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The following persons are at high risk to develop diabetes :
Individuals with positive family history of diabetes
Overweight individuals
Persons with
Hypertension
Hyperlipidaemia (Increase in cholesterol, triglyceride premature coronary artery disease etc.)
Those with previous bad obestetrical history
Recurrent abortion
Stillbirth
Congenital malformation
Big Baby etc.
DIAGNOSIS OF DIABETES BY BLOOD GLUCOSE CRITERIA
Diabetes is a state of chronic hyperglycaemia (rise in blood glucose levels). Correct and definitive diagnosis is mandatory by the proper glycaemic (blood glucose) criteria for the management of diabetes patients.
Glycaemic Criteria for non-pregnant adults and pregnant women are different and glucose load for OGTT in children is different than the adults.
Urine Glucose testing is not adequate for diagnosis of diabetes and positive results must be confirmed by the blood glucose estimation. Glycated Haemoglobin (HbAIC) and Fructosamine tests are highly specific but less sensitive, hence one could miss mild diabetes (these tests are supplementary tests and tests for monitoring diabetes should not be taken as a method of diagnosing diabetes).
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Type 1 diabetes is a genetically determined disorder, with an increased incidence in monozygotic twins and first-degree relatives or people with type 1 diabetes. Approximately 70% of monozygotic twins develop type 1 diabetes (with prolonged follow-up), and a first degrees relative of a person with type 1 diabetes has approximately one chance in twenty (5% risk) of developing the disease (vs. 1:300 in the general population). The responsible genes are within the major histocompatability complex (MHC) located on chromosome 6 (also called the HB locus). About 40% of the familial aggregation of autoimmune type 1 diabetes is explained by MHC genes, especially HLA class II molecules DQ and DR. Ninety-five percent of type 1 diabetics carry HLA D3, Dl or both compared with 45% of the general population. The presence! an aspartic acid residue at position 57 of the DQ 3 chain is protective for the development of type 1 diabetes. Clustering of long-term complications in families studied in the DCCT suggests that a genetic component contributes to vascular complications.
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The DCCT cohort was less than 39 years old at entry and was followed for only a mean of 6.5 years. Epidemiologic data had previously suggested that coronary artery disease may become apparent in most type 1 patients only after age 40. Therefore, the macrovascular disease rates in the DCCT were low, and no significant differences between intensive vs. standard management were seen. However, trends suggested a beneficial effect of intensive management to reduce the number of; pooled major macrovascular events. An event was defined as death secondary to cardiovascular disease or sudden death, acute myocardial infarction, coronary artery bypass surgery or angioplasty, angina confirmed by angiography, or ischemic changes on noninvasive testing. In addition, major cardiovascular events (fatal or nonfatal stroke) and major peripheral vascular events (amputation, bypass or angioplasty, or claudication with objective evidence) were included.
The number of macrovascular events (40) in the conventionally treated group was greater than that in the intensively treated group (23), but the differences were not statistically significant (p = 0.08). Mean total serum cholesterol and calculated low-density lipoprotein cholesterol were lower in the intensively treated group (p < 0.01), suggesting that long-term benefits may occur.
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It’s not just your pre-and post-event meals that influence your performance. Consuming a high carbohydrate diet every day will help you reach peak performance. The G.I. factor of the carbohydrate is not important here, only the amount of carbohydrate. It has been proven scientifically, unlike many other rumours involving dietary supplements, that eating lots of high carbohydrate foods will maximise muscle glycogen stores and thereby increase endurance.

The reason for this is that carbohydrate stores need to be replenished after each training session, not just after a race. If you train on a number of days per week, make sure you consume a high carbohydrate diet throughout the whole week.

Remember that alcohol interferes with glycogen re-synthesis and lowers blood glucose levels, sometimes to dangerous levels. Keep alcohol intake moderate—no more than one to three standard drinks per day and try to have two alcohol-free days a week. A standard drink is equivalent to one glass of wine (120 ml), one middy of beer (285 ml) or one nip of spirits (30 ml).

Beer is not a good source of carbohydrate. When athletes fail to consume adequate carbohydrate each day, muscle and liver glycogen stores may eventually became depleted. Dr Ted Costill at the University of Texas showed that the gradual and chronic depletion of stored glycogen may decrease endurance and exercise performance. Intense work-outs often two to three times a day, draw heavily on the athlete’s muscle glycogen stores. Athletes on a low carbohydrate diet will not perform their best because muscle stores of fuel are low.

If the diet provides inadequate amounts of carbohydrate, the reduction in muscle glycogen will be critical. A heavily training athlete should consume about 500 to 800 grams of carbohydrate a day (about two to three times normal) to help prevent carbohydrate depletion. In practice, few Australian athletes achieve this enormous figure. As a comparison, a typical Australian man or woman eats only 240 grams of carbohydrate each day.

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