Thursday, 30 October 2014

The physiological effects of alcohol

I have always been more concerned by the psychological power of alcohol than its physiological effects.

That was until I read about its physiological effects.

What follows is by no means a comprehensive list. It was taken, with kind permission, from Dr David Marjot's excellent book The Diseases of Alcohol. Much of it is copied (by hand) word for word.

I have tried to explain some of the medical language, and in doing so (or in the transcription), may have made some mistakes. Any mistakes, therefore, are my responsibility.

So, this is what booze does to you:

Nervous system disorders

Eyes - in moderation alcohol may protect against macular degeneration. In excess it may hasten its development. Alcohol increases the risk of cataracts.

Cerebellar atrophy (brain cell wasting) - a common companion of Korsakoff's psychosis (a disease for proper alcoholics). Moderate doses of alcohol (one bottle of wine daily over a long period) can lead to the loss of Purkinje cells (quite important bits of your brain) in the cerebellum.

Purkinje cell at the top

There is also a possible link between cerebral atrophy and (alcoholic) dementia. Alcohol, particularly in heavy drinkers does cause loss of brain substance - both white and grey matter. These changes can be partly reversed by abstinence.

Other brain disorders due to alcohol - Marchiafava-Bigami degeneration, myelosis of the corpus callosum and Central Pontine myelosis.

Nutritional disorders

Thiamine deficiency: Myopathy, encephalopathy (eg Wernike-Korsakoff disease, cerebellar atrophy and peripheral neuritis)
Folate deficiency: Raised mean corpuscular volume of red blood cells (MCV)
Niacin deficiency: Classic pellagra with pigmented dermatitis, diarrohea and dementia (all rare)
Vitamin D and calcium deficiency: Osteoporosis and osteomalacia (heavy drinkers only)
Protein deficiency: usually due to poor intake

Disordered digestion due to direct effects of alcohol on gut mobility, damage to the lining of the bowel, or pancreatic and liver disorders.

Malabsorption of nutrients associated with disorders of the liver and pancreas, nutritional deficiencies and gut bacterial activity.

High utilisation and poor retention of vital nutrients.

Metabolic changes

Hypoglycaemia (low blood sugar) - usually occurs after an alcohol binge or in children during one, a mechanism being the inhibition of gluconeogenesis.

Hyperglycaemia (high blood sugar) - alcohol can cause a rise in blood sugar due to activation of the sympathetic-medullary system with adequate glycogen stores in the liver. If the islet cells in the pancreas are damaged or lost due to alcoholic pancreatic damage, then insulin-dependent diabetes can occur.

Hyperlipidaemia (too many fat-soluble molecules in the blood) - can occur in heavy drinkers that may be also associated with other alcohol disorders such as pancreatic malfunction, renal disease, diabetes and liver insufficiency. There is a disturbed LDL/HDL ratio.

Hyeruricaemia (too much uric acid in the blood) - changes in the alcoholic liver (in particular the reddox shift) can lead to an excessive production of uric acid with high blood levels and associated gout. Most gout, though, does not come from heavy drinking.

Stroke - heavy drinking causes hypertension and arterial disease. This increases the risk of strokes and coronary artery disease.

Fits - Grand mal fits (jerking and muscle seizures) can happen during withdrawal/early abstinence, but withdrawal symptoms can also be seen while a patient is still drinking heavily. Tremors due to alcohol withdrawal can become clonic movements and pass into fit.

Peripheral Nervous System Disorders

Peripheral neuropathy - primarily an axonal sensorimotor wallerian degeneration. This is only associated with a long period of heavy drinking, and women may be more susceptible than men. The distal lower limbs are affected, in worse cases the proximal leg and distal arms. Symptoms include weakness and muscle wasting, particlarly of the small muscles in the foot. Foot drop may occur.

Sensory loss - touch, sensation (heat and cold) and pain. Gait may be affected with a wide base when walking. Tendon reflexes are diminished or absent. Burning pain, particularly in the feet, may be common.

Alcoholic autonomic neuropath - diarrhoea, constipation, bowel incontinence, bladder incontinence/retention, loss of sweating, peripheral vaso-dilation or vaso-contraction with heat or cold intolerance. Irregular heartbeat or even failure. Loss of control over blood vessels with postural hypotension and faints.

Pressure neuropathy - can occur if a patient becomes unconscious or comatose after a bout of heavy drinking. Prolonged pressure over many hours can lead to severe damage to a peripheral nerve.

Chronic or atrophic myopathy - muscle wastage. Not entirely clear how alcohol does this, but it is by far the most common skeletal muscle disorder in those dependent on alcohol. Cured by abstinence.

Gastro-intestinal system

Parotid Gland enlargement - common sign in heavy drinkers. The swelling is likely to be a direct effect of regular alcohol consumption and subsides with abstinence.

Mouth and pharynx disorders - Pre-cancerous changes such as leukoplakia and cancers themselves can be observed. Swallowing may be affected by alcohol-associated neuropathies (nerve diseases/problems) and encephalopathies (brain diseases).

Pancreatitis - quite common complication of heavy drinkers. Pancreatitis is most likely a chronic disease with exacerbations (ie acute pancreatitis). Acinar cells metabolise alcohol. This in turn may cause pancreatic stellate cells to produce fibrosis, changes very similar to those seen in cirrhosis of the liver.

Malabsorption syndromes - a number of changes can occur to the small bowel due to heavy drinking. Impaired pancreatic function often associated with hepatic dysfunction (liver failure) can lead to malabsorption. In some cases motility is affected by neuropathy. Alcohol (or it's metabolite acetaldehyde) has a direct toxic effect on small intestine cells causing villous atrophy and smooth muscle myopathy. It also causes a reduced synthesis of proteins.

Liver disorders

Alcoholic Liver Disease (ALD) - a major cause of morbidity and mortality in heavy drinkers which is in no way confined to alcoholics. Women develop cirrhosis at half the accumulated lifetime alcohol intake of men.

As little as 25 ml of alcohol (approx one 175ml glass of 12% wine) a day in women and 75ml (three 500ml cans of Kronenbourg) a day in men over several years can bring ALD on.

In men, 75ml a day over a period of weeks can bring fatty changes to the liver, 100ml (four cans of Kronenbourg) a day can cause Acute Alcohol Hepatitis (AAH) and 200ml (eight cans of Kronenbourg or just over two bottles of 12% wine) a day over around ten years can lead to cirrhosis.

When alcohol reaches the liver three enzymes are involved in its initial breakdown; alcohol dehydrogenase - responsible for 80% of the metabolism, cytochrome P-450 2E1 (CYP2E1) and catalose for the rest.

The metabolite is acetaldehyde that is broken down to acetate by mitochondrial aldehyde dehydrogenase. Hydrogen is produced that converts nicotinamide-adenine dinuclucleotide (NAD) to its reduced form NADH. This has the effect of increasing the redox potential in the liver. Fatty acids are replaced as  active energy-producing metabolites

The three types of Alcoholic Liver Disease:

Fatty liver or steatosis: probably the most common liver consequence of drinking too much. There is an accumulation of fat in large vesicles such that the nucleus is displaced to one side. Small vesicles can also occur that are more evenly distributed. This latter represents mitochondrial damage. The liver is enlarged and the cut surface is yellow. Abstinence will cause the condition to reverse.

Acute Alcoholic Hepatits: The source of inflammatory damage in ALD is probably acetaldehyde. It changes stellate cells lining the blood sinusoids to fibroblasts that are active products of collagen. This fills in the sinusoids with obstruction to the blood flow and associated metabolism. Kupffner cells respond by an inflammatory cytokine cascade, bringing about the release of tumor necrosis factor alpha (TNF alpha). Toxins including gut bacterial toxins are not broken down with the production of inflammatory cytokines and active leucocytes that further cause inflammation. This starts up a cycle of inflammation and scarring. The typical pictures is of macrovesicular fat, neutrophil, infiltration, Mallory bodies and liver cell necrosis.

AAH will often resolve through abstinence, if irreversible liver failure hasn't happened. AAH with liver failure may still respond to cortico-steroids.

Cirrhosis of the liver: These are features of fatty liver and acute inflammation but the picture is dominated by widespread fibrosis which destroys the liver architecture. Initially there are small island of regenerating liver cells (micro-nodular cirrhosis) and later with larger nodules (macro-nodular cirrhosis). The liver shirnks into a jaundiced scarred organ with surface marked by the nodules - the hobnail liver. The clinical picutre of ALD can be one or more of the following elements:

 - symptomatic hepatomegaly
 - acute hepatits with fever, upper right quadrant pain, liver tenderness, jaundice, prolonged INR, raised liver enzymes, hypoglycaemia, raised sedimentation rate.
- acute liver failure with acute encephalopathy.
- chronic liver failure.
- spider naevi, Dupuytrens' contractures, feminization in the make
- portal hypertension, oesophageal varices, GI bleeding, ascites, portal-systemic encephalopathy, hepato-renal syndrome.

The development of hepato-cellular cancer does make the prognosis grave.

Only around 15% of heavy drinkers develop ALD.  Abstinence will bring about a stabilisation in the majority of patients. If the cirrhosis is too severe, the disease will remain progressive, but at a slower rate. Transplant remains an option if liver failure persists.

Blood disorders

The effects of alcohol on the haemopoietic system are complex. There is a positive correlation between acetaldehyde modified haemoglobin, values for carbohydrate deficient transferring (CDT), raised gamma-glutamyl transferase, aspartate aminotransferase and haematological abnormalities in alcoholism. There is also evidence for folate deficiency in some patients.


Macrocytosis of alcoholism: The mean corpuscular volume of red cells is a frequent finding in heavy drinkers. Most patients are not anaemic so it could be related to folate deficiency, but it could equally be a direct toxic effect of the alcohol itself.

Blood loss: This may be direct, such as the result of damage in the gastro-intestinal tract such as bleeding oesophageal varices. Alcohol also lowers platelet counts, particularly if the spleen is enlarged.

Haemolytic anaemia and sidero-blastic anaemia.

Leucopenia (low white blood cells): The suppressive effect of alcohol on bone marrow leads to poorly functioning white blood cells and in some case to leucopenia. This has a marked effect of resistance to infection, typically in the lung.

Macrophage (groovy white blood cells) disorders: There is evidence that the initial cirrhotic effect of alcohol is on the liver macrophages with initial local inflammatory responses not only to harmed liver cells but to damage to the macrophages themselves. A similar mechanism could be at work in the lungs with impaired defences against infection.

Thrombocytopaenia: Alcohol suppresses the production of platelets by the bone marrow. The bone marrow shows a general loss of cellularity, megaloblastosis, vacuolation of developing red cells and sideroblasts. The peripheral blood picture reflects these changes.

Kidney disorders

Alcohol can be associated with a number of renal conditions:

Acute tubular dysfunction
Acute tubular necrosis after binge drinking
IgA nephropathy with glomerulonephritis
Hepato-renal syndrome
Inhibition of anti-diuretic hormone ADH
Hyponatraemia (low sodium in the blood) - secondary to high fluid intake
Hypokalaemia (low potassium in the blood) - due to poor retention of potassium
Hypophosphataemia (low phosphate in the blood) - due to poor renal absorption
Hypocalcaemia (low serum calcium in the blood) associated with loss in the urine, poor albumin binding, lack of vitamin D, muscle breakdown and magneisum deficiency.

Heart and blood vessels

Hypertension (high blood pressure) - even in non-alcoholic patients there is a connection between alcohol and high blood pressure. The effect of alcohol may be greater than that of salt intake. Low alcohol intake (less than a third of a bottle of 12% wine a day), has no effect on hypertension.

Arrhythmias - particularly atrial fibrillation can be associated with a bout of heavy drinking. This can occur in healthy subjects causing sudden death, particularly during exercise. The mechanisms are obscure but may be related to dys-regulation of cardiac rhythm by changes in adrenergic stimulation, or poor vagal control of heart rhythm.

Cardiomyopathy (heart muscle disease)

Alcoholic cardiomyopathy - not clear whether alcohol and/or acetaldehyde are the toxic agents. While there are increases in cardiac enzymes on biopsy it is not clear if these are an adaptive response or evidence of damage. Some patients show antibodies to acetaldehyde-protein adducts. Treatment is to reduce alcohol intake.

Thiamine deficiency cardiomyopathy - in some drinkers (not all alcohol dependent) thiamine deficiency can occur with the development of the syndromes of heart failure with oedema or wet beri-beri and peripheral neuritis or dry beri-beri. Both may occur at the same time. Thiamine deficiency may arise as a result of high utilization (as part of the hypermetabolic state induced by very heavy drinking), low intake of thiamine and poor retention of that little taken in.

Coronary heart disease

Alcohol in small doses may reduce the risk of coronary artery disease, possibly due to an increase in high density lipoproteins HDL associated with coagulation and fibronolysis. Alcohol reduces the chances of coronary artery clots and if clots occur there is a slightly more rapid fibrinolysis with attenuation of the clot.

The effect on coronary artery disease means that stable, moderate, regular drinkers not taking more than 30ml of alcohol (ie one pint of Stella or a third of a bottle of 12% wine) a day do show overall reduced mortality compared with non-drinkers. In practice this only benefits the middle-aged.

It seems from this study the best possible thing you can do with your life and alcohol is not drink until the age of 45 and then have one drink a day until you reach your sixties, then other things like cancer come into play and you are better off stopping.

Whoop. Tee. Doo.

Blood disorders

The effects of alcohol on the haemopoietic system are complex. How complex? There is positive correlation between acetaldehyde modified haemoglobin, values for carbohydrate deficient trasferring (CDT), raised gamma-glutamyl transferase, aspartate aminotransferase and haematological abnormalities in alcoholism. That complex.

There is also evidence for folate deficiency and an effect on developing blood cells with possible effects on haemapoietic growth factors.

Macrocytosis of alcoholism - the mean corpuscular volume of red cells is a frequent finding in heavy drinkers. This may be related to folate deficiency in some cases but a direct toxic effect of alcohol seems a simpler explanation.

Blood loss - this may be direct, such as the result of damage in the gastro-intestinal tract (ie bleeding oesophageal varices). Those with liver disease may suffer from low levels of vitamin-K dependent coagulation factors. Alcohol also lowers platelet counts particularly if the spleen is enlarged.

Haemolytic anaemia - there is Zieves syndrome in which there is a haemolytic anaemia, jaundice, hyperlipoporteinaemia associated with cirrhosis of the liver.

Sidero-blastic anaemia - can occur in poorly-nourished alcoholic patients. High iron with low folate readings. Responds to abstinence.

Leucopenia - the suppressive effect of alcohol on bone marrow leads to poorly functioning white blood cells and in some cases to leucopenia.

Macrophage disorders - there is evidence that the initial cirrhotic effect of alcohol on the liver macrophages with initial local inflammatory responses not only to harmed liver cells but to damage to the macrophages themselves. A similar mechanism could be at work in the lungs with impaired defences against infection.

Thrombocytopaenia - alcohol suppresses the production of platelets by the bone marrow. The bone marrow also shows a general loss of cellularity, megablastoisis, vacuolation of developing red cells and sideroblasts. The peripheral blood picture reflects these changes.

Dem bones

Chronic excessive alcohol use leads to increased nitrogen excretion associated with loss of lean tissue mass (becoming therefore, an effective, but incredibly unsafe way to lose weight). In animal studies alcohol caused loss of bone protein.

Osteoperosis - alcoholism is a risk factor for osteoperosis. If you abstain or take more than two drinks a day you are at higher risk of hip fracture. Bone density falls as alcohol intake rises.

Osteonecrosis - secondary to trauma but still a problem with alcoholics. Associated with osteonecrosis: vascular damage, cell death and defective repair.

Immunity and infectious disorders

Alcohol has many effects on the immune system. It inhibits the activity of the cellular non-specific response to infection. Among the cells affected are neutrophils, macrophages and natural killer cells. also involved are soluble mediators such as complement, cytokines, leukotrienes and prostaglandins.

One of the functions of the natural killer cells is to seek out and destroy the body's own damaged cells such as cancer cells. This may be one of the mechanism whereby alcohol 'causes' cancer

Alcohol affects the function of T-cells and B lymphocytes in transforming B lymphocytes into plasma cells and producing immunoglobulin antibodies.

There may be a an excess of antibody IgA that is associated with autoimmunity. This antibody can become deposited in tissues including the kidney. It can be associated with inflammatory liver disease and give rise to the hepato-renal syndrome.

Most humoral responses involve B lymphocytes, CD4 T lymphcytes and antigen presenting cells. If any of theses cells are affected then the immune response if reduced; as with B lymphocytes and alcohol. This refueced response is critical in the body's reaction to tuberculosis and pneumonia.

CD4 T and CD8 T lymphocytes are essential for cell medicated immune responses, particularly for viruses. The function of these cells is impaired by alcohol. The most significant co-factor in the progress of hepatitis C infections is alcohol.

The primary effects of alcohol are to create a functional immunodeficiency but also autoimmunity.

Endocrine disorders

The endocrine system is a collection of glands which secrete hormones into the bloodstream in order to target distant organs - pineal gland, pituitary gland, pancreas, ovaries, testes, hypothalamus stc

Corticotropin-releasing factor (CRF) is released in the brain in those central systems involved critical to the development of addiction, apparently in response to the stress of withdrawal. NPY is used to ;calm' these systems. Central effects doimpinge on the hypothalamus and on to the control of the hypothalamic-pituary adrenonocortial system.

Pseudo-Cushings Syndrome is the result of stimulation to the pituitary by CRF with the release of adrenocorticotropic hormone (ACTH) and the output of cortisol via the adrenal cortex. This can lead to the Cushing's picture of typical facies, abdomnial striae, proximal muscle wasting, bruising, hypertension and osteoperosis. You have to be drinking a lot for this (more than a 70cl bottle of 40% spirits a day) and it soon goes if you (can) stop.

Alcohol can produce hypoglycaemia if liver stores of gylcogen are low and/or glucose mobilisation is inhibited while alcohol is metabolised. The onset is 6 to 36 hours after a proper bender. In addiction sometimes insulin secretion is increased by alcohol. This effect is a serious risk if children, particularly small children, take an overdose of alcohol and must always be considered when children are seen to be intoxicated.

Those with insulin-dependent diabetes who are taking insulin may be at risk of hypoglycaemia if they drink at all heavily. Chronic heavy drinking can be associated with hyerglaycaemia as this type of drinking can reduce the responses to insulin; both exogenous and endogenous. This is particularly seen with impaired liver function whether or not showing frank alcohol liver disease.


Alcohol may inhibit the metabolism of Vitamin A, which is essential to sperm development.

The Hypothalamic-Pituitary-Gonadal Axis (good name for an indie band) is a system which involves feedback from the target organs, the gonads. The hypothalamus releases via the portal system the luteinising hormone release hormone (LHRH) that on reaching the pituitary gland sends the gonadotropin hormone's luteinising hormone (LH) and follicle stimulating hormone (FSH). LH is linked to the production of androgens. FSH is responsible for the maturation of sperm and the development of the ovarian follicle. In men, drinking alcohol leads to a fall in androgens with diminished sexual function. In women, mistimed and absent ovulation occurs with changes to the menstrual cycle.

Alcohol is toxic to Leydig cells and can be associated with testosterone deficiency. There is a reduction, but abstinence will pick it all up again.

Prolactin is secreted by the pituitary gland. It supports lactation and breast feeding. Its production is inhibited by dopaminergic neurones. Alcohol can increase the output of prolactin. This may lead to impotence in men and fertility problems in women.

Fertility is generally greatly affected by alcohol, through miscarriage, aneuploidy, structural congenital abnormalities, disordered foetal growth, perinatal death etc.

Alcohol is a teratogenic agent - it can cause foetal damage. Binge drinking in critical moments of the foetal nervous system can cause foetal damage. The rate at which the mother can metabolise alcohol may be a key factor. Whilst the greatest risk is during the first trimester, damage can occur throughout pregnancy.

Inter-uterine exposure to alcohol can lead to:

Death - miscarriage, stillborn babies, prematurity early mortality
Physical malformity - heart defects, spina bifida, cleft palate
Pre-natal growth deficiency
Central nervous defects from structural changes (eg foetal alcohol syndrome) to behavioural disorders (eg Alcohol-related Neurodevelopmental Disorders - ARND).

But the occasional unit of alcohol during pregnancy is unlikely to do any harm.

Growth and development

Calcium is stored in the bones and to some extent in the teeth. It is a key electrolyte in brain function. Calcium flux is regulated by the parathyroid hormone (PTH), vitamin D derivatives and calcitonin from the thyroid. Alcohol may by its action on the kidneys lead to a loss of calcium. Heavy drinking may lead to a shortage of vitamin D. Reproductive hormones may be low in drinkers with loss of calcium. Osteoperosis can occur in heavy drinkers.

Alcohol may lead to a diminution of growth hormone with impaired immunity and muscle weakness in the adult and problems at puberty in the adolescent.

A high alcohol intake can lead to a reduction in thyroid-stimulating hormone (TSH). The thyroid responds to TSH by putting out two hormones, theroxine-3 and thyroxine-4.

The following paragraph is taken from You and Your Hormones: "Too little production of thyroxine by the thyroid gland is known as hypothyroidism.  Hypothyroidism in adults causes a decreased metabolic rate.  This results in symptoms which include fatigue, intolerance of cold temperatures, low heart rate, weight gain, reduced appetite, poor memory, depression, stiffness of the muscles and infertility."


Alcohol is broken down in the liver into acetaldehyde, and acetaldehyde itself is toxic. Acetaldehyde modifies proteins and acetaldehyde-protein complex is a one of a number of possible cancer mechanisms.

Others are:

Direct damage by acetaldehyde
Genetic variation in aldehyde dehydrogenase ADH
Free radicals
DNA adducts
Changes in hormone metabolism
Altered response to commensal bacteria

Cancer of the aero-digestive system (ie mouth, tongue, pharynx, larynx and oesophagus) is exponentially likely if you drink and smoke.
Alcohol is a cause of liver cancer.
Alcohol is also one factor in a complex interaction of gut bacteria, tobacco, diet and genetic variation when it comes to colon and rectum cancer. Half of all colorectal cancers could be prevented by drinking in moderation, not smoking, exercising and eating a balanced diet.
Only a small proportion of breast cancers are due to alcohol, but the risk rises in linear fashion with dose. Binge drinking increases the risk. It's possible that alcohol initiates changes in oestrogen metabolism via a damaged liver.


More than 0.3% blood ethanol concentration in grams per litre will kill you.


Happy drinking!

Wednesday, 15 October 2014


From an ITV news website report today:

"The South East of England has the most "high risk" drinkers in England, with more than 1.6 million consuming dangerous levels of alcohol on a daily basis, fresh data has revealed."


"Research from the charity Alcohol Concern showed there at least 1.6 million "high or increasing risk" drinkers living in the wealthiest corner of England."

There are 8.7m people in the South East of England, so that means 18% of people in the South East of England, nearly a fifth, are "at risk"!

"High risk drinking is defined as people who have more than six to eight units of alcohol each day, while increasing risk is more than two to four units a day."

Hang on a minute. What? 

Does this mean high risk drinking is 6 to 8 units a day or more than 8 units a day? And are increasing risk drinkers drinking 2 to 4 units a day or more than 4 units a day?

According to the report if you are part of the "increasing risk" group of drinkers, you are drinking at dangerous levels. Yet "increasing risk" is defined as "more than two to four units a day". Is that 3? or 5?

Drinking "more than two units" and you are "at risk"? At risk of what? There are 2.2 units in this bottle of Doombar

4.3% vol, 500ml bottle.
According to the drinkaware website (which is funded by the drinks industry), drinking one of these a day marks you out as a lower risk drinker.
As it says on the drinkaware website: "No level of drinking is considered risk free". Well this is perfectly true. But as we know, breathing air also carries a risk, so no level of not drinking is risk free either.
So what is the real risk to our health of a bottle of Doom Bar a day?
According to the Alcohol Concern website (which is not funded by the drinks industry), a bottle of Doom Bar a day is actually well within "sensible drinking limits" for both men and women.
Yet according to today's report, people who drink a bottle of Doom Bar might be statistically part of the 1.6m "high or increasing risk" drinkers in the South East of England. 

Certainly anyone who drinks two bottles of Doom Bar a day is at "increasing risk". Really?

Now you're in trouble.
The South East of England has the highest population of any part of Britain. So it's unsurprising it has the highest number of people drinking at "increasing or high" risk levels. It has the largest number of people.
The South East also has the highest life expectancy for men. This must be in spite of our alcohol consumption. The South East also has the second highest life expectancy for women in the country (by 0.1 of a year from the South West, that well known bunch of teetotallers). 
I am not in any way disputing the statistics, and I don't have a problem with the way they are reported. I would just suggest our public health messages around alcohol are close to meaningless.

Tuesday, 14 October 2014

GUEST BLOGGER: The Downsides of Giving Up

Nick writes: I had a very unusual response to yesterday's blog post about trying to find out if I had liver damage as a result of my drinking. A number of people contacted me privately with their stories. 

Last night I asked one of my correspondents if she would write something for publication on this blog. When I woke up, this was waiting in my inbox (my correspondent wishes to remain anonymous, which is her prerogative):

"Nick's blog grabbed my attention. Without seeing or therefore having the chance to understand a set of blood test readings - Nick decided to quit drinking! A lot of people decide to take a day, a week, or a month off alcohol. Right now Stoptober is giving inspiration to many.

But of those who decide to quit (with or without a bit of worry about a blood test) and those that make it for a day, a week or a month, never mind a year - the period Nick set himself - is anyone's guess. We don't hear about those who sigh and open the next bottle or order another drink at the bar and give up giving up immediately. Not until they need a lot of help.

Like quitting cigs or any behaviour we can't control, we're suddenly in the realm of addiction and all the self-delusion that follows.

The first time I tried seriously to stop smoking I remember wanting to throw a chair out of the window of my second-floor flat ('I Love the Sound of Breaking Glass' was in the charts). My frustration as I realised that I could not stop even when I really wanted to was a terrible loss of confidence in myself. 

That was a long time ago. I did quit smoking cigarettes. It was the proudest achievement of my life when I managed it.

I remember saying so in a group for alcohol addiction. Other women there had babies they said they lived for and would do anything for. Their children were the proudest achievements of their lives, mine was that I had stopped smoking cigarettes. For twenty-five years. During that time I was made redundant and both my parents died.

My alcohol addiction group was a day programme. I attended faithfully for 12 weeks. I spoke in groups, I cooked soup, stirred porridge, meditated and only baulked at drumming.

And I started smoking again.

I remained abstinent from alcohol but the pull - probably about sixty per cent of those at the centre (including the staff) smoked - meant I felt pressured to join in.  I ended three months there clear of alcohol but re-addicted to smoking.

So, thanks alcohol rehab. 

I know I started smoking, no-one forced me."

Thank you, Anonymous Correspondent, for getting in touch and writing this. You might think you are weak, but you kicked drinking and there's no way I'm going to do that permanently. And if you kicked smoking once, you can do it again. Read Allen Carr's book. That really put me off.

If anyone else would like to write something about alcohol on this blog, preferably identifying yourself (but anonymously is fine), please get in touch with me on twitter or facebook.


Monday, 13 October 2014

Nick is not ill

As I mentioned in March, I went to the doctor. I wanted to see if 25 years of drinking had had any effect on my health.

Now, admittedly, I haven't drunk every day of those 25 years. But I have drunk more than the recommended weekly limit many times.

There's a Wonder Stuff song called The Size of a Cow which repeats the refrain "You know that I've been drunk a thousand times...."

I remember working out, with my bass-playing friend Aidan, what age we would have to be before we had been drunk a thousand times. I reckon I probably made it by the age of 25, certainly by 30.

In recent years, the Friday and Saturday night binge drinking has eased off, replaced by more regular, habitual drinking. Two pints here, three bottles of beer there, most of a bottle of wine on a Saturday night at home etc. That's not to say that if a drinking buddy came over I couldn't put away a lot more, but those nights are few and far too painful to do very often.

Knowing that any alcohol is unhealthy, you would have thought that over the years I might have done myself some damage, which is why I went to the doctor in March.

Blood test No 1

They took some blood. It came back with a slightly high bilirubin score. I wasn't told what that score was. The document in the link above says 17 is normal. A high bilirubin score can suggest liver damage. I didn't get to discuss the result with a doctor, I was just told over the phone I had a high bilirubin score and had to go for another test three months later.

Blood test No 2

I went for another test and the following week I got an email back telling me I had a low white blood cell count, which was probably due to a virus, but could I go back for another blood test the following  month. No mention of the bilirubin.

Blood test No 3

So back I went. This time my white blood cell count was higher, but still below normal. So could I go back for another blood test, this time in two months?

Blood test No 4

Eight days ago I did my most recent blood test, on 3 October 2014.

Time to go see the doctor and discuss the results.

As the set up at our medical centre means you rarely get to see the same GP twice in a row, I explained my initial request for a blood test and subsequent return visits to a slightly bemused Eastern European lady who I had never met before.

She looked at my results. Yes, my bilirubin score was initially 28. She thought 20 or 21 was about normal. By the second blood test it was 23. The other three tests of liver function:

GGT - Gamma Glutamyl Transferase
ALT - Alanine Aminotransferase
MCT - Mean Cell Volume

were all fine on both occasions. The doctor said if I had any alcohol-inflicted liver damage she would expect to see high levels in all three of the above measures before any increase in bilirubin levels. All three were normal. She was unconcerned. She said she wouldn't get even slightly worried unless a bilirubin score was consistently above 30 to 40, and that my varying levels hovering above normal could just be a genetic trait.

We had a chat about alcohol and safe limits and it was clear she wasn't going to endorse my drinking habits. I wasn't expecting her to.

We both agreed alcohol is not good for you. She told me she sees people younger than me coming to her with cirrhosis and that alcohol abuse is a real problem. I don't doubt it.

But... I would estimate I have drunk more than the recommended daily limit of 3 to 4 units of alcohol on at least a fifth of the 10,000 days that have passed since I first started drinking. On some of those 2,000 days my unit consumption was significantly higher than the recommended daily limit. Days when (and I feel curiously ashamed to admit this) I was drunk, your honour.

The long term effect this has had on my liver? Nil. Nothing. It is as perfectly healthy as if I were teetotal and had been all my life. Think about that for a moment.

Now, I haven't had any of my other organs tested. My adult drinking might have already set in motion a series of problems quietly gestating in my body.

Pancreatic cancer is linked to heavy drinking, as is throat cancer and brain damage. I am currently putting together a list of the conditions linked to excessive alcohol consumption, and believe me it ain't pretty.

But when I read the literature, and compare it to my own behaviour, I am starting to think maybe I just don't drink anywhere near enough. The liver is the one that tends to start throwing up red flags if your alcohol consumption is becoming problematic, and mine is just chipper, thanks.

What to make of this? Well here's an idea - the reason public health messages about alcohol are failing to hit home is because they are not relevant to the majority of the population.

Watch men in pubs on a Friday night. Many are drinking three to four units an hour. Telling them the limit is 3 to 4 units a day is like telling a journalist it's not a good idea to go round asking too many questions.

That's not to say the addictive nature of alcohol can't wear down your defences, take a hold of you and, over time, push you into a high level of consumption that causes problems. It's a powerful, seductive, liberally-available, socially-sanctioned drug.

But come on... tell me my real safe limit and I'll stick to it. Tell me I'm in danger after a couple of pints and I just will not believe you.

Oh and in case you were wondering, my white blood cell count is back to normal, too. So that's nice.

Wednesday, 1 October 2014


It's the first of October. There are three charity things happening this month which have all appropriated an otherwise innocent chunk of autumn.

The first is Stoptober, an NHS attempt to make us give up smoking.
The second is Go Sober for October, a MacMillan Cancer Nurses initiative which speaks for itself.
The third is Octobeardfest, which comes from the Prostate Project, and is "inspired" by Movember.

All are worthy causes. All can be achieved (for men, anyway) with minimal effort.

As I don't smoke, haven't had a drink since December, and will be filming a TV series throughout this month, I can't take part in any of the above October-related fun.

But that doesn't mean you can't. So join me in feeling better about yourself and raising money for good causes by doing nothing in October.

It's easy.

Right now I am not really thinking about not drinking at all, which is a deliberate ploy. Partly because there's no point and partly because the urge to have a drink simply does not exist any longer, almost to the extent that I am feeling a little daunted about starting again. This will change in December as I start hassling people for sponsorship and planning some exploratory visits to pubs with friends in January.

So making it three-quarters of the way through the year has been unremarkable save for one unexpected exception. The dawning realisation that I am going to watch an entire season of Strictly Come Dancing sober.

After Saturday night, that might be more of a struggle than I anticipated.