Fear God (UNDER CONSTRUCTION)

FEAR GOD

Revelation 14: 7 And I saw another angel fly in the midst of heaven, having the everlasting gospel to preach unto them that dwell on the earth, and to every nation, and kindred, and tongue, and people, 7Saying with a loud voice, Fear God, and give glory to him; for the hour of his judgment is come: and worship him that made heaven, and earth, and the sea, and the fountains of waters. 8And there followed another angel, saying, Babylon is fallen, is fallen, that great city, because she made all nations drink of the wine of the wrath of her fornication. 8And there followed another angel, saying, Babylon is fallen, is fallen, that great city, because she made all nations drink of the wine of the wrath of her fornication. 9And the third angel followed them, saying with a loud voice, If any man worship the beast and his image, and receive his mark in his forehead, or in his hand, 10The same shall drink of the wine of the wrath of God, which is poured out without mixture into the cup of his indignation; and he shall be tormented with fire and brimstone in the presence of the holy angels, and in the presence of the Lamb: 11And the smoke of their torment ascendeth up for ever and ever: and they have no rest day nor night, who worship the beast and his image, and whosoever receiveth the mark of his name. 12Here is the patience of the saints: here are they that keep the commandments of God, and the faith of Jesus.

Ecclesiastes 12:13 Let us hear the conclusion of the whole matter: Fear God, and keep his commandments: for this is the whole duty of man.14For God shall bring every work into judgment, with every secret thing, whether it be good, or whether it be evil.

Universality and Cosmology

ANALYZING UNDERLYING IMPETUSES AS REFLECTED IN HISTORY (1840's-present)
Religion Civil Rights Science and Technology Space Forms of government Wars and conflicts
Crimes against humanity Literature Entertainment

Universitarianism reflected in religions, military, and politics. (1800's) III

Showing posts with label ADHD. Show all posts
Showing posts with label ADHD. Show all posts

Friday, October 29, 2010

History of attention-deficit hyperactivity disorder [minimal brain disorder]

History of attention-deficit hyperactivity disorder

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Hyperactivity has long been part of the human condition. Sir Alexander Crichton describes "mental restlessness" in his 1798 book.[1][2] The terminology used to describe the symptoms of ADHD has gone through many changes over history including: "minimal brain damage", "minimal brain dysfunction", "learning/behavioral disabilities" and "hyperactivity". In the DSM-II (1968) it was the "Hyperkinetic Reaction of Childhood". In the DSM-III "ADD (Attention-Deficit Disorder) with or without hyperactivity" was introduced. In 1987 this was changed to ADHD in the DSM-III-R and subsequent editions.[3]

Contents

[show]

[edit] Terminology

"ADD" and "ADHD" are not the same thing, and do not constitute a single syndrome, with several important and distinctive variations. The clinical definition of "ADHD" dates to the mid-20th century, but was known by other names. Physicians developed a diagnosis for a set of conditions variously referred to as "minimal brain damage", "minimal brain dysfunction", "minimal brain disorder"[4], "learning/behavioral disabilities" and "hyperactivity". Some of these labels became problematic as knowledge expanded. For example, as awareness grew that many children with no indication of brain damage also displayed the syndrome, the label which included the words "brain damage" did not seem appropriate.
The DSM-II (1968) began to call it "Hyperkinetic Reaction of Childhood" even though the professionals were aware that many of the children so diagnosed exhibited attention deficits without any signs of hyperactivity. In 1980, the DSM-III introduced "ADD (Attention-Deficit Disorder) with or without hyperactivity." That terminology (ADD) technically expired with the revision in 1987 to ADHD in the DSM-III-R. In the DSM-IV, published in 1994, ADHD with sub-types was presented. The current version (as of 2008), the DSM-IV-TR was released in 2000, primarily to correct factual errors and make changes to reflect recent research; ADHD was largely unchanged.[5]
Under the DSM-IV, within the ADHD syndrome, there are three sub-types, including one which lacks the hyperactivity component.[6] Approximately one-third of people with ADHD have the predominantly inattentive type (ADHD-I), meaning that they do not have the hyperactive or overactive behavior components of the other ADHD subtypes.
Even today, the ADHD terminology is objectionable to many. There is some preference for using the ADHD-I, ADD, and AADD terminology when describing individuals lacking the hyperactivity component, especially among older adolescents and adults who find the term "hyperactive" inaccurate, inappropriate and even derogatory.

[edit] 18th century

In 1798, a Scottish-born physician and author, Sir Alexander Crichton (1763–1856), described what seems to be a mental state much like the inattentive subtype of ADHD, in his book An inquiry into the nature and origin of mental derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects. In the chapter "Attention", Crichton described a "mental restlessness".[1][2]
"The incapacity of attending with a necessary degree of constancy to any one object, almost always arises from an unnatural or morbid sensibility of the nerves, by which means this faculty is incessantly withdrawn from one impression to another. It may be either born with a person, or it may be the effect of accidental diseases.
"When born with a person it becomes evident at a very early period of life, and has a very bad effect, inasmuch as it renders him incapable of attending with constancy to any one object of education. But it seldom is in so great a degree as totally to impede all instruction; and what is very fortunate, it is generally diminished with age."[2]
Dr. Crichton further observed: "In this disease of attention, if it can with propriety be called so, every impression seems to agitate the person, and gives him or her an unnatural degree of mental restlessness. People walking up and down the room, a slight noise in the same, the moving of a table, the shutting a door suddenly, a slight excess of heat or of cold, too much light, or too little light, all destroy constant attention in such patients, inasmuch as it is easily excited by every impression."[7]
Crichton has noted that "they have a particular name for the state of their nerves, which is expressive enough of their feelings. They say they have the fidgets".[7] Dr. Crichton suggested that these children needed special educational intervention and noted that it was obvious that they had a problem attending even how hard they did try. "Every public teacher must have observed that there are many to whom the dryness and difficulties of the Latin and Greek grammars are so disgusting that neither the terrors of the rod, nor the indulgence of kind intreaty can cause them to give their attention to them."[8]
Alexander Crichton was almost two centuries ahead of his time in his observations of what is now known as the Inattention subtype of ADHD. He wrote about the salient features of this disorder, including attentional problems, restlessness, early onset, and how it can affect schooling, without any of the moralism introduced by George Still and later authors.[9][10]

[edit] 20th century

In March of 1902, the father of British paediatrics Sir George Frederick Still (1868–1941) gave a series of lectures to the Royal College of Physicians in London under the name “Goulstonian lectures” on ‘some abnormal psychical conditions in children’, which were published later the same year in the Lancet.[11]
He described 43 children who had serious problems with sustained attention and self-regulation, who were often aggressive, defiant, resistant to discipline, excessively emotional or passionate, which showed little inhibitory volition, had serious problems with sustained attention and could not learn from the consequences of their actions; though their intellect was normal. He wrote “I would point out that a notable feature in many of these cases of moral defect without general impairment of intellect is a quite abnormal incapacity for sustained attention.[11]
Dr. Still wrote: “there is a defect of moral consciousness which cannot be accounted for by any fault of environment” When Still was talking about Moral Control, he was referring to it as William James had done before him, but to Still, the moral control of behavior meant "the control of action in conformity with the idea of the good of all."[11]
"Another boy, aged 6 years, with marked moral defect was unable to keep his attention even to a game for more than a very short time, and as might be expected, the failure of attention was very noticeable at school, with the result that in some cases the child was backward in school attainments, although in manner and ordinary conversation he appeared as bright and intelligent as any child could be."[11] He proposed a biological predisposition to this behavioral condition that was probably hereditary in some children and the result of pre- or postnatal injury in others.[9][12]
George Still certainly did not use the current terminology for this disorder, but many historians of ADHD have inferred that the children he described in his series of three published lectures to the Royal College of Physicians would likely have qualified for the current disorder of ADHD combined type, among other disorders.[9][11][12]

[edit] Encephalitis epidemic 1917–1918

The treatment of children with similar behavioral problems who had survived the epidemic of encephalitis lethargica from 1917 to 1918 and the pandemic of influenza from 1919 to 1920 led to terminology which referred to "brain damage."[13]

[edit] References

  1. ^ a b [1] An Early Description of ADHD (Inattentive Subtype): Dr Alexander Crichton and `Mental Restlessness' (1798) Child and Adolescent Men i think star wars is cooltal Health, Volume 6, Number 2, May 2001 , pp. 66–73(8)
  2. ^ a b c p 271, An inquiry into the nature and origin of mental derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects.
  3. ^ Development of the DSM
  4. ^ Bland, J.,(2002) About Gender: Testosterone and Aggression - Childhood. http://www.gender.org.uk/about/06encrn/63gaggrs.htm
  5. ^ Development of the DSM
  6. ^ What is Adult ADD?
  7. ^ a b p 272, An inquiry into the nature and origin of mental derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects.
  8. ^ p 278, An inquiry into the nature and origin of mental derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects.
  9. ^ a b c Palmer, E. D., and Finger, S. 2001. An early description of ADHD(Inattention Subtype): Dr. Alexander Crichton and the "MentalRestlessness" (1798). Child Psychology and Psychiatry Reviews, 6, 66-73.
  10. ^ An inquiry into the nature and origin of mental derangement: comprehending a concise system of the physiology and pathology of the human mind and a history of the passions and their effects.
  11. ^ a b c d e Still GF. "Some abnormal psychical conditions in children: the Goulstonian lectures". Lancet, 1902;1:1008–1012
  12. ^ a b Russell A. Barkley: The Relevance of the Still Lectures to Attention Deficit Hyperactivity Disorder A Commentary. 2006; 10; 137 J Atten Disord.
  13. ^ ADHD - ADHD's Dynamic History: The Effects of Continuously Changing Diagnostic Criteria

Neurotoxicity

Neurotoxicity

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Neurotoxicity occurs when the exposure to natural or artificial toxic substances, which are called neurotoxins, alters the normal activity of the nervous system in such a way as to cause damage to nervous tissue. This can eventually disrupt or even kill neurons, key cells that transmit and process signals in the brain and other parts of the nervous system. Neurotoxicity can result from exposure to substances used in chemotherapy, radiation treatment, drug therapies, certain drug abuse, and organ transplants, as well as exposure to heavy metals, certain foods and food additives, pesticides, industrial and/or cleaning solvents, cosmetics, and some naturally occurring substances. Symptoms may appear immediately after exposure or be delayed. They may include limb weakness or numbness, loss of memory, vision, and/or intellect, uncontrollable obsessive and/or compulsive behaviors, delusions, headache, cognitive and behavioral problems and sexual dysfunction. Individuals with certain disorders may be especially vulnerable to neurotoxins.
The name implies the role of a neurotoxin although the term 'neurotoxic' may be used more loosely to describe states that are known to cause physical brain damage but where no obvious neurotoxin has been identified.
The term neurotoxic is used to describe a substance, condition or state that damages the nervous system and/or brain, usually by killing neurons. The term is generally used to describe a condition or substance that has been shown to result in observable physical damage. The presence of neurocognitive deficits alone is not usually considered sufficient evidence of neurotoxicity, as many substances exist which may impair neurocognitive performance without resulting in the death of neurons. This may be due to the direct action of the substance, with the impairment and neurocognitive deficits being temporary, and resolving when the substance is metabolised from the body. In some cases the level or exposure-time may be critical, with some substances only becoming neurotoxic in certain doses or time periods.

[edit] Prognosis

The prognosis depends upon the length and degree of exposure and the severity of neurological injury. In some instances, exposure to neurotoxins can be fatal. In others, patients may survive but not fully recover. In other situations, many individuals recover completely after treatment.

[edit]

Saturday, October 16, 2010

Dopaminergic (modern diseases)

Dopaminergic

Dopaminergic means related to the neurotransmitter dopamine.[1] For example, certain proteins such as the dopamine transporter (DAT), vesicular monoamine transporter 2 (VMAT2), and dopamine receptors can be classified as dopaminergic, and neurons which synthesize or contain dopamine and synapses with dopamine receptors in them may also be labeled as dopaminergic. Enzymes which regulate the biosynthesis or metabolism of dopamine such as aromatic L-amino acid decarboxylase (AAAD) or DOPA decarboxylasemonoamine oxidase (MAO), and catechol O-methyl transferase (COMT) may be referred to as dopaminergic as well. Lastly, any endogenous or exogenous chemical substance which acts to affect dopamine receptors or dopamine release through indirect actions (for example, on neurons that synapse onto neurons that release dopamine or express dopamine receptors) can also be said to have dopaminergic effects, two prominent examples being opioids which enhance dopamine release indirectly in the reward pathways, and amphetamines, which enhance dopamine release directly by binding to, and inhibiting VMAT2. (DDC),

[edit] Supplements and drugs

A complete list of dopaminergic substances used as supplements and drugs includes:
Others such as hyperforin and adhyperforin (both found in Hypericum perforatum (St. John's Wort (SJW))), L-theanine (found in Camellia sinensis (Tea Plant, also known as Black, White, Oolong, Pu-erh, or Green Tea)), and S-adenosyl-L-methionine (SAMe), which are all dietary supplements used mainly  for the remedification of depression and anxietyantidepressants and anxiolytics, respectively.

Friday, October 15, 2010

Dopamine Dopaminergic system (misinformation included)


 Dopamine

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Dopamine
Identifiers
CAS number 51-61-6 YesY,
62-31-7 (hydrochloride)
PubChem 681
ChemSpider 661
UNII VTD58H1Z2X YesY
SMILES
InChI
InChI key
Properties
Molecular formula C8H11NO2
Molar mass 153.18 g/mol
Density 1.26 g/cm3
Melting point 128 °C, 401 K, 262 °F
Boiling point decomposes
Solubility in water 60.0 g/100 ml
Hazards
R-phrases R36/37/38
S-phrases S26 S36
 Yes (what is this?)  (verify)
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
Y
Infobox references
Dopamine is a catecholamine neurotransmitter present in a wide variety of animals, including both vertebrates and invertebrates. In the brain, this phenethylamine functions as a neurotransmitter, activating the five types of dopamine receptors—D1, D2, D3, D4, and D5—and their variants. Dopamine is produced in several areas of the brain, including the substantia nigra and the ventral tegmental area.[1] Dopamine is also a neurohormonehypothalamus. Its main function as a hormone is to inhibit the release of prolactin from the anterior lobe of the pituitary. released by the
Dopamine is available as an intravenous medication acting on the sympathetic nervous system, producing effects such as increased heart rate and blood pressure. However, because dopamine cannot cross the blood-brain barrier, dopamine given as a drug does not directly affect the central nervous system. To increase the amount of dopamine in the brains of patients with diseases such as Parkinson's disease and dopa-responsive dystonia, L-DOPA, which is the precursor of dopamine, can be given because it can cross the blood-brain barrier.

Contents

[show]

[edit] History

Dopamine was first synthesized in 1910 by George Barger and James Ewens at Wellcome Laboratories in London, England.[2] It was named dopamine because it was a monoamine, and its synthetic precursor was 3,4-dihydroxyphenylalanine (L-DOPA). Dopamine's function as a neurotransmitter was first recognized in 1958 by Arvid Carlsson and Nils-Åke Hillarp at the Laboratory for Chemical Pharmacology of the National Heart Institute of Sweden.[3] Carlsson was awarded the 2000 Nobel Prize in Physiology or Medicine for showing that dopamine is not just a precursor of norepinephrine (noradrenaline) and epinephrine (adrenaline), but a neurotransmitter as well.

[edit] Biochemistry


Biosynthesis of dopamine

[edit] Name and family

Dopamine has the chemical formula C6H3(OH)2-CH2-CH2-NH2. Its chemical name is "4-(2-aminoethyl)benzene-1,2-diol" and its abbreviation is "DA."
As a member of the catecholamine family, dopamine is a precursor to norepinephrine (noradrenaline) and then epinephrine (adrenaline) in the biosynthetic pathways for these neurotransmitters.

The effects of drugs that reduce dopamine activity

In humans, drugs that reduce dopamine activity (neuroleptics, e.g. antipsychotics) have been shown to reduce motivation, cause anhedonia (inability to experience pleasure), and long-term use has been associated with the irreversible movement disorder, tardive dyskinesia.[26] Furthermore, antipsychotic drugs are associated with weight gain, diabetes, lactation, gynecomastia, drooling, dysphoria, fatigue, sexual dysfunction, and heart rhythm problems. Selective D2/D3 agonists pramipexole and ropinirole, used to treat restless legs syndrome[27] (RLS), have limited anti-anhedonic properties as measured by the Snaith-Hamilton Pleasure Scale (SHAPS).

[edit] Opioid and cannabinoid transmission

Opioid and cannabinoid transmission instead of dopamine may modulate consummatory pleasure and food palatability (liking).[28] This could explain why animals' "liking" of food is independent of brain dopamine concentration. Other consummatory pleasures, however, may be more associated with dopamine. One study found that both anticipatory and consummatory measures of sexual behavior (male rats) were disrupted by DA receptor antagonists.[29] Libido can be increased by drugs that affect dopamine, but not by drugs that affect opioid peptides or other neurotransmitters.

[edit] Sociability

Sociability is also closely tied to dopamine neurotransmission. Low D2 receptor-binding is found in people with social anxiety. Traits common to negative schizophrenia (social withdrawal, apathy, anhedonia) are thought to be related to a hypodopaminergic state in certain areas of the brain. In instances of bipolar disorder, manic subjects can become hypersocial, as well as hypersexual.[citation needed] This is credited to an increase in dopamine, because mania can be reduced by dopamine-blocking anti-psychotics.[30]

[edit] Processing of pain

Dopamine has been demonstrated to play a role in pain processing in multiple levels of the central nervous system including the spinal cord,[31] periaqueductal gray (PAG),[32] thalamus,[33] basal ganglia,[34][35] insular cortex,[36][37] and cingulate cortex.[38] Accordingly, decreased levels of dopamine have been associated with painful symptoms that frequently occur in Parkinson's disease.[39] Abnormalities in dopaminergic neurotransmission have also been demonstrated in painful clinical conditions, including burning mouth syndrome,[40] fibromyalgia,[41][42] and restless legs syndrome.[43] In general, the analgesic capacity of dopamine occurs as a result of dopamine D2 receptor activation; however, exceptions to this exist in the PAG, in which dopamine D1 receptor activation attenuates pain presumably via activation of neurons involved in descending inhibition.[44] In addition, D1 receptor activation in the insular cortex appears to attenuate subsequent pain-related behavior.

[edit] Salience

Dopamine may also have a role in the salience of potentially important stimuli, such as sources of reward or of danger.[45] This hypothesis argues that dopamine assists decision-making by influencing the priority, or level of desire, of such stimuli to the person concerned.

[edit] Behavior disorders

Deficient dopamine neurotransmission is implicated in attention-deficit hyperactivity disorder, and stimulant medications used to successfully treat the disorder increase dopamine neurotransmission, leading to decreased symptoms.[46] Consistent with this hypothesis, dopaminergic pathways have a role in inhibitory action control and the inhibition of the tendency to make unwanted actions.[47]
The long term use of levodopa in Parkinson's disease has been linked to dopamine dysregulation syndrome.[48]

[edit] Latent inhibition and creative drive

Dopamine in the mesolimbic pathway increases general arousal and goal directed behaviors and decreases latent inhibition; all three effects increase the creative drive of idea generation. This has led to a three-factor model of creativity involving the frontal lobes, the temporal lobes, and mesolimbic dopamine.[49]

[edit] Chemoreceptor trigger zone

Dopamine is one of the neurotransmitters implicated in the control of nausea and vomiting via interactions in the chemoreceptor trigger zone. Metoclopramide is a D2-receptor antagonist that functions as a prokinetic/antiemetic.

[edit] Dopaminergic mind hypothesis

The dopaminergic mind hypothesis seeks to explain the differences between modern humans and their hominid relatives by focusing on changes in dopamine.[50] It theorizes that increased levels of dopamine were part of a general physiological adaptation due to an increased consumption of meat around two million years ago in Homo habilis, and later enhanced by changes in diet and other environmental and social factors beginning approximately 80,000 years ago. Under this theory, the "high-dopamine" personality is characterized by high intelligence, a sense of personal destiny, a religious/cosmic preoccupation, an obsession with achieving goals and conquests, an emotional detachment that in many cases leads to ruthlessness, and a risk-taking mentality. High levels of dopamine are proposed to underlie increased psychological disorders in industrialized societies. According to this hypothesis, a "dopaminergic society" is an extremely goal-oriented, fast-paced, and even manic society, "given that dopamine is known to increase activity levels, speed up our internal clocks and create a preference for novel over unchanging environments."[50] In the same way that high-dopamine individuals lack empathy and exhibit a more masculine behavioral style, dopaminergic societies are "typified by more conquest, competition, and aggression than nurturance and communality."[50] Although behavioral evidence and some indirect anatomical evidence (e.g., enlargement of the dopamine-rich striatum in humans)[51] support a dopaminergic expansion in humans, there is still no direct evidence that dopamine levels are markedly higher in humans relative to other apes.[52] However, recent discoveries about the sea-side settlements of early man may provide evidence of dietary changes consistent with this hypothesis.[53]

[edit] Links to psychosis

Abnormally high dopaminergic transmission has been linked to psychosis and schizophrenia.[54] Increased dopaminergic functional activity, specifically in the mesolimbic pathway, is found in schizophrenic individuals. Anti-psychotic medications act largely as dopamine antagonists, inhibiting dopamine at the receptor level, and thereby blocking the effects of the neurochemical in a dose-dependant manner. The older, so-called typical antipsychotics most commonly act on D2 receptors,[55] while the atypical drugs also act on D1, D3 and D4 receptors.[56][57] The finding that drugs such as amphetamines, methamphetamine and cocaine, which can increase dopamine levels by more than tenfold,[58] can temporarily cause psychosis, provides further evidence for this link.[5

Therapeutic use

Levodopa is a dopamine precursor used in various forms to treat Parkinson's disease and dopa-responsive dystonia. It is typically co-administered with an inhibitor of peripheral decarboxylation (DDC, dopa decarboxylase), such as carbidopa or benserazide. Inhibitors of alternative metabolic route for dopamine by catechol-O-methyl transferase are also used. These include entacapone and tolcapone.

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