As we enter the festive season it’s a good time to think about what all those celebratory alcoholic drinks can do to your gut.

Alcohol can interfere with the time it takes for food to go through your gut (also known as the “transit time”). In particular, it can affect the muscles of the stomach and the small bowel (also known as the small intestine).

So, how and why does alcohol make your poos goes weird? Here’s what you need to know.

Diarrhoea and the ‘transit time’

Alcohol’s effect on stomach transit time depends on the alcohol concentration.

In general, alcoholic beverages such as whisky and vodka with high alcohol concentrations (above 15%) slow down the movement of food in the stomach.

Beverages with comparatively low alcohol concentrations (such as wine and beer) speed up the movement of food in the stomach.

These changes in gut transit explain why some people can get a sensation of fullness and abdominal discomfort when they drink vodka or whisky.

How long someone has been drinking a lot of alcohol can affect small bowel transit.

We know from experiments with rats that chronic use of alcohol accelerates the transit of food through the stomach and small bowel.

This shortened transit time through the small bowel also happens when humans drink a lot of alcohol, and is linked to diarrhoea.

Alcohol can also reduce the absorption of carbohydrates, proteins and fats in the duodenum (the first part of the small bowel).

Alcohol can lead to reduced absorption of xylose (a type of sugar). This means diarrhoea is more likely to occur in drinkers who also consume a lot of sugary foods such as sweets and sweetened juices.

Chronic alcohol use is also linked to:

• lactose intolerance
• overgrowth of small bowel bacteria and
• reduced absorption of fats from the pancreas not producing enough digestive enzymes.

This means chronic alcohol use may lead to diarrhoea and loose stools.

How might a night of heavy drinking affect your poos?

When rats are exposed to high doses of alcohol over a short period of time, it results in small bowel transit delay.

This suggests acute alcohol intake (such as an episode of binge drinking) is more likely to lead to constipation than diarrhoea.

This is backed up by recent research studying the effects of alcohol in 507 university students.

These students had their stools collected and analysed, and were asked to fill out a stool form questionnaire known as the Bristol Stool Chart.

The research found a heavy drinking episode was associated with harder, firm bowel motions.

In particular, those who consumed more alcohol had more Type 1 stools, which are separate hard lumps that look or feel a bit like nuts.

The researchers believed this acute alcohol intake results in small bowel transit delay; the food stayed for longer in the intestines, meaning more water was absorbed from the stool back into the body. This led to drier, harder stools.

Interestingly, the researchers also found there was more of a type of bacteria known as “Actinobacteria” in heavy drinkers than in non-drinkers.

This suggests bacteria may have a role to play in stool consistency.

But binge drinking doesn’t always lead to constipation. Binge drinking in patients with irritable bowel syndrom (IBS), for example, clearly leads to diarrhoea, nausea and abdominal pain.

What can I do about all this?

If you’re suffering from unwanted bowel motion changes after drinking, the most effective way to address this is to limit your alcohol intake.

Some alcoholic beverages may affect your bowel motions more than others. If you notice a pattern of troubling poos after drinking certain drinks, it may be sensible to cut back on those beverages.

If you tend to get diarrhoea after drinking, avoid mixing alcohol with caffeinated drinks. Caffeine is known to stimulate contractions of the colon and so could worsen diarrhoea.

If constipation after drinking is the problem, then staying hydrated is important. Drinking plenty of water before drinking alcohol (and having water in between drinks and after the party is over) can help reduce dehydration and constipation.

You should also eat before drinking alcohol, particularly protein and fibre-rich foods.

Food in the stomach can slow the absorption of alcohol and may help protect against the negative effects of alcohol on the gut lining.

Is it anything to worry about?

Changes in bowel motions after drinking are usually short term and, for the most part, resolve themselves pretty efficiently.

But if symptoms such as diarrhoea persist beyond a couple of days after stopping alcohol, it may signify other concerning issues such as an underlying gut disorder like inflammatory bowel disease.

Researchers have also linked alcohol consumption to the development of irritable bowel syndrome.

If problems persist or if there are alarming symptoms such as blood in your stool, seek medical advice from a general practitioner.

Vincent Ho, Associate Professor and clinical academic gastroenterologist, Western Sydney University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Before the COVID pandemic, the World Health Organization (WHO) had made a list of priority infectious diseases. These were felt to pose a threat to international public health, but where research was still needed to improve their surveillance and diagnosis. In 2018, “disease X” was included, which signified that a pathogen previously not on our radar could cause a pandemic.

While it’s one thing to acknowledge the limits to our knowledge of the microbial soup we live in, more recent attention has focused on how we might systematically approach future pandemic risks.

Former US Secretary of Defense Donald Rumsfeld famously talked about “known knowns” (things we know we know), “known unknowns” (things we know we don’t know), and “unknown unknowns” (the things we don’t know we don’t know).

Although this may have been controversial in its original context of weapons of mass destruction, it provides a way to think about how we might approach future pandemic threats.

Influenza: a ‘known known’

Influenza is largely a known entity; we essentially have a minor pandemic every winter with small changes in the virus each year. But more major changes can also occur, resulting in spread through populations with little pre-existing immunity. We saw this most recently in 2009 with the swine flu pandemic.

However, there’s a lot we don’t understand about what drives influenza mutations, how these interact with population-level immunity, and how best to make predictions about transmission, severity and impact each year.

The current H5N1 subtype of avian influenza (“bird flu”) has spread widely around the world. It has led to the deaths of many millions of birds and spread to several mammalian species including cows in the United States and marine mammals in South America.

Human cases have been reported in people who have had close contact with infected animals, but fortunately there’s currently no sustained spread between people.

While detecting influenza in animals is a huge task in a large country such as Australia, there are systems in place to detect and respond to bird flu in wildlife and production animals.

It’s inevitable there will be more influenza pandemics in the future. But it isn’t always the one we are worried about.

Attention had been focused on avian influenza since 1997, when an outbreak in birds in Hong Kong caused severe disease in humans. But the subsequent pandemic in 2009 originated in pigs in central Mexico.

Coronaviruses: an ‘unknown known’

Although Rumsfeld didn’t talk about “unknown knowns”, coronaviruses would be appropriate for this category. We knew more about coronaviruses than most people might have thought before the COVID pandemic.

We’d had experience with severe acute respiratory syndrome (SARS) and Middle Eastern respiratory syndrome (MERS) causing large outbreaks. Both are caused by viruses closely related to SARS-CoV-2, the coronavirus that causes COVID. While these might have faded from public consciousness before COVID, coronaviruses were listed in the 2015 WHO list of diseases with pandemic potential.

Previous research into the earlier coronaviruses proved vital in allowing COVID vaccines to be developed rapidly. For example, the Oxford group’s initial work on a MERS vaccine was key to the development of AstraZeneca’s COVID vaccine.

Similarly, previous research into the structure of the spike protein – a protein on the surface of coronaviruses that allows it to attach to our cells – was helpful in developing mRNA vaccines for COVID.

It would seem likely there will be further coronavirus pandemics in the future. And even if they don’t occur at the scale of COVID, the impacts can be significant. For example, when MERS spread to South Korea in 2015, it only caused 186 cases over two months, but the cost of controlling it was estimated at US$8 billion (A$11.6 billion).

The 25 viral families: an approach to ‘known unknowns’

Attention has now turned to the known unknowns. There are about 120 viruses from 25 families that are known to cause human disease. Members of each viral family share common properties and our immune systems respond to them in similar ways.

An example is the flavivirus family, of which the best-known members are yellow fever virus and dengue fever virus. This family also includes several other important viruses, such as Zika virus (which can cause birth defects when pregnant women are infected) and West Nile virus (which causes encephalitis, or inflammation of the brain).

The WHO’s blueprint for epidemics aims to consider threats from different classes of viruses and bacteria. It looks at individual pathogens as examples from each category to expand our understanding systematically.

The US National Institute of Allergy and Infectious Diseases has taken this a step further, preparing vaccines and therapies for a list of prototype pathogens from key virus families. The goal is to be able to adapt this knowledge to new vaccines and treatments if a pandemic were to arise from a closely related virus.

Pathogen X, the ‘unknown unknown’

There are also the unknown unknowns, or “disease X” – an unknown pathogen with the potential to trigger a severe global epidemic. To prepare for this, we need to adopt new forms of surveillance specifically looking at where new pathogens could emerge.

In recent years, there’s been an increasing recognition that we need to take a broader view of health beyond only thinking about human health, but also animals and the environment. This concept is known as “One Health” and considers issues such as climate change, intensive agricultural practices, trade in exotic animals, increased human encroachment into wildlife habitats, changing international travel, and urbanisation.

This has implications not only for where to look for new infectious diseases, but also how we can reduce the risk of “spillover” from animals to humans. This might include targeted testing of animals and people who work closely with animals. Currently, testing is mainly directed towards known viruses, but new technologies can look for as yet unknown viruses in patients with symptoms consistent with new infections.

We live in a vast world of potential microbiological threats. While influenza and coronaviruses have a track record of causing past pandemics, a longer list of new pathogens could still cause outbreaks with significant consequences.

Continued surveillance for new pathogens, improving our understanding of important virus families, and developing policies to reduce the risk of spillover will all be important for reducing the risk of future pandemics.

This article is part of a series on the next pandemic.

Allen Cheng, Professor of Infectious Diseases, Monash University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

People who are taller are at greater risk of developing cancer. The World Cancer Research Fund reports there is strong evidence taller people have a higher chance of of developing cancer of the:

• pancreas
• large bowel
• uterus (endometrium)
• ovary
• prostate
• kidney
• skin (melanoma) and
• breast (pre- and post-menopausal).

But why? Here’s what we know, don’t know and suspect.

A well established pattern

The UK Million Women Study found that for 15 of the 17 cancers they investigated, the taller you are the more likely you are to have them.

It found that overall, each ten-centimetre increase in height increased the risk of developing a cancer by about 16%. A similar increase has been found in men.

Let’s put that in perspective. If about 45 in every 10,000 women of average height (about 165 centimetres) develop cancer each year, then about 52 in each 10,000 women who are 175 centimetres tall would get cancer. That’s only an extra seven cancers.

So, it’s actually a pretty small increase in risk.

Another study found 22 of 23 cancers occurred more commonly in taller than in shorter people.

Why?

The relationship between height and cancer risk occurs across ethnicities and income levels, as well as in studies that have looked at genes that predict height.

These results suggest there is a biological reason for the link between cancer and height.

While it is not completely clear why, there are a couple of strong theories.

The first is linked to the fact a taller person will have more cells. For example, a tall person probably has a longer large bowel with more cells and thus more entries in the large bowel cancer lottery than a shorter person.

Scientists think cancer develops through an accumulation of damage to genes that can occur in a cell when it divides to create new cells.

The more times a cell divides, the more likely it is that genetic damage will occur and be passed onto the new cells.

The more damage that accumulates, the more likely it is that a cancer will develop.

A person with more cells in their body will have more cell divisions and thus potentially more chance that a cancer will develop in one of them.

Some research supports the idea having more cells is the reason tall people develop cancer more and may explain to some extent why men are more likely to get cancer than women (because they are, on average, taller than women).

However, it’s not clear height is related to the size of all organs (for example, do taller women have bigger breasts or bigger ovaries?).

One study tried to assess this. It found that while organ mass explained the height-cancer relationship in eight of 15 cancers assessed, there were seven others where organ mass did not explain the relationship with height.

It is worth noting this study was quite limited by the amount of data they had on organ mass.

Another theory is that there is a common factor that makes people taller as well as increasing their cancer risk.

One possibility is a hormone called insulin-like growth factor 1 (IGF-1). This hormone helps children grow and then continues to have an important role in driving cell growth and cell division in adults.

This is an important function. Our bodies need to produce new cells when old ones are damaged or get old. Think of all the skin cells that come off when you use a good body scrub. Those cells need to be replaced so our skin doesn’t wear out.

However, we can get too much of a good thing. Some studies have found people who have higher IGF-1 levels than average have a higher risk of developing breast or prostate cancer.

But again, this has not been a consistent finding for all cancer types.

It is likely that both explanations (more cells and more IGF-1) play a role.

But more research is needed to really understand why taller people get cancer and whether this information could be used to prevent or even treat cancers.

I’m tall. What should I do?

If you are more LeBron James than Lionel Messi when it comes to height, what can you do?

Firstly, remember height only increases cancer risk by a very small amount.

Secondly, there are many things all of us can do to reduce our cancer risk, and those things have a much, much greater effect on cancer risk than height.

We can take a look at our lifestyle. Try to:

• eat a healthy diet
• exercise regularly
• maintain a healthy weight
• be careful in the sun
• limit alcohol consumption.

And, most importantly, don’t smoke!

If we all did these things we could vastly reduce the amount of cancer.

You can also take part in cancer screening programs that help pick up cancers of the breast, cervix and bowel early so they can be treated successfully.

Finally, take heart! Research also tells us that being taller might just reduce your chance of having a heart attack or stroke.

Susan Jordan, Associate Professor of Epidemiology, The University of Queensland and Karen Tuesley, Postdoctoral Research Fellow, School of Public Health, The University of Queensland

This article is republished from The Conversation under a Creative Commons license. Read the original article.