Hyperglycemia Toxicity
Beta cell death resulting from hyperglycemia in diabetes Type II can cause insulin dependent diabetes in some cases. Hyperglycemia causes pancreatic beta cell damage in itself. From preliminary animal studies, it appears that beta cells fail to respond appropriately to glucose when glucose levels are kept above 120 mg/dl. By this mechanism, uncontrolled Type II diabetes can eventually turn into Type I. This is another example of how a pathology (hyperglycemia) can actually reinforce the illness itself by destroying the cells that counteract hyperglycemia. It is interesting to note that illnesses can often create feedback loops that are self-perpetuating.
The fasting glucose homeostasis is controlled by a balance between glucose utilization by peripheral tissues and hepatic glucose production. Non-diabetics are able to have fasting insulin levels that are sufficient to suppress hepatic gluconeogenesis through the production of glucagon. But insulin resistance and insulin deficiency found in Type I diabetes have no effective feedback loop for gluconeogenesis, and thus the liver will contribute to hyperglycemia.
The fasting glucose homeostasis is controlled by a balance between glucose utilization by peripheral tissues and hepatic glucose production. Non-diabetics are able to have fasting insulin levels that are sufficient to suppress hepatic gluconeogenesis through the production of glucagon. But insulin resistance and insulin deficiency found in Type I diabetes have no effective feedback loop for gluconeogenesis, and thus the liver will contribute to hyperglycemia.
Secondary Diabetes
Diabetes can be secondary to liver disease, due to the liver’s role in producing hepatic insulin sensitizing substrate. Diabetes can also be secondary to other diseases, such as pancreatectomy, hemochromatosis, cystic fibrosis, and chronic pancreatitis. Endocrinopathies, such as acromegaly, pheochromocytoma, Cushing’s syndrome, primary aldosteronism, and glucagonoma, are all potential causes of diabetes as well.
Clinical Trials
Milk Thistle and Secondary Diabetes
Milk thistle has been shown to be an effective treatment for patients with diabetes secondary to cirrhosis. In a trial done in Italy, 30 diabetic patients were given a regime of conventional therapy and 600 mg daily of silymarin, while 30 other patients were given only conventional therapy. After 4 months, the group who using 600 mg daily of silymarin had decreased fasting glucose levels, decreased glucosuria, decreased HbA1c values, and decreased fasting insulin levels, with a decreased exogenous insulin requirement. The control group had increased insulin levels after the study and stabilization of exogenous insulin needs. This study demonstrated that silymarin decreased endogenous insulin overproduction and decreased exogenous insulin requirements in patients with liver disease. Milk thistle stimulates protein synthesis, resulting in the regeneration of hepatic cells and new liver tissue.60
Iatrogenic Diabetes
Antihypertensive drugs, thiazide diuretics, glucocorticoids, estrogens, psychoactive medications, and pentamidine all can be causes of impaired glucose tolerance. Virtually all non-controlled diabetic patients end up on antihypertensive drugs due to diabetic induced high blood pressure, and many will need thiazide diuretics due to congestive heart failure initiated by the hypertension. Antihypertensive and thiazide diuretics drugs intensify insulin resistance, thereby further intensifying diabetic illness.61
Naturopathic Medical Alternatives [SH]
Botanical Medicine
Rauwolfia serpentina: Antihypertensive pharmacological alternatives do exist. For example, Rauwolfia serpentia can lower blood pressure very well without affecting glucose intolerance. In Ayurvedic medicine, this herb has been used in the treatment of insomnia and schizophrenia since 1,000 BC. In China, it had also been used for thousands of years in the treatment of a Chinese pathology called ‘liver fire rising’. Pharmacology studies indicates that it blocks the adrenergic transmitter vesicles, which take up and store the amines, resulting in depletion of norepinephrine, dopamine, and serotonin, and a consequent decrease in blood pressure.
Syndrome X
This condition of impaired glucose intolerance is often the precursor of Type II diabetes. Like Type II, it results from genetic, lifestyle, nutritional, and environmental factors. Syndrome X is associated with truncal obesity and accelerated fat deposition due to evolutionary adaptations from feast or famine conditions. In the modern Western world of food security, the body is often in the feast condition and is rarely ever in the famine condition. Patients with syndrome X will have insulin resistance, hyperinsulinemia, hypertension, and related dyslipidemias. Hyperinsulinemia results from ineffective insulin response and perhaps nitric oxide deficiency.62 Syndrome X can be effectively treated with natural medicines and lifestyle factors.
Acute Complications in Diabetes [A]
Diabetics need to be concerned about chronic complications and acute complications of diabetes. In general it is the chronic complications that do most of the damage. Chronic complications result from high glucose levels (hyperglycemia) reacting with different tissues of the body. Acute complications result from some extreme abnormality of blood sugar, causing either severe hyperglycemia or low blood sugar (hypoglycemia). The initial symptoms of acute hyperglycemia will involve excess urination (polyuria), excess thirst (polydipsia), fatigue, and blurry vision.
Hyperglycemia may result in a coma due to the high level of glucagon stimulation, which is a response to low serum insulin levels. Hyperglycemic comas are either diabetic ketoacidosis (DKA) or nonketotic hyperosmolar coma. Hypoglycemic coma results when the patient takes excess insulin relative to what the body needs during eating or exercise.
Diabetes Ketoacidosis [B]
Any disorder that affects the balance between insulin and counter-regulatory hormones can initiate diabetic ketoacidosis. Most patients already have been diagnosed with diabetes before they are diagnosed with DKA. Usually, only older people will have DKA without any prior diagnosis. Eighty percent of DKA occurs in people with diagnosed diabetes resulting from inadequate insulin or current stress or illness. DKA usually occurs in Type I patients and rarely in Type II patients. Symptoms include rapid respiration, acetone odor on breath, and diffuse abdominal pain. Metabolic acidosis of pH < 7.35, blood sugar levels of more than 250 mg/dl, and ketones in urine or blood are diagnostic of DKA.
The most common causes of DKA are infections, myocardial infarctions, and emotional stress. Even localized infections, such as urinary tract infections, including prostatitis, can trigger DKA. Prescription drugs, such as corticosteroids and pentamidine, or hormonal changes can also be also be triggers. The deficiency of insulin and the counter regulatory hormones (glucagons, epinephrine, growth hormone, and cortisol) result in gluconeogenesis in the liver and breakdown of fat (lipolysis), which is the basis of fatty acid breakdown that converts into ketones. The high levels of ketones cause metabolic acidosis.
The prognosis for a young healthy diabetic who is adequately managed is excellent. However, when the patient is old or weak and has other current illness (especially infection), or if the acidosis is very severe, there is significant mortality. If patients with DKA have fallen into a coma or hypothermia, prognosis is poor. In the hospital, electrolytes, bun, creatinine, glucose urinalysis, and electrocardiogram should be ordered. Treatment will mainly consist of IV fluids and insulin bolus of 10-20 units IV, followed by a continuous infusion of 5-10 units per hour.
Non-Ketotic Hyperosmolar Coma [B]
The NKH coma usually only occurs in the elderly. Altered mental status is the main reason that these patients are brought to the hospital. The patient’s blood sugar is consistently very high and alkaline. However, the most distinguishing feature is extreme dehydration caused by frequent urination. Symptoms include polydipsia, polyuria, and severe dehydration. Laboratory diagnostics reveal hyperglycemia equal or above to 600 mg/dl, hyperosmolarity >320 mOsm/L, arterial pH equal or over 7.3, and the absence of ketones. Mortality rates are much more severe than DKA, ranging from 20% to 80%. Rehydration is of utmost importance.
Hypoglycemia [B]
Hypoglycemia in a diabetic is primarily caused by incorrect dosage of insulin or hypoglycemic drugs. It is considered an acceptable complication of drug therapy. However, other factors need to be considered; for example, menstruating women can experience hypoglycemia due to the rapid fall in estrogen and progesterone. Other contributing disorders to hypoglycemia in diabetics include organ failure, hormonal deficiencies, B cell tumor, and hypoglycemia of infancy and childhood.
C-Peptide is the peptide connects the A and B chains of insulin. It is used to differentially diagnose patients with insulinoma versus factitious hypoglycemia. In hypoglycemic coma induced by an overdose of insulin medication, C-peptides may be lower than normal, while insulin levels are increased. If C-peptide is high – endogenous insulin is produced in high amounts, either from anti-hyperglycemic prescription drugs, such as sulphonylureas, that stimulate the pancreas to produce more insulin or an insulin-secreting tumor. To differentiate between these causes, drug urine tests must be done.
