An initiative of :



Stichting Food-Info

Food-Info.net> Food products > Olive oil

Health Effects of the Minor Components of Olive Oil

(Part II)

Authors:
Prof. Dr. med Gerd Assmann
Prof. Dr. troph. Ursel Wahrburg
The Institute of Arteriosclerosis Research, University of Münster, Germany

1 Introduction


In this second fact sheet on minor components of olive oil, the findings on the health benefits of hydrocarbons, particularly squalene, and sterols present in olive oil will be reviewed.

2 Minor components of olive oil

2.1 Hydrocarbons

The major hydrocarbon in olive oil is squalene, a triterpene and intermediate product of the cholesterol biosynthesis pathway. Extra virgin olive oil contains squalene in an amount of about 400-450 mg/100g, while refined olive oil contains about 25% less (1). Some papers have found squalene levels around 200-700 mg/100g in extra virgin olive oil (reviewed in (2)). According to the latter study, the average intake of squalene is 30 mg per day in the USA. However, with a high consumption of extra virgin olive oil, the intake can reach 200-400 mg per day as observed in Mediterranean countries (2). Individuals might even consume up to 1g of squalene per day with their diets, as suggested by Gylling and Miettinen (3).

In addition to squalene, other hydrocarbons are also present, e.g., the pro-vitamin A ß-carotene, albeit in very small quantities (ß-carotene: 0.03 - 0.36 mg/100g) (Kiritsakis and Markakis 1987).

2.2 Sterols

Sterols are an essential component of cell membranes, and both animals and plants produce them. The sterol ring is a common feature of all sterols; the differences are in the side chain. Cholesterol is exclusively an animal sterol. Over 40 phytosterols have been identified so far. The amount of total sterols in extra virgin olive oil found by different groups varies between 113-265 mg/100g oil (5;6). Two factors influencing this amount are the cultivar and the degree of ripeness of the olives (5). By far the major sterol in olive oil is ß-sitosterol, constituting up to 90-95% of total sterols (5;6). Campesterol and stigmasterol make up about 3% and 1%, respectively (5;6). Stanols are saturated sterols, which are virtually absent from typical diets (reviewed in (4)).

3 Impact of the minor constituents on human health

3.1 Hydrocarbons (squalene)

3.1.1 Squalene and serum cholesterol concentrations

As mentioned above, squalene is a metabolite of cholesterol synthesis. Thus, theoretically, dietary squalene can be transformed into cholesterol in the body and could therefore increase serum cholesterol levels. The first prerequisite for this effect would be that considerable quantities are absorbed. Evidence suggests that 60 to 80 percent of dietary squalene is absorbed from an oral dose (2;7). Furthermore, evidence indicates that a substantial amount of dietary squalene is indeed converted to cholesterol in humans. However, this increase in cholesterol synthesis is not associated with consistent increases in serum cholesterol levels, possibly as a result of a concomitant increase in faecal elimination (8). Although Miettinen and Vanhanen observed an increase in serum total and LDL-cholesterol concentrations after a dietary supplementation with a very high daily dose of squalene (1g), the values could be normalised when the squalene dose was subsequently reduced to a lower level (0.5g per day) (9). Of particular interest is a study indicating that squalene, added to a protocol with low-dose pravastatin, further enhanced the efficacy of pravastatin as a cholesterol-lowering drug (10). Taken together, the concern that low doses of squalene contribute to high serum cholesterol levels appears to be misplaced. At reasonable dietary levels of 0.5g or less per day, squalene appears to have no adverse effect on serum cholesterol concentrations.

3.1.2 Squalene and cancer

Epidemiological studies suggest a cancer-protective effect of dietary olive oil. In Greece, women with high total fat intake, mainly olive oil, have a breast cancer rate of only about one-third that of women in the United States (11). A case-control study in Spain showed a reduced risk for breast cancer in women with the highest olive oil consumption (12). In a large case-control study in Greece, breast cancer risk was 25% lower in women consuming olive oil more than once a day (13). In another case-control study in Spain, women in the highest third of monounsaturated fatty acid (MUFA) consumption (largely from olive oil) had a greatly reduced risk of breast cancer (14). A recent case-control study in Italy indicated a decreased risk of breast cancer with an increased intake of unsaturated fatty acids from edible oils. In Italy, about 80% of edible oil is olive oil, suggesting a protective effect of olive oil intake (15). Another recent case-control study in Italy reported a significant inverse trend of edible oil (mainly olive oil) intake and risk of pancreatic cancer (16). Two leading scientists in the field, Theresa J. Smith and Harold L. Newmark, suggested that this protective effect might be due to the large amount of squalene in extra virgin olive oil (2;11), an assumption supported by a considerable amount of experimental animal studies. The majority of these studies have investigated the effect of topically applied or systemically administered squalene on chemically-induced cancers of the skin, the colon and the lung of mice. Taken together, these results clearly show that dietary squalene has distinct anti-carcinogenic effects (17-21).

2.1.3 Other effects of dietary squalene

Firstly, studies indicate that the dietary intake of squalene might have other beneficial effects besides its anti-cancer properties. Kohno and colleagues observed that squalene is a highly potent quencher of reactive singlet oxygen on the human skin surface (22). In animal models, squalene also appears to play an important role in the health of the eye, especially the rod photoreceptor cells of the retina (23). Furthermore, several groups have reported that animals fed squalene show an enhanced capacity to excrete toxins such as hexachlorbenzene or strychnine (24-26), although some of these effects required very high doses of squalene.

2.2 Sterols (ß-sitosterol)

2.2.1 Effect on serum cholesterol concentrations

Both oral and parenteral administration of plant sterols and stanols result in reduced concentrations of plasma total and LDL-cholesterol (reviewed in (4;27)). It is likely that most of this reduction is due to the inhibition of intestinal cholesterol absorption. Also, hepatic and intestinal cholesterol metabolism might be affected. It must be noted, however, that significant reductions in serum cholesterol levels have been achieved only in those studies, in which phytosterol supplements have been used. The doses given were in the range of 1-3 g per day, an amount which cannot be achieved with natural foods. Most of the studies used margarines fortified with sterols or stanols. In general, the reduction in total and LDL-cholesterol increased with increasing daily doses of sterols up to a dose of 2g per day, beyond which no further cholesterol-lowering effect could be observed (28). A recent meta-analysis of all randomised, double-blind trials concluded that at daily intakes of 2g plant sterols or stanols, serum LDL-cholesterol concentrations were lowered by 9-14%, with no effects on HDL-cholesterol or triglycerides (27). Furthermore, the decrease in cholesterol concentrations is more distinct in hypercholesterolaemic subjects and in subjects on a cholesterol-rich diet (reviewed in (4;27)). In one study, significant lipid-lowering effects were observed with a relatively low dose of 740 mg phytosterols per day in subjects consuming a cholesterol-rich diet (29). Therefore, it cannot be excluded that the amounts of phytosterols taken up with a diet rich in extra virgin olive oil might be somewhat beneficial with regard to serum cholesterol concentrations, especially in hyperlipidaemic patients consuming diets rich in cholesterol.

3.2.2 Phytosterols and cancer

There are several reports on anti-tumor effects of phytosterols, especially ß-sitosterol. Von Holtz and colleagues observed that compared with cholesterol-treated controls, human prostate cancer cells treated with ß-sitosterol decreased their growth by 24% and induced apoptosis 4-fold (30). Apoptosis is the so-called programmed cell death, a prophylactic mechanism, by which cells commit suicide, e.g., when they have converted into cancer cells, in order to avert damage from the body. Furthermore, ß-sitosterol appears to be effective in the treatment of benign prostatic hyperplasia (31-33). In addition to these findings on prostate cancer or prostate hyperplasia, there have been reports on the health benefits of ß-sitosterol on colon cancer cells and breast cancer cells in vitro (34-36). Furthermore, ß-sitosterol was shown to nullify the effect of a carcinogen on the colon in rats (37). There are only a few studies investigating the relationship between phytosterols and cancer in humans. In a study in Uruguay, De Stefani and colleagues found a strong inverse relationship between the total intake of phytosterols and stomach cancer (38). In an observational study, a research group from California, U.S.A., compared the sterol intakes of Seventh-Day-Adventists, a group known for its very low total cancer morbidity and mortality, with that of the general population. They found that the Seventh-Day-Adventists not only consumed less cholesterol, but also far more phytosterols, and suggested that either the high total phytosterol intake or the high phytosterol-to-cholesterol-ratio of their diet contributed to the reduced occurrence of cancer (39).

The majority of the investigations referred to above are either in vitro studies using cell culture models of specific cancers or animal studies. Thus, the results on this topic must be considered in this light until there are more data available from studies in humans. Nevertheless, the findings are promising in that phytosterols, and particularly ß-sitosterol, might exert distinct anti-carcinogenic effects with regard to cancers of the prostate, colon, breast and stomach.

4 Summary and conclusions

Among the minor components of olive oil, there are hydrocarbons, particularly squalene, and phytosterols. In a wide range of studies, these substances have been shown to exert beneficial effects. Above all, anti-carcinogenic effects have been shown for both squalene and ß-sitosterol. Therefore, the relatively high content of squalene and phytosterols is another valuable feature of olive oil, which contributes to the oil imparting health benefits. Considering the possibility of additional synergistic effects between hydrocarbons, phytosterols, phenols, tocopherols, flavour compounds, and the favourable fatty acid composition, health benefits of the oil as a whole might even be higher than the sum of the single beneficial effects.

5 Reference list

  1. Owen RW, Mier W, Giacosa A, Hull WE, Spiegelhalder B, Bartsch H. Phenolic compounds and squalene in olive oils: the concentration and antioxidant potential of total phenols, simple phenols, secoiridoids, lignans and squalene. Food Chem.Toxicol. 2000;38:647-59.
  2. Smith TJ. Squalene: potential chemopreventive agent. Expert.Opin.Investig.Drugs 2000;9:1841-8.
  3. Gylling H, Miettinen TA. Postabsorptive metabolism of dietary squalene. Atheroscler. 1994;106:169-78.
  4. Jones PJ, MacDougall DE, Ntanios F, Vanstone CA. Dietary phytosterols as cholesterol-lowering agents in humans. Can.J Physiol Pharmacol. 1997;75:217-27.
  5. Gutierrez F, Jimenez B, Ruiz A, Albi MA. Effect of olive ripeness on the oxidative stability of virgin olive oil extracted from the varieties picual and hojiblanca and on the different components involved. J Agric.Food Chem 1999;47:121-7.
  6. Kiritsakis A, Markakis P. Olive oil: a review. Adv. Food Res. 1987;31:453-82.:453-82.
  7. Kelly GS. Squalene and its potential clinical uses. Altern.Med Rev. 1999;4:29-36.
  8. Strandberg TE, Tilvis RS, Miettinen TA. Metabolic variables of cholesterol during squalene feeding in humans: comparison with cholestyramine treatment. J Lipid Res. 1990;31:1637-43.
  9. Miettinen TA, Vanhanen H. Serum concentration and metabolism of cholesterol during rapeseed oil and squalene feeding. Am J Clin.Nutr. 1994;59:356-63.
  10. Chan P, Tomlinson B, Lee CB, Lee YS. Effectiveness and safety of low-dose pravastatin and squalene, alone and in combination, in elderly patients with hypercholesterolemia. J Clin.Pharmacol. 1996;36:422-7.
  11. Newmark HL. Squalene, olive oil, and cancer risk. Review and hypothesis. Ann.N Y.Acad.Sci. 1999;889:193-203.:193-203.
  12. Martin-Moreno JM, Willett WC, Gorgojo L et al. Dietary fat, olive oil intake and breast cancer risk. Int.J Cancer 1994;58:774-80.
  13. Trichopoulou A, Katsouyanni K, Stuver S et al. Consumption of olive oil and specific food groups in relation to breast cancer risk in Greece. J Natl.Cancer Inst. 1995;87:110-6.
  14. Landa MC, Frago N, Tres A. Diet and the risk of breast cancer in Spain. Eur.J Cancer Prev. 1994;3:313-20.
  15. Franceschi S, Favero A, Decarli A et al. Intake of macronutrients and risk of breast cancer. Lancet 1996;347:1351-6.
  16. La Vecchia C, Negri E. Fats in seasoning and the relationship to pancreatic cancer. Eur.J Cancer Prev. 1997;6:370-3.
  17. Van Duuren BL, Goldschmidt BM. Cocarcinogenic and tumor-promoting agents in tobacco carcinogenesis. J Natl.Cancer Inst. 1976;56:1237-42.
  18. Yamaguchi T, Nakagawa M, Hidaka K et al. Potentiation by squalene of antitumor effect of 3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-1-(2-chloroethyl)-nitros ourea in a murine tumor system. Jpn.J Cancer Res. 1985;76:1021-6.
  19. Rao CV, Newmark HL, Reddy BS. Chemopreventive effect of squalene on colon cancer. Carcinogenesis 1998;19:287-90.
  20. Smith TJ, Yang GY, Seril DN, Liao J, Kim S. Inhibition of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung tumorigenesis by dietary olive oil and squalene. Carcinogenesis 1998;19:703-6.
  21. Smith, T. J., Kim, S., Lee, M. J., Yang, G. Y., Newmark, H. L., and Yang, C. S. Inhibition of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NKK)-induced lung tumorigenesis and DNA oxidation by dietary squalene. Proceedings of the American Association for Cancer Research 40, 262. 1999.
    Ref Type: Journal (Full)
  22. Kohno Y, Egawa Y, Itoh S, Nagaoka S, Takahashi M, Mukai K. Kinetic study of quenching reaction of singlet oxygen and scavenging reaction of free radical by squalene in n-butanol. Biochim.Biophys.Acta 1995;1256:52-6.
  23. Fliesler SJ, Keller RK. Isoprenoid metabolism in the vertebrate retina. Int.J Biochem.Cell Biol. 1997;29:877-94.
  24. Kamimura H, Koga N, Oguri K, Yoshimura H. Enhanced elimination of theophylline, phenobarbital and strychnine from the bodies of rats and mice by squalane treatment. J Pharmacobiodyn. 1992;15:215-21.
  25. Richter E, Fichtl B, Schafer SG. Effects of dietary paraffin, squalane and sucrose polyester on residue disposition and elimination of hexachlorobenzene in rats. Chem Biol.Interact. 1982;40:335-44.
  26. Richter E, Schafer SG. Effect of squalane on hexachlorobenzene (HCB) concentrations in tissues of mice. J Environ.Sci.Health B 1982;17:195-203.
  27. Law MR. Plant sterol and stanol margarines and health. West J Med 2000;173:43-7.
  28. Plat J, Kerckhoffs DA, Mensink RP. Therapeutic potential of plant sterols and stanols. Curr.Opin.Lipidol. 2000;11:571-6.
  29. Pelletier X, Belbraouet S, Mirabel D et al. A diet moderately enriched in phytosterols lowers plasma cholesterol concentrations in normocholesterolemic humans. Ann.Nutr.Metab 1995;39:291-5.
  30. Von Holtz RL, Fink CS, Awad AB. beta-Sitosterol activates the sphingomyelin cycle and induces apoptosis in LNCaP human prostate cancer cells. Nutr.Cancer 1998;32:8-12.
  31. Klippel KF, Hiltl DM, Schipp B. A multicentric, placebo-controlled, double-blind clinical trial of beta-sitosterol (phytosterol) for the treatment of benign prostatic hyperplasia. German BPH-Phyto Study group. Br.J Urol. 1997;80:427-32.
  32. Carbin BE, Larsson B, Lindahl O. Treatment of benign prostatic hyperplasia with phytosterols. Br.J Urol. 1990;66:639-41.
  33. Wilt TJ, MacDonald R, Ishani A. beta-sitosterol for the treatment of benign prostatic hyperplasia: a systematic review. BJU.Int. 1999;83:976-83.
  34. Awad AB, Downie AC, Fink CS. Inhibition of growth and stimulation of apoptosis by beta-sitosterol treatment of MDA-MB-231 human breast cancer cells in culture. Int.J Mol.Med 2000;5:541-5.
  35. Awad AB, Chen YC, Fink CS, Hennessey T. beta-Sitosterol inhibits HT-29 human colon cancer cell growth and alters membrane lipids. Anticancer Res. 1996;16:2797-804.
  36. Awad AB, von Holtz RL, Cone JP, Fink CS, Chen YC. beta-Sitosterol inhibits growth of HT-29 human colon cancer cells by activating the sphingomyelin cycle. Anticancer Res. 1998;18:471-3.
  37. Raicht RF, Cohen BI, Fazzini EP, Sarwal AN, Takahashi M. Protective effect of plant sterols against chemically induced colon tumors in rats. Cancer Res. 1980;40:403-5.
  38. De Stefani E, Boffetta P, Ronco AL et al. Plant sterols and risk of stomach cancer: a case-control study in Uruguay. Nutr.Cancer 2000;37:140-4.
  39. Nair PP, Turjman N, Kessie G et al. Diet, nutrition intake, and metabolism in populations at high and low risk for colon cancer. Dietary cholesterol, beta-sitosterol, and stigmasterol. Am J Clin.Nutr. 1984;40:927-30

Source: http://europa.eu.int/comm/agriculture/prom/olive/medinfo/index.htm

Food-Info.net is an initiative of Stichting Food-Info, The Netherlands

Free counters!