Can dietary fat intake modify genetic associations with blood lipid level? Observations from a Swedish cohort study
(2014) KNLM01 20142Food Technology and Nutrition (M.Sc.)
- Abstract
- Humans have for a long time contemplated the link between diet and disease. As early as 400 BC, Hippocrates, commonly referred to as the father of western medicine, stated, “let food be thy medicine and let medicine be thy food”. Today, a poor diet is still considered one of the major risk factors for common complex diseases such as cardiovascular disease (CVD).
CVD refers to a class of diseases that involves heart and blood vessels. According to WHO, CVD is one of the leading causes of morbidity and mortality in the industrialized world [8]. The cause of CVD is multifactorial, of which dyslipidemia plays a central role. Dyslipidemia is a state of elevated low density lipoprotein cholesterol (LDL-C), triglycerides, and/or reduced high... (More) - Humans have for a long time contemplated the link between diet and disease. As early as 400 BC, Hippocrates, commonly referred to as the father of western medicine, stated, “let food be thy medicine and let medicine be thy food”. Today, a poor diet is still considered one of the major risk factors for common complex diseases such as cardiovascular disease (CVD).
CVD refers to a class of diseases that involves heart and blood vessels. According to WHO, CVD is one of the leading causes of morbidity and mortality in the industrialized world [8]. The cause of CVD is multifactorial, of which dyslipidemia plays a central role. Dyslipidemia is a state of elevated low density lipoprotein cholesterol (LDL-C), triglycerides, and/or reduced high density lipoprotein cholesterol (HDL-C). In the past, the treatment strategy of dyslipidemia has involved pharmacological intervention (e.g. statins or fibrates) to lower serum LDL-C and triglycerides. However, it is not until recently that the importance of diet and lifestyle are emphasized in clinical treatment and prevention of dyslipidemia. The classic ‘diet-heart’ hypothesis postulates that high intake of foods rich in fat raise the level of circulating cholesterol and triglycerides in the blood, thereby contributing to the risk of heart disease. However, recent research efforts have shown this hypothesis to be overly simplistic, where total fat intake as percentage of total energy intake is not as important as initially believed, whereas fat quality seems to be much more important. Studies have shown that replacement of saturated fat with mono- or poly- unsaturated fat appears to be beneficial for health whereas there seems to be no clear beneficial effect if saturated fat is replaced with (refined) carbohydrates.
Like many other complex diseases, dyslipidemia and CVD are products of a genetic predisposition and environmental risk factors. Large-scale population genetics studies have identified 164 common genetic variants (single nucleotide polymorphisms [SNPs]) associated with lipid levels. It is plausible that environmental factors, including diet, physical activity, alcohol consumption and smoking, may interact with genetic variants to modify circulating lipid levels in the context of dyslipidemia.
Studying gene-environment interactions may help explore novel mechanisms of disease, and inform future personalized nutrition/medicine based on genetic make-up. A new research field combining genetics, nutrition and biochemistry emerged in 2000, known as nutrigenetics, to study inter-individual variation in response to diet. If dyslipidemia can be effectively intervened upon through lifestyle, a large proportion of CVD cases could be delayed or even avoided. Furthermore, targeted diet and lifestyle interventions can protect against drug overconsumption, abuse or adverse side effects. Last but not least, compared to the massive costs related to disease diagnosis and treatment, the use of lifestyle interventions to control and prevent disease may prove to be a much more economical and effective way to improve public health interventions targeting populations susceptible to CVD and related traits.
The Nunavik Inuit Health Survey comprises a small cohort of adult Inuits (N=553), in which interactions between 35 SNPs (in 20 genes) and components of dietary fat intake on plasma lipid levels were investigated]. 14 interactions with total fat intake, and 13 interactions with saturated fat intake were observed on blood lipid traits (total cholesterol, LDL-C, HDL-C and triglycerides), with an additive effect observed when looking at the combined genetic burden. It is meaningful to replicate the same analysis within a population of European ancestry to verify the reliability of the findings by Rudkowska et al., thus furthering our understanding on the biological mechanism of dyslipidemia. (Less)
Please use this url to cite or link to this publication:
http://lup.lub.lu.se/student-papers/record/5014185
@misc{5014185,
abstract = {{Humans have for a long time contemplated the link between diet and disease. As early as 400 BC, Hippocrates, commonly referred to as the father of western medicine, stated, “let food be thy medicine and let medicine be thy food”. Today, a poor diet is still considered one of the major risk factors for common complex diseases such as cardiovascular disease (CVD).
CVD refers to a class of diseases that involves heart and blood vessels. According to WHO, CVD is one of the leading causes of morbidity and mortality in the industrialized world [8]. The cause of CVD is multifactorial, of which dyslipidemia plays a central role. Dyslipidemia is a state of elevated low density lipoprotein cholesterol (LDL-C), triglycerides, and/or reduced high density lipoprotein cholesterol (HDL-C). In the past, the treatment strategy of dyslipidemia has involved pharmacological intervention (e.g. statins or fibrates) to lower serum LDL-C and triglycerides. However, it is not until recently that the importance of diet and lifestyle are emphasized in clinical treatment and prevention of dyslipidemia. The classic ‘diet-heart’ hypothesis postulates that high intake of foods rich in fat raise the level of circulating cholesterol and triglycerides in the blood, thereby contributing to the risk of heart disease. However, recent research efforts have shown this hypothesis to be overly simplistic, where total fat intake as percentage of total energy intake is not as important as initially believed, whereas fat quality seems to be much more important. Studies have shown that replacement of saturated fat with mono- or poly- unsaturated fat appears to be beneficial for health whereas there seems to be no clear beneficial effect if saturated fat is replaced with (refined) carbohydrates.
Like many other complex diseases, dyslipidemia and CVD are products of a genetic predisposition and environmental risk factors. Large-scale population genetics studies have identified 164 common genetic variants (single nucleotide polymorphisms [SNPs]) associated with lipid levels. It is plausible that environmental factors, including diet, physical activity, alcohol consumption and smoking, may interact with genetic variants to modify circulating lipid levels in the context of dyslipidemia.
Studying gene-environment interactions may help explore novel mechanisms of disease, and inform future personalized nutrition/medicine based on genetic make-up. A new research field combining genetics, nutrition and biochemistry emerged in 2000, known as nutrigenetics, to study inter-individual variation in response to diet. If dyslipidemia can be effectively intervened upon through lifestyle, a large proportion of CVD cases could be delayed or even avoided. Furthermore, targeted diet and lifestyle interventions can protect against drug overconsumption, abuse or adverse side effects. Last but not least, compared to the massive costs related to disease diagnosis and treatment, the use of lifestyle interventions to control and prevent disease may prove to be a much more economical and effective way to improve public health interventions targeting populations susceptible to CVD and related traits.
The Nunavik Inuit Health Survey comprises a small cohort of adult Inuits (N=553), in which interactions between 35 SNPs (in 20 genes) and components of dietary fat intake on plasma lipid levels were investigated]. 14 interactions with total fat intake, and 13 interactions with saturated fat intake were observed on blood lipid traits (total cholesterol, LDL-C, HDL-C and triglycerides), with an additive effect observed when looking at the combined genetic burden. It is meaningful to replicate the same analysis within a population of European ancestry to verify the reliability of the findings by Rudkowska et al., thus furthering our understanding on the biological mechanism of dyslipidemia.}},
author = {{Chen, Yan}},
language = {{eng}},
note = {{Student Paper}},
title = {{Can dietary fat intake modify genetic associations with blood lipid level? Observations from a Swedish cohort study}},
year = {{2014}},
}