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You are right what i said was by far in a way an oversimplified and technically incorrect. As far as classifications the current American Diabetes Association (ADA) classification of diabetes mellitus does not reflect the clinical heterogeneity of patients with diabetes and the emergence of the concept and evidence that early beta cell dysfunction is likely to be a primary defect in the pathophysiology of diabetes, regardless of "type." Furthermore, The high prevalence of overweight/obesity in the population has further complicated classification systems with an added element of insulin resistance even in type 1 diabetes. So classifying diabetes into two or three types is technically incorrect because its far more complicated than that, but for most cases does not change the treatment and management. Currently one system used subdivides type one to type A(immune mediated) or type B with total insulin deficiency and no c-peptide levels but idiopathic in nature and without immune destruction or present of antibodies. Thus, genetic markers for type 1A diabetes are present from birth, immune markers are detectable after the onset of the autoimmune process, and metabolic markers can be detected with sensitive tests once enough ß-cell damage has occurred, but before the onset of symptomatic hyperglycemia. This long latent period is a reflection of the large number of functioning beta cells that must be lost before hyperglycemia occurs. As previously stated type 2 does not involve immune mediated destruction and their gene loci involved do not appear to overlap however, inflammation ( interleukin-1 mediated) may play a role in islet beta cell loss in both types. Type 1 is more likely to occur at a young age, but its not always the case as in latent autoimmune autoimmune in adults or LADA. Maturity onset diabetes of the young (MODY) is another subtype of type1 which is a clinically heterogeneous disorder characterized by non-insulin dependent diabetes diagnosed at a young age (<25 years) with autosomal dominant transmission and lack of autoantibodies however, only accounts for approximately 2-5% of total cases of diabetes. Whereas in the US type 2 which makes up about 90% is a result of complex polygenetic risk factors and environmental effects. Genetically the genes known to influence type 2 i believe there are maybe 14 don't influence your response to insulin which would make more sense, but rather how your pancreas makes insulin in the first place. Moreover, how healthy your pancreas starts out could determine how vulnerable you are to other diabetes triggers, like getting fat and obesity. In the past, poor metabolic control of type 1 diabetes prevented most patients from gaining weight. However, Intensive therapy now commonly used to manage type 1 diabetes has resulted in approximately 20 to 30 percent of type 1 diabetic patients becoming overweight or obese. Insulin resistance and other features of type 2 diabetes may be exhibited in overweight patients with type 1 diabetes, especially those who also have a family history of type 2 diabetes. Thus, need for insulin does not distinguish between type 1 and type 2 diabetes. The presence of GAD and islet cell antibodies in patients with presumed type 2 diabetes can identify patients who actually have type 1 diabetes (LADA) and more likely to require insulin as destruction progresses. Screening for LADA criteria are age of onset <50 years, acute symptoms, BMI <25 kg/m2, and personal or family history of autoimmune disease. Obesity by far in a way is the largest external risk factor especially those body type with predominate truncal obesity. However many other diseases contribute to the development of diabetes suchs as cystic fibrosis, hereditary hemochromatosis, chronic pancreatitis, and endocrine abnormalities such as cushings disease, acromegaly, somatostatin-secreating tumors, hyperthyroidism, and glucagon-secreting tumors. The problems of diabetes are by far in a way caused by non-enzymatic glycosylation like in diabetic retinopathy or osmotic damage. This is by far in a way not even close to being complete doesn't even touch on common things such as gestational diabetes or type 3 diabetes secondary to alzheimers disease.

for one thing type 1 and type 2 diabetes are no longer even used they are old terminology its insulin dependent diabetes and non-insulin diabetes mellitus. I was just trying to say 10-15 pounds weight loss makes a huge difference when your borderline to reverse insulin sensitivity. Based on her weight and recent weight gain it makes autoimmune destruction of the pancreas less likely. If she is pre diabetic starting on a low dose metformin can be very helpful at preventing the development of diabetes. exercise as simple as walking 15-20 minutes a day can dramatically changed your sugar levels, in increases the number of insulin receptors in the muscles and dramatically helps in the uptake of sugar from the bloodstream. Health is definitely number one, and all I'm saying is not to worry to much you are young and just a few small changes to your diet such as avoiding the breads eating a burger without the bun, take the crust off the pizza, and eating throughout the day versus a few large meals. If you lose even just 10-15 pounds and make it a routine to just walk everyday the next time you get your Hemaglobin A1c drawn you will not be borderline. simply just walking everyday will keep your health in check and vastly reduce your cholesterol. Most importantly help you to be feeling a lot better. I am not a doctor, but i will be in about 10 months

if you are indeed pre diabetic weight loss of 10-15 pounds is all you need to make substantial changes to your Hemoglobin A1c and sugar levels. Weight loss to improve sugar isn't 100 pounds just a little bit makes a huge impact. Also creatine oral tablets are great at dropping your sugar and improving Glucose uptake.