Acellular carbohydrates as a critical concept

English: different sorts of Pasta

English: different sorts of Pasta (Photo credit: Wikipedia)

A missing piece of the puzzle in understanding the health impacts of the carb-containing foods that we eat?

Dr. Ian Spreadbury presents an intriguing and potentially ground-breaking concept in a paper recently published.  The full text of the paper is available free online.

Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity.

Spreadbury I.  Diabetes Metab Syndr Obes. 2012;5:175-89.

PMID:  2282663   Free PMC Article

This is a scholarly and well argued thesis. His key conclusion?

“A dietary pattern with carbohydrates exclusively from cellular low-density sources may remove the root cause of a range of our most prevalent diseases.”

There is some risk that his research and theories will be used falsely as an argument in favor of foods that are simply low in carbohydrate density.  In fact, his focus is on both the density of carbs in foods AND on whether the carbs (starch and sugar) are present within cells.

He also does not propose that simply switching from a long-term intake of high-carbohydrate-density acellular foods will instantly fix the problems that have been set in motion – such as impacts on the gut microbe population (the microbiome), inflammation and leptin resistance – nor simply erase the downstream outcomes such as obesity and diabetes.  He does propose that such a dietary change might bring great benefits and that over time the body would likely slowly at least partially recover.  He calls for research into these questions.

My attention was first brought to this paper by Dr. Jay Wortman on his blog, and it has received other attention.

It is likely to become much more widely known now that Dr. Andrew Weil has commented on it HERE and HERE. (Note: Weil’s previously broken link they now have fixed)

I don’t agree fully with Dr. Weil’s comments.  For example, his statement

 “If Spreadbury is right, the obesity solution is straightforward.”

is just so wrong I don’t know where to start.

I love this at the bottom of Dr. Spreadbury’s paper

“This work was not supported by funding.”.

Of course, there are other aspects of carbohydrate intake that still need to be taken into consideration – especially the impact of per-meal carb total intake (not solely the form of the carbs) on blood glucose control in diabetes – where there is a combined impact from carb food form and total.

Increased Intestinal Permeability Shown in Obesity

There are an uncountable number of things that may contribute to obesity.  We also don’t have a good understanding of the causes of metabolic syndrome and why some people develop it and others don’t.

In this study of a small number of women (20 in the lean group, 20 in the obese group), there was increased intestinal permeability in the obese women.

Note that this study shows correlation, not causation.  That is, this does not indicate whether:

  • obesity increases the chance of developing higher intestinal permeability
  • higher intestinal permeability increases the chance of becoming or remaining obese, or
  • these two things happen together from some common cause.

In addition, the study showed that those with higher intestinal permeability tended to be those with indicators of metabolic syndrome.  Again, this study reports correlation and does not provide insight on causation.

Their Conclusions:

We demonstrated that intestinal permeability parameters in obese women are positively correlated with anthropometric measurements and metabolic variables. Therapeutic interventions focused on intestine health and the modulation of intestinal permeability should be explored in the context of obesity.

Intestinal permeability parameters in obese patients are correlated with metabolic syndrome risk factors.

Teixeira TF, Souza NC, Chiarello PG, Franceschini SC, Bressan J, Ferreira CL, Peluzio MD.   Clin Nutr. 2012 Mar 21. [Epub ahead of print]

PMID: 22444236

NOTE:  I did not read the full article (it is not open access).