Raynaud’s phenomenon (abbreviated "RP") occurs one percent of the general population. Patients usually report "cold fingers" accompanied by color changes of the skin (white, blue or red). Most people with RP note cold-induced numbness with a pins and needles sensation of the fingers and toes and occasional dull pain and sense of clumsiness of the hands.
It usually occurs as repeating attacks lasting an average of 15-20 minutes following rewarming. Although cold is the main trigger of an attack, rapidly changing temperature can be a prime cause even in a warm environment.
Blood flow studies have shown that during an attack there is no blood flowing through the arteries or the small capillaries of the fingers. This is probably an exaggeration of the normal mechanism which maintains core temperature by shunting blood away from the hands and feet and to the internal organs when we are cold. The cause of this exaggerated response in Raynaud’s is not totally understood but is likely secondary to chemical and neural factors acting on the fingers and toes.
Raynaud’s phenomenon can occur in otherwise normal individuals or can be associated with another disease. Raynaud’s often is an initial sign rheumatoid arthritis. Approximately 40 percent of patients with systemic lupus erythematosus (SLE or lupus), 50 percent of patients with dermatomyositis, and 90 percent of patients with scleroderma have Raynaud’s phenomenon.
Otherwise normal individuals who have RP usually have milder, less frequent attacks compared to patients with scleroderma. Those with scleroderma frequently develop painful ischemic ulcers or loss of their finger tips.
Conventional treatment involves the use of Prednisone and other corticosteroids. Often patients are unable to tolerate the toxic side effects of these drugs.
The alternative, nutritional medicine approach is to identify hidden allergies by blood test and avoid those allergens (primarily foods). Also hypothyropidism which is then treated as such. In the interim, before surgery, the condition can be managed on an temporary basis with Lugol’s solution. Theoretically enzyme potentiated desensitization holds hope for putting the disease in long term remission.