Triglycerides are an important class of naturally occurring fats. Triglycerides get their name from the fact that they consist of three molecules of fatty acids and one molecule of glycerine. Triglycerides are the major components of very low-density lipoproteins (VLDLs) and also are present in particles called chylomicrons. Triglycerides play an important part as a source of energy and transporters of dietary fat. Triglycerides are split into glycerine and fatty acids in the intestine. They are then packaged with cholesterol to produce chylomicrons, which are transported to the large vessels near the heart before being mixed with the blood. Tissues of the body capture the chylomicrons and release the triglycerides as a source of energy.1
Liver cells and fat cells manufacture and store triglycerides. When the liver and fat cells reach the point where they can no longer store excess triglycerides, they dump the excess triglycerides into the bloodstream, pushing normal blood triglyceride levels into dangerous levels.1
Until the 1990s, high serum triglycerides was merely a subject of debate and was not considered a great threat in regards to heart disease or cardiovascular disease in the medical or the scientific community. Triglycerides were overshadowed by concerns over total cholesterol and LDL cholesterol levels in the blood test results of patients. However, a 1994 study published in the journal Circulation ignited a controversy over triglycerides and disease that is still going on to this day. Researchers at USC reported in 1994 that high triglyceride containing lipoproteins called IDLs and VLDLs (intermediate density lipoproteins and very low density lipoproteins) damaged the artery wall more than LDL cholesterol. Moreover, LDLs were masking this effect of the damage caused by triglycerides.2
The evidence and extent of this damage by triglycerides began to grow, study by study. In 1997, a matched study of 340 patients with high triglycerides and patients with normal triglycerides (100 mg per dL) showed that the patients with abnormally high triglycerides (over 200 mg per dL) had three times the risk of heart attack, and people with the highest ratio of triglycerides to HDL (high density lipoproteins) had 16 times the risk of heart attack compared to those with the lowest ratio of triglycerides. The authors of the study concluded, “The ratio of triglycerides to HDL was the strongest predictor of a heart attack, even more accurate than the LDL/HDL ratio.”3
Various studies by numerous researchers have added debate and confusion over what the ideal and dangerous levels of serum triglycerides really are. The variations of the ideal fasting triglyceride safety zone levels vary from 60 mg/dL up to the American Heart Association’s recommendation of 150 mg/dL or below. Part of the confusion resides in the fact that fasting triglyceride levels are much lower than triglyceride levels after meals or any type of food consumption.4 For example, one study evaluating “desirable” fasting triglyceride levels in 32 non-obese women and men had their fasting triglycerides measured and were then given a milkshake with fructose, glucose or aspartame. Their triglycerides were measured after twelve hours of overnight fasting, and then at two, four, six, eight and ten hours after consuming the milkshake.5Patients with fasting serum triglyceride levels between 101-143 mg/dl had their triglyceride levels peak at four hours and averaged 200 mg/dl. The patients with less than 100 mg/dL fasting triglyceride levels averaged only 124 mg/dL after the milkshake, which was still considered in the “safe” range. The average of 200 mg/dL was considered a dangerous level by the researchers, although the subjects’ original fasting levels were considered within “safe levels.”5
The American Heart Association guidelines for triglyceride levels after fasting are specified in Table 1.
The average triglyceride level in the United States is approximately 134 mg/dL, which makes the average U.S. triglyceride level significantly higher than in countries that have low cardiovascular disease rates. Aside from increasing cardiovascular disease rates, however, high triglyceride levels correlate with increased body weight and the risk of developing diabetes.6
In addition, the first study linking high triglycerides with an increased risk of stroke was conducted in 2001. Nine hundred and forty one patients were followed for eight years to detect transient ischemic attack or ischemic stroke. Other contributing factors, such as smoking, complete medical history, total serum cholesterol levels and age were taken into consideration.7
The final results of the study were that patients with serum triglyceride levels over 200 mg/dL had a three times greater risk of suffering a transient ischemic stroke, the most common form of stroke. A transient ischemic stroke is also referred to as a “mini stroke,” which often precedes a major stroke.7
Triglyceride levels at or above 500 mg/dL are termed hypertriglyceridemia, which can lead to acute pancreatitis and fatty liver, also referred to as nonalcoholic fatty liver disease. Nonalcoholic fatty liver disease refers to whole spectrum of liver injury, which ranges from mild liver damage with no symptoms to very serious conditions, such as cirrhosis of the liver. Serum triglyceride levels above 1,000 mg/dL can result in attacks of acute pancreatitis, which results in elevated blood pancreatic enzymes and severe upper abdominal pain.8
Conclusive evidence accumulated since 1994 shows that blood triglyceride levels above 150 mg/dL constitute a greater risk factor for cardiovascular disease and other major diseases when triglyceride levels increase beyond that point.
Lowering Triglycerides
The question remains—what supplements are the most effective agents for reducing blood triglycerides? In fact, there is a very large body of accumulated human trial data that points to two effective triglyceride lowering agents—fish oil and niacin.9-10
As early as 1993, human trials testing the dietary n-3 fatty acids that occur in fish oil resulted in triglyceride reductions in normal subjects, hypertriglyceridemic patients, patients with combined hyperlipidemia and persons with types IV and V hyperlipidemia. In the authors’ words, “in these carefully controlled metabolic experiments, dramatic reductions occurred in plasma triglycerides and to a lesser extent in plasma total cholesterol. The synthesis of triglyceride and VLDL is greatly reduced by n-3 fatty acids. Fish oil combined with a low-cholesterol, low-saturated-fat diet has been shown to produce complimentary effects. In most situations, the use of fish oil supplements should be regarded as pharmacologic therapy, particularly effective in severe hypertriglyceridemic states. However, a lifelong diet rich in fish may be protective against atherosclerosis as well. Moreover, fish oil may prevent the “chylomicronemia” syndrome of type V hyperlipidemia.”11
A 2008 human trial found a significant reduction in serum triglycerides in a 4-week, placebo study, followed by an 8-week fish oil study. “Treatment with fish oils reduced significantly levels of plasma triglycerides 46%, very low density lipoproteins + intermediate density lipoprotein cholesterol by 21% … Whereas the triglyceride lowering is uniform, the liver response is more variable.”12
Niacin is another agent shown to lower triglyceride levels. A European review concluded in 1996 that “nicotinic acid is the more potent agent (compared to statins) for raising HDL-C (high density lipoprotein cholesterol) by up to 29% at clinically recommended doses. It also substantially reduces triglycerides and LDL-C, and promotes a shift from small, dense LDL to larger, more buoyant LDL particles. Nicotinic acid is also safe for use in patients with diabetes, with no evidence of clinically relevant deterioration in glycaemic control at recommended doses (< or = 2 g/day.)”13
A 2007 German review of niacin discussed its use as a successful lipid-lowering agent for five decades. The review stated that “it is effective in lowering low-density lipoprotein (LDL) cholesterol, triglycerides, and lipoprotein (a), and in increasing high-density lipoprotein (HDL)-cholesterol. All these effects are pronounced, and at present greater increase of HDL-cholesterol cannot be obtained by any other drug. Patients with hypertriglyceridemia/low HDL are the most suitable candidates for this drug.”14
The Carb Connection
It should also be kept in mind that diet and exercise play a role in the triglyceride levels of humans. Sugars and carbohydrates have an impact on increasing serum triglyceride levels as demonstrated in numerous human trials. In 2004, a clinical trial comparing the impact of glucose and fructose consumption in normal weight women showed that a fructose drink consumed for three days caused a “prolonged elevation of plasma triglycerides” compared to a glucose drink. The authors concluded that (fructose consumption) “as demonstrated in this study, could lead to increased caloric intake and ultimately contribute to weight gain and obesity during chronic consumption of diets high in fructose.” This study is important in view of the fact that soft drink manufacturers switched to high fructose corn syrup instead of sucrose in the late 1970s.15
A clinical trial in 2008 confirmed this earlier study with men and women consuming a fructose drink in the morning. In the words of the authors, “when fructose was consumed, absolute lipogenesis (fat manufacture) was 2-fold greater than when it was absent.” They also stated that “Acute intake of fructose … may create a metabolic milieu that enhances subsequent esterification of fatty acids flowing to the liver to elevate triglyceride synthesis.”16
A second 2008 clinical trial comparing three healthy diets, a higher percentage carbohydrate diet, a higher protein diet, or a higher unsaturated diet showed that the higher ratio protein diet reduced plasma apo B and triglycerides in VLDL (very low density lipoproteins) by 16 percent.17
Because of the connection between high blood sugar and high triglyceride levels it can often be helpful to consume a blood-sugar supporting supplement while at the same time reducing intake of high fructose corn syrup, sugar and refined carbohydrates. Clinically, a supplement that contains goat’s rue, cinnamon, N-acetyl cysteine, quercetin, biter melon and vanadyl sulfate (such as GluControl™) has been used successfully to support healthy triglyceride levels.
Bitter melon significantly lowers triglycerides in rodents fed a high-fat diet.18 Quercetin also has lowered high plasma concentrations of triglycerides that occur in obese rodents.19 NAC also appears to lower triglyceride levels in rodents fed a high-saturated-fat diet through its ability to reduce the expression of enzymes participating in biosynthesis of triglycerides.20
Cinnamon has reduced triglycerides by 23-30 percent in subjects with type 2 diabetes after 40 days of daily consumption of 1 to 6 grams, indicating that combining GluControl with additional cinnamon can be an effective approach.21
Conclusion
In conclusion, fasting serum triglyceride levels should ideally be kept below 150 mg/dL, because subsequent eating could push triglycerides near to or over the American Heart Association guidelines of 200 mg/ dL, which are considered high risk levels. Niacin and fish oil consumption are two safe supplements used to lower serum triglycerides, as demonstrated in very large numbers of human clinical trials. Fructose drinks and higher percentage carbohydrate diets also have a direct impact on raising people’s serum triglyceride levels, indicating that blood-sugar supporting supplements such as GluControl also may be an effective approach.
References
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