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Can the Hypotriglyceridemic Effect of Fish Oil Concentrate Be Sustained?

Gordon Schectman, MD; Sushma Kaul, MS; George D. Cherayil, PhD; Martha Lee, PhD; and Ahmed Kissebah, MD, PhD
[+] Article, Author, and Disclosure Information

Grant Support: Supported by Grant 77-33-03R from the Veterans Administration and by General Clinical Research Center grant RR00058.

Requests for Reprints: Gordon Schectman, MD, Division of General Internal Medicine, Medical College of Wisconsin, 8700 West Wisconsin Avenue, Milwaukee, WI 53226.

Current Author Addresses: Dr. Schectman: Division of General Internal Medicine, Medical College of Wisconsin, 8700 West Wisconsin Avenue, Milwaukee, WI 53226.

Drs. Kaul and Lee: Clinical Research Center, 9200 West Wisconsin Avenue, Milwaukee, WI 52336.

Dr. Cherayil: Department of Pathology, Medical College of Wisconsin, 8700 West Wisconsin Avenue, Milwaukee, WI 53226.

Dr. Kissebah: Department of Medicine, Medical College of Wisconsin, 8700 West Wisconsin Avenue, Milwaukee, WI 53226.

© 1989 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1989;110(5):346-352. doi:10.7326/0003-4819-110-5-346
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Study Objective: To determine whether high doses of fish oil concentrate followed by low-dose maintenance therapy can sustain the initial plasma triglyceride reductions.

Design: Before-and-after trial with 3-month treatment periods.

Setting: Outpatient lipid clinic at a university medical center.

Patients: Sixteen patients with hypertriglyceridemia recruited from the General Internal Medicine Clinics. Five had concomitant hypercholesterolemia (type IIb).

Intervention: Fish oil supplementation at two doses. After basal measurements, 9.8 g/d omega-3 fatty acids were provided for study months 1 to 3, and 3.9 g/d were provided for study months 4 to 6.

Measurements and Main Results: Blood was drawn monthly and plasma was analyzed for levels of triglycerides, low-density-lipoprotein (LDL) cholesterol and apolipoprotein B, high-density-lipoprotein (HDL) cholesterol and apolipoprotein A1, and glucose and glycohemoglobin. During therapy with the higher dose, mean plasma triglyceride levels were reduced from 3.65 ± 0.35 mmol/L at baseline to 1.85 ± 0.20 mmol/L at 1 month, but increased by 30% to 2.40 ± 0.30 mmol/L by the third month of therapy (P < 0.05); this increase could not be explained by changes in body weight or compliance. Plasma triglyceride levels continued to increase with low-dose therapy and remained only 11 % below baseline values by the sixth month of therapy (P = not significant). Although fish oil therapy increased HDL cholesterol levels ( + 18% at high dose; 99% CI, 5% to 31%), favorable changes were not seen in LDL cholesterol, apolipoprotein B, or apolipoprotein A1 levels.

Conclusions: Fish oil concentrate at high doses followed by low-dose maintenance therapy cannot sustain the initial large plasma triglyceride reductions. Moreover, the efficacy of the higher dose becomes less pronounced after the first month of therapy. This reduced efficacy during prolonged therapy, and the lack of beneficial effect on apolipoprotein and LDL cholesterol levels, may limit the practical benefit of fish oil in the treatment of hypertriglyceridemia.


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