Matthew Knuiman

Matthew Knuiman

Auto-generated profile, based on publicly available information

Matthew Knuiman

School of Population and Global Health, Faculty of Health and Medical Sciences, The University of Western Australia, Perth, Australia

Research Focus & Metrics

Academic Career Length

43Years (1984-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
1 February 2005 in American Journal of Preventive Medicine
Verified
Journal Article
Closed access
BGBillie Giles-Corti
Billie Giles-Corti
MBMelissa H. Broomhall
Melissa H. Broomhall
MKMatthew Knuiman
Matthew Knuiman
CCCatherine Collins
Catherine Collins
KDKate Douglas
Kate Douglas
RDRobert J. Donovan
Robert J. Donovan

1 April 2018 in The Lancet
Verified
Journal Article
Open access
AWAngela M Wood
Angela M Wood
SKStephen Kaptoge
Stephen Kaptoge
ABAdam S Butterworth
Adam S Butterworth
PWPeter Willeit
Peter Willeit
SWSamantha Warnakula
Samantha Warnakula
EGEmerging Risk Factors Collaboration/EPIC-CVD/UK Biobank Alcohol Study Group
Emerging Risk Factors Collaboration/EPIC-CVD/UK Biobank Alcohol Study Group
Low-risk limits recommended for alcohol consumption vary substantially across different national guidelines. To define thresholds associated with lowest risk for all-cause mortality and cardiovascular disease, we studied individual-participant data from 599 912 current drinkers without previous cardiovascular disease. We did a combined analysis of individual-participant data from three large-scale data sources in 19 high-income countries (the Emerging Risk Factors Collaboration, EPIC-CVD, and the UK Biobank). We characterised dose-response associations and calculated hazard ratios (HRs) per 100 g per week of alcohol (12·5 units per week) across 83 prospective studies, adjusting at least for study or centre, age, sex, smoking, and diabetes. To be eligible for the analysis, participants had to have information recorded about their alcohol consumption amount and status (ie, non-drinker vs current drinker), plus age, sex, history of diabetes and smoking status, at least 1 year of follow-up after baseline, and no baseline history of cardiovascular disease. The main analyses focused on current drinkers, whose baseline alcohol consumption was categorised into eight predefined groups according to the amount in grams consumed per week. We assessed alcohol consumption in relation to all-cause mortality, total cardiovascular disease, and several cardiovascular disease subtypes. We corrected HRs for estimated long-term variability in alcohol consumption using 152 640 serial alcohol assessments obtained some years apart (median interval 5·6 years [5th-95th percentile 1·04-13·5]) from 71 011 participants from 37 studies. In the 599 912 current drinkers included in the analysis, we recorded 40 310 deaths and 39 018 incident cardiovascular disease events during 5·4 million person-years of follow-up. For all-cause mortality, we recorded a positive and curvilinear association with the level of alcohol consumption, with the minimum mortality risk around or below 100 g per week. Alcohol consumption was roughly linearly associated with a higher risk of stroke (HR per 100 g per week higher consumption 1·14, 95% CI, 1·10-1·17), coronary disease excluding myocardial infarction (1·06, 1·00-1·11), heart failure (1·09, 1·03-1·15), fatal hypertensive disease (1·24, 1·15-1·33); and fatal aortic aneurysm (1·15, 1·03-1·28). By contrast, increased alcohol consumption was log-linearly associated with a lower risk of myocardial infarction (HR 0·94, 0·91-0·97). In comparison to those who reported drinking >0-≤100 g per week, those who reported drinking >100-≤200 g per week, >200-≤350 g per week, or >350 g per week had lower life expectancy at age 40 years of approximately 6 months, 1-2 years, or 4-5 years, respectively. In current drinkers of alcohol in high-income countries, the threshold for lowest risk of all-cause mortality was about 100 g/week. For cardiovascular disease subtypes other than myocardial infarction, there were no clear risk thresholds below which lower alcohol consumption stopped being associated with lower disease risk. These data support limits for alcohol consumption that are lower than those recommended in most current guidelines. UK Medical Research Council, British Heart Foundation, National Institute for Health Research, European Union Framework 7, and European Research Council.

7 July 2015 in JAMA
Verified
Journal Article
Open access
PDF file
EAEmanuele Di Angelantonio
Emanuele Di Angelantonio
SKStephen Kaptoge
Stephen Kaptoge
DWDavid Wormser
David Wormser
PWPeter Willeit
Peter Willeit
ABAdam S. Butterworth
Adam S. Butterworth
JDJohn Danesh
John Danesh
The prevalence of cardiometabolic multimorbidity (defined herein as a history of ≥2 of the following: diabetes mellitus, stroke, myocardial infarction [MI]) is increasing rapidly.1-3 Considerable evidence exists about the mortality risk of having any 1 of these conditions alone.4-7 However, evidence is sparse about life expectancy among people who have 2 or 3 cardiometabolic conditions concomitantly. Valid estimation of the associations of cardiometabolic multimorbidity with mortality requires comparison of people with multimorbidity with participants within the same cohorts who did not have any of the conditions at baseline. However, few population cohorts have had sufficient power, detail, and longevity to enable such comparisons.8-14

1 May 2002 in Diabetes Care
Verified
Journal Article
Closed access
PDF file
DDDavid Dunstan
David Dunstan
PZPaul Z Zimmet
Paul Z Zimmet
TWTimothy A Welborn
Timothy A Welborn
MCMaximilian P De Courten
Maximilian P De Courten
ACAdrian Cameron
Adrian Cameron
JSJonathan E Shaw
Jonathan E Shaw
OBJECTIVE—To determine the population-based prevalence of diabetes and other categories of glucose intolerance (impaired glucose tolerance [IGT] and impaired fasting glucose [IFG]) in Australia and to compare the prevalence with previous Australian data. RESEARCH DESIGN AND METHODS—A national sample involving 11,247 participants aged ≥25 years living in 42 randomly selected areas from the six states and the Northern Territory were examined in a cross-sectional survey using the 75-g oral glucose tolerance test to assess fasting and 2-h plasma glucose concentrations. The World Health Organization diagnostic criteria were used to determine the prevalence of abnormal glucose tolerance. RESULTS—The prevalence of diabetes in Australia was 8.0% in men and 6.8% in women, and an additional 17.4% of men and 15.4% of women had IGT or IFG. Even in the youngest age group (25–34 years), 5.7% of subjects had abnormal glucose tolerance. The overall diabetes prevalence in Australia was 7.4%, and an additional 16.4% had IGT or IFG. Diabetes prevalence has more than doubled since 1981, and this is only partially explained by changes in age profile and obesity. CONCLUSIONS—Australia has a rapidly rising prevalence of diabetes and other categories of abnormal glucose tolerance. The prevalence of abnormal glucose tolerance in Australia is one of the highest yet reported from a developed nation with a predominantly Europid background.

1 December 2012 in Journal of Environmental Psychology
Verified
Journal Article
Closed access
JFJacinta Francis
Jacinta Francis
BGBillie Giles-Corti
Billie Giles-Corti
LWLisa Wood
Lisa Wood
MKMatthew Knuiman
Matthew Knuiman

15 April 2014 in Journal of Clinical Sleep Medicine
Verified
Journal Article
Closed access
NMNathaniel Marshall
Nathaniel Marshall
KWKeith K.H. Wong
Keith K.H. Wong
SCStewart R.J. Cullen
Stewart R.J. Cullen
MKMatthew W. Knuiman
Matthew W. Knuiman
RGRonald R. Grunstein
Ronald R. Grunstein
To ascertain whether objectively measured obstructive sleep apnea (OSA) independently increases the risk of all cause death, cardiovascular disease (CVD), coronary heart disease (CHD), stroke or cancer. Community-based cohort. 400 residents of the Western Australian town of Busselton. OSA severity was quantified via the respiratory disturbance index (RDI) as measured by a single night recording in November-December 1990 using the MESAM IV device, along with a range of other risk factors. Follow-up for deaths and hospitalizations was ascertained via record linkage to the end of 2010. We had follow-up data in 397 people and then removed those with a previous stroke (n = 4) from the mortality/ CVD/CHD/stroke analyses and those with cancer history from the cancer analyses (n = 7). There were 77 deaths, 103 cardiovascular events (31 strokes, 59 CHD) and 125 incident cases of cancer (39 cancer fatalities) during 20 years follow-up. In fully adjusted models, moderate-severe OSA was significantly associated with all-cause mortality (HR = 4.2; 95% CI 1.9, 9.2), cancer mortality (3.4; 1.1, 10.2), incident cancer (2.5; 1.2, 5.0), and stroke (3.7; 1.2, 11.8), but not significantly with CVD (1.9; 0.75, 4.6) or CHD incidence (1.1; 0.24, 4.6). Mild sleep apnea was associated with a halving in mortality (0.5; 0.27, 0.99), but no other outcome, after control for leading risk factors. Moderate-to-severe sleep apnea is independently associated with a large increased risk of all-cause mortality, incident stroke, and cancer incidence and mortality in this community-based sample.