Tag: Food and Drug Administration

Electro-Convulsive Therapy

Post author By Mukul
Post date April 19, 2011
No Comments on Electro-Convulsive Therapy

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Definition:
Electroconvulsive therapy (ECT) is a procedure in which electric currents are passed through the brain, deliberately triggering a brief seizure. Electroconvulsive therapy seems to cause changes in brain chemistry that can immediately reverse symptoms of certain mental illnesses. It often works when other treatments are unsuccessful.

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Electroconvulsive therapy (ECT), formerly known as electroshock, is a psychiatric treatment in which seizures are electrically induced in anesthetized patients for therapeutic effect. Its mode of action is unknown. Today, ECT is most often recommended for use as a treatment for severe depression which has not responded to other treatment, and is also used in the treatment of mania and catatonia. It was first introduced in the 1938 and gained widespread use as a form of treatment in the 1940s and 1950s.

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Informed consent is a standard of modern electroconvulsive therapy. According to the Surgeon General, involuntary treatment is uncommon in the United States and is typically only used in cases of great extremity, and only when all other treatment options have been exhausted and the use of ECT is believed to be a potentially life saving treatment. However, caution must be exercised in interpreting this assertion as, in an American context, there does not appear to have been any attempt to survey at national level the usage of ECT as either an elective or involuntary procedure in almost twenty years. In one of the few jurisdictions where recent statistics on ECT usage are available, a national audit of ECT by the Scottish ECT Accreditation Network indicated that 77% of patients who received the treatment in 2008 were capable of giving informed consent

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Electroconvulsive therapy can differ in its application in three ways: electrode placement, frequency of treatments, and the electrical waveform of the stimulus. These three forms of application have significant differences in both adverse side effects and positive outcomes. After treatment, drug therapy is usually continued, and some patients receive continuation/maintenance ECT. In the United Kingdom and Ireland, drug therapy is continued during ECT.

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The treatment involves placing electrodes on the temples, on one or both sides of the patient’s head, and delivering a small electrical current across the brain, with the patient sedated or under anaesthetic. The aim is to produce a seizure lasting up to a minute, after which the brain activity should return to normal. Patients may have one or more treatment a week, and perhaps more than a dozen treatments in total.

Although ECT has been used since the 1930s, there is still no generally accepted theory to explain how it works. One of the most popular ideas is that it causes an alteration in how the brain responds to chemical signals or neurotransmitters.

Why & when it is done?
Electroconvulsive therapy (ECT) can provide rapid, significant improvements in severe symptoms of a number of mental health conditions. It may be an effective treatment in someone who is suicidal, for instance, or end an episode of severe mania.

ECT is used to treat:
*Severe depression, particularly when accompanied by detachment from reality (psychosis), a desire to commit suicide or refusal to eat.

*Treatment-resistant depression, long-term depression that doesn’t improve with medications or other treatments.

*Schizophrenia, particularly when accompanied by psychosis, a desire to commit suicide or hurt someone else, or refusal to eat.

*Severe mania, a state of intense euphoria, agitation or hyperactivity that occurs as part of bipolar disorder. Other signs of mania include impaired decision making, impulsive or risky behavior, substance abuse and psychosis.

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*Catatonia, characterized by lack of movement, fast or strange movements, lack of speech, and other symptoms. It’s associated with schizophrenia and some other psychiatric disorders. In some cases, catatonia is caused by a medical illness.

Electroconvulsive therapy is sometimes used as a last-resort treatment for:

#Treatment-resistant obsessive compulsive disorder, severe obsessive compulsive disorder that doesn’t improve with medications or other treatments

#Parkinson’s disease, epilepsy, and certain other conditions that cause movement problems or seizures

*Tourette syndrome that doesn’t improve with medications or other treatments

ECT may be a good treatment option when medications aren’t tolerated or other forms of therapy haven’t worked. In some cases ECT is used:

#During pregnancy, when medications can’t be taken because they might harm the developing fetus

#In older adults who can’t tolerate drug side effects

#In people who prefer ECT treatments over taking medications

#When ECT has been successful in the past

Risk factor:–
Patients are given short-acting anaesthetics, muscle relaxants and breathe pure oxygen during the short procedure in order to minimise the risks. However, although ECT is much safer than it was, there are still side effects to the treatment. The most common are headache, stiffness, confusion and temporary memory loss on awaking from the treatment – some of these can be reduced by placing electrodes only on one side of the head. Memory loss can be permanent in a few cases, and the spasms associated with the seizure can cause fractured vertebrae and tooth damage. However, the recommended use of muscle relaxant nowadays makes the latter a very rare occurrence. Patients can also experience numbness in the fingers and toes.

The death rate from ECT used to be quoted as one for every 1,000 patients, but with smaller amounts of electric current used in modern treatments, accompanied by more safety techniques, this has been reduced to as little as four or five in 100,000 patients.

Recomendations:–
A common argument against ECT is that it destroys brain cells, with experiments conducted on animals in the 1940s often cited as evidence. However, modern studies have yet to reproduce these findings in the human brain.

Some activists, however, still campaign against the widespread use of ECT in psychiatry, quoting those cases which have resulted in long-term damage or even death, whether because of the built-in chance of problems, or through errors by doctors.

Experts say that given the correct staff training, and when used for the right clinical conditions, ECT can ‘dramatically’ benefit the patient. An audit of ECT in Scotland between February 1996 and August 1999 said concerns about unacceptable side effects, effectiveness of the treatment and disproportionate use on elderly people were ‘largely without foundation’.

It said that in nearly three quarters of cases people with depressive illness showed ‘a definite improvement’ after ECT. Women were more likely to receive the treatment than men, but the auditors said this was because they were twice as likely to suffer from depression. Only 12 per cent of patients who got ECT were aged over 75. However, the Royal College of Psychiatrists has admitted that in the past the treatment has been administered by untrained, unsupervised junior doctors. However, modern guidelines have changed this and ECTAS (ECT Accreditation Services) exist to check that such treatment is being given safely and efficiently.

Guidelines on ECT from NICE (2003) recommend that it’s used only to achieve rapid and short-term improvement of severe symptoms after an adequate trial of other treatment. options has proven ineffective and/or when the condition is considered to be potentially life-threatening, in individuals with:

•Severe depressive illness
•Catatonia
•Prolonged or severe manic episode

NICE also says that ‘valid consent should be obtained in all cases where the individual has the ability to grant or refuse consent. The decision to use ECT should be made jointly by the individual and the clinician(s) responsible for treatment, on the basis of an informed discussion. This discussion should be enabled by the provision of full and appropriate information about the general risks associated with ECT and about the risks and potential benefits specific to that individual. Consent should be obtained without pressure or coercion, which may occur as a result of the circumstances and clinical setting, and the individual should be reminded of their right to withdraw consent at any point. There should be strict adherence to recognised guidelines about consent and the involvement of patient advocates and/or carers to facilitate informed discussion is strongly encouraged.’

Click to learn more in detail about Electro-Convulsive Therapy

You may click to see:-

Keep fighting even when depression treatments don’t work
Video:Electroconvulsive therapy

DSM-IV Codes
Harold A. Sackeim
Insulin shock therapy
History of electroconvulsive therapy in the United Kingdom
Psychiatric survivors movement
Consumer/Survivor/Ex-Patient Movement
List of people who have undergone electroconvulsive therapy

Resources:
http://www.mayoclinic.com/health/electroconvulsive-therapy/MY00129
http://www.bbc.co.uk/health/physical_health/conditions/electro_convulsive_therapy.shtml
http://en.wikipedia.org/wiki/Electroconvulsive_therapy

http://www.minddisorders.com/Del-Fi/Electroconvulsive-therapy.html

Electroconvulsive Therapy Under New Scrutiny (webmd.com)
The effectiveness of electroconvulsive therapy: A literature review (bipolarblast.wordpress.com)
FDA mulls future of electroshock therapy (cnn.com)
Shock Therapy: Old Treatment, New Scrutiny (cbsnews.com)
“FDA says ECT machines should undergo rigorous testing” and related posts (media-dis-n-dat.blogspot.com)
FDA panel deems electroshock devices high risk (cnn.com)
What Kind of Therapy is Out There? (try-therapy.com)
The Facts about Dysphoric Mania (brighthub.com)
Depression and Electroshock: 10 Surprising Truths (cbsnews.com)
Wednesday – Must be ECT Day (suddenlybipolar.wordpress.com)

Tags Askari, Behavior, Boston, Cognitive behavioral therapy, Compulsive behavior, Derealization, ECT, Electroconvulsive therapy, Exposure and response prevention, Exposure therapy, Food and Drug Administration, Fridays (TV series), Health, Major depressive disorder, Mania, Mental disorder, Obsessive Compulsive Disorder, Royal College of Psychiatrists

Ailmemts & Remedies

Cushing’s syndrome

Alternative Names: Itsenko-Cushing syndrome, hyperadrenocorticism or hypercorticism
Definition:
Cushing’s syndrome is a hormone disorder caused by high levels of cortisol in the blood. This can be caused by taking glucocorticoid drugs, or by tumors that produce cortisol or adrenocorticotropic hormone (ACTH) or CRH

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Cushing’s disease refers to one specific cause of the syndrome, a tumor (adenoma) in the pituitary gland that produces large amounts of ACTH, which in turn elevates cortisol. It is the most common cause of Cushing’s syndrome, responsible for 70% of cases.

This pathology was described by Harvey Cushing in 1932.

Cushing’s syndrome is not confined to humans and is also a relatively common condition in domestic dogs and horses.

Treatments for Cushing’s syndrome can return your body’s cortisol production to normal and noticeably improve your symptoms. The earlier treatment begins, the better your chances for recovery.

Symptoms:
SymptomsMost people with Cushing syndrome will have:

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•Upper body obesity (above the waist) and thin arms and legs
•Round, red, full face (moon face)
•Slow growth rate in children

Skin changes that are often seen:
•Acne or skin infections
•Purple marks (1/2 inch or more wide) called striae on the skin of the abdomen, thighs, and breasts
•Thin skin with easy bruising

Muscle and bone changes include:
•Backache, which occurs with routine activities
•Bone pain or tenderness
•Collection of fat between the shoulders (buffalo hump)
•Thinning of the bones, which leads to rib and spine fractures
•Weak muscles

Woman with cushing syndrome often have:

•Excess hair growth on the face, neck, chest, abdomen, and thighs
•Menstrual cycle becomes irregular or stops

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Men may have:
•Decreased fertility
•Decreased or no desire for sex
•Impotence

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Other symptoms that may occur with this disease:
*Mental changes, such as depression, anxiety and irritability or changes in behavior
*Fatigue
*Headache
*High blood pressure
*Increased thirst and urination
*Muscle weakness
*Loss of emotional control
*Cognitive difficulties
*New or worsened high blood pressure
*Glucose intolerance that may lead to diabetes
*Headache
*Bone loss, leading to fractures over time

Iatrogenic Cushing’s syndrome (caused by treatment with corticosteroids) is the most common form of Cushing’s syndrome. The incidence of pituitary tumors may be relatively high, as much as one in five people, but only a minute fraction are active and produce excessive hormones.

Adults with the disease may also have symptoms of extreme weight gain, excess hair growth in women, high blood pressure, and skin problems. In addition, they may show:

*muscle and bone weakness
*osteoporosis
*diabetes mellitus
*hypertension
*moodiness, irritability, or depression
*sleep disturbances
*menstrual disorders such as amenorrhea in women and decreased fertility in men
*baldness
*hypercholesterolemia

Cause:
There are several possible causes of Cushing’s syndrome.

Exogenous vs. endogenous Hormones that come from outside the body are called exogenous; hormones that come from within the body are called endogenous.

The most common cause of Cushing’s syndrome is exogenous administration of glucocorticoids prescribed by a health care practitioner to treat other diseases (called iatrogenic Cushing’s syndrome). This can be an effect of steroid treatment of a variety of disorders such as asthma and rheumatoid arthritis, or in immunosuppression after an organ transplant. Administration of synthetic ACTH is also possible, but ACTH is less often prescribed due to cost and lesser utility. Although rare, Cushing’s syndrome can also be due to the use of medroxyprogesterone.

Endogenous Cushing’s syndrome results from some derangement of the body’s own system of secreting cortisol. Normally, ACTH is released from the pituitary gland when necessary to stimulate the release of cortisol from the adrenal glands.

*In pituitary Cushing’s, a benign pituitary adenoma secretes ACTH. This is also known as Cushing’s disease and is responsible for 70% of endogenous Cushing’s syndrome.

*In adrenal Cushing’s, excess cortisol is produced by adrenal gland tumors, hyperplastic adrenal glands, or adrenal glands with nodular adrenal hyperplasia.

*Finally, tumors outside the normal pituitary-adrenal system can produce ACTH that affects the adrenal glands. This final etiology is called ectopic or paraneoplastic Cushing’s syndrome and is seen in diseases like small cell lung cancer.

Pseudo-cushing’s syndrome:
Elevated levels of total cortisol can also be due to estrogen found in oral contraceptive pills that contain a mixture of estrogen and progesterone. Estrogen can cause an increase of cortisol-binding globulin and thereby cause the total cortisol level to be elevated. However, the total free cortisol, which is the active hormone in the body, as measured by a 24 hour urine collection for urinary free cortisol, is normal.

Pathophysiology:
The hypothalamus is in the brain and the pituitary gland sits just below it. The paraventricular nucleus (PVN) of the hypothalamus releases corticotropin-releasing hormone (CRH), which stimulates the pituitary gland to release adrenocorticotropin (ACTH). ACTH travels via the blood to the adrenal gland, where it stimulates the release of cortisol. Cortisol is secreted by the cortex of the adrenal gland from a region called the zona fasciculata in response to ACTH. Elevated levels of cortisol exert negative feedback on the pituitary, which decreases the amount of ACTH released from the pituitary gland. Strictly, Cushing’s syndrome refers to excess cortisol of any etiology. One of the causes of Cushing’s syndrome is a cortisol secreting adenoma in the cortex of the adrenal gland. The adenoma causes cortisol levels in the blood to be very high, and negative feedback on the pituitary from the high cortisol levels causes ACTH levels to be very low. Cushing’s disease refers only to hypercortisolism secondary to excess production of ACTH from a corticotrophic pituitary adenoma. This causes the blood ACTH levels to be elevated along with cortisol from the adrenal gland. The ACTH levels remain high because a tumor causes the pituitary to be unresponsive to negative feedback from high cortisol levels.

Cushing’s Syndrome was also the first autoimmune disease identified in humans.

Diagnosis:-
When Cushing’s syndrome is suspected, either a dexamethasone suppression test (administration of dexamethasone and frequent determination of cortisol and ACTH level), or a 24-hour urinary measurement for cortisol offer equal detection rates. Dexamethasone is a glucocorticoid and simulates the effects of cortisol, including negative feedback on the pituitary gland. When dexamethasone is administered and a blood sample is tested, high cortisol would be indicative of Cushing’s syndrome because there is an ectopic source of cortisol or ACTH (e.g.: adrenal adenoma) that is not inhibited by the dexamethasone. A novel approach, recently cleared by the US FDA, is sampling cortisol in saliva over 24 hours, which may be equally sensitive, as late night levels of salivary cortisol are high in Cushingoid patients. Other pituitary hormone levels may need to be ascertained. Performing a physical examination to determine any visual field defect may be necessary if a pituitary lesion is suspected, which may compress the optic chiasm causing typical bitemporal hemianopia.

When any of these tests are positive, CT scanning of the adrenal gland and MRI of the pituitary gland are performed to detect the presence of any adrenal or pituitary adenomas or incidentalomas (the incidental discovery of harmless lesions). Scintigraphy of the adrenal gland with iodocholesterol scan is occasionally necessary. Very rarely, determining the ACTH levels in various veins in the body by venous catheterization, working towards the pituitary (petrosal sinus sampling) is necessary.

Mnemonic:
C – Central obesity, Cervical fat pads, Collagen fibre weakness, Comedones (acne)
U – Urinary free cortisol and glucose increase
S – Striae, Suppressed immunity
H – Hypercortisolism, Hypertension, Hyperglycemia, Hypercholesterolemia, Hirsutism
I – Iatrogenic (Increased administration of corticosteroids)
N – Noniatrogenic (Neoplasms)
G – Glucose intolerance, Growth retardation

Treatment:-
Most Cushing’s syndrome cases are caused by steroid medications (iatrogenic). Consequently, most patients are effectively treated by carefully tapering off (and eventually stopping) the medication that causes the symptoms.

If an adrenal adenoma is identified it may be removed by surgery. An ACTH-secreting corticotrophic pituitary adenoma should be removed after diagnosis. Regardless of the adenoma’s location, most patients will require steroid replacement postoperatively at least in the interim as long-term suppression of pituitary ACTH and normal adrenal tissue does not recover immediately. Clearly, if both adrenals are removed, replacement with hydrocortisone or prednisolone is imperative.

In those patients not suitable for or unwilling to undergo surgery, several drugs have been found to inhibit cortisol synthesis (e.g. ketoconazole, metyrapone) but they are of limited efficacy.

Removal of the adrenals in the absence of a known tumor is occasionally performed to eliminate the production of excess cortisol. In some occasions, this removes negative feedback from a previously occult pituitary adenoma, which starts growing rapidly and produces extreme levels of ACTH, leading to hyperpigmentation. This clinical situation is known as Nelson’s syndrome.

Lifestyle and home remedies:-

The length of your recovery from Cushing’s syndrome will depend on the severity and cause of your condition. Remember to be patient. You didn’t develop Cushing’s syndrome overnight and your symptoms won’t disappear overnight, either. In the meantime, these tips may help you on your journey back to health.

*Increase activities slowly. You may be in such a hurry to get your old self back that you push yourself too hard too fast, but your weakened muscles need a slower approach. Work up to a reasonable level of exercise or activity that feels comfortable without overdoing it. You’ll improve little by little, and your persistence will be rewarded.

*Eat sensibly. Nutritious, wholesome foods provide a good source of fuel for your recovering body and can help you lose the extra pounds that you gained from Cushing’s syndrome. Make sure you’re getting enough calcium and vitamin D. Taken together, they help your body absorb calcium, which can help strengthen your bones, counteracting the bone density loss that often occurs with Cushing’s syndrome.

*Monitor your mental health. Depression can be a side effect of Cushing’s syndrome, but it can also persist or develop after treatment begins. Don’t ignore your depression or wait it out. Seek help promptly from your doctor or a therapist if you’re depressed, overwhelmed or having difficulty coping during your recovery.

*Gently soothe aches and pains. Hot baths, massages and low-impact exercises, such as water aerobics and tai chi, can help alleviate some of the muscle and joint pain that accompanies Cushing’s syndrome recovery.

*Exercise your brain. If you’re recovering from any cognitive difficulties as a result of Cushing’s syndrome, mental exercises, such as math problems and crossword puzzles, may improve your brain function.

Coping and support:-
Support groups can be valuable in dealing with Cushing’s syndrome and recovery. They bring you together with other people who are coping with the same kinds of challenges, along with their families and friends, and offer a setting in which youe can share common problems.

Ask your doctor about support groups in your community. Your local health department, public library and telephone book and the Internet also may be good sources to find a support group in your area.

Prognosis:
Removing the tumor may lead to full recovery, but there is a chance that the condition will return.

Survival for people with ectopic tumors depends on the tumor type. Untreated, Cushing syndrome can be life-threatening.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://en.wikipedia.org/wiki/Cushing’s_syndrome
http://www.mayoclinic.com/health/cushings-syndrome/DS00470
http://www.nlm.nih.gov/medlineplus/ency/article/000410.htm
http://www.bbc.co.uk/health/physical_health/conditions/cushing1.shtml
http://nursingcrib.com/nursing-notes-reviewer/cushings-syndrome/
http://www.potbellysyndrome.com/documents/083EFB330BDDC27C6EEC8354AFFA139607633EB6.html
http://www.wrongdiagnosis.com/c/cushings_disease/book-diseases-7a.htm

http://www.nature.com/eye/journal/v20/n6/fig_tab/6701956f4.html

FDA review endorses efficacy of Novartis’ new drug for Cushing’s disease

Questions to Ask Your Doctor About Cushing’s Syndrome (everydayhealth.com)
How Stress Makes You Sick and Sad (psychologytoday.com)
What Exactly is Cushing’s Disease (dogfyi.wordpress.com)
When a Slow Metabolism Signals Illness (everydayhealth.com)
Fitness fanatic goes from size 10 to 18 in weeks after pituitary gland tumour (dailymail.co.uk)
Could My Daughter Have Cushing’s Disease? (everydayhealth.com)
Cortisol Levels and Weight Gain (bloomnaturalhealth.wordpress.com)
You: Book explains adrenal dysfunction; vegan magazine applauds herbivore heroes (washingtonpost.com)
Corcept Therapeutics Inc. Announces Key Secondary Endpoint Was Met in Phase 3 Study of Corlux for Cushing’s Syndrome (biospace.com)

Tags Adrenal gland, Adrenocorticotropic hormone, Cortisol, Cushing, Cushing's syndrome, European Medicines Agency, Food and Drug Administration, Health, Hsp90, Hypertension, Max Planck, Max Planck Institute of Psychiatry, Menstrual cycle, Munich, Nature Medicine, Osteoporosis, Pituitary gland, Silibinin

News on Health & Science

Health Claim Filed for Vitamin D

Post author By Mukul
Post date February 13, 2011
No Comments on Health Claim Filed for Vitamin D

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The Alliance for Natural Health USA is filing a Qualified Health Claim Petition with the FDA for vitamin D. For years, the FDA held that health claims could only be made if there was Significant Scientific Agreement (SSA) about the claim — a standard almost impossible to reach in science. Following court losses, the Agency finally acknowledged that consumers benefit from more information.
…..CLICK & SEE
As a result, the agency has established interim procedures whereby “qualified” health claims can be made, so long as the claims are not misleading.

According to the Alliance for Natural Health:
“It means that if the FDA accepts our petition, producers and sellers of vitamin D will be able to make certain specific claims about its ability to treat certain diseases or conditions.”

In the event you decide to supplement, vitamin D3 is 87 percent more potent at raising vitamin D blood levels than vitamin D2, according to a new study. Vitamin D3 also produces a 2- to 3-fold increase over D2 in the storage of the vitamin.

Scientists gave 33 healthy adults 50,000 International Units (IU) of either vitamin D2 or D3 each week for a total of 12 weeks. About 17 percent of the D3 ingested was stored by the subjects, and the rest was consumed or metabolized.

According to the study in the Journal of Clinical Endocrinology & Metabolism:

“Given its greater potency and lower cost, D3 should be the preferred treatment option when correcting vitamin D deficiency.”

You should also be aware that if you use strong sunscreen, it can lead to vitamin D deficiency. Take the case of Tyler Attrill, a 12-year-old girl whose condition came to light when she failed to recover properly from surgery.

According to BBC News:
“Tyler Attrill used factor 50 cream which, according to her consultant, could have deprived her of the essential vitamin and caused the bone disease rickets.”

The condition, which is likely shared by many others, caused Tyler pain for a number of years before it was diagnosed.

Reources:
The Alliance for Natural Health January 18, 2011
Journal of Clinical Endocrinology & Metabolism December 22, 2010
BBC News January 19, 2011

Posted By Dr. Mercola.Feb 10. 2011

Essential Vitamins for Digestive Health (everydayhealth.com)
The Truth About Vtiamin D: Why You Need Vitamin D (webmd.com)
Choice pours scorn on ‘expensive lolly waters’ (theage.com.au)
Sprung: nutrient waters full of sugar (theage.com.au)
The Benefits of Vitamin D for Children (everydayhealth.com)
What is the best kind of vitamins for kids? (zocdoc.com)
Extra Calcium, Vitamin D No Bone Booster for Men (nlm.nih.gov)
Vitamin Pills Unnecessary-Researchers. (ramanan50.wordpress.com)
90 percent of Americans are nutrient deficient, but processed milk is not the answer (gracemedeirosmj.wordpress.com)
Ontario nixes funding for vitamin D tests (theglobeandmail.com)

Tags BBC NEWS, Ergocalciferol, Food and Drug Administration, Health claims on food labels, International unit, Journal of Clinical Endocrinology & Metabolism, United States, Vitamin

Ailmemts & Remedies

Adrenoleukodystrophy

Alternative Names: Adrenoleukodystrophy; Adrenomyeloneuropathy; Childhood cerebral adrenoleukodystrophy; ALD; Schilder-Addison Complex

Definition:
Adrenoleukodystrophy (ALD), is a rare, inherited disorder that leads to progressive brain damage, failure of the adrenal glands and eventually death. ALD is a disease in a group of genetic disorders called leukodystrophies. Adrenoleukodystrophy progressively damages the myelin sheath, a complex fatty neural tissue that insulates many nerves of the central and peripheral nervous systems. Without functional myelin, nerves are unable to aid in the conduction of an impulse, which leads to increasing disability.

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Patients with X-linked ALD have defects in the ATP-binding cassette, sub-family D (ALD), member 1 transporter protein, which is encoded by the ABCD1 gene. The ABCD1 (aka ALDP) protein is indirectly involved in the break down of very long-chain fatty acids (VLCFAs) found in the normal diet. Lack of this protein can give rise to an over-accumulation of VLCFAs which can lead to damage to the brain, adrenal gland, and peripheral nervous system.

There are several different types of the disease which can be inherited, but the most common form is an X-linked condition. X-linked ALD primarily affects males, but about one in five women with the disease gene develop some symptoms. Adrenomyeloneuropathy is a less-severe form of ALD, with onset of symptoms occurring in adolescence or adulthood. This form does not include cerebral involvement, and should be included in the differential diagnosis of all males with adrenal insufficiency. Although they share a similar name, X-linked ALD and neonatal adrenoleukodystrophy (NALD), a peroxisome biogenesis disorder, are completely different diseases.

Although this disorder affects the growth and/or development of myelin, leukodystrophies are different from demyelinating disorders such as multiple sclerosis where myelin is formed normally but is lost by immunologic dysfunction or for other reasons.

Causes:
There are several types of ALD, which may be inherited in two different ways, and which can cause different patterns of disease even among people in the same families.

ALD is most commonly inherited as an X-linked condition. This means the abnormal gene is found on the X chromosome.

Because women have two X chromosomes, they have a spare normal gene as well as the abnormal one, so generally only carry the condition (although they may have a mild form of the disease). Men have only one X, so they are affected by the condition.

X-linked ALD may occur in three forms, with onset of symptoms in either childhood or adulthood.

Neonatal ALD is much less common. In this type of ALD the faulty gene isn’t X-linked but is found on one of the other chromosomes. This means both boys and girls can be affected.

Symptoms:
Childhood cerebral type:

•Changes in muscle tone, especially muscle spasms and spasticity
•Crossed eyes (strabismus)
•Decreased understanding of verbal communication (aphasia)
•Deterioration of handwriting
•Difficulty at school
•Difficulty understanding spoken material
•Hearing loss
•Hyperactivity
•Worsening nervous system deterioration
*Coma
*Decreased fine motor control
*Paralysis
•Seizures
•Swallowing difficulties
•Visual impairment or blindness

Adrenomyelopathy:
•Difficulty controlling urination
•Possible worsening muscle weakness or leg stiffness
•Problems with thinking speed and visual memory

.
Adrenal gland failure (Addison type):

•Coma
•Decreased appetite
•Increased skin color (pigmentation)
•Loss of weight, muscle mass (wasting)
•Muscle weakness
•Vomiting

Diagnosis:
The diagnosis is established by clinical findings and the detection of serum very long-chain free fatty acid levels. MRI examination reveals white matter abnormalities, and neuro-imaging findings of this disease are somewhat reminiscent of the findings of multiple sclerosis. Genetic testing for the analysis of the defective gene is available in some centers.

Neonatal screening may become available in the future, which may permit early diagnosis and treatment.

Genetics:
X-linkedX-linked ALD (X-ALD) is the most common form of ALD. In X-ALD, the defective ABCD1 gene resides on the X chromosome (Xq28). The incidence of X-ALD is at least 1 in 20,000 male births.[6] The ABCD1 (“ATP-binding cassette, subfamily D, member 1”) gene was discovered in 1993 and codes for a peroxisome membrane protein necessary for the ?-oxidation of VLCFAs.

X-ALD is characterized by excessive accumulation of very long-chain fatty acids (VLCFA), which are fatty acids with chains of 25–30 carbon atoms. The most common is hexacosanoate, with a 26 carbon skeleton. The elevation in (VLCFA) was originally described by Moser et al. in 1981.[8] The precise mechanisms through which high VLCFA concentrations in affected organs cause the disease is still unknown.

Autosomal
Neonatal adrenoleukodystrophy (NALD) is one of three autosomal dominant disorders which belong to the Zellweger spectrum of peroxisome biogenesis disorders (PBD-ZSD).The other two disorders are Zellweger syndrome (ZS), and infantile Refsum disease (IRD). NALD is most frequently caused by mutations in the PEX1, PEX5, PEX10, PEX13, and PEX26 genes.

Treatment:
There’s no cure for ALD, and the nervous system progressively deteriorates, with death usually occurring between one and ten years after the start of symptoms.

Research suggests that a mixture of oleic acid and euric acid, known as Lorenzo’s oil, may delay or reduce symptoms in boys with X-linked ALD by lowering levels of VLCFAs. The most benefit is seen when the treatment is used before symptoms develop, before irreversible damage has occurred.

Bone marrow transplants have also been used with some success in boys in the early stages of X-linked ALD but are not without considerable risk. Newer treatments that may lower brain levels of VLCFA are being tested. Treatment with docosahexanoic acid (DHA) may help young children with neonatal ALD.

Genetic research has identified the transporter proteins and their faulty genes, starting the path towards gene therapy.

Research directions:
Active clinical trials are currently in progress to determine if the proposed treatments are effective:

*Glyceryl Trioleate (Lorenzo’s oil) for Adrenomyelneuropathy.
*Beta Interferon and Thalidomide This study is closed.
*Combination of Glyceryl Trierucate and Glyceryl Trioleate (Lorenzo’s Oil) in assymptomatic patients.
*Hematopoietic stem cell transplantation.

Prognosis:
Treatment is symptomatic. Progressive neurological degeneration makes the prognosis generally poor. Death occurs within one to ten years of presentation of symptoms. The use of Lorenzo’s Oil, bone marrow transplant, and gene therapy is currently under investigation.

Possible Complications:
•Adrenal crisis
•Vegetative state (long-term coma)

Prevention:
Genetic counseling is recommended for prospective parents with a family history of X-linked adrenoleukodystrophy. Female carriers can be diagnosed 85% of the time using a very-long-chain fatty acid test and a DNA probe study done by specialized laboratories.

Prenatal diagnosis of X-linked adrenoleukodystrophy is also available. It is done by evaluating cells from chorionic villus sampling or amniocentesis.

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/adrenoleukodystrophy1.shtml
http://en.wikipedia.org/wiki/Adrenoleukodystrophy
http://www.nlm.nih.gov/medlineplus/ency/article/001182.htm

http://health.bwmc.umms.org/imagepages/17277.htm

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Natural Chelation Nutrient To Clean Arteries

Post author By Mukul
Post date January 23, 2011
No Comments on Natural Chelation Nutrient To Clean Arteries

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These days, the prescribed solution in the United States for heart problems is often invasive, dangerous and expensive surgery, with dubious results. The New England Journal of Medicine says open-heart surgery “appears neither to prolong life nor prevent myocardial infarction (heart attack).” This is a serious procedure that at its best addresses only a small part of the vascular system, leaving the rest of the problem unresolved. That allows the condition that causes the buildup to continue, which can often lead to a deadly outcome.

Instead of surgery, there are natural solutions to clear your arteries of plaque buildup. It’s called oral chelation. Chelation flushes toxic metals, calcium, plaque buildup and cholesterol deposits from the walls of your arteries. Accumulation of these substances means your arteries are gradually hardening. Chelation can be administered orally or by intravenous injection.

Oral chelation is safe, proven effective and inexpensive. It is non-invasive. It works on your whole vascular system, not just a confined part of it as in open-heart or bypass surgery. By clearing all the arteries in your body—even the micro-arteries in your eyes—the procedure helps protect your brain and your heart.

The main nutrient in oral chelation is EDTA (ethylene diamine tetraacetic acid). Since it was discovered in 1930, EDTA has been universally proven as an effective chelator. The designation “chelator” means it pulls, claws and dissolves plaque in the arteries, so that it can be flushed out of the body with the aid of the kidneys. EDTA helps support the cardiovascular system by flushing out toxins and heavy metals.

Both the American Heart Association (AHA) and the U. S. Food and Drug Administration have approved the use of EDTA chelation therapy for the removal of lead, aluminum and cadmium poisoning from the vascular system. It has actually been found to be 300 times safer than aspirin. EDTA works by reaching every blood vessel in your body, from the largest artery to the tiniest capillary and arteriole. Most of these blood vessels are much too small or too deep within the brain or other organs to be reached safely by surgery or other methods.

You may click to see :

What is Chelation

Natural Chelation Therapy

Natural affordable Chelation for All

Chelation Therapy

Source :Better Health Research