Posted by admin on January 15, 2011 under Diabetes | 
Type 2 diabetes results in genetically susceptible people from insulin resistance and diminished insulin secretion by the pancreas. Loss of first-phase insulin secretion after a glucose stimulus is the first recognizable pancreatic functional defect. Postnutrient hyperglycemia occurs, and the pancreas secretes an excess of insulin in an attempt to return plasma glucose to or toward normal. In this phase of type 2 diabetes, impaired glucose tolerance is usually demonstrated. Over time, insulin output by the pancreas diminishes, and at the time of diagnosis by fasting hyperglycemia, insulin secretion is approximately 50% of normal. With increasing duration of type 2 diabetes, further diminution of insulin secretion occurs, hepatic glucose output increases, and insulin resistance of muscle, fat, and liver is accentuated by “glucose toxicity.”
This sequence of events can be viewed as occurring in four stages. In stage 1, diminished first-phase insulin secretion and impaired glucose tolerance may be managed by oral drugs that stimulate an immediate insulin release. Insulin resistance can be addressed by an intensive diet and exercise program and by insulin-sensitizing drugs. As the disease progresses, combination therapy that addresses the dual issues of diminished insulin secretion and insulin resistance are indicated. Combination therapy with insulin stimulators (meglitinides or sulfonylureas) and insulin sensitizers (metformin, thiazolidinediones) is needed. Triple oral therapy with an insulin stimulator, a thiazolidinedione to increase insulin sensitivity, and metformin to inhibit hepatic glucose output may be effective. Some physicians advocate adding an alpha glucosidase inhibitor to blunt the absorption of dietary carbohydrates. Thus, serial addition of many oral antidiabetic agents to address the diabetic state is feasible. The final step is insulin therapy, which can be used as basal replacement with continued oral agent therapy or as the sole pharmacologic agent. Guidelines for glycemic regulation are the same as in type 1 diabetes: the goal for fasting blood glucose is 80-120 mg/dl. Action should be taken for HbA1 c > 8%, with a goal of < 7%.
In type 2 diabetes, hyperglycemia appears to be a major contributor to the progression of retinopathy, albuminuria, and neuropathy. In this respect, the main cause of the so-called “microvascular” complications of type 2 diabetes is comparable to type 1 diabetes. In both cases, prospective randomized trials have provided strong support for a policy of lowering HbAlc to as close to normal as safely possible. For every 1% lowering of an elevated HbAlc, there is about a 25% decrease in the risk for progression of diabetic retinopathy.
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Posted by admin on May 8, 2009 under Diabetes |
Ian was manager of the Victorian Under-18 Men’s Hockey Team. In addition to his role as manager, he was also in charge of the team’s fitness and nutrition programs. He had done quite a lot of reading about the glycaemic index and decided to base the whole diet around this.
Despite some early grumbling and moaning, the players stuck to the diet almost 100 per cent during the whole two weeks of the Australian championships in Darwin in July. Ian planned the diet very carefully so that they got all the right foods at the right time—low G.I. before the game and high G.I. immediately after, along with jelly beans at half time!
He noticed that the benefits became very apparent early in the championship. The players themselves were noticing that they were not running out of energy during the game and were recovering a lot quicker than they had in the past.
About half way through the tournament other people started to wonder just where this Victorian team was getting all its energy from! Ian said:
‘At first they thought it was amusing and perhaps a little strange that we were eating Coco Pops and Rice Bubbles at the team bus in the carpark immediately after each game, but soon their amusement turned to curiosity.
People kept commenting on how fit the team was. But I knew that it wasn’t just their fitness. I had not had as much time as I would have liked to work on their fitness, and in fact I remember being concerned just before we went away that their fitness levels may not have been high enough. I knew that what I as seeing in Darwin was not just their fitness—it was the combination of fitness and a sustained energy supply. A “whole body fitness” was what we had achieved. It clearly demonstrated to me that you cannot do one without the other.
We ended up winning the championship by a relatively easy margin, and our fitness and energy levels were certainly a major contributing factor.
One of the things I liked about using the Glycaemic Index as the basis of the diet was that the players were able to very quickly understand the basic principles and by the end of the first week they knew exactly what to do.
I gave the players a questionnaire to complete at the conclusion of the tounament, and I thought you would be interested to hear some of their comments.
• ‘ I felt that when I played each game I was at my peak. I believe the diet played a major part in this.’
• ‘I found I had more energy coming into and during the game.’
• ‘Energy and glycogen levels were at perfect level.’
• ‘I never felt flat or without energy.’
• ‘Felt really good after every game, never felt run down during the game.’
• ‘Everything made me feel good before, during and after the game.’
• ‘Diet was major reason we did do well in the championships.’
• ‘Feel better after games, recovery is better, better energy in the game.’
• ‘I was never short of energy. My glycogen levels were con stantly maintained and replenished at the necessary points. I always felt fit and healthy.’
• ‘Kept my energy level high in the game and also after the game.’
• ‘After the game, recovery is far more rapid.’
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