Health Issues with High Blood Triglyceride


These are fat molecules which come mostly from consuming refined carbohydrates (noodles, bread, buns, table sugar, breakfast cereals, white rice, sago, desserts, biscuits, cookies, sweet fruits, fruit juices, soft drinks), refined sugars, and from our dietary fats. Calories not immediately used by tissues of our body are converted to TGs, which are our body’s primary source of stored energy. When energy is required, TGs are broken down from our fat cells into their molecular components, namely glycerol and fatty acids.

TGs alone can be measured by a blood test but are most often ordered as part of a standard lipid (cholesterol) profile requiring some twelve-hour fast and is widely used as a blood marker to ‘determine’ risk for coronary artery disease (CAD), a condition that can cause heart attacks and angina (chest pain). A normal TG level, as defined by the U.S. National Cholesterol Education Adult Treatment, is less than 150 mg/dL. Both TG and the ‘bad’ low density lipoprotein (LDL) levels increase from an average of 50 – 60 mg/dL in children to about 140 mg/dL in adults. Hypertriglyceridemia (or HTG) (high blood triglyceride levels) may be defined as a fasting TG level of > 2.26 mmol/l (> 200 mg/dl) and is recognised as a primary indicator for treatment in type II(b) dyslipidemia (blood fat disorder) (Ryan et al. 1999).



More than 95% of our dietary fats are TGs converted from carbohydrates and/or sugars. The primary function of carbohydrates is to provide energy for our body, especially the brain and the nervous system. TGs differ from cholesterol, which our body does not use for energy. Whereas TGs are a form of stored energy, cholesterol is a steroid that contributes to the formation of our cell membranes and production of our sex hormones. High cholesterol foods also increase blood TG levels. Saliva enzyme amylase helps break down carbohydrates into glucose (blood sugar). Monosaccharides include glucose, fructose (fruit sugar) and galactose (dairy lactose) have single sugar unit; disaccharides include sucrose (table sugar), honey, maltose and lactose have two sugar units; and both polysaccharides and oligosaccharides which include starch, glycogen, and cellulose have multiple sugar units. Foods and beverages from the first category are considered “empty calories”, whereas the last two categories are known as “complex carbohydrates” such as legumes, peas, beans, starchy vegetables, whole-grains and cereals providing crucial vitamins and minerals, as well as dietary fiber that are important to health.

Triglycerides in fat tissues surround our body's organs to protect them from injury, and fat tissues under our skin acts as insulation to maintain body temperature. Our digestion, absorption and transportation of the fat-soluble vitamins A, E, D and K are dependent on TGs. A high-fat diet is a promoter of HTG and so is alcoholic beverage.



Diets consisting of 60 percent or more of mostly refined carbohydrates promote HTG in adults and in some children. Surprisingly, the USDA Food Pyramid seems to promote such a diet. Furthermore, high glycermic index (GI) carbohydrates, or food/beverages high in simple sugars, can cause a greater insulin response and consequently greater amounts of TGs being stored in our fatty tissues. The higher the quantity of high-GI foods/beverages consumed, the higher our fat storage. Therefore, people who consume large amounts of soft drinks, sweet fruits, fruit drinks, fruit juices, sports/isotonic drinks, alcohol and sugary/starchy desserts are more likely to have high blood TG levels.

Conditions causing elevated TGs are accompanied by low good HDL cholesterol levels. People with HTG usually do not have symptoms unless there is pancreatitis resulting from this condition. But if high TG levels are caused by a genetic condition, then xanthomas (yellowish fatty deposits under the skin) may be present.


Major causes of high blood triglyceride levels (HTG):

(a) Dietary Factors: excessive intake of alcohol (beer, wine, hard liquor), saturated fats (lard, butter, shortening, cream, refined palm oil), trans fat (hydrogenated and partly hydrogenated fats from margarine, salad cream, French fries, deep-fried food, and snack foods), sugar (jam, jellies, candies, sodas, fruit drinks/juices/punches, honey, sweetened beverages), desserts (pies, cakes, cookies, ice cream, chocolate drinks), sweetened cereals, fruit-flavored yogurts, energy bars, sports drinks, refined starch (pasta, white rice, white flour, corn flour), potato chips, popcorn, and high calorie foods. Excess calories from alcohol will also cause liver to turn ‘fatty’ by making more TGs, which in turn causes less fat to be removed from the blood stream.

(b) Lifestyle Factors: lack of exercise, being overweight, smoking, lack of sleep, skipping meals, and eating large portions of foods at one time.

(c) Weight: TG levels increase with the increased BMI (body mass index) (Assmann et al. 1998). People who are obese (BMI >27) will have more of their calories consumed converted into TGs and cholesterol due partly to their inactivity.

(d) Age: blood TG levels increase with one’s advancing age.

(e) Metabolic Conditions: such as hypothyroidism (under-active thyroid) or poorly controlled diabetes can place us at risk for HTG.


Other causes of HTG:

(a) Medical History: diabetes mellitus, insulin resistance (a precursor to diabetes), hypothyroidism (low metabolism), polycystic ovarian syndrome (PCOS), chronic renal insufficiency (kidney disease), liver disorder, Cushing syndrome, pregnancy, medications, hypercalcemia, multiple myeloma and systemic lupus erythematous (SLE) may cause secondary HTG (Castelli, 1986).

(b) Genetics: increased blood TG levels may be linked to some genetic diseases (Voyiaziakis et al. 1998).

(C) Medications: oral contraceptives, estrogen, corticosteroids, diuretics, Beta-blockers, Tamoxifen, steroids, and certain antidepressants may cause increased TG levels. Indeed, oral contraceptives can increase blood TG levels by up to 40% (La Rosa, 1997).




High blood triglyceride levels are linked to the numerous chronic health disorders including heart disease, diabetes, fatty liver, nerve damage, hypertension, and stroke. Fats converted from starch and sugars can accumulate in various internal organs, most prominently in cardiac tissues (Sarwar et al. 2010), which alters the heart’s left ventricular functions seen in people with metabolic disorders (de las Frentes et al. 2005). These stored fats may influence expression of their genes controlling the susceptibility to coronary artery disease (Kifali et al. 2010). Since this common dietary fat increases platelet activation and boosts blood clot formation, its elevation raises your risk of stroke (de Man et al. 2000). Elevated levels may also be a consequence of other health disorders such as poorly-treated Type II diabetes mellitus, lipid disorder, and obesity. Fortunately, these conditions may be partly reversed by drastically lowering levels of serum TGs (Ebinger et al. 2010) especially through nutritional therapy (ANMP 2013).

A most common symptom of coronary artery disease (CAD) is the accumulation of plaques on the arterial walls. These plaques are likely to compose of TGs, oxidized cholesterol, foam cells, calcium, and other debris that circulated in the blood. Plaques are known to result from arterial lesions (damages) inflicted primarily by chronic inflammation, and aggravated by hypertension, elevated serum ferritin, hyperhomocysteinemia, heavy metal toxicity, and elevated TG levels. The relationship between a high-fat diet and CAD incidence is strong in population studies (Castelli, 1986). Indeed, elevated TGs could contribute some 300% higher cardiovascular disease risk as evidenced from patients with metabolic syndrome (Syndrome X) (De Flines and Scheen, 2010). Patients with higher liver TG (fatty liver) tend to suffer poorer blood flow and impaired energy metabolism in their cardiac tissues (Rijzewijk et al. 2010). They often suffer from hypertension and insulin-resistance (Grundy, 1998). The Copenhagen Men Study also shown that a high fasting TG level is a strong risk factor for ischemic (poor blood flow) heart disease independent of other major risk factors such as good HDL cholesterol (Jeppesen, 1998). Consequently, HTG is a common form of dyslipidemia (blood fat disorder) that is useful in predicting premature CAD (Brunzell, 2008).

In the past 20 years or so, total cholesterol (TC) level alone has been known not to be an independent predictor of increased risk of cardiovascular events (Castelli et al. 1992), although clinically it is still a widely used marker. A 20-year study by Austin et al (2000) on CAD mortality in people with genes promoting HTG found that their baseline plasma triglyceride levels could predict their CAD mortality independently of TC.

TG molecules are stored in fat cells in the presence of insulin hormone. If TGs are not moved into cells for storage and remain in bloodstream, they may elevate the risk of heart attack and stroke in some individuals. When insulin levels are low, TGs are moved from fat cells to be used as energy.

In people already suffering from hepatitis, HTG is likely to worse their liver conditions. According to a 2006 American Family Physician review, non-alcoholic fatty liver disease is a most common cause of elevated liver enzymes. People with fatty liver disease may suffer 30 percent higher mortality rate than people without fatty liver disease.

A 2009 Study at the University of Michigan showed that diabetic patients with high TG levels were much more likely to develop nerve damage. This diabetic neuropathy is characterized by painful tingling and numbing in their extremities as nerves are damaged or lost. Consequently, elevated TG levels can predict diabetic nerve damage. Fortunately, a combination of diet, nutritional therapy, and regular exercise can reduce risk of developing neuropathy.



Besides eating too much starchy or sugary food, there are genetic (passed down through families) disorders that lead to abnormal blood levels of TGs such as:

• Familial combined hyperlipidemia (FCHL) (Type V hyperlipidemia);

• Familial hypertriglyceridemia (Type IV hyperlipidemia);

• Familial chylomicronemia (Type I hyperlipidemia);

• Familial dysbetalipoproteinemia;

• Familial hypercholesterolemia.

The first three primary hereditary disorders are capable of producing TG levels as high as 1,000 mg/dL.


Natural treatment for HTG:

(i) Dietary modification may include some of these measures:

(a) Selecting only low calorie or low glycemic index foods/beverages;

(b) Reducing long-chain saturated fats (mainly from animal products) and trans fat (deep-fried or foods containing hydrogenated fats);

(c) Using monounsaturated, medium-chain triglycerides (MCTs) and omega-3 fats such as virgin coconut oils, canola, olive, hazelnut, and flax seed.

(d) Having at least two servings of fish high in omega-3 fatty acids per week, such as cod, mackerel, sardines, and anchovies;

(e) Choosing other plant-based omega-3 fatty acids, such as fresh walnuts, almonds and flaxseed;

(f) Avoiding or reducing alcohol intake since even small amounts would raise blood triglyceride levels;

(g) Reducing all refined starches and sugars such as white flour, corn flour, white rice, pastries, biscuits, noodles, candy, soda, and fruit drinks/juices, which are rapidly converted into triglycerides by the body;

(h) Selecting low-fructose fruits in season (lemon, guava, kiwi, bitter melon, green star fruit, green mango, mangosteen), fresh ‘rainbow’ vegetables, complex root vegetables, unsweetened all-bran cereals, millet, quinoa, buckwheat, pearl barley, legumes, and lentils;

(i) Reducing desserts after meal, except for plain tea or coffee;

(j) Reducing ‘diet’ or ‘light’ cola or soft drinks since these too stimulate elevated insulin and promote fat gain;


Virgin coconut oil consumption reduces risk of heart disease. The MCTs the oil contains seem to offer a triple approach to weight loss, namely they (i) have a lower calorie content than other long-chain fats, (ii) are minimally stored as fat, and (iii) contribute to thermogenesis (enhanced metabolism) to burn more calories. Furthermore, they suppress appetite, a characteristic of obvious benefit to those attempting to lower their intake of total calories (Stubbs et al. 1996). Higher waist circumference contributes to high blood TG levels after eating, more so in men compared to women (Davies et al. 2002). Even modest weight loss could reduce serum triglycerides.


(ii) Lifestyle modifications may include:

(a) Enjoy around 45 minutes of physical activity for five or more days a week;

(b) Avoid or reduce cigarette smoking to reduce oxidative stress;

(c) Avoid or reduce alcohol consumption to reduce fatty liver conditions;

(d) Control hypertension, with medication and nutraceuticals prescribed;

(e) Weekly vegetable fast since triglycerides levels decrease naturally from fasting and bowel rest over a period of days;

(f) Obtain eight hours of sleep per night to help lower elevated mental stress; and

(g) Maintain hydration by drinking between two and three litres of mildly alkaline fluid every day with one or two glasses before each meal. Water before meal may mildly suppress one’s appetite too.


Research suggests 20 – 24% reductions in TG levels with reduced progression of CAD by following these life-style modifications (Miller, 2000).


Many natural nutrients (nutraceuticals) do exit to lower blood triglyceride levels and these should be taken only under supervision by a MOH-registered nutritional therapist ( Do not self-treat.



Association of Nutritional Medicine Practitioners Malaysia. Accessed: 23 Nov., 2013.

Assmann, G et al. The emergence of triglycerides as a significant independent risk factor in coronary artery disease. Eur Heart J 1998;19:M8-14.

Austin, M et al. Cardiovascular disease mortality in familial forms of hypertriglyceridemia: a 20-year prospective study. Circulation 2000;101:2777-82.

Brunzell JD. Clinical practice. Hypertriglyceridemia. N Engl J Med 2007;357:1009-17.

Castelli WP. The triglyceride issue: a view from Framingham. Am Heart J 1986;112:432-7.

Castelli, WP et al. Lipids and risk of coronary heart disease: The Framingham Study. Ann Epidemiol 1992;2:23-8.

Davies, M et al. Effects of moderate alcohol intake on fasting insulin and glucose concentrations and insulin sensitivity in postmenopausal women: a randomized controlled trial. JAMA. 2002;287(19):2559-62.

De Flines, J and Scheen, A. Management of metabolic syndrome and associated cardiovascular risk factors. Acta Gstro Belg 2010;73(2):261-6.

De las Fuentes, L et al. Plasma triglyceride level is an independent predictor of altered left ventricular relaxation. J Am Soc Encho 2005;18(12):1285-91.

De Man, F et al. Activated platelets in patients with severe hyper-triglycerides: effects of triglyceride-lowering therapy. Atherosclerosis 2000;152(2):407-14.

Ebinger, M et al. The Berlin “Cream and Sugar” Study: the prognostic impact of an oral triglyceride tolerance test in patients after acute ischaemic strokes. Int J Stroke 2010;5(2):126-30.

Jeppesen J, et al. Triglyceride Concentration and Ischemic Heart Disease: An Eight-Year Follow-up in the Copenhagen Male Study. Circulation. 1998;97:1029-1036.

Kisfali, P et al. Triglyceride level affecting shared susceptibility genes I metabolic syndrome and coronary artery disease. Curr Med Chem 2010;17(30):3533-41.

La Rosa JC. Triglycerides and coronary risk in women and the elderly. Arch Intern Med 1997;157:961-8.

Miller M. Current perspectives on the management of hypertrigly-ceridemia. Am Heart J 2000;140:232-40.

Poulter N. Lipid lowering: what about the other 75%? Br J Cardiol 2000;7:186-8.

Rijzewijk, L et al. Effects of hepatic triglyceride content on myocardial metabolism in type 2 diabetes. J Am Coll Cardiol 2010;56(3):225-33.

Ryan T et al. ACC/AHA guidelines for the management of patients with acute myocardial infarction. J Am Coll Cardiol 1999;34:890-911.

Sarwar, N et al. Triglyceride-mediated pathways and coronary disease: collaborative analysis of 101 studies. Lancet 2010;375(9726):1634-9.

Stubbs, R and Harbron, C. Covert manipulation of the ratio of medium-to long-chain triglycerides in isoenergetically dense diets: effect on food intake in ad libitum feeding men. Int J Obes Relat Metab Disord 1996;20(5):435-44.

Voyiaziakis, et al. Low high density lipoprotein levels due to apolipoprotein A-I deficiency exacerbated the development of atherosclerotic lesions in mice with elevated atherogenic lipoproteins. J. Lipid Res 1998;39:313-21.

Share this article

About Author

Dato’ Steve Yap

Masters’ in Metabolic & Nutritional Medicine (USF Med Sch);

Advanced Fellow, Anti-Aging Regenerative Functional Medicine (USA);

Fellow, Integrative Cancer Therapies (USA);

Nutritional Therapy Council Certified Practitioner (UK);

President, Federation of Complementary & Natural Medical Associations M’sia;

Complementary Medicine Director, DSY Wellness Longevity Center (

Login to post comments

Contact Us

Greenpower Empire Sdn Bhd (1010678-A)


Registered Address: 33-1-5, Mutiara Court, Lorong Delima 20, Green Lane, 11700 Jelutong, Pulau Pinang, Malaysia.


Email: [email protected]

Last Posts