Phytosterols 800mg.

Beta-sitosterol is normally the largest single sterol in a plant sterol blend, alongside campesterol and stigmasterol. Adding it raises the total sterol load acting at the same micellar step.

Brassicasterol is a rapeseed-derived sterol that competes with cholesterol for micellar space in the same way as sitosterol. It is part of the sterol mixture rather than a separate mechanism.

Plant sterols reduce how much cholesterol crosses the gut wall, while monacolin K restrains HMG-CoA reductase in the liver. Because the body compensates for a blocked absorption route by making more, the two act on the halves of one loop.

Sterols limit intestinal cholesterol uptake, and berberine raises hepatic LDL receptor expression by stabilising its messenger RNA. The two act at separate points of the same lipid handling loop.

Psyllium forms a viscous gel that carries bile acids out of the ileum, so the liver draws on cholesterol to rebuild them. Sterols meanwhile hold cholesterol out of the micelle, so the two reduce recycling at different steps.

Oat beta-glucan raises the viscosity of intestinal contents and reduces bile acid reabsorption. Plant sterols work on the micellar solubility of cholesterol itself, a separate lever in the same lumen.

Pectin binds bile acids and increases their loss in stool, while sterols displace cholesterol from the micelle. Both reduce how much cholesterol returns to the liver by separate routes.

Guar gum thickens intestinal contents and slows lipid and bile salt reabsorption. Sterols act inside the micelle, so the mechanisms do not overlap.

Bergamot polyphenols such as brutieridin carry an HMG-like side chain and act on hepatic cholesterol synthesis. Sterols act only in the gut lumen, so the pair covers two separate points.

EPA and DHA reduce hepatic triglyceride assembly and VLDL output, while plant sterols act on cholesterol absorption. The two address different lipid fractions and are commonly formulated together.

Plant sterols crowd carotenoids as well as cholesterol out of mixed micelles, which lowers circulating beta-carotene during regular sterol intake. Carotenoid-rich intake is normally raised alongside sterol use for this reason.

Lycopene shares the micellar route that sterols crowd, so plasma lycopene tends to fall with steady sterol intake. The interaction is a competition for solubilisation, not a chemical one.

Tocopherols enter the enterocyte through the same mixed micelles that sterols compete for. Lipid-adjusted vitamin E tends to move down modestly with sustained sterol intake.

Free sterols only compete with cholesterol once micelles have formed, which requires dietary fat and bile flow. Taken without a lipid load the same dose does much less.

Lutein reaches the enterocyte dissolved in the same mixed micelles that carry cholesterol, and plant sterols displace lipophilic passengers from those micelles. Sterol intake has been reported to lower circulating carotenoid concentrations, which is a marker change rather than a functional outcome. Separating intake across meals or taking carotenoids with a fat-containing meal is the usual formulation answer. The competition itself is established lipid absorption physiology.

Zeaxanthin is absorbed by the same micelle-dependent route as lutein, so the displacement effect of plant sterols applies to it in the same way. Reported effects are on blood carotenoid concentrations, a marker. The size of the effect depends on sterol dose, meal fat content and timing. This is transport competition, not chemical inactivation.

Astaxanthin needs bile-salt micelles and dietary fat to cross the intestinal barrier, the same dependency that plant sterols interfere with. Direct measurement of a sterol effect on astaxanthin specifically is thinner than for lutein or beta-carotene, so this is inference from a shared route. Dosing at a different meal reduces the overlap. Marked at Strong rather than Established for that reason.

Vitamin D3 is absorbed from mixed micelles and, like cholesterol, interacts with the NPC1L1 transporter and other intestinal lipid transporters. Sterols that compete for micellar space can therefore reduce how much is taken up from a given dose. Human data on sterols and vitamin D status are less consistent than for carotenoids, so this stays mechanistic. Taking the two at separate meals is the practical answer.

Phylloquinone is highly lipophilic and its absorption tracks the fat content of the meal it is eaten with. Plant sterols reduce the efficiency of that lipid absorption step. Any resulting change would show first as lower circulating vitamin K, a marker of status rather than a function measure. Separation in time keeps the two out of the same micelle pool.

Coenzyme Q10 has poor and saturable oral absorption that depends on bile and dietary lipid, the step plant sterols interfere with. A direct measurement of sterols lowering CoQ10 uptake is not established, so the concern is mechanistic rather than demonstrated. Formulators who combine them usually place CoQ10 in its own lipid vehicle or at a different meal. Recorded at Promising.

Free plant sterols are crystalline and almost insoluble, and they only act inside the intestinal micelle, so how well they disperse determines how much competition with cholesterol actually occurs. Phosphatidylcholine is a physiological emulsifier that participates in mixed micelle formation. Lecithin-based dispersions are a standard way to present crystalline sterols. The role is formulation and dispersion, not an added cholesterol effect of its own.

Sunflower lecithin supplies the same phosphatidylcholine-rich emulsifier function without soy-derived material, which matters for products positioned away from soy. Its purpose in a sterol formula is dispersing a poorly soluble crystalline solid so it can enter micelles. It contributes no independent effect on cholesterol handling. Confidence reflects standard formulation practice rather than a comparative trial.

Sterol competition happens inside bile-salt mixed micelles, so people with reduced bile delivery have less of the compartment the mechanism needs. Supplemental bile salts are used where bile flow is limited, for example after gallbladder removal. This is a dependency of the mechanism on normal fat digestion rather than a demonstrated additive benefit. Anyone in that situation should be working with a clinician.

Glucomannan forms a viscous gel that slows lipid and bile-salt diffusion toward the brush border, while sterols compete with cholesterol for micellar space. The two act on the same luminal step through independent physical mechanisms, so their effects on cholesterol absorption are not expected to overlap. Reported endpoints for both are blood lipid markers. Viscous fibres also reduce absorption of other nutrients taken at the same time.

Resistant starch is fermented in the colon, changing short-chain fatty acid production and bile acid pools further along the tract than where sterols act. Any interaction is indirect, through bile acid recycling rather than through micellar competition. Human evidence for the pairing is not established. Recorded as a modulating relationship at Promising.

Artichoke leaf has a long history of use for bile flow and appears in European monograph literature on that basis. Because sterol competition depends on bile-salt micelles, formulators pair the two on that reasoning. No combination study supports it and the size of any bile flow effect at supplement doses is unclear. Kept as a traditional pairing at Early confidence.

Aged garlic extract has been studied for effects on circulating lipid markers through mechanisms unrelated to intestinal sterol competition. Combining two independent mechanisms acting on the same marker is a common formulation logic. Whether the effects add in practice has not been measured for this pair. Both endpoints are markers, not outcomes.

Green tea catechins have been described as destabilising cholesterol-containing micelles and precipitating cholesterol in the lumen, a different physical route to the same step sterols act on. The two mechanisms are compatible in principle. Trial evidence for the combination specifically is not established. Catechin extracts also carry their own intake considerations at concentrated doses.