Effect of consumption of whole milk and skim milk on blood lipid profiles in healthy men.

A controlled crossover feeding study was conducted in eight males aged 20-36 y to compare the effects of skim milk and whole milk on blood lipids. For 6-wk diet periods, 236 mL/4191 kJ of skim or whole milk was consumed with a background diet designed according to the American Heart Association recommendations. Plasma lipids were analyzed at baseline and at 3 and 6 wk. After 6 wk, the mean total cholesterol concentration was 4.47 mmol/L with skim milk and 4.80 mmol/L with whole milk (P < or = 0.001); mean low-density-lipoprotein-cholesterol concentrations were 2.64 and 2.96 mmol/L, respectively (P < or = 0.001). Mean apolipoprotein B decreased with skim milk and increased with whole milk (P < or = 0.05). No statistically significant differences were observed for plasma high-density lipoprotein-cholesterol, triglyceride, apolipoprotein A-I, or fatty acids. Substitution of skim milk for whole milk may decrease the risk of coronary heart disease.

Effect of glyburide and omega 3 fatty acid dietary supplements on glucose and lipid metabolism in patients with non-insulin-dependent diabetes mellitus.

Using a random crossover design, we examined the effects of glyburide for 4 wk on glucose, insulin, lipid, and lipoprotein metabolism in 10 men with non-insulin-dependent diabetes (NIDDM) receiving dietary fish-oil concentrates containing omega 3 (n-3) fatty acids (8 g/d). Compared with glyburide alone, fasting plasma glucose concentrations increased with fish oil. Although glyburide with fish oil decreased fasting glucose concentrations, they did not return to baseline. Basal insulin concentrations were unaltered by fish oil without or with glyburide; however, postprandial insulin concentrations were decreased by fish oil. Although total cholesterol and triglyceride concentrations were unchanged, very-low-density-lipoprotein cholesterol concentrations decreased and low-density-lipoprotein cholesterol rose and apolipoprotein B concentrations trended higher. Thus, glyburide only partially rectified the impaired fuel homeostasis associated with fish-oil supplements in patients with NIDDM. Therefore, we do not recommend intake of fish oil concentrates containing n-3 fatty acids in patients with NIDDM.

Effects of n-3 and n-6 fatty acid-enriched diets on plasma lipoproteins and apolipoproteins in heterozygous familial hypercholesterolemia.

Polyunsaturated fatty acids in vegetable (n-6) and marine (n-3) oils have been shown to reduce cholesterol levels in normolipidemic individuals. However, there is relatively little information available on the lipoprotein responses to dietary n-6 and n-3 fatty acids in individuals with genetic forms of hyperlipidemia at risk for premature cardiovascular disease. We studied five subjects with heterozygous familial hypercholesterolemia (FH), as well as five normal controls, on three rigidly controlled diets differing primarily in their fatty acid composition. FH subjects reduced their total plasma cholesterol by 34% during the n-3 diet and by 26% with the n-6 diet (both p less than 0.001) when compared with values while on a butter diet. In addition, low density lipoprotein (LDL) cholesterol fell 31% and 29% (both p less than 0.001), and apolipoprotein B (apo B) levels dropped 28% and 27% (both p less than 0.01) during the n-3 and n-6 diets, respectively. A significant reduction of total and LDL cholesterol as well as of apo B was also noted in normal controls during n-3 and n-6 diets. Total plasma triglyceride and high density lipoprotein cholesterol fell significantly during n-3 diets in normal and FH subjects. Thus, FH and normal subjects respond in a similar fashion to diets low in saturated fatty acids and rich in n-3 and n-6, with decreased LDL cholesterol and apo B concentrations.

Divergent lipoprotein responses to fish oils with various ratios of eicosapentaenoic acid and docosahexaenoic acid.

To determine if the ratio of eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids in fish oil had an effect on plasma lipid responses, we randomly fed eight normolipidemic men three 36%-fat diets containing primarily butter, EPA-rich pollock oil, or DHA-rich tuna or salmon-blend oils. Plasma EPA and DHA reflected the amounts in the diets. Compared with values for the butter diet, very-low-density lipoprotein (VLDL) triglycerides decreased equally (71-78%) with all diets; low-density lipoprotein (LDL) cholesterol (LDL-C) and apolipoprotein B decreased 26% and 13%, respectively, on the tuna and salmon-blend oil but did not change (-1%) and increased 19% with the pollock diet; high-density lipoprotein cholesterol (HDL-C) and lipoproteins A-I and A-II decreased with all diets but more with the pollock diet than with the tuna and salmon diets. The 23-31% decrease in total cholesterol on the tuna and salmon diets resulted mostly from decreased LDL-C whereas the 16% decrease on pollock oil resulted mostly from a decrease in HDL-C.

Effects of shellfish consumption on lipoproteins in normolipidemic men.

Eighteen normolipidemic males were fed six different species of shellfish; each shellfish was fed so that protein in shellfish equalled that in animal foods in the normal diet, with less than one-half of the amount of fat in animal foods allowed for preparation of the shellfish. Oyster, clam, crab, and mussel diets, low in cholesterol and high in n-3 fatty acids, lowered VLDL triglycerides and cholesterol and, except for the mussel diet, LDL and total cholesterol. Squid and shrimp diets, higher in cholesterol and lower in n-3 fatty acids, did not change the blood lipids. The ratio of LDL to HDL cholesterol was decreased on the oyster and mussel diets. Oyster, mussel, and squid diets increased HDL2 cholesterol. Cholesterol absorption was decreased on the oyster, clam, and mussel diets. When consumed with moderate dietary fat restriction, oysters, clams, mussels, and crab appear to be useful in hypolipidemic diets for normolipidemic men.

Shellfish: proximate composition, minerals, fatty acids, and sterols.

Proximate composition, minerals, fatty acids, and sterols were determined for eight species of shellfish commonly marketed in the Northwest. Moisture and total lipid content varied with the size of the species, with more variation in mollusca than in crustacea; total lipid content ranged from 0.7% in sea scallops to 3.1% in blue mussels but only from 1.2% in Dungeness crab to 1.3% in pink shrimp. The mineral content was highly variable; the mineral content of Northwest samples tended to be lower than that reported in other studies. Generally, shellfish are good sources of zinc, and Pacific oysters, blue mussels, and Manila clams are also good sources of iron. Five fatty acids (16:0, 16:1, 18:1, 20:5n-3, and 22:6n-3) represented from 60% to 84% of the fatty acid content. Palmitic acid ranged from 13% to 32% of the total fatty acids. Long-chain n-3 polyunsaturated fatty acids were predominant (37.6% to 54.3%), with sea scallops containing more than 50%; n-6 polyunsaturated fatty acids ranged from 1.5% to 6.5%. In crustacea, cholesterol was the primary sterol, and brassicasterol was the only other measurable sterol. In all mollusca except California squid, cholesterol averaged 37 mg/100 gm and ranged from 23% to 39% of the total sterols. In squid, cholesterol, at 231 mg/100 gm, was the only measurable sterol. We conclude that shellfish vary widely in their nutrient content but, in general, are valuable additions to the diet.

Elevated plasma glucose and lowered triglyceride levels from omega-3 fatty acid supplementation in type II diabetes.

We studied the effect of omega-3 fatty acids (omega 3FA) on glucose homeostasis and lipoprotein levels in eight type II (non-insulin-dependent)-diabetic subjects ingesting 8 g/day omega 3FA for 8 wk as marine-lipid concentrate capsules. After omega 3FA supplementation, fasting plasma glucose levels increased 22% (P = .005) and meal-stimulated glucose increased 35% (P = .036). The percentage of glucose elevation correlated with percentage ideal body weight (r = .73, P = .04). No significant changes were seen in fasting or meal-stimulated plasma insulin, glucose disposal, or insulin-to-glucagon ratios. Very-low-density lipoprotein cholesterol and triglyceride (TG) levels showed consistent reductions of 56% (P less than .001) and 42% (P less than .001), respectively, after omega 3FA supplementation. Total cholesterol levels decreased 7% (P less than .05) without alteration in low- or high-density lipoprotein cholesterol. Thus, omega 3FA supplementation at a dose of 8 g/day significantly improves plasma TG levels but increases fasting and meal-stimulated glucose concentrations in the type II diabetic patient not treated with insulin or sulfonylurea agents. Marine-lipid concentrate capsules supplying large amounts of omega 3FAs should be used cautiously in the type II diabetic patient.

The effects of omega 3 and omega 6 fatty acid-enriched diets on plasma lipoproteins and apoproteins in familial combined hyperlipidemia.

There is abundant evidence that dietary omega 3 fatty acids effect a favorable change in lipoprotein profiles of normolipidemic individuals. However, there is relatively little information available on the lipoprotein responses of hyperlipidemic individuals at risk for premature coronary artery disease. We studied a group of subjects with familial combined hyperlipidemia (FCHL), as well as a group of normal controls, on three rigidly controlled diets differing primarily in their fatty acid composition. The normal subjects demonstrated significant reductions in total cholesterol, low density lipoprotein (LDL) cholesterol, and total apolipoprotein B (apo B) levels on both an omega 3 (salmon) and omega 6 (safflower) fatty acid-enriched diet when these were compared with a basal diet high in saturated fat. The primary difference in response to the polyunsaturated diets was the potent triglyceride-lowering effect of the salmon diet. The FCHL subjects demonstrated a response to the safflower diet similar to that observed in normals and also manifested a marked triglyceride lowering with the salmon diet. However, total cholesterol and total apo B levels were not lowered by the salmon diet, and LDL cholesterol and apo B levels exhibited an upward trend. Thus, individuals with FCHL, a common disorder associated with premature coronary artery disease, do not appear to have a favorable lipoprotein response to diets enriched in omega 3 fatty acids.

Effect of shellfish consumption on cholesterol absorption in normolipidemic men.

Noncholesterol marine sterols, abundant in molluscan shellfish, could inhibit cholesterol absorption. Eight normolipidemic males were fed for 3 weeks each three natural food diets in which a mixture of oysters and clams, crab, or chicken was served as the primary source of animal protein. The diets were equalized for caloric distribution, cholesterol, and n-3 fatty acids, leaving the noncholesterol marine sterols in the oyster/clam diet (444 mg/2,000 kcal) as the potential lipid-modifying variable. Cholesterol absorption was measured by plasma isotope ratio after doses of oral 14C- and intravenously infused 3H-labeled cholesterol. Cholesterol absorption was lower (42 +/- 4%) during the oyster/clam diet than during the chicken (54 +/- 3%, P less than 0.01) or crab (55 +/- 3%, P less than 0.01) diet periods. There was no difference between the chicken and crab diet periods. Total plasma cholesterol and triglycerides, very low density lipoprotein cholesterol and triglycerides, and low density and high density lipoprotein (HDL) cholesterol were not significantly different between any of the diets. The ratio of the HDL2-/HDL3-cholesterol was higher following the oyster/clam diet (0.46 +/- 0.09) than the chicken diet (0.32 +/- 0.06, P less than 0.05). Plasma and red cell membrane n-3 fatty acids were not significantly different among the three diets, but red cell membrane n-3 fatty acids increased as a function of time regardless of dietary sequence.

The effect of training and diet on lipoprotein cholesterol, tissue lipoprotein lipase and hepatic triglyceride lipase in rats.

Treadmill training for 1 hr/day for 10 wk did not significantly affect chylomicron, very low density, low density, or high density lipoprotein cholesterol in rats fed either a high carbohydrate (glucose) or high fat (coconut oil) diet. Lipoprotein lipase activity of heart, adipose tissue, and skeletal muscle fibers was also unaffected by training. Carbohydrate feeding, however, when compared to fat feeding significantly lowered all lipoprotein cholesterol values as well as heart and fast-oxidative-glycolytic muscle fiber lipase activity and, conversely, significantly elevated hepatic triglyceride lipase activity. Thus, in the rat, an alteration in the serum lipid profile did not occur as a result of training, but dietary differences did independently influence serum lipid levels and tissue enzyme activity. It is suggested that human studies need to control for the possible independent influence of dietary differences when investigating the effects of training on lipoprotein metabolism.

Lipid metabolism in pregnancy. VIII. Effects of dietary fat versus carbohydrate on lipoprotein and hepatic lipids and tissue triglyceride lipases.

UNLABELLED: We have asked, is hypertriglyceridemia in the fed state in pregnancy due to intolerance to exogenous fat, accumulation of endogenous triglycerides, or accumulation of remnants of d < 1.006 lipoprotein metabolism? To answer these questions, we fed fat-free diets high in starch or sucrose, or diets containing fat or fat plus cholesterol to pregnant and nonpregnant rats for 12 days until gestational day 21 (term = 22 days). Blood was obtained 0, 4, or 8 hr after removal of food from the cages. Lipid concentrations were determined in chylomicrons and very low, low, and high density lipoproteins. Hypertriglyceridemia in pregnancy exists on both starch and sucrose containing fat-free diets and is exaggerated 4 and 8 hr after food is removed from the cage. The triglyceride rise occurs in d < 1.006 lipoproteins. With fat feeding, chylomicron triglyceride concentrations are not significantly elevated in pregnant rats, 0 or 8 hr postabsorptively despite greater food intake in pregnancy. In contrast, very low density lipoprotein (VLDL) triglyceride concentrations are elevated at all times following fat feeding in pregnant compared to nonpregnant animals. A significant contribution of lipoprotein remnants to the triglyceride rise in d < 1.006 lipoproteins seems unlikely since an isolated increase in VLDL cholesterol is not observed. No statistically significant accumulation of hepatic triglycerides occurs on any diet in pregnancy. Diet induced shifts in adipose tissue and muscle lipoprotein lipase activity are exaggerated in pregnancy while hepatic lipase is unaffected. Fetal weight is similar on all diets except sucrose where weight is reduced. CONCLUSIONS: Hypertriglyceridemia in fed pregnant rats is due to an increase in endogenous triglycerides. Remnant lipid accumulation does not appear to contribute to the endogenous hypertriglyceridemia. There is no intolerance to exogenous (dietary) fat. The results are compatible with an unimpaired delivery of exogenous fat to fat oxidizing tissues thereby maximizing glucose availability for fetal growth.

Dietary management of the pregnant diabetic.

The tendency of the pregnant diabetic to fasting ketosis limits the extent to which calorie restriction (particularly negative calorie balance) can be used in the treatment of the obese, adult-onset, pregnant diabetic. In addition, the vagaries of measuring excess weight gain and detecting extraneous sources of weight gain in diabetic pregnancy, and the difficulty of accurately enforcing a caloric prescription without forcing the subject to weigh her food, make the determination of an accurate degree of caloric limitation difficult at best. A greater reliance on the mother's appetite center may be more accurate and rewarding in most instances than any devices available to the clinician. Important considerations in the diet of the pregnant diabetic are adequate protein, minerals, and vitamins, an amount of carbohydrate that is constant from day to day but not necessarily restricted, carbohydrate intake in an unrefined form that maximizes the intake of associated fiber, and a reproducible meal and snack schedule which complements in insulin regimen. Insulin must remain the primary therapeutic tool if the effects of maternal diabetes on fetal morbidity and mortality are to be minimized.

Egg substitutes: chemical and biologic evaluations.

The total lipid, cholesterol, phospholipid, and fatty acid content of dried whole egg (DWE), a refrigerated liquid egg substitute, a powdered egg substitute, and a commercial egg yolk replacer (EYR) were compared. All substitutes contained less total lipid, cholesterol, and phospholipid than DWE. The powdered substitute contained only half the total lipid content reported by the producers and only a fifth of the cholesterol of DWE, while the percentage distribution of fatty acids was similar to that of DWE. The liquid substitute and EYR had fatty acid distributions similar to soybean oil. Rat growth and lipid response were compared for diets containing either DWE or a mixture of EYR and egg white. Both diets were fed with and without vitamin and mineral supplements. Rat growth response was greatest on the DWE diets, either with or without the supplements, was intermediate on the supplemented EYR diets, and was least on the unsupplemented EYR diets. The consumption of DWE-containing diets, when compared with the EYR-containing diets, caused greater liver weight, greater liver total lipid and total cholesterol content, and slightly higher serum cholesterol.