TABLE 4.

Associations between dietary DHA and WMH burden in the studied population¹

Variable	Model	APOE-ε4 in the model	Estimate (95% CI)	P	R 2
DHA	Unadjusted	—	−375 (−1232, 483)	0.391	0.002
	Adjusted2	Carrier/noncarrier3	−250 (−1119, 618)	0.571	0.112
		Number of alleles4	−234 (−1102, 633)	0.596	0.113
		Homozygote/nonhomozygote5	−244 (−1107, 618)	0.578	0.123
DHA × APOE-ε4	Unadjusted	Carrier/noncarrier3	−1488 (−3235, 259)	0.095	0.012
	Adjusted6		−918 (−2624, 788)	0.291	0.115
	Unadjusted	Number of alleles4	−1089 (−2239, 62)	0.064	0.013
	Adjusted6		−661 (−1781, 459)	0.247	0.117
	Unadjusted	Homozygote/nonhomozygote5	−1511 (−3682, 659)	0.172	0.011
	Adjusted6		−845 (−2944, 1253)	0.429	0.124

¹ n = 340. Data are presented for 1 g/d of DHA, obtained by multiple linear regression analyses. WMH burden was rank-transformed. ALA, α-linolenic acid; WMH, white matter hyperintensity.

²Including APOE-ε4, total intracranial volume, gender, age, BMI, hypercholesterolemia, hypertension, self-reported energy intake, and ALA intake as covariates.

³Distributed into n = 218 carriers and n = 122 noncarriers.

⁴Distributed into n = 122 with 0 alleles, n = 157 with 1 allele, and n = 61 with 2 alleles.

⁵Distributed into n = 61 homozygotes and n = 279 nonhomozygotes.

⁶Including total intracranial volume, gender, age, BMI, hypercholesterolemia, hypertension, self-reported energy intake, and ALA intake as covariates.