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Query: UMLS:C0004352 (
autism
)
32,579
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The rise in
Infantile Autism
, learning problems, cognitive decline with age, Alzheimer's, Parkinson's Diseases and the
SIDS
epidemic, has a common cause in the rising dietary deficit in Omega-3 brain-food. This paper suggests that aside from the wider concept of Autism Spectrum Disorders (ASD) and Pervasive Developmental Disorders (PDD), the rise in
Infantile Autism
(IA) in the last decade is the effect of deficient brain-food (Omega-3). The consequent delay of development prolongs the 2nd regressive event in infancy to pruning of the centre in the Medial Frontal Lobe System that connects Hippocampus and Cingulum. With a consequently defective Supplementary Motor Area (SMA), the Delayed Response Function is affected leading to persistent psychosis. Post-Pubertal Episodic Psychoses are associated with acute reduction of excitation, a risk of breakdown of circuitry, insufficient fill-in mechanisms, and silent spots. An acute psychosis occurs if the silent spots comprise of SMA. Only two brain areas have continuous neurogenesis, indicating their important functions: the Hippocampus and Olfactory Bulb that belongs to the Lateral Frontal Lobe System essential to survival. Concerned with necessity of action in response to the environment, it relies upon short-term memory and Acute Feedback Mechanisms influenced by emotion and motivation from the external world. In contrast, the Medial Frontal Lobe network is controlled by Feed-Forward Predictive Mechanisms related to storage of information. The Delayed Response Function is mastered at 7 months, when 2nd event occurs with pruning of axons and dendrites. An abolished or defective Delayed Response Function seriously incapacitates an individual: A defective "Social Brain" with an inability for conscious action and to communicate, predominates in IA. There is a near lack of speech, despite normal vision and hearing in the minority without marked adversity in pregnancy, at delivery or in infancy. I propose that the recent rise in IA despite no rise in adversity signifies a rising deficiency in brain-food. That this is so is suggested by a changing clinical picture: no Mental Retardation in an IA majority. Deficit in Olfaction is pathognomonic in schizophrenia since 30 yrs and distinguishes the Asperger Syndrome. If brain-food deficiency alone sufficiently prolongs pruning to cause absent activity in SMA in infancy, less mentally retarded IA from other causes might be observed. Deficit in brain-food was evident in the Sudden Infant Death Syndrome: birthweight averaged 200-300 g lower than sibs, Omega-3 levels in brainstem were lower than controls. Only 20 %
SIDS
died in first hypoxic episode, suggesting such episodes are more frequent than we imagined. Children with learning-behaviour problems have similarly depressed birthweight. A general deficiency in Omega-3 contributes to the lacking reduction in Schizophrenia, despite early puberty predominates. Olfactory Bulb is first affected in the Alzheimer's and Parkinson's Disease. Cognitive decline with age, Hippocampal dysfunctions rise markedly irrespective of disease, but the major mental illnesses and
Infantile Autism
in particular, benefit from "brain-food" that might also prevent a development of these disorders. To secure optimal brain function in the coming generations, there is a need to change the diet now from its emphasis on protein for body growth to food for the brain. This means there is a need to increase fish and sea food consumption.
...
PMID:Infantile autism: a chronic psychosis since infancy due to synaptic pruning of the supplementary motor area. 1932 37
The Congress of the International Pediatric Sleep Association joint meeting with Pediatric Sleep Medicine Conference was held in Rome on December 3-5, 2010. It was chaired by the president of IPSA, prof. O. Bruni. About 400 participants taking part in 20 sessions could listen to lectures delivered by the most prominent specialists in pediatric sleep medicine. The presented issues related to sleep development, sleep-disordered breathing, abnormal behaviors and movements during sleep (restless legs syndrome, periodic limb movement disorder, bruxism), epilepsy, narcolepsy, insomnia, infant apnea, arousals and
SIDS
, sleep problems in children with other diseases (cancer,
autism
, ADHD, obesity), pharmacological treatment of pediatric sleep disorders, sleep habits, sleep education programs for children and families. This paper reports on the latest findings in the field of sleep medicine presented at the Congress. Particular attention was paid to practical issues in daily clinical work.
...
PMID:[The current state of knowledge of pediatric sleep medicine. Report from the Congress of the International Pediatric Sleep Association (IPSA) joint meeting with Pediatric Sleep Medicine Conference (Rome, 2010)]. 2154 92
The rise in
infantile autism
, learning problems, cognitive decline with age, Alzheimer's, Parkinson's diseases and the
SIDS
epidemic, has a common cause in the rising dietary deficit in Omega-3 brain-food. This paper suggests that aside from the wider concept of
autism
spectrum disorders (ASD) and pervasive developmental disorders (PDD), the rise in
infantile autism
(IA) in the last decade is the effect of deficient brain-food (Omega-3). The consequent delay of development, prolongs the 2nd regressive event in infancy to pruning of the centre in the Medial Frontal Lobe System that connects hippocampus and singulum. With a consequently defective supplementary motor area (SMA), the Delayed Response Function is affected leading to persistent psychosis. Post-pubertal episodic psychoses are associated with acute reduction of excitation, a risk of breakdown of circuitry, insufficient fill-in mechanisms, and silent spots. An acute psychosis occurs if the silent spots compromise SMA. Only two brain areas have continuous neurogenesis, indicating their important functions: the Hippocampus and Olfactory Bulb that belongs to the lateral frontal lobe system essential to survival. Concerned with necessity of action in response to the environment, it relies upon short-term memory and acute feedback mechanisms influenced by emotion and motivation from the external world. In contrast, the medial frontal lobe network is controlled by feed-forward predictive mechanisms related to storage of information The Delayed Response Function is mastered at 7 months, when 2nd event occurs with pruning of axons and dendrites. An abolished or defective delayed response function seriously incapacitates an individual: a defective "social brain" with an inability for conscious action and to communicate, predominates in IA. There is a near lack of speech, despite normal vision and hearing in the minority without marked adversity in pregnancy, at delivery or in infancy. The recent rise in IA despite no rise in adversity signifies a rising deficiency in brain-food. This is suggested by a changing clinical picture: no Mental Retardation in an IA majority. Deficit in olfaction is pathognomonic in schizophrenia since 30 yrs and distinguishes the Asperger syndrome. If brain-food deficiency alone sufficiently prolongs pruning to cause absent activity in SMA in infancy, less mentally retarded IA from other causes might be observed. Deficit in brain-food was evident in the Sudden Infant Death Syndrome: birthweight averaged 200-300g lower than sibs, Omega-3 levels in brainstem were lower than controls. Only 20%
SIDS
died in first hypoxic episode, suggesting such episodes are more frequent than we imagined. Children with learning-behaviour problems have similarly depressed birthweight. A general deficiency in omega-3 contributes to the lacking reduction in Schizophrenia, despite early puberty predominates. Olfactory bulb is first affected in the Alzheimer's and Parkinson's disease. Cognitive decline with age, hippocampal dysfunctions rises markedly irrespective of disease, but the major mental illnesses and
Infantile Autism
in particular, benefit from "brainfood" that might also prevent a development of these disorders. To secure optimal brain function in the coming generations, there is a need to change the diet now from its emphasis on protein for body growth to food for the brain. This means there is a need to increase fish and sea food consumption.
...
PMID:Infantile autism: a chronic psychosis since infancy due to synaptic pruning of the supplementary motor area. 2214 Nov 91
Starting with a brief history of beriberi and the discovery that thiamin deficiency is its cause, the symptoms and signs are reviewed. None are pathognomonic. The disease has a low mortality and a long morbidity. The appearance of the patient can be deceptive, often being mistaken for psychosomatic disease in the early stages. The chemistry of thiamin and the laboratory methodology for depicting its deficiency are outlined. The diseases associated with thiamin deficiency, apart from malnutrition, include a number of genetically determined conditions where mutations, either in the cofactor relationship or a transporter, provide the etiology. It is emphasized that such mutations are often epigenetically responsive to megadoses of thiamin or one of its derivatives. The use of thiamin in clinical practice requires a high index of suspicion on the part of the clinician since it has a part to play in eating disorders, diabetes, neurodegenerative disease, and cancer. A high rate of critical illness and postsurgery thiamin deficiency have been reported, particularly those associated with gastrointestinal bypass. Emphasis is placed on thiamin deficiency as a major cause of asymmetric dysautonomia, because of the high degree of sensitivity to thiamin deficiency in the brainstem, cerebellum, and hypothalamus. The relationship of thiamin with regional pain syndrome, eosinophilic esophagitis, its analgesic capacity, and its preventive use in obstetrics is raised as a potential issue. The role of thiamin in
SIDS
and
autism
is outlined. It is emphasized that megadose thiamin is being used as a drug, either in stimulating the damaged cofactor/enzyme combination, or mitochondria.
...
PMID:Thiamin. 2947 20