Reducing T2D, obesity risk: Fast eaters should slow down

Fast eating increases post-prandial glucose (PPG) concentration and glycaemic excursion in young, healthy women without diabetes, an interventional study has shown, thus underscoring the role of eating speed in the development of type 2 diabetes (T2D) and obesity.

Fast eating is reportedly associated with diabetes, obesity, and other metabolic syndromes. “[Specifically,] eating fast was associated with increased body weight and overeating, elevated blood pressure and fasting plasma glucose concentration, increased insulin resistance, and increased risk of impaired glucose tolerance and T2D,” said Saeko Imai from the Faculty of Home Economics at Kyoto Women’s University in Japan, who presented the findings at EASD 2020.

“However, … eating speed was entirely assessed by self-reported questionnaires, which might yield bias and lack objectivity, leaving the effect of eating speed on glycaemic response unclear,” she pointed out. As such, an objective evaluation is warranted to assess the acute effects of different eating speeds on glycaemic parameters.

For 6 days, 19 women (mean age 21 years, body mass index 20.6 kg/m², HbA_1c 34 mmol/mol) wore flash glucose monitoring systems to evaluate PPG responses at varying eating speeds. The women consumed identical test meals* either at a fast (10 minutes) or slow speed (20 minutes) on days 4 and 5. On day 4, half ate their meals fast, while the rest ate slowly; participants reversed this pattern on day 5. Slow eaters had to follow a certain sequence: vegetables first, main dish next, carbohydrates last. [EASD 2020, abstract 206]

Plasma glucose concentrations were similar between fast and slow eaters (mean, 4.76 vs 4.79 mmol/L).

However, compared with slow eaters, fast eaters had significantly higher MAGE** (3.67 vs 2.67 mmol/L; p<0.01), standard deviation of glucose (1.18 vs 0.92 mmol/L; p<0.05), post-meal IGP*** (2.30 vs 1.71 mmol/L; p<0.01 [breakfast], 4.06 vs 3.13 mmol/L; p<0.01 [lunch], and 3.87 vs 2.27 mmol/L; p<0.001 [dinner]), and dinner IAUC^# for glucose (256 vs 128 mmol/L x min; p<0.001 [2 hours], 336 vs 200 mmol/L x min; p<0.01 [3 hours], and 373 vs 260 mmol/L x min [4 hours]; p<0.01).

The lowdown on slowing down

“Post-prandial hyperglycaemia and higher MAGE are associated with increased risk of T2D and cardiovascular diseases (CVD) in people with and without diabetes. Therefore, decreasing PPG concentrations and MAGE [by eating slowly] may reduce the risk of developing impaired glucose tolerance, T2D, and CVD in people without diabetes,” explained Imai.

Slow eating may also enhance diet-induced thermogenesis, elevate serum adiponectin, and suppress endotoxins and non-esterified fatty acids, she added. “Eating slowly may also influence gastrointestinal satiety hormones^## … which control appetite and influence food consumption, suggesting that modifiable eating behaviours actually regulate the hormonal response to food.”

From a public health perspective, promoting awareness about the benefits of slow eating may be a cost-effective approach to promote weight management and glycaemic control, said Imai. “One practical approach … for promoting slow eating behaviour is to try eating slowly at lunch breaks in schools and workplaces.”

Nonetheless, she called for further evaluation to ascertain the mechanisms and long-term effects of eating speed on metabolic control in individuals with and without diabetes. “Real-world approaches are needed to better understand the negative influence of eating fast on glycaemic responses and to support approaches for slowing down eating speed in healthy individuals.”

“[Moreover,] we previously demonstrated that eating vegetables first, [followed by the] main dish and the carbohydrates last improves the decrease in PPG concentrations,” added Imai. As this sequence was observed by slow eaters, this might have influenced the results, she noted. Therefore, eating sequence should also be looked into in future trials.