Mom’s Soap Box

Nature of the disease

Diabetes is classically diagnosed as a failure of the body to properly metabolize carbohydrates. Its defining symptom is a high blood glucose level. Type 1 Diabetes results from insufficient insulin production by the pancreas. Type 2 Diabetes results from ineffective insulin. In both types, the blood glucose level remains elevated. Neither insufficient insulin nor ineffective insulin can limit post prandial (after eating) blood sugar to the normal range. In established cases of Type 2 Diabetes, these elevated blood sugar levels are often preceded by and accompanied by chronically elevated insulin levels and by serious distortions of other endocrine hormonal markers.

The ineffective insulin is no different from effective insulin. Its ineffectiveness lies in the failure of our cell population to respond to it. It is not the result of any biochemical defect in the insulin itself. Therefore, it is appropriate to note that this disease is a disease that affects almost every cell in the seventy trillion or so cells of our body. All of these cells are dependent upon the food that we eat for the raw materials that they need for self repair and maintenance.

The classification of diabetes as a failure to metabolize carbohydrates is a traditional classification that originated in the early 19th century when little was known about metabolic diseases or about metabolic processes. Today, with our increased knowledge of metabolic processes, it would appear quite appropriate to define Type 2 Diabetes more fundamentally as a failure of the body to properly metabolize fats and oils. This failure results in a loss of effectiveness of insulin and in the consequent failure to metabolize carbohydrates. Unfortunately, much medical insight into this matter, except at the research level, remains hampered by its 19th century legacy.

Thus Type II Diabetes and its early hyperinsulinemic symptoms are whole body symptoms of this basic cellular failure to properly metabolize glucose. Each cell of our body, for reasons which are becoming clearer, find themselves unable to transport glucose from the blood stream to their interior. The glucose then either remains in the blood stream, is stored as body fat or as glycogen, or is otherwise disposed of in urine.

It appears that when insulin binds to a cell membrane receptor, it initiates a complex cascade of biochemical reactions inside the cell. This causes a class of glucose transporters known as GLUT 4 molecules to leave their parking area inside the cell and travel to the inside surface of the plasma cell membrane. When in the membrane, they migrate to special areas of the membrane called caveolae areas. There, by another series of biochemical reactions, they identify and hook up with glucose molecules and transport them into the interior of the cell by a process called endocytosis. Within the cells interior, this glucose is then burned as fuel by the mitochondria to produce energy to power cellular activity.

Thus these GLUT 4 transporters lower glucose in the blood stream by transporting it out of the bloodstream into all of our bodily cells.

Many of the molecules involved in these glucose and insulin mediated pathways are lipids, also known as fatty acids. A healthy plasma cell membrane, now known  to be an active player in the glucose scenario, contains a complement of cis type w=3 unsaturated fatty acids. This makes the membrane relatively fluid and slippery. When these cis fatty acids are chronically unavailable because of our diet, trans fatty acids and short and medium chain saturated fatty acids are substituted in the cell membrane. These substitutions make the cellular membrane stiffer and more sticky and inhibit the glucose transport mechanism.

Thus, in the absence of sufficient cis omega 3 fatty acids in our diet, these fatty acid substitutions take place, the mobility of the GLUT 4 transporters is diminished, the interior biochemistry of the cell is changed and glucose remains elevated in the bloodstream.

Elsewhere in the body, the pancreas secretes excess insulin, the liver manufactures fat from the excess sugar, the adipose cells store excess fat, the body goes into a high urinary mode, insufficient cellular energy is available for bodily activity and the entire endocrine system becomes distorted. Eventually pancreatic failure occurs, body weight plummets and a diabetic crisis is precipitated.

Although there remains much work to be done to fully elucidate all of the steps in all of these pathways, this clearly marks the beginning of a biochemical explanation for the known epidemiological relationship between cheap engineered dietary fats and oils and the onset of Type 2 Diabetes.