IngredientesCampestanol is a naturally occurring phytostanol — the saturated form of a plant sterol — found in trace quantities across a wide range of plant foods and concentrated commercially from vegetable oils and tall oil. It is one of the minor but biologically significant members of the phytosterol family, and it has attracted sustained scientific and regulatory attention primarily because of its role, alongside its more abundant counterpart sitostanol, in reducing intestinal cholesterol absorption. Its safety and efficacy as a component of plant stanol ester functional foods have been evaluated by the U.S. Food and Drug Administration (FDA), the European Food Safety Authority (EFSA), the Joint FAO/WHO Expert Committee on Food Additives (JECFA), and other major regulatory and scientific bodies.
Campestanol is formally designated by the systematic IUPAC name 3β,5α-ergostan-3-ol and carries the Chemical Abstracts Service (CAS) registry number 474-60-2. It is also known by the synonym 24-methyl-5α-cholestan-3β-ol. The "campestanol" name derives from campesterol — its unsaturated precursor — which in turn takes its name from the rapeseed plant, Brassica campestris, from which that parent sterol was first isolated.
The chemical structure of phytosterols, including campestanol, consists of a sterol-derived tetracyclic core decorated with ring and/or C17 side-chain modifications; plant stanols such as campestanol are saturated plant sterols that possess no double bonds in the sterol ring moiety. Plant sterols differ from cholesterol only in the structure of their side chain, whereas saturated sterols termed stanols lack the Δ5 double bond in their B-ring. Campestanol is obtained from campesterol by hydrogenating the double bond between carbons 5 and 6 and removing carbon 242. Because this double bond saturation removes the one structural feature that distinguishes the most absorbed dietary sterols from stanols, campestanol is much more resistant to intestinal uptake than its parent campesterol.
Phytosterols are natural components of the human diet and are cholesterol-like and lipophilic, comprising both sterols and stanols; stanols are the hydrogenated products of sterols. Campestanol is therefore the stanol form of campesterol. The structures of sitosterol and campesterol, and the corresponding stanols sitostanol and campestanol, are directly related: each stanol is the fully saturated ring analog of its parent sterol.
Of more than 250 sterols and stanols known to exist in nature, only six — campesterol, campestanol, stigmasterol, sitosterol, sitostanol, and brassicasterol — are dominant in seed oils (rapeseed, soybean, corn, and sunflower oils), other grains (corn, rye, wheat, barley, millets, rice, oats, and peanuts), and tree oils.
The most abundant phytosterols in the human diet are sitosterol and campesterol; their saturated counterparts, sitostanol and campestanol, are found in much lower amounts. Good food sources of phytosterols include vegetable oils, cereal grains, nuts, legumes, and fruits and vegetables. Sitostanol and campestanol occur naturally in small quantities in the lipid fractions of cereal grains such as wheat, rye, and corn, and in vegetable oils such as corn and olive oil.
The most commonly occurring phytosterols in the human diet are β-sitosterol, campesterol, and stigmasterol, which account for about 65%, 30%, and 3% of dietary phytosterol content, respectively; the most common plant stanols in the human diet are sitostanol and campestanol, which combined make up about 5% of dietary phytosterol.
In cereal bran, sitostanol and campestanol have been reported to account for 13.9% and 9.9% of total sterols, respectively, in bran, and 3.9% and 3.1% in germ; the contribution of stanols to total sterols in bran has varied across studies from 26 to 37%.
The average western diet provides 20 to 50 mg of plant stanols daily. This is far below the quantities (approximately 1.5–3 g/day) required to produce measurable cholesterol-lowering effects in clinical studies.
In plant tissues, sterols and stanols can exist as conjugates, often esterified with fatty acids such as oleic or linoleic acid, in five distinct forms. The richest naturally occurring sources of phytosterols are vegetable oils and products made from them; sterols can be present in the free form and as fatty acid esters and glycolipids.
Commercially, phytosterols are isolated from vegetable oils such as soybean oil, rapeseed (canola) oil, sunflower oil, or corn oil, or from so-called "tall oil," a by-product of the manufacture of wood pulp. Phytosterols can be hydrogenated to obtain phytostanols.
The composition of the resulting stanol mixture depends significantly on the source material. Phytostanols produced from tall oil sterols typically contain approximately 90% sitostanol and approximately 10% campestanol, whereas a blend of stanols obtained from vegetable oils, typically from soybean oil, contains 68–75% sitostanol and 25–32% campestanol.
Starting with unsaturated phytosterols, pure saturated phytostanols can be obtained by hydrogenation, a process in which the double bond in the sterol molecule is saturated by the addition of hydrogen; this reaction is carried out in a suitable solvent under high hydrogen pressure, generally using a noble-metal-based catalyst such as palladium or platinum.
Both phytosterols and stanols, which are high-melting powders, can be esterified with fatty acids of vegetable (oil) origin; the resulting esters are liquid or semi-liquid materials having comparable chemical and physical properties to edible fats and oils, enabling supplementation of various processed foods with phytosterol and phytostanol esters.
The esterification process was patented by the Finnish company Raisio Group in 1989, resulting six years later in their marketing of Benecol margarine. Currently there are two main phytosterol-based ingredients used in commercial foods: plant stanol ester, based almost exclusively on plant stanols (sitostanol and campestanol), and plant sterol ester, based mainly on plant sterols (sitosterol and campesterol).
In a characterized commercial product investigated clinically, a plant stanol ester snack bar delivered 1.54 g of plant stanols and 0.1 g of plant sterols per day; the sterol composition was sitostanol 85.6%, campestanol 8.0%, sitosterol 3.0%, and campesterol 2.5%.
EFSA's specification for the authorised novel food category 'phytosterols/phytostanols' sets maximum composition limits: the authorised novel food concerns phytosterols extracted from plants that may be presented as free sterols and stanols or esterified with food-grade fatty acids; it must contain less than 81% β-sitosterol, less than 35% β-sitostanol, less than 40% campesterol, less than 15% campestanol, less than 30% stigmasterol, and less than 3% brassicasterol.
Phytosterols have a long history of safe use, dating back to Cytellin, the pharmaceutical preparation of phytosterols marketed in the US from 1954 to 1982; phytosterol esters have generally recognized as safe (GRAS) status in the US. The U.S. FDA has specifically identified campestanol as one of the phytosterols qualifying for a coronary heart disease health claim. Plant stanol esters are prepared by esterifying a mixture of plant stanols derived from edible oils or byproducts of the kraft paper pulping process with food-grade fatty acids; the plant stanol mixture must contain at least 80% sitostanol and campestanol (combined weight). Current science recognizes that the phytosterol substance for such health claims should consist of at least 80% sitosterol, campesterol, stigmasterol, sitostanol, and campestanol combined.
Campestanol itself was not identified or isolated as a discrete compound in traditional botanical medicine — traditional and historical use applies to the plant materials and crude phytosterol-containing preparations rather than to purified campestanol. The history of phytosterols as a therapeutic class is relevant, however, because campestanol is a constituent of all phytosterol-rich plant materials used historically.
The cholesterol-lowering properties of phytosterols were first demonstrated approximately 50 years ago by Peterson, who fed chicks plant sterols in their diet; shortly thereafter, Pollak showed the same effect in humans, to whom he administered crude sitosterol at 5 to 10 g/day for up to 8 months. These early studies used crude plant sterol mixtures in which campestanol was present as a minor component, alongside the dominant sitosterol.
Campestanol-containing plant foods — including whole grain cereals, vegetable oils, and legumes — have been integral to diets across many cultures for millennia, and the phytosterol content of such foods is now recognized to have contributed passively to cardiovascular health through reduced cholesterol absorption. However, there is no documented tradition of isolating or consciously concentrating plant stanols for medicinal purposes prior to the 20th century. The deliberate exploitation of campestanol and sitostanol as functional food ingredients is a product of late 20th-century nutritional science, not of traditional healing systems.
Phytosterols are plant sterols with chemical structure and biofunctionality similar to cholesterol; nonetheless, phytosterols differ from cholesterol by possessing an additional side chain with methyl or ethyl substituents. In campestanol specifically, the added methyl group at C-24 and the fully saturated ring system together render the molecule structurally analogous to cholesterol but with critically different behavior in the intestinal lumen.
Despite structural similarity to cholesterol, phytosterols are not absorbed in significant quantities; absorption is less than 2% for phytosterols, while it is 30–60% for cholesterol. The stanol form (campestanol) is even more poorly absorbed than the sterol form (campesterol). Absorption of sitostanol has been estimated to be between 0 and 3%, and serum levels are practically undetectable; the absorption of the other major stanol, campestanol, is also very low, in contrast to its unsaturated counterpart, campesterol.
Phytosterols and phytostanols lower LDL cholesterol by displacing cholesterol from mixed micelles in the small intestine so that cholesterol absorption is partially inhibited. Plant sterols appear to decrease the solubility of cholesterol in the oil and micellar phases, thus displacing cholesterol from bile salt micelles and interfering with its absorption. One theory suggests that cholesterol in the intestine, already marginally soluble, is precipitated into a nonabsorbable state by the presence of added phytosterols and stanols; a second theory is based on the fact that cholesterol must enter bile salt and phospholipid-containing "mixed micelles" to be absorbed into the bloodstream.
Phytosterols and phytostanols interfere with intestinal cholesterol absorption through several proposed mechanisms: by displacing cholesterol from mixed micelles (the micellar theory); by modifying the expression of genes encoding sterol transporter proteins Niemann-Pick C1-Like 1 (NPC1L1) or ATP-binding cassette transporters (ABCG5 and ABCG8) that promote cholesterol efflux from enterocytes back into the intestinal lumen; by decreasing cholesterol re-esterification in the enterocyte; or by increasing cholesterol removal via the transintestinal cholesterol efflux (TICE) pathway. Of these different theories, only the micellar theory has gained experimental support.
The effects of stanols and sterols probably also involve the ATP-binding cassette (ABC) subfamily G, member 5 (ABCG5) and ABCG8 transporter proteins; these membrane proteins selectively pump phytosterols from the enterocytes back into the intestinal lumen, thus keeping their absorption low.
The affinity of the sterol transporter NPC1L1 differs among sterols, and the intestinal absorption preference follows the order: cholesterol > cholestanol > campesterol > sitosterol > campestanol > sitostanol. This ordering confirms that campestanol, as a stanol, is among the least readily absorbed dietary sterols, a property that underlies its utility as a cholesterol absorption inhibitor.
The efficacy of phytosterols and phytostanols added to foods and food supplements in achieving significant non-pharmacologic serum and LDL cholesterol reduction is well documented; irrespective of age, gender, ethnic background, body weight, background diet, or the cause of hypercholesterolemia, and even when added to statin treatment, phytosterols and phytostanols at 2 g/day significantly lower LDL cholesterol concentration by 8–10%; they do not affect concentrations of HDL cholesterol, lipoprotein(a), or serum proprotein convertase subtilisin/kexin type 9. In some studies, phytosterols and phytostanols have modestly reduced serum triglyceride levels, especially in subjects with slightly increased baseline concentrations.
Overview of Evidence: The strongest and best-replicated evidence for campestanol-containing preparations concerns their ability to reduce LDL cholesterol when delivered as plant stanol esters. Campestanol does not exist in isolation in clinical trials — it is studied as a component of plant stanol ester mixtures, primarily alongside sitostanol.
It has been suggested, on largely theoretical grounds, that stanol esters derived from wood sources such as tall oil (which contains mainly sitostanol) might be more effective in inhibiting cholesterol absorption than stanol esters derived from vegetable sources (up to 33% of which is campestanol); however, the results of three separate studies have shown that there is no significant difference in the LDL-lowering effect of sitostanol ester-rich versus campestanol ester-rich preparations.
In human studies, for the first time demonstrating hypocholesterolemic effects of vegetable oil-based stanols, a stanol mixture with a substantial amount of campestanol (over 10%, and preferably about 30%) was shown to be at least as effective as stanol mixtures with high levels of sitostanol. Furthermore, the results of that study indicated that campestanol, contrary to what had been previously reported, is virtually unabsorbed.
It has been shown in several randomized, double-blind clinical studies that consumption of foods such as margarine or yoghurt-type drink with added plant stanol ester effectively reduce serum total cholesterol and LDL cholesterol; the Scientific Panel on Dietetic Products, Nutrition and Allergies to the European Commission stated that "a clinically significant LDL-C lowering effect of about 10% can be achieved by a daily intake of plant stanol esters equivalent to 2 g of plant stanols in an appropriate food."
Clinical studies consistently indicate that the intake of phytosterols at 2 g/day is associated with a significant reduction of 8–10% in LDL cholesterol levels.
A daily intake of 1.5 to 2.4 g of plant stanols has been scientifically evaluated to lower LDL cholesterol by 7 to 10% in different populations, ages, and disease states; based on earlier studies, a general understanding was that no further reduction may be achieved at intakes exceeding approximately 2.5 g/day, but recent studies suggest that plant stanols show a continuous dose–response effect in LDL cholesterol lowering.
EFSA concluded that blood cholesterol can be reduced on average by 7 to 10.5% if a person consumes 1.5 to 2.4 grams of plant sterols and stanols per day, an effect usually established within 2–3 weeks; longer-term studies extending up to 85 weeks showed that the cholesterol-lowering effect could be sustained.
Plant stanols reduce the absorption of both cholesterol and plant sterols such as sitosterol and campesterol in the gastrointestinal tract, with a subsequent serum cholesterol and plant sterol lowering effect.
Evidence Strength: Strong. Multiple randomized, double-blind, placebo-controlled clinical trials across diverse populations, combined with regulatory-level systematic review by the FDA and EFSA, support the LDL-lowering effect of plant stanol ester mixtures containing campestanol. The individual contribution of campestanol versus sitostanol cannot be precisely quantified from currently published clinical literature, but head-to-head comparisons of high-campestanol versus high-sitostanol mixtures show equivalent efficacy.
In an animal model using the heterozygous Watanabe hyperlipidemic rabbit challenged with cholesterol, rapeseed oil stanol esters (containing campestanol and sitostanol) significantly lowered LDL cholesterol (mean −50% in the high-dose groups); in all experimental groups, a significant reduction of the cholesterol content of the cranial aortic intima was observed, with a dramatically reduced number of animals with significant aortic atherosclerotic lesions (13 in the control group, compared with 3 in the stanol group).
Plant sterols and stanols are known to attenuate absorption of low-density lipoprotein cholesterol, a risk factor for premature atherosclerosis and cardiovascular disease. Human data on direct anti-atherosclerotic effects of stanol ester preparations containing campestanol are limited and largely confined to surrogate endpoints such as LDL cholesterol rather than clinical events such as myocardial infarction or stroke.
Evidence Strength: Moderate for surrogate endpoints; preliminary/indirect for actual cardiovascular events in humans. There are still no available studies with long-term follow-up ensuring the safety of regular consumption of products enriched with phytosterols, as highlighted in recent publications of the European Society of Cardiology/European Atherosclerosis Society and the American Heart Association/American College of Cardiology.
Even when added to statin treatment, phytosterols and phytostanols at 2 g/day significantly lower LDL cholesterol concentration by 8–10%. Clinical studies have demonstrated that plant stanol ester preparations (containing campestanol alongside sitostanol) provide an additive LDL-lowering effect on top of statin therapy, since statins reduce cholesterol synthesis while stanols reduce cholesterol absorption — two complementary mechanisms. This has been confirmed in multiple randomized controlled trials, though again campestanol has not been evaluated in isolation in this context.
Evidence Strength: Moderate to strong for additive LDL reduction when stanol esters are added to statin therapy, based on published randomized clinical trials. Evidence is for the stanol mixture class, not campestanol specifically.
Campestanol belongs to the broader phytostanol/phytosterol class for which emerging anticancer evidence exists. Considerable emerging evidence supports the inhibitory actions of phytosterols on lung, stomach, ovarian, and breast cancer; phytosterols seem to act through multiple mechanisms of action, including inhibition of carcinogen production; however, randomized cancer prevention trials in humans are unfeasible due to time and cost.
Phytosterols appear to act through multiple mechanisms of action, including inhibition of carcinogen production, cancer-cell growth, angiogenesis, invasion and metastasis, and through the promotion of apoptosis of cancerous cells.
Case-control studies have indicated that high dietary phytosterol/stanol intake has been associated with reduced odds of several cancers, including lung (odds ratio 0.29, 95% CI 0.14–0.63), stomach (OR 0.33, 95% CI 0.17–0.65), and colorectum (OR 0.50, 95% CI 0.41–0.61).
However, these epidemiological associations are for total phytosterol/stanol intake, not campestanol specifically. The broad consensus in published preclinical data indicates that phytostanols are anti-proliferative in vivo, and reduced tumor growth is associated with lower expression of proliferation markers such as Ki67 and PCNA; however, in some studies performed at very high doses, especially in mixtures containing high concentrations of campestanol or campesterol, phytostanols appeared to be either ineffective, led to gut health complications, or in two cases promoted tumor growth.
Evidence Strength: Preliminary and largely preclinical. Human evidence is epidemiological only (case-control studies) and cannot be attributed to campestanol alone. Randomized controlled trials in humans are absent for any cancer endpoint.
Phytosterols exhibit anti-inflammatory properties that complement their antioxidant actions; by reducing inflammation, phytosterols may indirectly contribute to the management of oxidative stress-related conditions; phytosterols' antioxidant effects may contribute to cancer prevention by neutralizing free radicals and inhibiting oxidative damage to DNA, with their potential anti-inflammatory properties further inhibiting the progression of certain cancers.
Phytosterols have garnered growing scientific and clinical interest due to their diverse pharmacological effects, including cholesterol-lowering, anti-inflammatory, antioxidant, antidiabetic, and chemopreventive actions. However, most of this evidence pertains to the phytosterol class broadly — or specifically to β-sitosterol — and has not been tested specifically for campestanol in human clinical trials.
Evidence Strength: Weak to preliminary. Anti-inflammatory and antioxidant effects are primarily derived from in vitro and animal studies of the broader phytosterol class. No human clinical trials specifically address these outcomes for campestanol.
The esterification of sitosterol or sitostanol with fatty acids increases both their solubility in food matrices such as mayonnaises and margarines, as well as their intestinal dispersion, thus maximizing their effectiveness. Campestanol is used predominantly in its esterified form — campestanol fatty acid esters — incorporated into functional food matrices including margarines, yoghurt-type drinks, milk, breakfast cereals, and snack bars. Free (unesterified) campestanol powder also exists as a research-grade material but is not the primary commercial format.
Incorporation of phytosterols and phytostanols into foods is difficult due to their high melting point (140–170°C) and their tendency to form insoluble crystals; they were originally added to high-fat foods such as edible oil spreads where solubilization and dispersion of the sterols are relatively simple.
Because campestanol is always studied within stanol mixtures rather than in isolation, no specific clinical dose for campestanol alone has been reported. Its proportion within typical commercial stanol ester preparations ranges from approximately 6–32%, depending on whether tall oil or vegetable oil is the manufacturing source.
Whereas about 50% of cholesterol is absorbed in the intestinal tract, plant stanols and sterols are absorbed much less: absorption is about 10–15% for campesterol and campestanol, 4–7% for sitosterol, and 1% for sitostanol; foods enriched with plant stanol or sterol esters lower serum cholesterol levels by reducing intestinal absorption of cholesterol.
Phytosterol absorption is of less magnitude than cholesterol and is preferably secreted in the intestinal lumen by ABCG5/G8 transporters; therefore, plasma levels of plant sterols/stanols are negligible compared with cholesterol under an ordinary diet.
Phytosterol supplementation is contraindicated in the rare patients presenting with phytosterolemia (or sitosterolemia). Sitosterolemia is an inherited metabolic disorder with an autosomal recessive pattern of inheritance, characterized by the accumulation of certain phytosterols — including sitosterol, campesterol, and stigmasterol — which are not effectively eliminated from the intestine or the liver; the aggregation of these sterols is believed to contribute to the development of cardiovascular disease and other related health complications. Recent research indicates that its frequency may be more prevalent than previously thought, with estimates suggesting a minimum occurrence of 1 in 50,000 individuals globally.
A consistently observed finding across phytosterol/phytostanol clinical trials is a modest reduction in certain fat-soluble nutrients. After standardization for LDL cholesterol, levels of the various tocopherols were significantly increased, those of various carotenoids were unchanged, and those of β-carotene were decreased. The European Commission's Scientific Committee on Food has noted the complexity of interpreting these changes in the context of reduced LDL particle number. No significant changes were found in serum fat-soluble vitamin and carotenoid concentrations when related to serum total cholesterol in stanol ester margarine studies, suggesting that apparent reductions are largely a consequence of lower cholesterol-carrying particles rather than direct nutrient malabsorption.
Feeding studies in rats with stanol mixtures containing sitostanol and campestanol showed no adverse effects on reproduction, pup mortality, or pup body weight at dietary concentrations up to 4.38% plant stanol esters (equivalent to 2.5% total stanols in the diet). Notwithstanding this, use in pregnant and breastfeeding women has not been established in human populations. Pregnant and breastfeeding women should avoid foods with added plant sterols, as the safety of these has not been studied in these groups.
JECFA noted that there is no evidence for genotoxicity of phytosterols or phytostanols and their esters, and no indication of potential for carcinogenicity. No evidence was found in the literature for the genotoxicity, subchronic toxicity, chronic toxicity and carcinogenicity, and reproductive toxicity of four phytosterols identified in the novel food phytosterol/phytostanol category.
In some animal studies performed at very high doses, especially in mixtures containing high campestanol or campesterol concentrations, phytostanols appeared to be either ineffective, led to gut health complications, or in two cases promoted tumor growth and activation of oncogene expression; a dose equivalent to 70 g per person per day of plant stanols, or plant sterols, was associated with intestinal tumor formation in animal models. These doses are several orders of magnitude above levels achieved through dietary or functional food consumption and are not considered relevant to normal human intake.
There are still no available studies with long-term follow-up ensuring the safety of regular consumption of products enriched with phytosterols; however, the consumption of foods enriched with phytosterols is associated with a much lower increase (around twice) in circulating plant sterols compared to the 50-fold increase seen in phytosterolemia. Based on available short- and medium-term studies — including 85-week efficacy/safety studies — plant stanol preparations containing campestanol have shown acceptable safety profiles at recommended consumption levels.
There is controversy about treatment with statins inducing a further increase in plasma non-cholesterol sterols, raising concerns about the safety of supplementing plant sterols to such drugs; an increase in plant sterols has also been reported upon consumption of plant sterol-enriched foods, regardless of other treatments. The clinical significance of mildly elevated plasma sitostanol and campestanol during stanol ester use is not established, but it is distinct from the pathological hyperabsorption seen in sitosterolemia. In stanol ester margarine trials, serum sitostanol and campestanol increased only modestly: increases of 0.11 and 0.19 mg/L, respectively, during active treatment.
Condiciones de salud que campestanol puede ayudar a apoyar.
Campestanol is a plant stanol (saturated form of campesterol) that inhibits intestinal cholesterol absorption as part of the phytosterol/stanol class. EFSA endorses a health claim for plant stanols including campestanol for LDL-C reduction at 2–3 g/day.
Sistemas corporales que campestanol puede ayudar a apoyar.
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