It is sheepish to admit, especially as I am normally a demure, diffident person – but nobody has ever accused me of being over-restrained at feasts, especially if fine food, lots of alcohol and good company are present. Needless to say, there are consequences, and in my case it often results in a hazy sense of bodily unease (which lasts for days), combined with a rock-solid bout of constipation.
Therefore I would not suggest anyone emulate this propensity for overindulgence – especially as I am not unaware of what is happening to the body in these situations. For example, there is increased risk of liver cirrhosis – and several million brain neurons were probably fried by the alcohol.
Perhaps up to 4% of all deaths worldwide are related to alcohol abuse, though surprisingly only around 20% of heavy drinkers actually develop cirrhosis. By heavy drinking, one definition is consuming 100ml (80g) or more of ethanol a day for a period of 10 years or longer.
Many countries use “units of alcohol” (UA) to measure alcohol consumption – a UA is 10ml (8g) of ethanol so a pint of beer would be 2 UA or more (it depends on the strength of the beer). Therefore 100ml (80g) of ethanol is simply 10 UA – and in case you are curious, the reason why 100ml of alcohol is only 80g by weight is because ethanol is lighter than water.
A bottle of wine has around 9-10 UA so to run a 20% chance of developing cirrhosis, statistically one has to drink at least a bottle of wine a day for several years. However, statistics do not really help if there is a genetic disposition for cirrhosis.
This might apply to a significant proportion of humans who are genetically unable to produce enzymes called Aldehyde Dehydrogenases (ALDH1 and ALDH2) which are needed to neutralise acetaldehyde, a toxic compound created during the processing of alcohol in the body.
Prime examples are most Asians who lack the ability to express ALDH1 and ALDH2, so excessive alcohol consumption may be considerably more toxic for them. If you are interested, please read “A cure for hangover and – hic! – other holiday tales“.
Also, statistics indicate that consuming more than 26g of ethanol a day (just over 3 UA) increases the chances of bowel cancer by 21% – as Britain’s general incidence of bowel cancer is 6%, this increases the risk to about 7.25% overall.
The Real Concern
Sobering as the facts about alcohol are, I have another more personal concern. The wooziness from drinking inevitably subsides after a while, but the disquiet is over the onset of intestinal issues after binging on food and alcohol – specifically the general feeling of corporeal unease and constipation which lasts for days.
The background for this worry is a little long-winded, so please bear with me.
My father eventually succumbed to complications after suffering for over 15 years from Parkinson’s Disease (PD). His PD was as severe as it was unexpected – nobody else in the family had the disease and it was immensely tragic watching him descend from an intelligent, outgoing human into someone who needed a handkerchief near the mouth at all times.
The severity of his condition meant that none of the usual PD drugs worked and he eventually contracted a severe infection in a hospital after treatment for respiratory issues. This finally killed him, and not in a pleasant way.
As such, PD is a subject which I keep an eye on – not least because as my father’s son, I have a statistically higher chance of developing this terrifying disease. There is some evidence that the disease may be hereditary (due to indeterminate research into various PARK genes) – but there is more evidence that PD can be caused by environmental factors.
Some characteristics of PD, apart from symptoms such as uncontrollable tremors and lack of motor control, are over-aggregations of proteins called alpha-synuclein (a-syn) in the nervous systems and the abundance of inflammatory compounds called cytokines in the brain – in combination, these compounds seemingly damage the brain neurons controlling motor functions.
Other lesser known symptoms of most PD patients are intestinal problems, mainly constipation.
The concern about intestinal well-being is based on sobering research which found links between PD and the human gastrointestinal microbiota (HGM), the colonies of bacteria present in all human intestines.
A 2016 paper from the University of Wisconsin-Madison discovered that patients with PD have a significantly different composition of gut bacteria from normal people – this supported a hypothesis published by the University of Frankfurt in 2003.
When gut material from PD patients were transplanted into the guts of germ-free mice without PD, the test mammals began to display symptoms of PD. Even more curious was an experiment at CalTech where mice specially engineered to overproduce a-syn in their brains did not develop PD symptoms until gut matter from PD patients was implanted into their guts – control faecal material from normal people had a much smaller impact on motor dysfunction on such mice.
Despite the dramatic inferences, I should add that none of this is conclusive proof as yet (there may be other indeterminate causes of PD) – but it is certainly plausible that some relationship exists between a defective HGM and PD.
Interestingly, the Wisconsin-Madison team also provided a possible explanation: the flawed HGM in PD patients may cause significant overproduction of certain short-chain fatty acids (SCFA) (such as acetate, butyrate, propionate, etc) which are known to activate immune responses in neurons.
This was based on experiments where (i) SCFAs were fed to mice; (ii) faecal material from PD patients were transplanted into mice; and (iii) gut matter from normal humans were transplanted into mice – only the first two groups of mice developed symptoms of PD.
The University of Luxembourg and University of Alabama have also detected similar connections between PD and HGM. The Luxembourg paper goes further and suggested a link between a problematic HGM and the sleeping condition called Idiopathic Rapid-Eye-Movement Sleep Behaviour Disorder (iRBD) – and people with iRBD have a higher risk of developing PD in later life.
They also identified a relationship between certain HGM bacteria and depression.
An earlier 2012 joint paper by Harvard Medical School and Oxford University proposed that dysbiosis (an impairment of the HGM) is the root cause of many illnesses, including Irritable Bowel Syndrome, metabolic diseases, allergies, cardiovascular issues and, once again, neurological diseases.
Experiments done on mice at CalTech in 2013 also suggested a link between autism and HGM bacteria called Bacteroides fragilis which are notably lacking in children with autism, though it was unclear whether the link was causal or consequential.
HGM And Bingeing
Amazingly, it is only within the last few years that science is starting to quantify how seriously important HGM is to overall health – previously it was mostly theories and anecdotal inferences.
You probably know that humans have a second brain called the Enteric Nervous System (ENS) which also significantly affects well-being – this was discovered less than 20 years ago, and the HGM is contained within the ENS. If you are interested, read this short story, “The nine-metre brain“.
Therefore, the concern is that a bad (or excessive) diet can cause some sort of damage to HGM – which in turn can cause problems affecting the health of the rest of the body, including the brain. It is a plausible explanation as to why I (and probably many other people) feel disquieted and constipated for days after serious bingeing on rich food and alcohol.
Note that the ENS is made up of neurons (like the brain) and any activity that can destroy ENS neurons can probably spread to the brain eventually.
As an aside, laxatives are often used to treat constipation, but overuse can cause side-effects and obscure underlying HGM issues. How various laxatives work depends on their chemicals (and it is complicated to explain everything) – but they can be extremely effective (eg. magnesium citrate) so I would not suggest taking laxatives with a sleeping pill.