NOVEMBER 20 — What’re Triglycerides (TGs)?

These are fat molecules from refined carbohydrates and sugars. Calories not immediately used are converted to TGs, which are our primary source of stored energy. When energy is required, TGs are broken down from fat cells into glycerol and fatty acids.

Blood TGs are usually tested as part of a standard lipid (cholesterol) profile, which is widely used as a blood marker to ‘determine’ risk for coronary artery disease (CAD). The US National Cholesterol Education defines ‘normal’ TG as less than 150 mg/dL. Both TG and ‘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 (HTG) (or chronically elevated blood triglyceride levels) is a fasting TG level of > 2.26 mmol/l (> 200 mg/dl) and represents a metabolic syndrome.

Functions of carbohydrates

Carbohydrates provide energy especially for our brain and the nervous system, but not our heart. TGs differ from cholesterol, which our body does not use for energy. Whereas TGs serve as stored energy, cholesterol is a steroid contributing to formation of cell membranes and sex hormone production. Saliva enzyme amylase helps break down carbohydrates into glucose. Monosaccharides include glucose, fructose (fruit sugar), and galactose (milk sugar) have single sugar unit; disaccharides include sucrose (table sugar), honey, maltose and lactose have two sugar units; and both polysaccharides and oligosaccharides which include complex starches and cellulose have multiple sugar units. Foods/beverages from monosaccharides are considered "empty calories”, whereas the last two categories are "complex carbohydrates” from legumes, peas, beans, starchy vegetables, and seeds providing vitamins, minerals and dietary fiber.

TGs as stored fat tissues promote abdominal obesity. However, our absorption and transportation of the fat-soluble vitamins such as A, E, D and K depends on intake of some dietary fats. A high-starch diet is a promoter of HTG and so are alcoholic beverages or soft drinks.

Excessive carbs intake

Diets consisting of 60 percent or more of mostly refined carbohydrates can promote HTG in adults and in some children. Surprisingly, the USDA Food Pyramid seems to promote such a diet. Furthermore, high glycermic index carbohydrates, or food/beverages high in simple sugars, can cause higher insulin response and consequently greater amounts of TGs being stored.

Conditions causing elevated TGs are accompanied by low good HDL cholesterol levels.

Major causes of HTG

1. Dietary factors: excessive intake of alcohol, sugar, desserts, sweetened cereals, energy bars, sports drinks, refined starch, potato chips, popcorn, and high calorie foods.
2. Lifestyle factors: lack of exercise, being overweight, elevated stress, lack of sleep, skipping meals, and eating large portions at one time.
3. Weight – TG levels increase with the increased BMI with oobesity measured as BMI >27.
4. Age: TG levels increase with advancing age, unless reversed by physical activities.

Metabolic conditions such as hypothyroidism or poorly controlled diabetes.

Health issues

High blood TG levels are linked to the numerous chronic health disorders including heart disease, diabetes, fatty liver, nerve damage, hypertension, stroke, and metabolic syndrome. Since this common dietary fat increases platelet activation and boosts blood clot formation, its elevation raises risk of stroke.

A most common symptom of CAD is accumulation in arterial wall of calcified plaques, which also compose of TGs, oxidized cholesterol, foam cells, immune cells, pathogens and other debris that circulated in the blood. Besides ApoE4 genotype, plaques result from arterial lesions inflicted primarily by chronic inflammation, and aggravated by hypertension, elevated serum ferritin, hyperhomocysteinemia, heavy metal toxicity, and elevated TG levels. Indeed, elevated TGs could contribute some 300% higher cardiovascular disease risk as evidenced from patients with metabolic syndrome. Patients with higher liver TG (fatty liver) tend to suffer poorer blood flow and impaired energy metabolism in their cardiac tissues. Fatty liver disease can raise mortality rate by 30%.

The Copenhagen Men Study showed high fasting TG level as strong risk factor for ischemic heart disease independent of good HDL cholesterol. Consequently, HTG representss a dyslipidaemia (blood fat disorder) useful in predicting premature CAD.

A 20-year study by Austin et al (2000) on CAD mortality in people with genes promoting HTG found that their baseline plasma TG levels could predict their CAD mortality independently of total cholesterol.