Liver cancer risk proportionate to waistline increase alcoholic cirrhosis

Dr Irengbam Mohendra Singh *

Unlike the portly satiric little man Mr Pickwick, with a portmanteau, in Charles Dickens's The Pickwick Papers, to whom we feel so charitable, and to which charitable institute I now belong, scientists have now discovered a sinister meaning in modern men with pot-belly.

The first serious cause in-inverted commas of waistline expansion is the crazy-but-true-yarn inactive lifestyle in the middle ages (40s), among the various facets of provocative style of living. As traditional rich food and alcoholic drink pep up a wonderful whirlwind of energy conservation, men lead the way to women in the race for a bulging tummy.

Researchers now say the increase in abdominal fat carries the risk of developing heart disease, stroke, type-2 (adult) diabetes and some cancers, especially liver cancer by deposition of excess fat in it. The famous paunch is called "beer belly" in the UK, though not do all beer drinkers have beer belly.

It also occurs in men who do not drink alcohol at all, eg north Indians and the Buddha, known as "truncate obesity". A few women also sport the hanging belly. I had a young smart married woman patient, who was PA to a firm, and when she sat her abdomen also sat in the chair. It took me 6 months to organise her tummy-tuck surgery under NHS that does not cater for cosmetic surgery.

There are many discussions about how obesity causes liver cancer. Though the exact cause of liver cancer is unknown, alcohol is a definite risk factor. This discourse relates to the findings of some researchers who suspect inflammation (hepatitis)of liver cells by deposition of fat as the cause of liver cancer, regardless of whether the patient drinks alcohol or not. Inflammation is a phenomenon caused by chemicals released by our body when a tissue (groups of cells) is damaged or simply stressed. It's a normal body's defence mechanism. It's however, good only for a short period but when it continues for long, it can stimulate cancer cells.

According to the journal Cancer Research, 1.57 million adults in US had increased risk of cancer in proportion to increased body mass index (BMI). Broadly, the risk of developing liver cancer increases by almost 10% for every two-inch growth in waistline. Peter Campbell, a director at the American Cancer Society, who conducted the research said: liver cancer is not just related to excess alcoholic intake and viral hepatitis (B & C).

Some researchers have confirmed that there is a link between abdominal obesity and liver cancer. To prove the point, they turned to mice that has a particular gene – prone to developing gene mutation (alteration)to trigger liver cancer. They fed some mice a high fat diet and the mice put on weight and developed more liver cancers than (control) mice fed on a healthy diet. Examination of their livers showed inflammatory cells near the cancer cells. When they blocked the production of these inflammatory cells they found the cancer cells developed slowly, meaning inflammation was precursor to producing cancer.

The question, now posed to researchers was, what actually caused the damage that turned the cells cancerous. They thought of bacteria, knowing that obese people have different range of bacteria in their guts than do people of a healthy weight. Normally, a group of bacteria, collectively called Clostridium cluster XI are present in higher numbers in the guts of obese mice. They destroyed the mice's gut bacteria with antibiotics, while feeding them a high-fat diet.

These mice developed liver cancer at the same rate as similar mice fed on normal diets but with no sign of liver inflammation. Further research showed that these bacteria convert the acids produced by our digestive system to a chemical called deoxycholic acid. And that these chemicals in the guts of obese mice caused inflammation and ultimately, cancer of the liver.

As liver cancer occurs commonly in the UK among chronic alcoholic British men, there have been many research on it. Cases of liver cancer have increased by more than 50% in the past decade, with around 6,000 diagnoses in the UK every year. They are mostly untreatable as symptoms often appear late in their existence.

The protruding belly or paunch in the West is historically associated with beer drinking men, as easy "extra fat" supplied by beer on top of the normal fat provided by food are deposited in the loose abdominal fatty tissue, as they have nowhere to go, unlike in women, who have large areas of subcutaneous fat that can accommodate further input.

To be fair, anybody who has beer belly is not an excessive beer drinker, or associated with liver cirrhosis. Many Indians, especially in the north have beer belly without drinking alcohol at all. While working in Delhi hospitals, I found a lot of very emaciated north Indian villagers suffering from liver cirrhosis, associated with poor nutrition (protein) that leads to deposition of fat in liver cells.

Liver, mainly produces bile (gall) to digest fat we eat. Any alcohol we drink (not just beer), as it enters our gut is converted into two things: fat and a chemical, acetate (acetic acid + an alkali). These acetates are taken into the blood stream and used as primary fuels to generate energy that keeps us going.

The fat also enters the blood stream and is carried to liver where it is metabolised ie broken down (see below). When drinking is in excess, the liver can't cope and fat molecules deposit inside liver cells and they cause inflammation in the long run.

Heavy drinking ie more than 14 units of alcohol a week (in practice, any drinker consumes more than this amount) is considered to be harmful to health. A unit of alcohol is a single measure (25ml) of whisky , or a third of a pint of beer, or half a standard glass (175ml) of red wine. It takes 10 years or more of heavy drinking before cirrhosis develops. Liver cirrhosis was quite uncommon in Manipur as Meiteis did not drink alcohol and there were no empirical evidence of it among hill dwellers.

When you drink alcohol it's absorbed from the gut and 98% are converted into energy (capacity for work) by liver, while producing a toxic chemical acetaldehyde as by-product, which is known to produce inflammation, cirrhosis and cancer of liver. This chemical is normally turned into water and carbon dioxide and goes out of body until the liver is overloaded with alcohol. The liver initially swells up and then shrinks when the cells turn into lifeless fibres (fibrosis). Ultimately, the liver stops functioning. Naturally, without a dead liver you are going to die.

Luckily, not everybody who drinks alcohol, does not develop cirrhosis; only about 20-30%. Out of these about 15% will develop liver cancer. Cirrhosis typically develops between the ages of 30 and 40 and patients will come to know its presence by becoming weak and tired, with loss of appetite and weight, abdominal discomfort and jaundice (yellow tinge of conjunctivae).

Doctors will make a diagnosis by clinical examination and blood tests, and if necessary, by examining a bit of liver tissue (biopsy) known as histological 'gold standard' to exclude or confirm alcoholic cirrhosis or other causes. Now there are tests to avoid unpleasant liver biopsy, such as serum and radiological markers of fibrosis.

Although a provisional clinical diagnosis of alcoholic hepatitis/cirrhosis can be made from patient's long association with alcoholic consumption, in guiding therapeutic decision, making and providing prognosis, doctors should be careful in labelling diagnosis of "alcoholic" cirrhosis on clinical suspicion, as the diagnosis may be inaccurate in up to 30% of patients, while it carries a 100% stigma to the patient and the family.

The further progress of the patient with known alcoholic cirrhosis depends on patient's overall state of health and his liver's capacity to compensate for the functional overload by the disease without complications, and his total abstinence from alcohol (this must be done in hospital as a sudden withdrawal of alcohol can be dangerous to patient).

The most important management of advanced cirrhosis is abstinence of alcohol when alcohol-related, and to treat complications, such as fluid in abdomen (ascites), bleeding from gastro-intestinal tract, which have specific therapies. A good nutrition with sufficient protein intake, treatment of zinc deficiency and clotting factors (to prevent bleeding) are essential. Regular walking exercise is helpful in preventing thinning of muscles. The liver should be screened by MRI scan yearly for cancer, and treated if so developed.

Not every patient with cirrhosis dies. The death rate is between 50-80%, depending on countries. With a liver transplant when liver fails completely, 70 out of 100 will live at least up to 5 years, according to Cleveland Clinic, Ohio, US,
Alcohol is enjoyable to drink socially, but by the middle age one must learn to be able to limit one's alcoholic intake. For those who drink alcohol regularly they should have an annual liver function tests that include "Gamma GT (GGT)" – that becomes positive first, showing very early liver damage. If positive, you should stop drinking alcohol altogether and the liver will heal itself in 6 months. You should also eat a good protein diet like chicken with your drinks. Eating a good amount of pulses (mung or mussorie dal proteins) will help.