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Twenty-three apparently healthy volunteers aged 35 to 60 years consumed closely monitored self-selected (SS) diets for five weeks followed by two low fat controlled diets (25% energy) for two six-week periods followed by another five-week SS diet. The two low fat diets, fed in a crossover design to one-half of the subjects per controlled diet period, had a polyunsaturated/saturated (P/S) fat ratio of either 0.3 or 1.0. Results are reported for bi-weekly measurements of energy and nutrients; blood profiles and plasma fatty acids; and for end-of-period values for stool characteristics. Blood chemistry profiles differed in the two groups. The low P/S diet produced significant increases not only in cholesterol, but in 16:0, 16:1, and percent saturated fatty acids and decreases in 18:2 and omega 6 fatty acids. The reverse was seen with the high P/S diet. The essential fatty acid (EFA) linoleic acid returned in the poststudy period to prestudy levels (all subjects), but arachidonic acid did not. The explanation for negative correlation between magnesium intake or excretion and percent plasma linoleic acid must await further research.

The effects of two low fat diets with differing ratios of polyunsaturated to saturated fatty acids (P/S) on blood lipids, lipoproteins (LP), and apolipoproteins (Apo) were studied in 23 adult men, 30-60 years old, using a crossover design. Both test diets had 25% fat calories with either a P/S of 0.3 (Diet 1) or a P/S of 1.0 (Diet 2) and equivalent amounts of cholesterol. The study consisted of four periods: a 5-week prestudy on self-selected diet (SS), two 6-week test diet periods followed by a second 5-week post-study period on the SS diet. When compared with the SS diet, Diet 2 lowered the mean plasma total cholesterol (TC) by about 20% (P less than 0.01). Low density lipoprotein (LDL) cholesterol was also decreased by about 18% by Diet 2 (P less than 0.01). The high P/S diet did not cause a change in total cholesterol in the high density lipoprotein (HDL) subclass2 (HDL2) when compared to the SS diet. Levels of triglycerides (TG) were slightly reduced in HDL2 but showed a greater reduction in HDL3 in both diets. Phospholipids (PL) were significantly reduced in HDL2 and in HDL3, but the reduction in HDL3 PL was not statistically significant. Apo A-I levels were not changed by either diet when compared with the SS diet, but Apo A-II levels of HDL2 and HDL3 were significantly decreased by the low fat diets, and there was no P/S effect. No other consistent changes in apoprotein levels occurred. Our data suggest that, in men with normal lipid levels, practical dietary changes involving a moderate increase in P/S from 0.3 to 1.0 in a low fat, low cholesterol diet do influence lipoprotein composition and apoprotein distribution in a short time. The reduction in cholesterol in total lipid composition and in LDL lipids which accompanied the reduction of dietary fat and cholesterol are considered to be beneficial.

This study demonstrates that a three-week stabilization period, in which all subjects eat an identical diet, produced a more uniform but different baseline of metabolic parameters than the subject's self-selected or "habitual" diets. Subjects required more food energy to maintain initial body weights during the stabilization period than when they ate their reported self-selected diets; average intakes of almost all nutrients were higher from the stabilization than from the self-selected diet. The switch to the stabilization diet produced small but significant reductions in blood pressure, in some serum enzymes, urine volume, and sodium; and statistically significant increases in serum LDL cholesterol, potassium, aldosterone, protein, albumin, phosphorus, BUN, and in urine potassium. The findings indicate that results must be interpreted with caution from studies in which the baseline for measuring metabolic variables is established by feeding subjects a standardized diet that differed markedly from their regular, self-selected diets.

This experiment was conducted to determine the relationships between modest changes in dietary linoleate, blood pressure (BP) response, and levels of eicosanoid synthesis in humans. Products of eicosanoids which appear in blood were measured in urine: PGI2, 6-keto-PGF1 alpha (KPGI2); TXA2, (TXB2); PGF2 alpha, 13,14-dihydro-15-keto-PGF2 alpha, (MPGF2 alpha). Twenty-three adult men were fed controlled diets having 25 energy percent fat, and having P/S ratios of either 0.3 (low-PUFA) or 1.0 (high-PUFA), for a total of 12 weeks, with a switchover between P/S ratios at 6 weeks. The results showed that, under the conditions of this study, BP was significantly reduced by reducing dietary fat intake from about 37 to 25 energy percent. However, no further effects on BP were produced by increasing the P/S ratio from 0.3 to 1.0. KPGI2 excretion was significantly lowered on both controlled diets as compared to the self-selected (SS) diet. However, MPGF2 alpha was lowered only on the low-PUFA diet as compared to the self-selected diet. No significant decrease in TXB2 excretion was observed. Both MPGF2 alpha and KPGI2 excretion were positively correlated with urine volume and sodium excretion. On the SS diet, but not on the controlled diets, MPGF2 alpha excretion was negatively correlated with plasma linoleate and positively correlated with stearate. On the low-PUFA diet, MPGF2 alpha excretion increased with the intake of linoleate, while, on the high-PUFA diet, it decreased. This may have been due to the limited amounts of linoleate available in the low-PUFA diet (3.2-3.4 energy percent) as compared to that in the high-PUFA diet. Both KPGI2 and MPGF2 alpha excretion were positively correlated with systolic and diastolic BP. These results suggest that the amount of dietary linoleate is an important factor in the regulation of prostaglandin synthesis in humans.