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Almond fatty acid bioavailability in hyperlipidemia: A randomized controlled crossover trial
Author(s) -
Nishi Stephanie K,
Kendall Cyril WC,
Bazinet Richard P,
Jenkins David JA,
Sievenpiper John L
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.146.4
Subject(s) - linoleic acid , bioavailability , crossover study , hyperlipidemia , food science , feces , chemistry , fatty acid , conjugated linoleic acid , zoology , medicine , biochemistry , biology , endocrinology , diabetes mellitus , pharmacology , paleontology , alternative medicine , pathology , placebo
Objective Almond intake is associated with reduced coronary heart disease (CHD) risk, yet concern remains that weight gain may occur due to their high fat content and subsequent energy density. Our aim was to assess fatty acid bioavailability of almond intake, using linoleic acid (18:2n‐6) as a marker of fat absorption, in individuals with hyperlipidemia as part of a secondary analysis of a randomized controlled clinical trial. Methods In a randomized crossover study, 27 hyperlipidemic men and women incorporated 3 isoenergetic (mean 423 kcal/d) supplements into a NCEP Step 2 diet each for 1 month. Supplements provided 22.2% of energy and consisted of full‐dose almonds (73±3 g/d), half‐dose almonds plus half‐dose muffins, and full‐dose muffins (control), matched for linoleic acid content. Fecal samples were collected at the end of each treatment period. Fatty acids were measured in the dietary supplements and freeze‐dried fecal samples using gas chromatography. Results Twenty‐two participants had fecal fatty acid data available from all 3 dietary phases for analyses. In the control supplement, linoleic acid comprised of 5.4 mg/g (536 mg/d), comparable to the linoleic acid content of the almond supplement of 5.7 mg/g (428 mg/d). There was a significantly greater amount of fecal linoleic acid following almond intake (7201±1147 mg/d) compared with the control (1802±1102 mg/d), adjusted for linoleic intake (P<0.01). For every half dose increase in almond intake (i.e. approximately 37.5 g almonds/day) there was a 2693 mg/day increase in linoleic acid excreted in the feces (P‐trend = 0.0024). Conclusions A dose‐response was observed with increasing linoleic acid excretion with increased almond intake. The fat content of almonds may not be as bioavailable as predicted by Atwater factors as suggested by the increased linoleic acid excretion with almond intake compared to the control. With less fat being bioavailable, meaning less kilocalories may be absorbed by the body, the concern of the ‘high energy density’ of almonds and risk of weight gain may be overstated. Protocol registration: clinicaltrials.gov identifier, [NCT00507520] Support or Funding Information Source of Research Support: Almond Board of California; PSI Foundation; Banting and Best Diabetes Centre; Canadian Diabetes Association