Flaxseed lignans, alpha-linolenic acid (ALA), and dietary fibre have been studied for effectiveness in reducing and preventing diabetes. High blood levels of glucose (hyperglycemia) due to defective insulin metabolism are associated with diabetes (1). Type 1 diabetes (T2D) is caused by an absence of insulin secretion. Type 2 diabetes which results from a combination of insulin resistance and inadequate compensatory insulin secretion is the most common type of the disease, accounting for 90-95% of cases.
The number of adults with diabetes is increasing yearly and is now estimated to be 8.3% of the global population, or 387 million people (1). By 2035 this will rise to 592 million. In Canada, diabetes will reach about 3.2 million people in 2016. In the United States, 29.1 million people or 9.3% of the population have diabetes, resulting in an estimated expenditure of $245 billion in 2012 (2).
Controlling blood glucose levels can significantly lower glycated hemoglobin (hemoglobin A1C) by approximately 1 – 2 % within three to six months (3). Glycated hemoglobin occurs when glucose molecules attach to the hemoglobin in red blood cells. A hemoglobin A1C value of ³6.5% is a criterion for the diagnosis of diabetes.
In human clinical trials, flaxseed lignans have been shown to reduce the risk of diabetes. T2D who received a flaxseed lignan supplement for 12 weeks had significantly reduced hemoglobin A1C compared to placebo (4). A flaxseed lignan extract (543 mg/d) improved metabolic syndrome composite score, including improving insulin resistance, in men after six months of treatment (5).
Measurements of plasma phospholipid fatty acids showed an inverse association between ALA and T2D (6). Samples were assessed from 12,132 incident T2D cases and 15,919 subcohort participants in the European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct study across eight European countries. These findings were similar to comparative findings from summary estimates from up to nine studies including between 71 to 2,499 T2D cases. Of note, there were no convincing associations found between levels of marine-derived omega-3 fatty acids and T2D.
The effect of flaxseed soluble fibre on blood glucose levels in patients with T2D has been examined. The addition of 5 g of flaxseed mucilage to flatbreads was assessed in 60 patients fed for 3 months (7). Fasting blood glucose significantly decreased in the flaxseed group after three months (8.4 ± 0.4mmol/L at baseline; 7.6 ± 0.4 mmol/L after treatment). Insulin sensitivity also improved in patients receiving flaxseed mucilage.
In a randomized cross-over study, overweight or obese men and women with pre-diabetes who consumed 13 g of ground flaxseed for 12 weeks showed improved fasting insulin and glucose as well as insulin sensitivity compared to control (8). Following one month on a 10 g/day supplement of ground flaxseed, fasting blood glucose and hemoglobin A1C were found to be significantly reduced in type 2 diabetics (9). And in another study, a large amount of flaxseed (40 g/day) improved insulin sensitivity in glucose intolerant people (10). After 12 weeks, a small but significant drop in insulin resistance was found. A mechanism proposed may be related to a decrease in oxidative stress due to the antioxidants in flaxseed.
These studies suggest both a therapeutic and protective role for lignans, ALA, fibre and ground flaxseed in diabetics and an ability to reduce diabetic complications.
- International Diabetes Federation. 2014. Diabetes Atlas: Key Findings 2014. http://www.idf.org/diabetesatlas/update-2014
- Centers for Disease Control and Prevention. 2014. National Diabetes Statistics Report, 2014. http://www.cdc.gov/diabetes/pubs/statsreport14/national-diabetes-report-web.pdf\
- Canadian Diabetes Association. Can J Diabetes 2013;37:S1-S216.
- Pan A, et al. PLoS ONE 2007;2:e1148.
- Cornish SM, et al. Appl Physiol Nutr Metab 2009;34:89-98.
- Forouhi NG, et al. PLoS Med. 2016 Jul 19;13(7):e1002094.
- Thakur G, et al. Int J Food Sci Nutr 2009;60 Suppl 6:126-136.
- Hutchins AM, et al. Nutr Res 2013;33:367-375.
- Mani UV, et al. J Diet Suppl 2011;8:257-265.
- Rhee Y and Brunt A. Nutr J. 2011; 10: 44.