Short communication: Daily intake of 125 g of cheese for 2 weeks did not alter amount or distribution of serum lipids or desaturase indexes in healthy adults in an exploratory pilot study.

Regular cheese contains saturated fat, consumption of which may negatively influence the amount of serum lipids. The American Dietary Guidelines (https://health.gov/dietaryguidelines/2015/guidelines/) recommend consumption of low-fat food. However, we observed a negative association between cheese intake and serum triglycerides and a positive association with high-density lipoprotein cholesterol. Cheese intake was also inversely related to metabolic syndrome and blunted the harmful association of intake of soft drinks with serum lipids. Cheese contains calcium and factors that may inhibit desaturases, thereby partly explaining why cheese might not have negative effects on serum lipids. Thus, opposing forces seem to govern the cheese effect but will any of these prevail? In an exploratory pilot study, 17 healthy subjects participated in a 4-wk crossover trial without washout. During the first 2 wk, 9 subjects were randomly assigned to add 125 g/d of regular cheese to their habitual diet. After 2 wk, cheese intake was discontinued and the subjects were instructed to return to their habitual diet. The other 8 subjects followed their habitual diet during the first 2 wk, and then added 125 g/d of cheese for the next 2 wk. Mean values (mmol/L) before and after 2 wk on habitual (cheese) diet were as follows: serum triglycerides: 0.91 (0.89) and 0.95 (0.91); total cholesterol: 5.25 (5.16) and 5.08 (5.24); low-density lipoprotein cholesterol: 3.18 (3.17) and 3.09 (3.22); and high-density lipoprotein cholesterol: 1.71 (1.64) and 1.61 (1.66). The fatty acid pattern in total serum lipids and desaturase indexes did not change significantly in response to high cheese intake. Thus, an appreciable increase in daily cheese intake for 2 wk may not alter concentrations of serum lipids, estimates of desaturases, or the distribution of serum fatty acids.

Short communication: Is consumption of a cheese rich in angiotensin-converting enzyme-inhibiting peptides, such as the Norwegian cheese Gamalost, associated with reduced blood pressure?

Epidemiological and clinical studies have shown that angiotensin-converting enzyme (ACE)-inhibiting peptides derived from dairy products may decrease blood pressure. These peptides have been identified in many cheeses, and Gamalost, a traditional Norwegian cheese, is particularly rich in these peptides. The aim of this cross-sectional study was to examine whether frequency of Gamalost intake was associated with blood pressure in a Norwegian population sample. Blood pressure and other clinical measurements, including the factors of metabolic syndrome, were obtained from 168 participants (56% female, mean age = 51 yr) who completed a questionnaire about dietary habits and other health-related factors. Mean Gamalost intake was 2 servings per week. The prevalence of hypertension was 23.8% in the population, with mean systolic and diastolic blood pressures of 128 and 78 mmHg, respectively. Intake of Gamalost was inversely associated with systolic blood pressure. Each increase in frequency unit of Gamalost intake corresponded to a reduction in systolic blood pressure of 0.72 mmHg, after controlling for sex, age, education, waist circumference, physical activity, smoking status, and dairy food intake. Results from this study indicate that consumption of Gamalost (or other foods rich in ACE-inhibiting peptides) may reduce blood pressure.

Relationship between Fecal Content of Fatty Acids and Cyclooxygenase mRNA Expression and Fatty Acid Composition in Duodenal Biopsies, Serum Lipoproteins, and Dietary Fat in Colectomized Familial Adenomatous Polyposis Patients.

A few familial adenomatous polyposis studies have focused upon faecal sterols and bile acids but none has analysed the fecal content of fatty acids. We report here findings of an observational study on 29 colectomized familial adenomatous polyposis patients that describe the fecal content of fatty acids, and relate this to the proportions of fatty acids and levels of cyclooxygenase mRNA expression in duodenal biopsies, levels of serum lipoproteins, and diet. In the ileostomy group separately (n = 12), the fecal content of arachidonic acid was correlated negatively to the proportions of eicosapentaenoic acid and docosahexaenoic acid in duodenal biopsies. Total serum-cholesterol was negatively correlated to the fecal content of saturates and monounsaturates. The fecal palmitoleic acid/palmitic acid ratio was positively correlated to the levels of cyclooxygease-2 expression in duodenal biopsies.In the ileal-pouch-anal anastomosis group separately (n = 17), significant correlations were found between the fecal contents of oleic acid, linoleic acid, and alpha-linolenic acid, and the proportions of myristic acid, oleic acid and eicosaenoic acid in duodenal biopsies. Dietary monounsaturates were positively correlated to different fecal fatty acids. Future studies should focus on molecular mechanisms relevant to fatty acid metabolism, inflammation, and angiogenesis, in addition to nutrition.

Daily energy expenditure and cardiovascular risk in Masai, rural and urban Bantu Tanzanians.

BACKGROUND: Several studies have revealed that the Masai, pastoralists in Tanzania, have low rates of coronary heart disease despite a diet high in saturated fat. It has also been suggested that they may be genetically protected. Recent studies detailing other potential protective factors, however, are lacking. METHODS: A cross-sectional investigation of 985 Tanzanian men and women (130 Masai, 371 rural Bantu and 484 urban Bantu) with mean age of 46 (9.3) years. Anthropometric measures, blood pressure, serum lipids, and the reported dietary pattern and physical activity level were assessed. RESULTS: 82% of Masai subjects reported a high fat/low carbohydrate intake, whereas 77% of the rural Bantu subjects reported a low fat/high carbohydrate intake, while a high fat/high carbohydrate intake was the main dietary pattern of the urban Bantu group as, reported by 55%. The most conspicuous finding for the Masai was the extremely high energy expenditure, corresponding to 2565 kcal/day over basal requirements, compared with 1500 kcal/day in the rural and 891 kcal/day for the urban Bantu. Mean body mass index among the Masai was lower than the rural and urban Bantu. Mean systolic blood pressure of the Masai was also lower compared with their rural and urban Bantu counterparts. The Masai revealed a favourable lipid profile. CONCLUSION: The potentially atherogenic diet among the Masai was not reflected in serum lipids and was offset probably by very high energy expenditure levels and low body weight.

ApoB but not LDL-cholesterol is reduced by exercise training in overweight healthy men. Results from the 1-year randomized Oslo Diet and Exercise Study.

OBJECTIVES: (i) To estimate changes in apoB and apoB/apoA-I, reflecting the balance between atherogenic and anti-atherogenic lipoprotein particles, by exercise training and compare with changes in LDL-C and TC/HDL-C ratio, and (ii) To compare strengths of relationships between physical fitness and various lipoprotein variables. DESIGN, SETTING, AND SUBJECTS: The study was a 1-year open randomized trial comprising 219 healthy middle-aged subjects aged 40-49 years who were allocated to exercise or no exercise, dietary advice or no advice in a 2 x 2 factorial design. This study includes 188 men who completed the trial, 45 to diet, 48 to exercise, 58 to diet + exercise and 37 to control. INTERVENTIONS: Exercise; supervised endurance exercise three times a week. Diet; reduce weight, increase intake of fish and reduce total fat intake. MAIN OUTCOME MEASURE: One-year change in apoB and apoB/apoA-I ratio. RESULTS: Exercisers decreased their ApoB and ApoB/ApoA-I values significantly compared to non-exercisers. LDL-C was not, but LDL-C/HDL-C was marginally but statistically significantly reduced by exercise. One-year change in ApoB and ApoB/ApoA-I correlated more strongly to 1-year changes in physical fitness than LDL-C or LDL-C/HDL-C. Adjusting for changes in LDL-C or LDL-C/HDL-C did not influence the correlation between changes in fitness and ApoB or ApoB/ApoA-I. However, adjusting for changes in ApoB or ApoB/ApoA-I wiped out the correlation between change in fitness and LDL-C or LDL-C/HDL-C. Relationships weakened when adjusting for changes in waist circumference, but Apo B or ApoB/ApoA-I still correlated significantly to changes in fitness. CONCLUSION: Physical exercise reduced the atherogenic burden as experienced by the reduction in apoB or apoB/apoA-I levels, but not by LDL-C in healthy middle-aged men. Possibly, regular physical activity might increase the LDL-C particle size, thereby making LDL less atherogenic. Monitoring of apolipoproteins rather than the cholesterol moiety of lipoproteins might improve the assessment of lipoprotein changes after exercise training.

Physical activity and blood lipids in rural and urban Tanzanians.

BACKGROUND: Physical inactivity and raised blood lipids are two powerful risk factors for coronary heart disease (CHD). Incidence and mortality from CHD are expected to increase in developing countries. However, studies on the prevalence of cardiovascular risk factors in Africa are rare. In this study we examined the level of physical activity and serum lipids in rural and urban Tanzanians. METHODS: Rural and urban inhabitants, n=985, mean age 43.8 years [SD, +/-8.9] were investigated. Physical activity level (PAL) was assessed by an interview-administered questionnaire and blood samples were collected and analysed for serum lipids. RESULTS: The rural population (n=501) reported a substantially higher PAL than the urban population (n=484). They also had significantly lower mean weight, body mass index (BMI), T-cholesterol, LDL-cholesterol, and HDL-cholesterol, T-cholesterol/HDL-cholesterol ratio, triglycerides and Apolipoprotein A-1. CONCLUSION: This study demonstrates that the urban Tanzanians have a considerably lower physical activity level and a more unfavourable lipid pattern than rural Tanzanians. These findings underline the importance of undertaking preventive measures to counter the increasing incidence of CHD in urban African populations.

Energy balance in weight stable athletes with and without menstrual disorders.

The energy balance and nutritional adequacy was assessed in a group of runners with irregular menstrual function (IR, n = 10) and in a comparable group of runners with normal menstrual function (R, n = 10). Based on computerized records of 3 days food intake, the mean content of energy and macronutrients were estimated. Excess energy expenditure (EEE) during training hours was estimated using HF monitoring and individual HF/VO2 nomograms. For the rest of a daily 24 h cycle, estimated values for basal metabolic rate (BMR) and sedentary metabolic rate were applied. Daily training-related excess energy expenditure (2.1 +/- 0.3 vs 2.2 +/- 0.4) MJ (Mean +/- SEM) and total energy expenditure (TEE) (11.0 +/- 0.3 vs 11.2 +/- 0.4) MJ in R vs IR were not different in the two groups. Calculated daily energy intake (EI) was, however, significantly lower in IR (9.7 +/- 0.5 MJ) than in R (12.3 +/- 0.7 MJ), (P = 0.007). Calculated EI and TEE were in balance in R athletes. When the same calculations were applied on IR athletes, a moderate but statistically significant negative energy balance was found (-1.5 +/- 0.6 MJ, P = 0.03). The calculated energy deficit was supported by significantly lower levels of free thyroxine in IR athletes, and may indicate an adaptive lower BMR in IR athletes. Mean intakes of carbohydrates (7.0 g/kg in R and 5.7 g/kg in IR) and protein (1.71 g/kg in R and 1.49 g/kg in IR) were close to guidelines. Intakes were not significantly different in the two groups. The most important difference in macronutrient intake was found in dietary fat (1.70 g/kg in R and 1.04 g/kg in IR) that was significantly lower in the IR group than in the R group (P = 0.007). The weight stable IR and R athletes seemed to meet the recommended intake of carbohydrates, protein and fat in their diet fairly well. However, according to the present calculations, a small energy deficit was observed in IR athletes but not in R athletes. Compared with the intake of the R athletes, this energy deficit seems primarily to be related to a lower intake of dietary fat in IR athletes.

Lipid peroxidation and growth inhibition of human microvascular endothelial cells.

Peroxidation products of polyunsaturated fatty acids may cause growth inhibition of cells in culture. This study was carried out to elucidate to what extent peroxidation products may be found in growth media, with and without cells and albumin, using thiobarbituric acid-reactive substances (TBARS) and protein carbonyl groups as measures of peroxidation. The growth of human microvascular endothelial cells was studied as influenced by docosahexaenoic (C22:6, n - 3), arachidonic acid (C20:4. n - 6), and serum albumin. Cell growth was strongly inhibited by the fatty acids, and the inhibition was related to the concentration of TBARS in the medium. Defatted albumin (0.5 g/100 ml) nullified the increase of TBARS in the medium and released the growth inhibition by the fatty acids. With polyunsaturated fatty acids (PUFA) there was a time- and concentration-dependent increase in media TBARS, observed both with and without cells, but the TBARS increase was somewhat greater in the presence of cells. Surprisingly, TBARS in cell-free media also increased somewhat upon increasing the albumin concentration from 0.5 to 5 g/100 ml, and the TBARS increase differed among various preparations of albumin. Unexpectedly, the albumin that had not been defatted gave the lowest TBARS values. The amount of protein carbonyl groups did not differ among various albumin preparations. It is concluded that PUFA may autooxidize in media used for cell cultures, and thereby cause an unspecific growth inhibition, which can be prevented by a low albumin concentration. However, even defatted albumin preparations may contain lipid peroxidation products, the causes and implications of which remain to be elucidated.

Effect of long-term storage on the concentration of albumin and free fatty acids in human sera.

Stored sera from healthy persons can be used to study relationships between blood variables at the time of sampling and disease appearing several years later but storage may influence the variables. In this work we measured the concentration of albumin and free fatty acids (FFA) in samples from the JANUS serum bank of Norway. Sera from blood donors and persons participating in health screening programs have been added to the bank since 1973. The concentration of albumin and FFA was measured in 443 JANUS bank sera. The material was divided into quartiles according to the length of storage: <3 years (n = 110), 3-6 years (n = 110), 6-12 years (n = 115) and >12 years (n = 108). Albumin was measured colorometrically using the bromcresol green method and FFA was determined enzymatically. The serum albumin concentrations (mean +/- SEM) in the four groups were 55.8+/-0.6, 56.2+/-0.5, 59.9+/-0.6 and 59.5+/-0.6 g/L. The values of groups 3 and 4 were significantly higher than those of groups 1 and 2 (p<0.001). The serum FFA concentrations in the four groups were 0.56+/-0.03, 0.64+/-0.03, 0.77+/-0.03 and 0.85+/-0.04 mmol/L, i.e. a significant storage effect. The Scheffé multiple comparison test showed that FFA values in groups 3 and 4 were significantly higher than those in groups 1 and 2 (p <0.001 for group 4 vs. 1 and 2, and 3 vs. 1; p<0.04 for group 3 vs. 2) Serum FFA and albumin levels were positively associated (r = 0.489, p <0.01). Using linear regression analysis, it was estimated that serum albumin values increased by 0.28 g/L per year (i.e. 0.5%) and FFA by 0.02 mmol/L (i.e. 3.8%). Thus, measured by standard methods, serum FFA and albumin could increase in response to several years of storage at -25 degrees C. It is suggested that the storage time dependent increase in FFA is due to FFA liberation from lipoprotein triglycerides, whereas the apparent increase in albumin concentration possibly could be attributed to an unfolding of the protein, allowing more bromcresol green to be bound.

Effect of acupuncture on smoking cessation or reduction: an 8-month and 5-year follow-up study.

BACKGROUND: This study was undertaken to examine whether acupuncture treatment may have a long-term effect on smoking cessation or reduction. METHODS: Altogether 46 healthy men and women who reported smoking 20 +/- 6 cigarettes per day (mean +/- SD) volunteered in the study. They were randomly assigned to a test group (TG) or to a control group (CG) in which presumed anti-smoking acupoints were stimulated (TG) or acupuncture was applied to acupoints considered to have no effect on smoking cessation (CG). Before each treatment, after the last one, and 8 months and 5 years after the last one, each subject answered questionnaires about his or her smoking habits and attitudes. Blood samples for measuring variables related to smoking, i.e., serum cotinine and serum thiocyanate, were taken. RESULTS: During the treatment period the reported cigarette consumption fell on average by 14 (TG) and 7 (CG) cigarettes per day (P < 0.001). For both groups the reported cigarette consumption rose on average by 5-7 cigarettes during the following 8 months, and there was no systematic change thereafter. Consequently, TG showed a maintained reduction in smoking; no lasting effect was seen for CG. The TG reported that cigarettes tasted worse than before the treatments, and also the desire to smoke fell. For TG the serum concentration of cotinine fell, and the values correlated with the reported smoking. CONCLUSIONS: This study confirms that adequate acupuncture treatment may help motivated smokers to reduce their smoking, or even quit smoking completely, and the effect may last for at least 5 years. Acupuncture may affect the subjects' smoking by reducing their taste of tobacco and their desire to smoke. Different acupoints have different effects on smoking cessation.

Apoptotic effects of dichloro stearic and dichloro myristic acid in human hepatoma cells (HepG2).

Chlorinated fatty acids represent the major fraction of extractable organically bound chlorine in fish. After dietary intake such fatty acids may accumulate in adipose tissue, and even be transferred from mother to child via breast milk. We have previously reported that 9,10-dichloro stearic acid and 5,6-dichloro myristic acid inhibited cell growth. The aim of the present work was to investigate whether the growth inhibitory effect of these modified fatty acids might involve apoptosis. Human hepatoma cells (HepG2) were cultured for 4 days before addition of chlorinated fatty acids, and then cultured for another day before harvested. Morphological analysis was mainly done by light microscopy. In addition, fluorescence microscopy and electrophoretic analysis of DNA were carried out. The effect of 0.3 and 0.6 mmol/l was studied. Both chlorinated fatty acids seemed to cause a concentration-dependent increase in the relative abundance of pycnotic and broken nuclei, as well as nuclear fragments, with the strongest effect of dichloro stearic acid. Apoptosis by the chlorinated fatty acids was however less than that of docosahexaenoic acid, a known apoptosis effector. In conclusion, chlorinated fatty acids seem to possess the ability to cause apoptosis.

Predictors of restenosis after coronary angioplasty. A study on demographic and metabolic variables.

OBJECTIVE: The major concern about percutaneous transluminal coronary angioplasty (PTCA) is the high incidence of restenosis. METHODS: Demographic, clinical and biochemical data were recorded 2 weeks prior to PTCA in 388 patients fulfilling the criteria for initial stenosis, successful PTCA, and angiographic follow-up after 6 months. Restenosis was evaluated by quantitative coronary angiography. RESULTS: Variables predictive of restenosis in univariate analysis were diabetes mellitus, male gender, and the levels of high density lipoprotein (HDL) cholesterol, apolipoprotein A1 (Apo A1) and thio-barbituric acid-reactive substances (TBARS). In trend analysis through quartiles TBARS and fasting glucose levels were significantly associated with restenosis (p = 0.016 and 0.044, respectively), whereas the negative predictivity of Apo A1 and HDL-cholesterol were of borderline significance. In multivariate analysis male gender and diabetes mellitus showed predictivity of significance, and a negative predictivity was also apparent for HDL-cholesterol. CONCLUSION: We conclude that diabetes mellitus, male gender, and low HDL-cholesterol are predictors of restenosis 6 months after PTCA. In addition, TBARS may be a marker for the development of restenosis after PTCA.

Active recovery and post-exercise white blood cell count, free fatty acids, and hormones in endurance athletes.

Strenuous endurance exercise in fasted subjects is accompanied by increased plasma levels of catecholamines, leucocytosis, low insulin, and elevated plasma free fatty acids (FFA). Immediately after such exercise, plasma FFA may rise to high and potentially harmful levels, whereas the white blood cell count (WBCC) rapidly decreases towards or below baseline values. The present work investigated how active recovery (AR) for 15 min at 50% of maximal oxygen consumption (VO2max), after 60 min of uphill running at 83% of VO2max, influenced plasma FFA, lymphocyte, neutrophil, granulocyte, and monocyte count, as well as adrenaline, noradrenaline, insulin and cortisol concentrations until 120 min post-exercise. Thirteen endurance athletes participated in the study [24.2 (3.7) years, 1.82 (0.06) m, 76.7 (7.9) kg and VO2max 69.2 (6.8) ml min-1 kg-1]. In a randomized order, the subjects completed two sets of strenuous workouts, followed by either AR or complete rest in the supine position (RR). Compared with RR, AR strongly counteracted the rapid increase in plasma FFA 5 min post-exercise. The decreases in neutrophil and monocyte counts post-exercise were nullified by AR, and the cell count stayed above resting values throughout the observation period. AR also counteracted the rapid return of hormone concentration towards baseline levels. It would appear that active recovery at low intensity after strenuous exercise can maintain sufficient adrenergic activation to counteract the post-exercise drop in WBCC. However, in spite of keeping the catecholamine concentration high and insulin levels low, AR can also maintain a low plasma FFA concentration, probably because of the continued use of FFA in muscle. It remains to be elucidated whether the observed high FFA and low WBCC values after RR have a negative effect on health. If so, AR could be a preventive measure.

Active recovery counteracts the post-exercise rise in plasma-free fatty acids.

The present study investigated the effect of active recovery (AR) as compared to rest recovery (RR) upon FFA concentrations following moderate- (MI) or high-intensity (HI) running. Fourteen well-trained males (23.7 +/- 6 years, VáO2max = 69.5 +/- 1.8ml á min-1 kg-1) were randomly assigned into two trials (HI = 30 min at 82% of VáO2max; MI = 60 min at 75% of VáO2max). Within each group, the subject completed two sets of experiments of running followed by either AR (15 min running at 50% of VáO2max) or RR (complete rest in the supine position). Plasma volume changes after the exercise did not deviate between the AR or RR trials. In both the HI and MI trials, AR resulted in lower FFA peaks and lower overall FFA concentrations while performing AR (p <.05). However, upon discontinuing AR, there was a rise in the FFA concentration. At 120-min post-exercise, the FFA concentrations after AR and RR were not significantly different. The changes in the FFA/albumin ratio were similar to the FFA responses. It is concluded that AR may counteract the rise in FFA 5-15 minutes after exercise.

[Physical activity, overweight and obesity]. / Fysisk aktivitet, overvekt og fedme.

Regular physical activity has profound effects on body composition and the utilisation of nutrients and help to maintain and increase skeletal muscle mass, with increased resting metabolic rate and enhanced capacity for lipid oxidation during rest and exercise. Regular exercise may also prevent or limit the loss of lean tissue (fat-free mass, FFM) during slimming regimens. Increased physical activity induces a number of favourable changes in the metabolism of lipoproteins: serum triglycerides are lowered by the increased lipolytic activity, the HDL concentration increases and the concentration of small dense LDL decreases. In addition, the enhanced metabolic capacity of skeletal muscle (metabolic fitness) will favorably influence risk factors such as insulin resistance and hypertension. Because regular physical activity has favorable effects on several of the comorbid conditions of obesity, particularly cardiovascular disease and type 2 diabetes, it is not surprising that the mortality rates seem to be lower in the overweight and moderately obese individuals who are physically fit compared with the unfit. The treatment of overweight and obese persons should perhaps be more focused on the level of regular physical activity than on body weight per se. For most of those who wish to reduce their body weight, it is recommended that they combine regular physical activity with a somewhat reduced energy intake, in particular of food rich in fat. Emphasis should be on promoting relatively low-intensity, long-duration physical activity which can be conveniently incorporated into daily life.

Active recovery reduces the decrease in circulating white blood cells after exercise.

This study was conducted to examine the effects of different recovery regimens on white blood cell count (WBCC) and muscle enzyme activities following strenuous, submaximal, steady state workouts on a treadmill. Fourteen endurance trained, healthy, non-smoking college-aged males participated in the study. The workouts were followed by either 15-min of rest recovery (RR), or active recovery (AR). The AR consisted of running at 50% of VO2max whereas RR implied complete rest. Seven subjects completed two sets of 60-min running at 70% of VO2max (moderate intensity group, MI) followed by either RR or AR. The other seven completed two sets of 30-min running at 80% of VO2max (high intensity group, HI) followed by either RR or AR. Blood samples were drawn at rest, immediately after exercise, and at 15- and 120-min post-exercise (PE). Blood lactate concentrations increased throughout the running trials. Creatine kinase (CK), lactate dehydrogenase (LD), white blood cell count (WBCC) and thrombocyte count increased between rest and 0-min PE (p<0.05). Between 0-15-min PE, there were several significant differences between RR and AR in the HI-trial. RR was associated with a 35% reduction in WBCC, compared to only 6% decrease in AR (p<0.02). Neither during 15-120-min PE this period, nor in the 120-min sample alone, were there any significant differences in WBCC between the RR and AR experiments. In conclusion, the results show that AR as opposed to rest recovery prevents the initial 0-15-min PE fall in WBCC after strenuous endurance exercise.

Growth-modulating effects of dichloro myristic and dichloro stearic acid in cell cultures.

Chloro-containing fatty acids are a major fraction of extractable, organically bound chlorine in fish. It has been suggested that dichloro stearic acid (9,10-dichlorooctadecanoic acid) (C18) is metabolized to dichloro myristic acid (5,6-dichlorotetradecanoic acid) (C14) which accumulates in tissues. Hence, the biological effects of the C18 dichloro fatty acid could be due to formation of the C14 dichloro fatty acid. In this study we have compared the effects of dichloro stearic and dichloro myristic acid on growth of three widely differing cell lines. Both fatty acids inhibited cell growth; however, dichloro myristic acid had a weaker growth inhibitory effect than dichloro stearic acid. Dichloro myristic acid had a biphasic effect (i.e. growth was stimulated at low concentrations, followed by inhibition at higher concentrations) on the growth of human hepatoma cells and immortalized human kidney epithelial cells, but no such effect on human microvascular endothelial cells. The order of potency for growth inhibition by dichloro myristic acid was consistently human hepatoma cells>immortalized human kidney epithelial cells >human microvascular endothelial cells, whereas the relative potency of dichloro stearic acid was variable. Albumin alone stimulated cell growth and had a stronger protective effect against growth inhibition by dichloro myristic acid than against that of dichloro stearic acid. It seems unlikely that a major part of the effect of dichloro stearic acid on cell growth is caused by conversion to dichloro myristic acid.

Luminal loss and restenosis after coronary angioplasty. The role of lipoproteins and lipids.

AIMS: Lipoproteins and lipids, especially lipoprotein(a), have been studied as risk factors for restenosis after coronary angioplasty with conflicting results. We investigated the association between serum levels of lipoprotein(a) apolipoprotein A-1, apolipoprotein B-100, total-cholesterol, high density lipoprotein-cholesterol, triglycerides, and coronary luminal loss and restenosis after angioplasty. METHODS: The lipoproteins and lipids were measured in 305 consecutive patients who underwent successful angioplasty and reangiography 20+/-3 weeks after angioplasty. Single-vessel dilatation was performed in 251 patients. Luminal loss was defined as minimal luminal diameter post-angioplasty minus minimal luminal diameter at follow-up, divided by the interpolated reference diameter of the vessel. Restenosis was defined according to three dichotomous categorical criteria: (1) >50% diameter stenosis at follow-up (2) loss of >50% of the gain achieved by angioplasty, (3) the need for target vessel revascularization. RESULTS: There was no significant association between the serum levels of lipoproteins and lipids and luminal loss. Univariate analysis did not show any significant difference in the serum levels of any of the lipoproteins and lipids between the restenosis and no-restenosis groups. Multivariate analysis revealed that only the angiographic variables (luminal gain and post-angioplasty minimal luminal diameter) were associated with luminal loss and restenosis after angioplasty. CONCLUSION: Lipoproteins and lipids were neither associated with luminal loss nor independent risk factors for restenosis after angioplasty.

Growth of human lung adenocarcinoma in nude mice is influenced by various types of dietary fat and vitamin E.

Studies have shown effects of dietary lipids on carcinogenesis and tumour progression. Different mechanisms for the inhibitory effect of n-3 fatty acids (FA) have been proposed. The inhibition of the growth of subcutaneously transplanted A427 lung adenocarcinoma cells in athymic nude mice may occur due to an increased level of lipid peroxidation products and is the object of this study. The nude mice were fed diets supplemented with corn oil (CO), olive oil (OO) or K85, a mixture of ethyl esters of n-3 FAs, mainly eicosapentaenoic acid (EPA, 20:5, n-3) and docosahexaenoic acid (DHA, 22:6, n-3). Tumours of the n-3 FA group showed reduced growth. Peroxidation products measured by the thiobarbituric acid reactive substances (TBARS) test showed higher levels in tumours from n-3 FA fed mice than in the other diet groups. The growth inhibitory effects and the elevated level of TBARS in the n-3 FA diet group were counteracted by vitamin E supplement in the diet. Cu/Zn-superoxide dismutase (SOD) activity in liver did not differ greatly among the diet groups. The Ki-67 labelling index (LI), indicating cell proliferation rate was significantly lower in the K85 diet group compared to the other diet groups.

The effect of supplementation with omega-3 fatty acids on soluble markers of endothelial function in patients with coronary heart disease.

During progression of atherosclerosis the overlying endothelial cells alter their expression of some surface molecules. Circulating levels of such molecules may be quantified. We investigated the effect of omega-3 fatty acids (n-3 FA) on the levels of tissue plasminogen activator antigen, von Willebrand factor, and the soluble forms of thrombomodulin, P-selectin, E-selectin, and vascular cell adhesion molecule-1 in 54 patients with coronary heart disease. Twenty-three of the patients had taken 5.1 g/d n-3 FA for 6 months (group I) and 31 were given corn oil as placebo (group II). For another 4 weeks ("the study period") they all got 5.1 g/d of n-3 FA. Compliance was confirmed by demonstration of changes in relevant fatty acids in serum phospholipids. At baseline, significant differences between the groups were found with lower median values of von Willebrand factor (128% versus 147%) and soluble thrombomodulin (24.9 versus 32.5 ng/mL) and higher median values of soluble E-selectin (41.4 versus 35.5 ng/mL) and soluble vascular cell adhesion molecule-1 (573 versus 473 ng/mL) in group I. During the study period differences in changes between the groups were found; tissue plasminogen activator antigen and soluble thrombomodulin decreased (P for difference between the groups 0.001 and 0.015, respectively), whereas soluble E-selectin and soluble vascular cell adhesion molecule-1 increased (P for difference between the groups <0.01 for both) in group II relative to group I. Our results indicate that n-3 FA supplementation decreases hemostatic markers of atherosclerosis, whereas markers of inflammation may be increased. The latter may be the result of lipid peroxidation as a simultaneous decrease of vitamin E and increase in thiobarbituric acid-reactive substances were observed.