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primary prevention strategy is unclear. Paradoxically, exposure to increased fuel supply in utero (and hence often a larger baby) may also be associated with the development of NIDDM, a hypothesis supported by animal models ( 15). Further support comes from the higher incidence of NIDDM among the offspring of women with diabetes in pregnancy rather than those developing NIDDM after pregnancy (16), if at all (8), the greater frequency of maternal rather than paternal transmission of NIDDM (S), and the greater chance of developing NIDDM in the offspring of women with a higher post-load glucose concentration (17). Animal models have suggested that even minor disturbances in glucose tolerance may be associated with an increased risk of diabetes in the offspring and this hypothesis is supported by a recent study demon- strating higher cord insulin/C-peptide ratio in the offspring of normal Polynesian mothers who had evidence of marginal hyperglycaemia ( 1 8).

Primary Prevention of GDMNIDDM in pregnancy Obesity and regular exercise have been identified as

the most important modifiable risk factors for NIDDM (4), in spite of the failure of most interventions to achieve reductions in body weight in either individuals or populations (19). There are 2 major approaches to implementing strategies to prevent diabetes: the population based approach or the high- risk approach. The former attempts to reduce weight and increase exercise over whole communities, while the latter identifies those at highest risk and focusses solely on those individuals. In reality, both are likely to be required for the control of NIDDWGDM in the community.

The high-risk approach is much more amenable to controlled, if not randomized, studies and such studies have now demonstrated that NIDDM can be delayed or possibly prevented. An early study among Australian Aborigines showed marked improvement in glucose tolerance after temporary reversion to a traditional lifestyle (20). A recent large randomized prospective study among Chinese with impaired glucose tolerance (IGT) in Da Qing province demon- strated a 30% reduction in progression to NIDDM by weight control and/or increased exercise (21) over 6 years. An earlier Swedish prospective study demon- strated 50% fewer subjects with IGT progressing to NIDDM over a 6 year period with a structured exercise programme (22). Finally, an American study of the massively obese with IGT who had undergone gastric bypass showed a reduction in progression to NIDDM by 95% over 4-6 years (23). Drug studies have also been attempted, but these demonstrated no effect and would be inappropriate in women wishing to become pregnant in the future(3).

Population based interventions, even if in high-risk populations, are difficult to randomize and control.

Acting as a control group within a study is an intervention itself, while Failing to include a control group suffers from doubts about the true impact of the intervention on the natural history of the disease in that population at that time. As few of the primary prevention programmes for ischaemic heart disease demonstrated significant weight reductions, achieving such a goal is likely to be extremely difficult. N o controlled population study has yet been published demonstrating that such strategies prevent NIDDM. The National Institutes of Health in the United States is funding a randomized study for the primary prevention of NIDDM in high-risk groups, including small high-risk communities. However, results will not be available for many years. Small uncontrolled studies of GDM among Alaskans (24) and NIDDM among Tanzanian Hindus (25) support the hypothesis that community-based lifestyle programmes in high- risk populations may be beneficial, but this remains unproven.

CONCLUSIONS NIDDM and GDM are growing public health

problems. If data from population and intervention studies in high-risk groups are taken together, it is likely that a reduction in weight, in most likelihood coupled with increased exercise will reduce the rate of increase in the numbers with NIDDM and GDM. Over a longer period of time, it may begin to reduce the numbers developing these conditions overall. In order to hasten the implementation of such interventions, methods for monitoring of GDM and NIDDM in populations are required. This requires the diagnosis of GDM in the first place (i.e. universal screening) and methods to follow-up such individuals. Whatever interventions are finally and unequivocally shown t o prevent GDMINIDDM (if indeed this is possible). their speedy implementation will require well integrated primary and secondary services for the care of those with diabetes. Finally, if reducing obesity is the key to preventing GDMNDDM (as it appears to be) then a practical understanding o f the cultural, psychosocial and sociological milieu within each ‘community’ will be required. Clearly only a multi- disciplinary approach with clinicians at the core, will ensure the speedy implementation of any primary prevention programme.

References I . McCarty D. Zirnrnet P. Diabetes 1YY4 to 2010: Global Estimates

and projections. International Diabetes Inbtitute. Melbourne. Australia. 1994: 46.

2. Jarrett RJ. Gestationdl diabetes niellitus: A non-entity:‘ Br Med J 15193; 306: 37-38.

3. Knowler WC. Narayan KMV, Hanson KL. Nelson RG. Bennett PH, Tuornilehto J. Schersren B. Pettitt DJ. Preventing noti- insulin dependent diabetes. Diabetes 1951.5: 44: 481 -487.

4. Manson JE, Spelsberg A. Primary prebention of non-insulin dependent diabetes rnellitus. Am J Prev Med 1991: 10: 172- 181.