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Looking beyond lipids: lifestyle is pivotal

Friday 28 April 2017   (0 Comments)
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Precision nutrition

Precision medicine is the new byword in cardiovascular prevention, aided by novel genomic insights. Can we also apply the same concept to nutritional approaches? 

This was a question raised by Professor Qi Sun (Harvard T.H. Chan School of Public Health, Boston, USA) during his plenary lecture. Recent research would support this possibility. Zeevi and co-workers showed marked interindividual variability in the postprandial glucose response, even when the same foods were eaten, leading them to suggest that tailoring nutritional interventions to the individual could be a viable approach in the future.1 Therefore rating certain foods as universally “good” or “bad” based on the average post prandial glucose response in the population may be inappropriate. The opportunity to precisely predict the glycaemic response in individuals could offer prove highly beneficial in optimising treatments for diabetes (both type 1 and type 2).

Dietary components cannot, however, be considered in isolation. There is evidence that a range of other factors, including when we eat and sleep, how much physical activity we do, intestinal disorders, and the quality of the gut microbiome, all impact individual variability in glycaemic response to a given food. The other part of the equation is the feasibility of translating algorithms based on individual response to the general population. To do so would require prospective information regarding the impact on cardiometabolic disease in the long-term.

For now, the focus should be on diet quality, adopting a Mediterranean diet that is high in whole grains, fruit, vegetables nuts ,and pulses, with limited intake of red or processed meat, as recommended in current guidelines.2 Additionally, when preparing food at home, it is important to consider how it is cooked, given evidence that methods such as roasting or cooking red meat on the barbeque are associated with a higher risk of developing type 2 diabetes than stewing or boiling.

Gut microbiome and cardiometabolic health

Discussion of diet and cardiometabolic health inevitably leads to the gut. As discussed by Professor Fredrik Bäckhed (The Wallenberg Laboratory, University of Gothenburg, Sweden) the gut microbiome can be considered as a second genome influencing cardiometabolic health.

There is now accumulating evidence that dietary factors influence the gut microbiome and ultimately cardiometabolic health. For example, dietary fibre is recognised as beneficial, whereas the bacterial metabolite trimethylamine-N-oxide (TMAO), formed by the oxidation of TMA, which is contained in choline-containing foods such as meat and eggs, is considered harmful, increasing the atherosclerotic burden.3 Understanding of the underlying mechanisms has been elusive, although recent studies have implicated signalling between bacterial products and cellular receptors involved in the regulation of bile acid homeostasis, and glucose and lipid metabolism in cross-talk between the gut microbiota and the host.4,5  

Similar crosstalk affecting the regulation of insulin signalling may contribute to insulin resistance in type 2 diabetes. For example, novel findings suggest that insulin signalling may in some way enhance production of imidazole propionate by the gut bacteria in individuals with pre-diabetes or type 2 diabetes. Elucidation of the mechanism of the gut-host crosstalk may offer potential therapeutic targets for the future.

The role of exercise

Beyond diet and weight loss, physical activity also affects metabolic health, as discussed by Professor Patrick Schrauwen (Maastricht University, the Netherlands). Studies have shown that exercise training not only decreases lipid content in the liver, but also increases fat storage in skeletal muscle.6-8 In athletes, this paradox is explained by restoration in muscle mitochondrial function and metabolic flexibility which accompanies the increase in skeletal muscle fat.8 However, in individuals with type 2 diabetes there is no compensatory increase in oxidative capacity. Thus, even without weight loss, there is a rationale that exercise improves metabolic health by increasing energy turnover. 

The key question then is how much exercise is needed to improve metabolic health?

As highlighted by Professor Schrauwen we are increasingly sedentary. Standing or walking could be just as important as structured exercise for improving metabolic health. Indeed, recent research suggests that breaking sitting time by standing or brisk walking is more effective, in terms of glycaemic control, than structured exercise.9

Another way of improving metabolic health is increasing brown adipose tissue activity. The recent “re-discovery” of brown adipose tissue in humans is one of the most intriguing findings in the research area of metabolic diseases. Studies have shown that short-term cold acclimation not only activates brown adipose tissue in lean humans but also improves the metabolic profile of skeletal muscle to benefit glucose uptake in patients with type 2 diabetes.10 Does activation of brown adipose tissue offer a ‘magic bullet’ for improving cardiometabolic health? Certainly, findings are encouraging.

In the meantime, as recommended by guidelines, we need to focus on improving diet quality, sitting less and increasing physical activity to improve our cardiometabolic health for now and the future.


1. Zeevi D, Korem T, Zmora N et al. Personalized nutrition by prediction of glycemic responses. Cell 2015;163:1079-94.

2. Catapano AL, Graham I, De Backer G et al. 2016 ESC/EAS guidelines for the management of dyslipidaemia. Atherosclerosis 2016;253:281-344.

3. Senthong V, Li XS, Hudec T et al. Plasma trimethylamine N-oxide, a gut microbe-generated phosphatidylcholine metabolite, is associated with atherosclerotic burden. J Am Coll Cardiol 2016;67:2620-8.

4.Schroeder BO, Bäckhed F. Signals from the gut microbiota to distant organs in physiology and disease. Nat Med 2016;22:1079-89.

5. Wahlström A, Kovatcheva-Datchary P, Ståhlman M et al. Crosstalk between bile acids and gut microbiota and its impact on Farnesoid X Receptor signalling. Dig Dis 2017;35:246-50.

6. Brouwers B, Hesselink MK, Schrauwen P, Schrauwen-Hinderling VB. Effects of exercise training on intrahepatic lipid content in humans. Diabetologia 2016;59:2068-79.

7. Meex RC, Schrauwen-Hinderling VB, Moonen-Kornips E et al. Restoration of muscle mitochondrial function and metabolic flexibility in type 2 diabetes by exercise training is paralleled by increased myocellular fat storage and improved insulin sensitivity. Diabetes 2010;59:572-9.

8. Goodpaster BH, He J, Watkins S, Kelley DE. Skeletal muscle lipid content and insulin resistance: evidence for a paradox in endurance-trained athletes. J Clin Endocrinol Metab 2001;86:5755-61.

9. Duvivier BM, Schaper NC, Hesselink MK et al. Breaking sitting with light activities vs structured exercise: a randomised crossover study demonstrating benefits for glycaemic control and insulin sensitivity in type 2 diabetes. Diabetologia 2017;60:490-8.

10. Hanssen MJ, van der Lans AA, Brans B et al. Short-term cold acclimation recruits brown adipose tissue in obese humans. Diabetes 2016;65:1179-89.

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