PENTAGON BRIEFING ON REMOVING "The God Gene"

[mgt23]

.............doing the rounds, claimed as fake. I wonder if anyone has more details on this conspiracy theory of a god gene (VMAT2)vaccine.

[youtube:30prxzy2]http://www.youtube.com/watch?v=nADFJlAggnY[/youtube]30prxzy2]



http://grantjkidney.com/alert-pentagon- ... ccination/

ALERT: Pentagon Plans to Remove 'God Gene' From Human Brain Via Vaccination
Published April 3, 2012

Grant J. Kidney— High level military intelligence is planning to turn every one in the United States in to an emotionless, atheistic zombie.

During a public press briefing, Pentagon officials showed charts and graphs of the human brain and detailed just exactly how they would remove the portion of the brain which gives way to religious experiences.

Under the guise of fighting radical Muslims, the process of reversing one's religious inclinations would be administered in the form of a vaccine. If successful, the Pentagon will no doubt use the vaccine to target other such spiritual or religious groups.

Whether one is theistic or atheistic is beyond the scope of this particular article. What matters most is folks' free choice to explore patterns of thought which come naturally to them. If an injection is forced upon the public so as to 'liberate' them from what some might consider 'delusions of grandeur', then we're all in a lot of trouble- atheist, Christian, Muslim, Jew, Buddhist, etc.

It has long since been the plan of the elite social planners to rewire and to reprogram the human brain so as to force subservient behavior upon the masses. With an awakening population geared up for all out war with the government, what may be considered last minute measures such as injecting folks with dangerous, mind altering vaccines, would be considered top priority for those who intend to dominate over our lives in a world which resembles the new film 'Hunger Games'.

Already vaccines exist which remove the brain's natural endorphin production processes. To feel good, to love, to hate- these emotions can now be wiped clean of the human 'hardware' by government funded research.

Just as in the movie 'Equilibrium', the true intent of the global elite is to pacify and dull the human experience so as to ensure that but two classes exist- the oligarchs and their pitiful, drone-like, worker slaves.

http://en.wikipedia.org/wiki/God_gene

God gene
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The God gene hypothesis proposes that a specific gene (VMAT2) predisposes humans towards spiritual or mystic experiences. The idea has been postulated by geneticist Dean Hamer, the director of the Gene Structure and Regulation Unit at the U.S. National Cancer Institute, and author of the 2005 book The God Gene: How Faith is Hardwired into our Genes.

The God gene hypothesis is based on a combination of behavioral genetic, neurobiological and psychological studies. The major arguments of the theory are: (1) spirituality can be quantified by psychometric measurements; (2) the underlying tendency to spirituality is partially heritable; (3) part of this heritability can be attributed to the gene VMAT2;[1] (4) this gene acts by altering monoamine levels; and (5) spiritual individuals are favored by natural selection because they are provided with an innate sense of optimism, the latter producing positive effects at either a physical and psychological level.

A number of scientists and researchers are highly critical of this theory; Carl Zimmer, writing in Scientific American, questions why "Hamer rushed into print with this book before publishing his results in a credible scientific journal."[2] In his book, Hamer also writes "Just because spirituality is partly genetic doesn't mean it is hardwired."[3]
Contents

    1 Proposal
    2 Scientific criticism
    3 Religious response
    4 See also
    5 References
    6 External links

Proposal

According to this hypothesis, the God gene (VMAT2) is a physiological arrangement that produces the sensations associated, by some, with mystic experiences, including the presence of God or others, or more specifically spirituality as a state of mind (i.e. it does not encode or cause belief in God itself in spite of the "God gene" moniker).

Based on research by psychologist Robert Cloninger, this tendency toward spirituality is quantified by the self-transcendence scale, which is composed of three sub-sets: "self-forgetfulness" (as in the tendency to become totally absorbed in some activity, such as reading); "transpersonal identification" (a feeling of connectedness to a larger universe); and "mysticism" (an openness to believe things not literally provable, such as ESP). Cloninger suggests that taken together, these measurements are a reasonable way to quantify (make measurable) how spiritual someone is feeling.

The self-transcendence measure was shown to be heritable by classical twin studies conducted by Lindon Eaves and Nicholas Martin. Interestingly, these studies show that specific religious beliefs (such as belief in Jesus) have no genetic basis and are instead memes, that is cultural units transmitted by non genetic means, as by imitation.

In order to identify some of the specific genes involved in self-transcendence, Hamer analyzed DNA and personality score data from over 1000 individuals and identified one particular locus, VMAT2, with a significant correlation. VMAT2 codes for a vesicular monoamine transporter that plays a key role in regulating the levels of the brain chemicals serotonin, dopamine and norepinephrine. These monoamine transmitters are in turn postulated to play an important role in regulating the brain activities associated with mystic beliefs.

What evolutionary advantage this may convey, or what advantageous effect it is a side effect of, are questions that are yet to be fully explored. However, Dr. Hamer has hypothesized that self-transcendence makes people more optimistic, which makes them healthier and likely to have more children.
Scientific criticism

Although it is always difficult to determine the many interacting functions of a gene, VMAT2 appears to be involved in the transport of monoamine neurotransmitters across the synapses of the brain. PZ Myers argues: "It's a pump. A teeny-tiny pump responsible for packaging a neurotransmitter for export during brain activity. Yes, it's important, and it may even be active and necessary during higher order processing, like religious thought. But one thing it isn't is a 'god gene.'"[4]

Carl Zimmer claimed that, given the low explanatory power of VMAT2, it can be characterized as a gene that accounts for less than one percent of the variance of self-transcendence scores. These, Zimmer says, can signify anything from belonging to the green party to believing in ESP. Zimmer also points out that the God Gene theory is based on only one unpublished, unreplicated study.[5] However Hamer notes that the importance of the VMAT2 finding is not that it explains all spiritual or religious feelings, but rather that it points the way toward one neurobiological pathway that may be important.
Religious response

John Polkinghorne, an Anglican priest, member of the Royal Society and Canon Theologian at Liverpool Cathedral, was asked for a comment on Hamer's theory by the British national daily newspaper, The Daily Telegraph. He replied: "The idea of a God gene goes against all my personal theological convictions. You can't cut faith down to the lowest common denominator of genetic survival. It shows the poverty of reductionist thinking." [6][7]

Walter Houston, the chaplain of Mansfield College, Oxford, and a fellow in theology, told the Telegraph: "Religious belief is not just related to a person's constitution; it's related to society, tradition, character—everything's involved. Having a gene that could do all that seems pretty unlikely to me."

Hamer responded that the existence of such a gene would not be incompatible with the existence of a personal God: "Religious believers can point to the existence of God genes as one more sign of the creator's ingenuity—a clever way to help humans acknowledge and embrace a divine presence."[7]

Hamer repeatedly notes in his book that, "This book is about whether God genes exist, not about whether there is a God."[8]
See also

    VMAT2
    Neurotheology
    Origin of religion
    Cognitive science of religion

References

    ^ Hamer, Dean (2005). The God Gene: How Faith Is Hardwired Into Our Genes. Anchor Books. ISBN 0-385-72031-9.
    ^ College Quarterly - Winter 2005
    ^ Hamer, Dean H. 2004. The God gene how faith is hardwired into our genes. New York: Doubleday. Pages 211-12.
    ^ Myers, PZ (2005-02-13). "No god, and no 'god gene', either". Pharyngula. Retrieved 2012-01-29.
    ^ Zimmer, Carl (October 2004). "Faith-Boosting Genes: A search for the genetic basis of spirituality". Scientific American.
    ^ The 'God Gene' Sales Stunt
    ^ a b Geneticist claims to have found 'God gene' in humans
    ^ Hamer, Dean (2005). The God Gene: How Faith Is Hardwired Into Our Genes. Anchor Books. Page 16

    The God Gene: How Faith is Hardwired into our Genes by Dean Hamer. Published by Doubleday, ISBN 0-385-50058-0.

External links

    Dean Hamer's website
    Daily Telegraph report
    Carl Zimmer's review

http://en.wikipedia.org/wiki/VMAT2

Vesicular monoamine transporter 2
From Wikipedia, the free encyclopedia
  (Redirected from VMAT2)
Jump to: navigation, search
Solute carrier family 18 (vesicular monoamine), member 2
Identifiers
Symbols    SLC18A2; SVAT; SVMT; VAT2; VMAT2
External IDs    OMIM: 193001 MGI: 106677 HomoloGene: 2298 ChEMBL: 1893 GeneCards: SLC18A2 Gene
[show]Gene Ontology
Orthologs
Species    Human    Mouse    
Entrez    6571    214084    
Ensembl    ENSG00000165646    ENSMUSG00000025094    
UniProt    Q05940    Q8BRU6    
RefSeq (mRNA)    NM_003054.4    NM_172523.3    
RefSeq (protein)    NP_003045.2    NP_766111.1    
Location (UCSC)    Chr 10:
119 – 119.04 Mb    Chr 19:
59.34 – 59.37 Mb    
PubMed search    [1]    [2]    
This box:

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The vesicular monoamine transporter 2 (VMAT2) also known as solute carrier family 18 member 2 (SLC18A2) is a protein that in humans is encoded by the SLC18A2 gene.[1] VMAT2 is an integral membrane protein that acts to transport monoamines—particularly neurotransmitters such as dopamine, norepinephrine, serotonin, and histamine—from cellular cytosol into synaptic vesicles.[2]
Contents

    1 Binding sites and ligands
    2 Inhibition of VMAT2
        2.1 VMAT2 function in mice
    3 Spirituality hypothesis
    4 References
    5 Further reading
    6 External links

Binding sites and ligands

One binding site is that of dihydrotetrabenazine (DTBZ) and reserpine. Lobeline binds at this site. Dextroamphetamine and dextromethamphetamine bind at distinct sites to the VMAT2, inhibiting its function. Although the amphetamines inhibit VMAT2 presynaptically leading to diminished neurotransmitter, the primary mechanism for the enhancement of extracellular monoamines, like dopamine, is reversal of the dopamine transporter (DAT).[3] Other VMAT2 inhibitors such as GZ-793A have been shown to inhibit the reinforcing effects of methamphetamine but without producing stimulant or reinforcing effects themselves.[4]
Inhibition of VMAT2

VMAT2 is essential in the presynaptic neuron's ability to facilitate the release of neurotransmitters into the synaptic cleft. If VMAT2 function is inhibited or compromised, neurotransmitters, such as dopamine, cannot be released via normal transport (exocytosis, action potential) into the synapse. VMAT2 function inhibition can have many various effects on neurotransmitter function. Specifically of importance is its effect on the neurotransmitter dopamine.

Dopamine, specifically, is highly neurotoxic to most cellular structures, due to its ability to auto-oxidize in the presence of oxygen radicals. Dopamine, and other neurotransmitters, are metabolized via various processes into various substances, by enzymes such as monoamine oxidase (MAO), catechol-O-methyl transferase (COMT), and dopamine beta hydroxylase (DBH).

Vesicles normally protect dopamine from auto-oxidation and metabolism by monoamine oxidase and COMT. Impaired VMAT2 function/activity may contribute to symptoms of depression, anxiety, restless leg syndrome, akathisia, Parkinson's disease, social anxiety, and many other conditions, via inhibition of normal dopamine release into the synapse. Long-term use of amphetamine and methamphetamine causes long-lasting reductions in VMAT2 expression/activity, similar to chronic use of cocaine. This reduction of VMAT2 activity contributes significantly to the neurotoxic effects of amphetamine and methamphetamine.

Cocaine users display a marked reduction in VMAT2 immunoreactivity. Sufferers of cocaine-induced mood disorders displayed a significant loss of VMAT2 immunoreactivity; this might reflect damage to dopamine axon terminals in the striatum. These neuronal changes could play a role in causing disordered mood and motivational processes in more severely addicted users.[5]
VMAT2 function in mice

Mice bred without VMAT2 display marked depression and hypoactivity symptoms, and die within a few days of birth. Their brains exhibit a significant decrease of monoamine and catecholamine content, compared to wild-type mice. Depolarization does not normalize behavior in VMAT2-KO mice, compared to wild-type mice. Amphetamine, however, decreases the functional deficits caused by VMAT-deletion, indicating that monoamines/catecholamines, such as dopamine, are still present in the presynaptic cytoplasm, but not packaged into vesicles necessary for normal depolarization/exocytosis-induced release. In wild-type mice and humans, amphetamine inhibits VMAT2 function and reverses the dopamine transporter (DAT), causing the release of unprotected free cytoplasmic dopamine into the synaptic cleft. VMAT-2 deletion mimics the VMAT-2 inhibition caused by amphetamine, allowing amphetamine to simply reverse the DAT, releasing dopamine, and subsequently reducing functional deficits in VMAT2-KO mice. VMAT2-KO mice also display significantly increased neurotoxicity in response to amphetamine, due to the unprotected metabolism and auto-oxidation of dopamine in the presynaptic cytoplasm of dopamine neurons.[6][7]
Spirituality hypothesis
Main article: God gene

Geneticist Dean Hamer has suggested that the VMAT2 gene correlates with spirituality using data from a smoking survey, which included questions intended to measure "self-transcendence". Hamer performed the spirituality study on the side, independently of the National Cancer Institute smoking study. His findings were published in the mass-market book The God Gene: How Faith Is Hard-Wired Into Our Genes.[8][9] However Hamer's claim that the VMAT2 gene contributes to spirituality is controversial.[10] Hamer's study has not been published in the peer reviewed literature.[11]
References

    ^ Surratt CK, Persico AM, Yang XD, Edgar SR, Bird GS, Hawkins AL, Griffin CA, Li X, Jabs EW, Uhl GR (March 1993). "A human synaptic vesicle monoamine transporter cDNA predicts posttranslational modifications, reveals chromosome 10 gene localization and identifies TaqI RFLPs". FEBS Lett. 318 (3): 325–30. doi:10.1016/0014-5793(93)80539-7. PMID 8095030.
    ^ Eiden LE, Schäfer MK, Weihe E, Schütz B (February 2004). "The vesicular amine transporter family (SLC18): amine/proton antiporters required for vesicular accumulation and regulated exocytotic secretion of monoamines and acetylcholine". Pflugers Arch. 447 (5): 636–40. doi:10.1007/s00424-003-1100-5. PMID 12827358.
    ^ Jones SR, Gainetdinov RR, Wightman RM, Caron MG. (March 1998). "Mechanisms of amphetamine action revealed in mice lacking the dopamine transporter.". J Neurosci. 18 (6): 1979–86. PMID 9482784.
    ^ Alvers, K. M.; Beckmann, J. S.; Zheng, G.; Crooks, P. A.; Dwoskin, L. P.; Bardo, M. T. (2012). "The effect of VMAT2 inhibitor GZ-793A on the reinstatement of methamphetamine-seeking in rats". Psychopharmacology. doi:10.1007/s00213-012-2748-3. PMID 22638813. edit
    ^ Little KY, Krolewski DM, Zhang L, Cassin BJ (January 2003). "Loss of striatal vesicular monoamine transporter protein (VMAT2) in human cocaine users". Am J Psychiatry 160 (1): 47–55. doi:10.1176/appi.ajp.160.1.47. PMID 12505801.
    ^ Takahashi N, Miner LL, Sora I, Ujike H, Revay RS, Kostic V, Jackson-Lewis V, Przedborski S, Uhl GR (September 1997). "VMAT2 knockout mice: heterozygotes display reduced amphetamine-conditioned reward, enhanced amphetamine locomotion, and enhanced MPTP toxicity". Proc. Natl. Acad. Sci. U.S.A. 94 (18): 9938–43. doi:10.1073/pnas.94.18.9938. PMC 23302. PMID 9275230.
    ^ Luo X, Persico AM, Lauder JM (2003). "Serotonergic regulation of somatosensory cortical development: lessons from genetic mouse models". Dev. Neurosci. 25 (2-4): 173–83. doi:10.1159/000072266. PMID 12966215.
    ^ Hamer, Dean H. (2004). The God gene: how faith is hardwired into our genes. Garden City, N.Y: Doubleday. ISBN 0-385-50058-0.
    ^ Kluger, Jeffrey; Jeff Chu, Broward Liston, Maggie Sieger, Daniel Williams (2004-10-25). "Is God in our genes?". TIME. Time Inc.. Retrieved 2007-04-08.
    ^ Silveira LA (2008). "Experimenting with spirituality: analyzing The God Gene in a nonmajors laboratory course". CBE Life Sci Educ 7 (1): 132–45. doi:10.1187/cbe.07-05-0029. PMC 2262126. PMID 18316816.
    ^ Zimmer, Carl (October 2004). "Faith-Boosting Genes: A search for the genetic basis of spirituality". Scientific American.

Further reading

    Need AC, Keefe RS, Ge D, et al. (2009). "Pharmacogenetics of antipsychotic response in the CATIE trial: a candidate gene analysis.". Eur. J. Hum. Genet. 17 (7): 946–57. doi:10.1038/ejhg.2008.264. PMC 2986499. PMID 19156168.
    Okamura N, Villemagne VL, Drago J, et al. (2010). "In vivo measurement of vesicular monoamine transporter type 2 density in Parkinson disease with (18)F-AV-133.". J. Nucl. Med. 51 (2): 223–8. doi:10.2967/jnumed.109.070094. PMID 20080893.
    Saisho Y, Harris PE, Butler AE, et al. (2008). "Relationship between pancreatic vesicular monoamine transporter 2 (VMAT2) and insulin expression in human pancreas.". J. Mol. Histol. 39 (5): 543–51. doi:10.1007/s10735-008-9195-9. PMC 2566800. PMID 18791800.
    Tsolakis AV, Grimelius L, Stridsberg M, et al. (2009). "Obestatin/ghrelin cells in normal mucosa and endocrine tumours of the stomach.". Eur. J. Endocrinol. 160 (6): 941–9. doi:10.1530/EJE-09-0001. PMID 19289536.
    Harris PE, Ferrara C, Barba P, et al. (2008). "VMAT2 gene expression and function as it applies to imaging beta-cell mass.". J. Mol. Med. 86 (1): 5–16. doi:10.1007/s00109-007-0242-x. PMID 17665159.
    Roe BE, Tilley MR, Gu HH, et al. (2009). "Financial and psychological risk attitudes associated with two single nucleotide polymorphisms in the nicotine receptor (CHRNA4) gene.". PLoS ONE 4 (: e6704. doi:10.1371/journal.pone.0006704. PMC 2724734. PMID 19693267.
    Sørensen KD, Wild PJ, Mortezavi A, et al. (2009). "Genetic and epigenetic SLC18A2 silencing in prostate cancer is an independent adverse predictor of biochemical recurrence after radical prostatectomy.". Clin. Cancer Res. 15 (4): 1400–10. doi:10.1158/1078-0432.CCR-08-2268. PMID 19228741.
    Watabe M, Nakaki T (2008). "Mitochondrial complex I inhibitor rotenone inhibits and redistributes vesicular monoamine transporter 2 via nitration in human dopaminergic SH-SY5Y cells.". Mol. Pharmacol. 74 (4): 933–40. doi:10.1124/mol.108.048546. PMID 18599602.
    Catlow K, Ashurst HL, Varro A, Dimaline R (2007). "Identification of a gastrin response element in the vesicular monoamine transporter type 2 promoter and requirement of 20 S proteasome subunits for transcriptional activity.". J. Biol. Chem. 282 (23): 17069–77. doi:10.1074/jbc.M611421200. PMID 17442673.
    Yosifova A, Mushiroda T, Stoianov D, et al. (2009). "Case-control association study of 65 candidate genes revealed a possible association of a SNP of HTR5A to be a factor susceptible to bipolar disease in Bulgarian population.". J Affect Disord 117 (1-2): 87–97. doi:10.1016/j.jad.2008.12.021. PMID 19328558.
    Tabakoff B, Saba L, Printz M, et al. (2009). "Genetical genomic determinants of alcohol consumption in rats and humans.". BMC Biol. 7: 70. doi:10.1186/1741-7007-7-70. PMC 2777866. PMID 19874574.
    Zheng G, Dwoskin LP, Crooks PA (2006). "Vesicular monoamine transporter 2: role as a novel target for drug development.". AAPS J 8 (4): E682–92. doi:10.1208/aapsj080478. PMC 2751365. PMID 17233532.
    Crowley JJ, Lipsky RH, Lucki I, Berrettini WH (2008). "Variation in the genes encoding vesicular monoamine transporter 2 and beta-1 adrenergic receptor and antidepressant treatment outcome.". Psychiatr. Genet. 18 (5): 248–51. doi:10.1097/YPG.0b013e3283052ff7. PMID 18797399.
    Guo JT, Chen AQ, Kong Q, et al. (2008). "Inhibition of vesicular monoamine transporter-2 activity in alpha-synuclein stably transfected SH-SY5Y cells.". Cell. Mol. Neurobiol. 28 (1): 35–47. doi:10.1007/s10571-007-9227-0. PMID 17985233.
    Talkowski ME, Kirov G, Bamne M, et al. (2008). "A network of dopaminergic gene variations implicated as risk factors for schizophrenia.". Hum. Mol. Genet. 17 (5): 747–58. doi:10.1093/hmg/ddm347. PMID 18045777.
    Verney C, Lebrand C, Gaspar P (2002). "Changing distribution of monoaminergic markers in the developing human cerebral cortex with special emphasis on the serotonin transporter.". Anat. Rec. 267 (2): 87–93. doi:10.1002/ar.10089. PMID 11997877.
    Perlis RH, Moorjani P, Fagerness J, et al. (2008). "Pharmacogenetic analysis of genes implicated in rodent models of antidepressant response: association of TREK1 and treatment resistance in the STAR(*)D study.". Neuropsychopharmacology 33 (12): 2810–9. doi:10.1038/npp.2008.6. PMID 18288090.
    Caudle WM, Richardson JR, Wang MZ, et al. (2007). "Reduced vesicular storage of dopamine causes progressive nigrostriatal neurodegeneration.". J. Neurosci. 27 (30): 8138–48. doi:10.1523/JNEUROSCI.0319-07.2007. PMID 17652604.

External links

    Vesicular+Monoamine+Transporter+2 at the US National Library of Medicine Medical Subject Headings (MeSH)

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Membrane transport protein: neurotransmitter transporters (TC 2.A.1.2)
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Membrane proteins, carrier proteins: membrane transport proteins solute carrier (TC 2A)