Ricky Williams interview

[forever in debt to mo lewis]

"In my experience, it's impossible to use either Josh Gordon or cocaine without getting "stoned" or its equivalent, whereas you can (and many people do) have a couple drinks and still be sober. I'm not arguing for legally mandated sobriety by any stretch, but this still strikes me as a pretty important distinction between alcohol and the other recreational drugs being discussed."

 

I see your point

 

but I also think its a matter of tolerance and potency...weed and cocaine vary in potency as well

[Skrappy1]

Id think if someone were truely addicted, theyd have a difficult time paying a mortgage and a car note on a car that isnt very cheap.To me an addict is someone who cant carry on a normal daily routine or make money. someone who cant control and urge.

Sounds more like you are trying to classify addiction as a correlation to social status. I wonder, when Dwight Gooden and Darryl Strawberry were in their primes with the Mets, did either of them ever have trouble making their car payments? I would think not.

 

You are the one who is failing to admit that some can use cocaine recreationally.

No, actually for the sake of argument I conceded there may be exceptions, remember?

 

You are saying they are exceptions, absolutely.

See?

 

How can you be so sure that they are just exceptions. Just as easily as someone can drink socially, someone can use coke recreationally.Just as easy as someone can be an alchy..someone can be a cokehead..it works both ways for everything that can be addictive

I can be so sure that they are exceptions from experience in that matter that is probably more so than most. Aren't you paying attention? For what it's worth, I am also now back in school after many years away...I am a justice studies major and have taken courses in drug abuse. I not only have witnessed personally with my own two eyes, I have also seen statistics that justify what I have said. Cocaine is much more physically addictive. There is no question, I am sorry if you feel otherwise, you are simply wrong.

Edited December 21, 2004 by Skrappy1

[forever in debt to mo lewis]

"Sounds more like you are trying to classify addiction as a correlation to social status. I wonder, when Dwight Gooden and Darryl Strawberry were in their primes with the Mets, did either of them ever have trouble making their car payments? I would think not."

 

no I was talking about someone who works 13 hours a day to pay bills..not someone paid millions to play a game...for about 5 hours a day.

 

"No, actually for the sake of argument I conceded there may be exceptions, remember"

 

only for the sake of argument..if you are only saying it for the sake of argument you are missing my point..my point is for every vice..there are recreational users and there are degenerates . and being "stoned" off Josh Gordon or cocaine is varied by amount of consumption,potency, and tolerance just like drinking

[godtomsatan]

I'm totally with Skrappy1 on this. With all due respect Brentastic I can't see how you can possibly compare cocaine with alcohol.  I spent 6 years in college studying the effects of drugs and there is no way you can compare the two.

 

 

I spent 6 years of college, and about 8 years after college, "studying" drugs as well.

 

Alcohol in moderation actually is beneficial to the body. Cocaine in moderation (outside of its anesthetic properties) is deadly. If the same amount of people who drank also did cocaine we wouldn't have enough space to bury them all.  Comparing cocaine to alcohol is like comparing a cobra bite to a bee sting.  It takes a lot of one to kill but it only takes a drop of the other and it's over. 

 

 

That's not a very scholarly analysis.

 

Just as people can sit around and have a couple of brewskies during happy hour Friday after work, people can take a quick toot off their housekey in the bathroom once they're ready to go out and hit the town. They might even have a good time.

 

They might not do it until six months later.

 

Just like alcohol (especially WITH alcohol), cocaine can bring on a good time. It's a danger and a problem when your lifestyle and responsibilities are effected. Just like everything else.

 

Also, back to the point of Ricky. I don't see how you can justify this guy's actions at all. He QUIT w/o any notice whatsoever. What would happen if you just gave a week's notice at your job. Would be people be upset? My guess is yes.

 

 

They might be upset, but I'm positive they will get over it. If they don't, ultimately, how is it my problem or responsibility? I have my reasons for quitting that are mine alone.

 

Considering Ricky was in a profession where seasons and careers end every week, his move can never really be completely viewed as a blindside event.

[godtomsatan]

only for the sake of argument..if you are only saying it for the sake of argument you are missing my point..my point is for every vice..there are recreational users and there are degenerates . and being "stoned" off Josh Gordon or cocaine is varied by amount of consumption,potency, and tolerance just like drinking

 

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I don't know if there are a lot of recreational meth heads or heroin users.

 

While I think Josh Gordon and cocaine are different than the above, I just don't think anyone probably ends up casually doing the above stuff.....

[Piles]

That's not a very scholarly analysis.

 

 

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Alcoholism: Clinical & Experimental Research

©2004Research Society on Alcoholism

Volume 28(5) May 2004 pp 786-791

Effect of Dealcoholized Beer (Bitburger Drive®) Consumption on Hemostasis in Humans

[Alcohol Effects on the Fetus, Brain, Liver, and Other Organ Systems]

 

Bassus, S.; Mahnel, R.; Scholz, T.; Wegert, W.; Westrup, D.; Kirchmaier, C. M.

From Deutsche Klinik fuer Diagnostik, Fachbereich Haemostaseologie, Wiesbaden, Germany.

Received for publication September 9, 2003; accepted January 23, 2004.

Supported, in part, by a grant from Bitburger Brauerei Th. Simon GmbH.

Reprint requests: Steffen Bassus, Deutsche Klinik fuer Diagnostik, Fachbereich Haemostaseologie, Aukammalle 33, D-65191 Wiesbaden, Germany; Fax: 0611-577-417; E-mail: bassus.hst@dkd-wiesbaden.de.

 

Abstract

 

Background: The beneficial effect of moderate alcohol consumption in lowering the risk of cardiovascular disease has been shown in several epidemiologic studies. Such studies have also shown, however, that the protective effect of alcoholic beverages like wine and beer is not only due to the ethanol content but also to the presence of nonalcoholic constituents. The positive effect of alcoholic beverages has been attributed to changes in lipoprotein metabolism, but there is substantial evidence that effects on hemostasis play an important role. Whether the effects of alcoholic beverages on hemostasis are due exclusively to ethanol or are due, in part, to nonalcoholic components, is still under debate.

 

Methods: We have examined the hemostatic effects of 3 liters of beer, dealcoholized beer, and ethanol/water (v/v 4%), consumed over a period of 3 hr, in 12 young healthy volunteers. Platelet parameters CD62, PAC-1, and monocyte platelet aggregates were analyzed using flow cytometric measurements. The activity of factor VII was determined with a prothrombin time (PT) assay and plasminogen activator inhibitor activity using a chromogenic substrate. Thrombin generation was determined according to the method of Hemker.

 

Results: All three fluids administered, dealcoholized beer, beer, and ethanol, reduced the expression of activated fibrinogen receptor, the platelet activation marker CD62, and the formation of monocyte-platelet-aggregate. In addition, dealcoholized beer also showed significant inhibitory effects on thrombin generation, whereas beer and ethanol showed procoagulatory effects.

 

Conclusions: This study has shown that the acute consumption of dealcoholized beer inhibits thrombogenic activity in young adults. This action could have a beneficial effect on the development of coronary artery disease. Thus, the consumption of dealcoholized beer could provide cardiovascular benefit without the negative effects of alcohol.

 

AN INVERSE ASSOCIATION between moderate alcohol consumption and vascular risk has been shown in many epidemiologic studies (Castelnuovo et al., 2002). All-cause mortality, as a function of alcohol use, has been depicted as a J-shaped curve, reflecting a lower risk of coronary heart disease (CHD) on consumption of moderate amounts of wine and beer and an increased risk of certain types of cancer when the consumption of these beverages is high (Fagrell et al., 1999). It has been suggested that the effect of alcohol beverages on cardiovascular disorders is not due to alcohol alone but also, at least in part, to other, so-called confounding factors or nonalcoholic components, for example, resveratrol, which is present in red wine (Rimm et al., 1996). Some studies have examined whether alcoholic beverages differ in their ability to protect against CHD and whether some types of beverage might produce stronger cardiovascular protection than others, but data obtained so far are inconclusive (Cleophas, 1999). There are data showing that the benefits are less marked in beer drinkers (relative risk 0.78) than wine drinkers (relative risk 0.68), but a possible pitfall in comparing different studies is that important covariates may not be treated equally across the studies, and this could have a major effect on the conclusions reached (Rimm et al., 2002). For example, after controlling for drinking patterns (frequency of alcohol consumption), diet, and social class, it was found that beer and the particular wine used did not differ in terms of the beneficial effects produced. Indeed, the evidence suggests that, regardless of the type of beverage consumed, the pattern of intake is one of the most important determinants, where the lowest relative risk is seen in those who consume small or moderate amounts of alcohol on at least 3 days a week. (Mukamal et al., 2003).

 

The mechanisms that underlie the protective effects of moderate alcohol consumption on CHD risk are not fully understood. Moderate alcohol consumption affects lipoprotein metabolism via elevating plasma high-density lipoprotein concentrations (Rakic et al., 1998) and mediating an increase in the total antioxidant capacity of plasma (Ghiselli et al., 2000). Furthermore, there is substantial evidence that the effects on hemostasis play a key role in the protective effect of alcohol on cardiovascular risk (Rimm et al., 1999). The consumption of alcoholic beverages is significantly and positively correlated with changes in hemostatic and fibrinolytic parameters, but other factors such as inflammatory processes, which participate in the development of atherosclerosis and CHD, could be also be involved (Ross, 1999). Data published recently on C-reactive protein show that moderate alcohol consumption has anti-inflammatory effects, and this may represent a link between moderate consumption of alcoholic beverages and a lower cardiovascular risk (Albert et al., 2003;Imhof et al., 2001). Moreover, there is a direct relationship between thrombosis and inflammation involving the formation of platelet-monocyte aggregates at sites of vascular lesions (Freedman and Loscalzo, 2002).

 

To our knowledge, none of the studies dealing with the effects of alcoholic beverages on hemostasis and inflammation have examined the relative contribution of alcohol alone and that of the nonalcoholic compounds in beer. The aim of this study therefore, was to determine whether the confounding factors in beer contribute to the antithrombotic and anti-inflammatory effects of this beverage. Several hemostatic parameters have been measured after the acute consumption of beer, dealcoholized beer, and ethanol alone.

 

 

RESULTS

Ethanol Concentration

 

Consumption of alcohol in the form of beer increased the mean ethanol serum levels to 42 mg/100 ml at 1.5 hr and 100 mg/100 ml after 3.5 hr, and corresponding values for ethanol alone were 32 mg/100 ml and 99 mg/100 ml. The subjects showed moderate signs of alcohol intoxication like incoordination, flushing, and changes in speech and behavior.

PAC-1 and CD62 Expression

 

After consumption of 3 liters of dealcoholized beer, the expression of the activated fibrinogen receptor (PAC-1) and the platelet activation marker CD62 was significantly reduced to 90% and 81% of the baseline, respectively. In the case of ethanol, there was a decrease in the expression of both platelet activation markers, but these changes did not reach significance due to the large interindividual variation. Beer had no effect on CD62 and PAC-1 expression, indicating that the effects of ethanol and nonalcoholic components on PAC-1 and CD62 are antagonistic. After 24 hr, the changes in PAC-1-and CD62 expression had returned to baseline in all groups (Figs. 1 and 2). These data indicate that ethanol reduces the inhibitory effects of nonalcoholic compounds.

 

 

After ingestion of dealcoholized beer, there was a slight decrease in FVIIc, whereas ethanol and beer consumption led to a moderate increase with the change at 3.5 hr being statistically significant (Table 1). In the case of all beverages, a relationship between dose and response was seen up to 3.5 hr, after which values returned to baseline after 24 hr. Beer and ethanol appear to have an activating effect on FVIIc, whereas the nonalcoholic components have no effect on FVII coagulant activity.

 

 

Ingestion of 3 liters of dealcoholized beer (3.5 hr) had a low inhibitory effect on PAI-1 activity (Table 2). Consumption of 3 liters of ethanol and beer (3.5 hr) had a stimulating effect on PAI-1 activity, and in the case of ethanol this change was statistically significant. At all other time points there were no or only minor differences compared with baseline. High ethanol concentration led to an enhanced PAI-1 activity and therefore to an inhibition of fibrinolysis. Nonalcoholic components in beer had no effect on PAI-1 activity.

 

All investigated beverages showed statistically significant effects on the ETP in PRP at 1.5 hr and 3.5 hr (Fig. 4). In the case of dealcoholized beer, the 1.5 hr and 3.5 hr values showed a significant reduction in ETP (Fig. 4a). The acute consumption of ethanol-containing beverages caused an activation of coagulation leading to an significantly enhanced ETP (Fig. 4aa and 4c). None of the beverages showed a relationship between dose and response. All beverages exhibited a significant effect after ingestion of 1 liter, and this effect on ETP and the inhibition of thrombin generation appeared to be maximal because an increase in the amount ingested to 2 liters produced no further effect. The change in this parameter with all beverages returned to baseline after 24 hr.

 

Maximum aggregation was measured in terms of percent change in optical density in response to collagen and arachidonic acid. Both activators in the two concentrations used showed no effect on maximum aggregation (data not shown).

 

None of the beverages had a significant effect on hematocrit, prothrombin time, activated partial thromboplastin time, and fibrinogen level (data not shown).

 

DISCUSSION

 

Consumption of alcoholic beverages has a large impact on public health, and negative implications of alcohol use and abuse are important areas of investigation. However, there is substantial evidence that the moderate intake of alcoholic beverages is associated with reduced morbidity and mortality rates in the case of several cardiovascular conditions, particularly CHD (Mukamal et al., 2003;Thun et al., 1997). It is still under debate whether this protective effect is due to alcohol alone or, in part, due to confounding factors. Three major effects are observed after consuming alcoholic beverages: alterations in lipid metabolism, inhibition of hemostasis, and stimulation of fibrinolysis. Our study focused on the acute effects of dealcoholized beer on hemostasis, fibrinolysis, and inflammation.

 

Recently published studies have shown that moderate alcohol consumption has an inhibitory effect on coagulation (Fagrell et al., 1999;Marques-Vidal et al., 2001;Rimm et al., 1999). Moreover, beer consumption causes a decrease in activity of FVII and PAI-1 in patients with CHD (Gorinstein et al., 1997). Both factors are known to be predictive markers for cardiovascular events (Hamstein et al., 1987;Meade et al., 1980). The results of the present study demonstrated that the acute effect of alcoholic beverages promotes coagulation and that the activities of FVII and PAI-1 and the generation of thrombin are enhanced. The apparent inconsistencies between our findings and the previously cited studies regarding coagulation are presumably due to differences in study design: the long-term alcohol ingestion in the case of CHD patients and the acute effects of alcoholic beverages in young healthy volunteers. The findings suggest that the protective effect of ethanol after long-term intake is primarily mediated by alterations in lipid metabolism, antioxidant effects, and platelet inhibition, whereas the anticoagulatory effect is presumably a secondary phenomenon affecting the endothelium. Furthermore, the effect of ethanol alone is probably dependent on the vascular status of the subjects in the study. However, the finding that the consumption of dealcoholized beer causes a significant decrease in thrombin generation is of considerable interest. Nonalcoholic compounds in beer seem to inhibit coagulation, but the mechanisms involved and substances responsible are subjects for speculation. One of the factors associated with CHD is a high level of plasma homocysteine, and it is known that the levels of homocysteine can be lowered by the intake of folate (Boushey et al., 1995). Because epidemiologic studies have shown a link between the consumption of beer and low homocysteine levels (Ubbink et al., 1998), it might be speculated that folate, which is a constituent in beer, is responsible for low homocysteine concentrations. Other ingredients in beer affecting hemostasis are the substances found in hops such as phytoestrogens, daidzein, genistein, 6-prenylnaringenin, and 8-prenylnaringenin (Milligan et al., 1999). These substances are thought to protect against CHD (Knight and Eden, 1996). The benefit that can be gained from the intake of phytoestrogens is difficult to assess. Mandli (1997) has estimated that for a significant estrogenic effect, the amount consumed would have to approach 175 liters of beer a day. It is also known that beer increases antioxidant capacity on human plasma (Ghiselli et al., 2000), and this effect is thought to account for some of the protective effects against CHD. In an animal model, the antioxidant properties of polyphenols in beer appear to be responsible for slowing the development of atherosclerosis (Vinson et al., 2003). Together, the findings in this and other recently published studies suggest that the ingredients in beer have a clinically relevant effect on hemostasis, but the molecular mechanisms are still under debate.

 

Platelet activation results in a change in the shape of the platelets, secretion of granule contents, and platelet aggregation. Secretion of [alpha] granule contents leads to expression of glycoprotein CD62 on the surface of platelets, followed by CD62 interactions with monocyte PSGL1 receptor leading to the formation of MPAs. Furthermore, platelet activation leads to activation of glycoprotein (GP) IIb/IIIa, which is essential for fibrinogen binding and platelet aggregation. Activated GP IIb/IIa is measured with monoclonal antibody PAC-1, which binds exclusively to activated GP IIb/IIIa. Measurements of CD62 and activated GP IIb/IIIa expression as well as the measurement of MPA formation are indirect markers of platelet activation. Moreover, MPA formation stimulates coagulation due to the enhanced expression of TF in both cell types (Zillmann et al., 2001) and recruits the immune system in arterial wall remodeling (Ross, 1999;Sarma et al., 2002). In clinical practice it has been shown that increased CD62 expression, and therefore MPA formation, is associated with acute coronary syndrome (Sarma et al., 2002). It remains unclear, however, whether blocking CD62 improves clinical outcome, but experimental data show beneficial effects in animal models (Phillips et al., 2003). Our data confirm other studies showing that ethanol reduces CD62 expression (Nguyen et al., 1998) and demonstrate that nonalcoholic compounds in beer have an important role in the decrease in CD62 and MPA. The observed reduction in CD62 expression and MPA formation after the ingestion of dealcoholized beer may therefore lead to a decreased plasma hemostasis via reduction in the expression of tissue factor and alleviation of inflammatory response in the arterial wall (Prescott et al., 2001). It is conceivable that because of these changes there is a reduced vascular risk. It is of interest that in high-risk cardiovascular patients, concomitant with the elevation in the expression of CD62, there is an increase in the binding of fibrinogen to the GPIIb/IIIa receptor on activated platelets, and a number of therapeutic strategies are widely used to block this receptor. Ethanol alone is known to reduce GPIIb/IIIa expression in vitro (McKenzie et al., 2002), but in our studies in vivo, only dealcoholized beer produced a significant reduction of approximately 10% in the expression of GPIIb/IIIa, whereas ethanol and beer had no significant effects. However, whether a reduction of 10% in the expression of GPIIb/IIIa inhibits atherosclerosis and decreases the risk of CHD risk in the long term remains unclear. The aggregation results are in agreement with recent reports on the effect of ethanol consumption on platelet aggregation (Zhang et al., 2000). In PRP, the acute intake of alcohol had no significant effect on platelet aggregation after stimulation with collagen and arachidonic acid. In contrast, measurements in whole blood showed significant inhibitory effects with collagen as an agonist. However, the reasons for this observations are unknown, and measurements in whole blood could not be performed in this study because of technical reasons.

 

The results of the present study show antiplatelet effects with all beverages tested, whereas coagulation is inhibited by dealcoholized beer and stimulated by beer and ethanol. The effect of dealcoholized beer on platelets and coagulation might contribute to the known beneficial effects of moderate beer consumption in CHD. The limitations in our study are that only acute effects were measured, whereas protective effects during long-term consumption are more important. In addition, it is not known whether moderate but prolonged intake of dealcoholized beer has similar and longer lasting effects on hemostasis than the acute consumption of relatively large amounts. More studies are required to fully evaluate the effect of the nonalcoholic compounds in beer on the hemostatic system.

 

 

 

 

 

Is this more scholarly????

Edited December 21, 2004 by Piles

[CaptainHook]

I'm guessing that was the longest post ever.

 

I'm also guessing nobody read it all.

[Big John]

I'm guessing that was the longest post ever.

Not by a longshot. skins articles in the Tailgate are a lot longer.

[Piles]

I'm guessing that was the longest post ever.

 

I'm also guessing nobody read it all.

 

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I'm guessing you are right but it proved my point... Just read the abstract and conclusion.....

[Gunther]

Not by a longshot.  skins articles in the Tailgate are a lot longer.

 

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:bigshock:

[Bill Swerski]

I'm guessing that was the longest post ever.

 

I'm also guessing nobody read it all.

 

623155[/snapback]

 

 

 

 

I think it's pretty funny that the Germans are doing research on alcoholism. I'm sure they won't have much difficulty finding volunteers for their studies.

[Piles]

I think it's pretty funny that the Germans are doing research on alcoholism.  I'm sure they won't have much difficulty finding volunteers for their studies. 

 

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Aint that the truth....

[Brentastic]

I'm also guessing nobody read it all.

 

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Got that right!

[Piles]

Got that right!

 

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Here's a brief synopsis just for you Brentastic....

 

 

Conclusions: This study has shown that the acute consumption of dealcoholized beer inhibits thrombogenic activity in young adults. This action could have a beneficial effect on the development of coronary artery disease. Thus, the consumption of dealcoholized beer could provide cardiovascular benefit without the negative effects of alcohol.

 

Consumption of alcoholic beverages has a large impact on public health, and negative implications of alcohol use and abuse are important areas of investigation. However, there is substantial evidence that the moderate intake of alcoholic beverages is associated with reduced morbidity and mortality rates in the case of several cardiovascular conditions, particularly CHD

Edited December 21, 2004 by Piles