Some Should Like it Spicy

Cinnamon, one of the oldest and most commonly used spices, is long known as a good anti-bacterial and antioxidant agent. Perhaps it might help millions of sufferers of type 2 diabetes, too. A research conducted at the Beltsville Human Nutrition Research Center in Maryland, USA, and the University of Peshawar, Pakistan, published in 2003, dealt with this question.

Although the causes of type 2 diabetes and cardiovascular diseases are multifactorial, dietary intake certainly plays a role in the frequency and severity of these diseases. The dietary components which might be of benefit in prevention and treatment have not been clearly defined, but botanical products seem to belong to these components. They can improve glucose metabolism and the overall condition of individuals with diabetes, not only by reducing blood glucose but also by improving lipid metabolism, antioxidant status, and capillary function. A number of medicinal and/or culinary herbs have been reported to lead to hypoglycaemic effects in patients with diabetes, triggering the insulin activity in vitro, and cinnamon is one of these. Cinnamon (Cinnamomum sp.) is the dried inner bark of the cinnamon trees.

Because insulin has an important role in lipid metabolism, too, the researchers from Maryland and Pakistan considered that consumption of cinnamon would lead not only to improved blood glucose, but also lipid levels. Therefore, this study was designed to determine whether there is a reaction of clinical figures related to diabetes and cardiovascular diseases (the prevalence of which is increased from two- to fourfold in people with type 2 diabetes).

The trial investigated whether cinnamon improves levels of blood glucose, triglycerides, total cholesterol, HDL cholesterol, and LDL cholesterol in type 2 diabetes. An overall of 60 patients were divided randomly into six groups. Groups 1, 2, and 3 consumed 1, 3, or 6 g of cinnamon daily, respectively, and groups 4, 5, and 6 got placebo capsules. Besides, people had their normal diet and medications. Cinnamon intake lasted for 40 days followed by a 20-day washout period. Results after 40 days showed that all three dosages of cinnamon had lead to a significant decrease in:

  • mean fasting serum glucose (18–29%)
  • triglycerides (23–30%)
  • LDL cholesterol (7–27%)
  • total cholesterol (12–26%)

No significant changes were noted in the placebo groups. Changes in HDL cholesterol were not significant. The response was not dose-dependent, meaning that also small amounts of cinnamon do as good as bigger ones. The lower blood glucose and lipid levels were maintained during the cinnamon-free interval, too, indicating that it would not be necessary to intake cinnamon every day.

The mode of action of cinnamon in reducing blood glucose still has to be determined. It is known that in type 2 diabetes, insulin sensitivity and glycogen synthesis are reduced. The altered activity of enzymes playing important roles in glycogen synthesis is involved in some cases of diabetes. Extracts of cinnamon can activate glycogen synthesis, increased glucose uptake, and inhibited glycogen synthase kinase-3, an enzyme leading to decreased activity of the insulin receptor. Cinnamon has been shown also to activate insulin receptor kinase and to inhibit dephosphorylation of the insulin receptor, all effects leading to an increased insulin sensitivity.

Because cinnamon would not increase the caloric intake, patients with type 2 diabetes or subjects with elevated glucose, triglyceride, LDL cholesterol, or total cholesterol levels may have a benefit from the regular inclusion of cinnamon in their daily diet. In addition, cinnamon may have positive effects for the general population, too, to prevent and/or control elevated glucose and blood lipid levels, so the final conclusion of the researchers.

Autoantibodies in Diabetes: Useful also for Prevention?

Until diabetes can be cured or prevented, the early identification of individuals at increased will provide the opportunity for early education. In turn, this education will be the foundation to ensure good disease management and minimise future complications associated with diabetes.

Type 1 diabetes mellitus is an organ-specific autoimmune disease which leads to the destruction of pancreatic islet cells. Specific antibodies against islet-cell antigens, such as insulin (IAA), glutamic acid decarboxylase autoantibodies (GADA) and the protein tyrosine phosphatase-like molecule (IA-2A), play an important role in the pathogenesis of type 1 diabetes mellitus, all of them being linked to insulin secretion by the b -cells, and are established markers in diagnosis and in the pre-diagnostic phase. GADA is the immune marker of higher diagnostic sensitivity in adult patients, whilst in childhood diabetes IAA and IA-2A are the dominating antibodies.

GADA identifies the so-called „late-onset diabetes in adults“, LADA. LADA means type 1 diabetes only diagnosed in adulthood (in contrary to the more frequent diagnosis in childhood), having a prevalence of an estimated 0.15–0.25% in the general population, which means a similar frequency as typical type 1 diabetes. In over 80% of cases, LADA patients develop insulin dependency within a few years after the diagnosis.

The advice nowadays is to determine GADA in all patients with adult onset of diabetes mellitus to check diagnosis of potential LADA (and not the typically diagnosed type 2 in adult onset diabetes). and so predicting development of insulin dependence. In addition, because there is a high frequency of other endocrine autoimmune diseases, in this subtype of diabetes, screening for other organ-specific autoantibodies (against e.g. thyroid gland, gastric mucosa cells, adrenal gland) should be performed in every LADA patient.

Prediction of diabetes risk

There are also interesting suggestions in another recent publication which discusses the screening of non-diabetic persons for their risk of developing type 1 diabetes by looking for these autoantibodies as markers. It bases on the knowledge that islet autoimmunity can precede manifestation diabetes by years–and early diagnosis, even before clinical outbreak of the disease, could help prevent complications by prevention of unnoticed hyperglycaemic states. The prevalence of the islet autoantibodies IAA, GADA, or IA-2A in euglycaemic subjects is between 5 and 5% in relatives of type 1 diabetes patients. For the general population, determination of more than one antibody is necessary for a meaningful risk prediction, out of statistical reasons. Prevalence of multiple islet antibodies in recent population studies was measured as 0.3–0.8%.

As far as the predictive value of autoantibodies for type 1 diabetes relatives is concerned (i.e. the probability to develop diabetes if autoantibodies are present), the figures of several trials are extremely different, reaching from 1–100%, depending on kind and number of determined antibodies, time of first determination, follow-up time etc. In summary, the article under discussion says, type 1 diabetes risk can be predicted only by using a variety of autoantibody characteristics, which in turn can be used in different combinations to select subjects of defined diabetes risk for intervention trials.

It is not sure, yet, whether these results are applicable to islet autoantibody-positive subjects in the general population, who not have relatives with type 1 diabetes. Some data suggest that multiple islet autoantibody positivity bears a similar risk for development of type 1 diabetes regardless of the family history, but the numbers of individuals studied to date are too small to allow accurate risk estimations in this subgroup.

At the time being, so the final conclusion, screening for such markers in the general population should be undertaken only in defined research studies. For individuals at increased risk for type 1 diabetes, it may be offered outside of such studies, but should be limited to centres with sufficient experience in testing, providing exact risk information and psychological counselling.

Diabetes Management: Self-Monitoring of Blood Glucose Might Be Effective also in NIDDM

Self-monitoring of blood glucose is an important component of modern therapy for diabetes and of proven efficacy for glucose control in type 1 diabetes (insulin-dependent diabetes mellitus) and type 2 diabetes patients using insulin. The benefit in patients with type 2 diabetes not in need for insulin therapy, though, has not yet been conclusively demonstrated. The authors of the Cochrane Collaboration have reviewed the scientific literature on this topic.

Diabetes mellitus is a rather common disease in the Western industrialized countries: 6 to 8% of the total population have diabetes (2000: 177 million patients worldwide), and these numbers are estimated to become even higher in the future. Self-monitoring of blood glucose (SMBG) is recommended for people with diabetes and their health care professionals in order to achieve glycemic control–to prevent hypoglycaemia as well as hyperglycaemia and, by the latter, so preventing (mainly microvascular) diabetes complications, as retinopathy, nephropathy, and neuropathy. The aim of SMBG is to get detailed information about blood glucose levels at many time points and so to enable maintenance of a glucose level as constant as possible by more precise regimens: by adjustment of diet, physical activity, and insulin doses to improve glycemic control on a day-to-day basis.

There is an ongoing debate on the benefit of SMBG in non-insulin dependent diabetes mellitus (NIDDM). At the time being, these patients should have a visit to a general practitioner or diabetes nurse in a three-month interval for the evaluation of glycemic control. It has been suggested that SMBG might possibly replace these 3-monthly visits, leading to greater independence for the patients, a better understanding of their disease and therefore a better compliance with medical treatment and better motivation for lifestyle changes.

The authors of a recent Cochrane review have chosen data from six randomised controlled (one additionally blinded for outcome assessor) studies from 1990 up to 2005 to search for a final conclusion. Four of the trials compared SMBG with usual laboratory testing, one trial compared SMBG with self-monitoring of urine glucose and one three-armed trial compared SMBG with self-monitoring of urine glucose and usual care.

The mean methodological quality of studies was low (assessment by a score list by two independent reviewers). Two of the six studies reported a statistical significant lowering effect on levels of haemoglobin A1c (HbA1c). One of these trials, though, included also changes of diet and lifestyle by additional educational programs, so a clear assignment of result to intervention could not be made. There were only two studies reporting other outcome measures (quality of life, well-being, patients‘ satisfaction), and these effects did not reach statistic significance.

The authors conclude, as far as the level of evidence is concerned, from the reviewed studies that there is only moderate evidence for SMBG having a positive effect on HbA1c levels in NIDDM patients, and no proven evidence for such effects on fasting plasma glucose, quality of life, patients‘ satisfaction and well-being.

There are several possible explanations for this only moderate evidence: The group sizes varied largely between studies (from 12 to 689), with the two biggest largest showing the significant effects (113 and 345 patients in the intervention groups, respectively). Furthermore, the frequency of monitoring blood glucose differed between the studies, diabetes duration and baseline HbA1c levels were also different between the studies, which all may have contributed to the different results. Additionally, patients taking part in a randomised controlled trial might be more motivated in both the intervention and control group to improve their behaviour by the knowledge that outcome measures are being observed.

Overall, to assess these potential benefits a large and well designed randomised controlled (control group versus intervention group) trial is required. This long-term trial should also investigate additional patient-related outcomes like quality of life, well-being and patient satisfaction, and provide adequate education to the patient to allow SMBG to be effective. Furthermore, there should be studied subgroups of patients according to age, diabetes duration and baseline HbA1c values. With these analyses it can be determined whether SMBG is more effective in a special group of patients, like newly diagnosed patients or poorly controlled patients.

Höhere Lebensqualität für Diabetiker

Langfristige Folgeschäden des Diabetes mellitus treten vor allem an Augen, Nerven und Niere auf. Zur Behandlung dieser Schädigungen gibt es verschiedene neue Ansätze.

Bei der Entstehung der diabetischen Folgeschäden kommen mehrere Stoffwechselprozesse zum Tragen, an denen unter anderem die so genannte Proteinkinase C beteiligt ist. Erfolg versprechend in der Therapie dieser Spätschäden erscheint demnach vor allem der Einsatz spezifischer Hemmstoffe dieses Enzyms. Ruboxystaurin hat in ersten klinischen Tests im Rahmen einer oralen Therapie zu einer Normalisierung der Durchblutungsverhältnisse in der Netzhaut geführt. Diabetische Nerven- und Nierenschäden können damit möglicherweise ebenfalls zumindest in ihrer Entwicklung zum Stillstand gebracht oder sogar rückbildungsfähig zu werden.
Eine weitere Folge des erhöhten Blutzuckerspiegels ist ein vermehrter „oxidativer Stress“. Sinnvoll scheint daher eine Therapie mit Antioxidanzien, die in ersten Untersuchungen das Fortschreiten der Netzhautschädigung hemmen konnten.
Die synthetische Aminosäure Harkoserid könnte bald eine Möglichkeit zur Behandlung von diabetischen Nervenschmerzen sein. Erste klinische Untersuchungen erscheinen Erfolg versprechend. Ergebnisse einer weiteren Studie sollen 2005 vorliegen.
Benfotiamin, ein Vorläufer von Vitamin B1, kann die Erneuerungsfähigkeit diabetisch geschädigter Nerven fördern. Auch die Netzhautschäden können möglicherweise durch die Substanz verhindert werden.