Diabetic neuropathy occurs when prolonged elevation of blood sugar levels damages nerve fibers causing problems with sensation and nerve function.

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Diabetic neuropathy occurs when prolonged elevation of blood sugar levels damages nerve fibers causing problems with sensation and nerve function. There are several types of diabetic neuropathy, categorized by which nerves are affected. Diabetic neuropathy occurs in both type 1 and type 2 diabetes, and about 40–70% of diabetics will develop the condition.

Fortunately, research shows that lifestyle modification along with natural interventions, such as lipoic acid and B vitamins, can modulate the complex pathways that underlie the development and progression of diabetic neuropathy.

Causes and Risk Factors

Diabetic neuropathy is caused by a combination of the direct effects of high blood sugar on nerve cells as well as damage to the small blood vessels that provide blood to the nerves.

Risk Factors include:

  • Long-term poor blood sugar control (primary risk factor)
  • Cardiovascular disease
  • Age
  • Male gender
  • Elevated triglycerides
  • High body mass index
  • Smoking and excess alcohol consumption

Diagnosis and Treatment


  • Presence of characteristic symptoms including lower extremity numbness, pain, sensitivity, dryness, muscle weakness/wasting, difficulty walking, and loss of temperature sensation
  • Physical exam
  • Fasting blood glucose, hemoglobin A1C, CBC/Chemistry panel, others
  • Nerve conduction studies or electromyograms on the foot


  • Judicious tight blood sugar control is paramount in controlling progression of diabetic neuropathy.
  • For painful peripheral neuropathy, pregabalin and/or duloxetine may be prescribed.
  • Wound care in limbs affected by peripheral neuropathy is important.

Novel and Emerging Therapies

  • Stem cells. Research suggests stem cell transplantation can protect and restore pancreatic cells, improve blood flow to damaged nerves, and may reduce inflammation and thus relieve diabetic neuropathy pain.
  • Nabilone. Two studies found nabilone, a synthetic cannabinoid, relieves pain and improves sleep in patients with diabetic neuropathy.
  • Botulinum toxin. Studies suggest injection of botulinum toxin, a neurotoxin secreted by the bacterium Clostridium botulinum, to sites of painful diabetic neuropathy may significantly reduce pain and improve sleep quality.

Dietary and Lifestyle Considerations include:

  • Diet. Eating a healthy, balanced diet rich in fibrous plant foods and healthy fats can help keep blood glucose levels under control and may reduce risk of diabetes and its complications.
  • Exercise. One study found that aerobic exercise, in the form of walking on a treadmill for four hours per week, slowed the progression of diabetic neuropathy.

Targeted Natural Interventions

  • Lipoic acid. In clinical trials, doses of 600 – 1,800 mg/day of lipoic acid have led to symptom improvement in people with diabetic neuropathy.
  • Acetyl L-carnitine and L-carnitine. One study found that two grams of L-carnitine daily for 10 months improved nerve conduction velocity, which is impaired in diabetic neuropathy. Other studies have found that acetyl-L-carnitine reduced pain, improved vibration sensation in the legs, and increased nerve regeneration in patients with diabetic neuropathy.
  • Omega-3 fatty acids. Two studies on animal models found that supplementation with omega-3 fatty acids improved signs of diabetic neuropathy.
  • Curcumin. Curcumin may modulate pain associated with diabetic neuropathy.
  • Vitamin D. One study on 51 patients with diabetic neuropathy found vitamin D supplementation reduced reported pain levels by 50%. In a case report of a patient with severe pain, vitamin D supplementation provided substantial relief from pain due to diabetic neuropathy.

Mechanisms Involved in the Development of Diabetic Neuropathy:

The development and progression of diabetic neuropathy is complex. There are a number of metabolic, vascular, and hormonal mechanisms involved.


One key factor involved in the development and progression of diabetic neuropathy is increased glycation, a process in which glucose and other sugars interact with proteins. Glycation causes proteins throughout the body to become dysfunctional. The dysfunctional molecules created by glycation are termed advanced glycation end products (AGEs).

Because people with diabetes have elevated blood glucose levels, they usually also have higher levels of AGEs. These glycation end products have the capacity to destroy cells or disrupt function in many tissues, including nerve. The damage done to nerves by glycation occurs via two different mechanisms. First, the glycation of nerve proteins inhibits their function, which directly affects nerve activity. Second, AGEs can bind to the surfaces of nerve cells and trigger an inflammatory response, further damaging the neurons . Increased levels of reactive oxygen species also contribute to the formation of AGEs .


Inflammation also plays a critical role in diabetic neuropathy, as people with both type 1 and type 2 diabetes have higher levels of C-reactive protein and tumor necrosis factor-alpha (TNF-α), which are two chemicals involved in the inflammatory response. Higher levels of TNF-α are associated with diabetic neuropathy . All of these different pro-inflammatory chemicals lead to the presence of an increased number of immune cells, called macrophages, around the nerves. These macrophages contribute to neuropathy by several mechanisms, including the production of reactive oxygen species and enzymes that break down myelin, which is a protein that forms a protective coating around nerves .

Vascular Dysfunction

Elevated blood glucose levels also cause vascular dysfunction, leading to circulatory problems. High glucose levels activate a protein called protein kinase C, which triggers the constriction of blood vessels; these constricted blood vessels lead to reduced blood flow to neurons . Blood vessels are also damaged by AGEs, further disrupting blood flow. This impaired blood flow to neurons deprives them of oxygen, also known as ischemia. Oxygen deprivation can damage and destroy neurons.

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