FADS1 FADS2 Gene Cluster, PUFA Intake and Blood Lipids in Children: Results from the GINIplus and LISAplus Studies

Abstract

BackgroundElevated cholesterol levels in children can be a risk factor for cardiovascular diseases in later life. In adults, it has been shown that blood lipid levels are strongly influenced by polymorphisms in the fatty acid desaturase (FADS) gene cluster in addition to nutritional and other exogenous and endogenous determinants. Our aim was to investigate whether lipid levels are determined by the FADS genotype already in children and whether this association interacts with dietary intake of n-3 fatty acids.MethodsThe analysis was based on data of 2006 children from two German prospective birth cohort studies. Total cholesterol, HDL, LDL and triglycerides were measured at 10 years of age. Six single nucleotide polymorphisms (SNPs) of the FADS gene cluster were genotyped. Dietary n-3 fatty acid intake was assessed by food frequency questionnaire. Linear regression modeling was used to assess the association between lipid levels, n-3 fatty acid intake and FADS genotype.ResultsIndividuals carrying the homozygous minor allele had lower levels of total cholesterol [means ratio (MR) ranging from 0.96 (p = 0.0093) to 0.98 (p = 0.2949), depending on SNPs] and LDL [MR between 0.94 (p = 0.0179) and 0.97 (p = 0.2963)] compared to homozygous major allele carriers. Carriers of the heterozygous allele showed lower HDL levels [β between −0.04 (p = 0.0074) to −0.01 (p = 0.3318)] and higher triglyceride levels [MR ranging from 1.06 (p = 0.0065) to 1.07 (p = 0.0028)] compared to homozygous major allele carriers. A higher n-3 PUFA intake was associated with higher concentrations of total cholesterol, LDL, HDL and lower triglyceride levels, but these associations did not interact with the FADS1 FADS2 genotype.ConclusionTotal cholesterol, HDL, LDL and triglyceride concentrations may be influenced by the FADS1 FADS2 genotype already in 10 year old children. Genetically determined blood lipid levels during childhood might differentially predispose individuals to the development of cardiovascular diseases later in life.

Fatty acid status in infancy is associated with the risk of type 1 diabetes-associated autoimmunity

“…Limitations Fatty acids found in the peripheral circulation of infants originate from infant and maternal diets and adipose tissue storage, as well as metabolic processes, some of which are affected by genetic factors [38,39]. It can be considered a limitation that it was not possible to account for genetic factors involved in fatty acid metabolism.…”

The impact of fatty acid desaturase genotype on fatty acid status and cardiovascular health in adults

“…The majority of studies to date suggest that FADS minor alleles (associated with decreased desaturase activity) are associated with reduced inflammation, total cholesterol, LDL-cholesterol and coronary artery disease risk (Tables 1 and 2) (18,(27)(28)(29)(30)(31) . In the Verona Heart Study (2008), a coronary artery disease incidence of 84 v. 66 % was evident in individuals with six to seven v. two to three risk alleles and a higher AA:LA ratio was an independent risk factor for coronary artery disease (18) .…”

Dietary arachidonic acid in perinatal nutrition: a commentary

“…The differences in the observations may be explained by the observed variable associations between different FADS SNPs and blood levels, especially for DHA (60) as indicated by the most recent studies (64,68). The importance of FADS genotypes has also been investigated in relation to plasma lipid profile in childhood (69,70) and atopic development, specifically of asthma (71)(72)(73). Furthermore, daily margarine intake (amongst the major sources of n-6 PUFA) has been found to be associated with increased asthma in children who were major allele homozygotes, indicating that FADS gene variants may modulate risk of allergic diseases possibly via a reduction in AA (72).…”