E Siguel, MD, PhD, R Lerman, MD, PhD.
We report that Essential Fatty Acid (EFA) abnormalities are highly prevalent in patients with elevated Total/HDL cholesterol (TC/HDLC) and correction of abnormal EFA profiles improves abnormal lipid levels far better than current recommended nutritional treatments.
Methods. Using a newly developed and highly sensitive patented method to identify EFA abnormalities, we analyzed fasting plasma at several intervals from 10+ patients with abnormal lipids and elevated TC/HDLC, who had been previously treated in accordance with conventional medical practice.
Results. Compared with healthy subjects with normal lipids, the patients had: 1) reduced % polyunsaturated fatty acids (PUFA) (p < 0.01), 2) increased % monounsaturated fatty acids (MUFA) (p < 0.01), and higher values of 20:3w9/20:4w6 and 16:1w7. On indices of EFA status or on the production of abnormal fatty acids, the patients had biochemical evidence of Relative EFA insufficiency (average to high plasma concentrations of EFAs but cells do not receive enough EFAs). The TC/HDLC was inversely proportional to plasma PUFA. When patients were placed on a diet high in EFAs, plasma PUFA levels increased, MUFA decreased, and TC/HDLC decreased in proportion to the increase in plasma PUFA.
Conclusions. All patients have biochemical evidence of EFA abnormalities. While conventional treatment may reduce total cholesterol 10%-15%, correction of biochemical evidence of EFA abnormalities is associated with major reductions in TC/HDLC and triglycerides. Patients also have w3/w6 abnormalities that must be considered to prevent either excessive bleeding or clot formation. We present specific new guidelines for the care of EFA abnormalities, which in our experience is the most frequently overlooked nutritional abnormality in these patients, and implications for enteral nutrition practice and health care costs.
E Siguel, MD, PhD, R Lerman, MD, PhD.
We report that Essential Fatty Acid (EFA) deficiency (EFAD) and EFA abnormalities are highly prevalent in patients with Short Bowel Syndrome even when those patients receive EFA supplements.
Methods. Using a newly developed and highly sensitive patented method to identify EFAD and EFA abnormalities, we analyzed fasting plasma at several intervals from 20+ patients with Crohn's disease, Cystic Fibrosis and Short Bowel Syndrome, who were being treated in accordance with established medical practice.
Results. Compared with healthy subjects, the patients had: 1) reduced % polyunsaturated fatty acids (p < 0.01), 2) increased % monounsaturated fatty acids (p < 0.01), 3) higher ratios of Mead (20:3w9) to arachidonic (20:4w6) acid (p < 0.01), 4) increased % of 16:1w7 (p < 0.01). On indices of EFA status or on the production of abnormal fatty acids, the patients had biochemical evidence of EFA insufficiency. We characterize the condition of Absolute EFAI (low plasma concentrations of EFAs) and Relative EFAI (plasma concentrations are adequate or high but cells do not receive enough EFAs).
Conclusions. Practically all patients have biochemical evidence of EFAI. Although conventional treatment is sometimes sufficient to temporarily correct observable clinical symptoms of EFAD, most patients have huge whole body deficits of EFAs and require far more EFAs than currently provided. Patients also have w3/w6 abnormalities that must be considered to prevent either excessive bleeding or clot formation. We present specific new guidelines for the care of EFA abnormalities, which in our experience is the most frequently overlooked nutritional abnormality in these patients.
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© 1998 Edward Siguel. All rights reserved |
modified 9/14/98 |