Nutritional and Vitamin Deficiency Neuropathy

Vitamin B12 is an essential dietary nutrient—a B12 deficiency can lead to a number of serious conditions including peripheral neuropathy.

Vitamin B12 deficiency is common in the United States, especially among the elderly. It is estimated that between 10% and 25% of the people over 80 years of age may have a B12 deficiency. There are several causes of vitamin B12 deficiency. A strict vegetarian diet may promote a B12 deficiency because animal-based foods such as red meat, dairy products, fish, poultry and eggs are the only recognized source of dietary B12. A lack of B12, or the inability of stomach acids to aid in the absorption, also causes this deficiency. Consequently, drugs that reduce stomach acid should not be taken with B12 supplements. A number of other conditions, procedures, and drugs are associated with a reduced the ability to absorb B12. These include autoimmune diseases, pernicious or unexplained anemia, pancreatic diseases, ileal resection, Crohn’s disease, HIV infection, gastritis, gastric or small intestine surgeries, malabsorption syndromes, multiple sclerosis, and use of histamine2 receptor antagonists or proton pump inhibitors.

More recently, the chronic use of nitrous oxygen, also known as laughing gas, has been related to severe cases of B12 deficiency.

Symptoms of lack of vitamin B12 can cause serious anemia, nerve damage and degeneration of the spinal cord. It is common for anemia to develop first, but this is not always the case, especially if a person is taking a folate supplement. A lack of B12 damages the myelin sheath that surrounds and protect nerves. Without this protection, nerves cease to function properly and conditions such as peripheral neuropathy occur. Even B12 deficiency that is relatively mild may affect the nervous system and the proper functioning of the brain. Several types of neurological manifestations are described: progressive degeneration of spinal cord, optic nerve neuropathy, cognitive disorders and polyneuropathy. The nerve damage caused by a lack of B12 may become permanently debilitating, if the underlying condition is not treated.

Today, doctors are exploring a link between pre-diabetes (also known as impaired glucose tolerance or IGT) and peripheral neuropathy. Approximately 10% of adults in America have what is being called “pre-diabetes” or “borderline diabetes”—a condition where the body has higher than normal blood sugar levels, but not high enough to be diagnosed as true diabetes. If left untreated, people with pre-diabetes are at risk of developing type 2 diabetes, heart disease, and nerve damage (which could result in peripheral neuropathy.)

People with pre-diabetes or IGT can significantly reduce their risk of developing type 2 diabetes through diet, exercise and learning to control their blood sugar levels.

The first sign of diabetic neuropathy is usually numbness, tingling or pain in the feet, legs or hands.

Over a period of several years, the neuropathy may lead to muscle weakness in the feet and a loss of reflexes, especially around the ankle.

As the nerve damage increases, the loss of sensation in the feet can reduce a person’s ability to detect temperature or to notice pain. Because the person can no longer notice when his/her feet become injured, people with diabetic neuropathy are more likely to develop foot problems such as skin lesions and ulcers that may become infected.

Diabetic neuropathy may suddenly flare up and affect a specific nerve or group of nerves. When this occurs, the result may be weakness and muscle atrophy in various parts of the body, such as involvement of the eye muscles or eyelid (e.g., causing double vision or a drooping eyelid) or thigh muscles. Alternatively, neuropathy caused by diabetes may slowly progress over time. It also can interfere with the normal functioning of the digestive system and sexual organs.