snip
> Can i present the argument put forward by 'unreasonable people' that
> although the component parts of the human body is described by genes
> myopia itself does not show a genetic relationship?
You can present it, but finding evidence will be tougher.
> First some statements that i imagine we can agree on? Please let me
> know.
[quoted text clipped - 21 lines]
>
> Can you let me know if we are in aggreement so far?
I don't agree with your description of the refractive error bell curve; it
is a normal distribution curve with steep slope, slightly skewed to
hyperopia with a very small secondary peak (with normal distribution around
that peak) in the high myopia area
It is not just the emmetropization process that causes the bell curve, the
natural variation of the eye components before emmetropization takes place
means that the refractive error of newborns and very young children follows
a normal curve. Emmetropizaton steepens the slope of the curve so that
higher percentages are at "normal" or near "normal".
We will never separate genetic from environmental, that is Ridley's point.
It is like the old chicken and egg question.
Is refractive error genetic or environmental if:
Baby inherits steep cornea gene and strong emmetropization gene from
parents, so that the neonatal myopia present due to steep cornea is quickly
compensated for by slowing growth of the eye in response to myopic defocus
during babyhood?
Baby has gene that causes rapid growth of eye if baby eats too much sugar, a
sluggish emmetropization gene and indulgent grandparents who visit daily and
give him sweets. After every visit with Grannie, the eye grows rapidly and
the emmetropization process has a limited response to the resulting myopic
defocus.
Female baby has gene that causes growth of eye is response to high estogren
levels and a emmetropizaton gene that stops working at age 6. At puberty,
myopia develops.
Male baby has gene that causes growth of eye is response to high estogren
levels and a emmetropizaton gene that stops working at age 6. At puberty,
no myopia develops.
Female fetus has the sluggish emmetropization gene, the rapid growth
stimulated at puberty gene and a gene that causes steep corneas if mother
eats asparagus six times in one week during the second trimesterand .
Second trimester starts in April when asparagus is at it's peak and Mom
loves asparagus. Baby born with steep corneas and low hyperopia,
emmetropization doesn't respond well.
I'm sure we could think up lots of other possiblities, the point is made:
how can we separate genes and environment.
Dr Judy
> Cheers
>
> Andrew
andrewedwardjudd@hotmail.com - 20 Mar 2005 21:43 GMT
> I'm sure we could think up lots of other possiblities, the point is made:
> how can we separate genes and environment.
Dear Dr Judy,
I suppose the uncertain area is:
How capable is the emmetropisation process if all
environmentally/behaviourally negative factors were altered to be
posative factors?
It appears that those who are aware of genetic and environmental
influences can be divided into essentially two opposites camps
1. Myopia cannot be improved - possibly it can be halted for some forms
of myopia. It can vary up or down but generally it varies down until
middle age, improves slightly for several decades and then varies down
again.
2. Myopia can be improved if environmentally/behaviourally negative
effects are changed to environmentally/behaviourally posative effects.
So then we come to Twin studies to decide this one way or another.
In the context of these studies I am interested in the relationship of
family habits, family anxiety, twin dominance/rivalry/birth order,
loneliness etc etc etc in the development of myopia.
If these influences are very important in myopia we would expect the
most *similar* refractions in the following order when studying MZ and
DZ twins.
1. MZ Raised together in the same family who are treated *most*
identically by care givers (inside the family and at school ect) and
other family members **and** who have the most supportive relationship
with each other **and** who are most alike physically. These twins
may be so alike that outsiders particularly could not treat each twin
as a different person because they could not tell the difference
between them.
2. Then some kind of confusion in ordering of differently treated (MZ
twins who are *not* supportive of each other) and similarly treated (DZ
twins who *are* supportive of each other)
3. Finally the *most* differently treated DZ twins who are not
supportive of each other and most unalike physically.
To my knowledge this has never been tested in this manner.
Genetic studies of twins assume environment/behaviour is not relevant,
and yet a test of environmental/behavioural factors in a twin study
would produce the same statistical results in favour of
environmental/behavioural factors.
Similarly "Familial high myopia" is said to be inherited in a
"Mendelian" manner. This is assumed because it occurs in 3
generations with some members having high myopia over -6D.
Meanwhile environmentally/behaviourally we can conclude that "family
habits, family anxiety,dominance/rivalry etc etc etc"
are likely to be passed from generation to generation.
In conclusion:
1. If we are in the genetic camp the 'Classical twin study' method and
"familial high myopia" are concrete 'very scientific evidence' that
myopia has a very strong genetic component influencing it so that
emmetropisation is unable to restore normal sight.
2. If we are in the environmental/behavioural camp we notice that
current gene studies are concluding that "different genes seem to be
the cause of high myopia in different families" (but still no genes
yet found for these families)
I have written to the British Twin study group to ask them if they are
prepared to examine the most refractively different set of MZ twins for
behavioural differences. These twins seem to have the capability of
providing some very useful data on the environmental/behavioural
reasons why myopia developes.
Andrew