Managing your diet is essential to feeling great and performing at your best. Ever wonder why some people can have bad eating habits and not gain weight while others starve themselves and struggle to lose weight? Like many medical conditions, excess weight is caused by a combination of genetic and environmental factors. While you can’t control your genetic predisposition towards gaining weight, knowledge about your genes can help you make educated decisions about what foods are most suitable for you. Some of the gene variations produce a change in the amount of fat absorbed from a meal, change carbohydrate metabolism or even affect the body’s ability to regulate blood sugar with insulin. Knowledge is power.
Next, we will discuss genetic variations related to:
As a general rule eliminate refined sugars and trans fats from your diet. How do you accomplish this? Avoid fried foods prepared in hydrogenated oil, baked goods, candy, chips and other processed foods. These are all likely to contain refined sugar and trans-fat. Refined sugar is composed of simple carbohydrates, which are converted into glucose for energy. Any unused glucose is stored as fat cells in your body. Trans fat is solidified in a way that makes it harder for your body to break down. In this state, it helps preserve food – good for food manufacturers, but very bad for you. Replace trans fats with unsaturated fats. Eat undamaged mono and polyunsaturated fats rich in omega-3 fatty acids. Foods rich in unsaturated fats include avocados, nuts, fish, and unrefined plant-based oils.
Your body metabolizes dietary carbohydrates as its first source of fuel. They are the most important source of energy for your body. Your digestive system changes carbohydrates into glucose (blood sugar). Your body uses this sugar as energy for cells, tissues and organs. Carbohydrates are often considered simple (like sugars) or complex (fiber, vitamins and starches). Complex carbohydrates with a lower glycemic load help maintain a consistent, low blood glucose level and offer many health benefits.
Variations in this gene panel may result in increased sensitivity to dietary carbohydrates, which can lead to an increased tendency to weight gain, particularly abdominal fat, as well as lower success rates with weight loss regimens. Variations have also been linked to a greater risk of obesity, insulin resistance, metabolic syndrome, type 2 diabetes, and cardiovascular disease.
Genes that have been associated with the ability to process dietary carbohydrates are:
ABCC9: Variation in this gene is associated with poor insulin sensitivity and weight gain around your waist.
LRP1: Participates in the movement of glucose transporters to the cell surface where they can internalize glucose. Directly regulates the insulin signaling pathway. It is the link between lipoprotein and glucose metabolism.
MC4R: Linked to dominant obesity, increased BMI, problematic eating behaviour, insulin resistance, and type 2 diabetes.
PLIN1: Encodes a protein that coats fat droplets and prevents their breakdown. Variations in this gene impact glucose tolerance, insulin sensitivity, BMI and the amount of complex carbohydrates tolerated.
PPARG: Influences the regulation of genes involved in carbohydrate and fat metabolism and insulin production—factors that moderate the risk of obesity and type 2 diabetes. Plays a key role in fat cell formation and metabolism.
Figure 6-1 Researchers identify variants affecting carbohydrate metabolism in samples of 450 patients with Metabolic syndrome (MetS), a condition characterized by altered energy metabolism, insulin resistance, and elevated cardiovascular risk https://academic.oup.com/jcem/article/99/2/E384/2537265.
Insulin production and regulation affect your blood glucose levels. Normally a small amount of insulin released from the pancreas absorbs glucose into the cells to create energy. When the genes that control this have variations, more insulin is needed to absorb glucose, also known as insulin resistance. Insulin resistance can lead to type 2 diabetes. Insulin resistance and insulin sensitivity are two sides of the same coin. If you are insulin resistant, then you have low insulin sensitivity. If you have a predisposition, there are lifestyle changes you can make to prevent issues with this disease.
Insulin resistance can lead to a variety of health problems. The body will attempt to compensate for having a low sensitivity to insulin by producing more insulin. However, the increased level of circulating insulin can damage blood vessels, increase blood pressure, and has been associated with heart disease, obesity, osteoporosis and even cancer.
While insulin resistance does not always have noticeable symptoms one of the earliest and most noticeable symptoms is weight gain, particularly around the midsection. Further symptoms include lethargy, hunger and thirst that persist after meals, difficulty concentrating, and high blood pressure.
Examples of genes that have been associated with the ability to regulate blood sugar through insulin are:
AGER: Interacts with molecules implicated in homeostasis, development, inflammation, and certain diseases, such as diabetes and Alzheimer’s disease. Variation is associated with increased risk of insulin resistance.
CEBPA: Modulates the expression of genes involved in cell cycle regulation as well as in body weight homeostasis. Involved in the creation of fat cells and energy homeostasis. Caloric restriction reduces CEBPA protein expression in patients with metabolic syndrome. Variation is associated with increased risk of insulin resistance and lower insulin production.
IGF1: Promotes growth, this variation is associated with decreased IGF1 levels. Low levels of IGF1 are associated with increased insulin resistance, metabolic syndrome, and predict development of glucose intolerance and type 2 diabetes.
LRP1: Encodes a member of the low-density lipoprotein receptor family of proteins. Participates in the movement of glucose transporters to the cell surface where they can internalize glucose. Directly regulates the insulin signaling pathway. It is the link between lipoprotein and glucose metabolism.
PPARG: Influences the regulation of genes involved in carbohydrate metabolism and insulin production—two factors that moderate the risk of obesity and type 2 diabetes. Variations in this gene are associated with insulin resistance. Plays a key role in fat cell formation and metabolism.
SH2B1: Expressed in the hypothalamus, a crucial center for energy balance and regulation of food intake. Variations can disrupt hormonal signaling and are associated with obesity, increased snacking and fat intake, type 2 diabetes, insulin dependence, and BMI.
TCF7L2: Regulates blood glucose through insulin. Variations are related to insulin resistance, risk for type 2 diabetes, and increased fat.
Figure 6-2 Study finds that risk for type 2 diabetes and insulin sensitivity associated with PPARG SNPs can be attenuated with physical activity. https://journals.lww.com/acsm-msse/Fulltext/2008/01000/SNPs_in_PPARG_Associate_with_Type_2_Diabetes_and.5.aspx
High-density lipoprotein (HDL) is a cholesterol carrier that transports excess fats and cholesterol from cells within the artery walls and peripheral tissues to the liver for excretion or re-utilization. HDL also regulates inflammation of blood vessels and has antioxidant properties. Having high levels of HDL cholesterol can help reduce the risk of stroke, heart attack and heart disease; low levels of HDL could increase your risk.
High cholesterol and HDL-LDL cholesterol imbalance often have no symptoms. The American Heart Association recommends that all adults aged 20 or older have their cholesterol and other traditional risk factors checked every four to six years. The National Institute of Health suggests that women should have their cholesterol checked regularly starting at age 45, and men beginning at 35. If you smoke, have diabetes, if heart disease runs in your family, or if you have genetic risk indicated by this report consider having your cholesterol checked earlier rather than later.
Some examples of genes that have been associated with the ability to regulate HDL cholesterol are:
CEBPA: Modulates the expression of genes involved in cell cycle regulation as well as in body weight homeostasis. Involved in the creation of fat cells and energy homeostasis. Caloric restriction reduces CEBPA protein expression in patients with metabolic syndrome. Associated with insulin sensitivity and secretion and HDL cholesterol concentration.
CETP: A key determinant in lipid metabolism, mainly for high-density lipoprotein but also for triglycerides. Variation is associated with an increase in HDL cholesterol levels and a decreased risk of heart attack.
FADS1: Encodes fatty acid desaturase 1, a key enzyme in the synthesis of long-chain polyunsaturated fatty acids. Associated with HDL cholesterol, triglycerides, and risk of coronary heart disease.
LIPC: Regulates HDL levels and is associated with lowering ‘high hepatic lipase’ activity, which is linked to abdominal fat accumulation. Also associated with lower risk for coronary artery disease. Variation is associated with an increase of HDL (good) cholesterol levels, and a greater increase in HDL cholesterol following vigorous physical activity.
SCARB1: Facilitates the uptake of HDL cholesterol in the liver. This movement of cholesterol is a protective mechanism against the development of atherosclerosis, which is the principal cause of heart disease and stroke.
Figure 6-3 Study finds that diet interacts with FADS1 variants to modulate HDL-cholesterol and obesity related traits. https://www.sciencedirect.com/science/article/abs/pii/S0261561417302534#abs0010
Cholesterol is carried in the blood attached to proteins called lipoproteins. There are two main forms, low-density lipoprotein (LDL) and high-density lipoprotein (HDL). Knowing your levels of these can help understand your risk of heart disease.
Too much LDL cholesterol is bad because it contributes to plaque, a thick, hard deposit that can clog arteries and make them less flexible. This condition is known as atherosclerosis. If a clot forms and blocks a narrowed artery, heart attack or stroke can result.
Many factors play a part in raised or unhealthy patterns of blood cholesterol, these include genes inherited from parents, diet, lifestyle, weight, gender, age, ethnicity and medical history. Having unhealthy cholesterol levels, together with other risk factors for heart and circulatory disease such as smoking or high blood pressure, can put you at high risk of early heart disease.
Some examples of genes that have been associated with the ability to regulate LDL cholesterol are:
APOB: Involved in the metabolism of lipids, it is the main protein constituent of LDL lipoproteins. Associated with insulin resistance, metabolic syndrome and cardiovascular disease.
APOE: Transports lipoproteins, fat-soluble vitamins, and cholesterol into the lymph system and then into the blood. It mediates cholesterol metabolism and is involved in cardiovascular disease.
LPA: Increased LPA in blood is a risk factor for coronary heart disease, cerebrovascular disease, atherosclerosis, thrombosis, and stroke. LPA concentrations may be affected by disease, and are only slightly affected by diet, exercise, and other environmental factors.
Figure 6-4 Meta-analysis finds ABOB variants are associated with higher levels of lipids including LDL cholesterol. Read more at https://lipidworld.biomedcentral.com/articles/10.1186/s12944-017-0558-7?utm_campaign=BSLB_TrendMD_2019_LSGR_LipidsHealth&utm_source=TrendMD&utm_medium=cpc
Fats are an essential part of our body’s ability to function. They are involved in key functions ranging from body temperature to weight management. Maintaining a good level of healthy fats in our diet is important for long-term health. The genes in this panel are associated with processing beneficial unsaturated fats in your diet. There are two main types:
Diets with MUFA and PUFA correlate with healthy hearts, fewer strokes and less belly fat. Foods containing MUFA may reduce LDL cholesterol and increase HDL cholesterol thereby lowering the risk of heart disease and stroke.
Variations in these genes may indicate your body takes longer to metabolize/ breakdown dietary fats which would result in a lower metabolic rate.
Some examples of genes that have been associated with the ability to metabolize unsaturated fats in your diet are:
APOA5: Associated with metabolic syndrome and risk of coronary heart disease due to its role in regulating plasma triglycerides.
FABP2: Involved in absorption and metabolism of dietary fats.
PPARG: Influences the regulation of genes involved in carbohydrate and fat metabolism and insulin production—factors that moderate the risk of obesity and type 2 diabetes. Plays a key role in fat cell formation and metabolism.
TCF7L2: Regulates blood glucose through insulin. Variation is related to insulin resistance, risk for type 2 diabetes, and increased body fat. Suggested that macronutrients may modify these effects.
Figure 6-5 FABP2 encodes a protein in the intestinal mucus responsible for the absorption and transport of fat. FABP2 variant has twice the affinity for long-chain fatty acids. Researchers hypothesize that the variant allele increases the absorption of dietary fat. https://www.sciencedirect.com/science/article/pii/S0899900717300333.
Dietary fat contains varying proportions of saturated fat. Examples of foods containing a high proportion of saturated fat include animal fat products such as cream, cheese, butter, other whole milk dairy products and fatty meats which also contain dietary cholesterol. Many prepared foods are high in saturated and trans-fat content such as pizza, dairy desserts, and sausage.
The genes in this panel are associated with the processing of fats in your diet. Variations in these genes may result in a lower resting metabolic rate, meaning that the body takes longer to metabolize dietary fats.
Depending on the amount of saturated fat consumed, this can result in difficulty losing body fat and lead to an increased risk of obesity, higher BMI, increased susceptibility to type 2 diabetes and cardiovascular disease. Health organizations encourage people to switch where possible from saturated to unsaturated and polyunsaturated fats.
Regardless of your genetic type, it can be beneficial to limit saturated fats from animal sources in your diet.
Some examples of genes that have been associated with metabolization of saturated fats are:
ACSL1: Plays an important role in triacylglycerol production and breaking down of fatty acid. Variations may influence risk of metabolic syndrome via disturbances in fatty acid metabolism.
APOA2: Critical part of the fat-burning process. Linked to craving foods with higher carbohydrates, proteins, and saturated fats. Variation is associated with risk of obesity with high saturated fat intake.
APOB: Involved in the metabolism of lipids, it is the main protein constituent of LDL lipoproteins. Associated with insulin resistance, metabolic syndrome and cardiovascular disease. Variation influences triacylglyceride response to monounsaturated fatty acid rich diet.
APOE: Transports lipoproteins, fat-soluble vitamins, and cholesterol into the lymph system and then into the blood. Mediates cholesterol metabolism and is involved in cardiovascular disease.
FTO: Encodes the fat mass and obesity-associated protein. Affects the hypothalamus region of the brain which regulates appetite, energy intake and satiety.
LPL: Found in the blood vessels of fatty tissue and muscles. It plays a critical role in breaking down triglycerides and the partitioning of fatty acids towards storage or oxidation, involved in obesity.
Is saturated fat good for you?
Arguably one of the most controversial nutrients, fats, has been riding the health rollercoaster for decades. After spending years on the naughty nutrition list, fat is making a comeback.
Both meat and plant-based foods contain fats. You will find dietary fat is found in two forms: saturated fats and unsaturated fats. Most fats contain a combination of saturated and unsaturated fats in different proportions.
Saturated fats tend to be solid at room temperature found in foods such as, meat (such as beef, pork, chicken, lamb, and turkey), dairy products (dairy, cheese, butter, yogurt, sour cream, ice cream). lard (animal fat). and coconut oil.
Unsaturated fats are typically liquid at room temperature found in foods such as olives and olive oil, vegetable oils such as canola, grapeseed, and avocado, avocados, nuts and seeds, fish, especially salmon, mackerel, and sardines.
Saturated fats are saturated with hydrogen molecules and contain only single bonds between carbon molecules.
Often listed as “bad” fats, health organizations recommend keeping saturated fat intake low to lower heart disease risks and to promote overall health. Despite these recommendations, we have seen a dramatic rise in cardiovascular disease rates in the last 40 years.
Why your genetics matter when it comes to saturated fat
Your genetic makeup determines how your body processes and reacts to certain nutrients. For instance, the APOA2 gene plays a critical role in the fat-burning process. Variations in this gene have a higher risk of obesity if saturated fat intake is greater than 22 grams per day.
Other genetic factors may affect how your body breaks down fatty acid and triacylglycerol production. For example, variations in the ACSL1 gene may influence the risk of metabolic syndrome due to disturbances in fatty acid metabolism.
Your tolerance to saturated fat may be impacted by how well your genes metabolize and process dietary fats. Luckily, you now have easy access to DNA testing that can provide personalized insights on the diet that is right for you.
7 nutritionist-approved ways to add healthy fats to your diet
Genetic analysis is the easiest way to determine your body’s ability to process saturated fats, unsaturated fats and stored body fat. But without that information, it is still important to introduce healthy fats into your diet with a few of these nutritionist-approved tips!
Eat 1-2 servings of fish per week (1 serving of fish is about the size of your palm). Unfortunately, fish and chips don’t count! Deep-frying destroys the beneficial properties of the fatty acid found in fresh fish. The best way to prepare fish is to steam or bake it.
A plant-based alternative to fish is 1 tbsp of chia seeds per day, ¼ cup walnuts per day, 2 tbsp of flaxseed oil per day or omega-3 supplements derived from algae sources.
Try ¼ cup raw and unsalted nuts or seeds as a snack – they’re a good source of unsaturated fats, and they are high in fiber and protein.
However, when cooking, saturated fats have a higher smoke point than unsaturated fats and are more tolerant to heat exposure than unsaturated fats. For cooking, you may be better with fats such as coconut oil, butter, and ghee.
Olive oil is a form of unsaturated fat that is best used as a salad dressing, drizzled over cooked dishes or soups. This way of preparation preserves the beneficial properties of the fats found in olive oil.
Trim visible fat off of meats. Choose lean cuts often.
Add half an avocado to your meal for a good source of fiber and healthy fats to keep you feeling full for longer.
Excess fat is stored in your body and is broken down and used as energy when carbohydrates are not available. The genes in this panel impact fat storage, the metabolism of stored fat, and BMI. They have an effect on health and body composition.
Variations in this panel can lead to excess energy from food to be stored as fat and difficulty in metabolizing or burning off the stored fats. This may lead to higher body mass and a greater likelihood of abdominal obesity and cardiovascular disease.
Some examples of genes that have been associated with breaking down stored body fat are:
ADRB1: Increases cardiac output by increasing heart rate. Plays a vital role in lipolysis, the breakdown of fats and other lipids, which provides the body with energy and affects body mass. Variation is associated with trouble breaking down stored fat.
ADRB2: Binds epinephrine and is involved in the fight or flight response. Plays a key role in weight balance as determined by gaining and burning stored fat. Variation is associated with difficulty burning stored fat once it has been gained.
ADRB3: Breaks down stored fats for energy consumption. Dissipates excess energy through heat production in adipose tissue, where the majority of body fat is stored. Variation is associated with onset of type 2 diabetes, visceral fat accumulation, and insulin resistance.
TNFA: Involved in the inflammatory state of the body, having pro- and anti-inflammatory components. Variations in this gene are associated with efficient fat storage.
Protein is an essential nutrient necessary for almost every tissue in our body, it is also important if you are trying to build muscle.
High-intensity exercise, particularly strength training and resistance training, can result in micro-injury or trauma to skeletal muscles. When muscles undergo trauma, the body uses protein to repair them, causing muscle cells to increase in number and thickness.
Variations in these genes are common and may respond well to higher protein diets.
Some examples of genes that have been associated with dietary protein are:
IGF1: Has growth-promoting effects on almost every cell in the body. The IGF1 variant tested in this panel is associated with decreased IGF1 levels. Low levels of IGF1 are associated with increased insulin resistance, metabolic syndrome, and predict development of glucose intolerance and type 2 diabetes. Dietary protein intake can increase IGF1 levels.
NADSYN1: Variation is associated with greater positive changes in insulin regulation (fasting insulin and insulin resistance) in response to a high protein diet.
PPARGC1A: Regulates mitochondrial biogenesis, fatty acid oxidation, glucose utilization and thermogenesis. Variation is associated with greater reduction of cholesterol on a high-protein diet than on a low-fat diet.
An appropriate protein intake can promote the reduction of body fat stores because the thermic effect of protein is greater than that of carbohydrate or fat. Protein also exerts a greater satiety effect in combination with other macronutrients, although this effect is partly mediated by satiety hormones released from the small intestine.
During weight loss, higher protein diets preserve lean body tissue. This is the major determinant of resting and 24-hour energy expenditure, which in turn prevents an excessive reduction in energy expenditure. This is particularly significant when higher protein diets are used in combination with complex carbohydrates and physical training.
An example of a gene that has been associated with weight response to high protein diet is:
TFAP2B: Expressed mainly in adipose tissue, encodes for the transcription factor activating enhancer binding protein 2b which has been associated with obesity and insulin resistance. Variation is associated with weight gain on a high-protein diet.