Fat
and Cardiovascular Disease
The hypothesis
that consuming a great amount of fat in diet will lead to cardiovascular disease
is outdated and needs further understanding.
While some fats are essential for good health, like MUFA and PUFA, other such
as trans fat is harmful to our bodies. Therefore,
it is the type of dietary fat that matters and not the total amount of fat consumed
that decides the cardiovascular disease risk.
This has been well documented in
population studies. For example, Greeks consume much lesser SFA and more MUFA
(in olive oil) as compared to the Americans, even though they may have similar
fat intakes. They also have one of the lowest rates of heart attacks in the
world. Japanese who live in Japan have the lowest rate of heart attacks in the
world. They also consume an abundance of raw fish (sashimi) that are high in
natural SFA and N3 EFA (from the PUFA in the meat of the fish).
The lower rates of cardiovascular disease is not directly related to total fat
intake, but more with the kind of fat consumed. This is further
confirmed by studies within Japan, where it is found that the incidence of cardiovascular
disease among fishing villages is lower than farming villages, where the diet
is higher in grain.
" Traditional medical wisdom
since the 1970s encourages a reduction of fat intake as a way to reduce cholesterol
level. Americans are consuming more than 40%
of its calories in fat; this should be reduced to 30% and not
lower. While some people restrict fat to 20%, there are other enthusiaststhat
even considered reducing fat intake to 10% or less of caloric intake. Extreme
low fat intake level is difficult to achieve without foregoing food and appetizing
choices. A diet extremely low in fat has been linked to an increase in cancer
and strokes, primarily through the free radical pathology pathway. It should
be noted up to 30% of the adult population should not be on a low-fat ,high
carbohydrate diet. Instead, they should be on a high-fat (45%, comprising mostly
of monounsaturaed and polyunsatuated fat), low protein (15%), and moderate complex
carohydrate (40%) dietbecause they suffer from insulin resistance ( or Syndrome
X). This condition is caused by over conconsumption of carbohydrate over a long
period of time, and it is linked to a high risk of cardiovascular disease. "
Any focus on a single dietary
discipline should be taken with care. The proper choice of fat in the diet
is more important than the absolute amount. The general delusion that low fat
diet causes low cardiovascular risk without considering the kind of fat taken
in must be dismissed. Sad to say, most people
replace fat with protein and carbohydrates when they reduce their fat intake.
Carbohydrate such as pasta, rice, cereal, and potato are chosen. This is actually
worse as a high carbohydrate diet increases insulin, reduces HDL cholesterol,
and increases triglycerides. Knowing the details on what to eat is therefore
critical. The
popular notion of a high carbohydrate diet of the last 30 years has produced
an obese population never seen before in human history and an epidemic of adult
onset diabetes.
Fat
Recommendation
A well-balanced proportion of fat
is the key to healthy aging. A diet too low in fat may actually bring harm to
health. The correct way is to discern the right type to take and those to avoid.
The overall fat intake as a percentage of
dietary calories should not fall below 30%. To have plenty of
"good" MUFA like olive oil, seeds, nuts, and cold-water fish that
have high N3 content. Saturated fat is necessary for good health. It could come
from animal or plant sources. If animal source is desired, choose free-range
poultry or beef, organic eggs, and deep-water fatty fish such as salmon. It
is very important to avoid "bad" trans fat, like margarine and fried
foods. Moreover, the use of processed PUFA such as corn, safflower or sunflower
oil should be restricted.
Out of
the 30 % recommended daily calorie from fat sources, less than one third should
be saturated fat, the rest should come from mono-unsaturated fat as much as
possible.
Here are some practical tips:
- Trim visible fat from
all cuts of meat.
- Include one to two fish or
seafood meals a week (total 8 ounces). Open water cold-water oily fish
such as salmon or tuna is preferred.
- Don't batter or fry fish
in animal or hydrogenated vegetable fats; pan-frying and deep-frying may decrease
the omega-3 content of the fish.
- Switch to low fat or non-fat
varieties of milk and other dairy products.
- Instead of frying foods, try
steaming, stir-frying, or baking.
- Limit take-out foods,
butter, potato chips, biscuits and cake, and other processed food containing
vegetable shortening (trans fat).
- Choose fat from unrefined
sources - for example, oily fish, nuts, soy, avocado, seeds (in bread),
and virgin/cold pressed oils.
- Use a virgin olive oil,
if available.
- Use non-stick cooking pans to
cut back on the amount of fats that are used solely to stop the food from
sticking.
Cholesterol
A waxy substance consisting of fats
(lipids) and proteins, cholesterol is a necessity for life. Cholesterol
is carried around in the blood on carrier molecules called lipoproteins.
The main lipoproteins categories are namely very-low-density lipoprotein (VLDL),
low-density lipoprotein (LDL), and high-density-lipoprotein (HDL). Once bound
to the carrier HDL, the cholesterol is known as HDL cholesterol. HDL in effect
transports fat from the cell to the liver. When the HDL cholesterol level is
high, it is more cardio protective. Therefore, HDL cholesterol is considered
"good " cholesterol. LDL is the carrier of oxidized cholesterol
as LDL cholesterol from the liver to cell. Elevated LDL cholesterol is directly
correlated with increased cardiovascular risk. LDL cholesterol is therefore
called the "bad" cholesterol.
Cholesterol, when unoxidized,
is an antioxidant and free radical scavenger in its naturally occurring state.
In fact, cholesterol guards the cell membranes' phospholipid from free radical
damage and protects it against atherosclerosis, cancer, and other free radical
attack. Also, cholesterol is a predecessor to many steroid hormones and vitamin
D. Cholesterol is produced at the liver at
the rate of 3,000 to 4,000 mg daily in the liver.
The
notion that total blood cholesterol level alone is the key determinant of cardiovascular
heath should be dispelled. Polar bears, for example, maintain a total blood
cholesterol of over 400 mg/dl and they seldom develop heart attacks.
There is obviously a lot more to learn about cholesterol and its link to cardiovascular
disease that we currently know.
Cholesterol
and Free Radical Activity
While the exact mechanism of how
cholesterol affects our body is still under intense investigation, it is clear
that the unified theory of free radical damage caused by unhealthy foods such
as processed fat and cholesterol is the most likely mechanism.
Free Radical damage to our blood vessels is one of the primary causes of atherosclerosis.
The most important cause of free
radical pathology is the excessive dietary fat consisting of processed PUFA
trans fat frequently used in fried foods, margarine, and cooking oil, and oxidized
cholesterol from commercially prepared foods.
In the event that dietary fat and oil is retrieved from fresh, whole, and unprocessed
foods, no lipid peroxidation will take place and the cell membrane will remain
healthy in a normal cis-configuration without any free radical damage.
One theory advanced by the late Nobel
laureate Dr. Linus Pauling, together with his resereach cohort Dr. Matthias
Rath, is that the total serum cholesterol is really an indicator of the amount
of free radical damage in the body. Our body maintains an optimum level of total
cholesterol level as well as a delicate balance among its subcomponents. A negative
feedback mechanism exists within the body that decreases the rate of endogenous
synthesis when the dietary intake is exceeds what is needed.
The total circulating cholesterol therefore remains relatively constant at between
170-200 mg/dl for the normal adult. The higher the free radical level, the higher
the body needs to produce cholesterol internally from the liver to act as an
antioxidant and free radical scavenger. In fact, a low total cholesterol level
(below 150 mg/dl) has been linked with an increased risk of cancer and stroke.
Cholesterol in its natural state
is therefore actually good for us. During commercialization, lipid (including
fat and cholesterol) peroxidation takes place as soon as fats and oils are extracted
from the foods in which they naturally occur. This commercialization process
is speeded up by metallic ions, particularly iron and copper. Extensive lipid
peroxidation can occur without an apparent stale or flavor, like in peanut butter,
the making of salad and cooking oil, and also in so-called cold-pressed oils.
During the processing of PUFAs to make cooking oil, rapid peroxidation can
take place and free radicals are released. This process is accelerated by heat,
atmospheric oxygen, light, and trace amounts of unbound metallic elements.
Oxidized cholesterol is a free
radical generator. It is attached particularly to low-density lipoproteins
as LDL cholesterol as it goes from the liver to the cell. Hamburgers and other
cooked and processed foods contain animal fats that are usually high in oxidized
cholesterol when cooked. Foods cooked in animal fat and fried in processed PUFA
(such as corn oil) also have high oxidized-cholesterol content. As a result,
the higher the LDL cholesterol level, the higher the risk of cardiovascular
disease. Research has shown that rabbits that consumed a small amount of
oxidized cholesterol for merely 12 weeks had atherosclerosis plaques that were
two times as big as the control population. Studies reveal that heart attack
risk falls 2% for every 1% drop in LDL cholesterol level.
One of the most important causes
of free radical pathology is the excessive dietary fat consisting of processed
PUFA or trans fat frequently used in fried foods, margarine, and cooking oil.
In the event that dietary fat and oil is retrieved from fresh, whole, and unprocessed
food, no peroxidation will take place and cell membrane will remain healthy
in a normal cis-configuration without any free radical damage. Studies have
shown that 20% of dietary calories as commercially available fat will not surpass
the control threshold of endogenous free radical protection. bUnfortunately,
the current contribution from such fat to our diet exceeds 40 percent.
Lipoprotein(a)
Some of the natural cholesterol produced
by the liver in response to free radical damage is converted into LDL cholesterol
and its relative lipoprotein(a) (Lp(a)).
While LDL cholesterol maybe known as the "bad" cholesterol, Lp(a)
is even worse. Lp(a) is a plasma lipoprotein that structurally resembles
LDL, but with an additional adhesive protein. Lp(a) is also made in the liver
and transported to the cell. Studies have shown that Lp (a) holds fast to damaged
blood vessel, attracting other Lp(a) molecules, and finally constituting the
athrosclerotic plaques. In fact, a high Lp(a)
level (more than 30 mg/dl) has been revealed to carry a 10 times greater risks
for heart disease that LDL cholesterol level. Lp(a) level should
be part of a routine blood screening test for cardiovascular disease risk.
Lp(a), according to Drs. Pauling
and Rath, is the body's way of repairing its damaged vessel wall that has micro
leakages caused at least in part by free radical damage and vitamin deficiencies
(more specifically vitamin C ). Humans do not make any endogenous vitamin
C and have no self-repair mechanism of the vascular system. Lp(a) is used by
the body as a surrogate vitamin C, so to say. Lp(a), unfortunately, has a sticky
characteristic and adheres to each other, forming an atherosclerotic plaque
over time. The body, at the interim, is unaware. As long as the damage
persists due to free radical presence (either from improper diet, aging, pollution,
lack of vitamins, or toxins), the body responds by making more cholesterol endogenously
in the liver, feeding a viscous cycle of ever increasing Lp(a).
Cholesterol
and Cardiovascular Disease
It is proven that single focused
dietary strategy of lowering dietary cholesterol does not reduce coronary heart
disease risks. To make matters worse, such "low-fat, high carbohydrate"
diets are often high in the wrong type of carbohydrate. Instead of taking in
complex, paleo type carbohydrates such as green leafy vegetables, the ignorant
consumer often ends up eating foods such as pasta, soda, processed foods, and
fast foods. These types of food are rich in sugar and starch (carbohydrate).
They actually lower the important "good" HDL cholesterol. An
HDL cholesterol level is inversely proportional to the cardiovascular disease
risk. It should be remembered that cholesterol and fat are concentrated sources
of calories and can lead to obesity if consumed too much.
In the Framingham study for example,
men and women consumed an average cholesterol intake of 700 mg and 500 mg per
day respectively were studied (one egg provides 200 mg). The average serum concentration
of cholesterol for men and women with higher than average cholesterol intake
were found to be 237 and 245 mg/dl respectively. Subjects with lower than average
intakes were found to be 237 and 241 mg/dl. The difference is statistically
insignificant. Statistically, studies have
showed that people who consume 4 eggs per week (one egg provides 200mg cholesterol)
actually have average serum cholesterol (193 mg/dl) same than those who reported
consuming only 1 egg per week (197 mg/dl). Clearly dietary cholesterol in and
of itself is not the critical link to heart disease risks as we once thought.
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