ReversingAUTISM.org: Progressive research to find answers.

I think I finally found the real answer and truth why children cannot tolerate CASEIN and it's because they don't have the enzyme tyrosine hydroxylase to metabolize tyrosine that is found in large quantities in casein. Tyrosine is the precursor of octopamine. I personally have observe that asperger children very high functioning are still not capable of eating products containing casein or tyramine, and those people are the ones having the most challenge with social impairment problems. Interestingly enough the absent of octopamine in invertebrates is directly connected to social impairment. Andrea Lalama.

Octopamine, it’s my latest research. I been trying to find what can possibly cause the social detachment our children suffer from. Everything started by the fact that I cannot tolerate red wine. It gives me a headache. Convinced by the Sulphur and sulfites theory I didn’t explore any further regarding this issue. But a few days ago a man (a stranger) told me corporations have been using genetically modified bacteria to make red wine, and that it’s his believe that the byproduct of this bacteria when it get’s mix with the natural sulphites in wine makes a really bad combination and that it’s the reason of the headaches. I gave him the benefit of the dubt because I do not get headaches with ORGANIC red wine nor sulfites free. So, further researching I found this info to be truth! NOW I’m desperate for finding the answers within this information. MY FIRST concerns and ideas are...what if.... The logical explanation is that maybe what it’s affecting our children ability to metabolize Sulphur in their bodies could be do to the same problem. The new GM fungus they are using may have the answer we are looking for to solve the Sulphur problem. Or the excess of a biogenic amine like tyramine causes the Sulphur problem or the lack of Octopamine causes what we call autistic social impearment by the lack of the enzyme that metabolizes tyramine to Octopamine or simply the spinal fluid is not producing enough Octopamine. SECOND. We maybe can ask NASA for cooperation to find out if our children has this toxic substances causing the autistic characteristics, the main one that worries me is excessive Tyramine, more than histamine for a lot of reasons, but the main one I describe in my third thought. In my further research I found that NASA found out that: NASA Data Helps Avoid Red Wine Headaches BERKELEY, Calif., Nov. 2, 2007 ________________________________________ ...NASA-funded technology ...created a device they say can easily detect ... chemicals, called biogenic amines, occur naturally in a wide variety of aged, pickled and fermented foods prized by gourmet palates, including wine, chocolate, cheese, olives, nuts and cured meats... ... The researchers found the highest amine levels in red wine and sake, and the lowest in beer. For now, the device only works with liquids. ... a clinical dietitian and co-author of "Handbook of Food-Drug Interactions," a book cited by the study for its descriptions of the effects of amines on the brain. ... MAOI inhibitors, which block the body's ability to break down amines, ... News of this gourmand's use for space technology was described in an article published Thursday in the journal Analytical Chemistry. Biogenic amines include tyramine, histamine, and phenylethylamine, ... ...The highest levels of tyramine were found in red wine, and the highest levels of histidine were found in sake, the researchers note. The beer tested contained only small amounts of these biogenic amines, they say. THIRD Tyramine is the precursor of Octopamine. So I have two concerns, does our children have a lack of octopamine or they don’t have the enzyme to metabolize tyramine? THIS IS MY MAIN CONCERN: OCTOPAMINE, because the behaviors our children have is so similar to the absent of octopamine produces in invertebrates, specially pay attetion to the FAT METABOLISM!!! And the fight or flight respons!! ALSO IT CONTROLS THE ADRENALINE, MY BIGGEST PROBLEM!! Also helps the Acetycholine to be released meaning more in the synapse wich is what we are trying to do with the intravenous phosphatydilcholine to beging with, maybe giving octopamine will eliminate the need for phos.choline. The biogenic monoamine octopamine (OA) gained sub- stantial interest because it has widespread modulatory actions in invertebrates (Orchard, 1982; Evans, 1985; Bicker & Menzel, 1989; Roeder, 1994; 1999). OA is believed to play an important role for the general control of behaviour, regulating the motivational state of the animal (Hoyle, 1986; Sombati & Hoyle, 1984a,b; Bacon et al., 1995; Roeder et al., 1998). Octopamine is a biogenic amine which is closely related to noradrenaline, and has a similar action to dopamine. Octopamine is a major neuromodulator with neurotransmitter and neurohormone functions that mediates diverse physiological processes in the peripheral nervous system and CNS of invertebrates. Octopamine is derived from tyramine, another trace amine that is derived from tyrosine or from tyramine-containing food. Octopamine can also be further metabolized into synephrine via the enzyme pheylethanolamine N-methyltransferase. In invertebrates, the role of octopamine is analogous to that of norepinephrine (NE) in vertebrates, and it is responsible for the "fight or flight" effect and fat mobilizing. In mammals, octopamine exists in low concentrations in the central and sympethatic nervous systems [3]. Octopamine is a trace amine, a class of molecules that naturally occur in both vertebrate and invertebrate species. Octopamine was first identified 50 years ago in the octopus [1], and while the biological role it plays in many invertebrate species is well established, the physiological role octopamine plays in mammals is not well known. The two isomers para-octopamine (p-octopamine) and meta-octopamine (m-octopamine) tend to be found together in the same tissues [4]. Levels of octopamine and other trace amines can become elevated in certain pathological states, and are also elevated by inhibition of monoamine oxidase (MAO) [2]. Until recently, the primary role of trace amines was assumed to be as "false neurotransmitters," as they can concentrate in nerve terminals containing neurotransmitters such as dopamine (DA), NE, and serotonin, thus changing receptor function or neurotransmitter uptake. However, a class of receptors called trace amine receptors (TARs) was recently discovered, but the relevance of these receptors has not yet been established [2]. Because of this, the known actions of octopamine on the better understood receptors will be the focus of this article. Octopamine may have effects outside of the adrenergic system in mammals, primarily related to the dopaminergic system. Octopamine is a selective antagonist at the D1 receptor [15-16]. It also inhibits reuptake in vitro, leading to higher concentrations of dopamine [17-18]. In turn, one of these effects may be responsible for the reduction of prolactin secretion seen with octopamine [18]. There is also a report of octopamine decreasing acetylcholine release by rat peripheral nerves. This effect seems to be downward of the effects at alpha(2) and/or D1 receptors [19]. octopamine has low oral bioavailability. Not only is it readily broken down by MAOI, it is extensively metabolized by the gut wall [23]. This does not mean it is completely ineffective orally, only that large doses are required for an effect (probably much larger than those found in most supplements). Octopamine is a naturally occurring selective beta-3 adrenergic receptor agonist, and has been shown in studies to exhibit strong lipolytic activity in fat cells. At this point if we assume this Octopammine is the problem there are a few things it has it in a naturally. And those are: Bitter Orange, which of course it’s regulated by FDA! No wonder. FOUR Further investigation led me to an experiment done in BEES and a particular wasp. LEADING ME TO BELIEVE OUR CHILDREN MAY HAVE TOO MUCH TYROAMINE AND TOO LOW OCTOPAMINE, WHICH LOGICALLY MAY BE BECAUSE A LACK OF AN ENZYME THAT METABOLIZE THE PRECURSOR Tyramine to OC. A Role for Octopamine in Honey Bee Division of Labor David J. Schulza,, Andrew B. Barrona,, Gene E. Robinsonab Departments of aEntomology, and bNeuroscience Program, University of Illinois at Urbana-Champaign, Urbana, Ill., USA Efficient division of labor is one of the main reasons for the success of the social insects. In honey bees the division of labor is principally achieved by workers changing tasks as they age. Typically, young adult bees perform a series of tasks within the colony before ultimately making the transition to foraging outside the hive for resources. This lifelong behavioral development is a well-characterized example of naturally occurring behavioral plasticity, but its neural bases are not well understood. Two techniques were used to assess the role of biogenic amines in the transition from in-hive work to foraging, which is the most dramatic and obvious transition in honey bee behavioral development. First, associations between amines and tasks were determined by measuring the levels of amines in dissected regions of individual bee brains using HPLC analysis. Second, colonies were orally treated with biogenic amines and effects on the onset of foraging were observed. Octopamine concentration in the antennal lobes of the bee brain was most reliably associated with task: high in foragers and low in nurses regardless of age. In contrast, octopamine in the mushroom bodies, a neighboring neuropil, was associated with age and not behavior, indicating independent modulation of octopamine in these two brain regions. Treating colonies with octopamine resulted in an earlier onset of foraging in young bees. In addition, octopamine levels were not elevated by non-foraging flight, but were already high on return from the first successful foraging trip and subsequently remained high, showing no further change with foraging experience. This observation suggests that octopamine becomes elevated in the antennal lobes in anticipation of foraging and is involved in the release and maintenance of the foraging state. Foraging itself, however, does not modulate octopamine levels. Behaviorally related changes in octopamine are modulated by juvenile hormone, which has also been implicated in the control of honey bee division of labor. Treatment with the juvenile hormone analog methoprene elevated octopamine and octopamine treatment 'rescued' the delay in behavioral development caused by experimentally depleting juvenile hormone in bees. Although the pathways linking juvenile hormone and octopamine are presently unknown, it is clear that octopamine acts 'downstream' of juvenile hormone to influence behavior and that juvenile hormone modulates brain octopamine levels. A working hypothesis is that octopamine acts as an activator of foraging by modulating responsiveness to foraging-related stimuli. This is supported by the finding that octopamine treatment increased the response of bees to brood pheromone, a stimulator of foraging activity. Establishing a role for octopamine in honey bee behavioral development is a first step in understanding the neural bases of this example of naturally occurring, socially mediated, behavioral plasticity. The next level of analysis will be to determine precisely where and how octopamine acts in the nervous system to coordinate this complex social behavior. Copyright © 2003 S. Karger AG, Basel We found that T hnM18 mutants, with elevated tyramine levels and reduced octopamine levels, had a severe locomotion phenotype. Mutant larvae spent much more time in pausing episodes than wild-type larvae and displayed a reduction in speed and linear translocation. The locomotion phenotype was partially rescued by feeding T hnM18 larvae octopamine, an effect that could be nullified with simultaneous feeding of tyramine. FIFTH ALA and R-lipoic acid has proven to be one of the most significant supplements helping the children just as much as DMSA from which I deduce the succinic acid was the actual piece helping the children eliminating the aunnesesarely effect of dimercapto compound that it’s not beneficial because it pulls good minerals and trace elements that our children actually needs. So OCTOPAMINE seems to be a lot better than ALA without the side effects ALA produces. ALSO the olfactory issues we see in the children in fact I just made acoment to anju regarding this issue, they get so sensitive to olfactory and sometimes the opposite, they don’t smell at all. Octopamine has the ability to improve insulin sensitivity. This is a huge plus since increased insulin sensitivity not only improves one's fat loss efforts but also induces a myriad of other healthy benefits including preventing and treating diabetes, lowering cholesterol and having more strength and energy. alpha-lipoic acid increase the insulin sensitivity. Octopamine could be a major breakthrough. Imagine obtaining the effects of alpha-lipoic acid while it increases metabolism, lipolysis and insulin secretion and decreases catabolism of proteinaceous tissues. Honeybees: Implications for Olfactory Dysfunction in Humans Tahira Farooqui Department of Entomology, The Ohio State University, Columbus, Ohio, farooqui.2@osu.edu Biogenic amines, such as norepinephrine (in vertebrates) and octopamine (in invertebrates), have structural and functional similarities. These amines play crucial roles in animal behavior by modifying the synaptic output of relevant neurons. Increased levels of norepinephrine in the olfactory bulb preferentially increase mitral cell excitatory responses to olfactory nerve inputs, suggesting its critical role in modulating olfactory function including memory formation and/or recall of specific olfactory memories. Increased levels of octopamine in the antennal lobe play an important role in a reinforcement pathway involved in olfactory learning and memory in honeybees. Similar to adrenergic receptors in the human brain, activation of octopaminergic receptors in the honeybee brain induces specific second messenger pathways that change protein phosphorylation and/or gene expression, altering the activity and/or abundance of proteins responsible for neuronal signaling leading to changes in olfactory behavior. The author's studies in honeybees Apis mellifera indicate that oxidative stress plays a major role in olfactory dysfunction. A similar mechanism has been proposed for olfactory abnormalities in patients of Alzheimer disease and Parkinson disease. Due to similarities in cellular and molecular processes, which govern neuronal plasticity in humans and honeybees, the author proposes that the honeybee can be used as a potential and relatively simple model system for understanding human olfactory dysfunction during aging and in neurodegenerative diseases. NEUROSCIENTIST 13(4):304—322, 2007. DOI: 10.1177/1073858407303676 SIXTH Finally we can maybe use a homeopathic of a wasp’s venom to help the children upregulate the Octopamine. Because the venom produces a stage like autism in the roach’s brain so similar that really shock me. By other hand I try to figure out what could possibly cause IF something the lack of OCTOPAMINE in our children, and that I mention in idea seven. Zombie cockroaches revived by brain shot 10:10 30 November 2007 , NewScientist.com news service, Nora Schultz There is a cure for zombies after all – if you are a cockroach. A new study has shown that cockroaches that turned into "zombies" after being stung by a parasitic wasp can be revived with an antidote. Cockroaches can lose their ability to walk when stung by jewel wasps (Ampulex compressa) – the females of which use the cockroaches to feed their young. The wasp, being much smaller than the cockroach, has evolved a fine sting that can deliver a venom cocktail directly into the cockroach’s brain. The poisons effectively turn the cockroach into a zombie. The cockroach is not entirely paralysed, but loses its ability to escape. The wasp then grabs it by the antennae and pulls it into its burrow and lays an egg on its abdomen. The cockroach sits still while the wasp's larva hatches, chews a hole into its belly, and slowly eats its living host from the inside over a period of eight days. Brain injection To find out if he could revive the cockroaches, Frederic Libersat from Ben-Gurion University in Be'er Sheva, Israel, injected stung zombie cockroaches with candidate chemicals that resembled various neurotransmitters in the brain. Libersat found that one of the drugs, a mimic of the neurotransmitter octopamine, succeeded in bringing the roaches back to life. "The cockroach begins to walk spontaneously again, especially when injected directly into the brain," says Libersat. He had previously discovered that octopamine-producing neurons elsewhere in the cockroach’s body show reduced activity when stung by the wasps. Libersat thinks that the same thing may happen in the brain. Zombie humans "I think the most likely explanation is that a component of the toxin affects the expression of genes that regulate the activity of these neurons", he says. So could octopamine become a possible antidote for future humans turned into zombies by, say, invading aliens? Not quite, says neuroscientist Hans-Joachim Pflüger at the Freie Universität Berlin, Germany. "Our brain is of course much more complex, and we use different neurotransmitters,” he says. “But new research shows tiny quantities of octopamine exist in the vertebrate spinal cord and do affect leg movement, so it will be interesting to see what exactly octopamine does in humans." Journal reference: The Journal of Experimental Biology (vol 210, p 4411) SEVEN OCTOPAMINE agonist-perfect compound of a pesticide BT mixture with CHLORDIMEFORM!!!! A MERCURY-COMPOUND!!!! I raise my case  Chlordimeform- a chemical that is an agonist of Octopamine Mercury-compound pesticides Acute hemorrhagic cystitis. Industrial exposure to the pesticide chlordimeform. Folland DS, Kimbrough RD, Cline RE, Swiggart RC, Schaffner W. An outbreak of hematuria occurred from May 20 to May 23, 1975, among employees of a chemical packaging plant. Nine of 22 workers who packaged the insecticide chlordimeform in a separate shed became severely ill with abdominal pain, dysuria, urgency to void, or hematuria. None of 18 persons who worked in other areas of the plant were affected. Four additional workers who had packaged the chemical during the previous year had a history of similar symptoms. Bladder biopsy specimens from three affected persons showed severe hemorrhagic cystitis; chlordimeform and 2-methyl-4-chloroaniline, a metabolite of chlordimeform, were present in urine specimens collected three days after exposure. The illness lasted from one week to two months; the workers recovered completely. Chlordimeform that was injected subcutaneously into three cats produced similar, though less severe, changes in the bladders of two animals. Andrea Lalama. http://www.reversingautism.org For the record, all original ideas like BT connection and Other opinions and hypothesis like Octopamine, succinic acid, and more created by Andrea Lalama, relevant to autism and expressed in this email are Copyright by Andrea Lalama 2005-2008.