How does stress affect type 2 diabetes?

Stress tends to increase adrenaline levels in our blood, which in turn releases glucose from our liver and muscles back into our blood stream. This response is there to prepare us for “flight” or “fight”. This was hugely helpful in the days that we were “hunter-gatherers”, but these days we often do not have the same chances in using up this extra glucose and of course our stressors are very different.
When the level of sugar in the blood rises above a certain level (usually above 15 mmol/L), your body will try and get rid of this excess glucose by pushing it out in the urine. In other words, you will be going to the toilet a lot more. As a result of the frequent urination you will lose a lot of fluid from your body which can cause dehydration. You may start to feel thirsty, maybe develop a headache and possibly a dry mouth. You may not have noticed these symptoms if your BGL rises, but remains below 15, or if your BGL has been really high for a long time. Sugars below 15 mmol/L rarely give clear symptoms.
Stress is a normal phenomenal; it is impossible to avoid stress completely, so we have to be clever in how we deal with stress. Regular physical activity can help burn off some of the excess sugar in our blood and can help to normalise adrenaline levels at the same time. 

I will take a slightly different tack to Helen and Carolein. Omental Fat and Chronic Diseases.
In today’s society stress is treated as though it is evil in itself, just like fat it appears to serve no useful purpose. Of course, life without stress could be harmful because individuals would lose their ability to react to the challenges in life. Fat also has its uses and can vary in function depending on its location and volume.
People all have an optimal stress level known as Eustress whereas too much stress is referred to as distress. Excessive Omental fat seems to be associated with several chronic diseases like Diabetes, Hypertension, Depression and even some forms of cancer (Maglione-Garves et al)
Reaction to stress can take varied forms. If the stressor is perceived as a challenge the “fight” hormone Norepinepherine is released. A loss of control may release the “flight” hormone epinephrine. Prolonged stress which is seen as hopeless activates the hypothalamus and cortisol is released from the adrenal cortex. The brain has the ability to selectively activate fight, flight or defeat responses (Maglione-Garves et al). The defeat response can activate the cortisol receptors in the omentum and lead to increased omental fat (Wettstein).
In the animal kingdom stress tends to be of short duration and to be of the fight or flight nature. In modern society our stressors are not often physical and tend to be prolonged such as fear of loss of a job or breakdown of a relationship and can result in Omental fat.  
Epel et al. demonstrated that when more cortisol is secreted in response to stress the person tends to consume more foods high in sugar and fat. It has been thought that cortisol directly influences food consumption by binding to receptors in the hypothalamus. This can stimulate an individual to eat food that is high in fats and or sugars, what we know a comfort foods. Wettstein also suggests that cortisol causes fat receptors in the omentum to be activated and accumulates fat.
Measurement of fat:
One of the criteria for the Metabolic Syndrome  suggested by Stöppler and Mathur is Abdominal Obesity. The criteria they suggest is a waist circumference over 102 cm in men and over 88 cm in women. This appears to me, to be pretty loose because it makes no allowance for the persons height or structure. Again it would also include the subcutaneous fat on the sides of the body which does not have the same deleterious effects as Omental fat. Even the very popular scale of BMI does not account for body composition or the location or type of fat. Several athletes are classed as obese according to this scale, though they have a very low percentage of body fat especially in the omentum. A person may have skinny limbs, a large waistline and yet be the ideal BMI. A simpler and perhaps more accurate way of measuring central obesity is the measurement of waist over hips. It has been suggested that the ratio should be 0.8 for women and 0.9 for men (See Welborn et al below).
I would like to see central adiposity measured with callipers along the sagital plane . I feel this would give a clearer measure of central obesity or Omental fat and reduce the inclusion o f subcutaneous fat to a minimum.
Reducing Omental Fat:
If “distress” can cause Omental fat (Wettstein) then setting realistic life goals would help tof optimise the level of stress. In the short term Yogic practices such as meditation would be helpful.  Meditation has several advantages from soothing the parasympathetic nervous system to reducing blood pressure and assisting with sleep disorders.
 
Waist–hip ratio is the dominant risk factor predicting cardiovascular death in Australia
Timothy A Welborn, Satvinder S Dhaliwal and Stanley A Bennett
MJA 2003; 179 (11/12): 580-585
Results:
Of the modifiable risk factors, obesity, as measured by waist–hip ratio, is a dominant, independent, predictive variable for CVD and CHD deaths in Australian men and women. Self-reported angina/myocardial infarction in both sexes, and cigarette smoking in women, are also independent risk factors.
Conclusions:
Obesity assessed by waist–hip ratio is a better predictor of CVD and CHD mortality than waist circumference, which, in turn, is a better predictor than BMI. The recognition of central obesity is clinically important, as lifestyle intervention is likely to provide significant health benefits.
If anyone would like further details about reduction of Omental fat I could send them diagrams explaining how these Yogic practices are performed.
cine 62:623-632, 2000
James W Fix Protruding Gut Syndrome
Wettstein MaxRuchi Mathur, MD, FRCP(C)Ruchi Mathur, MD, FRCP(C) is an Attending Physician with the Division of Endocrinology, Diabetes and Metabolism and Associate Director of Clinical Research, Recruitment and Phenotyping with the Center for Androgen Related Disorders, Department of Obstetrics and Gynecology at Cedars-Sinai Medical Center. 
Melissa Conrad Stöppler, MD 
 
Melissa Conrad Stöppler, MDMelissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
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