Pub medic - Warning: Christmas can seriously damage your health

Every year we’re inundated with information about the inherent dangers of the festive season—and apparently with good reason. A study in the United States showed a mortality spike on Christmas and New Year’s Day due to cardiac and respiratory conditions.¹ Oddly, European figures don’t show this, and a similar study in the United Kingdom (based in the north east) showed that we have a higher than average mortality on New Year’s Day but not on Christmas Day.² Bizarre as this discrepancy is, over the holiday period, binge drinking goes up, leading to more drink fuelled crimes and road traffic injuries and sparking fresh debates about heart disease, stroke, and liver disease.

We also eat too many mince pies and Yorkshire puddings, piling on the pounds; then we spend January frantically trying to lose them, wreaking havoc with our metabolism and perpetuating the general trend towards obesity. The endless round of present buying, social engagements and visits from the in-laws, not to mention “spouse saturation syndrome,”³ resulting from prolonged overexposure to your nearest and dearest, all lead to increased stress, fatigue, and depression. And that’s just if you’re healthy.

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Is there still a reason to celebrate?

A wide variety of chronic illnesses require careful management around the holiday season. Here are a few snippets with which to while away the hours (and presumably the pints) in the pub on Christmas Eve.

Diabetes: a delicate balancing act

Around Christmas or any other party season, this gets a lot more difficult, partly because there’s so much more food around to be tempted with, and, secondly, because the increased stress levels that Christmas shopping, parties, and in-law visits bring activates the hypothalamic-pituitary-adrenal cortex axis, leading to an increase in cortisol release. Cortisol, a steroid hormone, opposes the action of insulin, promoting the release of glucose into the bloodstream to provide an energy substrate for the “fight or flight” response, via lipolysis and proteolysis in peripheral sites and gluconeogenesis in the liver. This happens in people who don’t have diabetes as well, of course, but they are able to produce more insulin to cope with the increased discharge of glucose into the bloodstream.

Judging the right dosage of insulin when eating patterns, stress levels, and exercising are all interrupted can be much more difficult. Incidentally, higher levels of stress may leave us all vulnerable to infections because raised cortisol has an immunosuppressive effect by altering gene expression and therefore production or operation of interleukins and various immune cells such as macrophages. This is an area of contention, however, and the steroid dose usually has to be far higher than that found in normal physiological states to induce significant immunosuppression.

The effects of excessive alcohol consumption are even more complex and probably more dangerous. If the liver is occupied with the 10 pints of beer you have just ingested, the hepatocytes will be using all their NAD+ to oxidise the ethanol, and producing lots of NADH as a result. This inhibits gluconeogenesis by preventing the conversion of lactate, a major gluconeogenic substrate, to pyruvate, which then goes on to make glucose, and also inhibits the conversion of glycerol to glucose, because both reactions require NAD+ and are inhibited by higher concentrations of NADH. Therefore, you won’t be releasing glucose into the bloodstream.

In non-diabetic people, it doesn’t matter so much because you just won’t produce any insulin to counter it. If you’re on insulin replacement therapy, however, you don’t have that level of control and the chances are you’ll have a crashing hypoglycaemic attack in the middle of the night. It’s the one time when a doctor will probably recommend a trip to the kebab shop on the way home, to keep your carbohydrate concentrations up.

Hypertension and the heart

Your mates may not thank you for bringing this one up in the pub, but alcohol is easily the most important recognised morbidity marker for a whole range of conditions, not to mention the scourge of the health and law authorities who have to deal with the surge of drink related events around party season. Alcohol and the cardiovascular system have a long and fraught association and the literature on the subject is exhaustive.⁴ 

Although regular light drinking is meant to be cardioprotective (increased high density lipoprotein, decreased platelet activation and plasma fibrinogen) binge drinking certainly is not, and evidence shows that heavy drinking in one session can precipitate cardiac arrythmias⁵ and myocardial infarctions even in young healthy people with no previous heart conditions.⁶ Imagine, then, what it may do if you already have underlying coronary artery disease, dysrhythmias, or hypertension.

Whole chapters of biochemistry textbooks are devoted to alcohol metabolism, but the main acute effects on the cardiovascular system seem to be mediated by a rise in adrenaline. Adrenaline is released from the adrenal medulla and has various actions including peripheral vasoconstriction and increased cardiac output, both of which increase blood pressure. The neural input to the adrenal medulla has traditionally been regarded as sympathetic, but research has shown that there are receptors for gamma aminobutyric acid (GABA),⁷ which is known to medical students as an inhibitory neurotransmitter. Alcohol is a GABA receptor agonist, which may explain why it causes a release of adrenaline.^{8 9}

Acute increases in blood pressure in someone with underlying cardiovascular disease, such as atherosclerosis, are much more likely to precipitate myocardial infarction from thromboembolism in a coronary artery, presumably from the increase in haemodynamic stress exerted on the atherosclerotic plaque. It’s been suggested that platelet activation is also enhanced by acute excessive alcohol intake, leading to an increased risk of thrombosis and consequent myocardial infarction.¹⁰

Strokes are slightly more complicated. The risk of an embolic stroke may actually reduce with heavy drinking, but the risk of an intracerebral haemorrhage goes up, especially with underlying hypertension.¹¹ There’s also a difference between people who drink heavily all the time and people who binge on weekends or on holidays. In the withdrawal period after a binge, platelet aggregation becomes hyper-reactive after being inhibited by alcohol, and this may cause the increased risk of thromboembolic stroke as opposed to haemorrhagic in binge drinkers.

Party poopers

A whole host of other conditions need special consideration around Christmas and New Year, of course. Inflammatory bowel disease and malabsorptive digestive syndromes, such as coeliac disease, can be affected by the amount and type of food eaten, as well as the irregular hours of the social scene. Musculoskeletal disorders, including the arthritides (rheumatoid arthritis and osteoarthritis) and back pain can be exacerbated by long journeys, stress, and tiredness. And gout attacks can be precipitated by eating lots of high purine foods (such as meat, including turkey)¹² and drinking alcohol.¹³ Psychiatric disorders can also be worsened, especially depression and anxiety syndromes. Calls to the Samaritans (a charity helpline for people who want to talk about their problems) go up by around 10% in the festive period.

Your very good health

Even if you’re in top shape and without any type of illness, chronic or otherwise, Christmas is still a risky business. The number of drink-related road injuries soars compared with most other months (except, bizarrely, October and November). December has about 20% more casualties than March, for example.¹⁴ Unintentional domestic injuries also go up. Just before Christmas 2004, the NHS was expecting 80 000 emergency admissions from festive mishaps over the 12 day Christmas period.

And finally

Here’s one last snippet for you: Christmas disease has nothing to do with the festival, but is a rare form of haemophilia discovered in 1952 by doctors treating a young boy called Stephen Christmas. It results from a deficiency in clotting factor IX and, like haemophilia A (which is a deficiency in factor VIII), presents clinically with bleeding into joints and soft tissues.¹⁵ Merry Christmas and Happy New Year!

Competing interests: None declared.

Stephanie Gapper, second year medical student, University of Nottingham
Email: Mzyysg1@nottingham.ac.uk


studentBMJ 2006;14:1-44 January ISSN 0966-6494

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