TOWARD A UNIFIED THEORY OF AMETROPIA:

REFRACTIVE ERROR AS A LESION

 

(Original title: Preventing Refractive Error: What’s a Doctor to DO?)

 

[Available from The Optometric Extension Program as Tape #WK-4

from the 3rd International Congress of Behavioral Optometry]

 

Merrill D. Bowan, O.D.

 

INTRODUCTION

 

My premise is that refractive error is disease.  Myopia is a lesion. Astigmia is a lesion.  Hyperopia (in the range of adverse hyperopia, which clinically appears to be that greater than 1.00), is a lesion.

 

Myopia, astigmia and hyperopia have already been described as adaptive stress diseases.  You have a list of my papers in the program that will give you a more in-depth understanding of how I have come to the conclusions you are about to hear.   I invite you to listen carefully to see if you find exception with what I am about to say.

 

[ OVERHEAD #1  - Paradigm Shift]

 

[CHICK, standing beside open eggshell: "Oh WOW! Paradigm shift!"]

 

Optometry has been in a shell for too long: the shell of the medical model, or the classic eye-ball model, or the merchandising model. It is time for optometry to come out of its shell and open its professional eyes to a whole new paradigm: Refractive Error As Adaptive Disease.

 

Skeffington was only one of the first of our professional fathers to point out that;

 

[OVERHEAD #2 - Refractive Error]

 

[Refractive error is the last stage of a visual problem.]

 

 People may think that it is a bad thing to be myopic, or hyperopic, or astigmatic, but to the body, these are good things, not bad.  They reflect and reinforce the way the body has chosen to cope.  Myopia is a wonderful way of pulling a spatial problem in to assimilate it.  Hyperopia is a wonderful way of pushing it away, glossing it over, or running away from the problem.  Astigmatism is tricky - it is part of the transition to myopia, or the body’s concession when it wants to run away, but is being constrained to perform.

 

The trigger is stress, and its impact on the individual.

 

[OVERHEAD #3 - Stress Adaptation]

 

[VISUAL STRESS --> ESCAPE (COPE) -->

1) RETREAT: FT./FLIGHT; STOP WORKING;

DAYDREAM = "LEAVE"

2) TOLERATE: UNDERACHIEVE; SOMATICIZE; SWITCH MODES

3) ADAPT: MYOPIA; ASTIGMIA; ADVERSE HYPEROPIA; AMBLYOPIA; STRABISMUS]

 

But, wait!

 

What about genetics?  What about animal deprivation studies?  What about nutrition? And, What about Naomi? What role do we play as clinicians?

 

Let’s take the last question first. Since ametropia is almost certainly a disease process, we clinicians need to concern ourselves less with what an eye is, myopic or hyperopic, sick or healthy, but instead look at what the visual system is becoming - whether it is "sicking" or not.

 

So then, if we are going to be looking for disease, then we have to talk about the disease process.

 

DISEASE

 

There is a spectrum to health and "normal" and "abnormal" are the polar opposites on that continuum of health.  Disease can be defined as the changes within individuals that cause their health parameters to fall outside of the range of normal.  When the structures or function of an organ or tissue system deviates so much that normal homeostatic processes can not restore the balance or if they are destroyed, or cannot meet the environmental challenge, then a disease is said to exist. 1

 

Diseases are extensions or distortions of the life processes.  The stressing agent itself does not constitute the disease - it merely evokes the response, the changes, that are manifested as disease.  A disease therefore is actually the sum of the physiological processes that have been distorted. The elements of a disease actually lie within the very mechanism of adaptation.

 

The symptoms of a disease are subjective, and the individual must be questioned to elicit them.  But when they are visible to the observer or examiner, they are called signs of a disease.  When there is a demonstrable structural change, we call it a lesion.  Ametropias fit the description of lesions.

 

Our optometric patients live, somewhat comfortably, in the sub-clinical or pre-clinical stages of disease, until the problem manifests itself - frequently on a school Snellen screening test. It takes an advanced stage of a visual problem to show as a visual acuity impairment.  The pathophysiology has been in place for some time before we can see the signs.

 

Learning disabled children have a notorious lack of myopia, the literature shows2 -- is this perhaps a reflection of their failure, or inability -- or unwillingness -- to convert symptoms into a disease?  It looks suspiciously so.

 

What are the causes of Ametropia, and as clinicians, what can we do to intervene?  As doctors, it is our responsibility to create the environment for healing to take place - or to prevent disease in the first place.

 

ETIOLOGIES

 

[OVERHEAD #4 Etiologies]

 

[ 1) GENETICS: INADEQUATE, UNAMENABLE

2) NUTRITION: FRUSTRATING, SOMEWHAT AMENABLE

3) FUNCTION: MOST RECURRENT, MOST AMENABLE]

 

 

There are only three possible causes of Ametropia:

 

1) Genetics are involved, for sure.  However, a genetic model allows for little means of amenability - we can’t intervene in meaningful ways if our Genesis is totally responsible for all Ametropia.  We have little or nothing to talk about, with the current understanding.  Mutti and Zadnik found that a parental history of myopia had a 25% predictive validity.3  Angi and Clementi (et al) found, by comparing mono- and dizygotic twins that heritablity of refractive error was low - from .08 to .14.4

 

Hauge holds that heretabiltity studies have limited value;5 and after an initially moderately strong initial coincidence, the identical twin studies show a growing inter-pair difference as the twins grow older.6  So while genetics is indeed a factor, it certainly isn’t the only factor, and may not be even a particularly strong factor. 

 

Zadnik’s Orinda longitudinal study7 began with a great idea: to study the genetic background of a cohort and the follow the group’s refractive status for an extended period. Unfortunately, as critics have pointed out, there are a number of flaws: the parents’ refractive error was not determined in a fully scientific way. There was only a questionnaire of what age the parents began wearing any glasses, and classifications made from that information.8 It dilutes the importance of any conclusions that will be reached. There are at least four other areas of concern about that study. 8  Hopefully these can be corrected.

 

All in all, genetics is an inadequate argument for ametropia.  Young’s Eskimo studies,9 his point that atropine and other cycloplegics shouldn’t work,10 and the advent of larger than ever numbers of late onset myopes11 all point to extra-genetic mechanisms for a significant number of myopes. The question isn’t nature or nurture, its nature and nurture: what is the mix in this disease process?

  

2) Nutrition is a frustrating possibility of an etiology.  We are what we eat, just like our mothers told us, and Lane’s work has implicated a number of processes involving magnesium, chromium, calcium, and vitamin C. He also implicated diets high in refined carbohydrates. 12.13,14 British studies have suggested diets low in protein.15  (That study may have actually been factoring calcium, not protein, but that is a discussion for some other half hour).

 

In 1995, Dr. Lane reported that food folates (folic acid) were strongly associated with reversal of myopia, with a correlation of .935 and a confidence level of .001 from ages 18-38.  From ages 6-17, the relationship was a bit weaker, with a correlation of .82 and confidence of less than .005.  Pharmacological additives did not get equivalent results.16 We must eat foods in their nearest to natural states, he is still saying.

 

Why do I say that nutrition is frustrating?  Well, we can change our diets, but how do we change a child’s tastes? And our American soils are depleted in minerals since 1936, according to a Government publication?17  We need to eat well, but what? I will give you a handout later that helps work through this dilemma. So we have to consider that nutritional distortions are at least somewhat amenable.

 

3)  Functional - this etiology is the most recurrent theme in the literature of the last 15 years or so.18-22  The impact of the environment is right now, in fact, the most discussed of all the factors.  Animal deprivation studies and pharmacological studies are testimony that we can alter the eye’s environment and function as well as observe changes in the eye. A functional approach to control of myopia is the clinician’s only really productive tool in ametropia prevention. 

 

Unfortunately there is no coordinated effort in exploring the domain or scope of refractive error. Hyperopia is treated as a non-problem, astigmatism is a nuisance and myopia is regrettable.

 

Any discounting of refractive error is in error.  Scientists and clinicians call for proofs yet many of them are just defending their own inertia.  They do almost nothing for their patients’ welfare while they take the money to the bank and wait for "George to do it" - ametropia research, that is.

 

The literature supports no fewer than 19 different possibilities for the etiology of myopia. That means any of millions of possible combinations may be at play in the patient before me.  What can any doctor do, really? In my paper, Stress and Eye, I showed how the 19 combinations can be reduced to just seven, with Genetics at the top of the list. 23

 

[OVERHEAD #5: 7 Classes]

 

[ 1) GENETICS; 2) MALNUTRITURE; 3) STRESS AND APPERCEPTION; 4) ENVIRONMENTAL FACTORS; 5) INFORMATION PROCESSING; 6) PATHOLOGICAL SEQUELLAE; 7) EXPERIMENTAL ESCAPADES]

 

All seven, the paper goes on, reduce to one: Stress.  Stress is a component of all disease.

 

 However, to paraphrase Herbert Weiner’s observation on disease, may I say that, "Refractive Errors are mere abstractions.  They cannot be understood without appreciation of the person who is ill."

 

Robert Sapolsky, a notable physiologist from Stanford,. observes that the psychology impinging upon a system is as decisive a factor as the physiology of that system. If we can change the way even a rat perceives his world, he says, you will dramatically alter the likelihood of its getting a disease. 24

 

Because of observations like these, we must investigate Who the ametrope is, What his environment is like, and How much time he spends in stressing environments, both visual and emotional.

 

ANIMAL RESEARCH

 

But what about all the animal research? Well what about it? Let’s consider the deprivation studies.

 

The study of chicks may be a poor choice of species to generalize from, since bird eyes are quite different than mammalian eyes.  The scleras are comprised of Type 1 collagen, not Type 2.  The ciliary muscle is striated, not smooth and thus under different control.  And studies with species that do not have a frontal, binocular visual system, so that all parameters can be studied, is a liability, as well.

 

Zadnik pointed out that the ages of these animals is nowhere near comparable to human ages for the onset of myopia.25

 

The pharmacological studies with pirenzipine seem promising, but Devadas and Morgan found last year that its action is dose-dependent, working only at very high concentrations, rendering it and others that they studied as physiologically insignificant, they said.26

 

McBrien, Leech and Cottrial found about the same thing, with intravitreally-injected pirenzepine working well, but with subconjunctivally placed pirezepine not working nearly as well.27

 

McBrien also did an interesting study with chicks and atropine which may have far-reaching implications.  They found that form deprivation myopia was prevented by intravitreally placed atropine.28  The study is long and complex, but I found it very interesting that not only the posterior, but the anterior chamber was smaller in the atropinized experimental and control animals.  It suggest that in addition to any retinal/scleral effect, that the whole eye may be shrunk by the chemical. If that is so - that the atropine directly affects the collagen protein of the sclera -  then it would lend indirect support to the physiological difference between  myopes and hyperopes, since atropine only reveals latent hyperopia in hyperopes and causes very mixed results in myopes, actually increasing myopia in some.29

 

Returning for a moment to consider the animal studies, the results are quite exciting (one hardly knows what to expect, actually).  The results vary on whether you use white or black occluders, minus or plus lenses (which has been hit or miss within studies), form deprivation only, total deprivation or partial deprivation, what animal and what species of animal (Rhesus and Stump-tailed Macaques have different responses). It is all a bit mind-boggling in complexity.25

 

Then, once again, as Zadnik questions, is it relevant to humans? These animals correspond to humans under six months of age and with some rare exceptions that will produce form deprivation myopia in humans, no visual deprivation of similar magnitude occurs in children. 25

 

These experiments are distracting to the average clinician who wants to help prevent visual problems and enhance a person’s visual and cognitive performance. It is as if we have left sound and productive methods and research behind because of various investigators who are infatuated with novelty. We need to have reasonable approaches:  we would like perfect, proven approaches, but we are not going to have these for another 10-20 years - and only if we can get out of the experimental rut we are in.  We have lost valuable time, I believe, because we as neuro-developmental optometrists have not been assertive about what we know and do every day.  It is time to stop being wimpy and get to the research labs with the old models that worked so well. Not perfectly, mind you, but well.

 

We can prevent about 2/3rds of refractive error, it seems, from the literature and clinical experience.29 Our alternative is to do nothing and watch them get worse.  This should be found unethical and morally intolerable by the caring clinician. We do know what to do - it’s almost too late, but we need to begin to do it.

 

TONIC STUDIES

 

Studies of dark focus and dark vengeance (tonic focus and tonic vergence) show that both are intermediate values - anywhere from about 1.0D. to 2.5 D in front of the individual, with myopes having the higher values.30,31  While studies of dark vergence show loose association with dark focus, one study revealed a good correlation of the two under the condition of mental processing.32 That should make the ears of those of you who do perceptual therapy perk up, because it supports the old wisdom that when we look at the functioning of the visual system, we are looking at how the brain is functioning in very real, direct and indirect ways. 

 

Since seeing takes place in the CNS, we must probe the CNS to determine as best we can what interference is occurring and what direction it wants to move.  We can then devise a treatment plan to intervene or eliminate, if not just reduce, the movement of the organism to cope with the interference (or, stress). 

 

TWO WORLDS

 

 Philosophically speaking, we may say that humans exist in two space worlds: distance and near.  If one has trouble operating in - accommodating (both optically and cognitively) - the nearspace world, you must either adapt - become myopic - or guard against encroachment into that space. To study an object, one must be able to bring it in and attend to it in nearspace, not farspace.

 

Thus, hyperopes would derive much motivation from the farpoint world, guarding the estate, and myopes derive much of their motivation from analysis and processing of nearspace.

 

One writer believes that it appears as if the visual system always tends to myopia,33 if so, we are fighting how the environment impacts us by emmetropizing.  (I called it "hyperopization" in my paper, Stress and Eye.23) Because the animal research appears to have validated the presence of a regulatory system, Van Alphen’s comment in his paper on Emmetropia and Ametropia becomes valid.  That is:

 

[OVERHEAD #6 Van Alphen]

 

["Only when the brain is invested with a regulatory capacity that a unified concept for the origin of ametropia becomes feasible". 34(p. 84)]

 

Because animal research has demonstrated that there is an emmetropizing mechanism with regulatory capacity, we can look for a unified concept of ametropia.  Perhaps then as clinicians, we can be "real doctors" working to prevent and, to some extent, cure, ametropia.

 

[OVERHEAD #7 - PERSONALITY: MYOPIA AND HYPEROPIA]

 

BEHAVIOR	HYPEROPES	MYOPES
Problem solving style	Actors	Thinkers
Physiological style	Adrenaline	Cortisol
Motor responses	Approach	Withdraw
Neurological Style	Peripheral	Central
Spatial response	Distancing	Absorbing
Distress response	Fight/Flight	Worry/Adapt
Affect response	Assertion	Depression
Life perception	Must control	Out of Control
Motivations	Goal/task	Relational

 

 

PERSONALITY

 

As Aristotle said, "Nothing is in the mind that did not pass through the senses." Ward Halstead, a Chicago psychiatrist, called vision "One of the major contacts with reality in the early experience of the child.  The outcome of the future development of the personality is to a great degree a function of the extent and quality of that visual contact."  Seeing takes place in the CNS. (Importantly, we also seem to be observing that what passes through the visual sense also affects the sensory structure.)

 

Studies of the relationships of personality style and ametropia have suffered from some basic problems and disagreement.  The different researchers have all used many different personality probes that are not necessarily equal.  Additionally, the tests may not have been looking at the attributes that clinicians associate with the various ametropias. 

 

What are the attributes associated with myopia?  Myopes seem to have a profile that makes them: worry, depress, fear and they are lent to withdrawn-ness, a sedentary lifestyle, a detailed analytical nature, and a higher degree of desire for inter-personal relations.35,36 Angi and Rupelo described their myopic population as "sufferers".37

 

What are the attributes associated with hyperopia?  The candidates for adverse hyperopia are more likely to be: assertive, alarmable and hot-reacting; action-oriented; global analytical approach.36 These and a higher degree of goal, problem and task-orientedness would seem to predispose one for progressive hyperopia.

 

There are individuals who mix these: they will do the opposite of one or the other, but statistics should prove an association of the above factors, generally speaking.  The problem is to get personality inventories that are accurate in measuring the qualities being looked for.36

 

Researchers before Van Alphen’s seminal paper - and since - have asserted a relationship between anxiety and myopia.38,39   Just how to sort out what kind of, and how much, anxiety is required to trip the pre-myope into the active distortion is the problem before researchers now.