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Media Stories / Diana inquest: Henri Paul's parents were told he wasn't drunk
« Last post by zebb on August 07, 2017, 07:33:19 am »
http://www.dailymail.co.uk/news/article-485544/Diana-inquest-Henri-Pauls-parents-told-wasnt-drunk.html

Diana inquest: Henri Paul's parents were told he wasn't drunk
Last updated at 23:49 03 October 2007

Henri Paul
Lord Stevens told Henri Paul's grieving parents that their son had not been drinking heavily on the night of the crash only because they were upset at accusations he had been as 'drunk as a pig'.

His remarks were contradicted a month later in the offical Operation Paget report into the tragedy which concluded Diana and Dodi died because Paul was drunk and speeding.

The clash has been seized on by Mohamed al Fayed who says it is proof that 'Establishment' figures want to cover up their murders.

Yesterday, however, the coroner revealed that the former police chief's comments had been taken out of context.

He had, he said, only been trying to 'reassure' Jean and Gisele Paul who had been deeply upset by newspaper reports that he was an alcoholic who had been drinking heavily in the hours before the accident.

He also confirmed that tests had shown Paul was twice the French drink drive limit and traces of Prozac were found in his blood.

Lord Justice Scott Baker said: "Henri Paul was the acting head of security at The Ritz Hotel.

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It is alleged he worked for security services in France or in the UK and was instrumental in carrying out the plan, either inadvertently or otherwise, to have Diana and Dodi murdered in the underpass - a plan which, of course, resulted in his own death.

"It is further said that it was publicly and erroneously put about that he was unfit to drive through drink in order to cover up the real cause of the crash.

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diana crash scene inquest pictures
"Henri Paul's role and his actions leading up to the crash in the early hours of Sunday 31 August are critical to assessing the conspiracy to murder allegations."

As acting head of security at the Ritz, the 41-year-old worked closely with both Dodi Fayed and Mohamed, though he was not normally used as a driver. He joined the hotel in 1986 and had been in his new job for just two months when he died.

He was described by fellow employees as a conscientious member of staff who, the coroner said, "would find it difficult to say No".

On the night of the accident, Paul left work at 7pm but was called back after Diana and Dodi unexpectedly returned to the hotel.

No-one has ever been able to fill in what he did during those "missing hours".

What is beyond doubt, however, is that Paul was seen in the bar of the Ritz Hotel between 10pm and midnight consuming at least two glasses of Ricard, an aniseed liqueur.

And while there is no evidence to prove that he had consumed any alcohol before then, it was perfectly likely as at that stage Paul did not know he would be called back to work - let alone to drive his boss's car.

Tests carried out on blood and other body samples after his death indicate that Paul was twice the legal limit when he died.

These range between 1.74g to 1.87grammes per litre of blood. The legal limit in France is 0.5 per litre.

Further tests showed that Paul had been taking a cocktail of drugs including prozac to combat depression and sleeping pills for insomnia.

His close friend and doctor, Dominic Melo, has told how he also prescribed him Aotol, a drug to stop cravings for alcohol after Paul said he had become concerned about his drinking and was suffering feelings of 'isolation'.

Mr al Fayed, the court heard, firmly believes that Paul's samples were tampered with or swopped with those of an unnamed person, although DNA tests have proved they were from him.

What does continue to puzzle investigators, however, is the level of carbon dioxide in his blood.

Although this could have been affected by smoking, levels of the gas in the driver's blood samples were 'very high', more than 20 per cent.

Lord Justice Scott Baker admitted yesterday that Paul should have shown noticeable signs of impairment before his death. "If the sample is from him, how did it get to that level?" he said.

He also outlined outstanding questions about Paul's finances at the time of his death. In his pockets were a surprising 12,565 French francs - around £1,256 --while a further £170,000 was discovered in several bank accounts. His salary at The Ritz was around £1,500 a month.

Mr al Fayed claims this is proof that he was an intelligence informant. Paul's mother, however, says hotel clients tipped him lavishly.

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Read more: http://www.dailymail.co.uk/news/article-485544/Diana-inquest-Henri-Pauls-parents-told-wasnt-drunk.html#ixzz4p4XGF2DS
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16
http://www.dailymail.co.uk/news/article-4766332/Henri-Paul-says-British-police-told-Diana-murdered.html?login#comments

Henri Paul was on Prozac and been drinking on the night of the crash.

Father of Princess Diana's death crash driver Henri Paul claims British police told him she was murdered and his son was 'collateral damage'
Henri Paul's father Jean, 85, has claimed UK police told him Diana was murdered
He fears he will die without knowing the full story behind the August 1997 crash
An official inquest in 2008 ruled Diana and Dodi were unlawfully killed due to the 'gross negligence' of Mr Paul, who had been drinking
By Thomas Burrows for MailOnline
PUBLISHED: 23:15, 6 August 2017 | UPDATED: 00:21, 7 August 2017
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The father of Henri Paul, Princess Diana's driver on the night she died, has claimed UK police told him she was murdered.

Henri's elderly father Jean, 85, fears he will die without knowing the full story behind the crash.

Mr Paul, the acting head of security at the Ritz Hotel in Paris, was at the wheel of the Mercedes which crashed in the Alma Tunnel in the early hours of August 31, 1997 with Diana and Dodi Al Fayed in the back.

He said: 'Diana was killed and my son was killed. I believe they were both murdered. My son was simply ­collateral damage of a plot to kill Diana and they killed him as well.

'I am 100% sure he [Henri] was not involved in this plot. He was too honourable and too honest.'

Henri Paul was at the wheel of the Mercedes which crashed in the Alma Tunnel in the early hours of August 31, 1997 with Diana and Dodi Al Fayed in the back   +2
Henri Paul was at the wheel of the Mercedes which crashed in the Alma Tunnel in the early hours of August 31, 1997 with Diana and Dodi Al Fayed in the back

Despite an official inquest ruling Diana and Dodi were unlawfully killed due to the 'gross negligence' of Mr Paul, who had been drinking, Jean remains convinced it was part of an Establishment plot.

He even claimed some officers inside Scotland Yard believe there was a secret plot to kill Diana.

In an interview with the Daily Mirror he said: 'I have no real hope to know what really happened. Perhaps it will be known in 30 or 50 years. But I would really like to know before I die. But I don't think it will happen.'

The 85-year-old even sensationally suggested his son's blood sample was switched or tampered with to make it look like he had drink in his system.

He said: 'On that day there were over 20 autopsies that took place and it was easy for the authorities to switch blood samples to show alcohol was present in the sample they said was Henri's.

'That is what I believe happened.'

Many conspiracy theories have surrounded Diana's death, and Dodi's father, former Harrods owner Mohamed Al Fayed, has always insisted he believes the couple were murdered.

However an inquest in 2008 found Diana and Dodi were unlawfully killed due to the 'gross negligence' of Mr Paul, who had been drinking. A lack of seatbelts also contributed to their deaths.

And in 2013, the Met dismissed reports claiming SAS troops were behind the couple's death, ­insisting there was 'no credible evidence' of secret service involvement.

Diana's first lover after her marriage to Prince Charles, bodyguard Barry Mannakee, was killed in a 1987 motorcycle accident three weeks after being sacked by the Royal Family following rumours of their romance.

Some of his family believe the secret services were behind the death, but that has never been proven.

Jean's wife, former teacher Giselle, 87, was traumatised by their son's death and is now living in a care home.

In a previous interview she said: 'We believe there was a plot to kill the Princess that terrible night in August 1997.

'We know in our hearts that our son was murdered and we still live with the hope that one day the truth will be known.'

The couple have outlived all but one of their five sons. 

 

Read more:
'British police told me Princess Diana was murdered': Death crash driver's dad claims son was 'collateral damage' in plot - Mirror Online
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17
https://www.sciencedaily.com/releases/2011/11/111115175354.htm

Serotonin system in women's brains is damaged more readily by alcohol than that in men’s brains, study finds
Date:
November 17, 2011
Source:
University of Gothenburg
Summary:
After only four years of problem drinking, a significant decrease in the function of the serotonin system in women’s brains can be seen. This is the system that regulates such functions as impulse control and mood. It takes 12 years before a corresponding decrease is seen in men.
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FULL STORY
After only four years of problem drinking, a significant decrease in the function of the serotonin system in women's brains can be seen. This is the system that regulates such functions as impulse control and mood. It takes 12 years before a corresponding decrease is seen in men. This is the conclusion of multidisciplinary research carried out at the Department of Psychology and the Sahlgrenska Academy at the University of Gothenburg, Sweden.

The research group in the multidisciplinary project Gothenburg Alcohol Research Project (GARP) has studied for the first time three of the major neurotransmitter substances in the brain in a single individual. They have studied a group of women and a group of men with alcohol dependence. The results will be published in January 2012 in the journal Alcoholism: Clinical & Experimental Research.

"We have used what is known as neuroendocrine techniques to show that it is principally the serotonergic system in the brain that is seriously impaired by alcohol. This is the system that regulates impulse control and mood, among other functions," says Kristina Berglund, scientist at the Department of Psychology and representative for the research group.

Both men and women suffer adverse effects, but the effects arise much more rapidly in women. The results show that the function of women's serotonin system has fallen by 50% after as little as four years with problematic alcohol consumption, while it takes 12 years before the function of men's systems is halved.

"It is important to note that the damage is just as serious in men and women, but the time courses are different. We still don't know whether the serotonin system can repair itself, but there are research results showing that other damage to the brain can heal after a certain period without alcohol," says Ulf Berggren of the Sahlgrenska Academy, University of Gothenburg.

Story Source:

Materials provided by University of Gothenburg. Note: Content may be edited for style and length.

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University of Gothenburg. "Serotonin system in women's brains is damaged more readily by alcohol than that in men’s brains, study finds." ScienceDaily. ScienceDaily, 17 November 2011. <www.sciencedaily.com/releases/2011/11/111115175354.htm>.
18
https://www.ncbi.nlm.nih.gov/pubmed/26311211

Alcohol Alcohol. 2016 Mar;51(2):164-71. doi: 10.1093/alcalc/agv090. Epub 2015 Aug 26.
Variation in the Serotonin Transporter Gene and Alcoholism: Risk and Response to Pharmacotherapy.

Thompson MD1, Kenna GA2.
Author information
Abstract
SLC6A4, the gene encoding the serotonin transporter protein (5-HTT), has been extensively examined as a risk factor for alcohol dependence (AD). More recently, variability in the transporter gene was identified to be a potential moderator of treatment response to serotonergic medications such as ondansetron and sertraline. There is an insertion-deletion polymorphism in the promoter region (5-HTTLPR) of the SLC6A4, with the most common alleles being a 14-repeat short (S) allele and a 16-repeat long (L) allele. The S allele has often been associated with AD. By contrast, the L allele has been associated with pharmacological responsiveness in some individuals with AD. Differences in clinical phenotype may determine the utility of the 5-HTTLPR polymorphism as a moderator of pharmacological interventions for AD. We review the AD typology and disease onset in the context of pharmacogenetic and genomic studies that examine the utility of 5-HTTLPR in improving treatment outcomes.
© The Author 2015. Medical Council on Alcohol and Oxford University Press. All rights reserved.

PMID: 26311211 PMCID: PMC4755552 [Available on 2017-03-01] DOI: 10.1093/alcalc/agv090
[Indexed for MEDLINE] Free PMC Article
19
Normalizing Dopamine Levels in the Brain Can Reduce Alcohol Cravings Study Shows (2015)

https://www.yourbrainonporn.com/normalizing-dopamine-levels-brain-can-reduce-alcohol-cravings-study-


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Normalizing Dopamine Levels in the Brain Can Reduce Alcohol Cravings Study Shows (2015)

Submitted by admin on Wed, 10/14/2015 - 17:01
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More than 16 million adults in the U.S. have an alcohol-use disorder
A scientific study has shown alcohol dependency can be treated by targeting the dopamine system.
Gautam Naik Oct. 14, 2015 12:27 p.m. ET
Scientists have shown that a drug that normalizes dopamine levels in the brain can reduce alcohol cravings in people dependent on drink.
The finding was based on two studies, one conducted on people and one on rats. In the human trial, patients who took the experimental drug showed a marked reduction in alcohol craving. A separate animal study suggested that the drug works by acting on dopamine levels.
“It is proof of concept” that alcohol dependency can be treated by targeting the dopamine system, said Pia Steensland, neuroscientist at Karolinska Institute in Sweden and co-author of both studies. “We need to do larger trials” to validate the results.
Current drugs for alcohol dependency aren’t especially effective. The population of patients is genetically diverse, so only certain subgroups benefit. Prescription rates are low. As a result, the need for better medicines is huge.
Alcohol makes the brain’s reward system release more dopamine than normal, triggering a feeling of well-being. But as more alcohol is drunk, the more the reward system is desensitized and the less dopamine is released. Eventually, a person drinks more alcohol not just to feel euphoric, but to attain a state of physical and emotional normality. Thus, addiction sets in.
More than 16 million adults in the U.S. have an alcohol-use disorder and nearly 88,000 people die each year from alcohol-related causes, according to the National Institutes of Health. In 2006, alcohol misuse cost the U.S. economy $223.5 billion, the NIH said.
For the human study, published Wednesday in the journal European Neuropsychopharmacology, scientists recruited 56 Swedish alcohol dependent men and women, who typically would drink the equivalent of a bottle of wine a day.
The participants abstained from drink for at least four days. Half were then given a placebo and half got OSU6162, a drug believed to stabilize dopamine levels. The patients were randomized and neither they nor the researchers knew who was getting the experimental drug and who was getting the placebo.
For two weeks, the participants could drink as much as they liked. On day 15, each person was offered a glass of their favorite drink. According to the study, the OSU group reported not enjoying their first sip as much as the placebo group. After the drink was finished, the OSU group reported a lower craving for alcohol compared to the placebo group.
In addition, those with the poorest impulse control—and thus at greater risk of relapse after a period of abstinence—responded best to the experimental drug.
Both the OSU and placebo groups reported only mild side effects. This is significant because other dopamine-based medicines, such as those used to treat schizophrenia, completely block dopamine and can lead to nasty side-effects, such as nausea.
The rights to OSU6162 are owned by Arvid Carlsson, professor emeritus at the Sahlgrenska Academy in Sweden and co-author of the human study. Dr. Carlsson, 92 years old, shared in the 2000 Nobel Prize for medicine for discovering that dopamine is a transmitter in the brain. His team also developed OSU6162.
To better understand how OSU6162 might work, Dr. Steensland and other researchers did a separate study on rats, also published Wednesday in the journal Addiction Biology. Rats that voluntarily drank alcohol over the course of almost a year had lower dopamine levels than animals that drank no alcohol. When OSU6162 was given to the “alcohol rats,” their dopamine levels returned to normal.
The human trial wasn’t designed to comprehensively evaluate whether the experimental drug could help people drink less. But because of the promising early-stage results, Dr. Steensland and her colleagues now hope to do a longer-term trial involving many more patients.
 
One step closer to a new drug for alcohol dependence
October 14, 2015
Researchers at Karolinska Institutet and the Sahlgrenska Academy in Sweden might be one step closer to finding an effective drug for alcohol dependence. In two separate studies, they show that the dopamine stabilizer OSU6162 can reduce the craving for alcohol in alcohol dependent people and normalises the level of dopamine in the brain reward system of rats that have consumed alcohol over a long period of time. However, thorough clinical studies are needed to determine if the OSU6162 also can help alcohol dependent people drink less alcohol.
"The results of our studies are promising, but there is still a long way to go before we have a marketable drug," says Pia Steensland, PhD, Associate Professo at the Department of Clinical Neuroscience of Karolinska Institutet, and co-author of both studies. "The socioeconomic costs of alcohol are huge, not to mention the human suffering. It is inspiring to continue working."
Roughly a million Swedes over 15 years of age drink so much alcohol that they risk damaging their health, and it is estimated that some 300,000 of these people are dependent. Despite the pressing need, there are only a few approved drugs for the treatment of alcohol dependence, but their effects vary from person to person and the prescriptions rates are low. Consequently the hunt for new, more efficacious drugs for alcohol dependence continues.
The studies of OSU6162 are based on the knowledge of how the brain reward system stimulates us to act in the interests of our own survival. Since dopamine creates a feeling of wellbeing, such as when we exercise or eat good food, the memory associates the two so that we will repeat the behaviour. Alcohol makes the brain reward system release more dopamine than normal, creating a pleasant euphoric sensation. However, the more alcohol drunk, the more the reward system is desensitised and the less dopamine is released. With time, greater volumes of alcohol are needed to cause intoxication and eventually to attain a state of physical and emotional normality - addiction has set in.
In the clinical study, which is published in the scientific journal European Neuropsychopharmacology¸ the scientists examined for the first time if OSU6162 can reduce the craving for alcohol in people with alcohol dependence. Half the participants were treated with OSU6162 and half with placebo for a fortnight, after which both groups were exposed to different situations that could be assumed to elicit a craving for alcohol. The results show that the experimental group experienced less of a craving for alcohol after drinking one glass of an alcoholic beverage.
"At the same time, the OSU6162 group reported not enjoying the first zip of alcohol as much as the placebo group," says Dr Steensland. "One interesting secondary finding was that those with the poorest impulse control, that is those thought to be most at risk of relapse after a period of abstinence, were those who responded best to the OSU6162 treatment."
A study of rats published at the same time in the scientific journal Addiction Biology adds to the understanding of how OSU6162 works, as it shows that rats that voluntarily consumed alcohol for almost a year had lower levels of dopamine in their brain reward system than rats that had never drunk alcohol. However, when the "alcohol rats" were treated with OSU6162 it was found that the substance counteracted the low concentrations of dopamine in the brain reward system.
"We therefore think that OSU6162 can reduce the alcohol craving in dependent people by returning the downregulated levels of dopamine in their brain reward system to normal," says Dr Steensland.
More information: 'The Effects of the Monoamine Stabilizer (-)-OSU6162 on Craving in Alcohol Dependent Individuals: A Human Laboratory Study', Lotfi Khemiri, Pia Steensland, Joar Guterstam, Olof Beck, Arvid Carlsson, Johan Franck, Nitya Jayaram-Lindström, European Neuropsychopharmacology, online 6 October 2015, doi:org/10.1016/j.euroneuro.2015.09.018.
'The Monoamine Stabilizer (-)-OSU6162 Counteracts Down-Regulated Dopamine Output in the Nucleus Accumbens of Long-Term Drinking Wistar Rats', Kristin Feltmann, Ida Fredriksson, Malin Wirf, Björn Schilström, Pia Steensland, Addiction Biology, online 14 October 2015, DOI: 10.1111/adb.12304.
20
Media Stories / Understanding Paxil, Alcohol, and Abuse
« Last post by zebb on July 23, 2017, 09:21:02 am »
http://www.healthline.com/health/depression/paxil-alcohol#overview1


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Understanding Paxil, Alcohol, and Abuse
Paxil and alcohol Effect on alcohol abuse Other interactions Takeaway
Overview
Paroxetine (Paxil) is an antidepressant. It’s used to treat many conditions, including:

depression
generalized anxiety disorder
social anxiety disorder
panic disorder
post-traumatic stress disorder
obsessive-compulsive disorder
Paxil is a selective serotonin reuptake inhibitor (SSRI). It helps increase the levels of serotoninin, a chemical messenger that affects your mood. Mixing alcohol with Paxil can lead to some unwanted side effects. Paxil may also affect alcohol cravings, though findings on this influence are still unclear.

Read more: What to know about SSRIs »

PAXIL AND ALCOHOL

Risks of mixing Paxil and alcohol
Increased symptoms
Alcohol can make the symptoms of depression worse. It may also make Paxil less effective at treating depression. If the drug doesn’t work as well, your symptoms may come back. Because of these factors, people should avoid drinking alcohol while they take Paxil.

Increased side effects
Alcohol also can increase some of Paxil’s side effects, especially dizziness, sleepiness, and trouble concentrating. Other side effects of Paxil that alcohol can increase include:

agitation
changes in vision
hallucinations (seeing or hearing things that aren’t real)
high or low blood pressure
decreased sex drive
mood swings
irregular heart rhythm
joint pain
loss of emotional feeling
nausea
vomiting
diarrhea
paranoia
mania (racing thoughts or excess energy)
rigid muscles, poor muscle control, or uncontrolled muscle movements
suicidal thoughts or actions
unintentional weight gain
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EFFECT ON ALCOHOL ABUSE

Paxil’s relationship to alcohol abuse
The relationship between Paxil and alcohol misuse is unclear. Some information seems to indicate that Paxil use helps curb the reliance on alcohol in people with anxiety disorders, while other information has indicated just the opposite.

A study in the journal Alcoholism: Clinical & Experimental Research investigated the relationship between social anxiety and alcohol use disorders. For people with social anxiety disorders who misused alcohol to make them feel more comfortable in social settings, the results suggest taking Paxil allowed them to engage more easily without drinking alcohol. In other words, Paxil reduced their need for alcohol to ease discomfort in social situations. This effect may have reduced alcohol dependence and misuse in these people.

On the other hand, some research has linked the use of SSRIs like Paxil to increased alcohol cravings and misuse. In a review of studies on SSRIs and alcohol dependence, researchers found that SSRIs actually led to an increase in alcohol consumption in some groups. This risk might be higher in people who have certain genes that already make them more prone to alcohol misuse.

OTHER INTERACTIONS

Other interactions
Paxil can also interact with a number of drugs. While you’re taking Paxil, you should avoid taking MAO inhibitors and the antipsychotic thioridazine (Mellaril). You should also avoid the antipsychotic drug pimozide (Orap). All of these drugs can cause severe side effects when you take them with Paxil.

Other drugs that can cause problems if you take them with Paxil include:

cimetadine (Tagamet), used to treat gastroesophageal reflux disease (GERD)
fentanyl, an opioid pain reliever
drugs that thin the blood such as warfarin, rivaroxaban, and apixaban
nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin and ibuprofen
epilepsy medications
drugs used to treat irregular heartbeats, schizophrenia, and HIV infection
metoprolol (Lopressor, Toprol XL), a blood pressure lowering drug
other antidepressants such as tricyclics, lithium, SNRIs, or SSRIs
procyclidine (Kemadrin), a drug used to treat Parkinson’s disease
tamoxifen, a breast cancer drug
triptans, used to treat migraine headaches
You should let your doctor know about all drugs you take, including over-the-counter drugs as well as herbal remedies, vitamins, and supplements.

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TAKEAWAY

Talk to your doctor
If your doctor has prescribed Paxil or another antidepressant, ask about all the possible side effects and interactions it can cause. Be careful about using alcohol or drugs that might interact with your antidepressant.

If you think that Paxil is increasing your alcohol use, talk about it with your doctor. They may be able to recommend a drug that is better suited for you.
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