Kaitlin Day, RMIT University and Sharayah Carter, RMIT University

Intermittent fasting has gained popularity in recent years as a dietary approach with potential health benefits. So you might have been surprised to see headlines last week suggesting the practice could increase a person’s risk of death from heart disease.

The news stories were based on recent research which found a link between time-restricted eating, a form of intermittent fasting, and an increased risk of death from cardiovascular disease, or heart disease.

So what can we make of these findings? And how do they measure up with what else we know about intermittent fasting and heart disease?

The study in question

The research was presented as a scientific poster at an American Heart Association conference last week. The full study hasn’t yet been published in a peer-reviewed journal.

The researchers used data from the National Health and Nutrition Examination Survey (NHANES), a long-running survey that collects information from a large number of people in the United States.

This type of research, known as observational research, involves analysing large groups of people to identify relationships between lifestyle factors and disease. The study covered a 15-year period.

It showed people who ate their meals within an eight-hour window faced a 91% increased risk of dying from heart disease compared to those spreading their meals over 12 to 16 hours. When we look more closely at the data, it suggests 7.5% of those who ate within eight hours died from heart disease during the study, compared to 3.6% of those who ate across 12 to 16 hours.

We don’t know if the authors controlled for other factors that can influence health, such as body weight, medication use or diet quality. It’s likely some of these questions will be answered once the full details of the study are published.

It’s also worth noting that participants may have eaten during a shorter window for a range of reasons – not necessarily because they were intentionally following a time-restricted diet. For example, they may have had a poor appetite due to illness, which could have also influenced the results.

Other research

Although this research may have a number of limitations, its findings aren’t entirely unique. They align with several other published studies using the NHANES data set.

For example, one study showed eating over a longer period of time reduced the risk of death from heart disease by 64% in people with heart failure.

Another study in people with diabetes showed those who ate more frequently had a lower risk of death from heart disease.

A recent study found an overnight fast shorter than ten hours and longer than 14 hours increased the risk dying from of heart disease. This suggests too short a fast could also be a problem.

But I thought intermittent fasting was healthy?

There are conflicting results about intermittent fasting in the scientific literature, partly due to the different types of intermittent fasting.

There’s time restricted eating, which limits eating to a period of time each day, and which the current study looks at. There are also different patterns of fast and feed days, such as the well-known 5:2 diet, where on fast days people generally consume about 25% of their energy needs, while on feed days there is no restriction on food intake.

Despite these different fasting patterns, systematic reviews of randomised controlled trials (RCTs) consistently demonstrate benefits for intermittent fasting in terms of weight loss and heart disease risk factors (for example, blood pressure and cholesterol levels).

RCTs indicate intermittent fasting yields comparable improvements in these areas to other dietary interventions, such as daily moderate energy restriction.

So why do we see such different results?

RCTs directly compare two conditions, such as intermittent fasting versus daily energy restriction, and control for a range of factors that could affect outcomes. So they offer insights into causal relationships we can’t get through observational studies alone.

However, they often focus on specific groups and short-term outcomes. On average, these studies follow participants for around 12 months, leaving long-term effects unknown.

While observational research provides valuable insights into population-level trends over longer periods, it relies on self-reporting and cannot demonstrate cause and effect.

Relying on people to accurately report their own eating habits is tricky, as they may have difficulty remembering what and when they ate. This is a long-standing issue in observational studies and makes relying only on these types of studies to help us understand the relationship between diet and disease challenging.

It’s likely the relationship between eating timing and health is more complex than simply eating more or less regularly. Our bodies are controlled by a group of internal clocks (our circadian rhythm), and when our behaviour doesn’t align with these clocks, such as when we eat at unusual times, our bodies can have trouble managing this.

So, is intermittent fasting safe?

There’s no simple answer to this question. RCTs have shown it appears a safe option for weight loss in the short term.

However, people in the NHANES dataset who eat within a limited period of the day appear to be at higher risk of dying from heart disease. Of course, many other factors could be causing them to eat in this way, and influence the results.

When faced with conflicting data, it’s generally agreed among scientists that RCTs provide a higher level of evidence. There are too many unknowns to accept the conclusions of an epidemiological study like this one without asking questions. Unsurprisingly, it has been subject to criticism.

That said, to gain a better understanding of the long-term safety of intermittent fasting, we need to be able follow up individuals in these RCTs over five or ten years.

In the meantime, if you’re interested in trying intermittent fasting, you should speak to a health professional first.

Kaitlin Day, Lecturer in Human Nutrition, RMIT University and Sharayah Carter, Lecturer Nutrition and Dietetics, RMIT University

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

An article published this week in the prestigious journal Nature Medicine documents what is believed to be the first evidence that Alzheimer’s disease can be transmitted from person to person.

The finding arose from long-term follow up of patients who received human growth hormone (hGH) that was taken from brain tissue of deceased donors.

Preparations of donated hGH were used in medicine to treat a variety of conditions from 1959 onwards – including in Australia from the mid 60s.

The practice stopped in 1985 when it was discovered around 200 patients worldwide who had received these donations went on to develop Creuztfeldt-Jakob disease (CJD), which causes a rapidly progressive dementia. This is an otherwise extremely rare condition, affecting roughly one person in a million.

What’s CJD got to do with Alzehimer’s?

CJD is caused by prions: infective particles that are neither bacterial or viral, but consist of abnormally folded proteins that can be transmitted from cell to cell.

Other prion diseases include kuru, a dementia seen in New Guinea tribespeople caused by eating human tissue, scrapie (a disease of sheep) and variant CJD or bovine spongiform encephalopathy, otherwise known as mad cow disease. This raised public health concerns over the eating of beef products in the United Kingdom in the 1980s.

Human growth hormone used to come from donated organs

Human growth hormone (hGH) is produced in the brain by the pituitary gland. Treatments were originally prepared from purified human pituitary tissue.

But because the amount of hGH contained in a single gland is extremely small, any single dose given to any one patient could contain material from around 16,000 donated glands.

An average course of hGH treatment lasts around four years, so the chances of receiving contaminated material – even for a very rare condition such as CJD – became quite high for such people.

hGH is now manufactured synthetically in a laboratory, rather than from human tissue. So this particular mode of CJD transmission is no longer a risk.

What are the latest findings about Alzheimer’s disease?

The Nature Medicine paper provides the first evidence that transmission of Alzheimer’s disease can occur via human-to-human transmission.

The authors examined the outcomes of people who received donated hGH until 1985. They found five such recipients had developed early-onset Alzheimer’s disease.

They considered other explanations for the findings but concluded donated hGH was the likely cause.

Given Alzheimer’s disease is a much more common illness than CJD, the authors presume those who received donated hGH before 1985 may be at higher risk of developing Alzheimer’s disease.

Alzheimer’s disease is caused by presence of two abnormally folded proteins: amyloid and tau. There is increasing evidence these proteins spread in the brain in a similar way to prion diseases. So the mode of transmission the authors propose is certainly plausible.

However, given the amyloid protein deposits in the brain at least 20 years before clinical Alzheimer’s disease develops, there is likely to be a considerable time lag before cases that might arise from the receipt of donated hGH become evident.

When was this process used in Australia?

In Australia, donated pituitary material was used from 1967 to 1985 to treat people with short stature and infertility.

More than 2,000 people received such treatment. Four developed CJD, the last case identified in 1991. All four cases were likely linked to a single contaminated batch.

The risks of any other cases of CJD developing now in pituitary material recipients, so long after the occurrence of the last identified case in Australia, are considered to be incredibly small.

Early-onset Alzheimer’s disease (defined as occurring before the age of 65) is uncommon, accounting for around 5% of all cases. Below the age of 50 it’s rare and likely to have a genetic contribution.

The risk is very low – and you can’t ‘catch’ it like a virus

The Nature Medicine paper identified five cases which were diagnosed in people aged 38 to 55. This is more than could be expected by chance, but still very low in comparison to the total number of patients treated worldwide.

Although the long “incubation period” of Alzheimer’s disease may mean more similar cases may be identified in the future, the absolute risk remains very low. The main scientific interest of the article lies in the fact it’s first to demonstrate that Alzheimer’s disease can be transmitted from person to person in a similar way to prion diseases, rather than in any public health risk.

The authors were keen to emphasise, as I will, that Alzheimer’s cannot be contracted via contact with or providing care to people with Alzheimer’s disease.

Steve Macfarlane, Head of Clinical Services, Dementia Support Australia, & Associate Professor of Psychiatry, Monash University

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