January 2003

Vol. 2   No. 1

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Taming Elevated Triglycerides, Insulin Resistance, and Syndrome X

Triglycerides are the fats in the blood.  To visualize their appearance, think of chicken soup left overnight in the refrigerator.  The next morning you find an upper layer of yellowish fat, which has formed over the brownish liquid below.   When blood is drawn into a tube during venepuncture, and then left on the counter for a while, light-yellow fat (triglycerides) will rise to the top, leaving the more watery red blood below.  When someone has very high triglycerides, you can actually see the fat separate from the blood in the tube even before the needle is removed from the patient’s arm.

People often confuse triglycerides with cholesterol, possibly because both are commonly elevated to unhealthy levels by life-long consumption of the American diet.  Another reason is these two distinct substances subsist together in the blood in packages called lipoproteins.  Even though people with high cholesterol often have high triglycerides, this does not have to be the case – each can be elevated independently.

Even with these associations, cholesterol is very different from triglycerides.  Whereas, triglycerides (fats) are chemically long chains of carbon atoms, cholesterol is a carbon structure made of 4 attached rings.  Fats are primarily used to meet our future energy needs and are stored in our adipose (fatty) tissues.  Cholesterol has many useful functions in the body including roles in membrane structure, brain tissue, fetal development, and the synthesis of bile acids and steroid hormones, like progesterone and vitamin D.  When present in excess it collects in our tissues and plays a pivotal role in artery damage, known as atherosclerosis.

Sources of Triglycerides:

There are two common dietary sources of these blood fats.  They can be derived directly from the fats in the foods we eat or the body can make them by turning carbohydrates into new fats (primarily in the liver) by a process called de novo lipogenesis.  Although this process of new fat synthesis can make enough new fat to raise triglyceride levels (fats in the blood), production is so limited that it does not contribute significantly to body fat (weight) gain.1   Therefore, people who say sugars turn into fats, and thus eating sugar is the primary reason people living under usual conditions become obese, are dead wrong, based upon the preponderance of scientific research.1

Triglyceride elevation caused by eating fats is associated with an increased risk of developing diseases of atherosclerosis, such as heart attacks.  Whether or not this relationship holds true for triglycerides elevated by their synthesis from excess carbohydrate intake is still unknown (but I doubt it).  Elevated triglycerides also cause the blood to clot – increasing the risk of heart attacks, strokes and deep vein thrombosis.  With very high elevation of triglycerides, the risk of pancreatitis is also increased.

Dietary Fats Become Triglycerides:

Saturated fat from the foods we eat moves through the intestinal wall into the bloodstream and becomes what is known as triglycerides.2 Saturated fat also raises cholesterol, and most importantly the risk of heart disease.  When polyunsaturated fats (especially omega-3 fats found in vegetable fats and fish oils) are substituted for saturated fats the triglycerides decrease.3 In addition, high-fat diets (of both the saturated and unsaturated kinds) have been found to raise insulin and sugar (glucose) levels in the blood, when compared to low-fat diets (which are also low in simple sugars).4  Insulin sensitivity improves when fat is removed from the diet; therefore, insulin resistance (as discussed below) is reduced.

Carbohydrate Converted into Triglycerides:

A common teaching is that carbohydrates are bad for you because they cause your blood triglycerides to increase.  These findings are based upon experiments where the carbohydrate provided was primarily in the form of simple sugars and/or people were required to eat more food than they can comfortably consume – they were force-fed.4,5   The rise in triglycerides is caused by an increase in synthesis of these blood fats in the liver and a decrease in removal of these fats from the body (primarily by the liver).

When people eat only as much as they want – as would be found in normal living conditions – of foods high in complex carbohydrate, their total cholesterol, LDL “bad” cholesterol and weight decrease and their triglycerides do not increase (as they do when overfed).5

One study looked directly at the effects of substituting sugar for starch in normal volunteers.  The diet of simple sugars raised triglyceride levels; however, when starch was substituted for the simple carbohydrate, the triglyceride levels did not increase.2 Therefore, on a healthy diet, high in complex carbohydrates (starches and vegetables), total and LDL “bad” cholesterol decrease and triglycerides do not increase.  In fact, combining a diet high in complex carbohydrates with exercise, as we do in our program, results in dramatic reductions in the triglyceride levels.6  More specifically, results from our program show an average reduction in triglycerides of approximately 10 mg/dl in 11 days of healthy eating.  Furthermore, people starting with high triglycerides – say over 600 mg/dl – accomplish, on average, over 300 mg/dl reduction in triglycerides in 11 days of our diet and daily exercise program.

One special note for those of you who are trying to lower your triglycerides; fruit raises triglycerides in sensitive people and needs to be severely limited – at least for several weeks – in people trying to lower triglycerides.7  Fruit (natural, dried, and as juice) is made of simple sugars and the primary sugar is fructose.

Syndrome X, the Metabolic Syndrome:

Elevated triglycerides are frequently associated with a set of complex metabolic abnormalities, including decreased high-density lipoprotein (HDL-“good”) cholesterol, an increase in small (dense) low-density lipoprotein (LDL-“bad”) cholesterol, central (abdominal) obesity, insulin resistance, hypertension, and type-2 diabetes. (Small, dense, low-density lipoprotein (LDL) cholesterol, is more likely to produce artery damage than large, more buoyant, LDL cholesterol.)  This common complex of signs has been called Syndrome X, and is also known as the metabolic syndrome and the insulin-resistance syndrome.  Insulin resistance is considered by many researchers to be the central component of this syndrome.

Insulin resistance develops as a protective response to the fattening effects of the American diet and lack of exercise.  One of the main functions of insulin is to store fat in the body’s fat cells.  As people get fatter, the efficiency of insulin decreases (insulin resistance develops) in an attempt to slow down the ever-expanding body fat stores (so people don’t get so fat they can’t fit through the doorway).  Elevated triglycerides cause the insulin to become less effective, and therefore this change is a key player in the development of insulin resistance.8 Another very recent and important observation has been that the deposition of fat into skeletal muscle cells causes insulin resistance; and most importantly, the reduction of this muscle fat by a change in diet reverses insulin resistance.9

National surveys suggest syndrome X is very common, affecting about 25% to 35% of US adults. The syndrome is more common in older people and in Mexican Americans. People with the syndrome are about twice as likely to develop cardiovascular disease and over four times as likely to develop type-2 diabetes, compared with people who do not have this metabolic syndrome.  While this syndrome may, to a small extent, have a genetic basis, an unhealthy diet and lack of exercise are the primary controllable causes.10

Many researchers believe the way to treat this problem is by substituting monounsaturated fats (olive oil) and polyunsaturated fats (vegetable and fish oils) for the saturated fats (animal fats) and carbohydrates in the diet.3 While many studies show some improvement with this kind of substitution, this approach never cures the syndrome – of more concern is the fact that these kinds of fats actually encourage weight gain, oily skin, diabetes, life-threatening bleeding, and cancer.11

The correct way to treat syndrome X is to correct the causes: a high-fat, low-carbohydrate diet and lack of exercise.  This approach has been used with excellent benefits in experimental animals and people,6,12  For example, the effects of an intensive, 3-week dietary and exercise program (the Pritikin Program) were studied in 3 separate groups of people – those who had diabetes, insulin resistance and with normal insulin.  The results were remarkable, with weight loss and reductions in triglycerides, cholesterol and insulin levels – essentially curing syndrome X.6

Lowering Triglycerides Naturally:

What the Numbers Mean:

Normal:  Less than 150 mg/dl

Borderline (but acceptable): 150 –199 mg/dl

Slightly High: 200 – 350 mg/dl

High: 350 to 600 mg/dl

Very High: Above 600 mg/dl*

* I have seen levels as high as 5688 mg/dl.  Diet and exercise alone has reduced these very high levels to less than 1000 mg/dl in 2 weeks.  Medication was required to further reduce them.

A diet high in complex carbohydrates (low fat) and low in simple sugars (even fruits and fruit juice) reduces triglycerides very effectively.  It may be especially important to reduce the intake of the simple sugar fructose. Fructose has an especially potent effect on de novo lipogenesis; causing insulin resistance, raising glucose, insulin, and triglycerides, and causing hypertension in animal models.1,13 Fructose probably makes a much greater contribution to human obesity than does any other sugar.13   The per capita fructose consumption (mostly as sucrose and high-fructose corn syrup) has increased by 26%, from 64 g/d in 1970 to 81 g/d in 1997.  You will find this kind of sugar in soft drinks and many packaged foods.

Exercise is a very important approach for fighting elevated triglycerides. Exercise burns these fats in the muscle tissues, lowering triglyceride levels.14,15

Medications to Lower Triglycerides:

Several medications have been successfully used to lower triglycerides.  These include the “natural” cholesterol-lowering medications, like gugulipid and niacin; and prescription medications like “statins” (Mevacor, Lipitor, Zocor, Pravachol, etc.) and fibrates (Lopid –gemfibrozil).16  Medications should be used as a last resort after all benefits from diet and exercise have been achieved.

Niacin is one of the least expensive and most effective medications to lower triglycerides (and cholesterol).17,18 You can buy it over-the-counter.  However, this vitamin (B3) can be very potent and toxic, and for these reasons I usually recommend people take it under doctor’s supervision.  The most common side effect is flushing (a burning sensation all over the body). This side effect is reduced when niacin is taken with meals and when an aspirin is taken beforehand.  The body adjusts to the flushing effects with time.  Therefore, you should start with a low dose (say 250 mg a day) and gradually increase the dose based upon your ability to tolerate the flushing.  Effective dosages are commonly in the 1000 to 3000 mg/day range (in divided doses).  This drug can also cause liver inflammation (chemical hepatitis), especially when taken in time-released forms, and cause increases in blood sugar levels.

Summary in a Few Sentences:

Finally, to put all of this discussion together into a few concise sentences this is what happens:  Simple sugars from the diet cause the liver to synthesize fat through de novo lipogenesis, which reduces the sugar in the blood, but raises the triglycerides.  Fats in our foods also make a large contribution to blood triglycerides. Fat which accumulates in our muscles, and the high triglycerides in our blood, inhibit the actions of insulin – all this contributes to insulin resistance, which slows down the accumulation of body fat, but allows the blood sugars to rise and heralds the onset of diabetes. A diet high in complex carbohydrates (starches and vegetables) and exercise, with associated weight loss, reverses (cures) these problems.


1)  McDevitt R.  De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women.  Am J Clin Nutr. 2001 Dec;74(6):737-46.

2)  Hudgins CH.  Human fatty acid synthesis is reduced after the substitution of dietary starch for sugar.  Am J Clin Nutr. 1998 Apr;67(4):631-9.

3)  Griffin BA.  The effect of n-3 fatty acids on low density lipoprotein subfractions.
Lipids. 2001;36 Suppl:S91-7.

4)  Vidon C.  Effects of isoenergetic high-carbohydrate compared with high-fat diets on human cholesterol synthesis and expression of key regulatory genes of cholesterol metabolism.  Am J Clin Nutr. 2001 May;73(5):878-84.

5)  Schaefer EJ.  Body weight and low-density lipoprotein cholesterol changes after consumption of a low-fat ad libitum diet.  JAMA. 1995 Nov 8;274(18):1450-5.

6)  Barnard RJ.  Role of diet and exercise in the management of hyperinsulinemia and associated atherosclerotic risk factors.  Am J Cardiol. 1992 Feb 15;69(5):440-4.

7)  Truswell AS.  Food carbohydrates and plasma lipids--an update.  Am J Clin Nutr. 1994 Mar;59(3 Suppl):710S-718S.

8)  Daly ME.  Dietary carbohydrates and insulin sensitivity: a review of the evidence and clinical implications.  Am J Clin Nutr. 1997 Nov;66(5):1072-85.

9)  Greco AV.  Insulin resistance in morbid obesity: reversal with intramyocellular fat depletion.  Diabetes. 2002 Jan;51(1):144-51.

10)  Meigs JB.  Epidemiology of the metabolic syndrome, 2002. Am J Manag Care. 2002 Sep;8(11 Suppl):S283-92.

11)  McDougall J. Vegetable Fat as Medicine. https://www.drmcdougall.com/vegetable_fat.html

12)  Roberts CK.  Reversibility of chronic experimental syndrome X by diet modification.  Hypertension. 2001 May;37(5):1323-8.

13)  Elliott SS.  Fructose, weight gain, and the insulin resistance syndrome. Am J Clin Nutr. 2002 Nov;76(5):911-22.

14)  Sidossis LS.  Regulation of plasma fatty acid oxidation during low- and high-intensity exercise.  Am J Physiol. 1997 Jun;272(6 Pt 1):E1065-70.

15)  Seip RL.  Skeletal muscle lipoprotein lipase: molecular regulation and physiological effects in relation to exercise.  Exerc Sport Sci Rev. 1998;26:191-218. Review.

16)  McDougall J.  The McDougall Program for a Healthy Heart.  Plume, New York, NY, 1996.

17)  Capuzzi DM.  Niacin dosing: relationship to benefits and adverse effects.  Curr Atheroscler Rep. 2000 Jan;2(1):64-71.

18)  Xydakis AM.  Combination therapy for combined dyslipidemia.  Am J Cardiol. 2002 Nov 20;90(10B):21K-29K.

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