Wilsons Temperature Syndrome
- The hallmark symptoms of Wilson’s temperature syndrome (WTS) – persistent or relapsing fatigue, anxiety, depression, headaches, insomnia, muscle aches, cognitive dysfunction, and an overall lack of well-being – are indistinguishable from chronic fatigue syndrome (CFS) and hypothyroidism, except that WTS requires low body temperature as diagnostic of WTS.
- Wilson’s temperature syndrome is a diagnosis of exclusion and is confirmed by a therapeutic trial of WT3 therapy. Thyroid tests have no role in diagnosing this condition other than to rule out decreased thyroid gland function.
- Although WTS does not require the strict definition of fatigue lasting for more than 6 months as in the diagnosis of CFS, in most cases the definition is indistinguishable from CFS, except that WTS includes patients who have mild fatigue and low body temperature and it does not require other symptoms to be present at the same time.
- Dr. Denis Wilson developed the SR-T3 treatment protocol over a 2-year period via empirical observations of treating patients with intractable fatigue (treating more than 5,000 people over 4 years).
- The Wilson’s Temperature Syndrome website (wilsonssyndrome.com), established in 1997, provides information to the general public regarding Wilson’s temperature syndrome.
Thyroid Treatment in Chronic Fatigue and Fibromyalgia Syndrome
- CFS shares many features with fibromyalgia syndrome (FMS).
- The predominance of pain or fatigue is the primary means of distinguishing between these two syndromes.
- Precedence for the use of T3 to treat CFS can be found in recent successful FMS studies.
Quick Overview of Major Parathyroid Metabolism Disorders
|Parathyroid Metabolism Disorder||Major Signs and Symptoms||Key Laboratory Tests||Conventional Therapies||Restorative Medicine|
|Hyperparathyroidism||Commonly asymptomatic Muscle weakness, kidney stones||Serum calcium Serum phosphorous Serum PTH MRI||Surgery||Magnesium supplementation (750 mg q.i.d. or to bowel tolerance), avoiding excess phosphorous intake.|
|Hypoparathyroidism||Often asymptomatic Paresthesias Modd disturbances Muscle tetany Monitro for hypercalcemia||Serum calcium Serum phosphorous Serum PTH||Calcium and Vitamin D supplements||Supplementation with calcium, vitamin, D, and magnesium supplementation (750 mg q.i.d. or to bowel tolerance) while avoiding excess phosphorous|
|Osteoporosis||Often asymptomatic||DEXA bone density scan||Calcium, vitamin D, hormone replacement therapy, various medications||Multi-vitamin and mineral treatment|
- Osteoporosis is a disease of the bone that leads to increased risk of fracture.
- Osteoporosis occurs when the normal cycle of bone remodeling is interrupted.
Osteoclasts carve out cavities in bone surface>osteoblasts form new bone
- In bones affected with osteoporosis, new bone formation does not keep up with one removal, leaving the bone progressively brittle.
- As bone is lost, the skeleton continues to have normal composition, but it becomes more porous, hyper-mineralized, and more fragile.
- The World Health Organization has declared osteoporosis the second largest medical problem, next to cardiovascular disease, and is the most common bone disorder in America.
- More than 25 million Americans, primarily women, are candidates for developing osteoporosis.
- The disease leads to 1.5 million fractures per year, including hip, spinal compression and vertebral fractures which often lead to surgical intervention.
- These fractures are associated with varying degrees of pain, deformed spine, height loss, loss of appetite, heartburn, bloating, and difficulty sleeping, breathing and walking.
- Other metabolic bone and joint diseases and disorders (osteoarthritis, rheumatoid arthritis, cancer, endocrine disorders, Paget’s disease, and amenorrhea) account for an additional 12 million cases of accelerated bone loss per year.
- Treatment is only partially successful (at best) once progressive bone weakening has occurred, therefore it is important to identify women in danger and those who are currently losing bone at an accelerated rate so that effective treatment can begin in the prevention rather than reversal of one loss.
- If prevention is the goal, it is important to start treatment in young women in their 30’ and 40s, as most women over age 30 slowly loose bone, with menopause marking the onset of more rapid bone loss.
- Preventive measures, such as diet, exercise, and nutritional supplements are known to help prevent and partially reverse the effects of osteoporosis.
Relationship of PTH to Osteoporosis
- PTH induces osteoclastic activity (bone breakdown which allows for bone formation), freeing calcium ions.
- PTH also promotes the synthesis of the active form of vitamin D, 1,25-dihydroxy.
- Thus, PTh increases calcium absorption in the GI tract and decerses calium loss in the urine.
- PTH levels are modulated via a negative feedback loop by serum calcium ion levels. Normal muscle activity and blood clotting depend on normal muscle activity in the plasma.
- Reduced parathyroid function lowers calcium levels and, below, certain levels, causes muscle stiffness, cramps, and convulsions.
- Reduced PTH contributes to rickets, osteomalacia and osteoporosis formation in susceptible individuals.
Causes of Osteoporosis
- Genetics – Caucasian or Asian ancestry
- Family history of osteoporosis
- Gender – women 4 times more likely than men
- Fair skinned, slender, small boned women who have a close relative with the disease have the greatest risk
- Diet and nutrition, physical activity, excessive alcohol consumption and cigarette smoking can all increase the risk of osteoporosis
- Physiological states and disease can increase the risk.
Laboratory Tests for Osteoporosis Measurements of bone mass assess the short term likelihood of fractures, however few tools are available to assist healthcare professionals in assessment of bone resorption before it has become excessive. Bone biopsies provide this information but are too invasive for routine use. One urinary excretion test, pyridinium crosslinks, has been found to be the most accurate are specific markers of bone resorption and provides a valid parameter in the diagnosis of osteoporosis. Other useful tests to assess abnormal calcium metabolism include:
- ESR (erythrocyte sedimentation rate)
- Alkaline phosphatase
- 24 urine
Another test which can assess bone mass, but not the dynamics of bone formation is photon absorptiometry. This test is excellent for identifying women who are in immediate danger of developing fractures. It has limited value, however, in predicting those who will lose bone, develop osteoporosis, or are more likely to suffer fractures in the future. Diagnosis of Osteoporosis Diagnosis of osteoporosis is made by evaluating a “T” score and a “Z” score. A “T” score compares a patient’s bone mass to a young, normal subject, and a “Z” score is a comparison of patients’ bone mass to age matched normal subjects. The differential diagnosis of osteoporosis includes a thorough exam for other calcium metabolism disorders such as osteomalacia, osteogenesis imperfecta, hyperparathyroidism, hyperthyroidism, hypogonadism, Cushing’s syndrome, multiple myeloma, rheumatoid arthritis, and renal failure.
Conventional Medical Treatment for Osteoporosis
Pharmacological agents for osteoporosis fall into two categories; they either inhibit bone resorption or stimulate bone formation. Bone resorption inhibitors include estrogen, phosphates, and calcitonin. Bone formation stimulators include sodium fluoride, androgens, parathyroid hormone, and growth hormone. Other conventional treatment of osteoporosis includes estrogen replacement therapy (ERT), calcium supplements, and weight bearing exercise. ERT inhibits bone resorption in postmenopausal women and has been shown to reduce the incidence of osteoporotic fractures by about 50%. Although the conventional approach reduces the incidence of osteoporosis, many women cannot or will not use ERT because of the risks and side effects associated with it.