Enhancement of platelet 12-HETE production in the presence of polymorphonuclear leukocytes during calcium ionophore stimulation.

This study investigates the effect of platelet/neutrophil interactions on eicosanoid production. Human platelets and polymorphonuclear leukocytes (PMNs) were stimulated alone and in combination, with calcium ionophore A23187 and the resulting eicosanoids 12S-hydroxy-(5Z,8Z,10E,14Z)-eicosatetraenoic acid (12-HETE), 12S-heptadecatrienoic acid (HHT), 5S,12R-dihydroxy-(6Z,8E,10E,14Z)-eicosatetraenoi c acid (LTB4) and 5S-hydroxy-(6E,8Z,11Z,14Z)-eicosatetraenoic acid (5-HETE) were measured by HPLC. The addition of PMNs to platelet suspensions caused a 104% increase in 12-HETE, a product of 12-lipoxygenase activity, but had only a modest effect on the cyclooxygenase product HHT (increase of 18%). By using PMNs labelled with [14C]arachidonic acid it was shown that the increases in these platelet eicosanoids could be accounted for by translocation of released arachidonic acid from PMNs to platelets and its subsequent metabolism. The observation that 12-lipoxygenase was about five times more efficient than cyclooxygenase at utilising exogenous arachidonic acid during the platelet/PMN interactions was confirmed in experiments in which platelets were stimulated with A23187 in the presence of [14C]arachidonic acid. Stimulations of platelets with thrombin in the presence of PMNs resulted in a decrease in 12-HETE and HHT levels of 40% and 26%, respectively. The presence of platelets caused a small increase in neutrophil LTB4 output but resulted in a decrease in 5-HETE production of 43% during stimulation with A23187. This study demonstrates complex biochemical interactions between platelets and PMNs during eicosanoid production and provides evidence of a mechanism to explain the large enhancement in 12-HETE production.

Dietary modification of fatty acid and prostaglandin synthesis in the rat. Effect of variations in the level of dietary fat.

Dietary supplements with safflower oil, linseed oil, cod liver oil and hydrogenated coconut oil were given to rats at levels of 5, 20 and 40 energy % to simultaneously assess the effects of both type and level of dietary fat on tissue fatty acid composition and prostanoid synthesis. There was no significant change in weight gain or blood pressure between the dietary groups after the 4-week dietary regimen. The liver oil and linseed oil diets depressed the arachidonic acid content of kidney phospholipids at all levels of supplementation. The arachidonic acid content of plasma lipids was significantly elevated in animals on the safflower oil diet at 20 and 40 energy % while those on the same level of liver oil diet showed a marked reduction in arachidonic acid. Whole blood synthesis of thromboxane B2 varied significantly at all levels of fat supplementation, with the 20 energy % safflower oil fed group showing maximally enhanced thromboxane B2 production compared to the coconut oil group (P less than 0.001). Conversely, the liver oil groups showed depressed thromboxane B2 synthesis at 20 and 40 energy % (P less than 0.01) compared to the coconut oil group and at 5 energy % compared to the safflower oil group (P less than 0.05). Production of 6-ketoprostaglandin F1 alpha and prostaglandin E2 by incubated kidney homogenates only differed significantly between the dietary groups at 40 energy %. Urinary excretion of 6-ketoprostaglandin F1 alpha was increased by 45% and 55% in rats fed the safflower oil diet at 20 and 40 energy %, respectively compared to the saturated fat diet, while in the liver oil groups excretion was reduced by 20% and 32%. Dietary suppression of prostanoid synthesis is explained in part by changes in available arachidonic acid and competitive inhibition of cyclooxygenase by (n - 3) fatty acids. Thus, minor changes in dietary fat can readily alter tissue fatty acid composition, but both the extent and nature of changes in phospholipid and prostanoid metabolism vary markedly according to the tissue site.

Onset of changes in phospholipid fatty acid composition and prostaglandin synthesis following dietary manipulation with n-6 and n-3 fatty acids in the rat.

A synthetic diet preparation supplemented with 10% by weight of either safflower oil, hydrogenated coconut oil containing 3% safflower oil, or 'max EPA' fish oil was fed to rats over a 8-week period. Serial measurements of serum fatty acids, serum thromboxane B2 and urinary prostaglandin excretion were taken during the treatment period to assess the rate of change in fatty acid composition and prostaglandin synthesis following dietary manipulation. There was no significant change in weight gain between the dietary groups during the treatment period. Significant changes in serum fatty acids occurred within 48 h of treatment, with the 'max EPA' oil group having arachidonic acid levels reduced by 23% (P less than 0.01) compared to the coconut oil group. Conversely, rats fed safflower oil had an 18% enhancement of arachidonic acid during the same time period. Whole blood synthesis of thromboxane B2 was significantly depressed (P less than 0.01) after 48 h in rats fed 'max EPA' oil compared to the safflower oil or coconut oil groups. This suppression reached a maximum of 65% (P less than 0.001) after 7 days of dietary 'max EPA' oil treatment. The safflower oil and coconut oil-fed groups showed the same levels of serum thromboxane B2 production over the treatment period. Urinary excretion of both 6-ketoprostaglandin F1 alpha and prostaglandin E2 varied significantly (P less than 0.01) between the groups after 7 days of dietary treatment. Rats fed 'max EPA' oil had depressed urinary prostanoid excretion compared to the safflower and coconut oil groups which remained very similar to each other. After the 8-week treatment period rats were killed and the phospholipid fatty acid composition and prostaglandin-generating capacity of platelets, aorta and renal tissue was examined. Prostanoid production by kidney cortex and medulla and segments of aorta was consistently suppressed in rats fed 'max EPA' oil. These observations correlated well with changes in the phospholipid fatty acid profiles in these tissues. This study shows rapid changes in serum fatty acids and thromboxane B2 generation following dietary manipulation, while changes in urinary excretion or prostanoid metabolites occur only after a longer time period.

Differential effect of aspirin on platelet aggregation in IDDM.

Diabetes mellitus is associated with a high incidence of cardiovascular diseases not directly attributable to hyperlipidemia, smoking, or hypertension, but which in part may be explained by an enhanced tendency to thrombosis due to increased platelet activity. The aim of this study was to evaluate platelet function and compare the effectiveness of the antiplatelet drug aspirin on platelet aggregation in diabetic and nondiabetic subjects. Platelet aggregation and composition were examined in 20 male insulin-dependent diabetes mellitus (IDDM) patients and 20 nondiabetic control subjects matched for age and body mass index. All were normotensive with serum total cholesterol less than 6.5 mM. Although within the clinically acceptable normal range, blood pressure was significantly higher in diabetic patients (130/75 mmHg) than in control subjects (123/70 mmHg) (P less than 0.05). Serum thromboxane B2 and ex vivo aggregation of platelets in response to two doses of the agonists collagen and platelet-activating factor (PAF) were similar to nondiabetic subjects. However, after taking 100 mg/day aspirin for 5 days, platelet aggregation to collagen was reduced by 76% in control subjects compared to 56% in IDDM patients (P less than 0.001). Aspirin treatment also reduced the slope of the aggregation curve and increased the lag time (the period between the addition of collagen and the start of irreversible aggregation) significantly more in control than in diabetic platelets. This difference in platelet aggregation could not be attributed to differences in platelet serotonin or thromboxane A2 secretion, the latter being almost completely suppressed by aspirin in each group. Platelet aggregation to PAF was similar in both groups and was not affected by aspirin.(ABSTRACT TRUNCATED AT 250 WORDS)

Fish oil-induced changes in apolipoproteins in IDDM subjects.

The aim of this study was to examine the effect of Max EPA (a commercially available fish oil preparation) on serum cholesterol lipoproteins and apolipoproteins in insulin-dependent diabetic (IDDM) men with dosages that were likely to be acceptable to patients. Twenty-two male IDDM patients aged 20-41 yr, 6 of whom had retinopathy, were recruited from the Royal Perth Hospital diabetic clinic. After screening, subjects were divided into three groups. Six of the subjects without retinopathy were randomly selected and allocated to a control group. The remaining 16 patients (10 without and 6 with retinopathy) received a fish oil supplement. All subjects were advised to maintain their usual dietary patterns. Sixteen patients, including the 6 with retinopathy, were instructed to take 15 Max EPA fish oil capsules/day with meals. Patients in the control group did not take Max EPA. Three weeks of Max EPA supplementation without other dietary modification led to a significant rise in total cholesterol (P less than 0.01), which could be accounted for by increases in low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol. The increase in HDL cholesterol was explained by a 33% rise (P less than 0.001) in its HDL2 subclass. Changes in apolipoproteins were examined and showed that the level of apolipoprotein A-I increased after ingestion of fish oil and correlated significantly (P less than 0.05) with the rise in HDL cholesterol.(ABSTRACT TRUNCATED AT 250 WORDS)

Potentiation of bradykinin by captopril during suppression of prostacyclin synthesis.

The effect of captopril on blood pressure and on the depressor responses to intravenously administered bradykinin was examined in anesthetized normotensive rats during inhibition of prostaglandin synthesis. The hypotensive action of captopril persisted after treatment with indomethacin in doses that markedly suppressed urinary excretion of the prostacyclin metabolite 6-keto prostaglandin F1 alpha. Captopril markedly potentiated the vasodepressor responses to intravenous bradykinin given by bolus injection or continuous infusion. Neither the magnitude nor the duration of the blood pressure fall were affected by treatment with indomethacin. It is concluded that in the anesthetized rat the hypotensive action of captopril and its augmentation of the depressor response to bradykinin is independent of prostacyclin synthesis.

Fluid temperature and volume dependence of the dissociated plasma epinephrine and norepinephrine response to drinking.

The ingestion of cold fluids results in a rise in plasma norepinephrine (NE) and a fall in plasma epinephrine (E). To assess the relative roles of fluid volume and temperature in mediating this dissociated sympathetic response to drinking, NE and E levels were measured on 3 separate occasions in 10 men before and after ingestion of either 750 ml distilled water at 4 C, 750 ml at 25 C, or 150 ml at 4 C. An increase in plasma NE occurred after drinking 750 ml water at both 4 C and 25 C. Levels rose during ingestion of fluid and fell again when drinking was completed, consistent with a sympathetic response to deglutition. There was no change after 150 ml at 4 C. In contrast, plasma E fell after the men drank 750 ml water at 4 C, but it did not change after they drank 750 ml water at 25 C or 150 ml at 4 C. The fall was maximal 10 min after drinking was completed and levels remained depressed for a further 30 min. These findings suggest that the fall in E is temperature dependent and is a response to the presence of cold fluid in the stomach rather than to deglutition. We conclude that the dissociation of the plasma NE and E response after drinking cold fluids is therefore a result of independent and contrasting influences of, respectively, the volume and temperature of the fluid ingested.

Alcohol stimulation of renin release in man: its relation to the hemodynamic, electrolyte, and sympatho-adrenal responses to drinking.

Alcohol stimulation of the renin-angiotensin axis has been proposed as an explanation for the higher blood pressure in drinkers. This study examines the acute effects of moderate alcohol intake on PRA in relation to change in fluid and electrolyte balance, sympatho-adrenal activity, blood pressure, and heart rate in 20 normal men, aged 20-24 yr. They consumed either 750 ml nonalcoholic beer as a control or the same beverage with 1 ml/kg alcohol added, which increased the plasma alcohol concentration to 16.7 +/- 1.0 (+/- SE) mM within 70 min. PRA increased more than 2-fold 90 min after the ingestion of alcohol. This was accompanied by a decrease in diastolic blood pressure and a fall in plasma potassium, both possible stimuli to the rise in PRA. A late increase in plasma sodium, also occurring 90 min after alcohol ingestion, was attributed to plasma volume contraction after an alcohol-induced diuresis. This may have been an additional factor in stimulating renin release. Norepinephrine levels increased during both alcohol and control studies. In contrast, plasma epinephrine decreased significantly during the control study, but did not change after alcohol ingestion. Hence, alcohol stimulation of sympathetic nervous activity is unlikely to have mediated the renin release. We conclude that the acute increase in PRA associated with moderate alcohol consumption is predominantly a secondary response to changes in fluid and electrolyte balance and blood pressure. Although a direct action of alcohol on renin release was not excluded, the possibility that repeated activation of the renin-angiotensin system mediates the pressor effect of regular moderate alcohol consumption is, therefore, diminished.

Free and sulfate-conjugated catecholamines during exercise in man.

The study examined the plasma concentration of free and sulfate-conjugated norepinephrine (NE) and epinephrine (E) at rest and after vigorous bicycle exercise. Free and total catecholamines were measured by a modified radioenzymatic assay using external standards. This assay was less costly and, in subjects with normal renal function, plasma levels were highly comparable to those obtained using internal standards. Exercise was associated with a predictable rise in plasma free NE and E concentration, which correlated with the hemodynamic changes, and a significant decrease in the levels of catecholamine sulfate conjugates. There was an inverse relationship between the degree of conjugation and the free levels of NE and E both at rest and after exercise. This suggests that the degree of conjugation is another factor determining the concentration of free amines in plasma.

Changes in prostanoid synthesis in response to diet and hypertension in one-kidney, one clip rats.

This study was designed to examine the effects of diets that alter prostaglandin biosynthesis on the blood pressure in one-kidney, one clip rats with established hypertension and to compare the prostanoid generating capacity of hypertensive animals with those that remained normotensive. Rats attaining blood pressures of at least 180 mm Hg within 8 weeks of nephrectomy and renal artery stenosis were paired by weight and blood pressure and then placed on either a safflower oil or a prostaglandin I2 inhibitory diet (cod liver oil-linseed oil mix) for 4 weeks. Animals with blood pressures of less than 150 mm Hg were also paired for the same two dietary regimens. Comparison between the two blood pressure groups revealed that on both dietary regimens hypertensive rats produced significantly more aortic 6-keto-prostaglandin F1 alpha and serum thromboxane B2. Rats on the cod liver oil-linseed oil diet incorporated eicosapentaenoic acid into tissue stores with a corresponding decrease in arachidonic acid and significantly impaired ability to generate serum thromboxane B2 (36%), aortic 6-keto-prostaglandin F1 alpha (65%), renal homogenate 6-keto-prostaglandin F1 alpha (64%) and prostaglandin E2 (58%), and urinary prostaglandin E2 (70%) and 6-keto-prostaglandin F1 alpha (52%). Despite these differences in prostanoid synthesizing capacity, no differences in blood pressure were observed between the safflower oil-fed rats and rats fed cod liver oil-linseed oil within either the hypertensive or normotensive groups. These results suggest that prostanoids do not play a major role in maintaining blood pressure in established one-kidney, one clip hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Two-way factorial study of alcohol and salt restriction in treated hypertensive men.

The aim of this study was to determine whether moderate restriction of dietary salt intake leads to an additional fall in blood pressure in treated hypertensive men who are asked to simultaneously reduce their usual alcohol intake. Sixty-three subjects entered an initial 2-week familiarization period during which they continued their usual alcohol intake and commenced a "low sodium" diet (less than 60 mmol/day) supplemented with 100 mmol sodium chloride per day as enteric-coated tablets. Subjects were then randomly assigned to either drink a low alcohol beer alone for a 4-week period (reducing their self-reported alcohol consumption from 537 to 57 ml/week) or to continue their usual alcohol intake (543 versus 557 ml/week). Within the low and normal alcohol intake groups, subjects were assigned to either a low or normal sodium intake. The low sodium groups continued the sodium-restricted diet but were switched to placebo sodium chloride tablets for the 4 weeks. This resulted in a fall in the 24-hour urinary sodium excretion from 144 to 69 mmol/day. The normal sodium groups continued the low sodium diet but kept taking 100 mmol/day of the sodium chloride tablets, and their urinary sodium excretion remained unchanged (125 versus 142 mmol/day). Regular antihypertensive therapy was continued throughout. Fifty-nine subjects completed the trial. In those who reduced their alcohol intake there was a fall in both systolic blood pressure (-5.4 mm Hg supine, p less than 0.01) and diastolic blood pressure (-3.2 mm Hg supine, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Platelet activating factor and one-kidney, one clip hypertension.

The reduction in blood pressure to normotensive levels within 3 hours of unclipping the one-kidney, one clip Goldblatt hypertensive rat has been attributed to the release of potent blood pressure-lowering lipids, one of which is thought to be identical to platelet activating factor. The specific platelet activating factor receptor antagonist WEB 2086 was infused intravenously into hypertensive one-kidney, one clip rats, and the mean arterial blood pressure changes after unclipping were examined. Before infusion, blocking doses of WEB 2086 were confirmed to effectively abolish the fall in blood pressure induced by exogenous platelet activating factor. Serotonin release in response to exogenous platelet activating factor was also inhibited in platelets preincubated with plasma from rats infused with the antagonist. Hypertensive rats were given a bolus blocking dose of WEB 2086 (5 mg/kg i.v.) and the same dose by infusion (5 mg/kg/hr i.v.) before they were unclipped. A control group was given a bolus volume of saline and infused with saline before unclipping. In WEB 2086-treated rats, blood pressure fell from a baseline mean of 181 +/- 13.0 to 125 +/- 23 mm Hg after 4 hours, a fall of 28%. Saline-treated rats fell from a mean of 194 +/- 23 to 127 +/- 25 mm Hg (33%). There was no significant difference in the blood pressure fall between the two groups. Therefore, platelet activating factor is unlikely to be responsible for the restoration of normal blood pressure after unclipping the Goldblatt hypertensive rat. We attribute the fall in blood pressure to other presently unidentified renomedullary lipids.

Genetic influences on plasma catecholamines in human twins.

We examined the relative genetic and environmental influences on the variability in plasma epinephrine, norepinephrine, and dopamine levels in 109 twin pairs. Epinephrine levels were lower in females (P = 0.048). The norepinephrine concentration increased with age (r = 0.40; P < 0.001). Blood pressure (BP) was not associated with epinephrine levels in either sex or with norepinephrine levels in females. In males, there was a positive association between norepinephrine concentration and diastolic BP (r = 0.31; P = 0.020). A negative association between dopamine levels and systolic and diastolic BP in females (r = -0.22; P = 0.014 and r = -0.20; P = 0.027, respectively) was not maintained after accounting for age, body mass index, and sex. Using path analysis and maximum likelihood model fitting, genetic, unique environment, and age effects contributed 57% (P < or = 0.001), 27% (P < or = 0.001), and 16% (P < or = 0.001) to the variability in norepinephrine, respectively. Genetic effects explained 64% (P < 0.1) and 74% (P < 0.1) of the variability in epinephrine concentrations in females and males, respectively. Unique environmental influences explained the remainder. Genetic and unique environmental effects explained 72% (P < 0.01) and 28% (P < or = 0.001) of the variability in dopamine levels. These results indicate a substantial genetic influence on plasma catecholamine levels. Although consistent associations between plasma catecholamines and BP were not evident in this study, the observed genetic influence on circulating catecholamines may be relevant to the potential role of the sympathetic nervous system in the early stages of essential hypertension.

Evidence for a direct effect of alcohol consumption on blood pressure in normotensive men. A randomized controlled trial.

A direct pressor effect of alcohol is proposed as the basis for the association between regular alcohol consumption and an increase in blood pressure found in population studies. To examine this further, a randomized controlled crossover trial of the effects of varying alcohol intake on blood pressure in 46 healthy male drinkers was conducted. From an average of 336 ml of ethanol per week, alcohol consumption was reduced by 80% for 6 weeks by drinking a low alcohol content beer alone. This reduction was associated with a significant reduction in systolic and diastolic blood pressure (p less than 0.001 and p less than 0.05 respectively). The mean difference in supine systolic blood pressure during the last 2 weeks of normal or low alcohol intake was 3.8 mm Hg, which correlated significantly with change in alcohol consumption (r = 0.53, p less than 0.001). Reduction of alcohol intake also caused a significant decrease in weight (p less than 0.001). After adjustment for weight change, an independent effect of alcohol on systolic but not diastolic blood pressure was still evident, with a 3.1 mm Hg fall predicted for a decrease in consumption from 350 ml of ethanol equivalent per week to 70 ml per week (p less than 0.01). Systolic blood pressure rose again when normal drinking habits were resumed. These results provide clear evidence for a direct and reversible pressor effect of regular moderate alcohol consumption in normotensive men and suggest that alcohol may play a major role in the genesis of early stages of blood pressure elevation.

Effects of alcohol and caloric restrictions on blood pressure and serum lipids in overweight men.

We have examined the independent and combined effects on blood pressure and blood lipids of alcohol restriction and weight loss in overweight male drinkers with a view to assessing overall effects on cardiovascular risk of two widely promoted nonpharmacological approaches for hypertension. Eighty-six men with a mean age of 44.3 years, a mean regular alcohol intake of 440 ml/wk (five or six standard drinks per day), a mean blood pressure of 137.4 mm Hg systolic and 84.8 mm Hg diastolic, and a mean body mass of 92.5 kg entered a controlled two-way factorial study. The subjects were randomly assigned to four groups for an 18-week intervention in which members of two groups drank only low-alcohol beer, thereby reducing their alcohol intake by 374 ml/wk, while those of the other two groups continued their normal alcohol intake. Within the low and normal alcohol intake groups subjects either continued their usual diet or reduced their caloric intake by 4,200-6,300 kJ/day (1,000-1,500 kcal/day) (with protein, fat, and carbohydrate provided as 15%, 30%, and 55% of total calories, respectively). Calorie reduction and alcohol restriction caused weight losses of 7.5 (p less than 0.001) and 2.1 (p less than 0.01) kg, respectively. Calorie reduction and alcohol restriction were associated with decreases in systolic blood pressure of 5.4 (p less than 0.001) and 4.8 (p less than 0.01) mm Hg, respectively, and in diastolic blood pressure of 4.2 (p less than 0.001) and 3.3 (p less than 0.01) mm Hg, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects on blood pressure of omega 3 fats in subjects at increased risk of cardiovascular disease.

This study was conducted to compare the effects of omega 3 fatty acids, taken as fish or fish-oil supplements in the setting of a high- or low-fat dietary background, on blood pressure and heart rate in men with moderate cardiovascular risks. One hundred twenty men were randomly allocated to five high-fat (40% of daily energy) and two low-fat (30% of energy) groups to undertaken a 12-week dietary intervention period involving fish, fish oil, or a combination of these. Sodium intake was restricted to less than 90 mmol/d. The five high-fat groups were assigned to take either 6 or 12 fish-oil capsules daily, fish or a combination of fish oil and fish, or placebo capsules. The two low-fat groups took either fish or placebo capsules. Fish meals were devised to provide 1.3 g of eicosapentaenoic acid daily, equivalent to that contained in 6 fish-oil capsules. Subjects were instructed to eat a selection of fish that provided an average of 3.65 g/d (range, 3.2 to 4.1 g/d) of total omega 3 fatty acids. Subjects were seen at regular intervals during the baseline and dietary intervention periods for measurement of weight, blood pressure, heart rate, dietary compliance, urinary electrolyte excretion, platelet phospholipid fatty acids, blood glucose, and insulin concentration. There was a greater fall in both systolic and diastolic blood pressures in subjects allocated fish or fish oil, particularly in the low-fat groups, compared with control subjects. However, there was no significant group effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Vegetarian diet in mild hypertension: effects of fat and fiber.

Recently, a relatively small reduction in systolic blood pressure (approximately 5 mm Hg) was estimated to substantially reduce the numbers of major coronary events. The blood pressure reduction is about the same as the difference seen between typical ovolactovegetarians and omnivores. This paper reviews the evidence for the blood pressure-lowering effects of a vegetarian diet on those with elevated blood pressure. It also reviews whether the effect on blood pressure of a vegetarian diet can be attributed either to elevation of the dietary P:S ratio or to fiber intake alone.

Effects of a lacto-ovo vegetarian diet on serum concentrations of cholesterol, triglyceride, HDL-C, HDL2-C, HDL3-C, apoprotein-B, and Lp(a).

The effect of intervention with a lacto-ovo vegetarian diet on serum concentrations of cholesterol, triglyceride, total high-density lipoprotein cholesterol (HDL-C), HDL2-C, HDL3-C, low-density lipoprotein cholesterol, apoprotein-B, apoprotein-HDL, and Lp(a) was studied in 19 men and 17 women. Most weekday meals were obtained from a single source and dietary records were completed to assess the changes in nutrient intakes. Blood was collected in the 6th wk of each dietary period. Because of strong correlations between many of the changes in nutrient intakes, principal component (factor) analysis was used followed by stepwise multiple regression analysis to identify associations between changes in diet and changes in lipid, lipoprotein or apoprotein levels. Three principal components accounted for 92.0% of the variation in lipid levels: factor 1 represented an increase in saturated fat, total fat, monounsaturated fat, cholesterol, and energy intake: factor 2 represented an increase in fiber and polyunsaturated fat, and decrease in protein intake; factor 3 an increase in total carbohydrate, complex carbohydrate, and energy intake. Where a change in a variable was significantly associated with change in diet, one factor appeared primarily responsible for the change; total cholesterol (factor 2, p = 0.034); triglyceride (factor 3, p = 0.005); apo-HDL (factor 1, p = 0.014); HDL2-C (factor 2, p = 0.023), HDL3-C (factor 3, p = 0.015). A borderline significant association was seen for total HDL-C (factor 2, p = 0.055).

Effects of varying dietary fat, fish, and fish oils on blood lipids in a randomized controlled trial in men at risk of heart disease.

This study aimed to determine the effects of incorporating fish with 40%- or 30%-fat diets and the differences in response to fish or fish oil omega 3 fats. Men with high-normal blood pressure and elevated serum cholesterol were randomly allocated to one of seven diets for 12 wk. Fish or fish oil with a 40%-fat diet increased total cholesterol, HDL cholesterol, HDL2 cholesterol, and LDL cholesterol, and reduced triglycerides. The 30%-fat diet alone reduced cholesterol, LDL cholesterol, and HDL cholesterol, with triglycerides unchanged. Fish with the 30%-fat diet reduced cholesterol, LDL cholesterol, and triglycerides and increased HDL2 cholesterol. This study has shown that plasma lipids are affected similarly by fish or fish oil in men consuming a 40%-fat diet. Adverse effects of omega 3 fats on total and LDL cholesterol are reversed by a 30%-fat diet, whereas one daily fish meal substantially lowers triglycerides and reverses the fall in HDL cholesterol that is usual with a low-fat diet.

Vegetarian diet and blood pressure levels: incidental or causal association?

Evidence that nutrients other than the major cations may influence blood pressure levels stems from studies of acculturated vegetarians and from randomized controlled dietary trials. Earlier studies of vegetarians focused on religious groups and on vegans, making it difficult to know whether their lower blood pressures were due to diet per se or to other aspects of lifestyle. Seventh-day Adventist vegetarians showed significantly less hypertension and lower blood pressures compared with Mormon omnivores, effects which were independent of differences in obesity and not due to altered sodium intake. Subsequently, controlled dietary intervention studies in healthy normotensive omnivores provided more direct evidence for a blood pressure-lowering effect of a lactoovovegetarian diet with reversible changes of 5-6 mm Hg systolic and 2-3 mm Hg diastolic occurring over 6-wk periods. Similar dietary effects in mild hypertensive subjects provides impetus for identifying the responsible nutrients.