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  1. #1
    Bojangles69's Avatar
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    Sorry guys didnt mean to do this to ya..

    I know how much you hate alcohol threads but I really need a quick consensus on something.
    I drink maybe 7 or 8 times a year (+ or -)

    I actually went out Sun night and got drunk (lastnight)
    My question though because this is maybe the 3rd or 4th time this has happened.

    I take high doses vitamin c and pantothenic acid (8 gms C and 4-5 grams B-5)
    They are BOTH acids.
    Ones obviously an anti-oxidant. HOWEVER, i noticed vitamin c has the ability to act as a cataylst in certain potencies, like causing iron to rust in your blood.

    My thing is ANYTIME i drink now when i wake up i dont really get the worst headache but my WHOLE body (joints, back, EVERYTHING) are in IMMENSE pain. I could barely walk today because my joints hurt so bad. I was also shaky and kinda dizzy.
    Thats NOT typical for me.

    And i was wondering, this started happening when I began taking the C & B-5, im starting to think alcohol is reacting with one of them and producing some sort of poison or toxin anytime i drink. So the solutions obvious. ONly drinking on major holidays and just 2 or 3 drinks at the most.

    But the reason i post this here is to see if anyone is taking the same vitamins and has had a similar affect in the past. Im not one to bitch about pain but I've been draggin myself around all day in agony.

    And if you cant answer that question maybe you can tell me wahts good for burns? I just accidentally missed a cup and poured boiling water all over my fingers, when i dropped the pot even more shot up and soaked my hand. Anyone know any home remedies because i wana cry right now. Bo's not having a good day today, guess he gets waht he deserves.

  2. #2
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    i think its called a hangover...jp....but becuase u only drink once in a while ur bodies not used to it...if u do drink just dont take so many pills...i would put some a cold pack on ur burns...

  3. #3
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    Quote Originally Posted by salmon1
    don't drink at all... ever
    hell no u need it once in awhile...goin out and gettin drunk...helps from gettin burnt out..

  4. #4
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    I take about 4grams of vit c daily and now that I think about it I get the shakes the next day but I think that is due to dehydration from the alcohol? I also get a headache but these soon subside when I drink some gatorade or water and have a nice meal.

    I think Johan would no more about this than anyone since he has done extensive vitamin C research, Try pmming him this link so he can answer.

  5. #5
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    Quote Originally Posted by salmon1
    don't drink at all... ever

    Dude the pope even drinks wine.

  6. #6
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    Quote Originally Posted by lucabratzi
    hell no u need it once in awhile...goin out and gettin drunk...helps from gettin burnt out..
    I definately agree with that. Everyone's different I guess.

  7. #7
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    For the burns, run it under cold water and you can get brn cream, as for the joints, were ya workin out a ton before you drank? Maybe the dehydration caused more soreness? Just a guess, I'm no doctor.

  8. #8
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    i drink more frequently than you and eveerytime i do it i have 3g of vitc and 3 b complexes in my pocket which i take out throughout the night(about every hour or so). it helps me alot and i never get the aches you are talking about. it has to be something else. maybe the hangover has compromized your immune system and you are coming down with a cold.

  9. #9
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    I think it is stemming from dehydration! I wake up in the middle of the night fater drinking and my mouth feels like cement is drying in it. I have to drink about a half gallon of water and some gatorade and then I am set.

  10. #10
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    Bo.. would you like me to move this thread to the steroid forum?

    Holla

    As to your question(s)

    Could me a number of factors contributing to the pain.. I have some ideas.. but i'll do some reading and get back to you.

  11. #11
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    Quote Originally Posted by Narkissos
    Bo.. would you like me to move this thread to the steroid forum?

    Holla

    As to your question(s)

    Could me a number of factors contributing to the pain.. I have some ideas.. but i'll do some reading and get back to you.
    If you think it'll get more responses im game.

    Muchos gracias.

  12. #12
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    And about the dehydration, only way i can see dehyration causeing pain is that is prevents toxins from being diluted and they linger longer and are more potent.

    Its very well possible because i do lots of cardio and even though i drink on those days ive only had a couple glasses of water today. BUt for some reason i still think this is beyond dehydration.

    Ive been dehydrated and hungover far worse and never had pain like this. It has to be some type of acid byproduct with the ascorbic acid or pantothenic acid with the alcohol. Whatever it is. It SUCKS.

  13. #13
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    Off the top of my head.. It isn't the Vitamin C causing the prob.

    It is possibly the High dose of Vitamin B-5.. or rather, the lack of an equivalent (or at least supplementary) dose of the additional B-vitamins.

    The B-vitamins are a complex as you know..and while the supplementation of individual substrates can serve to benefit specific conditions.. in the end they work 'better' together.

    They're the 'stress vitamins'.. namely due to the fact that stress states deplete their concentrations.

    Alcohol ingestion and the subsequent metabolism.. and the post-metabolism scavenging of alcohol's metabolites..requires (and depletes) the b-complex.

    The pain you experience could be a high level of free radicals/toxins post-event. It could be due to dehydration..both fluid and mineral depletion from the alcohol.. Vitamin C can have a diuretic effect also. This could compound it. It could be from the systemic depletion of key substrates.

    Heck it could be a lot of things.

    My advise... add a b-complex (200 mg at regular intervals) tru-out the night of drinking..and the following day or two. Add an additional anti-oxidant.. alpha-lipoic acid etc.

    Nark

  14. #14
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    Quote Originally Posted by Bojangles69
    If you think it'll get more responses im game.

    Muchos gracias.
    Np...moved...

    I'm here reading an article that may shed some light.

    I may edit it and post it.

  15. #15
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    Quote Originally Posted by Narkissos
    Off the top of my head.. It isn't the Vitamin C causing the prob.

    It is possibly the High dose of Vitamin B-5.. or rather, the lack of an equivalent (or at least supplementary) dose of the additional B-vitamins.

    The B-vitamins are a complex as you know..and while the supplementation of individual substrates can serve to benefit specific conditions.. in the end they work 'better' together.

    They're the 'stress vitamins'.. namely due to the fact that stress states deplete their concentrations.

    Alcohol ingestion and the subsequent metabolism.. and the post-metabolism scavenging of alcohol's metabolites..requires (and depletes) the b-complex.

    The pain you experience could be a high level of free radicals/toxins post-event. It could be due to dehydration..both fluid and mineral depletion from the alcohol.. Vitamin C can have a diuretic effect also. This could compound it. It could be from the systemic depletion of key substrates.

    Heck it could be a lot of things.

    My advise... add a b-complex (200 mg at regular intervals) tru-out the night of drinking..and the following day or two. Add an additional anti-oxidant.. alpha-lipoic acid etc.

    Nark
    Someone give this m/fker a PHD. Thats some good shit Nark. Ever since I started taking high does of B-5 my skin has been clearer than its ever been.
    I could have done more research however, which is what I'll be doing for the next week or 2.
    Thank you.

  16. #16
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    Living with Alcohol

    Living with Alcohol
    by Steven Wm. Fowkes

    Edited: Narkissos

    Alcohol is everywhere within Western culture. Since the dawn of recorded history, the art of fermenting fruit and grain into wine and beer has been a much-prized skill. As technology advanced, distillation of alcoholic beverages into refined spirits became quite popular. The high alcohol content of refined spirits made them exceptionally stable for long-term storage and commerce.

    Along with fermentation technology came drunkenness, hangovers and alcoholism. Drunkenness is caused by alcohol’s pharmacological effect on the human central nervous system. This effect causes incoordination, slowed reaction time, muscle relaxation, behavioral disinhibition and impaired judgment, all of which last for several hours after alcohol is consumed. There is no simple and effective way to prevent drunkenness other than to avoid alcohol consumption in the first place.

    Hangovers are the result of alcohol’s toxicity. Hangover symptoms include headaches, dehydration, irritability, sleep disturbances, liver toxicity, nerve and tissue hypersensitivity, etc. These symptoms can be prevented or significantly reduced by simple interventions that will be discussed in this article. These interventions augment natural detoxification mechanisms that would otherwise be overwhelmed by the sheer volume of alcohol intake.


    Acetaldehyde Toxicity

    Alcohol’s effects are not limited to those of alcohol alone. Alcohol is metabolized in a multi-step process into various metabolites which have unique biochemical effects of their own. The first step in this process is the conversion of alcohol to acetaldehyde [see Figure A].



    Since acetaldehyde is approximately 30 times more toxic than alcohol, acetaldehyde is a major cause of alcohol-associated side effects. If acetaldehyde is not efficiently converted into acetic acid (the second step in the metabolism of alcohol), severe toxicity can result. This is a common problem among certain people of Asian extraction (notably Innuit and American Indians) who have a genetic weakness in the acetaldehyde dehydrogenase enzyme [see Figure A]. Even in people who do not have this genetic trait, acetaldehyde dehydrogenase is often unable to fully keep up with the production of acetaldehyde during alcohol intoxication.

    Cross-Linking

    One of the most significant mechanisms of alcohol toxicity is the powerful cross-linking activity of acetaldehyde. Cross-linking is a process by which “molecular bridges” are formed between “reactive sites” on different molecules. These cross-links “tie up” the affected molecules and interfere with their normal function. In some circumstances, molecular function can be completely blocked by cross-linking.

    A good example of the effect of cross-linking in action is the “tanning” of leather. The tanning process involves applying large amounts of a cross-linking agent (like tannic acid) to animal hides to cross-link the flexible collagen and elastin proteins in the animal skin to produce tough, inflexible, abrasion-resistant leather. This same process happens — at a slower rate — in people. Cross linking is largely responsible for age-related changes in human skin that make it inflexible, wrinkled and dry. Some of the most leathery skin you will ever see is found on alcoholics who stay outdoors a lot of the time. The ultraviolet (UV) and near-ultraviolet components of sunlight activate the cross-linking process.

    There are many substances that can act as cross-linking agents. Aldehydes are one class of cross-linker, of which acetaldehyde is a member. Acetaldehyde is used in making plastics, adhesives and fabrics. The closely related chemical formaldehyde is used in insulating foams, plywood, particle board and embalming fluid.
    Attached Thumbnails Attached Thumbnails Sorry guys didnt mean to do this to ya..-c45alco.gif  

  17. #17
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    Stewed, Not Pickled

    The primary detoxification mechanism for scavenging unmetabolized acetaldehyde is sulfur-containing antioxidants [see Figure A]. The two most important are cysteine, a conditionally essential amino acid, and glutathione, a cysteine-containing tripeptide (a three-amino-acid polymer) [see Figure B]. Cysteine and glutathione are active against acetaldehyde (and formaldehyde) because they contain a reduced (unoxidized) form of sulfur called a sulfhydryl group, which contains a sulfur atom bonded to a hydrogen atom (abreviated SH).

    Sulfhydryl groups interact with aldehydes to render tham incapable of forming cross links. This “mops up” or scavenges any stray acetaldehyde that is not properly metabolized into acetate (acetic acid) [see Figure A]. Although this is a powerful aldehyde detoxification mechanism, it is easily overwhelmed by the relatively large amounts of alcohol that are typically consumed with alcoholic beverages as compared to the amounts of alcohol and acetaldehyde that are produced through normal metabolism.

    Fortunately, sulfhydryl antioxidants can easily be fortified through dietary supplementation.

    In one experiment with rodents [Sprince et al., 1974], a LD-90 dose of acetaldehyde (the dose that would normally kill 90% of the animals) was completely blocked by pretreatment of the animals with cysteine and vitamins B-1 and C. In other words, none of the cysteine-treated animals succumbed to the lethal dose of acetaldehyde! N-Acetylcysteine (NAC) protected almost as well as cysteine.

    In another rodent experiment [Busnel & Lehman, 1980], alcohol’s ability to inhibit swimming after the alcohol had been completely metabolized was blocked by vitamin C. What this and the previous study suggests is that the pharmacologic and toxic effect of alcohol are different. The pharmacological effect (i.e., intoxication or drunkenness) is not inhibited by vitamin C or cysteine, but the toxic effect (e.g., the hangover, nervous irritability, swimming difficulty) is inhibited. This suggests that, with
    alcohol, you can “have your cake and eat it too.”

    Dosage Suggestions

    Typical doses of cysteine that are sufficient to block a major portion of the toxic effect of alcohol/acetaldehyde are about 200 mg per ounce of alcohol consumed. However, the rapid assimilation and metabolism of alcohol requires both prior and concurrent dosing of cysteine to maintain protection. Furthermore, a multifold excess of vitamin C is required to keep the cysteine in it’s reduced state and “on the job” against acetaldehyde. I use capsules (because they dissolve fast) containing 200 mg cysteine plus 600 mg of vitamin C (with or without extra B-1). I take one before I start drinking, one with each additional drink and one when I’m finished. It works remarkably well.

    Additional Nutrients

    There are several other nutrients which may synergize with cysteine and vitamin C. Glutathione, the predominant sulfhydryl antioxidant in the human body, should be considered. Although it is probably quite effective, it is many times more expensive than cysteine and it is not as concentrated; it contains only 10% sulfur compared to 26% sulfur in cysteine. Much larger doses of glutathione must be taken to get the same sulfhydryl concentration, and a significant but unknown amount of glutathione is broken down in the stomach into its component amino acids (glutamate, cysteine and glycine).

    So while glutathione is a great idea, it’s an expensive great idea.
    Thiamine (vitamin B-1) and lipoic (thioctic) acid are key sulfur-containing nutrients that may be depleted by alcohol and/or may help with acetaldehyde detoxification. Thiamine was tested by Sprince and colleagues [1974] and found to offer protective benefit to acetaldehyde toxicity when combined with C and cysteine. Whether this is due to a direct interaction between acetaldehyde and the thiamine-bound sulfur or an enhancement of cellular energy production by the active thiamine cofactor (thiamine pyrophosphate) is not known. Alcoholics are known to be thiamine depleted, but whether this depletion is caused by diminished intestinal absorption of thiamine by alcohol or by destruction of thiamine by acetaldehyde is not known. Even under normal circumstances, intestinal absorption of thiamine is not very efficient.



    In its reduced form, lipoic acid is a powerful sulfhydryl antioxidant. Due to lipoic acid’s twin sulfhydryl groups, it should scavenge aldehydes even more effectively that either cysteine or glutathione (see Figure B). However, supplemental lipoic acid is commercially available only in its oxidized form which contains no sulfhydryl sulfur. It is converted into the reduced form within the mitochondria after absorption from the bloodstream into the cell. So while lipoic acid may be a good cellular protector, it is not as efficient at scavenging acetaldehyde from the bloodstream as cysteine and glutathione. Lipoic acid is also fairly expensive.

    Within the cells of the liver, however, lipoic acid and acetaldehyde may be readily interacting. The liver metabolizes the largest percentage of ingested alcohol and acetaldehyde levels may be quite high in liver cells. Acetaldehyde may bind to reduced lipoamide (the active lipoic acid factor) to render it inactive (see Figure B). Due to this potential problem, it may be a good idea not to take one’s regular dose of lipoic acid near when one drinks alcohol but rather several hours before and after.

    Two combination formulas are available: Twin Labs and Vitamin Research Products make a C-and-cysteine formula, and VRP makes a B-1, C and N-acetylcysteine formula.
    Attached Thumbnails Attached Thumbnails Sorry guys didnt mean to do this to ya..-c45all.gif  

  18. #18
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    The NADH Connection

    When alcohol is metabolized, it has a powerful effect on cellular energy production pathways. The conversion of alcohol into acetaldehyde by alcohol dehydrogenase and acetaldehyde into acetate by acetaldehyde dehydrogenase results in the generation of NADH (reduced nicotinamide adenine dinucleotide). NADH is the hydrogen-transfer chemical (i.e., electron transporter) that enables oxidative phosphorylation to take place (i.e., the production of ATP energy within the mitochondria through the utilization of oxygen). This process is too complex to discuss in detail here, but an etensive review article can be found in Smart Drug News Volume 5, No. 2.

    Suffice it to say that NADH production generates lots of energy. This is why drinking alcohol warms people up. The extremely rapid NADH production from the alcohol dramatically increases energy availability and body temperature, especially in people who are chilled. After alcohol has been converted into acetate, the acetate enters the citric acid cycle to generate even more NADH. Vinegar is about 5% acetic acid (acetate).
    For people with compromised mitochondrial function, alcohol may provide a temporary shot of energy that can energize the brain for dealing with stressful circumstances. This increased energy, combined with muscle relaxation and behavioral disinhibition, can be percieved as a valuable aid to social interaction.

    Mitochondrial energy production can be supported through diet and supplements instead of alcohol. NADH is now available as a supplement in 2.5 and 5 mg doses. Dosages range from 2.5 mg to more than 10 mg. NAD (the oxidized form of NADH) is also available as a supplement. NAD is made in the human body in two ways: primarily from the essential amino acid L-tryptophan, and secondarily from niacinamide (vitamin B-3). Both of these can be taken supplementally.

    In addition to making NAD, tryptophan also makes serotonin, a brain neurotransmitter involved in the regulation of carbohydrate feeding behaviors, mood and emotional control. Elevated serotonin levels suppress the appetite for carbohydrates (“sugar cravings”) and promote calmness and equanimity. Low serotonin levels increase carbohydrate appetite, aggressive and violent behaviors, and depression. Maybe this factor is involved in the difference between “happy” and “angry” drunks.

    The natural production of NADH (in the absence of alcohol) depends on lipoic acid, thiamine and riboflavin. Since lipoic acid and thiamine contain sulfur which may become bound to acetaldehyde, I wonder whether the use of alcohol compromises the very energy pathways it stimulates.

    References

    Busnel RG and Lehman AG, Behavioral Brain Research 351-6, 1980.

    Sprince H et al., Protectants against acetaldehyde toxicity: Sulfhydryl compounds and ascorbic acid. Fed Proc 33(3) (Part 1): March 1974. See also: Sprince H et al., Agents and Actions 5(2): 164-73, 1975 and Sprince H et al., Intl J Vit Nutr Res 47 (Supplement 1G): 185-212, 1977.

  19. #19
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    GREAT post Nark .. learn something new everyday!

  20. #20
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    great NARK very informative.

    I have to find the artical that shows sesame seed oil speeds acetylaldehyde metabolism.

    Ill get back to you BO

  21. #21
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    Quote Originally Posted by AnabolicAndre
    great NARK very informative.

    I have to find the artical that shows sesame seed oil speeds acetylaldehyde metabolism.

    Ill get back to you BO
    That'd be an interesting read indeed

    Maybe we can build an anti-hangover cocktail...and test it on Bo

    No orals in your cycles for a while Bo.. we need your liver

  22. #22
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    Bo is our new gineau pig

  23. #23
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    Get to reading and posting.

    Beef it up and i'll move it to the educational forum

  24. #24
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    " Sesamin and episesamin have been shown to raise aldehyde dehydrogenase levels by more than 3 fold. When alcohol is consumed, it enters cells and is broken down into a toxic compound known as acetaldehyde. An enzyme called aldehyde dehydrogenase 2 (ALDH2) converts the acetaldehyde into acetic acid, which is non-toxic and can be readily used by your body to provide energy."

    Now if I'm reading correctly it says ALDH is raised more than 3 fold. ALDH is the enzyme which as a first step breaks down alcohol into acetaldehyde (which is actually even more toxic than alcohol itself I have read elsewhere). Then the second step is breaking down the acetaldehyde with the enzyme ALDH2. It isn't mentioned that the ALDH2 levels are increased by using sesamin. So I'm worried, if ALDH2 is not increased, than that would mean alcohol is first broken down faster/better into acetaldehyde due to the larger amount of ALDH enzyme available. But now the second step goes just as fast as before supplementing sesamin due to unchanged amount of ALDH2, so the level of (the more toxic) acetaldehyde will stay higher for longer in the body.

  25. #25
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    I searched on Pubmed and after reading this maybe I understand it better. The first step is done by alcohol dehydrogenase, the second step by aldehyde dehydrogenase. So with the 3 fold increase in aldehyde dehydrogenase occuring from sesamin supplementation, it would mean first step goes just as fast/good as without sesamin, but second step goes faster/better.


    Antioxidative roles of sesamin, a functional lignan in sesame seed, and it's effect on lipid- and alcohol-metabolism in the liver: a DNA microarray study.

    Kiso Y.

    Institute for Health Care Science, Suntory Ltd., 1-1-1 Wakayamadai, Shimamoto-cho, Mishima-gun, Osaka 618-8503, Japan. [email protected]

    Sesamin was orally administered to rats, and blood, bile and urine were collected periodically. Over 40% of the dose of sesamin was detected in bile as glucuronides of 2-(3, 4-methylenedioxyphenyl)-6-(3, 4-dihydroxyphenyl)-cis-dioxabicyclo[3.3.0] octane and 2-(3, 4-dihydroxyphenyl)-6-(3, 4-dihydroxyphenyl)-cis-dioxabicyclo[3.3.0] octane by 24 hr after administration. Antioxidant activities of these metabolites were compared and catechol metabolites showed strong radical scavenging activities against not only superoxide anion radical but also hydroxyl radical. It was suggested that sesamin was absorbed by the route of portal vein and metabolized to mono- or di-catechol metabolite by drug metabolizing enzymes in the liver cells. Both metabolites exhibited antioxidant activity in the liver and were finally conjugated with glucuronic acid and to excrete in bile. Sesamin can be classified as a pro-antioxidant. The profiles of gene expression of the liver in rats given sesamin or vehicle were compared. The gene expression levels of the late stage enzymes of beta-oxidation including trifunctional enzyme, acyl-CoA oxidase, bifunctional enzyme and 3-ketoacyl-CoA thiolase were significantly increased by sesamin. On the other hand, the transcription of the genes encoding the enzymes for fatty acid synthesis was decreased. Moreover, in sesamin rats, the gene expression of aldehyde dehydrogenase was increased about 3-fold, whereas alcohol dehydrogenase, liver catalase and CYP2E1 were not changed. These results suggested that sesamin ingestion regulated the transcription levels of hepatic metabolizing enzymes for lipids and alcohol.

    PMID: 15630196 [PubMed - indexed for MEDLINE]


    http://www.ncbi.nlm.nih.gov/entrez/...0196&query_hl=1

  26. #26
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    Quote Originally Posted by salmon1
    don't drink at all... ever
    same here.

  27. #27
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    interesting stuff!!! Wish I new all this when I drank!!

  28. #28
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    Quote Originally Posted by salmon1
    don't drink at all... ever
    2nd this
    you cant mix the 2 lifestyles
    get big or go party
    pick a path

  29. #29
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    ill Bump this for nark

  30. #30
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    Good bump Dre...

    Tomorrow night's a beer bash at school..time to put the theory to practise

    LMAO.

  31. #31
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    lol this thread is much appreciated bo, nark and dre

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