ALCOHOL

PROF. DR. SHAH MURAD shahmurad65@gmail.com

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Social problem

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Legal issue

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TEMPERANCE

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Accept

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Not accept

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Intellectual STIGMA !!!!!

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Should take

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Should not !!!!

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SIN

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WORSHIP

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Increase IQ

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DECREASE IQ !!!

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Mind Depressant

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Mind Stimulant !!!

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WHERE IS THE TRUTH about ALCOHOL then ???????????

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Same conflicts in MEDICAL SCIENCES about ALCOHOL

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‡ Ethanol (alcohol, ethyl alcohol) is the world's most commonly used recreational drug, yet, despite many years of research, ethanol's exact pharmacological mechanism remains somewhat elusive.

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‡ Ethanol has been shown to affect a member of nearly every type of ion channel in the body, but often at concentrations far above those found in recreational users.

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‡ In order to make sense of the huge amount of research into the effects of ethanol on neurons, one must gauge it against the threshold plasma concentration of ethanol needed to produce an effect and a rough estimation of the fatal concentration in humans, i.e. the range of ethanol's concentration found during 20 recreational usage

‡ It is estimated that the plasma concentration necessary to cause threshold effects in humans is 5mM (40mg/100mL) while in a review of 808 fatal alcohol poisonings, the mean plasma concentration was 72mM. ‡ To put blood concentrations further in context, the blood-alcohol limit in most states in the US is 17.4 mM. 21

GABA-A receptors
‡ Because of ethanol's depressive effects, there has been constant speculation that its site of action is the GABA-A receptor (the major inhibitory receptor in the brain, the same receptor enhanced by benzodiazepines and barbiturates).
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‡ Many experiments have looked into this possibility, and they broadly fit into two categories: ones that found no effect and ones that found a relatively high potency effect, well within recreational concentrations.
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‡ Exactly why there is this stark dichotomy is unclear, though it may have something to do with more recently discovered facts about the distribution of "subunits" of GABA-A receptors.

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NMDA receptors
‡ Inhibition of NMDA receptors by ethanol is another theme that has received a lot of attention, because of the similar anaesthetic nature of ethanol and the classical NMDA receptor antagonists, >>>>>>>>>>> the dissociative anaesthetics (ketamine).

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‡ The NMDA receptor is a compelling site for explaining ethanol's actions, as the concentrations of ethanol that start to cause a significant inhibition of the NMDA receptor are the same concentrations at which the effects of ethanol are beginning to be registered in humans (~5mM).
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‡ NMDA receptor antagonists are classically known for their ability to block the formation of memories, an effect that larger amounts of ethanol are renowned for. ‡ However, one problem with this theory is the lack of similarity between alcohol's intoxication state and that induced by ketamine 27

Nicotinic Acetylcholine Receptors ‡ The nicotinic acetylcholine receptor is another interesting target of ethanol. ‡ Ethanol potentiates the alpha7 subtype of the nicotinic acetylcholine receptor at concentrations that overlap the concentration needed to intoxicate.
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‡ The alpha7 subtype is one of the most common nicotinic acetylcholine receptor subtypes in the brain, the other common subtype, the alpha-4beta-2 subtype, is not affected by ethanol.
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‡ It is almost certain that ethanol's classical "depressant" effects are not mediated by this receptor, as the classical nicotinic acetylcholine receptor agonist nicotine is not depressant. ‡ However, one effect that nicotine and ethanol share is their addictive 30 nature.

‡ It has been demonstrated that nicotinic acetylcholine receptor antagonists inhibit the increase in dopamine release in the brain caused by ethanol and the rewarding effects in humans

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Voltage-Gated Sodium Channels
‡ Ethanol has been shown to inhibit voltage-gated sodium channels (the same channel local anesthetics inhibit), but only at very high concentrations

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Potassium Channels and GIRKS
‡ ethanol modulates potassium channels. ‡ Potassium channels are very important in reducing neuronal excitability. ‡ The G-protein coupled inward rectifying (GIRK) channel is a channel modulated by CB1-cannabinoid and Mu-opioid receptors (as well as many others).
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‡ Ethanol has been shown to directly open (or at least potentiate the opening of) this channel at concentrations starting at ~20-75mM. ‡ While this puts the GIRK channel outside the range for mediating ethanol's recreational effects, it could be responsible for some of the effects of ethanol seen at higher doses, such as analgesia. 34

‡ In mice lacking a functional GIRK channel, ethanol had severely reduced potency as an analgesic. ‡ Ethanol has also been shown to enhance the activity of calciumactivated potassium channels. ‡ These channels become active when a neuron fires repetitively, slowing and eventually stopping the neuron 35 from firing.

‡ Ethanol activates these receptors in the high range of ethanol blood concentrations, and so may be responsible for some of the depressant effects of ethanol at high concentrations.

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Glycine Receptor
‡ The glycine receptor is an inhibitory receptor distributed largely in the spinal cord and brainstem.

‡ Ethanol potentiates this receptor at concentrations directly overlaying its recreational plasma concentrations.
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‡ This could cause a variety of effects like inhibition of signaling from the brain to the body, and might also be responsible for respiratory depression at high doses, but is unlikely to mediate the classical cognitive effect of ethanol
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Voltage-Gated Calcium Channels
‡ The effect of ethanol on voltage-gated calcium channels is one effect that has received a lot of press.

‡ Ethanol inhibits these channels at concentrations very similar to its recreational plasma concentration and has an IC50 in the middle of the recreational range. 39

‡ The opening of voltage-gated calcium channels is responsible for the release of neurotransmitters throughout the body and, by inhibiting this, ethanol will decrease neurotransmitter release. ‡ This inhibition causes a decrease in both excitatory and inhibitory synaptic transmission
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Serotonin 5-HT3 Activation
‡ Ethanol has also been shown to potentiate the serotonin 5-HT3 receptor. ‡ This receptor is somewhat enigmatic, but is believed to modulate excitation in some parts of the brain, and to facilitate vomiting.
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‡ The ethanol concentrations that are needed to potentiate the 5HT3 receptor are outside the range reached during recreational usage

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‡ Despite ethyl alcohol being one of the most widely used psychoactives, the pharmacology of its altering effects is still not yet fully understood.

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‡ There are many systems that it is known to affect, but many of the documented neurophysiological effects only occur at plasma concentrations outside the range that ethanol is used in humans.
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‡ Its effects on GABA-A receptors seem tantalizing, but generally unlikely, due to either a far too high or too low potency, depending on the subunit makeup.

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‡ Ethanol's inhibition of NMDA receptors seems likely to be a contributor to its effects.

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Is alcohol a Poison?
‡ A poison is any substance that is capable of causing injury, illness or death to an organism.

‡ Salt, water and oxygen are all poisons because in high enough quantities they can harm 47 people.

‡ Too much salt in a diet can cause serious health problems, hyper hydration can kill athletes, and too much oxygen given to a premature infant can cause permanent blindness.

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‡ Toxicologists emphasize that ´the dosage makes the poison.µ ‡ Although salt, water, oxygen, aspirin, alcohol beverages, and many other substances can cause poisoning in excessive amounts, it makes no sense to call them poisons.
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ETHYL ALCOHOL IS A POISON
‡ ´ETHYL ALCOHOL IS A POISON.

‡ >>>>>>>>>>>> ¶No intelligent person knowingly ingests poison unless they want to die prematurely·
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‡ So why do so many groups and organizations insist on calling alcohol a poison?

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‡ Apparently to stigmatize alcoholic beverages and frighten people into alcohol abstinence.

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‡ The tactic was first used effectively by the Anti-Saloon League, the Women¶s Christian Temperance Union, the KKK and other anti-alcohol groups. The technique is still widely used today.

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‡ Governmental efforts to promote the belief that alcohol beverages are harmful and to censor any evidence to the contrary have continued for many decades, often under pressure from special interest groups.
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"When news leaked that the two scientists' report contained language to the effect that moderate drinking was unharmful, temperance organizations in the state immediately rallied and deluged the legislature and the governor's office with cries of objection."
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‡ The National Institutes of Health much later funded a study that found moderate drinkers to be less likely to suffer heart disease, but refused to allow the Harvard researchers to publish the results because it considered them "socially undesirable."
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