Tom Cruise says He knows the history of Psychiatry

[PFTSOF]

[PFTSOF]

[Mr. G]

As I have said before, I have answered many questions but have not once pushed Scientology on anyone. Not once. I don't care what you think of it, at all. No really. This thread was started with the idea that Tom Cruise doesn't know Psychiatry. So that means that some of the people here do. Fair enough? So I posed the question that they should post just ONE scientific study on the theory on chemical imbalances. Of course everyone ran from that challange because they know it doesn't exist. I even posted neurologists and Psychiatrists who said that it is a scam. This is them saying it, not me. If you want to be pro Psychiatry be my guest but know that it is based on your opinion not science.

[rustoffa]

LMMFAO!


The Chemical Imbalance in Mental Health Problems
Joseph M. Carver, Ph.D. of www.drjoecarver.com by Joseph M. Carver, Ph.D.



Introduction

Over the years, advances in neurology and research have simplified the way psychologists, psychiatrists, and others diagnosis and treat mental health problems. In over one hundred years of mental health treatment, the symptoms and behaviors associated with certain mental health conditions have remained the same. Psychotic disorders, where the individual often can’t distinguish between reality and their fantasies, still have auditory hallucinations. Depressed individuals still can’t sleep and remain preoccupied with the past. Hyperactive children (Attention-Deficit Hyperactivity Disorder or ADHD) still exhibit uncontrollable restlessness.

When patients first began reclining on the couches of psychoanalytic psychiatrists, the depressed folks talked about their past. This led the founders of psychology and psychiatry to believe that issues that began in childhood caused many mental health problems. But questions were still not answered. Why would a bad relationship with your mother create the appetite loss found in depression, especially when eating problems only started several months prior to the session? By what strange mechanism would a childhood issue create an auditory hallucination, often years after the reported traumatic event? Many people had difficult childhoods, but they didn’t hallucinate and have a great appetite. It became clear that many mental health problems also had a physical component that involved changes in concentration, sleep, appetite, speech pattern, energy level, perceptions (hallucinations), and motivation. Studies began to determine the connection, if indeed one was present, between the condition of the patient and the physical signs/symptoms that were also present.

The picture became easier to understand when chemicals in the brain called “neurotransmitters” were discovered. The brain consists of billions of neurons or cells that must communicate with each other. The communication between neurons maintains all body functions, informs us when a fly lands on our hand, or when we have pain. The communication between neurons is controlled by the brain’s type and level of neurotransmitters. Neurotransmitters are chemical substances that control and create signals in the brain both between and within neurons. Without neurotransmitters, there would be no communication between neurons. The heart wouldn’t get a signal to beat, arms and legs wouldn’t know to move, etc.

As we discovered more about neurotransmitters, we began to identify which neurotransmitters controlled certain bodily functions or which were related to certain emotional/psychiatric difficulties. Serotonin, a neurotransmitter, was found to be related to body temperature and the onset of sleep. Research also identified Serotonin as related to depression and later to a variety of mental health conditions such as anorexia and obsessive-compulsive disorder.

As research in neurotransmitters continued, studies between neurotransmitters and mental conditions revealed a strong connection between amounts of certain neurotransmitters in the brain and the presence of specific psychiatric conditions. Using an everyday example, our automobile operates by using a variety of fluids such as engine oil, transmission fluid, brake fluid, and coolant (anti-freeze). Every automobile has a way to measure the levels or amounts of each of these needed liquids such as the dipstick for oil and transmission fluid and marked indicators for anti-freeze and brake-fluid levels. Using our dipstick to measure engine oil, for an example, we can find our engine to be found one, two, or even three quarts low. After a recent oil change, the dipstick may also tell us that we have excessive oil in the engine. To work properly, all fluid levels must be in the “normal range” as indicated by the dipstick. When we receive a blood test, values of certain blood components are given with the “normal range” also provided, indicating if a blood chemical is below or above the average range.

Neurological research has identified over fifty (50) neurotransmitters in the brain. Research also tells us that several neurotransmitters are related to mental health problems – Dopamine, Serotonin, Norepinephrine, and GABA (Gamma Aminobutyric Acid). Too much or too little of these neurotransmitters are now felt to produce psychiatric conditions such as schizophrenia, depression, bi-polar disorder, obsessive-compulsive disorder, and ADHD.

Unfortunately, the body doesn’t have a built-in dipstick for neurotransmitters, at least one that’s inexpensive enough for community mental health practice. There are advanced imaging techniques such as Positron Emission Tomography (PET Scans) that are being utilized in research and in the development of medications that directly influence changes in specific neurotransmitters. Lacking a PET Scanner, most professionals evaluate neurotransmitter levels by looking for indicators in thought, behavior, mood, perception, and/or speech that are considered related to levels of certain neurotransmitters.

This is perhaps best illustrated in individuals with depressed mood. The mental health professional is often required to separate those who would benefit from counseling and those who may require counseling and an antidepressant medication. The key is looking for those symptoms that are known to be related to chemical changes in the brain. For example, situational depression often produces sad expressions, worry, pessimistic attitude and other features but does not create prolonged changes in the physical symptoms such as changes in sexual interest, appetite, or sleep. The continued presence of physical symptoms tells us that the brain’s neurotransmitter levels have changed.

The technical aspects of neurotransmitter levels, the psychiatric symptoms they produce, and how medications have been developed to raise or lower the brain levels of these neurotransmitters can be very complicated. For this reason, the same procedure of explaining other medical conditions where medication brings symptoms back to the “normal range” is often used. Medical patients with high blood pressure, high blood sugar, or high cholesterol are informed that their body chemistry is too high, or in some cases, too low and must be corrected with medication.

For many years, mental health professionals have used the term “chemical imbalance” to explain the need for medications that are used to treat mental health conditions. This simple and commonly used explanation recognizes that the condition is a medical problem and that it can be treated with medication. The “chemical imbalance” explanation also reflects the overall theme of treatment – identifying what neurotransmitters are involved in the clinical symptom picture and with medication, attempting to return that neurotransmitter level back to the “normal range”.

Your Neurotransmitter Levels and Emotional Health

Your emotional health is a combination of attitudes, personality, support systems, and your brain’s neurotransmitter levels. Positive attitudes and a healthy personality help us through life’s difficulties and a good support system of family and friends is also valuable during times of trouble. Despite having these resources, there are times when coping with our experiences and life events changes our neurotransmitter status. Like an overheated automobile, we begin to have difficulty operating properly.

We are all at-risk for changes in our brain’s chemistry. Mostly commonly, we will experience depression, anxiety, or stress reactions. As our neurotransmitters change, they bring with them additional symptoms, behaviors, and sensations that add to our on-going difficulties. Recognizing these changes is an important part of treatment and returning your life to normal and reducing our stress.

This discussion is offered to explain how the neurotransmitter system in the brain can create psychiatric conditions and mental health problems. It is hoped the discussion will provide information that will be of value to those who suspect their neurotransmitter system is creating problems.

[rustoffa]

Bull Terrier Neurological Disorder Resources

This site was last updated Tuesday, June 07, 2005 . Most of the pages can be accessed from the navigation menus to the left and top of this page, and from links within those main category pages. For an ordered list of all files on the site, please see our Site Map.
Welcome!

The primary focus of this site is to help owners of dogs with a neurologically based behavioral disorder such as Compulsive Tail Chasing learn more about these issues and find out where they need to go to get help. We also provide a support group hosted by Yahoo! Groups where people can share their experiences with other owners of affected dogs.

Another goal of this site is to provide details on the Bull Terrier Compulsive Tail Chasing study coordinated by Dr. Alice Moon-Fanelli at Tufts. Dr. Moon-Fanelli, who has spent over a decade studying spinning and helping affected dogs, has made available to us all the necessary forms and information for those interested in participating in the study.

Let us know what you think of this site - sign our guestbook.
Not Just for Bull Terriers...

While much of the information on this site is geared towards Bull Terriers and the neurological disorders most common to this breed, problems such as Sudden Onset Aggression and Canine Compulsive Disorders also affect many other breeds. Our Yahoo! Group--which, to the best of our knowledge, is the only resource of its' kind for any breed at this time-- is open everyone and we have quite a few members who have breeds other than Bull Terriers.
Please Help!

Dr. Alice Moon-Fanelli needs Bull Terriers to take part in the Compulsive Tail Chasing study. We implore all owners and breeders to take the time to help us find the cause of this disorder - dogs' lives depend on it.

[Rebel]

Originally posted by Mr. G
Well here is the point. The Psychs have been saying for decades that there IS a chemical imbalance and a lot of people have decided that it is true without one study. A sheep is someone who just goes along and doesn't have thier own point of view based on reason, sound familiar? Feel free to think I am brainwashed but I am asking a simple question, I am not telling you your point of view I am asking you to back it up. Simple no?

I can point you to thousands of studies which show the effectiveness of SSRIs, TCAs, and MAOIs. All of these drugs alter the chemical layout of your brain, whether it's norepi, serotonin, epi, etc. People are quick to point a finger and say "There's no PROOF of a chemical imbalance." It's basically saying the same thing as "I don't believe the car is out of gas until I pull the gas tank out and look in it", at least IMO. If it works, it works, and they do work.

Are they overused? In many cases, yes, in some cases they aren't used enough IMO. Many docs like to cover up problems with benzos and narcs, and not treat the real issue, but that's a whole other arguement there.

What has me bothered is the effect things like this have (the Cruise incident). There is a small percentage of people who will see this, and believe him. Then who has to deal with them all night at the ER when they stop taking their Effexor (and don't tell me different, I see it literally every night I work). It's really sad when things like this occur. Just because they can write a song, or act in a movie, they think they are all of a sudden political experts, or can diagnose people's problems during a Matt Lauer interview.

Yes psychs have said for decades there is chemical imbalance, and I don't have to look in the gas tank to see it. I've seen it work, and I've seen it work miracles, literally. So I don't need Cruise or some scientology crackpot telling me how medicine should be practiced.

[Rebel]

Here's a study under the recruitement phase that the NIMH is currently running. There have been studies like this previously, which do show certain imbalances, but PROOF.....is a strange word.

Pretty much, this study is just looking to prove the basis of the MOA of SSRIs and some of the other antidepressants currently used.

Just check out the purpose section to get an idea of what the study is. This stuff isn't new, of course there's never PROOF

------------------------------

Examination of Brain Serotonin Receptors in Patients with Mood Disorders

This study is currently recruiting patients.

Sponsored by: National Institute of Mental Health (NIMH)
Information provided by: Warren G Magnuson Clinical Center (CC)


Purpose

The purpose of this study is to evaluate the function of certain brain chemicals and receptors in patients with mood disorders. This study will also examine how the stress hormone cortisol affects brain function.
Data suggest that serotonin 1A (5-HT1A) receptor function is abnormal in patients with mood disorders, such as major depressive disorder (MDD) and bipolar disorder (BP). However, these data are limited because they are based on small sample sizes. In this study, PET scans will be used to compare 5-HT1A receptor binding potential between mood disorder patients and healthy volunteers.
All participants will have an initial medical and psychiatric evaluation. Depression severity, anxiety, negative thinking, level of functioning, intelligence, and cognitive functions will be measured. Urine, saliva, and blood will be collected. Women will have a pregnancy test and tests to determine menstrual phase and time of ovulation. Participants will undergo magnetic resonance imaging (MRI) and PET scans of the brain. Some participants will have other procedures such as a lumbar puncture. Participants with Cushing's disease will undergo imaging as a comparison group.
Condition Intervention
Mood Disorder
Drug: 15 O-water
Drug: FCWAY


Study Type: Observational
Study Design: Natural History

Official Title: Serotonin1A Receptor and Serotonin Transporter Imaging In Mood Disorders

Further Study Details:

Expected Total Enrollment: 286
Study start: October 4, 2001


Multiple lines of evidence suggest that serotonin1A (5-HT1A) receptor and serotonin transporter (5-HTT) function is abnormal in major depressive disorder (MDD) and that somatic antidepressant treatments effect changes the function of these systems that are relevant to their therapeutic mechanisms. The data supporting these hypotheses have been obtained by assessing neuroendocrine and temperature responses to 5-HT1A agonists in MDD subjects, measuring 5-HT1A receptor and 5-HTT binding in brain tissue acquired post mortem from small samples of MDD subjects, and examining effects on 5-HT1A receptor function in rats following antidepressant drug (AD) administration. The recent development of highly selective 5-HT1A receptor and 5-HTT radioligands for positron emission tomography (PET) imaging made direct, noninvasive exploration of the central serotonin sites binding possible. Two studies conducted using one of these, [carbonyl-11C]-WAY-100635, found reduced 5-HT1A receptor binding potential (BP) in the mesiotemporal cortex, the raphe, and the prefrontal cortex (PFC). Pilot data from these studies suggested that the abnormal reduction in 5-HT1A receptor BP is more prominent in bipolar disorder (BD) than MDD subjects (i.e., unipolar depressives) who did not have bipolar relatives, and that it exists independently of mood state.
However, these data have the limitations that the subject samples studied in these preliminary post mortem and PET series have been small, and that [carbonyl-11C]WAY-100635 uptake is difficult to quantitate in PET images. Therefore, these observations require replication in subject samples large enough to establish main effects of diagnostic subtype using a 5-HT1A receptor radioligand that can be validly quantitated. A selective 5-HT1A receptor radioligand suitable for this purpose, [18F]FC-WAY100635 ([18F]FCWAY), has recently been developed at the NIH. In addition, a recently developed selective 5-HTT ligand, [11C] DASB provides a unique opportunity to image the 5-HTT in the same depressed sample.
The proposed study will advance knowledge regarding the neurobiology of mood disorders by employing PET and [18F]FCWAY and [11C] DASB to compare 5-HT1A receptor BP between mood disordered and healthy control subjects in the mesiotemporal cortex, raphe, anterior cingulate gyrus, and left orbital cortex. The following hypotheses, based upon pilot data acquired using [carbonyl-11C]-WAY-100636, will be tested: 1) Depressives have reduced 5-HT1A receptor binding relative to healthy controls. 2) Bipolar depressives will have significantly greater reductions in 5-HT1A receptor binding than unipolar depressives with only unipolar relatives. A pilot study in which bipolar depressives are treated with lithium or divalproex and then re-imaged will test the third hypothesis, that 5-HT1A receptor binding will increase in bipolar subjects during mood stabilizer therapy.
Finally, because central 5-HT1A receptor density is down-regulated in rodents by corticosterone administration and by stress-mediated corticosterone secretion, assessments of hypothalamic-pituitary-adrenal (HPA) axis activity (which is commonly elevated in MDD and BD), will be assessed to determine whether down-regulation of 5-HT1A receptors correlates with cortisol hypersecretion in mood disorders. Because this down-regulation may play a compensatory role to reduce cortisol secretion, neuroendocrine assessments of long-standing rather than acute hypercortisolism and of the pathophysiological diathesis to hypersecrete cortisol will be emphasized as providing the most sensitive correlates of reduced 5-HT1A receptor binding. A medical control group with Cushing's Disease will also be imaged to determine whether pathological elevation of glucocorticoid levels down-regulates 5-HT1A receptor expression in humans, as it does in rats.
Eligibility

Genders Eligible for Study: Both
Accepts Healthy Volunteers

Criteria
INCLUSION CRITERIA:
MDD SAMPLES:
Sixty subjects (ages 18 to 60) with MDD will be selected who additionally meet criteria for one of 3 subgroups:
A) MDD, Currently depressed with FPDD, as defined by DSM-IV criteria for recurrent MDD, currently in a major depressive episode, who have a first degree relative with MDD but no first degree relatives with mania, alcoholism, or antisocial personality disorder.
B) MDD, Currently in remission with a history of FPDD, defined as a period of at least six months with no more than one clinically significant symptom, and during which time subjects were not taking an AD agent. Subjects will thus meet the historical criteria for recurrent MDD (DSM-IV). We will also require that subjects previously had a least one antidepressant drug trial, to ensure that the severity of previous episodes warranted treatment.
C) MDD, Currently depressed, non-FPDD. To assess the specificity of the findings in MDD to FPDD, a sample meeting criteria for MDD, currently in a depressive episode, but not FPDD will also be imaged.
BIPOLAR DEPRESSED SAMPLE:
Twenty subjects (ages 18 to 60) who meet DSM-IV criteria for bipolar disorder and are currently in a major depressive episode. Subjects may be inpatients or outpatients. Because effective treatment will not be discontinued for the purposes of this protocol, subjects will be identified who have never been treated or who have discontinued medication due to lack of efficacy, noncompliance, physician order or other reasons prior to study entry.
HEALTHY, LOW RISK, CONTROL SAMPLE:
Forty subjects (ages 18 to 60) who have not met criteria for any major psychiatric disorder. The control subjects will have no known first or second degree relatives with mood disorders.
CUSHINGS DISEASE CONTROL SAMPLE:
Ten subjects (ages 18 to 60) with probable Cushing's Disease will be recruited who have both clinical and biochemical evidence of hypercortisolism (including urinary free cortisol excretion higher than the upper limit of normal (greater than 248) nmole/day, and marked central adiposity, cutaneous atrophy, proximal myopathy, and large purple striae). The diagnosis of probable Cushing's Disease will also have been established prior to referral via CRH and ACTH.
MENSTRUALLY-RELATED DYSPHORIC DISORDER SAMPLE:
(n equals 30; ages 18-50). These females are recruited, screened and diagnosed by collaboration under protocol number 81-M-0126, previously approved by IRB, entitled 'The Phenomenology and Biophysiology of Menstrually Regulated Mood and Behavioral Disorders', principal investigator, David Rubinow, M.D. As described in that protocol these subjects must have a regular menstrual cycle lasting 21 - 33 days and meet the following criteria: 1) history within the last two years of at least six months with menstrually-related mood or behavioral disturbances of at least moderate severity - that is, disturbances that are distinct in appearance and associated with a notable degree of subjective distress; 2) a 30 percent increase in mean negative mood ratings (relative to the range of the scale employed) in the premenstrual week compared with the week following the end of menses in at least two of the three cycles; 3) age 18 to 50; 4) not pregnant and in good medical health; 5) regular menses.
REMITTED MDD WITH AND WITHOUT A HISTORY OF PPD:
(n=40; ages 18-40). These subjects are recruited, screened and diagnosed by collaboration under 95-M-0097, previously approved by IRB entitled An Endocrine Modal for Postpartum Mood Disorders. These subjects will have a history of DSM-IV MDD. Twenty will also have had a hypomanic/manic episode that occurred within three months of childbirth and twenty will have not had the latter within three months of childbirth. Women will have been well for a minimum of one year, have a regular menstrual cycle for at least three months, medication free (including birth control pill), have no history of puerperal suicide attempts or psychotic episodes requiring hospitalization. Any women with a current axis I psychiatric diagnosis will be excluded from participating in this protocol.
HEALTHY FEMALE CONTROLS UNDER 95-M-0097:
(n=20, age 18-40). These healthy control women are under an identical drug administration regimen as the 40 remitted MDD women above and will similarly be recruited and screened under 95-M-0097. They will meet the same criteria specified for the remitted MDD group above but will not have any past or present Axis I diagnosis or evidence of menstrually related mood disorders. This healthy sample of females will have given birth.
EXCLUSION CRITERIA:
Subjects must not have taken antidepressant or other medications likely to alter monoamine neurochemistry or cerebrovascular function for at least 3 weeks (8 weeks for fluoxetine) prior to scanning. Subjects being scanned at two points or the same point twice in their menstrual cycle must not have taken birth control pills for at least 6 months prior to scanning. However, effective medications will not be discontinued for the purposes of this study. Instead, subjects will be recruited who are not currently receiving psychotropic drugs. Subjects will also be excluded if they have:
a) serious suicidal ideation or behavior;
b) psychosis to the extent that the ability to provide informed consent is in doubt;
c) medical or neurological illnesses likely to affect physiology or anatomy;
d) a history of drug or alcohol abuse within 1 year or a lifetime history of alcohol or drug dependence (DSM IV criteria);
e) current pregnancy
f) current breast feeding;
g) general MRI exclusion criteria;
h) previous exposure to ecstasy (i.e. MDMA) which has neurotoxic effects on 5-HTT expressing neurons.
Subjects beyond age 50 are excluded from the MRMD sample due to peri-menopausal status and subjects beyond age 60 are excluded to reduce the biological heterogeneity encompassed by the MDD criteria, since depressives whose age-at MDD-onset is later than 60 have a far greater likelihood of having MRI correlates of cerebrovascular disease than age-matched, healthy controls or age-matched, early-onset depressives.
Subjects whose first major depressive episodes arose temporally after other major medical or psychiatric conditions will also be excluded.
Location and Contact Information

Please refer to this study by ClinicalTrials.gov identifier NCT00026832


Maryland
National Institute of Mental Health (NIMH), 9000 Rockville Pike, Bethesda, Maryland, 20892, United States; Recruiting
Patient Recruitment and Public Liaison Office 1-800-411-1222 prpl@mail.cc.nih.gov
TTY 1-866-411-1010

More Information

Detailed Web Page

Publications

Drevets WC, Frank E, Price JC, Kupfer DJ, Holt D, Greer PJ, Huang Y, Gautier C, Mathis C. PET imaging of serotonin 1A receptor binding in depression. Biol Psychiatry. 1999 Nov 15;46(10):1375-87.

Gunn RN, Sargent PA, Bench CJ, Rabiner EA, Osman S, Pike VW, Hume SP, Grasby PM, Lammertsma AA. Tracer kinetic modeling of the 5-HT1A receptor ligand [carbonyl-11C]WAY-100635 for PET. Neuroimage. 1998 Nov;8(4):426-40.

Sargent PA, Kjaer KH, Bench CJ, Rabiner EA, Messa C, Meyer J, Gunn RN, Grasby PM, Cowen PJ. Brain serotonin1A receptor binding measured by positron emission tomography with [11C]WAY-100635: effects of depression and antidepressant treatment. Arch Gen Psychiatry. 2000 Feb;57(2):174-80.

Study ID Numbers: 020047; 02-M-0047
Record last reviewed: October 4, 2004
Last Updated: June 23, 2005
Record first received: November 14, 2001
ClinicalTrials.gov Identifier: NCT00026832
Health Authority: United States: Federal Government
ClinicalTrials.gov processed this record on 2005-07-18

U.S. National Library of Medicine, Contact NLM Customer Service
National Institutes of Health, Department of Health & Human Services
Copyright, Privacy, Accessibility, Freedom of Information Act

[Rebel]

oops, taken from clinicaltrials.gov

sponsored by the National Institute for Mental Health

can't have anybody coming down on us lol

[Mr. G]

Yes I am sure there are many people who feel they have been benefited by these drugs, I am not debating that. One thing I have noticed in psych drug commercials is they say the problem "might" be caused by a chemical imbalance. Key word "might". Since Cruise came out against unecessary drugging many Psychs and Neurologiests have also come out exposing the scam as you may have seen posted here. This is just one post at one website but just watch what happens as more and more people become educated in this subject. You gotta hand it to Tom for sticking his neck out about something he cares about. He didn't have to.

[Rebel]

I'm sure Tom has studied the drug commercials very hard to gain his clinical expertise.

I've read literally thousands of studies, and I wouldn't claim to have the knowledge he CLAIMS to have in this area, thing is the general public doesn't know better.

Tom can go dive off of the damn Eiffel Tower in the name of Ewoks, Klingons, R2D2 or whatever other scientology beliefs he has for all I care. It bothers me when he on national tv trying to push this stuff on an innocent public.

It's amazing how regulated the statements a drug company can/can't make, but any yahoo can go on the news and say whatever. I saw some guy advertising that seaweed can cure cancer the other day, he should be locked up for that.

[Mr. G]

Well I guess we agree on one thing, the general public doesn't know any better. Psychiatry is going to be brought to task. It's put up or shut up. They shot themselves in the foot years ago, as they were making progress up to around 1870 when Wundt decided that man was an animal. Before that they thought man was a spiritual being: Psych (greek word meaning spirit) ology (study of). So it used to mean the study of the spirit. Since then it has become a cash cow i.e insurance fraud, involuntary commitment ect. If it wasn't for tax money Psychiatry would wither and die as very few people would voluntarily have part of their brain cut out or electrocuted.

[Rebel]

Electroshock therapy is very, very effective. I've seen that personally as well. I know it seems primitive, but it is still very effective and still used.

[Seshmeister]

Originally posted by Mr. G
As I have said before, I have answered many questions but have not once pushed Scientology on anyone. Not once.

You also haven't answered any of the questions asked about scientology or defended the dozens of accusations here which makes it look as though you have been completely brainwashed.

That pretty much invalidates your opinion on anything whether it's drug therapy or Sammy Hagar because we don't know if it's your thoughts you're posting or those of your controllers.

Cheers!

[Mr. G]

Fine with me. How you feel about me isn't important. I have answered many questions about Scientology if you read the post. I am not here to defend Scientology as I am sure your mind is made up. All I have done is ask for one scientific study, one blood test or one lab report to validate their (psychiatry's) claims. You have completely avoided that. So lets see it. By the way I know why you are avoiding it but lets see you explain it. Start

[rustoffa]

Originally posted by Mr. G
You gotta hand it to Tom for sticking his neck out about something he cares about. He didn't have to.

Arguably, he IS the most "untouchable" of the bunch...not to mention a huge Speelburg vision looking at the clock.

The whole fucking thing screams publicity....grab a young starlet, start some cuntroversy....it's laughable.

IMO, you gotta hand it to Matt Lauer.

Go over to the NBC boards.

Lauer's sig:

"Owning Cruise like a Top-Gun Mig"