The human liver is hardly a thing of beauty but it deserves some TLC. It’s the largest single organ in the body, weighs about 1.5 kg and is roughly the size of a football. Its functions are to filter blood coming from the gastrointestinal tract, detoxify chemicals and metabolise drugs. In other words, it comes in for a lot of abuse, and alcohol is up there at the top with all the other potential nasties.
A healthy liver looks smooth and glistening – just like the pig’s liver displayed on marble slabs at the meat counter – but a cirrhotic liver looks gnarled and blotchy. Even Dr Lector wouldn’t be tempted by this pickled monstrosity:
That’s because of a process called fibrosis, which is the body’s healing response to all the maltreatment. However, it isn’t all or nothing, and there’s a spectrum of changes between a normal liver and one that’s cirrhotic. The good news is that much of it is potentially reversible if the nasties are got to in time.
A fatty liver comes in for a lot of bad press and it’s not only about its owner being overweight. Other causes are diabetes, high blood pressure and high cholesterol – plus excessive alcohol consumption. Over time, the liver can become very fatty. While that in itself doesn’t harm the liver, the fat deposits and alcohol injure the liver cells themselves.
Inflammation follows and then the fibrosis, which, left untreated, may progress on to cirrhosis. If you’re particularly unlucky, hepatocellular carcinoma may succeed that, which is probably because of liver cell death and the organ’s unchecked attempts at regeneration.
Fibrosis is similar to what happens when the skin is cut. First off the starting line are cells in the blood called macrophages that trigger fibroblasts to lay down a mesh-like protein called fibrin. Just as a larger skin wound may form a visible scar, it’s the excessive scarring that sets the liver on the course to cirrhosis. However, unlike the healing of skin, the process in the liver is two way: the fibrin can be dissolved as well as deposited. But there are limits to the repair process.
In fact, the liver can function entirely normally with a certain amount of fibrosis. That’s why liver function tests aren’t a reliable monitor of earlier stages of damage. But once the fibrosis becomes thicker and more extensive, then the flow of blood in the liver becomes compromised, cells die and liver function suffers. Left untreated, there’s no way back apart from a transplant, and they’re in short supply.
One important question is whether fibrosis is a consequence of ageing. If that’s the case, then abstaining from alcohol can only achieve so much. Some might also argue that alcohol isn’t such a bad boy if its effect is only contributory rather than causative.
The answer is complicated. The ability of older people to metabolise alcohol isn’t as good as in the young, so the alcohol lingers in the system. All the medication that older people are prescribed may also make alcohol more toxic.
Age-related fibrosis itself, irrespective of alcohol and other toxic agents, is difficult to quantify. However, there’s little doubt that an older person with alcohol-related liver disease tends to do worse than someone younger, including an increased risk of developing liver cancer. Like the rest of the body, the liver simply isn’t so good at repairing itself.
Personally, I’m not going to risk it – particularly as I’m waiting for my ELF re-test. Henry is making acquaintance with his ELF, too.