I still dont drink like I used to b4 jail. I hate not being in control, and drunk dudes always get knocked the fuck out at bars.
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I still dont drink like I used to b4 jail. I hate not being in control, and drunk dudes always get knocked the fuck out at bars.
You're native american though yeah?Quote:
Originally Posted by V4D3R
Its the worst shit to happen to Aboriginals here, still killing them by the thousands. Put a total ban on drinking in one part because of kids dying from neglect, shits fucked up.
DJ Methods...we are just going to have to agree to disagree.
Yes people who drink teach at my university. And alot of them are along way from being anything but ROTE parrots. Alot have OBVIOUS health problems from over working....and they are not my example of a well based mind.
Yes, they rule my country....lol that should be enough said.
Also, any person who thinks the ONLY harm in drinking is what it does to you mentally or physically is thinking shallowly. Drinking once a month or whatever may have a minimal effect....but propogating the use of a substance which ruins families, causes alot of violence, mental problems etc is an evil.
Also, if you read my earlier threads, I gave up caffeine (hard as that was) coz it caused depression among other things in me pretty severely. Also, I do not smoke weed, and I am very concious of what excess refine sugars does to me, and I try not to eat them - but this is my current vice. I agree 100%, all of these should be avoided. (BTW I actually only do drink water...I don't even drink juice....all my sugars come in foods).
And I also have to disagree about the good not being grey. Alcohol only inhibits certain parts of the brain - please explain what is so beneficial about that? A sense of escapism, that's all and that is what I have a problem with.
Also, my theory is hardly debunked. You can probably expect to see depression and senility in your mum over the coming years. I hope it is fun :) Also, my mum hasn't drunk and she gets picked as in her 20s....I am sure your mum well and truly shows the signs of her party days. Also, my mothers kids didn't end up with psychosis.
As for poetry etc....I don't deny it can enhance creativity - but it is at a cost. ALOT of the best poets and writers have been manic depressants who basically destroyed themselves. With effort the same creativity could have been aroused more naturally. Also, I hardly implied I think mathematics MAKES humanity...but it is extremely practical. I love poetry and art and so on....but intoxication isn't a necessity to this.
You are NOT in a better position to judge than me. Imagine giving a group of people heroin and getting one of the USERS to observe the changes in the other people! LMAO was your mum drunk when she dropped you on your head or what?
Also, it is a FACT both aboriginals and american indians don't handle alcohol as well as Europeans. This is part of the reason there is such abuse in these communities. But that's cool hey? Coz we need it to catch up with friends once a month....
The way I see it is like this. If something can cause violence or stupidity, or be involved in like 1/4 car accidents, or ruin a persons life or a family it should NOT be encouraged in society even if it had large benefits. Not only does alcohol do all this (these are FACTS - it happens...and should be unacceptable in ANY proportion) its benefits are what? Escapism? Wow.... And anyone who doesn't actively denounce it is as guilty as anyone else when these things happen. You think it is just aboriginals? My grandfather died from it, my grandmother killed herself coz her husband got drunk and beat her - he is now dying from it, my mums twin brother has been told he will die soon if he continues drinking....but he can't stop coz it is now his method of dealing with shit. But had he never started to drink he would have dealt with stuff properly instead of hiding from it and adding an additional problem.
If you think this stuff is worth the "social lubrication" it offers people (who should maybe work on there fucking self-esteem instead) then you don't deserve to be on this planet. But anyone who holds this mentality will soon bring their own demise upon themselves :)
Effects of alcohol on the body
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Alcohol consumption and healthAlcohol and cancerAlcohol and cardiovascular diseaseAlcohol and weightAlcoholic liver diseaseAlcoholismEffects of alcohol on the bodyFetal alcohol syndromeThe effects of alcohol on the human body can take several forms.
Alcohol, specifically ethanol, is a potent central nervous system depressant, with a range of side effects. The amount and circumstances of consumption play a large part in determining the extent of intoxication; e.g., consuming alcohol after a heavy meal is less likely to produce visible signs of intoxication than consumption on an empty stomach. Hydration also plays a role, especially in determining the extent of hangovers. The concentration of alcohol in blood is usually measured in terms of the blood alcohol content.
Alcohol has a biphasic effect on the body, which is to say that its effects change over time. [1] Initially, alcohol generally produces feelings of relaxation and cheerfulness, but further consumption can lead to blurred vision and coordination problems. Cell membranes are highly permeable to alcohol, so once alcohol is in the bloodstream it can diffuse into nearly every biological tissue of the body. After excessive drinking, unconsciousness can occur and extreme levels of consumption can lead to alcohol poisoning and death (a concentration in the blood stream of 0.55% will kill half of those affected). Death can also occur through asphyxiation by vomit. An appropriate first aid response to an unconscious, drunken person is to place them in the recovery position.
Intoxication frequently leads to a lowering of one's inhibitions, and intoxicated people will sometimes do things they would not do while sober, often overlooking social, moral, and legal considerations. Conversely, some studies have suggested that intoxicated people have much greater control over their behavior than is generally recognized. [1]
http://upload.wikimedia.org/wikipedi...FASbrains2.gif http://en.wikipedia.org/skins-1.5/co...gnify-clip.png
The image shows the brains of two six-week-old infants. The left brain is confirmed no alcohol exposure, while the right brain is of an infant with fetal alcohol syndrome.
This article primarily covers the short-term effects of alcohol on the adult human body. For the potential long-term cumulative effects of alcohol on the adult human body, please refer to alcohol consumption and health, alcohol and cardiovascular disease, alcohol and cancer, alcohol and weight and alcoholic liver disease. The potential impact of alcohol consumption by pregnant women on their fetuses is discussed in the article fetal alcohol syndrome.
Contents
[hide]
- <LI class=toclevel-1>1 Metabolism of alcohol and action on the liver
<LI class=toclevel-1>2 Beneficial effects of alcohol <LI class=toclevel-1>3 Effects by doses
- <LI class=toclevel-2>1.1 Dehydration
- 1.2 Hangovers
<LI class=toclevel-1>4 Pharmacology <LI class=toclevel-1>5 Animal and Insect Models <LI class=toclevel-1>6 References
- <LI class=toclevel-2>3.1 Moderate doses
- 3.2 Excessive doses
- 7 External links
[edit] Metabolism of alcohol and action on the liver
The liver breaks down alcohols into acetaldehyde by the enzyme alcohol dehydrogenase, and then into acetic acid by the enzyme acetaldehyde dehydrogenase. Next, the acetate is converted into fats or carbon dioxide and water. Chronic drinkers, however, so tax this metabolic pathway that things go awry: fatty acids build up as plaques in the capillaries around liver cells and those cells begin to die, which leads to the liver disease cirrhosis. The liver is part of the body's filtration system which, if damaged, allows certain toxins to build up, leading to symptoms of jaundice.
Some people's DNA code calls for a different acetaldehyde dehydrogenase, resulting in a more potent alcohol dehydrogenase. This leads to a buildup of acetaldehyde after alcohol consumption, causing the alcohol flush reaction with hangover-like symptoms such as flushing, nausea, and dizziness. These people are unable to drink much alcohol before feeling sick, and are therefore less susceptible to alcoholism.[2][3] This adverse reaction can be artificially reproduced by drugs such as disulfiram, which are used to treat chronic alcoholism by inducing an acute sensitivity to alcohol.
[edit] Dehydration
Overconsumption can therefore lead to dehydration (the loss of water).
[edit] Hangovers
Main article: Hangover
A common after-effect of ethanol intoxication is the unpleasant sensation known as hangover, which is partly due to the dehydrating effect of ethanol. Hangover symptoms include dry mouth, headache, nausea, and sensitivity to light and noise. These symptoms are partly due to the toxic acetaldehyde produced from alcohol by alcohol dehydrogenase, and partly due to general dehydration. The dehydration portion of the hangover effect can be mitigated by drinking plenty of water between and after alcoholic drinks. Other components of the hangover are thought to come from the various other chemicals in an alcoholic drink, such as the tannins in red wine, and the results of various metabolic processes of alcohol in the body, but few scientific studies have attempted to verify this. Consuming water between drinks and before bed is the best way to prevent or lessen the effects of a hangover.
[edit] Beneficial effects of alcohol
The World Health Organization (WHO) reports that there is convincing evidence that "low to moderate alcohol intake" results in a decreased risk of coronary heart disease.[4] However, the WHO cautions that "other cardiovascular and health risks associated with alcohol do not favour a general recommendation for its use."[5]
Moderate alcohol consumption has been found to be associated with a lower risk of Alzheimer’s disease and other dementia, angina pectoris, bone fractures and osteoporosis, diabetes, duodenal ulcer, gallstones, hepatitis A, Hodgkin’s lymphoma, intermittent claudicating (IC), kidney stones, non-Hodgkin’s lymphoma, metabolic syndrome, pancreatic cancer, Parkinson's Disease, peripheral arterial disease (PAD), rheumatoid arthritis, and type B gastritis. [6] Also it has been suggested that moderate consumption can reduce the risk of dementia, facilitate memory and learning,[7] and even improve IQ scores.[8]
However, a study of red wine published in the American Journal of Clinical Nutrition, found that alcohol-free red wine had the same health benefits as the alcoholic wine, and that the alcohol may actually shorten the benefits.[9] Flavonoids believed to be protective against coronary heart disease and some types of cancer, are present in wine due to its fermentation from grapes. These left the blood more quickly when alcohol was consumed.[9]
Moderate drinkers tend to have better health and live longer than those who abstain from alcohol or are heavy drinkers[citation needed], but this average difference may possibly be explained in part by the fact that a fraction of abstainers from alcohol are ex-alcoholics or those who have health problems or take drugs that preclude the use of alcohol. See Alcohol consumption and health.
[edit] Effects by doses
Different concentrations of alcohol in the human body have different effects on the subject. The following lists the effects of alcohol on the body, depending on the blood alcohol concentration or BAC.[10][11][12] Also, tolerance varies considerably between individuals.
Please note: the BAC percentages provided below are just estimates and used for illustrative purposes only. They are not meant to be an exhaustive reference; please refer to a healthcare professional if more information is needed.
- Euphoria (BAC = 0.03 to 0.12%)
- Subject may experience an overall improvement in mood and possible euphoria.
- They may become more self-confident or daring.
- Their attention span shortens. They may look flushed.
- Their judgment is not as good — they may express the first thought that comes to mind, rather than an appropriate comment for the given situation.
- They have trouble with fine movements, such as writing or signing their name.
- Lethargy (BAC = 0.09 to 0.25%)
- Subject may become sleepy
- They have trouble understanding or remembering things, even recent events. They do not react to situations as quickly.
- Their body movements are uncoordinated; they begin to lose their balance easily, stumbling; walking is not stable.
- Their vision becomes blurry. They may have trouble sensing things (hearing, tasting, feeling, etc.).
- Confusion (BAC = 0.18 to 0.30%)
- Profound confusion — uncertain where they are or what they are doing. Dizziness and staggering occur.
- Heightened emotional state — aggressive, withdrawn, or overly affectionate. Vision, speech, and awareness are impaired.
- Poor coordination and pain response. Nausea and vomiting sometimes occurs.
- Stupor (BAC = 0.25 to 0.40%)
- Movement severely impaired; lapses in and out of consciousness.
- Subjects can slip into a coma; will become completely unaware of surroundings, time passage, and actions.
- Risk of death is very high due to alcohol poisoning and/or pulmonary aspiration of vomit while unconscious.
- Coma (BAC = 0.35 to 0.50%)
- Unconsciousness sets in.
- Reflexes are depressed (i.e., pupils do not respond appropriately to changes in light).
- Breathing is slower and more shallow. Heart rate drops. Death usually occurs at levels in this range.
- Death (BAC more than 0.50%)
- Can cause central nervous system to fail, resulting in death.
[edit] Moderate doses
Although alcohol is typically thought of purely as a depressant, at low concentrations it can actually stimulate certain areas of the brain. Alcohol sensitises the N-methyl-D-aspartate (NMDA) system of the brain, making it more receptive to the neurotransmitter glutamate. Stimulated areas include the cortex, hippocampus and nucleus accumbens, which are responsible for thinking and pleasure seeking. Another one of alcohol's agreeable effects is body relaxation, possibly caused by heightened alpha brain waves surging across the brain. Alpha waves are observed (with the aid of EEGs) when the body is relaxed. Heightened pulses are thought to correspond to higher levels of enjoyment.
A well-known side effect of alcohol is lowering inhibitions. Areas of the brain responsible for planning and motor learning are dulled. A related effect, caused by even low levels of alcohol, is the tendency for people to become more animated in speech and movement. This is due to increased metabolism in areas of the brain associated with movement, such as the nigrostriatal pathway. This causes reward systems in the brain to become more active, and combined with reduced understanding of the consequences of their behavior, can induce people to behave in an uncharacteristically loud and cheerful manner.
Behavioral changes associated with drunkenness are, to some degree, contextual. A scientific study found that people drinking in a social setting significantly and dramatically altered their behavior immediately after the first sip of alcohol, well before the chemical itself could have filtered through to the nervous system. Likewise, people consuming non-alcoholic drinks often exhibit drunk-like behavior on a par with their alcohol-drinking companions even though their own drinks contained no alcohol whatsoever. [citation needed]
[edit] Excessive doses
The effect alcohol has on the NMDA receptors, earlier responsible for pleasurable stimulation, turns from a blessing to a curse if too much alcohol is consumed. NMDA receptors start to become unresponsive, slowing thought in the areas of the brain they are responsible for. Contributing to this effect is the activity which alcohol induces in the gamma-aminobutyric acid system (GABA). The GABA system is known to inhibit activity in the brain. GABA could also be responsible for the memory impairment that many people experience. It has been asserted that GABA signals interfere with the registration and consolidation stages of memory formation. As the GABA system is found in the hippocampus, (among other areas in the CNS), which is thought to play a large role in memory formation, this is thought to be possible.
Blurred vision is another common symptom of drunkenness. Alcohol seems to suppress the metabolism of glucose in the brain. The occipital lobe, the part of the brain responsible for receiving visual inputs, has been found to become especially impaired, consuming 29% less glucose than it should. With less glucose metabolism, it is thought that the cells aren't able to process images properly.
Often, after much alcohol has been consumed, it is possible to experience vertigo, the sense that the room is spinning (sometimes referred to as 'The Spins'). This is associated with abnormal eye movements called nystagmus, specifically positional alcohol nystagmus. In this case, alcohol has affected the organs responsible for balance (vestibular system), present in the ears. Balance in the body is monitored principally by two systems: the semicircular canals, and the utricle and saccule pair. Inside both of these is a flexible blob called a cupula, which moves when the body moves. This brushes against hair cells in the ear, creating nerve impulses that travel through the vestibulocochlear nerve (Cranial nerve VIII) in to the brain. However, when alcohol gets in to the bloodstream it distorts the shape of the cupola, causing it to keep pressing on to the hairs. The abnormal nerve impulses tell the brain that the body is rotating, causing disorientation and making the eyes spin round to compensate. When this wears off (usually taking until the following morning) the brain has adjusted to the spinning, and interprets not spinning as spinning in the opposite direction causing further disorientation. This is often a common symptom of the hangover.[citation needed]
Anterograde amnesia, colloquially referred to as "blacking out", is another symptom of heavy drinking.
Another classic finding of alcohol intoxication is ataxia, in its appendicular, gait, and truncal forms. Appendicular ataxia results in jerky, uncoordinated movements of the limbs, as though each muscle were working independently from the others. Truncal ataxia results in postural instability; gait instability is manifested as a disorderly, wide-based gait with inconsistent foot positioning. Ataxia is responsible for the observation that drunk people are clumsy, sway back and forth, and often fall down. It is probably due to alcohol's effect on the cerebellum.
Extreme overdoses can lead to alcohol poisoning and death due to respiratory depression.
A rare complication of acute alcohol ingestion is Wernicke encephalopathy, a disorder of thiamine metabolism. If not treated with thiamine, Wernicke encephalopathy can progress to Korsakoff psychosis, which is irreversible.
Chronic alcohol ingestion over many years can produce atrophy of the vermis, which is the part of the cerebellum responsible for coordinating gait; vermian atrophy produces the classic gait findings of alcohol intoxication even when its victim is not inebriated.
Severe drunkenness and hypoglycemia can be mistaken for each other on casual inspection, with potentially serious medical consequences for diabetics. Measurement of the serum glucose and ethanol concentrations in comatose individuals is routinely performed in the emergency department or by properly-equipped prehospital providers and easily distinguishes the two conditions.
[edit] Pharmacology
At low or moderate doses, alcohol primarily acts as an unselective GABAA agonist. Alcohol binds to several different subtypes of GABAA, but not to others. The main subtypes responsible for the subjective effects of alcohol are the α1β3γ2, α5β3γ2, α4β3δ and α6β3δ subtypes, although other subtypes such as α2β3γ2 and α3β3γ2 are also affected. Activation of these receptors causes most of the effects of alcohol such as relaxation and relief from anxiety, sedation, ataxia and increase in appetite and lowering of inhibitions which can cause a tendency towards violence in some people.[13][14][15][16][17][18][19]
At higher dose ranges, other targets also become important. Alcohol at high doses acts as an antagonist of the NMDA receptor, and since the NMDA receptor is involved in learning and memory, this action is thought to be responsible for the "memory blanks" that can occur at extremely high doses of alcohol. People with a family history of alcoholism may exhibit genetic differences in the response of their NMDA glutamate receptors as well as the ratios of GABA-A subtypes in their brain. Alteration of NMDA receptor numbers in chronic alcoholics is likely to be responsible for some of the symptoms seen in delerium tremens during severe alcohol withdrawal, such as delerium and hallucinations. Other targets such as sodium channels can also be affected by high doses of alcohol, and alteration in the numbers of these channels in chronic alcoholics is likely to be responsible for the convulsions that can occur in acute alcohol withdrawal, as well as other effects such as cardiac arrhythmia. Also chronic NMDA receptor blockade may produce apoptosis in neurons which is likely to one of the factors involved in producing the brain damage seen in long-term alcoholic patients. Other targets that are affected by alcohol include cannabinoid, opioid and dopamine receptors, although it is unclear whether alcohol affects these directly or if they are affected by downstream consequences of the GABA/NMDA effects.[20][21][22][23][24][25][26][27]
[edit] Animal and Insect Models
There have been some attempts to use animal and insect models to study the effects of ethanol on humans. Other creatures are not immune to the effects of alcohol:
Many of us have noticed that bees or yellow jackets cannot fly well after having drunk the juice of overripe fruits or berries; bears have been seen to stagger and fall down after eating fermented honey; and birds often crash or fly haphazardly while intoxicated on ethanol that occurs naturally as free-floating microorganisms convert vegetable carbohydrates to alcohol.[28] Birds may have even been killed by excessive consumption of alcohol.[29]
In Sweden, drunken moose have been observed. The theory is that they had eaten large amounts of overly ripe berries.
As a result, animal and insect models are fairly attractive. Heberlein et al. conducted studies of fruit fly intoxication at the University of California, San Francisco in 2004.[30] The brains and nervous systems of bees bear similarities to those of humans, so honey bees are used in studies of the effect of alcohol.[31][32][33] The value of antabuse (disulfiram) as a treatment for alcoholism has been tested using a bee model.[34]
Ulrike Heberlein's group at University of California, San Francisco has used fruit flies as models of human inebriation and even identified genes that seem to be responsible for alcohol tolerance accumulation (believed to be associated with veisalgia, or hangover), and produced genetically engineered strains that do not develop alcohol tolerance[35][36][37][38]
University of Minnesota Biology Professor PZ Myers is using zebrafish to study ethanol teratogenesis and ethanol gametogenesis.[39] A wide range of other animal models have been used,[40][41] including primate,[42] mouse,[43] and rat models.[44]
Alcohol consumption and health
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Alcohol consumption and healthAlcohol and cancerAlcohol and cardiovascular diseaseAlcohol and weightAlcoholic liver diseaseAlcoholismEffects of alcohol on the bodyFetal alcohol syndrome
The relationship between alcohol consumption and health has been the subject of formal scientific research since at least 1926, when Dr. Raymond Pearl published his book, Alcohol and Longevity, in which he reported his finding that drinking alcohol in moderation was associated with greater longevity than either abstaining or drinking heavily.[1] Since that time
- “Data have come in from all over the world. Studies have focused on both men and women, various age groups, and people of many ethnic groups. The conclusion remains the same: those who drink moderately live longer and have less risk of developing heart disease than those who abstain from alcohol. Published papers now total in the many hundreds." [2] [3] [4][5].
- To determine if moderate drinkers have fewer heart attacks because they might lead more healthful lifestyles than do abstainers or heavy drinkers, Harvard scientists recently reported their study of only healthy men who led healthful lifestyles. For up to 16 years the doctors monitored the health of 8,867 men who didn't smoke, were of normal weight, exercised at least 30-60 minutes per day, and ate a balanced healthful diet. Among these healthy men with healthy lifestyles, those who consumed anywhere from 1/2 to two alcoholic drinks of beer, wine or liquor per day had significantly decreased risk of heart attacks. Those who averaged slightly more (one to two drinks per day) had the lowest risk. This study strongly suggests that the beneficial effects of drinking alcohol in moderation comes from the alcohol itself rather than from differences in lifestyle [6] Other research also addresses this question.
- Another study found that when men increased their alcohol intake from very low to moderate, they significantly reduced their risk of coronary heart disease. The study monitored the health of 18,455 males for a period of seven years. [7]
- Drinking in moderation has also been found to help those who have suffered a heart attack survive it. [8] Alcohol helps reduce damage after heart attacks
Such widely different types of evidence based on different methodologies largely rule out the possibility that some factor or factors other than the alcohol itself is causing the significant reductions in fatalities found among moderate drinkers around the world.
- Much evidence is not simply correlational or time sequence in nature. Some of the many specific ways by which alcohol leads to improved cardiovascular health are now understood, often in great detail. [9]
While it is widely recognized that alcoholism has negative health effects, moderate consumption, frequently defined as the consumption of 1-4 alcoholic drinks in a day (depending on the age and gender of the subjects) has been found in much research to have a positive effect on longevity[10] (Doll & Peto). See the main article Recommended maximum intake of alcoholic beverages for a list of governments' guidances on alcohol intake which, for a man, range from 140 to 280g per week.
However, some research suggests to some that the benefits of moderate alcohol consumption may not be large enough or certain enough to recommend to those who do not already drink, even if not contraindicated. There is a concern that doing so might lead to symptoms of alcoholism in those who previously did not imbibe or that those who drink heavily would interpret the advice as support for heavy drinking.[11][12] Dr. Tim Naimi and some others at the US Centers for Disease Control and Prevention (CDC) speak widely concerning what they consider the supposed benefits of moderate alcohol intake, pointing out that the research designs that have led to such conclusions are not generally indicative of a cause and effect.[13]
On the other hand, Dr. R. Curtis Ellison, a physician and leading medical researcher, says that adults should have a drink a day, unless contraindicated. “The bottom line is, never go more than 24 hours without a drink” says Dr. Ellison, who is chief of preventive medicine and epidemiology at Boston University School of Medicine. Dr. Ellison recommends that other doctors prescribe a drink a day to their patients to promote better health and greater longevity. [14] Similarly, well-known medical authority Dean Edell, M.D., asserts that “you would have to be living on another planet not to know that alcohol -- in moderation -- is good for your health.” [15]
Contents
[hide]
- <LI class=toclevel-1>1 Controversy <LI class=toclevel-1>2 Mortality <LI class=toclevel-1>3 Overall longevity <LI class=toclevel-1>4 Cancer <LI class=toclevel-1>5 Cardiovascular diseases
<LI class=toclevel-1>6 Gastrointestinal disease
- <LI class=toclevel-2>5.1 Coronary artery disease <LI class=toclevel-2>5.2 Peripheral Vascular Disease
- 5.3 Stroke
<LI class=toclevel-1>7 Hematologic diseases
- <LI class=toclevel-2>6.1 Gastritis and bacterial contamination <LI class=toclevel-2>6.2 Pancreatitis
- 6.3 Peptic ulcer disease
<LI class=toclevel-1>8 Hepatobiliary disease
- <LI class=toclevel-2>7.1 Anemia
- 7.2 Thrombocytopenia
<LI class=toclevel-1>9 Neurologic disease
- <LI class=toclevel-2>8.1 Alcoholic liver disease <LI class=toclevel-2>8.2 Gallstones
- 8.3 Gallbladder disease
<LI class=toclevel-1>10 Obesity <LI class=toclevel-1>11 Other diseases
- <LI class=toclevel-2>9.1 Brain development <LI class=toclevel-2>9.2 Cognition <LI class=toclevel-2>9.3 Dementia and Alzheimer’s Disease <LI class=toclevel-2>9.4 Essential tremor <LI class=toclevel-2>9.5 Myopathy
- 9.6 Neuropathy
<LI class=toclevel-1>12 Issues
- <LI class=toclevel-2>11.1 Diabetes <LI class=toclevel-2>11.2 Kidney stones <LI class=toclevel-2>11.3 Osteoporosis <LI class=toclevel-2>11.4 Rheumatoid arthritis
- 11.5 Miscarriage
<LI class=toclevel-1>13 Alcohol compared to other drugs <LI class=toclevel-1>14 See also <LI class=toclevel-1>15 References
- <LI class=toclevel-2>12.1 Health effect and type of alcohol consumed <LI class=toclevel-2>12.2 Recommending alcohol consumption to "teetotalers" <LI class=toclevel-2>12.3 Comparison with health benefits of exercise and diet <LI class=toclevel-2>12.4 Moderate consumption
- 12.5 Heavy consumption
- 16 External links
[edit] Controversy
Some research suggests to some that the benefits of moderate alcohol consumption may not be large enough or certain enough to recommend to those who do not already drink, even if not contraindicated. There is a concern that doing so might lead to symptoms of alcoholism in those who previously did not imbibe or that those who drink heavily would interpret the advice as support for heavy drinking.[16][17] Dr. Tim Naimi and some others at the US Centers for Disease Control and Prevention (CDC) speaks widely concerning what they consider the supposed benefits of moderate alcohol intake, pointing out that the research designs that have led to such conclusions do not prove a cause and effect.[18]
On the other hand, Dr. R. Curtis Ellison, a physician and leading medical researcher, says that adults should have a drink a day, unless contraindicated. “The bottom line is, never go more than 24 hours without a drink” says Dr. Ellison, who is chief of preventive medicine and epidemiology at Boston University School of Medicine. Dr. Ellison recommends that other doctors prescribe a drink a day to their patients to promote better health and greater longevity. [19] Similarly, well-known medical authority Dean Edell, M.D., asserts that “you would have to be living on another planet not to know that alcohol -- in moderation -- is good for your health.” [20]
[edit] Physiological effects of ethanol
Alcohol appears to be hormetic.[21] Medical research demonstrates that, consumed in moderation, alcohol increases HDL (“good cholesterol”), decreases thrombosis (blood clotting), reduces fibrinogen (a blood clotter), increases fibrinolysis (clot dissolving), reduces artery spasm from stress, increases coronary blood flow and increases insulin sensitivity -- all good for heart health[22][23] (Rimm; Zhang).
[edit] Alcohol production in the body
It is inevitable that all humans always have some amount of alcohol in their bodies at all times, even if they never drink alcoholic beverages in their lives. This is because of a process called endogenous ethanol production. Many of the bacteria in the intestines use alcohol fermentation as a form of respiration. This metabolic method produces alcohol as a waste product, in the same way that metabolism results in the formation of carbon dioxide and water. Thus, human bodies always contain some quantity of alcohol produced by these benign bacteria.
[edit] Mortality
Light and moderate drinking saves more lives in England and Wales than are lost through the abuse of alcohol according to scientists at the University of London. The researchers determined that if everyone abstained from alcohol, death rates would be significantly higher. In the words of the lead author, "alcohol saves more lives than it costs." [25]
- United Kingdom: "In 2004 there were 8,221 alcohol-related deaths in the UK, almost double the total of 4,144 in 1991."[24]
Other researchers, led by Dr. Ian White, found that, in the United Kingdom, 15,080 deaths were prevented through the use of alcohol, while 13,216 were caused by its abuse. Thus, the use of alcohol led to a net gain of 1,864 lives. [26]
Research by the U.S. Centers for Disease Control and Prevention (CDC) and the National Institute on Alcohol Abuse and Alcoholism (NIAAA) reveals that the benefits of moderate drinking outweigh the harms from abusive drinking. The NIAAA calculates that if all drinkers in the U.S. became abstainers, there would be an additional 80,000 deaths per year. Abstaining dramatically increases the risks of heart attack, ichemic stroke, and many other diseases and life-threatening conditions. The CDC calculates that abusive drinking lead to about 75,766 deaths from all causes in 2001, a number that continues to decline. Therefore, these analyses indicate that moderate alcohol consumption saves more lives than are lost as a result of alcohol abuse. [28]
- United States: A 2001 report estimates that medium and high consumption of alcohol led to 75,754 deaths in the USA. Low consumption has some beneficial effects so a net 59,180 deaths were attributed to alcohol.[27]
- Australia:The Cancer Council of New South Wales concludes that “If the net effect of total alcohol consumption on Australian society is considered, there is a net saving of lives due to the protective effect of low levels of consumption on cardiovascular disease.” [29]
[edit] Overall longevity
Studies support the finding that moderate alcohol consumption is associated with benefits in longevity because of reductions in coronary heart disease, stroke and other diseases such as Alzheimer’s disease, diabetes, duodenal ulcer, hepatitis A, Hodgkin’s lymphoma, non-Hodgkin’s lymphoma, metabolic syndrome, pancreatic cancer, Parkinson's Disease and peripheral arterial disease (PAD) [30][22][31][32][33][34][35](Wang & Barker) .[36] Apparent mechanisms of these benefits include the effect of alcohol on improving blood lipid profile [37] (it raises HDL or “good” cholesterol [38] and lowers LDL or “bad” cholesterol [39]). It improves blood insulin levels and activity, [40] reduces blood pressure, [41] reduces coronary artery spasm in response to stress and increases coronary blood flow, [42] reduces platelet aggregation, [43] reduces fibrinogen (a blood clotter) [44] increases fibrinolysis (the process by which clots dissolve), [45] Frequently, such studies qualify these findings with admonitions against heavy alcohol consumption or abuse, due to the negative health effects often associated with this behavior.
The U.S. National Institute on Alcohol Abuse and Alcoholism (NIAAA) has completed an extensive review of current scientific knowledge about the health effects of moderate alcohol consumption. It found that the lowest death rate from all causes occurs at the level of one to two drinks per day. That is, moderate drinkers have the greatest longevity.[46][47]
Research in various countries has found the all-cause mortality rates range from 16 to 28% lower among moderate drinkers than among abstainers[48][49][50][51] (Yuan).
The medical studies establishing this relationship are large (some include over 200,000 people), cross-cultural (have been conducted in countries around the world), and are sometimes long-term (the longest beginning in 1948 and continuing to this day).[52]
To test the hypothesis that the results may reflect the poor health of alcoholics who now abstain, some studies have restricted the abstainers studied to lifelong teetotalers. Others have controlled for lifestyle factors, income levels, educational levels and other factors. The results have remained the same: moderate drinkers tend to live longer than abstainers or heavy drinkers.[53] Other studies contradict this view.[54]
A 23-year prospective study of 12,000 male British physicians aged 48–78, found that overall mortality was significantly lower in the group consuming an average of 2–3 "units" (British unit = 8g) per day than in the non-alcohol-drinking group (relative risk 0.81, confidence interval 0.76-0.87, P = 0.001).[55] The authors noted that the causes of death that are already known to be augmentable by alcohol accounted for only 5% of the deaths (1% liver disease, 2% cancer of the mouth, pharynx, larynx, or oesophagus, and 2% external causes of death) and were significantly elevated only among men consuming >2 units/day.
In a 1996 American Heart Association scientific statement, Thomas A. Pearson, MD, Ph.D noted, "A large number of observational studies have consistently demonstrated a U-shaped relation between alcohol consumption and total mortality. This relation appears to hold in men and women who are middle aged or older. The lowest mortality occurs in those who consume one or two drinks per day. In teetotalers or occasional drinkers, the rates are higher than in those consuming one or two drinks per day. In persons who consume three or more drinks per day, total mortality climbs rapidly with increasing numbers of drinks per day."
[edit] Cancer
Main article: Alcohol and cancer
The U.S. Department of Health & Human Services’ National Toxicology Program listed alcohol as a known carcinogen in 2000 .[56] The National Institute on Alcohol Abuse and Alcoholism (NIAAA) reports that "Although there is no evidence that alcohol itself is a carcinogen, alcohol may act as a cocarcinogen by enhancing the carcinogenic effects of other chemicals. For example, studies indicate that alcohol enhances tobacco's ability to stimulate tumor formation in rats (Garro & Lieber). In humans, the risk for mouth, tracheal, and esophageal cancer is 35 times greater for people who both smoke and drink than for people who neither smoke nor drink (Blot et al.), implying a cocarcinogenic interaction between alcohol and tobacco-related carcinogens (Garro & Lieber)."[57]
"3.6% of all cancer cases worldwide are related to alcohol drinking, resulting in 3.5% of all cancer deaths."[58]
The NIAAA states that "Although epidemiologic studies have found a clear association between alcohol consumption and development of certain types of cancer, study findings are often inconsistent and may vary by country and by type of cancer."[57]
Chronic heavy abuse of alcohol increases risk of certain cancers. "Considerable evidence suggests a connection between heavy alcohol consumption and increased risk for cancer, with an estimated 2 to 4 percent of all cancer cases thought to be caused either directly or indirectly by alcohol (Rothman)" indicates the NIAAA.[57]
Drinking alcohol, especially along with smoking, increases the risk of cancers of the mouth, esophagus, pharynx, larynx and liver, and of breast cancer, according to the National Cancer Institute. Except for breast cancer, these cancers are all rare (NIAAA). Moderate consumption does not significantly increase the risk of the most common cancers, except for breast cancer.
The moderate consumption of alcohol increases the risk of several cancers, might decrease the risk of a few others, and is unrelated to the incidence of many forms of cancer – see Alcohol and cancer for details.
[edit] Cardiovascular diseases
Main article: Alcohol and cardiovascular disease
The World Health Organization Technical Committee on Cardiovascular Disease asserted that the relationship between moderate alcohol consumption and reduced death from heart disease could no longer be doubted.[59] Consumption of red wine may be particularly favourable, since red wines contain certain polyphenol antioxidants associated with cardiovascular health.
Pearson reviewed the evidence supporting the effect of alcohol consumption on coronary heart disease (CHD): "More than a dozen prospective studies have demonstrated a consistent, strong, dose-response relation between increasing alcohol consumption and decreasing incidence of CHD. The data are similar in men and women in a number of different geographic and ethnic groups. Consumption of one or two drinks per day is associated with a reduction in risk of approximately 30% to 50%. Studies of coronary narrowings defined by cardiac catheterization or autopsy show a reduction in atherosclerosis in persons who consume moderate amounts of alcohol. In general, the inverse association is independent of potential confounders, such as diet and cigarette smoking. Concerns that the association could be an artifact due to cessation of alcohol consumption in persons who already have CHD have largely been disproved."[60]
Other studies cast doubt on this hypothesis.[61]
[edit] Coronary artery disease
- Angina Pectoris (myocardial infarction). Moderate drinking has been found to reduce the risk of angina pectoris.[62]
[edit] Peripheral Vascular Disease
- Peripheral Artery Disease (Peripheral Vascular Disease – PAD). "Moderate alcohol consumption appears to decrease the risk of PAD in apparently healthy men.".[63] "In this large population-based study, moderate alcohol consumption was inversely associated with peripheral arterial disease in women but not in men. Residual confounding by smoking may have influenced the results. Among nonsmokers an inverse association was found between alcohol consumption and peripheral arterial disease in both men and women."[64][65]
In heart attack patients who are treated with alcohol, the tissues affected by low blood flow are healthier and stronger than those who receive no alcohol because of alcohol's positive effects on artery walls.[67] Similarly, drinking alcoholic beverages in moderation may help patients recover from coronary stenting. Healing appears to be promoted by the inflammation inhibiting effects of alcohol. [68]
- Thrombosis (formation of undesirable blood clots anywhere in the body) is lower among moderate drinkers than teetotalers. [66]
The cardiovascular effects of alcohol are not all beneficial, however; studies show that large-quantity consumption of alcohol can lead to alcoholic cardiomyopathy, commonly known as "holiday heart syndrome." Alcoholic cardiomyopathy presents in a manner clinically identical to idiopathic dilated cardiomyopathy, involving hypertrophy of the musculature of the heart that can lead to a form of cardiac arrythmia. These electrical anomales, represented on an EKG, often vary in nature, but range from nominal changes of the PR, QRS, or QT intervals to paroxsysmal episodes of ventricular tachycardia. The pathophysiology of "holiday heart syndrome" has not been firmly identified, but certain hypotheses cite an increased secretion of epinephrine and norepinephrine, increased sympathetic output, or a rise in the level of plasma free fatty acids as possible mechanisms.[69]
To determine if moderate drinkers have fewer heart attacks because they might lead more healthful lifestyles than do abstainers or heavy drinkers, Harvard scientists recently reported their study of only healthy men who led healthful lifestyles. For up to 16 years the doctors monitored the health of 8,867 men who didn't smoke, were of normal weight, exercised at least 30-60 minutes per day, and ate a balanced healthful diet. Among these healthy men with healthy lifestyles, those who consumed anywhere from 1/2 to two alcoholic drinks of beer, wine or liquor per day had significantly decreased risk of heart attacks. Those who averaged slightly more (one to two drinks per day) had the lowest risk. This study strongly suggests that the beneficial effects of drinking alcohol in moderation comes from the alcohol itself rather than from differences in lifestyle [70] Other research also addresses this question.
- Another study found that when men increased their alcohol intake from very low to moderate, they significantly reduced their risk of coronary heart disease. The study monitored the health of 18,455 males for a period of seven years. [71]
- Drinking in moderation has also been found to help those who have suffered a heart attack survive it. [72] Alcohol helps reduce damage after heart attacks
Such widely different types of evidence based on different methodologies largely rule out the possibility that some factor or factors other than the alcohol itself is causing the significant reductions in fatalities found among moderate drinkers around the world.
- Much evidence is not simply correlational or time sequence in nature. Some of the many specific ways by which alcohol leads to improved cardiovascular health are now understood, often in great detail. [73]
[edit] Stroke
Compared to abstaining, drinking in moderation is associated with a reduced risk of stroke, whereas abusing alcohol is associated with an increased risk of stroke.[74]
A study of over 22,000 male physicians aged 40-84 years old over an average of 12 years, concluded, "Light-to-moderate alcohol consumption reduces the overall risk of stroke and the risk of ischemic stroke in men. The benefit is apparent with as little as one drink per week. Greater consumption, up to one drink per day, does not increase the observed benefit."[75]
A meta-analysis of 35 previous studies of the effect of alcohol consumption on stroke risk found that "compared with abstainers, consumption of more than 60 g of alcohol per day (i.e., over four standard drinks -- heavy drinking) was associated with an increased relative risk of total stroke, 1.64 (95% confidence interval [CI], 1.39-1.93); ischemic stroke, 1.69 (95% CI, 1.34-2.15); and hemorrhagic stroke, 2.18 (95% CI, 1.48-3.20), while consumption of less than 12 g/d was associated with a reduced relative risk of total stroke, 0.83 (95%, CI, 0.75-0.91) and ischemic stroke, 0.80 (95% CI, 0.67-0.96), and consumption of 12 to 24 g/d was associated with a reduced relative risk of ischemic stroke, 0.72 (95%, CI, 0.57-0.91). The meta-regression analysis revealed a significant nonlinear relationship between alcohol consumption and total and ischemic stroke and a linear relationship between alcohol consumption and hemorrhagic stroke."[76]
[edit] Gastrointestinal disease
[edit] Gastritis and bacterial contamination
"The link between alcohol use and chronic gastritis (stomach inflammation) is clear, although progression from chronic gastritis to neoplasia is less well understood and probably involves other factors in addition to alcohol."[77][78]
Drinking strong alcoholic beverages with a meal may offer some protection against bacterial contamination. "The antibacterial activity of red and white wine against enteropathogens may protect against bacterial diarrhoea in a similar way to bismuth salicylate. This protective effect helps explain wine's legendary reputation as a digestive aid."[79] "Limited data indicate that drinking alcoholic beverages along with eating food contaminated with Shigella or Salmonella decreases the risk and/or the severity of illness. … During an oyster-borne outbreak of hepatitis A, we studied the effect of ingestion of alcoholic beverages concomitant with consumption of contaminated oysters. … After controlling for potential confounders, we found a protective effect for beverages that have an alcohol concentration of greater than or equal to 10% (odds ratio = 0.1, 95% confidence interval = 0.02-0.9), but not for beverages with an alcohol concentration of less than 10% (odds ratio = 0.7, 95% confidence interval = 0.2-2.9)."[80]
[edit] Pancreatitis
Heavy alcohol consumption is a major cause of pancreatitis, in both its chronic and acute forms.
[edit] Peptic ulcer disease
"These results suggest a protective effect of alcohol consumption against active infection with H pylori…".[81] Another study concluded, "Adjusting for other risk factors, alcohol intake (comparing those who drink > 30 gm of alcohol per day to nondrinkers) was not associated with higher risk of duodenal ulcer (RR = 0.74; 95% CI = 0.42-1.29)."[82]
[edit] Hematologic diseases
[edit] Anemia
Alcoholics may have anemia from several causes:[83]
- Aggregated iron stores (chronic inflammation )
- Frequency as the sole cause of anemia - 37%
- Frequency as the contributing to anemia - 43%
- Megaloblastic anemia (presumably due to folate deficiency as only 5% had low B12 levels)
- Frequency as the sole cause of anemia - 1%
- Frequency as the contributing to anemia - 34%
- Regarding diagnosis, MCV>100 had sensitivity=66%
- Acute blood loss
- Frequency as the sole cause of anemia - 2%
- Frequency as the contributing to anemia - 25%
- Sideroblastic changes
- Frequency as the sole cause of anemia - 0%
- Frequency as the contributing to anemia - 23%
- Iron deficiency anemia
- Frequency as the sole cause of anemia - 4%
- Frequency as the contributing to anemia - 13%
- Regarding diagnosis, ferritin<100 had sensitivity=65%; ferritin<200 has sensitivity=80%
[edit] Thrombocytopenia
Alcoholics may have thrombocytopenia from direct toxic effect on megakaryocytes, or from hypersplenism.
[edit] Hepatobiliary disease
[edit] Alcoholic liver disease
Main article: Alcoholic liver disease
- Alcohol is one cause of cirrhosis and hepatitis.
- Roughly one in four people who consume more than three drinks per day during a period of 10–15 years will experience some level of alcoholic hepatitis.
[edit] Gallstones
Research has found that drinking reduces the risk of developing gallstones. "Compared with alcohol abstainers, the relative risk of gallstone disease, controlling for age, sex, education, smoking, and body mass index, was 0.83 … for occasional and regular moderate drinkers (< 25 ml of ethanol per day), 0.67 … for intermediate drinkers (25-50 ml per day), and 0.58 … for heavy drinkers. This inverse association was consistent across strata of age, sex, and body mass index."[84] Frequency of drinking also appears to be a factor. "An increase in frequency of alcohol consumption also was related to decreased risk. Combining the reports of quantity and frequency of alcohol intake, a consumption pattern that reflected frequent intake (5-7 days/week) of any given amount of alcohol was associated with a decreased risk, as compared with nondrinkers. In contrast, infrequent alcohol intake (1-2 days/week) showed no significant association with risk. … Recommendations regarding the benefit of moderate quantities of alcohol for gallstone disease should be weighed against the potential health hazards of alcohol consumption."[85]
[edit] Gallbladder disease
Consumption of alcohol is unrelated to gallbladder disease.[86] However one study suggested that drinkers who take Vitamin C (ascorbic acid) might reduce their risk. "After adjustment for potential confounding variables, use of ascorbic acid supplements among drinkers was associated with a decreased prevalence of gallbladder disease … and cholecystectomy …. Use of ascorbic acid supplements among non-drinkers was not significantly associated with either prevalence of gallbladder disease or cholecystectomy. Further study is necessary to confirm our findings and, specifically, to examine the combined effects of ascorbic acid and alcohol on cholesterol metabolism."[87]
[edit] Neurologic disease
[edit] Brain development
Consuming large amounts of alcohol over a period of time can impair normal brain development in both rats and humans. Research is lacking on the possible brain effects of light or moderate alcohol consumption among young humans.[88] "Deficits in retrieval of verbal and nonverbal information and in visuospatial functioning were evident in youths with histories of heavy drinking during early and middle adolescence."[89] "Heavy, chronic drinking appears to produce adverse neural effects that are detectable by functional magnetic resonance imaging."[90] "The data suggest that CIE [chronic-intermittent ethanol] exposure during adolescence has a lasting impact on sensitivity to ethanol-induced motor impairments. This effect might stem from a disruption of normal developmental processes."[91]
Abstinence from chronic heavy alcohol consumption encourages new brain cell development, according to a study.[92]
[edit] Cognition
Research has demonstrated a positive association between moderate drinking and cognition or thinking ability. A study of 6,033 British civil servants who were followed an average of 11 years found that those who consumed at least one drink in the previous week, compared with those who did not, were significantly less likely to have poor cognitive function. The beneficial effect extended to those drinking more than 240 g per week (approximately 30 drinks). Higher levels of consumption were not investigated. [93] A three-year longitudinal study of several hundred men in the Netherlands found that low-to-moderate alcohol drinking was associated with a significantly lower risk for poor cognitive function than abstaining. [94] A large prospective study that examined the effects of alcohol consumption on men 18 years later found that non-drinkers and heavy drinkers had the poorest cognitive ability. Moderate alcohol consumption was associated with the highest cognitive performance later in life.(82) [95] A longitudinal study in France found that, among the women studied, moderate alcohol consumption was associated with higher cognitive function. Moderate drinkers were 2.5 times more likely to receive the highest cognitive ability scores than were abstainers. [96]
Two recent studies have added to the evidence that drinking in moderation is associated with better cognitive ability. Researchers in Australia studied 7,485 people age 20 to 64. They found that moderate drinkers performed better than abstainers on all ,measures of cognitive ability. [97]
A 2003 John Hopkins study has linked moderate alcohol use to brain shrinkage and did not find any reduced risk of stroke among moderate drinkers.[1]
[edit] Dementia and Alzheimer’s Disease
Research has found moderate drinking to be associated with lower risk of dementia, including Alzheimer’s disease. A study of about 6,000 people age 65 and older found that moderate drinkers had a 54% lower chance of developing dementia than did abstainers. [98] A study in the Netherlands of 7,983 people age 55 or older over a period averaging six years found that those who consumed one to three drinks per day had a significantly lower risk of dementia (including Alzheimer’s) than did non-drinkers. [99] Over one thousand persons age 65 and older were studied over a period of seven years. Researchers found, that overall, light and moderate drinkers suffered less mental decline than did teetotalers. [100] A study of 1,018 men and women age 65-79 whose mental health was monitored for an average of 23 years found that “drinking no alcohol, or too much, increases risk of cognitive impairment.” [101] In Italy researchers examined 15,807 people 65 years of age and older. Among the drinkers only 19% showed signs of mental impairment compared to 29% of the abstainers. [102] In a study of 402 people at least 75 years of age who were followed almost six years found that light to moderate drinking was significantly associated with a decreased risk of dementia and Alzheimer's disease compared with non-drinkers. [103] The results of a study of 12,480 women age 70-81 beginning in 1980 found that women who consumed alcohol moderately on a daily basis were about 20% less likely than non-drinkers to experience poor memory and decreased thinking abilities. [104] A study of 7,469 women age 65 and older found that those who consumed up to three drinks per day scored significantly better than non-drinkers on global cognitive function, including such things as concentration, memory, abstract reasoning, and language. [105] A study of over 9,000 women age 70-79 over a four-year period. After adjusting for other factors that might effect mental function, the researchers found that the women who drank in moderation performed significantly on five of seven tests. They also performed significantly better on a global score that combined all seven tests [106] A study of older women found that moderate drinkers (those who consumed up to two drinks per day) demonstrated better memory abilities than abstainers. The performance memory tests included such things as remembering a story, a route, hidden objects, future intentions and connecting random numbers and letters. In all cases, the group who drank scored better than those who did not drink. They also performed better on concentration, verbal-associative capacities and oral fluency. [107]
In people with mild cognitive impairment, consuming up to a drink of alcohol per day reduced the development of dementia by 85% compared to teetotalers. The Italian study participants, age 65 to 84, were studied over a period of three and one-half years. [108]
Studies have found the risks of Alzheimer's disease to be as much as 75% lower among drinkers than among teetotalers. A study of found that those who drank regularly, including those who consumed in excess of U.S. recommend levels (one drink per day for women and two for men) had a significantly lower risk of Alzheimer’s disease than did non-drinkers. [109] A French study of 2,273 subjects over a period of three years found that moderate drinkers were significantly less likely than non-drinkers to develop either dementia or Alzheimer’s disease. [110]
A review of existing research to identify how dementia can be reduced found that that both abstaining from alcohol and abusing it are risk factors for cognitive decline and dementia. [111]
[edit] Essential tremor
Essential tremors can be temporarily and dramatically relieved in up to two-thirds of patients by drinking small amounts of alcohol, thus avoiding the serious side effects of the most effective and expensive medications or the dangers of surgery. (Charles P. D., et al. Classification of tremor and update on treatment. American Family Physician, 1999, 59(6), 565-72; Bain, P. G., et al. A study of hereditary essential tremor. Brain, 1994, 117(Pt 4), 805-24 ; Lou, J.S., & Jankovic J. Essential tremor: clinical correlates in 350 patients. Neurology, 1991, 41(2 Pt 1), 234-8; Singer C, et al. Gait abnormality in essential tremor. Movement Disorders, 1994, 9(2), 193-6; Wasielewski PG, et al. Pharmacologic treatment of tremor. Movement Disorders, 1998, 13(Suppl 3), 90-100; Boecker, H., et al. The effect of ethanol on alcoholic-responsive essential tremors: a positron emission tomography study. Annals of Neurology, 1996, 39, 650-658, 1996; Setting a steady course for benign essential tremor. The Johns Hopkins Medical Letter, 1999 (December), 11(10).)
[edit] Myopathy
Nearly half of chronic alcoholics may have myopathy.[112] Proximal muscle groups are especially affected.
[edit] Neuropathy
25% of alcoholics may have peripheral neuropathy, including autonomic.[113]
[edit] Obesity
Main article: Alcohol and weight
Contrary to common belief, drinking alcohol does not necessarily lead to weight gain. Most research studies find no increase in body weight, some find an increase, and some find a small decrease among women who begin consuming alcohol (references for this statement are listed in Alcohol and weight). Some of these studies are very large; one involved nearly 80,000 and another included 140,000 subjects.
A study of 14 male subjects concluded that "In free-living subjects over a 6-week period, the addition of two glasses of red wine to the evening meal does not appear to influence any measured variable which may adversely affect body weight or promote the development of obesity during this time period."[114]
A Mayo clinic study of 8,236 men and women found that people who had one or two alcoholic drinks a day were about half as likely to be obese than teetotalers.[115]
[edit] Other diseases
[edit] Diabetes
Moderate drinkers may have a lower risk of diabetes than non-drinkers. "Alcohol intake increases insulin sensitivity and may partly explain both the J-shaped relationship between the prevalence of diabetes and the amount of alcohol consumption and the decreased mortality for myocardial infarction."[116] "Compared with abstainers men who drank 30.0-49.9 g of alcohol daily had a relative risk of diabetes of 0.61."[117] "Consumption of 30 g/d of alcohol (2 drinks per day) has beneficial effects on insulin and triglyceride concentrations and insulin sensitivity in nondiabetic postmenopausal women."[118] After adjustment for age, randomized treatment assignment, smoking, physical activity, and body mass index, the relative risk estimates of diabetes for those reporting alcohol use of rarely/never were 1.00 (referent), 1 to 3 drinks per month 1.03, 1 drink per week 0.89, 2 to 4 drinks per week 0.74, 5 to 6 drinks per week 0.67, and 1 or more drinks per day 0.57.[119] "The results of this study suggested that moderate alcohol consumption may reduce the risk of type 2 diabetes. On the other hand, binge drinking and high alcohol consumption may increase the risk of type 2 diabetes in women."[120]
[edit] Kidney stones
Research indicates that drinking alcohol is associated with a lower risk of developing kidney stones. One study concludes, "Beer consumption was inversely associated with risk of kidney stones; each bottle of beer consumed per day was estimated to reduce risk by 40% …. Since beer seemed to be protective against kidney stones, the physiologic effects of other substances besides ethanol, especially those of hops, should also be examined."[121] "…consumption of coffee, alcohol, and vitamin C supplements were negatively associated with stones."[122] "After mutually adjusting for the intake of other beverages, the risk of stone formation decreased by the following amount for each 240-ml (8-oz) serving consumed daily: caffeinated coffee, 10%; decaffeinated coffee, 10%; tea, 14%; beer, 21%; and wine, 39%."[123] "…stone formation decreased by the following amount for each 240-mL (8-oz) serving consumed daily: 10% for caffeinated coffee, 9% for decaffeinated coffee, 8% for tea, and 59% for wine." (CI data excised from last two quotes.).[124]
[edit] Osteoporosis
Moderate alcohol consumption is associated with higher bone mineral density in postmenopausal women. "…alcohol consumption significantly decreased the likelihood [of osteoporosis]."[125] "Moderate alcohol intake was associated with higher BMD [bone mineral density] in postmenopausal elderly women."[126] "Social drinking is associated with higher bone mineral density in men and women [over 45]."[127]
[edit] Rheumatoid arthritis
Light to moderate alcohol consumption appears to reduce the risk of developing rheumatoid arthritis, according to research. [128]
[edit] Miscarriage
Spontaneous abortion is linked to alcohol consumption. [citation needed]
[edit] Issues
[edit] Health effect and type of alcohol consumed
A study concluded, "Results from observational studies, where alcohol consumption can be linked directly to an individual's risk of coronary heart disease, provide strong evidence that all alcoholic drinks are linked with lower risk. Thus, a substantial portion of the benefit is from alcohol rather than other components of each type of drink."[129]
Dr. Dean Edell writes that there are “differences of opinion about whether beer, wine, or liquor offers the quickest route to a longer life. Of ten major studies, one-third found this true for wine, one-third for beer, and one-third for liquor. Most researchers now believe that it is the alcohol in all of them that provides the magic, but they don’t rule out other components of alcoholic beverages”.[130]
One review suggests that red wine, particularly from areas of cold climate, seems to offer increased cardio-vascular protection and speculates that the effect results from polyphenols, chemical components contained in grape skin.[131]
[edit] Recommending alcohol consumption to "teetotalers"
Recommendation to an abstainer to become a moderate drinker is controversial because of the potential health hazards of alcohol abuse.[132]
"Given that there is a vast panoply of very effective and under-used cardiovascular drugs and that the beneficial effects of alcohol are small and ill-understood, all those present at the Novartis Foundation meeting concurred that global recommendations such as '1-3 drinks per day are good for you' are not only meaningless but also irresponsible."[133]
"People who choose not to drink alcohol should not be urged to drink to gain any potential health benefit… Non-drinkers can use other strategies, such as regular exercise, giving up smoking, and a healthy diet, to gain protection against heart disease."[134]
[edit] Comparison with health benefits of exercise and diet
Some of the benefits of moderate drinking can be obtained from having a low-fat diet, exercising regularly (for heart health), and eliminating excess salt from the diet. On the other hand, Dr. Eric Rimm of Harvard reports that people have increases of 10 to 30 percent in HDL in a week from drinking alcohol. He says that “nothing else in the diet can have such a dramatic impact on HDL in such a short time”.[135]
Drinking alcohol in moderation can have a greater impact on reducing heart disease than any factor other than the cessation of smoking. And both drinking in moderation and not smoking contribute to the effectiveness of other lifestyle improvements.[136]
Moreover, a prospective study concluded in 2007 comparing the effects of moderate alcohol consumption in otherwise similar cohorts of men who were in the lowest-risk categories in a variety of health indicators, such as weight, dietary habits, exercise habits, blood pressure, and cholesterol, became the first study to show that even for such men in optimum health, those who consumed moderate doses of alcohol received significant health benefits over those who abstained from alcohol, suggesting that moderate consumption of alcohol has independent health benefits that do not substitute for and cannot be substituted by other positive lifestyle interventions. [citation needed]
[edit] Moderate consumption
Moderate consumption of alcohol is defined by the U.S. Department of Agriculture and the Dietary Guidelines for Americans as no more than two drinks for men and one drink for women per day. It is defined by the U.S. National Institute on Alcohol Abuse and Alcoholism (NIAAA) as four drinks per day, not to exceed 14 per week for a man and three per day, not to exceed 14 per week for a woman. The UK equivalent is 3-4 units per day for men and 2-3 units for women. See the main article Recommended maximum intake of alcoholic beverages for a list of governments' guidances on alcohol intake which, for a man, range from 140 to 280g per week.
An exhaustive review of all major heart disease studies has found that "moderate consumers (1 to 2 drinks/day) were at a lower risk of coronary heart disease than nonconsumers or heavy consumers. Evaluation of total mortality in relationship to alcohol consumption reveals that a similar U-shaped relationship to longevity exists."[137] "A substantial portion of the benefit is from alcohol rather than other components of each type of drink." [138] However, studies have also shown that episodic heavy drinking increases the risk of major coronary events such as coronary heart disease and stroke, even in users whose overall volume of drinking was low.[citation needed]
Other possibilities are that moderate drinkers have more healthful lifestyles (making them healthier), higher economic status (giving them greater access to better foods or better healthcare), higher educational levels (causing them to be more aware of disease symptoms), etc. However, when these and other factors are considered, the conclusion again remains the same: moderate drinkers are less likely to suffer cardiovascular disease, which is the leading cause of death in Europe and the Americas.[139] In addition, research has demonstrated specific mechanisms whereby alcohol significantly reduces cardiovascular disease [140] [141] [142] [143] [22] [144] [145] [146] [147] [148], may reduce the risk of dementia, and even indirectly facilitate memory and learning.[149] However, a study published in the British Medical Journal found that, after adjusting for other potentially confounding factors, alcohol consumption had no noticeable effect on the risk of coronary heart disease.[150] This was true for the full range of the test group, including both non-drinkers and heavy drinkers. The study's authors state that the difference may be explained by the exclusion of people who were of ill health who in other studies may have been included in the non-drinker category, as well as other variables, particularly socioeconomic background.
According to the New England Journal Of Medicine, compared to abstainers, those who drink alcohol regularly have higher death rates from injuries, violence, suicide, poisoning, cirrhosis, certain cancers, and possibly hemorrhagic stroke.[146][151] Also according to the NEJM, for men under the age of 34 and women under the age of 45, those reporting no alcohol intake have the lowest mortality rate.[151] The British Medical Journal found that the risks of several types of cancer increase for those who consume alcohol in comparison to lifelong abstainers.[152] This was true even for moderate drinkers.
Alcohol consumption can cause a magnesium deficiency or reduce magnesium levels, as well as reduce levels of zinc and other minerals. These deficiencies may contribute to, or explain, many resulting diseases related to the overconsumption of alcohol. Moderate or heavy consumers of alcohol may want to ensure a healthy diet containing adequate magnesium and other minerals to help reduce the risk of diseases caused by alcohol consumption.
[edit] Heavy consumption
Heavy consumption is detrimental to the user's health. People under the influence of alcohol sometimes find themselves in dangerous or compromising situations where they would not be had they remained sober.
Some people are predisposed to developing a chemical dependency to alcohol, alcoholism. The results of alcoholism are considered a major health problem in many nations. The development of alcoholism does not take place in the absence of alcohol, but neither does the presence of alcohol cause it.
Children of alcoholic parents have 4 times more chance to becoming addicted themselves.
Alcohol is said to be a factor in about 50% of deaths in car accidents, 50% of homicides and 25% of suicides. [2]
The neurological effects of alcohol use are often a factor in deadly motor vehicle accidents. Operating a motor vehicle or heavy machinery under the influence of alcohol is a serious crime in almost all developed nations.
RISK OF TRAFFIC ACCIDENTS[citation needed]DOSAGERISK0.6 g/l1.5 times the risk0.8 g/l4 times the risk1.5 g/l25 times the risk
[edit] Alcohol compared to other drugs
A 2007 paper in The Lancet attempted to classify drugs by the harm they do; it puts alcohol in fifth place behind heroin, cocaine, barbiturates, and street methadone.[153][154]
Alcohol and cancer
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Alcohol consumption and healthAlcohol and cancerAlcohol and cardiovascular diseaseAlcohol and weightAlcoholic liver diseaseAlcoholismEffects of alcohol on the bodyFetal alcohol syndrome"Considerable evidence suggests a connection between heavy alcohol consumption and increased risk for cancer, with an estimated 2 to 4 percent of all cancer cases thought to be caused either directly or indirectly by alcohol[1]" indicates the NIAAA.[2]" 3.6% of all cancer cases worldwide are related to alcohol drinking, resulting in 3.5% of all cancer deaths."[3]
Contents
[hide]
- <LI class=toclevel-1>1 Alcohol as a carcinogen and cocarcinogen <LI class=toclevel-1>2 Alcohol as risk factor for cancers
<LI class=toclevel-1>3 Effect of alcohol on the progress of cancer when established <LI class=toclevel-1>4 Recommended maximum alcohol intake <LI class=toclevel-1>5 See also <LI class=toclevel-1>6 References <LI class=toclevel-1>7 Source
- <LI class=toclevel-2>2.1 Alcohol is a risk factor for these cancers
<LI class=toclevel-2>2.2 Heavy alcohol drinking appears to be a risk factor for these cancers
- <LI class=toclevel-3>2.1.1 Head and neck cancers <LI class=toclevel-3>2.1.2 Breast cancer
- 2.1.3 Colorectal cancer
<LI class=toclevel-2>2.3 Evidence appears to be inconsistent regarding these cancers
- <LI class=toclevel-3>2.2.1 Liver cancer <LI class=toclevel-3>2.2.2 Ovarian cancer
- 2.2.3 Breast cancer in men
<LI class=toclevel-2>2.4 Alcohol appears to reduce risk of these cancers
- <LI class=toclevel-3>2.3.1 Leukemia <LI class=toclevel-3>2.3.2 Malignant melanoma <LI class=toclevel-3>2.3.3 Prostate cancer
- 2.3.4 Thyroid cancer
<LI class=toclevel-2>2.5 Alcohol appears not to be a risk factor for these cancers
- <LI class=toclevel-3>2.4.1 Hodgkin's lymphoma (HL) <LI class=toclevel-3>2.4.2 Kidney cancer (Renal cell carcinoma) (RCC)
- 2.4.3 Non-Hodgkin's lymphoma
- <LI class=toclevel-3>2.5.1 Bladder cancer <LI class=toclevel-3>2.5.2 Endometrial cancer <LI class=toclevel-3>2.5.3 Gallbladder cancer <LI class=toclevel-3>2.5.4 Lung cancer <LI class=toclevel-3>2.5.5 Pancreatic cancer <LI class=toclevel-3>2.5.6 Small intestine cancer <LI class=toclevel-3>2.5.7 Stomach cancer
- 2.5.8 Vulvar cancer
- 2.5.9 Thirty other cancers
- 8 External links
[edit] Alcohol as a carcinogen and cocarcinogen
The International Agency for Research on Cancer (Centre International de Recherche sur le Cancer) of the World Health Organization has classified alcohol as a Group 1 carcinogen. Its evaluation states, "There is sufficient evidence for the carcinogenicity of alcoholic beverages in humans.… Alcoholic beverages are carcinogenic to humans (Group 1)."[4]
The U.S. National Institute on Alcohol Abuse and Alcoholism (NIAAA) reports that "Although there is no evidence that alcohol itself is a carcinogen, alcohol may act as a cocarcinogen by enhancing the carcinogenic effects of other chemicals. For example, studies indicate that alcohol enhances tobacco's ability to stimulate tumor formation in rats.[5] In humans, the risk for mouth, tracheal, and esophageal cancer is 35 times greater for people who both smoke and drink than for people who neither smoke nor drink,[6] implying a cocarcinogenic interaction between alcohol and tobacco-related carcinogens."[2]
The NIAAA emphasizes that "Although epidemiologic studies have found a clear association between alcohol consumption and development of certain types of cancer, study findings are often inconsistent and may vary by country and by type of cancer."[2]
"Studies have suggested that high concentrations of acetaldehyde, which is produced as the body breaks down ethanol, could damage DNA in healthy cells. … Researchers at the National Institute on Alcohol Abuse and Alcoholism in Bethesda, Maryland, have added weight to this idea by showing that the damage occurs at concentrations of acetaldehyde similar to those in saliva and the gastrointestinal tract while people drink alcohol. Acetaldehyde appears to react with polyamines - naturally occurring compounds essential for cell growth - to create a particularly dangerous type of mutagenic DNA base called a Cr-Pdg adduct…"[7]
[edit] Alcohol as risk factor for cancers
[edit] Alcohol is a risk factor for these cancers
[edit] Head and neck cancers
Head and neck cancers are a collective term for cancers of the:
The U.S. National Cancer Institute's (NCI) Cancer Trends Progress Report Alcohol Consumption states that drinking alcohol increases the risk of these cancers in both men and women. In general, these risks increase above the recommended maximum intake (see below). "Heavy alcohol use … leads to greater increases in risk for most of the alcohol-related cancers. … Also, using alcohol with tobacco is riskier than using either one alone, because it further increases the chances of getting cancers of the mouth, throat, and esophagus."
The International Head and Neck Cancer Epidemiology (INHANCE) Consortium co-ordinates research on this topic – see Pooled analysis investigating the effects of beer, wine and liquor consumption on the risk of head and neck cancers.
A study looking at laryngeal cancer and beverage type concluded, "This study thus indicates that in the Italian population characterized by frequent wine consumption, wine is the beverage most strongly related to the risk of laryngeal cancer."[8]
The American Cancer Society estimates that, as a proportion of all cancer deaths in the US in 2006, cancer of the mouth (oral cavity) will represent 1.3 percent, of the esophagus will be 2.4 percent, of the pharynx will constitute slightly under one-half of one percent, and of the larynx will be about six-tenths of one percent.[9]
Although they are also located in the head or neck, alcohol consumption is not a risk factor for brain cancer, eye cancer, pituitary gland cancer, thymus cancer, salivary gland cancer, thyroid cancer, nasal cavity and paranasal sinus cancer, or adenoid cancer. (see below).
[edit] Breast cancer
Alcohol increases the risk of breast cancer in women. A review concludes that "studies confirm previous observations that there appears to be an association between alcohol intake and increased risk of breast cancer in women. On balance, there was a weak association between the amount of alcohol consumed and the relative risk."[10]
The National Institute on Alcohol Abuse and Alcoholism (NIAAA) concludes that "Chronic alcohol consumption has been associated with a small (averaging 10 percent) increase in a woman's risk of breast cancer[11][12] .[13] According to these studies, the risk appears to increase as the quantity and duration of alcohol consumption increases. Other studies, however, have found no evidence of such a link[14][15][16] .[2] " The nature and inconsistency of the evidence has called into question the existence of any causal link between moderate alcohol consumption and breast cancer [1]
The Committee on Carcinogenicity of Chemicals in Food, Consumer Products concludes, "The new research estimates that a woman drinking an average of two units of alcohol per day has a lifetime risk of developing breast cancer 8% higher than a woman who drinks an average of one unit of alcohol per day. The risk of breast cancer further increases with each additional drink consumed per day. … The research also concludes that approximately 6% (between 3.2% and 8.8%) of breast cancers reported in the UK each year could be prevented if drinking was reduced to a very low level (i.e. less than 1 unit/week)."[17]
It has been reported that "Two drinks daily increase the risk of getting breast cancer by about 25 percent." (NCI) but the evidence is inconsistent. The Framingham study has tracked individuals since the 1940s. Data from that research found that drinking alcohol moderately did not increase breast cancer risk.[18] Similarly, research by the Danish National Institute for Public Health found that moderate drinking had virtually no effect on breast cancer risk.[19] Breast cancer constitutes about 7.3% of all cancers.[9] Among women, breast cancer comprises 60% of alcohol-attributable cancers.[20] One study suggests that women who frequently drink red wine may have an increased risk of developing breast cancer.[21]
Alcohol consumption has been shown to increase the rate of breast cancer in women.[22]
A study of 17,647 nurses found that high drinking levels more than doubled risk of breast cancer. "The relative risk of breast cancer was 2.30 … for alcohol intake of 22–27 drinks per week, compared to 1–3 drinks per week. Among alcohol consumers, weekly alcohol intake increased the risk of breast cancer with 2% for each additional drink consumed. Weekend consumption increased the risk with 4% for each additional drink consumed Friday through Sunday." Binge drinking of 4–5 drinks on the last weekday increased risk by 55%.[23]
"The findings from this prospective study suggest that moderate alcohol consumption increases breast cancer risk."[24]
A study showed that one or two alcoholic drinks a day increases the risk of breast cancer by 10 per cent compared with light drinkers who drank less than one drink a day. Women who have three or more drinks a day increase their risk of breast cancer by 30 per cent. The type of drink was not a factor.[25]
"Folate intake counteracts breast cancer risk associated with alcohol consumption"[26] and "women who drink alcohol and have a high folate intake are not at increased risk of cancer".[27] Those who have a high (200 micrograms or more per day) level of folate (folic acid or Vitamin B9) in their diet are not at increased risk of breast cancer compared to those who abstain from alcohol.[28] A study of over 17,000 Australian women aged 40-69 over a period of about ten years found that those who consumed 40 grams of alcohol (about three to four drinks) per day have a higher risk of breast cancer than do women who abstain from alcohol. However, in women who take 200 micrograms of folate or folic acid (Vitamin B9) every day, the risk of breast cancer drops below that of alcohol abstainers. (Baglietto, Laura, et al. Does dietary folate intake modify effect of alcohol consumption on breast cancer risk? Prospective cohort study. British Medical Journal, August 8, 2005) See Folic acid for more.
A study on mice suggests that, when breast cancer is established, drinking as little as two alcoholic drinks a day increases the growth rate of tumors. Alcohol causes cancer cells' blood vessels to grow which in turn fuels the growth of the tumor, a process known as angiogenesis.[29]
[edit] Colorectal cancer
Colorectal cancer refers to cancers of the colon or rectum. Colorectal cancer constitutes about 9.7% of all cancers.[9]The National Cancer Institute does not list alcohol as a risk factor.[30]
The NIAAA reports that, "Epidemiologic studies have found a small but consistent dose-dependent association between alcohol consumption and colorectal cancer[31][32]even when controlling for fiber and other dietary factors.[33][34] Despite the large number of studies, however, causality cannot be determined from the available data."[2]
"Heavy alcohol use may also increase the risk of colorectal cancer" (NCI). One study found that "People who drink more 30 grams of alcohol per day (and especially those who drink more than 45 grams per day) appear to have a slightly higher risk for colorectal cancer."[35][36] Another found that "The consumption of one or more alcoholic beverages a day at baseline was associated with approximately a 70% greater risk of colon cancer."[37][38][39]
One study found that "While there was a more than twofold increased risk of significant colorectal neoplasia in people who drink spirits and beer, people who drank wine had a lower risk. In our sample, people who drank more than eight servings of beer or spirits per week had at least a one in five chance of having significant colorectal neoplasia detected by screening colonoscopy.".[40]
Other research suggests that "to minimize your risk of developing colorectal cancer, it's best to drink in moderation"[2]
The EPIC study suggests that "people who drink 15 grams of alcohol a day - equivalent to about two units - have about a 10 per cent increased risk of bowel cancer. Those who drank more than 30 grams of alcohol - equivalent to three to four units which is less than a couple of pints of strong lager - increased their bowel cancer risk by around 25 per cent." [41][42]
In “Moderate Alcohol Consumption Protects Against Colorectal Adenoma, ” Dr. Gregory Austin of the University of North Carolina at Chapel Hill and his colleagues found from an analysis of a case control study of patients who underwent a full colonoscopy that abstainers or non-drinkers had a 40% higher risk of adenoma than did those who consumed beer, wine, or liquor (distilled spirits) in moderation. The researchers conclude that “Individuals who consume moderate amounts of alcohol are at lower risk of colorectal adenomas than nondrinkers and heavy drinkers.” (Austin, Gregory, et al. Moderate Alcohol Consumption Protects Against Colorectal Adenoma. Paper presented at Digestive Diseases Week (DDW), May 24, 2006 , abstract M2263) [2]
Drinking may be a cause of earlier onset of colorectal cancer.[43]
[edit] Heavy alcohol drinking appears to be a risk factor for these cancers
[edit] Liver cancer
The NIAAA reports that "Prolonged, heavy drinking has been associated in many cases with primary liver cancer." However, it is liver cirrhosis, whether caused by alcohol or another factor, that is thought to induce the cancer."[44][45]
"The chances of getting liver cancer increase markedly with five or more drinks per day" (NCI). However, the risk is cut dramatically by consuming coffee daily.[46] Research has now demonstrated that drinking four cups of coffee per day reduces alcoholic cirrhosis risk by 80% among both men and women of different racial categories (Klatsky et al., Coffee, cirrhosis, and tranaminase enzymes. Archives of Internal Medicine, 2006, 166, 1190-1195).
In areas of Africa and Asia, liver cancer afflicts 50 or more people per 100,000 per year, usually associated with cirrhosis caused by hepatitis viruses. In the United States, liver cancer is relatively uncommon, afflicting approximately 2 people per 100,000, but excessive alcohol consumption is linked to as many as 36% of these cases by some investigators[1][47][2] "Mortality rates of hepatocellular carcinoma (HCC) are high in Italy compared with other Western countries. … Overall, 61% of HCC were attributable to HCV [hepatitis C virus], 13% to HBV [hepatitis B virus], and 18% to heavy alcohol drinking."[48] A study in the province of Brescia, northern Italy concluded, "On the basis of population attributable risks (AR), heavy alcohol intake seems to be the single most relevant cause of HCC in this area (AR: 45%), followed by HCV (AR: 36%), and HBV (AR: 22%) infection."[49]
Liver and intrahepatic bile duct cancers combined account for about 2.8% of all cancers.[9]
[edit] Ovarian cancer
"Associations were also found between alcohol consumption and cancers of the ovary …, but only for 50 g and 100 g a day."[50] "Thus, the results of this study suggest that relatively elevated alcohol intake (of the order of 40 g per day or more) may cause a modest increase of epithelial ovarian cancer risk."[51]
[edit] Breast cancer in men
"Heavy alcohol intake increases the risk of breast cancer in men."[52] "If you drink heavy amounts of alcohol, you have a greater risk of breast cancer."[53]
Male breast cancer is very rare and, in Western populations, the incidence is less than one case per 100,000 men. Male Breast Cancer
[edit] Evidence appears to be inconsistent regarding these cancers
[edit] Leukemia
Leukemia (British spelling: leukaemia). There is no association between drinking alcohol and adult leukemia.
“Results from the few studies that have examined the association between alcohol use during pregnancy and childhood leukemia are conflicting,” reported a study that found an association."[54] A review published by the National Cancer Institute placed maternal alcohol consumption during pregnancy in the category of “suggestive” and asserts that it is “unlikely to be an important risk factor.” [55]
Leukemia constitutes about 7.8% of all cancers.[9]
[edit] Malignant melanoma
"In interview data from the U.S.A.'s Third National Cancer Survey, alcohol ingestion was associated with a higher occurrence of cancers of the breast, thyroid, and malignant melanoma. Data from other studies support the first two associations."[56] "High alcohol consumption was associated with an increased risk for melanoma, which remained after adjustment for confounders…".[57] Other studies suggest there is no association for melanoma. "The risk of malignant melanoma was not influenced by alcohol consumption or smoking habits."[58] "There was no evidence that … alcohol or polyunsaturated fats were associated with an increased risk."[59]
There is no association between alcohol and Nonmelanoma skin cancer.
[edit] Prostate cancer
"Associations were also found between alcohol consumption and cancers of the ovary and prostate, but only for 50 g and 100 g a day."[50] However, one study concludes, "In contrast to the majority of previous studies, we found a positive association between moderate alcohol consumption and the risk of prostate cancer. Liquor, but not wine or beer, consumption was positively associated with prostate cancer."[60]
The Fred Hutchinson Cancer Research Center "found that men who consumed four or more glasses of red wine per week reduced their risk of prostate cancer by 50 percent". They "found no significant effects — positive nor negative — associated with the consumption of beer or hard liquor and no consistent risk reduction with white wine, which suggests that there must be a beneficial compound in red wine that other types of alcohol lack. That compound … may be an antioxidant called resveratrol, which is abundant in the skins of red grapes.".[61][62]
Prostate cancer accounts for about 4.8% of all cancers.[9]
[edit] Thyroid cancer
"In interview data from the U.S.A.'s Third National Cancer Survey, alcohol ingestion was associated with a higher occurrence of cancers of the breast, thyroid, and malignant melanoma. Data from other studies support the first two associations."[56] Another study suggests that drinking in moderation significantly reduces the risk of some malignant tumors such as thyroid cancer in women.[63] However, another study concludes, "A reduced risk associated with alcohol was eliminated after adjustment for smoking…".[64]
[edit] Alcohol appears to reduce risk of these cancers
[edit] Hodgkin's lymphoma (HL)
"Our study indicates a protective effect of alcohol consumption for nonsmoking HL cases."[65]
The National Cancer Institute does not list alcohol consumption as a risk factor for Hodgkin's lymphoma.[3]
[edit] Kidney cancer (Renal cell carcinoma) (RCC)
Moderate alcohol consumption appears to reduce the risk of kidney cancer. An analysis of data from 760,044 men and women who were tracked for seven to 20 years found that moderate drinkers are about 30% less likely to develop renal cell cancer than are abstainers. (Lee, J. E. et al. Alcohol intake and renal cell cancer in a pooled analysis of 12 prospective studies. Journal of the National Cancer Institute, 2007, 99, 811-822.)
A large prospective study of 59,237 Swedish women age 40-76 found that those who consumed at least one drink per week had a 38% lower risk of kidney cancer than did abstainers or those who drank less. For women over 55, the risk dropped by two-thirds (66%). [66]
A small study concluded that its "findings suggest an inverse association of alcohol consumption and RCC development among women but not among men."[67] Another small study concluded that "No significant relationship emerged, nor any differences between the sexes."[68]
[edit] Non-Hodgkin's lymphoma
A review of findings from nine international studies suggests that drinking alcohol reduces the risk of non-Hodgkin’s lymphoma (NHL) by 27%. The protective effect of alcohol did not vary by beverage type. "People who drink alcoholic beverages might have a lower risk of NHL than those who do not, and this risk might vary by NHL subtype. Further study designs are needed to determine whether confounding lifestyle factors or immunomodulatory effects of alcohol explain this association.".[69] The research also found that, in addition, alcohol's protective effect varies by form or subtype of non-Hodgkin‘s lymphoma. Drinkers were about half as likely as non-drinkers to develop Burkitt's lymphoma.
The cancer is the sixth most common in the USA.
[edit] Alcohol appears not to be a risk factor for these cancers
[edit] Bladder cancer
"Our data suggest that total and beverage-specific alcohol consumption are not associated with an increased risk of bladder cancer."[70] A Dutch study concludes, "The results of this study do not suggest an important association between alcohol consumption and bladder cancer risk."[71] Bladder cancer represents about 2.3% of all cancers.
[edit] Endometrial cancer
"Thirteen studies to date have reported on the relationship between endometrial cancer and alcohol consumption. Only two of these studies have reported that endometrial cancer incidence is associated with consumption of alcohol; all the others have reported either no definite association, or an inverse association." (Six studies showed an inverse association; that is, drinking was associated with a lower risk of endometrial cancer) "…if such an inverse association exists, it appears to be more pronounced in younger, or premenopausal, women."[72]
Endometrial plus all other uterine cancers account for about 1.9% of all cancers.[9]
[edit] Gallbladder cancer
The National Cancer Institute does not list alcohol as a risk factor for gallbladder cancer (National Cancer Institute. General Information about Gallbladder Cancer).
A letter to the editor of the International Journal of Cancer [4] suggested that “incidence differences for gallbladder cancer between occupational groups suggest an etiological role for alcohol.” The investigators did not use any direct measure of alcohol consumption and their surrogate indicator was confounded by smoking. They reported that “Occupations with high consumption of alcohol and/or high prevalence of smoking associated with a risk of liver and gallbladder cancers” which led to their conclusion that “alcohol drinking is a risk factor of gallbladder cancer because of the covariation of primary liver and gallbladder cancers in occupational groups.” (Ji, J; Hemminki K (2005 Sep). "Variation in the risk for liver and gallbladder cancers in socioeconomic and occupational groups in Sweden with etiological implications". Int Arch Occup Environ Health 78 (8): 641-9) However covariation alone cannot establish that any variable is a risk factor.
Researchers using direct measures of drinking have not found alcohol to be a risk factor for the disease. A French study of female gallbladder patients found that only 2% consumed alcohol [5] and a Polish case-controlled study found no relationship between alcohol consumption and the disease .[6]
A large multicultural case-control study of gallbladder cancer was conducted in Australia, Canada, the Netherlands and Poland with the Surveillance of environmental Aspects Related to Cancer in Humans (SEARCH) Program of the International Agency for Research on Cancer (IARC). It found no evidence that alcohol is a risk factor for gallbladder cancer. [7]
[edit] Lung cancer
"Globally, lung cancer is the most frequent malignancy in males, while it is the fifth most common cancer in females." [8] It is a major cause of death, constituting about 28.8% of all cancers.[9] The NIAA reports that “A few studies have linked chronic heavy drinking with cancers of the stomach, pancreas, and lungs (International Agency for Research on cancer). However, the association is consistently weak and the majority of studies have found no association (International Agency for Research on Cancer).”[2]
Chronic heavy alcohol consumption possibly increases the risk of lung cancer, but the evidence is inadequate to date.[73] Commenting on a study by Freudenheim et al[74] R. Curtis Ellison MD writes, "This study, like others, suggests a weak, positive association between consuming larger amounts of alcohol (>2 drinks a day) and lung cancer risk."[75]
[edit] Pancreatic cancer
"A few studies have linked chronic heavy drinking with cancers of the stomach, pancreas, and lungs. However, the association is consistently weak and the majority of studies have found no association", write the NIAAA,[2] citing the International Agency for Research on Cancer..[76] Alcohol has been reported as a possible risks in some (but not in most) studies.[77] Drinking alcohol excessively is a cause of acute pancreatitis and chronic pancreatitis. "About 7 out of 10 cases of chronic pancreatitis are due to long term heavy drinking. Chronic pancreatitis is a known risk factor for cancer of the pancreas. But chronic pancreatitis that is due to alcohol doesn't increase risk as much as other types of chronic pancreatitis. So if there is a link with alcohol and pancreatic cancer risk, it is only very slight."[78]
Pancreatic cancer constitutes about 5.7% of all cancers.
[edit] Small intestine cancer
The National Cancer Institute does not list alcohol as a possible risk factor for cancer of the small intestine. [9]
[edit] Stomach cancer
As indicated above, the NIAA reports that “A few studies have linked chronic heavy drinking with cancers of the stomach, pancreas, and lungs (International Agency for Research on cancer). However, the association is consistently weak and the majority of studies have found no association (International Agency for Research on Cancer).”[2]
Alcohol consumption, even when chronic and heavy, probably does not affect the risk of stomach cancer.[73]
[edit] Vulvar cancer
The American Caner Society does not list alcohol as a risk factor for this disease [10] "No consistent association emerged between milk, meat, liver, alcohol and coffee consumption and risk of vulvar cancer."[79]
[edit] Thirty other cancers
Alcohol is not listed as a risk factor for any of the following cancers
- Adenoid cancer [11] [12]
- Adrenal gland cancer [13]
- Anal cancer [14]
- Appendix cancer[80]
- Bile duct cancer [15]
- Bone cancer [16]
- Brain cancer [17]
- Central nervous system cancer (craniopharyngioma) [18]
- Cervical cancer [19]
- Ewing's family of tumors [20]
- Extragonal germ cell cancer [21]
- Extrahepatic bile duct cancer [22]
- Eye cancer [23] [24]
- Fallopian tube cancer [25]
- Kaposi's sarcoma [26]
- Malignant mesothelioma [27]
- Nasal cavity and paranasal sinus cancer [28]
- Penile cancer[29]
- Pituitary gland cancer [30]
- Pleuropulmonary blastoma [31]
- Salivary gland cancer [32]
- Skin cancer [33]
- Soft tissue cancers [34]
- Spinal cancer [35]
- Testicular cancer[36]
- Thymus cancer [37]
- Transitional cell cancer of renal pelvis and ureter [38]
- Urethral cancer [39]
- Vaginal cancer [40]
[edit] Effect of alcohol on the progress of cancer when established
A study of the influence of alcohol intake on tumor growth of hepatocellular carcinoma (HCC) in patients with type C cirrhosis, found that alcohol influenced tumor volume doubling time (TVDT). "In conclusion we found that alcohol intake was closely related to the tumor growth of HCC in patients with type C cirrhosis."[81]
A study of chick embryos suggests that alcohol stimulates their tumor growth by fueling the production of a growth factor that stimulates blood vessel development in tumors.[82][83] A 2006 study in mice showed moderate drinking resulted in larger and more robust tumors.[84]
A study where high amounts of alcohol were given to mice suggests that it accelerates their cancer growth by speeding up the loss of body fat and depressing immune activity - particularly that of 'killer t-cells'.[85][86]
[edit] Recommended maximum alcohol intake
Main article: Recommended maximum intake of alcoholic beverages
As outlined above, there is no recommended alcohol intake with respect to cancer risk alone as it varies with each individual cancer. See Recommended maximum intake of alcoholic beverages for a list of governments' guidances on alcohol intake which, for a man, range from 140–280g per week.
One meta-analysis suggests that risks of cancers may start below the recommended levels. "Risk increased significantly for drinkers, compared with non-drinkers, beginning at an intake of 25 g (< 2 standard drinks) per day for the following: cancers of the oral cavity and pharynx (relative risk, RR, 1.9), esophagus (RR 1.4), larynx (RR 1.4), breast (RR 1.3), liver (RR 1.2), colon (RR 1.1), and rectum (RR 1.1)"[87][88]
Alternatively, the actual quantities of alcohol associated with negative effects may be substantially higher than generally reported because participants in medical research studies tend to underestimate and underreport their usual amounts of alcohol consumption.[89]
[edit] Relative health risks
An increase in risk of a particular cancer through drinking needs to balanced against the benefits of moderate drinking on reducing heart attacks. See Alcohol and heart attacks for more. There are, of course, many ways of reducing your risk of a heart attack either without, or in addition to, drinking alcohol, such as controlling your weight and exercising. Balancing such risks is a personal decision that should be discussed with one’s own physician.
Alcoholic liver disease
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Alcoholic liver disease
Classification & external resourceshttp://upload.wikimedia.org/wikipedi..._hepatitis.jpg
Microscopy of liver showing fatty change, cell necrosis, Mallory bodiesICD-10K70.ICD-9571.1MedlinePlus000281MeSHD008108Alcoholic liver disease is the major cause of liver disease in Western countries, (in Asian countries, viral hepatitis is the major cause). It arises from the excessive ingestion of alcohol.
Alcohol consumption and healthAlcohol and cancerAlcohol and cardiovascular diseaseAlcohol and weightAlcoholic liver diseaseAlcoholismEffects of alcohol on the bodyFetal alcohol syndromeContents
[hide]
- <LI class=toclevel-1>1 Pathophysiology
- <LI class=toclevel-2>1.1 Fatty change <LI class=toclevel-2>1.2 Alcoholic hepatitis <LI class=toclevel-2>1.3 Liver fibrosis
- 1.4 Cirrhosis
- 2 References
[edit] Pathophysiology
http://upload.wikimedia.org/wikipedi...ver_injury.jpg http://en.wikipedia.org/skins-1.5/co...gnify-clip.png
Pathogenesis of alcohol induced liver injury
Fatty change and alcoholic hepatitis are probably reversible. The later stages of fibrosis and cirrhosis tend to be irreversible but can usually be quite well managed for long periods of time.
[edit] Fatty change
Main article: Fatty liver
Fatty change, or steatosis is the accumulation of fat in liver cells which can be seen as fatty globules under the microscope. Alcoholism causes large fatty globules (macrovesicular steatosis). Small fatty globules have different causes. Other causes of macrovesicular steatosis include diabetes, obesity and starvation. Alcoholic fatty change is probably dose related.
[edit] Alcoholic hepatitis
Main article: Alcoholic hepatitis
Some people get an acute hepatitis or inflammatory reaction to the cells affected by fatty change. This is not directly related to the dose of alcohol. Some people seem more prone to this reaction than others. This is called alcoholic steatonecrosis and the inflammation probably predisposes to liver fibrosis.
[edit] Liver fibrosis
Liver fibrosis, in itself, is largely asymptomatic but as it progresses it can turn into cirrhosis, where the fibrosis alters the architecture and impairs the function of the liver.
[edit] Cirrhosis
Main article: cirrhosis
Cirrhosis is a late stage of liver disease marked by fibrosis and altered liver architecture. It is often progressive and may eventually lead to liver failure. Late complications of cirrhosis or liver failure include portal hypertension, coagulation disorders, ascites and other complications including hepatic encephalopathy and the hepatorenal syndrome.
Cirrhosis also has number of other causes, such as hepatitis and toxins. The late stages of cirrhosis (say from viral hepatitis or alcohol) may look similar. This phenomenon is termed a "final common pathway" for a disease.
Fetal alcohol syndrome
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Jump to: navigation, search
Fetal Alcohol Syndrome (FAS)
Classification & external resourceshttp://upload.wikimedia.org/wikipedi...px-FASbaby.jpg
A baby with Fetal Alcohol Syndrome (FAS)ICD-10Q86.0.ICD-9760.71DiseasesDB32957MedlinePlus000911eMedicineped/767 MeSHD005310Alcohol consumption and healthAlcohol and cancerAlcohol and cardiovascular diseaseAlcohol and weightAlcoholic liver diseaseAlcoholismEffects of alcohol on the bodyFetal alcohol syndromeFetal alcohol syndrome or FAS is a disorder of permanent birth defects that occurs in the offspring of women who drink alcohol during pregnancy. It is unknown whether amount, frequency or timing of alcohol consumption during pregnancy causes a difference in amount of damage done to the fetus. Thus, the current recommendation is not to drink at all during pregnancy. Alcohol crosses the placental barrier and can stunt fetal growth or weight, create distinctive facial stigmata, damage neurons and brain structures, and cause other physical, mental, or behavioural problems.[1][2][3]
The main effect of FAS is permanent and nonsubsequinciel central nervous system damage, especially the brain. Developing brain cells and structures are underdeveloped or malformed by prenatal alcohol exposure, often creating an array of primary cognitive and functional disabilities (including poor memory, attention deficits, impulsive behavior, and poor cause-effect reasoning) as well as secondary disabilities (for example, mental health problems, and drug addiction).[3][4] The risk of brain damage exists during each trimester, since the fetal brain develops throughout the entire pregnancy.[5]
Fetal alcohol exposure is the leading known cause of mental retardation in the Western world.[6] In the United States alone, the FAS prevalence rate is estimated to be between 0.2 and 2.0 cases per 1,000 live births, comparable to or higher than other developmental disabilities such as Down syndrome or Spina Bifida.[7] The lifetime medical and social costs of each child with FAS are estimated to be as high as US$800,000.[8] While prenatal alcohol exposure does not automatically result in FAS, the U.S. Surgeon General advises pregnant women to abstain from alcohol use due to the risk of FAS.[9]
Contents
[hide]
- <LI class=toclevel-1>1 History
<LI class=toclevel-1>2 Diagnosis <LI class=toclevel-1>3 Signs and symptoms
- <LI class=toclevel-2>1.1 Historical references
- 1.2 Recognition as a syndrome
<LI class=toclevel-1>4 Prognosis
- <LI class=toclevel-2>3.1 Growth deficiency <LI class=toclevel-2>3.2 Facial features <LI class=toclevel-2>3.3 Central nervous system damage
<LI class=toclevel-2>3.4 Prenatal alcohol exposure
- <LI class=toclevel-3>3.3.1 Structural <LI class=toclevel-3>3.3.2 Neurological
- 3.3.3 Functional
- <LI class=toclevel-3>3.4.1 Confirmed exposure
- 3.4.2 Unknown exposure
- 3.5 Related signs
<LI class=toclevel-1>5 Treatment
- <LI class=toclevel-2>4.1 Primary disabilities <LI class=toclevel-2>4.2 Secondary disabilities
- 4.3 Protective factors and strengths
<LI class=toclevel-1>6 Prevention <LI class=toclevel-1>7 See also <LI class=toclevel-1>8 References <LI class=toclevel-1>9 Further reading
- <LI class=toclevel-2>5.1 Medical interventions <LI class=toclevel-2>5.2 Behavioral interventions <LI class=toclevel-2>5.3 Developmental framework <LI class=toclevel-2>5.4 Advocacy model <LI class=toclevel-2>5.5 Neurobehavioral approach
- 5.6 Public health and policy
- 10 External links
[edit] History
[edit] Historical references
Anecdotal accounts of prohibitions against maternal alcohol use from biblical, ancient Greek, and ancient Roman sources imply a historical awareness of links between maternal alcohol use and negative child outcomes.[10] This assertion has been repeated in articles and books, but a more recent review of the original source material does not support such ancient knowledge.[11]
The earliest known observation of possible links between maternal alcohol use and fetal damage was made in 1899 by Dr. William Sullivan, a Liverpool prison physician who noted higher rates of stillbirth for 120 alcoholic female prisoners than their sober female relatives; he suggested the causal agent to be alcohol use.[12] This contradicted the predominating belief at the time that heredity caused mental retardation, poverty, and criminal behavior, which contemporary studies on the subjects usually concluded.[3] A case study by Henry H. Goddard of the Kallikak family — popular in the early 1900s — represents this earlier perspective,[13] though later researchers have suggested that the Kallikaks almost certainly had FAS.[14] General studies and discussions on alcoholism throughout the mid-1900s were typically based on a heredity argument.[15]
Prior to fetal alcohol syndrome being specifically identified and named in 1973, a few studies had noted differences between the children of mothers who used alcohol during pregnancy or breast-feeding and those who did not, but identified alcohol use as a possible contributing factor rather than heredity.[3]
[edit] Recognition as a syndrome
Fetal Alcohol Syndrome was named in 1973 by two dysmorphologists, Drs. Kenneth Lyons Jones and David W. Smith of the University of Washington Medical School in Seattle, United States. They identified a pattern of "craniofacial, limb, and cardiovascular defects associated with prenatal onset growth deficiency and developmental delay" in eight unrelated children of three ethnic groups, all born to mothers who were alcoholics.[16] The pattern of malformations indicated that the damage was prenatal. News of the discovery shocked some, while others were skeptical of the findings.[17]
Dr. Paul Lemoine of Nantes, France had already published a study in a French medical journal in 1968 about children with distinctive features whose mothers were alcoholics,[2] and in the U.S., Christy Ulleland and colleagues at the University of Washington Medical School[1] had conducted an 18-month study in 1968-1969 documenting the risk of maternal alcohol consumption among the offspring of 11 alcoholic mothers. The Washington and Nantes findings were confirmed by a research group in Gothenburg, Sweden in 1979.[18] Researchers in France, Sweden, and the United States were struck by how similar these children looked, though they were not related, and how they behaved in the same unfocused and hyperactive manner.[18]
Within four years of the Washington discovery, animal studies, including non-human primate studies carried out at the University of Washington Primate Center by Dr. Sterling Clarren, had confirmed that alcohol was a teratogen. By 1978, 245 cases of FAS had been reported by medical researchers, and the syndrome began to be described as the most frequent known cause of mental retardation.
While many syndromes are eponymous, i.e. named after the physician first reporting the association of symptoms, Dr. Smith named FAS the causal agent of the symptoms.[19] He reasoned that doing so would encourage prevention, believing that if people knew maternal alcohol consumption caused the syndrome, then abstinence during pregnancy would follow from patient education and public awareness.[19] Nobody was aware of the full range of possible birth defects from FAS or its prevalence rate at that time,[19] but admission of alcohol use during pregnancy can feel stigmatizing to birth mothers and complicate diagnostic efforts[7] of a syndrome with its preventable cause in the name.
Over time, as subsequent research and clinical experience suggested that a range of effects (including physical, behavioral, and cognitive) could arise from prenatal alcohol exposure, the term Fetal Alcohol Spectrum Disorder (FASD) was developed to include FAS as well as other conditions resulting from prenatal alcohol exposure.[19] Currently, FAS[16][20][21] is the only expression of prenatal alcohol exposure defined by the International Statistical Classification of Diseases and Related Health Problems and assigned ICD-9 and ICD-10 diagnoses.
[edit] Diagnosis
Several diagnostic systems have been developed in North America:
Fetal alcohol syndrome is the only expression of FASD that has garnered consensus among experts to become an official ICD-9 and ICD-10 diagnosis. To make this diagnosis (or determine any FASD condition), a multi-disciplinary evaluation is necessary to assess each of the four key features for assessment. Generally, a trained physician will determine growth deficiency and FAS facial features. While a qualified physician may also assess central nervous system structural abnormalities and/or neurological problems, usually central nervous system damage is determined through psychological, speech-language, and occupational therapy assessments. Prenatal alcohol exposure risk may be assessed by a qualified physician, psychologist, social worker, or chemical health counselor. These professionals work together as a team to assess and interpret data of each key feature for assessment and develop an integrative, multi-disciplinary report to diagnose FAS (or other FASD conditions) in an individual.
- The Institute of Medicine's guidelines for FAS, the first system to standardize diagnoses of individuals with prenatal alcohol exposure,[21]
- The University of Washington's "The 4-Digit Diagnostic Code," which ranks the four key features of FASD on a Likert scale of one to four and yields 256 descriptive codes that can be categorized into 22 distinct clinical categories, ranging from FAS to no findings,).[22]
- The Centers for Disease Control's "Fetal Alcohol Syndrome: Guidelines for Referral and Diagnosis," which established general consensus on the diagnosis FAS in the U.S. but deferred addressing other FASD conditions,[7] and
- Canadian guidelines for FASD diagnosis, which established criteria for diagnosing FASD in Canada and harmonized most differences between the IOM and University of Washington's systems.[23]
The following criteria must be fully met for an FAS diagnosis:[22][21][7][23]
- Growth deficiency — Prenatal or postnatal height or weight (or both) at or below the 10th percentile[24]
- FAS facial features — All three FAS facial features present[25]
- Central nervous system damage — Clinically significant structural, neurological, or functional impairment
- Prenatal alcohol exposure — Confirmed or Unknown prenatal alcohol exposure
[edit] Differential diagnosis
The CDC reviewed nine syndromes that have overlapping features with FAS; however, none of these syndromes include all three FAS facial features, and none are the result of prenatal alcohol exposure:[7]
- Aarskog syndrome
- Williams syndrome
- Noonan's syndrome
- Dubowitz syndrome
- Brachman-DeLange syndrome
- Toluene syndrome
- Fetal hydantoin syndrome
- Fetal valproate syndrome
- Maternal PKU fetal effects
[edit] Signs and symptoms
[edit] Growth deficiency
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Newborn infant with FAS.
Growth deficiency is defined as significantly below average height, weight or both due to prenatal alcohol exposure, and can be assessed at any point in the lifespan. Growth measurements must be adjusted for parental height, gestational age (for a premature infant), and other postnatal insults (e.g., poor nutrition), although birth height and weight are the preferred measurements.[22] Deficiencies are documented when height or weight falls at or below the 10th percentile of standardized growth charts appropriate to the patient's population.[24]
The CDC and Canadian guidelines use the 10th percentile as a cut-off to determine growth deficiency.[7][23] The "4-Digit Diagnostic Code" allows for mid-range gradations in growth deficiency (between the 3rd and 10th percentiles) and severe growth deficiency at or below the 3rd percentile.[22] Growth deficiency (at severe, moderate, or mild levels) contributes to diagnoses of FAS and PFAS (Partial Fetal Alcohol Syndrome), but not ARND (Alcohol-Related Neurodevelopmental Disorder) or static encephalopathy.
Growth deficiency is ranked as follows by the "4-Digit Diagnostic Code:"[22]
- Severe — Height and weight at or below the 3rd percentile.
- Moderate — Either height or weight at or below the 3rd percentile, but not both.
- Mild — Either height or weight or both between the 3rd and 10th percentiles.
- None — Height and weight both above the 10th percentile.
[edit] Facial features
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A thin upper lip and smooth philtrum are diagnostic of FAS.
Several characteristic craniofacial abnormalities are visible in individuals with FAS.[26] The presence of FAS facial features indicates brain damage, though brain damage may also exist in their absence. FAS facial features (and most other visible, but non-diagnostic, deformities) are believed to be caused mainly during the 10th and 20th week of gestation.[27]
Refinements in diagnostic criteria since 1975 have yielded three distinctive and diagnostically significant facial features known to result from prenatal alcohol exposure and distinguishes FAS from other disorders with partially overlapping characteristics.[28][29] The three FAS facial features are:
Measurement of FAS facial features uses criteria developed by the University of Washington. The lip and philtrum are measured by a trained physician with the Lip-Philtrum Guide,[30] a 5-point Likert Scale with representative photographs of lip and philtrum combinations ranging from normal (ranked 1) to severe (ranked 5). Palpebral fissure length (PFL) is measured in millimeters with either calipers or a clear ruler and then compared to a PFL growth chart, also developed by the University of Washington.[25]
- A smooth philtrum — The divot or groove between the nose and upper lip flattens with increased prenatal alcohol exposure (see photo at right).
- Thin vermilion — The upper lip thins with increased prenatal alcohol exposure (see photo at right).
- Small palpebral fissures — Eye width shortens with increased prenatal alcohol exposure.
Ranking FAS facial features is complicated because the three separate facial features can be affected independently by prenatal alcohol. A summary of the criteria follows:[22][31]
These distinctive facial features in a patient does strongly correlate to brain damage. Sterling Clarren of the University of Washington's Fetal Alcohol and Drug Unit told a conference in 2002:
- Severe — All three facial features ranked independently as severe (lip ranked at 4 or 5, philtrum ranked at 4 or 5, and PFL less than or equal to two standard deviations below average).
- Moderate — Two facial features ranked as severe and one feature ranked as moderate (lip or philtrum ranked at 3, or PFL between one and two standard deviations below average).
- Mild — A mild ranking of FAS facial features covers a broad range of facial feature combinations:
- Two facial features ranked severe and one ranked within normal limits,
- One facial feature ranked severe and two ranked moderate, or
- One facial feature ranked severe, one ranked moderate and one ranked within normal limits.
- None — All three facial features ranked within normal limits.
I have never seen anybody with this whole face who doesn't have some brain damage. In fact in studies, as the face is more FAS-like, the brain is more likely to be abnormal. The only face that you would want to counsel people or predict the future about is the full FAS face. But the risk of brain damage increases as the eyes get smaller, as the philtrum gets flatter, and the lip gets thinner. The risk goes up but not the diagnosis.At one-month gestation, the top end of your body is a brain, and at the very front end of that early brain, there is tissue that has been brain tissue. It stops being brain and gets ready to be your face ... Your eyeball is also brain tissue. It's an extension of the second part of the brain. It started as brain and "popped out." So if you are going to look at parts of the brain from alcohol damage, or any kind of damage during pregnancy, eye malformations and midline facial malformations are going to be very actively related to the brain across syndromes ... and they certainly are with FAS.[32][edit] Central nervous system damage
http://upload.wikimedia.org/wikipedi...FASbrains2.gif http://en.wikipedia.org/skins-1.5/co...gnify-clip.png
The image shows the brains of two six-week-old infants. The left brain is confirmed no alcohol exposure, while the right brain is of an infant with FAS. [1]
Central nervous system (CNS) damage is the primary feature of any FASD diagnosis. Prenatal alcohol exposure, a teratogen, can damage the brain across a continuum of gross to subtle impairments, depending on the amount, timing, and frequency of the exposure as well as genetic predispositions of the fetus and mother.[21][33] While functional abnormalities are the behavioral and cognitive expressions of the FAS disability, CNS damage can be assessed in three areas: structural, neurological, and functional impairments.
All four diagnostic systems allow for assessment of CNS damage in these areas, but criteria vary. The IOM system requires structural or neurological impairment for a diagnosis of FAS.[21] The "4-Digit Diagnostic Code" and CDC guidelines state that functional anomalies must measure at two standard deviations or worse in three or more functional domains for a diagnoses of FAS.[22][7] The "4-Digit Diagnostic Code" further elaborates the degree of CNS damage according to four ranks:
- Definite — Structural impairments or neurological impairments for FAS or static encephalopathy.
- Probable — Significant dysfunction of two standard deviations or worse in three or more functional domains.
- Possible — Mild to moderate dysfunction of two standard deviations or worse in one or two functional domains or by judgment of the clinical evaluation team that CNS damage cannot be dismissed.
- Unlikely — No evidence of CNS damage.
[edit] Structural
Structural abnormalities of the brain are observable, physical damage to the brain or brain structures caused by prenatal alcohol exposure. Structural impairments may include microcephaly (small head size) of two or more standard deviations below the average, or other abnormalities in brain structure (e.g., agenesis of the corpus callosum, cerebellar hypoplasia).[21]
Microcephaly is determined by comparing head circumference (often called occipitofrontal circumference, or OFC) to appropriate OFC growth charts.[24] Other structural impairments must be observed through medical imaging techniques by a trained physician. Because imaging procedures are expensive and relatively inaccessible to most patients, diagnosis of FAS is not frequently made via structural impairments, except for microcephaly.
Evidence of a CNS structural impairment due to prenatal alcohol exposure will result in a diagnosis of FAS, and neurological and functional impairments are highly likely.[21][22][7][23]
During the first trimester of pregnancy, alcohol interferes with the migration and organization of brain cells, which can create structural deformities or deficits within the brain.[34] During the third trimester, damage can be caused to the hippocampus, which plays a role in memory, learning, emotion, and encoding visual and auditory information, all of which can create neurological and functional CNS impairments as well.[35]
As of 2002, there were 25 reports of autopsies on infants known to have FAS. The first was in 1973, on an infant who died shortly after birth.[10] The examination revealed extensive brain damage, including microcephaly, migration anomalies, callosal dysgenesis, and a massive neuroglial, leptomeningeal heterotopia covering the left hemisphere.[36]
In 1977, Dr. Clarren described a second infant whose mother was a binge drinker. The infant died ten days after birth. The autopsy showed severe hydrocephalus, abnormal neuronal migration, and a small corpus callosum (which connects the two brain hemispheres) and cerebellum.[36] FAS has also been linked to brainstem and cerebellar changes, agenesis of the corpus callosum and anterior commissure, neuronal migration errors, absent olfactory bulbs, meningomyelocele, and porencephaly.[36]
[edit] Neurological
When structural impairments are not observable or do not exist, neurological impairments are assessed. In the context of FAS, neurological impairments are caused by prenatal alcohol exposure which causes general neurological damage to the central nervous system (CNS), the peripheral nervous system, or the autonomic nervous system. A determination of a neurological problem must be made by a trained physician, and must not be due to a postnatal insult, such as a high fever, concussion, traumatic brain injury, etc.
All four diagnostic systems show virtual agreement on their criteria for CNS damage at the neurological level, and evidence of a CNS neurological impairment due to prenatal alcohol exposure will result in a diagnosis of FAS, and functional impairments are highly likely.[21][22][7][23]
Neurological problems are expressed as either hard signs, or diagnosable disorders, such as epilepsy or other seizure disorders, or soft signs. Soft signs are broader, nonspecific neurological impairments, or symptoms, such as impaired fine motor skills, neurosensory hearing loss, poor gait, clumsiness, poor eye-hand coordination, or sensory integration dysfunction. Many soft signs have norm-referenced criteria, while others are determined through clinical judgment.
[edit] Functional
When structural or neurological impairments are not observed, all four diagnostic systems allow CNS damage due to prenatal alcohol exposure to be assessed in terms of functional impairments.[21][22][7][23] Functional impairments are deficits, problems, delays, or abnormalities due to prenatal alcohol exposure (rather than hereditary causes or postnatal insults) in observable and measurable domains related to daily functioning, often referred to as developmental disabilities. There is no consensus on a specific pattern of functional impairments due to prenatal alcohol exposure[21] and only CDC guidelines label developmental delays as such,[7] so criteria vary somewhat across diagnostic systems.
The four diagnostic systems list various CNS domains that can qualify for functional impairment that can determine an FAS diagnosis:
- Evidence of a complex pattern of behavior or cognitive abnormalities inconsistent with developmental level in the following CNS domains — sufficient for an PFAS or ARND diagnosis using IOM guidelines[21]
- Learning disabilities, academic achievement, impulse control, social perception, communication, abstraction, math skills, memory, attention, judgment
- Performance at two or more standard deviations on standardized testing in three or more of the following CNS domains — sufficient for an FAS, PFAS or static encephalopathy diagnosis using 4-Digit Diagnostic Code[22]
- Executive functioning, memory, cognition, social/adaptive skills, academic achievement, language, motor skills, attention, activity level
- General cognitive deficits (e.g., IQ) at or below the 3rd percentile on standardized testing — sufficient for an FAS diagnosis using CDC guidelines[7]
- Performance at or below the 16th percentile on standardized testing in three or more of the following CNS domains — sufficient for an FAS diagnosis using CDC guidelines[7]
- Cognition, executive functioning, motor functioning, attention and hyperactive problems, social skills, sensory problems, social communication, memory, difficulties responding to common parenting practices
- Performance at two or more standard deviations on standardized testing in three or more of the following CNS domains — sufficient for an FAS diagnosis using Canadian guidelines
- Cognition, communication, academic achievement, memory, executive functioning, adaptive behavior, social skills, social communication
[edit] Prenatal alcohol exposure
Prenatal alcohol exposure is determined by interview of the biological mother or other family members knowledgeable of the mother's alcohol use during the pregnancy (if available), prenatal health records (if available), and review of available birth records, court records (if applicable), chemical dependency treatment records (if applicable), or other reliable sources.
Exposure level is assessed as Confirmed Exposure, Unknown Exposure, and Confirmed Absence of Exposure by the IOM, CDC and Canadian diagnostic systems. The "4-Digit Diagnostic Code" further distinguishes confirmed exposure as High Risk and Some Risk:
- High Risk — Confirmed use of alcohol during pregnancy known to be at high blood alcohol levels (100mg/dL or greater) delivered at least weekly in early pregnancy.
- Some Risk — Confirmed use of alcohol during pregnancy with use less than High Risk or unknown usage patterns.
- Unknown Risk — Unknown use of alcohol during pregnancy.
- No Risk — Confirmed absence of prenatal alcohol exposure, which rules out an FAS diagnosis.
[edit] Confirmed exposure
Amount, frequency, and timing of prenatal alcohol use can dramatically impact the other three key features of FAS. While consensus exists that alcohol is a teratogen, there is no clear consensus as to what level of exposure is toxic.[21] The CDC guidelines are silent on these elements diagnostically. The IOM and Canadian guidelines explore this further, acknowledging the importance of significant alcohol exposure from regular or heavy episodic alcohol consumption in determining, but offer no standard for diagnosis. Canadian guidelines discuss this lack of clarity and parenthetically point out that "heavy alcohol use" is defined by the National Institute on Alcohol Abuse and Alcoholism as five or more drinks per episode on five or more days during a 30 day period.[37]
"The 4-Digit Diagnostic Code" ranking system distinguishes between levels of prenatal alcohol exposure as High Risk and Some Risk. It operationalizes high risk exposure as a blood alcohol concentration (BAC) greater than 100mg/dL delivered at least weekly in early pregnancy. This BAC level is typically reached by a 55kg female drinking six to eight beers in one sitting.[22]
[edit] Unknown exposure
For many adopted or adult patients and children in foster care, records or other reliable sources may not be available for review. Reporting alcohol use during pregnancy can also be stigmatizing to birth mothers, especially if alcohol use is ongoing.[7] In these cases, all diagnostic systems use an unknown prenatal alcohol exposure designation. A diagnosis of FAS is still possible with an unknown exposure level if other key features of FASD are present at clinical levels.
[edit] Related signs
Other conditions may commonly co-occur with FAS, stemming from prenatal alcohol exposure. However, these conditions are considered Alcohol-Related Birth Defects[21] and not diagnostic criteria for FAS.
- Cardiac — A heart murmur that frequently disappears by one year of age. Ventricular septal defect most commonly seen, followed by an atrial septal defect.
- Skeletal — Joint anomalies including abnormal position and function, altered palmar crease patterns, small distal phalanges, and small fifth fingernails.
- Renal — Horseshoe, aplastic, dysplastic, or hypoplastic kidneys.
- Ocular — Strabismus, optic nerve hypoplasia[38] (which may cause light sensitivity, decreased visual acuity, or involuntary eye movements).
- Occasional abnormalities — Ptosis of the eyelid, microophthalmia, cleft lip with or without a cleft palate, webbed neck, short neck, Tetralogy of Fallot, coarctation of the aorta, Spina bifida, and hydrocephalus.
[edit] Prognosis
[edit] Primary disabilities
The primary disabilities of FAS are the functional difficulties with which the child is born as a result of CNS damage due to prenatal alcohol exposure.[4] Often, primary disabilities are mistaken as behavior problems, but the underlying CNS damage is the originating source of a functional difficulty[39] (rather than a mental health condition, which is considered a secondary disability).
The exact mechanisms for functional problems of primary disabilities are not always fully understood, but animal studies have begun to shed light on some correlates between functional problems and brain structures damaged by prenatal alcohol exposure.[3] Representative examples include:
Functional difficulties may result from CNS damage in more than one domain, but common functional difficulties by domain include:[39][3][43][44] (This is not an exhaustive list of difficulties.)
- Learning impairments are associated with impaired dendrites of the hippocampus[40]
- Impaired motor development and functioning are associated with reduced size of the cerebellum[41]
- Hyperactivity is associated with decreased size of the corpus callosum[42]
- Achievement — Learning disabilities
- Adaptive behavior — Poor impulse control, poor personal boundaries, poor anger management, stubbornness, intrusive behavior, too friendly with strangers, poor daily living skills, developmental delays
- Attention — Attention-Deficit/Hyperactivity Disorder (ADHD), poor attention or concentration, distractible
- Cognition — Mental retardation, confusion under pressure, poor abstract skills, distinguishing between fantasy and reality, slower cognitive processing
- Executive functioning — Poor judgment, Information-processing disorder, poor at perceiving patterns, poor cause and effect reasoning, inconsistent at linking words to actions, poor generalization ability
- Language — Expressive or receptive language disorders, grasp parts not whole concepts, lack understanding of metaphor, idioms, or sarcasm
- Memory — Poor short-term memory, inconsistent memory and knowledge base
- Motor skills — Poor handwriting, poor fine motor skills, poor gross motor skills, delayed motor skill development (e.g., riding a bicycle at appropriate age)
- Sensory integration and soft neurological problems — Sensory integration (SI) disorders, tactile defensiveness, under-sensitive to stimulation
- Social communication — Intrude into conversations, inability to read nonverbal or social cues, "chatty" but without substance
[edit] Secondary disabilities
The secondary disabilities of FAS are those that arise later in life secondary to CNS damage. These disabilities often emerge over time due to a mismatch between the primary disabilities and environmental expectations; secondary disabilities can be ameliorated with early interventions and appropriate supportive services.[4]
Six main secondary disabilities were identified in a University of Washington research study of 473 subjects diagnosed with FAS, PFAS (partial fetal alcohol syndrome), and ARND (alcohol-related neurodevelopmental disorder):[4][3]
Two additional secondary disabilities exist for adult patients:[4][3]
- Mental health problems — Diagnosed with ADHD, Clinical Depression, or other mental illness, experienced by over 90% of the subjects
- Disrupted school experience — Suspended or expelled from school or dropped out of school, experienced by 60% of the subjects (age 12 and older)
- Trouble with the law — Charged or convicted with a crime, experienced by 60% of the subjects (age 12 and older)
- Confinement — For inpatient psychiatric care, inpatient chemical dependency care, or incarcerated for a crime, experienced by about 50% of the subjects (age 12 and older)
- Inappropriate sexual behavior — Sexual advances, sexual touching, or promiscuity, experienced by about 50% of the subjects (age 12 and older)
- Alcohol and drug problems — Abuse or dependency, experienced by 35% of the subjects (age 12 and older)
- Dependent living — Group home, living with family or friends, or some sort of assisted living, experienced by 80% of the subjects (age 21 and older)
- Problems with employment — Required ongoing job training or coaching, could not keep a job, unemployed, experienced by 80% of the subjects (age 21 and older)
[edit] Protective factors and strengths
Eight factors were identified in the same study as universal protective factors that reduced the incidence rate of the secondary disabilities:[4][3]
Malbin (2002) has identified the following areas of interests and talents as strengths that often stand out for those with FASD and should be utilized, like any strength, in treatment planning:[43]
- Living in a stable and nurturant home for over 72% of life
- Being diagnosed with FAS before age six
- Never having experienced violence
- Remaining in each living situation for at least 2.8 years
- Experiencing a "good quality home" (meeting 10 or more defined qualities) from age 8 to 12 years old
- Having been found eligible for developmental disability (DD) services
- Having basic needs met for at least 13% of life
- Having a diagnosis of FAS (rather than another FASD condition)
- Music, playing instruments, composing, singing, art, spelling, reading, computers, mechanics, woodworking, skilled vocations (welding, electrician, etc.), writing, poetry
[edit] Treatment
There is no cure for FAS, because the CNS damage creates a permanent disability, but treatment is possible. Because CNS damage, symptoms, secondary disabilities, and needs vary widely by individual though, there is no one treatment type that works for everyone. Instead, comprehensive, multi-model approaches based on the needs of the patient must be used. Several treatment models have been identified, but regardless of the predominant approach, most in the current literature recommend multiple types of interventions to ameliorate the negative effects.
[edit] Medical interventions
Traditional medical interventions (i.e., psychoactive drugs) are frequently tried on those with FAS because many FAS symptoms are mistaken for or overlap with other disorders, most notably ADHD.[45] For instance, an FAS patient who is inattentive, does not complete schoolwork, and cannot stay seated has characteristics that an untrained person could easily mistake as ADHD, especially if the patient is not yet diagnosed with FAS. A common course of action would be a medication referral to a pediatrician, who might recommend a trial of Ritalin for the symptoms.
Medications are often important in treating FAS, but should be used in conjunction with other intervention approaches to address the multiple disabilities that arise from FAS.
[edit] Behavioral interventions
Traditional behavioral interventions are predicated on learning theory, which is the basis for many parenting and professional strategies and interventions.[43] Along with ordinary parenting styles, such strategies are frequently used by default for treating those with FAS, as the diagnoses Oppositional Defiance Disorder (ODD), Conduct Disorder, Reactive Attachment Disorder (RAD), etc. often overlap with FAS (along with ADHD), and these are sometimes thought to benefit from behavioral interventions. Frequently, a patient's poor academic achievement results in special education services, which also utilizes principles of learning theory, behavior modification, and outcome-based education.
Because the "learning system" of a patient with FAS is damaged, however, behavioral interventions are not always successful, or not successful in the long run, especially because overlapping disorders frequently stem from or are exacerbated by FAS.[43] Kohn (1999) suggests that a rewards-punishment system in general may work somewhat in the short-term but is unsuccessful in the long-term because that approach fails to consider content (i.e., things "worth" learning), community (i.e., safe, cooperative learning environments), and choice (i.e., making choices versus following directions).[46] While these elements are important to consider when working with FAS and have some usefulness in treatment, they are not alone sufficient to promote better outcomes.[43] Kohn's minority challenge to behavioral interventions does illustrate the importance of factors beyond learning theory when trying to promote improved outcomes for FAS, and supports a more multi-model approach that can be found in varying degrees within the advocacy model and neurobehavioral approach.
[edit] Developmental framework
Many books and handouts on FAS recommend a developmental approach, based on developmental psychology, even though most do not specify it as such and provide little theoretical background. Optimal human development generally occurs in identifiable stages (e.g., Jean Piaget's theory of cognitive development, Erik Erikson's stages of psychosocial development, John Bowlby's attachment framework, and other developmental stage theories). FAS interferes with normal development,[44] which may cause stages to be delayed, skipped, or immaturely developed. Over time, an unaffected child can negotiate the increasing demands of life by progressing through stages of development normally, but not so for a child with FAS.[44]
By knowing what developmental stages and tasks children follow, treatment and interventions for FAS can be tailored to helping a patient meet developmental tasks and demands successfully.[44] If a patient is delayed in the adaptive behavior domain, for instance, then interventions would be recommended to target specific delays through additional education and practice (e.g., practiced instruction on tying shoelaces), giving reminders, or making accommodations (e.g., using slip-on shoes) to support the desired functioning level. This approach is an advance over behavioral interventions, because it takes the patient's developmental context into account while developing interventions.
[edit] Advocacy model
The advocacy model takes the point of view that someone is needed to actively mediate between the environment and the person with FAS.[3] Advocacy activities are conducted by an advocate (for example, a family member, friend, or case manager) and fall into three basic categories. An advocate for FAS: (1) interprets FAS and the disabilities that arise from it and explains it to the environment in which the patient operates, (2) engenders change or accommodation on behalf of the patient, and (3) assists the patient in developing and reaching attainable goals.[3]
The advocacy model is often recommended, for example, when developing an Individualized Education Program (IEP) for the patient's progress at school.[45]
An understanding of the developmental framework would presumably inform and enhance the advocacy model, but advocacy also implies interventions at a systems level as well, such as educating schools, social workers, and so forth on best practices for FAS. However, several organizations devoted to FAS also use the advocacy model at a community practice level as well.[47]
[edit] Neurobehavioral approach
The neurobehavioral approach focuses on the neurological underpinnings from which behaviors and cognitive processes arise.[43] It is an integrative perspective that acknowledges and encourages a multi-modal array of treatment interventions that draw from all FAS treatment approaches. The neurobehavioral approach is a serious attempt at shifting single-perspective treatment approaches into a new, coherent paradigm that addresses the complexities of problem behaviors and cognitions emanating from the CNS damage of FAS.
The neurobehavioral approach's main proponent is Diane Malbin, MSW, a recognized speaker and trainer in the FASD field, who first articulated the approach with respect to FASD and characterizes it as "Trying differently rather than trying harder."[48] The idea to try differently refers to trying different perspectives and intervention options based on effects of the CNS damage and particular needs of the patient, rather than trying harder at implementing behavioral-based interventions that have consistently failed over time to produce improved outcomes for a patient. This approach also encourages more strength-based interventions, which allow a patient to develop positive outcomes by promoting success linked to the patient's strengths and interests.[43]
[edit] Public health and policy
Treating FAS at the public health and public policy levels promotes FAS prevention and diversion of public resources to assist those with FAS.[3] It is related to the advocacy model but promoted at a systems level (rather than with the individual or family), such as developing community education and supports, state or province level prevention efforts (e.g., screening for maternal alcohol use during OB/GYN or prenatal medical care visits), or national awareness programs. Several organizations and state agencies in the U.S. are dedicated to this type of intervention.[47]
[edit] Prevention
Alcohol is a teratogen, and the only certain way to prevent FAS is to avoid drinking alcohol during pregnancy.[3] Some studies have shown that small amounts of alcohol during pregnancy might not pose a risk to the fetus, although no amount of alcohol during pregnancy can be guaranteed to be absolutely safe.[49][50] In the United States, the Surgeon General recommended in 1981, and again in 2005, that women abstain from alcohol use while pregnant or while planning a pregnancy, the latter to avoid damage in the earliest stages of a pregnancy, as the woman may not be aware that she has conceived.[9] In the United States, federal legislation has required that warning labels be placed on all alcoholic beverage containers since 1988 under the Alcoholic Beverage Labeling Act.
Alcohol and mental health
People drink for all sorts of reasons, but if you're persistently boozing to blot out problems in your life, things could go from bad to worse.
- Alcohol may relieve stress in the short term, but it is a depressant drug. This means if you're feeling down when you drink, chances are the issues are going to seem worse when you sober up.
- Drinking interferes with sleep patterns, which can leave you feeling ragged when you need to be needle sharp. Bad sleep also has an effect on mental agility and stress management. So if you're life's a chaotic mess, stop getting so trolleyed for a bit and see if helps to restore some order.
- Regular boozing is usually a factor in worsening existing mental problems. It is often linked to depression, especially because people tend to turn to alcohol in a bid to improve their mood.
- Alcohol interferes with the way antidepressants work, which makes it bad news for anyone taking medication for a mental health problem. Mixing booze with any kind of medication carries risks, and can be fatal in some cases
From: http://www.thesite.org/drinkanddrugs...ndmentalhealth
:)9:(
holy shit mang a link would've done the trick too you're blinding me
Consuming large amounts of alcohol over a period of time can impair normal brain development in both rats and humans. Research is lacking on the possible brain effects of light or moderate alcohol consumption among young humans.[88] "Deficits in retrieval of verbal and nonverbal information and in visuospatial functioning were evident in youths with histories of heavy drinking during early and middle adolescence."[89] "Heavy, chronic drinking appears to produce adverse neural effects that are detectable by functional magnetic resonance imaging."[90] "The data suggest that CIE [chronic-intermittent ethanol] exposure during adolescence has a lasting impact on sensitivity to ethanol-induced motor impairments. This effect might stem from a disruption of normal developmental processes."[91]
Abstinence from chronic heavy alcohol consumption encourages new brain cell development, according to a study.[92]
Wow.......I was right...who would have thought that a brain dulling substance could actually make you dumber hey? Yes, maybe in moderate (which most young Australians are NOT) the problems are reduced....but it is really no case for how acceptable alcohol is.
Yeah sorry but it seems certain people bent on defending things with bias do not READ things that don't agree with them...so I thought I would just shove them right in their face.
I have to admit though...the heart disease reduction in moderate drinkers is interesting....I wonder why it is...
ppl are evil regardless..with or without alcohol..i think it has alot to do with the person 2...