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Campesterol is a phytosterol whose chemical structure is similar to that of cholesterol, and is one of the ingredients for E numberE499.
Natural occurrences
Many vegetables, fruits, nuts,[1] and seeds contain campesterol, but in low concentrations. Banana, pomegranate, pepper, coffee, grapefruit, cucumber, onion, oat, potato, and lemon grass (citronella) are few examples of common sources containing campesterol at roughly 1–7 mg/100 g of the edible portion. In contrast, canola and corn oils contain as much as 16–100 mg/100 g. Levels are variable and are influenced by geography and growing environment. In addition, different strains have different levels of plant sterols. A number of new genetic strains are currently being engineered with the goal of producing varieties high in campesterol and other plant sterols.[2] It is also found in dandelion coffee.
It is so named because it was first isolated from the rapeseed (Brassica campestris).[3]
Precursor of anabolic steroid boldenone
Campesterol can serve as a precursor to a wide range of steroid hormones. This is because it has structural similarity to cholesterol. Anabolic steroids like testosterone and boldenone are among the compounds that can be biosynthesized from either cholesterol or phytosterols like campesterol through a process called steroidogenesis.
Boldenone undecylenate is commonly used in veterinary medicine to induce growth in cattle, but it is also one of the most commonly abused anabolic steroids in sports. This led to suspicions that some of the athletes that have tested positive on boldenone undecylenate did not actually abuse the hormone itself, but had increased levels because they consumed food rich in campesterol or similar phytosteroids.[4][5][6]
Effect on blood lipids
Plant sterols were first shown in the 1950s to lower LDLs and cholesterol.[7] Since then, numerous studies have reported the lipid-lowering effects of dietary phytosterols, including campesterol.[8]
In basic research, campesterol competes with cholesterol, thus reducing the absorption of cholesterol in the human intestine.[9] Plant sterols may also act directly on intestinal cells and affect transporter proteins. In addition, an effect on the synthesis of cholesterol-transporting proteins may occur in the liver cells through processes including cholesterol esterification and lipoprotein assembly, cholesterol synthesis, and apolipoprotein (apo) B100-containing lipoprotein removal.[10]
Serum levels of campesterol and the ratio of campesterol to cholesterol have been proposed as measures of cardiac risk. Some studies have suggested that higher levels predict lower cardiac risk. However, extremely high levels are thought to be indicative of higher risk, as indicated by genetic disorders, such as sitosterolemia.[11]
Study results of serum levels have been conflicting. A 2012 meta-analysis found that no clear relationship exists between campesterol or sitosterol blood levels and risk of cardiovascular disease, and that perhaps previous studies have been confounded by other factors.[12] For example, people who have a higher campesterol level related to a diet high in fruits and nuts may be consuming a Mediterranean-style diet, thus have lower risk because of other lipids or lifestyle factors.[13]
Adverse effects
Nutrient levels
Excessive supplementation with plant sterols may be associated with reductions in beta-carotene and lycopene levels.[14] Excessive long-term consumption of plant sterols may have a deleterious effect on vitamin E, possibly leading to vitamin E deficiency.[15]
Increased risk of disease
Excessive use of plant sterols has been associated with an increased risk of cardiovascular disease,[9] and genetic conditions that cause extremely elevated levels of some phytosterols, such as sitosterol, are associated with higher risks of cardiovascular disease. However, this is an active area of debate, and no data suggest that modestly elevated levels of campesterol have a negative cardiac impact.[16]
^Fernholz, Erhard; MacPhillamy, H. B. (1941). "Isolation of a New Phytosterol: Campesterol". Journal of the American Chemical Society. 63 (4): 1155. doi:10.1021/ja01849a079.
^Boldenone, Boldione, and Milk Replacers in the Diet of Veal Calves: The Effects of Phytosterol Content on the Urinary Excretion of Boldenone Metabolites, G. Gallina, G. Ferretti, R. Merlanti, C. Civitareale, F. Capolongo, R. Draisci and C. Montesissa, J. Agric. Food Chem., 2007, 55 (20), pp 8275–8283
^Food Addit Contam. 2007 Jul;24(7):679-84.;Phytosterol consumption and the anabolic steroid boldenone in humans: a hypothesis piloted; Ros MM, Sterk SS, Verhagen H, Stalenhoef AF, de Jong N.;National Institute for Public Health and the Environment (RIVM), the Netherlands.
^Excretion profile of boldenone in urine of veal calves fed two different milk replacers; R. Draisci, R. Merlanti, G. Ferretti, L. Fantozzi, C. Ferranti, F. Capolongo, S. Segato, C. Montesissa; Analytica Chimica Acta, Volume 586, Issues 1–2, 14 March 2007, Pages 171–176
^Heggen, E.; Granlund, L.; Pedersen, J.I.; Holme, I.; Ceglarek, U.; Thiery, J.; Kirkhus, B.; Tonstad, S. (2010). "Plant sterols from rapeseed and tall oils: Effects on lipids, fat-soluble vitamins and plant sterol concentrations". Nutrition, Metabolism and Cardiovascular Diseases. 20 (4): 258–65. doi:10.1016/j.numecd.2009.04.001. hdl:10852/55512. PMID19748247.
^ abChoudhary, SP; Tran, LS (2011). "Phytosterols: Perspectives in human nutrition and clinical therapy". Current Medicinal Chemistry. 18 (29): 4557–67. doi:10.2174/092986711797287593. PMID21864283.
^Calpe-Berdiel, Laura; Escolà-Gil, Joan Carles; Blanco-Vaca, Francisco (2009). "New insights into the molecular actions of plant sterols and stanols in cholesterol metabolism". Atherosclerosis. 203 (1): 18–31. doi:10.1016/j.atherosclerosis.2008.06.026. PMID18692849.
