Oxnard - Port Hueneme Optometrist Dr. Don Steensma 465 W. Channel Islands Blvd, Port Hueneme, CA 805/486-3585
Type 1 results from a lack of insulin production in the pancreas. These people must take insulin injections or they will die. Approximately 0.12% of Americans (400,000) have this type. We do not know it’s cause, but it might be genetic or viral. It is usually diagnosed in children and young adults.
Type 2 results from insulin resistance. The cells do not respond normally to the insulin and do not allow the glucose into the cell. Approximately 5.8% of Americans (18 million) have this type and it is often associated with obesity. It is sometimes controlled with diet, exercise and weight loss, but oral medications or even insulin are often needed. Approximately 19% of Americans (57 million) have pre-diabetes in which the blood glucose levels are higher than normal but not high enough for a diagnosis of type 2 diabetes. Many of these people will eventually become diabetic.
The American diet has changed drastically in the last three decades. A large part of the average American diet consists of super-sized fast foods and simple carbohydrates. We sit at the computer or the TV and do not get the exercise we need. Just look around and you can see that we are in the midst of an obesity epidemic. Look at our kids. Many are obese. It’s no wonder the incidence of diabetes has doubled in the last three decades.
Type 1 diabetes tends to come on rapidly with the classic symptoms of frequent urination, excessive thirst and fatigue while type 2 diabetes comes on more slowly, often over a course of years.
Type 3 sometimes occurs because pregnancy hormones can block insulin from doing its job. When this happens, glucose levels may increase in a pregnant woman's blood.
You are at greater risk for gestational diabetes if you are older than 25 when you are pregnant; Have a family history of diabetes; Gave birth to a baby that weighed more than 9 pounds or had a birth defect; Have sugar (glucose) in your urine when you see your doctor for a regular prenatal visit; Have high blood pressure;
Have too much amniotic fluid; Have had an unexplained miscarriage or stillbirth; Were overweight before your pregnancy.
Usually there are no symptoms, or the symptoms are very mild. Usually, the glucose level returns to normal after delivery. Gestational diabetes usually starts halfway through the pregnancy. All pregnant women should receive an oral glucose tolerance test between the 24th and 28th week of pregnancy to screen for diabetes.
Measurement of HbA1c (glycated hemoglobin) (Commonly referred to as A1c) is the standard for the diagnosis and monitoring of diabetes. A measurement of HbA1c indicates the patient’s average blood glucose level during the last three months. Unlike blood sugar levels, HbA1c is not largely affected by what the patient ate in recent hours. Glucose reacts with hemoglobin in the red blood cell, and form glycated hemoglobin. Once glycated, the hemoglobin molecule remains that way for the 120-day lifespan of the red blood cell.
The 2010 HbA1c benchmark for healthy individuals is 6.5%. A measurement that is between 6.5% to 7.0% is considered pre-diabetic.
This is the most common complication. It results from excess glucose in the blood (normal blood sugar levels range from 70mg/dL to 120mg/dL), and may be caused by the ingestion of too many carbohydrates or sugars, high stress, lack of physical activity, illness, or skipped medication doses. Chronic hyperglycemia leads to micro-vascular and macro-vascular complications. In the short term hyperglycemia can lead to diabetic ketoacidosis (DKA) or hyperglycemic hyperosmolar non-ketotic syndrome (HHNS).
This is the result of breakdown of muscle, fat and liver cells for glucose, resulting in ketone production. It usually occurs with total insulin deficiency, as seen in type 1 diabetes. It leads to profound dehydration, vomiting, respiratory distress and ultimately coma. It is usually associated with sickly-sweet breath.
This is a state of dehydration and hyperglycemia that is seen mainly in older patients with type 2 diabetes and without significant production of ketones. It occurs when fluid intake cannot keep pace with increased urinary output from marked hyperglycemia. It leads to altered mental status, coma and death in 10% to 50% of cases. It is now being seen with increasing frequency in obese children with type 2 diabetes.
This is an elevated lactic acid with acidosis, without ketones It results from impaired tissue oxygenation and increased anaerobic metabolism. LA in diabetes may result from poor circulation coupled with vigorous exercise, thiamine deficiency or certain medications. Common symptoms include nausea, hyperventilation and lethargy. Metformin - the most commonly prescribed diabetes medication rarely cause LA. Mortality rates for LA are more than 50% when associated with circulatory failure or septic shock.
This is defined as an episode of abnormally glucose concentration (with or without symptoms) that expose the individual to harm. It occurs very frequently in patients with type 1 diabetes as well as in type 2 patients who are treated with insulin or a sulfonylurea drug Hypoglycemia symptoms are confusion, tremor, sweating and sleepiness. These sympt0oms are reversible with prompt treatment. However, severe hypoglycemia may cause long-term damage.
This the most important complication of diabetes. Diabetes is a major risk factor for cardiovascular disease. Coronary artery disease and cerebral vascular disease are most common problems. heart failure and peripheral arterial disease can also occur. Adults with diabetes have mortality rates that are about two to four times higher than adults without diabetes. Survival rates for individuals with diabetes are lower once they have had a cardiovascular event. Also, the risk for stroke is two to four times higher among people with diabetes.
The hyperglycemia, free fatty acids and insulin resistance alters the function and structure of blood vessels. Blood clots form leading to atherosclerosis. Cardiovascular risk increase with the presence of obesity hypertension, high fat and triglyceride blood levels. Other risk factors include smoking, physical inactivity, increased age, male gender, menopause, family history and race.
Diabetes is the leading cause of end-stage kidney disease in the U.S. Nearly a third of diabetic patients develop nephropathy. Chronic hyperglycemia causes inflammation, which leads to fibrosis and hyperactivity of the renin-angiotensin-aldosterone hormone balance that damage the nephrons. High protein levels in the urine (Macroalbuminura) is the earliest sign of nephropathy. This can lead to kidney failure over 5 -10 years
There is evidence that use of both angiotensin conversion enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) in treating hypertension, prevent or delay progression to macroalbuminuria. These classes of drugs are now considered first-line therapy for any diabetes patient with high blood pressure and/or kidney disease. Diabetic kidney disease results in 2-3 times more cardiovascular disease compared to diabetes patients without kidney disease. Vitamin D supplementation may help in patients with macroalbuminuria.
The degree of kidney disease appears to be linked with the severity of diabetic retinopathy.
Approximately 8% of diabetics develop diabetic retinopathy. Often diabetic retinopathy (eye damage) occurs at the same time as diabetic nephropathy (kidney damage), Diabetic polyneuropathy (nerve damage) periodontal disease (gum damage).
Proliferative Diabetic Retinopathy (NPDR). As the blood glucose levels rise and fall in diabetics the retinal blood vessels begin to leak small amounts of blood and fluid. There are usually no symptoms in the early stages of diabetic retinopathy.
Proliferative Diabetic Retinopathy (PDR). Over time as the disease process progresses, poor blood circulation leads to hypoxia (lack of oxygen). This stimulates new blood vessels to grow on the retinal surface in order to bring more oxygen to the hypoxic area. Often these new blood vessels (neovascularzation) will shrink pulling on the retina and may lead to a retinal detachment and blindness. Proliferative retinopathy can be treated with lazers that destroy the neovascularization. A fairly new therapy is the injection of drugs into the eye which slow the development of neovascularization.
Macular edema. Vision may not be effected until the disease becomes severe, or if a hemorrhage occurs in the macula (that part of the retina that provides sharp, central vision) This condition is called
More than half of patients with diabetes also have dry eye disease. The most common dry eye symptoms reported by patients with diabetes as well as non-diabetics are burning and foreign body sensation.
Dry eyes. We think that there are three causes of dry eye in the diabetic patient.
Peripheral neuropathy secondary to hyperglycemia. In the eye, hyperglycemia causes micro-vascular damage to the corneal nerves. This can block the feedback mechanism that controls tear secretion, so the tear glands do not secrete tears properly. A similar effect happens temporally after LASIK. When the nerves are cut the eye becomes much dryer for up to 6 months when the nerve regenerates.
Insulin insufficiency. Insulin exerts important effects on glands that are located throughout the body which produce saliva, milk and human tears. In the eye, corneal and lacrimal gland metabolism, growth, epithelial cell proliferation and culture maintenance are influenced by insulin. A low insulin level generally disrupts the bio-mechanical balance of these tissues and results in ocular dryness.
Inflammation is another problem. Hyperglycemia triggers inflammation. Tear gland inflammation leads to a reduction in the quantity and quality of the tears..
Cataracts. Diabetic patients often develop cataracts about 10 years earlier than non-diabetics.
It is very important that all diabetic patients get a thorough eye examination at least every year.
Neuropathy (nerve damage) is a common complication of diabetes. About 65% of Americans with diabetes have some form of neuropathy. Pain and burning are the most common symptoms It can occur at any time, in the diabetic progression but risk rises with age and longer duration of diabetes. Neuropathy often occur in people who have had diabetes for at least 25 years.
There are four types of diabetic neuropathy:
Peripheral (distal polyneuropathy) may lead to podiatric problems, including foot deformities, infections, ulcers and amputations.
Proximal (diabetic amyotrophy) is characterized by weakness followed by wasting of hip and leg muscles, either unilaterally or bilaterally, with associated pain.
Autonomic (autonomic neuropathy) can affect any of the body’s involuntary functions, including heart rate, blood pressure, perspiration and digestion, among others.
Focal (mononeuropathy) is damage to a single nerve or nerve group, which results in loss of movement, sensation, or other function of that nerve. Symptoms depend on the specific nerve affected.
Of all the treatments, tight and stable glycemic control is probably the most important. In the Diabetes Control and Complications Trial (DCCT), the occurrence of diabetic neuropathy was reduced by 60% over a 10-year period with rigorous blood glucose control in patients with type 1 diabetes. Similar findings were noted in the Stockholm Diabetes Intervention Study. Depending on the type of nerve problem and symptoms, additional treatments include various medications, orthotics, infrared light therapy (Anodyne), nutritional supplements and dietary changes.
The degree of nerve disease appears to be linked with the severity of diabetic retinopathy.
Both men and women with diabetes are affected by bladder problems (infection, incontinence and inefficient voiding) as well as sexual dysfunction (erectile dysfunction, decreased libido, painful intercourse and infertility). The causes include autonomic neuropathy, myopathy, reduced immunologic response, vascular insufficiency and low levels of testosterone. is a strong association between erectile dysfunction and cardiovascular disease, nephropathy and neuropathy, and a possible association with retinopathy. Incontinence is particularly a problem for female patients.
Drugs for erectile dysfunction have been shown to improve sexual response in men with diabetes, and in one study showed that Viagra (sildenafil, Pfizer) significantly lowered glycosylated hemoglobin (HbA1c).
Damage to blood vessels and nerves, and abnormal collagen accumulation in skin result in changes in connective tissue. These complications are most often seen in patients with longstanding type 1 diabetes, but also may be seen in patients with type 2 diabetes.
Hand, wrist and shoulder abnormalities are common. Common hand syndromes include: diabetic cheiroarthropathy (stiff hand syndrome), Dupuytren’s contracture (affecting the fourth and fifth digits), flexor tenosynovitis (trigger finger) and carpal tunnel syndrome-all of which may cause deformity and severe restriction of hand mobility. Carpal tunnel syndrome may be more common in those with pre-diabetes and may be seen up to 10 years before a diagnosis of diabetes. Adhesive capsulitis (frozen shoulder) has been reported in 19% of diabetes patients, appearing at a younger age and with less pain than in other patients.
Diffuse idiopathic skeletal hyperostosis is a calcification of spinal ligaments, most often in the thoracic spine. It is most commonly seen in obese type 2 patients. Although diabetes is not a clear risk factor for osteoarthritis, obesity is a risk factor for both and may help explain increased risk of large and small joint ostheoarthritis in type 2 diabetes. Fracture risk appears to be higher in both type 1 and type 2 diabetes. Type 1 diabetes has been associated with low bone density, though its role in increased fracture risk is debated.
Muscle complications from diabetes may be secondary to limb/ digit contracture and/or motor neuropathy that results in disuse and muscle atrophy. Atherosclerosis may cause claudication with muscle cramping and painful walking. Diabetic muscle infarction is a rare condition that is generally seen in patients with longstanding, poor control and multiple micro-vascular complications. It presents with pain and swelling (commonly in the thigh or calf muscles). Therapy consists of rest and analgesia.
Neuropathy decreases the ability to feel pain or discomfort, while poor circulation decreases the ability to heal and resist infection. Foot ulcers may lead to gangrene and amputation. More than 60% of all lower-leg amputations in this country unrelated to an accident are performed because of diabetes.
Several other foot problems are associated with diabetes, including athlete’s foot; calluses and corns; dry, cracked skin; and nail disorders. Nerve damage causes muscle weakness and loss of tone in the feet, possibly resulting in hammertoes and bunions.
A severe podiatric complication is Charcot’s foot, (neurogenic arthropathy). It results in disintegration of ligaments, joint surfaces and bone, which leads to deformity, loss of function and ulceration. Because of neuropathy, pain goes unnoticed and the patient continues to walk on the damaged joint. Surgery and occasionally amputation may be warranted.
The air sacs of our lungs (alveoli) are microvascular tissue. Gas exchange in the lungs is adversely impacted and forced expiratory volume (FEV) worsens with diabetes duration and poorer blood glucose control In most cases this does not lead to functional exercise capacity or quality of life except in instances of coexisting chronic obstructive pulmonary disease (COPD). There does not appear to be a link between reduced FEV and diabetic retinopathy.
Patients with diabetes often have dry, cracked skin and blistering that facilitates infection. Elevated tissue glucose and compromised immunological response may lead to bacterial or fungal infection. Any ulceration of the extremities in any patient with diabetes requires an urgent consult to reduce the risk of limb loss. Acanthosis nigricans, which is hyper-pigmentation secondary to excess insulin production, is particularly noteworthy. Its appearance may precede a diagnosis of diabetes by several years.
Diabetes often affects the small blood vessels in the soft tissue and bone that support the teeth. About one third of patients experience severe gum disease. Severe gum disease has a strong link to cardiovascular risk in diabetics. Improvement in periodontal disease has been linked to improved blood glucose control. Diabetes patients are often experience dry mouth as a result of hyperglycemia and autonomic neuropathy. The degree of periodontal disease appears to be linked with the severity of diabetic retinopathy.
GI disorders are common in diabetics. As many as 75% of patients report significant symptoms, including difficulty swallowing, reflux, constipation, abdominal pain, nausea, vomiting and diarrhea. Impaired autonomic motility in the intestines may also lead to bloating, pain and bacterial overgrowth. Elevated blood glucose leads to fungal overgrowth resulting in Candida infections in the digestive tract. Obesity and type 2 diabetes are strongly associated with an increased risk for digestive tract cancers as well as reproductive organ cancers in women.
Type 1 diabetes usually is an autoimmune disease and 20% also have other autoimmune disorders such as celiac disease, Hashimoto’s hypothyroidism, Graves’ disease, autoimmune gastritis, pernicious anemia, Addison’s disease and vitiligo. Multiple sclerosis is more common in both type 1 and type 2 diabetes.
The incidence of several psychiatric disorders such as depression, anxiety, schizophrenia and dementia. Are more common in diabetics. Depression is 2-3 times more common in people with diabetes. Dementia seems to be associated with obesity in middle-aged individuals who develop diabetes later in life. Diabetes may be associated with Alzheimer’s disease. Recent studies may indicate that insulin deficiency and resistance within the brain are early bio-markers for Alzheimer’s.
All diabetes pills sold today in the United States are members of six classes of drugs.
Sulfonylureas stimulate the beta cells of the pancreas to release more insulin. Sulfonylurea drugs have been used since the 1950s. Chlorpropamide (Diabinese) is the only first-generation sulfonylurea still in use today. There are three second-generation drugs: glipizide (Glucotrol and Glucotrol XL), glyburide (Micronase, Glynase, and Diabeta), and glimepiride (Amaryl). These drugs are 1-2 times a day, before meals. All sulfonylurea drugs have similar effects on blood glucose levels, but they differ in side effects, how often they are taken, and drug interactions. Because they stimulate the release of insulin, they may induce hypoglycemia (low blood glucose levels).
Meglitinides are drugs also stimulate the beta cells to release insulin. Repaglinide (Prandin) and nateglinide (Starlix) are meglitinides. They are taken before each of meal. Because they stimulate the release of insulin, they may induce hypoglycemia (low blood glucose levels).
Metformin (Glucophage) lowers blood glucose levels by decreasing the amount of glucose produced in the liver. Metformin also helps by making muscle tissue more sensitive to insulin so glucose can be absorbed more easily. It is usually taken two times a day. A side effect of metformin is diarrhea, but this is better if taken with food.
Rosiglitazone (Avandia) and pioglitazone (ACTOS) help insulin work better in the muscle and fat and also reduce glucose production by the liver. patients taking these medications must be monitored for liver problems. They also increase the risk for heart failure in some individuals.
Acarbose (Precose) and meglitol (Glyset) lower blood glucose levels by blocking the breakdown of starches, such as bread, potatoes, and pasta in the intestine. They also slow the breakdown of some sugars. Their action slows the rise in blood glucose levels after a meal. They should be taken with the first bite of a meal. They may cause gas and diarrhea.
DPP-4 inhibitors help improve A1C without causing hypoglycemia. They work by by preventing the breakdown of a naturally occuring compound in the body, GLP-1. GLP-1 reduces blood glucose levels in the body, but is broken down very quickly so it does not work well when injected as a drug itself. By interfering in the process that breaks down GLP-1, -4 inhibitors allow it to remain active in the body longer, lowering blood glucose levels only when they are elevated. -4 inhibitors do not tend to cause weight gain and tend to have a neutral or positive effect on cholesterol levels. Sitagliptin (Januvia) and saxagliptin (Onglyza) are the two -4 inhibitors currently on the market.
There are more than 20 types of insulin sold in the United States. They differ in how they are made, how they work in the body, and how much they cost.
Rapid-acting insulin (lispro, Novo Nordisk, and sanofi-aventis), begins to work about 5 minutes after injection, peaks in about 1 hour, and continues to work for 2 to 4 hours.
Regular or Short-acting insulin usually reaches the bloodstream within 30 minutes after injection, peaks anywhere from 2 to 3 hours after injection, and is effective for approximately 3 to 6 hours.
Intermediate-acting insulin generally reaches the bloodstream about 2 to 4 hours after injection, peaks 4 to 12 hours later, and is effective for about 12 to 18 hours.
Long-acting insulin (ultralente) reaches the bloodstream 6 to 10 hours after injection. It is usually effective for 20 to 24 hours. There are also two long-acting insulin analogues: glargine and detemir. They both tend to lower glucose levels fairly evenly over a 24-hour period with less of a peak of action than ultralente.
Exenatide (Byetta) Mimics incretins, the peptides that are secreted when a person eats. Incretins stimulate insulin production and help the person feel full by delaying emptying of the stomach. It can cause nausea and vomiting. It helps with losing weight. It can lead to hypoglycemia if is used with insulin or a sulfonylurea.
Pramlintide (Symlin) is a synthetic version of amylin, a peptide that is secreted along with insulin when a person eats. It helps the person feel full by delaying emptying of the stomach. It can cause nausea and vomiting. Symlin is indicated for patients who have Type 1 diabetes and for those who have Type 2 diabetes and require insulin. It helps with losing weight.
Omega-3 essential fatty acids have been shown to prevent cardiac arrhythmia’s and also decrease clinical depression in people with diabetes. They have been shown to decrease plasma triglyceride, visceral fat, free fatty acid, C-reactive protein, glucose and insulin levels.
Lutein, zeaxanthin and lycopene antioxidents. Patients with high levels of serum lutein, zeaxanthin and lycopene are 67% less likely to develop diabetic retinopathy than those with low levels.
Vitamin D. A daily intake of 2,000 IU of 25-hydroxyvitamin D is required to maintain healthy serum concentrations in patients who either have type 1 or type 2 diabetes.
Benfotiamine. This is a form vitamin B1 which decreases the incidence of micro-vascular complications secondary to diabetes. Animal studies revealed that benfotiamine supplementation prevented the onset of diabetic retinopathy.
Alpha lipoic acid. ALA is a super-antioxidant that blocks glycosylation of proteins, improves glucose transport and reduces blood vessel complications of diabetes.
Pycnogenol. Pycnogenol is an extract of French maritime pine bark. It is thought that pycnogenol retards capillary leakage in patients with diabetic retinopathy.
Taurine. Taurine may lower blood glucose. Taurine has been shown to minimize diabetic retinopathy in an animal model by suppressing excessive glutamate excitotoxicity.
In addition to nutritional supplementation, regular exercise can reduce a patient’s risk for diabetes by burning off excess caloric energy and accumulated fat. Basic lifestyle changes to increase physical activity include maintaining a workout schedule, taking the stairs instead of the elevator, parking further away from your destination and taking walks. Coaching and fitness testing by personal trainers may also be helpful.