3 PUFAs, which is consistent with krill oil containing a high percentage of phosphatidylcholine-bound DHA/EPA compared with fish oil, which is primarily comprised of triglyceride-bound DHA/EPA. This small study did not evaluate clinical outcomes and was not a therapeutic trial.
The mechanism for demyelination involves the integration of LPC into the cell membrane, which induces permeability and necrotic cell death. This effect has been demonstrated experimentally when LPC is injected directly into neural tissue at supraphysiological concentrations; it is the basis for widely used animal models of demyelinating disease. The relevance of this finding to oral ingestion of LPC at typical supplement dosages is unknown and has not been directly tested.
Many of the discrepancies in the published studies are due to the investigation of different species or mixtures of lysophosphatidylcholines and the use of supra-physiological concentrations in the absence of serum or other carrier proteins. In vivo, LPC in plasma is distributed between albumin or other carrier serum proteins and lipoproteins. Carrier proteins substantially modulate biological activity.
Interpretation of LPC effects is complicated by the rapid metabolism of lysophosphatidylcholine (LPC) in cells and tissues to pro-inflammatory lysophosphatidic acid. The downstream conversion to LPA by autotaxin adds a layer of biological complexity that affects how LPC effects should be interpreted.
Researchers have found increased levels of LPC in atherosclerosis, inflammatory disease, diabetes, adrenoleukodystrophy, and squamous cervical cancer, while lower concentrations of LPC have been reported in infectious diseases, ovarian cancer, and colorectal cancer. This non-linear relationship between LPC levels and disease states reflects both the species-specific nature of LPC biology and the context-dependency of its effects.
There are suggestions that some experimental studies in vitro of lysophosphatidylcholines may be flawed because insufficient levels of carrier proteins were used. This caveat applies to interpreting a substantial proportion of the in vitro safety and toxicology data for LPC.
Elevated levels of 26:0-lysophosphatidylcholine in blood are reported to be a robust biomarker for Zellweger spectrum disorders such as X-linked adrenoleukodystrophy, which is caused by pathogenic variants in the ABCD1 gene encoding an ATP-binding cassette membrane protein that transports very-long-chain saturated fatty acids into peroxisomes for β-oxidation. If this lipid biomarker is detected in dried blood spots during newborn screening, it can identify potential patients and prevent disease onset. This illustrates that quantitative monitoring of specific LPC species is clinically meaningful in the context of peroxisomal disorders.
No specific human safety trials or toxicological dose-finding studies of oral LPC supplementation were identified in the peer-reviewed literature at the time of this writing. LPC is an endogenous human metabolite present at micromolar concentrations throughout life. Its safety as an isolated oral supplement at doses above those achievable from food has not been formally characterized in controlled human studies.
Health conditions that Lysophosphatidylcholine may help support.
Body systems that Lysophosphatidylcholine may help support.
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