What is Diabetic Retinopathy

I have just heard that one of my relatives who has diabetes has just be diagnosed with a vision problem called Diabetic Retinopathy, so I have done some research and here is a short explanation that may help you or someone you know.

Diabetic retinopathy is a complication of diabetes which affects the tiny blood vessels in the light-sensitive tissue called the retina that lines the back of the eye. The retina detects light and converts it to signals sent through the optic nerve to the brain. Diabetic retinopathy can cause the blood vessels to bleed or leak fluid, thereby distorting vision. Without treatment, diabetic retinopathy can cause loss of vision and blindness.


Diabetes interferes with the body’s ability to use and store sugar. The disease is characterised by too much sugar in the blood, which can cause damage throughout the body. Low vision is one symptom of diabetes, other symptoms include:

  • increased thirst and hunger
  • weight gain or loss
  • fatigue
  • frequent urination
  • skin infections, and wounds that heal slowly

Diabetic retinopathy affects a large percentage of all patients who have had diabetes for 20 years or more. It is also one the leading causes of blindness for people aged 20 to 64 years.

Often diabetic retinopathy may not be detected until vision loss occurs so people with diabetes should get a comprehensive eye examination when diabetes is first diagnosed and then these tests should be repeated on a regular basis. Early diagnosis and treatment can usually prevent severe vision loss.


Studies have shown that controlling diabetes can slow the onset and worsening of diabetic retinopathy. People who monitor and maintain a normal glucose level are significantly less likely to develop the disease than those who don’t. Good glucose control also reduces the likelihood of developing other health problems including kidney and nerve diseases. Trials have also shown that controlling blood pressure and cholesterol levels and avoiding tobacco can also reduce the risk of vision loss.

There are several therapies that may be used alone or in combination for treating the disease and reducing vision loss, however they are not a cure for the disease. These treatments are:

  • Laser surgery – the heat from a laser is used to seal or destroy the leaking blood vessels in the retina.
  • Medication – several medications are available to be used in the treatment of diabetic retinopathy. These medications are injected into the eye.
  • Vitrectomy – this treatment involves the use of surgical instruments to remove the damaged blood vessels. Removing this material allows light rays to focus on the retina again.

Vision lost caused by diabetic retinopathy is sometimes irreversible. However, early detection, regular monitoring and treatment can reduce the risk of blindness by a significant amount.

Our goal at EZiD is to assist all people living with low vision by simplifying some of the decisions they have to make every day, for more information about how we can help please use this link.

by John Owens – john@ezidlabels.com

The Braille Alphabet

Louis Simon Braille (1809 – 1852) was born in Coupvray, France, the fourth child and only son of Simon-René Braille, a saddle and horse tack maker, and his wife Monique.


When Braille was three years old, he injured one of his eyes while playing with his father’s leather making tools. This resulted in both his eyes becoming infected, and by the time Braille was five, he was completely blind. Although there were few options for blind children his parents wanted Braille to be educated, first at the local village school then via a scholarship to attend the National Institute for Blind Youth in Paris.

This was the first school of its kind to educate blind students using a combination of oral instruction and raised-print books developed by the school’s founder. Braille did well at his studies and became an accomplished musician. And the crude raised-print books gave Braille the idea that a tactile alphabet would allow blind people to read and write.

In 1821, a retired soldier named Charles Barbier visited the school to share his invention called sonography. This was a complicated code used by soldiers to write and decode messages at night, using a system of twelve raised dots, without having to use a light. The army decided the system was too complicated, however Barbier thought the system might assist blind people.

Braille and some of the other students recognised the possibilities of sonography and over the next three years Braille worked to develop a much simpler system using six dots lined up in two columns of three dots each.


Braille became an apprentice teacher at the school when he was 19 and in 1837 the school published the first book in braille. However, the school did not adopt the system. Nonetheless, by 1850, when tuberculosis forced Louis Braille to retire from teaching, his six-dot method was on its way to widespread acceptance.

Louis Braille died of his illness on January 6, 1852, in Paris, at the age of 43. Today, in most languages, braille is the standard form of communication used by blind people.

“Access to communication in the widest sense is access to knowledge, and that is vitally important for us if we are not to go on being despised or patronised by condescending sighted people. We do not need pity, nor do we need to be reminded that we are vulnerable. We must be treated as equals – and communication is the way we can bring this about.” Louis Braille 1841.

See the EZiD braille label here.

What is Glaucoma?


Glaucoma is a complicated disease in which the optic nerve at the back of the eye is damaged which leads to progressive, irreversible vision loss. Glaucoma is one of the leading causes of blindness.

There are two main types of glaucoma: primary open angle glaucoma and acute angle closure glaucoma.

The most common form is primary open angle glaucoma. This is often associated with an increase in eye pressure. Eye pressure refers to the tissue pressure within the human eye and is typically caused by the continual drainage and production of aqueous humour.


The aqueous humour is the watery fluid between the cornea and the lens. It maintains the pressure needed to inflate the eye and provides nutrition for the central cornea and lens as they do not have their own blood supply. It circulates from behind the iris into drainage channels between the iris and the cornea. If it cannot drain away correctly, then there can be a fluid build-up leading to a rise in eye pressure and ultimately damage to the optic nerve.

Eye pressure is usually shown as millimetres of mercury (mm Hg). The standard eye pressure should measure less than 21 mm Hg. Ocular hypertension occurs when the eye pressure increases. Vision damage occurs very slowly and the first signs may be the loss of some parts of the visual field, most commonly the peripheral, or side vision.

Acute angle closure glaucoma occurs when the drainage system becomes completely blocked and the fluid pressure rises quickly as more fluid continues to be made. The usual symptoms are sudden and severe eye pain, a red eye and blurred, haloed or decreased vision. The sufferer may feel sick and vomit and it can rapidly lead to blindness in the affected eye if not treated promptly.

Glaucoma can affect young children also; it is called congenital, paediatric or infantile glaucoma. It is usually diagnosed within the first year of life. Symptoms include enlarged eyes, cloudiness of the cornea and sensitivity to light.

Glaucoma can be treated with eye drops, pills, laser surgery, traditional surgery or a combination of these methods. All are intended to decrease eye pressure and, thereby, protect the optic nerve. The goal of any treatment is to prevent loss of vision, as vision loss from glaucoma is irreversible. The good news is that glaucoma can be managed if detected early, and with medical and/or surgical treatment, most people with glaucoma will not lose their sight.


John Owens –

A Short History of Bifocals and Multifocals


Multifocal eyeglass lenses contain two or more lens powers to help you see objects at all distances if you lose the ability to naturally change the focus of your eyes due to age. This condition is called Presbyopia and it is caused by the hardening of the lens of the eye. This causes the eye, when looking at close objects, to focus light behind the retina instead of on the retina.


Presbyopia occurs from age 40 and everyone is affected to some degree. Many people complain their arms have ‘become too short’ because they cannot hold reading material in a comfortable position. Other symptoms include eyestrain, blurred vision when looking at one object up close then another object further away, and difficulty reading small print.

Bifocal and multifocal lenses provide clear vision at all distances. Bifocals have two prescriptions in the same lens and multifocal have a range of powers; distance, intermediate and near vision. Your pupil alternates between the powers as your gaze moves up or down. The top part of the lens is for distance vision and the bottom part for near vision.


The invention of bifocals has long been credited to Benjamin Franklin (1705 – 1790) the American politician, statesman and diplomat. He was also an inventor so this may be true or it could be a myth. He was certainly one of the first to wear bifocals. Franklin was involved in the optical business before he left America. He imported spectacles and records of his advertisements in newspapers still exist. From the mid 1750s to the mid 1770s he spent much of his time in London and it was during this time that he was first said to have invented bifocals.

It is likely that London opticians were making ‘split lenses’ also known as ‘divided lenses’ for artists including Benjamin West (1738 – 1820) and Sir Joshua Reynolds (1723 – 1792). Both these men were in London at the same time as Benjamin Franklin and both of them have also been named as the inventor of bifocals.

There is also one recorded example of bifocal use in the animal world, Thermonectus marmoratus. This is a species of diving beetle also known as the sunburst diving beetle and the spotted diving beetle. These beetles live in ponds and lakes in Southern California, Arizona, New Mexico, Texas and Mexico. If their water source dries up they fly to a new one. Adult male beetles are about ½” or 1cm in length and females are slightly bigger. They are unique because they have, within their principal eyes, two retinas and two separate focal planes so they can switch their vision from close to distance when they are searching for food.


Thermonectus marmoratus – the Diving Beetle

John Owens

How Do Your Eyes Work?

It may seem a bit odd as your brain produces the image you ‘see’, however your eyes collect all the information the brain uses to create the image. They take pictures of the world around you and send them to your brain, and your brain then works out what your eyes are seeing.


The cornea is the see-through skin covering the front of your eyes. It bends, or refracts, the rays that pass through the round hole of the pupil.

The iris controls the amount of light entering your eye. It is the coloured part of the eye surrounding the front of the pupil.

The rays then pass through the lens, focuses them on the retina.

The retina, which sits at the back of the eye, is a thin layer of tissue containing millions of tiny light-sensing nerve cells. These nerve cells are called rods and cones because of their distinct shapes. Rods ‘see’ black and white and cones are responsible for colour vision.

Cones are concentrated in the centre of the retina, in an area called the macula, and function best in relatively bright light. Rods are located outside the macula and extend all the way to the edge of the retina. They provide peripheral vision and allow the eyes to detect motion and help us see in dim light and at night.

Once light meets the retina the process of sight begins. They turn the picture into an electrical message for the brain. The optic nerve sends these messages to a part of the brain called the thalamus via the optic nerve. This area combines information from both your eyes and then sends it to another area of your brain called the visual cortex. This is a specialised part of the brain which processes visual information and is located at the back of the brain. It interprets the electrical signals to obtain information about the object’s colour, shape and depth. Other parts of the brain then put this information together to create the whole picture.


Humans have five senses: the eyes to see, the tongue to taste, the nose to smell, the ears to hear, and the skin to touch. By far the most important organs of sense are our eyes.  We perceive up to 80 per cent of all impressions by means of our sight. And if other senses such as taste or smell stop working, it’s the eyes that best protect us from danger”. Quote from

John Owens –



A Short History of Spectacles, Eyeglasses and Glasses

The Wikipedia definition is: “Glasses, also known as eyeglasses or spectacles, are devices consisting of lenses mounted in a frame that holds them in front of a person’s eyes.” The French called early versions pince-nez which literally means ‘pinch the nose.’ The term spectacles was the name given when arms were added to the lenses so that the ears could provide more comfortable support than a squashed nose. 


The word spectacle may have been adapted from the Latin words specere (to look at) or spectare (to observe). The word glasses may have evolved from the word spyglass, the name often given to telescopes.

Magnifying glasses had been around for a very long time. However the relationship between the shape of a lens and its magnifying qualities was a more recent discovery. The scientist, mathematician, astronomer and philosopher Ibn al-Haitham (965-1039) was the first to recognise the correlation between the curved surface of a semi-spherical lens and its powers of magnification when he published his seven volume thesis The Book of Optics.


Robert Grosseteste (c. 1175-1253) the English statesman, scientist, theologian and philosopher became interested in experiments with magnifying lenses, and passed this interest onto his most famous pupil, Roger Bacon (1213 – 1292). Bacon made the first recorded reference to the magnifying properties of lenses in 1262. He was a young lecturer at Oxford University where he carried out experiments with lenses and mirrors. In 1268 he suggested that properly shaped lenses might assist people with low vison.

Glasses appeared first in Florence about 1280 and their use spread rapidly across Europe. Credit for the invention is usually given to a monk called Alessandro di Spina who died in the Italian city of Pisa in 1313. Salvino degli Armati, is also credited as having some involvement. Although I have read several accounts that suggest his involvement was a hoax.


It took another three hundred years before anyone was able to explain why glasses actually worked. In 1604 the work of the German astronomer, mathematician and astrologer Johannes Kepler (1571 – 1630) was published. In the course of his astronomical investigations Keppler provided a correct explanation of vision and the functions of the pupil, cornea and retina.

In 1784 Benjamin Franklin (1706 – 1790) invented bifocals. Benjamin suffered from both myopia (short-sightedness) and presbyopia (reduced ability with age to clearly focus on close objects). In his invention the two lens sections were held by the frame; the middle and lower portion of the lens having different focal lengths.

John Owens – November 2016

What is Macular Degeneration?


Macular degeneration is the leading cause of severe vision loss in people over age 60. Because the disease develops as a person ages, it is often referred to as age-related macular degeneration (AMD) and it can be a source of significant visual disability. I have AMD. It occurs when the retina’s small central portion, known as the macula, deteriorates. The retina, which sits at the back of the eye, is a thin layer of tissue containing millions of tiny light-sensing nerve cells. It records the images we see and sends them via the optic nerve from the eye to the brain.

The macula is responsible for central vision in the eye, and it controls your ability to read, drive a car, recognise faces and colours, and see objects in fine detail.


When the macula’s cells deteriorate, images are not received correctly. Initially macular degeneration does not affect vision. However, if the disease progresses, people experience a gradual decline in their ability to see object clearly and distorted vision. If the condition continues to worsen they will see dark or empty spaces blocking the central field of vision and diminished colour vision central vision.

Even so, because the rest of the retina is still working, they retain their peripheral vision, which is not as clear as central vision. At present macular degeneration is considered an incurable eye disease.

There are two main types of age-related macular degeneration:

Dry form. The “dry” form of macular degeneration is characterised by the presence of deposits, called drusen, in the macula. A few small drusen may not cause changes in vision; however, if they grow in size and number they may lead to the symptoms people find most noticeable when they read. In more advanced stages there is also a thinning of the light-sensitive layer of cells in the macula leading to tissue death.


Photo taken in 2014 showing the drusen in my right eye.

Wet form. The “wet” form of macular degeneration is characterised by the growth of abnormal blood vessels underneath the macula. These blood vessels leak blood and fluid into the retina, causing distortion of vision that makes straight lines look wavy, as well as blind spots and loss of central vision.

How is AMD Treated? Some doctors recommend vitamin supplements to reduce the progression of Dry AMD. I live in Sydney Australia and the treatment I adhere to includes taking vitamin supplements daily and I can confirm that my AMD has not deteriorated since I was first diagnosed 5 years ago.

The main treatment for wet AMD is injections of Lucentis. This treatment targets the VEGF protein (Vascular Endothelia Growth Factor). This protein promotes the growth of abnormal blood vessels in the retina. These injections may prevent further loss of vision.


John Owens – 2016