Dietary Interventions And Autism

Children and adults with autism can get just as sick from poor diets and nutrition as anyone else can.  When weight becomes an issue or health risks are apparent and need to be avoided, dietary interventions are the only things that work.   They are absolutely necessary when children and adults, with or without autism, develop diseases like insulin resistant diabetes, or Crohn’s disease.

The very first step is a proper diagnosis with a family doctor or pediatrician.  Blood tests are the quickest means of assessing just exactly what health problems the patient is facing or may be facing in the not too distant future.  Current health problems can be treated as soon as doctors are aware that they exist, and parents of children with autism have several different diets out there to choose from which may or may not work for their children.  It’s important to note that three of the most popular dietary interventions for autism are already used for other health issues, and therefore may not work the same for a child with autism.

The first is a gluten-free, casein-free diet, more commonly referred to as GFCF.  It is a diet used with children and adults who are allergic and have extreme reactions to to any food that involves grain gluten, which is in practically every cereal, baked goods, breads, and carbohydrate rich foods.  Thankfully, food companies have begun to realize that this particular food sensitivity needs specially made products and only those products are going to increase sales for them.  Now supermarkets and grocery stores have at least one entire aisle devoted to GFCF foods for people who have been diagnosed with Celiac’s disease.  As for children and adults with autism, there are random reports that it has worked for some, but not for others.  It remains a trial and error process.

Another type of diet, which originated in the 70’s and was meant for children with ADHD,  has shown some signs of effectiveness when used to control hyperactivity and impulse issues in children with autism.  It’s referred to as the Feingold diet, named for the guy who designed it.  It’s an attempt at getting kids to eat more of certain kinds of foods and significantly less of others.  It has worked with ADHD kids and has had some limited results with kids with autism.

The last most popular dietary intervention parents have tried, again with mixed results, is the Specific Carbohydrate Diet, or SCD.  This diet is extremely limiting and hard to implement with children who already are very picky eaters.  The theory behind it suggests that balancing out the flora in the GI tract leads to less aggressive behaviors; at the very least it solves any bowel issues the child with autism may have.

Other diets that limit the fine sugar a child can consume or eliminate milk and dairy and substitute for soy or rice products are also on the list of popular dietary interventions.  The problem with any dietary changes is that the parents have to commit to it for no less than three months before they are able to see any differences, if there will be any at all.  Usually after a month, people give up because it becomes too difficult to plan and buy special meal items for just one person in the house, and it’s not something everyone else in the house is willing to commit to.

Dietary changes with autism also have to be gradual.  Parents who have a child with autism understand that routine and expectations of the status quo remain so, and sudden and complete upheaval of a diet or nutrition program can make things worse, not better.  For instance, say a parent wants to remove milk and dairy to see if lactose intolerance is a possibility for behavior triggers.  One third of all the regular milk the child normally drinks is replaced with soy, rice, or almond milk.  After a week, it becomes half, and after another two weeks, it becomes two thirds, and after another two weeks the child is completely off cow’s milk.  That’s just one food item gradually replaced.  If the child enjoys cheese, yogurt, and ice cream, all of those have to be gradually replaced on their own as well.  This entire process could take a year or more to get the autistic child completely off traditional dairy foods.  That’s a long time to dedicate to a single dietary intervention that may or may not work.

Still, for parents who would rather treat behaviors and moods by finding causes and cures that don’t involve medication, it’s worth the effort.  Hundreds of thousands of parents globally have tried at least one or two dietary changes for their autistic children in the hopes it will help.  The results vary as much as children on the spectrum do, and that should be the expectation for any parent who wants to give it a go.

Above all else, parents should not neglect the total nutrition needs of their children.  The children, despite their special needs, are children with the same nutrition needs as their peers.  Keeping that in mind, parents should notify their pediatrician that they will be placing their child on a special diet, and any advice would be helpful.   Many pediatricians would agree that the diets are met with mixed results, and the only help they can offer is to make sure the child is getting the bare minimum in vitamins and minerals through supplements every day.   Consulting with a pediatric dietician, if there is one in the area where they live, is also an excellent approach to any diet plans.

Check these articles, too.
1. Nutritional Therapies For Autism
2. Autism and Diet

Autism and Aging

Because autism diagnoses have become more prevalent than they were thirty years ago, many children who currently are on the spectrum and adults who are just finding out that they are on the spectrum too are not old enough to show what happens to the autistic person in old age.   Currently, the oldest living people worldwide with autism are in their sixties, so there’s at least another two decades before any questions can be answered with regards to aging and autism.  There are some theories out there that might point the way as far as what types of research might be conducted on the topic a few decades down the road.

There is some assumption that skills will decrease as adults with autism reach their seventh and eight decades in life, but since that is normal for anyone, that doesn’t mean much.  Children and adults with autism now will have a higher risk for dementia and Alzheimer’s as they get older because of the fact that their brains are already quite different from those who don’t have autism.  The structures of the brain as well as the hormones and chemicals produced are as vastly different on the spectrum as they are in comparison to non-autistic peers.

In addition, medications or alcohol use/abuse can add to the problems that aging autistics will encounter.  Since alcohol and drug use and abuse is already to tied to altered brain chemistry and physiology, the risks of changes in personality and moods almost doubles in people with autism.  For those who suffer from anxiety and depression and have autism, suicide is a constant possibility the older they get.  In short, many of the challenges they face are expected to increase or become more problematic with age, which is why it is so necessary for them to have an excellent support system when they  are younger.

Many mid to high functioning adults on the spectrum currently lead fairly normal and extremely productive lives.  They appear very normal to the outside world, and it is only through interaction with them that anyone can tell that they are just a little bit different.  The majority have high I.Q.’s and work for government agencies where they are not required to interact with people, only solve problems, build, and invent things.  Several others work in the capacity of engineers, logistics, programmers or they work with animals as vets.  Their jobs are very high stress, and high stress jobs are linked to Alzheimers, which is why so many adults with autism are expected to be diagnosed with the disease later in life.

Brain shrinkage, often associated with dementia and other diseases that attack the brain in the late stages of life, is already present in people with autism.  It’s on a much smaller scale and only affects certain areas, but it’s there.  The brain still works, but is more compressed within the skull, and is a sign of the alterations the brain took starting at age two.  This is another reason why scientists hypothesize that adults with autism will likely suffer two to three times more from dementia and Alzheimer’s as they age.  Again, it’s only a hypothesis, and not something that as of yet can be proven.  Only adults with autism who choose to participate in this type of research in the future or donate their bodies to science will be able to help confirm or deny that this hypothesis holds any weight.

Other groups of scientists and researchers, such as the group at the University of Amsterdam, are already under way, even though they do not have a large enough population of volunteers who have autism and fall within the right age category.  They are actually hypothesizing that the opposite is true, that the autism symptoms get better in the golden years.  They plan to conduct a five year study to see if this is true, and certainly, attempting to prove that there are improvements at the end of the autism rainbow of life will be most interesting to see.

Other research and support groups, like Aging With Autism, or AWA for short, are conducting ongoing research in this area, which should be much more effective in the long run.  During the interlude between the young adults who have autism and the elderly adults with autism further on down the road, AWA provides much needed support to individuals and their families.  They have programs to help autistic children transition into adulthood and lead as normal and unrestrictive lives as possible, which on the trajectory of life, may indeed impact the end of life for many of these young adults.  Along the way, those that are supported are encouraged to give back in the form of data to show how the positive effects of lifelong support can impact an elderly adult with autism.  There is no pressure to do so, but in an area where very little is known about a disorder, participants are more than happy to contribute.

Several other autism agencies, whether directly or indirectly, are currently contributing what they can to the study of autism and aging.  The concern is more on how to financially support adults with autism rather than on how aging changes their bodies and minds.  Money donated to these charitable organizations is handed over to researchers who are  working on the problem before it becomes a problem.

The American Speech-Language-Hearing Association publishes articles on a number of topics.  One in particular that readers might find useful is the Perspectives on Gerontology: Aging and Autism, by Pamela A. Smith.  Readers do have to buy the article for short term reading duration, as only the excerpt is available for free.  For $7, readers can “check out” the article for about a week, and discover what many doctors and researchers are thinking with regards to autism and aging.

Autism, Epilepsy and Seizures

What is epilepsy?

Autism, Epilepsy and Seizures
Autism, Epilepsy and Seizures

Epilepsy is a combination of diverse chronic neurological disorders, which is usually characterized by unpredictable and unprovoked recurrent seizures.  The disease is caused by eternal alteration in brain tissue, which results in over impulsive brain. The overexcited brain thus conveys abnormal signals, which in turn causes repeated and unpredictable seizures. However, a single seizure that does not repeat again is not considered as epilepsy. Although,in some cases of epilepsy, a single seizure in combination with brain alteration can increase the likelihood of future seizures.The disease affect a variety of mental and physical functions such assensory, motor, and autonomic function; consciousness; emotional state; memory; cognition or behavior. Epilepsy is represented as one of the most common neurological diseases that affect about 50 million of people worldwide. The onset of epileptic seizure is manifested by unusual, excessive and hypersynchronous discharge of neurons in the over excited brain.The cause of epileptic seizure may be genetic background or the severe brain injury or family propensity towards the disease.However the exact cause of epilepsy largely remains unknown. Some of the possible common causes of epilepsy include stroke, Alzheimer’s disease, trauma, brain injury, congenital birth defect, metabolism disorder, brain tumor, brain infection (e.g. meningitis, encephalitis and brain abscess) and medication (amphetamines cocaine, tramadol, and antidepressants). The onset of epileptic seizure typically begins at the age between 5 to 20, but not strictly adheres to this age group and can happen at any age.The symptoms of epilepsy may vary from patient to patient and comprise from simple staring spells to violent shaking and loss of consciousness. The Physical examination such as electroencephalogram (EEG) and Head CT or MRI can be performed to check the abnormal electrical activity and its accurate location in the brain. The treatment of epilepsy is principally based on seizure preventing medications. However, in case of unsuccessful medication, other therapy such as surgery, complementary therapy, or vagus nerve stimulation, changes in diet or special diet are also tried.

Is epilepsy and seizures the same thing?

The term epilepsy and seizure closely resembles each other and therefore erroneously interchanged. However, in spite of the close association between the epilepsy and seizure, they should not be considered the identical or same clause. In this respect, a precise distinction and delineation between seizures and epilepsy is highly essential. A seizure is medically described as a brain dysfunction that results in altered attention or behavior. Seizures are mainly caused due to episodes of disturbed brain activity, which result in unnecessary hypersynchronous discharge of a population of cortical neurons. A seizure can beoften encountered under the condition of brain injuries or chemical imbalances, or infections which can irritate the brain. Whereas Epilepsy is marked as a disorder of the central nervous system in which a person has multiple or repeated seizures over time. Therefore, a person with epilepsy has seizures, but seizure patient don’t necessarily has epilepsy. The precise distinction between epilepsy and seizures is essential to focus the diagnostic approach and to select the appropriate drug therapy. Since, in case of epilepsy chronic treatment, such as antiepileptic medication or surgery might be required, whereas for an isolated seizure the common therapy is directed towards the underlying cause and not towards antiepileptic drugs (AEDs). The concepts of seizures and epilepsy become more obvious in view of the basic anatomic and electrophysiologic properties of the cerebral cortex. The major criteria of clear delineation comprise the factors that determine the level of neural activity at the cellular and cell network level and electroencephalogram (EEG). Clinical studies suggested several kinds of seizures, which areattributed with specific behavioural changes and electrophysiological disturbances and detected by electroencephalographic (EEG) recordings. Doctors recommend that a single seizure does not essentially signify that a person has epilepsy. According to them, approximately 10 percent of adults experience a seizure at some point in their lifetime, but the two-third of them will never experience it again.The characteristic symptoms of epileptic seizures include a loss or change of alertness, jerking and ripple movements of the arms or legs, difficulty in speaking and lip-smacking. Non-epileptic seizures, or pseudo-seizures or psychogenic seizures, also closely resemble with epilepsy thus making diagnosis difficult.

Connection between Autism and epilepsy

Epilepsy and autism represent a group of heterogeneous clinical disorders associated with behaviorally defined, neurodevelopmental disorders. Seizures are relatively common and most prevalent neurological disorder associated with epilepsy and autism or autistic spectrum disorder. It has been observed that epilepsy is frequently developed in individuals with autism or autistic spectrum disorders (ASD). Prevalence studies suggested that seizures in autistic patients develop either in childhood or at puberty or adulthood. However, the risk of seizure particularly remains high at adulthood in autistic patients. Clinical data estimated that the frequency of epilepsy is comparatively larger than the prevalence of active epilepsy in the general population. Studies on autistic patients has established that as many as ~ one third of children with autism also have epilepsy. This risk is comparatively higher in autistic patients with severe mental retardation, genetic abnormalities and brain malformations. It has been proposed that abnormalities in brain of autistic patients can disrupt the cortical neuron and therefore alter brain activity. Overload or disturbances in brain neurons result in unusual, excessive hypersynchronous electrical discharge of a population of cortical neurons, thus contribute to increased risk of seizure. Clinical studies suggest that during epilepsy regression of language, behaviour and cognition further develops the clinical manifestations that resemble with the behavioral syndrome of autism. The common risk factors which increased the probability of coexistence of both epilepsy and autism comprisegenetic factors, language impairment, severe cognitive dysfunction, motor deficits, symptomatic etiology, and onset of seizure.

Clinical studies suggested a possible association between epilepsy and autism. Recent studies suggested the sharing of common predisposing genes between epileptic and autistic individuals. Studies conducted by Patrick Cossette and research team reported that nonsense andmissense mutations in synapsin gene (SYN1) were associated with ASDs, epilepsy, or both. Cossette and co-workers observed that these mutations were associated with functional defects in nerve terminal function. The synapsin 1 is the member of synapsin family of neuronal phosphoproteins, which are associated with the synaptic vesicles present in the central and peripheral nervous systems.This family of proteins are implicated in synaptogenesis and in modulation of neurotransmitter release, thereby playing a potential role in neuropsychiatric diseases.More recently, in year 2012, studies conducted by Joseph G. Gleeson and team suggested the possible involvement of another gene BCKDK (Branched Chain Ketoacid Dehydrogenase Kinase) in consanguineous families with intellectual disability such as autism and epilepsy. The research team has identified inactivating mutations in the gene BCKDK in autistic and epileptic patients. The protein encoded by BCKDK (Branched Chain Ketoacid Dehydrogenase Kinase) is accountable for phosphorylation-mediated inactivation of the E1α subunit of branched-chain ketoacid dehydrogenase. It has been observed that BCKDK knock-out mice display abnormal amino acid profile in brain and neurobehavioral shortfalls.Apart from this, the likelihood of interaction among the pathophysiology of neural circuits could lead to autistic or conversely could predispose the brain to seizures. However, the possibilities are not mutually exclusive and the underlying mechanisms responsible for increased seizure susceptibility in autistic individual are not yet clear. The clinical and neurobiological aspects as well as the mechanisms answerable for cellular hyperexcitability in autism and epilepsy are likely to involve the interplay of genetic, epigenetic, and environmental factors. It has been postulated that the possible relationships between brain development, epilepsy and ASD might be a common neurobiological antecedent. This includes genetic susceptibilities or structural or developmental abnormalities or environmental insults, which possibly lead to abnormal brain development. The varied etiologies of autism and epilepsy make it improbable that single universal machinery can explain seizure tendency in both disorders.In view of this, future studies point to potential genetic links of neural circuits and cellular signaling pathways directed to neural hyperexcitability in epilepsy and autism and need to be reviewed in detail.

Suggested References

Epilepsy: Medical Encyclopedia. Pubmed health

Berg, A. T. and S. Plioplys (2012). “Epilepsy and autism: is there a special relationship?” Epilepsy Behav 23(3): 193-198. Abstract

Thompson, A. W., R. Kobau, et al. (2012). “Epilepsy care and mental health care for people with epilepsy: California Health Interview Survey, 2005.” Prev Chronic Dis 9: E60.Abstract

Stafstrom, C. E., P. J. Hagerman, et al. (2012). “Pathophysiology of Epilepsy in Autism Spectrum Disorders.”Abstract

Novarino, G., P. El-Fishawy, et al. (2012). “Mutations in BCKD-kinase lead to a potentially treatable form of autism with epilepsy.” Science 338(6105): 394-397.Abstract

Berg, A. T., S. Plioplys, et al. (2011). “Risk and correlates of autism spectrum disorder in children with epilepsy: a community-based study.” J Child Neurol 26(5): 540-547.Abstract

Theoharides, T. C. and B. Zhang (2011). “Neuro-inflammation, blood-brain barrier, seizures and autism.” J Neuroinflammation 8: 168.Abstract

Fassio, A., L. Patry, et al. (2011). “SYN1 loss-of-function mutations in autism and partial epilepsy cause impaired synaptic function.” Hum Mol Genet 20(12): 2297-2307.Abstract

Levisohn, P. M. (2007). “The autism-epilepsy connection.” Epilepsia 48 Suppl 9: 33-35.Abstract

Tuchman, R. (2006). “Autism and epilepsy: what has regression got to do with it?” Epilepsy Curr 6(4): 107-111. Abstract

Fisher, R. S., W. van Emde Boas, et al. (2005). “Epileptic seizures and epilepsy: definitions proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE).” Epilepsia 46(4): 470-472.Abstract

Suggested Articles:
1. Autism and Vaccines
2. Autism and Depression
3. Autism and Bad Behavior
4. Autism and Schizophrenia
5. Autism and Alzheimer’s
6. Autism and Crohn’s disease
7. Autism and Dyslexia

The connections between Autism and TV

The connections between Autism and TV

Does Television trigger childhood autism?

Autism is a social and psychological disorder that currently affects 1 in every 300 children. Currently there is no proof of one specific cause of autism. Studies show that autism manifests through a mutated gene called MET; however doctors firmly believe there are environmental triggers that actually bring the disorder out. The only problem is, the triggers have not yet been determined.

Recently a study focused on Television as the believed trigger of childhood autism. In reality, there has only been this one study on this claim, and it was very limited on its gatherings. The researchers discovered that the rate of autism diagnosis drastically increased with the introduction of cable television. They also showed that areas with greater access to cable had the highest autism rates. Researchers than demonstrated how children in rainier areas had to stay inside more, which likely led to additional TV viewing, and higher autism risk.

The above findings were the sum of the entire study. This study did not show the high numbers of autistic children in environments without TV. Overall this study failed to give adequate evidence that TV causes autism.

Do autistic children watch a lot of TV?

Autistic children thrive on sensory stimulation. They long to interact in a world with which they do not know how to communicate. Autistic children are commonly found soothing themselves by various self-stimulatory behaviors. These behaviors could include hand flapping, rocking, twirling, or other squirmy movements. No matter the behavior, the sensation is the same… they are looking for much needed comfort and interaction. Television opens a world of interactive stimulation that autistic children are otherwise lacking.

Autistic children enjoy that they can gather cues and skills from television that they cannot seem to pick up from other humans. Television teaches them concepts and emotional responses that they can find pleasure in. It also teaches them life skills that they may not otherwise learn.

Another benefit of television that seems to make the child happy is its assistance in social situations like school and play. Autistic children have a difficult time finding ways to communicate with their peers. Popular TV shows offer a common ground for conversation between the autistic child and his schoolmates. TV also offers an otherwise private and distant child an outlet for cuddles and play time with their parents.

Autistic children connect best with their visions and sounds. Words are generally lost to the minds of the autistic. Television offers an array of colors and sounds; songs and play that delight the usually straight forward mind of an autistic child. They find the giddiness and imagination of the shows absolutely fascinating, and once they are focused in on it, they simply cannot turn away.

This attraction to TV comes from its ability to allow the child to feel the pleasures of interaction without actually interacting. Autistic children tend to connect deeper with the characters, and can frequently be caught repeating phrases and songs from their favorite shows. In the end, it isn’t necessarily that autistic kids watch more TV than others; it is simply that they find a deeper pleasure in the overall experience.

Possible Links to Autism
1). Link between autism and circumcision
2). Link between air pollution and autism
3). Link between autism and crohn’s disease
4). Link between cellphones use and autism
5). Link between autism and alzheimer’s

Autism And Aerobic Exercise

The effects of autism on your child

Autism is a widely varying disorder that affects nearly one in every 166 people. It is absolutely phenomenal how many levels and variances there are between each autistic child, however one thing remains constant; Autism always affects the child’s ability to function and behave in social and changing environments. Another consistent factor of autism is Vestibular System Dysfunction. This dysfunction inhibits the child’s ability to maintain proper and effective movement and coordination.

A healthy and natural treatment for autism

Because of the varying levels, symptoms, and effects of autism, medications can become a difficult thing to prescribe. Studies show that the most commonly advised treatment is vigorous physical activity. Specialists recommend this treatment because of its consistent effectiveness on all variances of autism.

The varying benefits of exercise for your autistic child

Continuous exercise gives the child an outlet for their energy and aggression, decreasing the hyperactive and self- destructive behaviors they generally use to stimulate themselves. Autistic children have constantly wandering minds and fidgeting behaviors, with little ability to effectively communicate their thoughts and needs. This can cause great anxiety and stress for both the child and the parents. In addition to the physical advantages, exercise has been shown to alleviate these mental and emotional issues by improving sleep, attention span, reaction time, and by calming and focusing the child’s mind.

Dedication to ensuring activity in your child’s life

Adding physical activity to your child’s daily life will have many beneficial results other than the release of energy and frustrations; including but not limited to better sleep patterns and a decrease in depression or other emotional disorders. Also, autistic children tend to put on excess weight very easily, which could only add to their social disadvantages. With the incorporation of regular exercise, you are ensuring that your child receives the activity needed to maintain a stable weight and healthy lifestyle.

To gain adequate results, your child needs only 20 minutes of aerobics or other strenuous activity 3 days a week. Autistic children thrive with consistency, and actually fall apart in the midst of change; therefore habits are easily maintained in the lives of the autistic. Make sure your child latches onto healthy habits by incorporating fun and energetic activities into your daily routine.

Another great way to guarantee your child receives the exercise they need is to discuss with their teacher the possibility of including a physical regimen into their Individualized Education Program. The best way to establish normalcy for the autistic child is to add these activities in a way that includes the other children in their class. This will enable the child to embrace a non-vocal play and socialization with their peers.

Medications and other treatments can be monotonous. They can easily end up being very expensive and rather ineffective; not to mention the possible dangerous side effects of various drugs. It only makes sense to test the more natural, safe, and inexpensive measures, such as exercise, before introducing anything else into your child’s mind and body. In the end you have nothing to lose, other than your child’s pent up stress; rather you have everything to gain.

Learn more about, “Autism Movement Therapy

Autism and Dyspraxia

Autism and Dyspraxia: A Common Pair

Developmental Dyspraxia is a disorder that is often present in those with autism. It is also known as Developmental Coordination Disorder or Motor Learning Disability. It is seen in children with autism from a very early age as fine motor skills and gross motor skills fail to develop. While it is not completely understood, it is seen as a treatable condition. Many people born with dyspraxia will gain control of their fine and large motor skills through occupational therapy.

Dyspraxia is known to hinder the fine motor skills. Movements may be made involuntarily, with little control even in the gross motor skills. Dyspraxia usually manifests itself in this way when the child is beginning to develop. If a parent suspects that their child might have Dyspraxia, they should see a clinical Psychologist, Educational Psychologist, Pediatrician or occupational therapist.

Assessment of a child may include how well the child uses fine motor skills, the smaller muscles. These skills include tying shoes, buttoning buttons, and cutting with scissors. The child’s gross motor skills are also observed. These skills include running, jumping, balancing when standing, and throwing. If these skills are impaired, it usually means the child has dyspraxia.

Scientifically, it is not quite known how dyspraxia happens. Some scientists think that it is related to a developmental defect in the cerebellum part of the brain. This is usually due to injury during fetal development. Some scientists found that when the cerebrum was injured in premature babies, the cerebellum failed to develop successfully. This shows how the cerebellum could possibly be damaged in utero as well. Some scientists think that a deficiency in Omega 3 fatty acids in their last months of pregnancy show a higher risk for having a child with dyspraxia.

There is treatment for dyspraxia, but it is a long road ahead for those who have the disorder. Occupational therapy is the most common. An occupational therapist will see how the child uses his or her motor skills daily, and will work with them to start using them to their potential. In this respect it is much like physical therapy for those with injuries.

Often times, dyspraxia affects the child’s speech as well. Speech requires use of fine motor skills in the face, and therefore is affected by this disease. For this reason, a speech therapist is often employed in addition to the occupational therapist. It is not uncommon for a child, or adult, with dyspraxia to use a communication device rather than speak in the traditional sense.

Occupational therapists strongly encourage outdoor play and movement for children with this disorder. This get’s their motor skills moving and even under control as time goes on. This play time allows the child to explore their own body movements and gain control over them. However, outdoor play can often lead to certain dangers for the child. For example, if a child lives near a busy street, the child may lose their balance and stumble into the street. The parents need to weigh the risks with the possible benefits of outdoor play. Closely monitored outdoor play is the most promising way to improve gross motor skills.

Fine motor skills are a little harder to deal with. The tying of the child’s shoe is often a very integral point. If a child with this disorder can master the tying of their shoe, they have gotten farther than most with this disorder ever will.

Those with autism often have dyspraxia (although not everyone with dyspraxia has autism or vice versa) as one of their symptoms, but it can, in some cases, be controlled and worked on until the disorder ceases to hinder the person’s ability to function normally.

Autism and Circumcision

There is a possible link between autism and circumcision. Autism is a disorder that affects the brain and manifests itself at an early age. Circumcision is the removal of the foreskin from the penis of a newborn male. This is one of the most bizarre connections to autism made, and many do not take the theory seriously. There is some evidence that there may be truth to this theory. The thought process goes by population, and the percentage of that population that is circumcised. The most obvious reason for this thought process is the fact that there is more autism in nations where circumcision is more commonplace. For instance, the United States.

One theory is that the trauma of a circumcision is to blame. The argument states that the trauma from the surgical procedure with no anaesthetic puts the young mind in a state of shock. The young mind, being so underdeveloped, stays in a state of shock to a certain extent. This is the supposed reason the person turns out to be a person with autism. The mind is trying to keep itself in a state of good health, but it is difficult to do this when such trauma is experienced when the brain is forming its first memories and cognitive developmental abilities.

Another theory is that if an anesthetic is used during circumcision, it can take a toll on the brain. Remember, at this point the brain is very susceptible to anything. It is still developing and can be swayed in any direction. Anesthetic may have a negative effect on the brain of a young child.

It seems like a “no win” situation for this case. Without anesthetic you risk trauma, and with it you risk brain damage. Either way, the brain is affected. Whether or not it is affected in a way that promotes autism is still unknown. Also, this is generalized only amongst the male population, since females are not circumcised. Furthermore, there are uncircumcised males who have autism. In the end, it may not be the only cause, but may very well contribute to autism. The extra care for a penis with foreskin left intact is also harder for the autistic child to take care of and clean properly. This presents yet another problem for the autistic child and the autistic child’s caretaker and/or parents. Whether or not there is a link between circumcision and autism is still unclear, but the evidence shows that it may. However, a circumcised penis is probably more manageable for an autistic child. Again, this is a no win situation.

If female circumcision is performed, the female newborn is much more likely to become traumatized by the incident. In female circumcision, which is relatively uncommon, the clitoris is most often removed. This is much more likely to end in neuron damage and a state of shock that permanently damages the brain to cause symptoms of autism. While, again, this seems to only affect the genital area, it does have an affect on the brain as the nerves are connected to the central nervous system.

In conclusion, while it would seem that the majority of children with autism are circumcised, there seems to be little evidence to prove that the the circumcision is to blame. However, while female circumcision is uncommon, it would seem that this is more likely to cause brain damage than male circumcision (although both are traumatic). The general verdict is that there is no connection between circumcision and autism. However, circumcision may be the better choice for a male with autism in terms of care and cleaning.

More connections to autism
1). Autism caused by breast milk?
2). Do vaccines cause autism?
3). Does air pollution cause autism?

Autism and Dyslexia

Many people wonder about the co-morbidity between autism and dyslexia.  Autism is an illness that causes social interaction issues and communication problems in the sufferers, while dyslexia causes children to have difficulty learning to read and write.  However, it seems these two afflictions have much in common and can potentially occur together.

Both autism and dyslexia can occur on a spectrum, that is, both of these conditions can be less or more severe depending on the child and diagnosis.  For example, severe cases of autism can prevent those who have it from communicating using words and they require special technology to communicate via symbols or pictures.  Additionally, dyslexia can be more or less severe and, in many cases, can go overlooked or undiagnosed.

Additionally, both diseases are known to be based in the brain and affect neural processes and chemical communication between neurons.  The exact cause of both of these illnesses is unknown but in both cases it affects processing.

It has been hypothesized that there are shared genetic causes of both autism and dyslexia.  Researchers in 2010 found that people affected with either disorders had “missing” segments of DNA on the same two chromosomes.  Instead of coding for the proteins necessary for the neural processing involved in reading or, for autistic subjects, interpersonal communication, the proteins were missing or, at best, inactive.  What’s interesting about this is that the same missing DNA was found in autistic subjects as in dyslexic subjects, but was not found at all in subjects pulled from the general population.  This suggests that there is possibly a genetic predisposition one can have toward having dyslexia or autism.  However, this doesn’t guarantee someone with this mutation will have one or either of these conditions, it just shows that this genetic marker may signal a higher probability of this problem.

Other environmental and physical issues, such as pollution or stomach problems, have been correlated with the conditions.  While autism can be a condition from birth when a baby fails to develop at the pace expected, it also can be “regressive.”  A child who has been developing normally can suddenly regress and lose verbal or physical skills he or she had previously demonstrated.  Generally, dyslexia is considered to be a disorder that begins at birth, but is only recognized when a child is in school learning to read.

The cause of autism and dyslexia, while well documented and often diagnosed, are still shrouded in mystery.  It is not certain how either condition is caused and it seems that there are many symptoms that can characterize both of them.  For instance, dyslexia is often described as a visual processing disorder where the person with the condition doesn’t “see” the word or sentence correctly.  Some studies suggest that dyslexia is caused by an inability of the brain to process moving images in the same way as the general population.  Many others describe the condition as a difficulty determining “phonemes” or sounds made by the letters in a word.  It’s possible that both these definitions are somewhat correct, which leads to a further obfuscation of the true cause behind the disorder.

Often, due to the varying spectrum of dyslexia “symptoms” teachers and parents confuse dyslexia with laziness, lack of motivation, or being only slightly behind.  Generally, children with dyslexia are of average or even above average intelligence and only struggle in the subjects that require extensive reading and writing.

Since autism occurs on a spectrum as well, it can often be misidentified as “awkwardness” and difficulty socializing at their age level.  Like dyslexia, children affected with mild symptoms of autism or Asperger’s (a less-invasive form of autism) can be seen as just a little behind their peers.  However, due to a boom in diagnosis in recent years, more and more children with the disorder are recognized and treated.

Unlike children with autism, who can’t help their symptoms from showing, especially if they have severe iteration of the condition, children with dyslexia can often hide their condition deftly.  It can be hard to diagnose a child with the disorder because they often adopt strategies that mask their difficulties.  This is one major difference between the disorders and could account for a difference in the rates of correct diagnoses.

Children with dyslexia don’t process written words (and some believe it may also have an auditory component), but other than this difficulty, affected children are of average or above average intelligence.  This differs slightly from autism.  Though many children with Asperger’s are of average or even above average intelligence, other forms of autism are often co-morbid with Intellectual Disability.  These children do not learn at the same speed as other children their age.  This is another major difference between autism and dyslexia.

Luckily both autism and dyslexia are treatable and symptoms can be mitigated, especially when diagnosed early.  While conventional teaching doesn’t work for students with dyslexia, when the disorder is recognized, children can become literate with special help and attention.  Autism, as well, may be treated successfully with intensive treatment.  Autistic children also need to learn many social skills that come to other children naturally.  It is important to note that the effectiveness of treatments depends upon both how early it begins, and the severity of the condition.

Autism and Cell Phones

Autism rates are continuing to climb and many people attribute this to a connection between autism and cell phones. While others scoff at this notion, it is a connection that needs to be explored more fully to really understand if it is a credible idea or whether it is just a coincidence that autism seems to be have risen with the advent of cell phones and increased cellphone usage.

Do cell phones cause autism? There is no real way to know for sure, but many studies are being done and have been done trying to answer that very question. Detractors say that the cell phone autism link is foolish and contribute the rise in autism diagnoses to earlier intervention and a greater knowledge about the symptoms, which means that it is diagnosed earlier and more frequently.  Whatever the true cause, it is important to consider the link between increased cell phone usage and the increased number of children diagnosed with autism.

cell phone radiation facts Autism

The studies that support a cell phone autism link attribute it to the electromagnetic radiation (EMR) that is found with cell phone usage and other electronic device usage. This radiation is said to cause changes in the cell membranes, which allows heavy metal toxins, which have long been associated with autism, to build up in the body. This is a pretty accepted idea that heavy metal toxins have some link with autism, so if EMR is causing changes in the cell membranes that keep the body from removing the toxins naturally, it is essential that it be further explored.

In normal cells, the body will remove most of the toxins, but if cell damage occurs, these toxins can build up in the body causing all sorts of different illnesses and conditions, including autism. This is why researchers are trying to solidify this connection between autism and cell phones to encourage changes in the way cell phones are made and used.

Autism and cell phone towers, as well as phones and other wireless devices, are continuing to increase in usage. Children younger and younger are getting their own devices and using their parent and caregiver’s devices. This means that they are being exposed to EMR younger and younger, which could account for the rise in autism.

Babies and young children are most susceptible to EMR, say some researchers, simply because their skull is not fully formed and as dense as an adult skull is. This makes their brain more susceptible to the EMR and to the changes that occur in cells. For this reason, it is essential to keep babies away from wireless devices as much as possible just to be on the safe side.

Experts recommend that you decrease your usage of wireless devices like phones, tablets, etc. to help reduce the exposure to the radiation that the information carrying waves naturally has. This is probably not realistic to most people, however, as their dependence upon their devices is quite significant and the link is not accepted as fact in most circles.

Radio waves and autism have a very strong connection, but it is one that has not been fully proven to be credible. That is why you want to be sure that you take the information and use it wisely. Whether there is truly a link between autism and cell phones, it is certain that the radiation that we are exposed to each and every day from wireless device usage is sure to have some effect upon our bodies. The key is to be wise about usage and to be wise about exposing our children to the devices and EMR as well.

Some claims these surprising factor may cause Autism.
1). Do environmental factors cause autism?
2). Does air pollution cause autism?
3). Does circumcision cause autism?
4). Can a gut bacteria imbalance really cause autism?
5). Does breast milk cause autism?

Autism and Alzheimer’s

Alzheimer and Autism: A tale of shifting hypothesis

The Alzheimer disease is rewarded as one of the most prevalent neurodegenerative disease in the world.  It is characterized in medical literature as a progressive form of dementia, typically known as loss of brain function. The disease is immedicable and begins with slight and poorly recognized loss of memory, which become more severe over time and eventually leads to death. The common symptoms include difficulty in remembering recent events, perplexity, thinking and judgement, language disorder, agitation, and hallucinations. The regional specificity of neurological abnormality in Alzheimer disease is linked with higher level cognitive functions in the neocortex and hippocampus. Clinical diagnosis of Alzheimer disease is based on signs of gradually progressive dementia and usually relies on behavioural/judgment examination, neuro-imaging and clinical-neuropathologic evaluation. Neuropathologic observations such as intra-neuronal neurofibrillary tangles (containing tau protein), β-amyloid neuritic plaques and gross cerebral cortical atrophy (on CT and MRI) and diffuse cerebral hypometabolism (on PET) by neuroimaging are some of the accurate standards for diagnosis of Alzheimer disease. Molecular and genetic testing in early-onset familial Alzheimer disease (EOFAD, caused by mutations in one of three genes APPPSEN1PSEN2) are also considered affirmative for diagnosis. The cause and progression of disease is a subject of debate and poorly understood. Supportive treatment such as medication is used to hold up the disease progression rate. The presently available drug therapies for Alzheimer are based on drugs that boost cholinergic activity by inhibiting acetylcholinesterase. The fundamental theory behind their usage is based on the fact that Alzheimer disease is caused by reduced synthesis of the neurotransmitter acetylcholine. The use of these drugs have been reported to generate a modest but useful cognitive benefit in a minority of affected individuals (e.g., donepezil, rivastigmine,  galantamine etc).

Genetic basis of Alzheimer’s disease

Majority of studies suggests sporadic nature of Alzheimer disease (~ 75%). However, nearly 25% of all cases of Alzheimer’s disease are familial and out of which  around 95% cases are observed  at  late onset (age >60-65 years) and remaining 5%  at early onset (age <65 years). It has been observed that hereditary (chromosomal and genetic) factors are directly involved in the pathogenesis of the disease. A number of genes have been reported to be directly involved in increasing the risk of disease. The most well studied and established genetic association came from familial early-onset Alzheimer disease (FEOAD). The familial early-onset Alzheimer disease is inherited in an autosomal dominant pattern and credited due to mutations beta-amyloid precursor protein (APP) and presenilins  (PSEN1 and 2) genes. The beta-amyloid precursor protein after cleavage produces amyloid β.  It has been observed that mutations in APP gene results in abnormal cleavage of beta-amyloid precursor protein, thus generating a close relative of the beta-amyloid protein that results in plaque formation. It has been observed that ~10-15% cases of familial early-onset are due to mutation in beta-amyloid precursor protein (APP). The proteins encoded by PSEN (presenilin) genes work in cleavage of amyloid precursor protein. Mutations in either one or both PSEN1 and PSEN2 gene result in inaccurate cleavage of APP. Thus, PSEN (presenilin) genes are also allied with advancement of familial early-onset Alzheimer disease. It has been observed that mutations in PSEN1 and PSEN2 account for around 30%-70% and 5% of familial early-onset Alzheimer disease. However, mutations in PSEN (1 and 2) and APP are not always associated with all cases of familial early-onset Alzheimer disease. Therefore, it is noteworthy that other genes (yet not described) may play an essential role in familial early-onset Alzheimer disease.

Alzheimer and Autism: Associations between neurodevelopmental and neuropsychiatric disorder

At psychological level, both Autism and Alzheimer share a number of features including, catatonic state, disrupted sleep, difficulty with balance and language comprehension, and attention transition issues and a lot. Studies conducted on neurodevelopmental and neuropsychiatric disorders develop a strong belief of genetic overlapping between Alzheimer and Autism. There is growing interest among researchers and clinicians concerning association between Alzheimer and Autism, the two clinically divergent disorders. Both Alzheimer’s and Autism patients have significantly similar abnormal findings in the brain including, extreme deposition of metal ions such as mercury (Hg), reduced Acetylcholine (neurotransmitter), existence of viral or bacterial infection and markedly increase in ß-amyloid (1-42). Although, Alzheimer and Autism are caused by divergent mechanism but a number of genes have been found to be common among the two diseases. This conceptual framework of involvement of same genes is based on recent experimental evidences. A large number of genes have been proposed to contribute in pathology of both Alzheimer and Autism. These include, Catechol-O-methyltransferase (involved in degradation of catecholamines such as dopamine, epinephrine, and norepinephrine), Fragile X mental retardation protein (FMRP), Major histocompatibility complex, class I, A (HLA-A), Phosphatase and tensin homolog (PTEN), and Solute carrier family 6 member (SLC6A4, neurotransmitter transporter, serotonin).

However, the most extensively established hypothesis is centralized around the beta-amyloid (βA), widely studied in Alzheimer disease. Support for this assumption comes from the frequent studies which report the increased level of secreted beta-amyloid precursor protein (APP), in patients with autistic behaviour and aggression. Studies conducted by Lahiri and co-workers at Department of Psychiatry, Indiana University School of Medicine observed that plasma level of secretary beta-amyloid precursor protein- alpha form (sAPPa) was drastically higher in autistic patients. Furthermore, it has also been observed that brain-derived neurotrophic factor (BDNF) and sAPPβ levels are appreciably decreased in plasma of autistic patients. It is suggested that increased levels of sAPPα and decreased level of sAPPβ or imbalance in levels of sAPPα and sAPPβ (proteolytic products of APP by α- and β-secretase) directly contribute in brain overgrowth in autistic patients. These studies were further supported by Wegie and co-workers working at New York State Institute for Basic Research in Developmental Disabilities. They have observed the accumulation of beta-amyloid precursor protein (APP) in brain tissue of children with Autism. Wegie and co-workers reported the accumulation of intracellular N-terminally truncated Aβ-42 in brain neurons of cortex and cerebellar cortex and dentate nucleus. Taken together, these studies provide evidences of common similarities and active participitation of abnormal processing or defective non-amyloidogenic processing of APP in both Alzheimer and Autism disorder.

Another common link between Alzheimer and Autism is mercury relationship. It has been suggested that mercury directly affect the neurological system and causes disastrous neurological damage via disturbing immune system and lithium level in brain, inflicting oxidative burden and depleting glutathione level. It has been observed that mercury has a tendency to accumulate at very high levels in the cerebral cortex and hippocampus. Studies have shown that mercury concentration is found to be altered in the brain and body fluids in Alzheimer and Autistic patients. Furthermore, mercury toxicity induces subtle changes in brain morphology similar to that of Alzheimer and Autism disorder. Studies conducted by Hock and collageous at Psychiatric University Hospital, Basel, Switzerland highlighted a direct relationship between mercury toxicity and beta amyloid secretions. They have shown that mercury inflicts the release of beta-amyloid peptide 1-40 and 1-42 into cell culture supernatants and suggested mercury implication in pathophysiological mechanisms of Alzheimer diseases. Meanwhile, studies conducted by Geier and co-workers at Institute of Chronic Illnesses, USA suggested that mercury in synergism of toxins and pathogens inflicts brain pathology in ASD. Apart from this, elevated immune responses have been observed in the brain of patients from Alzheimer and Autism diseases. The underlying studies demonstrated that increased cytokines level in the brain tissue specially tumor necrosis factor alpha (TNF-alpha) can affect immune response, brain inflammation and possibly the susceptibility to Alzheimer and Autism disorders.

It has been a long time since the first case of Alzheimer and Autism were reported. A number of presumptions have been proposed so far concerning the molecular and genetic link of the two diseases. Conclusion materialize from literature studies suggested that abnormal processing or defective non-amyloidogenic processing of APP represent one of the most affirmative and frequent link between the Autism and Alzheimer disease. Thus, beta amyloid production could be a milestone in the pathophysiological mechanisms of Autism and Alzheimer disease.

Suggested Literature

Alzheimer’s disease. Pubmed health

Bird, T. D. (1993). “Alzheimer Disease Overview.”Book

Brookmeyer, R., S. Gray, et al. (1998). “Projections of Alzheimer’s disease in the United States and the public health impact of delaying disease onset.” Am J Public Health 88(9): 1337-1342.Abstract

Wenk, G. L. (2003). “Neuropathologic changes in Alzheimer’s disease.” J Clin Psychiatry 64 Suppl 9: 7-10. Abstract

Berchtold, N. C. and C. W. Cotman (1998). “Evolution in the conceptualization of dementia and Alzheimer’s disease: Greco-Roman period to the 1960s.” Neurobiol Aging 19(3): 173-189. Abstract

Ray, B., J. M. Long, et al. (2011). “Increased secreted amyloid precursor protein-alpha (sAPPalpha) in severe autism: proposal of a specific, anabolic pathway and putative biomarker.” PLoS One 6(6): e20405. Abstract

Sokol, D. K., D. Chen, et al. (2006). “High levels of Alzheimer beta-amyloid precursor protein (APP) in children with severely autistic behavior and aggression.” J Child Neurol 21(6): 444-449. Abstract

Sokol, D. K., B. Maloney, et al. (2011). “Autism, Alzheimer disease, and fragile X: APP, FMRP, and mGluR5 are molecular links.” Neurology 76(15): 1344-1352.Abstract

Alzheimer’s & Autism: The Mercury Connection. Article

Accumulation of Amyloid-Beta Peptide Species In Four Brain Structures In Children with Autism. Article

Olivieri, G., C. Brack, et al. (2000). “Mercury induces cell cytotoxicity and oxidative stress and increases beta-amyloid secretion and tau phosphorylation in SHSY5Y neuroblastoma cells.” J Neurochem 74(1): 231-236. Abstract

Wu, G., S. Sankaranarayanan, et al. (2011). “Decrease in brain soluble amyloid precursor protein beta (sAPPbeta) in Alzheimer’s disease cortex.” J Neurosci Res 89(6): 822-832.Abstract