If you do a search on Google with the autism-remedy key, there will obviously be a series of anecdotal explanations about children with autism that with a gluten-free diet have healed miraculously, because, not so?, gluten is the mother of all the troubles and so to get rid of any illness, starting from bloating to headaches, dizziness, joint pain and teeth, it’s enough to get rid of gluten and we’re cured. The bones will regain their density, the joints the mobility….and we will live happily ever after, unless we become immortal.
Obviously, gluten free madness does not leave either autistic people alone.
Not to mention the other anecdotes that explain the causes of autism on the net, starting with the MMR vaccinations to glyphosate, genetically modified foods, circumcision all these and others trigger autism. It seems like we are in a train that has gone mad and the end is an expected one. The train will derail.
The problem is not the train but the passengers. Whenever someone appears to explain emotionally the causes of autism , even without a touch of science, the world believes.
Autism spectrum disorder (ASD) is a condition that appears very early in childhood development, varies in severity, and is characterized by impaired social skills, communication problems, and repetitive behaviors. These difficulties can interfere with affected individuals’ ability to function in social, academic, and employment settings. People with ASD also have an increased risk of psychiatric problems such as anxiety, depression, obsessive-compulsive disorder, and eating disorders.
ASD is a common condition, and affects almost five times as many males as females.
The number of children diagnosed with ASD has been increasing rapidly in the past few decades. The prevalence of the disorder in the United States was estimated as 1 in 68 children in 2014, up from 1 in 88 only two years earlier. In the 1980s, before the term ASD was used, the prevalence of autism was reported to be about 1 in 2,000. However, it is unclear whether this represents a true increase in the prevalence of ASD or reflects changes in the way behaviors characteristic of the disorder have been diagnosed and categorized.
Genetics of ADS
ASD is a serious pathology in which the genetic component has more than 60% of the role, and this is scientifically demonstrated.
Rare gene mutations or chromosome abnormalities are thought to be the cause of the condition, often as a feature of syndromes that also involve additional signs and symptoms affecting various parts of the body. For example, mutations in the ADNP gene cause a disorder called ADNP syndrome. In addition to ASD and intellectual disability, this condition involves distinctive facial features and a wide variety of other signs and symptoms. Some of the other genes in which rare mutations are associated with ASD, often with other signs and symptoms, are ARID1B, ASH1L, CHD2, CHD8, DYRK1A, POGZ, SHANK3 and SYNGAP1. In most individuals with ASD caused by rare gene mutations, the mutations occur in only a single gene.
A team of scientists from John Hopkins led by Chakravarti identified 4 genes potentially responsible for autism and focused on one of them CTNND2 because it falls into a region of the genome known to be associated with mental retardation and other intellectual disorders. The research team says the CTNND2 protein influences the regulation of other genes and is much larger in the brains of newborns than in adults or other tissues, which makes them believe it has a key role in brain development.
Many of the genes associated with ASD are involved in the development of the brain. The proteins produced from these genes affect multiple aspects of brain development, including production, growth, and organization of nerve cells. Some affect the number of neurons that are produced, while others are involved in the development or function of the connections between neurons where cell-to-cell communication takes place, or of the cell projections (dendrites) that carry signals received at the synapses to the body of the neuron. Many affect development by controlling (regulating) the activity of other genes or proteins.
The specific ways that changes in these and other genes relate to the development of ASD are unknown. However, studies indicate that during brain development, some people with ASD have more neurons than normal and overgrowth in parts of the outer surface of the brain (the cortex). In addition, there are often patchy areas where the normal structure of the layers of the cortex is disturbed. Normally the cortex has six layers, which are established during development before birth, and each layer has specialized neurons and different patterns of neural connection. The neuron and brain abnormalities occur in the frontal and temporal lobes of the cortex, which are involved in emotions, social behavior, and language. These abnormalities are thought to underlie the differences in socialization, communication, and cognitive functioning characteristic of ASD.
What about gluten free(GF) diet and Casein Free(CF) diet in ADS?
Much has been said about the gluten free, casein free (GFCF) diet and its use to help individuals with autism. Many families with children newly identified with autism wonder if it’s something their child should follow, and others who have been following the diet wonder if they should continue to adhere to it. Let’s try to answer these questions.
The GFCF diet was first developed for people with celiac disease, a disorder that involves a severe reaction to gluten in the diet. Gluten is found in wheat products such as bread and other bakery goods but also in a wide variety of other food products. Casein is a protein most associated with dairy products and also has potential to cause severe reactions in certain individuals. When used appropriately, the GFCF diet is safe and can help avoid these severe health problems.
The theory behind its use in autism?
Gluten is a big protein and there are fragments of gluten that cannot be completely digested. Some investigators believe that a few of these fragments bear a structural resemblance to chemicals called endorphins, which are produced in our brain. Endorphins share a similar chemical structure to morphine, and they naturally relieve pain and reduce stress.
Supporters of this theory call the gluten fragments “gliadorphins.” They hypothesize that the gliadorphins somehow cross the intestinal barrier, enter the bloodstream, and cross the blood-brain barrier. Once across the blood-brain barrier, the gliadorphins interact with the endorphin receptors and cause the behavioral changes described above. This theory can explain the behavioral changes experienced by patients with celiac disease and gluten sensitivity. It doesn’t adequately explain, however, symptoms like neuropathy, an abnormal and usually painful state of the nervous system, or the tingling of the hands and feet that I often detect in these patients. This apparent contradiction can be explained by the second theory, which suggests that brain involvement in gluten-relate disorders is secondary to an inflammatory process. This inflammation is a continuum of immune responses starting in the gut. The first few steps in the process overlap with the first theory: specific gliadin peptides are generated from gluten, and they cross the intestinal barrier. But the picture changes after that. The breakdown of the gliadin peptides generates a chain of events that leads to an inflammatory response. When these fragments “breach the walls of the city” by crossing the intestinal barrier into places they don’t belong, the immune soldiers mount a response to get rid of the enemy. The immediate immune response (or the innate immune response) in the intestine is the first step leading to what could become symptoms of gluten-related disorders.
If only the innate immune system is involved, the outcome is likely to be gluten sensitivity. If the more sophisticated adaptive immune system is involved , then the autoimmune response of celiac disease will most likely emerge.
Prof. dr. Alessio Fasano in his book “Gluten freedom”, said: the gut is not like Las Vegas: What happens in the gut doesn’t stay in the gut. These immune cells may leave the intestine and travel to other districts, including the peripheral nerves or the brain. There they can cause inflammation leading to the behavioral and/or neurological symptoms . Clinical trials and research studies supporting this second theory have increased in recent.
In a recent survey involving more than 27,000 parents of autistic kids, avoidance of gluten (approximately 9,000 cases) and/or casein (approximately 7,000 cases) were the most frequent treatments they implemented with their children. The survey results from the Autism Research Institute showed a better to worse ratio of thirty to one and thirty-two to one, respectively, for these dietary interventions. This means that for every one child whose behavior deteriorated on the gluten-free diet, thirty children had improved behavior (from a total of 4,340 children), and for every one child whose behavior deteriorated on the casein-free diet, thirty-two children improved (from a total of 6,950 children). Therefore, from the point of view of caretakers who experience firsthand the burden of ASD, the gluten-free diet is judged to be one of the most effective interventions to treat the condition. To challenge these conclusions, scientists have performed several double-blind studies. In these studies, both the family of the ASD child and the investigator are unaware if the child is in the treatment group (gluten-free diet) or the placebo group. A recent systematic review reported in the literature by researchers for the Cochrane Collaboration identified six double-blind randomized trials. Three studies showed that a gluten-free diet was beneficial. The remaining three studies detected no improvement in the behavior of ASD children after implementation of the diet. The authors concluded: Research has shown of high rates of use of complementary and alternative therapies for children with autism including gluten and/or casein exclusion diets. Current evidence for efficacy of these diets is poor. Large-scale, good-quality randomized controlled trials are needed.
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