Lisa Te Morenga

Dr. Lisa Te Morenga

Department of Human Nutrition, University of Otago, Dunedin, New Zealand 9054
orcid
Centre for Public Health Research, Massey University

Research Focus & Metrics

Academic Career Length

17Years (2010-Present)

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

Representative Publications

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1 February 2019 in The Lancet
Verified
Journal Article
Open access
ARAndrew Reynolds
Andrew Reynolds
JMJim Mann
Jim Mann
JCJohn Cummings
John Cummings
NWNicola Winter
Nicola Winter
EMEvelyn Mete
Evelyn Mete
LMLisa Te Morenga
Lisa Te Morenga
Previous systematic reviews and meta-analyses explaining the relationship between carbohydrate quality and health have usually examined a single marker and a limited number of clinical outcomes. We aimed to more precisely quantify the predictive potential of several markers, to determine which markers are most useful, and to establish an evidence base for quantitative recommendations for intakes of dietary fibre. We did a series of systematic reviews and meta-analyses of prospective studies published from database inception to April 30, 2017, and randomised controlled trials published from database inception to Feb 28, 2018, which reported on indicators of carbohydrate quality and non-communicable disease incidence, mortality, and risk factors. Studies were identified by searches in PubMed, Ovid MEDLINE, Embase, and the Cochrane Central Register of Controlled Trials, and by hand searching of previous publications. We excluded prospective studies and trials reporting on participants with a chronic disease, and weight loss trials or trials involving supplements. Searches, data extraction, and bias assessment were duplicated independently. Robustness of pooled estimates from random-effects models was considered with sensitivity analyses, meta-regression, dose-response testing, and subgroup analyses. The GRADE approach was used to assess quality of evidence. Just under 135 million person-years of data from 185 prospective studies and 58 clinical trials with 4635 adult participants were included in the analyses. Observational data suggest a 15-30% decrease in all-cause and cardiovascular related mortality, and incidence of coronary heart disease, stroke incidence and mortality, type 2 diabetes, and colorectal cancer when comparing the highest dietary fibre consumers with the lowest consumers Clinical trials show significantly lower bodyweight, systolic blood pressure, and total cholesterol when comparing higher with lower intakes of dietary fibre. Risk reduction associated with a range of critical outcomes was greatest when daily intake of dietary fibre was between 25 g and 29 g. Dose-response curves suggested that higher intakes of dietary fibre could confer even greater benefit to protect against cardiovascular diseases, type 2 diabetes, and colorectal and breast cancer. Similar findings for whole grain intake were observed. Smaller or no risk reductions were found with the observational data when comparing the effects of diets characterised by low rather than higher glycaemic index or load. The certainty of evidence for relationships between carbohydrate quality and critical outcomes was graded as moderate for dietary fibre, low to moderate for whole grains, and low to very low for dietary glycaemic index and glycaemic load. Data relating to other dietary exposures are scarce. Findings from prospective studies and clinical trials associated with relatively high intakes of dietary fibre and whole grains were complementary, and striking dose-response evidence indicates that the relationships to several non-communicable diseases could be causal. Implementation of recommendations to increase dietary fibre intake and to replace refined grains with whole grains is expected to benefit human health. A major strength of the study was the ability to examine key indicators of carbohydrate quality in relation to a range of non-communicable disease outcomes from cohort studies and randomised trials in a single study. Our findings are limited to risk reduction in the population at large rather than those with chronic disease. Health Research Council of New Zealand, WHO, Riddet Centre of Research Excellence, Healthier Lives National Science Challenge, University of Otago, and the Otago Southland Diabetes Research Trust.

15 January 2012 in BMJ
Verified
Journal Article
Open access
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LMLisa Te Morenga
Lisa Te Morenga
SMSimonette Mallard
Simonette Mallard
JMJim Mann
Jim Mann
Objective To summarise evidence on the association between intake of dietary sugars and body weight in adults and children. Design Systematic review and meta-analysis of randomised controlled trials and prospective cohort studies. Data sources OVID Medline, Embase, PubMed, Cumulative Index to Nursing and Allied Health Literature, Scopus, and Web of Science (up to December 2011). Review methods Eligible studies reported the intake of total sugars, intake of a component of total sugars, or intake of sugar containing foods or beverages; and at least one measure of body fatness. Minimum duration was two weeks for trials and one year for cohort studies. Trials of weight loss or confounded by additional medical or lifestyle interventions were excluded. Study selection, assessment, validity, data extraction, and analysis were undertaken as specified by the Cochrane Collaboration and the GRADE working group. For trials, we pooled data for weight change using inverse variance models with random effects. We pooled cohort study data where possible to estimate effect sizes, expressed as odds ratios for risk of obesity or β coefficients for change in adiposity per unit of intake. Results 30 of 7895 trials and 38 of 9445 cohort studies were eligible. In trials of adults with ad libitum diets (that is, with no strict control of food intake), reduced intake of dietary sugars was associated with a decrease in body weight (0.80 kg, 95% confidence interval 0.39 to 1.21; P<0.001); increased sugars intake was associated with a comparable weight increase (0.75 kg, 0.30 to 1.19; P=0.001). Isoenergetic exchange of dietary sugars with other carbohydrates showed no change in body weight (0.04 kg, −0.04 to 0.13). Trials in children, which involved recommendations to reduce intake of sugar sweetened foods and beverages, had low participant compliance to dietary advice; these trials showed no overall change in body weight. However, in relation to intakes of sugar sweetened beverages after one year follow-up in prospective studies, the odds ratio for being overweight or obese increased was 1.55 (1.32 to 1.82) among groups with the highest intake compared with those with the lowest intake. Despite significant heterogeneity in one meta-analysis and potential bias in some trials, sensitivity analyses showed that the trends were consistent and associations remained after these studies were excluded. Conclusions Among free living people involving ad libitum diets, intake of free sugars or sugar sweetened beverages is a determinant of body weight. The change in body fatness that occurs with modifying intakes seems to be mediated via changes in energy intakes, since isoenergetic exchange of sugars with other carbohydrates was not associated with weight change.

1 July 2014 in The American Journal of Clinical Nutrition
Verified
Journal Article
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LMLisa Te Morenga
Lisa Te Morenga
AHAlex J Howatson
Alex J Howatson
RJRhiannon M Jones
Rhiannon M Jones
JMJim Mann
Jim Mann
Background: Dietary sugars have been suggested as a cause of obesity, several chronic diseases, and a range of cardiometabolic risk factors, but there

4 July 2016 in Current Nutrition Reports
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Journal Article
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HEHelen Eyles
Helen Eyles
AJAndrew Jull
Andrew Jull
RDRosie Dobson
Rosie Dobson
RFRidvan Firestone
Ridvan Firestone
RWRobyn Whittaker
Robyn Whittaker
Cliona Ni MhurchuCliona Ni Mhurchu
Cliona Ni Mhurchu

17 November 2017 in PLOS ONE
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Journal Article
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LMLisa Te Morenga
Lisa Te Morenga
JMJason M Montez
Jason M Montez
Elevated cholesterol has been linked to cardiovascular disease in adults and preclinical markers of atherosclerosis in children, thus reducing saturated (SFA) and trans-fatty acids (TFA) intake from an early age may help to reduce cholesterol and the risk of cardiovascular disease later in life. The aim of this review is to examine the evidence for health effects associated with reducing SFA and TFA intake in free-living children, adolescents and young adults between 2 to 19 years of age. Systematic review and meta-analysis of randomised controlled trials (RCTs) and prospective cohort studies. Study selection, assessment, validity, data extraction, and analysis were undertaken as specified by the Cochrane Collaboration and the GRADE working group. Data were pooled using inverse variance models with random effects. EMBASE; PubMed; Cochrane Central Register of Controlled Trials; LILACS; and WHO Clinical Trial Registry (up to July 2016). RCTs involving dietary interventions aiming to reduce SFA or TFA intakes and a control group, and cohort studies reporting the effects of SFA or TFA exposures, on outcomes including blood lipids; measures of growth; blood pressure; insulin resistance; and potential adverse effects. Minimum duration was 13 days for RCTs and one year for cohort studies. Trials of weight loss or confounded by additional medical or lifestyle interventions were excluded. Compared with control diets, there was a highly statistically significant effect of reduced SFA intake on total cholesterol (mean difference (MD) -0.16 mmol/l, [95% confidence interval (CI): -0.25 to -0.07]), LDL cholesterol (MD -0.13 mmol/l [95% CI:-0.22 to -0.03]) and diastolic blood pressure (MD -1.45 mmol/l [95% CI:-2.34 to -0.56]). There were no significant effects on any other risk factors and no evidence of adverse effects. Advice to reduce saturated fatty acids intake of children results in a significant reduction in total and LDL-cholesterol levels as well as diastolic blood pressure without evidence of adverse effects on growth and development. Dietary guidelines for children and adolescents should continue to recommend diets low in saturated fat.

26 November 2012 in Diabetic Medicine
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MKM. Kataoka
M. Kataoka
BVB. J. Venn
B. J. Venn
SWS. M. Williams
S. M. Williams
LMLisa Te Morenga
Lisa Te Morenga
IHI. M. Heemels
I. M. Heemels
JMJim Mann
Jim Mann