Table 1.

Pooled analyses cited as the primary evidence base for CHD benefits of n-6 linoleic acid (LA): no clear distinction made between n-3 and n-6 PUFA species (adapted with permission from Ramsden et al.⁽¹¹⁾)^*

Pooled analysis	Outcome	Quote defining the independent variable	Exposure variable(s)	Mixed n-3/n-6 PUFA† or n-6 specific PUFA‡
Mozaffarian et al.(8) Meta-analysis of RCT	Non-fatal MI + CHD death	‘[total] PUFA consumption as a replacement for SFA’	LA + ALA + EPA and DHA	Mixed (n-3 + n-6)
Jakobsen et al.(9)§ Pooled analysis of eleven observational cohorts	CHD events + CHD death	‘[total] PUFAs; including both n-3 and n-6 fatty acids, also known as omega-3 and omega-6 fatty acids; primarily n-6 linoleic acid’	LA + ALA + EPA and DHA	Mixed (n-3 + n-6)
Mensink et al.(10) Meta-analysis of RCT	LDL-cholesterol	‘total PUFAs may be considered to equal the n-6 PUFAs with 18 carbon atoms (linoleic acid plus some α-linolenic acid)’	LA + ALA	Mixed (n-3 + n-6)

RCT, randomised controlled trial; MI, myocardial infarction; ALA, α-linolenic acid.

^*None of these pooled analyses evaluated the specific effects of n-6 LA or n-6 PUFA; however, their concordant benefits have been attributed to n-6 LA.

^†Mixed n-3/n-6 PUFA indicates RCT interventions that substantially increased both n-3 and n-6 PUFA, or exposure variables in observational cohorts that included both n-3 and n-6 PUFA.

^‡n-6 Specific PUFA indicates RCT interventions that increased n-6 LA without substantially increasing n-3 PUFA.

^§Individual prospective cohorts included in the pooled analysis by Jakobsen et al. have limited ability to disentangle the respective intakes of n-3 ALA and n-6 LA, particularly for foods eaten away from home and packaged foods⁽¹¹⁾ (see Table 2).