Associations between dietary fiber and inflammation, hepatic function and risk of type 2 diabetes in older men: potential mechanisms for benefits of fiber on diabetes risk

Dietary fiber is important in regulating blood sugar and several prospective studies have shown dietary fiber to have a protective effect on risk of type 2 diabetes1, 2. How much fiber is required and whether some kinds of fiber are better than others, remains uncertain. Moreover why fiber may be protective for diabetes is not clear. Several studies have shown inverse associations between dietary fiber and markers of inflammation, insulin sensitivity and hepatic function3, factors which have been linked to the development of type 2 diabetes4. It has thus been proposed that the mechanisms by which fibre may reduce risk of diabetes may relate to it effect on hepatic function, improving insulin sensitivity or reducing inflammation. We examined prospectively the relationship between dietary fiber and the risk of type 2 diabetes in older men and evaluated the role of insulin and inflammatory and hepatic markers5.

British Regional Heart Study

The subjects included 3,428 men aged 60 to 79 years without a diagnosis of diabetes who were originally enrolled in the British Regional Heart Study (BRHS) when aged 40-59 years6. The men were re-examined in 1998-2000 when aged 60-79 years. The population studied consisted almost entirely of white Europeans (>99%). The men completed a questionnaire which included questions on medical history, lifestyle behaviour and socioeconomic status. Information on fiber intake was obtained from a seven day recall food frequency questionnaire that was developed for use in the World Health Organisation MONICA survey. Anthropometric measurements including body weight, height and waist circumferences were carried out. Blood measurements were taken in the fasting state. Inflammatory markers including c-reactive protein (CRP), interleukin 6 (IL-6) and tissue plasminogen activator (t-PA) were measured. Gammaglutamyl tranferase (GGT) was used as a marker of hepatic function. The men were followed up for all cause mortality, cardiovascular morbidity and development of type 2 diabetes. During the mean seven years follow up from rescreening in 1998-2000 to July 2006 there were 162 incident diabetes cases.

Dietary fiber and risk of type 2 diabètes

The average intake of total fiber was 25.85g/day. There was a trend towards lower levels of inflammation and hepatic function with increasing intake of total fiber. Those with high fibre intake showed significantly lower levels of inflammation (CRP, IL-6, t-PA) and hepatic function GGT than those with low intake even after taking into account age, lifestyle and demographic characteristics. We observed no significant association between dietary fiber and insulin levels. After adjustment for total energy intake and lifestyle and demographic factors, the lowest quartile of total dietary fiber (≤ 20 g/day) was associated with significantly increased risk for diabetes (relative risk [RR], 1.47; 95% confidence interval [CI], 1.03 – 2.11). Low cereal and low vegetable/fruit fiber intake were both associated with increased risk of diabetes. Dietary fiber was inversely associated with the inflammatory markers CRP and IL-6, as well as with t-PA and GGT. After adjusting for these markers, the increased risk for diabètes seen with low dietary fiber was attenuated (RR, 1.28; 95% CI, 0.89 – 1.86).


The data suggest a diet high in fiber (including both high cereal and high vegetable/fruit fiber intake) may reduce the risk of diabetes via favorable effects on reducing inflammation and attenuating or preventing hepatic fat accumulation. The mechanism for these associations between fiber intake and hepatic function and the inflammatory process however, requires further study. The available evidence suggests that high fiber intake (at least 20 grams/day) should be promoted to help offset diabetes risk.

  1. Schulze MB et al. Arch Intern Med 2007;167:956-65.
  2. Barclay AW et al. Diabetes care 2007;30:2811-3.
  3. Wieckert M et al. J Nutr 2008;138:439-442.
  4. Sattar et al. Diabetologia 2008 ;51 :926-40.
  5. Wannamethee SG et al. Diabetes Care 2009 ;32:1823-5.
  6. Shaper et al. BMJ 1981;283:179-186.