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Herbs & Plants

American ginseng

 

Botanical Name: Panax quinquefolius
Family: Araliaceae ( ivy family)
Subfamily: Aralioideae
Genus: Panax
Species: P. quinquefolius
Kingdom: Plantae
Order: Apiales

Synonyms: Aralia quinquefolia. Five Fingers. Tartar Root. Red Berry. Man’s Health

Common Name: American  ginseng

Habitat :American ginseng is native to eastern North America, though it is also cultivated in places such as China,Korea and Japan. The plant grows in rich woods throughout eastern and central North America, especially along the mountains from Quebec and Ontario, south to Georgia.
Description:
American ginseng is a smooth herbaceous perennial herb, with a large, fleshy, very slow-growing root, 2 to 3 inches in length (occasionally twice this size) and from 1/2 to 1 inch in thickness. Its main portion is spindle-shaped and heavily annulated (ringed growth), with a roundish summit, often with a slight terminal, projecting point. At the lower end of this straight portion, there is a narrower continuation, turned obliquely outward in the opposite direction and a very small branch is occasionally borne in the fork between the two. Some small rootlets exist upon the lower portion. The colour ranges from a pale yellow to a brownish colour. It has a mucilaginous sweetness, approaching that of liquorice, accompanied with some degree of bitterness and a slight aromatic warmth, with little or no smell. The stem is simple and erect, about a foot high, bearing three leaves, each divided into five finely-toothed leaflets, and a single, terminal umbel, with a few small, yellowish flowers. The fruit is a cluster of bright red berrles….CLICK & SEE THE PICTURES

Cultivation: On account of the growing scarcity of the American Ginseng plant, experiments have been made by the State of Pennsylvania to determine whether it can be grown profitably, resulting in the conclusion that in five years, starting with seeds and one year plants (or sooner if a start were made with older plants), an acre of ground would yield a profit of 1,500 dollars, without allowance for rental, but many precautions are necessary for success. The cultivated plants produced larger roots than those of the wild plant.

In 1912 it was estimated that the acreage of cultivated Ginseng in the United States was about 150 acres, and it is calculated that to supply China with twenty million dollars’ worth of dry root would require the American growers to plant 1,000 acres annually for five years, before this estimated annual supply could be sold. The cultivation of Ginseng would therefore appear to offer a rich field to American agriculture. It presents, however, considerable difficulty, owing to the great care and special methods required and to the fact that it is a very slow-growing crop, so that rapid returns can hardly be anticipated, and it is doubtful if its cultivation can be carried on profitably except by specialists in the crop. None the less, the percentage returns for the industrious, patient and painstaking farmer are large, and the demand for a fine article for export is not at all likely to be exceeded by the supply.

Part Used: The Root.

Chemical Constituents: Like Panax ginseng, American ginseng contains dammarane-type ginsenosides, or saponins, as the major biologically active constituents. Dammarane-type ginsenosides include two classifications: 20(S)-protopanaxadiol (PPD) and 20(S)-protopanaxatriol (PPT). American ginseng contains high levels of Rb1, Rd (PPD classification), and Re (PPT classification) ginsenosides—higher than that of P. ginseng in one study.

A large amount of starch and gum, some resin, a very small amount of volatile oil and the peculiar sweetish body, Panaquilon. This occurs as a yellow powder, precipitating with water a white, amorphous substance, which has been called Panacon.

Medicinal uses:
American ginseng or Panax quinquefolius is commonly used as Chinese or herbal medicine. In Western medicine, it is considered a mild stomachic tonic and stimulant, useful in loss of appetite and in digestive affections that arise from mental and nervous exhaustion.

A tincture has been prepared from the genuine Chinese or American root, dried and coarsely powdered, covered with five times its weight of alcohol and allowed to stand, well-stoppered, in a dark, cool place, being shaken twice a day. The tincture, poured off and filtered, has a clear, light-lemon colour, an odour like the root and a taste at first bitter, then dulcamarous and an acid reaction.

There is no evidence that American ginseng is effective in those infected with the common cold. The effect of preventive use is not clear. When used preventively it makes no difference on the rate of infections. It also appears to have no effect on how bad the infections are. There is tentative evidence that it may lessen the length of sickness when used preventively.

For detail medicinal uses you may click & see 
Cautions: : Individuals requiring anti-coagulant therapy such as warfarin should avoid use of American ginseng. Not recommended for individuals with impaired liver or renal function. It is not recommended in those who are pregnant or breastfeeding. Other adverse effects include: headaches, anxiety, trouble sleeping and an upset stomach.

Recent studies have shown that through the many cultivated procedures that American ginseng is grown, fungal molds, pesticides, and various metals and residues have contaminated the crop. Though these contaminating effects are not considerably substantial, they do pose health concerns that lead to neurological problems, intoxication, cardiovascular disease, and cancer.

Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplement, it is always advisable to consult with your own health care provider.

Resources:
https://en.wikipedia.org/wiki/American_ginseng
http://www.botanical.com/botanical/mgmh/g/ginsen15.html

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Categories
Ailmemts & Remedies

Kidney transplant

Introduction:
A kidney transplant is an operation that places a healthy kidney in your body. The transplanted kidney takes over the work of the two kidneys that failed, and you no longer need dialysis.

CLICK  & SEE
During a transplant, the surgeon places the new kidney in your lower abdomen and connects the artery and vein of the new kidney to your artery and vein. Often, the new kidney will start making urine as soon as your blood starts flowing through it. But sometimes it takes a few weeks to start working.

If you have advanced and permanent kidney failure, kidney transplantation may be the treatment option that allows you to live much like you lived before your kidneys failed. Since the 1950s, when the first kidney transplants were performed, much has been learned about how to prevent rejection and minimize the side effects of medicines.

But transplantation is not a cure; it’s an ongoing treatment that requires you to take medicines for the rest of your life. And the wait for a donated kidney can be years long.

Many transplanted kidneys come from donors who have died. Some come from a living family member. The wait for a new kidney can be long. People who have transplants must take drugs to keep their body from rejecting the new kidney for the rest of their lives.

A successful transplant takes a coordinated effort from your whole health care team, including your nephrologist, transplant surgeon, transplant coordinator, pharmacist, dietitian, and social worker. But the most important members of your health care team are you and your family. By learning about your treatment, you can work with your health care team to give yourself the best possible results, and you can lead a full, active life.

Around 40 per cent of patients with end-stage renal failure (ESRF) need a transplant which frees people from the need for dialysis treatments.

A successful kidney transplant has ten times the function of dialysis (for example ten times the ability to remove toxins and extra water from the blood). It means that transplant patients have a better quality of life, with more energy than they did on dialysis.

How transplants work:-
An assessment is necessary to determine whether your body will accept an available kidney. This may require several visits over four to six months, and all potential recipients must be healthy enough for surgery.

Although there is no age limit, few units will transplant patients over 70 years – unless very fit.

If a family member, partner or friend wants to donate a kidney, they will need to be evaluated for general health too.

If there is no potential living donor, you will need to register with hospital and be put on a national waiting list to receive a kidney from a deceased donor. but this varies considerably around the country. Kidneys can also be donated by strangers.

If there is a suitable living donor, the operation can be scheduled in advance, when it suits both sides. If you’re on a waiting list for a deceased donor kidney, as soon as it becomes available, you must go to the hospital quickly – where a test is carried out to check the kidney won’t be rejected. If it’s suitable, the transplant can proceed. The operation usually takes three to four hours.

A surgeon places the new kidney inside your lower abdomen and connects the artery and vein of the new kidney to your artery and vein. Your blood flows through the new kidney, which makes urine, just like your own kidneys did when they were healthy. Unless they are causing infection or high blood pressure, your own kidneys are left in place.

During the operation, the transplant kidney is inserted into the lower abdomen and connected to an artery and vein (to the leg). The blood flows through the new kidney, which makes urine, just like the old kidneys did when they were healthy. The old kidneys are usually left in place.

CLICK & SEE

Often the new kidney will start making urine as soon as blood starts flowing through it, but about one third of patients will require dialysis for around a week. Most patients leave hospital two weeks after the operation.

To prevent the immune system from seeing the new kidney as foreign and rejecting it, you’ll have to take drugs that turn off (or suppress) your immune response (immunosupressants). It’s important to understand the instructions for taking these medicines before leaving hospital, as missing the tablets for just 24 hours can cause rejection and the loss of the kidney.

Recovery From Surgery:-
As after any major surgery, you’ll probably feel sore and groggy when you wake up. However, many transplant recipients report feeling much better immediately after surgery. Even if you wake up feeling great, you’ll need to stay in the hospital for about a week to recover from surgery, and longer if you have any complications.

Posttransplant Care:-
Your body’s immune system is designed to keep you healthy by sensing “foreign invaders,” such as bacteria, and rejecting them. But your immune system will also sense that your new kidney is foreign. To keep your body from rejecting it, you’ll have to take drugs that turn off, or suppress, your immune response. You may have to take two or more of these immunosuppressant medicines, as well as medications to treat other health problems. Your health care team will help you learn what each pill is for and when to take it. Be sure that you understand the instructions for taking your medicines before you leave the hospital.

If you’ve been on hemodialysis, you’ll find that your posttransplant diet is much less restrictive. You can drink more fluids and eat many of the fruits and vegetables you were previously told to avoid. You may even need to gain a little weight, but be careful not to gain weight too quickly and avoid salty foods that can lead to high blood pressure

Rejection:-
You can help prevent rejection by taking your medicines and following your diet, but watching for signs of rejection—like fever or soreness in the area of the new kidney or a change in the amount of urine you make—is important. Report any such changes to your health care team.

Even if you do everything you’re supposed to do, your body may still reject the new kidney and you may need to go back on dialysis. Unless your health care team determines that you’re no longer a good candidate for transplantation, you can go back on the waiting list for another kidney.

Side Effects of Immunosuppressants:
Immunosuppressants can weaken your immune system, which can lead to infections. Some drugs may also change your appearance. Your face may get fuller; you may gain weight or develop acne or facial hair. Not all patients have these problems, though, and diet and makeup can help.

Immunosuppressants work by diminishing the ability of immune cells to function. In some patients, over long periods of time, this diminished immunity can increase the risk of developing cancer. Some immunosuppressants cause cataracts, diabetes, extra stomach acid, high blood pressure, and bone disease. When used over time, these drugs may also cause liver or kidney damage in a few patients.

Hope through Research:-
The NIDDK, through its Division of Kidney, Urologic, and Hematologic Diseases, supports several programs and studies devoted to improving treatment for patients with progressive kidney disease and permanent kidney failure, including patients who receive a transplanted kidney.

•The End-Stage Renal Disease Program promotes research to reduce medical problems from bone, blood, nervous system, metabolic, gastrointestinal, cardiovascular, and endocrine abnormalities in kidney failure and to improve the effectiveness of dialysis and transplantation. The program seeks to increase kidney graft and patient survival and to maximize quality of life.

•The NIH Organ/Tissue Transplant Center, located at the NIH Clinical Center in Bethesda, MD, is a collaborative project of NIH, the Walter Reed Army Medical Center, the Naval Medical Research Center, and the Diabetes Research Institute at the University of Miami. The site includes a state-of-the-art clinical transplant ward, operating facility, and outpatient clinic designed for the study of new drugs or techniques that may improve the success of organ and tissue transplants.

•The U.S. Renal Data System (USRDS) collects, analyzes, and distributes information about the use of dialysis and transplantation to treat kidney failure in the United States. The USRDS is funded directly by NIDDK in conjunction with the Centers for Medicare & Medicaid Services. The USRDS publishes an Annual Data Report, which characterizes the total population of people being treated for kidney failure; reports on incidence, prevalence, mortality rates, and trends over time; and develops data on the effects of various treatment modalities. The report also helps identify problems and opportunities for more focused special studies of renal research issues.

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://www.topnews.in/health/kidney-transplant-patients-low-physical-activity-likely-die-early-211177
http://www.nlm.nih.gov/medlineplus/kidneytransplantation.html
http://www.kidney.niddk.nih.gov/kudiseases/pubs/transplant/
http://www.bbc.co.uk/health/physical_health/conditions/in_depth/kidneys/kidneys_transplant.shtml

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Categories
Ailmemts & Remedies

Gorlin syndrome

Alternative Names:Nevoid basal cell carcinoma syndrome (NBCCS),basal cell nevus syndrome, multiple basal cell carcinoma syndrome and Gorlin–Goltz syndrome

Definition:
Gorlin syndrome is an inherited medical condition involving defects within multiple body systems such as the skin, nervous system, eyes, endocrine system, and bones. People with this syndrome are particularly prone to developing a common and usually non-life-threatening form of non-melanoma skin cancers.

You may click to see more pictures of  Gorlin syndrome

People with the syndrome have a predisposition to multiple basal cell carcinomas (a form of skin cancer), jaw cysts and other generally harmless abnormalities in the bone. The severity of the disease can be wide-ranging.

About 10% of people with the condition do not develop basal cell carcinomas (BCCs). the name Gorlin syndrome refers to researcher Robert J. Gorlin (1923–2006).

First described in 1960, NBCCS is an autosomal dominant condition that can cause unusual facial appearances and a predisposition for basal cell carcinoma, a malignant type of skin cancer. The prevalence is reported to be 1 case per 56,000-164,000 population. Recent work in molecular genetics has shown NBCCS to be caused by mutations in the PTCH (Patched) gene found on chromosome arm 9q. If a child inherits the defective gene from either parent, he or she will have the disorder

Incidence:
About 750,000 new cases of sporadic basal cell carcinomas (BCCs) occur each year in the United States. Ultraviolet (UV) radiation from the sun is the main trigger of these cancers, and people with fair skin are especially at risk. Most sporadic BCCs arise in small numbers on sun-exposed skin of people over age 50, although younger people may also be affected. By comparison, NBCCS has an incidence of 1 in 50,000 to 150,000 with higher incidence in Australia. One aspect of NBCCS is that basal cell carcinomas will occur on areas of the body which are not generally exposed to sunlight, such as the palms and soles of the feet and lesions may develop at the base of palmer and plantar pits. One of the prime features of NBCCS is development of multiple BCCs at an early age, often in the teen years. Each person who has this syndrome is affected to a different degree, some having many more characteristics of the condition than others.

Components:-
Some or all of the following may be seen in someone with Gorlin Syndrome:

1.Multiple basal cell carcinomas of the skin
2.Odontogenic keratocyst: Seen in 75% of patients and is the most common finding. There are usually multiple lesions found in the mandible. They occur at a young age (19 yrs average).
3.Rib and vertebrae anomalies
4.Intracranial calcification
5.Skeletal abnormalities: bifid ribs, kyphoscoliosis, early calcification of falx cerebri (diagnosed with AP radiograph)
6.Distinct faces: frontal and temporopariental bossing, hypertelorism, and mandibular prognathism

What genes are related to Gorlin syndrome?
Mutations in the PTCH1 gene cause Gorlin syndrome. This gene provides instructions for making a protein called Patched-1, which functions as a receptor. Receptor proteins have specific sites into which certain other proteins, called ligands, fit like keys into locks. Together, ligands and their receptors trigger signals that affect cell development and function. A protein called Sonic Hedgehog is the ligand for the Patched-1 receptor. Patched-1 prevents cell growth and division (proliferation) until Sonic Hedgehog is attached.

The PTCH1 gene is a tumor suppressor gene, which means it keeps cells from proliferating too rapidly or in an uncontrolled way. Mutations in this gene prevent the production of Patched-1 or lead to the production of an abnormal version of the receptor. An altered or missing Patched-1 receptor cannot effectively suppress cell growth and division. As a result, cells proliferate uncontrollably to form the tumors that are characteristic of Gorlin syndrome.

You may click to learn more about the PTCH1 gene.

How do people inherit Gorlin syndrome?
Gorlin syndrome is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the features that are present from birth, such as large head size and skeletal abnormalities. An affected person often inherits a PTCH1 mutation from one affected parent. Other cases may result from new mutations in the gene. These cases occur in people with no history of the disorder in their family. For tumors to develop, a mutation in the other copy of the PTCH1 gene must occur in certain cells during the person’s lifetime. Most people who are born with one PTCH1 mutation eventually acquire a second mutation in certain cells and develop basal cell carcinomas and other tumors.

Causes:-
Gorlin syndrome is an autosomal dominant condition. The abnormal gene is found on chromosome 9. New mutations (where neither parent carries the gene) are common.

Diagnosis:
Diagnosis of NBCCS is made by having 2 major criteria or 1 major and 2 minor criteria.

The major criteria consist of the following:

1.more than 2 BCCs or 1 BCC in a person younger than 20 years;
2.odontogenic keratocysts of the jaw
3.3 or more palmar or plantar pits
4.ectopic calcification or early (<20 years) calcification of the falx cerebri
5.bifid, fused, or splayed ribs
6.first-degree relative with NBCCS.

.
The minor criteria include the following:

1.macrocephaly.
2.congenital malformations, such as cleft lip or palate, frontal bossing, eye anomaly (cataract, colobma, microphtalmia, nystagmus).
3.other skeletal abnormalities, such as Sprengel deformity, pectus deformity, polydactyly, syndactyly or hypertelorism.
4.radiologic abnormalities, such as bridging of the sella turcica, vertebral anomalies, modeling defects or flame-shaped lucencies of hands and feet.
5.ovarian and cardio fibroma or medulloblastoma (the latter is generally found in children below the age of two).
People with NBCCS need education about the syndrome, and may need counseling and support, as coping with the multiple BCCs and multiple surgeries is often difficult. They should reduce UV light exposure, to minimize the risk of BCCs. They should also be advised that receiving Radiation therapy for their skin cancers may be contraindicated. They should look for symptoms referable to other potentially involved systems: the CNS, the genitourinary system, the cardiovascular system, and dentition.

Genetic counseling is advised for prospective parents, since one parent with NBCCS causes a 50% chance that their child will also be affected.

Treatment:
Although there’s no cure, the carcinomas can be treated by surgery, lasers or photodynamic therapy, which reduces scarring.

If there’s a family history of the syndrome, it’s possible for family members to be tested to see if they carry the faulty gene.

Those with Gorlin syndrome are now advised to avoid – or to take advice before undergoing – any radiation treatment, as it’s thought it may exacerbate the condition.

Treatment is usually supportive treatment, that is, treatment to reduce any symptoms rather than to cure the condition.

*Enucleation of the odontogenic cysts can help but new lesions, infections and jaw deformity are usually a result.
*The severity of the basal cell carcinoma determines the prognosis for most patients. BCCs rarely cause gross disfigurement, disability or death .

*Genetic counseling

Advice and support:-
•Gorlin Syndrome Group
•Tel: 01772 496849
•Email: info@gorlingroup.org
•Website: www.gorlingroup.org

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://www.bbc.co.uk/health/physical_health/conditions/gorlinsyndrome1.shtml
http://en.wikipedia.org/wiki/Nevoid_basal_cell_carcinoma_syndrome
http://ghr.nlm.nih.gov/condition/gorlin-syndrome
http://dermnetnz.org/systemic/gorlins.html

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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.

click & see the pictures

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.

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://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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Categories
Herbs & Plants

Ma Huang (Ephedra sinica)

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Botanical Name: Ephedra sinica
Family: Ephedraceae
Genus: Ephedra
Kingdom: Plantae
Division: Gnetophyta
Class: Gnetopsida
Order: Ephedrales
Common Names: Ephedra, Ma Huang,Joint-pine, Jointfir, Mormon-tea or Brigham Tea.
The Chinese name is má huáng, which means “yellow hemp”. Ephedra is also sometimes called sea grape (from the French raisin de mer), although that is also a common name for Coccoloba uvifera.

Ephedra sinica Stapf. Engl.: Chinese ephedra, Chinese joint-fir. Suom.: efedra. Sven.: efedra. TCM: ma huang, cao ma huang

Habitat :These plants occur in dry climates over a wide area mainly in the northern hemisphere, across southern Europe, north Africa, southwest and central Asia, southwestern North America, and, in the southern hemisphere, in South America south to Patagonia.

Description: Ephedra is a shrublike plant found in desert regions throughout the world. It is distributed from northern China to Inner Mongolia. The dried green stems of the three Asian species (E. sinica, intermedia, equisetina) are the plant parts employed medicinally. The North American species of ephedra does not appear to contain the active ingredients of its Asian counterparts. The plants are 1.5 to 4 foot high. They typically grow on dry, rocky, or sandy slopes. The many slender, yellow green branches of ephedra have two very small leaf scales at each node. The mature, double seeded cones are visible in the fall.

click to see the pictures…..>…….(01).…….(1)..……...(2).………………….

Species
Ephedra alata Decne
Ephedra altissima Desf.
Ephedra americana Humb. & Bonpl. ex Willd.
Ephedra antisyphilitica Berl. ex C.A.Meyer – Clapweed, Erect Ephedra
Ephedra aspera Engelm. ex S.Wats. – Boundary Ephedra, Pitamoreal
Ephedra boelckei F.A.Roig
Ephedra californica S.Wats. – California Ephedra, California Jointfir
Ephedra campylopoda C. A. Mey.
Ephedra chilensis C. Presl
Ephedra ciliata Fisch. ex C. A. Mey.
Ephedra coryi E.L.Reed – Cory’s Ephedra
Ephedra cutleri Peebles – Navajo Ephedra, Cutler’s Ephedra, Cutler Mormon-tea, Cutler’s Jointfir
Ephedra dahurica Turcz.
Ephedra distachya L. – Joint-pine, Jointfir
Ephedra distachya L. subsp. distachya
Ephedra distachya subsp. helvetica (C.A.Meyer) Aschers. & Graebn.
Ephedra distachya L. subsp. monostachya (L.) Riedl
Ephedra equisetina Bunge – Ma huang
Ephedra fasciculata A.Nels. – Arizona Ephedra, Arizona Jointfir, Desert Mormon-tea Photo
Ephedra fedtschenkoae Pauls.
Ephedra foliata Boiss. ex C.A.Mey.
Ephedra fragilis Desf.
Ephedra fragilis subsp. campylopoda (C.A.Meyer) Aschers. & Graebn.
Ephedra frustillata Miers – Patagonian Ephedra
Ephedra funerea Coville & Morton – Death Valley Ephedra, Death Valley Jointfir
Ephedra gerardiana Wallich ex C.A.Meyer – Gerard’s Jointfir, Shan Ling Ma Huang
Ephedra holoptera Riedl
Ephedra intermedia Schrenk ex C.A.Meyer
Ephedra lepidosperma C.Y.Cheng

Ephedra distachyaEphedra likiangensis Florin
Ephedra lomatolepis Shrenk
Ephedra macedonica Kos.
Ephedra major Host
Ephedra major subsp. procera Fischer & C.A.Meyer
Ephedra minuta Florin
Ephedra monosperma C.A.Meyer
Ephedra multiflora Phil. ex Stapf
Ephedra nevadensis S.Wats. – Nevada Ephedra, Nevada Jointfir, Nevada Mormon-tea
Ephedra pachyclada Boiss.
Ephedra pedunculata Engelm. ex S.Wats. – Vine Ephedra, Vine Jointfir
Ephedra procera Fisch. & C. A. Mey.
Ephedra przewalskii Stapf
Ephedra przewalskii var. kaschgarica (B.Fedtsch. & Bobr.) C.Y.Cheng
Ephedra regeliana Florin – Xi Zi Ma Huang
Ephedra saxatilis (Stapf) Royle ex Florin
Ephedra sinica Stapf – Cao Ma Huang, Chinese ephedra
Ephedra strobilacea Bunge
Ephedra torreyana S.Wats. – Torrey’s Ephedra, Torrey’s Jointfir, Torrey’s Mormon-tea, Cañutillo
Ephedra trifurca Torrey ex S.Wats. – Longleaf Ephedra, Longleaf Jointfir, Longleaf Mormon-tea, Popotilla, Teposote
Ephedra viridis Coville – Green Ephedra, Green Mormon-tea

Active Compounds:
Ephedra’s active medicinal ingredients are the alkaloids ephedrine and pseudoephedrine. The stem contains 1-3% total alkaloids, with ephedrine accounting for 30-90% of this total, depending on the plant species employed. Both ephedrine and its synthetic counterparts stimulate the central nervous system, dilate the bronchial tubes, elevate blood pressure, and increase heart rate. Pseudoephedrine (the synthetic form) is a popular over-the-counter remedy for relief of nasal congestion.

Biochemistry and pharmacology
The alkaloids ephedrine and pseudoephedrine are the active constituents of the plant. Pseudoephedrine is used in over-the-counter decongestants. Derivatives of ephedrine are used to treat low blood pressure, but alternatives with reduced cardiovascular risk have replaced it for treating asthma. Ephedrine is also considered a performance-enhancing drug and is prohibited in most competitive sports. Some species in the Ephedra genus have no alkaloid content; however, the most commonly used species, E. sinica, has a total alkaloid content of 1–3% by dry weight. Ephedrine constitutes 40–90% of the alkaloid content, with the remainder consisting of pseudoephedrine and the demethylated forms of each compound.

Medical uses:
Plants of the Ephedra genus, including E. sinica and others, have traditionally been used by indigenous people for a variety of medicinal purposes, including treatment of asthma, hay fever, and the common cold. They have also been proposed as a candidate for the Soma plant of Indo-Iranian religion. The alkaloids ephedrine and pseudoephedrine are active constituents of E. sinica and other members of the genus. These compounds are sympathomimetics with stimulant and decongestant qualities and are related chemically to the amphetamines. Ephedra nevadensis contains ephedrine in its roots, stems and branches. Ephedra distachya contains up to 3% ephedrine in the entire plant. Ephedra sinica contains approximately 2.2% ephedrine.

The stems of the ephedra plant can be brewed into a pungent, bitter, herb tea that dilates the bronchial vessels while stimulating the heart and central nervous system.

The active chemical components of ephedra, or ma huang, the alkaloids ephedrine and pseudo ephedrine, are found in over the counter allergy and cold medications as over-the-counter decongestants. . An internal review of FDA records between 1969 and September 2006 found 54 reports of deaths in children associated with decongestant medicines containing pseudoephedrine, phenylephrine or ephedrine, prompting the recent recall of these medications in children’s cold care products.

The phytochemical ephedrine possesses properties similar to adrenaline that serves a critical role in our system as a neurotransmitter and a modulator of our metabolic rate. This powerful stimulant action is the major reason why it is so dangerous when misused. Ephedra has fallen into disfavor because of its misuse in the west as a diet drug. A handful of people have died over the last few years prompting the FDA to ban its use.

Herbalists, however, use the whole plant which contains six other related alkaloids, one of which, pseudoephedrine, actually reduces the heart rate and lowers blood pressure. This plant has been used in China for thousands of years, yet no undesirable side-effects have been recorded from the proper administration of the whole plant. Mabey, Richard ,48 Those wishing to use the whole herb to treat allergies and asthma can still buy bulk ephedra from reputable whole herb sources such as Mountain Rose, however it is recommended that it be used under only under supervision of a qualified herbalist.

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Traditional Chinese Medicine

Ma Huang has a 5,000 year history of use in Chinese medicine as an asthma treatment and is traditionally prescribed in TCM as an effective treatment of hay fever, edema, arthritis, colds, asthma, bronchitis and hives.

Weight Loss Aid: Ephedrine suppresses the appetite and increases the metabolic rate of adipose tissue. Ephedrine activates the sympathetic nervous system, increasing the metabolic rate and increasing the amount of the food converted to heat (thermogenesis). This prevents the body from converting these foods to fat, thus helping in the control of weight gain by those who have low metabolism.

Ephedrine is often used in conjunction with methylxanthine sources such as coffee, tea, cola nut, and guarana. The methylxanthines enhances the thermogenic effect of ephedrine. Clinical studies have also shown that aspirin may be effective in increasing the thermogenic effect of ephedrine.


Side Effects:

The herb and its extracts are potentially addictive, and can disrupt regular heart rhythm, induce cardiac arrest, and raise blood pressure. They are very likely to make you sweat profusely, become irritable, nervous, nauseous and cause insomnia.

Disclaimer:The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.

Resources:
http://www.holisticonline.com/herbal-med/_herbs/h53.htm
http://en.wikipedia.org/wiki/Ephedra_sinica
http://www.anniesremedy.com/herb_detail298.php
http://en.wikipedia.org/wiki/Ephedra