Originally posted by Dr. Davis on 2015-01-24
on the Wheat Belly Blog,
sourced from and currently found at: Infinite Health Blog.
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of WB Blog articles.
How NOT to have HIGH TRIGLYCERIDES
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
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.