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Low carbohydrate-high protein diet and incidence of cardiovascular diseases in Swedish women: prospective cohort study

BMJ 2012; 344 doi: (Published 26 June 2012) Cite this as: BMJ 2012;344:e4026

Re: Low carbohydrate-high protein diet and incidence of cardiovascular diseases in Swedish women: prospective cohort study

As someone who studies diet from an evolutionary perspective - and its impact on the human microbiome - I always find diet studies that draw a correlation between increased protein or fat intake (or some combination of the two) with some unfavorable outcome. The implication always ending in some cautionary tale of the woes of eating too many animals.

In the current study, the authors suggest a low-carb high protein diet is significantly associated with increasing incidence of cardiovascular disease. In conclusion, they suggest attention be given in future studies to the nature of the protein - that is, plant versus animal. The implication is that one is better than the other and the reader can only assume the latter given the current wind direction in dietary advise on meat consumption. Interestingly, even though the conclude with this cautionary tale, their own study found no significant difference in cardiovascular health based on the difference of protein intake from either animal or plant origin.

That aside, a recent paper published in JAMA found that an extreme low-carb Atkins-like diet increased biomarkers of inflammation (e.g., CRP), even though the diet resulted in greater weight loss compared to other diets. The current study and its increase cardiovascular risk from low-carb intake and the JAMA study may be pointing us to the role of the microbiome.

In a series of elegant studies, Cani and colleagues ( 2-4) have shown that holding calories constant and varying macro levels of fat can induce low-grade metabolic endotoxemia which can lead to complications associated with cardiovascular health. As fat intake, so do serum levels of LPS and associated biomarkers. However, in high-fat diets with prebiotic oligosaccharides added (derived from chicory roots), serum levels of LPS drop, as do the metabolic markers of inflammation.

In the current study, the implication that increased protein – implied to be a bad thing if derived from animal sources – will increase risk of cardiovascular disease. By default, as either protein or fat intake go up and carbohydrates go down in ANY diet, we can assume that the physical and chemical diversity of what plants that are being consumed will decrease. With a drop in diversity comes a drop in the diversity of available fermentable oligo- and polysaccharides available to the microbiota.
In the Cani studies (and there are numerous others), a prebiotic oligosaccharide was shown to stimulate the growth of the LAB Bifidobacterium, which in turn improved gut permeability through several well-known mechanisms (5).

Rather than implying that higher protein and fat consumption may have a less than desirable outcome in cardiovascular health, maybe we should be talking more about the diversity and quantity of fermentable substrates that is lacking in the diet.(6) In other words, let us not always conclude that an association between high protein (and fat) and cardiovascular disease is the result of meat consumption.

(1) JAMA. 2012;307(24):2627-2634. doi:10.1001/jama.2012.6607

(2) Cani, Patrice D., Rodrigo Bibiloni, Claude Knauf, Aurélie Waget, Audrey M. Neyrinck, Nathalie M. Delzenne, and Rémy Burcelin. 2008. "Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice." Diabetes no. 57 (6):1470-1481. doi: 10.2337/db07-1403.

(3) Cani, Patrice D., Jacques Amar, Miguel Angel Iglesias, Marjorie Poggi, Claude Knauf, Delphine Bastelica, Audrey M. Neyrinck, Francesca Fava, Kieran M. Tuohy, Chantal Chabo, Aurélie Waget, Evelyne Delmée, Béatrice Cousin, Thierry Sulpice, Bernard Chamontin, Jean Ferrières, Jean-François Tanti, Glenn R. Gibson, Louis Casteilla, Nathalie M. Delzenne, Marie Christine Alessi, and Rémy Burcelin. 2007. "Metabolic Endotoxemia Initiates Obesity and Insulin Resistance." Diabetes no. 56 (7):1761-1772. doi: 10.2337/db06-1491.

(4) Cani, P. D. 2012. "Crosstalk between the gut microbiota and the endocannabinoid system: impact on the gut barrier function and the adipose tissue." Clinical Microbiology and Infection no. 18:50-53. doi: 10.1111/j.1469-0691.2012.03866.x.

(5) Tuohy KM, Rouzaud GC, Bruck WM, Gibson GR (2005) Modulation of the human gut microflora towards improved health using prebiotics—assessment of efficacy. Curr Pharm Des 11:75– 90

(6) Leach, J.D., K. D. Sobolik (2010). High dietary intake of prebiotic inulin-type fructans in the prehistoric Chihuahuan Desert. British Journal of Nutrition, 103 , pp 1558-1561 doi:10.1017/S0007114510000966

Competing interests: No competing interests

02 July 2012
Jeff Leach
Human Food Project
48 Swallow, New Orleans LA 70124