Hostname: page-component-cd9895bd7-jn8rn Total loading time: 0 Render date: 2024-12-26T22:38:00.904Z Has data issue: false hasContentIssue false

Effects of takeaway food consumption on postprandial lipaemia and diet quality: a study on cardiovascular disease risk

Published online by Cambridge University Press:  24 November 2016

H.G. Janssen
Affiliation:
Nutrition and Health Research Group, Liverpool John Moores University, Faculty of Education, Health & Community, Barkhill Road, Liverpool, L17 6BS
I.G. Davies
Affiliation:
Nutrition and Health Research Group, Liverpool John Moores University, Faculty of Education, Health & Community, Barkhill Road, Liverpool, L17 6BS
Rights & Permissions [Opens in a new window]

Abstract

Type
Abstract
Copyright
Copyright © The Authors 2016 

Postprandial lipaemia (PPL) is a risk factor for cardiovascular disease (CVD) due to its atherogenic tendencies(Reference Adiels, Matikainen and Westerbacka1, Reference Pirillo, Norata and Catapano2). PPL is characterised by an increase in the concentration of blood triglycerides and the metabolic events that occur following the digestion and absorption of a meal containing fat(Reference Jackson, Poppitt and Minihane3). Consumption of takeaway food (TF) has been on the rise over the past few decades(Reference Jaworowska, Blackham and Davies4), often containing a range of ingredients associated with a risk of developing CVD(Reference Jaworowska, Blackham and Long5). To date there have been no studies which compare differences in TF consumption and the effects, if any, on postprandial responses to a high calorie test meal (HCTM). The aim of the present study was to investigate the effect of TF consumption on markers of postprandial lipid metabolism and risk of developing CVD later on in life. The objectives were to identify the dietary patterns of two groups, measure their lipid profiles, and assess whether regular TF consumers (RTFC) had a higher intake of unhealthy foods compared to non-TF consumers (NTFC).

Ethical approval and written informed consent were obtained prior to participation. Thirteen healthy volunteers were split into two groups; RTFC and NTFC. The HCTM was administered and bloods were analysed across a two hour period using Cholestech LDX point of care to assess PPL between groups. Usual dietary intake was assessed by using the EPIC-Norfolk food frequency questionnaire and responses were processed using FETA software. Demographical characteristics and anthropometrics were recorded. All data were analysed using descriptive statistics; SQRT transformations were applied to data not normally distributed. Mixed between-within subjects ANOVA, to compare variables, and independent t-tests, to differentiate nutrient intakes, were carried out between RTFC and NTFC. PPL response was measured as area under the curve and incremental area under the curve according to the trapezoid rule.

Notes: n = number of participants. P Value = difference between TF groups. Data was represented as mean (M) and standard deviation (SD). *Salt content was calculated from sodium concentration by multiplying by 2·542

PPL was not significantly different between groups. However, regular TF intake was positively associated with higher intakes of total carbohydrate (p = 0·016), sugar (p = 0·019) and salt (p = 0·032). These findings could be attributed to the TF composition reported as high in fats, salt and sugar(Reference Jaworowska, Blackham and Davies4), or they may be a marker for a high risk diet. In conclusion, a diet high in TF has not been shown to effect PPL in a sample of young adults. However, regular TF consumption has been shown to increase intake of some nutrients which have been associated with CVD risk when consumed in large quantities over a long period of time.

References

1.Adiels, M, Matikainen, N, Westerbacka, J et al. (2012) Atherosclerosis, 222(1), 222228.10.1016/j.atherosclerosis.2012.02.001Google Scholar
2.Pirillo, A, Norata, G & Catapano, A (2014) Curr Med Res Opin, 30(8), 14891503.10.1185/03007995.2014.909394Google Scholar
3.Jackson, KG, Poppitt, SD & Minihane, AM (2012) Atherosclerosis, 220(1), 2233.10.1016/j.atherosclerosis.2011.08.012Google Scholar
4.Jaworowska, A, Blackham, T, Davies, I et al. (2013) Nutr Rev, 71(5), 310318.10.1111/nure.12031Google Scholar
5.Jaworowska, A, Blackham, T, Long, R et al. (2014) Nutrition & Food Science, 44(5), 414430.10.1108/NFS-08-2013-0093Google Scholar