Although I was never what could be described as a heavy drinker, I was partial to a good red wine and a good gin and tonic. Being short, I never had the highest tolerance for alcohol, but after the med-induced brain weirdness, I stopped wanting to drink entirely.
Then, when I started getting massive digestive issues last year, I thought alcohol would help move things along a little bit. So I would have wine with meals. However, once I finally decided to change my diet, I cut out alcohol, and haven’t had any this year. And it’s strange, unlike many foods (read: bread), I have no desire to drink anymore.
Most people are (or at the very least should be) aware of the he negative social consequences of alcohol, so today I’m going to be focussing on the direct health effects. Additionally, I’m going to make the assumption that most of my readers aren’t alcoholics and are therefore able to choose their ‘dose’ and take appropriate measures to negate any of the known indirect dangers (impaired driving, missing work, exposure to violence, etc.) associated with alcohol consumption.
Short Term Effects
A typical sleep study administers alcohol 30–60 minutes before bedtime, so that peak blood alcohol concentration is reached at the moment of falling asleep. In general, studies tell us that the tolerance level to the effects of alcohol on sleep occurs within three nights. But, as we all know, alcohol decreases sleep latency. In other words, it made the subjects fall asleep faster.
Once alcohol has been completely metabolised, multiple studies have found a ‘rebound effect’ of disruption of the second half of sleep, and it also suppresses REM sleep in the first half of sleep.
Did you know that drinking 50g of alcohol in 250mL of water causes elimination of 600-1000mL of water over several hours? That’s why you can spend so much time running to and from the loo when you drink. This is caused by the inhibition of the release of vasopressin (anti-diuretic hormone), and vasopressin signals for the kidneys to reabsorb water. I need to guzzle water like a fish (wait, do fish guzzle water?!) and often find that I don’t retain water anyway, so I know that alcohol exacerbates the situation. If I don’t drink enough before going to bed (a fine line between hydration and several trips to the loo) I often wake up feeling hungover. It’s not the most pleasant experience!
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As someone with a particularly sensitive gut, I found this of real interest, and it definitely has cemented my decision that alcohol probably isn’t the best thing for my body.
Alcohol consumption can damage mucous membranes of the GI tract, which can lead to inflammation of the stomach lining (gastritis).
Mucous membrane lesions
Mucous membranes of the GI tract from the mouth to the stomach are especially affected because the alcohol is undiluted when it touches these membranes.
The dose at which mucosal lesions appear varies, but risk seems to increase above 2oz/d (approx. 57g/d). In the stomach and small intestines, hemorrhagic (bleeding) lesions and mucosal inflammation can occur after a single episode of heavy drinking
Luckily, this is rapidly reversible, but with chronic exposure (aka lotsa drinkin’) the damage becomes progressive and can cause long term problems.
Alcohol interferes with gastric motility, causing delayed gastric emptying at concentrations above 15% ABV. As a result, food may begin to be digested by bacteria while still in the stomach (think about that ‘drunk night food’ we often have while drinking), and the gaseous byproducts of this process can cause bloating and discomfort.
Additionally, alcohol consumption decreases ‘impeding wave motility’ in the small intestine. This means that the muscle movements which keep food in the small intestine while it is being digested are less active. At the same time, ‘propulsive wave motility’ (the movements which keep the food moving through the small intestine) is undisturbed. And this combination leads to diarrhoea. Sexy.
Alcohol increases the production of stomach acid (but only from drinks with low alcohol content, such as wine and beer)2 and a single episode of consumption is enough to weaken the lower oesophageal sphincter, causing heartburn.
Alcohol impairs the digestion of other nutrients in the intestines (such as sodium), as well as the functioning of enzymes such as lactase.
Susceptibility to bacterial toxins
According to Alcohol’s Role in Gastrointestinal Tract Disorders: “alcohol induces the release of noxious signalling molecules, such as cytokines, histamine, and leukotrienes.”
These substances can set off a chain reaction that leads to the destruction of the tips of the villi (the finger-like bodies that line the intestinal wall), and the lesions that result allow bacterial toxins to enter the bloodstream.
It’s also worth noting the histamine release here, as it can play a role in reactions for those of us with histamine sensitivity.
The links between the short-term effects (where we can measure the mechanisms of effect more easily) and long-term effects (where we can often only measure the outcome) are often a matter of debate.
Just so you can get an idea of what we’re talking about when doses are referenced:
- light: <2.5 g/day (<0.5 drink)
- moderate: 2.5–14.9 g/day (about 0.5–1 drink)
- heavy: 15–29.9 g/day (about 1–2.5 drinks)
- extremely heavy: 30–60 g/day (about 2.5–5 drinks), and >60 g/day (≥5 drinks)
A meta-analysis of risk of alcohol consumption (25g/d, 50g/d, 100g/d) on various cancers shows that no cancer risk is reduced by alcohol consumption, even at 25g/d. In fact, many increased, even at 25g/d:
- oral cavity and pharynx (relative risk 1.75 ± 0.06)
- oesophagus (1.51 ± 0.04)
- liver (1.17 ± 0.06)
- larynx (1.38 ± 0.06)
- breast (1.31 ± 0.04)
That being said, there is no threshold effect for these cancers: in general, the more alcohol consumed, the more risk there is.
We’ve all heard the saying that alongside an apple, a glass of red wine a day keeps the doctor away, right? Well, let’s look into that a bit further!
In a meta-analysis of the effect of alcohol consumption on cardiovascular outcomes, it was shown that consumption is associated with a lower risk of mortality, by all causes (0.87 ± 0.04).
Alcohol consumption was associated with lower risk of cardiovascular disease mortality (relative risk 0.75 ± 0.05), and consumption associated with lower risk of coronary heart disease incidence (relative risk 0.71 ± 0.06), mortality (relative risk 0.75 ± 0.065).
Consumption associated with same risk of stroke incidence (relative risk 0.98 ± 0.08), mortality (1.06 ± 0.16).
Again, this is all dependent on the dose. According to the analysis, 2.5–14.9g/d is protective against cardiovascular disease mortality, coronary heart disease incidence and mortality, and stroke incidence and mortality.
All doses protective against coronary heart disease incidence and mortality. However, higher doses can be harmful for stroke incidence and mortality, cardiovascular disease mortality (U/J curve).
Interestingly, the same group did a meta-analysis of effect of alcohol on biological markers of heart disease. The findings are consistent with the outcome-based study: light to moderate alcohol consumption is associated with reduction in biological markers of heart disease.
Light/moderate consumption increased high density lipoprotein (‘good cholesterol’), apolipoprotein A1, adinopectin levels; reduced fibrinogen levels.
These higher levels of high density lipoprotein associated with lower risk of atherosclerosis (artery hardening). Apolipoprotein A1 “is considered to be the ‘active ingredient’ in HDL-C”, and higher levels of adinopectin associated with a lower risk of diabetes and coronary heart disease.
However, high fibrinogen levels considered risk factor for cardiovascular disease. That being said, light/moderate consumption does not appear to increase triglyceride levels, as was previously suspected. High levels of triglycerides in bloodstream are associated with atherosclerosis (a disease of the arteries), but all the evidence points towards low-to-moderate consumption of alcohol as protecting against heart disease.
Alcoholic liver disease is a spectrum.
Fatty liver (steatosis) usually presents no symptoms and resolves itself with 4–6 week abstinence from alcohol. It can appear after only a few days of heavy drinking, increasing the risk of cirrhosis.
With alcoholic hepatitis, fatty liver changes can cause inflammation of the liver, which can range from mild to life-threatening. This is typically only noticed after decades of heavy consumption; and by this point it often leads to death as the damage has been going on unnoticed. Luckily, this can be reversible with abstinence.
With cirrhosis, the replacement of liver cells with scar tissue leads to a lessening of the liver’s ability to detoxify. Unlike steatosis and alcoholic hepatitis, this is irreversible, and can be fatal without abstinence.
- evidence of threshold effect:13
- for women, >24 g/d
- for men, >36 g/d
Risk factors for alcoholic liver disease to consider are:
- women are twice as sensitive to alcohol-mediated liver toxicity16
- in one large study conducted in China, it was found that drinking outside of mealtimes carries higher risk (2.71) of alcoholic liver disease compared to drinking only at mealtimes5
- one study found that excess body weight (BMI >25 for women, >27 for men) over the past 10 years is an independent risk factor for the development of fatty liver, cirrhosis, and alcoholic hepatitis10
The bottom line?
I’d like to thank the awesome Colin Gorrie of Not That Kind of Dr for the wonderful research. If you haven’t checked out his blog, please make sure you do. He covers the science behind health in more detail and is an invaluable resource for those of us trying to dig deeper into how our bodies work…especially when dealing with chronic illness.
We’d both love to hear if there are any foods that you’d be interested in being featured in this series. Do leave a comment below and we’ll see what we can dig up for you!