**1. Introduction**

Sugar forms an integral part of the human eye, and can be found in different parts of the eye including the tears, aqueous humour, and the lens. Its primary function in the eye includes; maintenance of the structural component of the eye, and the provision of nourishment to the surrounding structures of the eye wherein it is found. For instance, glucose found in the aqueous humour forms part of the required nourishment to the avascular lens, and cornea [1]. In the tears, sugar in the form of glucose forms part of the nutrients that supply the avascular cornea. The sugar in the vitreous is present as hyaluronic acid which is a molecular unit of glucusonite, and N-acetylglucosamine. Its function is to maintain the point of vitreous attachment to the retina. In general, sugar is important for the normal functioning of the human eye. In the lens, sugar is found as polysaccharides. Meyer *et al* [2] showed that there are at least three different polysaccharides in the cornea stroma - keratin sulfate, chondroitin-4-sulfate, and chondroitin, and may play a role in cornea healing.

Despite the role of sugar in maintaining the metabolic requirements of the human body, excessive sugar consumption can lead to high sugar concentration in blood circulation within the body system which can be detrimental to human health. Sustained high sugar level results in hyperglycaemia, and if left unchecked can result in Diabetes Mellitus. Diabetes mellitus is a group of metabolic diseases, characterized by chronic hyperglycaemia due to deficiency in the production, and/or usage of insulin. Diabetes mellitus can occur as either Type 1 (due to poor secretion of insulin) or Type 2 (due to poor usage of insulin for glucose metabolism).

Diabetes Mellitus presents with a myriad of ocular complications and has been identified as the leading cause of legal blindness globally. Complications secondary to diabetes affects almost every part of the eye and could result in diabetic retinopathy, cataracts, glaucoma, keratopathy, dry eye syndrome, and so many others (**Figure 1**).

**Figure 1.** *Fundus picture of a proliferative diabetic retinopathy.*

In recent years, diabetes mellitus has become a serious public health concern as the number of diabetic patients worldwide has more than doubled over the last three decades. In 2010, 286 million people were said to be diabetic, and this was projected to increase to 439 million by 2030 [3]. As the prevalence of DM, duration, and onset increases, the number of patients with ocular complications due to the condition is also expected to increase.

## **2. Mechanism of action of the effect of hyperglycaemic on the eyes**

The mechanism of action of hyperglycaemia on the eyes and the consequential damage to the eyes have been likened to that of the effect of ageing on the eye [4]. Various factors such as pro-inflammation, oxidative stress, glycosylated crosslinkages, the formation of advanced glycelated end-products (AGE), vascular permeability, vascular endothelial growth factor (VEGF), and epigenetic factors have been found to cause to ageing changes in the eye. Similarly, these factors have been implicated in the development of ocular complications secondary to sustained increased sugar levels in the body [5–7].

Further, Insulin resistance as may be seen in diabetic patients has been associated with the repression of a Sirtuin 1(Sirt 1) [8], which is the gene responsible for the regulation of appetite in the geriatric population. Sirt 1 is also known as the anti-ageing gene due to its ability to alleviate oxidative stress [8–10]. Repression of Sirt 1 gene may lead to mitochondrial apoptosis, and in diabetic patients can also lead to diabetic retinopathy due to oxidative stress [8, 10, 11].

#### **3. Sugar, and the lens: an overview**

The human crystalline lens is the structure directly behind the iris, and in front of the vitreous humour [1]. The lens thickness and curvature allows it to

**23**

*Impact of Sugar on Vision*

and alignment.

diffusion.

**3.1 Sugar, and cataract**

nent bonds, and eventually cataract.

effective way of manageing diabetic cataracts.

fewer complications, and better prognosis.

*DOI: http://dx.doi.org/10.5772/intechopen.96325*

contribute significantly to refraction [12]. It is also responsible for accommodation in non-presbyopic, and pre-presbyopic people. Its transparent nature allows for the passage of light to the retina. Physiologically, the lens contains 2/3 water, and 1/3 protein (water-soluble and water-insoluble proteins) [13]. Water-soluble proteins are responsible for maintaining the lens optical properties. On the other hand, water-insoluble protein maintains cellular structures, architectural arrangement,

The lens lacks blood vessel supplies to it and is therefore regarded as avascular. Due to the lack of blood vessels in the lens, it acquires most of its nutrition from the aqueous humour, through the aerobic glycolysis, or through the pentose phosphate pathway (sorbitol pathway). The sorbitol pathway is believed to be a pathway through which glucose, and galactose from the aqueous humour is absorbed into the lens [14]. When glucose is absorbed, it is reduced to sorbitol by the aldose reductase enzyme. Further to this, sorbitol is metabolized by the sorbitol dehydrogenase, whereas galacititol remains in the lens nearly not metabolized for a prolonged period. In diabetes, the increased presence of sugar in the blood results in increased glucose level in the aqueous, therefore bringing about increased sugar inflow into the lens through the sorbitol pathway [15]. Unfortunately, the sorbitol is produced faster than it is converted to fructose by the sorbitol dehydrogenase. This, therefore, means an increased amount of sorbitol in the lens. The prolonged presence of sorbitol in the lens results in increased intracellular fluid as a response to increased osmotic pressure, therefore causing the swelling of the lens material. Further, because sorbitol is polar, it is hardly removed from the lens through simple

Sustained hyperglycaemia causes the inflow of sugar into the lens resulting in the swelling of the lens material. This also results in the loss of the lens structural arrangement (lens fibres), precipitation of the water-insoluble proteins, oxidation of the water-insoluble proteins, hardening of the lens fibres, formation of perma-

Sugar induced cataract is a common occurrence, and a significant cause of visual impairment among diabetic patients. According to the Framingham study findings, diabetic patients under 65 are four times more likely to develop cataracts than their normal age mates. The onset of cataract in diabetes is often associated with fluctuations in the sugar level of a sufferer, and the cataract progresses rapidly once initiated. Even though the process of cataract formation in a diabetic patient is known, however, there is no known mechanism to delay its formation in the presence of Hyperglycaemic [16]. Nevertheless, cataract surgery is a recommended, and

Early cataract extraction in diabetic patients though recommended, should be approached with caution, and is advisable to be done with regulated blood sugar levels as healing may be delayed due to Hyperglycaemic [17, 18]. Although, a study in Nigeria reported no significant difference in the visual outcome of diabetic patients post-cataract when compared to age-matched nondiabetic controls, however, complications such as rubeosis, acceleration in the formation of retinopathy, post-operative inflammation,, and incidence of clinical, and angiographic cystoid oedema has been reported to occur more in diabetic patients following cataract extraction [19]. Given these complications, the preferred method of cataract extraction in diabetic patients is phacoemulsification as this has been associated with

#### *Impact of Sugar on Vision DOI: http://dx.doi.org/10.5772/intechopen.96325*

*Sugar Intake - Risks and Benefits and the Global Diabetes Epidemic*

In recent years, diabetes mellitus has become a serious public health concern as the number of diabetic patients worldwide has more than doubled over the last three decades. In 2010, 286 million people were said to be diabetic, and this was projected to increase to 439 million by 2030 [3]. As the prevalence of DM, duration, and onset increases, the number of patients with ocular complications due to the

**2. Mechanism of action of the effect of hyperglycaemic on the eyes**

The mechanism of action of hyperglycaemia on the eyes and the consequential damage to the eyes have been likened to that of the effect of ageing on the eye [4]. Various factors such as pro-inflammation, oxidative stress, glycosylated crosslinkages, the formation of advanced glycelated end-products (AGE), vascular permeability, vascular endothelial growth factor (VEGF), and epigenetic factors have been found to cause to ageing changes in the eye. Similarly, these factors have been implicated in the development of ocular complications secondary to sustained increased

Further, Insulin resistance as may be seen in diabetic patients has been associated with the repression of a Sirtuin 1(Sirt 1) [8], which is the gene responsible for the regulation of appetite in the geriatric population. Sirt 1 is also known as the anti-ageing gene due to its ability to alleviate oxidative stress [8–10]. Repression of Sirt 1 gene may lead to mitochondrial apoptosis, and in diabetic patients can also lead to diabetic

The human crystalline lens is the structure directly behind the iris, and in front of the vitreous humour [1]. The lens thickness and curvature allows it to

condition is also expected to increase.

*Fundus picture of a proliferative diabetic retinopathy.*

**Figure 1.**

sugar levels in the body [5–7].

retinopathy due to oxidative stress [8, 10, 11].

**3. Sugar, and the lens: an overview**

**22**

contribute significantly to refraction [12]. It is also responsible for accommodation in non-presbyopic, and pre-presbyopic people. Its transparent nature allows for the passage of light to the retina. Physiologically, the lens contains 2/3 water, and 1/3 protein (water-soluble and water-insoluble proteins) [13]. Water-soluble proteins are responsible for maintaining the lens optical properties. On the other hand, water-insoluble protein maintains cellular structures, architectural arrangement, and alignment.

The lens lacks blood vessel supplies to it and is therefore regarded as avascular. Due to the lack of blood vessels in the lens, it acquires most of its nutrition from the aqueous humour, through the aerobic glycolysis, or through the pentose phosphate pathway (sorbitol pathway). The sorbitol pathway is believed to be a pathway through which glucose, and galactose from the aqueous humour is absorbed into the lens [14]. When glucose is absorbed, it is reduced to sorbitol by the aldose reductase enzyme. Further to this, sorbitol is metabolized by the sorbitol dehydrogenase, whereas galacititol remains in the lens nearly not metabolized for a prolonged period. In diabetes, the increased presence of sugar in the blood results in increased glucose level in the aqueous, therefore bringing about increased sugar inflow into the lens through the sorbitol pathway [15]. Unfortunately, the sorbitol is produced faster than it is converted to fructose by the sorbitol dehydrogenase. This, therefore, means an increased amount of sorbitol in the lens. The prolonged presence of sorbitol in the lens results in increased intracellular fluid as a response to increased osmotic pressure, therefore causing the swelling of the lens material. Further, because sorbitol is polar, it is hardly removed from the lens through simple diffusion.

#### **3.1 Sugar, and cataract**

Sustained hyperglycaemia causes the inflow of sugar into the lens resulting in the swelling of the lens material. This also results in the loss of the lens structural arrangement (lens fibres), precipitation of the water-insoluble proteins, oxidation of the water-insoluble proteins, hardening of the lens fibres, formation of permanent bonds, and eventually cataract.

Sugar induced cataract is a common occurrence, and a significant cause of visual impairment among diabetic patients. According to the Framingham study findings, diabetic patients under 65 are four times more likely to develop cataracts than their normal age mates. The onset of cataract in diabetes is often associated with fluctuations in the sugar level of a sufferer, and the cataract progresses rapidly once initiated. Even though the process of cataract formation in a diabetic patient is known, however, there is no known mechanism to delay its formation in the presence of Hyperglycaemic [16]. Nevertheless, cataract surgery is a recommended, and effective way of manageing diabetic cataracts.

Early cataract extraction in diabetic patients though recommended, should be approached with caution, and is advisable to be done with regulated blood sugar levels as healing may be delayed due to Hyperglycaemic [17, 18]. Although, a study in Nigeria reported no significant difference in the visual outcome of diabetic patients post-cataract when compared to age-matched nondiabetic controls, however, complications such as rubeosis, acceleration in the formation of retinopathy, post-operative inflammation,, and incidence of clinical, and angiographic cystoid oedema has been reported to occur more in diabetic patients following cataract extraction [19]. Given these complications, the preferred method of cataract extraction in diabetic patients is phacoemulsification as this has been associated with fewer complications, and better prognosis.

#### **3.2 Sugar, and refractive error**

Refractive changes have been noted to occur in diabetic patients. A number of earlier clinical studies had reported an association between sustained hyperglycaemia, and refractive shift towards increased myopia [12, 19, 20]. Myopic shift occurs when a diabetic patient experiences more myopia than the regular refractive error status. This happens due to an increase in the inflow of sugar into the lens through the sorbitol pathway catalysed by the aldose reductase activity [21, 22]. People with diabetes have been observed to have a higher prevalence of myopia compared to those without diabetes [23]. In a study conducted by Jacobsen *et al* [24] it was determined that the prevalence of myopia (spherical equivalent 0.5 D) was 53.3% among 252 type 1 diabetic patient age 16–26 years old. The relative risk of a myopic shift was determined to be 1.7 in patients aged 16–21 years, and 1.6 in patients with HbA1c above 8.8%. Insulin dosage was not related to myopia. Klein et al. [21] showed that persons of similar age with T1D were likely to be more myopic than those with T2D. In general, myopia associated with diabetes reverses when sugar control is instituted.

Although past studies had reported a myopic shift in refractive status following an increase in sugar level, however, recent studies have also noted a hyperopic shift associated with glycaemic control [25, 26]. Hyperopic shift following hyperglycaemia control has been reported to occur when glucose levels fall a few days or weeks after the initiation of glycaemic control [12, 27]. This hyperopia was associated with increased lens thickness, and a decrease in anterior chamber depth [22]. Lin *et al* [12] reported the development of hyperopia in 4 men and 1 woman who was treated with insulin. According to their report, the hyperopia peaked at 11.7 days after initiation of glycaemic control and tapered off at 64.0 days after treatment initiation. From this it can be deduced that institution of treatment in diabetic patients is often followed by two refractive changes; one involving a rapid refractive change towards the direction of hyperopic, and the other is a gradual change to the patient's normal refractive status.

In general, both myopic, and hyperopic shifts are transient, and patients' refractive status gradually returns to the baseline values a few days or weeks after sugar stabilizes. Thus, it can be said that both myopic, and hyperopic shift may occur with changes in sugar levels in a hyperglycemic patient [25]. Hence, change in prescription glasses should be approached with caution as glasses prescribed during this time will only be durable during the said sugar fluctuations [28].

#### **3.3 Sugar, and accommodation**

Several studies have reported on biometric changes such as lens thickening, increase in the lens surface curvature and a decrease in the refractive index secondary to diabetes [29]. According to Mathebula, and Makunyane "people with diabetes have accelerated age-related biometric ocular changes compared to people without diabetes" [4]. Elevated sugar levels in pre-presbyopic patients have been associated with a reduction in the amplitude of accommodation. According to Huntjens and O'Donnell, amplitude of accommodation is lower in people living with Type I patients than that of their non-diabetic age-matched, even in the absence of non-detectable retinal damage [25].

Amplitude of accommodation is important for maintaining images on the retina while doing near work. A reduction in amplitude of accommodation means that the near point becomes receded, and a patient will have difficulties reading things at near as seen in presbyopic patients. This has unfortunately been found in prepresbyopic diabetic patients who show signs of presbyopia earlier than their age

**25**

*Impact of Sugar on Vision*

accommodation.

polysaccharides.

diabetic retinopathy.

**4. Sugar, and the cornea**

*DOI: http://dx.doi.org/10.5772/intechopen.96325*

match nondiabetic counterparts. The effect of hyperglycaemia on the accommodative system may be due to changes in lens glucose metabolism, ischemic hypoxia on the oculomotor nerve, and ciliary muscles. Some studies have noted that the longer the duration of diabetes, the more likely the reduction in the amplitude of

The cornea is a superficial organ most affected by high sugar levels [30]. The impact of sugar on the cornea varies with its level and duration, and may underpin specific systemic complications that may be associated with diabetes. At normal glycaemic levels, sugar serves as one of the dissolved nutrients in the tears, and aqueous humour that nourishes the cornea. Sugar is also found in the cornea stroma in the form of polysaccharides (glycosaminoglycan GAG) [31]. GAG reduces the effects of diffraction when light is directed towards the eye. Chondroitin sulphate an element that plays a role in cornea wound healing is also made from

However, in diabetes, sugar promises to be detrimental to the anatomical and physiological wellbeing of the cornea. Structural components such as the epithelium, the nerves, immune cells, and the endothelium of the cornea are often negatively affected. Sustained hyperglycaemia reduces cornea sensitivity and innervation due to peripheral neuropathy. These nerve alterations occur all over the cornea including at the cornea scleral junction (limbal region) where new epithelial cells are formed [31]. When there is a reduction in corneal sensitivity, affected patients experiences various symptoms, and in most cases become susceptible to further damages to the eye. Reduction in corneal sensitivity has been identified as a

predictor for the development of peripheral neuropathy in diabetic patients.

Other cornea complications such as corneal infections, ulcers, and oedema have been reported in diabetic patients with poorly controlled glycaemic levels. Sugar induced cornea swelling increases the fragility of the cornea epithelium and can result in stroma oedema [32]. This for unknown reasons affects the stromal collagen bundles and increases corneal autofluorescence level. The variation between the normal fluorescence level and increased autofluorescence in the corneal may be an indicator of changed corneal metabolism due to impaired corneal mitochondria metabolism. Corneal fluorescence may also be an indicator of a pathological breakdown of the blood-aqueous- barrier as may be seen in patients with proliferative

Sustained hyperglycaemic levels in the body also increases the chances of corneal erosions, persistent epithelial defects, corneal endothelial damage, and dry eye [6, 22, 32]. With Sustained hyperglycaemia the cornea faces difficulties with wound healing, and most times there is incomplete wound healing, thus small corneal erosions become persistent as wound healing is delayed. Delayed wound healing has been linked to a reduction in cornea epithelium regeneration secondary to a decrease in cornea sensitivity, which occurs as a result of peripheral neuropathy [6]. linked Further, because the ability of the cornea to ward off infections is reduced,

The lids and conjunctiva are tissues in the body that protects the eye against external invaders. Sustained high blood sugar level increases the susceptibility

infections like fungal keratitis occurs and remains recurrent [33].

**5. Sugar, and the lids, and conjunctiva**

match nondiabetic counterparts. The effect of hyperglycaemia on the accommodative system may be due to changes in lens glucose metabolism, ischemic hypoxia on the oculomotor nerve, and ciliary muscles. Some studies have noted that the longer the duration of diabetes, the more likely the reduction in the amplitude of accommodation.
