![]() But tart cherries deliver a much greater content of various anthocyanins than sweet cherries, as well as higher amounts of other phenolic compounds and other nutrients 1. It’s also often referred to as sour cherry or pie cherry because it’s the variety of cherry that’s commonly used to make cherry pie.Īll cherries provide substantial quantities of antioxidants and other nutrients. ![]() The juice used was a combination of Prunus cerasus, Prunus acida, Prunus avium, and Prunus fructicosa, imported from the Caucasus and sold commercially as “100% cherry juice from concentrate.Contrary to the popular sweet cherry that everyone likes to buy around Christmas time and gorging ourselves silly with, the tart cherry is the other main type of cherry, which as its name suggests carry’s a more 'tarty' taste. All patients drank 4 oz of tart cherry juice 2 ×/d for 14 d. Presumed etiologies of the peripheral neuropathies in the study group were: 3 HIV, 2 chemotherapy-induced, 5 spinal disorders, and 2 idiopathic. There were no restrictions on diet or activity. The patients agreed not to use NSAIDs, steroids, lidocaine, and narcotic pain relievers during the study. All study patients were allowed to remain on their prescribed doses of gabapentin, pregabalin, SNRIs, tricyclics, and SSRIs during the study. All study patients had been on multiple antiepileptics, analgesics, and antidepressants for more than 2 y without significant improvement of symptoms. All patients described 9–10 out of 10 pain more than 50% of the time. All study patients had carried a diagnosis of peripheral neuropathy for 5–10 y. Patients with diabetic peripheral neuropathy were excluded due to the potentially confounding effect of the increased glycemic load from cherry juice. The study group consisted of 12 primary care patient volunteers with painful lower extremity peripheral neuropathy. Most patients are on more than 1 of these medications but, even with polypharmacy and optimal dosing, only 40%–60% of patients report partial relief of symptoms, and many have significant adverse effects, such as somnolence, constipation, and drug dependence. These medications alter ion channels and neurotransmitters, decrease the sensitivity of nociceptive receptors, and desensitize C fibers. Common conventional treatments include antiepileptics, antidepressants, NSAIDs, and narcotics. It is believed that these symptoms are caused by alterations in ion channels, alterations in neurotransmitters and their receptors, and altered gene expression. While weakness and loss of sensation are common in many peripheral polyneuropathies, “gain of function” symptoms, such as paresthesias and allodynia, are the most distressing and are very difficult to treat. The pathophysiology of polyneuropathies is complex and not fully understood, but 3 common patterns of damage occur: (1) distal axonopathy, where the cell bodies remain intact, but axons degenerate from distal to proximal, usually as the result of toxic or metabolic injury (2) demyelination neuropathy, where damage to the myelin sheath from autoimmune, infectious, or other causes disrupts electrical signaling and (3) ganglionopathies, where damage occurs at the cell body or neuron, a relatively rare occurrence. No cause is identified in approximately 30% of patients. ![]() These neuropathies may develop from direct compression of peripheral nerves, toxic or metabolic injury to nerve tissue, autoimmune attack, or nutritional deficiency. Peripheral polyneuropathies are common and are believed to affect up to 9% of the US population older than 50 y.
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