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COFFEE AND DIABETES

The only cell in the body able to synthesise and secrete insulin is the β cell of the endocrine pancreas. In type 1 diabetes, sometimes known as insulin -dependent diabetes (IDDM) or juvenile onset diabetes, this cell has been selectively destroyed by the immune system. Although type 1 diabetes is an inherited disease an environmental factor is required to trigger it. Environmental factors hypothesised to trigger the disease include viral infections, cow’s milk protein and coffee. The evidence for a role for coffee in triggering type 1 diabetes is weak and comes from a single ecological study showing a correlation between the incidence of type 1 diabetes and the annual consumption of coffee in 13 countries (1).

In type 2 diabetes, also known as non-insulin dependent diabetes (NIDDM) or maturity onset diabetes, the target tissues for insulin (muscle, liver and adipose tissue) become insensitive or resistant to the action of insulin. This means that more insulin is needed to obtain the same response from the target tissues. A Dutch cohort study of 17,111 adults identified 306 new cases of type 2 diabetes and showed that those subjects drinking at least 7 cups of coffee per day were half as likely to develop the disease (2). This association was statistically significant. By contrast, a cohort study of 2,680 Pima Indians in Arizona identified 824 new cases of type 2 diabetes but found no significant association between coffee consumption and disease risk (3). An intervention trial has also reported that a single dose of 3 mg caffeine/kg body weight significantly decreased ). An intervention trial has also reported that a single dose of 3 mg caffeine/kg body weight significantly decreased insulin sensitivity in 12 healthy subjects (4). Clearly available data on the relationship between type 2 diabetes incidence and coffee or caffeine consumption are contradictory.

Both types of diabetes are characterised by glucose intolerance that is a higher than normal blood glucose concentration after a meal. One study reported that coffee consumption improved glucose tolerance (5) whereas two other studies reported that coffee consumption resulted in a deterioration in glucose tolerance (6, 7). In addition, a single dose of 200 mg caffeine has been shown to impair glucose tolerance in 30 healthy subjects (8). The available results on effects of coffee or caffeine intake on glucose tolerance are also contradictory.

Hypoglycaemia is a characteristic short-term metabolic complication of diabetes. Any agent that improves the perception of hypoglycaemic symptoms or increases the effectiveness of the counter-regulatory hormonal responses designed to raise the blood glucose concentration would be valuable in the management of diabetes. After 72 hours abstinence, ingestion of 250-400 mg caffeine improved the perception of hypoglycaemic symptoms and the counter-regulatory responses in non-diabetics and type 1 diabetics (9, 10). However, the longer-term effects of caffeine are more complex. When the effects of abstinence were compared with ingestion of 400 mg caffeine/day for 7 days it was found that counter-regulatory responses were unaffected. At onset the perception of hypoglycaemic symptoms was greater after caffeine abstinence but as the symptoms continued perception was greater in response to caffeine (11).  Researchers of a study conducted in Sweden and published in 2004 (12) also found a reduced risk of type 2 diabetes and impaired glucose tolerance with increased coffee consumption.  

Research into the relationship between coffee drinking and the development of type 2 diabetes continues with three studies being published in the early months of 2006. A prospective cohort study (13)including 88,529 women as part of the US Nurses Health Study found that moderate consumption of both caffeinated and decaffeinated coffee may lower the risk of type 2 diabetes in younger and middle aged women. The authors suggest, as have others before them, that coffee constituents other than caffeine may be responsible for the observed effect. Van Dam, who was one of the authors of this study, conducted an extensive review (14) of 71 published studies and recommended further research to establish the constituent responsible for the observed effect, and to identify the exact mechanism of action. Another study (15) evaluated the effects of coffee consumption on glucose tolerance, and on serum glucose and insulin levels. After adjustment for potential confounding factors (age, body mass index, systolic blood pressure, occupational, commuting and leisure time physical activity, alcohol intake, tea drinking, and smoking), coffee consumption was significantly inversely associated with fasting glucose, two-hour plasma glucose, and fasting insulin in men and women. These authors concluded that in this cross sectional analysis, coffee showed positive effects on several glycaemic markers.  

Throughout 2006 several studies have been conducted, and published, in different populations, all of which suggest a strong inverse association between coffee consumption and the onset of type 2 diabetes. Iso et al (16) in thier study of a Japanese population consisting on 17,413 participants found an inverse association of green tea and coffee consumption with the risk of type 2 diabetes in women and over-weight men. Gruber (17) in the Netherlands evaluated various lifestyle factors in relation to diabetes prevention, and found that individuals who drank 4 to 7 cups of coffee per day had the smallest risk. A study on a Finnish population set (18) of over 21,000 men and women examined the joint associations of coffee consumption and other lifestyle factors, including physical activity, obesity and alcohol consumption with the risk of type 2 diabetes. Coffee drinking was associated with a reduced risk of type 2 diabetes in both men and women, and this association was observed regardless of levels of physical activity, body mass index and alcohol consumption. Pereira et al (19) as part of the IOWA Womens Health Study in the USA consisiting of over 28,000 women, examined the association between total, caffeinated and decaffeinated coffee consumption, and risk of incident type 2 diabetes. In this cohort, coffee intake, especially decaffeinated, was inversely associated with the risk of type 2 diabetes. A further US study (20) analysed data from a prospective, community-based cohort to assess the risk of incident type 2 diabetes associated with coffee and sweetened beverage consumption. Both men and women who drank more than 4 cups of coffee per day had a risk of developing type 2 diabetes that was about 67% less than that of their counterparts who drank no coffee. Finally, Smith et al (21) investigated the association between coffee drinking and incident type 2 diabetes based on an oral glucose test and examined coffee drinking habits in those with impaired glucose separately from those with normal glucose at baseline. These authors found a 'striking protective effect of caffeinated coffee against incident type 2 diabetes'.

Research continues to suggest that coffee drinking lowers the risk of developing type 2 diabetes.  

References:

1. Tuomilehto, J. et al. British Medical Journal, 300, 642-643, 1990.

2. Van Dam, R.M. and Feskens, E.J.M. Lancet, 360, 1477-1478, 2002.

3. Saremi, A. et al. Diabetes Care, 26, 2211-2212, 2003.

4. Keijzers, G.B. et al. Diabetes Care, 25, 364-369, 2002.

5. Feinberg, L.J. et al. Metabolism, 17, 916-922, 1968.

6. Jankelson, O.M. et al. Lancet, 1, 527-529, 1967. 

7. Wachmann, A. et al. Metabolism, 19, 539-546, 1970.
8. Pizziol, A. et al. European Journal of Clinical Nutrition, 52, 846-849, 1998.
9. Debrah, K. et al. Lancet, 347, 19-24, 1996.
10. Kerr, D. et al. Annals of Internal Medicine, 119, 799-804, 1993.
11. Watson, J.M. et al. Clinical Science, 104, 447-454, 2003
12. Agargh  et al. Journal of Internal Medicine, 255, 645-652, 2004.
13. Van Dam, R. et al. Diabetes Care, 29, 398-403, 2006
14. Van Dam, R. et al. Nutrition, Metabolism and Cardiovascular Disease, 16, 69-77, 2006.
15. Bidel, S. et al, Horm, Metab, Research, 38, 38-43, 2006.
16. Iso, H. et al, Annals of Internal Medicine, 144, 2006.
17. Gruber, A. et al, International Journal of Clinical Practice, 60, 2006.
18. Hu,G et al, International Journal of Obesity, 2006
19. Pereira,M.A. et al, Archives of Internal Medicine, 166, 2006.
20. Paynter, N.P. et al, American Journal of Epidemiology, IN PRESS/Online 2006
21. Smith, B. et al, Diabetes Care, Volume 29, 2006