Beth A MacIntosh1, Christopher E Ramsden2, Gilson Honvoh3, Keturah R Faurot4, Olafur S Palsson5, Angela D Johnston4, Chanee Lynch4, Paula Anderson4, Daria Igudesman6, Daisy Zamora7, Mark Horowitz8, Susan Gaylord4, John D Mann9. 1. Metabolic and Nutrition Research Core, UNC Medical Center, 102 Mason Farm Rd., CB#7777, NC, 27599, USA. Electronic address: beth.macintosh@unchealth.unc.edu. 2. Lipid Peroxidation Unit, Laboratory of Clinical Investigation, National Institute on Aging, NIH, Baltimore, MD, USA; Intramural Program of the National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA; Department of Physical Medicine and Rehabilitation, University of North Carolina, Chapel Hill, NC, USA. 3. Department of Physical Medicine and Rehabilitation, University of North Carolina, Chapel Hill, NC, USA; Department of Biostatistics, Gillings School of Global Public Health, Program on Integrative Medicine, Department of Physical Medicine and Rehabilitation, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. 4. Department of Physical Medicine and Rehabilitation, University of North Carolina, Chapel Hill, NC, USA. 5. Division of Gastroenterology and Hepatology, Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. 6. Department of Nutrition, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. 7. Department of Psychiatry, UNC School of Medicine, Chapel Hill, NC, USA; Lipid Peroxidation Unit, Laboratory of Clinical Investigation, National Institute on Aging, NIH, Baltimore, MD, USA. 8. Lipid Peroxidation Unit, Laboratory of Clinical Investigation, National Institute on Aging, NIH, Baltimore, MD, USA. 9. Department of Neurology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Abstract
BACKGROUND & AIMS: Increasing dietary intake of n-3 EPA+DHA and lowering dietary n-6 LA is under investigation as a therapeutic diet for improving chronic pain syndromes as well as other health outcomes. Herein we describe the diet methodology used to modulate intake of n-3 and n-6 PUFA in a free living migraine headache population and report on nutrient intake, BMI and diet acceptability achieved at week 16 of the intensive diet intervention and week 22 follow-up time-point. METHODS: A total of 178 participants were randomized and began one of three diet interventions: 1) a high n-3 PUFA, average n-6 PUFA (H3) diet targeting 1500 mg EPA+DHA/day and 7% of energy (en%) from n-6 linoleic acid (LA), 2) a high-n-3 PUFA, low-n-6 PUFA (H3L6) targeting 1500 mg EPA+DHA/day and <1.8 en% n-6 LA or 3) a Control diet with typical American intakes of both EPA+DHA (<150 mg/day) and 7 en% from n-6 LA. Methods used to achieve diet change to week 16 include diet education, diet counseling, supply of specially prepared foods, self-monitoring and access to online diet materials. Only study oils and website materials were provided for the follow-up week 16 to week 22 periods. Diet adherence was assessed by multiple 24 h recalls administered throughout the trial. Diet acceptability was assessed in a subset of participants at 4 time points by questionnaire. RESULTS: At week 16 H3 and H3L6 diet groups significantly increased median n-3 EPA+DHA intake from 48 mg/2000 kcals at baseline to 1484 mg/2000 kcals (p < 0.0001) and from 44 mg/2000 kcals to 1341 mg/2000 kcals (p < 0.0001), respectively. In the Control group, EPA+DHA intake remained below the typical American intake with baseline median at 60 mg/2000 kcals and 80 mg/2000 kcals (p = 0.6) at week 16. As desired, LA intake was maintained in the H3 and Control group with baseline median of 6.5 en% to 7.1 en% (p = 0.4) at week 16 and from 6.5 en% to 6.8 en% (p = 1.0) at week 16, respectively. In the H3L6 group, n-6 LA decreased from 6.3 en% at baseline to 3.2 en% (p < 0.0001) at week 16. There were no significant changes in BMI or diet acceptability throughout the trial or between diet groups. CONCLUSIONS: We find this diet method to be acceptable to research participants and successful in altering dietary n-3 EPA+DHA with and without concurrent decreases in n-6 LA. If n-6 LA of less than 3 en% is desired, additional techniques to limit LA may need to be employed.
BACKGROUND & AIMS: Increasing dietary intake of n-3 EPA+DHA and lowering dietary n-6 LA is under investigation as a therapeutic diet for improving chronic pain syndromes as well as other health outcomes. Herein we describe the diet methodology used to modulate intake of n-3 and n-6 PUFA in a free living migraine headache population and report on nutrient intake, BMI and diet acceptability achieved at week 16 of the intensive diet intervention and week 22 follow-up time-point. METHODS: A total of 178 participants were randomized and began one of three diet interventions: 1) a high n-3 PUFA, average n-6 PUFA (H3) diet targeting 1500 mg EPA+DHA/day and 7% of energy (en%) from n-6 linoleic acid (LA), 2) a high-n-3 PUFA, low-n-6 PUFA (H3L6) targeting 1500 mg EPA+DHA/day and <1.8 en% n-6 LA or 3) a Control diet with typical American intakes of both EPA+DHA (<150 mg/day) and 7 en% from n-6 LA. Methods used to achieve diet change to week 16 include diet education, diet counseling, supply of specially prepared foods, self-monitoring and access to online diet materials. Only study oils and website materials were provided for the follow-up week 16 to week 22 periods. Diet adherence was assessed by multiple 24 h recalls administered throughout the trial. Diet acceptability was assessed in a subset of participants at 4 time points by questionnaire. RESULTS: At week 16 H3 and H3L6 diet groups significantly increased median n-3 EPA+DHA intake from 48 mg/2000 kcals at baseline to 1484 mg/2000 kcals (p < 0.0001) and from 44 mg/2000 kcals to 1341 mg/2000 kcals (p < 0.0001), respectively. In the Control group, EPA+DHA intake remained below the typical American intake with baseline median at 60 mg/2000 kcals and 80 mg/2000 kcals (p = 0.6) at week 16. As desired, LA intake was maintained in the H3 and Control group with baseline median of 6.5 en% to 7.1 en% (p = 0.4) at week 16 and from 6.5 en% to 6.8 en% (p = 1.0) at week 16, respectively. In the H3L6 group, n-6 LA decreased from 6.3 en% at baseline to 3.2 en% (p < 0.0001) at week 16. There were no significant changes in BMI or diet acceptability throughout the trial or between diet groups. CONCLUSIONS: We find this diet method to be acceptable to research participants and successful in altering dietary n-3 EPA+DHA with and without concurrent decreases in n-6 LA. If n-6 LA of less than 3 en% is desired, additional techniques to limit LA may need to be employed.
Authors: John Douglas Mann; Keturah R Faurot; Beth MacIntosh; Olafur S Palsson; Chirayath M Suchindran; Susan Ann Gaylord; Chanee Lynch; Angela Johnston; Kristen Maiden; David A Barrow; Joseph R Hibbeln; Christopher E Ramsden Journal: Prostaglandins Leukot Essent Fatty Acids Date: 2017-11-16 Impact factor: 4.006
Authors: Christopher E Ramsden; Amit Ringel; Sharon F Majchrzak-Hong; Jun Yang; Helene Blanchard; Daisy Zamora; James D Loewke; Stanley I Rapoport; Joseph R Hibbeln; John M Davis; Bruce D Hammock; Ameer Y Taha Journal: Mol Pain Date: 2016-03-10 Impact factor: 3.395