Polygonum bistorta

Botanical Name :Polygonum bistorta or Persicaria bistorta
Family: Polygonaceae
Genus: Persicaria
Species: P. bistorta
Kingdom: Plantae
Order: Caryophyllales
Synonyms: Persicaria bistorta (L.) Samp., Polygonum ampliusculum Gand., Polygonum bistorta L., Polygonum bourdinii Gand., Polygonum carthusianorum Gand., Polygonum ellipticum Willd. ex Spreng., Polygonum pilatense Gand.

Common Name : Bistort or Common Bistort,  Meadow bistort, Snakeweed

Numerous other vernacular names have been recorded for the species in historical texts, though none is used to any extent. Many of the following refer to the plant’s use in making puddings: Adderwort, Dragonwort, Easter giant, Easter ledger, Easter ledges, Easter magiant, Easter man-giant, Gentle dock, Great bistort, Osterick, Oysterloit, Passion dock, Patience dock (this name is also used for Rumex patientia), Patient dock, Pink pokers, Pudding grass, Pudding dock, Red legs, Snakeweed, Twice-writhen, Water ledges.

Habitat :     Polygonum bistorta is native to northern and central Europe, including Britain, mountains of S. Europe, western and central Asia. It grows in damp meadows and by water, especially on acid soils.

Polygonum bistorta is a perennial plant, growing to 0.5 m (1ft 8in) by 0.5 m (1ft 8in) at a fast rate.   It  blooms  late spring into mid summer, producing tall stems ending in single terminal racemes that are club-like spikes of pink-rose colored flowers.  The seeds ripen from Aug to October. The flowers are hermaphrodite (have both male and female organs) and are pollinated by Insects.  The racemes are about 2 cm thick and 5-9 cm long and end 1 meter tall,upright growing stems. Plants grow in moist soils and under dry conditions go dormant, losing their foliage until adequate moisture exists again. This species is grown as an ornamental garden plant, especially the form ‘Superba’ which has larger, more showy flowers. Typically alpine plants growing from short, thick rhizomes that branch. The foliage is normally basal with a few smaller leaves produced near the lower end of the flowering stems. The leaves are oblong-ovate or triangular-ovate in shape and narrow at the base. The petioles are broadly winged.

The Latin name “bistorta” refers to the twisted appearance of the root. In Northern England the plant was used to make a bitter pudding in Lent from a combination of the plant’s leaves, oatmeal, egg and other herbs. It is the principal ingredient of dock pudding or Easter-Ledge Pudding.  The root of Bistort can be used to produce an astringent that was used in medicine.

Landscape Uses: Container, Ground cover. Succeeds in an ordinary garden soil[1] but prefers a moisture retentive not too fertile soil in sun or part shade. The plant repays generous treatment. A very cold-hardy plant, tolerating temperatures down to at least -25°c. Bistort was formerly cultivated as a medicinal and edible plant, though it has now fallen into virtual disuse. Plants are somewhat spreading, forming quite extensive colonies especially in low-lying pastures. They seem to be immune to the predations of rabbits. Special Features: Attractive foliage, Edible, Not North American native, Invasive, Suitable for cut flowers, Suitable for dried flowers.


Edible Uses::…Edible Parts: Leaves; Root; Seed.
Leaves (Fresh weight)

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*0 Calories per 100g
* Water : 82.6%

Medicinal Uses:



Other Uses:......Tannin.……The roots contain up to 21% tannin





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Peptic ulcers may also occur.



Abnormal parathyroid gland function:
*primary hyperparathyroidism
*solitary parathyroid adenoma
*primary parathyroid hyperplasia
*parathyroid carcinoma
*multiple endocrine neoplasia (MEN)
*familial isolated hyperparathyroidism
*lithium use
*familial hypocalciuric hypercalcaemia/familial benign hypercalcaemia

*haematologic malignancy (multiple myeloma, lymphoma, leukaemia)

Vitamin-D metabolic disordershyper:
*vitaminosis D (vitamin D intoxication)
*idiopathic hypercalcaemia of infancy
*rebound hypercalcaemia after rhabdomyolysis

Disorders related to high bone-turnover rateshyperthyroidism:
*prolonged immobilization
*thiazide use
*vitamin A intoxication
*Paget’s disease of the bone
*multiple myeloma

Renal failure
*severe secondary hyperparathyroidism:
*aluminium intoxication
*milk-alkali syndrome

Risk Factors:










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Molar Pregnancy












*Dark brown to bright red vaginal bleeding during the first trimester

*Severe nausea and vomiting

*Vaginal passage of grape-like cysts

*Rarely, pelvic pressure or pain



*High blood pressure


*Ovarian cysts


*Overactive thyroid (hyperthyroidism)





Risk Factors:







Treatment :














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Cymopterus bulbosus

Botanical Name :Cymopterus bulbosus
Family :Apiaceae
Genus : Cymopterus Raf.
Species : Cymopterus bulbosus A. Nelson
Kingdom : Plantae
Subkingdom :Tracheobionta
Superdivision : Spermatophyta
Division : Magnoliophyta
Class : Magnoliopsida
Subclass : Rosidae
Order : Apiales

Common Name :Biscuit Root





Edible Uses
Edible Parts: Condiment;  Leaves;  Root.


Medicinal Uses:
The plant has been eaten as a stomach medicine.



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Hydrocephalus, also known as “water on the brain,” is a medical condition in which there is an abnormal accumulation of cerebrospinal fluid (CSF) in the ventricles, or cavities, of the brain  and is an excessive amount of fluid that surrounds the brain and spinal cord called cerebrospinal fluid (or CSF).

This may cause increased intracranial pressure inside the skull and progressive enlargement of the head, convulsion, tunnel vision, and mental disability.The excess fluid can compress surrounding, fragile brain tissue, causing brain damage. Left untreated, hydrocephalus can be fatal. Hydrocephalus can also cause death.
Hydrocephalus is sometimes present at birth, although it may develop later. About 1 out of 500 children is born with the disorder. The outlook if you have hydrocephalus depends on how quickly the condition is diagnosed and whether any underlying disorders are present.

The name derives from the Greek words  hudro means “water”, and kephalos means “head”.

The clinical presentation of hydrocephalus varies with chronicity. Acute dilatation of the ventricular system is more likely to manifest with the nonspecific signs and symptoms of increased intracranial pressure. By contrast chronic dilatation (especially in the elderly population) may have a more insidious onset presenting, for instance, with the Hakim triad.




In infants with hydrocephalus, CSF builds up in the central nervous system, causing the fontanelle (soft spot) to bulge and the head to be larger than expected. Early symptoms may also include:

*Eyes that appear to gaze downward (Sundowning)
*Separated sutures

Symptoms that may occur in older children can include:

*Brief, shrill, high-pitched cry
*Changes in personality, memory, or the ability to reason or think
*Changes in facial appearance and eye spacing
*Crossed eyes or uncontrolled eye movements
*Difficulty feeding
*Excessive sleepiness
*Irritability, poor temper control
*Loss of bladder control (urinary incontinence)
*Loss of coordination and trouble walking
*Muscle spasticity (spasm)
*Slow growth (child 0–5 years)
*Slow or restricted movement


In hydrocephalus, CSF builds up and puts pressure on the brain, squashing the delicate tissues and causing the chambers or ventricles within the brain to swell. Without treatment damage or destruction of the brain tissues may occur.

Our brain is the consistency of gelatin, and it floats in a bath of cerebrospinal fluid. This fluid also fills large open structures, called ventricles, which lie deep inside your brain. The fluid-filled ventricles help keep the brain buoyant and cushioned.



There are two types of hydrocephalus:
Non-communicating hydrocephalus – the flow of CSF through the brain is blocked.
Communicating hydrocephalus – either too much CSF is produced, or it isn’t reabsorbed back into the tissues as it should be, so volume increases.

There are many causes of hydrocephalus and some of them are:
•Bleeding in the brain (for example if a baby is born very preterm)
•Congenital malformations (structural abnormalities that are present from birth)
•After infections in the brain
•Brain tumours
•Abnormalities in the blood vessels in the brain


Risk Factors:

*An infection within the uterus


Other factors that increase your risk of hydrocephalus include:
*Lesions or tumors of the brain or spinal cord
*Central nervous system infections
*Bleeding in the brain
*Severe head injury



In newborns and toddlers with hydrocephalus, the head circumference is enlarged rapidly and soon surpasses the 97th percentile. Since the skull bones have not yet firmly joined together, bulging, firm anterior and posterior fontanelles may be present even when the patient is in an upright position.




Because hydrocephalus can injure the brain, thought and behavior may be adversely affected. Learning disabilities including short-term memory loss are common among those with hydrocephalus, who tend to score better on verbal IQ than on performance IQ, which is thought to reflect the distribution of nerve damage to the brain. However the severity of hydrocephalus can differ considerably between individuals and some are of average or above-average intelligence. Someone with hydrocephalus may have motion and visual problems, problems with coordination, or may be clumsy. They may reach puberty earlier than the average child (see precocious puberty). About one in four develops epilepsy.



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Prickly Heat? Don’t Try Talc

Sweat (Hadise album)
Sweat (Hadise album) (Photo credit: Wikipedia)

A genuine “Indian summer” is upon us now with temperatures all over the country in the high thirties and forties. Earlier, Indians used to wear white cotton clothes in summer but now most prefer to dress in synthetic silks, and polyester fabrics, little realising that those clothes are totally inappropriate in this weather.


Even school children — who are issued uniforms with the material and tailoring regulated by the school — end up wearing thick synthetic clothes when ideally they should wear pure cotton or at least a 60 per cent cotton and 40 per cent polyester mix.

To survive, our bodies need to maintain an average internal temperature of 98.6ºF or 36.6ºC and it uses sweating to regulate the temperature. When the outside temperature is high, the body secretes sweat from glands situated in the layer below the skin. The sweat reaches the surface through coiled tubes and forms a thin film of fluid. As this layer evaporates, the body cools down. Sweating can be excessive when the temperature is high, there is increased physical exertion, there is little or no circulation of air and if the clothes are made of synthetic material that traps the sweat. (Nowadays many sports companies manufacture sports clothes out of special material that “wicks” away the sweat).

If sweat pores get blocked (by dead skin cells, dirt or talcum powder), the trapped sweat forms tiny clear bumps below the surface of the skin called miliria crystalline (prickly heat). These look unsightly but do not really cause any symptoms. Eventually, they turn red (miliria rubra), and evolve into a brown scaly rash which can be confused with pimples, folliculitis or chicken pox.

Prickly heat usually appears in covered areas where sweat cannot evaporate easily or the pores are blocked. The forehead is affected if it is covered with a fringe or cap. The upper back and chest, and the arms are other common locations. In adults the rash sometimes appears on the inner thighs or in areas where there are body folds. It is aggravated by friction between the skin and tight fitting non-absorbent synthetic clothing. The continuous rubbing can lead to the skin eventually peeling off, leaving a raw red area.

Prickly heat causes itching and a tingling sensation but scratching can cause secondary infection with bacteria. The appearance of the rash then changes and there can be a yellow pus discharge. The person may develop fever. Uninfected prickly heat, however, does not cause fever. Although prickly heat is uncomfortable and unsightly, with a little care it can be easily prevented.

• Stay away from the direct heat of the sun as far as possible

• Wear loose fitting cotton clothes or at least a 60-40 mix of cotton and polyester

• Make sure school uniforms are stitched out of natural materials, preferably thin materials

• Try to ensure that schools have fans and ventilation.

• Do not scratch. The more you scratch, the more it will itch.

• Use a mild dose of antihistamine to control itching.

• Do not apply thick oil-based creams and talc. They will only block the pores further.

Bathe two or three times a day in tepid water. Add a teaspoon of sodium bicarbonate to a bucket of water before bathing till the prickly heat disappears.

• Use soap containing trichlorhexidine (Dial, Neko) Do not apply soap directly to the skin. Use a moist wash rag, a herbal scrubber or a loofah.

• If prickly heat becomes red and pustular, changes appearance or the temperature rises, consult a doctor immediately.

Contrary to advertisements on television, talc does not soothe, relieve or prevent prickly heat. Talc is made up of finely powdered combinations of ground zinc stearate, and silicates. It blocks the skin pores, increasing the sweat build up and aggravating prickly heat.

Talc causes other medical problems as well. The size of the particles is so small that they can easily be inhaled. The particles can reach the smallest areas of the lung and cause pneumonia, inflammation or swelling of the airways. This can be fatal in babies. If applied to the groin and genital areas, talc can migrate through the vagina, uterus, and fallopian tubes to the ovary. Some scientific studies have found a relationship between the use of talcum powder and cancer of the ovary.

Baby powder is talc based and should not be used. Nappy rash is different from prickly heat and the treatment is different too.

If you get prickly heat, bathe two to three times a day. Use plain calamine lotion (not creams and ointment) to relieve the itching. If secondary infection has occurred, consult a doctor.

You may click to see :
*Remedies for Prickly Heat
*Natural Remedy for Prickly Heat

* Two baths a day keep bacteria at bay

Source : The Telegraph ( Kolkata, India)

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Huntington’s Disease


Most people with Huntington’s disease develop signs and symptoms in their 40s or 50s, but the onset of disease may be earlier or later in life. When disease onset begins before age 20, the condition is called juvenile Huntington’s disease. Earlier onset often results in a somewhat different presentation of symptoms and faster disease progression.


Medications are available to help manage the symptoms of Huntington’s disease, but treatments can’t prevent the physical, mental and behavioral decline associated with the condition.


Symptoms of Huntington’s disease commonly become noticeable between the ages of 35 and 44 years, but they can begin at any age from infancy to old age. In the early stages, there are subtle changes in personality, cognition, and physical skills. The physical symptoms are usually the first to be noticed, as cognitive and psychiatric symptoms are generally not severe enough to be recognized on their own at the earlier stages. Almost everyone with Huntington’s disease eventually exhibits similar physical symptoms, but the onset, progression and extent of cognitive and psychiatric symptoms vary significantly between individuals.

The most characteristic initial physical symptoms are jerky, random, and uncontrollable movements called chorea. Chorea may be initially exhibited as general restlessness, small unintentionally initiated or uncompleted motions, lack of coordination, or slowed saccadic eye movements. These minor motor abnormalities usually precede more obvious signs of motor dysfunction by at least three years. The clear appearance of symptoms such as rigidity, writhing motions or abnormal posturing appear as the disorder progresses. These are signs that the system in the brain that is responsible for movement is affected.[6] Psychomotor functions become increasingly impaired, such that any action that requires muscle control is affected. Common consequences are physical instability, abnormal facial expression, and difficulties chewing, swallowing and speaking. Eating difficulties commonly cause weight loss and may lead to malnutrition.  Sleep disturbances are also associated symptoms. Juvenile HD differs from these symptoms in that it generally progresses faster and chorea is exhibited briefly, if at all, with rigidity being the dominant symptom. Seizures are also a common symptom of this form of HD.

Cognitive abilities are impaired progressively. Especially affected are executive functions which include planning, cognitive flexibility, abstract thinking, rule acquisition, initiating appropriate actions and inhibiting inappropriate actions. As the disease progresses, memory deficits tend to appear. Reported impairments range from short-term memory deficits to long-term memory difficulties, including deficits in episodic (memory of one’s life), procedural (memory of the body of how to perform an activity) and working memory. Cognitive problems tend to worsen over time, ultimately leading to dementia. This pattern of deficits has been called a subcortical dementia syndrome to distinguish it from the typical effects of cortical dementias e.g. Alzheimer‘s disease.

Reported neuropsychiatric manifestations are anxiety, depression, a reduced display of emotions (blunted affect), egocentrism, aggression, and compulsive behavior, the latter of which can cause or worsen addictions, including alcoholism, gambling, and hypersexuality.  Difficulties in recognizing other people’s negative expressions have also been observed. Prevalence of these symptoms is also highly variable between studies, with estimated rates for lifetime prevalence of psychiatric disorders between 33% and 76%.  For many sufferers and their families these symptoms are among the most distressing aspects of the disease, often affecting daily functioning and constituting reason for institutionalisation. Suicidal thoughts and suicide attempts are more common than in the general population.


Reported prevalences of behavioral and psychiatric symptoms in Huntington’s disease :
Irritability 38–73%
Apathy 34–76%
Anxiety 34–61%
Depressed mood 33–69%
Obsessive and compulsive 10–52%
Psychotic 3–11%








Risk Factors:
If one of your parents has Huntington’s disease, you have a 50 percent chance of developing the disease. In rare cases, you may develop Huntington’s disease without having a family history of the condition. Such an occurrence may be the result of a genetic mutation that happened during your father’s sperm development.

After the onset of Huntington’s disease, a person’s functional abilities gradually worsen over time. The rate of disease progression and duration varies. The time from disease onset to death is often about 10 to 30 years. Juvenile onset usually results in death in fewer than 15 years.


Eventually, a person with Huntington’s disease requires help with all activities of daily living and care. Late in the disease, he or she will likely be confined to a bed and unable to speak. However, a person’s understanding of surroundings and interactions remain intact for a long time.

Common causes of death include:

*Pneumonia or other infections
*Injuries related to falls
*Complications related to the inability to swallow


A physical examination, sometimes combined with a psychological examination, can determine whether the onset of the disease has begun. Excessive unintentional movements of any part of the body are often the reason for seeking medical consultation. If these are abrupt and have random timing and distribution, they suggest a diagnosis of HD. Cognitive or psychiatric symptoms are rarely the first diagnosed; they are usually only recognized in hindsight or when they develop further. How far the disease has progressed can be measured using the unified Huntington’s disease rating scale which provides an overall rating system based on motor, behavioral, cognitive, and functional assessments. Medical imaging, such as computerized tomography (CT) and magnetic resonance imaging (MRI), only shows visible cerebral atrophy in the advanced stages of the disease. Functional neuroimaging techniques such as fMRI and PET can show changes in brain activity before the onset of physical symptoms.


A pre-symptomatic test is a life-changing event and a very personal decision. The main reason given for choosing testing for HD is to aid in career and family decisions. Over 95% of individuals at risk of inheriting HD do not proceed with testing, mostly because there is no treatment. A key issue is the anxiety an individual experiences about not knowing whether they will eventually develop HD, compared to the impact of a positive result.  Irrespective of the result, stress levels have been found to be lower two years after being tested, but the risk of suicide is increased after a positive test result. Individuals found to have not inherited the disorder may experience survivor guilt with regard to family members who are affected. Other factors taken into account when considering testing include the possibility of discrimination and the implications of a positive result, which usually means a parent has an affected gene and that the individual’s siblings will be at risk of inheriting it. Genetic counseling in HD can provide information, advice and support for initial decision-making, and then, if chosen, throughout all stages of the testing process. Counseling and guidelines on the use of genetic testing for HD have become models for other genetic disorders, such as autosomal dominant cerebellar ataxias. Presymptomatic testing for HD has also influenced testing for other illnesses with genetic variants such as polycystic kidney disease, familial Alzheimer’s disease and breast cancer

Embryos produced using in vitro fertilisation may be genetically tested for HD using preimplantation genetic diagnosis. This technique, where a single cell is extracted from a 4 to 8 cell embryo and then tested for the genetic abnormality, can then be used to ensure embryos with affected HTT genes are not implanted, and therefore any offspring will not inherit the disease. It is also possible to obtain a prenatal diagnosis for an embryo or fetus in the womb.

Differential diagnosis:
About 90% of HD diagnoses based on the typical symptoms and a family history of the disease are confirmed by genetic testing to have the expanded trinucleotide repeat that causes HD. Most of the remaining are called HD-like disorders.  Most of these other disorders are collectively labelled HD-like (HDL). The cause of most HDL diseases is unknown, but those with known causes are due to mutations in the prion protein gene (HDL1), the junctophilin 3 gene (HDL2), a recessively inherited HTT gene (HDL3—only found in one family and poorly understood), and the gene encoding the TATA box-binding protein (HDL4/SCA17). Other autosomal dominant diseases that can be misdiagnosed as HD are dentatorubral-pallidoluysian atrophy and neuroferritinopathy. There are also autosomal recessive disorders that resemble sporadic cases of HD. Main examples are chorea acanthocytosis, pantothenate kinase-associated neurodegeneration and X-linked McLeod syndrome







The length of the trinucleotide repeat accounts for 60% of the variation in the age of onset and the rate of progression of symptoms. A longer repeat results in an earlier age of onset and a faster progression of symptoms. For example, individuals with a trinucleotide repeat greater than sixty repeats often develop the disease before twenty years of age, and those with less than forty repeats may not develop noticeable symptoms. The remaining variation is due to environmental factors and other genes that influence the mechanism of the disease.

Life expectancy in HD is generally around 20 years following the onset of visible symptoms.  Most of the complications that are life-threatening result from muscle coordination issues, or to a lesser extent from behavioural changes resulting from the decline in cognitive function. The largest risk is pneumonia, which is the cause of death of one-third of those with HD. As the ability to synchronise movements deteriorates, difficulty clearing the lungs and an increased risk of aspirating food or drink both increase the risk of contracting pneumonia. The second greatest risk is heart disease, which causes almost a quarter of fatalities of those with HD. Suicide is the next greatest cause of fatalities, with 7.3% of those with HD taking their own lives and up to 27% attempting to do so. It is unclear to what extent suicidal thoughts are influenced by psychiatric symptoms, as they may be considered to be a response of an individual to retain a sense of control of their life or to avoid the later stages of the disease.  Other associated risks include choking, physical injury from falls, and malnutrition.





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Human Papilloma Virus (HPV)

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•vulval cancer
•cancer of the vagina
•cancer of the penis
•anal cancer
•head and neck (tongue, tonsils and throat) cancers






Risk Factors:
*You had sexual contact at an early age.



*Any of your sexual partners did not wear a condom.

HPV and cancer risks:


•cervical cancer (the most common HPV-associated cancer)
•penile cancer (possibly 40 per cent linked)
•anal cancer (around 85 per cent linked)





Other testing:





•Genital warts, which can be cauterised or treated chemically.













Oral infection:








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Lomatium dissectum

Botanical Name: Lomatium dissectum
Family: Apiaceae
Tribe: Selineae
Genus: Lomatium
Species: L. dissectum
Kingdom: Plantae
Order: Apiales

Common Name: Fernleaf biscuitroot.

Habitat :It is native to much of western North America, where it grows in varied habitat. It is found in the eastern Transverse Ranges and the Sierra Nevada in California.

Lomatium dissectum is a perennial herb reaching up to 1.4 meters tall, growing from a thick taproot. The leaves are mostly attached near the base of the plant, spreading with petioles up to 30 centimeters long and large blades divided into many small, narrow segments. The inflorescence is an umbel of many small yellow or reddish flowers, each cluster on a ray up to 10 centimeters long. The fruits resemble pumpkin seeds.

click & see the pictures

Medicinal Uses:
Both Lomatium and Ligusticum were used by Native Americans and early American medical practitioners for a variety of chronic or severe infectious disease states, particularly those of viral origin. Modern research is rather limited, but clinical trials have supported the inclusion of these botanicals for viral infections including HIV and condyloma.  Traditionally it’s demonstrated efficacy against a variety of bacterial infections including tuberculosis.   Lomatium contains an oleoresin rich in terpenes. It acts as a stimulating expectorant, enhancing the liquification and consequent elimination of mucus from the lungs. It also appears to exert a strong antibacterial activity, interfering with bacterial replication and inducing increased phagocytosis. The resin also contains a number of furanocoumarins including nodakenetin, columbianin and pyranocoumarin. These resins may be responsible for the plant’s antiviral effect. They may also be partly responsible for the phagocytic action lomatium causes.

Based on empirical evidence and discussions with clinical herbalists, lomatium can be used as an antimicrobial, especially in the lungs and upper respiratory tract. It provides quick-acting relief in cases of viral or bacterial infection, particularly when there is a large amount of thick or sticky mucus and infection is deep-seated and persistent. Consider taking lomatium for pneumonia, infective bronchitis and tuberculosis.

As an immunostimulant, this herb is traditionally used to treat colds and flus. Many cases during the 1920s U.S. influenza epidemic were successfully treated with lomatium by the professional herbalists of the time, and it has been used for this purpose by Native Americans since the introduction of influenza to the Americas.  Its infection-fighting ability makes lomatium valuable as a mouthwash and gargle for oral and throat infections, as a douche for bacterial and viral infections or candida, as a skin wash for infected cuts or wounds, and in many other first- aid situations.  Both tea and tincture forms are commonly used. For acute bacterial or viral infections, 2.5 ml of the tincture diluted in water can be used three to four times daily. A painful, itchy full-body rash that can persist for days occurs frequently when the crude tincture is used.  It seems to occur more commonly with the strong, fresh-root preparation and disappears when treatment stops.



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Aristolochia debilis


Botanical Name :Aristolochia debilis
Family: Aristolochiaceae
Subfamily: Aristolochioideae
Genus: Aristolochia
Species: Aristolochia debilis
Regnum: Plantae
Cladus: Angiosperms
Cladus: Magnoliids
Order: Piperales

Synonyms : A. recurvilabra. Hance.

Common Name : Ma Dou Ling,  Birthwort, Frail

Habitat :Aristolochia debilis is native to  E. Asia – C,hina, Japan. It grows in the roadside thickets and meadows in lowland, C. and S. Japan and in China.

Aristolochia debilis is a perennial herb growing to 1 m (3ft 3in) by 1 m (3ft 3in).


You may click to see the pictures


Prefers a well-drained loamy soil, rich in organic matter, in sun or semi-shade. Succeeds in ordinary garden soil. This species is not very hardy in Britain, tolerating temperatures down to about -5°c. Most species in this genus have malodorous flowers that are pollinated by flies.

Seed – best sown in a greenhouse as soon as it is ripe in the autumn. Pre-soak stored seed for 48 hours in hand-hot water and surface sow in a greenhouse. Germination usually takes place within 1 – 3 months at 20°c. Stored seed germinates better if it is given 3 months cold stratification at 5°c. When large enough to handle, prick the seedlings out into individual pots and grow them on in the greenhouse for their first winter. Plant out in late spring or early summer after the last expected frosts. Division in autumn. Root cuttings in winter[

Edible Uses:Leaves are edible.They are cooked. It is said that the leaves of this species are not poisonous but caution is advised.

Medicinal Uses:
Alterative;  Anodyne;  Antibacterial;  Antifungal;  AntiinflammatoryAntitussiveCarminative;  Cytotoxic;  Diuretic;  Expectorant;  Hypotensive;
Stomachic;  Tonic.

Alterative, antibacterial, antifungal, diuretic. Stimulates energy circulation. The fruit and its capsule are antiasthmatic, antiseptic, antitussive and expectorant. It is used internally in the treatment of asthma and various other chest complaints, haemorrhoids and hypertension. The root is anodyne and anti-inflammatory. It is used internally in the treatment of snakebite, gastric disorders involving bloating, and is clinically effective against hypertension. It is harvested in the autumn and dried for later use. The whole plant is antitussive, carminative, stimulant and tonic. The root contains aristolochic acid. This has anti-cancer properties and can be used in conjunction with chemotherapy and radiotherapy. Aristolochic acid can also be used in the treatment of acute and serious infections such as TB, hepatitis, liver cirrhosis and infantile pneumonia. It also increases the cellular immunity and phagocytosis function of the phagocytic cells. Aristolochic acid is said to be too toxic for clinical use

Internally used for arthritis, purulent wounds, hypertension, snake and insect bites, and gastric disorders involving bloating (roots); for asthma, wet coughs, bronchitis, hypertension and hemorrhoids (fruits). Indications: heat in the lungs manifested as cough with profuse yellow sputum and asthma.  The fruit (Madouling) is used with Loquat Leaf, Peucedanum root, Mulberry bark and Scutellaria root.  Deficiency of the lungs manifested as cough with scanty sputum or with bloody sputum and shortness of breath.  Fruit is used with Glehnia root, Ophiopogon root, Aster root and Donkey hide gelatin.

Known Hazards: No specific details for this species is known  but most members of this genus have poisonous roots and stems. The plant contains aristolochic acid, this has received rather mixed reports on its toxicity. According to one report aristolochic acid stimulates white blood cell activity and speeds the healing of wounds, but is also carcinogenic and damaging to the kidneys. Another report says that it is an active antitumour agent but is too toxic for clinical use. Another report says that aristolochic acid has anti-cancer properties and can be used in conjunction with chemotherapy and radiotherapy and that it also increases the cellular immunity and phagocytosis function of the phagocytic cells




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