I have some learning difficulties but when I was young there was no such thing; there was the idea that you had a child that was a late bloomer. A much more appropriate term than slow learner.
I also had a tumble out of a slow moving car when I was about 3; something the parents kept under wraps.
Now that I am over 65, and have the internet at my fingertips, I have developed an interest in my difficulty which centers around my not being able to make figures ‘stay’ in my head so I can manipulate them mentally like I can ideas. The problem with us late bloomers is that we don’t know we are different or how the workings of our mind are not like others. So we are late in investigating why this is so.
I have a large cafe au lait, an iris nevis, a weak left ankle and a problem with not being able to hear clearly out of my left ear. Not deaf, just not hear distinctly. I have looked at the various sites for MS, MD, MG, and others to the dismay of my doctors.
The most important information I have gained is from the NF sites. Neurofibromatosis 1 & 2 are both genetic, NF 1 a defect on chromosome 17 and NF 2 a defect on chromosome 22. While they are different, and while the Wiki site among others says that some symptomatic aspects of NF 1 & 2 are common in the populace, the fact that it is a dominant gene which means your children inherit, and the fact that the doctors tell us that even tho it is a genetic condition, about half the cases are spontaneous upon birth.
NF 1 has as one of its primary sysptoms learning disabilities. Ask any educational professional or physician for that matter and you will be told there is no known cause of learning disabilities. Yet, there is the primary symptom of NF1, learning disabilities.
As any of us parents of a child identified by the school system as being learning deficient know, inattention, distractability, impulsivity and other like occupy the mind of our child. And we are told by family members we often demonstrated the same. The conclusions to be drawn from this experience is that the child adopts coping skills to make it in the adult world just as we ourselves did.
The worrisome part is that the coping skills are necessary as the brain remains in its late blooming condition. Even now articles call our attention to the possibility that we are adults with learning disabilities.
Another facet is that science tells us we have so many genetic changes that it is impossible to identify and treat a single one.
The Ritalin epidemic in North America is astounding in its enormity. How can so many children be victims of a learning disability? The assurance of the educational institution that learning disabilities are not genetic falls flat in the face of the NF 1 symptoms.
The current interest of science in epigenetics is a breath of fresh air. The ability of methyl groups to be ’emplaced’ and silence genetic areas is only one of the valuable aspects. The other being a protein Histone that winds up or loosen to allow the dna gene to be expressed or hidden. The aspects are also reversible.
How did the NA continent become the hot bed of learning disabilities proving the massive pharma response?
If NF1 is the culprit, it would be clear that the settlers of NA would have been the risk takers, the adventurers, the darers, the dissatisfied wanderers. These individuals carrying the NF1 would have been the majority of settlers of NA. And the dominant gene would have produced the disasterous learning disability segment we see today. The answer then would not be pharma Ritalin but creation of methyl groups and histones which are social creations through mothering and parenting.
The NA continent was depopulated even when early explorers arrived. Perhaps this indicates that there was an element in the environment that was not beneficial in the long term. It has long been known that the Great Lakes area is more prone to radon gas in the rocks. It cannot be dismissed. Areas of Texas with naturally occurring lithium in the water seems not to be a benefit in not only calming but encouraging neuronal growth as well.
Science has begun several avenues into determining how to minimize learning disabilities and emphasize maximize brain capabilities. To this end there is CNS research that includes spinal tapping.
It would seem obvious that the next step is collecting dna that does not have the widespread chromosome 17 and 22 deficit. And to determine how often this ‘spontaneous’ genetic defect occurs. Although no estimates are available as to how often this occurs, the fact that it is dominant means that it is already so widespread the only option is to find the undamaged gene.