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Is Smoking a Risk Factor for AMD?

Info: 7789 words (31 pages) Dissertation
Published: 13th Dec 2019

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Tagged: HealthMedicine


Age-related macular degeneration (AMD) is the leading cause of vision loss affecting central vision. It is directly proportional to age and thus the older you get, the more likely you are to have AMD. AMD is linked to several factors leading to its cause, such as gender, family history and alcohol. This study assesses the link between smoking and AMD. Smoking can be carried out in different ways, the most common being the cigarette which contains tobacco. There are many harmful chemicals released into the body system when cigarette smoke is inhaled. Smoking is already known to be directly linked to diseases, for example, lung cancer and coronary heart disease.

Studies were looked into to see if there was a relationship. All the studies showed that those who are current smokers were more at risk of developing wet AMD than those who used to smoke (ex-smokers) and those who have not smoked before.

There are treatment available for those who have wet AMD, the most effective being anti-VEGF injections. Those who smoke have different methods available to help them stop smoking and reduce the risk of them getting AMD.


Age-related macular degeneration (AMD) is a condition which causes changes to a part of the back of the eye, called the macula, resulting in severe visual loss in typically older people. The macula is responsible for central vision and is densely populated with cone cells.

There are 2 types of photoreceptor cells; cone and rod cells. Rod cells are much more sensitive than cone cells and thus used in dark/dull vision. Cone cells on the other hand are used to give high resolution, colour vision in light conditions. These cone cells are therefore used for colour perception which are damaged when effected by AMD.

AMD has many contributing factors such as genetics, age and gender. The older you get, the more likely it is for you to get AMD. If an immediate family member has AMD, there is a bigger possibility that you could get AMD. Studies have also shown women are more likely to get AMD than males. These factors cannot be changed, however a modifiable factor with risk of AMD is said to be smoking.

Smoking is a practice in which a substance is burned and the resulting smoke breathed in to be tasted and absorbed into the bloodstream. There are different types of smoking and later on in this study, they will be discussed.

There is also an indirect way smoking can cause harm without being the intended active smoker; passive smoking. Passive smoking (also known as second-hand smoking) is inhaling mainstream smoke which is exhaled by the active smoker.

The aim of this elective study is to establish whether smoking is a risk factor for AMD. Going through different researches carried out. The harms of smoking and how it is related to AMD.

21,000 new cases each year in UK by the macular disease society

26,000 eligible for anti-VEGF treatments

The table above shows how big of an effect AMD has on the population. Listed are the four most common ways of visual impairment; AMD, cataract, glaucoma and diabetes. Both male and females were included in the sample used for the study aged 75 and over. Results show that AMD is the leading disease to cause visual impairment in men and women. A common theme in both male and female groups was a big increase in the number of people suffering from AMD as the age group increased.

2. Types of Smoking & AMD

Smoking is very common amongst society. Many start off in their teens and then progress into adulthood. Some do try to stop but they are addicted and begin to suffer from withdrawal symptoms, leading them to resume their bad habit. Here we will look into why people smoke, different types of products they smoke and what is their influence.

The most common product which is smoked is the cigarette. A cigarette is a substance derived from the tobacco plant rolled up in thin rice paper as a cylindrical shape. Cigarettes are widely available to the public to anyone over 18 years of age in England.

Tobacco is the leading cause of preventable cancers. WHO estimated over 1.1 billion people smoked tobacco worldwide in 2015. Tobacco consumption accounts for nearly 6 million deaths per year and around 10% of these deaths are due to non-smokers being exposed to second-hand smoke.

Other popular types of smoking include tobacco pipe, hookah, cannabis and heroin.

Tobacco pipe is the oldest method of smoking. It consists of a pipe usually made of wood or clay. There is a chamber where the tobacco is placed for it to be lit and the smoke is inhaled through the mouthpiece. This equipment comprises of the same substance as the cigarette.

Hookah (also known as sheesha) is smoked using a water pipe where the tobacco is burnt using coal and inhaled through a hose-like pipe. The coal is ignited to burn the tobacco at its correct temperature. When the hookah is inhaled using the hose, hot air, from the charcoal vaporising the tobacco, is passed through the body into the water jar where it is cooled down and fills the top of the jar. The change in pressure when the air enters the lungs allows more charcoal to be burnt in the hookah which continues the process. Hookah is widely available and popular around the world including the United Kingdom, more so in the Arabian Peninsula and south Asia.

Hookah is frequently smoked in “sheesha bars” where usually a group of people pass around the hose around a table taking turns in inhaling the tobacco. There has been a recent increase in the number of shisha bars – the numbers have risen from 179 in 2007 to 556 in 2012 in the UK.

Some tobacco used in hookah comes in a range of flavours including apple, strawberry, grape, lemon, mint and many others (predominantly fruit flavours)

When a cigarette burns, it releases many harmful chemicals into our system. Not only is the smoker inhaling these chemicals but also any one inhaling the smoke released from the cigarette will breathe in these chemicals too. Some of these chemicals are naturally in the tobacco plant, some of the chemicals are added by the industry, some are absorbed by the plant from fertilisers and some only form when the tobacco is burnt as a chemical reaction. Below are a list of chemicals and their uses:

  • Benzene – an industrial solvent found in rubber cement, refined from crude oil
  • Arsenic – a poison, used in wood preservatives and rat poison
  • Cadmium and lead – used in batteries
  • Formaldehyde – used in mortuaries and paint manufacturing
  • Polonium-210 – a highly radioactive element
  • Chromium – used to manufacture dye, paints and alloys
  • 1,3-Butadiene – used in rubber manufacturing
  • Nickel – used to protect metals from corrosion
  • Vinyl chloride – used to produce plastic and vinyl products
  • Beryllium – used in nuclear reactors
  • Ethylene oxide – a disinfectant used to sterilise hospital equipment
  • Tar – material used for paving roads

The main ingredient in cigarettes are tobacco. Although tobacco smoke contains many different harmful substances, the following 3 are the most detrimental to one’s health.

Nicotine One of the main reasons people find it difficult to quit smoking is because they are addicted to the nicotine. Without nicotine, the number of smokers would drop drastically and as a result the tobacco trade would lose a lot of profits.

Excessive exposure of nicotine leads to symptoms such as vomiting, nausea, drowsiness, seizures; and also starts affecting cell proliferation, apoptosis, oxidative stress & DNA mutation by various mechanisms which leads to cancer.


When a person is smoking a cigarette, the particles inhaled carry the nicotine to the lungs where it is absorbed into the bloodstream by diffusion via the bronchiole and alveoli. The nicotine then enters the blood circulation around the body and quickly makes its way to the brain, where it binds to nicotinic cholinergic receptors (ligand-gated ion channels that normally bind acetylcholine). The binding opens up the channels and this allows sodium or calcium to enter. The entry of the positive ions initiates more calcium ions to enter to even out the charge. Subsequently this causes the release of neurotransmitters.


When the brain is stimulated by nicotine, a variety of neurotransmitters are released in the brain. One of these neurotransmitters is dopamine. Dopamine is triggered when someone is having a pleasurable experience and is desiring something such as times like eating. In this case, it is nicotine. Smoking, therefore, give someone immediate pleasure and as we would like to have more of this feeling, a smoker will continue to smoke. Just how when you are hungry you have the need and urge to eat, a similar reaction is taking place when the brain is deprived of nicotine and would want to go back to smoking.


Nicotine addiction is due to other elements in the cigarette smoke other than nicotine.

Monoamine oxidases, enzymes located in catecholaminergic and other neurons, catalyze the metabolism of dopamine, norepinephrine, and serotonin. Condensation products of acetaldehyde in cigarette smoke with biogenic amines inhibit the activity of monoamine oxidase type A and monoamine oxidase type B, and there is evidence that inhibition of monoamine oxidase contributes to the addictiveness of smoking by reducing the metabolism of dopamine.22,23

Carbon Monoxide – is a deadly gas which is poisonous and cannot be detected using our senses as it is not identifiable with its smell or taste. It is emitted by faulty boilers and car exhausts. When we breathe, carbon monoxide enters our air pathway along with oxygen and the other gases we draw in. It is then diffused into the bloodstream just like oxygen is; by going through the mouth/nose, down the trachea, into the lungs.

Carbon monoxide is lethal here as it binds to haemoglobin in the red blood cells to create carboxyhaemoglobin. There is a large number of red blood cells in blood and that’s why it appears red. Haemoglobin is a protein molecule responsible for transporting oxygen around the body. Carbon monoxide mimics the role of oxygen and is diffused mover from the blood to tissue and muscles instead of oxygen. The lack of oxygen is harmful for cells to function properly, leading to possible cell death and leaving the body in a state of asphyxiation. This precedes to muscle and heart dysfunction – making the body and muscles feel weak. This could go unnoticed in a regular lifestyle, but would be noticed when doing intense exercise.

In addition, 10% to 15% of carbon monoxide binds to other proteins, particularly myoglobin within cardiac muscle. This hinders binding with oxidative phosphorylation, which is necessary for myocardial contraction. Chest pain, arrhythmias, hypoperfusion, and myocardial injury/ischemia can occur with moderate exposure.6

Prolonged carbon monoxide exposure can be more brutal as it is linked to coronary heart disease. This is when the blood supply to the blood is disrupted or blocked, leading to chest pain. It can also effect the brain and cause memory problems, concentration difficulty, and vision or hearing loss.

Tar is a sticky substance produced when tobacco is burnt during smoking and contains many cancer-causing chemicals. It does not become a gas and stays in a solid state in the lungs. It damages many biochemical and mechanical processes. Tar coats the cilia in the lungs, making them not work or die. Cilia in the lungs are used to help clean the pathway by stopping build-up of mucus/unwanted particles. As the cilia are covered by tar, their function is lost, toxic particles in tobacco smoke can travel directly to the alveoli without the being trapped in the cilia. As a result of this, breathing is troubled and there are possibilities of lung cancer. Tar also damages the mouth by rotting and blackening teeth, damaging gums, and desensitizing taste buds.

Tobacco use is associated with increased risk of several cancers, including lung, larynx, oesophagus, oral cavity and pharynx, bladder, pancreas, kidney, liver, stomach, bowel, cervix, leukaemia, and ovarian cancers.


Smoking also is a big risk of major heart diseases such as coronary heart disease, heart attacks, strokes and some vascular diseases. The increased heart rate due to carbon monoxide and nicotine intake increases the risk of a blood clot. Other chemicals can damage the lining of blood vessels by the depositing of plaques. If these build up, it can cause the narrowing of the vessels. Smoking doubles the risk of having a heart attack and smokers have twice the risk of dying from coronary heart disease than those who have not smoked before.

Each puff of a cigarette contains more than 60 well-established carcinogens. Considerable evidence indicates that in human cancers caused by cigarette smoking, PAHs, N-nitrosamines, aromatic amines, and certain volatile organic agents play a major role. The most common type of cancer death in the UK is lung cancer. There are around 35,900 lung cancer deaths in the UK in 2014 and there were 46, 403 new cases of lung cancer, 2014. Smoking tobacco is one of the biggest causes of lung cancer. More than 8 out of 10 lung cancers (80%) are caused by smoking.

The picture below shows what area of the body smoking can cause cancer to and also the number of cases of each part getting cancer is represented by the circles. The bigger the circle, the higher the number of cancer cases in the UK linked to smoking.  Lung cancer has the biggest circle meaning it is the most common cancer which is linked to smoking in the UK. Ovaries and cervix cancer have the smallest circles, indicating the least common cancer linked to smoking.

cancers caused by smoking

There are 2 types of AMD; dry and wet. Dry AMD affects approximately 80-90% of individuals with AMD. This occurs when the layer of retinal pigment epithelial cells are broken down or have begun to break down. These RPE cells support the rods and cones (see introduction). Degeneration of these cells are called atrophy. We can examine the retina for signs of AMD and will see yellowy white deposits in the macula region called drusen. Drusen are lipids and build-up of waste materials broken off from the photoreceptors. Vision loss is usually not noticed when drusen first appear. However, as the macular degeneration worsens and becomes more advanced, larger drusen will appear in size and more in quantity.

Wet AMD is more severe than dry AMD. Wet AMD accounts for only 10% of all AMD cases. However 90% of severe visual loss is due to wet AMD. It occurs when Bruch’s membrane underneath the retina breaks, causing the oxygen supply to not be stable. Our immune system reacts by growing new blood vessels from underneath the retina, the vessels abnormally grow which then leak fluid causing the macula to bulge as it is pushed against and disrupting central vision.  Unlike dry AMD which is a gradual process, wet AMD can develop quickly over a few days or weeks.


At the top of the picture we can see the macular photoreceptors and then underneath is the retinal pigment epithelium and then there is Bruch’s membrane. Most cases of AMD are due to abnormalities in Bruch’s membrane which is between the retinal pigment epithelium and the choroid. The retinal pigment epithelium cells and Bruch’s membrane and in responsible for important functions such as the maintenance of the microenvironment of the photoreceptors.

Bruch’s membrane allows transmission of materials through and from the RPE. For example, metabolic waste is transported from the photoreceptors to the choroid via Bruch’s membrane. As Bruch’s membrane becomes abnormal, becomes thick and drusen build up, it begins to compromise the function of the retinal pigment epithelial cells and thus compromising the function of the photoreceptors leading to problems in vision.

From the picture above, we can see Bruch’s membrane is being used as a barrier between the choroid and the retinal epithelium cells. In AMD, the choroidal blood supply penetrates the weak Bruch’s membrane (due to ageing changes). Vessels grow from underneath the retina in response to increased VEGF secretion from ischemia. The blood vessels grow upwards, pushing the retinal epithelium cells and the photoreceptors up, thus misaligning the photoreceptors and causing vision to be distorted.

Visible light is the only part of the electromagnetic spectrum which is visible to the human eye. It falls between infrared and ultra violet radiation, with wavelengths between 390nm and 700nm. How we see colour is partially explained by the trichromatic theory (also called the Young-Helmholtz theory).

Firstly, Thomas Young suggested that there are three different receptors responsible for colour vision. Hermann von Helmholtz later discovered that colour vision requires three different wavelengths of light to create a variety of colours.

The three primary colours (primaries) are derived from three different cone receptors:

  • Short-wavelength cone receptors (Blue),
  • Middle-wavelength cone receptors (Green), and
  • Long-wavelength cone receptors (Red).


The graph above shows us that although the wavelengths are close together, especially the long and middle one, the difference is noticeable with our colour vision. The shortest wavelength for a cone receptor is blue – having a peak at 420 nm (represented by the blue curve). The next cone receptor is green at the medium wavelength, with a peak at 534 nm (represented by the green curve). And finally the longest wavelength for a cone receptor is red, with a peak at 564 nm (represented by a red curve). All three wavelengths combine in different ways to form different colours, e.g. yellow, orange, cyan, etc.

Those suffering from AMD will have majority of these cone receptors disrupted, leading to colour deception difficulty.

3583 people aged 43-86 years had a baseline examination between 1988 and 1990, then a 5 year follow up between 1993 and 1995. The sample was questioned about cigarette smoking in the past, present, duration of smoking and the number of cigarettes smoked per day. The age-related maculopathy grading was determined by grading the stereoscopic colour fundus photographs using the Wisconsin Age-related Maculopathy Grading System. Age, gender, vitamin supplement use and alcohol consumption was kept controlled.

Results showed that men who smoked more cigarettes were more likely to develop early age-related maculopathy (odds ratio (OR) per 10 pack-years smoked = 1.06, 95% confidence interval (CI) 1.00-1.13, p = 0.06) than men who had smoked less. This relationship was not found in women.

Men (OR = 3.21, 95% CI 1.09-9.45) and women (OR = 2.20, 95% CI 1.04-4.66) who were current smokers at the time of the baseline examination had significantly higher odds of developing large drusen (> or = 250 microns in diameter) after 5 years than those who had never smoked or who quit before the baseline study.

The authors have concluded based on these findings that smoking appears to be linked to early age-related maculopathy.

Another Beaver Dam Eye study carried out investigated the relationship of cigarette smoking and the progression of AMD. Examinations were carried out every 5 years over 20 years on a total of 4439 participants. The extent of AMD was determined by grading retinal photographs.

Current smokers showed to have an increased risk of going from minimal to moderate early AMD. A greater number of pack-years smoked was associated with an increased risk of transitioning from no AMD to minimal early AMD and from severe early AMD to late AMD.

The findings illustrated that the incidence of early AMD over the 20-year period was 24.4%, and the incidence of late AMD was 4.5%. And also current smoking and a greater number of pack-years smoked increases the risk of progression of AMD.

This beaver dam eye study examined 3684 people who were between 43 and 86 years old over a 10-year period starting from 1988-1990. The aim was to see if there was an association between smoking and alcohol consumption and the long term incidence of age-related maculopathy. The condition was determined by grading fundus photographs.

The authors found that people who had smoked more were more likely to develop large (> or =250 micro m in diameter) soft drusen (risk ratio (RR) per 10 pack-years smoked = 1.08, 95% confidence interval (CI): 1.02, 1.14) and pigmentary abnormalities (RR = 1.09, 95% CI: 1.04, 1.14) and to have progression of early ARM (RR = 1.05, 95% CI: 1.00, 1.10) than people who had smoked less and thus have deduced that smoking has a positive link early signs of age-related maculopathy.

Alcohol was also part of this study. Although my dissertation does not involve alcohol, this study concluded with heavy drinkers of alcohol to be more likely to develop late age-related maculopathy than those who have reported never to be heavy drinkers. This could be a big contributing factor and was not used as a control in other studies.

4750 people were randomly sampled who were aged 65 and older from 7 different European countries (Norway, Estonia, United Kingdom, France, Italy, Greece, and Spain) to find out the association between cigarette smoking and age-related maculopathy (ARM) which includes AMD.

Participants of the study underwent an eye examination and digital retinal photography. Images of the fundi were assessed and graded at a single centre. Smoking history was taken by conducting a structured questionnaire to the partakers. Multinomial and binary logistic regressions were used to examine the association between smoking history and ARM grade and type of AMD.

The fundi images were graded according to the International Classification System for ARM and stratified using the Rotterdam staging system into 5 exclusive stages (ARM 0-3 and ARM 4, also known as AMD).

158 cases were categorized as AMD (109 being wet AMD and 49 being dry AMD); 2260 had no signs of ARM. Current smokers showed increased odds of wet AMD (odds ratio [OR], 2.6; 95% confidence interval [CI], 1.4-4.8) or dry AMD (OR, 4.8; 95% CI, 2.1-11.1). However ex-smokers had odds of approximately 1.7. Compared with people who had unilateral AMD, bilateral AMD sufferers were more likely to have a history of heavy smoking in the previous 25 years (OR, 5.1; 95% CI, 1.3-20.0).

The results meant that current smokers had higher odds of suffering from AMD than ex-smokers. These findings highlight the need for increasing public awareness of the risks associated with smoking and the benefit of quitting smoking. Patients with unilateral disease who are current smokers should be advised of the risk of second-eye disease.

The aim of this study was to assess the association between age-related maculopathy (ARM) and current and passive smoking. A cross-sectional study of a sample of 3654 people from a defined west area of Sydney, Australia. Questionnaires regarding smoking history were made to get background information of the smokers’ past. Logistic regression, adjusting for age and sex, and 2-way analysis of variance were used to assess associations.

Current tobacco smoking had a significant relationship with wet AMD (odd ratio (OR), 3.92) and dry AMD (OR, 4.54). Smoking was also seen to have a significant association with late AMD (OR, 1.83) but not early ARM. Passive smoking was associated with increased but insignificant odds for late AMD.

These results have provided the authors with sufficient evidence to suggest that smoking is causally linked to ARM. The highest risk found from the study was those who were current smokers and have concluded it would be beneficial to advise and educate older patients who smoke about the risk of ARM/AMD.

6174 elderly people aged 55 years and older from the city district of Rotterdam, Netherlands.

Subjects were interviewed to identify their smoking history. Age-related macular degeneration was diagnosed by evaluating the fundi. Relative risks and 95% confidence intervals (CIs) were calculated using multivariate logistic regression analysis.

In subjects younger than 85 years old, current smokers had a 6.6-fold increased risk of wet AMD than those who had never smoked before (95% CI, 2.8-15.9). Former smokers had a 3.2-fold increased risk of wet AMD than those who have not smoked (95% CI, 1.4-7.4). Smoking was not associated with dry AMD in this study. A strong increased risk of wet AMD was present in those who had smoked more than 10 pack-years (relative risk, 6.5; 95% CI, 2.9-14.8). Those who had quit smoking 20 or more years before the eye examination had no increased risk.

These outcomes resulted in evidence supporting the relationship between smoking and AMD, especially in people with wet AMD.

The title of this study is “A prospective study of cigarette smoking and age-related macular degeneration in women”. There were 31 843 registered nurses participated in the Nurses’ Health Study who were aged 50 to 59 years old in 1980 who took part in the experiment in 11 states in the United States of America. These nurses did not report a diagnosis of AMD at the beginning of the study. Every 2 years, their information on smoking habits were collected and updated.

Women who currently smoked 25 or more cigarettes per day had a relative risk (RR) of AMD of 2.4 (95% confidence interval [CI], 1.4-4.0) compared with women who never smoked.  Past smokers of this amount also had a 2-fold increased risk (RR=2.0; 95% CI, 1.2-3.4) relative to never smokers. Risk of AMD also increased with an increasing number of pack-years smoked (P for trend <.001); among women who smoked for 65 or more pack-years, the risk was 2.4 times the risk of never smokers (95% CI, 1.5-3.8).

21 157 male physicians from the US enrolled in the Physicians’ Health Study were followed for at least 7 years with an average of 12.2 years follow up. 11% of the sample were current smokers, 39% were ex-smokers and 50% had not smoked previously.

The main outcome which would be measured is incident AMD, which is defined by self-report that was confirmed by medical record, review, first diagnosed after randomization, and responsible for vision loss to 20/30 (6/9 UK) or worse.

There were 268 incident cases of AMD where vision loss were confirmed. In multivariate analysis, current smokers of 20 or more cigarettes per day, compared with those that have not smoked before, had an increased risk of AMD (relative risk [RR], 2.46; 95% confidence interval [CI], 1.60-3.79). Past smokers had a slight increase in risk of AMD (RR, 1.30; 95% CI, 0.99-1.70).


A study titled “Risk Factors for Progression of Early Age-Related Macular Degeneration in Koreans” involved 10 890 participants who are older than 50 years old. 318 began the study with early AMD. From these 318 people, 172 were re-examined after a mean duration of 4.4 years. The progression was defined by the Age-Related Eye Disease Study (AREDS) simplified AMD severity scale. Multivariable logistic regression was used to examine associations between AMD progression and baseline physical, demographic, behavioural, and ocular characteristics.

34 (19.8%) of the 172 people that were re-examined had progression in AMD severity. Multivariable analyses revealed that current smoking (odds ratio, OR, 7.0, 95% confidence interval, CI, 1.4-34.4, adjusted for age, alcohol consumption, body mass index, BMI, blood pressure, BP, total cholesterol, and high density lipoprotein, HDL, cholesterol) and hypertension (OR 10.3, 95% CI 1.9-55.7, adjusted for age, smoking status, alcohol consumption, BMI, total cholesterol, and HDL cholesterol) were independently associated with progression of early AMD.

The results of this study show that smoking is also linked to AMD in the Korea, East Asia and this indicates the association between smoking and AMD isn’t constrained only to the countries in the West.

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The graph below was taken from a study called Neovascular Age-Related Macular Degeneration Risk Based on CFH, LOC387715/HTRA1, and Smoking. This graph compares how early the participants of the study were diagnosed with end-stage AMD in those that are non-smokers, ex-smokers and current smokers. There is a clear pattern illustrated in the graph showing a general trend which is current smokers being the earliest to have end-stage AMD (approximately 72 years old), followed by those people who are ex-smokers (i.e. have previously smoked and now stopped) having end-stage AMD later on in life (approximately 74 years old); and then the participants who are non-smokers (have not previously smoked and currently do not smoke) with the age of end-stage AMD onset being at its latest (approximately 76 years old).

There is a distinct theme in the graph and study, however the difference between the 3 different groups are very close together and some results overlap. For example, some current smokers were at the end-stage AMD after some people who were ex-smokers. Therefore although there are some downfalls of the results, the overall outcome supports the other studies which have been mentioned previously.

This literature written is titled: Smoking and age-related macular degeneration: a review of association. It evaluates the epidemiological evidence associating smoking with AMD. They used 17 studies which were cross-sectional studies, prospective cohort studies and case-control studies. 13 out of the 17 studies used found a statistically significant association between smoking and AMD with an increased risk of AMD of 2-3 times more in current smokers than those who have not smoked before. The review confirmed a strong relationship between smoking and AMD, which established the causality criteria.


Your Treatment Options

There aren’t any cures for AMD. Patients with dry AMD may be referred to a low vision clinic for trying different types of magnifying lenses or large-print books or telescopes. A large study carried out by the National Eye Institute of the National Institutes of Health, called AREDS (Age-Related Eye Disease Study) showed there were improvements to those suffering from AMD who took supplements containing vitamin C and E, zinc and copper. There’s some evidence to suggest a diet high in vitamins A (beta-carotene) may slow the progression of dry AMD. An updated AREDS2 formula, to make it safer for smokers, added lutein, zeaxanthin, and omega-3 fatty acids and removed beta-carotene because it was linked to a high risk of lung cancer in smokers.

Getting in contact with an ECLO (eye clinic liaison officer) is also beneficial as they will be able to help those who need advice or need any questions to be answered or would need support and counselling. Also registering the patient as partially sighted or severely sight impaired would help them claim benefits.

The first treatment available for wet AMD was Laser photocoagulation in the 1980s. If the new blood vessels are outside the fovea, it was treated with an intense laser which obliterated the choroidal neovascular membrane. The problem was only a few cases had the blood vessels growing outside the central fovea. Majority of the cases already had the CNM within the fovea. Therefore this treatment is not advised as it would destroy the central fovea. Even if it wasn’t in the centre, Ophthalmologists would be wary of using an intense laser near the fovea as the scars spread towards the fovea – causing (central) vision problems. Thus they would undertreat patients which leads to 50% recurrence rate within 12 months. A consequence of using the intense laser is it will create a scotoma in vision resulting in a blank area.

The photodynamic therapy (PDT) laser was introduced in the late 1990s.This was the first time wet AMD was able to be treated involving the fovea. It’s not as damaging as laser photocoagulation. It is a two-step process which cleverly uses light to activate the drug in the CNM. Verteporfin drug is infused intravenously by the drip method. At a precise time after infusion, when drug at maximum concentration in choroid, a special laser at 690 nm is applied to the CNV and the drug is then activated. Upon activation, the laser damages the abnormal blood vessels, thus stopping growth. The CNV then heals up as a scar. It is more likely damage limitation rather than vision improvement. It’s still used for for some retinal conditions but now superseded by pharmacotherapy for wet AMD.

Anti-VEGF injection began in 2006. VEGF is a protein released by cells when signalled which stimulates the growth of new arteries and veins. High levels of VEGF have been found in CNV surgically excised from humans or animal experimental CNV. There are a few types of anti-VEGF drugs used in treatment of wet AMD, these are: Ranibizumab (Lucentis), Bevacizumab (Avastin) and Pegaptanib (Macugen). The best one from these is Lucentis. It is a monoclonal antibody against VEGF and has the ability to inhibit all kinds of VEGF. The intravitreal injection consists of 0.5mg of Lucentis and the liquid is 0.05ml. It is a licenced regime by NICE (National Institute for Health and Care Excellence). These drugs have been able to help people suffering from wet AMD to regain their vision but follow-up visits likely needed for the treatment to be effective. The treatment commences with a loading dose of 3 intravitreal injections at monthly intervals (0.5mg monthly for 3 months). Thereafter further injections will be given in response to the outcome of the first injections; assessing visual acuity and examining with an OCT (Optical Coherence Tomography).

The graphs below shows the results carried out by MARINA. Both graphs contain the same results but illustrated slightly differently. The MARINA study compared the treatment of Lucentis against a control group who had no treatment on their AMD to see if their visual acuity got better or worse over 12 months on an ETDRS chart (logMAR). The experiment was done over a 12 month period. The results showed that those who did not have any treatment (represented by the black line) had their visual acuity decreased after 12 months and could read on average 10.4 letters less than when started. However, those participants who had taken Lucentis had an improvement in their visual acuity and was able to read 6.5 letters more (represented by the orange line with 0.3mg Lucentis) and 7.2 more letters (represented by the red line with 0.5mg Lucentis). This clearly shows how effective Lucentis is as a treatment with the visual acuity improving immensely.


The ANCHOR study is comparing the effectiveness of treatment of AMD patients with Lucentis against those treated with a PDT laser to see if their visual acuity got better or worse over 12 months on an ETDRS chart (logMAR). The experiment was done over a 12 month period. The results showed that those who were treated using the PDT laser method (represented by the green line) had their visual acuity get better after the first month then vigorously started to decrease and over the 12 months, the average letters seen were 9.5 letters less than when starting the treatment. This was an improvement than the results of those who weren’t treated in the MARINA study. However compared to those who had taken Lucentis had an improvement in their visual acuity and was able to read 8.5 letters more (represented by the orange line with 0.3mg Lucentis) and 11.3 more letters (represented by the red line with 0.5mg Lucentis). This study demonstrates the anti-VEGF therapy is superior to PDT laser treatment.


The main reason people smoke is because they are addicted to nicotine. Treatment for smoking is done by gradually taking the smoker off nicotine. This is done in the following ways:

  • Nicotine Replacement Therapy
  • Varenicline (Champix)
  • E-cigarettes

The Nicotine Replacement Therapy (NRT) is a way of taking in low levels of nicotine without smoking a cigarette containing the harmful substances like tar and carbon monoxide. NRT can be bought from pharmacies and can also be prescribed by your doctor. NRT is taken in different ways depending on the smoker’s preference. It is available in adhesive skin patches, chewing gum, tablets, lozenges, nasal/mouth spray. Patches release nicotine at a slow and stable pace; the problem with this is it doesn’t copy how the body received nicotine while smoking in a big amount during a short amount of time. The other methods give an instant supply of nicotine to the body and can be beneficial when one is craving nicotine. NRT does increase the chance of quitting smoking and best results are found when NRT is taken with counselling.

Varenicline is a medicine first licenced in the UK in December 2006. It’s similar to how NRT works but is effective in two ways. Firstly it stimulates nicotine receptors to reduce cravings and the withdrawal effects. It then also cleverly blocks the receptors and prevents nicotine from attaching to the receptors. This shuns the effects of nicotine in those who give in to the temptation and begin to smoke.

E-cigarettes are an electronic handheld device which vaporises flavoured liquid usually containing nicotine and have recently hit the market. Using this device is sometimes called vaping. The use of an e-cigarette is mimicking smoking a cigarette but vapour is inhaled rather than harmful cigarette chemicals. The long term effects are unknown but it is likely to be safer than tobacco cigarettes as no serious adverse effects have been reported in trials.

In conclusion, there is sufficient evidence from the range of studies carried out to suggest smoking is a modifiable risk factor of age-related macular degeneration. There have been flaws in some studies, for example:

  • Not all studies mentioned the pack-years smoked by the participants
  • Family history of the participants were not take into account
  • Not all studies took alcohol consumption into account
  • Sample size may not account for the entire population
  • Those that partook the study may not be truthful regarding their smoking past
  • Some studies took place roughly 25 years ago, do the results still stand as science have developed over this time period and become more sophisticated and accurate methods have been introduced to assess the fundus

Even though there are these imperfections, due to the overwhelming collective results, this elective study supports smoking being a risk factor in AMD (especially wet AMD). Therefore optometrists should make a mental note to advise patients to refrain from smoking, especially when early signs of AMD have been seen at the back of the eye.


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