My 3 year old son is out of
controlControl
Control rx, and we dont know why! He seems completely
hyperHyper-sal from 5am til 8pm, he throws
tantrumsTemper tantrums with no reasoning, and has to be held incase he causes injury to himself both in public at home or anywhere, he
bitesAnimal bite
Animal bite - first aid - series
Animal bites
Brown recluse spider bite on the hand
Chigger bite - close-up of blisters
Flea bite - close-up
Frostbite
Frostbite - hands
Human bites
Inhibited sexual desire
Insect bite reaction - close-up kicks and hits other children for no reason and shouts at people when we are out aggressively, we have asked our gp's and advice had his diet checked been to see
familyBirth control and family planning
Choosing a primary care provider
Ewing’s sarcoma
Family troubles - resources counsellors, yet no one can tell us what is wrong, we are a
familyBirth control and family planning
Choosing a primary care provider
Ewing’s sarcoma
Family troubles - resources with 2 other children and have a great loving home, but our 3 year old is destroying it, both our 8 year old and 1 year old dont have any behavoiur problems, this has been going on for 18 months, and we have tried e4very thing,discipline, we have tried talking we have tried shouting smacking but nothing works, he just laughs or runs, we are at our wits ends, all we want to know is if our son has a medical problem, or if it is our fault, or if its just the way he is, but i dont know what kind of doctor we need to see in order for us to get a diagnosis. can you advise please
My 6 yr old is going through the same thing and is currently taking Risperdal to calm down these rages. He has been diagnosed with Bipolar - Manic Depression. You may want to check out the web site I go to www.bpkids.org There are alot a folks who will give you a prompt response on this disorder or may lead to where you need to go to find help for your child.
Chris
Symtpoms of the deficiency are dry itchy skin, excessive thirst, asthma and allergies, vision problems at an early age, dyslexia and dyspraxia, excema and psoriasis, and extreme behavior problems. If your child has a combination of these symptoms an EFA deficiency could be the problem. Try reading "The LCP Solution" by Jacqueline Stordy PhD and Malcolm Nicholl. There have been scientific studies that show an essential fatty acid deficiency can be the cause of behavior problems. A large percentage of ADHD kids (my son has ADHD) have an essenital fatty acid deficiency.
Clinical characteristics and serum essential fatty acid levels in hyperactive children.
Mitchell EA, Aman MG, Turbott SH, Manku M.
This study compared 48 hyperactive children with 49 age-and-sex-matched controls. Significantly more hyperactive children had auditory, visual, language, reading, and learning difficulties, and the birth weight of hyperactive children was significantly lower than that of controls (3,058 and 3,410 g, respectively; p less than 0.01). In addition, significantly more hyperactive children had frequent coughs and colds, polydypsia, polyuria, and a serious illness or accident in the past year than controls, but there was no increase in asthma, eczema, or other allergies. Serum essential fatty acid (EFA) levels were measured in 44 hyperactive subjects and 45 controls. The levels of docasahexaenoic, dihomogammalinolenic, and arachidonic acids were significantly lower in hyperactive children than controls (docosahexaenoic: 41.6 and 49.5 micrograms/ml serum respectively, p = 0.045; dihomogammolinolenic: 34.9 and 41.3 micrograms/ml serum, p = 0.007; arachidonic: 127.1 and 147.0 micrograms/ml serum, p = 0.027). These findings have possible therapeutic and diagnostic implications, but further research is needed to attempt to replicate these differences.
Long-chain polyunsaturated fatty acids in children with attention-deficit hyperactivity disorder.
Burgess JR, Stevens L, Zhang W, Peck L.
Department of Foods and Nutrition, Purdue University, West Lafayette, IN 47907-1264, USA. ***@****
Attention-deficit hyperactivity disorder (ADHD) is the diagnosis used to describe children who are inattentive, impulsive, and hyperactive. ADHD is a widespread condition that is of public health concern. In most children with ADHD the cause is unknown, but is thought to be biological and multifactorial. Several previous studies indicated that some physical symptoms reported in ADHD are similar to symptoms observed in essential fatty acid (EFA) deficiency in animals and humans deprived of EFAs. We reported previously that a subgroup of ADHD subjects reporting many symptoms indicative of EFA deficiency (L-ADHD) had significantly lower proportions of plasma arachidonic acid and docosahexaenoic acid than did ADHD subjects with few such symptoms or control subjects. In another study using contrast analysis of the plasma polar lipid data, subjects with lower compositions of total n-3 fatty acids had significantly more behavioral problems, temper tantrums, and learning, health, and sleep problems than did those with high proportions of n-3 fatty acids. The reasons for the lower proportions of long-chain polyunsaturated fatty acids (LCPUFAs) in these children are not clear; however, factors involving fatty acid intake, conversion of EFAs to LCPUFA products, and enhanced metabolism are discussed. The relation between LCPUFA status and the behavior problems that the children exhibited is also unclear. We are currently testing this relation in a double-blind, placebo-controlled intervention in a population of children with clinically diagnosed ADHD who exhibit symptoms of EFA deficiency.
Plasmalogens, phospholipase A2, and docosahexaenoic acid turnover in brain tissue.
Farooqu AA, Horrocks LA.
Department of Molecular and Cellular Biochemistry The Ohio State University, Columbus 43210, USA.
Plasmalogens are glycerophospholipids of neural membranes containing vinyl ether bonds. Their synthetic pathway is located in peroxisomes and endoplasmic reticulum. The rate-limiting enzymes are in the peroxisomes and are induced by docosahexaenoic acid (DHA). Plasmalogens often contain arachidonic acid (AA) or DHA at the sn-2 position of the glycerol moiety. The receptor-mediated hydrolysis of plasmalogens by cytosolic plasmalogen-selective phospholipase A2 generates AA or DHA and lysoplasmalogens. AA is metabolized to eicosanoids. The mechanism of signaling with DHA is not known. The plasmalogen-selective phospholipase A2 differs from other intracellular phospholipases A2 in molecular mass, kinetic properties, substrate specificity, and response to glycosaminoglycans, gangliosides, and sialoglycoproteins. A major portion of [3H]DHA incorporated into neural membranes is found at the sn-2 position of ethanolamine glycerophospholipids. Studies with a mutant cell line defective in plasmalogen biosynthesis indicate that the incorporation of DHA is reduced in this RAW 264.7 cell line by 50%. In contrast, the incorporation of AA remains unaffected. This is reversed completely when the growth medium is supplemented with sn-1-hexadecylglycerol, suggesting that DHA can be selectively targeted for incorporation into plasmalogens. We suggest that deficiencies of DHA and plasmalogens in peroxisomal disorders, Alzheimer's disease (AD), depression, and attention deficit hyperactivity disorders (ADHD) may be responsible for abnormal signal transduction associated with learning disability, cognitive deficit, and visual dysfunction. These abnormalities in the signal-transduction process can be partially corrected by supplementation with a diet enriched with DHA