Our paper on setting weight loss targets in a commercial weight management group has been accepted for publication in the Journal of Human Nutrition and Dietetics. It will be available through the journal website within 6 weeks- see Early View.
Setting targets leads to greater long-term weight losses and ‘unrealistic’ targets increase the effect in a large community-based commercial weight management group.
Amanda Avery, Michaela Carrington, Simon Langley-Evans and Judy Swift
Background. Setting personal targets is an important behavioural component in weight management programmes. Normal practice is to encourage ‘realistic’ weight loss but the under-pinning evidence base for this is limited and controversial. This study investigates the effect of number and size of weight loss targets on long-term weight loss in a large community sample of adults.
Methods. Weight change, attendance and target weight data for all new UK members, joining January to March 2012 was extracted from a commercial slimming organisation’s electronic database.
Results. Of the 35 380 members who had weight data available at 12 months after joining, 69.1% (n=24 447) had a starting BMI≥30kg/m2. Their mean weight loss was 12.9±7.8% and for both sexes, weight loss at 12 months was greater for those who set targets (p<0.001). Those that set ≥ 4 targets achieved the greatest loss (p<0.001). OR for weight loss ≥10% at 12 months was 10.3 (CI 9.7- 11.1, p<0.001) where targets had been set compared to none. At the highest quintile of target size, the size of the first target explained 47.2% (p<0.001) of the variance in weight loss achieved at 12 months. The mean BMI reduction in those with a target >25% was 7.6±4.0 kg/m2. A higher percentage of obese members did not set targets (p<0.001) compared to those with a BMI below 30kg/m2.
Conclusions. Much of the variance in achieved weight loss in this population was explained by the number of targets set and the size of the first target. Whilst obese people were less likely to set targets, doing so increased the likelihood of achieving clinically significant weight loss and for some ‘unrealistic’ targets improved results.
Our paper entitled Maternal high-fat feeding in pregnancy programmes atherosclerotic lesion size in the ApoE*3 Leiden mouse has been accepted for publication by the Journal of the Developmental Origins of Health and Disease. Study authors are Liz Tarling, Ruth Austin, Kevin Ryan, Susanne Kugler, Simon Langley-Evans and Andy Salter.
The paper describes the impact of feeding a high fat diet during pregnancy upon development of atherosclerosis in the adult ApoE*3 Leiden offspring of wild type mice. ApoE*3 Leiden mice are mice carrying a human mutation of the ApoE gene. This gene predisposes to atherosclerosis in mice that are fed a high cholesterol diet. In our study transgenic males were mated with wild type females and the pregnant mice were either fed a low fat or a high fat ‘Western’ type diet. Atherosclerosis prone ApoE*3 Leiden female offspring were then fed either low fat, low cholesterol diet or a high cholesterol atherogenic diet.
All mice fed the atherogenic diet developed atherosclerotic plaques, but those whose mothers were fed the high fat diet developed significantly larger plaques. This study confirms our earlier work that showed that maternal diet during pregnancy can programme atherosclerosis in the offspring, but importantly showed that a typical high fat Western diet is as effective in this programming as is undernutrition (our previous work showed programming by feeding a low protein diet). The data are consistent with the hypothesis that maternal fat intake may result in the development of atherosclerotic plaques during fetal development, but other mechanisms may be at work, including programming of inflammatory processes.
We are very pleased to welcome Nagehan Ertugrul Bilgili to the lab. Nagehan will be working under the supervision of myself and Simon Welham to investigate the role of amino acids in renal development.
The University of Nottingham has formed a new partnership with the University of Adelaide and as part of this the universities have created some new PhD studentships. Our lab has been fortunate enough to secure one of these studentships and we have now appointed Sally Draycott to be our student. Sally, a recent graduate from the School of Biosciences (Animal Science) will spend 2 years of her project here at Sutton Bonington and 2 years in Adelaide. Her supervisor in Australia will be Professor Robert Gibson. The project will examine the effect of fatty acids in the maternal diet upon fetal development and later health.
Calling course leaders and module organisers everywhere. Although it may be August and you are maybe sitting with your feet up listening to England destroy Australia in the cricket (as am I), climbing a mountain, walking the Pennine Way, perhaps lazing on a beach or paddling in the surf, you just know that it will soon be over and the students will be returning to campus hungry for your wisdom. It. Is. Going. To. Happen.
I am aware that many courses will be teaching lifespan nutrition at various stages of their degrees. Many of those courses make use of my book, Nutrition: A lifespan approach. I have extensively updated that first edition now and the second edition, entitled Nutrition Health and Disease: A lifespan approach will be available in a couple of weeks. If your libraries are now updating their stock, or you are renewing your reading lists then now might be a good time to take the details (ISBN:978-1-118-90709-2) and get some orders in.
As well as an updated text which will refer students to the current state-of-the-art in the subject, buying the book will give lecturers access to pre-prepared lecture slides which can be used in teaching.
The second edition of my book finally plopped onto the doormat yesterday, as Wiley delivered the first advance copy. It looks really good and the cover is so much more interesting than the abstract yellow and grey spirograph horror of the first edition.
The official publication date is now the 4th September, which is hopefully in good time for university libraries everywhere to invest in a copy or ten. It can be pre-ordered now on Amazon, or at the Wiley-Blackwell website.
The Universities of Nottingham and Adelaide (Australia) have provided funding for a PhD studentship to myself and Matt Elmes in Nottingham and Bob Gibson and Beverly Muhlhauser in Adelaide. The project is entitled, ‘Long-term health effects of fatty acids in pregnancy‘ and the student will spend 2 years in Nottingham and 2 in Adelaide. An overview of the project is provided below. If you are interested in learning more about the project or wish to apply for the studentship then please contact me at Simon.Langley-Evans@nottingham.ac.uk. Note that the position is only open to students from the UK or EU due to the funding arrangements.
Linoleic acid is the most abundant polyunsaturated fatty acid in human diets this has been associated with a rise in auto-immune disease and cardiovascular disease. Linoleic acid (LA), consumption has increased world wide and this fatty acid is a major component of human tissues, and the direct precursor to the oxidized linoleic acid metabolites including (OXLAMs) 9- and 13-hydroperoxy-octadecadienoic acid (9- and 13-HpODE) and 9- and 13-hydrox-octadecadienoic acid (9- and 13-HODE) Lowering dietary linoleic acid reduces bioactive oxidized linoleic acid metabolites in humans Randomized Controlled Trial. Relatively large quantities of these OXLAMs are formed when vegetable oils rich in LA are cooked or otherwise heated. After consumption, these preformed OXLAMs are readily absorbed and incorporated into human tissues.
OXLAMs have been mechanistically linked to several pathological conditions including steatohepatitis. Consumption of heated vegetable oils rich in LA has also been linked to development of cerebellar ataxia in chicks, suggesting that dietary OXLAMs could have unfavorable effects on the developing brain. However, the effects of exposure to high levels of OXLAMs during pregnancy on the mother, or on the later metabolic, immune and neurodevelopmental outcomes in the child are unknown.
Work in our laboratories has firmly established that exposure to adverse nutritional environments during fetal development is associated with poor health outcomes in later life, including cardiovascular disease and the metabolic syndrome. Much of this work has focused on effects of maternal obesity or specific components of undernutrition such as protein restriction or iron deficiency. This novel project will consider whether maternal fatty acid consumption during impacts upon metabolic and cardiovascular health of the resulting offspring, using established rodent models. Measurements of OXLAMs will enable the relationship between exposure to high levels may have a mechanistic role in the early life programming of disease.
Daniel ZC, Akyol A, McMullen S, Langley-Evans SC (2014) Exposure of neonatal rats to maternal cafeteria diet during suckling alters hepatic gene expression and DNA methylation in the insulin signalling pathway. Genes and Nutrition9, 365.
Wood KE, Lau A, Mantzioris E, Gibson RA, Ramsden CE, Muhlhausler BS. A low omega-6 polyunsaturated fatty acid (n-6 PUFA) diet increases omega-3 (n-3) long chain PUFA status in plasma phospholipids in humans. Prostaglandins Leukot Essent Fatty Acids. 2014 Apr;90(4):133-8.