I have a 7 year old boy whose
temperTemper tantrums is out of
controlControl
Control rx mainly when there are
majorMajor tears
Major-gesic stressors in his life (the
firstFirst progesterone mc10
First progesterone mc5
First-progesterone vgs 100
First-progesterone vgs 200
First-progesterone vgs 25
First-progesterone vgs 400
First-progesterone vgs 50
First-testosterone
First-testosterone mc week of chool, my difficult 2nd pregnancy), but occasionally during "
normalNormal saline flush" times as well. He has been like this since he was 3. We consulted a psycologist when the "terrible 3s" didn't end at 3 and his opinion was that our son was maturing emotionally slowly but would come around. He still has HUGE
temperTemper tantrums tantrums, including hitting and kicking, and does not respond well to anything, discipline or love, when he's in the midst of a tantrum. I have done a small amount of reading on ODD and I think he shows a majority of the symptoms. The only catch is that he seems to be a perfect child (mostly) in public. He's not a behavior problem in school and he has many friends, though I have noticed he tends to be bossy. He is argumentative, negative, and easily irritated, especially by his little brother. But there are times when he is a wonderful child, too. There is a history of mental disorders in both my own and my husband's family (OCD, alcoholism, etc.) and I am concerned about my son. Does this sound like ODD? What steps shall we take?
Sallymg - could you give me the titles of some other books to get my hands on? I'm in the process of getting "The Explosive Child" - I found some info on the Net and the characteristics fit my son exactly.
Thank you again.
I went to the library and found "The Explosive Child" and have read most of it. I think I need to re-read it several times to ingest it all. I have already tried the "compromising" approach on several things that I think I would put in the B basket and have had some success!! Hooray. We'll see what happens 2 months from now.
I will look up the "Defiant Child" books, too.
Thank you very much.
g
My son does have an appointment with a therapist coming up and I intend to go in with book in hand. I hope that if she is unfamiliar with Dr. Greene that at least she will be open to his ideas. At this point I am not willing to go for any more motivational stuff as I have been trying everything under the sun for years. Fortunately, my mom is very supportive and also well educated in young child stuff and I can bounce things off her. I was telling her the highlights of the book and she agreed that this all seems to make sense in relation to what we know about my boy's personality and quirks. I'm not sure that I have a grip on what may be causing his behavior but I do know that he has some sensory issues. So I guess that's somewhere to start. I'm going to have to read Dr. G at least once more to get a grip on where to begin with the "home program".
We are a religious family too, and I believe that God will lead us where we need to be. All we need to do is pay close attention.
Thank you for everything. Hope all is well with you.
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