The role of nutrition in myopia control

Many nutrients are required for proper growth and development. Some vitamins have been associated with the development of myopia, specifically vitamin A, vitamin B2, vitamin C, and vitamin D. (Adobe Stock / Seventyfour)

Within the eyecare community, there is a predominant consensus that the cause of juvenile onset myopia—a significant worldwide public health concern—involves both genetic and environmental elements. The rise in the prevalence of myopia has been too rapid to be explained by genetic factors alone and thus suggests a substantial role of environmental influences.

However, the interaction of these 2 components to create refractive error remains speculative. It is becoming more apparent that myopia is not only a benign refractive error but also has long-term medical and visual consequences, yet little attention has been paid to the possible role of nutrition in the development and advancement of myopia.

Numerous studies have demonstrated that near work is related to myopia; however, all individuals in industrialized countries must do regular near work during childhood education, yet only a certain percentage of the population ultimately develops myopia.

There are several factors that have been explored as potential environmental contributors to myopia development, including the spectrum of exposed light, outdoor time, circadian rhythms, spatial frequency characteristics of written material, vitamin levels, dietary intake, physical activity, excessive near work, intraocular pressure, form deprivation, and binocular vision disorders.

We will review the role of nutrition and how it interacts with the expression of genes to create the conditions thatmight lead to the development of myopia.

The evolutionary perspective

When considering the genetic influence on ocular growth and function, it must be considered to first analyze our ancestral genetic makeup. We can infer that significant myopia was not likely present in the population of the early Homosapiens, as these early humans required clear distance vision to escape predators, find food, and recognize members of other species and a host of environmental dangers. Thus, any gene or genes that would producehigh myopia would be lethal and rapidly eliminated by natural selection.

Studies by Morgan and Monroe¹ suggested that increased near work among younger individuals was the environmental factor that may have influenced the higher rates of myopia. However, they also hypothesized that dietary changes, especially higher carbohydrate intake, might affect the structure of the growing eye.

In rural areas with little exposure to modern lifestyles, the near work of reading indicates the rate of myopia reaches much beyond the rates of that of hunter-gatherers—typically less than 4%.¹ The quantity and intensity of education in these rural areas are less than in urban settings. Other environmental factors could have effects on myopia development and progression, most specifically a high availability of processed foods.

Studies of nonwesternized Eskimos indicate those who have engaged in long hours of near work (eg, sewing, tool making) in dimly lit houses did not develop myopia.^2-4 The few studies carried out in existing hunter-gatherer societies and in recently westernized hunter-gatherer groups indicate that the incidence of myopia normally occurs in less than 2% of the population, and most refractive errors are less than –1.00D. Moderate to high myopia (–3.00 to –9.00D) is either nonexistent or occurs in approximately 1in1000 individuals.

Diet-induced hyperinsulinemia and myopia

The diets of hunter-gatherer civilizations are typically considered to have high protein, moderate levels of fat, and low levels of carbohydrates when compared with modern western diets.^5,6 Additionally, the carbohydrates present in hunter-gatherer diets were typically of a low glycemic index (GI); they are slowly absorbed and produce a gradual and minimal rise in plasma glucose and insulin levels when compared with the sugars and refined starches in western diets. 

The GI is a ranking of carbohydrates on a scale from 0 to 100 according to the extent to which they raise blood glucoselevels after eating. High GI foods are those that are rapidly digested and absorbed and result in marked fluctuations in blood glucose levels. Low GI foods, by virtue of their slow digestion and absorption, produce gradual rises in blood glucose and insulin levels and have proven health benefits. A GI of more than 70 is considered high, 55 to 70 is medium, and of less than 55 is low.⁷

Figure 1.

The glycemic load (GL), which is a function of the net carbohydrate intake and its GI, estimates how much a food raises a person’s blood glucose level following its consumption. It is calculated by multiplying the GI and the carb content, and dividing that by 100 of each food. For example, a high glycemic food such as watermelon (index=72) only contains 11 net carbohydrates and thus has a GL of only 8, whereas white rice (index=64) contains 52 net carbohydrates and has a GL of 33. A GL of 20 or higher is considered high (Figure 1).⁷ 

The average GL of foods in industrialized countries has continually increased, primarily from consumption of refined cereals and sugars.⁸ Populations in more rural areas of both industrialized and non-industrialized countries typically have limited access to these processed foods, sugars, and refined cereal products.⁹ Accordingly, their diets usually consist of locally grown, minimally processed foods; hence, the GL of these traditional foods is generally lower than highly processed and packaged foods.

Over the past 30-plus years, evidence has shown that the consumption of a westernized diet promotes the development of both acute and chronic hyperinsulinemia, which has also been termed prediabetes. Numerous studies have demonstrated that the addition of sucrose in the diet of both individuals with and without hyperinsulinemia causes an increase in postprandial insulin levels.^10-12 There is evidence that insulin has both direct and indirect ocular growth promoting effects via the induction of insulin-like growth factors (IGFs), leading to decreases in IGF binding proteins (IGFBPs), which is also implicated in ocular growth.¹³

Collectively, these studies show that increasing consumption of high levels of refined carbohydrates, especially those considered high-calorie foods, is particularly responsible for the worsening of glycemic control, which may in turn promote insulin resistance and compensatory hyperinsulinemia.

Hyperinsulinemia, IGF, and IGFBPs 

The metabolic reactions that accompany hyperinsulinemia are complex and have profound effects on growth and development, including within the eye. Postprandial levels of insulin are produced by the pancreas, whereas the liver secretes IGF-1 as well as the IGFBP-1, which controls the action of IGF-1. Hyperinsulinemia suppresses the secretion of IGFBP-1 from the liver, which in turn increases free IGF-1 in the serum.¹⁴ Also, growth hormone (GH) levels are reduced via a negative feedback loop from free IGF-1 on GH secretion, resulting in reductions in IGFBP-3. Increased circulating levels of free IGF-1 is a potent stimulator of growth in all tissues (Figure 2).

Figure 2.

Myopia is a result of abnormal thinning and axial elongation of both the sclera and choroid of the eye. It is now well known that the biomechanical properties of the sclera are closely related to its structural and biochemical makeup, and that specific changes in scleral biochemistry promote ocular enlargement and therefore myopia.¹⁵

Studies in animal models confirm that in form-deprivation myopia, there is a differentiation of scleral cartilage brought about by production of both scleral chondrocytes and fibroblasts, which in turn leads to axial elongation.^16-18

Because consuming foods with refined sugars and starches promote both short- and long-term hyperinsulinemia, these foods have the potential to elevate free IGF-1 and reduce the levels of IGFBP-3 in the tissues, including the sclera. Enhanced scleral growth and effective thinning may result from both elevations in free IGF-1 and reductions in IGFBP-3. This reduction in IGFBP-3, stimulated by elevated serum insulin levels with excessive intake of high glycemic carbohydrates, may also contribute to unregulated cell proliferation in scleral tissue.^19,20

Retinoic acidreceptors and hyperinsulinemia

Retinoic acid, a metabolite of vitamin A that mediates the functions of the vitamin, is required for growth and development. The all-transretinoic acid (ATRA) form is essential in the growth of more highly developed animals. In the sclera, ATRA inhibits glycosaminoglycan synthesis, thereby thinning the sclera and promoting axial elongation.²¹ 

Hyaluronic acid (HA)is one of the non-sulfated glycosaminoglycans distributed widely throughout connective, epithelial, and neural tissues. HA binds cells together, lubricates joints, and helps maintain the shape of the eyeballs. HA is responsible for strength and integrity of scleral collagen; thus low concentrations of IGFBP-3 may enhance axial elongation by further impeding glycosaminoglycan and HA synthesis.²²

Additional nutrients that affect myopia development

Many nutrients are required for proper growth and development. Some vitamins have been associated with the development of myopia, specifically vitamin A, vitamin B2, vitamin C, and vitamin D.

Vitamin B2 (riboflavin) is essential to energy metabolism, cell respiration, and antibody production, growth, and development. It is also essential for the metabolism of carbohydrates, proteins, and fats. Additionally, riboflavin is involved in the metabolism of niacin (vitamin B3), vitamin B6, and folate. Thus, it is important to ingest all the B vitamins together, as an excess in any 1 of these can create a deficiency in the others.

Riboflavin is used in collagen cross-linking, which is an effective method for halting the progression of keratectasia. The cornea and sclera are made of a similar type of collagen fibers. In the cornea, the fibers are arranged in sheets and layers, which makes the cornea clear. In the sclera, the fibers are arranged randomly. Riboflavin functions as a photosensitizer for the production of oxygen free radicals, which induce physical cross-linking of collagen.^23,24 Thus, hyperinsulinemia might be a factor in the development of keratoconusand myopia. 

Vitamin C is essential for collagen production in the body. A deficiency leads to impaired collagen synthesis; however, the effect is increased with the addition of bioflavonoids. Vitamin C is watersoluble and flushes out of the body in 2 to 3 hours, so a single daily dose is not very effective.

Vitamin D has been studied in several trials because of its association to sunlight. However, this effect has not been born out in studies.^25,26 One possible mechanism for the effects of bright light is through pupillary constriction, which increases depth of focus, thereby reducing the demand on accommodation.

Proposed model of juvenile-onset myopia

Reduced synthesis of retinoic acid increases scleral growth, whereas increased synthesis of retinoic acid slows growth.²⁷ Excessive near work may induce myopia because form deprivation causes the choroid to produce too little retinoic acid. This would create a similar situation, as diet-induced hyperinsulinemia chronically elevates IGF-1 and therefore may synergistically act with plasma reductions in IGFBP-3 to accelerate scleral tissue growth.

Given the unprecedented rise in myopia in individuals of Asian and Chinese descent, it is important to review possible trends in their dietary habits. It is documented that this demographic tends to be more insulin resistant than individuals of European descent.^28-33

Figure 3.

Reviewing the demographics of diabetes worldwide, it should be noted that more than half of the world’s population with diabetes is centered in Western Pacific and South-East Asia regions (Figure 3). It is possible that the higher rates of myopia in Asian populations may in part be due to their increased genetic susceptibility to insulin resistance. It is important to note that white rice, which has a GL of 33, is a staple ofthe diet in Asia.

It is possible that the etiology of juvenile-onset myopia does not have a single cause but might be a result of several factors. It has been established that newborns typically exhibit low hyperopia.³³ When taking in a westernized diet that includes highly refined grains and carbohydrates, they could likely tend toward development of hyperinsulinemia.

The growth pattern of the sclera thins and continues to elongate due to the excessive carbohydrate influences combined with a lack of bright lighting and an increase of near point tasks, especially the digital display variety. This depleted nutrition pattern might continue with a vitamin B2 deficiency and an increase in intraocular pressure, with the excessive accommodation leading to continued scleral elongation and subsequent myopia. Real-world human studies would be required to confirm how these interactions might lead to the current state of myopia development.

In conclusion, a review of the above referenced studies suggest that high GL carbohydrate diets may alter the genetic influence of growth of the sclera and choroid, which will in turn induce permanent changes in the development and progression of myopia, particularly during periods of growth.

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