In Depth

Falsified data and diabetes: Grizzly bears, chocolate and serious misconduct

A scientific paper investigating diabetes and obesity in grizzly bears was retracted from the journal Cell Metabolism on Tuesday. The reason: a scientist manipulated data. This is by no means the first time falsified data and diabetes research have crossed paths.

This paper was originally published in August 2014. Amge, a biotech company, was investigating how the metabolisms of grizzly bears adjust to hibernatio, to further understand the biology behind diabetes and obesity.

The researchers reported that when the bears were at their fattest, they managed to remain highly sensitive to insulin. During hibernatio, the bears entered a similar state to type 2 diabetes as insulin sensitivity reduced, which enabled them to break down fat stores to survive.

This was due to a protein called PTEN in fat cells, according to Amgen researchers. PTEN allowed the bears to become more or less insulin sensitive when needed, and upon waking from hibernatio, the bears recovered from their diabetic state.

The study suggested that diabetes and obesity “could exist naturally on opposite ends of the metabolic spectrum,” according to lead investigator Dr Kevin Corbit.

However, late last year, Amgen discovered that some experimental data had been changed.

“We know data were actually manipulated, and that just cannot stand,” said Alexander Kamb, Amgen’s research chief. Lamb was not one of the 12 authors of the study.

Cell Metabolism was quickly contacted for a retraction, and following a review by the journal, it was retracted on Tuesday. A lone company scientist was reportedly to blamen, and while Amgen claim the data manipulation did not affect the overall findings, the paper’s explanation of how PTEN is involved in fat cells has since been called into question.

Lynne Nelso, a professor of cardiology at Washington State and one of the paper’s lead authors, insisted: “We did nothing wrong, and we’re still going to pursue the hibernation physiology in bears because we think it’s an important thing to do.”

“Chocolate will help you lose weight”

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Journalist Johannes Bohannon fooled several publications with his study suggesting chocolate can help you lose weight

The grizzly bear study is grossly unfortunate, as a fascinating set of results on diabetes and obesity has been plunged into doubt.

But, in another compelling saga, one science journalist set about deliberately misleading the scientific community when he reported that chocolate can help you lose weight.

A 100 per cent authentic study riddled with “terrible science” was conducted by John Bohanno, whose researcher name was Johannes Bohannon.

Soon after it was published in the International Archives of Medicine, an online open-access journal, German tabloid Bild went bold with their headline: “Those who eat chocolate stay slim!”

Bohanno, a journalist with a PhD in the molecular biology of bacteria, wanted to expose how science journalism can be focused on attention-grabbing headlines. “Readers just can’t get enough stories about the benefits of red wine or the dangers of fructose,” he explained.

While the study was fraught with inaccuracy, it “did indeed find a statistically significant effect on weight loss, it was designed to do exactly that,” according to Business Insider, defending those who were caught out by the study.

The termination of DiaPep277

The news that chocolate can’t help you lose weight wasn’t particularly surprising, or damaging to the diabetes community, but the cancellation of DiaPep277 was much more serious.

The type 1 diabetes drug was being manufactured by Hyperion Therapeutics – specifically, at Andromeda Biotech, an Israeli-based subsidiary of the company.

DiaPep277 was designed to be a therapeutic vaccine for type 1, given to newly-diagnosed patients. But, when it was revealed that Andromeda employees had shared and analysed un-blinded data from a trial, the employees were suspended, and development of DiaPep277 was ceased.

As a result, a prospective new drug which hoped to stop the immune system attacking its own beta cells, and could have been a potential cure, is no more.

Falsifying data is not a common event in diabetes research, thankfully. It is still disappointing, though, when promising findings are forever tainted due to the regrettable actions of one or more individuals.

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