Natural Treatments for Diabetes Insipidus

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Natural Treatments for Diabetes Insipidus

By Dr. Jeffrey Shapiro, MD, Category : General Health * October 21, 2015
Diabetes Insipidus When you think of the word diabetes, what comes to mind?

Maybe you think of insulin injections, since type 1 diabetes occurs as a result of the body being unable to create insulin. Or perhaps you think of controlling high blood sugar through a low glycemic index diet?

What if I told you that the name diabetes has nothing to do with blood sugar control or insulin injections? Let me explain...

What is Diabetes Insipidus?
In general, diabetes is a term that causes the body to produce a large amount of urine. Excessive urination is a symptom that is highly characteristic of all types of diabetes, especially diabetes insipidus. It is a chronic endocrine disorder that is distinctive of intense thirst--known as polydipsia. In other words, this form of diabetes has absolutely nothing to do with blood sugar or insulin.

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Causes of Diabetes Insipidus
There are two main types of diabetes insipidus--nephrogenic diabetes insipidus and central diabetes insipidus (neurogenic diabetes insipidus).

Central diabetes insipidus results from a lack of antidiuretic hormone (ADH)--also called vasopressin--it's basically a hormone that promotes the retention of water by the kidneys. It can be characterized by pituitary gland damage caused by inflammation, surgery, a tumor, a head injury, or an illness such as meningitis. The cause is usually genetic with children. Also, in some cases the cause of central diabetes insipidus is not known.

On the other hand, your body will often make enough vasopressin with nephrogenic diabetes insipidus; however, your kidneys will not respond to the ADH due to a kidney tubules defect. The cause may be due to a chronic kidney disorder or an inherited genetic disorder from an X-linked trait that will affect the arginine vasopressin (AVP) receptor 2 gene. Nephrogenic diabetes insipidus is also thought to affect men more than women; however, women can pass the gene that causes the disease to their children.

Certain drugs can lead to nephrogenic diabetes insipidus, including lithium and a tetracycline antibiotic called demeclocycline. Other disorders can also make the kidneys sensitive to ADH such as autosomal dominant polycystic kidney disease, sickle cell nephropathy, hypercalcemia (high calcium levels), low potassium levels, amyloidosis, Sjogren syndrome, pyelonephritis, Bardet-Biedl syndrome, chronic hypokalemic nephropathy, release of obstructing periureteral fibrosis, and nephronophthisis and medullary cystic kidney disease complex, and certain cancers like sarcoma and myeloma.

Gestational diabetes insipidus is a type of diabetes insipidus that happens during pregnancy. It also occurs when an enzyme made by the placenta destroys the vasopressin before the baby is born. Primary polydipsia is another condition also called psychogenic polydipsia or dipsogenic diabetes insipidus. The condition can cause a large amount of diluted urine. This form of diabetes insipidus is caused by excessive intake of fluids rather than an issue with damage or vasopressin production. Prolonged excessive water intake can suppress ADH and cause kidney damage, and therefore the body cannot concentrate urine. Other causes or primary polydipsia include mental illness and abnormal thirst.

Symptoms of Diabetes Insipidus
As mentioned, excessive thirst and frequent urination are the main symptoms of diabetes insipidus.

Other symptoms related with diabetes insipidus include:

Bed-wetting
Colorless urine instead of pale yellow
Constipation
Frequent desire to wake up throughout the night to urinate
Young children and infants will also experience unusually:

Wet diapers
Delayed growth
Weight loss
Dry skin with cool extremities
Inconsolable crying or unexplained fussiness
Vomiting
Diarrhea
Fever
Others will also experience dehydration, and if the person loses too much water, they may also show signs of irritability, muscle pains, lethargy, and unexplained weakness.

How Is Diabetes Insipidus Diagnosed?
There are a number of ways diabetes insipidus is diagnosed. For instance, a fluid deprivation test can help differentiate between the types of diabetes insipidus, including an ADH production defect (central diabetes insipidus), a defect in the kidney response to ADH (nephrogenic diabetes insipidus), or excessive fluid intake (primary polydipsia). The test will measure changes in urine output and urine composition when fluids are withheld. Sometimes blood ADH levels are also measured during a fluid deprivation test.

Diabetes insipidus is also sometimes determined when urine is less concentrated in a urinalysis test. A magnetic resonance imagining (MRI) of the brain is also considered a non-invasive test that can help detect pituitary gland abnormalities related to central diabetes insipidus. Genetic screening may also be suggested in those with a family history of diabetes insipidus.

Without diabetes insipidus treatment, the condition can lead to fatigue, weight loss, increased heart rate, low body temperature, chronic dehydration, consistent headaches, low blood pressure, brain damage, and kidney damage.

The most common conventional treatments will depend on the type of diabetes insipidus:

Central diabetes insipidus
Treatment is usually desmopressin--a synthetic replacement for vasopressin that reduces urine production. People should only take desmopressin as needed since taking excessive desmopressin can result in low sodium levels in the blood and large amounts of water retention. Low sodium symptoms include nausea, confusion, lethargy, and possibly seizures.

Nephrogenic diabetes insipidus
Desmopressin is not a treatment option since the kidneys are not functioning properly from ADH. The main treatment options include water intake to avoid dehydration, a low-salt diet to lower the urine made by your kidneys, and a low protein diet. If symptoms don't stop, drugs are often given to reduce urine output, including thiazide diuretics, amiloride, and non-steroidal anti-inflammatory drugs (NSAIDs).

Gestational diabetes insipidus
Desmopressin is also used to treat gestational diabetes insipidus. The noted side effects of desmopressin include nausea, belly pain, headaches, vomiting, sudden face redness and a slight increase in blood pressure. In rare cases gestational diabetes insipidus is caused by a thirst mechanism abnormality, and in these cases desmopressin is not prescribed.

Primary polydipsia
The main diabetes insipidus treatment method involves reducing your fluid intake. However, when mental illness causes primary polydipsia, treating the mental illness may relieve the primary polydipsia symptoms.

Natural Treatments for Diabetes Insipidus
There are natural treatments available for diabetes insipidus, especially when it comes to diet changes. The best natural approach for diabetes insipidus treatment should be to address the symptoms of frequent urination and excessive thirst. The following are some natural diet changes that can go a long way:

The diabetes insipidus diet
This is a low-salt diet and low-protein diet. It is thought that eating salty foods will enhance thirst associated with diabetes insipidus. Excessive salt intake creates instant thirst that causes you to drink more than necessary. All salty snacks and foods should be eliminated from the diet such as pretzels, peanuts, potato chips, and condiments. Since people with diabetes insipidus may urinate more frequently, avoidance of salty foods helps prevent the problem from getting worse.

Although a low protein diet is also recommended, it is believed that it may lead to nutritional deficiencies. Overall, the diet should contain mostly nutrient-dense whole foods with plenty of water-heavy fruits and vegetables. The best water-based foods to include as part of the diabetes insipidus diet includes cucumbers, zucchini, radishes, blueberries, strawberries, sweet bell peppers, red cabbage, and dark green leafy vegetables such as spinach and kale.

Replenish with adequate fluids
It is important for those with nephrogenic diabetes insipidus to increase their water consumption. However, chronic water intake can be an issue with polydipsia and kidney damage. It is important for diabetes insipidus patients to drink enough liquids to replace their urine losses and to relieve excessive thirst. It is recommended that fluid replacement not exceed 500 ml to 750 ml per hour. It is a good idea to carry a water bottle with you to prevent dehydration associated with diabetes insipidus.

Vitamin D supplementation
In a published case study in the journal Archives of Diseases in Childhood, a patient with nephrogenic diabetes insipidus also featured low levels of vitamin D3 (cholecalciferol). It makes sense then that vitamin D3 supplementation would help balance the deficiency in those with nephrogenic diabetes insipidus.

Also Read : Why Women Need More Vitamin D

Herbal remedies
Diabetes insipidus natural treatments also include herbal remedies. In particular plantain, catechu, and black sesame seed are considered effective for excessive urination. Herbal remedies that are often used for excessive thirst include quince fruit seeds, Indian barberry, green cardamom peel, coriander seeds, lemon juice, tamarind pulp, mango tree young shoots, neem leaves, cucumber seeds, cloves, nutmeg, sandalwood, turmeric, holy basil, fennel seed, and mint leaves.

Homeopathic remedies
There are also some homeopathic remedies that can help relieve diabetes insipidus naturally. For instance, the remedy uranium nitrate can help treat excessive thirst and frequent urination related with diabetes insipidus. Phosphoric acid is also considered when the person with diabetes insipidus experiences symptoms of nervousness, anxiety, worry, and grief. Other appropriate homeopathic remedies for diabetes insipidus include causticum, silicea, strophanthus, phosphorus, lactic acid, and bryonia.

Lifestyle Changes for Diabetes Insipidus
There are key lifestyle changes that can help patients with diabetes insipidus, including:

Avoiding processed foods: Avoiding processed foods reduces your intake of sodium, and the chemicals and preservatives associated with packaged food items.
Removing caffeine from the diet: Try removing caffeine from the diet, especially coffee and carbonated soft drinks. Caffeine can also be found in chocolate, black tea, energy drinks, and over-the-counter drugs such as aspirin.
Final Thoughts on Diabetes Insipidus Treatment
Although nephrogenic diabetes insipidus and central diabetes insipidus can be difficult to treat, there are options that successfully treat the condition. To recap, the dietary options include a low-salt and low-protein diet. It is also important to consume a nutrient dense diet that is high in vegetables and fruits. It is a good idea to drink more water in the treatment of diabetes insipidus, especially with central diabetes insipidus.

Read Next:

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Sources for Today's Article:
Zelman, M., et al., Human Diseases: A Systemic Approach (Upper Saddle River: Pearson Education, 2015), 273.
"Treatments and drugs," Mayo Clinic web site, March 14, 2013; http://www.mayoclinic.org/diseases-conditions/diabetes-insipidus/basics/treatment/con-20026841.
"Diabetes insipidus," Mayo Clinic web site, March 14, 2013; http://www.mayoclinic.org/diseases-conditions/diabetes-insipidus/basics/causes/con-20026841.
Chapman, I.M., "Central Diabetes Insipidus (Vasopressin-Sensitive Diabetes Insipidus)," Merck Manual Professional Version web site; http://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/pituitary-disorders/central-diabetes-insipidus, last accessed October 20, 2015.
McMillan, J.I., "Nephrogenic Diabetes Insipidus," Merck Manual Professional Version web site; http://www.merckmanuals.com/professional/genitourinary-disorders/renal-transport-abnormalities/nephrogenic-diabetes-insipidus, last accessed October 20, 2015.
"Homeopathy for Diabetes," Hpathy.com, May 16, 2014; http://treatment.hpathy.com/homeo-medicine/homeopathy-diabetes/.
Katzir, Z., et al., "Nephrogenic diabetes insipidus, cystinosis, and vitamin D," Archives of Disease in Childhood, 1988; 63(5): 548-550.
Khardori, R., "Diabetes Insipidus Treatment & Management," Medscape web site; http://emedicine.medscape.com/article/117648-treatment, last accessed October 20, 2015.
"Natural Tips to Quench Excessive Thirst," Natural Fitness Tips web site; http://www.nftips.com/2014/06/natural-tips-to-quench-excessive-thirst.html, last accessed October 20, 2015.
"Diet for Diabetes Insipidus Insipidus," Diabetes Insipidus web site; http://diabetesinsipidus.org/diet-for-diabetes-insipidus, last accessed October 20, 2015.

Tags: DIABETES INSIPIDUS DIABETES INSIPIDUS DIET DIABETES INSIPIDUS NATURAL REMEDIES DIABETES INSIPIDUS NATURAL TREATMENTS DIABETES INSIPIDUS TREATMENT
Dr. Jeffrey Shapiro, MD
About the Author, Browse Jeffrey's Articles
After receiving athletic and academic awards at Yale and Stanford, Jeff has coached those seeking peak wellness, appeared on ABC News 20/20 and served as a consultant for CBS News 60 Minutes and The Late Show with David Letterman. As the author of many research studies and practicing anesthesiology/critical care medicine for more than 20 years, Jeff can be your guide to common sense decision making regarding drugs, supplements and vitamins.

With no corporate sponsors and no vitamins or supplements to sell, Jeff can tell the truth regarding marketing versus science.

Jeff's states: "my personal and selfish reason for speaking is that if I can convince a single person to make a healthier choice, it makes my day job (in the operating room) easier."

As the editor of The Vitamin Doctor, Dr. Shapiro uses this same "marketing versus science" approach to give you the straight facts on the vitamins and supplements you may be taking daily.




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Nephrogenic diabetes insipidus



Related Terms
Acquired nephrogenic diabetes insipidus, ADH-resistant diabetes insipidus, arginine vasopressin, AVP, diabetes insipidus renalis, hyperchloremia, hypernatremia, NDI, polydipsia, polyuria, vasopressin-resistant diabetes insipidus.

Background
Nephrogenic diabetes insipidus (NDI) is a rare disorder that is caused by large amounts of dilute urine produced by the nephrons, which are found in the kidneys. Normally, the kidneys control the concentration of the urine by absorbing water and returning it to the blood in response to the body's need for water. In a healthy person, an antidiuretic (urine-limiting) hormone called arginine vasopressin (AVP) sends a signal to the kidneys to control the concentration of urine. In patients with NDI, the kidneys are unable to respond to AVP, which causes a problem with water retention. A substantial amount of water that is needed by the body is lost in large quantities as dilute urine. This leaves NDI patients continuously thirsty and in danger of dehydration.
NDI may be either acquired or inherited. Acquired NDI is more common and is usually caused by certain drugs, severe dehydration, or an electrolyte imbalance, such as elevated sodium or chlorine levels in the blood. Inherited NDI is caused by defects in the AVPR2 or AQP2 genes. NDI can be inherited in an X-linked or an autosomal fashion. X-linked mutations are carried on the X chromosome, which is one of the two sex chromosomes. Females have two X chromosomes, whereas males have one X and one Y chromosome. Males are most likely to have symptoms of inherited X-linked NDI because they receive only one X chromosome, compared to females who inherit two X chromosomes. Autosomal mutations are located on one of the 22 non-sex chromosomes. Males and females are equally likely to display symptoms of the autosomal forms of inherited NDI because this form of the disorder is not linked to a sex chromosome.
Symptoms of NDI include extreme thirst (polydipsia), excessive urination (polyuria), short stature, and a failure to develop during infancy. NDI patients require a steady supply of water to alleviate their thirst and to prevent dehydration. With early diagnosis and proper management, the quality and duration of life can be normal for patients with NDI.
NDI is different from diabetes mellitus, which involves problems with insulin and blood sugar regulation. The symptoms can be similar and may include extreme thirst and frequent urination. However, NDI is related to how the kidneys handle fluids. Urine and blood tests can determine if a patient has NDI or diabetes mellitus.

Signs and symptoms
General: The main symptoms of nephrogenic diabetes insipidus (NDI) are extreme thirst (polydipsia) and excretion of large amounts of dilute urine (polyuria). The symptoms are similar for both the acquired and the inherited forms of the disease. When NDI is inherited, these symptoms appear at birth and are usually diagnosed before one year of age. When the condition is acquired, symptoms may not occur until adulthood.
Inherited NDI: Infants born with NDI may become dehydrated if they do not receive enough fluids to replace the water lost through the urine. If left untreated, NDI can cause brain damage and stunted growth. Symptoms in infants may include poor feeding and development, rapid onset of severe dehydration, and a swollen bladder caused by the high urine volume. Some infants also have vomiting, gagging, constipation or diarrhea, unexplained fevers, weakness, and irritability.
Acquired NDI: The initial symptoms of acquired NDI may include rapid onset of severe dehydration, vomiting, diarrhea, fever, seizures, or coma. Other symptoms may include a swollen kidney (hydronephrosis), a swollen ureter (hydroureter), and an abnormally large bladder (megalocystis). If a person has normal thirst mechanisms and drinks enough fluids, NDI may have no significant effects on the fluid and electrolyte balance of the body. If the person does not drink enough fluids, the high urine output may cause high blood sodium levels, dry skin, sunken eyes, fatigue, headache, irritability, low body temperature, muscle pains, rapid heart rate, weight loss, and shock.

Diagnosis
General: Nephrogenic diabetes insipidus (NDI) should be considered in people with polyuria (excessive urine production) and/or polydipsia (excessive thirst). Blood and urine tests are performed to test for abnormal levels of water, sodium, and arginine vasopressin (AVP).
Blood test: Blood is tested for sodium levels and plasma concentration, which is the ratio of plasma solutes to plasma solvent. Increased blood sodium or blood plasma concentration indicate NDI.
Urine test: Because output of a large volume of dilute urine is the main symptom of NDI, many types of urine testing are performed when diagnosing NDI. These include testing the total amount of urine produced in a 24-hour period and the concentration of the urine, which is measured by testing the urine specific gravity. In patients with NDI, the volume of urine is higher than normal, and the urine has a low concentration and specific gravity. Although an overnight urinary concentration test in female relatives has been proposed as a method of carrier detection, it has been proven unreliable. Failure to concentrate the urine normally in the presence of high blood AVP levels or when given desmopressin (DDAVP), a synthetic antidiuretic hormone, indicates NDI.
Water deprivation test: Patients with NDI tend to produce urine that has a low concentration despite being deprived of water. On administration of AVP, patients with NDI will show little or no increase in urine concentration. During the water deprivation test, the patient is carefully monitored to make sure his or her body weight and blood plasma concentration stay within a safe range. The patient goes without water for less than six hours while the blood plasma concentrations and urine volume are measured. If the patient has NDI, he or she will be resistant to the antidiuretic action of AVP. Immediately following the water deprivation period, a patient with NDI will still have concentrated blood plasma and dilute urine despite the fact that he or she will be fairly dehydrated at that point. At the end of the water fast, the patient's response to an infusion of DDAVP is measured. If the patient does not respond to DDAVP, he or she may have NDI. If the patient shows highly concentrated urine in response to DDAVP, he or she may have a different form of diabetes insipidus called pituitary diabetes insipidus, which is also called central or neurogenic diabetes insipidus. Following DDAVP administration, a patient with NDI caused by a mutant AQP2 gene will display an increased heart rate and blood pressure, whereas the patient who has NDI caused by a mutated V2R gene will not.
Ultrasound: An ultrasound may be performed to examine for swelling of the kidney, the urinary tract, and the bladder to establish the extent of disease in an individual diagnosed with NDI. Some degree of urinary tract swelling may be seen on ultrasound examination even in infants.
DNA test: If a person has a family history of NDI, a sample of the patient's blood is analyzed in a laboratory for the mutated AVPR2 or AQP2 genes. If a mutation is present, a positive diagnosis is made. Although a carrier does not have NDI disease, he or she may pass a copy of the mutated gene to his or her children. Molecular genetic testing of the AVPR2 gene detects approximately 95% of disease-causing mutations in individuals with X-linked NDI. Molecular genetic testing of the AQP2 gene detects about 95% of disease-causing mutations in individuals with autosomal recessive NDI.

Complications
Dehydration: Rapid and severe dehydration occurs when not enough water is consumed to make up for water lost in the urine. If this happens rapidly or if it is present for a long time, permanent brain damage and poor growth may occur. Dehydrated individuals may be treated with intravenous (IV) administration of normal saline, especially in emergency situations. However, saline infusion may elevate sodium in the blood to dangerous levels. Repeated or prolonged episodes of severe dehydration may result in seizures, shock, developmental delay, mental decline, and death.
Urinary tract swelling: The large and constant flow of urine over many years can expand the urinary tract and the bladder. This may cause a variety of potential problems, including rupture of the urinary tract, infection, pain, improper bladder function, and/or kidney failure. In addition, reversible NDI may progress to irreversible NDI in these patients.



Treatment


General: There is currently no known cure for nephrogenic diabetes insipidus (NDI). Treatment involves preventing dehydration by drinking water on a regular basis and especially at the first signs of thirst. In infants and children who may not readily communicate their thirst, water must be offered frequently, even during the night. Reducing or stopping medications that can cause NDI may improve symptoms. Friends, teachers, and neighbors should be educated about the condition. Infants and children should be monitored for abnormal growth and blood sodium concentrations and should have a yearly ultrasound evaluation to monitor for a swollen urinary tract. Continuous or intermittent bladder catheterization may be necessary when the bladder does not completely empty on its own.
Intravenous (IV) hydration: Healthcare providers generally treat dehydration with normal saline, which can be dangerous to individuals with NDI because of the sodium content. Acute blood loss or shock may be treated with isotonic fluid until the blood pressure and heart rate are stabilized, after which 2.5% dextrose in water is the preferred solution. Whenever possible, rehydration should occur through drinking water.
Drinking: The goal of treatment is to regulate fluid levels in the body. Treatment should involve regular intake of a high volume of fluid. The volume of fluids consumed should be about equal to the volume of urine produced.
Lifestyle changes: NDI patients require constant access to drinking water and toilet facilities, which may disrupt school and other social or group activities.
Patients with NDI are advised to adopt a low-sodium diet. A low-sodium diet maximizes the effectiveness of thiazide diuretics in reducing urine output. Although previously a diet low in protein was recommended for NDI patients, severe limitation of dietary protein may introduce nutritional deficiencies.
Diuretics: Thiazide (hydrochlorothiazide and chlorothiazide) and amiloride diuretics deplete total body salt, allowing the kidneys to more readily absorb water and decrease urine output. This improved water absorption can be reversed by consuming a high-salt diet. Therefore, low-sodium diets are prescribed for NDI patients. Thiazide diuretics may also deplete the body's stores of potassium. When taking thiazide diuretics, the patient's potassium levels must be monitored. To maintain sufficient potassium in the body, the addition of potassium supplements may be required. Combining a thiazide diuretic with a potassium-sparing diuretic (such as amiloride) may be more effective than using a thiazide alone. Sometimes thiazides are used in combination with the prostaglandin inhibitor, indomethacin, which treats pain.
Acquired NDI may be caused by taking lithium. Thiazide diuretics should be used with care in cases of lithium-induced NDI because they reduce the degree to which the kidney can excrete lithium. Amiloride is more widely used in these cases because it inhibits the accumulation of lithium while blunting lithium's inhibiting action on water reabsorption.
Nonsteroidal anti-inflammatory drugs (NSAIDs): NSAIDS, such as indomethacin, are often prescribed to improve the ability to concentrate urine and to reduce urine output in individuals with NDI. NSAIDs have been used individually and in combination with thiazide diuretics (with or without amiloride). Because NSAIDs have undesirable effects, such as gastric and renal tubular damage, and because the incidence of complications has not been studied in individuals with NDI, caution is warranted in the chronic use of NSAIDs for treatment of NDI. Indomethacin often causes headaches and dizziness and may increase the risk of gastrointestinal disorders. If administered in the first year of life, indomethacin increases the risk of kidney disease.

Integrative therapies
Traditional or theoretical uses lacking sufficient evidence:
Low sodium diet: Patients with nephrogenic diabetes insipidus (NDI) are advised to adopt a low-sodium diet. A low-sodium diet maximizes the effectiveness of thiazide diuretics in reducing urine output. Although previously a diet low in protein was recommended for NDI patients, severe limitation of dietary protein may introduce nutritional deficiencies.
Psychomotor therapy, physical therapy: Children with a history of severe dehydration, delayed development, or a delay in establishing the correct diagnosis and management of NDI should be considered for behavioral and physical therapy before school age.

Prevention
General: Prevention of nephrogenic diabetes insipidus (NDI) includes taking measures such as drinking water on a regular basis and especially at the first signs of thirst. In infants and children who may not communicate their thirst, water must be offered frequently, even during the night. Medications that could cause acquired NDI should be avoided in families at risk for the disease. Friends, teachers, and neighbors should be educated about the condition. Infants and children should be monitored for abnormal growth and blood sodium concentrations and should have a yearly ultrasound evaluation to monitor for a swollen urinary tract to prevent symptom development.
Genetic testing: Genetic testing may be performed to determine if a person carries the mutated genes that cause NDI. Although carriers do not have the disease, they may pass a copy of their mutated genes to their children. Genetic testing of children or newborns with NDI symptoms is valuable because early diagnosis and treatment can prevent the physical and mental decline associated with repeated episodes of dehydration.
Prenatal DNA testing may be performed if there is a family history of NDI. However, there are health risks associated with prenatal testing, including miscarriage. Therefore, patients should discuss the potential health risks and benefits with their healthcare provider before making any health-related decisions. A genetic counselor can also explain the different types of genetic tests, including their potential risks and benefits. These counselors can help patients understand the results and limitations of these tests.

Author information
This information has been edited and peer-reviewed by contributors to the Natural Standard Research Collaboration (www.naturalstandard.com).

Bibliography
Bichet DG. Nephrogenic diabetes insipidus. Adv Chronic Kidney Dis. 2006 Apr;13(2):96-104.
Garofeanu CG, Weir M, Rosas-Arellano MP, et al. Causes of reversible nephrogenic diabetes insipidus: a systematic review. Am J Kidney Dis. 2005 Apr;45(4):626-37.
Khanna A. Acquired nephrogenic diabetes insipidus. Semin Nephrol. 2006 May;26(3):244-8.
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The Diabetes Insipidus Foundation. .

Causes
General: The body naturally produces an antidiuretic or urine-limiting hormone called arginine vasopressin (AVP). AVP signals the kidneys to return water to the blood and helps to control the concentration of the urine. In people with nephrogenic diabetes insipidus (NDI), the kidneys cannot properly respond to this hormonal signal and produce abnormally high amounts of dilute urine. NDI may be either acquired or inherited.
Acquired NDI: Acquired NDI is usually caused by certain drugs, such as lithium and certain antibiotic, antifungal, chemotherapy, and antiviral drugs. It can also be caused by severe dehydration, urinary blockage, or an electrolyte imbalance, such as an elevated blood sodium level (hypernatremia) or an elevated blood chlorine level (hyperchloremia). When NDI is induced by a drug, the drug damages the kidneys in such a way that they are unable to respond to AVP. Disturbance of the aquaporin-2 shuttle, a channel that makes the kidneys collect more water, is the cause of acquired NDI.
Inherited NDI: Inherited NDI is caused by defects in either the AVPR2 or the AQP2 gene. About 90% of patients with inherited NDI are males with X-linked recessive NDI who have mutations in the AVP receptor 2 (AVPR2) gene, which provides instructions for making the AVP V2 receptor in the kidney. Other modes of inheritance are autosomal recessive (9%) or autosomal dominant (1%). These forms of the disease are caused by mutations in the aquaporin-2 (AQP2) gene, which provides instructions for making the vasopressin-sensitive water channel in the kidney. Males are more likely than females to be affected by inherited X-linked NDI, whereas males and females are equally likely to display symptoms of NDI that is inherited as an autosomal recessive or an autosomal dominant trait.

Risk factors
Acquired NDI: Acquired nephrogenic diabetes insipidus (NDI) is usually caused by certain drugs, such as lithium, demeclocycline, and aminoglycosides. It can also be caused by severe dehydration or an electrolyte imbalance, such as an elevated blood sodium level (hypernatremia) or elevated blood chlorine level (hyperchloremia).
Inherited NDI: Inherited NDI is caused by mutations or defects in the AVPR2 or AQP2 genes. NDI can be inherited in several ways. Most people inherit NDI as an X-linked recessive trait. About 90% of people with inherited NDI are males who have inherited the disease as an X-linked recessive trait. About 10% of people with inherited NDI inherit the disease as an autosomal recessive or autosomal dominant trait. X-linked recessive NDI is caused by mutations in the AVP receptor 2 (AVPR2) gene, which provides instructions for making the AVP V2 receptor in the kidney. Autosomal dominant and autosomal recessive forms of NDI are caused by mutations in the aquaporin-2 (AQP2), which provides instructions for making the AVP-sensitive water channel in the kidney.
X-linked inheritance: X-linked NDI is estimated to affect 1 in 200,000 males. Females have two X chromosomes while males have one X and one Y chromosome. Because males inherit an X chromosome from the mother and a Y chromosome from the father, males can only inherit X-linked diseases from the mother. In females who have one copy of the defective gene that causes NDI, the normal copy of the gene on the other X chromosome can compensate. Because males have only one X chromosome, they are more likely than females to show symptoms of X-linked NDI.
Females with one copy of the defective gene that causes NDI do not generally show symptoms but are called carriers because they may pass the defective gene to their children. If a female carrier has daughters with an unaffected male, their daughters have a 50% chance of being carriers for the disease. These daughters may show some symptoms, but are unlikely to have a serious form of the disease. If a female carrier has sons with an unaffected man, the sons have a 50% chance of getting the disease.
Autosomal recessive inheritance: To inherit NDI as an autosomal recessive trait, one must inherit two mutated alleles of the causative gene (one from each parent). A person who has only one mutated allele does not generally experience symptoms and is called a carrier. If one parent is a carrier, there is a 50% chance with each birth that the child will also be a carrier and a 0% chance that the child will inherit the disease. If both parents are carriers, there is a 25% chance with each birth that the child will inherit the disease and a 50% chance that each child will be a carrier.
Autosomal dominant inheritance: To inherit NDI as an autosomal dominant trait, one must inherit only one copy of the mutated gene for the disease to manifest. If one parent has the condition, therefore, there is a 50% chance that each of his/her children will have the disorder.

Types of the disease
Acquired NDI: Acquired nephrogenic diabetes insipidus (NDI) occurs more frequently than inherited NDI but is still a rare disorder. It is usually less severe than inherited NDI and can occur at any time during the life cycle. Acquired NDI is usually caused by certain drugs, such as lithium and certain antibiotic, antifungal, chemotherapy, and antiviral drugs. It can also be caused by severe dehydration, urinary blockage, or an electrolyte imbalance, such as an elevated blood sodium level (hypernatremia) or an elevated blood chlorine level (hyperchloremia). When NDI is induced by a drug, the kidneys become damaged in such a way that they are unable to respond to anti-diuretic hormone. Disturbance of the aquaporin-2 shuttle, a channel that makes the kidneys collect more water, is the cause of acquired NDI.
Acquired NDI can also occur as a consequence of more fundamental disorders, such as kidney disease, abnormally low levels of potassium, abnormally high levels of calcium, or sickle cell disease. Acquired NDI may also be caused by one or more of the ureters becoming blocked during pregnancy or as a result of protein starvation. Acquired NDI can be either permanent or temporary, depending on the length of exposure to the drug or condition that caused the symptoms to occur.
Inherited NDI: Inherited NDI is caused by defects in either the AVP receptor 2 gene (AVPR2) or theaquaporin-2 gene (AQP2). Approximately 90% of patients with inherited NDI are males with X-linked recessive NDI who have mutations in the AVPR2 gene, which provides instructions for making the AVP V2 receptor in the kidney. Other modes of inheritance are autosomal recessive (9%) or autosomal dominant (1%), in which the defective gene is AQP2, which provides instructions for making the vasopressin-sensitive water channel in the kidney. Males are more likely than females to be affected by X-linked NDI, whereas males and females are equally likely to display symptoms of the autosomal forms of inherited NDI.
Other: Some doctors have described a third type of NDI called partial NDI. Individuals with partial NDI are diagnosed later in childhood. These individuals usually do not have delayed growth or development, and they are able to concentrate the urine in response to dehydration but not as well as unaffected individuals.

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The information in this monograph is intended for informational purposes only, and is meant to help users better understand health concerns. Information is based on review of scientific research data, historical practice patterns, and clinical experience. This information should not be interpreted as specific medical advice. Users should consult with a qualified healthcare provider for specific questions regarding therapies, diagnosis and/or health conditions, prior to making therapeutic decisions.


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HOMOEO TRICKS



DIABETES INSIPIDUS


This condition is characterized by relative or absolute deficiency of ADH or inability of kidney to respond to normal ADH resulting in polyuria of very dilute urine with polydipsia.

ETIOLOGY (Causes of Diabetes Insipidus)
Central (neurogenic) diabetes insipidus (CDI)
Familial
Manifested as autosomal dominant
Associated with
Diabetes mellitus
Optic atrophy
Nerve deafness
Bladder atony
Acquired
Idiopathic
Tumor, e.g craniopharyngioma
Inflammatory e.g basal meningitis
Head trauma
Surgery causing disruption of pituitary
stalk
Irradiation
Sheehan s syndrome
Nephrogenic diabetes insipidus (NDI)
Familial
Manifested as sex-linked recessive
Acquired
Iatrogenic e.g lithium demeclocycline meth oxyflurane colchicine
After pyelonephritis
Polycystic kidney disease
Obstructive uropathy
Hypokalaemia
Hypercalcaemia
Sickie cell anaemia
PATHOLOGY
ADH regulatory mechanism
- Inappropriate ADH Secretion implies
Persistent release of ADH unrelated to plasma osmolarity.
- AS a conseqence, there is
Excessive reabsorption of water kidneys
Expansion of extracellular fluid volume
- These lead to
Haemodilution
Hyponatraemia
Inability to excrete dilute urine

Central (neurogenic) diabetes insipidus (CDI)
Complete or partial ADH deficiency
Results in polyuric state in which
- Kidney is unable to concentrate urine
- Large amounts of dilute urine are excreted
Nephrogenic diabetes insipidus (NDI)
ADH is produced normally
There is ineffectual response of ADH on distal tubule or Collecting tubule
ADH levels are elevated in face of
- Hypertonic plasma.
- Dilute urine.
CLINICAL FEATURES
Symptoms
Onset: Sudden or insidious
Polyuria
- Increased frequency, day and night
- May pass 15-20 liters of urine in 24 hours
Polydipsia
- Compensatory mechanism to prevent dehydration
- excessive incessant thirst
- Craving for ice- cold water
- Disturbs night sleep
- patient may consume in excess of 10 litres of fluid per day
- Attempts to limit fluid intake may lead to se vere dehydration
Other features
- Weakness
- Fatigue
- Irritability
- Muscular pains
- Headache
- Constipation
In prolonged cases
- Weight loss
- Exhaustion
- If intracranial tumor associated features of
- Increased intracranial tension
- Endocrine disturbances


Signs
- Drowsiness
- Sunken eyes
- Dry skin
- Dry tongue
- Temperature subnormal
- Pulse fast
- Blood pressure low
- Emaciation in prolonged cases
COMPLICATIONS
- Severe dehydration
- Shock
- Coma with or without convulsions
INVESTIGATIONS
- Diagnosis of DI requires assessment of ADH Secretion
- Random measurement of ADH is of little use
- Any ADH measurement must take into account serum and urine osmolarity.
Tests used are:
- Indirect test.
- Direct test.
Indirect or water deprivation test:
It is done by measuring effect of dehydration on serum and osmolarity.
It is called indirect because it measures effect of ADH, not level itself.
Patient is dehydrated until serum becomes hypertonic.
If the patient has DI
Specific gravity is not in creases by 50% in CDI.
Specific gravity is not increased in NDI.
After decompressing:
Produced anti -diuresis in CDI.
Failure of response indicates NDI.
Direct or hypertonic saline test:
It is done by measuring ADH after dehydration.
Patient is made hypertonic by saline infusion.
ADH levels are then measured.
In normal parsons
Serum ADH increases in relatively Linear Fashion with serum osmolarity .
In DI, this linearity is lost
If ADH levels are decreased, patient has CDI.
If ADH levels are elevated, patient has NDI.
Urinalysis :
Increased daily output.
Specific gravity low.
No sugar.
X-ray skull
Deformed or enlarged sella.
IVP shows :
Enlargement of ureters, kidneys, bladder.
PROGNOSIS
- Variable according to cause
If caused by tumor, it is reversible with surgery.
If caused by head trauma spontaneous recovery is likely within one year.
If caused by brain infection symptoms may persist indefinitely.
- Acute cases have better prognosis than those which start insidiously
- Patients who have an intact thirst mechanism
Do not require medication to live as long as they have free access to water.
However this can be very disruptive to their life style.
In due course of time can result in renal damage.
PREDOMINAT MIASM
- Sycotic disorder

THERAPEUTIC AIM
- To treat underlying cause, if possible.
- To replace hormone deficiency.
- To maintain baseline hormonal levels.
- To prevent/control complications.
GENERAL MANAGEMENT
- Maintain fluid, electrolyte balance.
- Monitor for signs of dehydration.
- Well balanced nutritious diet.

HOMEOPATHIC MEDICINE FOR DIABETES
Hormone replacement therapy.
Complimentary homeopathic drugs for symptomatic treatment
Arnica Montana (Head Trauma)
Arsenicum Album
Conium Maculatum (Tumor)
Gelsemium
Lachesis (sheehan's syndrome)
Natrium Sulphuricum (head trauma)
Phosporus
Phosphoric Acid
Pituitary Extract
Lycopodium
Thuja Occidentalis (anti-miasmatic)
Tuberculinum (basal meninggitis).




http://www.homoeotricks.com/diabetes-insipidus/

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Diabetes insipidus - Homeopathy Treatment and Homeopathic Remedies
Date: August 6, 2008 Author: Dr. Manish Bhatia
Diabetes insipidus (DI) is a condition characterized by excretion of large amounts of severely diluted urine, which cannot be reduced when fluid intake is reduced. It denotes inability of the kidney to concentrate urine. DI is caused by a deficiency of antidiuretic hormone (ADH), also known as vasopressin, due to the destruction of the back or "posterior" part of the pituitary gland where vasopressin is normally released from, or by an insensitivity of the kidneys to that hormone. It can also be induced iatrogenically by various drugs.

Signs and symptoms of Diabetes insipidus
Excessive urination and extreme thirst (especially for cold water and sometimes ice or ice water) are typical for DI. Symptoms of diabetes insipidus are quite similar to those of untreated diabetes mellitus, with the distinction that the urine is not sweet as it does not contain glucose and there is no hyperglycemia (elevated blood glucose). Blurred vision is a rarity. Signs of dehydration may also appear in some individuals since the body cannot conserve much (if any) of the water it takes in.

The extreme urination continues throughout the day and the night. In children, DI can interfere with appetite, eating, weight gain, and growth as well. They may present with fever, vomiting, or diarrhea. Adults with untreated DI may remain healthy for decades as long as enough water is drunk to offset the urinary losses. However, there is a continuous risk of dehydration.


Diagnosis for Diabetes insipidus
In order to distinguish DI from other causes of excess urination, blood glucose levels, bicarbonate levels, and calcium levels need to be tested. Measurement of blood electrolytes can reveal a high sodium level (hypernatremia as dehydration develops). Urinalysis demonstrates a dilute urine with a low specific gravity. Urine osmolarity and electrolyte levels are typically low.

A fluid deprivation test helps determine whether DI is caused by:

excessive intake of fluid
a defect in ADH production
a defect in the kidneys' response to ADH
This test measures changes in body weight, urine output, and urine composition when fluids are withheld and as dehydration occurs. The body's normal response to dehydration is to concentrate urine and conserve water, so urine becomes more concentrated and urination becomes less frequent. Those with DI continue to urinate large amounts of dilute urine in spite of not drinking any fluids. Sometimes measuring blood levels of ADH during this test is also necessary.

To distinguish between the main forms, desmopressin stimulation is also used; desmopressin can be taken by injection, a nasal spray, or a tablet. While taking desmopressin, a patient should drink fluids or water only when thirsty and not at other times, as this can lead to sudden fluid accumulation in central nervous system. If desmopressin reduces urine output and increases osmolarity, the pituitary production of ADH is deficient, and the kidney responds normally. If the DI is due to renal pathology, desmopressin does not change either urine output or osmolarity.

If central DI is suspected, testing of other hormones of the pituitary, as well as magnetic resonance imaging (MRI), is necessary to discover if a disease process (such as a prolactinoma, or histiocytosis, syphilis, tuberculosis or other tumor or granuloma) is affecting pituitary function. Thankfully most people with this form either have experienced past head trauma or simply have stopped ADH production for no apparent reason.

Habit drinking (in its severest form termed psychogenic polydipsia) is the most common imitator of diabetes insipidus at all ages. While many adult cases in the medical literature are associated with mental disorders, most patients with habit polydipsia have no other detectable disease. The distinction is made during the water deprivation test, as some degree of urinary concentration above isosmolar is usually obtained before the patient becomes dehydrated.


Pathophysiology
Electrolyte and volume homeostasis is a complex mechanism that balances the body's requirements for blood pressure and the main electrolytes sodium and potassium. In general, electrolyte regulation precedes volume regulation. When the volume is severely depleted, however, the body will retain water at the expense of deranging electrolyte levels.

The regulation of urine production occurs in the hypothalamus, which produces antidiuretic hormone (ADH or vasopressin) in the supraoptic and paraventricular nuclei. After synthesis, the hormone is transported in neurosecretory granules down the axon of the hypothalamic neuron to the posterior lobe of the pituitary gland where it is stored for later release. In addition, the hypothalamus regulates the sensation of thirst in the ventromedial nucleus by sensing increases in serum osmolarity and relaying this information to the cortex.

The main effector organ for fluid homeostasis is the kidney. ADH acts by increasing water permeability in the collecting ducts and distal convoluted tubule, specifically it acts on proteins called aquaporins which open to allow water into the collecting duct cells. This increase in permeability allows for reabsorption of water into the bloodstream, thus concentrating the urine.

There are several forms of DI:

Central diabetes insipidus is due to damage to the hypothalamus or pituitary due to a tumor, stroke, neurosurgery or some rather rare causes (which include hemochromatosis, sarcoidosis, histiocytosis, diseases that can form masses in the vicinity like a tuberculoma or syphilis and some genetic disorders). If the hypothalamus is damaged, the feeling of thirst may be completely absent.
Nephrogenic diabetes insipidus is due to the inability of the kidney to respond normally to ADH. There are hereditary causes (90% are due to mutations of the ADH V2 receptor, and 10% mutations of the aquaporin 2 water channel), but these are rare (incidence is around 4 per million live births). Most are male, because V2 receptor mutations are x-linked recessive defects. More common are acquired forms of NDI, which occur as a side-effect to some medications (such as lithium citrate and amphotericin B), as well as in polycystic kidney disease (PKD) and sickle-cell disease, and electrolyte disturbances such as hypokalemia and hypercalcemia. In some cases, no cause is found.
Dipsogenic DI is due to a defect or damage to the thirst mechanism, which is located in the hypothalamus. This defect results in an abnormal increase in thirst and fluid intake that suppresses ADH secretion and increases urine output. Desmopressin is ineffective, and can lead to fluid overload as the thirst remains.
Gestational DI only occurs during pregnancy. While all pregnant women produce vasopressinase in the placenta, which breaks down ADH, this can assume extreme forms in GDI. Most cases of gestational DI can be treated with desmopressin. In rare cases, however, an abnormality in the thirst mechanism causes gestational DI, and desmopressin should not be used.

Treatment of Diabetes insipidus
Central DI and gestational DI respond to desmopressin. Also gestational DI tends to abate on its own 4 to 6 weeks following labour, though some women may develop it again in subsequent pregnancies. In dipsogenic DI, desmopressin is not usually an option.

Desmopressin will be ineffective in nephrogenic DI. Instead, the diuretic hydrochlorothiazide (HCT or HCTZ) or indomethacin can improve nephrogenic diabetes insipidus; HCT is sometimes combined with amiloride to prevent hypokalemia. Again, adequate hydration is important for patients with DI, as they may become dehydrated easily.

Homeopathy Treatment for Diabetes insipidus
Keywords: homeopathy, homeopathic, treatment, cure, remedy, remedies, medicine

Homeopathy treats the person as a whole. It means that homeopathic treatment focuses on the patient as a person, as well as his pathological condition. The homeopathic medicines are selected after a full individualizing examination and case-analysis, which includes the medical history of the patient, physical and mental constitution, family history, presenting symptoms, underlying pathology, possible causative factors etc. A miasmatic tendency (predisposition/susceptibility) is also often taken into account for the treatment of chronic conditions. A homeopathy doctor tries to treat more than just the presenting symptoms. The focus is usually on what caused the disease condition? Why 'this patient' is sick 'this way'. The disease diagnosis is important but in homeopathy, the cause of disease is not just probed to the level of bacteria and viruses. Other factors like mental, emotional and physical stress that could predispose a person to illness are also looked for. No a days, even modern medicine also considers a large number of diseases as psychosomatic. The correct homeopathy remedy tries to correct this disease predisposition. The focus is not on curing the disease but to cure the person who is sick, to restore the health. If a disease pathology is not very advanced, homeopathy remedies do give a hope for cure but even in incurable cases, the quality of life can be greatly improved with homeopathic medicines.

The homeopathic remedies (medicines) given below indicate the therapeutic affinity but this is not a complete and definite guide to the homeopathy treatment of this condition. The symptoms listed against each homeopathic remedy may not be directly related to this disease because in homeopathy general symptoms and constitutional indications are also taken into account for selecting a remedy. To study any of the following remedies in more detail, please visit the Materia Medica section at www.Hpathy.com.

None of these medicines should be taken without professional advice and guidance.

Homeopathy Remedies for Diabetes insipidus :
Apis., apoc., kali-n., phos., squil., uran-n.



http://www.doctorbhatia.com/diseases-and-treatment/endocrine-disorders/diabetes-insipidus-homeopathy-treatment-and-homeopathic-remedies/

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Lifestyle and home remedies
By Mayo Clinic Staff

If you have diabetes insipidus:

Prevent dehydration. As long as you take your medication and have access to water when the medication's effects wear off, you'll prevent serious problems. Plan ahead by carrying water with you wherever you go, and keep a supply of medication in your travel bag, at work or at school.
Wear a medical alert bracelet or carry a medical alert card in your wallet. If you have a medical emergency, a health care professional will recognize immediately your need for special treatment.


http://www.mayoclinic.org/diseases-conditions/diabetes-insipidus/basics/lifestyle-home-remedies/con-20026841

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Thomas, 1907: the Eclectic Practice of Medicine. > Part VI - Constitutional Diseases. >


Diabetes Insipidus.

Synonyms.--Polyuria; Hydruria; Hyperuresis; Diuresis.
Definition.--A constitutional disease characterized by an excessive flow of urine of low specific gravity, and devoid of sugar and albumin, thirst, and loss of flesh and strength.
Etiology.--Age predisposes to diabetes insipidus, it being more frequent during childhood and early maturity, the disease becoming more rare after reaching the age of thirty. Heredity also plays an important part. Weil notes twenty-three cases in a family running back four generations. It has occurred during' convalescence of acute infectious diseases, and is often associated with abdominal tumors, tuberculosis, and syphilis. The ingestion of large quantities of water or malt liquors, is not infrequently followed by polyuria.
Disorders of the nervous system, however, are more largely responsible than all other causes combined. Bernard discovered a spot in the floor of the fourth ventricle of animals, which, when irritated, is followed by polyuria. Tumors of the brain, blows on the head, great mental excitement, fright, sunstroke, apoplexy, and paralysis of the sixth nerve, have all been followed by diabetes insipidus. Epileptics not infrequently have this lesion.
Pathology.--No characteristic anatomical lesions are found. In some cases the bladder is hypertrophied owing to constant overdistention. The ureters and pelvis of the kidneys have been found dilated, due to backward pressure due to an overdistended bladder. The kidneys are sometimes enlarged and congested. Various lesions of the nervous system have been found, but none peculiar to polyuria.
Symptoms.--Diabetes insipidus may come on gradually or develop suddenly. When due to shock or traumatism, it develops quickly, otherwise it is insidious in its appearance. The patient's attention is first attracted to the disease by the frequent calls to urinate and the large quantity voided, and that he is compelled to micturate several times during the night. The urine is clear, light in color, and of low specific gravity, ranging from 1,001 to 1,008, and varying in quantity from three to thirty quarts every twenty-four hours. Thirst is a prominent symptom, and large quantities of water are consumed. The mouth, owing to deficient secretion of saliva, becomes dry, and the skin is dry and constricted. Usually there is but little disturbance of the digestive system, although persistent constipation, due to the excessive quantity of water voided, is a common feature.
The only complaint made by the patient is that of aching in the loins and weariness on slight exertion. Although there is gradual loss of flesh, there is not the emaciation that is seen in diabetes mellitus. The surface and the extremities are inclined to be cool, and a subnormal temperature is not uncommon.
The course of the disease depends to a great extent upon the primary lesion. Where due to tuberculosis or organic disease of the brain or abdomen, the general health fails, the patient becomes much emaciated, and the disease terminates fatally in from a few months to one or two years, while in idiopathic cases, the patient may live for years in comparatively good health.
Diagnosis.--The large quantity of urine voided, the low specific gravity and absence of sugar, enables one to recognize diabetes insipidus from diabetes mellitus, and the continued polyuria day after day enables one to recognize it from polyuria due to hysteria, which is always more or less transient.
Prognosis.--When due to organic lesions of the brain or abdomen, the prognosis is unfavorable. If idiopathic, the patient may live for years and enjoy comparatively good health, and a good per cent of cases will entirely recover.
Treatment.--The idiopathic form of the disease yields readily to medication, which is simple and positive.
Belladonna.--A belladonna plaster is ordered across the loins, and the specific tincture of belladonna given internally. Ten to fifteen drops of the specific tincture are added to four ounces of water, and a teaspoonful given every three hours. Where there is a feeble capillary circulation, this remedy will not disappoint in its action.
Rhus Aromatica.--This is an excellent remedy in polyuria, but should be given in fifteen to twenty drop doses, four times a day. Ergot in drop doses every hour is also a good agent in many cases. A general tonic treatment is frequently very beneficial in bringing; about a cure. In addition to the tonic diuretics, hydrangia, collinsonia, hamamelis, achillea, and like remedies, the administration of the compound tonic mixture (the triple phosphate of iron, quinia, and strychnia), in half teaspoonful doses, will give good results.
The diet should be nourishing, but easily digested, and as little fluid taken as is consistent with good health. Moderate exercise in the open air, and a sponge-bath daily, is to be advised. An equable climate assists materially in effecting a cure.
The Eclectic Practice of Medicine, 1907, was written by Rolla L. Thomas, M. S., M. D.



http://www.henriettes-herb.com/eclectic/thomas/diabetes-insi.html

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Urinating Too Much?
What is the best treatment for diabetes insipidus? Is there any cure? What are the best herbs to use?


A
Answer (Published 1/27/2009)
Diabetes insipidus (DI) is a rare disease that causes increased urination (indeed, the literal meaning of the Greek term "diabetes" is "excessing urine discharge"). The kind of diabetes that we usually encounter is diabetes mellitus (from the Greek word for "sweet"), also known as DM and "sugar diabetes." In DM, the increased urinary output is a symptom of excess sugar in the blood (and urine) due to problems with insulin, whereas in DI, the urine is insipid (tasteless) because it is very dilute. The large volume excreted is mostly water. Blood sugar and insulin levels are normal in DI, which has nothing in common with DM except the name.

Related Weil Products
Weil Vitamin Advisor for Diabetes - If you have type II diabetes, a healthful diet and lifestyle and specific supplements and herbs may help manage symptoms. Learn more and get your free, personalized vitamin and supplement recommendation today from the Weil Vitamin Advisor.
There are several forms of DI. The most common is called central or pituitary DI and stems from damage to the pituitary gland as a result of head injury, brain surgery or, sometimes, a tumor. The disease can run in families and can also be caused by certain drugs like lithium. In 25 percent of all cases, no cause can be found.

Whatever the cause, the pituitary damage disrupts the normal release of antidiuretic hormone (ADH). Made in the adjacent hypothalamus, ADH is stored in the pituitary and released into the bloodstream as necessary. It controls water balance in the body by directing the kidneys to reabsorb water and decrease urinary output when necessary. The ADH deficiency that characterizes DI results in constant water loss through excessive production of dilute urine. Affected individuals may feel thirsty all the time. The frequent urination continues at night, disrupting sleep and, sometimes, causing bedwetting. And you risk dehydration if you don't drink enough water to make up for what you lose. (Always have a water supply with you.)

If the symptoms don't bother you, you may not need treatment - but you should see your physician for regular monitoring. When necessary, pituitary DI is treated with the synthetic hormone desmopressin, in the form of a nasal spray. It acts much like natural ADH. I'm afraid I know of no herbs or supplements that can aid in the treatment of any form of DI.

Andrew Weil, M.D.



http://www.drweil.com/drw/u/QAA400516/Urinating-Too-Much-Diabetes-Insipidus.html

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Urocyon's Meanderings
"The Truth Shall Make Ye Fret." -- T. Pratchett

Vicious circles: Diabetes, and vitamin and mineral deficiencies


This started out as an endnote to another post I'm working on, and kept growing. It's important enough stuff to move over to a post of its own, anyway.

Diabetes can lead to lots of nutritional deficiencies, through obvious mechanisms such as peeing out lots of vitamins and minerals. Very few doctors seem to even think about how frequently this happens. I had to figure out and correct these deficiencies on my own.

Polyuria will pretty obviously mess up your electrolyte balance-a lot like a stomach virus, or sweating really heavily-and you also pee out an awful lot of water-soluble vitamins. The more you drink to make up for losing fluid, the more vitamins and minerals you end up losing in urine. Apparently, "thiamine concentration in blood plasma was decreased 76% in type 1 diabetic patients and 75% in type 2 diabetic patients", regardless of blood glucose management. Diabetic kidneys are a little too good at filtering it out. I would be amazed if other B vitamins were not similarly affected. Being low on B vitamins will also make you depressed and tired all the time.

I got symptoms of more than one B vitamin deficiency (there's a lot of overlap in symptoms, and they work togther a lot), including signs of full-blown "dry" beriberi: "However, because doctors may not consider beriberi in non-alcoholics, this diagnosis is often missed." As another overview points out: "Probably the best diagnostic test is a good clinical response to administration of thiamine." I feel confident saying that this was the problem, because my system did respond quickly to thiamine supplementation.

Like with potassium and especially magnesium, getting low on B vitamins can make your blood glucose control much worse, setting up a vicious cycle. Lack of all these nutrients will also cause muscle spasms/pain/weakness, besides hypertension and any number of cardiovascular and neurological problems generally written off as diabetic complications. Making sure you have enough thiamine can fend off all kinds of cellular damage from high blood glucose. Low magnesium and potassium levels are risk | factors for developing Type 2 diabetes and high blood pressure in the first place, and are also implicated in any number of "diabetic complications". Besides hideous muscle cramps, I started getting disturbing heart arrhythmias which went away within an hour when I took in enough combined potassium and magnesium.

Here's one interesting article I ran across, illustrating some connections: Hypertension, Hypokalemia, and Thiazide-Induced Diabetes: A 3-Way Connection:

Hypertension treated with thiazides [diuretics], especially in higher doses, can cause hypokalemia. Hypokalemia, in turn, can aggravate hypertension and also lead to diabetes mellitus via mechanisms discussed in the text. Diabetes, in turn, can cause hypertension, and people with hypertension are more likely to get diabetes mellitus. Correcting potassium stores may, therefore, be beneficial for both diabetes mellitus and hypertension.

From another article, "38% of diabetic outpatient clinic visits involve hypomagnesemia". "Also hypomagnesemia is related to thiamine deficiency because magnesium is needed for transforming thiamine into thiamine pyrophosphate." It's all connected. You can substitute magnesium in that above study, just as easily (there has been similar research). Also, if you are low on magnesium, you can't use your potassium properly; this happens with other nutrients, too, like a chain missing links. Being low on potassium will also make you insatiably thirsty, which will make you pee out more nutrients; it's also easy to blame on the diabetes itself, and took me a while to figure out.

This is one of the reasons the renewed all-or-nothing sodium hating here in the UK appalls me; it's all about balance between electrolytes, and the ones trying to scare people away from sodium bloody well ought to know this by now. My mom almost killed herself ca. 1980, when they were still pushing this approach back in the US: she was told "cut out the salt, or DIE!" and wound up in the hospital over it. She took the ill-considered advice seriously and stayed away from things like tomatoes (high in both sodium and potassium!), and baked her own salt-free bread; high doses of diuretics probably helped, as well. ´Most of the seriously impairing "side effects" she experienced later, for many years, can easily be attributed to serious dehydration and electrolyte imbalances-no doubt lack of some vitamins, as well-from the combo of diuretics and increasingly-difficult-to-manage diabetes.

That includes the same near-constant feverish feeling and flu-like symptoms I also experienced for nigh on 15 years. I assumed I just had a lousy immune system (like my mom's) and kept catching colds and flu, until I replaced some minerals. So far this winter, I have had one cold.

Even without diabetes to make people excrete more magnesium and reduce their stores, a lot of people are low on it. Intensive farming practices without proper replacement have led to serious soil depletion of a lot of minerals, so we get much less in foods than was the case even 50 years ago. Note how over this same time period, a number of chronic illnesses, including diabetes, cardiovascular problems, and osteoporosis have gone "epidemic". In the US, "According to recent USDA surveys, the average intake of magnesium by women 19 to 50 years of age was about 74 percent of the RDA. Men of the same age got about 94 percent of the recommended amount. About 50 percent of women had intakes below 70 percent of their RDA."

Looking at the UK, "Dietary intakes of magnesium in the United States have been declining over the last 100 years from about 500mg/day to 175-225mg/day (10) and a recent national survey suggested that the average magnesium intake for women is as low as 228mgs per day (11). But since this figure is derived using a one-day diet recall method, it may actually be an overestimate of actual magnesium intakes (12). Meanwhile, the UK's Food Standards Agency estimates that the average daily intake of magnesium in Britain for both men and women is just 227mgs - only two thirds of the US recommended daily amount (RDA)." The picture looks similar elsewhere, from quick glances while looking for those figures.

Diabetes is associated with a disturbingly long list of complications. That's what will reduce your lifespan. Having seen how this played out with relatives and other people she knew suffering a lot, and then dying early, was what made my mom's diabetes diagnosis more frightening than the later cancer one; she was suicidal for weeks after hers got diagnosed. (If you think you're inevitably going to get serious neuropathic pain, lose your feet, and die of a heart attack if you're lucky, why not?!) Most people-including medical professionals, who should know better by now-just think of these complications as the unavoidable wages of diabetes. (This is also related to the atmosphere of blame around Type 2 diabetes, but that is a different story.) From the research I have done, it looks as though pretty much all of this suffering is preventable, and I can't help but get frustrated and sad about how little attention this gets in the trenches.

Throw in malabsorption from Glucophage/metformin, and you can quickly have a real mess. It can also interfere with thiamine, and given that a lot of the malabsorption is caused by chronic | explosive diarrhea, fat-soluble vitamins are also affected. Metformin carries warnings about B12 and folic acid deficiency-and the rest ought to be obvious!-but not many doctors even seem to be considering this when people come in with blatant deficiency symptoms. I know this firsthand. Not only was I sick the whole time I took the stuff, to the point that I almost stopped leaving the house, my glucose control got really horrible-and the GP kept telling me the "side effects" would subside with time.

Right now, I'm making sure to eat enough salt (got headaches, nausea, and strange dreams before thinking of this!), drinking a lot of tomato juice with a pinch of Epsom salts and KCl salt substitute added, and taking a lot of supplements. Benfotiamine ("a fat-soluble composition and is better absorbed and utilized") seems to be the way to go if you think you're low on thiamine-which you probably are if you're diabetic. I also take a mutivitamin and high-potency B complex, just in case.

Not surprisingly, I'm feeling a lot better in general these days. It's only been about a month since I recognized the need to get more potassium and (even more) magnesium, and that greatly improved the hideous leg/hip muscle spasms I'd been getting again (much like what Kaninchen ZERO describes as "turning to stone"). The difference was clear: drink some doctored tomato juice, be able to go lie down and go to sleep within an hour! I remembered to order in more benfotiamine last week-having stopped taking it because things had improved so much before-and by the next day after taking it again, a lot of the residual leg/hip cramping was gone. My mood started improving, too, and I'm experiencing much less fatigue and brain fog.

Also see The Role of Magnesium in Fibromyalgia, and Association between magnesium intake and depression and anxiety in community-dwelling adults: the Hordaland Health Study. I also wonder about how much muscle wasting-especially involving limbs-among diabetics is really coming from nutrient deficiencies known to cause this. I am hoping to be able to get back some of the muscle mass I've lost, now that I'm not seriously malnourished.

At this point, I am wondering whether I ever had "mild" generalized tardive dystonia, or whether the problems with muscle tone and spasm-which started when I was on medications known for doing that-have mostly been coming from drug-induced diabetes. Time and continued improvement of my nutritional status will tell.

ETA 13 July 2011: I forgot to update this earlier, but noticed that it had gotten a number of hits today. The pain and spasms did improve for a while with the supplements I talked about in this post, but never got totally better and came back worse than before. I kept wondering what I was doing wrong, and got very discouraged. Besides the factors mentioned here-which still play in-it turns out that I have had a confirmed underlying vitamin D deficiency and osteomalacia from it, causing low blood levels of calcium and magnesium. The effects of hypocalcemia and hypomagnesemia look very similar, which is probably how I missed the low calcium symptoms before.

For an overview of how calcium, magnesium, and vitamin D interact in the body, see Magnesium: A Key to Calcium Absorption, Taking Calcium with Magnesium Is CRUCIAL to Absorb that Calcium and Take Magnesium AND Vitamin D To Avoid Vitamin D Side Effects, also Magnesium is more than a co-factor for vitamin D. They all work together (along with trace minerals and some vitamins), and if you are not getting enough magnesium you won't be able to absorb and use the vitamin D or calcium properly-and so forth. The minerals are electrolytes, and being low on them or otherwise having them out of balance will send your whole neuromuscular system haywire from improper electrical conduction.

All this can cause severe muscle spasms, cramps, twitches, passing-out level menstrual cramps and flooding from that, migraines and cluster headaches, even seizures, and pain which is often dismissed and misdiagnosed-since vitamin D deficiency is frequently considered a much rarer problem than it really is, so they don't even check for that. That is also very dangerous, because your heart is a muscle too, besides all the research showing that these deficiencies contribute to/cause a lot of chronic illnesses and cancers. (I will try to add a link here when I finish a post on vitamin D deficiency and chronic pain, but I did talk about that some in the earlier post linked above.) This reached a crisis point, to the point of a pelvic fracture from getting kicked by the dog (!), after years of living in the UK and not getting nearly as much sun exposure as my burn-resistant "Mediterranean" skin type needs. I thought I was getting enough vitamin D from a 100% RDA cod liver oil capsule, and also had a seriously false sense of security because my skin is as light as most native British people's when I have been out of the sun for a long time. (In reality, UV treatment for both skin problems and vitamin D synthesis is calculated to the point of a very mild burn, so if you tan easily and do not burn easily, you will need a lot more exposure than someone who does burn more quickly.) Also, it seems that the majority of the White British population is low on vitamin D year round-and no wonder!

But now that I know the symptoms and more about how vitamin D works, I suspect this has been going on, to one degree or another, for about 15 years, since I got put on medications that made me photosensitive and prone to overheating in the sun. So, if you're on any that will do that, please watch out! There are also not that many food sources, and requirements are turning out to be higher than most doctors still think, as I went into some in the vitamin D post linked above.

My blood sugar control also seems to have improved a lot. I was very frustrated and more than a little scared before, since nothing I did (besides taking Januvia/sitagliptin when I was back in the US) made much difference to my blood sugar levels. None of the things that are supposed to help, did, including a very low carb diet. Vitamin D deficiency is also linked to insulin resistance (through causing magnesium deficiency, at least partly, no doubt) and poor glucose control in diabetics. For more info, please have a look at Vitamin D and Diabetes: Let the Sunshine In. Their summary:

Vitamin D is an important nutrient for all persons, particularly for those with diabetes. Epidemiologic evidence suggests that an adequate intake of vitamin D may prevent or delay the onset of diabetes. There is also evidence to indicate that it may help to reduce some of the complications associated with diabetes (cardiovascular disease, renal insufficiency, and peripheral neuropathies). Small clinical studies have demonstrated that vitamin D may help with metabolic control, particularly as it relates to beta cell function. The information regarding vitamin D receptor activity as well as the genetic variations that may predispose individuals to problems with vitamin D synthesis and utilization will be important areas of clinical research.

It appears that diet alone will not provide sufficient amounts of vitamin D, and that treatment with supplements is probably necessary for most individuals with diabetes. However, given the possible benefit, it may be an easy and cost-effective therapy which could improve their long-term health outcomes as well as their quality of life.

(Earlier) Edit: A very relevant link I ran across a while after posting this: Diabetes on rise in young aboriginal women:

"Diabetes is a disease of young First Nations adults with a marked predilection for women; in contrast, diabetes is a disease of aging non-First Nations adults that is more common in men," Dr. Roland Dyck of Royal University Hospital in Saskatoon and his coauthors wrote...

A tuberculosis survey of 1,500 First Nations people in 1937, for example, did not detect diabetes. By 1990, almost 10 per cent of the province's native people had diabetes, and by 2006, 20 per cent did...

"What is clear is that the rapid appearance of Type 2 diabetes particularly among First Nations people and other indigenous and developing populations has been precipitated by environmental rather than genetic factors," the researchers said.

Eating a more traditional diet seems to help. The Tohono O'odham on the U.S. side of the border are well known as the group with the world's highest rate of Type 2 diabetes-estimated at 80%-while their relatives on the other side have a fifth the rate. A lot in the U.S. are also fatter than they used to be. The apparent difference? Living more traditional lifestyles, with access to more traditional foods. I can't find the reference right now, but I saw one study admitting that "you're fat and diabetic because you're lazy and don't go to the gym" was a very bad (and lazy) assumption; someone working at the health clinic bothered to find out what people were actually doing, and most were pretty physically active in their everyday lives-doing heavy gardening work, walking some distance to go fishing, etc. If there had been a gym readily available there at that point, they'd have been too busy working their asses off to go there! (In other words, about what I would expect.) The kneejerk blaming is persistent, though, as ideology-based approaches to the world usually are.

As far as I can tell, the current "more saturated fat leading to obesity and heart problems" dogma (not necessarily based in reality, when people were eating a lot of fatty foods before!) is far less applicable here than the fact that traditional foods are much richer in all kinds of nutrients. There's also the slow-release carbohydrate factor from whole grains and tubers to take into account. Tying back in well, beans, nuts, sunflower seeds, pumpkin seeds, fruits, and assorted green leafy stuff will give you an awful lot of magnesium and potassium-among other good things!-and I have been eating more of all of them. They're also delicious. :)

There's an amazing variety of nuts back home -even after the chestnuts got blight, and many kinds of nut trees plundered for timber-and they used to be a staple. Now they are very expensive if you can't gather them yourself, so people eat other things which are not nearly as nutritious. Nuts are just one example.

And, in another example of truly wrong-headed advice, the NHS diabetic nutrition sheet I was given (which did not even distinguish between Type 1 and Type 2) warned people to eat things like nuts and salmon maybe once a week if they must eat them at all, because of the (rich in omega-3) fat content. Thank goodness I knew better, in general; it made me feel sorry for the majority who wouldn't.





https://urocyon.wordpress.com/2010/01/18/diabetes-and-vitamin-and-mineral-deficiencies/