Vitamin E can delay the progression of atherosclerosis
Vitamin E keeps blood vessels free of deposits and prevents
accumulation of harmful lens proteins
The fat-soluble antioxidant vitamin E protects body cells,
other vitamins, hormones, and enzymes from harmful free radicals.
Cell damage induced by such radicals is found in tumours,
diabetes mellitus, atherosclerosis, and cataract and may possibly
also occur in arthritis and Alzheimer’s disease. Vitamin E
plays an important role in the prevention of such diseases
and in particular in the prevention of coronary heart disease,
the consequences of which kill over 26,000 people each year
in Switzerland alone. The development of cataract, an eye
disease that is responsible for the blindness of 16 million
people throughout the world, can likewise be positively influenced
by regular intake of vitamin E.
1. Cataracts mostly develop with increasing age
A cataract is any opacity of the crystalline lens
of the eye. Cataracts are the leading cause of blindness in
the world, affecting millions of people especially in developing
countries, where poor medical infrastructure makes operations
difficult to perform.
The most common form, accounting for over 90 percent of cases,
is senile cataract, which can develop in the elderly
in the absence of any specific cause. The development
of cataracts can also be favoured by previous eye injuries,
exposure to x-rays or infrared or ultraviolet irradiation,
prolonged use of medications such as corticosteroids, chronic
choroiditis, and diabetes mellitus. In some cases it dates
back to a prenatal infection such as maternal rubella, and
in many cases it is due to dietary vitamin deficiency.
As cataract is a slowly progressive condition, the patient
is often unaware of any impairment until the disease is well
advanced, by which time the environment appears blurred, dull,
hazy, and distorted as if seen through frosted glass. The
patient experiences glare in sunlight or when looking at objects
against the light, and suffers double vision. This is due
to a change in the refractive properties of the lens as a
result of the opacity. The patient generally becomes more
short-sighted, a change that is initially offset by the simultaneously
present presbyopia (farsightedness of old age).
The diagnosis of cataract is an easy one for the ophthalmologist,
generally requiring no more than an examination with a slit
lamp. This instrument permits microscopic examination of the
eye and, thanks to the narrow flat beam of light that it projects,
can illuminate an optical section through the eye, so that
changes in the localization and range of depth of the various
structures can be easily assessed.
In patients with mature or hypermature cataracts the pupil
may appear white under slit-lamp examination, as it does to
the naked eye. At such advanced stages of cataract the lens
may swell and liquefy, releasing lens fragments into the anterior
chamber and thereby possibly inducing glaucoma.
2. The basic need is for an operation
No drug is able to cause regression of a cataract. In order
to restore the patient’s former visual acuity, the opacified
lens must be removed by means of an operation. This can be
done by either of two basic techniques, namely intracapsular
or extracapsular extraction.
In the intracapsular method the lens is extracted
whole together with its capsule. This technique is now used
only rarely, as it more commonly leads to complications than
does extracapsular lens extraction. In the latter technique
the anterior lens capsule is first opened and then the inside
of the lens is removed, the posterior capsule being left in
place. In this way the natural barrier between the anterior
and posterior ocular segments is retained. The most modern
form of the extracapsular method is phacoemulsification. In
this technique the nucleus of the lens is fragmented by
ultrasonic vibrations and then removed by aspiration.
Lens extraction leaves the eye with an optical deficit that
must be corrected. This can be achieved by any one of three
basic methods: use of a cataract lens, use of a contact lens,
or implantation of an artificial intraocular lens. The latter
option is the best, as it most closely mimics natural conditions.
3. Loss of lens transparency due to oxidation and crosslinking
of lens proteins
Expressed in simplified terms, cataract is due to an accumulation
of harmful lens proteins. This in turn can be due to
metabolic disorders such as diabetes or to infections, mechanical
damage, or congenital lens opacities. Free radicals and other
chemical substances present in the environment can also cause
accumulation of damaged proteins, scattering of light, and
ultimately the various forms of cataract.
This can be explained by reference to certain peculiarities
of the structure of the crystalline lens, which is composed
of proteins and water with inorganic salts and contains no
nerves or blood vessels. Nutrition and removal of metabolic
end-products are achieved via the aqueous humour. The lens
contains only two types of cells, namely epithelial cells
and fibres of the lens. The former divide in the germinal
layer, migrate posteriorly, and finally become fibres (fibrae
lentis). These contain no nucleus or other organelles,
but have large amounts of certain structural proteins known
as crystallin. The arrangement of these protein molecules
ensures a uniform refractive index and allows light to pass
through the lens in a straight line.
Crystalline lenses grow throughout life. When new fibres
are produced, they overlie the older fibres and push them
towards the centre of the lens. During this process the older
fibres are dehydrated and compressed, however in adults they
are no longer removed and can become opacified.
The results of long-term studies suggest that a diet rich
in vitamin E, vitamin C, and other antioxidants may provide
protection against premature cataract formation. Results of
animal experiments have even shown that antioxidative vitamins
help prevent the development of the crosslinks between lens
proteins that result from oxidative processes.
4. Excessive cholesterol levels are critical
Vitamin E is also important in terms of prevention of cardiovascular
diseases, which are often initiated by critically high levels
of cholesterol in the blood. Water-insoluble lipids such as
the steroid alcohol cholesterol are transported by
lipoproteins (L) in the blood to the various organ
systems of the body. Lipoproteins are classified as either
VLDL (very-low-density lipoprotein), LDL (low-density lipoprotein),
or HDL (high-density lipoprotein). They all contain triglycerides,
phospholipids, and cholesterol in various concentrations.
HDLs contain relatively greater amounts of phospholipids,
VLDLs contain relatively greater amounts of triglycerides,
and LDLs and HDLs contain relatively more cholesterol.
VLDLs are generally released continuously from the liver
into the blood, thus ensuring a constant supply of triglycerides
to other cells of the body. While in the bloodstream they
release a large proportion of their neutral fats and in so
doing become smaller. This gives rise to cholesterol-richer
lipoprotein particles known as LDLs which, because they favour
the development of arteriosclerosis, are known as “bad”
cholesterol. HDLs are likewise released from the liver into
the blood-stream, where they become enriched with cholesterol
before returning to the liver. In this way they transport
cholesterol in the opposite direction, i.e. from the cells
of the body to the liver. They thus tend to prevent deposition
of cholesterol in the blood vessels and are therefore known
as “good” cholesterol. In fact, the risk for cardiac infarction
is often estimated on the basis of the ratio of total cholesterol
to HDL-cholesterol. This should be less than 4.0. Values above
5.0 indicate an increased risk for infarction. Atherosclerosis
is a slowly progressive alteration of the inner cell layers
of the walls of arteries such as the carotid, renal, and coronary
arteries and the arteries of the legs.
Arteriosclerosis, to which atherosclerosis can lead,
is known popularly as “hardening of the arteries”. In medical
terms it consists of a reduction in the internal diameter
and a hardening of the walls of arterial blood vessels. This
results in the blood flow being greatly reduced or even —
if the narrowing of the vessel is compounded by the formation
of a thrombus (clot) — coming to a complete halt. Involvement
of the coronary arteries reduces the supply of oxygen to the
heart muscle (myocardium). Should a coronary artery become
completely occluded, the area of heart muscle that it supplies
is starved of oxygen and therefore dies, i.e. the patient
suffers a myocardial infarction. Coronary heart disease
is one of the leading causes of death in industrialized countries.
5. Oxidized lipoproteins get the process going
Along with risk factors such as elevated plasma cholesterol
levels, high blood pressure, smoking, diabetes, and lack of
exercise, oxidatively altered low-density lipoproteins (LDLs)
play a part in the development of arteriosclerosis.
In this process LDL is deposited on the endothelium (inner
lining) of blood vessels and migrates from there into the
intima (inner cell layer) of the vessel. This process attracts
monocytes (cells of the immune system that circulate in the
blood). When oxidized, LDL can be harmful to vessels (atherogenic).
Oxidatively modified LDL promotes migration of monocytes into
the arterial wall and conversion of them into macrophages
(“eating cells”). This process leads at a later stage to the
formation of lipid-laden foam cells that accumulate
in the wall of the aorta and other vessels and form plaques.
Thickening of the arterial wall leads to the formation of
fatty streaks or plaques composed of cholesterol, oxidized
lipids, phospholipids, and insoluble protein complexes. Attachment
of blood platelets to the endothelium can then lead to the
secretion of growth factors that cause uncontrolled growth
of the smooth muscle cells of the arterial wall. An inflammatory
reaction is initiated, the vessel walls lose their elasticity,
and the clinical picture of arteriosclerosis develops.
Epidemiological data indicate that vitamin E and other antioxidative
substances present in food provide protection against atherosclerosis.
The WHO project MONICA (MONItoring of trends and determinants
in CArdiovascular disease) has found a negative correlation
between level of vitamin E in the blood plasma and risk of
death from cardiovascular disease.
Platelet thrombi and arteriosclerosis
Source: PRPV-D, Roche
Cataract
Progressive lens opacification makes the pupil appear white.
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