Lipid metabolism is extremely important as heart disease remains the number one killer in America. In fact, over 600,000 people die each year from heart disease. As of late, research has shown the intense connection between our environmental factors and the influences it has on cardiac diseases and public health. Through lifestyle and diet, we have the ability to modify the way our genes are expressed, ultimately lowering our chances of developing serious diseases like cardiovascular disease.
Lipid components are insoluble in water and serve as enzyme cofactors and help in lipid transport and their uptake into tissues. We have good cholesterol (HDL) and bad cholesterol (LDL). HDL removes damaged cholesterol and helps to lower the risk of cardiovascular disease. However, the more LDL an individual has, the higher their chances are for developing cardiovascular disease. We all have specific genes that either increase or decrease our risk of developing cardiovascular disease. These genes can have SNPs, and each has the ability to influence lipid metabolism. These influences can be modulated by the gene’s metabolism. There is heavy evidence that suggests environmental factors will influence most premature cardiovascular cases if action is taken in favor of an individual’s genetic predisposition.
We use DNA Health by DNA Life to test our patients for their genetic variations and to create a personalized healthcare plan for them to better lower their risk of developing diseases. An example of the test is shown below:
The first gene considered is LPL. This stands for Lipoprotein Lipase. Lipoprotein lipase is found in many tissue types throughout the body and is a key enzyme in metabolizing triglyceride-rich lipoproteins. It is mainly attached to the vascular endothelium and removes lipids from the circulation. There are beneficial SNPs that can result in a slightly shortened form of the protein due to an insertion of a premature stop codon, which can help decrease triglycerides and include HDL. For more information, please refer to GeneCards, The Human Gene Database for LPL.
If you have the CC genotype, the wild type allele, there is no impact. If you have the CG genotype, the heterozygous allele, or the GG homozygote allele, you have a beneficial impact. Those who have a CC genotype do better when they avoid refined carbohydrates and use complex carbohydrates like sweet potatoes instead.
This gene stands for Cholesterol Ester Transfer Protein. This impacts the metabolism of HDL (high-density lipoproteins) and mediates the exchange of lipids between lipoproteins, leading to the eventual uptake of cholesterol. Having a high plasma concentration of CETP concentration has been associated with reduced HDL concentrations. This genetic risk factor shows a strong indication for coronary artery disease. For more, please refer to GeneCards, The Human Gene Database for CETP.
For those who have the wild genotype of GG, you have a moderate risk. This is due to the fact that the G allele is associated with increase plasma CETP and lower HDL. The heterozygous genotype GA has a mild impact, whereas the homozygote AA has a beneficial impact. For individuals who possess a G allele, it is best to decrease saturated fat sources and instead use mono-unsaturated fats and increase omega 3 fatty acids. Exercise has also been proven to be beneficial and to reduce stress in all ways possible to better decrease excess inflammation.
Apolipoprotein C3 helps with lipid and triglyceride metabolism. It is regulated by insulin and inhibits LDL while delaying the catabolism and slows down the VLDL uptake and production. Individuals with the wild type, CC have no impact. The heterozygote CG has a mild impact, and the homozygous GG has a moderate impact. Studies show the G allele is associated with elevated triglyceride levels. For more information, please refer to the GeneCards, The Human Gene Database for APOC3.
For those who have the C allele, we have seen a positive responsiveness to dietary interventions such as decreasing carbohydrate intake, increasing exercise and avoiding the western diet. We also want to optimize their omega index to reduce the inflammation by focusing on the nutritional aspects first. Ideally, we want the omega index to be in a range of 8-12.
Apolipoprotein E has two SNPs that account for protein receptor binding. This is important because it plays a role in the transport of cholesterol, including the transfer of cholesterol to the brain. This gene has an impact on cognition. For this gene, exercise and lifestyle interventions are highly critical. Those who have E3 show no impact, E4 shows a high impact, and E2 shows a moderate impact. E3 is the neutral isoform, but E4 holders are hyper-responsive to toxins. Due to increased LDL binding, these carriers have an increased risk for higher levels of increased cholesterol. Additionally, this has an increased risk of overall inflammation and lower activity of glutathione. To best stay ahead on this gene, it is best to increase your antioxidant intake. For more information on APOE, refer to the GeneCards, The Human Gene Database for APOE.
Paraoxonase 1 helps to break down rancid fats. This helps to protect against damaged particles and helps to maintain substantial HDL levels. PON1 is also able to catalyze the hydrolysis of lipid peroxides. Having low PON1 has been associated with metabolic syndrome and coronary artery disease risk. Ideally, we want to have more PON1 to have more HDL. Those who have the wild type of AA show no impact. Those with the AG heterozygote have low impact and GG homozygous have a moderate impact. For more information, please refer to the GeneCards, The Human Gene Database for PON1.
The intake of high fruits and vegetables can help increase the expression of PON1, inhibiting LDL and helping to improve the hydrolysis of organic compounds. Despite the genotype, it is always important to upregulate this gene. Organic foods are the best way to do this and switching to a Mediterranean diet will aid in decreasing your risk for atherosclerosis.
Understanding the genotypes one possesses is just the beginning. From here, it is just as important to do test pairing for optimal health outcomes. These tests help us put more definitive numbers to the genotype as a reference point. One test we run is Lipoprotein Particle Testing (LPP) from Spectracell. This test shows the risk of cardiovascular disease by measuring the dense LDL and the HDL2b. A sample is shown below:
The second test we pair our genetic types with is an Omega-3 Index Complete Test from The Great Plains Laboratory. This test provides us with the omega 6: omega 3 ratio and lets us know more about their risk factor and specific levels. A sample is shown below:
These tests are extremely important as environmental factors not only influence lipid metabolism, but overall health as well. By knowing these genetics and test pairing, we are using our resources to reduce our patients risk of stroke, dementia, depression, and improve bone health. It should be noted that inflammation is the real silent killer to all chronic health conditions. Inflammation is a factor that influences lipometabolism as well as our musculoskeletal health. These go hand in hand as no body system works alone. Rather, all of our body systems work together and rely on the health and communication between each other to properly perform. A great article to read providing more information on the effects of lipid metabolism and the musculoskeletal system is: Effects of exercise on lipid metabolism and musculoskeletal fitness in female athletes.
Curious about your health? Fill out this metabolic assessment form to get started:
Being able to help patients by assessing their DNA and comparing them to direct measurable labs decreases a patients risk for certain diseases by a significant amount. This method of healthcare allows us to truly make a difference and impact peoples lives. -Kenna Vaughn, Senior Health Coach
Chen, K. T., & Yang, R. S. (2004). Effects of exercise on lipid metabolism and musculoskeletal fitness in female athletes. World journal of gastroenterology, 10(1), 122–126. https://doi.org/10.3748/wjg.v10.i1.122
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