Biomedical subjects
Publications and source records attributed to M B Katan.
A new study shows no significant associations between n-3 fatty acids or fish intake and heart disease among men who are initially free of cardiovascular disease. These conclusions may somewhat diminish enthusiasm for fish and fish oil as a panacea against heart disease.
Trans fatty acids raise plasma low-density lipoprotein (LDL) cholesterol levels in volunteers when exchanged for cis unsaturated fatty acids in the diet. In addition, trans fatty acids may lower high-density lipoprotein (HDL) cholesterol levels and raise triglyceride and lipoprotein(a) levels in plasma. Trans and cis unsaturated fatty acids are thus not equivalent, and diets aimed at reducing the risk of coronary heart disease should be low in both trans and saturated fatty acids.
Foods contain isomers of unsaturated fatty acids that have double bonds in unusual configurations (trans instead of cis) or unusual positions, or both. Such fatty acids arise through biohydrogenation in the rumen of cows and sheep or catalytic hydrogenation in industrial hardening of oils. The effects of transmonounsaturates on lipoproteins in man are opposite to those of their cis-isomer, oleic acid: trans fatty acids raise low density lipoprotein (LDL) cholesterol and lipoprotein Lp(a) and lower high density lipoprotein (HDL) cholesterol, all in a dose-dependent fashion. Trans fatty acids raised serum cholesteryl ester transfer activity in 52 of 55 volunteers (mean change 18%, P < 0.02), and lowered the ratio of cholesteryl esters to triglycerides in HDL. Lecithin cholesterol acyl transferase was unchanged. The effects of trans fatty acids on HDL and LDL may thus be mediated through cholesterol ester transfer protein.
OBJECTIVE: It has been suggested that certain foods of plant origin contain milligram-quantities of acetylsalicylate which could exert an anti-thrombotic effect. Acetylsalicylic acid prevents cardiovascular diseases through inhibition of platelet endoperoxide thromboxane production and platelet aggregation. We investigated whether a daily intake of 3 mg acetylsalicylic acid causes a measurable decrease of platelet cyclo-oxygenase activity assessed by in vitro thromboxane B2 production. DESIGN: We carried out a randomised, double-blind, placebo-controlled cross-over study. SUBJECTS: Ten healthy volunteers (5 men, 5 women) aged 22 +/- 3 years (mean +/- s.d) participated in the study; there were no drop-outs. INTERVENTIONS: Participants took 3 mg/d of acetylsalicylic acid or a placebo for 2 weeks each. At the end of each treatment period venous blood was drawn, and platelet-rich plasma was stimulated with arachidonic acid. RESULTS: Treatment with acetylsalicylic acid caused a 39 +/- 8% decrease in maximal thromboxane B2 production (P = 0.000), which was independent of treatment order. CONCLUSIONS: Quantitative data on acetylsalicylate in foods and the possible antithrombotic action of a diet rich in acetylsalicylate deserve closer investigation.
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Flavonoids are polyphenolic antioxidants naturally present in vegetable foods. Some flavonoids, such as quercetin, inhibit carcinogenesis in rodents, but their effect in humans is unknown. We measured the flavonoids quercetin, kaempferol, myricetin, apigenin, and luteolin in foods and assessed flavonoid intake in 1985 by dietary history in 738 men aged 65-84 years without a history of cancer, who were then followed for five years. Mean flavonoid intake was 25.9 mg/day. The major sources of flavonoid intake were tea at 61% and vegetables and fruits (mainly onions, kale, endive, and apples) at 38%. Between 1985 and 1990, 75 men developed cancer (all sites) and 34 men died from cancer. Flavonoid intake in 1985 was not associated with incidence of all-cause cancer (p for trend = 0.54) or with mortality from all-cause cancer (p for trend = 0.51). Flavonoid intake was also not associated with risk of cancers of the alimentary and respiratory tract (p for trend = 0.92). Adjustment for age, body mass index, smoking, physical activity, and vitamin C, vitamin E, beta-carotene, and dietary fiber intake did not change the relative risks. A high intake of flavonoids from vegetables and fruits only was inversely associated with risk of cancer of the alimentary and respiratory tract (relative risk of highest vs. lowest tertile = 0.51, 95% confidence interval 0.25-1.05); these results suggest the presence of other nonvitamin components with anticarcinogenic potential in these foods. We conclude that intake of flavonoids, mainly from tea, apples, and onions, does not predict a reduced risk of all-cause cancer or of cancer of the alimentary and respiratory tract in elderly men. The effect of flavonoids on risk of cancer at specific sites needs further investigation in prospective cohort studies.
Colonic fermentation of dietary carbohydrates and fiber might produce a protective effect against the development of large bowel cancer. Resistant starch, ie, starch that escapes small bowel digestion, is a candidate fermentable substrate that has been hitherto little studied. We supplemented 19 healthy volunteers with 15 g native amylomaize (Hylon-VII) three times a day, containing 28 g type II resistant starch, or with dextrins as a placebo for 7 d in a crossover design. Pre-experimentally, 11 subjects regularly produced breath methane and 8 did not. Resistant starch increased 24-h integrated excretion of breath hydrogen. The mean rise relative to placebo was 35% (P = 0.03) for all subjects and 60% for eight subjects not producing methane (P = 0.02). The 11 methane producers showed a 93% increase in breath-methane excretion on resistant starch (P = 0.03). Continued consumption of 28 g type II resistant starch/d is well tolerated and increases colonic fermentation in healthy volunteers.
Differences in dietary fatty acid structure induce marked differences in lipid and lipoprotein concentrations in plasma from fasting subjects. Under metabolic-ward conditions, replacement of carbohydrates by lauric, myristic, and palmitic acids raise both low-density-lipoprotein (LDL) and high-density-lipoprotein (HDL) cholesterol whereas stearic acid has little effect. Oleic and linoleic acids raise HDL and slightly lower LDL; all fatty acids lower fasting triglycerides when substituted for carbohydrates. Trans monounsaturates lower HDL and raise LDL and lipoprotein(a). The fatty acids in unhydrogenated fish oil potently lower triglycerides, with variable effects on LDL. Of the commercial fats, palm-kernel and coconut oil are the most hypercholesterolemic, followed by butter and palm oil. Replacement of hard fats rich in lauric, myristic, or palmitic acids or trans fatty acids by unsaturated oils will lower LDL, but replacement by carbohydrates will in addition decrease HDL and increase triglycerides. In free-living subjects, high-oil diets could lead to obesity, undoing the favorable effects on HDL and triglycerides.
We assessed how accurately participants in dietary trials reported their free-living energy intake. We compared self-reported energy intake, calculated from 3-d food records, with actual intakes needed to maintain body weight during controlled trials lasting 6-9 wk. In 269 free-living healthy male (n = 119) and female (n = 150) adults with mean body weights close to ideal values (mean +/- SD body mass index in kg/m2, 22.1 +/- 2.4), energy intake reported in food records was 1.2 +/- 1.6 MJ/d (277 +/- 378 kcal/d) lower than actual energy requirements during the experiments. The relative bias was significantly smaller (P = 0.01) for men (-8.0 +/- 13.4%) than for women (-12.2 +/- 13.7%). Body mass index, daily energy intake, and age were not significantly related to the extent of underestimation. We conclude that food records systematically underestimate energy needs in young, nonobese well-educated adults.
The Serbian cohorts of the Seven Countries Study were examined four times during a 25-year period. Large changes were observed in average serum cholesterol, blood pressure and the prevalence of smoking in these ageing cohorts. Comparison of men of the same age strata e.g. men aged 50-59 examined at baseline and after 10 years of follow-up and of men aged 65-69 examined after 10 and 25 years of follow-up showed that serum cholesterol increased by about 45% in Zrenjanin, 35% in Velika Krsna and 15% in Belgrade over the last 25 years. Systolic blood pressure increased by 9% in Zrenjanin and 7% in Velika Krsna. No significant increase in systolic blood pressure was observed in Belgrade. There was no major secular trend in smoking and the changes observed during 25 years were mainly due to ageing. No major change was observed in body mass index. The increases in serum cholesterol and blood pressure observed in the Serbian cohorts during the last 25 years are compatible with the increase in cardiovascular disease mortality observed in Yugoslavian men aged 30-69 during the period 1970-1984.
The cholesterol-raising effect of dietary saturated fatty acids is largely accounted for by lauric, myristic, and palmitic acids. Dairy fat is a major source of myristic acid, and palm oil is especially rich in palmitic acid. Myristic acid is suspected of being much more cholesterolemic than palmitic acid, but direct comparisons have been lacking. We therefore fed 36 women and 23 men three diets that differed from each other in palmitic, oleic, and myristic acid content by about 10% of total energy. We used palm oil, high-oleic acid sunflower oil, and a specially produced high-myristic acid fat to achieve these differences. Each diet was consumed for 3 weeks in random order. Mean serum cholesterol was 4.53 mmol/L on the high-oleic acid diet, 4.96 mmol/L on the palmitic acid diet, and 5.19 mmol/L on the myristic acid diet (P < .0001 for all comparisons). Myristic acid raised low-density lipoprotein (LDL) cholesterol by 0.11 mmol/L, high-density lipoprotein (HDL) cholesterol by 0.12 mmol/L, and apolipoprotein (apo) A-I by 7.2 mg/dL relative to palmitic acid; increases relative to oleic acid were 0.50 mmol/L for LDL cholesterol, 0.15 mmol/L for HDL cholesterol, 6.0 mg/dL for apoB, and 8.9 mg/dL for apoA-I (P < .01 for all comparisons). The HDL cholesterol and apoA-I levels on the palmitic and oleic acid diets were the same. None of the responses differed significantly between woman and men. Myristic acid and palmitic acid both caused high LDL cholesterol and apoB levels and low HDL to LDL ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
Boiled coffee contains an unidentified lipid that raises serum cholesterol. We studied the effects of the ingestion of coffee oil fractions of increasing purity in volunteers in order to identify the cholesterol-raising factor. In 15 volunteers who ingested 0.75 g/d of a non-triglyceride-fraction from coffee oil for 4 weeks, mean cholesterol increased by 48 mg/dl (1.2 mmol/l) relative to placebo. In contrast, a coffee oil stripped of the non-triglyceride lipids cafestol and kahweol had no effect. In three volunteers, purified cafestol (73 mg/d) plus kahweol (58 mg/d) increased cholesterol by 66 mg/dl (1.7 mmol/l) after 6 weeks. Oil from Robusta beans, which contains cafestol but negligible kahweol, also raised serum cholesterol. These findings show that cafestol is at least partly responsible for the cholesterol-raising effect of boiled coffee. Coffee oils and brews containing cafestol consistently increased serum triglycerides and alanine amino-transferase, and depressed serum creatinine and gamma-glutamyl-transferase (GGT). After withdrawal GGT activity rose above baseline. Norwegians who habitually consumed 5-9 cups of boiled coffee per day had higher serum cholesterol levels and lower GGT but no higher alanine aminotransferase activity than controls. Thus, serum cholesterol is raised by cafestol and possibly also kahweol, both natural components of coffee beans. The mechanism of action is unknown but is accompanied by alterations in liver function enzymes.
Flavonoids are polyphenolic antioxidants naturally present in vegetables, fruits, and beverages such as tea and wine. In vitro, flavonoids inhibit oxidation of low-density lipoprotein and reduce thrombotic tendency, but their effects on atherosclerotic complications in human beings are unknown. We measured the content in various foods of the flavonoids quercetin, kaempferol, myricetin, apigenin, and luteolin. We then assessed the flavonoid intake of 805 men aged 65-84 years in 1985 by a cross-check dietary history; the men were then followed up for 5 years. Mean baseline flavonoid intake was 25.9 mg daily. The major sources of intake were tea (61%), onions (13%), and apples (10%). Between 1985 and 1990, 43 men died of coronary heart disease. Fatal or non-fatal myocardial infarction occurred in 38 of 693 men with no history of myocardial infarction at baseline. Flavonoid intake (analysed in tertiles) was significantly inversely associated with mortality from coronary heart disease (p for trend = 0.015) and showed an inverse relation with incidence of myocardial infarction, which was of borderline significance (p for trend = 0.08). The relative risk of coronary heart disease mortality in the highest versus the lowest tertile of flavonoid intake was 0.42 (95% CI 0.20-0.88). After adjustment for age, body-mass index, smoking, serum total and high-density-lipoprotein cholesterol, blood pressure, physical activity, coffee consumption, and intake of energy, vitamin C, vitamin E, beta-carotene, and dietary fibre, the risk was still significant (0.32 [0.15-0.71]). Intakes of tea, onions, and apples were also inversely related to coronary heart disease mortality, but these associations were weaker. Flavonoids in regularly consumed foods may reduce the risk of death from coronary heart disease in elderly men.
Serum cholesterol in man rises when cholesterol intake increases, but the extent of the elevation varies between subjects. Part of the variation between subjects is spurious and not reproducible; it is caused by random diet-independent fluctuations of serum lipid levels. Part is due to consistent metabolic differences between subjects. We have earlier found that responsiveness was associated with higher initial total and HDL cholesterol, lower habitual cholesterol consumption, and lower body mass index, and unrelated to gender, age, or apo E phenotype. We have now investigated the metabolic basis of variability by measuring turnover rates of low density lipoprotein (LDL) apolipoprotein B (apo B) on a low-cholesterol diet (140 mg/day) and a high-cholesterol diet (900 mg/day) in 8 volunteers with well-defined differences in the responsiveness of their serum cholesterol to diet. Autologous 125I-LDL was injected on day 23 of each diet period. Its fractional catabolic rate (FCR) was estimated from the ratio of 125I in urine over that in plasma, seven days after injection. FCR (mean +/- SD) increased from 0.24 +/- 0.02 pools/day on the low- to 0.31 +/- 0.20 on the high-cholesterol diet. LDL-apo B concentration rose from 49 +/- 13 to 63 +/- 12 mg/dl, and LDL-apo B production rate, calculated as FCR x concentration/body weight, from 4.8 +/- 1.2 to 8.0 +/- 1.4 mg/kg/day. The individual rise in production rate was significantly correlated with the rise in the serum concentration of LDL-apo B (r = 0.90) or LDL-cholesterol (r = 0.75), and also with the rise in total serum cholesterol measured in these same subjects in similar experiments 3-4 years earlier (r = 0.74). Degradation of LDL by freshly isolated blood mononuclear cells and by mononuclear cells incubated for 72 h in lipoprotein-deficient medium (derepressed cells) was measured on both diets in these and in additional volunteers. The rate of degradation (mean +/- SD) of standard human LDL by fresh cells was 336 +/- 166 ng LDL protein/mg cell protein per 8 h on the low-cholesterol diet, and decreased by 147 +/- 180 ng/mg per 8 h or 44% on the high-cholesterol diet (n = 23, p < 0.01). The catabolic activity of derepressed cells obtained when subjects were on the low-cholesterol diet was negatively related to the LDL cholesterol response (r = -0.57, n = 18, p < 0.05), and to the total cholesterol response in earlier experiments (r = -0.45, n = 18, p < 0.10).(ABSTRACT TRUNCATED AT 400 WORDS)
The hypothesis that lean persons are more responsive than fat persons to the effects of dietary cholesterol was investigated in 1,903 middle-aged employed men who were examined in 1958 and 1959 as participants in the Chicago Western Electric Study. Change in intake of dietary cholesterol was positively associated with change in serum cholesterol for men in the lowest tertile of body mass index (defined as weight (kg)/height (m)2) (< 24.2) but not for men in the highest tertile (> 26.6) after adjustment for change in body mass index and change in intakes of energy and saturated and polyunsaturated fatty acids. A decrease of 150 mg/1,000 kcal in dietary cholesterol was associated with mean changes of -0.46, -0.18, and 0.13 mmol/liter in serum cholesterol for men with body mass indices of < 24.2, 24.2-26.6, and > 26.6, respectively. Body mass index was strongly correlated with subscapular skinfold thickness; thus, these differences in body mass index reflect true differences in adiposity. These results may help to explain inconsistencies that have occurred in feeding experiments with dietary cholesterol, and they suggest that a reduction in dietary cholesterol should have a more favorable effect on the serum cholesterol levels of fat persons after they have lost weight.