This is enlightening, thanks. To understand it properly I transcribed her talk as best I could, added screen dumps of the illustrations and looked up the long words (or the nearest I could find). I'd be grateful if someone would cast an eye on the text below (I removed the references to the diagrams) and correct mistakes. Thanks again.
Type 1 is usually the autoimmune system attacking the pancreatic beta cells and usually affects people in adolescence, but 10% of newly diagnosed Type 1 diabetics are adults. Dr Wendy Pgozelski is one.
Her dietician insisted that we need to eat at least 130 grams of carbs a day because the brain needs 130 grams of glucose. Dr P, who was eating half this amount of carbs daily and keeping her blood sugar levels perfectly steady, mentioned gluconeogenesis (the body makes its own sugar)(from protein??), which fell on deaf ears. One of the health team nurses said, "I want you to eat chocolate. I want you to live."
The US diabetes advice for Type 1s is that although carbs turn into sugar easily, and the more you eat the higher your blood glucose goes, you need 6-8 servings of bread, rice, pasta & cereal a day and should compensate with insulin.
Carbohydrate is the biggest dietary contributor to higher glucose. It is really made up of glucose molecules. These have to metabolize to release energy, so the glucose has to enter cells.
To penetrate a cell membrane, the glucose has to have a protein transporter. Red blood cells for instance have transporters that are pretty much always open. Other cells like muscle and fat need insulin.
In muscle and fat the glucose receptor is sequestered inside the cell and the insulin must bind to the insulin receptor to activate the glucose receptor to move to the membrane. So you really need insulin for that to work.
In Type 2 diabetes the insulin is present but the downstream reactions quoted above in muscle and fat cells are affected. We call this insulin resistance. Insulin is made but the cells no longer respond. Broadly the difference between Type 1 & 2 would be either the presence or absence of insulin.
In Type 1 there's too little insulin to let glucose into cells and too little to limit gluconeogenesis; in Type 2 cells become insensitive to insulin, but because there is biological feedback going on, initially the body churns out more insulin, and at first Type 2 diabetics are hyperinsulinaemic; eventually however there is insulin insufficiency.
Insulin is a powerful fat storage hormone, so in Type 2 the extra insulin is driving obesity (while obesity is driving the insulin resistance to a certain extent)
Glucose is very reactive, and one of the things it reacts with is protein – basically it gums it up & makes protein molecules very sticky. One of these is haemoglobin, which carries oxygen from the lungs to the red cells. Oxygen delivery is worst at the extremities of the body, notably the toes, and the cells begin to die.
Kidney cells are also affected; there's also an asthmatic effect: the presence of lots of glucose molecules means water rushes in to try to dilute the glucose, which is the reason for increased thirst. There are also many diseases associated with hyperinsulinaemia with damage to blood vessels and risk of heart disease.
People think that avoiding sugar means sweets, but there's very little difference in the effects of sweets and bread (or crackers, rice and potatoes) on blood sugar.
The haemoglobin A1c test measures how much a diabetic's haemoglobin is gummed up with glucose – ie has a glucose molecule sticking to it. Most non-diabetic people have 4-5% of their haemoglobin glycosylated at any one time. An untreated diabetic might have as much as 14%. Targets for treating diabetics are usually below 7%.
Dr P's "higher carb" diet was about 80grams and the lower was about 50. Remember she was balancing up with insulin too.