We’ve got a corker to dissect this week. The title of this note was the verbatim title of a press release issued on the back of a study commissioned by Kellogg’s – yes – that well known producer of cereals/grain fibre.
The Australian government’s press release, on the same topic, was entitled “Tackle chronic disease by eating more fibre“.
The full document, which inspired these headlines, can be seen here. The first sentence of the report states “Kellogg Australia commissioned Nutrition Research Australia to conduct this research.” I bet they did!
Where the claim comes from
The Executive Summary of the report (p10) states the following [CVD is cardiovascular disease and T2D is type 2 diabetes]:
“This research demonstrates that if Australian adults use grain fibre to increase their intake of dietary fibre to target intake levels for chronic disease risk reduction (28g for women, 38g for men):
• The potential healthcare expenditure savings would be approximately $1 billion for CVD and over $285 million for T2D in 2015–16. The savings for CVD would represent approximately 0.6% of total Australian health expenditure and savings for T2D would be around 0.2% of health expenditure.
• The potential productivity cost savings were estimated to be approximately $600 million for CVD and $1.4 billion for T2D. The savings for CVD represent approximately 0.04% of gross domestic product (GDP) and for T2D, approximately 0.08% of GDP.
The total combined economic savings could potentially reach $3.3 billion.”
That’s where the claimed $3.3 billion comes from. (Please note that the terms grain fibre and cereal fibre are often used interchangeably).
The DART study
What puzzled me, as soon as I saw the press releases, was that there has only been one long, large randomised controlled trial where (cereal) fibre was a specific intervention and that didn’t go well for (cereal) fibre manufacturers. The 1989 Diet And Reinfarction Trial (DART) (Ref 1) was a 2 year trial designed to examine the effects of 3 different dietary interventions in 2,033 men who had already had a heart attack. The men were randomly allocated to receive, or not to receive, advice on each of three dietary factors: fish; fat and/or fibre.
The fibre advice was to increase the intake of cereal fibre to 18g daily. 1,017 men were given fibre advice; 1,016 were given no-fibre advice. There were 123 deaths (12.1%) in the fibre advice group vs. 101 (9.9%) in the no-fibre advice group. There were 109 deaths (10.7%) from heart disease in the fibre advice group and 85 deaths (8.4%) from heart disease in the no-fibre advice group. These results were not statistically significant, but they clearly provided no support whatsoever for cereal fibre.
The Cochrane evidence
I was also puzzled because I happen to know that there are three Cochrane systematic reviews (the ‘gold standard’), which have reviewed fibre, CVD and T2D. The first was a systematic review of 23 randomised controlled trials (RCTs) entitled “Dietary fibre for the primary prevention of cardiovascular disease” (Ref 2). None of the RCTs reported on deaths (total, or from CVD). Thus there was no evidence on CVD outcomes. The Cochrane conclusion was that there was a need for longer term, well-conducted, RCTs to determine the effects of fibre on CVD events.
The second was closely related to the first (Ref 3). It was a systematic review of nine RCTs entitled “Whole grain cereals for the primary or secondary prevention of cardiovascular disease.” None of the RCTs reported on CVD mortality or events. There was no evidence even for assumed CVD risk factors, such as blood lipids or blood pressure. The Cochrane conclusion again was that there was a need for longer term, well-conducted, RCTs to determine the effects of whole grains on CVD events or risk factors.
The third Cochrane review was on T2D and it was a systematic review of 1 randomised controlled trial and 11 cohort studies entitled “Whole grain foods for the prevention of type 2 diabetes mellitus” (Ref 4) The verbatim conclusion of this study was: “The evidence from only prospective cohort trials is considered to be too weak to be able to draw a definite conclusion about the preventive effect of whole grain foods on the development of T2DM. Properly designed long-term randomised controlled trials are needed.”
So, what did the Kellogg’s study do to conclude the opposite of the one long, large randomised controlled trial that is available? And to conclude something that independent Cochrane researchers could not?
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