Effects of Dietary Coconut Oil, Butter and Safflower Oil on Plasma Lipids, Lipoproteins and Lathosterol Levels
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European Journal of Clinical Nutrition (1998) 52, 650±654 ß 1998 Stockton Press. All rights reserved 0954±3007/98 $12.00 http://www.stockton-press.co.uk/ejcn Effects of dietary coconut oil, butter and safflower oil on plasma lipids, lipoproteins and lathosterol levels C Cox1, W Sutherland2, J Mann1, S de Jong2, A Chisholm1 and M Skeaff1 Departments of 1Human Nutrition and 2Medicine, University of Otago, Dunedin, New Zealand Objective: The aim of this present study was to determine plasma levels of lathosterol, lipids, lipoproteins and apolipoproteins during diets rich in butter, coconut fat and saf¯ower oil. Design: The study consisted of sequential six week periods of diets rich in butter, coconut fat then saf¯ower oil and measurements were made at baseline and at week 4 in each diet period. Subjects: Forty-one healthy Paci®c island polynesians living in New Zealand participated in the trial. Interventions: Subjects were supplied with some foods rich in the test fats and were given detailed dietary advice which was reinforced regularly. Results: Plasma lathosterol concentration (P < 0.001), the ratio plasma lathosterol/cholesterol (P 0.04), low density lipoprotein (LDL) cholesterol (P < 0.001) and apoB (P < 0.001) levels were signi®cantly different among the diets and were signi®cantly lower during coconut and saf¯ower oil diets compared with butter diets. Plasma total cholesterol, HDL cholesterol and apoA-levels were also signi®cantly (P 0.001) different among the diets and were not signi®cantly different between buffer and coconut diets. Conclusions: These data suggest that cholesterol synthesis is lower during diets rich in coconut fat and saf¯ower oil compared with diets rich in butter and might be associated with lower production rates of apoB-containing lipoproteins. Sponsorship: The study was supported by the Health Research Council of New Zealand and the Anderson Telford Trust. Descriptors: diet; fat type; lathosterol; lipoproteins; polynesians Introduction SAFA in the diet. A suggested (Glatz & Katan, 1993) explanation for these varying ®ndings is that the gas Diets rich in saturated fatty acids (SAFA) raise plasma chromatographic (GC) separation of faecal plant sterols cholesterol and low density lipoprotein (LDL) cholesterol and endogenous sterols, a vital step in the cholesterol levels compared with diets rich in polyunsaturated fatty balance method of measuring cholesterol synthesis, may acids (PUFA). Saturated fatty acids with different chain not have been achieved in the earlier studies before the lengths vary in their hypercholesterolemic effect in the advent of capillary GC. Cholesterol balance estimates order of increasing potency myristate, palmitate and laurate whole body cholesterol synthesis as the difference between (Denke & Grundy, 1992; Zock et al, 1994; Cox et al, dietary intake and excretion of cholesterol and its metabo- 1995). Differences in plasma LDL cholesterol when these lites in the faeces in the steady state. In view of the fatty acids are predominant in the diet are theoretically due technical dif®culties and the requirement for steady-state to differences in the rates of very low density lipoprotein conditions in the cholesterol balance technique, alternative (VLDL) production and conversion to LDL or the catabol- methods for measuring cholesterol synthesis have been ism of LDL by hepatic receptors or both. There is limited developed. evidence that diets rich in palmitic acid stimulate the Plasma lathosterol levels and the ratio plasma latho- production of very low density lipoproteins (VLDL) and sterol/cholesterol have been established as excellent indices LDL (Cortese et al, 1983). The rate of VLDL secretion of cholesterol synthesis. They correlate closely with human from the liver is closely linked to cholesterol synthesis rates hepatic 3-hydroxy-3-methylglutaryl Coenzyme A (HMG in normolipidemic subjects (Watts et al, 1995). Whether CoA) reductase activity, the rate limiting step in cholesterol cholesterol synthesis varies during diets rich in SAFA of biosynthesis (BjoÈrkhem et al, 1987) and with whole-body different chain lengths has not been widely studied. cholesterol synthesis rates measured by cholesterol balance The effect of changing the quality of dietary fat on (Kempen et al, 1988). Also, levels of the sterol are cholesterol synthesis is controversial. While several studies decreased when cholesterol synthesis is reduced during have indicated that whole-body cholesterol synthesis is treatment with drugs that inhibit the HMG CoA reductase unchanged (Shepherd et al, 1980; Spritz et al, 1965; enzyme (Kempen et al, 1988) and are increased under Grundy & Ahrens, 1970; Nestel et al, 1976) others have conditions of increased cholesterol synthesis (Miettinen, documented decreased (Glatz & Katan, 1993) and 1985). Lathosterol is a cholesterol precursor that is formed increased (Jones et al, 1994) rates when PUFA replace after the rate-limiting step in cholesterol biosynthesis and `leaks' from cells at rates which are proportional to Correspondence: Dr W Sutherland, Department of Medicine, Dunedin School of Medicine, PO Box 913, Dunedin, New Zealand. rates of cellular cholesterol synthesis. Plasma lipoproteins Received 4 December 1997; revised 24 April 1998; accepted 9 May 1998 are acceptors for precursor sterols released from cells. Dietary fat type and lathosterol levels C Cox et al 651 Consequently, the ratio plasma lathosterol/cholesterol has naire. Body weight was measured and fasted venous blood been frequently used to correct for the effect of varying samples were taken on two occasions during the baseline numbers of lipoprotein acceptors on plasma lathosterol period and at weeks four and six of each diet period. levels. When PUFA are substituted for SAFA in the diet Plasma lipids and HDL cholesterol levels were measured in plasma latho-sterol levels and the ratio lathosterol/choles- all blood samples collected. Plasma lathosterol, very low terol are reduced (Glatz & Katan, 1993) suggesting that density lipoprotein (VLDL) cholesterol and apolipopro- cholesterol synthesis is also reduced. teins A±I, A±II and B were measured on one occasion The aim of the present study was to determine the effect during the baseline period and at the four-week point of of diets rich in coconut fat, butter and saf¯ower oil on each diet period. An earlier study from our laboratories plasma levels of lathosterol. The study was conducted in (Cox et al, 1995) suggested that plasma lipid and lipo- Paci®c Islanders because these types of diets have parti- protein levels had attained equilibrium by four weeks after cular relevance in that population. Traditionally, they eat a change in the type of fat in the diet. diets rich in coconut fat but on migration to New Zealand they increase their intake of other types of fat (Stanhope et al, 1981). Diets The experimental diets were designed to provide approxi- mately 17% protein, 47% carbohydrate and 36% fat as a Subjects and methods fraction of total energy intake. Target values for fat intake based on an 8.4 MJ/d diet were 84 g total fat for all diets Subjects and including; 39 g fat from butter plus fat from palmitic Forty-seven Paci®c Islanders from two Paci®c Island acid-rich foods to give an intake of approximately 17 g churches in Dunedin, New Zealand were recruited. Six palmitic acid (butter diet); 39 g fat from coconut oil to give subjects dropped out immediately after initial screening and an intake of approximately 17 g lauric acid (coconut diet); 41 subjects started the dietary phase of the study. The 41 and 24 g fat from saf¯ower oil to give an intake of subjects included 24 men and 17 women ages 19±72 y (31 approximately 17 g linoleic acid (saf¯ower diet). Calcu- Western Samoans and 10 Cook Islanders) with plasma lated intakes of myristic acid and linoleic acid were cholesterol levels between 4.2 mmol/l and 7.5 mmol/l and approximately similar in the coconut and butter diets. To plasma triglycerides less than 3 mmol/l. None was receiv- encourage dietary compliance, participants were supplied ing drugs known to in¯uence lipid metabolism. Character- with butter and cream during the butter diet, coconut istics of the subjects at baseline are shown in Table 1. All cream, coconut oil and monounsaturated margarine subjects gave informed consent and the study was approved during the coconut diet and saf¯ower oil and polyunsatu- by the Ethics committee of the Otago Area Health Board. rated margarine during the saf¯ower diet. Specially baked bread including similar amounts of butter, coconut oil or Study design saf¯ower oil were supplied to the study participants during The study included a run in period of six weeks followed the appropriate diet period. Egg yolk was added to the by three consecutive six week periods when diets rich in coconut diet and the saf¯ower diet to maintain approxi- butter (butter diet), coconut fat (coconut diet) then saf- mately similar cholesterol intake (250±300 mg/d) during ¯ower oil (saf¯ower diet) were consumed without washout the experimental diets. Subjects assigned to the butter diet periods between the experimental diet periods. A sequen- were instructed to eat butter, cream, butter bread, cheese, tial study design rather than the preferred randomized meat, ®sh, chicken, fruit and vegetables, rice, noodles, full crossover design was used to encourage compliance with cream milk and milk products and were instructed not to the diets because participants frequently ate communally eat coconut cream or products, margarine and cooking oils. within the church group. During the run in period partici- Those assigned to the coconut diet were instructed to eat pants completed a food frequency questionnaire to assess coconut cream, coconut bread, monounsaturated margarine, their usual food and nutrient intake and a health question- coconut, ®sh, meat cheese, chicken, fruit and vegetables, rice, noodles, trim milk and other low fat dairy products Table 1 Characteristics of the subjects at baseline and not to eat butter, cream, other margarines, chicken skin, deep-fried takeway foods and vegetable oils.