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Attention Deficit Hyperactivity Disorder (ADHD)

Definition:

Attention Deficit Hyperactivity Disorder, ADHD, is one of the most common mental disorders that develop in children. Children with ADHD have impaired functioning in multiple settings, including home, school, and in relationships with peers. If untreated, the disorder can have long-term adverse effects into adolescence and adulthood.

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It is a neurobehavioral developmental disorder affecting about 3-5% of the world’s population under the age of 19. It typically presents itself during childhood, and is characterized by a persistent pattern of inattention and/or hyperactivity, as well as forgetfulness, poor impulse control or impulsivity, and distractibility. ADHD is currently considered to be a persistent and chronic condition for which no medical cure is available, although medication can be prescribed. ADHD is most commonly diagnosed in children and, over the past decade, has been increasingly diagnosed in adults. About 60% of children diagnosed with ADHD retain the condition as adults. It appears to be highly heritable, although one-fifth of all cases are estimated to be caused from trauma or toxic exposure. Methods of treatment usually involve some combination of medications, behavior modifications, life style changes, and counseling.

The scientific consensus in the field, and the consensus of the national health institutes of the world, is that ADHD is a disorder which impairs functioning, and that many adverse life outcomes are associated with ADHD. It has been frequently said by a minority of news sources, social critics, certain religions, and individual medical professionals, to be a controversial disorder. These criticisms fall outside of majority or minority viewpoint and question its causes, its treatment, and even the existence of ADHD.

Classification:
ADHD is a developmental disorder, in that, in the diagnosed population, certain traits such as impulse control significantly lag in development when compared to the general population. Using magnetic resonance imaging, this developmental lag has been estimated to range between 3 years, to 5 years in the prefrontal cortex of those with ADHD patients in comparison to their peers; consequently these delayed attributes are considered an impairment. ADHD has also been classified as a behavior disorder and a neurological disorder or combinations of these classifications such as neurobehavioral or neurodevelopmental disorders.
Three forms of ADHD are thought to exist, ADHD-PI or ADHD Primarily Inattentive (previously known as ADD or Attention Deficit Disorder), ADHD-PH/I or ADHD Primarily Hyperactive/Impulsive, and ADHD-C or combined type. The majority of studies have looked at ADHD-C, with much less work done on ADHD-PI. To determine or rule out ADHD information from several key sources is required.


Symptoms:

The most common symptoms of ADHD are distractibility, difficulty with concentration and focus, short term memory loss, procrastination, problems organizing ideas and belongings, tardiness, impulsivity, and weak planning and execution. Not all people with ADHD have all the symptoms. The Diagnostic and Statistical Manual of Mental Disorders categorises the symptoms of ADHD into two clusters: Inattention symptoms and Hyperactivity/Impulsivity symptoms. Most ordinary people exhibit some of these behaviors but not to the point where they seriously interfere with the person’s work, relationships, or studies or cause anxiety or depression. Children do not often have to deal with deadlines, organization issues, and long term planning so these types of symptoms often become evident only during adolescence or adulthood when life demands become greater.

Symptoms of ADHD will appear over the course of many months, and include:

* Impulsiveness: a child who acts quickly without thinking first
* Hyperactivity: a child who can’t sit still, walks, runs, or climbs around when others are seated, talks when others are talking.
* Inattention: a child who daydreams or seems to be in another world, is sidetracked by what is going on around him or her.

Causes:-
According to a majority of medical research in the United States, as well as other countries, ADHD is today generally regarded as a chronic disorder for which there are some effective treatments, but no true cure. Evidence suggests that hyperactivity has a strong heritable component, and in all probability ADHD is a heterogeneous disorder, meaning that several causes could create very similar symptomology. Candidate genes include dopamine transporter (DAT), dopamine receptor D4 (DRD4), dopamine beta-hydroxylase (DBH), monoamine oxidase A (MAOA), catecholamine-methyl transferase (COMT), serotonin transporter promoter (SLC6A4), 5-hydroxytryptamine 2A receptor (5-HT2A), and 5-hydroxytryptamine 1B receptor (5-HT1B). Researchers believe that a large majority of ADHD arises from a combination of various genes, many of which affect dopamine transporters. Suspect genes include the 10-repeat allele of the DAT1 gene, the 7-repeat allele of the DRD4 gene, and the dopamine beta hydroxylase gene (DBH TaqI).

Genome wide surveys have shown linkage between ADHD and loci on chromosomes 7, 11, 12, 15, 16, and 17. If anything, the broad selection of targets indicates the likelihood that ADHD does not follow the traditional model of a “genetic disease” and is better viewed as a complex interaction among genetic and environmental factors. As the authors of a review of the question have noted, “Although several genome-wide searches have identified chromosomal regions that are predicted to contain genes that contribute to ADHD susceptibility, to date no single gene with a major contribution to ADHD has been identified.”

Studies show that there is a familial transmission of the disorder which does not occur through adoptive relationships.  Twin studies indicate that the disorder is highly heritable and that genetics contribute about three quarters of the total ADHD population.[8] While the majority of ADHD is believed to be genetic in nature,[8] roughly one-fifth of all ADHD cases are thought to be acquired after conception due to brain injury caused by either toxins or physical trauma prenatally or postnatally.

Additionally, SPECT scans found people with ADHD to have reduced blood circulation, and a significantly higher concentration of dopamine transporters in the striatum which is in charge of planning ahead. Medications focused on treating A.D.H.D.(such as methylphenidate) work because they force blood to flow in certain areas of the brain, those that control and regulate concentration, which usually don’t receive a normal or sufficient amount blood flow or circulation in the brains of A.D.H.D. en companying individuals. A study by the U.S. Department of Energy’s Brookhaven National Laboratory in collaboration with Mount Sinai School of Medicine in New York suggest that it is not the dopamine transporter levels that indicate ADHD, but the brain’s ability to produce dopamine itself. The study was done by injecting 20 ADHD subjects and 25 control subjects with a radiotracer that attaches itself to dopamine transporters. The study found that it was not the transporter levels that indicated ADHD, but the dopamine itself. ADHD subjects showed lower levels of dopamine across the board. They speculated that since ADHD subjects had lower levels of dopamine to begin with, the number of transporters in the brain was not the telling factor. In support of this notion, plasma homovanillic acid, an index of dopamine levels, was found to be inversely related not only to childhood ADHD symptoms in adult psychiatric patients, but to “childhood learning problems” in healthy subjects as well.

Although there is evidence for dopamine abnormalities in ADHD, it is not clear whether abnormalities of the dopamine system are the molecular abnormality of ADHD or a secondary consequence of a problem elsewhere. Researchers have described a form of ADHD in which the abnormality appears to be sensory overstimulation resulting from a disorder of ion channels in the peripheral nervous system.

An early PET scan study found that global cerebral glucose metabolism was 8.1% lower in medication-naive adults who had been diagnosed as ADHD while children. The image on the left illustrates glucose metabolism in the brain of a ‘normal’ adult while doing an assigned auditory attention task; the image on the right illustrates the areas of activity in the brain of an adult who had been diagnosed with ADHD as a child when given that same task; these are not pictures of individual brains, which would contain substantial overlap, these are images constructed to illustrate group-level differences. Additionally, the regions with the greatest deficit of activity in the ADHD patients (relative to the controls) included the premotor cortex and the superior prefrontal cortex.[24] A second study in adolescents failed to find statistically significant differences in global glucose metabolism between ADHD patients and controls, but did find statistically significant deficits in 6 specific regions of the brains of the ADHD patients (relative to the controls). Most notably, lower metabolic activity in one specific region of the left anterior frontal lobe was significantly inversely correlated with symptom severity.[25] These findings strongly imply that lowered activity in specific regions of the brain, rather than a broad global deficit, is involved in ADHD symptoms. However, these readings are of subjects doing an assigned task. They could be found in ADHD diagnosed patients because they simply were not attending to the task. Hence the parts of the brain used by others doing the task would not show equal activity in the ADHD patients.[citation needed]

The estimated contribution of non genetic factors to the contribution of all cases of ADHD is 20 percent.[26] The environmental factors implicated are common exposures and include alcohol, in utero tobacco smoke and lead exposure. Lead concentration below the Center for Disease Control’s action level account for slightly more cases of ADHD than tobacco smoke (290 000 versus 270 000, in the USA, ages 4 to 15). Complications during pregnancy and birth—including premature birth—might also play a role. It has been observed that women who smoke while pregnant are more likely to have children with ADHD. This could be related to the fact that nicotine is known to cause hypoxia (lack of oxygen) in utero, but it could also be that ADHD women have more probabilities to smoke both in general and during pregnancy, being more likely to have children with ADHD due to genetic factors.

Head injuries can cause a person to present ADHD-like symptoms, possibly because of damage done to the patient’s frontal lobes. Because these types of symptoms can be attributable to brain damage, one earlier designation for ADHD was “Minimal Brain Damage”.

There is no compelling evidence that social factors alone can create ADHD. Many researchers believe that attachments and relationships with caregivers and other features of a child’s environment have profound effects on attentional and self-regulatory capacities. It is noteworthy that a study of foster children found that an inordinate number of them had symptoms closely resembling ADHD. An editorial in a special edition of Clinical Psychology in 2004 stated that “our impression from spending time with young people, their families and indeed colleagues from other disciplines is that a medical diagnosis and medication is not enough. In our clinical experience, without exception, we are finding that the same conduct typically labelled ADHD is shown by children in the context of violence and abuse, impaired parental attachments and other experiences of emotional trauma.” Furthermore, Complex Post Traumatic Stress Disorder can result in attention problems that can look like ADHD, as can Sensory Integration Disorders.

It is believed that there are several different causes of ADHD. Roughly 80 percent of ADHD is considered genetic in nature and the estimated contribution of non genetic factors to the contribution of all cases of ADHD is believed to be 20 percent.. Environmental agents also cause ADHD. These agents, such as alcohol, tobacco, and lead, are believed to stress babies prenatally and cause ADHD. Studies have found that malnutrition is also correlated with attention deficits. Diet seems to cause ADHD symptoms or make them worse. Many studies point to synthetic preservatives and artificial coloring agents aggravating ADD & ADHD symptoms in those affected. Older studies were inconclusive quite possibly due to inadequate clinical methods of measuring offending behavior. Parental reports were more accurate indicators of the presence of additives than clinical tests. Several major studies show academic performance increased and disciplinary problems decreased in large non-ADD student populations when artificial ingredients, including artificial colors were eliminated from school food programs.. Professor John Warner stated, “significant changes in children’s hyperactive behaviour could be produced by the removal of artificial colourings and sodium benzoate from their diet.” and “you could halve the number of kids suffering the worst behavioural problems by cutting out additives”.

In 1982, the NIH had determined, based on research available at that time, that roughly 5% of children with ADHD could be helped significantly by removing additives from their diet. The vast majority of these children were believed to have food allergies. More recent studies have shown that approximately 60-70% of children with and without allergies improve when additives are removed from their diet,   that up to almost 90% of them react when an appropriate amount of additive is used as a challenge in double blind tests,and that food additives may elicit hyperactive behavior and/or irritability in normal children as well.

Diagnosis:
If ADHD is suspected, the diagnosis should be made by a professional with training in ADHD. After ruling out other possible reasons for the child’s behavior, the specialist checks the child’s school and medical records and talks to teachers and parents who have filled out a behavior rating scale for the child. A diagnosis is made only after all this information has been considered.

Many of the symptoms of ADHD occur from time to time in everyone. In those with ADHD the frequency of these symptoms occurs frequently and impairs regular life functioning typically at school or at work. Not only will they perform poorly in task oriented settings but they will also have difficulty with social functioning with their peers. No objective physical test exists to diagnose ADHD in a patient. As with many other psychiatric and medical disorders, the formal diagnosis is made by a qualified professional in the field based on a set number of criteria. In the USA these critera are laid down by the American Psychiatric Association in their Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), 4th edition. Based on the DSM-IV criteria listed below, three types of ADHD are classified:

1. ADHD, Combined Type: if both criteria 1A and 1B are met for the past 6 months
2. ADHD Predominantly Inattentive Type: if criterion 1A is met but criterion 1B is not met for the past six months
3. ADHD, Predominantly Hyperactive-Impulsive Type: if Criterion 1B is met but Criterion 1A is not met for the past six months.

The terminology of ADD expired with the revision of the most current version of the DSM. Consequently, ADHD is the current nomenclature used to describe the disorder as one distinct disorder which can manifest itself as being a primary deficit resulting in hyperactivity/impulsivity (ADHD, predominately hyperactive-impulsive type) or inattention (ADHD predominately inattentive type) or both (ADHD combined type).

Treatment:
Effective treatments for ADHD are available, and include behavioral therapy and medications.
Singularly, stimulant medication is the most efficient and cost effective method of treating ADHD. Over 200 controlled studies have shown that stimulant medication is an effective way to treat ADHD. Methods of treatment usually involve some combination of medications, behaviour modifications, life style changes, and counseling. Behavioral Parent Training, behavior therapy aimed at parents to help them understand ADHD, has also shown short term benefits. Omega-3 fatty acids, phosphatidylserine, zinc and magnesium may have benefits with regard to ADHD symptoms.

Comorbid disorders or substance abuse can make finding the proper diagnosis and the right overall treatment more costly and time-consuming. Psychosocial therapy is useful in treating some comorbid conditions.

ADHD Medications:

Another part of the treatment program often involves the prescribed use of certain medications. Parents sometimes worry about their children having to rely on medication. But it’s more important to realize that these can help the ADHD child function at his best, and will consequently help him avoid even greater problems.

Parents should expect to receive detailed information about any prescribed medication from their health professional, including the possible side-effects. This information should then be shared with everyone entrusted with the child’s care. Let’s now look at the most common of ADHD medication.

Methylphenidate

The most commonly prescribed ADHD medication is Methylphenidate. This medication is in fact a stimulant, which interestingly in ADHD children often has the reverse effect of calming them down.

Methylphenidate, also known as Ritalin, is commonly taken in pill form. It takes effect quickly, and lasts three to four hours. The child’s prescribed dosage needs to be administered by an informed adult, two or three times a day, depending on the child’s age – usually in the morning before school, and at lunchtime. Methylphenidate is now also available in a single dose, long acting forms. Dextroamphetamine is another medication used to treat ADHD.

Before medication therapy begins, the diagnosis should be well established, and individualized behaviour and educations plans should be in place. In the absence of these other forms of treatment, drug therapy alone is ineffective.

What about “drug holidays”?

In the past, children being treated for ADHD were sometimes given an extended break from taking medication – usually during the summer months when not in school – to minimize potential side effects. But today, most physicians suggest that current ADHD medication therapy can be safely followed year-round, and can continue to be very helpful outside of school as well. The benefits offered by modern ADHD medications as part of a greater treatment plan, usually outweigh the minimized potential for adverse side effects.

What about alternative treatments?

Alternative treatments for the child’s ADHD may be suggested to you, but it’s important to realize there is no significant scientific evidence that any are effective. Some of these controversial treatments include: biofeedback, mega-vitamin and mineral supplements, anti-motion sickness medication, and optometric exercises. Again, none of these approaches have ever been scientifically proven to have any significant effect on ADHD, so they should probably not be relied on.

The need for on-going monitoring

Whatever treatment strategies are undertaken, the child’s condition needs to be regularly monitored by a health professional. It is especially important to check for side-effects; confirm the on-going effectiveness of the program; and if necessary, make adjustments to the treatment plan.

Prognosis:
The diagnosis of ADHD implies an impairment in life functioning. Many adverse life outcomes are associated with ADHD.

During the elementary years, an ADHD student will have more difficulties with work completion, productivity, planning, remembering things needed for school, and meeting deadlines. Oppositional and socially aggressive behavior is seen in 40-70% of children at this age. Even ADHD kids with average to above average intelligence show “chronic and severe under achievement”. Fully 46% of those with ADHD have been suspended and 11% expelled. 37% of those with ADHD do not get a high school diploma even though many of them will receive special education services. The combined outcomes of the expulsion and dropout rates indicate that almost half of all ADHD students never finish highschool.Only 5% of those with ADHD will get a college degree compared to 27% of the general population. (US Census, 2003)

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/Attention-deficit_hyperactivity_disorder
http://www.lipsychiatric.com/common-disorders.asp#adhd
http://www.drpaul.com/behaviour/adhdmedi.html

Collagenous Colitis and Lymphocytic Colitis

What are collagenous colitis and lymphocytic colitis?

Inflammatory bowel disease is the general name for diseases that cause inflammation in the intestines, most often referring to Crohn’s disease and ulcerative colitis. Collagenous colitis and lymphocytic colitis are two other types of bowel inflammation that affect the colon. The colon is a tube-shaped organ that runs from the first part of the large bowel to the rectum. Solid waste, or stool, moves through the colon to be eliminated. Collagenous colitis and lymphocytic colitis are not related to Crohn’s disease or ulcerative colitis, which are more severe forms of inflammatory bowel disease....CLICK & SEE 

Collagenous colitis and lymphocytic colitis are also called microscopic colitis. Microscopic colitis means there is no sign of inflammation on the surface of the colon when viewed with a colonoscopy or flexible sigmoidoscopy two tests that let a doctor look inside your large intestine. Because the inflammation isn’t visible, a biopsy is necessary to make a diagnosis. A doctor performs a biopsy by removing a small piece of tissue from the lining of the intestine during a colonoscopy or flexible sigmoidoscopy.

What are the symptoms?

The symptoms of collagenous colitis and lymphocytic colitis are the same—chronic, watery, non-bloody diarrhea. Abdominal pain or cramps may also be present. People with collagenous colitis and lymphocytic colitis may suffer from ongoing diarrhea while others have times when they are symptom free.

What causes collagenous colitis and lymphocytic colitis?

Scientists are not sure what causes collagenous colitis or lymphocytic colitis. Bacteria and their toxins, or a virus, may be responsible for causing inflammation and damage to the colon. Some scientists think that collagenous colitis and lymphocytic colitis may result from an autoimmune response, which means that the body’s immune system destroys healthy cells for no known reason.

Who gets collagenous colitis and lymphocytic colitis?

Collagenous colitis is most often diagnosed in people between 60 and 80 years of age. However, some cases have been reported in adults younger than 45 years and in children. Collagenous colitis is diagnosed more often in women than men.

People with lymphocytic colitis are also generally diagnosed between 60 and 80 years of age. Both men and women are equally affected.

How are they diagnosed?

Some scientists think that collagenous colitis and lymphocytic colitis are the same disease in different stages. The only way to determine which form of colitis a person has is by performing a biopsy.

A diagnosis of collagenous colitis or lymphocytic colitis is made after tissue samples taken during a colonoscopy or flexible sigmoidoscopy are examined with a microscope.

Collagenous colitis is characterized by a larger-than-normal band of protein called collagen inside the lining of the colon. The thickness of the band varies; so several tissue samples from different areas of the colon may need to be examined.

With lymphocytic colitis, tissue samples show an increase of white blood cells, known as lymphocytes, between the cells that line the colon. The collagen is not affected.

Treatment

Treatment for collagenous colitis and lymphocytic colitis varies depending on the symptoms and severity of the case. The diseases have been known to resolve on their own, although most people suffer from ongoing or occasional diarrhea.

Lifestyle changes are usually tried first. Recommended changes include reducing the amount of fat in the diet, eliminating foods that contain caffeine and lactose, and avoiding over-the-counter pain relievers such as ibuprofen or aspirin.

If lifestyle changes alone are not enough, medications can be used to help control symptoms.

  • Treatment usually starts with prescription anti-inflammatory medications, such as mesalamine (Rowasa or Canasa) and sulfasalazine (Azulfidine), in order to reduce swelling.
  • Steroids, including budesonide (Entocort) and prednisone are also used to reduce inflammation. Steroids are usually only used to control a sudden attack of diarrhea. Long-term use of steroids is avoided because of side effects such as bone loss and high blood pressure.
  • Anti-diarrheal medications such as bismuth subsalicylate (Pepto Bismol), diphenoxylate atropine (Lomotil), and loperamide (Imodium) offer short-term relief.
  • Immunosuppressive agents such as azathioprine (Imuran) reduce the inflammation but are rarely needed.

For extreme cases of collagenous colitis and lymphocytic colitis that have not responded to medication, surgery to remove all or part of the colon may be necessary. However, surgery is rarely recommended. Collagenous colitis and lymphocytic colitis do not increase a person’s risk of getting colon cancer.

Collagenous colitis and lymphocytic colitis do not increase a person’s risk of getting colon cancer.

Colitis -Natural Cure

Treat Ulcerative Colitis

For More Information

Crohn’s & Colitis Foundation of America Inc.
386 Park Avenue South, 17th floor
New York, NY 10016–8804
Phone: 1–800–932–2423 or 212–685–3440
Fax: 212–779–4098
Email: info@ccfa.org
Internet: www.ccfa.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

Source:http://digestive.niddk.nih.gov/ddiseases/pubs/collagenouscolitis/index.htm

Purslane

Botanical Name: Portulaca sativa
Family: Portulacaceae
Genus: Portulaca
Species: P. oleracea
Kingdom: Plantae
Order: Caryophyllales

Synonyms:Garden Purslane. Pigweed.
Common Names: Common purslane, Verdolaga, Pigweed, Little hogweed, Red root, Pursley, and Moss rose
Parts Used: Herb, juice, seeds.
Habitat: Purslane   is  native to S. Europe. A not infrequent casual in Britain. It grows in fields, waste ground, roadside verges, cultivated ground and by the sea.

Now it is distributed all over the world. Portulaca oleracea, the Garden, or Green Purslane, is a herbaceous annual, native of many parts of Europe, found in the East and West Indies, China, Japan and Ascension Island, and though found also in the British Isles is not indigenous there.

Other Species:
Professor Hulme, in Familiar Wild Flowers, speaks of a variety which he calls the SEA PURSLANE (Atriplex portulacoides), common enough on the sea-shores of England and Ireland, though much less so in Scotland. It grows in saline marshes and muddy foreshores. It is a shrubby and much-branching plant, attaining to no great height, usually a foot to 18 inches – though occasionally to 2 feet. The lower portion of the stem is often somewhat creeping and rooting, which gives it a greater grip of the ground in view of fierce gales. The stems are often of a delicate purple colour, more or less covered with a grey bloom. The foliage is of pointed, lancehead form, thick and fleshy, and entirely silvery white in colour. The minute flowers are in little clusters that succeed one another at intervals on the short branches near the top of the plant and form a terminal head. The flowers are of two kinds: one is stamen-bearing, these stamens being five in number and within a five-cleft perianth; the other is pistilbearing and consists of two flattened segments, closing somewhat like the leaves of a book, and contained within the ovary. After the flowering is over, this flattened perianth considerably enlarges. This construction of the seed-bearing flower is of some specific importance, for in the present species and the A. pedunculata the two segments are united nearly to the top, while in another species, the A. rosea, these segments are not joined above their centres; and in a third, the A. hortensis, they are not joined at all.

An entirely different plant, one of the great Pink family, the Houckenya peploides, is sometimes called the ‘ovate-leaved Sea Purslane.’ It is a common plant on seabeaches, with large white five-petalled blossoms. Another name for it is ‘ovate Sandwort.’

The generic title of the Sea Purslane, Atriplex, is one of Pliny’s plant names. It is derived from two Greek words signifying ‘not to flourish,’ the meaning of the word applied to the plant is obscure. The specific name, Potrulacoides, signifies ‘resembling the purslane plant,’ the portulaca. Another name for the Sea Purslane is ‘Shrubby Orache.’

The origin of the name ‘Purslane’ is unknown. Turner calls the plant ‘purcellaine,’ and in the Grete Herball, 1516, it is ‘procelayne.’

In the North American prairies Purslane is called ‘Pussly.’

Description: Purslane is an annual plant growing to 0.3 m (1ft) by 0.3 m (1ft in) at a fast rate.
It is frost tender. It is in flower from Jun to September, and the seeds ripen from Jul to September. The flowers are hermaphrodite (have both male and female organs) and are pollinated by Insects, self.The plant is self-fertile.

It has a round, smooth, procumbent, succulent stem, growing about 6 inches high, with small, oblong, wedgeshaped, dark-green leaves, thick and stalked, clustered together, destitute of the bristle in their axils which others of the genus have. The flowers are small, yellow, solitary or clustered, stalkless, placed above the last leaves on the branches, blooming in June and July, and opening only for a short time towards noon.
The growth of the plant somewhat resembles Samphire, and the rich red colour of the stems is very striking and most decorative in herb borders. The Golden Purslane (Portulaca sativa) is a variety of Purslane with yellow leaves, less hardy than the Green Purslane, but possessing the same qualities. The seeds of an individual plant have been known to produce both green and goldenleaved plants.

click to see the pictures……..

A Purslane cultivar grown as a vegetable

A Purslane cultivar grown as a vegetable (Photo credit: Wikipedia)

Purslane is a pleasant salad herb, and excellent for scorbutic troubles. The succulent leaves and young shoots are cooling in spring salads, the older shoots are used as a pot-herb and the thick stems of plants that have run to seed are pickled in salt and vinegar to form winter salads. Purslane is largely cultivated in Holland and other countries for these purposes. It is used in equal proportion with Sorrel to make the well-known French soup bonne femme. Gerard said of this herb: ‘Raw Purslane is much used in sallads, with oil, salt and vinegar. It cools the blood and causes appetite;’ and Evelyn tells us that, ‘familiarly eaten alone with Oyl and Vinegar,’ moderation should be used, adding that it is eminently moist and cooling, ‘especially the golden,’ and is ‘generally entertained in all our sallets. Some eate of it cold, after it has been boiled, which Dr. Muffit would have in wine for nourishment.’

Most of the plants in this order are mucilaginous. The root of one species, Lewisia rediviva, the Tobacco root, a native of North America, so called from its odour when cooked, possesses great nutritive properties. It is boiled and eaten by the Indians, and Hogg tells us that it proves most sustaining on long journeys, and that 2 or 3 OZ. a day are quite sufficient for a man, even while undergoing great fatigue. Claytonia tuberosa, another plant belonging to the same order as the Purslanes, likewise a native of North America, has also an edible root.

Purslane in ancient times was looked upon as one of the anti-magic herbs, and strewn round a bed was said to afford protection against evil spirits. We are told that it was a sure cure for ‘blastings by lightening or planets and burning of gunpowder.’

Portulaca oleracea (Common Purslane, also known as Verdolaga, Pigweed, Little Hogweed or Pusley), is an annual succulent in the family Portulacaceae, which can reach 40 cm in height.. It is a native of India and the Middle East, but is naturalised elsewhere and in some regions is considered an invasive weed, but there is evidence that the species was in Crawford Lake deposits (Ontario) in 1430-89, suggesting that it reached North America in the pre-columbian era. It has smooth, reddish, mostly prostrate stems and alternate leaves clustered at stem joints and ends. The yellow flowers have five regular parts and are up to 6 mm wide. The flowers first appear in late spring and continue into mid fall. The flowers open singly at the center of the leaf cluster for only a few hours on sunny mornings. Seeds are formed in a tiny pod, which opens when the seeds are ready. Purslane has a taproot with fibrous secondary roots and is able to tolerate poor, compacted soils and drought

History

Widely used in Greece, archaeobotanical finds are common at many prehistoric sites. In historic contexts, seeds have been retrieved from a protogeometric layer in Kastanas, as well as from the Samian Heraion dating to 7th century BC. Theophrastus in the 4th century BC names purslane, andrákhne, as one of the several summer pot herbs that must be sown in April (H.P 7.12).

Known as “Sanhti or Punarva” in North India it is known to act as a liver tonic and is used in diseases of the liver.

Culinary uses:
Although purslane is considered a weed in the United States, it can be eaten as a leaf vegetable. It has a slightly sour and salty taste and is eaten throughout much of Europe and Asia. It can be used fresh as a salad, or cooked like spinach, and because of its mucilaginous quality it is also suitable for soups and stews. Australian Aborigines used to use the seeds to make seedcakes.

Purslane contains more Omega-3 fatty acids than any other leafy vegetable plant. It also contains vitamins (mainly vitamin C, and some vitamin B and carotenoids), as well as dietary minerals, such as magnesium, calcium, potassium and iron. Also present are two types of betalain alkaloid pigments, the reddish betacyanins (visible in the coloration of the stems) and the yellow betaxanthins (noticeable in the flowers and in the slight yellowish cast of the leaves). Both of these pigment types are potent antioxidants and have been found to have antimutagenic properties in laboratory studies.

Cultivation: Sow the seeds in drills, on a bed of rich light earth, during any of the summer months, from May onwards. To have it early in the season, it should be sown upon a hot bed, at the end of March and planted out in a warm border in May. The Green Purslane is quite hardy, the Golden Purslane less so.

Keep the plants clear from weeds, and in dry weather water them two or three times a week. The Purslanes need rather more watering than most herbs.

In warm weather, they will be fit for use in six weeks. When the leaves are gathered, the plants must be cut low and then a fresh crop will appear.

To continue a succession, sow three or four times, at an interval of a fortnight or three weeks.

If the seeds are to be saved, leave some of the earliest plants for that purpose.

* April to August is the ideal season to sow the seeds when frost does not pose a threat.

*Press the seeds into the surface of the soil and leave uncovered. Roots can also develop on parts of existing plants that are inserted into the soil. In fairly moist soil, two or three successive plantings can be made.

*Keep the herb well watered always. Thin the seedlings to 10cm apart and when they reach 5-7cm in height cut them back close to the ground. The seeds germinate very quickly.

* Purslane can also be grown in a container. Purslane prefers the sun and sandy soil for growth. One must water these herbs during dry spells and feed lightly once in a while.

*It is important to note that it is ideal to consume Purslane when it is young. The flavor apparently deteriorates as it starts to bloom.

* Purslane grows well at day or night temperatures of 27 or 22oC and when days are long (16 hours).

* Purslane can also be used as rotation crop when gardening as they bring up subsoil minerals and protect against many insects.

*Because of its inherent ability to tolerate different light intensities, temperature ranges and soil types. Purslane is ideal for home gardens and provides a ready supply of greens for the salad.

Medicinal Action and Uses: It was highly recommended for many complaints. The expressed juice, taken while fresh, was said to be good for strangury, and taken with sugar and honey to afford relief for dry coughs, shortness of breath and immoderate thirst, as well as for external application in inflammation and sores.

It was supposed to cool ‘heat in the liver’ and to be excellent for ‘hot agues,’ and all pains in the head ‘proceeding from the heat, want of sleep or the frenzy,’ and also to stop haemorrhages.

The herb, bruised and applied to the forehead and temple, was said to allay excessive heat, and applied to the eyes to remove inflammation. Culpepper says: ‘The herb if placed under the tongue assuayeth thirst. Applied to the gout, it easeth pains thereof, and helps the hardness of the sinews, if it come not of the cramp, or a cold cause.’

The juice, with oil of Roses, was recommended for sore mouths and swollen gums and also to fasten loose teeth. Another authority declared that the distilled water took away pains in the teeth, both Gerard and Turner telling us too, that the leaves eaten raw are good for teeth that are ‘set on edge with eating of sharpe and soure things.’

The seeds, bruised and boiled in wine, were given to children as a vermifuge.

In Greek popular medicine, purslane is used as a remedy for constipation and inflammation of the urinary system. In antiquity its healing properties were thought so reliable that Pliny advised wearing the plant as an amulet to expel all evil (Natural History 20.120).

Benefits and Uses of Purslane Herb:

Purslane herb presents a wide variety of therapeutic uses and each part of the herb is consumable and beneficial. Here is a compilation of the known benefits and uses of Purslane herb that is widely used the world over:

Key Benefits:

*Purslane is known as an excellent source of vitamins A, C and E and the essential amino acids. Reports describe Purslane as a “power food of the future” because of its high nutritive and antioxidant properties.

* Purslane leaves contain Omega-3 fatty acid which regulate the body’s metabolic activities. Purslane herb is known to have one of the highest known concentrations of Omega-3 fatty acid in any plant.

*The stems of Purslane herb are known to be high in vitamin C.

Therapeutic Uses:

*Purslane is widely used as a potherb in Mediterranean, central European and Asian countries.

* Purslane is also widely used as an ingredient in a green salad. Tender stems and leaves are usually eaten raw, alone or with other greens. They are also cooked or pickled for consumption.

* Purslane is used in various parts of the world to treat burns, headaches, stomach, intestinal and liver ailments, cough, shortness of breath and arthritis.

*Purslane herb has also been used as a purgative, cardiac tonic, emollient, muscle relaxant, and in anti-inflammatory and diuretic treatments.

* Purslane is popularly preserved for winter by pickling Purslane in apple cider vinegar with garlic cloves and peppercorns.

* Purslane appears among a list of herbs considered to help benefit conditions such as osteoporosis and psoriasis.
Medicinal Uses:
The sticky, broken leaves of fresh purslane sooth burns, stings and swellings.  The juice was once used for treating earaches and to “fasten” teeth and soothe sore gums.  Purslane has been considered valuable in the treatment of urinary and digestive problems.  The diuretic effect of the juice makes it useful in the alleviation of bladder ailments-for example, difficulty in passing urine. The plant’s mucilaginous properties also make it a soothing remedy for gastrointestinal problems such as dysentery and diarrhea.  In Chinese herbal medicine, purslane is employed for similar problems and for appendicitis.  The Chinese also use the plant as an antidote for wasp stings and snake bite.  Clinical trials in China indicate that purslane has a mild antibiotic effect.  In one study, the juice was shown to be effective in treating hookworms.  Other studies suggest that it is valuable against bacillary dysentery.  When injected, extracts of the herb induce powerful contractions of the uterus.  Taken orally, purslane juice weakens uterine contractions.    In Europe it’s been turned into a cough syrup for sore throats.  Purslane is the richest known plant source of Omega-3 acids, found mostly in fish oils.  These fatty acids reduce blood cholesterol and pressure, clotting, and inflammation and may increase immunity.   Recommended medicinal dosage is 15-30 grams.   Use for scours in goats.

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://botanical.com/botanical/mgmh/p/prugol77.html
http://en.wikipedia.org/wiki/Portulaca_oleracea

http://www.birdflusafetysite.com/Article/Purslane—A-Therapeutic-Herb/1069

http://www.herbnet.com/Herb%20Uses_OPQ.htm

Why do some people have vertigo?

Vertigo is a certain kind of dizziness, often wrongly used to describe a fear of heights (actually called acrophobia). Vertigo is not a disease, but only a symptom. It refers to the sensation of spinning or whirling one experiences when there is a disturbance in the body equilibrium    the feeling that you or the environment is moving when there is actually no movement. The sensation of movement is called subjective vertigo while the perception of movement in objects around is called objective vertigo. The term may also be used to describe lightheadedness, faintness or unsteadiness.

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Vertigo usually occurs due to a disorder in the vestibular system (comprising the inner ear, the vestibular nerve, brainstem and cerebellum). This system is responsible for integrating sensory stimuli and movement and keeping objects in visual focus as a person moves.

When the head moves, signals are transmitted to the labyrinth, an apparatus in the inner ear that is made up of three semicircular canals surrounded by fluid. The labyrinth then transmits the information to the vestibular nerve which in turn passes it to the brainstem and cerebellum (areas of the brain that control balance, posture and motor coordination). There are a number of reasons for dizzy spells.

Benign paroxysmal positional vertigo is the most common form, caused by sudden head movements. Vertigo can also be caused by certain problems in the brain or the inner ear. It may also be caused by inflammation within the inner ear. Other causes include migraine, head trauma, decreased blood flow to the brain and base of the brain, fluctuating pressure of the inner ear fluid, systemic diseases, certain antibiotics, environmental chemicals, etc.

Source:The Telegraph(Kolkata,India)