Scandinavian Somersaults … or As You Were?

Talking about diets in the last post may have brought to mind the publicity about weight-reducing diets created by a recent Swedish study Dietary Treatment for Obesity.”

This report, incorrectly described by some of the press as providing national guidelines, has been interpreted as earth-shaking in turning conventional wisdom on its head by advocating a switch from low-fat to high-fat/low-carb nutrition.

lg-raspberry_chipotle_meatballsHelp yourself: Swedish meat balls:

pork and beef with lots of cream

But did it really say anything remotely revolutionary? Well, no. First, it was concerned only with diets aimed at reducing weight for obese people – and the central point was that a low-carbohydrate, high-fat diet, was the most effective in the short-term – over about 6 months – after which there’s not much difference compared with other dietary regimens.

So to summarise: eating lots of sugar and starch is bad for you – as anyone with much of a clue about metabolism knew anyway (see Biting the Bitter Bullet & A Small Helping For Australia) – and substituting artificial sweeteners won’t help either (The Best Laid Plans in Mice and Men..).

ShowImageVB.aspxA reminder from The Food Standards Agency


SBU. Food in obesity. A systematic literature review. Stockholm: Swedish Council on Technology Assessment in Health Care (SBU); 2013. SBU Report No. 218. ISBN 978-91-85413-59-1.


Fast Food Fix Focuses on Fibre

If you’re like me you’re probably more bored than absorbed by the seemingly continuous stream of ‘studies’ telling us what we should and shouldn’t eat. No one’s going to argue it’s unimportant but gee, I wish they’d make their minds up. Of course the study of diet and its effects is tricky – as we noted in Betrayed by Nature – not least because you generally need enormous numbers of people to tease out significant effects.

Fortunately authoritative sources like The American Heart Association offer generally sane and simple advice: “eat a balanced diet and do enough exercise to match the number of calories you take in.”

A balanced diet includes fibre, sometimes called roughage, the stuff we eat but can’t digest that assists in taking up water and generally keeping our insides working. There’s much evidence that eating plenty of fibre helps to prevent bowel cancer – usually accumulated from vast numbers (e.g., the European Prospective Investigation into Cancer and Nutrition study involved over half a million people from ten European countries). But even for fibre, when you might just be thinking the answer’s clear-cut, there are other studies showing no protective effect.

So hooray for Stephen O’Keefe and friends from the University of Pittsburgh and Imperial College London for coming up with a dead simple experiment – and some pretty astonishing results (though to prevent panic we should reveal at the outset that they confirm that a high fibre diet can substantially reduce the risk of colon cancer).

Doing the obvious

The experiment compared what happened to two groups of 20, one African Americans, the other from rural South Africa, when they swapped diets for two weeks. So, in principle ‘dead simple’ but to describe it thus does a great injustice to the huge amount of effort involved – for a start they had to find two lots of 20 volunteers willing to have a colonoscopy examination before and after the diet swap. The Western diet was, of course, high protein, high fat, low fibre, whereas the typical African diet was high in fibre and low in fat and protein. Just to be clear, the American diet included beef sausage and pancakes for breakfast, burger and chips for lunch, etc. The traditional African diet comprises corn based products, vegetables, fruit and pulses, e.g., corn fritters, spinach and red pepper for breakfast.

B'fast jpegCompare and contrast.

A rural South African diet (corn fritters for breakfast) and the American diet (Getty images)

Shock – and horror

Almost incredibly, within the two weeks of these experiments there were significant, reciprocal changes in both markers for cancer development and in the bug army – the microbiota – inhabiting the digestive tracts of the volunteers. That is, the dreaded colonoscopy revealed polyps (tumour precursors) in nine Americans (that were removed) but none in the Africans. Cells sampled from bowel linings had significantly higher proliferation rates (a biomarker of cancer risk) in African Americans than in Africans. After the diet switch the proliferation rates flipped, decreasing in African Americans whilst the Africans now had rates even higher than in the starting African American group. These changes were paralled by an influx of inflammation-associated cells (lymphocytes and macrophages) in the now high-fat diet Africans whilst these decreased in the Americans on their new, high-fibre diet.

Equally amazing, these reciprocal shifts were also associated with corresponding changes in specific microbes and their metabolites. You may recall meeting our microbiota (in The Best Laid Plans of Mice and Men and It’s a Small World) – the 1000 or so assorted species of bacteria that have made you their home, mostly in your digestive tract, of which there are two major sub-families, Bacteroidetes and Firmicutes (Bs & Fs). We saw that artificial sweeteners in the form of saccharin shifts our bug balance: Fs down, Bs up. Here feeding Americans high-fibre diet was associated with a shift from Bs To Fs. As we noted before, the composition of the bug army is important because of the chemicals (metabolites) they produce – in this case the diet switch resulted in more short chain fatty acids (e.g., butyrate) in the American group and a reciprocal drop therein for the Africans.

The bottom line

It really is quite remarkable that these indicators of cancer risk manifest themselves so rapidly following a change to a typical Western diet. Of course ‘markers’ are one thing, cancer is another. As one of the authors, Jeremy Nicholson of Imperial College London, said: “We can’t definitively tell from these measurements that the change in their diet would have led to more cancer in the African group or less in the American group, but there is good evidence from other studies that the changes we observed are signs of cancer risk.”

Put less scientifically, “a nod’s as good as a wink to a blind horse.”


O’Keefe, S.J.D. et al. (2015). Fat, fibre and cancer risk in African Americans and rural Africans. Nature Communications 6, Article number: 6342 doi:10.1038/ncomms7342

Put A Cap On It

If you’re not too selective in your reading you may have spotted ‘a new test which can predict with 100 per cent accuracy whether a person will develop cancer up to 13 years in the future’ trumpeted, needless to say, by The Telegraph and The Independent. No one with much of a clue about biology would write such a line and, somewhat surprisingly, it was left to the Daily Mail to produce a more balanced account of a study from Northwestern University that measured the length of telomeres in blood over time to see if that could be used as a marker for cancer development.

How long is a cap?

Telomeres: protective DNA caps on the ends of chromosomes

Telomeres: protective DNA caps on the ends of chromosomes

Telomeres are short, repeated sequences of DNA that ‘cap’ the ends of our 46 chromosomes but the cell machinery that makes DNA can’t manage to replicate the tips of the caps, so every time a new cell is made the ends of each telomere get lost. Which is of no matter to individual cells (as telomeres don’t code for protein) but their continuing loss in all cells would mean the species couldn’t survive. Accordingly, germline cells (through which sexual reproduction occurs) make an enzyme called telomerase that can achieve the trick of replicating the ends of chromosomes. In all other types of cell, however, telomerase is almost undetectable—its gene is still present, of course, but its almost completely ‘switched off,’ never to be turned on again. Never, that is, unless the cell becomes a tumor cell – most primary tumours make substantial amounts of telomerase, so they can maintain the length of their telomeres and can grow indefinitely.

The new study showed, as expected, that the telomeres in white blood cells get shorter with age but the striking finding was that, on average, shortening happens a shade more rapidly in individuals who went on to develop cancer than in those who did not. However, for the cancer group in the three to four years before diagnosis telomere attrition ceased, cap length becoming relatively stable, presumably as a result of telomerase being switched on. In other words, it seems that cancer development may actually increase telomere shortening in the period before telomerase kicks in to maintain ‘immortality’ in the tumour cell. The presumption is that this effect shows up in white cells in circulating blood because at least some of them will have encountered the ‘tumour microenviroment’ that we visited last time.

And the truth of the matter …

Do these results justify the headlines that (yet again) so annoyed me? As ever, it’s not a bad idea to read what the boffins who did the work actually said about their study, to wit, that it “… enabled us to establish temporal associations between blood telomere length and cancer risk … However, our findings should be confirmed in future studies. Our sample size limited our ability to analyze specific cancer subtypes other than prostate cancer. Thus, caution should be exercised in interpreting our results as different cancer subtypes have different biological mechanisms, and our low sample size increases the possibility of our findings being due to random chance and/or our measures of association being artificially high.”

Well said lads: no hype there, just an honest assessment – but bear in mind if you ever tire of science you’ll never get a job as a journalist.


Hou, L. et al. (2015). Blood Telomere Length Attrition and Cancer Development in the Normative Aging. EBioMedicine doi:10.1016/j.ebiom.2015.04.008.