What are cataracts?
When most people hear the word cataract, they think of a film or layer growing over the surface of the eye that causes blurred vision and which, if left untreated, can result in blindness. In fact, cataracts actually develop within the eye itself. A cataract is a hardening and clouding of the lens of the eye, which prevents light reaching the inside of the eye.
It is essential that the lens is clear if you are to be able to see properly because it is the lens that is responsible for focusing light, or images, on the retina at the back of the eye. Once the light has reached the retina, the retina changes the light into nerve signals that are transmitted directly to the brain enabling you to see the image. In the normal eye, the lens is clear and the image that you see is sharp and defined. However, when a cataract causes the lens to become cloudy, the image will be blurred. It’s a bit like constantly looking through a pane of frosted glass.
Over a period of years, one or both lenses cloud over. If left untreated and both lenses are affected, total blindness may result although the amount of vision lost depends on the part of the eye affected. If the central part of the eye is clouded by a cataract you may become short sighted. When the condition becomes serious, a cataract is clearly visible to anyone looking at an affected eye as it appears as a darkened lens clouding over the pupil. Ironically, although the effects of developing cataracts can be devastating, the process itself is painless.
The myths about cataracts
There many common misconceptions about cataracts. They only affect the lens of the eye, leaving all the other important structures of the eye such as the optic nerve and retina intact. Specifically cataracts are not:
What are the symptoms of cataracts?
n its early stages a cataract may not cause any vision problems at all. Often the first signs do not appear until the cataract is more advanced although an early symptom maybe the sudden ability to read without previously needed reading glasses. There are a number of common symptoms associated with more advanced cataracts. They include:
What causes cataracts?
Unfortunately, the ageing process is the most common reason why people develop cataracts. Cataracts that form due to ageing are often referred to as senile cataracts. They are the leading cause of visual loss among those aged 55 and above. By the age of 60 about half of all people will have some cataract formation although it may be minor and not noticeable. By 70 years of age almost everyone will have some degree of cataract formation (University of Melbourne Centre for Eye Research Australia). According to the National Eye Institute (USA), by the age of 80, more than half of all Americans either have a cataract or have had cataract surgery. Bearing in mind that more and more people are living longer and longer, the incidence of cataract is set to reach epidemic proportions.
Whilst cataracts resulting from the ageing process are the most common form of cataracts, there are other types of cataracts. These are:
Advancing age isn’t, therefore, the only risk factor for developing cataracts. The other risk factors include:
For most people, however, cataracts are just part and parcel of growing old.
The ageing process and eye problems
Given that ageing is by far and away the leading cause of cataracts, what is it about the ageing process that results in so many people developing cataracts?
The lens itself is primarily made up of water and proteins. The proteins are arranged in a perfect physiochemical balance which ensures that the lens is kept transparent. By keeping the lens clear, light can pass through it.
Unfortunately, as we age, some of the proteins in the lens may clump together and start to cloud a small area of the lens. This is a cataract. Over time, the cataract may grow larger and cloud more of the lens, making it harder to see.
What causes the proteins in the lens to change with age and form cataracts?
Glycation explained
Research has shown that a process known as glycation is likely to play a large role in the changes that occur to the proteins in the lens. Glycation isn’t restricted to the eye but occurs throughout the body. Glycation, which is sometimes referred to as non-enzymatic glycosylation, is the name given to the “uncontrolled, non-enzymatic reaction of sugars with proteins”1 and plays an important part in the “damage done to (the) critical proteins of long-lived nerve cells in aging.” 1
Put simply, glycation can be described as the binding of a protein molecule to a glucose molecule. “The initial product of this chemical reaction is called a Schiff base, which spontaneously rearranges itself into an Amadori product.”2
A series of chemical reactions follows. The Amodori products undergo dehydration and rearrangement to form cross-links between neighbouring proteins. Eventually, the changes lead to the formation of advanced glycation end products (AGEs).3 Throughout our lives, starting in early embryonic development, AGEs are being formed in the body at a constant, albeit slow, rate. For diabetics, the rate of formation of AGEs is noticeably increased. This is because glucose, that provides the fuel for glycation, is available in greater amounts in diabetics than in the normal body.
Over time AGEs accumulate within the body, as the body does not rid itself of glycated substances quickly. This means that long lived cells and proteins can suffer significant damage as a result of glycation. Although some AGEs are benign, many are more reactive than the sugars they are derived from, and are implicated in many age-related chronic diseases such as type II diabetes mellitus (where there is beta cell damage), Alzheimer's Disease (amyloid proteins are side-products of the reactions progressing to AGEs), and cancer (acrylamide and other side-products are released).
Cardiovascular diseases are also affected by glycation. “The epithelial cells of the blood vessels are damaged directly by glycations, which are implicated in atherosclerosis, for example. Atherosclerotic plaque tends to accumulate at areas of high blood flow (such as the entrance to the coronary arteries) due to the increased presentation of sugar molecules, glycations and glycation end-products at these points.”4
Glycation damage may result in the stiffening and weakening of the collagen in the blood vessel walls. The stiffening leads to high blood pressure. The weakening may lead to micro- or macro-aneurisms. If this happens in the brain, it can result in a stroke.
Glycation specific to the eye
In the lens of the eye, it is the effect of glycation on the proteins and the accumulation of AGEs that is implicated in the development of cataracts. Glycation alters the structure of the proteins and this plays a crucial role in the development of cataracts. “Since the lens proteins are long-lived, they are highly susceptible to post-translational modification such as glycation.”3
Research into the role of glycation and AGEs and their relation to the formation of cataracts is increasingly providing the scientific evidence to support this theory. In a study carried out by a team lead by Sybille Franke and published in 2003, 44 cataractous lenses and 6 noncataractous control lenses were examined. The researchers concluded that “advanced glycation end products (AGEs) formed oxidatively and nonoxidatively occurred to a higher degree in cataractous lenses than in noncataractous lenses. The strong relationship between the lenses’ AGE content, color/opacity, and the state of the cataract may indicate that advanced glycation plays a pivotal role in cataract formation.”5
In research carried out at the University of Essex in the United Kingdom, the concentrations of AGEs in the human lens were detected, quantified and compared. The study showed that not only are the concentrations of AGEs increased in lenses affected by cataracts when compared with cataract free lenses, but that there is also a significant link between cataract and age.6
Free Radical Damage
Unfortunately, the damage from glycation is worsened by the action of free radicals and the damage that they can cause. To properly appreciate the action of free radicals in the body, it helps to understand a little bit about cells and molecules.
The human body is made up of many different types of cells, with the cells being made up different types of molecules. The molecules themselves are made up of one or more atoms of one or more elements joined together by chemical bonds. An atom consists of a nucleus, neutrons, protons and electrons. The number of protons (positively charged particles) in the atom’s nucleus determines how many electrons (negatively charged particles) surround the atom in one or more shells. It is the electrons that bond atoms together to form molecules and the number of electrons in the outer shell of an atom are the most important feature for determining how an atom will behave. Atoms seek to fill their outer shells in order to make the molecule as stable as possible. To do this an atom will either gain or lose electrons in order to either fill or empty it’s outer shell or an atom will bond with other atoms in order to complete it’s outer shell. The bonds created by sharing atoms are not usually split so as to leave a molecule with an odd unpaired electron, but if this does happen, a free radical is formed.
A free radical is very unstable. To become stable, it needs an electron to pair up with its odd unpaired electron. To get the electron that it needs, the free radical will “steal” an electron from another molecule – usually from the nearest stable molecule. The upshot of this is, of course, that a once stable molecule now loses an electron and becomes an unstable free radical itself. The whole process then repeats itself. It can happen over and over again eventually resulting in damage to the living cell. Excessive free radical damage – or oxidation – destroys proteins, enzymes and DNA, and can cause chronic tissue damage.
Free radical damage can be halted by anti- oxidants but as we age our bodies produce more harmful free radicals and less natural antioxidants. The damage from free radicals gradually begins to accumulate. Such free radical damage can happen in the cells of the eye, which, coupled with the damage caused by glycation, worsens the situation with regard to cataracts.
Is surgery the only cure?
When a cataract only causes mild symptoms, a change in glasses may be all that your health professional advises. However once vision has been affected to such an extent that daily life is becoming difficult or your own safety is at risk, surgery is the only course of action that will be offered to you. Cataract removal is the most commonly performed eye operation and, if the eye is otherwise healthy, the majority of operations will result in significant improvements in vision.
However, there is a significant complication rate. In the USA alone each year about 2% of patients develop serious complications such as retinal detachments, corneal edema which requires corneal transplant and endopthalmitis. Whilst 2% does not sound very much it actually equates to about 27,000 patients because so many cataract operations are performed in the first place. Furthermore some 30 – 50 % of patients have been found to require further laser treatment within 2 years of their original surgery because they have developed opacification of the posterior lens capsule.
And, although considered to be one of the safest surgical procedures, it is still surgery and, as with any surgery, it carries with it potential risks.
Most people believe that once a cataract has started to form, surgery is inevitable if they are ever to see clearly again but as the frontiers of science are pushed further, advances in treatment are made and with them has come Can-C, the real alternative to cataract surgery.
CataractEyeDrop.com want to provide you with all the information so you can make an informed decision.
