Orthostatic hypotension is one of the mechanisms found in CFIDS/ME.  It was first discovered in 1995 by P.C. Rowe and J. Bou-Holalgah  (Lancet, 345, JAMA, 274) using a tilt table testing method.  Streeten, et al found that the tilt table testing method was not necessary to show the abnormality and the test could be done in any physician's office if they were willing to take the time for the test. The late Dr. David Streeten was called the "father of orthostatic hypotension" in the United States as he wrote the medical text still used today in medical school on orthostatic hypotension. (See material's section to order the testing method by David S. Bell, M.D.) The late Dr. Streeten felt that the tilt table is not needed since "People don't tilt!"

     Delayed orthostatic hypotension that is sometimes combined with orthostatic tachycardia is caused by venous pooling.  In plain English, when your body changed position from lying to sitting and then to standing, the messengers in your body are supposed to demand that more blood be sent to your heart to compensate for the body's change.  Instead, the wrong message is sent to direct more blood to the extremities, particularly the legs.  The result is discomfort, pain, and, sometimes, even a blue-purplish coloring along with dizziness, altered vision, nausea, fatigue, neurocognitive difficulty, headache, sweating and pallor differences and, occasionally, fainting.  The patient may experience tachycardia, a loud thumping of the heart, as it struggles with the problem of too little blood to compensate for the change in position. While the symptoms will vary among patients, it is found in all patients as one of the key difficulties that they must face with CFIDS/ME.  Just standing in one place (orthostatis) has been found to be particularly difficult. 

Although this has nothing to do with cardiovascular deconditioning, the most recent research has found that this mechanism cannot be explained by a central or autonomic nervous system irregularity.  While no answers are yet definitive, vascular dysfunction seems to be the most favored by the data currently available.  The blood flow has been disturbed and is altered.  Research has been concentrating on the involvement of inflammatory cytokines including IL-1 (interleukin 1), IL-6 and tumor necrosis factor along with nitric oxide.  There seems to be sufficient factors indicating an imbalance between the endothelial and the immunological areas along with, perhaps, autoimmune mechanisms. 

In a 2004 article in Biologist (June, 51/2), Dr. Vance Spence from the University of Dundee in England and Dr. Julian Stewart, from New York Medical College, wrote "Standing up for ME" where they concluded that a treatment for this orthostatic problem will not be possible until the mechanism that creates the problem has been revealed.  The role of endothelial-dependent vasodialation and the pathways of the body that surround acetylcholine sensitivity is currently a targeted area of research.  They state that "there is clearly a problem with local vasodilator and vasoconstrictor mechanisms in these patients."  Specialists recommend drinking a lot of fluid and adding salt to the diet but, although important, will not rectify the problem.

Another part of CFIDS/ME is diabetes insipidus.  This metabolic disorder is characterized by extreme thirst along with the passing of high amounts of urine.  It is caused by the pituatary gland's failure to produce or to secrete sufficient amounts of an antidiuretic hormone (ADH) which can lead to dehydration and electrolyte imbalance.  Diabetes insipidus should not be confused with diabetes melitus since this condition has nothing to do with sugar in the urine.  It does not prevent one from being a victim of diabetes melitus where there is a problem with lack of insulin secretion from the beta cells of the pancreas although excessive thirst and urination are seen in both.  The treatment of diabetes insipidus as well as orthostatic hypotension is  eliminating the cause of the problem which is now being researched with funding from the National CFIDS Foundation.