Jaakko Tuomilehto

Physical inactivity is a modifiable risk factor for cardiovascular (CV) and metabolic disorders. VO₂max is the best method to assess cardio-respiratory fitness level but it is poorly adopted in clinical practice. Sudomotor dysfunction may develop early in metabolic diseases. This study aimed at comparing established CV risk evaluation techniques with SUDOSCAN; a quick and non-invasive method to assess sudomotor function. A questionnaire was filled-in; physical examination and VO₂max estimation using a maximal test on a bicycle ergometer were performed on active Finish workers. Hand and foot electrochemical skin conductance (ESC) were measured to assess sudomotor function. Subjects with the lowest fitness level were involved in a 12 month training program with recording of their weekly physical activity and a final fitness level evaluation. Significant differences in BMI; waist and body fat were seen according to SUDOSCAN risk score classification. Correlation between the risk score and estimated VO₂max was r = −0.57, p < 0.0001 for women and −0.48, p < 0.0001 for men. A significant increase in estimated VO₂max, in hand and foot ESC and in risk score was observed after lifestyle intervention and was more important in subjects with the highest weekly activity. SUDOSCAN could be used to assess cardio-metabolic disease risk status in a working population and to follow individual lifestyle interventions.

In the emerging landscape of cardiovascular (CV) outcome trials evaluating the effects of blood glucose lowering drugs in individuals with type 2 diabetes, it is becoming increasingly apparent that since the promising signals coming from the United Kingdom Prospective Diabetes Study (UKPDS) no unequivocal benefits have been established for any single therapy thus far. There is an unmet need for introducing an effective pharmacological agent which could target both correlates of glycaemic regulation and CV risk factors, to ameliorate the enormous burden of fatal and non-fatal CV events in diabetic patients. Acarbose, like other alpha-glucosidase inhibitors (AGIs), has been proven to be an effective antidiabetic treatment for decades, but the overall significant impact of this class of drugs on modulating CV risk has only recently been appreciated. Accumulating evidence has shown that apart from its multiple effects on primarily postprandial glucose dysmetabolism, a key component of mechanisms linked to increased incidence of CV events, acarbose therapy also associates with a favorable impact on an array of surrogate markers of CV disease. Data stemming from in vitro testing of human cell lines as well as from preliminary trials in diabetic populations, like the Study to Prevent Non-Insulin-Dependent Diabetes Mellitus (STOP-NIDDM) trial, have highlighted – though not undisputed – the potential beneficial effects of the drug on CV morbidity. Large scale trials, like the ongoing Acarbose Cardiovascular Evaluation (ACE) trial, aim at conclusively establishing such a positive effect in patients with coronary heart disease and impaired glucose tolerance. In view of its usually acceptable level of side effects that are, if they occur, mostly limited to transient gastrointestinal symptoms, acarbose could well be a strong future player in CV disease secondary prevention. Current discouraging results from many trials of antidiabetic medications to significantly lower CV event rates in diabetic patients, should only draw further attention on alternative glucose lowering agents, among which acarbose is indeed promising.

Type 1 diabetes mellitus (T1D) can occur at any age, with a peak in incidence around puberty. Classification between T1D and type 2 diabetes becomes more challenging with increasing age of onset of T1D over time develops in genetically predisposed individuals. The main susceptibility is conferred with human leukocyte antigen (HLA) genes. Some of the geographic variation in incidence and familial aggregation is explained by differences in HLA haplotypes. In many populations, the incidence is somewhat higher in males than in females, and a 1.3- to 2.0-fold male excess in incidence after about 15 years of age exists in most populations. The incidence of childhood-onset T1D varies markedly among countries. East Asian and native American populations have low incidences (approximately 0.1–8 per 100 000/year), while the highest rates are found in Finland (>60 per 100 000/year), Sardinia (40 per 100 000/year), and Sweden (47 per 100 000/year). The risk is highest in European-derived populations. About 10 %–20 % of newly diagnosed childhood cases of T1D have an affected first-degree relative. Those with an affected sibling or parent have a cumulative risk of 3 %–7 % up to about 20 years of age, as compared with <1 % in the general population. The cumulative incidence among the monozygotic co-twins of persons with T1D is less than 50 %. Thus, the majority of genetically predisposed people do not develop T1D. Studies assessing temporal trends have shown that the incidence of childhood-onset T1D has increased in all parts of the world. The average relative increase is 3 %–4 % per calendar year. For instance, in Finland, the incidence today is 5 times higher than 60 years ago. At the same time, the age at onset of T1D in children has become younger. It is strongly believed that nongenetic factors are important for the development of T1D and its increase, but the causative evidence is missing. The causes for this increasing trend and current epidemic still remain unknown.