A little while ago I wrote a blog about my own experience with Type 2 Diabetes, where I made a point about unnecessary deaths due to this illness, but further reading has increased my awareness that many people in this country (and maybe elsewhere) are not taking the diagnosis of diabetes seriously enough!
Therefore, I thought I should write another blog about health problems associated with having Type 2 Diabetes in an attempt to explain the science behind the disease and clarify the risks involved.
First, let me summarise (you may also find the animation on this webpage useful) what diabetes is about and how it occurs – diabetes is a result of a misalignment between insulin levels and glucose levels in the bloodstream, which leads to incorrect glucose levels in the blood. Blood glucose, which is the primary energy source for all the cells of the body, is produced from digestion of carbohydrates, sugars and fatty food and enters the bloodstream from the stomach or liver. However, while the blood can circulate the glucose to all of the cells of the body, the glucose is not automatically taken up by these cells. To enable uptake into muscle and other cells insulin is required, which is secreted by the pancreas and coexists in the bloodstream in balance with the level of glucose. In Type 1 Diabetes the pancreas does not produce insulin, which means that the cells are unable to take up glucose, in turn this leads to high levels of blood sugar (hyperglycemia). Type 2 Diabetes is more complex, but is primarily because the pancreas either produces insufficient insulin, or the insulin produced fails to function normally – often this is due to increased levels of fats within the bloodstream that have blocked insulin uptake by the muscle cells. This also leads to hyperglycemia, but also to increased insulin levels as the pancreas continues to release insulin in an attempt to enable muscle uptake of the increased glucose levels. While the onset of Type 1 Diabetes (in terms of symptoms) is rapid, the onset of the symptoms of Type 2 Diabetes is often slow and can take as long as a decade, which means people often “live” with an undiagnosed condition and tend to ignore the problem (as was the case for me). One molecular-based theory as to the cause of Type 2 diabetes is that aggregation of islet amyloid polypeptide (IAPP) leads to loss of the insulin-producing beta cells in the pancreas. This theory has recent support from a biophysical study of the interaction of IAPP and the lipid membranes of the beta cells (Lee C-C et al., 2012. Biophys. J. 102(5):1059-1068).
One of the major symptoms of both types of diabetes in an increased likelihood of infection (Muller et al. (2005). Clinical Infectious Diseases, 2005. 41(3): p. 281-288) and slow healing of injuries or wounds. Hyperglycemia is thought to enable or encourage bacterial growth in the bloodstream (perhaps through increased cell adhesion); although there is little direct evidence of this and a more likely explanation is that obesity, leading to the development of Type 2 Diabetes, impairs the immune response through an inflamation-related pathway (Geerlings & Hoepelman (1999). FEMS Immunology & Medical Microbiology, 26(3-4): p. 259-265; Wellen & Hotamisligil (2005). J Clin Invest, 2005. 115(5): p. 1111-9). In addition, recovery from infection is slower in diabetic patients. Yet this situation seems to be ignored by many patients, which may contribute to the incidence of infection. Typical problems that arise from this situation are:
- An increased incidence of yeast infection (Candida or Thrush).
- Urinary infections.
- MRSA.
- Foot infections (foot ulcers).
- Diabetic neuropathy (nerve damage) causes problems with sensation.
- Diabetic retinopathy.
However, I am writing this blog to deliver a very specific message, one that I hope will make readers realise how serious this disease is and how easy it is to avoid serious complications through careful control of diet and exercise. Diabetes has been linked to a wide range of complications, but one that I read about recently made me think – Alzheimer’s Disease (AD)! Meakin et al (2012. Biochemical Journal 441(1):285-296) have studied a mouse model with total absence of BACE1 ( a protein responsible for cleavage of the amyloid forming precursor protein, which leads to amyloidosis and AD). Both AD patients and Type 2 diabetics have an increased incidence of obesity in later life and AD patients have an increased likelihood of Type 2 diabetes, but more importantly, AD patients also have increased insulin resistance and impaired glucose metabolism.
Alzheimer’s Disease is thought to be initiated by cleavage of amyloid precursor protein (APP) by the gene product of BACE1, this increases the basal levels of beta-amyloid proteins, which aggregate into the amyloids that form the plaques in the brain of AD patients. Deletion of the BACE1 gene in mice avoids this process and leads to loss of plaque formation. In contrast, increased levels of BACE1 production has been observed in AD patients.
So, the question remains does obesity and type 2 diabetes link with an increased risk to Alzheimer’s Disease and can this process be reversed through diet and drug-based control of BACE1 levels? The answer seems to be yes, but more work is needed. However, the message I want to get across is that anyone with Type 2 diabetes, whether they are on medication or not, and anyone who is obese, should seriously control the situation through diet (Eriksson & Lindgärde 1991. Diabetologia 34(12):891-898) and exercise (Kopp et al 2012. Diabetes Research and Clinical Practice 95(1):25-29), or you run the risk of serious outcomes!
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