Concordance for Dyslipidemic Hypertension in Male Twins

Selby, Joseph V.; Newman, Beth; Quiroga, Jose; Christian, Joe C.; Austin, Melissa A.; Fabsitz, Richard R.

doi:10.1001/jama.1991.03460160057029

Cited by 78 publications

(36 citation statements)

References 19 publications

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“…Others have demonstrated a higher incidence of the syndrome of insulin resistance in FCH subjects but this was found to be associated with obesity ( 15,18). In the present study, obesity was not a feature in FCH subjects since the mean body mass index in the tertiles was lower than in the study ofHunt et al ( 15) and Selby et al ( 18). Nonetheless, in the present study insulin concentrations correlated significantly with the body mass index in FCH relatives.…”

Section: Discussioncontrasting

confidence: 55%

“…Insulin resistance which has been associated to increased atherosclerotic risk ( 14), has also been associated with FCH ( 15 ). In subjects with the syndrome ofinsulin resistance, also known as "syndrome X" ( 16,17), "familial dyslipidemic hypertension" ( 15,18), or the "deadly quartet" ( 19), clustering of risk factors may be found. This atherosclerotic state has also been called the "atherogenic lipoprotein phenotype" (20) and a candidate gene cluster comprising the insulin receptor and LDL receptor genes has been found on the short arm of chromosome 19 (21).…”

Section: Introductionmentioning

confidence: 99%

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Impaired fatty acid metabolism in familial combined hyperlipidemia. A mechanism associating hepatic apolipoprotein B overproduction and insulin resistance.

Cabezas

Bruin²,

Valk³

et al. 1993

J. Clin. Invest.

185

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To establish whether insulin resistance and/or postprandial fatty acid metabolism might contribute to familial combined hyperlipidemia (FCH) we have examined parameters of insulin resistance and lipid metabolism in six FCH kindreds. Probands and relatives (n = 56) were divided into three tertiles on the basis of fasting plasma triglycerides (TG). Individuals in the highest tertile (TG > 2.5 mM; n = 14) were older and had increased body mass index, systolic blood pressure, and fasting plasma insulin concentrations compared with individuals in the lowest tertile (n = 24). The former also presented with decreased HDL cholesterol and increased total plasma cholesterol, HDL-TG, and apoprotein B, E, and CIII concentrations.Insulin concentrations were positively correlated with plasma apo B, apo CIII, apo E, and TG, and inversely with HDL cholesterol. Fasting nonesterified fatty acids (NEFA) were elevated in FCH subjects compared to six unrelated controls and five subjects with familial hypertriglyceridemia. Prolonged and exaggerated postprandial plasma NEFA concentrations were found in five hypertriglyceridemic FCH probands. In FCH the X2 minor allele of the AI-CIII-AIV gene cluster was associated with increased fasting plasma TG, apo CIII, apo AI, and NEFA concentrations and decreased postheparin lipolytic activities. The clustering of risk factors associated with insulin resistance in FCH indicates a common metabolic basis for the FCH phenotype and the syndrome of insulin resistance probably mediated by an impaired fatty acid metabolism. (J.

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Section: Discussioncontrasting

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Impaired fatty acid metabolism in familial combined hyperlipidemia. A mechanism associating hepatic apolipoprotein B overproduction and insulin resistance.

Cabezas

Bruin²,

Valk³

et al. 1993

J. Clin. Invest.

185

View full text Add to dashboard Cite

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“…4,19,20 Castelli and Anderson 19 found that BP and serum cholesterol were strongly correlated among hypertensive patients, which led to early recommendations to treat elevated cholesterol in patients with hypertension. 5,19 Gaziano et al 21 also noted a potential interaction between elevated cholesterol and hypertension in the development of MI that suggested a direct relationship rather than the effect of 2 independent predictors.…”

Section: Discussionmentioning

confidence: 99%

Dyslipidemia and the Risk of Incident Hypertension in Men

Halperin

Sesso²,

Ma³

et al. 2006

Hypertension

286

190

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Abstract-Evidence suggests that hypertension may share a similar pathophysiology with cardiovascular disease (CVD).Thus, dyslipidemia, a strong predictor of CVD, may also predict incident hypertension. We analyzed 3110 men free of hypertension, CVD, and cancer from the Physicians' Health Study, who provided baseline blood samples from which we measured total cholesterol (TC) and HDL cholesterol (HDL-C), and calculated non-HDL-C and the TC/HDL-C ratio. We categorized each lipid parameter into quintiles and considered National Cholesterol Education Project clinical cut points. Other risk factor information was provided from self-reports on the baseline questionnaire. Incident hypertension was defined as either the initiation of antihypertensive treatment, self-reported systolic blood pressure Ն140 mm Hg, or diastolic blood pressure Ն90 mm Hg. Over a mean follow-up of 14.1 years, 1019 men developed hypertension. In Cox proportional hazards models adjusted for lifestyle and clinical risk factors, men in the highest quintile of TC, non-HDL-C, and TC/HDL-C ratio had increased risks of developing hypertension of 23%, 39%, and 54%, respectively, compared with participants in the lowest quintile. Furthermore, men in the highest quintile of HDL-C had a 32% decreased risk of developing hypertension compared with those in the lowest quintile. Models using National Cholesterol Education Project cut points demonstrated similar associations with hypertension. Models excluding men with diabetes and obesity maintained an independent association between baseline lipids and hypertension. These prospective cohort data suggest that dyslipidemias may lead to the subsequent development of hypertension. Thus, plasma lipids may be useful in the identification of men at risk for hypertension. Key Words: cholesterol Ⅲ lipids Ⅲ hypertension Ⅲ blood pressure Ⅲ men Ⅲ prospective studies H ypertension is a common condition that affects Ͼ50 million Americans 1 and is an important risk factor for cardiovascular disease. Although several risk factors for the development of hypertension have been identified, 2 its etiology is still not fully understood. 1 Hypertension is commonly associated with other cardiovascular risk factors, such as obesity, diabetes, and dyslipidemia. 3 The presence of these cardiovascular risk factors and the resulting endothelial dysfunction may play a role in the pathophysiology of hypertension. 4 Dyslipidemia, a strong predictor of cardiovascular disease, 5 causes endothelial damage, 6 -8 and the loss of physiological vasomotor activity that results from endothelial damage may become manifested as increased blood pressure (BP). Therefore, factors like dyslipidemia that cause endothelial dysfunction may lead to hypertension. Cross-sectional studies have suggested a link between abnormal lipids and hypertension. 4,9,10 A few studies have prospectively examined the relationship between plasma lipids and the future development of hypertension, finding that there is an association between plasma lipids and development of hyp...

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“…To date, multivariate approaches to the MMS have only been demonstrated in a number of twin [32][33][34][35] and family studies [36]. These studies have pointed towards strong genetic or shared environmental influences on the joint occurrence of MMS components [32,33]. Recently, Mitchell et al [36] suggested that a common gene or set of genes may influence components of the MMS such as insulin, BMI, triglycerides, and HDL-cholesterol.…”

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confidence: 99%

Familial components of the multiple metabolic syndrome: the ARIC Study

et al. 1997

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The clustering of multiple metabolic abnormalities including obesity, insulin resistance, non-insulin-dependent diabetes mellitus (NIDDM), hypertension, and dyslipidaemias has become known as the insulin resistance syndrome [1,2] or multiple metabolic syndrome (MMS) [3,4]. Genetic as well as shared environmental influences on insulin, insulin resistance, and obesity have been reported in family and twin studies [5][6][7][8][9][10][11]. Familial aggregation of NIDDM [12,13], elevated blood pressure levels [14,15], and lipid disorders [16,17] is well established. Metabolic disorders such as familial hypercholesterolaemia [18,19], familial combined hyperlipidaemia [20][21][22], and familial dyslipidemic hypertension [23] require a positive family history as part of their definition.Particularly within genetic epidemiology, studies on the MMS have frequently had a primary focus on a single, continuously distributed metabolic characteristic such as insulin [8,9]. Others have compared multiple metabolic variables among offspring of affected and unaffected parents [24][25][26][27][28][29][30][31]. Focusing on a single metabolic characteristic, however, limits the Diabetologia (1997) Summary The association of a parental history of diabetes mellitus and hypertension with the multiple metabolic syndrome (MMS) was studied in a population survey of middle-aged adults. The eligible population was drawn from the baseline examination of the Atherosclerosis Risk in Communities Study, a population-based, bi-ethnic, multi-centre cohort study. The MMS was defined as a multivariate, categorical phenotype of co-occurring diabetes, hypertension, and dyslipidaemia. MMS cases (n = 356) were compared to disorder-free control subjects (n = 6797) with respect to their parental history of diabetes and hypertension. MMS cases were more likely to report a history of diabetes in both parents (odds ratio [OR] 4.7, 95 % confidence interval (CI) 1.5-14.7) or a history of hypertension in both parents (OR 1.9, 95 % CI 1.1-3.0) than control subjects, adjusting for BMI, waist-to-hip ratio, age, gender, and ethnicity/centre. A parental history of diabetes and hypertension in both parents was associated with the greatest increase in odds of MMS (OR 8.3,. A dose-response relationship between the number of parental disorders (one; two; three to four) and the odds of MMS was observed (OR 1.2, 95 % CI 0.9-1.7; OR 2.0, 95 % CI 1.4-2.8; OR 4.0, 95 % CI 2.5-6.2). Based on the marked associations observed between a parental history of MMS components and the clustering of these metabolic disorders in the offspring generation, we conclude that genetic and/or non-genetic familial influences play a role in the development of the multiple metabolic syndrome. [Diabetologia (1997) 40: 963-970]

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Concordance for Dyslipidemic Hypertension in Male Twins

Cited by 78 publications

References 19 publications

Impaired fatty acid metabolism in familial combined hyperlipidemia. A mechanism associating hepatic apolipoprotein B overproduction and insulin resistance.

Impaired fatty acid metabolism in familial combined hyperlipidemia. A mechanism associating hepatic apolipoprotein B overproduction and insulin resistance.

Dyslipidemia and the Risk of Incident Hypertension in Men

Familial components of the multiple metabolic syndrome: the ARIC Study

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