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Results for “STEARIC ACID”

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PubMed1989

Changes of electron spin resonance membrane fluidity in hexadecane-induced hyperproliferative epidermis.

To study some of the biochemical and physical states of membranes associated with hyperproliferation, the effect of topical hexadecane on membrane fluidity in guinea pig epidermis was investigated by electron spin resonance using a 5-doxylstearic acid spin labeling agent. Guinea pig epidermal cells were separated into three regions of keratinocytes by Percoll density gradient centrifugation. Membrane fluidity and Na+, K+-ATPase activity were higher in hyperproliferating epidermal cells than in control. The free cholesterol content and the molar ratio of free cholesterol to phospholipid were found to decrease significantly. Also elevated levels of palmitic acid, stearic acid and omega-3 unsaturated fatty acid derived from phospholipid were observed. Normal differentiation of epidermis was found to be accompanied by a decrease in membrane fluidity, whereas a relatively high membrane fluidity was maintained in the hexadecane-induced hyperproliferation.

Alkanes↗

PubMed1997

Suppression of nitric oxide production in lipopolysaccharide-stimulated macrophage cells by omega 3 polyunsaturated fatty acids.

Although nitric oxide (NO) is an important biological mediator, its excessive production in inflammation is thought to be a causative factor for cellular injury and, over the long term, cancer. In the present study, the effects of several fatty acids on NO production in murine macrophage cell line RAW264 cells stimulated with lipopolysaccharide were examined. Suppression of NO production was observed with the omega 3 polyunsaturated fatty acids (PUFAs), docosahexaenoic acid, eicosapentaenoic acid and alpha-linolenic acid, in a dose-dependent fashion. In contrast, no inhibition was observed with omega 6 PUFA (linoleic acid), omega 9 PUFA (oleic acid) or a saturated fatty acid (stearic acid). Western and northern blot analyses suggested that suppression of the induction of inducible NO synthase gene expression is responsible for the inhibition of NO production by omega 3 PUFAs. The inhibitory effect of omega 3 PUFA on NO production in activated macrophages could contribute to their cancer chemopreventive influence.

Animals↗

PubMed2004

Triglyceride accumulation and altered composition of triglyceride-associated fatty acids in the skin of tenascin-X-deficient mice.

Tenascin-X (TNX) is a member of the tenascin family of glycoproteins of the extracellular matrix. Here, we observed abnormalities in the skin of TNX-deficient mice in comparison with that of wild-type mice. Histological analysis with Oil Red O staining demonstrated that there was considerable accumulation of lipid in the skin of TNX-deficient (TNX-/-) mice. By thin-layer chromatography of total lipids, it was found that the level of triglyceride was significantly increased in TNX-/- mice. The mRNA levels of most of the lipogenic enzyme genes examined were remarkably increased in TNX-/- mice. By gas chromatography-mass spectrometry analysis of triglyceride-associated fatty acids in the skin, saturated fatty acid palmitoic acid was decreased, whereas unsaturated fatty acids palmitoleic acid and oleic acid were increased in TNX-/- mice compared with those in wild-type mice. Conversely, fibroblast cell lines transfected with TNX showed a significant decrease in the amount of triglyceride. An increase in the saturated fatty acid stearic acid and decreases in the unsaturated fatty acids palmitoleic acid, oleic acid and linoleic acid, compared to those in mock-transfected cells were also caused by over-expression of TNX. These results indicate that TNX is involved in the regulation of triglyceride synthesis and the regulation of composition of triglyceride-associated fatty acids.

Adipose Tissue↗

PubMed1996

Abnormality in membrane fatty acid compositions of cells measured on erythrocyte in alcoholic liver disease.

It has been proven that the fatty acids of esterified phospholipids in the cell membrane play an important role in membrane fluidity. Our previous in vitro experiment indicated that the impairment of erythrocyte membrane fluidity might be largely because of the change in fatty acids. The aim of this study is to clarify changes of cell membrane fatty acids in more detail in relation to various stages and pathology of alcoholic liver disease. For the analysis, erythrocyte membranes were exploited on the assumption that their fatty acid compositions may be similar to those of other organs. In alcoholic liver disease, unsaturated fatty acids in the erythrocyte membrane decreased and saturated fatty acids increased. Consequently, the unsaturated fatty acid/saturated fatty acid ratio decreased significantly. When fractions of saturated fatty acids were studied, myristic acid (C14:0) increased markedly in the alcoholic group, and the increase was striking particularly in the cases of alcoholic hepatitis concurrently with hemolysis. Palmitic acid (C16:0) also tended to increase in the alcoholic liver disease group. A longer chain saturated fatty acid, stearic acid (C18:0), showed a moderate but significant increase in the alcoholic fatty liver and hepatic fibrosis group, but it decreased significantly in the alcoholic liver cirrhosis, as with the finding in viral liver cirrhosis. As with unsaturated fatty acids, linoleic acid (C18:2), arachidonic acid (C20:4), and eicosapentanoic acid (C20:5) decreased significantly. The arachidonic acid/linoleic acid ratio, which indicates microsomal elongation activity of liver cells, was found to be broadly distributed. No significant change was found in each group of alcoholic liver disease. However, the cases showing a decrease in this ratio had severe hepatic dysfunction concurrently. Thrombogenic Index, serving as an indicator for fatty acids in food, and that is concerned with formation of thrombus, was studied, using fatty acid fractions of the erythrocyte membrane. The index was significantly increased in alcoholic liver disease. It was suggested that the chronic alcohol intake and the resultant liver diseases might enhance the abnormality of the membrane fatty acid composition. These changes may affect cell membrane fluidity and eventually metabolic functions of the cell.

Alcoholism↗

PubMed1993

Stimulation of enterocyte protein kinase C by laxatives in-vitro.

To elucidate the role of protein kinase C in the mechanism of action of stimulatory laxatives, experiments were performed with preparations of rat lysed enterocytes. The phorbol ester 4-beta-phorbol 12-myristate 13-acetate (PMA) concentration-dependently (2-200 micrograms mL-1) stimulated the activity of protein kinase C in this preparation. Ricinoleic acid, the active principle of castor oil, deacetylbisacodyl, the active principle of bisacodyl, and deoxycholic acid exerted the same effect, although less efficiently. This reflects their potency for inducing intestinal fluid secretion and prostaglandin release, effects that are also induced more potently by PMA. Accordingly, the potency of the three C18 fatty acids, ricinoleic acid, stearic acid and oleic acid on protein kinase C activity in-vitro, on prostaglandin E2 release and on net fluid secretion in-vivo runs in parallel. It is therefore concluded that stimulatory laxatives activate protein kinase C, leading to prostaglandin E2 release, thus resulting in net fluid secretion.

Animals↗

PubMed1975

Cell envelope of Neisseria gonorrhoeae: outer membrane and peptidoglycan composition of penicillin-sensitive and-resistant strains.

The cell envelope of Neisseria gonorrhoeae, colony type 4, was studied. Outer membrane was isolated by lysozyme and ethylenediaminetetraacetic acid treatment of plasmolyzed cells according to Wolf-Watz et al. (1973). The degree of purity of the membrane preparations was checked by electron microscopy. The membrane fraction obtained had a density of 1.25 g/cm(3), was rich in phospholipase A and lysophospholipase, and contained only 10% of the total membrane activity of succinate dehydrogenase and d-lactate dehydrogenase. The outer membrane protein profile after sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed at least six major proteins. The predominating protein showed a molecular weight of 35,000. The lipopolysaccharide component was characterized by gas chromatography. The carbohydrates found were galactose, glucose, and glucosamine. d-Glycero-l-manno-heptose was present in very low amounts. Lipid A contained lauric acid, stearic acid, and beta-hydroxy-myristic acid. About 20% of the fatty acids in the outer membrane was derived from lipid A. The phospholipids were characterized as phosphatidylethanolamine, phosphatidylglycerol, and diphosphatidylglycerol. There was no evidence for a lipoprotein anchored to the peptidoglycan. The peptidoglycan of N. gonorrhoeae was of the chemotype I. The cell envelope of N. gonorrhoeae was found to be highly permeable to gentian violet. Cell envelopes of one penicillin-resistant and two penicillin-sensitive strains were compared. Only moderate differences in fatty acid composition were found.

Carbohydrates↗

PubMed2005

Potent block of inactivation-deficient Na+ channels by n-3 polyunsaturated fatty acids.

A voltage-gated, small, persistent Na(+) current (I(Na)) has been shown in mammalian cardiomyocytes. Hypoxia potentiates the persistent I(Na) that may cause arrhythmias. In the present study, we investigated the effects of n-3 polyunsaturated fatty acids (PUFAs) on I(Na) in HEK-293t cells transfected with an inactivation-deficient mutant (L409C/A410W) of the alpha-subunit (hH1(alpha)) of human cardiac Na(+) channels (hNav1.5) plus beta(1)-subunits. Extracellular application of 5 microM eicosapentaenoic acid (EPA; C20:5n-3) significantly inhibited I(Na). The late portion of I(Na) (I(Na late), measured near the end of each pulse) was almost completely suppressed. I(Na) returned to the pretreated level after washout of EPA. The inhibitory effect of EPA on I(Na) was concentration dependent, with IC(50) values of 4.0 +/- 0.4 microM for I(Na) peak (I(Na peak)) and 0.9 +/- 0.1 microM for I(Na late). EPA shifted the steady-state inactivation of I(Na peak) by -19 mV in the hyperpolarizing direction. EPA accelerated the process of resting inactivation of the mutant channel and delayed the recovery of the mutated Na(+) channel from resting inactivation. Other polyunsaturated fatty acids, docosahexaenoic acid, linolenic acid, arachidonic acid, and linoleic acid, all at 5 microM concentration, also significantly inhibited I(Na). In contrast, the monounsaturated fatty acid oleic acid or the saturated fatty acids stearic acid and palmitic acid at 5 microM concentration had no effect on I(Na). Our data demonstrate that the double mutations at the 409 and 410 sites in the D1-S6 region of hH1(alpha) induce inactivation-deficient I(Na) and that n-3 PUFAs inhibit mutant I(Na).

Cell Line↗

PubMed1986

Potentiated susceptibility of ascites tumor to acyl derivatives of ascorbate caused by balanced hydrophobicity in the molecule.

Orders of susceptibility of Ehrlich ascites tumor to L-ascorbic acid (Asc), its 6-stearoyl (6S), 6-palmitoyl (6P) and 2,6-dipalmitoyl (DP) derivatives were assessed in vitro and in vivo: 6P (a 50% growth inhibitory concentration (IC50) for cultured cells, 12 microM; an increased life-span of treated mice, 283%) greater than 6S (61 microM; 240%) much greater than Asc (430 microM; 122%) greater than or equal to DP (greater than 200 microM; 89%), indicating that the enhanced susceptibility was due to acyl moiety substituted at C6-hydroxyl group of Asc, but was retracted by further substitution at C2-hydroxyl group. Equimolar mixture of Asc and palmitic acid, stearic acid or their methyl esters was much less cytotoxic than 6P or 6S. Thus the enhanced susceptibility was not primarily due to an additive cytotoxic effect of ascorbyl and acyl moieties, but to a balanced hydrophobicity introduced into the molecule by a poorly cytotoxic acyl moiety.

Animals↗

PubMed1991

Lipid intake and atherosclerosis.

The importance of diet in the prevention and treatment of atherosclerosis is well known. Among the different nutrients, lipids certainly have a primary role. Dietary cholesterol can influence the progression of atherosclerosis by increasing cholesterol levels or by modifying the composition of lipoproteins. Epidemiological and clinical studies have clearly demonstrated a relationship between the intake of saturated fatty acids and atherosclerosis. Among these fatty acids, stearic acid has the smallest effect on cholesterol levels. Until a few years ago it was though that monounsaturated fatty acids (MUFA) did not affect lipoprotein metabolism. However, very recently it has been shown that MUFA have the same hypocholesterolemic effect as polyunsaturated fatty acids; moreover they do not induce a decrease in high-density lipoprotein cholesterol. Therefore the overall metabolic effect of MUFA seems to be beneficial.

Arteriosclerosis↗

PubMed1996

Serum fatty acids and blood pressure.

To examine the relation between serum fatty acids and blood pressure, we conducted a cross-sectional study of 156 men who were enrolled in the Multiple Risk Factor Intervention Trial. After confirming the stability of the stored serum samples, we measured serum fatty acid levels by gas-liquid chromatography and examined their association with blood pressure. Using stepwise linear regression, we determined that each SD increase (1.9%) in the serum level of cholesterol ester palmitoleic acid (16:1) was associated with a systolic pressure increase of 3.3 mm Hg (95% confidence interval, 0.9 to 5.6 mm Hg) and each SD increase (0.1%) in phospholipid omega 9 eicosatrienoic acid (20:3) was associated with a diastolic pressure increase of 1.7 mm Hg (95% confidence interval, 0.5 to 2.9 mm Hg). Serum level of cholesterol ester steric acid (18:0) was inversely associated with diastolic pressure: each SD increase (0.2%) was associated with a decrease of 1.4 mm Hg (95% confidence interval, -2.5 to -0.2 mm Hg). In multivariate models that included dietary fat intake, cholesterol ester dihomogammalinolenic acid (20:3) was also associated with diastolic pressure: each SD increase (0.16%) was associated with an increase of 1.2 mm Hg (95% confidence interval, 0.1 to 2.4 mm Hg). Our results indicate that three nonessential fatty acids--stearic acid, palmitoleic acid, and omega 9 eicosatrienoic acid, and one essential fatty acid--dihomogammalinolenic acid, are independent correlates of blood pressure among middle-aged American men at high risk of coronary heart disease.

Adult↗

PubMed1993

Lung surfactant phospholipids associate with polymerizing fibrin: loss of surface activity.

Intraalveolar fibrin formation is a hallmark of many acute and chronic lung inflammatory processes. We investigated the influence of fibrin polymerization on biochemical and biophysical properties of a calf lung surfactant extract (CLSE) used for therapy of neonatal distress syndrome. Thrombin-induced coagulation of human fibrinogen (range, 0.04 to 4 mg/ml) in the presence of CLSE (2 mg/ml phospholipids) resulted in progressive loss of surface tension-lowering properties and adsorption facilities of this surfactant preparation; the CLSE-inhibitory capacity of desAABB-fibrin surpassed that of fibrinogen by more than two orders of magnitude. In parallel with the loss of surface activity, association of the predominant surfactant phospholipid dipalmitoylphosphatidylcholine (DPPC) (14C-labeled, admixed to 2 mg/ml CLSE) with polymerizing desAABB-fibrin occurred. A volume of 0.3 mg/ml insoluble fibrin effected a approximately 50% loss, and 0.6 mg/ml a > 90% loss, of DPPC from the aqueous phase. Dioleoylphosphatidylcholine, dipalmitoylphosphatidic acid, stearic acid, palmitic acid, and arachidonic acid, admixed to CLSE as labeled compounds, as well as total CLSE phospholipids were retained in polymerizing desAABB-fibrin with dose-effect curves superimposable to that of DPPC; no fibrin association was noted for 14C-glycerol-3-phosphate. Polymerizing desAA-fibrin, generated by incubation of CLSE-fibrinogen mixtures with arvin, captured DPPC and resulted in loss of surface properties at even lower concentrations, compared with desAABB-fibrin. In contrast, CLSE incubation with preformed desAABB- and desAA-fibrin polymers did not cause substantial phospholipid coupling with the clot material or loss of surface properties. Microtiter plate-immobilized fibrinogen and desAABB- and desAA-fibrinomonomers did not bind CLSE phospholipids enriched with 14C-DPPC.(ABSTRACT TRUNCATED AT 250 WORDS)

1,2-Dipalmitoylphosphatidylcholine↗

PubMed1998

Factors determining drug residence in skin during transdermal absorption: studies on beta-blocking agents.

The factors determining drug residence in skin during penetration across rat abdominal skin were investigated using five beta-blocking agents with different lipophilicities as model drugs in vivo and in vitro. The amount of beta-blocking agent in the skin at steady state correlated well with lipophilicity. The distribution of beta-blocking agents to the stratum corneum and the contribution of intercellular lipids in the stratum corneum to their skin distribution were also correlated with their lipophilicity, suggesting that the stratum corneum, especially intercellular lipids in the stratum corneum, would be responsible for the residence of beta-blocking agents in the skin. Furthermore, cholesterol-3-sulfate, palmitic acid, stearic acid and oleic acid were found to interact with the beta-blocking agents, which are cationized under the physiological condition, and were assumed to play an important role in the skin accumulation. On the other hand, the binding to keratinocyte was so small that keratinocyte might have little effect on the skin accumulation of the beta-blocking agents. Drug transport from the stratum corneum to viable skin was suggested to be regulated by the lipophilicity of these agents. To investigate the residence of these drugs in viable skin, in vitro transport studies using stripped skin were performed. The transport rate constant across viable skin to receptor cells (k23) was inversely correlated with the lipophilicity of the drugs. The elimination rate constants from viable skin (k(vs)) obtained in the in vivo study were much smaller than the values of k23 obtained in the in vitro study, and they were inversely correlated with the binding to cytosol components of viable skin but not the lipophilicity. The viable skin-to-muscle concentration ratio of these drugs, obtained at the beta-phase of the plasma concentration-time curve after intravenous administration, was also inversely correlated with the binding to the cytosol components of viable skin. These results suggest that k(vs) reflects the transport from viable skin to muscle rather than to blood circulation and that the binding of drugs to cytosol components in viable skin would be one of the important factors determining the residence in viable skin.

Administration, Cutaneous↗

PubMed2002

Production of gamma-lactones by the brown-rot basidiomycete Piptoporus soloniensis.

A wild strain of brown-rot basidiomycete Piptoporus soloniensis produced a sweet flavor similar to tropical fruits in liquid cultures. The major and minor compounds were identified to be gamma-decalactone and gamma-octanolactone by gas chromatography-mass spectrometry analysis, respectively. The growth and production of gamma-decalactone by P. soloniensis in broth to which fatty acids had been added were investigated. The addition of 12-hydroxystearic acid and ricinoleic acid to the culture markedly enhanced the production of gamma-decalactone. On the other hand, addition of myristic acid, palmitic acid, stearic acid and oleic acid to the culture resulted in a higher production of gamma-octanolactone. The addition of hexanoic acid, octanoic acid, decanoic acid, lauric acid, linoleic acid and linolenic acid to the culture reduced the growth of P. soloniensis and production of gamma-decalactone and gamma-octanolactone. This strain accumulated oxalic acid in liquid culture and grew sufficiently under strongly acidic conditions.

Journal Article↗

PubMed1992

[Allosterism of acidic alcohol dehydrogenase (class III ADH) of mouse liver and its role in alcohol metabolism].

Two major ADH isozymes of mouse liver, basic ADH (Class I) and acidic ADH (Class III) were purified and the effects of various hydrophobic substances (t-butanol, butyramide, trifluoroethanol, trichloroacetic acid, stearic acid, oleamide, phenylalanine and norleucine) on their activities were investigated. All these hydrophobic substances activated acidic ADH with a range of from 15 to 560%, and reversely inactivated basic ADH activity with a range of from 10 to 100%, when 150 mmol/l ethanol was used as a substrate. Among these substances, t-butanol, which was the most potent activator of acidic ADH, enhanced the activity by 560% and completely inactivated basic ADH at a concentration of 1.0 mol/l. Kinetics studies demonstrated that the activation of acidic ADH by the hydrophobic substances was due to marked decreases of Km for ethanol in spite of decreases of Vmax, suggesting these substances were positive allosteric effectors for the isozyme. The inactivation of basic ADH by the hydrophobic substances was due to a decrease of Vmax without changing Km for ethanol. These results indicate that the activities of two ADH isozymes are regulated reversely by the hydrophobicity of the reaction environment which changes their kinetics constants. The ELISA method using the isozyme-specific antibody demonstrated that the content of acidic ADH in mouse liver was about 7 times larger than that of basic ADH (5.3 +/- 0.86 vs 0.72 +/- 0.06 mg/g-liver). In the light of the hydrophobic regulation of ADH isozyme activities and their liver contents, the role of acidic ADH on alcohol metabolism may be more predominant than basic ADH in the liver under hydrophobic condition.

Aldehyde Oxidoreductases↗

PubMed2004

Iron utilization and liver mineral concentrations in rats fed safflower oil, flaxseed oil, olive oil, or beef tallow in combination with different concentrations of dietary iron.

Diets with a higher proportion of polyunsaturated fatty acids (i.e., linoleic acid) have decreased iron absorption and utilization compared with diets containing a higher proportion of the saturated fatty acid stearic acid (e.g., beef tallow). However, less is known regarding the influence of other polyunsaturated or monounsaturated fatty acids, along with higher dietary iron, on iron absorption and utilization. The present study was conducted to compare the effects of dietary fat sources known to vary in (n-3), (n-6), and (n-9) fatty acids on iron utilization and liver mineral concentrations. Male weanling rats were fed a diet containing 10, 35, or 100 microg/g iron in combination with safflower oil, flaxseed oil, olive oil, or beef tallow for 8 wk. Indicators of iron status, iron utilization, and liver iron concentrations were unaffected by an interaction between the fat source and iron concentration. Plasma copper was the only variable affected by an interaction between the fat source and dietary iron. Findings of this study demonstrate that flaxseed oil and olive oil may alter tissue minerals and affect iron utilization. Further studies should be conducted to establish the effect of varying (n-3), (n-6), and (n-9) fatty acids on trace mineral status and iron utilization.

Animals↗

PubMed1998

Thermogenesis and fatty acid composition of brown adipose tissue in rats rendered hyperthyroid and hypothyroid-with special reference to docosahexaenoic acid.

The effects of hyperthyroidism and hypothyroidism on brown adipose tissue (BAT) thermogenesis and phospholipid fatty acid composition were investigated in rats. Chronic triiodothyronine (T3) treatment (hyperthyroidism) increased the interscapular BAT pad weight, its triacylglycerol content, and its DNA content. It did not affect basal and noradrenaline-stimulated in vitro oxygen consumption of BAT expressed per microg DNA, although it significantly increased the oxygen consumption of the whole BAT pad. T3 treatment had little effect on phospholipid content and phospholipid fatty acid composition. In contrast, chronic methimazole treatment (hypothyroidism) decreased the BAT pad weight and the triacylglycerol content, but did not significantly change the DNA content in comparison with the control. It significantly decreased the noradrenaline-stimulated BAT oxygen consumption expressed per microg DNA and per BAT pad, but did not change the basal oxygen consumption. Methimazole treatment significantly affected phospholipid content and phospholipid fatty acid composition. Among the major fatty acids of BAT, it decreased docosahexaenoic acid (DHA), arachidonic acid, palmitic acid, palmitoleic acid, and oleic acid, and it increased linoleic acid, stearic acid, and eicosapentaenoic acid. A regression analysis revealed a positive relationship between in vitro respiration and DHA levels in phospholipids (r = 0.404, p<0.05). These results suggest that thyroid hormones have trophic action on BAT and are necessary for BAT thermogenic activity. This study also suggests that DHA is involved in the regulation of BAT thermogenic activity, as we previously indicated.

Adipose Tissue, Brown↗

PubMedDate not supplied

Effect of surfactants on the stability of modified egg-yolk phosphatidyl choline liposomes.

Disintegration by surfactants on egg-yolk phosphatidyl choline (PC) vesicles, stabilized with polycholesteryl methacrylate and carboxy methyl chitosan, was investigated by measuring the amount of marker dye (bromothymol blue) released from the vesicles. In all the studies at pH 7.4 anionic and nonionic surfactants caused vesicle disintegration at low concentrations while cationic surfactants produced breakdown of vesicles at high concentrations. It was found that the modified liposomes disintegrated in the following order: Polymeric liposomes less than carboxymethyl chitosan coated/stearic acid/oleic acid containing PC liposomes less than cholesteryl methacrylate monomer containing PC liposomes/PC liposomes Polymeric liposomes were found to be the most stable compared with all other types. This may be explained due to the filling of the pores in the lipid structure which in turn block the surfactant penetration into phospholipid bilayers. In contrast to unsaturated fatty acid (oleic acid) saturated fatty acid (stearic acid) containing liposomes are more stable.

Drug Carriers↗

PubMed1992

Traditional risk-factor profile fails to explain striking geographical differences in IHD mortality among middle-aged men. The project "myocardial infarction in mid-Sweden".

An east-west gradient in cardiovascular mortality has been reported from the region of mid-Sweden. Postal questionnaire studies found that the risk factor distributions among middle-aged men were similar in areas with striking differences in cardiovascular mortality. In this study, 120 randomly selected 50-year-old men in two high mortality communities in the west and 120 men from two low mortality communities in the east were invited to a health survey in which serum lipids and other risk factors were analysed. Total serum cholesterol, LDL-cholesterol, HDL-cholesterol, and triglyceride levels were similar. Among fatty acids, stearic acid was high and arachidonic acid was low in the high mortality area. The levels of other traditional risk factors were the same. After taking these differences into account, the mortality differences remain large.

Coronary Disease↗