The bioavailability of phosphatidylserine

Phosphatidylserine (PS) is a phospholipid widely present in cell membranes, particularly abundant in brain neurons. It plays physiological roles such as regulating neural signal transmission and improving cognitive function. However, its bioavailability is significantly influenced by molecular structure, intake form, and in vivo metabolic processes. Enhancing absorption efficiency has long been a core issue in research and applications. Below are key strategies to improve phosphatidylserine bioavailability from four aspects: formulation optimization, intake methods, synergistic ingredients, and source selection.

I. Formulation Optimization: Breaking Absorption Barriers

Phosphatidylserine has a large molecular weight (approximately 800–900 Da) and amphiphilic properties (containing hydrophobic fatty acid chains and hydrophilic phosphate groups). Free phosphatidylserine is easily degraded by digestive enzymes in the gastrointestinal tract and struggles to cross the lipid barrier of intestinal epithelial cells. Formulation modification can significantly enhance its absorption efficiency:

Liposome encapsulation: Encapsulating phosphatidylserine in liposomes (vesicles composed of phospholipid bilayers) protects it from gastric acid and digestive enzymes. Liposomes can fuse with intestinal mucosal cells to directly release their contents, improving transmembrane transport efficiency. Studies show that liposome-encapsulated phosphatidylserine has a 30%–50% higher absorption rate in rats compared to the free form.

Nanoemulsions or microencapsulation: Dispersing phosphatidylserine in oil phases to form nano-sized droplets, or encapsulating it in biodegradable polymers (e.g., chitosan) as microcapsules, increases its solubility in the gastrointestinal tract and prolongs release. For example, nanoemulsions containing phosphatidylserine exhibit higher peak blood concentrations in human trials, with a half-life extended by approximately 1.5 times.

Combination with surfactants: Adding small amounts of food-grade surfactants (e.g., lecithin, Tween 80) reduces the interfacial tension between phosphatidylserine and gastrointestinal contents, promoting dispersion into smaller particles and increasing contact area with intestinal mucosa, thereby indirectly enhancing absorption.

II. Intake Methods: Matching Physiological Rhythms and Digestive Environments

The absorption efficiency of phosphatidylserine is closely related to intake timing and dietary status. Rational intake methods can reduce damage from the gastrointestinal environment:

Taking with meals, preferably with high-fat foods: The hydrophobic structure of phosphatidylserine makes it more soluble in lipid environments. Postprandial bile secretion increases, and bile salts emulsify phosphatidylserine into mixed micelles, facilitating passive diffusion across intestinal epithelial cells. Studies indicate that co-administration with high-fat meals (e.g., foods containing olive oil) increases absorption by 20%–40% compared to fasting intake.

Avoiding co-administration with strong acids or alkalis: Phosphatidylserine is most stable in a neutral environment (pH 6.0–7.0). Fasting gastric juice has an extremely low pH (approximately 1.0–2.0), which may cause partial hydrolysis of phosphatidylserine molecules; co-administration with alkaline drugs (e.g., antacids) also disrupts structural integrity. Thus, taking it with meals (when gastric pH rises to 3.0–5.0 due to food buffering) is preferable.

III. Synergistic Ingredients: Leveraging Nutrient Enhancement

Certain nutrients can indirectly improve phosphatidylserine bioavailability by regulating the intestinal environment or promoting transporter expression:

B vitamins and antioxidants: Vitamins B6 and B12 enhance the metabolic activity of intestinal mucosal cells, facilitating transmembrane transport of phosphatidylserine; antioxidants like vitamins E and C reduce degradation caused by oxidative stress during absorption, with a more significant protective effect on plant-sourced phosphatidylserine (vulnerable to free radical attack).

Synergy with other phospholipids: Coexistence with natural phospholipids such as phosphatidylcholine (PC) and phosphatidylethanolamine (PE) forms more stable lipid complexes, reducing hydrolysis rates in the gastrointestinal tract. For example, natural phosphatidylserine extracted from soybeans or egg yolks, often accompanied by other phospholipids, has 15%–25% higher bioavailability than chemically synthesized pure phosphatidylserine.

IV. Source and Purity: Natural Extraction Over Chemical Synthesis

The source and preparation process of phosphatidylserine directly affect its structural stability and absorption characteristics:

Naturally sourced phosphatidylserine is more absorbable: Phosphatidylserine extracted from egg yolks or soybeans retains natural fatty acid chain compositions (e.g., rich in unsaturated fatty acids), exhibiting better compatibility with human cell membranes and higher emulsification/transport efficiency in the intestine compared to chemically synthesized forms. For instance, egg yolk-derived phosphatidylserine has an absorption rate approximately 20% higher than synthetic counterparts in humans.

Moderate purification preserves active structures: Over-purification may damage fatty acid chains or phosphate groups in phosphatidylserine, reducing biological activity. Studies show that naturally extracted phosphatidylserine with 70%–80% purity has better absorption efficiency and physiological activity than highly purified products (>95% purity).

Improving phosphatidylserine bioavailability requires multi-dimensional coordination: protecting its structure through liposomes or nanoemulsions; utilizing bile emulsification by taking it with high-fat meals; enhancing stability with natural phospholipids or antioxidants; and prioritizing moderately purified phosphatidylserine from egg yolk or soybean sources. These strategies collectively enhance intestinal absorption efficiency, enabling phosphatidylserine to better exert neuroprotective and other physiological functions.