Obesity: Narkiewicz K

Redon J, Cifkova R, Laurent S, Nilsson P, Narkiewicz K, Erdine S, Mancia G, Anonymous00057. · University of Valencia and CIBER 06/03 Physiopathology of Obesity and Nutrition, Institute of Health Carlos III, Madrid, Spain. · J Hypertens. · Pubmed #18806611 No free full text.

Abstract: The metabolic syndrome considerably increases the risk of cardiovascular and renal events in hypertension. It has been associated with a wide range of classical and new cardiovascular risk factors as well as with early signs of subclinical cardiovascular and renal damage. Obesity and insulin resistance, beside a constellation of independent factors, which include molecules of hepatic, vascular, and immunologic origin with proinflammatory properties, have been implicated in the pathogenesis. The close relationships among the different components of the syndrome and their associated disturbances make it difficult to understand what the underlying causes and consequences are. At each of these key points, insulin resistance and obesity/proinflammatory molecules, interaction of demographics, lifestyle, genetic factors, and environmental fetal programming results in the final phenotype. High prevalence of end-organ damage and poor prognosis has been demonstrated in a large number of cross-sectional and a few number of prospective studies. The objective of treatment is both to reduce the high risk of a cardiovascular or a renal event and to prevent the much greater chance that metabolic syndrome patients have to develop type 2 diabetes or hypertension. Treatment consists in the opposition to the underlying mechanisms of the metabolic syndrome, adopting lifestyle interventions that effectively reduce visceral obesity with or without the use of drugs that oppose the development of insulin resistance or body weight gain. Treatment of the individual components of the syndrome is also necessary. Concerning blood pressure control, it should be based on lifestyle changes, diet, and physical exercise, which allows for weight reduction and improves muscular blood flow. When antihypertensive drugs are necessary, angiotensin-converting enzyme inhibitors, angiotensin II-AT1 receptor blockers, or even calcium channel blockers are preferable over diuretics and classical beta-blockers in monotherapy, if no compelling indications are present for its use. If a combination of drugs is required, low-dose diuretics can be used. A combination of thiazide diuretics and beta-blockers should be avoided.

Narkiewicz K. · No affiliation provided · Nephrol Dial Transplant. · Pubmed #16311261 links to  free full text

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Narkiewicz K. · No affiliation provided · J Hypertens. · Pubmed #12131519 No free full text.

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Redon J, Cífková R, Narkiewicz K. · Hypertension Clinic, Internal Medicine, Hospital Clinico, University of Valencia, Valencia, Spain. · Pol Arch Med Wewn. · Pubmed #19413186 links to  free full text

Abstract: Arterial hypertension is often part of a larger constellation of anthropometric and metabolic abnormalities that includes abdominal (or visceral) obesity, characteristic dyslipidemia (low high-density lipoprotein cholesterol and high triglycerides), glucose intolerance, insulin resistance and hyperuricemia. Using Adult Treatment Panel III criteria, prevalence is higher than in the general population and the metabolic syndrome (MS) can be found in as many as one third of patients. In hypertensives with MS, a high prevalence of hypertension-induced target organ damage and a negative prognostic value have been described. Dietary advice and life style changes should be strongly recommended and prompt pharmacologic treatment is required to control high blood pressure and to reduce risk. The effect of particular antihypertensive drugs on other components of the MS is an important clinical issue with consequences for the success of the treatment.

Redon J, Cifkova R, Laurent S, Nilsson P, Narkiewicz K, Erdine S, Mancia G. · University of Valencia, CIBER 06/03 Fisiopatología de la Obesidad y Nutrición, Institute of Health Carlos III, Madrid, Spain. · J Hypertens. · Pubmed #19262221 No free full text.

Abstract: Arterial hypertension is often part of a constellation of anthropometric and metabolic abnormalities that occur simultaneously to a higher degree than would be expected by chance alone, supporting the existence of a discrete disorder, the so-called metabolic syndrome. It is the result of interactions among a large number of interconnected mechanisms, which eventually lead to both an increase in cardiovascular and renal risk, and the development of diabetes. Mechanisms involved in the metabolic syndrome are obesity, insulin resistance, and a constellation of independent factors, which include molecules of hepatic, vascular, and immunologic origin with pro-inflammatory properties. At each of these key points are interactions of demographics, lifestyle, genetic factors, and environmental fetal programming. Superimposing upon these are infections or chronic exposure or both to certain drugs that can also make their contribution. Skeletal muscle and the liver, not adipose tissue, are the two key insulin-response tissues involved in maintaining glucose balance, although abnormal insulin action in the adipocytes also plays a role in development of the syndrome. Factors commonly associated with and partly dependent on obesity, insulin resistance, such as overactivity of the sympathetic, stimulation of the renin-angiotensin-aldosterone systems, abnormal renal sodium handling, endothelial dysfunction, and large vessels' alterations, may play a key role in the blood pressure elevation of the syndrome.

Jordan J, Engeli S, Redon J, Sharma AM, Luft FC, Narkiewicz K, Grassi G, Anonymous00199. · Franz Volhard Clinical Research Center and Department of Nephrology, HELIOS Klinikum Berlin and Medical Faculty of the Charité, Berlin, Germany. · J Hypertens. · Pubmed #17351387 No free full text.

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Wolf J, Lewicka J, Narkiewicz K. · Hypertension Unit, Department of Hypertension and Diabetology, Medical University of Gdansk, Debinki 7c, 80-952 Gdansk, Poland. · Nutr Metab Cardiovasc Dis. · Pubmed #17314035 No free full text.

Abstract: BACKGROUND AND AIM: There is growing recognition of the widespread incidence and health consequences of obstructive sleep apnea (OSA). This review examines the evidence linking sleep apnea with cardiovascular disease and discusses potential mechanisms underlying this link. DATA SYNTHESIS: The weight of evidence provides increasing support for a causal relationship between OSA and hypertension. Furthermore, OSA may contribute to the initiation and progression of cardiac ischemia, heart failure and stroke. Chronic sympathetic activation appears to be a key mechanism linking OSA to cardiovascular disease. Other potential mechanisms include inflammation, endothelial dysfunction, increased levels of endothelin, hypercoagulability and stimulation of the renin angiotensin system. OSA, hypertension and obesity often coexist and interact, sharing multiple pathophysiological mechanisms and cardiovascular consequences. Effective treatment of OSA may attenuate neural and humoral abnormalities in circulatory control, improve blood pressure control and conceivably reduce the risk of future cardiovascular events. CONCLUSION: Patients with OSA are at increased risk for cardiovascular disease. OSA should be considered in the differential diagnosis of hypertensive patients who are obese. In particular, OSA should be excluded in patients with hypertension resistant to conventional drug therapy.

Chrostowska M, Szczech R, Narkiewicz K. · Department of Hypertension and Diabetology, Medical University of Gdańsk, Gdańsk, Poland. · Curr Opin Nephrol Hypertens. · Pubmed #16914960 No free full text.

Abstract: PURPOSE OF REVIEW: Obesity is becoming recognized as one of the most important risk factors for the development of hypertension. The purpose of the review is to examine the latest evidence linking hypertension to obesity, summarize the benefits of weight reduction and present results of recent clinical trials evaluating antihypertensive treatment in obese patients. RECENT FINDINGS: Adipose tissue has been directly implicated in the pathogenesis of hypertension. Obesity has been associated with unequivocal changes in cardiovascular structure and function. In contrast to earlier studies, several recent trials included overweight and obese patients. Evidence of potential benefits of angiotensin blockade in the management of obesity hypertension is growing. Hypertension management in obese individuals is complicated by poorer response to treatment, and the increased need for multiple medications. It is important to consider obstructive sleep apnea in obese patients with resistant hypertension. SUMMARY: Several new lines of evidence suggest that drugs blocking the renin-angiotensin system might be considered as first-line therapy of obesity-related hypertension. Recent progress in understanding the mechanisms of obesity and associated disease processes might lead to development of novel therapeutic strategies. Further research in this area holds great promise for prevention of obesity-related cardiovascular disease.

Narkiewicz K. · Department of Hypertension and Diabetology, Medical University of Gdañsk, Debinki 7c, 80-952 Gdañsk, Poland. · Obes Rev. · Pubmed #16629872 No free full text.

Abstract: Cardiovascular risk in a patient with obesity hypertension increases with the extent of risk factor clustering. It is therefore important to determine the global risk of a patient with hypertension rather than to focus solely on blood pressure. Every hypertensive should be screened for other than blood pressure risk factors, target organ damage and concomitant diseases or accompanying clinical conditions. Assessment of blood pressure and target organ damage might be more difficult in obese hypertensives than in normal-weight patients. Intensive lifestyle interventions can reduce weight, and decrease blood pressure and cardiovascular risk in obese hypertensive patients. Current guidelines do not provide specific recommendation for pharmacological management of the hypertensive patients with obesity. Recent trials have consistently shown that therapy involving beta-blockers and diuretics may induce more new-onset diabetes compared with other combination therapies. Several lines of evidence suggest that anti-hypertensive agents that block the renin-angiotensin system may be especially beneficial in treating obese hypertensive patients. Hypertension management in obese individuals is complicated by poorer response to treatment, and the increased need for multiple medications. It is important to consider obstructive sleep apnoea in the differential diagnosis of hypertensive patients who respond poorly to combination therapy with anti-hypertensive medications.

Narkiewicz K, Somers VK. · Department of Hypertension and Diabetology, Medical University of Gdańsk, Debinki, Poland. · Acta Physiol Scand. · Pubmed #12609010 No free full text.

Abstract: The mechanisms underlying the link between obstructive sleep apnoea (OSA) and cardiovascular disease are not completely established. However, there is increasing evidence that autonomic mechanisms are implicated. A number of studies have consistently shown that patients with OSA have high levels of sympathetic nerve traffic. During sleep, repetitive episodes of hypoxia, hypercapnia and obstructive apnoea act through chemoreceptor reflexes and other mechanisms to increase sympathetic drive. Remarkably, the high sympathetic drive is present even during daytime wakefulness when subjects are breathing normally and no evidence of hypoxia or chemoreflex activation is apparent. Several neural and humoral mechanisms may contribute to maintenance of higher sympathetic activity and blood pressure. These mechanisms include chemoreflex and baroreflex dysfunction, altered cardiovascular variability, vasoconstrictor effects of nocturnal endothelin release and endothelial dysfunction. Long-term continuous positive airway pressure treatment decreases muscle sympathetic nerve activity in OSA patients. The vast majority of OSA patients remain undiagnosed. Unrecognized OSA may contribute, in part, to the metabolic and cardiovascular derangements that are thought to be linked to obesity, and to the association between obesity and cardiovascular risk. Furthermore, acting through sympathetic neural mechanisms, OSA may contribute to or augment elevated levels of blood pressure in a large proportion of the hypertensive patient population.

Kara T, Narkiewicz K, Somers VK. · Mayo Clinic, Rochester, MN 55905, USA. · Acta Physiol Scand. · Pubmed #12609009 No free full text.

Abstract: The chemoreflexes are important modulators of sympathetic activation. The peripheral chemoreceptors located in the carotid bodies respond primarily to hypoxaemia. Central chemoreceptors located in the region of the brainstem respond to hypercapnia. Activation of either the hypoxic or hypercapnic chemoreflex elicits both hyperventilation and sympathetic activation. During apnoea, when the inhibitory influence of stretch of the pulmonary afferents is eliminated, there is a potentiation of the sympathetic response to both hypoxia and hypercapnia. This inhibitory influence of the pulmonary afferents is more marked on the sympathetic response to peripheral compared with central chemoreceptor activation. The arterial baroreflexes also have a powerful inhibitory influence on the chemoreflexes. This inhibition is again more marked with respect to the peripheral compared with central chemoreflexes. In patients with hypertension, there is a marked increase in the sympathetic and ventilatory response to hypoxaemia. During apnoea, with elimination of the inhibitory influence of breathing, the sympathetic response in untreated mild hypertensive patients is strikingly greater than that seen in matched normotensive controls. This potentiated peripheral chemoreflex sensitivity in hypertension may be explained in part by impaired baroreflex function in these patients. Enhanced peripheral chemoreflex sensitivity is also evident in patients with obstructive sleep apnoea. This peripheral chemoreflex enhancement is not explained by obesity, as obese individuals have a selective potentiation of the central chemoreceptors with peripheral chemoreflex responses similar to those seen in lean controls. Increased sensitivity to hypoxaemia has important implications in patients with obstructive sleep apnoea who experience repetitive and severe hypoxaemic stress. Tonic activation of the chemoreflex may also contribute to the high levels of sympathetic activity evident even during normoxic daytime wakefulness in sleep apnoea patients. Administration of 100% oxygen in patients with sleep apnoea results in reductions in heart rate, blood pressure and central sympathetic outflow. In patients with heart failure, the central chemoreflex response to hypercapnia is markedly and selectively enhanced. This increased central chemoreflex sensitivity may contribute to the development of central sleep apnoea in heart failure patients. Administration of 100% oxygen does not lower sympathetic activity in patients with heart failure, providing further evidence against any peripheral chemoreflex potentiation. The peripheral and central chemoreflexes have powerful effects on sympathetic activity in both health and disease and may contribute importantly to disease pathophysiology, particularly in conditions such as hypertension, obstructive sleep apnoea and heart failure.

Narkiewicz K, Somers VK. · CV Division, Department of Internal Medicine, University of Iowa College of Medicine, 200 Hawkins Drive, Iowa City, IA 52242, USA. · Curr Hypertens Rep. · Pubmed #10981077 No free full text.

Abstract: Abnormalities in neural circulatory control may contribute importantly to the hypertensive state. The sympathetic nervous system in particular is a key mechanism for increasing blood pressure. Patients with obstructive sleep apnea have increased sympathetic activity. Obesity or other coexisting disease states do not explain the heightened sympathetic drive. This review examines the evidence linking sleep apnea with hypertension and the possible role of excessive sympathetic drive as a mediator of higher blood pressure in sleep apnea. Abnormalities in reflex circulatory control that could act to increase sympathetic activity in sleep apnea are also discussed.

Schlaich MP, Grassi G, Lambert GW, Straznicky N, Esler MD, Dixon J, Lambert EA, Redon J, Narkiewicz K, Jordan J, Anonymous00069, Anonymous00070. · Neurovascular Hypertension and Kidney Disease Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, VIC, Australia. · J Hypertens. · Pubmed #19155773 No free full text.

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Windak A, Gryglewska B, Tomasik T, Narkiewicz K, Grodzicki T. · Department of Internal Medicine and Gerontology, Jagiellonian University Medical College, Kraków, Poland. · Med Decis Making. · Pubmed #18936294 No free full text.

Abstract: OBJECTIVE: The aim of this study was to assess the advice about lifestyle changes that general practitioners (GPs) gave hypertensive patients with different levels of cardiovascular risk. DESIGN: and METHODS: A stratified sample of primary health care physicians in Poland completed a questionnaire consisting of 8 case vignettes that differed with regard to 3 major variables: 1) the level of blood pressure (high-normal blood pressure or grade 2 hypertension), 2) the presence of selected risk factors such as smoking and obesity, and 3) diabetes mellitus. The case vignettes were followed by a series of open questions. RESULTS: The response rate was 65% (125/192 selected physicians responded). The mean age was 45.2 +/- 8.1 years, and the average length of professional experience in primary care was 14.7 +/- 9.3 years. For 1000 potential clinical decisions considered, all expected pieces of advice were given in 18.3% of situations, whereas in 11.5%, no advice concerning nonpharmacological treatment was provided. In 70.2% of situations, Polish primary health physicians gave incomplete advice. The average percentage of expected advice in all cases was 57.2% +/- 30.8%. The presence of hypertension along with other risk factors of cardiovascular disease was associated with better quality advice (P < 0.001), but the coexistence of diabetes mellitus had opposite consequences (P<0.001). CONCLUSIONS: Despite the existence of well-known guidelines for the treatment of hypertension in Poland, GPs rarely give complete lifestyle advice, particularly for patients with cardiovascular risk due to high-normal blood pressure and diabetes.

Rutkowski M, Zdrojewski T, Bandosz P, Wierucki L, Piwoński J, Piwońska A, Narkiewicz K, Opolski G, Drygas W, Korewicki J, Wyrzykowski B. · Medical University, Gdańsk, Poland. · Kardiol Pol. · Pubmed #17577845 links to  free full text

Abstract: BACKGROUND: Cardiovascular diseases are the most common cause of mortality in Poland. To improve the situation in this area, a national cardiovascular preventive project is necessary, and it can be done by close cooperation between medical and political agencies. AIM: To present the current epidemiological situation in Poland to political and key opinion leaders and also to assess individual cardiovascular risk among Members of Polish Parliament. METHODS: The Project was carried out on 23-24 May 2006 in the residence of the Polish Parliament. Anthropometric, blood pressure and cholesterol measurements and a short questionnaire were performed. RESULTS: Survey and educational programme were carried out on 310 out of 460 Members of the Polish Parliament (females 59, males 251). Awareness of one's own blood pressure was declared by 70% of subjects, 39% declared earlier detected arterial hypertension, 21% had new detected elevated blood pressure, 31% declared earlier detected elevated cholesterol level and 32% had new detected elevated cholesterol level. Obesity was found in 40%, smoking was declared by 16.5%. The results were compared with those obtained in corresponding age-groups in the general population. CONCLUSIONS: 1. The results of screening survey in the Polish Parliament in 2006 indicate that, in comparison with nationwide adult population and Parliament Members examined in the year of 2000, present Parliament Members are more often diagnosed with obesity. However, they present with a better awareness of their own blood pressure and better control of arterial hypertension, as well as much lower percentage of those who admit smoking cigarettes. 2. Drawing Parliament Members attention to the problem of high prevalence and insufficient control of cardiovascular risk factors should result in positive outcome of future legislation process and make the battle with the epidemic of heart attacks and strokes in Poland more successful.

Narkiewicz K. · No affiliation provided · Herz. · Pubmed #12608390 No free full text.

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Phillips BG, Kato M, Narkiewicz K, Choe I, Somers VK. · Division of Clinical and Administrative Pharmacy, College of Pharmacy, University of Iowa, Iowa City, Iowa 52242, USA. · Am J Physiol Heart Circ Physiol. · Pubmed #10899061 links to  free full text

Abstract: Patients with obstructive sleep apnea (OSA) are frequently obese and are predisposed to weight gain. They also have heightened sympathetic drive. We reasoned that noradrenergic activation of beta(3)-receptors on adipocytes would inhibit leptin production, predisposing to obesity in sleep apnea. We therefore tested the hypothesis that obesity and predisposition to weight gain in OSA are associated with low levels of plasma leptin. We prospectively studied 32 male patients (43 +/- 2 yr) with OSA who were newly diagnosed and never treated and who were free of any other diseases. Control measurements were obtained from 32 similarly obese closely matched male subjects (38 +/- 2 yr). Leptin levels were 13.7 +/- 1.3 and 9.2 +/- 1.2 ng/ml in patients with OSA and controls, respectively (P = 0.02). Weight gain over the year before diagnosis was 5.2 +/- 1.7 and 0.5 +/- 0.9 kg in sleep apnea patients and similarly obese control subjects, respectively (P = 0.04). Muscle sympathetic activity was 46 +/- 4 and 30 +/- 4 bursts/min in patients with OSA (n = 16) and control subjects (n = 18), respectively (P = 0.01). Plasma leptin levels are elevated in newly diagnosed otherwise healthy patients with untreated sleep apnea beyond the levels seen in similarly obese control subjects without sleep apnea. Higher leptin levels in OSA, independent of body fat content, suggest that OSA is associated with resistance to the weight-reducing effects of leptin.

Phillips BG, Hisel TM, Kato M, Pesek CA, Dyken ME, Narkiewicz K, Somers VK. · Division of Clinical and Administrative Pharmacy, University of Iowa College of Pharmacy, Iowa City 52242, USA. · J Hypertens. · Pubmed #10489107 No free full text.

Abstract: OBJECTIVE: Patients with obstructive sleep apnea are often obese. Obesity may contribute to both sleep apnea itself and to the cardiovascular risk associated with sleep apnea. Weight loss in obese patients with sleep apnea may alleviate symptoms and decrease the severity of sleep apnea. Whether patients with obstructive sleep apnea are indeed predisposed to recent weight gain, as compared with similarly obese subjects without sleep apnea, is not known. PATIENTS AND METHODS: We compared 1-year weight histories in 53 male and female patients newly diagnosed with obstructive sleep apnea, compared with 24 controls matched for gender, age, body mass index, and percent body fat. Sleep apnea patients had never been treated. Control subjects were proven to be free of sleep-disordered breathing by overnight polysomnography. RESULTS: Patients with obstructive sleep apnea (n = 53) had a significant recent weight gain of 7.4 +/- 1.5 kg compared with a weight loss of 0.5 +/- 1.7 kg (P = 0.001) in similarly obese controls (n = 24). Male patients with obstructive sleep apnea (n = 28) had a history of significant weight gain (6.8 +/- 2.3 kg) over the year preceding the study compared with male control subjects (n = 13), in whom average weight fell by 0.58 +/- 2.4 kg (P = 0.03). Female patients (n = 25) with obstructive sleep apnea had an 8.0 +/- 1.9 kg weight gain compared with female controls (n = 11) who had a history of weight loss of 0.46 +/- 2.6 kg (P = 0.02). CONCLUSION: These findings support the concept that patients with obstructive sleep apnea may be susceptible to increasing obesity in the period preceding the diagnosis of obstructive sleep apnea.

Narkiewicz K, Kato M, Pesek CA, Somers VK. · Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, USA. · Hypertension. · Pubmed #10334803 links to  free full text

Abstract: The chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function. Obesity is associated with an increased risk of alveolar hypoventilation and carbon dioxide retention, suggesting that abnormalities in chemoreflex control mechanisms may be implicated. We tested the hypothesis that chemoreflex function is altered in obesity. We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypercapnia, hypoxia, and the cold pressor test in 14 obese subjects and 14 normal-weight subjects matched for age and gender. During hypercapnia, the increase in minute ventilation was significantly greater in obese subjects (7.0+/-0.3 L/min) than in normal-weight subjects (3.3+/-1.1 L/min; P=0.03). Despite higher minute ventilation during hypercapnia in obese subjects, the increase in muscle sympathetic nerve activity was similar in obese and normal-weight subjects. When the inhibitory influence of breathing during hypercapnia was eliminated by apnea, the increase in sympathetic nerve activity in obese subjects (99+/-16%) was greater than in normal-weight subjects (44+/-16%; P=0.02). The magnitude of the ventilatory and autonomic responses to hypoxia and the cold pressor test was similar in obese and normal-weight subjects. We conclude that chemoreflex responses to hypercapnia are potentiated in eucapnic obese subjects. In contrast, responses to hypoxia and to the excitatory cold pressor stimulus in obese subjects are similar to those in normal-weight subjects. Thus, obesity is characterized by selective potentiation of central chemoreflex sensitivity.

Narkiewicz K, Szczech R, Winnicki M, Chrostowska M, Pawlowski R, Lysiak-Szydlowska W, Choe I, Kato M, Sivitz WI, Krupa-Wojciechowska B, Somers VK. · Institute of Internal Medicine, Medical University of Gdansk, Poland. · J Hypertens. · Pubmed #10100090 No free full text.

Abstract: OBJECTIVE: To examine the influence of genetic factors on plasma leptin levels. SUBJECTS AND METHODS: We measured plasma leptin levels, body mass index and body fat distribution in healthy young female monozygotic (n = 19) and dizygotic (n = 14) twins. The twin zygosity was verified by determination of short tandem repeat and amplified fragment length polymorphism systems. The genetic analysis included analysis of variance-based and maximum likelihood-based methods. RESULTS: Plasma leptin levels were correlated significantly with body mass index (r = 0.59, P < 0.001), waist circumference (r = 0.54, P < 0.001) and hip circumference (r = 0.63, P < 0.001), but not with age (r = -0.17) or the waist:hip ratio (r = 0.02). The heritability estimates derived from intraclass correlations were significant for body mass index (P = 0.001), waist circumference (P = 0.004), hip circumference (P = 0.01) and plasma leptin levels (P = 0.005), but not for the waist:hip ratio (P = 0.22). In the maximum likelihood-based path analysis, heritability was estimated at 79% for body mass index and at 73% for plasma leptin levels. After adjustment for body mass index, the heritability estimate for leptin levels from the model-fitting approach was 55%. CONCLUSIONS: Genetic factors are major determinants of plasma leptin levels in humans and may account for as much as half of the variance in leptin levels.