What causes diabetes? I usually hear from people, it is due to tension and stress. But if I look around the diabetic patients are fond of every type of food. Is it true?

"What causes diabetes? I usually hear from people, it is due to tension and stress. But if I look around the diabetic patients are fond of every type of food. Is it true?"

To start... the issue with your query is that you don't specify - which TYPE of diabetes are you asking about? There are two completely different versions of diabetes - DI, or Diabetes Insipidus, and DM, or diabetes Mellitus. DI is a condition involving a failure in the fluid-control system, and stems from issues with the body using/producing/storing the hormone vasopressin. DM is a condition involving a failure in the gluco-regulatory system, and stems from issues with the production and use of the hormone insulin.

Since DI is quite rare, while DM is quite common, and only DM involves what one eats - I'll give you an outline of the three types of DM (fyi - there are four types of DI) in the hopes I'll hit the one you're interested in. It is important to understand... all are COMPLETELY DIFFERENT DISEASES from one another.

DM refers to one of three conditions that cause BG (Blood Glucose) levels to become elevated. The three basic types of DM are T1 (Type 1), T2 (Type 2), and T3c (Type 3c). People with these diseases are all D's (Diabetics), but more specifically - T1's, T2's, and T3c's.

Type 1 diabetes, which used to be called Juvenile Diabetes or IDDM (Insulin Dependent Diabetes Mellitus) is caused by one of a group of genetic anomalies in the HLA (Human Leukocyte Antigen) complex on Chromosome 6 of the DNA structure; in those that have one of these anomalies, a "trigger" is needed to start the disease process - the known triggers (not all are known) so far are several different viruses (enteroviruses and mumps are some of the most common).

When triggered, the disease causes the immune system to destroy a tiny portion (about 1% to 2%) of the pancreatic tissue - the part that produces the hormones insulin and amylin. We can live without amylin - but NOT without insulin. Until the extraction and purification of insulin from animal pancreases in 1921, ALL T1's died shortly after dx's (diagnosis). T1 is known as an "autoimmune" disease - because it's caused by the immune system attacking its own body, which it's not supposed to do. T1, while typically occurring in children (and being the most common chronic childhood disease) can occur at any age. Currently, the "median age" at dx's is 14 years old. The short summary of T1 is that people with T1 can produce no insulin because the insulin-producing cells of the pancreas have been destroyed. T1 is a rapid developing disease; but there is a slow-forming version usually seen in adults called LADA (Latent Autoimmune Diabetes in Adults), which is also referred to as T1.5 (Type 1.5) - which while in common usage, is not a valid diagnostic code.
 
Type 2 diabetes, which used to be called Maturity Onset Diabetes or NIDDM (Non-Insulin Dependent Diabetes Mellitus) is caused by cellular resistance to the action of insulin. In essence, even though a T2 produces plenty of insulin (actually, a lot more than non-D's do), it doesn't work right. Insulin's job is to move glucose (a simple sugar) from the bloodstream (the body's delivery system) into the cells of the body, which need it for fuel. When this transfer is too slow, the BG level gets too high - and the cells of the body don't get the fuel they need as fast as it's needed. T2 is caused by an anomalous sequencing of genetic variants located throughout over 80 areas of the human genome, but there are so far THREE that are absolutely confirmed as causative. All three are located near IRS1 (Insulin Receptor Substrate 1) on chromosome 2 of the human genome; these are SNPs (Single Nucleotide Polymorphisms) rs2943650, rs2943634, and rs2972146. These all cause the underlying biochemical issue of IR... but also, they pre-dispose the carrier to a tendency to gain weight easily, and fatigue readily.

There are 13 slightly different versions of the disease known as MODY (Maturity Onset Diabetes of the Young) each of which are associated with a single genetic anomaly in various places in the human genome.
 
Type 3c diabetes, or pancreatogenic diabetes, is caused by disease or injury to the pancreas that induces the condition - and is very similar to T1 in that insulin production is destroyed or severely limited. Physical injury or one of several diseases can cause this (pancreatitis, cystic fibrosis, pancreatic cancer, and many more). In any event - it is treated like T1 - with insulin injections.
 
To diagnose which type you have, the T3c is easily dismissed if you don't have one of the diseases or conditions that cause it. But T2 and T1 MUST be tested for - fortunately, that is easy. The C-peptide test is a test for a type of peptide (Connecting peptide) that is produced in conjunction with, and proportionately to, insulin. Since T1's produce virtually no insulin - they also have little or no C-peptide. T2's, however, have more-than-normal amounts of insulin and C-peptide. So a test for the presence of C-peptide (a simple blood test, and very cheap) is used as a proxy for an insulin test (a complex blood test, and very expensive). Dx'g (diagnosing) by age is a bad method, and is the reason the vast majority of LADA T1's are mis-dx'd as T2's at first - until they continue to sicken (T2 treatments and meds do NOT work for T1's) and the doc's finally do the C-peptide test and start insulin treatment.
 
There are also several tests for autoantibodies, which may be present in T1s... but often, they are no longer present by the time the testing is done. But docs often have these tests performed just to "confirm" the C- peptide result; unfortunately, a negative test result is NOT a guarantee that the patient is not T1.

In all forms of D, the most common symptoms are polydipsia (excessive thirst), polyurea (excessive urination) and fatigue. These are ALL caused by elevated BG levels. When your blood retains too much glucose that isn't getting into your body's cells, your kidneys try to "screen" it out - dumping the glucose into your bladder, which needs water to dilute it into, which becomes urine. Your kidneys "steal" the fluids from your body tissue, and use it to make sweetened urine; you get dehydrated, and have to pee a lot. In T1, there is usually a lot of un-sought weight-loss immediately before dx's - because without the fuel your body's cells need, your body fuels itself with its own fat and muscle tissue - "burning" those off instead of using the glucose in your bloodstream. In T2 - the weight loss usually doesn't happen, and in any event, never to the extent it does in T1. BUT... in LADA T1's, the weight loss, if any, may be very slow.

Lastly - on the issue about eating. As T2 develops, the victim (er, patient) experiences prolonged hunger even when they've eaten what SHOULD have been "enough". When their cells aren't getting the glucose they need - they signal the brain to feed them! EVEN WHEN BG IS ALREADY TOO HIGH! As a result - the victim (er... patient, developing T2) will overeat. Then, when sleeping... the body "catches up" with the excess glucose in the blood, by over-producing insulin while there's no food present, and the excess glucose gets stored - as fat tissue. THIS is the reason T2s are overweight at dx's (in those cases that are) - it has NOTHING TO DO with some sort of moral depravity; it's a disease... a metabolic disorder wherein their bodies aren't getting the fuel they need as fast as they need it. THIS is another factor that leads to weight gain BEFORE diagnosis. Ergo... it's more of a symptom.


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