Fatty acid consumption pattern of Americans: 1987–1988 USDA Nationwide Food Consumption Survey

Jonnalagadda, Satya S.; Egan, S. K.; Heimbach, James T.; Harris, Suzanne; Kris-Etherton, P. M.

doi:10.1016/0271-5317(95)02046-2

Cited by 52 publications

(15 citation statements)

References 11 publications

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“…The habitual AA intake of subjects in the current study was in the range of 100-200 mg/d, which is consistent with earlier reports for other Western populations (25)(26)(27). The amount of AA provided in the supplement in the current study (680 mg/d) increased AA intake almost 5-fold.…”

Section: Discussionsupporting

confidence: 81%

Dietary supplementation with eicosapentaenoic acid, but not with other long-chain n−3 or n−6 polyunsaturated fatty acids, decreases natural killer cell activity in healthy subjects aged >55 y

Thiès

Nebe-von-Caron

Powell

et al. 2001

The American Journal of Clinical Nutrition

169

130

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Section: Discussionsupporting

confidence: 81%

Dietary supplementation with eicosapentaenoic acid, but not with other long-chain n−3 or n−6 polyunsaturated fatty acids, decreases natural killer cell activity in healthy subjects aged >55 y

Thiès

Nebe-von-Caron

Powell

et al. 2001

The American Journal of Clinical Nutrition

169

130

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“…In addition, we (22) found changes in the metabolism of the polyunsaturated FA in the presence of elevated dietary AA. Furthermore, while the amount of AA fed in this study was 5 to 10 times that in the typical Western diet (6,35), it was still well below that used in the study reported by Seyberth et al (17). We cannot predict whether higher levels of dietary AA, or longer feeding period, will have major metabolic and physiological consequences.…”

Section: Discussionmentioning

confidence: 68%

“…The average amount of AA in Western diets is not certain but has been estimated at between 50 and 300 mg per day (4,5). Jonnalagadda et al (6) reported that the U.S. diet contains approximately 100 mg/d of AA based on the USDA Nationwide Food Consumption Survey for 1987-1988. Sinclair and O'Dea (7) reported that the Australian diet contained between 80 and 100 mg/d of AA.…”

mentioning

confidence: 98%

A human dietary arachidonic acid supplementation study conducted in a metabolic research unit: Radionale and design

Nelson

Kelly

Emken

et al. 1997

Lipids

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While there are many reports of studies that fed arachidonic acid (AA) to animals, there are very few reports of AA feeding to humans under controlled conditions. This 130-d study was conceived as a controlled, symmetrical crossover design with healthy, adult male volunteers. They lived in the metabolic research unit (MRU) of the Western Human Nutrition Research (WHNRC) for the entire study. All food was prepared by the WHNRC kitchen. The basal (low-AA) diet consisted of natural foods (30 en% fat, 15 en% protein, and 55 en% carbohydrate), containing 210 mg/d of AA, and met the recommended daily allowance for all nutrients. The high-AA (intervention) diet was similar except that 1.5 g/d of AA in the form of a triglyceride containing 50% AA replaced an equal amount of high-oleic safflower oil in the basal diet. The subjects (ages 20 to 39) were within -10 to +20% of ideal body weight, nonsmoking, and not allowed alcohol in the MRU. Their exercise level was constant, and their body weights were maintained within 2% of entry level. Subjects were initially fed the low-AA diet for 15 d. On day 16, half of the subjects (group A) wee placed on the high-AA diet, and the other group (B) remained on the low-AA diets. On day 65, the two groups switched diets. On day 115, group B returned to the low-AA diet. This design, assuming no carryover effect, allowed us to merge the data from the two groups, with the data comparison days being 65 (low-AA) and 115 (high-AA) for group B and 130 (low-AA) and 65 (high-AA) for group A. The main indices studied were the fatty acid composition of the plasma, red blood cells, platelets, and adipose tissue; in vitro platelet aggregation, bleeding times, clotting factors; immune response as measured by delayed hypersensitivity skin tests, cellular proliferation of peripheral blood mononuclear cells in response to various mitogens and antigens, natural killer cell activity, and response to measles/mumps/rubella and influenza vaccines; the metabolic conversion of deuterated linoleic acid to AA and the metabolic fate of deuterated AA in the subjects on and off the high-AA diet; and the production of eicosanoids as measured by excretion of 11-DTXB2 and PGI2-M in urine. The results of these studies will be presented in the next five papers from this symposium.

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“…The only positive findings were for palmitic acid (C16:0) in Japanese Americans. Major food sources of palmitic acid (C16:0) are meat, fish, milk, and cheese [42]. However, in our previous papers, we found no association between consumption of these foods and prostate cancer risk in Japanese Americans, or in the overall cohort [19, 43].…”

Section: Discussionmentioning

confidence: 90%

Circulating fatty acids and prostate cancer risk in a nested case–control study: the Multiethnic Cohort

Park

Wilkens

Henning

et al. 2008

Cancer Causes Control

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Objective-Dietary fat, including specific fatty acids, has been proposed to contribute to prostate cancer pathogenesis, but findings from the studies based on biomarkers have been conflicting.Methods-We examined the association between erythrocyte membrane fatty acid composition and prostate cancer risk in a nested case-control study within a multiethnic cohort of African Americans, Native Hawaiians, Japanese Americans, Latinos, and Whites. Analyses included 376 cases and 729 matched controls. Conditional logistic regression was used to estimate the odds ratios and 95% confidence intervals with adjustment for multiple covariates.Results-No significant association was found for saturated, mono-and polyunsaturated fatty acid, or for specific n-3 and n-6 fatty acids, even when the analysis was limited to advanced or high grade prostate cancer. In ethnic specific analyses, there was a positive association with palmitic acid in Japanese Americans that was significantly different from the null results in other groups. There was also an increased risk with n-3 fatty acids and the ratio of n-3/n-6 fatty acids in Whites. Conclusion-Although there was a suggestion of ethnic specific associations with some fatty acids, our overall findings do not support a role for fatty acids in prostate carcinogenesis.

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Fatty acid consumption pattern of Americans: 1987–1988 USDA Nationwide Food Consumption Survey

Cited by 52 publications

References 11 publications

Dietary supplementation with eicosapentaenoic acid, but not with other long-chain n−3 or n−6 polyunsaturated fatty acids, decreases natural killer cell activity in healthy subjects aged >55 y

Dietary supplementation with eicosapentaenoic acid, but not with other long-chain n−3 or n−6 polyunsaturated fatty acids, decreases natural killer cell activity in healthy subjects aged >55 y

A human dietary arachidonic acid supplementation study conducted in a metabolic research unit: Radionale and design

Circulating fatty acids and prostate cancer risk in a nested case–control study: the Multiethnic Cohort

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