Scientists in Sweden have investigated the increased risk of both latent autoimmune diabetes in adults (LADA) and Type 2 Diabetes (T2D) associated with the intake of sugar sweetened or artificially sweetened beverages and found interesting results (Löfvenborg et al., 2016, Reference 1).
This document is for informational purposes only and cannot be taken to make medical or other personal decisions
Diabetes is a heterogeneous disease whose main hallmark is an elevated blood glucose concentration. It is classified in two major categories, referred to as Type 1 Diabetes (T1D) and Type 2 Diabetes (T2D) representing about 5-10% and 90-95% of all cases, respectively.
Type 2 Diabetes (T2D) is a disease that has a significant genetic component, and is largely related to an unhealthy diet which includes excessive amounts of carbohydrates, stress, and lack of exercise. An unhealthy lifestyle brings overweight and obesity which leads to insulin-resistance (Footnote 1) and often to T2D. Type 2 Diabetes is not an autoimmune disease and typically develops in adult age. Its treatment includes drugs that: (1) promote insulin sensitivity; (2) stimulate the pancreas to secrete more insulin; and (3) reduce the glucose absorption rate from the gastrointestinal tract. After many years into the disease, the β-cells of many T2D patients wear off and these people may need insulin to control their blood glucose. Moreover, drug therapy is much more effective when combined with lifestyle changes which include physical exercise, adoption of a healthy diet low in carbohydrates, and elimination of vices such as smoking and excessive alcohol consumption.
Type 1 Diabetes is an autoimmune disease triggered by environmental factors in genetic predisposed people. In T1D the insulin-producing β-cells, housed within the islets of Langheran, are mistakenly recognized as foreign entities and killed, or impaired, by misguided immune cells; therefore, their ability to produce insulin is compromised and blood glucose rises. While T1D was originally considered a disease of the childhood and adolescence and referred to as Juvenile Diabetes, it can show up at any age. Though, as recent data have shown, very young children experience a more aggressive form of T1D than teenagers and adults (References 2 and 3; see blog post here). Type 1 Diabetes that develops after age 30 is called adult-onset type 1 diabetes and comes in two forms: one requires insulin immediately after diagnosis (insulin-dependent), while the other, referred to as latent autoimmune diabetes of adulthood (LADA), does not require insulin for at least six months because, at diagnosis, the patient still has β-cells that produce sufficient insulin to keep glucose within the physiological range. Moreover, β-cells may continue to produce insulin for several more years, but eventually they cannot keep up with demand and exogenous insulin needs to be injected. Latent autoimmune diabetes of adulthood (LADA) occurs much more frequently than the insulin-dependent form. Scientists at the University of Exeter Medical School, United Kingdom, have recently reported that half of all cases of type 1diabetes (T1D) develop after age 30 (Reference 4). These statistics are troublesome because they underline that this immune disease shows up in the first 30 years and second 30 years of our lives with the same frequency. Even more troublesome are various studies showing that up to 12% of the diabetes cases diagnosed as T2D in people above age 30, are actually adult-onset type 1 diabetes (LADA and insulin dependent diabetes), but are, in many instances, treated as T2D until sometime later it is realized that therapy does not work and new tests reveal that it is T1D. To solve the “is it T1D or T2D?” ambiguity and help people to get the correct diagnosis and the proper treatment, a battery of tests can be run; they include testing for: (1) autoantibodies to insulin, Glutamic Acid Decarboxylase 65 (GAD65, particularly useful to diagnose LADA), the tyrosine phosphatases IA-2, and the Zinc Transporter 8 (ZnT8), (2) the amount of C-peptide in the blood, and (3) the A1C value.
The Swedish Study linking sweetened drinks to both LADA and T2D (Löfvenborg et al., 2016, Reference 1)
This study was carried out by scientists at five research centers in Sweden and one in Finland and was based on analyses of data from the ESTRID study (Epidemiological Study of Risk Factors for LADA and Type 2 Diabetes), a Swedish population-based case-control study initiated in 2010 (Löfvenborg et al., 2016, Reference 1). It included only those people who were able to fill out a questionnaire regarding information about their education, their health and lifestyle which included physical activity, smoking, alcohol intake, body mass index (BMI), and their family history of diabetes; of course, critical to the study were people’s answers regarding their usage of sweetened beverages during the year before diagnosis, specifically their average number of 200 mL (one can equals 355ml) servings consumed per day or per week, and the type of beverage, e.g., cola, other soft drinks/soda, diet cola and other diet soft drinks/soda.
The analyses data was obtained from 357 people diagnosed with LADA (average age 58.3), 1136 people with T2D (average age 63.2), and 1371 people with neither disease (average age 58.5); the latter group served as a control. The LADA and T2D people had their disease diagnosis 7.5 and 5.3 months, respectively, prior their dates of participation.
It was found that drinking more than two 200ml servings per day of either sugar-sweetened or artificially sweetened beverages resulted in doubling the risk of developing LADA; and an additional 15% increased risk was observed for each increment of daily serving. On the other hand, it was observed that people who drank two servings or less per day had no greater risk of developing the disease compared to people who did not drink the sweetened soda at all. The risk of developing T2D had more than doubled (i.e., 2.4 fold) with more than two 200ml servings per day; and an additional 20% increased risk was observed for each increment of daily serving. Another important aspect of this research is that high intake of sweetened beverages presented also insulin resistance and low β-cell function for both LADA and T2D, but with quantitative differences. Specifically, LADA showed that high consumption of sweetened beverages presented insulin resistance, but less than that of T2D patients and lower beta cell function than that of T2D patients.
Earlier studies (cited in Reference 1) had already established that a high intake of sugar sweetened or artificially sweetened beverages are unhealthy and may increase the risk of developing T2D. When these earlier studies and the present one (Löfvenborg et al., 2016, Reference 1) are considered together, they indicate that excessive sugar-sweetened beverage intake increases diabetes risk through factors that include: (1) insulin resistance; (2) increased insulin demand due to both insulin resistance and increased blood sugar which force β-cells to produce more insulin, thus causing a stressful situation for these cells which may cause their deaths; (3) addition of pounds to the person’s weight; and (4) increased inflammation. It is well established that the factors at (3) and (4) not only foster diabetes, but also other serious diseases. With regard to artificially sweetened beverages intake, they add neither sugar nor calories to the diet, but Löfvenborg et al. (Reference 1) explain that they may bring “alterations in gut microbiota” and trigger biochemical pathways that stimulate appetite.
In conclusion, with respect to T2D the work of Löfvenborg et al., 2016, (Reference 1) produced results that are valuable, but that essentially confirm and strengthen past findings rather than adding new discoveries.
On the other hand, the findings that sugar sweetened or artificially sweetened beverages increase the incidence of LADA (Löfvenborg et al., 2016, Reference 1) are novel and very interesting, though not entirely surprising, since an earlier study concluded that “sugar intake may exacerbate the later stage of type 1 diabetes development; and sugar-sweetened beverages may be especially detrimental to children with the highest genetic risk of developing type 1 diabetes” (Lamb et al., 2015, Reference 5). And another study “revealed that daily consumption of sugar-sweetened beverages was related with increased homeostasis model assessment–insulin resistance index (HOMA-IR) in adolescents” (Kondaki et al., 2016, Reference 6).
These authors (Löfvenborg et al., 2016, Reference 1) suggest that “the excess risk of LADA among high consumers of sweetened beverages is related to mechanisms involving insulin resistance or other pathophysiological features shared with type 2 diabetes”. And also suggest that insulin resistance cause β-cell stress which activates the immune system to accelerate killing of β-cell and bring about diabetes; the latter process being faster in people genetically predisposed due to their HLA genes variants.
Löfvenborg and co-workers (Reference 1) conclude: “This is important as the identification of modifiable risk factors could aid in preventing autoimmune diabetes. It is especially urgent in times when diabetes prevalence is on the rise and sweetened beverage consumption continues to be high”.
We have to keep in mind that these are retrospective studies and may have some drawbacks especially regarding to the recall of amounts of beverage intake. Moreover, the high consumers of sweetened beverages had also unhealthier lifestyle in general and had gained more weight and BMI since age 20. Then the study is limited to a specific geographic area in Finland, but with respect to T2D it confirms results of similar studies performed in other populations. On the other hand, the study of people affected by LADA remains limited and needs to be expanded to cover people living in other parts of the world.
Insulin resistance occurs when insulin loses its ability to effectively foster glucose uptake by cells such as fat and muscle cells
(1) Löfvenborg, J.E. et al (2016). Sweetened beverage intake and risk of latent autoimmune diabetes in adults (LADA) and type 2 diabetes. Eur J Endocrinolvol. 175 no. 6 pp 605-614.
(2) Leete P, Willcox A, Krogvold L, Dahl-Jørgensen K, Alan K. Foulis AK, Richardson SJ and Morgan NG. (2016) Differential insulitic profiles determine the extent of beta cell destruction and the age at onset of type 1 diabetes. Diabetes published ahead of print February 8, 2016, doi:10.2337/db15-1615.
(3) Arif S, Leete P, Nguyen V, Marks K, Nor NM, Estorninho M, Kronenberg-Versteeg D, Bingley PJ,Todd JA, Guy C, Dunger DB, Powrie J, Willcox A, Foulis AK, Richardson SJ, de Rinaldis E, Morgan NG,Lorenc A, Peakman M: (2014) Blood and islet phenotypes indicate immunological heterogeneity in type 1 diabetes. Diabetes; 63:3835-3845.
(4) Nicholas JM Thomas of the Institute of Biomedical and Clinical Science, University of Exeter Medical School, United Kingdom, presented the data at the European Association for the Study of Diabetes (EASD), held in Munich, Germany on September 16-18, 2016.
(5) Lamb MM, Frederiksen B. Seifert JA, Kroehl M, Rewers M & Norris JM. Sugar intake is associated with progression from islet autoimmunity to type 1 diabetes: the Diabetes Autoimmunity Study in the Young. Diabetologia 2015 58 2027–2034. (doi:10.1007/s00125-015-3657-x).
(6) Kondaki K, Grammatikaki E, Jiménez-Pavón D, De Henauw S, González-Gross M, Sjöstrom M, Gottrand F, Molnar D, Moreno LA & Kafatos A et al. Daily sugar-sweetened beverage consumption and insulin resistance in European adolescents: the HELENA (Healthy Lifestyle in Europe by Nutrition in Adolescence) Study. Public Health Nutrition 2013 16 479–486. (doi:10.1017/S1368980012002613)