Dyslipidaemia is a disorder of lipoprotein metabolism which is characterized by high concentrations of TC, LDL and triglyceride (TG) and low levels of HDL. It is one of the main risk factors for coronary heart disease and its prevalence in the Omani population is very high, which is around 41%. It was found that polymorphisms in some apolipoproteins (major protein components of lipoproteins) may cause variations in the level of lipid parameters. This study aimed to determine the effect of apolipoprotein Al, MI and M2, and apolipoprotein E polymorphisms on lipid parameters. The total number of samples included in this study was 833. These samples represented three large, extended, and highly consanguineous families of Omani origin, with well identified phenotypes. These families were Al-Radah, Farq and Karsha. In order to determine the apo Al genotypes at the two polymorphic sites (M1 and M2), DNA was amplified by PCR and digested with Mspl. The apo E polymorphism genotypes were determined by PCR amplification of the DNA and digestion with Cfol. The statistical analysis was carried out for the individual families and for the pooled population. The Ml- allele frequency of the apo Al MI polymorphism was 0.19 for the total samples, 0.23 for Al-Radah, 0.196 for Farq and 0.14 for Karsha. The allelic frequencies of M2- were 0.0072, 0.0041, 0.0085, and 0.0085 for the population, Al-Radah, Farq, and Karsha, respectively. The frequency of E3 allele of the apo E polymorphism was 0.917 in the population, 0.976 in Al Radah, 0.867 in Farq and 0.920 in Karsha. The frequency of carriers of E4 allele was 0.032 in the population, 0.0183 in Al-Radah, 0.0580 in Farg and 0.0171 in Karsha and the frequency of E2 allele was 0.051 in the population, 0.0061 in Al Radah, 0.0751 in Farg and 0.0631 in Karsha. The alleles frequencies for Mi polymorphism and apo E polymorphism were significantly different between the three families. The individuals with M1- allele in the total samples had significantly higher HDL (P = 0.002) and a trend of high apo Al levels compared to M1+ carriers. Al-Radah family showed an association between M1- allele and HDL (P = 0.037). On the other hand, M1- allele in Farq was associated with increased apo Al level (P = 0.012). Karsha family did not show any association with this polymorphism. Generally, it was found that M1 polymorphism causes 1.1% of the variation in HDL levels. There were no differences in lipid parameters between the subjects with M2+ and subjects with M2- allele for the population and the three families. Individuals with E2 allele had low levels of total cholesterol, LDL and apo B in the total population (P < 0.001) and in Farq family (P < 0.001). However, in Karsha E2 was associated with decreased levels of LDL and apo B (P = 0.025 and 0.05, respectively) but not total cholesterol. Al-Radah had no association with this polymorphism. The apo E polymorphism, in general, explained 1.7% of the variation in TC, 2.4% of the variation in LDL, and 1.3% of the variation in apo B. The haplotype analysis of both apo A1 polymorphisms showed that there was no interaction between these two polymorphisms. In conclusion, the M1 polymorphism had a significant effect on the level of HDL and apo Al whereas apo E polymorphism was associated with TC, LDL and apo B.