Re: Alcohol reducing symptoms of autism in some individuals

January 16, 2008

Thanks for posting this. Although my son is only 5, he has always

craved alcoholic beverages from early on. If my husband leaves a beer

out on the table, our son is always trying to drink out of the glass.

Of course, we take the beer immediately away from him, but now I am

wondering if I should let him have a sip or two.

>

> forwarding this from another list - are there any people on this

list

> with adult ASD kids? I was wondering if any tended to drank wine (or

> other alcohol), and if noticed any changes in 'autism'?

>

> ....I was very intrigued by something posted on another

> board. In this link a woman is saying her child (adult Aspie) seems

more

> typical after

> drinking alcohol and that he doesn't seem drunk at all. If this was

> across the board with all ASD kids/adults or even very common it

might

> point to something in that is worth looking into.

>

> Indeed one comment left on board confirmed the effects in another

ASD

> individual. http://youtube.com/watch?v=MWXLiTcq4y0

> <http://youtube.com/watch?v=MWXLiTcq4y0>

>

> I have had a quick look through literature and it turns up alcohol,

esp.

> some types of drinks, decrease inflammatory responses. Sometimes

> dramatically. It is well know that chronic long-term

> consumption/intoxification messes up the immune system…

>

> I have copied some most interesting abstracts here, wonder if anyone

> would have any thoughts on this, or maybe some other mechanisms that

> could be at work…

>

> Natasa

>

> Atherosclerosis. 2007 Jun;192(2):335-41. Epub 2006 Sep 12.

>

> Ethanol beverages containing polyphenols decrease nuclear factor

kappa-B

> activation in mononuclear cells and circulating MCP-1

concentrations in

> healthy volunteers during a fat-enriched diet.

>

> Blanco-Colio LM..

>

> AIMS: Different epidemiological studies have demonstrated that some

> ethanol containing beverages intake could be associated with a

reduction

> of cardiovascular mortality, effect attributed in part to its

> antioxidant properties. Nuclear factor-kappa B (NF-kappaB) is a

redox

> sensitive transcription factor implicated in the pathogenesis of

> atherosclerosis. We have examined the effect of four different

ethanol

> containing beverages on the activation of NF-kappaB in peripheral

blood

> mononuclear cells (PBMC) and circulating concentrations of monocyte

> chemoattractant protein-1 (MCP-1) in healthy volunteers receiving a

> fat-enriched diet. METHODS AND RESULTS: Sixteen volunteers received

16

> g/m(2) of ethanol in form of red wine, spirits (vodka, rum, and

brandy)

> or no ethanol intake along with a fat-enriched diet during 5 days

and

> all of them took all alcohols at different periods. NF-kappaB

activation

> (electrophoretic mobility shift assay) and circulating MCP-1 levels

> (ELISA) were examined in blood samples taken before and after 5

days of

> ethanol intake. Subjects receiving a fat-enriched diet had increased

> NF-kappaB activation in PBMC at day 5. Furthermore, MCP-1 levels

were

> increased in plasma at day 5. Red wine intake and some ethanol

beverages

> containing polyphenols (brandy and rum) prevented NF-kappaB

activation

> and decreased MCP-1 release. CONCLUSION: Consumption of moderate

amounts

> of alcoholic drinks containing polyphenols decreases NF-kappaB

> activation in PBMCs and MCP-1 plasma levels during a fat-enriched

diet.

> Our results provide additional evidence of the anti-inflammatory

effects

> of some ethanol containing beverages, further supporting the idea

that

> its moderate consumption may help to reduce overall cardiovascular

> mortality.

>

> Publication Types: * Research Support, Non-U.S. Gov't

> PMID: 16970955 [PubMed - indexed for MEDLINE]

>

> 2: Alcohol Clin Exp Res. 2005 Jul;29(7):1198-205.

>

> Effects of systemic and local CXC chemokine administration on the

> ethanol-induced suppression of pulmonary neutrophil recruitment.

>

> Quinton LJ, S, Zhang P, Happel KI, Gamble L, Bagby GJ.

> Department of Physiology, Louisiana State University Health Sciences

> Center, New Orleans, Louisiana 70112, USA.

>

> BACKGROUND: Acute alcohol intoxication impairs the neutrophil

> response to intrapulmonary infection, resulting in impaired host

defense

> and increased patient morbidity and mortality. We recently showed

that

> intratracheal (IT) chemokine administration promotes pulmonary

> neutrophil migration in rats and that this process is enhanced by

> systemic administration of the Glu-Leu-Arg (ELR+) and CXC chemokine

> cytokine-induced neutrophil chemoattractant (CINC). Here we

hypothesized

> that exogenous chemokine administration would mitigate the

suppressive

> effect of alcohol on neutrophil recruitment into the lung. METHODS:

> Macrophage inflammatory protein-2 (MIP-2), a rat ELR+ CXC

chemokine, or

> live Klebsiella pneumoniae (K. pneumoniae) was administered it to

induce

> alveolar neutrophil migration in the absence or presence of acute

> ethanol intoxication. Depending on the experimental protocol, rats

> received either intravenous (IV) CINC or IT chemokines (CINC and

MIP-2)

> 20 min after it MIP-2 or K. pneumoniae. Rats were euthanized 90 min

or

> four hr after the first IT injection for sample collection. RESULTS:

> Neutrophil counts were significantly elevated in bronchoalveolar

lavage

> fluid (BALF) of rats receiving IT MIP-2 compared with vehicle-

treated

> rats, and this response was significantly decreased in animals

> pretreated with ethanol. CINC IV enhanced the neutrophil response

to IT

> MIP-2 in both the absence and presence of acute ethanol

intoxication. In

> rats challenged with K. pneumoniae, ethanol pretreatment

significantly

> reduced BALF levels of CINC and MIP-2, suppressed alveolar

neutrophil

> recruitment, and decreased whole-lung myeloperoxidase activity.

CINC IV

> did not alter BALF neutrophil counts in the absence or presence of

> ethanol administration 4 hr after IT K. pneumoniae. Alternatively,

IT

> chemokine instillation partially restored BALF neutrophil

recruitment

> but not whole-lung myeloperoxidase activity in ethanol-treated rats.

> CONCLUSIONS: Ethanol significantly inhibits the pulmonary

inflammatory

> responses to both MIP-2 and K. pneumoniae. Exogenous chemokine

> administration may be a useful means to enhance host defenses in the

> ethanol-intoxicated host, although the results of this study also

> indicate that ethanol intoxication can impair neutrophil

recruitment,

> independent of its effects on local chemotactic gradients.

>

> Publication Types: PMID: 16046875 [PubMed - indexed for MEDLINE]

>

> 3: Am J Physiol Heart Circ Physiol. 2005 Oct;289(4):H1669-75. Epub

2005

> May 20.

>

> Ethanol inhibits monocyte chemotactic protein-1 expression in

> interleukin-1{beta}-activated human endothelial cells.

>

> Cullen JP, Sayeed S, Jin Y, Theodorakis NG, Sitzmann JV, Cahill PA,

> Redmond EM. Department of Surgery, University of Rochester Medical

> Center, Rochester, New York 14642, USA.

>

> The aim of this study was to determine the effect of ethanol (EtOH)

> on endothelial monocyte chemotactic protein-1 (MCP-1) expression.

> IL-1beta increased the production of MCP-1 by human umbilical vein

> endothelial cells from undetectable levels to approximately 900

pg/ml at

> 24 h. EtOH dose-dependently inhibited IL-1beta-stimulated MCP-1

> secretion as determined by ELISA: 25 +/- 1%, 35 +/- 7%, and 65 +/-

5%

> inhibition for 1, 10, and 100 mM EtOH, respectively, concomitant

with

> inhibition of monocyte adhesion to activated endothelial cells.

> Similarly, EtOH dose-dependently inhibited IL-1beta-stimulated MCP-1

> mRNA expression. Experiments with actinomycin D demonstrated that

EtOH

> decreased the stability of MCP-1 mRNA. In addition, EtOH

significantly

> reduced NF-kappaB and AP-1 binding activity induced by IL-1beta and

> inhibited MCP-1 gene transcription. Binding of (125)I-labeled MCP-1

to

> its receptor (CCR2) on THP-1 human monocytic cells was not affected

by

> EtOH treatment. Modulation of the expression of MCP-1 represents a

> mechanism whereby EtOH could inhibit atherogenesis by blocking the

> crucial early step of monocyte adhesion and subsequent recruitment

to

> the subendothelial space. These actions of EtOH may underlie, in

part,

> its cardiovascular protective effects in vivo.

>

> Publication Types:

> PMID: 15908470 [PubMed - indexed for MEDLINE]

>

> 4: J Immunol. 2004 Nov 15;173(10):6376-83.

>

> Ethanol blocks leukocyte recruitment and endothelial cell

activation in

> vivo and in vitro.

>

> Saeed RW, Varma S, Peng T, Tracey KJ, Sherry B, Metz CN.

> Laboratories of Medical Biochemistry, North Shore-Long Island Jewish

> Research Institute, 350 Community Drive, Manhasset, NY 11030, USA.

>

> Immune system impairment and increased susceptibility to infection

> among alcohol abusers is a significant but not well-understood

problem.

> We hypothesized that acute ethanol administration would inhibit

> leukocyte recruitment and endothelial cell activation during

> inflammation and infection. Using LPS and carrageenan air pouch

models

> in mice, we found that physiological concentrations of ethanol (1-5

> g/kg) significantly blocked leukocyte recruitment (50-90%). Because

> endothelial cell activation and immune cell-endothelial cell

> interactions are critical regulators of leukocyte recruitment, we

> analyzed the effect of acute ethanol exposure on endothelial cell

> activation in vivo using the localized Shwartzman reaction model. In

> this model, ethanol markedly suppressed leukocyte accumulation and

> endothelial cell adhesion molecule expression in a dose-dependent

> manner. Finally, we examined the direct effects of ethanol on

> endothelial cell activation and leukocyte-endothelial cell

interactions

> in vitro. Ethanol, at concentrations within the range found in human

> blood after acute exposure and below the levels that induce

cytotoxicity

> (0.1-0.5%), did not induce endothelial cell activation, but

> significantly inhibited TNF-mediated endothelial cell activation, as

> measured by adhesion molecule (E-selectin, ICAM-1, VCAM-1)

expression

> and chemokine (IL-8, MCP-1, RANTES) production and leukocyte

adhesion in

> vitro. Studies exploring the potential mechanism by which ethanol

> suppresses endothelial cell activation revealed that ethanol blocked

> NF-kappaB nuclear entry in an IkappaBalpha-dependent manner. These

> findings support the hypothesis that acute ethanol overexposure may

> increase the risk of infection and inhibit the host inflammatory

> response, in part, by blocking endothelial cell activation and

> subsequent immune cell-endothelial cell interactions required for

> efficient immune cell recruitment.

>

> Publication Types: * Research Support, Non-U.S. Gov't

> * Research Support, U.S. Gov't, P.H.S.

> PMID: 15528377 [PubMed - indexed for MEDLINE]

>

> 5: J Immunol. 2004 Aug 15;173(4):2715-24.

>

> Suppression of innate immunity by acute ethanol administration: a

global

> perspective and a new mechanism beginning with inhibition of

signaling

> through TLR3.

>

> Pruett SB, Schwab C, Zheng Q, Fan R. Department of Cellular

> Biology and Anatomy, Louisiana State University Health Sciences

Center,

> Shreveport, LA 71130, USA. spruet@

> <../../../../../Autism-Immune/post?postID=9WFTsImPguepQk7vUh-

tlQEpL4hNuO\

> fWD74gdTCFYTIxPEdz7jJnZOuyY1aBYvFL6I5Wa7juVthG>

>

> Excessive consumption of ethanol (EtOH) suppresses innate immunity,

> but the mechanisms have not been fully delineated. The present

study was

> conducted to determine whether EtOH suppresses TLR signaling in

vivo in

> mice and to characterize the downstream effects of such suppression.

> Degradation of IL-1R-associated kinase 1 induced by a TLR3 ligand in

> peritoneal cells ( approximately 90% macrophages) was suppressed by

> EtOH. Phosphorylation of p38 kinase in peritoneal macrophages (F4/80

(+))

> was suppressed, as was nuclear translocation of p-c-Jun and p65 in

> peritoneal cells. EtOH decreased IL-6 and IL-12 (p40), but did not

> significantly affect IL-10 in peritoneal lavage fluid or in lysates

of

> peritoneal cells. Changes in cytokine mRNAs (by RNase protection

assay)

> in macrophages isolated by cell sorting or using Ficoll were

generally

> consistent with changes in protein levels in cell lysates and

peritoneal

> lavage fluid. Thus, suppression of TLR signaling and cytokine mRNA

> occurred in the same cells, and this suppression generally

corresponded

> to changes in i.p. and intracellular cytokine concentrations. DNA

> microarray analysis revealed the suppression of an IFN-related

> amplification loop in peritoneal macrophages, associated with

decreased

> expression of numerous innate immune effector genes (including

cytokines

> and a chemokine also suppressed at the protein level). These results

> indicate that EtOH suppresses innate immunity at least in part by

> suppressing TLR3 signaling, suppressing an IFN-related amplification

> loop, and suppressing the induction of a wide range of innate

effector

> molecules in addition to proinflammatory cytokines and chemokines.

>

> Publication Types: * Research Support, U.S. Gov't, P.H.S.

> PMID: 15294990 [PubMed - indexed for MEDLINE]

>

> 6: Atherosclerosis. 2004 Jul;175(1):117-23.

>

> Different effects of red wine and gin consumption on inflammatory

> biomarkers of atherosclerosis: a prospective randomized crossover

trial.

> Effects of wine on inflammatory markers.

>

> Estruch R, Sacanella E, Badia E, Antúnez E, Nicolás JM,

> Fernández-Solá J, Rotilio D, de Gaetano G, Rubin E,

> Urbano-Márquez A. Department of Internal Medicine, Hospital

> Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer

> (IDIBAPS), University of Barcelona, Barcelona, Spain.

>

> BACKGROUND: No intervention studies have explored the

> anti-inflammatory effects of different alcoholic beverages on

markers of

> atherosclerosis. We embarked on a randomized, crossover, single-

blinded

> trial to evaluate the effects of wine and gin on inflammatory

biomarkers

> of atherosclerosis. METHODS AND RESULTS: Forty healthy men (mean

age,

> 37.6 years) consumed 30 g ethanol per day as either wine or gin for

28

> days. Before and after each intervention, we measured the

expression of

> lymphocyte function-associated antigen 1 (LFA-1), Mac-1, very late

> activation antigen 4 (VLA-4), and monocyte chemoattractant protein

> (MCP-1) in monocytes, as well as the soluble vascular cell adhesion

> molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1),

> interleukin-1alpha (IL-1alpha), C-reactive protein (hs-CRP) and

> fibrinogen. After either gin or wine consumption, plasma fibrinogen

> decreased by 5 and 9%, respectively, and cytokine IL-1alpha by 23

and

> 21%. The expression of LFA-1 (-27%), Mac-1 (-27%), VLA-4 (-32%) and

> MCP-1 (-46%) decreased significantly after wine, but not after gin.

Wine

> reduced the serum concentrations of hs-CRP (-21%), VCAM-1 (-17%) and

> ICAM-1 (-9%). CONCLUSIONS: Both wine and gin showed anti-

inflammatory

> effects by reducing plasma fibrinogen and IL-1alpha levels. However,

> wine had the additional effect of decreasing hs-CRP, as well as

monocyte

> and endothelial adhesion molecules.

>

> Publication Types:

> PMID: 15186955 [PubMed - indexed for MEDLINE]

>

> 7: Scand J Gastroenterol. 2004 Mar;39(3):277-82.

>

> Alcohol modulates circulating levels of interleukin-6 and monocyte

> chemoattractant protein-1 in chronic pancreatitis.

>

> Pedersen N, Larsen S, Seidelin JB, Nielsen OH Dept. of Medicine

> M, Division of Gastroenterology, Glostrup Hospital, University of

> Copenhagen, Denmark.

>

> BACKGROUND: Cytokines are markers of acute pancreatic inflammation

> and essential for distant organ injury, but they also stimulate

> pancreatic fibrogenesis and are thus involved in the progression

from

> acute pancreatitis to chronic pancreatic injury and fibrosis. The

aim of

> this study was to evaluate the circulating levels of IL-6, MCP-1,

> TGF-beta1, IGF-1 and IGFBP-3 in patients with alcoholic chronic

> pancreatitis (CP). METHODS: Twelve male patients with severe CP and

11

> matched controls ingested 40 g alcohol. Plasma cytokine

concentrations

> were measured for 24 h and assessed by sandwich ELISA techniques.

> RESULTS: IL-6 was higher in CP at fasting and 1, 4 and 24 h after

> alcohol intake (P < 0.04), and a significantly greater rise was

found at

> 1 h compared to pre-stimulatory conditions and controls (P < 0.01).

> MCP-1 plasma levels in CP were significantly decreased at I h (P <

0.01)

> and 4 h (P < 0.001) compared to pre-stimulatory levels and

controls, and

> a variance analysis showed significantly (P < 0.001) lower

> post-stimulatory levels at 1 h and 4 h both in CP and in controls.

> Alcohol consumption (40 g), however, did not influence plasma

levels of

> TGF-1beta, IGF-I or IGFBP-3 in either of the two groups at the time

> frame applied. CONCLUSIONS: Acute alcohol intake induces a rise in

the

> plasma levels of IL-6 in CP as compared to controls. The low

circulating

> concentrations of MCP-1 1 and 4 h following alcohol consumption

might

> possibly reflect that this mediator acts locally via autocrine

> mechanisms.

>

> Publication Types: * Research Support, Non-U.S. Gov't

> PMID: 15074399 [PubMed - indexed for MEDLINE]

>

> 8: Alcohol Clin Exp Res. 2003 Nov;27(11):1838-45.

>

> Alcohol-induced suppression of lung chemokine production and the

host

> defense response to Streptococcus pneumoniae.

>

> Boé DM, S, Zhang P, Quinton L, Bagby GJ. Department of

> Physiology, Alcohol Research Center, Louisianna State University

Health

> Sciences Center, New Orleans 70112, USA.

>

> BACKGROUND: Acute alcohol intoxication impairs neutrophil migration

> in response to intrapulmonary infection with Streptococcus

pneumoniae,

> the most common bacterial cause of pneumonia. Many of the same host

> defense functions that are impaired in the alcohol-intoxicated host

are

> mechanistically associated with chemokines, a group of

proinflammatory

> molecules that enhance neutrophil adhesion and direct neutrophil

> migration to sites of inflammation. The purpose of this study was to

> determine whether alcohol-induced chemokine suppression is

responsible

> for impaired neutrophil recruitment into the lung during infection

of

> the alcohol-intoxicated host. METHODS: S. pneumoniae was

administered

> (107 colony-forming units) intratracheally 30 min after

intraperitoneal

> injection of 20% alcohol (5.5 g/kg) or saline. Four hours after

> bacterial challenge, bronchoalveolar lavage fluid (BALF) was

collected,

> and the ability of BALF to induce neutrophil chemotaxis and adhesion

> molecule expression was measured by using chemotactic and flow

> cytometric assays. In another experiment, intratracheal challenge

was

> performed by using recombinant macrophage inflammatory protein-2

> (MIP-2), and BALF neutrophils were measured. RESULTS: BALF MIP-2 and

> cytokine-induced neutrophil chemoattractant were decreased by

alcohol,

> and BALF from alcohol-intoxicated animals had decreased chemotactic

> activity for neutrophils, as well as a decreased ability to up-

regulate

> neutrophil adhesion molecule expression, compared with controls.

This

> decreased chemotactic activity was significantly increased in the

> alcohol group by repletion of chemokines to control levels. Alcohol

also

> suppressed neutrophil recruitment after intrapulmonary challenge

with

> MIP-2, suggesting that mechanisms other than chemokine suppression

> contribute to the alcohol-induced effect. CONCLUSIONS: At least two

> mechanisms, suppressed chemokine production and impaired neutrophil

> adhesion molecule expression, likely work in concert in the

> alcohol-intoxicated host to impair neutrophil adhesion and migration

> into the lung during pneumococcal infection. These alterations in

> neutrophil function likely increase the susceptibility of

> alcohol-consuming hosts to pneumonia.

>

> Publication Types: * Comparative Stu* Research Support, U.S.

> Gov't, P.H.S. PMID: 14634502 [PubMed - indexed for MEDLINE]

>

> 9: J Infect Dis. 2001 Nov 1;184(9):1134-42. Epub 2001 Sep 20.

>

> Acute ethanol intoxication suppresses lung chemokine production

> following infection with Streptococcus pneumoniae.

>

> Boé DM, S, Zhang P, Bagby GJ.

>

> Department of Physiology, Section of Pulmonary and Critical Care

> Medicine, Louisiana State University Health Sciences Center, New

> Orleans, LA 70112, USA.

>

> Alcohol intoxication impairs neutrophil function and increases host

> susceptibility to Streptococcus pneumoniae. In a rat model of

pneumonia,

> the effects of acute intoxication were monitored for lung chemokine

> responses, neutrophil recruitment, and bactericidal activity.

Alcohol

> delayed lung neutrophil recruitment, increased bacterial burden, and

> decreased survival. Before neutrophil recruitment, bronchoalveolar

> lavage (BAL) macrophage inflammatory protein-2 (MIP-2) and

> cytokine-induced neutrophil chemoattractant (CINC) were decreased by

> alcohol. This alcohol-induced effect was reversed at 6 h, when there

> were large numbers of neutrophils in control BAL fluid, compared

with

> the alcohol-treated group. Cyclophosphamide-induced neutropenia

> decreased neutrophil recruitment, minimizing the effects of

recruited

> neutrophils on chemokine levels, and extended the alcohol-induced

> chemokine suppression. MIP-2 and CINC mRNA contents also were

suppressed

> by alcohol 4 and 6 h after infection. Thus, alcohol suppresses lung

> chemokine activity in response to S. pneumoniae, which is associated

> with delayed neutrophil delivery, elevated bacterial burden, and

> increased mortality.

>

> Publication Types: * Research Support, U.S. Gov't, P.H.S.

> PMID: 11598836 [PubMed - indexed for MEDLINE]

>

January 17, 2008

My adult ASD child doesn't drink much, but I'll

have to pay more attention when he does.

--- jenniferreif1 wrote:

> Thanks for posting this. Although my son is

> only 5, he has always

> craved alcoholic beverages from early on. If my

> husband leaves a beer

> out on the table, our son is always trying to

> drink out of the glass.

> Of course, we take the beer immediately away

> from him, but now I am

> wondering if I should let him have a sip or

> two.

>

> >

> > forwarding this from another list - are there

> any people on this

> list

> > with adult ASD kids? I was wondering if any

> tended to drank wine (or

> > other alcohol), and if noticed any changes in

> 'autism'?

> >

> > ....I was very intrigued by something posted

> on another

> > board. In this link a woman is saying her

> child (adult Aspie) seems

> more

> > typical after

> > drinking alcohol and that he doesn't seem

> drunk at all. If this was

> > across the board with all ASD kids/adults or

> even very common it

> might

> > point to something in that is worth looking

> into.

> >

> > Indeed one comment left on board confirmed

> the effects in another

> ASD

> > individual.

> http://youtube.com/watch?v=MWXLiTcq4y0

> > <http://youtube.com/watch?v=MWXLiTcq4y0>

> >

> > I have had a quick look through literature

> and it turns up alcohol,

> esp.

> > some types of drinks, decrease inflammatory

> responses. Sometimes

> > dramatically. It is well know that chronic

> long-term

> > consumption/intoxification messes up the

> immune system…

> >

> > I have copied some most interesting abstracts

> here, wonder if anyone

> > would have any thoughts on this, or maybe

> some other mechanisms that

> > could be at work…

> >

> > Natasa

> >

> > Atherosclerosis. 2007 Jun;192(2):335-41. Epub

> 2006 Sep 12.

> >

> > Ethanol beverages containing polyphenols

> decrease nuclear factor

> kappa-B

> > activation in mononuclear cells and

> circulating MCP-1

> concentrations in

> > healthy volunteers during a fat-enriched

> diet.

> >

> > Blanco-Colio LM..

> >

> > AIMS: Different epidemiological studies have

> demonstrated that some

> > ethanol containing beverages intake could be

> associated with a

> reduction

> > of cardiovascular mortality, effect

> attributed in part to its

> > antioxidant properties. Nuclear factor-kappa

> B (NF-kappaB) is a

> redox

> > sensitive transcription factor implicated in

> the pathogenesis of

> > atherosclerosis. We have examined the effect

> of four different

> ethanol

> > containing beverages on the activation of

> NF-kappaB in peripheral

> blood

> > mononuclear cells (PBMC) and circulating

> concentrations of monocyte

> > chemoattractant protein-1 (MCP-1) in healthy

> volunteers receiving a

> > fat-enriched diet. METHODS AND RESULTS:

> Sixteen volunteers received

> 16

> > g/m(2) of ethanol in form of red wine,

> spirits (vodka, rum, and

> brandy)

> > or no ethanol intake along with a

> fat-enriched diet during 5 days

> and

> > all of them took all alcohols at different

> periods. NF-kappaB

> activation

> > (electrophoretic mobility shift assay) and

> circulating MCP-1 levels

> > (ELISA) were examined in blood samples taken

> before and after 5

> days of

> > ethanol intake. Subjects receiving a

> fat-enriched diet had increased

> > NF-kappaB activation in PBMC at day 5.

> Furthermore, MCP-1 levels

> were

> > increased in plasma at day 5. Red wine intake

> and some ethanol

> beverages

> > containing polyphenols (brandy and rum)

> prevented NF-kappaB

> activation

> > and decreased MCP-1 release. CONCLUSION:

> Consumption of moderate

> amounts

> > of alcoholic drinks containing polyphenols

> decreases NF-kappaB

> > activation in PBMCs and MCP-1 plasma levels

> during a fat-enriched

> diet.

> > Our results provide additional evidence of

> the anti-inflammatory

> effects

> > of some ethanol containing beverages, further

> supporting the idea

> that

> > its moderate consumption may help to reduce

> overall cardiovascular

> > mortality.

> >

> > Publication Types: * Research Support,

> Non-U.S. Gov't

> > PMID: 16970955 [PubMed - indexed for MEDLINE]

> >

> > 2: Alcohol Clin Exp Res. 2005

> Jul;29(7):1198-205.

> >

> > Effects of systemic and local CXC chemokine

> administration on the

> > ethanol-induced suppression of pulmonary

> neutrophil recruitment.

> >

> > Quinton LJ, S, Zhang P, Happel KI,

> Gamble L, Bagby GJ.

> > Department of Physiology, Louisiana State

> University Health Sciences

> > Center, New Orleans, Louisiana 70112, USA.

> >

> > BACKGROUND: Acute alcohol intoxication

> impairs the neutrophil

> > response to intrapulmonary infection,

> resulting in impaired host

> defense

> > and increased patient morbidity and

> mortality. We recently showed

> that

> > intratracheal (IT) chemokine administration

> promotes pulmonary

> > neutrophil migration in rats and that this

> process is enhanced by

> > systemic administration of the Glu-Leu-Arg

> (ELR+) and CXC chemokine

> > cytokine-induced neutrophil chemoattractant

> (CINC). Here we

> hypothesized

> > that exogenous chemokine administration would

> mitigate the

> suppressive

> > effect of alcohol on neutrophil recruitment

> into the lung. METHODS:

> > Macrophage inflammatory protein-2 (MIP-2), a

> rat ELR+ CXC

> chemokine, or

> > live Klebsiella pneumoniae (K. pneumoniae)

> was administered it to

> induce

> > alveolar neutrophil migration in the absence

> or presence of acute

> > ethanol intoxication. Depending on the

> experimental protocol, rats

> > received either intravenous (IV) CINC or IT

> chemokines (CINC and

> MIP-2)

> > 20 min after it MIP-2 or K. pneumoniae. Rats

> were euthanized 90 min

>

=== message truncated ===

________________________________________________________________________________\

____

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January 17, 2008

remember on Stan's 1 hour long conference video, he had a different

reading on the mom's fillings(amalgams) than the other mom's. And they

were regular drinkers, Alcohol might subdue bacteria for a while, or

help with that particular person's brain chemistry, Anyways,

bacteria=Autistic behaviors because PROPIONIC acid = autistic

behaviors, and propionic acid is a bacteria bi product or excrement,

so before everyone rushes to the store to give kids alcohol, remember,

there are many ways to subdue bacteria, good bacteria(probiotic),

prescription grade antibacterials etc..

>

> forwarding this from another list - are there any people on this list

> with adult ASD kids? I was wondering if any tended to drank wine (or

> other alcohol), and if noticed any changes in 'autism'?

>

> ....I was very intrigued by something posted on another

> board. In this link a woman is saying her child (adult Aspie) seems more

> typical after

> drinking alcohol and that he doesn't seem drunk at all. If this was

> across the board with all ASD kids/adults or even very common it might

> point to something in that is worth looking into.

>

> Indeed one comment left on board confirmed the effects in another ASD

> individual. http://youtube.com/watch?v=MWXLiTcq4y0

> <http://youtube.com/watch?v=MWXLiTcq4y0>

>

> I have had a quick look through literature and it turns up alcohol, esp.

> some types of drinks, decrease inflammatory responses. Sometimes

> dramatically. It is well know that chronic long-term

> consumption/intoxification messes up the immune system…

>

> I have copied some most interesting abstracts here, wonder if anyone

> would have any thoughts on this, or maybe some other mechanisms that

> could be at work…

>

> Natasa

>

> Atherosclerosis. 2007 Jun;192(2):335-41. Epub 2006 Sep 12.

>

> Ethanol beverages containing polyphenols decrease nuclear factor kappa-B

> activation in mononuclear cells and circulating MCP-1 concentrations in

> healthy volunteers during a fat-enriched diet.

>

> Blanco-Colio LM..

>

> AIMS: Different epidemiological studies have demonstrated that some

> ethanol containing beverages intake could be associated with a reduction

> of cardiovascular mortality, effect attributed in part to its

> antioxidant properties. Nuclear factor-kappa B (NF-kappaB) is a redox

> sensitive transcription factor implicated in the pathogenesis of

> atherosclerosis. We have examined the effect of four different ethanol

> containing beverages on the activation of NF-kappaB in peripheral blood

> mononuclear cells (PBMC) and circulating concentrations of monocyte

> chemoattractant protein-1 (MCP-1) in healthy volunteers receiving a

> fat-enriched diet. METHODS AND RESULTS: Sixteen volunteers received 16

> g/m(2) of ethanol in form of red wine, spirits (vodka, rum, and brandy)

> or no ethanol intake along with a fat-enriched diet during 5 days and

> all of them took all alcohols at different periods. NF-kappaB activation

> (electrophoretic mobility shift assay) and circulating MCP-1 levels

> (ELISA) were examined in blood samples taken before and after 5 days of

> ethanol intake. Subjects receiving a fat-enriched diet had increased

> NF-kappaB activation in PBMC at day 5. Furthermore, MCP-1 levels were

> increased in plasma at day 5. Red wine intake and some ethanol beverages

> containing polyphenols (brandy and rum) prevented NF-kappaB activation

> and decreased MCP-1 release. CONCLUSION: Consumption of moderate amounts

> of alcoholic drinks containing polyphenols decreases NF-kappaB

> activation in PBMCs and MCP-1 plasma levels during a fat-enriched diet.

> Our results provide additional evidence of the anti-inflammatory effects

> of some ethanol containing beverages, further supporting the idea that

> its moderate consumption may help to reduce overall cardiovascular

> mortality.

>

> Publication Types: * Research Support, Non-U.S. Gov't

> PMID: 16970955 [PubMed - indexed for MEDLINE]

>

> 2: Alcohol Clin Exp Res. 2005 Jul;29(7):1198-205.

>

> Effects of systemic and local CXC chemokine administration on the

> ethanol-induced suppression of pulmonary neutrophil recruitment.

>

> Quinton LJ, S, Zhang P, Happel KI, Gamble L, Bagby GJ.

> Department of Physiology, Louisiana State University Health Sciences

> Center, New Orleans, Louisiana 70112, USA.

>

> BACKGROUND: Acute alcohol intoxication impairs the neutrophil

> response to intrapulmonary infection, resulting in impaired host defense

> and increased patient morbidity and mortality. We recently showed that

> intratracheal (IT) chemokine administration promotes pulmonary

> neutrophil migration in rats and that this process is enhanced by

> systemic administration of the Glu-Leu-Arg (ELR+) and CXC chemokine

> cytokine-induced neutrophil chemoattractant (CINC). Here we hypothesized

> that exogenous chemokine administration would mitigate the suppressive

> effect of alcohol on neutrophil recruitment into the lung. METHODS:

> Macrophage inflammatory protein-2 (MIP-2), a rat ELR+ CXC chemokine, or

> live Klebsiella pneumoniae (K. pneumoniae) was administered it to induce

> alveolar neutrophil migration in the absence or presence of acute

> ethanol intoxication. Depending on the experimental protocol, rats

> received either intravenous (IV) CINC or IT chemokines (CINC and MIP-2)

> 20 min after it MIP-2 or K. pneumoniae. Rats were euthanized 90 min or

> four hr after the first IT injection for sample collection. RESULTS:

> Neutrophil counts were significantly elevated in bronchoalveolar lavage

> fluid (BALF) of rats receiving IT MIP-2 compared with vehicle-treated

> rats, and this response was significantly decreased in animals

> pretreated with ethanol. CINC IV enhanced the neutrophil response to IT

> MIP-2 in both the absence and presence of acute ethanol intoxication. In

> rats challenged with K. pneumoniae, ethanol pretreatment significantly

> reduced BALF levels of CINC and MIP-2, suppressed alveolar neutrophil

> recruitment, and decreased whole-lung myeloperoxidase activity. CINC IV

> did not alter BALF neutrophil counts in the absence or presence of

> ethanol administration 4 hr after IT K. pneumoniae. Alternatively, IT

> chemokine instillation partially restored BALF neutrophil recruitment

> but not whole-lung myeloperoxidase activity in ethanol-treated rats.

> CONCLUSIONS: Ethanol significantly inhibits the pulmonary inflammatory

> responses to both MIP-2 and K. pneumoniae. Exogenous chemokine

> administration may be a useful means to enhance host defenses in the

> ethanol-intoxicated host, although the results of this study also

> indicate that ethanol intoxication can impair neutrophil recruitment,

> independent of its effects on local chemotactic gradients.

>

> Publication Types: PMID: 16046875 [PubMed - indexed for MEDLINE]

>

> 3: Am J Physiol Heart Circ Physiol. 2005 Oct;289(4):H1669-75. Epub 2005

> May 20.

>

> Ethanol inhibits monocyte chemotactic protein-1 expression in

> interleukin-1{beta}-activated human endothelial cells.

>

> Cullen JP, Sayeed S, Jin Y, Theodorakis NG, Sitzmann JV, Cahill PA,

> Redmond EM. Department of Surgery, University of Rochester Medical

> Center, Rochester, New York 14642, USA.

>

> The aim of this study was to determine the effect of ethanol (EtOH)

> on endothelial monocyte chemotactic protein-1 (MCP-1) expression.

> IL-1beta increased the production of MCP-1 by human umbilical vein

> endothelial cells from undetectable levels to approximately 900 pg/ml at

> 24 h. EtOH dose-dependently inhibited IL-1beta-stimulated MCP-1

> secretion as determined by ELISA: 25 +/- 1%, 35 +/- 7%, and 65 +/- 5%

> inhibition for 1, 10, and 100 mM EtOH, respectively, concomitant with

> inhibition of monocyte adhesion to activated endothelial cells.

> Similarly, EtOH dose-dependently inhibited IL-1beta-stimulated MCP-1

> mRNA expression. Experiments with actinomycin D demonstrated that EtOH

> decreased the stability of MCP-1 mRNA. In addition, EtOH significantly

> reduced NF-kappaB and AP-1 binding activity induced by IL-1beta and

> inhibited MCP-1 gene transcription. Binding of (125)I-labeled MCP-1 to

> its receptor (CCR2) on THP-1 human monocytic cells was not affected by

> EtOH treatment. Modulation of the expression of MCP-1 represents a

> mechanism whereby EtOH could inhibit atherogenesis by blocking the

> crucial early step of monocyte adhesion and subsequent recruitment to

> the subendothelial space. These actions of EtOH may underlie, in part,

> its cardiovascular protective effects in vivo.

>

> Publication Types:

> PMID: 15908470 [PubMed - indexed for MEDLINE]

>

> 4: J Immunol. 2004 Nov 15;173(10):6376-83.

>

> Ethanol blocks leukocyte recruitment and endothelial cell activation in

> vivo and in vitro.

>

> Saeed RW, Varma S, Peng T, Tracey KJ, Sherry B, Metz CN.

> Laboratories of Medical Biochemistry, North Shore-Long Island Jewish

> Research Institute, 350 Community Drive, Manhasset, NY 11030, USA.

>

> Immune system impairment and increased susceptibility to infection

> among alcohol abusers is a significant but not well-understood problem.

> We hypothesized that acute ethanol administration would inhibit

> leukocyte recruitment and endothelial cell activation during

> inflammation and infection. Using LPS and carrageenan air pouch models