Peter M Nilsson

Skåne University Hospital, Malmö, Skåne, Sweden

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Publications (740)3397.19 Total impact

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    ABSTRACT: Experimental studies have suggested possible protective effects of dimethylglycine (DMG) on glucose metabolism. DMG is degraded to glycine through a DMG-dehydrogenase (DMGDH)-catalyzed reaction and this is the only known pathway for the breakdown of DMG in mammals. In this study we aimed to identify the strongest genetic determinant of circulating DMG concentration and to investigate its associations with metabolic traits and incident diabetes. In the cohort with full metabolomics data (n=709), low plasma levels of DMG were significantly associated with higher blood glucose levels (p=3.9E-4). In the genome-wide association study (GWAS) of the discovery cohort (n=5,205) the strongest genetic signal of plasma DMG was conferred by rs2431332 at the DMGDH-locus where the major allele was associated with lower DMG levels (p=2.5E-15). The same genetic variant (major allele of rs2431332), was also significantly associated with higher plasma insulin (p=0.019), increased insulin resistance (HOMA-IR) (p=0.019), as well as increased risk of incident diabetes (p=0.001) in the pooled analysis of the discovery cohort together with the two replication cohorts ((n=20,698) and (N=7,995). These data are consistent with a possible causal role of DMG deficiency in diabetes development and encourages for future studies examining if inhibition of DMG-dehydrogenase, or alternatively supplementation of DMG, might prove useful for the treatment/prevention of diabetes. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
    Diabetes 03/2015; DOI:10.2337/db14-1863 · 7.90 Impact Factor
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    ABSTRACT: Previous studies of prostate cancer (PCa) risk and anthropometrics (ie, body measurements) were based on single measurements or obtained over limited time spans. To study the association between anthropometrics measured at multiple time points in life and their relation to later diagnosis, metastasis, or death from PCa. This case-control study includes 27 167 Swedish men enrolled in two population-based projects from 1974 to 1996. PCa diagnosis up to December 31, 2006, disease information, gestation time, and anthropometrics at birth, military conscript testing, and adulthood were collected. A total of 1355 PCa cases were matched with 5271 controls. Univariate conditional logistic regression was used to determine whether clinical diagnosis, metastasis, or PCa death was associated with low birth weight (weight <2500g); with small size for gestational age; or with weight, length, or body mass index (BMI) at birth, adolescence (aged 16-22 yr), or early middle age (aged 44-50 yr). Apart from weight at adolescence, which was associated with an increased risk of PCa diagnosis (odds ratio [OR] per 5kg: 1.05; 95% confidence interval [CI], 1.01-1.09; p=0.026), preadulthood measurements were not associated with any PCa end point. Adulthood parameters were not associated with diagnosis. In contrast, weight and BMI at early middle age were significantly associated with metastasis (OR per 5kg: 1.13; 95% CI, 1.06-1.20; p<0.0001, and OR: 1.09; 95% CI, 1.05-1.14; p<0.0001) and death (OR per 5kg: 1.11 (95% CI, 1.03-1.19; p=0.005, and OR: 1.08; 95% CI, 1.03-1.13; p=0.003), respectively. It remains unclear whether these results apply to men of nonwhite origin, to populations with active PCa screening programs, or to countries without socialized health care. The analyses of these large data sets demonstrate that significant effects of body characteristics (with links to metabolic syndrome) measured at early middle age are associated with PCa disease severity, metastatic progression, and outcome. Conversely, measurements at birth and adolescence are not associated with PCa prevalence or outcome. Increased weight and body mass index in adults is associated with a higher risk of prostate cancer metastasis and death. Copyright © 2015 European Association of Urology. Published by Elsevier B.V. All rights reserved.
    European Urology 03/2015; DOI:10.1016/j.eururo.2015.03.017 · 10.48 Impact Factor
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    ABSTRACT: Do women who have diabetes before menopause have their menopause at an earlier age compared with women without diabetes? Although there was no overall association between diabetes and age at menopause, our study suggests that early-onset diabetes may accelerate menopause. Today, more women of childbearing age are being diagnosed with diabetes, but little is known about the impact of diabetes on reproductive health. We investigated the impact of diabetes on age at natural menopause (ANM) in 258 898 women from the European Prospective Investigation into Cancer and Nutrition (EPIC), enrolled between 1992 and 2000. Determinant and outcome information was obtained through questionnaires. Time-dependent Cox regression analyses were used to estimate the associations of diabetes and age at diabetes diagnosis with ANM, stratified by center and adjusted for age, smoking, reproductive and diabetes risk factors and with age from birth to menopause or censoring as the underlying time scale. Overall, no association between diabetes and ANM was found (hazard ratio (HR) = 0.94; 95% confidence interval (CI) 0.89-1.01). However, women with diabetes before the age of 20 years had an earlier menopause (10-20 years: HR = 1.43; 95% CI 1.02-2.01, <10 years: HR = 1.59; 95% CI 1.03-2.43) compared with non-diabetic women, whereas women with diabetes at age 50 years and older had a later menopause (HR = 0.81; 95% CI 0.70-0.95). None of the other age groups were associated with ANM. Strengths of the study include the large sample size and the broad set of potential confounders measured. However, results may have been underestimated due to survival bias. We cannot be sure about the sequence of the events in women with a late age at diabetes, as both events then occur in a short period. We could not distinguish between type 1 and type 2 diabetes. Based on the literature, an accelerating effect of early-onset diabetes on ANM might be plausible. A delaying effect of late-onset diabetes on ANM has not been reported before, and is not in agreement with recent studies suggesting the opposite association. The coordination of EPIC is financially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by Danish Cancer Society (Denmark); Ligue Contre le Cancer, Institut Gustave Roussy, Mutuelle Générale de l'Education Nationale, Institut National de la Santé et de la Recherche Médicale (INSERM) (France); German Cancer Aid, German Cancer Research Center (DKFZ) and Federal Ministry of Education and Research (BMMF) (Germany); Ministry of Health and Social Solidarity, Stavros Niarchos Foundation and Hellenic Health Foundation (Greece); Italian Association for Research on Cancer (AIRC) and National Research Council (Italy); Dutch Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund (WCRF), Statistics Netherlands (The Netherlands); ERC-2009-AdG 232997 and Nordforsk, Nordic Centre of Excellence programme on Food, Nutrition and Health (Norway); Health Research Fund (FIS), Regional Governments of Andalucía, Asturias, Basque Country, Murcia (no. 6236) and Navarra, ISCIII RETIC (RD06/0020) (Spain); Swedish Cancer Society, Swedish Scientific Council and Regional Government of Skåne and Västerbotten (Sweden); Cancer Research UK, Medical Research Council, Stroke Association, British Heart Foundation, Department of Health, Food Standards Agency, and Wellcome Trust (UK). None of the authors reported a conflict of interest. © The Author 2015. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
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    ABSTRACT: To examine whether increasing fasting plasma glucose (FPG) levels were associated with worsening left ventricular (LV) diastolic function, independently of LV mass index (LVMI) in elderly, otherwise healthy subjects. We tested cross-sectional associations between echocardiographically determined averaged E/é ratio/diastolic function, LVMI, cardiovascular risk factors, and FPG categorized as normal (NFG), impaired (IFG), and new-onset diabetes mellitus (DM), in 483 men and 208 women aged 56-79years without overt cardiovascular disease, who received no cardiovascular, anti-diabetic, or lipid-lowering drugs and had a preserved LV ejection fraction >50%. Median E/é was significantly higher among subjects with diabetes than those without (8 vs. 7; p=0.03), as was the prevalence of grade 2 or 3 diastolic dysfunction (25% vs. 16%; p=0.02). E/é and diastolic function were significantly associated with LVMI (p≤0.002), but not FPG category, on multivariable analysis. However, interaction analyses revealed that increasing LVMI was primarily associated with worsening diastolic function (higher E/é) in subjects with FPG>6mmol/L (β=0.005 for IFG and DM vs. 0.001 for NFG; p=0.02), whereas increasing systolic blood pressure was primarily associated with worsening diastolic function (higher E/é) in subjects with FPG≤6.9mmol/L (β=0.005 for NFG and 0.003 for IFG vs. -0.001 for DM; p=0.001). Diastolic dysfunction was significantly more prevalent among patients with DM than those without. The importance of LVMI increased, but the importance of systolic blood pressure decreased with higher FPG category. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
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    ABSTRACT: Current cardiovascular risk scores do not include obesity or fat distribution as independent factors, and may underestimate risk in obese individuals. Assessment of early vascular ageing (EVA) biomarkers including arterial stiffness, central blood pressure, carotid intima-media thickness and flow-mediated vasodilation may help to refine risk assessment in obese individuals in whom traditional cardiovascular risk scores and factors suggest no need for specific medical attention. A number of issues need to be addressed before this approach is ready for translation into routine clinical practice. Methodologies for measurements of vascular markers need to be further standardized and less operator-dependent. The utility of these nontraditional risk factors will also need to be proven in sufficiently large and properly designed interventional studies. Indeed, published studies on vascular markers in obesity and weight loss vary in quality and study design, are sometimes conducted in small populations, use a variety of differing methodologies and study differing vascular beds. Finally, current vascular measurements are still crude and may not be sufficient to cover the different aspects of EVA in obesity.
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    ABSTRACT: Observational studies have reported different effects of adiposity on cardiovascular risk factors across age and sex. Since cardiovascular risk factors are enriched in obese individuals, it has not been easy to dissect the effects of adiposity from those of other risk factors. We used a Mendelian randomization approach, applying a set of 32 genetic markers to estimate the causal effect of adiposity on blood pressure, glycemic indices, circulating lipid levels, and markers of inflammation and liver disease in up to 67,553 individuals. All analyses were stratified by age (cutoff 55 years of age) and sex. The genetic score was associated with BMI in both nonstratified analysis (P = 2.8 × 10(-107)) and stratified analyses (all P < 3.3 × 10(-30)). We found evidence of a causal effect of adiposity on blood pressure, and fasting levels of insulin, C-reactive protein, interleukin-6, HDL cholesterol, and triglycerides in a nonstratified analysis and in the <55-year stratum. Further, we found evidence of a smaller causal effect on total cholesterol (P for difference = 0.015) in the ≥55-year stratum than in the <55-year stratum, a finding that could be explained by biology, survival bias, or differential medication. In conclusion, this study extends previous knowledge of the effects of adiposity by providing sex- and age-specific causal estimates on cardiovascular risk factors. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
    Diabetes 02/2015; DOI:10.2337/db14-0988 · 7.90 Impact Factor
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    ABSTRACT: To evaluate the progression of carotid intima-media thickness (IMT) in the common carotid artery (CCA) and the bifurcation over a mean follow-up of 16 years in relation to cardiovascular risk factors. The study population included 3426 middle-aged Swedish men and women participating in the 1991-1994 (baseline) and the 2007-2012 (re-examination) investigation of the cardiovascular cohort of the Malmö Diet and Cancer Study (MDCS). There were differences in risk factor patterns in arterial segments in that diabetes and male sex were associated with the progression of IMT in the bifurcation, but not in the CCA, and high-density lipoprotein cholesterol (HDL) was associated with the progression of IMT in the CCA, but not in the bifurcation. Favourable changes in systolic blood pressure (SBP), low-density lipoprotein cholesterol (LDL) and HDL during follow-up decreased the IMT progression rate in the CCA. There was a cumulative relationship between traditional cardiovascular risk factors (i.e., regular smoking, LDL/HDL-ratio ≥ 3, hypertension) and IMT progression rates. The odds ratio (OR) of high IMT CCA progression rate (>75th percentile) was 1.0 (reference), 1.4 (95% CI: 1.1, 1.7), 1.7 (95% CI: 1.3, 2.2) and 2.1 (95% CI: 1.4, 3.1), respectively, for individuals with none, one, two, and three risk factors. There were differences in the associations between risk factors and progression rate in different arterial segments. Favourable changes in SBP and lipids during the follow-up period were associated with reduced IMT progression rates in the CCA. Copyright © 2015 The Authors. Published by Elsevier Ireland Ltd.. All rights reserved.
    Atherosclerosis 01/2015; 239(2):615-621. DOI:10.1016/j.atherosclerosis.2015.01.030 · 3.71 Impact Factor
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    ABSTRACT: Increased blood pressure and high dietary salt are leading risks for death and disability globally. Reducing the burden of both health risks are United Nations' targets for reducing noncommunicable disease. Nongovernmental organizations and individuals can assist by ensuring widespread dissemination of the best available facts and recommended interventions for both health risks. Simple but impactful fact sheets can be useful for informing the public, healthcare professionals, and policy makers. The World Hypertension League has developed fact sheets on dietary salt and hypertension but in many circumstances the greatest impact would be obtained from national-level fact sheets. This manuscript provides instructions and a template for developing fact sheets based on the Global Burden of Disease study and national survey data.
    Journal of Clinical Hypertension 01/2015; DOI:10.1111/jch.12479 · 2.36 Impact Factor
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    ABSTRACT: Arterial stiffness plays a fundamental role in the development of hypertension and is a risk factor for both cardiovascular disease and mortality. The stiffening that occurs with increasing age has, in numerous cross-sectional studies, been shown to be associated with several cardiovascular risk factors. This observational study aims to characterize the predictive and cross-sectional markers focusing on the non-hemodynamic component of arterial stiffness. In all, 2679 men and women from Malmö, Sweden, were examined at baseline during 1991-1994, and again at follow-up during 2007-2012 (mean age 72 years, 38% men). Follow-up examination included measurement of arterial stiffness by carotid-femoral pulse wave velocity (c-fPWV), after a mean period of 17 years. The associations between c-fPWV and risk markers were calculated with multiple linear regression. The results indicated that for both sexes, waist circumference (β = 0.17, P < 0.001), fasting glucose (β = 0.13, P < 0.001), Homeostatic Model Assessment - Insulin Resistance (β = 0.10, P < 0.001), triglycerides (β = 0.10, P < 0.001), and high-density lipoprotein cholesterol (β = -0.08, P < 0.001) were all predictors of cfPWV adjusted for mean arterial pressure and heart rate, as well as for classical cardiovascular risk factors and drug treatment. There were no associations between baseline or follow-up low-density lipoprotein cholesterol, smoking, or eGFR and c-fPWV. The non-hemodynamic cluster of risk markers and predictors of arterial stiffness in a middle-aged population includes abdominal obesity, hyperglycemia, and dyslipidemia, but not smoking and low-density lipoprotein cholesterol. This pattern existed in both sexes.This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License, where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially. http://creativecommons.org/licenses/by-nc-nd/4.0.
    Journal of Hypertension 01/2015; DOI:10.1097/HJH.0000000000000520 · 4.22 Impact Factor
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    ABSTRACT: To describe healthcare resource use patterns and estimate healthcare costs of newly diagnosed Type 2 diabetes mellitus (T2DM) patients in Sweden.
    Primary Care Diabetes 01/2015; DOI:10.1016/j.pcd.2015.01.001 · 1.29 Impact Factor
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    ABSTRACT: Background Obesity, type 2 diabetes and atrial fibrillation (AF) are closely associated, but the underlying mechanisms are not fully understood. We aimed to explore associations between body mass index (BMI) or weight change with risk of AF in patients with type 2 diabetes.MethodsA total of 7,169 participations with newly diagnosed type 2 diabetes were stratified according to baseline BMI, and after a second BMI measurement within 18 months, further grouped according to relative weight change as ¿weight gain¿ (>1 BMI unit), ¿stable weight¿ (+/¿ 1 BMI unit) and ¿weight loss¿ (<1 BMI unit). The mean follow-up period was 4.6 years, and the risk of AF was estimated using adjusted Cox regression models.ResultsAverage age at diabetes diagnosis was 60 years and the patients were slightly obese (mean BMI 30.2 kg/m2). During follow-up, 287 patients developed incident AF, and those with overweight or obesity at baseline had 1.9-fold and 2.9-fold higher risk of AF, respectively, than those with normal BMI. The 14% of the patients with subsequent weight gain had 1.5-fold risk of AF compared with those with stable weight or weight loss.Conclusions In patients with newly diagnosed type 2 diabetes, baseline overweight and obesity, as well as modest weight increase during the first 18 months after diagnosis, were associated with a substantially increased risk of incident AF. Patients with type 2 diabetes may benefit from efforts to prevent weight gain in order to reduce the risk of incident AF.Trial registrationClinicalTrials.gov: NCT01121315.
    Cardiovascular Diabetology 01/2015; 14(1):5. DOI:10.1186/s12933-014-0170-3 · 3.71 Impact Factor
  • Peter M Nilsson
    BMJ Clinical Research 12/2014; 349:g6843. DOI:10.1136/bmj.g6843 · 14.09 Impact Factor
  • Artery Research 12/2014; 8(4). DOI:10.1016/j.artres.2014.09.078
  • Journal of Clinical Hypertension 12/2014; 17(1). DOI:10.1111/jch.12469 · 2.36 Impact Factor
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    ABSTRACT: Aim To examine the association of sialic acid (SA) with first recorded diabetes mellitus-related hospitalization. Methods From a population-based study in Värmland, Sweden, between 1962 and 1965, 87,035 men and women were selected and followed for first recorded diabetes-related hospitalization until 2005. The association of SA was calculated and stratified for gender by Cox's proportional hazards models. Adjustments were made for conventional risk factors and socioeconomic status. Association analyses were made for comparisons between SA-levels above and below median. Results The mean age was 47.2 (SD 13.0) years and the total numbers of incident diabetes-related hospitalizations in men and women were 3445 and 3273, respectively. Hazard ratios per one standard deviation of SA were 1.12 (95% CI: 1.08–1.17, p < 0.0001) in men and 1.17 (95% CI: 1.13–1.22, p < 0.0001) in women. Interaction analyses indicated a relatively higher SA-associated risk in women than in men with above median SA levels. Conclusions In this large population-based cohort followed for more than 40 years, elevated SA, as a marker of systemic inflammation, was independently associated with risk of diabetes and diabetes-related hospitalizations.
    Primary Care Diabetes 12/2014; 8(4). DOI:10.1016/j.pcd.2014.06.002 · 1.29 Impact Factor
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    ABSTRACT: To estimate cardiovascular disease (CVD) mortality in relation to obesity and gender. Data from 11 prospective cohorts from four European countries including 23 629 men and 21 965 women, aged 24 to 99 years, with a median follow-up of 7.9 years were analyzed. Hazards ratios (HR) for CVD mortality in relation to baseline body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR) and waist-to-height ratio (WHtR) were estimated using Cox proportional hazards models with age as the timescale. Men had higher CVD mortality than women in all four BMI categories (<25.0, 25.0-29.9, 30.0-34.9 and ≥35.0 kg/m(2)). Compared with the lowest BMI category in women, multivariable adjusted HRs (95% confidence intervals) for higher BMI categories are 1.0 (0.8-1.4), 1.6 (1.1-2.1) and 2.8 (2.0-3.8) in women and 2.8 (2.2-3.6), 3.1 (2.5-3.9), 3.8 (2.9-4.9) and 5.4 (3.8-7.7) in men, respectively. Similar findings were observed for abdominal obesity defined by WC, WHR or WHtR. The gender difference was slightly smaller in obese than in non-obese individuals; but the interaction was statistically significant only between gender and WC (p = 0.02), and WHtR (p = 0.01). None of the interaction terms was significant among non-diabetic individuals. Men had higher CVD mortality than women across categories of anthropometric measures of obesity. The gender difference was attenuated in obese individuals, which warrants further investigation.
    Cardiovascular Diabetology 12/2014; 13(1):144. DOI:10.1186/s12933-014-0144-5 · 3.71 Impact Factor
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    ABSTRACT: Background/Objectives:Diets high in saturated and trans fat and low in unsaturated fat may increase type 2 diabetes (T2D) risk, but studies on foods high in fat per unit weight are sparse. We assessed whether the intake of vegetable oil, butter, margarine, nuts and seeds and cakes and cookies is related to incident T2D.Subjects/Methods:A case-cohort study was conducted, nested within eight countries of the European Prospective Investigation into Cancer (EPIC), with 12 403 incident T2D cases and a subcohort of 16 835 people, identified from a cohort of 340 234 people. Diet was assessed at baseline (1991-1999) by country-specific questionnaires. Country-specific hazard ratios (HRs) across four categories of fatty foods (nonconsumers and tertiles among consumers) were combined with random-effects meta-analysis.Results:After adjustment not including body mass index (BMI), nonconsumers of butter, nuts and seeds and cakes and cookies were at higher T2D risk compared with the middle tertile of consumption. Among consumers, cakes and cookies were inversely related to T2D (HRs across increasing tertiles 1.14, 1.00 and 0.92, respectively; P-trend <0.0001). All these associations attenuated upon adjustment for BMI, except the higher risk of nonconsumers of cakes and cookies (HR 1.57). Higher consumption of margarine became positively associated after BMI adjustment (HRs across increasing consumption tertiles: 0.93, 1.00 and 1.12; P-trend 0.03). Within consumers, vegetable oil, butter and nuts and seeds were unrelated to T2D.Conclusions:Fatty foods were generally not associated with T2D, apart from weak positive association for margarine. The higher risk among nonconsumers of cakes and cookies needs further explanation.European Journal of Clinical Nutrition advance online publication, 26 November 2014; doi:10.1038/ejcn.2014.249.
  • Journal of Clinical Hypertension 11/2014; 17(2). DOI:10.1111/jch.12437 · 2.36 Impact Factor
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    ABSTRACT: Background: Arterial stiffness has been hypothesized to contribute to cognitive decline. However, previous studies have reported inconsistent results. The aim of this cross-sectional study was to investigate the association between carotid-femoral pulse wave velocity (cfPWV), a marker of arterial stiffness, and cognitive function. Methods: The study population comprised 2637 individuals from the population-based Malmo "Diet and Cancer Study (mean age 72.1 years, 60.8% women). During the follow-up examinations between 2007 and 2012, cfPWV and results on the a quick test of cognitive speed (AQT) and Mini Mental State Examination (MMSE) cognitive tests were measured. Results: After adjustments for demographics and traditional cardiovascular risk factors, a linear association was found between cfPWV and AQT (B = 0.37; P = 0.039). On the basis of hypothesis that individuals with high cfPWV values have worse cognitive function than can be inferred from a linear association, cfPWV was dichotomized at the 90th percentile (the binary variable denoted cfPWV >13.8). When cfPWV >13.8 was added to the model, the linear association between continuous cfPWV and AQT disappeared (B = -0.08; P = 0.72), but cfPWV >13.8 was highly significant (B = 4.81; P = 0.004). In the adjusted model with MMSE as outcome variable, cfPWV >13.8 also reached a statistically significant effect. Conclusion: Arterial stiffness was inversely associated with cognitive function in a nonlinear fashion, with individuals in the top decentile of cfPWV explaining the association. Results from linear regressions should thus be interpreted with caution because, even when statistical significance is reached, they can be explained by pronounced nonlinearity.
    Alzheimer's and Dementia 11/2014; 32(11):2152-2157. DOI:10.1097/HJH.0000000000000329 · 17.47 Impact Factor

Publication Stats

26k Citations
3,397.19 Total Impact Points

Institutions

  • 2012–2015
    • Skåne University Hospital
      Malmö, Skåne, Sweden
    • University of Oxford
      • Wellcome Trust Centre for Human Genetics
      Oxford, ENG, United Kingdom
    • University Medical Center Utrecht
      • Julius Center for Health Sciences and Primary Care
      Utrecht, Provincie Utrecht, Netherlands
  • 1987–2015
    • Lund University
      • • Department of Clinical Sciences, Malmö
      • • Department of Diagnostic Radiology
      • • Department of Community Health Sciences
      • • Department of Health Sciences
      Lund, Skåne, Sweden
  • 2014
    • Örebro universitet
      Örebro, Örebro, Sweden
    • Danderyds Sjukhus AB
      Tukholma, Stockholm, Sweden
  • 2013
    • European Spallation Source (ESS)
      Lund, Skåne, Sweden
    • Medical Research Council (UK)
      Londinium, England, United Kingdom
    • University of Cambridge
      • Department of Public Health and Primary Care
      Cambridge, England, United Kingdom
  • 2010–2013
    • University of Freiburg
      • Faculty of Mathematics and Physics
      Freiburg, Lower Saxony, Germany
    • Örebro University Hospital
      Örebro, Örebro, Sweden
    • Memorial Sloan-Kettering Cancer Center
      • Epidemiology & Biostatistics Group
      New York City, NY, United States
  • 2011
    • Keele University
      Newcastle-under-Lyme, England, United Kingdom
  • 2010–2011
    • Università di Pisa
      • Department of Physics "E.Fermi"
      Pisa, Tuscany, Italy
  • 2004–2011
    • CERN
      • Physics Department (PH)
      Genève, Geneva, Switzerland
  • 1998–2011
    • Malmö University
      • Department of Cariology
      Malmö, Skåne, Sweden
  • 2008–2010
    • University of Texas at Arlington
      • Department of Physics
      Arlington, TX, United States
    • Karolinska University Hospital
      Tukholma, Stockholm, Sweden
  • 2003–2010
    • Uppsala University
      • Department of Public Health and Caring Sciences
      Uppsala, Uppsala, Sweden
    • Comenius University in Bratislava
      Presburg, Bratislavský, Slovakia
    • Iowa State University
      Ames, Iowa, United States
    • Aarhus University
      Aarhus, Central Jutland, Denmark
  • 1997–2010
    • University of Gothenburg
      • • Institute of Medicine
      • • Occupational Therapy Unit (OT)
      • • Unit of Social Medicine
      Göteborg, Vaestra Goetaland, Sweden
  • 2009
    • University of Valencia
      Valenza, Valencia, Spain
    • Landstinget i Kalmar län
      Kalmar, Kalmar, Sweden
  • 2005–2008
    • Akademiska Sjukhuset
      Uppsala, Uppsala, Sweden
  • 2004–2008
    • Panjab University
      • Department of Physics
      Chandigarh, Chandīgarh, India
  • 2007
    • Justus-Liebig-Universität Gießen
      Gieben, Hesse, Germany
  • 2005–2007
    • Sahlgrenska University Hospital
      • Department of Cardiology
      Goeteborg, Västra Götaland, Sweden
  • 2003–2007
    • Brookhaven National Laboratory
      • Physics Department
      New York City, NY, United States
  • 2006
    • AHEPA University Hospital
      Saloníki, Central Macedonia, Greece
  • 2000–2005
    • Uppsala University Hospital
      • Department of Geriatrics
      Uppsala, Uppsala, Sweden
  • 1999–2003
    • University of Münster
      Muenster, North Rhine-Westphalia, Germany
  • 2002
    • Region Skåne
      Malmö, Skåne, Sweden
    • Academia Sinica
      • Institute of Physics
      Taipei, Taipei, Taiwan
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France
  • 2001–2002
    • Vanderbilt University
      Nashville, Michigan, United States
    • Banaras Hindu University
      • Department of Physics
      Benares, Uttar Pradesh, India