Tuesday, March 20, 2007

here i am

here i am in 2007
i used to day dream about what i would be like in the "distant" future of the year 2000!
well there is a lot to think about now a days but some times i am tired of thinking and anyway
a lot still appears to be illogical anyway.
my wife and me appear to be doing very well as far as getting along with each other and there
really is not too many more people in our life as it just has turned out with out pointing any
fingers.
best wishes all the rest of you, call anytime.
love and peace,
and,
peace and love,
(kirk) kirk gregory czuhai

Sunday, February 11, 2007

bp/md myths

bp/mdmyths
Myths Facts "It's easy to tell who has bipolar" 7 of 10 people with bipolar disorder are misdiagnosed (1) On average a person had to visit 4 doctors to get the right name for the problem, and that took 10 years for 1 in 3 people. "Bipolar illness is rare" Not that rare: .4% to 1.4% are bipolar (2) Bipolar starts often between 21-30 years of age (3) "It's easy to see who is manic" Not really. 40% of mood swings are a mix of depressed feeling with mania, and women more often than men have this. This may make it harder for women to get the right diagnosis and treatment.(4) "It's not a big deal to get the right diagnosis" About one in six persons with untreated bipolar illness will commit suicide (3) but medication such as lithium dramatically lowers that risk. "If you take medication it won't help anyway" Scientific studies have found the following medications can help: lithium, depakote, tegretol, topomax, verapamil, risperdol, zyprexa, neurontin, seroquel. "They just need to act normal" Putting on an act won't change the abnormal activity levels of G signaling proteins and Protein Kinase C in nerve cell bodies, which are thought to drive the mood swings. "They'll get over it" It can be life long. Left untreated, bipolar illness will cycle an average of 10 times into mania or depression. That is suffering.(3) And six in 10 bipolar patients abuse street drugs or alcohol, worsening their illness.(5) "It's better not to talk about it" It's hard to fight a problem if you don't know it's name. Then you don't have the right name or the right medication. "A regular person can't figure it out" Mood swings can be up (manic), down (depressed) or mixed (a mix of both) "You can't tell if a person is manic" Mania is marked by at least four of these symptoms: decreased need for sleep, rapid pressured speech, hyperactivity, pressure to stay busy, a mood that is either euphoric or expansive or irritable, lack of conscience,poor concentration, racing thoughts one can't stop,poor impulse control, buying sprees. Appearance is often eccentric, such as bright colored clothing, excessive makeup.(2) "You can't tell if someone is depressed" Sure you can. It's the opposite of depression. Either increased or decresed sleep but a person is tired, energy is lower, it's harder to be motivated and well focused. There is a tendency for inappropriate guilt. Thoughts are slowed and speech is slower and strained, with lower physical energy.(2) "You wouldn't know what to talk about" Look at the table above. "It just scarey stuff" I don't think so. Bipolar illness does dramatically increase the risk for violence to self or others. Yet manic depression has given the world acres upon acres of great painting (Van Gogh), poetry (Lord Gordon Byron), novels, playwriting, and sculpture, to say nothing of great music. Depression may let them feel our human condition more deeply, mania may let them leap to creative heights most people cannot reach.(6) "Regular people can't tell what to do anyway" Wrong. Read "The practice guideline for treatment of patients with bipolar disorder."(7) "They'd fill you full of drugs" Wrong. A cornerstone of treatment is: reduce stress, set time limits on activities, regular exercise, relaxation, psychotherapy, support groups (7 PM Tuesdays at Mountain Crest Hospital), avoiding high levels of expressed emotion (especially for teens), avoiding street drugs (marijuana can calm racing thoughts but not other manic symptoms and depression). "It'd be like One Flew Over The Cuckoo's Nest" New medications work much better. Hospitalization is often avoided. Better than that: so is suicide. What's cuckoo about that? "You'd be a walking zombie" Not with new medications. One is a salt (lithium), four are usually used for seizures (depakote, tegretol, neurontin, topamax), and three are new atypical antipsychotics that are designed to have few or no side effects (zyprexa, risperdol, seroquel), and one is in the same family as valium (klonopin). In one zyprexa study 7 of 113 patients stopped medication because of side effects.(13) "Nothing would happen anyway" Lithium calms mania in 78% (8), depakote in about 65% (9), tegretol in about 50% (10), and neurontin can improve their effectiveness (10). Risperdol also can calm mania (11) as can zyprexa (12). "What they do for mood stuff is hocus pocus--nobody know what works or why Not now days. New science informs us. In bipolar illness there appears to be a problem with the proteins that send signals within nerve cells: they tend to send too many (in mania) or too few (in depression) and both lithium and depakote attach directly on the G signaling proteins and protein kinase C. (13-16) 1. NDMDA. Outreach. 2000;4:1. 2. DSM-IV.Washington, DC:APA;1994. 3. Goodwin FK, Jamison KR. Manic-Depressive Illness. New York, NY:Oxford University Press; 1990. 4. Burt VK. Concise Guide to Women's Mental Health. Washington, DC: American Psychiatric Press; 1997. 5. Brady KT. J Clin Psychopharmacol. 1992;12(1suppl):17S-22S. 6. Jamison KR. Touched by Fire. 7. See my website: Or, Expert Consensus Panel for Bipolar Disorder. J Clin Psychiatry 1996;57(suppl 12A):3-88. 8. APA. Practice Guideline for Treatment of Patients with Bipolar Disorder. Washingtonb, DC: American Psychiatric Press; 1995. 9. Bowden CL, et al. Am J Psychiatry. 1996; 153(6):765-770. 10. Clinical Breakthroughs in Psychiatry, Optima Educational Solutions, Arlington Heights, IL. 11. Sachs GS, et al. 38th American College of Neuropsychopharmacology Annual Meeting; Dec 13-17, 1999; Acapulco, Mexico. 12. Physicians Desk Reference. 55th ed. Montvale, NJ: Medical Economics Co; 2001. 13. Young LT, et al. Cerebral cortex G(s protein levels and forskolin-stimulated cyclid AMP formation are increased in bipolar affective disorder. J Neurochem. 1993;61:890-898. 14. Wang HY, et al. Enhanced protein kinase C activity and translocation in bipolar affective disorder brains. Biological Psychiatry. 1996 40:568-575. 15. Manji HK, et al. Regulation of signal transduction pathways by mood stabilizing agents: implications for the pathophysiology and treatment of bipolar affective disorder. In: Manji HK, et al. Eds. Bipolar Medications: Mechanisms of Action. Washington, DC: American Psychiatric Press, 2000; 129-177.

Religiosity and intelligence - Wikipedia, the free encyclopedia

Religiosity and intelligence - Wikipedia, the free encyclopedia: "The examples and perspective in this article or section may not represent a worldwide view of the subject.
Please improve this article or discuss the issue on the talk page.

In 1986, an essay in the magazine Free Inquiry, which is published by Paul Kurtz's Council for Secular Humanism, summarized studies on religiosity and intelligence.[1] In it Burnham Beckwith, the author of self-published and subsidy-published books on socialism and futurism,[2] summarized studies on religiosity and its relation with attributes that he considered positively linked with intelligence: IQ, SAT scores, 'success', and academic certification. Although conceding that it was easy to find fault with the studies he reviewed, 'for all were imperfect,' he contended that the studies he examined, taken together, provided strong evidence for an inverse correlation between intelligence and religious faith in America. Beckwith's essay in a political magazine dedicated to the promotion of atheism[2] should not be confused with a scientific study of the topic, however"

Religiosity and intelligence - Wikipedia, the free encyclopedia

Religiosity and intelligence - Wikipedia, the free encyclopedia: "per capita were far stronger inverse correlations.) No significant inverse correlation showed up for scientific literacy[6] or reading literacy, however.[7]"

Religiosity and intelligence - Wikipedia, the free encyclopedia

Religiosity and intelligence - Wikipedia, the free encyclopedia: "u"

Wednesday, January 31, 2007

1234 now its yours

http://1234.WS

peace and love,
and,
love and peace,
(kirk) kirk gregory czuhai

i have a friend named Al !

this is not the Al i was talking about
love and peace,
and,
peace and love,
(kirk) kirk gregory czuhai

Thursday, November 23, 2006

i betcha !

i betcha
I betcha someones read this and furthermore YOU who reads this that someones occasionally read this that are getting someone(s) to pay them while they are reading this!

so in that regard as foolish or as crazy as it sounds i am doing a useful service at all times in my fingering of this keyboard, keeping people employed and at THIS TIME HELPING THE BUSH economy!

So that sOb should not be taking ALL the credit!

peace and love,

(kirk) kirk

i need a new drug

I want to say that cannabis use can induce psychosis in exactly the way
described. It's happened to me on two different occasions and both followed
the exact same pattern: heavy use over the span of months, sudden abstinence
for about two weeks, and then trying to smoke no more than about a single
bud. I didn't know that THC-induced psychosis was possible until it happened
to me, but it is. (It's in the DSM-IV.) We're talking clocks going
backwards, walls moving, total divorce from reality, the whole deal. There's
a window of time there where one can be very, very sensitive to the effects
of THC.

tvp

"davon96720" wrote in message
news:rwrFd.20234$lG.3218@trnddc03...
> http://www.ukcia.org/research/can-psychosis.htm
>
>
>
>
> Cannabis Use and Psychosis
> Wayne Hall
>
> National Drug and Alcohol Research Centre
> (Funded by the National Drugs Strategy)
> The University of New South Wales, Sydney, Australia
>
> Paper presented at:
> Problematic Alcohol & Drug Use & Mental Illness
> Melbourne, February 1998.
> ISBN: 0947229884
>
> Copyright NDARC 1988
>
> [Please Note: Originally published as Technical Report No. 55. This was a
> mistake, it is an internal report only. - Alcohol and other Drug Council
of
> Australia]
>
>
>
> --------------------------------------------------------------------------
------
>
>
> Table of Contents
>
> a.. SUMMARY
> b.. Cause for Concern
> c.. Making Causal Inferences
> d.. A Cannabis Psychosis
> a.. Controlled Studies
> e.. Overall Evaluation
> f.. Cannabis Use and Schizophrenia
> a.. CIinical Studies
> b.. Correlates of cannabis use in schizophrenia
> c.. Population Studies
> g.. Explanations of the Association
> h.. Precipipation of Schizophrenia
> i.. Exacerbation of Schizophrenia
> j.. Intervention Studies
> k.. Self-Medication
> l.. An Overall Evaluation
> m.. Implications for Patients and their Families
> n.. REFERENCES
>
>
> --------------------------------------------------------------------------
------
>
>
> SUMMARY
> This report reviews evidence on two hypotheses about the relationship
> between cannabis use and psychosis. The first hypothesis is that heavy
> cannabis use may cause a "cannabis psychosis" - a psychosis that would not
> occur in the absence of cannabis use, the symptoms of which are preceded
by
> heavy cannabis use and remit after abstinence. The second hypothesis is
that
> cannabis use may precipitate schizophrenia, or exacerbate its symptoms.
>
> Evaluation of these hypotheses requires evidence of an association between
> cannabis use and psychosis, that is unlikely to be due to chance, in which
> cannabis use precedes psychosis, and in which we can exclude the
hypothesis
> that the relationship is due to other factors, such as, other drug use, or
a
> personal vulnerability to psychosis.
>
> There is some clinical support for the first hypothesis. If these
disorders
> exist they seem to be rare, because they require very high doses of THC,
the
> prolonged use of highly potent forms of cannabis, or a pre-existing (but
as
> yet unspecified) vulnerability. There is more support for the second
> hypothesis in that a large prospective study has shown a linear
relationship
> between the frequency with which cannabis had been used by age 18 and the
> risks over the subsequent 15 years of a diagnosis of schizophrenia. It is
> still unclear whether this means that cannabis use precipitates
> schizophrenia, whether it is a form of "self-medication", or whether the
> association is due to the use of other drugs, such as amphetamines, which
> heavy cannabis users are more likely to use. There is better evidence that
> cannabis use can exacerbate the symptoms of schizophrenia. Mental health
> services should identify patients with schizophrenia who use alcohol,
> cannabis and other drugs and advise them to abstain or to greatly reduce
> their drug use.
>
>
>
> --------------------------------------------------------------------------
------
>
> CAUSE FOR CONCERN
>
> There are good reasons to be concerned about the possibility that cannabis
> use may be a cause of psychotic disorders. Psychoses are serious and
> disabling disorders [1]. Cannabis is widely used by young Australians
during
> late adolescence[2], and high doses of tetrahydrocannabinol -the
> psychoactive substance in cannabis - have been reported to produce
psychotic
> symptoms, such as, visual and auditory hallucinations, delusional ideas,
and
> thought disorder, in normal volunteers [3).
>
> There are a number of hypotheses about the relationship between cannabis
use
> and psychosis that need to be distinguished [4]. The strongest hypothesis
is
> that heavy cannabis use causes a specific "cannabis psychosis". This
assumes
> that these psychoses would not occur in the absence of cannabis use, and
> that the causal role of cannabis use can be inferred from the symptoms and
> their relationship to cannabis us; e.g. they are preceded by heavy
cannabis
> use and remit after abstinence.
>
> A weaker type of hypothesis is that cannabis use may precipitate an
episode
> of schizophrenia. This hypothesis assumes that cannabis use is one factor
> among many others (including genetic predisposition and other unknown
> causes) that bring about schizophrenia It does not assume that the role of
> cannabis can be inferred from the symptoms of the disorder, or that it
will
> remit when cannabis use ceases.
>
> Finally, if cannabis use can precipitate schizophrenia it is also likely
> that it can exacerbate the symptoms of the disorder. It may exacerbate
> symptoms of schizophrenia (even if it is not a precipitant of the
disorder)
> if it reduces compliance with treatment, or interferes with the effects of
> the drugs used to treat it.
>
> MAKING CAUSAL INFERENCES
>
> In order to infer that cannabis use is a cause of psychosis in any of
these
> ways we need evidence: that there is an association between cannabis use
and
> psychosis; that chance is an unlikely explanation of the association; that
> cannabis use preceded the psychosis; and that plausible alternative
> explanations of the association can be excluded [5).
>
> Evidence that cannabis use and psychosis are associated and that chance is
> an unlikely explanation of the association are readily available. There
are
> a smaller number of prospective studies that show cannabis use precedes
> psychoses. The most difficult task is excluding the hypothesis that the
> relationship between cannabis use and psychosis is due to other factors
> (e.g. other drug use, or a genetic predisposition to develop schizophrenia
> and use cannabis).
>
> Since ethical reasons preclude experimental humans studies and there are
no
> suitable animal models, epidemiological methods must be used to rule out
> common causal hypotheses. These estimate the relationship between cannabis
> use and the risk of developing a psychosis after adjusting for variables
> that may affect the risk (e.g. personal characteristics prior to using
> cannabis, family history of psychotic illness, and other drug use). If the
> relationship persists after statistical adjustment, then we can be
confident
> that it is not due to the variables for which statistical adjustment has
> been made.
>
> "A Cannabis Psychosis"
>
> There are a substantial number of case reports of cannabis psychoses
[6-18].
> These describe individuals who develop psychotic symptoms or disorders
after
> using cannabis.
>
> Chopra and Smith [9], for example, described 200 patients who were
admitted
> to a psychiatric hospital in Calcutta between 1963 and 1968 with psychotic
> symptoms following the use of cannabis. The most common symptoms "were
> sudden onset of confusion, generally associated with delusions,
> hallucinations (usually visual) and emotional lability... amnesia,
> disorientation, depersonalisation and paranoid symptoms" (p 24). Most
> psychoses were preceded by the ingestion of a large dose of cannabis and
> there was amnesia for the period between ingestion and hospitalisation.
They
> argued that it was unlikely that excessive cannabis use was a sign of
> pre-existing psychopathology because a third of their cases had no prior
> psychiatric history, the symptoms were remarkably uniform regardless of
> prior psychiatric history, and those who used the most potent cannabis
> preparations experienced psychotic reactions after the shortest period of
> use.
>
> The findings of Chopra and Smith [9] have received some support from other
> case series which suggest that large doses of potent cannabis products can
> be followed by a "toxic" psychotic disorder with "organic" features of
> amnesia and confusion. These disorders have been reported from a variety
of
> different places including: the Caribbean [19-20], India [9], New Zealand
> [11], Scotland [18], South Africa [14], Sweden [8, 17, 21], the United
> Kingdom [6-7, 13] and the United States [15-16].
>
> These disorders have been attributed to cannabis use for combinations of
the
> following reasons: the onset of the symptoms followed closely upon
ingestion
> of large quantities of cannabis; the affected individuals often exhibited
> "organic" symptoms, such as, confusion, disorientation and amnesia; some
had
> no reported personal or family history of psychoses prior to using
cannabis;
> their symptoms rapidly remitted after a period of enforced abstinence from
> cannabis use, usually within several days to several weeks; recovery was
> usually complete with the person having no residual psychotic symptoms of
> the type often seen in persons with schizophrenia; and if the disorder
> recurred it was after the individual starting using cannabis.
>
> Some commentators have been critical of this evidence [4, 22-25]. They
> criticise the poor quality of information on cannabis use and its
> relationship to the onset of psychosis, and the person's premorbid
> adjustment and their family history of psychosis. They also emphasise the
> wide variety of clinical pictures of "cannabis psychoses" reported by
> different observers. These weaknesses impair the evidential value of these
> case series.
>
> Controlled Studies
>
> A small number of controlled studies have been conducted over the past 20
> years. Some case-control studies have either compared persons with
"cannabis
> psychoses" with persons who have schizophrenia, or compared psychoses
> occurring in persons who do and do not have biochemical evidence of
cannabis
> use prior to presenting for treatment. Their results have been mixed.
>
> Thacore and Shuckla [26], for example, reported a case control study that
> compared 25 cases who had a "cannabis psychosis" with 25 controls who were
> diagnosed as having paranoid schizophrenia with no history of cannabis
use.
> Their cases had a paranoid psychosis resembling schizophrenia in which
there
> was a clear temporal relationship between the prolonged use of cannabis
and
> the development of psychosis on more than two occasions. Patients with the
> "cannabis psychosis" displayed more odd and bizarre behaviour, violence,
> panic, and insight, and less evidence of thought disorder, than those with
> schizophrenia. They also responded swiftly to neuroleptic drugs and
> recovered completely.
>
> Rottanburg et at [27] conducted a similar study in which 20 psychotic
> patients with cannabinoids in their urine were compared with 20 psychotic
> patients who did not have cannabinoids in their urine. Psychotic patients
> with cannabinoids in their urine had more symptoms of hypomania and
> agitation, and less auditory hallucinations, flattening of affect,
> incoherent speech and hysteria than controls. They also showed marked
> improvements in symptoms by the end of a week, whereas there was no change
> in the patients whose urine did not contain cannabinoids.
>
> Chaudry et al [28] reported a comparison of 15 psychotic "bhang" users
with
> 10 bhang users without psychosis. They found that their cases were more
> likely to have a history of chronic cannabis use and past psychotic
> episodes. They also were more likely to be uncooperative and to have
> symptoms of excitement, hostility, grandiosity, hallucinations,
> disorientation and unusual thought content. All cases remitted within 5
days
> and had no residual psychotic symptoms.
>
> Mathers et al [29] reported a study of patients presenting to two London
> hospitals whose urine was analysed for the presence of cannabinoids. They
> found a relationship between the presence of cannabinoids in urine and
> having a psychotic diagnosis. Rolfe et al [30] reported a similar
> association between urinary cannabinoids and psychosis in 234 patients
> admitted to a Gambian psychiatric unit.
>
> In contrast to these positive findings, a number of controlled studies
have
> not found such a clear association. Imade and Ebie [31], compared the
> symptoms of 70 patients with cannabis-induced functional psychoses, 163
> patients with schizophrenia, and 39 patients with mania. They reported
that
> there were no symptoms that were unique to cannabis psychosis, and none
that
> enabled them to distinguish a "cannabis psychosis" from schizophrenia.
>
> Thornicroft et al [32] compared 45 cases who had a psychosis and a urine
> positive for cannabinoids with 45 controls who had a psychosis but either
> had a urine negative for cannabinoids or reported no cannabis use. They
> found very few demographic or clinical differences between the groups.
>
> McGuire et al [33-34] compared 23 cases of psychoses occurring in persons
> whose urines were positive for cannabinoids with 46 psychotic patients
whose
> urines were negative for cannabinoids or who reported no cannabis use. The
> two groups did not differ in their psychiatric histories or symptoms
> profile, as assessed by "blind" ratings of clinical files using the PSE
> (McGuire et al [33]). The cases, however, were more likely to have a
family
> history of schizophrenia.
>
> Two studies have examined the relationship between cannabis use and
> psychotic symptoms in the general population. Tien and Anthony [35] used
> data from the Epidemiologic Catchment Area study to compare the drug use
of
> individuals who reported "psychotic experiences" during a twelve month
> period. These psychotic experiences comprised 4 types of hallucinations
and
> seven types of delusional belief. They compared 477 cases who reported one
> or more psychotic symptoms in the one year follow-up with 1818 controls
who
> did not. Cases and controls were matched for age and social and
demographic
> characteristics. Daily cannabis use was found to double the risk of
> reporting psychotic symptoms (after statistical adjustment for alcohol use
> and psychiatric diagnoses at baseline).
>
> Thomas [36] reported the prevalence of psychotic symptoms among cannabis
> users in a random sample of people drawn from the electoral role of a
large
> city in the North Island of New Zealand. One in seven (14%) cannabis users
> reported "strange, unpleasant experiences such as hearing voices or
becoming
> convinced that someone is trying to harm you or that you are being
> persecuted" after using cannabis.
>
> Two studies have reported no difference in the prevalence of psychotic
> disorders in chronic cannabis users and controls. Beaubruhn and Knight
[37]
> compared the rate of psychoses in 30 chronic daily Jamaican cannabis users
> with that in 30 non-cannabis using controls. Stefanis et al [38] reported
a
> study of 47 chronic cannabis users in Greece and 40 controls. The small
> number of cases and the low prevalence of psychosis in the population make
> these negative findings unconvincing.
>
> Overall Evaluation
>
> The existence of a "cannabis psychosis" is still a matter for debate. In
its
> favour are case series of "cannabis psychoses", and a small number of
> controlled studies that compare the characteristics of "cannabis
psychoses"
> with those of psychoses in individuals who were not using cannabis at the
> time of hospital admission (e.g. [39]). Critics of the hypothesis
emphasise
> the fallibility of clinical judgements about aetiology, the poorly
specified
> criteria used in diagnosing these psychoses, the dearth of controlled
> studies, and the striking variations in the clinical features of "cannabis
> psychoses" [24).
>
> It is a plausible hypothesis that high doses of cannabis can produce
> psychotic symptoms. There is no compelling evidence, however, that there
is
> a specific clinical syndrome that is identifiable as a "cannabis
psychosis".
> The clinical symptoms reported by different observers have been mixed.
These
> symptoms seem to rapidly remit, with full recovery, after abstinence from
> cannabis.
>
> If cannabis-induced psychoses exist, they are rare or they only rarely
> receive medical intervention in Western societies (e.g. [40-41]). The
total
> number of cases of putative "cannabis psychoses" in the 12 case series
> reviewed was 397 and 200 of these came from a single series (Chopra and
> Smith [9]) collected over 6 years from a large geographic area in which
> heavy cannabis use was endemic (e-g. [9]).
>
> There are a number of likely reasons for the rarity of "cannabis
psychoses"
> in Western societies. One is that they occur after the use of large doses
of
> THC, or long periods of sustained heavy use. Although lifetime use of
> cannabis has increased in Western societies, the pattern of heavy cannabis
> use remains rare [2]. A second possibility (discussed below) is that
> cannabis psychoses only occur in persons who have a pre-existing
> vulnerability to psychotic disorder A third possibility is that heavy
> sustained use and vulnerability are both required.
>
>
>
> --------------------------------------------------------------------------
------
>
> CANNABIS USE AND SCHIZOPHRENIA
>
> Clinical studies
>
> In case-control studies of cannabis and other psychoactive drug use among
> schizophrenic patients [42-43], schizophrenic patients are more likely to
> have used psychotomimetic drugs such as amphetamines, cocaine, and
> hallucinogens than other psychiatric patients [42, 44-45] or normal
controls
> [46, 30]. The prevalence of substance use in schizophrenic patients varies
> between studies but it is generally higher than comparable figures in the
> general population [47). Rates of alcohol and stimulant use among
> schizophrenic patients also appear to have increased over the past several
> decades [48]. These variations are probably due to differences in the
> sampling of patients, with younger samples of newly incident cases
reporting
> higher rates than older samples of chronic cases. Studies have also
differed
> in the criteria for diagnosing schizophrenia and in way that substance use
> has been assessed [49].
>
> Alcohol use abuse and dependence are probably more common in the
> schizophrenic population than in the general population [42,48-49]. The
> findings on cannabis use have been more mixed (e.g. [29, 42, 44, 49, 50].
> Generally, cannabis is the next most commonly used drug after alcohol and
> tobacco, although it is usually used with alcohol [49, 52].
>
> Correlates of cannabis use in schizophrenia
>
> The controlled clinical studies disagree about the correlates of substance
> abuse in schizophrenia. Most have found that young males are
> over-represented among cannabis users (e.g. [49, 53-54]), as in the
general
> community [55]. In some studies, substance abusers have been reported to
> have an earlier onset of psychotic symptoms, a better premorbid
adjustment,
> more episodes of illness, and more hallucinations (e.g. [44, 46, 50, 54,
> 56]). But other well controlled studies have failed to replicate some or
all
> of these findings [53, 57-58].
>
> Population studies
>
> Surveys of psychiatric disorders in the community have reported higher
rates
> of substance abuse disorders among persons with schizophrenia The ECA
study
> found an association between schizophrenia and alcohol and drug abuse and
> dependence [55]. Nearly half of the patients identified as schizophrenic
in
> the ECA study had a diagnosis of substance abuse or dependence (34% for an
> alcohol disorder and 28% for another drug disorder) [59]. These rates were
> higher than the rates in general population, namely, 14% for alcohol
> disorders [60] and 6% for drug abuse [55]. The ECA findings have also been
> replicated in Edmonton, Alberta [61].
>
> More recently, Cuffel et al [53] have reported on patterns of substance
> abuse among 231 cases of schizophrenia identified in the ECA study. They
> found that the most commonly used substances were: alcohol (37%) and
> cannabis (23%), followed by stimulants and hallucinogens (13%), narcotics
> (10%) and sedatives (8%). Multiple drug use was common and the most common
> combinations of drugs was alcohol and cannabis (31%).
>
> Explanations of the Association
>
> One possible explanation of the association is that cannabis use
> precipitates schizophrenic disorders in vulnerable persons (e.g. [62]).
> Proponents of this hypothesis cite the earlier age of onset of psychotic
> symptoms among cannabis users (with their drug use typically preceding the
> onset of symptoms), their better premorbid adjustment their fewer negative
> symptoms, and their better treatment response (e.g. [42, 44, 63]).
>
> Another suggestion is that the associations between cannabis use and an
> early onset and good prognosis are spurious. Arndt et al [56] argue that
> schizophrenics with a better premorbid personality are more likely to be
> exposed to illicit drug use among peers than persons with schizophrenia
who
> are socially withdrawn. There is also evidence (e.g. [1, 64]) that persons
> with acute onset psychoses usually have a better premorbid adjustment and
a
> better prognosis. They also have greater opportunities to use cannabis and
> other illicit drugs than persons who have an insidious onset and are
> socially withdrawn.
>
> A third possibility is that cannabis use is a consequence (rather than a
> cause) of schizophrenia. For example, cannabis and other drugs may be used
> to medicate the unpleasant symptoms of schizophrenia, such as, depression,
> anxiety, lethargy, and anhedonia, or the unpleasant side effects of the
> neuroleptic drugs that are often used to treat the disorder [44].
>
> Precipitation of Schizophrenia
>
> The most convincing evidence that cannabis use may precipitate
schizophrenia
> comes from a 15-year prospective study of cannabis use and schizophrenia
in
> 50,465 Swedish conscripts [65]. This study investigated the relationship
> between self-reported cannabis use at age 18 and the risk of receiving a
> diagnosis of schizophrenia in the subsequent 15 years, as indicated by
> inclusion in the Swedish psychiatric case register.
>
> Andreasson et al [67] found that the relative risk of receiving a
diagnosis
> of schizophrenia was 2.4 times higher among those who had tried cannabis
by
> age 18 compared to those who had not. There was also a dose-response
> relationship between a diagnosis of schizophrenia and the number of times
> that cannabis had been used by age 18. Compared to those who had not used
> cannabis, the risk of developing schizophrenia was 1.3 times higher for
> those who had used cannabis one to ten times, 3 times higher for those who
> had used cannabis between one and fifty times, and 6 times higher for
those
> who had used cannabis more than fifty times.
>
> These risks were substantially reduced after statistical adjustment for
> variables that were independently related to the risk of developing
> schizophrenia, namely, having a psychiatric diagnosis at conscription, and
> having parents who had divorced (as a proxy for parental psychiatric
> disorder). Nevertheless, after adjustment, the dose response relationship
> remained statistically significant The adjusted relative risk of a
diagnosis
> of schizophrenia for those who had smoked cannabis from one to ten times
was
> 1.5 times, and that for those who had used ten or more times was 2.3
times,
> the risk for those who had never used cannabis. Andreasson et al [65] and
> Allebeck [62] have concluded that cannabis use precipitates schizophrenia
in
> vulnerable individuals.
>
> A number of alternative explanations of the Swedish finding have been
> offered by other authors. First, there was a large temporal gap between
> self-reported cannabis use at age 18 and the development of schizophrenia
> over the next 15 years or so [66-67]. Because the diagnosis of
schizophrenia
> was based upon a case register there was no data on how many individuals
> used cannabis up until the time that their schizophrenia was diagnosed.
> Andreasson et al [65] argued that cannabis use persisted because cannabis
> use at age 18 was also strongly related to the risk of attracting a
> diagnosis of drug abuse.
>
> A second possibility is that schizophrenia was misdiagnosed. On this
> hypothesis, the excess rate of "schizophrenia" among the heavy cannabis
> users was due to cannabis-induced psychoses which were mistakenly
diagnosed
> as schizophrenia [66, 67-8] examined 21 cases of schizophrenia among
> conscripts in the case register (8 of whom had used cannabis and 13 of
whom
> had not). They found that 80% of these cases met the DSM-III requirement
> that the symptoms had been present for at least six months, thereby
> excluding the diagnoses of transient drug-induced psychotic symptoms.
>
> A third hypothesis is that the relationship between cannabis use and
> schizophrenia is due to the use of other drugs. Longitudinal studies of
> illicit drag use indicate that persons who had used cannabis a large
number
> of times by late adolescence were at increased risk of subsequently using
> other illicit drugs, such as, amphetamine [66, 69]. Amphetamines which can
> produce an acute paranoid psychosis [70-72] were the major illicit drugs
of
> abuse in Sweden during the study period [73-75]. On this hypothesis,
> amphetamine-induced psychoses may explain the spurious association between
> cannabis use and schizophrenia. The evidence that psychotic symptoms
> persisted beyond 6 months [68] would also seem to exclude this hypothesis.
>
> A fourth hypothesis is that cannabis use at age 18 was a symptom of
emerging
> schizophrenia. Andreasson et al [68] rejected this hypothesis, noting that
> the cannabis users who developed schizophrenia had better premorbid
> personalities, a more abrupt onset, and more positive symptoms than the
> non-users who developed schizophrenia [68]. Moreover, although 58% of the
> heavy cannabis users had a psychiatric diagnosis at the time of
> conscription, there was still a dose-response relationship between
cannabis
> use and schizophrenia among those who had no such history. The
> persuasiveness of this evidence depends upon how confident we can be that
a
> failure to identity a psychiatric disorder at conscription meant that no
> disorder was present.
>
> A fifth hypothesis depends upon the validity of the self-reported cannabis
> use at conscription. Andreasson et al [66] acknowledged that there
probably
> was under-reporting of cannabis use because this information was not
> collected anonymously. They argued, however, that this would produce an
> under-estimate of the relationship between cannabis use and the risk of
> schizophrenia. This will be true if the schizophrenic and
non-schizophrenics
> conscripts were equally likely to under-report. If, for example,
> pre-schizophrenic subjects were more candid about their drug use, then the
> apparent relationship between cannabis use and schizophrenia could be due
to
> response bias [67]. This seems unlikely in view of the strong
dose-response
> relationship between the frequency of cannabis use by age 18, and the
large
> unadjusted relative risk of schizophrenia among heavy users.
>
> Exacerbation of Schizophrenia
>
> Clinical reports suggest that schizophrenic patients who continue to use
> cannabis experience more psychotic symptoms [76], respond poorly to
> neuroleptic drugs [77], and have a worse clinical course than those
patients
> who do not [78-80]. These reports have been supported by controlled
studies.
>
> Negrete et al [81] conducted a retrospective study of the relationship
> between self-reported cannabis use and symptoms. They used clinical
records
> of symptoms and treatment seeking among 137 schizophrenic patients who had
a
> disorder of at least six months duration, and who had made three visits to
> their psychiatric service during the previous six months. Negrete et al
[81]
> compared the prevalence of hallucinations, delusions and hospitalisations
> among the active cannabis users with that in patients who had previously
> used cannabis, and those who had never used cannabis. There were higher
> rates of continuous hallucinations and delusions, and more
hospitalisations
> among active cannabis users. These relationships persisted after
statistical
> adjustment for age and sex differences between the user groups.
>
> Negrete et al [81] argued that cannabis use exacerbated schizophrenic
> symptoms. They rejected the alternative hypothesis that patients with a
> poorer prognosis were more likely to use cannabis because those who no
> longer used cannabis experienced fewer symptoms, and reported a high rate
of
> adverse effects when they did use it. They also discounted the possibility
> that these were toxic psychoses because the minimum duration of symptoms
had
> been six months.
>
> Cleghorn et al [82] compared the symptom profiles of schizophrenic
patients
> with histories of substance abuse, among whom cannabis was the most
heavily
> used drug. Drug abusers had a higher prevalence of hallucinations,
delusions
> and positive symptoms than those who did not abuse drugs.
>
> Jablensky et al [64] reported a two year follow-up of 1202 first episode
> schizophrenic patients enrolled in 10 countries as part of a WHO
> Collaborative study. They found that the use of "street drugs", including
> cannabis and cocaine, during the follow up period predicted more psychotic
> symptoms and periods of hospitalisation. Martinez-Arevalo et al [83] also
> reported that continued use of cannabis during a one year follow up of 62
> DSM-diagnosed schizophrenic patients predicted a higher rate of relapse
and
> poorer compliance with anti-psychotic drug treatment.
>
> Linszen et al [84] recently reported a prospective study of outcome in 93
> psychotic patients whose symptoms were assessed monthly over a year.
Twenty
> four of their patients were cannabis abusers (11 were less than daily
users
> and 13 were daily cannabis users). Despite the small sample sizes, they
> found that the cannabis users as a whole relapsed to psychotic symptoms
> sooner, and had more frequent relapses. in the year of follow up, than the
> patients who had not used cannabis. There was also a dose response
> relationship, with the daily users relapsing earlier, and more often, than
> the less than daily users who, in turn, relapsed sooner, and more often,
> than the patients who did not use cannabis. These relationships persisted
> after multivariate adjustment for premorbid adjustment, and alcohol and
> other drug use during the follow up period.
>
> Most but not all studies [58], indicate that cannabis use exacerbates
> psychotic symptoms in patients with schizophrenia. The major cause of
> uncertainty about this relationship is assessing the contribution of
> confounding factors. It may be, for example, that the difference in
> psychotic symptoms between schizophrenia patients who do and do not use
> cannabis is due to differences in premorbid personality, family history,
and
> other characteristics [52]. This is unlikely in the WHO schizophrenia
study
> [64] and the recent study of Linzen [84], both of which used multivariate
> statistical methods to adjust for many of these confounders.
>
> The other difficulty is separating the contributions that cannabis and
> alcohol make to exacerbations of schizophrenic symptoms. It is rare for a
> schizophrenic patient to only use cannabis [49]. The concurrent use of
> alcohol is common, and the heavier their cannabis use, the more likely
they
> are to use psychostimulants and hallucinogens. Only the Linszen et al [84]
> study statistically adjusted for the effects of concurrent alcohol and
drug
> use and found that the relationship persisted. Our confidence that the
> effect is attributable to cannabis would be increased by replications of
the
> Linszen et al [84] finding.
>
> Intervention Studies
>
> If we could reduce cannabis use among patients with schizophrenia who use
> cannabis, then we could discover whether their disorders improved and
> whether the risks of relapse were substantially reduced. The major
> difficulty with this strategy is that it presupposes that we can
> successfully treat substance abuse in persons with schizophrenia. Alcohol
> and other substance abuse are difficult to treat [85], and many persons
with
> schizophrenia have characteristics that predict a poor treatment outcome,
> namely, they lack social support, they may be cognitively impaired, they
are
> unemployed, and they do not comply with treatment [49, 52].
>
> There are very few controlled outcome studies of substance abuse treatment
> in schizophrenia [86]. Few of these have produced large enough benefits of
> treatment, or treated a large enough number of patients, to provide an
> adequate chance of detecting any positive impacts of abstinence on the
> course of disorders [49, 52]. The few that have been large enough [87]
have
> not reported results separately by diagnosis.
>
> Self-Medication
>
> The reasons that most persons with schizophrenia give for using alcohol,
> cannabis and other illicit drugs are similar to those given by persons who
> do not have schizophrenia, namely, to relieve boredom, to provide
> stimulation, to feel good and to socialise with peers (e.g. [49, 88-90]).
> The drugs that are most often used by schizophrenic patients are also
those
> that are most readily available [48-49].
>
> In favour of the self-medication hypothesis, is the evidence that some
> schizophrenic patients report using cannabis because its euphoric effects
> relieve negative symptoms and depression (e.g. [42, 44, 91]). Dixon et al
> [44], for example; surveyed 83 patients with schizophrenia who reported
that
> cannabis reduced anxiety and depression, and increased a sense of calm but
> at the cost of increased suspiciousness.
>
> More recently, Hamera et at [90] have reported a time series study that
> examined correlations over 84 consecutive days between self-reported:
> psychotic symptoms, licit and illicit drug use, and medication compliance
in
> 17 persons with schizophrenia. They only found relationships between
> nicotine and prodromal psychotic symptoms and between caffeine use and
> symptoms of anxiety and depression. No relationships were found between
> psychotic symptoms and alcohol or cannabis use.
>
> This study does have limitations. The difficulty of the self-monitoring
task
> probably selected patients who were more compliant and less disordered
than
> a representative sample of schizophrenics. There were also relatively low
> rates of heavy drug use. The time period of 84 days may have been too
short
> to examine the relationship between drug use and major exacerbations of
the
> illness, and the task of self-monitoring may have had reactive effects on
> drug use.
>
> An Overall Evaluation
>
> The epidemiological evidence is strongest that cannabis use exacerbates
the
> symptoms of schizophrenia in affected individuals. This is supported by
the
> findings of a number of retrospective and prospective studies which have
> controlled for confounding variables. It is also biologically plausible.
> Psychotic disorders involve disturbances in the dopamine neurotransmitter
> systems since drugs that increase dopamine release produce psychotic
> symptoms when given in large doses, and neuroleptic drugs that reduce
> psychotic symptoms also reduce dopamine levels [93]. Cannabinoids, such as
> THC, increase dopamine release [92].
>
> It is also likely that cannabis use precipitates schizophrenia in persons
> who are vulnerable because of a personal or family history of
schizophrenia
> (e.g. [22, 39, 41]). This hypothesis is consistent with the
stress-diathesis
> model of schizophrenia [39, 95] in which the likelihood of developing
> schizophrenia is the product of stress acting upon a genetic "diathesis"
to
> develop schizophrenia.
>
> Although plausible, there is very little direct evidence that genetic
> vulnerability increases the risk that cannabis users will develop
psychosis.
> McGuire et al [34] reported that persons with a history of heavy cannabis
> use who developed a psychosis were 10 times more likely to have a family
> history of schizophrenia than persons. with a psychosis who had not used
> cannabis. It is also difficult to identify a genetic diathesis in the
> majority of cases of schizophrenia. Having a first degree relative (parent
> or sibling) who has schizophrenia increases the risks of developing the
> disorder between 9 and 18 times [95]. But, according to Gottesman [95],
81%
> of persons with schizophrenia will not have a first degree relative with
the
> disorder, and 63% will not have an affected first or second degree
relative.
>
> The most contentious issue is whether cannabis use can cause schizophrenia
> that would not have occurred in its absence. One cannot rule it out but it
> is unlikely to account for more than a minority of cases. Most of the 274
> conscripts who developed schizophrenia had not used cannabis, and only 21
> were heavy cannabis users and at most 7% of cases of schizophrenia could
be
> attributed to cannabis use. The treated incidence of schizophrenia, and
> particularly early onset, acute cases, has declined (or remained stable)
> during the 1970s and 1980s [94] when cannabis use increased among young
> adults in Australia and North America [2]. Although there are
complications
> in interpreting such trends [97-99] a large reduction in treated incidence
> has been observed in a number of countries and it cannot be explained as a
> diagnostic artefact [100].
>
>
>
> --------------------------------------------------------------------------
------
>
> IMPLICATIONS FOR PATIENTS AND THEIR FAMILIES
>
> Mental health services should identify patients with schizophrenia who use
> alcohol, cannabis and other drugs, and discuss its impact on their
disorder
> with them. Although this paper has primarily focused on cannabis we, the
> role alcohol should not be neglected. Cannabis is most often used with
> alcohol and heavy alcohol use is a stronger predictor of psychotic
symptoms
> (OR = 7.9) than regular cannabis use (OR = 2.0) [35].
>
> Patients whose drug use may be exacerbating their symptoms should be
advised
> to trial abstinence. Advice to abstain or to substantially reduce use may
be
> better received if accompanied by alternative suggestions about how to
deal
> with the negative symptoms and depression [52, 49]. if they are not
prepared
> to abstain, they may be prepared to reduce the frequency and quantity of
> drug use [52]. A positive effect on well-being and social functioning may
> motivate patients to consider longer term abstinence or a sustained
> reduction in use.
>
> In assisting patients who wish to become abstinent, we may need to notify
> some traditional treatment methods [49, 52]. Alcoholics Anonymous and
> Narcotics Anonymous group based approaches [52] may pose difficulties for
> many patients with schizophrenia who find social interaction difficult.
> These groups may also be opposed to using anti-psychotic medication.
>
>
>
> --------------------------------------------------------------------------
------
>
>
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> with acute or chronic psychosis. Hospital and Community Psychiatry,
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> consumption as a prognostic factor in schizophrenia. British Journal of
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> Parkus TS. Subjective experiences related to alcohol use among
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> 1989;15:465-476.
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> [91] Peralta V, Cuesta MJ. Influence of cannabis abuse on schizophrenic
> psychopathology. Acta Psychiatrica Scandinavica 1992;85:127-30.
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> caffeine use and symptom distress in schizophrenia. Journal of Nervous and
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> Cambridge, 1996.
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> [94] Adams IB, Martin BR. Cannabis: pharmacology and toxicology in animals
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> [95] Gottesman II. Schizophrenia Genesis: The origins of madness. W.H.
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>
>
> --
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Monday, September 11, 2006

some reasons Adam lived over 900 years

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-- Site Contents --BodyBurden HomeExecutive SummaryIndiv. Test ResultsHealth EffectsProducts/ManufacturersFindings & RecommendationsWhat's in your body?BodyBurden Table of ContentsRelated News Coverage-- Print Report Excerpts --How do chemicals end up in me?How many chemicals are in me?Can low doses hurt me?Health effects of low doses?Aren't chemicals well-tested?What must industry do?What should government do?What can you do?MethodologyStudy ParticipantsOther Internet ResourcesReferences: Health EffectsReferences: Chemical Info



EWG Home >> BodyBurden >> Executive Summary || Next Page: Test Results







KEY TO CONTAMINANTS



PCBs — Industrial insulators and lubricants. Banned in the U.S. in 1976. Persist for decades in the environment. Accumulate up the food chain, to man. Cause cancer and nervous system problems.



Dioxins — Pollutants, by-products of PVC production, industrial bleaching, and incineration. Cause cancer in man. Persist for decades in the environment. Very toxic to developing endocrine (hormone) system.



Furans — Pollutants, by-products of plastics production, industrial bleaching and incineration. Expected to cause cancer in man. Persist for decades in the environment. Very toxic to developing endocrine (hormone) system.



Metals — Lead, mercury, arsenic and cadmium — Cause lowered IQ, developmental delays, behavioral disorders and cancer at doses found in the environment. For lead, most exposures are from lead paint. For mercury, most exposures are from canned tuna. For arsenic, most exposures are from arsenic (CCA) treated lumber and contaminated drinking water. For cadmium, sources of exposure include pigments and bakeware.



Organochlorine insecticides. DDT, chlordane and other pesticides. Largely banned in the U.S. Persist for decades in the environment. Accumulate up the food chain, to man. Cause cancer and numerous reproductive effects.



Organophosphate insecticide metabolites — Breakdown products of chlorpyrifos, malathion and others. Potent nervous system toxicants. Most common source of exposure is residues in food. Recently banned for indoor uses.



Phthalates — Plasticizers. Cause birth defects of male reproductive organs. Found in a wide range of cosmetic and personal care products. Some phthalates recently banned in Europe.



Volatile and Semi-volatile organic chemicals. — Industrial solvents and gasoline ingredients like xylene and ethyl benzene. Toxic to nervous system, some heavily used SVOCs (benzene) cause cancer.



THE LATEST ON BODY BURDEN
Newsfeed from
Environmental Health News

11 September Toxic exposure bill clears hurdles. A bill that would set up the nation's first statewide program to measure exposure to toxic chemicals by testing thousands of volunteers has overcome industry opposition and reached the desk of Gov. Arnold Schwarzenegger. San Jose Mercury News, California.

11 September Babies in womb exposed to 'gender-bending' chemicals. Tests on blood taken from the placentas of pregnant women revealed up to fifteen different types of pesticide, new research found. Daily Mail, UK.

10 September Green bills await governor's pen. Emboldened by the success of California's anti-global warming initiative, environmentalists are now eyeing other green bills that they believe can help save the planet. Sacramento Bee, California.

5 September Toxic nation, toxic families. For some, ignorance is bliss. But a small group of Canadians swallowed their fears and had their blood tested to find out just how many environmental toxins are flowing through their veins. Vancouver 24 Hours, British Columbia.

22 August Elevated dioxin levels found in people living near Dow plant. People living in parts of two counties near the massive Dow Chemical complex in Midland, Mich., have slightly higher levels of dioxins in their blood than do people who live elsewhere in the state. Chemical & Engineering News.


In a study led by Mount Sinai School of Medicine in New York, in collaboration with the Environmental Working Group and Commonweal, researchers at two major laboratories found an average of 91 industrial compounds, pollutants, and other chemicals in the blood and urine of nine volunteers, with a total of 167 chemicals found in the group. Like most of us, the people tested do not work with chemicals on the job and do not live near an industrial facility.

Scientists refer to this contamination as a person’s body burden. Of the 167 chemicals found, 76 cause cancer in humans or animals, 94 are toxic to the brain and nervous system, and 79 cause birth defects or abnormal development. The dangers of exposure to these chemicals in combination has never been studied.



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TABLE 1: The chemicals we found are linked to serious health problems

Health Effect or Body System Affected
Number of chemicals found in 9 people tested that are linked to the listed health impact

Average number found in 9 people
Total found in all 9 people
Range
(lowest and highest number found in all 9 people)

cancer [1]
53
76 [2]
36 to 65

birth defects / developmental delays
55
79 [3]
37 to 68

vision
5
11 [4]
4 to 7

hormone system
58
86 [5]
40 to 71

stomach or intestines
59
84 [6]
41 to 72

kidney
54
80 [7]
37 to 67

brain, nervous system
62
94 [8]
46 to 73

reproductive system
55
77 [9]
37 to 68

lungs/breathing
55
82 [10]
38 to 67

skin
56
84 [11]
37 to 70

liver
42
69 [12]
26 to 54

cardiovascular system or blood
55
82 [13]
37 to 68

hearing
34
50 [14]
16 to 47

immune system
53
77 [15]
35 to 65

male reproductive system
47
70 [16]
28 to 60

female reproductive system
42
61 [17]
24 to 56



* Some chemicals are associated with multiple health impacts, and appear in multiple categories in this table.

Source: Environmental Working Group compilation
Footnotes | References: Health Effects



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These results represent the most comprehensive assessment of chemical contamination in individuals ever performed. Even so, many chemicals were not included in the analysis that are known to contaminate virtually the entire U.S. population. Two examples are Scotchgard and the related family of perfluorinated chemicals, and a group of compounds known collectively as brominated flame retardants.

A more precise picture of human contamination with industrial chemicals, pollutants and pesticides is not possible because chemical companies are not required to tell EPA how their compounds are used or monitor where their products end up in the environment. Neither does U.S. law require chemical companies to conduct basic health and safety testing of their products either before or after they are commercialized. Eighty percent of all applications to produce a new chemical are approved by the U.S. EPA with no health and safety data. Eighty percent of these are approved in three weeks.

Only the chemical companies know whether their products are dangerous and whether they are likely to contaminate people. As a first step toward a public understanding of the extent of the problem, the chemical industry must submit to the EPA and make public on the web, all information on human exposure to commercial chemicals, any and all studies relating to potential health risks, and comprehensive information on products that contain their chemicals.




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.
FOOTNOTES

[1] Chemicals listed as linked to cancer are those classified by the National Toxicology Program as "known" human carcinogens, or "reasonably anticipated" to be human carcinogens; or those classified by the Environmental Protection Agency as "known" or "probable" human carcinogens.

[2] Cancer: 3 heavy metals, 1 phthalate, 9 organochlorine pesticides, 8 furans, 7 dioxins and 48 PCBs

[3] Birth defects / developmental delays: 4 heavy metals, 2 phthalates, 7 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 3 other semivolatile or volatile organic compounds

[4] Vision: 1 heavy metal, 1 phthalate, 2 organochlorine pesticides and 7 other semivolatile or volatile organic compounds

[5] Hormone system: 4 heavy metals, 5 phthalates, 3 organophosphate pesticides and metabolites, 9 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 2 other semivolatile or volatile organic compounds

[6] Stomach or intestines: 3 heavy metals, 3 phthalates, 2 organophosphate pesticides and metabolites, 9 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 4 other semivolatile or volatile organic compounds

[7] Kidney: 4 heavy metals, 5 phthalates, 3 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 5 other semivolatile or volatile organic compounds

[8] Brain, nervous system: 4 heavy metals, 4 phthalates, 7 organophosphate pesticides and metabolites, 9 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 7 other semivolatile or volatile organic compounds

[9] Reproductive system: 4 heavy metals, 2 phthalates, 8 organochlorine pesticides, 8 furans, 7 dioxins and 48 PCBs

[10] Lungs/breathing: 4 heavy metals, 3 phthalates, 2 organophosphate pesticides and metabolites, 5 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 5 other semivolatile or volatile organic compounds

[11] Skin: 3 heavy metals, 5 phthalates, 2 organophosphate pesticides and metabolites, 4 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 7 other semivolatile or volatile organic compounds

[12] Liver: 4 heavy metals, 6 phthalates, 3 organochlorine pesticides, 48 PCBs and 8 other semivolatile or volatile organic compounds

[13] Cardiovascular system or blood: 4 heavy metals, 2 phthalates, 2 organophosphate pesticides and metabolites, 7 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 4 other semivolatile or volatile organic compounds

[14] Hearing: 1 heavy metal, 48 PCBs and 1 other semivolatile or volatile organic compound

[15] Immune system: 4 heavy metals, 1 phthalate, 6 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 3 other semivolatile or volatile organic compounds

[16] Male reproductive system: 4 heavy metals, 5 phthalates, 2 organochlorine pesticides, 7 dioxins, 48 PCBs and 4 other semivolatile or volatile organic compounds

[17] Female reproductive system: 2 heavy metals, 2 phthalates, 1 organochlorine pesticide, 7 dioxins, 48 PCBs and 1 other semivolatile or volatile organic compound













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Sunday, August 27, 2006

Kirk Gregory Czuhai

imitation is the sincerest form of flattery.
do you think, Kirk Gregory Czuhai, will make the Funk'n Wagnels soon?
ha ha har lol,
watch out its catching!
peace and love,
and,
love and peace,
(kirk) kirk grgory czuhai
Heaven Sense
kirk

Saturday, August 05, 2006

relax

relax