High triglyceride levels are common, as common as muffin tops and man breasts. You will find a triglyceride level among the four values on any standard cholesterol panel. High triglycerides are either ignored by most doctors or reflexively “treated” with drugs, such as fibrates (Lopid, fenofibrate) or prescription fish oil (Lovaza). But buried in this single value is tremendous insight into diet, metabolic efficiencies, and cardiovascular risk, with control using natural, non-medication means very easy to accomplish.
Why are triglycerides important? Triglyceride levels of 60 mg/dl or higher will:
- Block insulin, thereby adding to weight gain and higher blood sugars
- Cause formation of small LDL particles. Triglycerides occur in the bloodstream mostly as Very Low-Density Lipoproteins, VLDL, that interact with other lipoprotein particles. Abundant triglycerides in VLDL encounter LDL particles and make them triglyceride-rich. This leads to the formation of small LDL particles that causes coronary heart disease and heart attack.
- At levels above normal, the pancreatic beta cells that produce insulin are subjected to lipotoxicity, irreversible damage that can lead to inadequate insulin production by the pancreas over time.
- At very high levels above 1000 mg/dl, triglycerides cause pancreatitis, pancreatic inflammation that damages the delicate pancreatic tissues.
The higher the triglycerides, the higher the cardiovascular risk. This may work through formation of small LDL particles or by other means. Labs typically quote 150 mg/dl or higher as the cutoff for “normal,” but this is not true: a level of 150 mg/dl is associated with a substantial quantity of the above metabolic distortions. Only at 60 mg/dl or below, for instance, do small LDL particles drop to much lower levels or zero.
What causes triglycerides to rise?
First of all, dietary fats are triglycerides, by definition. Fat on pork, the fat in olive oil, the fat in other foods occur as triglycerides. When we consume fats and oils, there is therefore a modest and nearly immediate rise in blood triglycerides as particles called chylomicrons, large particles formed by the intestinal tract to “package” fats for digestion. Chylomicrons are cleared rapidly and efficiently by the liver over several hours. In most people, fat intake is–counterintuitively–only a minor contributor to blood triglyceride levels, a non-contributor to high fasting triglycerides.
There are two processes that are much larger determinants of both fasting and after-meal (“postprandial” or “non-fasting”) triglyceride levels:
- Whenever the liver has fatty acids delivered to it, it manufactures triglycerides (each triglyceride molecule contains 3–tri–fatty acids). Visceral fat–deep abdominal fat in the abdomen–is resistant to insulin and thereby provides a continual flow of fatty acids to the liver, a process that runs 24 hours a day.
- Carbohydrates in the diet are converted to triglycerides by the process of liver de novo lipogenesis, the creation of fat from carbohydrates.
These last two processes yield much greater rises in both fasting and postprandial triglycerides than that provided by dietary fat. These two processes explain why, for example, someone has a triglyceride level of 210 mg/dl fasting, 400 mg/dl 6 hours after eating. It also explains why some of the triglycerides manufactured by the liver stay there and accumulate, causing fatty liver.
Understanding these phenomena thereby lead us to practical dietary and natural methods to reduce triglycerides to a level of 60 mg/dl or less:
- Eliminate grains and sugars–Contrary to the conventional advice to reduce fat and eat plenty of “healthy whole grains,” the amylopectin A carbohydrate unique to grains provides dietary carbohydrates to fuel liver de novo lipogenesis. High blood sugars that result from grain amylopectin A also lead to insulin resistance. The result: high triglycerides. Eliminate grains and sugars and both processes unwind quickly and dramatically. Most people need to also limit carbohydrate consumption to no more than 15 grams net carbohydrates per meal (net carbs = total carbs – fiber) to prevent liver de novo lipogenesis from proceeding. Do not reduce dietary fat, as this raises triglycerides substantially. (When I was an ultra low-fat vegetarian, my triglycerides rose to 350 mg/dl; they are now 40 mg/dl.)
- Reverse insulin resistance–Beyond grain and sugar elimination, vitamin D restoration, getting adequate sleep, and physical activity all help reverse insulin resistance. A very quick way to reverse insulin resistance is through intermittent fasting, fasting for periods of 15-36 hours (while hydrating very well).
- Supplement omega-3 fatty acids from fish oil–The EPA and DHA of fish oil activate the enzyme lipoprotein lipase that helps accelerate clearance of both postprandial chylomicrons and VLDL particles. This does not apply to the omega-3 fatty acid, linolenic acid, from chia, flaxseed, or walnuts, nor can it be accomplished by the trivial quantity of EPA and DHA in krill oil; it must come from fish oil. It also requires greater supplemental total daily intakes of 3000-3600 mg EPA + DHA per day (divided into two doses). And not only do you not need the 10-fold more costly prescription fish oil, you can actually purchase fish oil that is superior to prescription fish oil (such as the liquid triglyceride form found in the brands Ascenta NutraSea and Nordic Naturals).
- Cultivate healthy bowel flora–“Feeding” bowel microorganisms the fibers they need allow them to convert fiber into butyrate, a fatty acid that yields metabolic effects that include reduction of insulin resistance, reduced blood sugar, reduced LDL values, and reduced triglycerides. This important strategy is discussed further in this Wheat Belly Blog post, as well as a full discussion in Wheat Belly Total Health.
Fibrate drugs and prescription fish oil are not necessary to reduce triglycerides. This is yet another example (among many) where the pharmaceutical industry has managed to persuade physicians that high triglycerides are a reason for prescribing drugs, not a reason to fix the cause. I have prescribed neither agent for high triglycerides in years, despite managing many complex hyperlipidemias that included many people with high triglyceride levels.