Fats: the Good, the Bad, and the Ugly
E.J. Schaefer
Lipid Metabolism Laboratory,Tufts University, Boston, MA
Fats are an integral part of the diet and comprise about 20-40% of
caloric intake in the U.S (mean about 34%). Fats are eaten as
triglyceride (TG, 3 fatty acids attached to a glycerol backbone),
absorbed as fatty acids (FA) after lipolysis, reconstituted as TG,
transported as chylomicrons, which undergo lipolysis in the capillary
bed, where FA goes to muscle and fat cells, and the chylomicrons become
remnant particles which pick up cholesterol ester (CE), and then deliver
the CE along with fat soluble vitamins to the liver. The liver makes TG
rich particles known as very low density lipoproteins (VLDL) which
undergo lipolysis to form low density lipoproteins (LDL). VLDL is the
major TG carrying lipoprotein in fasting plasma, while LDL is the major
cholesterol carrying lipoprotein, and delivers cholesterol to tissues.
A protein known as apo(a) can attach itself to VLDL and LDL to form
lipoprotein (a) or Lp(a). High density lipoproteins (HDL) serve as
acceptors of cholesterol from tissues, and can deliver CE to the liver
or it can be transferred to other lipoproteins via cholesterol ester
transfer protein. Risk factors for coronary heart disease (CHD) include
increased age, hypertension, smoking, diabetes, elevated LDL C (> 160
mg/dl), and decreased HDL C (< 40 mg/dl). Emerging risk factors for CHD
include elevated Lp(a) (>30 mg/dl), remnant cholesterol (>10 mg/dl), C
reactive protein (> 3.0 mg/L) and homocysteine (> 12 micromoles/L)
levels. LDL is the bad cholesterol particles; HDL is the good
cholesterol particle, TG, remnants, and Lp(a) are the ugly particles
that also confer increased risk. FA are also found on phospholipids and
CE, and are critical for determining membrane fluidity. Saturated fat
(mainly palmitic 16:0), has no double bonds, raises LDL, and decreases
membrane fluidity, monounsaturated fat (mainly oleic 18:1n9) has one
double bond, and has little effect on LDL or membrane fluidity, while
the polyunsaturated n6 fatty acids (mainly linoleic, 18:2n6) have two or
more double bonds, lower LDL C, and increase membrane fluidity. The
polyunsaturated n3 fatty acids (eaten mainly as alpha linolenic acid
18:3n3 in vegetable oils or as eicosapentaenoic acid or EPA 20:5n3 and
docosahexaenoic acid or DHA 22:6n3 in cold water fish or fish oil) lower
TG, decrease CHD risk, and increase membrane fluidity. Replacing
saturated fat with polyunsaturated fat has been shown to reduce CHD
risk. Fish oil supplementation has been shown to decrease CHD death. Low
plasma DHA levels, associated with low fish intake, in our studies in
Framingham are associated with an increased risk of Alzheimer's disease
and all-cause dementia. When polyunsaturated fats are hydrogenated
through long term heating, the double bonds can be converted from the
cis (hydogens on the same side) to the trans (hydrogen on opposite sides
of the carbon chain) position, and then they behave in a deleterious
manner by raising LDL C. Therefore the good fats are the essential fatty
acids and their derivatives (linoleic, alpha linolenec, EPA, and DHA) in
the right balance, the bad fats are the saturated fatty acids
(especially palmitic, myristic, and lauric acids), and the ugly fatty
acids are the trans fats (trans versions of linoleic and oleic). The top
of the USDA food pyramid should be changed to read: "Use animal fats,
trans fats, and sugars sparingly."
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