Botanical Name : Anemone chinensis Family: Ranunculaceae Genus: Anemone Species: A. chinensis Kingdom: Plantae Order: Ranunculales
Common Name : Bai Tou Weng, , Pulsatilla chinensis
Habitat : Anemone chinensis is native to E. Asia – N. China to E. Siberia. It grows in dry grassy places and rocky hillsides. Forest margins and slopes at elevations of 200 – 3200 metres in China. Description:
Pulsatilla chinensis is a perennial plant, growing to 0.3 m (1ft). It is in flower from Mar to May, and the seeds ripen from Jun to July. The flowers are hermaphrodite (have both male and female organs) and are pollinated by Insects. CLICK & SEE THE PICTURES..
Requires a well-drained humus-rich gritty soil and a sunny position. Tolerates alkaline soils. Plants are hardy to about . They are said to be difficult to grow in Britain, requiring a dry winter and spring followed by a warm humid summer. Large plants have a deep woody rootstock and transplant badly. A greedy plant, inhibiting the growth of nearby plants, especially legumes.
Seed – best sown as soon as it is ripe in early summer in a cold frame. The seed usually germinates in about 2 – 3 weeks. Sow stored seed in late winter in a cold frame. Germination takes about 1 – 6 months at 15°c. When they are large enough to handle, prick the seedlings out into individual pots and grow them on in the greenhouse for at least their first winter. Plant them out into their permanent positions in the spring. Root cuttings, 4cm long taken in early winter, potted up in a mixture of peat and sand. They can also be taken in July/August, planted vertically in pots in a greenhouse or frame. Chemical composition: The whole herb contain protoanemonin; Root contain triterpene saponins. Contain anemonin, saponin about 9%. In addition, contain Anemonin, is a kind of strong heart poison, but remove root whole herb have strong heart effect, its strong heart composition have Okinalin, C32 H64 O2, Okinalein, C4 H6 O2. Congener Pulsatilla cernua root contain Stigma- sterol, C29 H46 O and B-Sitosterol, and contain Hederagenin, Oleanolic acid and minute quantity of Acetyloleanolic acid. And from the
Ulsatilla nigricans root separate a kind of glycoside, named Pulsatoside A, its aglucone is Hederagenin, its sugar is arabinose, galactose, glucose and rhamnose. Root contain: Okinalin. Medicinal Uses:
In Traditional Chinese Medicine, pulsatilla is used as an anti-inflammatory and is considered specific for amoebic and bacterial dysentery with bloody stool, abdominal pain and tenesmus and is often used with phellodendron bark, coptis rhizome and ash bark, known as Pulsatilla Decoction (Baitouweng Tang). It is most commonly taken as a decoction to counter infection within the gastrointestinal tract. The root is also used to treat malarial fever. In addition, this herb can be used with flavescent sophora to prepare a lotion for the treatment of trichomoniasis vaginalis. The root contains the lactone protoanemonin which has an irritant and antibacterial action. Protoanemonin is destroyed when the root is dried. The fresh herb is a cardiac and nervous sedative, producing a hypnotic state with a diminution of the senses followed by a paralyzing action. A constituent similar to digitalis can be extracted from the whole herb with the roots removed. This is cardiotonic.
Bai Tou Weng is thought to clear toxicity and to lower fever. It is most commonly taken as a decoction to counter infection within the gastro-intestinal tract. The root is anodyne, anti-inflammatory, antispasmodic, astringent and sedative. The root is an effective cure for bacterial and amoebic dysentery. It is also used in the treatment of malaria, nose bleeds and haemorrhoids and is used externally to treat Trichomonas vaginitis. The root is harvested in the autumn or before the plant comes into flower in the spring, it can be dried for later use. The root contains the lactone protoanemonin which has an irritant and antibacterial action. Protoanemonin is destroyed when the root is dried. The fresh herb is a cardiac and nervous sedative, producing a hypnotic state with a diminution of the senses followed by a paralysing action. A constituent similar to digitalis can be extracted from the whole herb with the roots removed. This is cardiotonic
Known Hazards : Although no mention has been seen for this species, at least one member of the genus is slightly toxic, the toxins being dissipated by heat or by drying the plant
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.
Definition: Gastroparesis (gastro-, “stomach” + -paresis, “partial paralysis”), also called delayed gastric emptying, is a medical condition consisting of a paresis (partial paralysis) of the stomach, resulting in food remaining in the stomach for an abnormally long time. Normally, the stomach contracts to move food down into the small intestine for additional digestion. The vagus nerve controls these contractions. Gastroparesis may occur when the vagus nerve is damaged and the muscles of the stomach and intestines do not properly function. Food then moves slowly or stops moving through the digestive tract….CLICK & SEE
YOU MAY CLICK & SEE : Our Digestive System and How It Works Symptoms: The most common symptoms of gastroparesis are the following:
*Chronic nausea (93%)
*Vomiting (especially of undigested food) (68-84%)
*Abdominal pain (46-90%)
*A feeling of fullness after eating just a few bites (60-86%)
Other symptoms include the following:
*Erratic blood glucose levels
*Lack of appetite
*Spasms of the stomach wall
*Weight loss and malnutrition
Morning nausea may also indicate gastroparesis. Vomiting may not occur in all cases, as sufferers may adjust their diets to include only small amounts of food.
Symptoms may be aggravated by eating greasy or rich foods, large quantities of foods with fiber—such as raw fruits and vegetables—or drinking beverages high in fat or carbonation. Symptoms may be mild or severe, and they can occur frequently in some people and less often in others. The symptoms of gastroparesis may also vary in intensity over time in the same individual. Sometimes gastroparesis is difficult to diagnose because people experience a range of symptoms similar to those of other diseases.
Transient gastroparesis may arise in acute illness of any kind, as a consequence of certain cancer treatments or other drugs which affect digestive action, or due to abnormal eating patterns.
It is frequently caused by autonomic neuropathy. This may occur in people with type 1 or type 2 diabetes. In fact, diabetes mellitus has been named as the most common cause of gastroparesis, as high levels of blood glucose may affect chemical changes in the nerves.The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in gastroparesis. Other possible causes include anorexia nervosa and bulimia nervosa, which may also damage the vagus nerve. Gastroparesis has also been associated with connective tissue diseases such as scleroderma and Ehlers-Danlos syndrome, and neurological conditions such as Parkinson’s disease. It may also occur as part of a mitochondrial disease.
Chronic gastroparesis can be caused by other types of damage to the vagus nerve, such as abdominal surgery. Heavy cigarette smoking is also a plausible cause since smoking causes damage to the stomach lining.
Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection. “Stomach flu”, mononucleosis, and other ailments have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.
Gastroparesis sufferers are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men.A hormonal link has been suggested, as gastroparesis symptoms tend to worsen the week before menstruation when progesterone levels are highest. Neither theory has been proven definitively.
Gastroparesis can also be connected to hypochlorhydria and be caused by chloride, sodium and/or zinc deficiency, as these minerals are needed for the stomach to produce adequate levels of gastric acid (HCL) in order to properly empty itself of a meal.
Other identifiable causes of gastroparesis include intestinal surgery and nervous system diseases such as Parkinson’s disease or multiple sclerosis. For reasons that are not very clear, gastroparesis is more commonly found in women than in men.
The complications of gastroparesis can include
*severe dehydration due to persistent vomiting
*gastroesophageal reflux disease (GERD), which is GER that occurs more than twice a week for a few weeks; GERD can lead to esophagitis— irritation of the esophagus
*bezoars, which can cause nausea, vomiting, obstruction, or interfere with absorption of some medications in pill form
*difficulty managing blood glucose levels in people with diabetes
*malnutrition due to poor absorption of nutrients or a low calorie intake
*decreased quality of life, including work absences due to severe symptoms
Gastroparesis is diagnosed through a physical exam, medical history, blood tests, tests to rule out blockage or structural problems in the GI tract, and gastric emptying tests. Tests may also identify a nutritional disorder or underlying disease. To rule out any blockage or other structural problems, the doctor may perform one or more of the following tests:
*Upper gastrointestinal (GI) endoscopy. This procedure involves using an endoscope—a small, flexible tube with a light—to see the upper GI tract, which includes the esophagus, stomach, and duodenum—the first part of the small intestine. The test is performed at a hospital or outpatient center by a gastroenterologist—a doctor who specializes in digestive diseases. The endoscope is carefully fed down the esophagus and into the stomach and duodenum. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining. A person may receive a liquid anesthetic that is gargled or sprayed on the back of the throat. An intravenous (IV) needle is placed in a vein in the arm if general anesthesia is given. The test may show blockage or large bezoars—solid collections of food, mucus, vegetable fiber, hair, or other material that cannot be digested in the stomach—that are sometimes softened, dissolved, or broken up during an upper GI endoscopy.
Ulcerative colitis (Colitis ulcerosa, UC) is a form of inflammatory bowel disease (IBD). Ulcerative colitis is a form of colitis, a disease of the colon (the largest portion of the large intestine), that includes characteristic ulcers, or open sores. The main symptom of active disease is usually constant diarrhea mixed with blood, of gradual onset. IBD is often confused with irritable bowel syndrome (IBS). CLICK & SEE THE PICTURES
It is a disease that causes inflammation and sores (ulcers) in the lining of the large intestine (colon ). It usually affects the lower section (sigmoid colon) and the rectum. But it can affect the entire colon. In general, the more of the colon that’s affected, the worse the symptoms will be.
Ulcerative colitis shares much in common with Crohn’s disease, another form of IBD, but Crohn’s disease can affect the whole gastrointestinal tract while ulcerative colitis only attacks the large intestine, and while ulcerative colitis can be treated by performing a total colectomy (i.e., removing the entire large intestine), surgery for Crohn’s disease involves removing the damaged parts of the intestine and reconnecting the healthy parts, which does not cure Crohn’s, as it can recur after surgery, mostly at the site of the intestinal anastomosis (connection) or in other areas. Ulcerative colitis is an intermittent disease, with periods of exacerbated symptoms, and periods that are relatively symptom-free. Although the symptoms of ulcerative colitis can sometimes diminish on their own, the disease usually requires treatment to go into remission. Ulcerative colitis has an incidence of 1 to 20 cases per 100,000 individuals per year, and a prevalence of 8 to 246 per 100,000 individuals.
The disease is more prevalent in northern countries of the world, as well as in northern areas of individual countries or other regions. Rates tend to be higher in more affluent countries, which may indicate the increased prevalence is due to increased rates of diagnosis. It may also indicate that an industrial or Western diet and lifestyle increases the prevalence of this disease, including symptoms which may or may not be related to ulcerative colitis. Although UC has no known cause, there is a presumed genetic component to susceptibility. The disease may be triggered in a susceptible person by environmental factors. Although dietary modification may reduce the discomfort of a person with the disease, ulcerative colitis is not thought to be caused by dietary factors.
Ulcerative colitis, like its sister condition Crohn’s disease, is treated as an autoimmune disease. Treatment is with anti-inflammatory drugs, immunosuppression, and biological therapy targeting specific components of the immune response. Colectomy (partial or total removal of the large bowel through surgery) is occasionally necessary if the disease is severe, does not respond to treatment, or if significant complications develop. A total proctocolectomy (removal of the entirety of the large bowel and rectum) can cure ulcerative colitis (extraintestinal symptoms will remain), as the disease only affects the large bowel and rectum. While extra intestinal symptoms will remain, complications may develop.
As ulcerative colitis is believed to have a systemic (i.e., autoimmune) origin, patients may present with comorbidities leading to symptoms and complications outside the colon. The frequency of such extraintestinal manifestations has been reported as anywhere between 6 and 47 percent. These include the following:
*Aphthous ulcer of the mouth
*Ophthalmic (involving the eyes):
*Iritis or uveitis, which is inflammation of the iris Episcleritis
#Seronegative arthritis, which can be a large-joint oligoarthritis (affecting one or two joints), or may affect many small joints of the hands and feet
#Ankylosing spondylitis, arthritis of the spine
#Sacroiliitis, arthritis of the lower spine
*Cutaneous (related to the skin):…CLICK & SEE
#Erythema nodosum, which is a panniculitis, or inflammation of subcutaneous tissue involving the lower extremities
#Pyoderma gangrenosum, which is a painful ulcerating lesion involving the skin
*Deep venous thrombosis and pulmonary embolism
*Autoimmune hemolytic anemia
*Clubbing, a deformity of the ends of the fingers.
*Primary sclerosing cholangitis, a distinct disease that causes inflammation of the bile ducts
The clinical presentation of ulcerative colitis depends on the extent of the disease process. Patients usually present with diarrhea mixed with blood and mucus, of gradual onset that persists for an extended period (weeks). They may also have weight loss and blood on rectal examination. The inflammation caused by the disease along with chronic loss of blood from the GI tract leads to increased rates of anaemia. The disease may be accompanied with different degrees of abdominal pain, from mild discomfort to painful bowel movements or painful abdominal cramping with bowel movements.
Ulcerative colitis is associated with a general inflammatory process that affects many parts of the body. Sometimes these associated extra-intestinal symptoms are the initial signs of the disease, such as painful arthritic knees in a teenager and may be seen in adults also. The presence of the disease may not be confirmed immediately, however, until the onset of intestinal manifestations.
Extent of Involvement:
Ulcerative colitis is normally continuous from the rectum up the colon. The disease is classified by the extent of involvement, depending on how far up the colon the disease extends:
*Distal colitis, potentially treatable with enemas:
#Proctitis: Involvement limited to the rectum.
#Proctosigmoiditis: Involvement of the rectosigmoid colon, the portion of the colon adjacent to the rectum.
#Left-sided colitis: Involvement of the descending colon, which runs along the patient’s left side, up to the splenic flexure and the beginning of the transverse colon.
*Extensive colitis, inflammation extending beyond the reach of enemas:
#Pancolitis: Involvement of the entire colon, extending from the rectum to the cecum, beyond which the small intestine begins.
Severities of the diseases:..>...click & see
In addition to the extent of involvement, people may also be characterized by the severity of their disease.
#Mild disease correlates with fewer than four stools daily, with or without blood, no systemic signs of toxicity, and a normal erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP). There may be mild abdominal pain or cramping. Patients may believe they are constipated when in fact they are experiencing tenesmus, which is a constant feeling of the need to empty the bowel accompanied by involuntary straining efforts, pain, and cramping with little or no fecal output. Rectal pain is uncommon.
#Moderate disease correlates with more than four stools daily, but with minimal signs of toxicity. Patients may display anemia (not requiring transfusions), moderate abdominal pain, and low grade fever, 38 to 39 °C (100 to 102 °F).
Severe disease, correlates with more than six bloody stools a day or observable massive and significant bloody bowel movement, and evidence of toxicity as demonstrated by fever, tachycardia, anemia or an elevated ESR or CRP.
#Fulminant disease correlates with more than ten bowel movements daily, continuous bleeding, toxicity, abdominal tenderness and distension, blood transfusion requirement and colonic dilation (expansion). Patients in this category may have inflammation extending beyond just the mucosal layer, causing impaired colonic motility and leading to toxic megacolon. If the serous membrane is involved, colonic perforation may ensue. Unless treated, fulminant disease will soon lead to death. Causes:
Experts aren’t sure what causes it. They think it might be caused by the immune system overreacting to normal bacteria in the digestive tract. Or other kinds of bacteria and viruses may cause it.
Some factors are indicative:
*A genetic component to the etiology of ulcerative colitis can be hypothesized based on the following:
#Aggregation of ulcerative colitis in families.
#Identical twin concordance rate of 10% and dizygotic twin concordance rate of 3%
#Ethnic differences in incidence
#Genetic markers and linkages
There are 12 regions of the genome that may be linked to ulcerative colitis, including, in the order of their discovery, chromosomes 16, 12, 6, 14, 5, 19, 1, and 3, but none of these loci have been consistently shown to be at fault, suggesting that the disorder arises from the combination of multiple genes. For example, chromosome band 1p36 is one such region thought to be linked to inflammatory bowel disease.
Some of the putative regions encode transporter proteins such as OCTN1 and OCTN2. Other potential regions involve cell scaffolding proteins such as the MAGUK family. There may even be human leukocyte antigen associations at work. In fact, this linkage on chromosome 6 may be the most convincing and consistent of the genetic candidates.
Multiple autoimmune disorders have been recorded with the neurovisceral and cutaneous genetic porphyrias including ulcerative colitis, Crohn’s disease, celiac disease, dermatitis herpetiformis, diabetes, systemic and discoid lupus, rheumatoid arthritis, ankylosing spondylitis, scleroderma, Sjogren’s disease and scleritis. Physicians should be on high alert for porphyrias in families with autoimmune disorders and care must be taken with potential porphyrinogenic drugs, including sulfasalazine.
Many hypotheses have been raised for environmental contributants to the pathogenesis of ulcerative colitis. They include the following:
#Diet: as the colon is exposed to many dietary substances which may encourage inflammation, dietary factors have been hypothesized to play a role in the pathogenesis of both ulcerative colitis and Crohn’s disease. There have been few studies to investigate such an association, but one study showed no association of refined sugar on the prevalence of ulcerative colitis. High intake of unsaturated fat and vitamin B6 may enhance the risk of developing ulcerative colitis. Other identified dietary factors that may influence the development and/or relapse of the disease include meat protein and alcoholic beverages. Specifically, sulfur has been investigated as being involved in the etiology of ulcerative colitis, but this is controversial. Sulfur restricted diets have been investigated in patients with UC and animal models of the disease. The theory of sulfur as an etiological factor is related to the gut microbiota and mucosal sulfide detoxification in addition to the diet.
#Breastfeeding: There have been conflicting reports of the protection of breastfeeding in the development of inflammatory bowel disease. One Italian study showed a potential protective effect.
Several scientific studies have posited that Accutane is a possible trigger of Crohn’s disease and ulcerative colitis in some individuals. Three cases in the United States have gone to trial thus far, with all three resulting in multi-million dollar judgements against the makers of isotretinoin.
Ulcerative colitis is an autoimmune disease characterized by T-cells infiltrating the colon. In contrast to Crohn’s disease, which can affect areas of the gastrointestinal tract outside of the colon, ulcerative colitis usually involves the rectum and is confined to the colon, with occasional involvement of the ileum. This so-called “backwash ileitis” can occur in 10–20% of patients with pancolitis and is believed to be of little clinical significance. Ulcerative colitis can also be associated with comorbidities that produce symptoms in many areas of the body outside the digestive system. Surgical removal of the large intestine often cures the disease.
Levels of sulfate-reducing bacteria tend to be higher in persons with ulcerative colitis. This could mean that there are higher levels of hydrogen sulfide in the intestine. An alternative theory suggests that the symptoms of the disease may be caused by toxic effects of the hydrogen sulfide on the cells lining the intestine.
An increased amount of colonic sulfate-reducing bacteria has been observed in some patients with ulcerative colitis, resulting in higher concentrations of the toxic gas hydrogen sulfide. Human colonic mucosa is maintained by the colonic epithelial barrier and immune cells in the lamina propria. N-butyrate, a short-chain fatty acid, gets oxidized through the beta oxidation pathway into carbon dioxide and ketone bodies. It has been shown that N-butyrate helps supply nutrients to this epithelial barrier. Studies have proposed that hydrogen sulfide plays a role in impairing this beta oxidation pathway by interrupting the short chain acetyl CoA dehydrogenase, an enzyme within the pathway. Furthermore, it has been suggested that the protective benefit of smoking in ulcerative colitis is due to the hydrogen cyanide from cigarette smoke reacting with hydrogen sulfide to produce the nontoxic isothiocyanate, thereby inhibiting sulfides from interrupting the pathway. An unrelated study suggested that the sulphur contained in red meats and alcohol may lead to an increased risk of relapse for patients in remission.
The doctor will likely diagnose ulcerative colitis after ruling out other possible causes for your signs and symptoms. To help confirm a diagnosis of ulcerative colitis, he or she may want to have one or more of the following tests and procedures:
*Blood tests.The doctor may suggest blood tests to check for anemia — a condition in which there aren’t enough red blood cells to carry adequate oxygen to the patient’s tissues — or to check for signs of infection.
*Stool sample. White blood cells in stool can indicate ulcerative colitis. A stool sample can also help rule out other disorders, such as infections caused by bacteria, viruses and parasites.
*Colonoscopy. This exam allows the doctor to view the entire colon using a thin, flexible, lighted tube with an attached camera. During the procedure,the doctor can also take small samples of tissue (biopsy) for laboratory analysis. Sometimes a tissue sample can help confirm a diagnosis.
*Flexible sigmoidoscopy.The doctor uses a slender, flexible, lighted tube to examine the sigmoid, the last portion of the patient’s colon. If the colon is severely inflamed, the doctor may perform this test instead of a full colonoscopy.
*X-ray. If the patient have severe symptoms, the doctor may use a standard X-ray of the abdominal area to rule out serious complications, such as a perforated colon.
*CT scan. A CT scan of your abdomen or pelvis may be performed if the doctor suspects a complication from ulcerative colitis or inflammation of the small intestine. A CT scan may also reveal how much of the colon is inflamed.
Treatment for ulcerative colitis depends on the severity of the disease. Most people are treated with medication. If there is significant bleeding, infection, or complications, surgery may be required to remove the diseased colon. Surgery is the only cure for ulcerative colitis.
Ulcerative colitis may affect patients in different ways, and treatment is adjusted to meet the needs of the specific patient. Emotional and psychological support is also important.
The symptoms of ulcerative colitis come and go. Periods of remission, in which symptoms resolve, may last for months or years before relapsing. Patients and physicians need to decide together whether medications will be continued during remission times. In some patients, it may be the case that the medications keep the disease under control, and stopping them will cause a relapse.
Ulcerative colitis is a lifelong illness and cannot be ignored. Routine medical check-ups are necessary and scheduled colonoscopies are important to monitor the health of the patient and to make certain that the ulcerative colitis is under control and not spreading.
Ulcerative colitis can be treated with a number of medications including 5-ASA drugs such as sulfasalazine and mesalazine. Corticosteroids such as prednisone can also be used due to their immunosuppressing and short term healing properties, but due to the risks outweighing the benefits, they are not used long term in treatment. Immunosuppressive medications such as azathioprine, and biological agents such as infliximab and adalimumab are given lastly, only if people cannot achieve remission with 5-ASA and corticosteroids, due to their possible risk factors, including, but not limited to increased risk of cancers in teenagers and adults, TB and new or worsening heart failure (these side effects are rare). A formulation of budesonide was approved by the FDA for treatment of active ulcerative colitis in January 2013.The evidence on methotrexate does not show a benefit in producing remission in those with ulcerative colitis.
Alternative medicine and experimental treatment avenues:
About 21% of inflammatory bowel disease patients use alternative treatments. A variety of dietary treatments show promise, but they require further research before they can be recommended.
In vitro research, animal evidence, and limited human study suggest that melatonin may be beneficial.
Dietary fiber, meaning indigestible plant matter, has been recommended for decades in the maintenance of bowel function. Of peculiar note is fiber from brassica, which seems to contain soluble constituents capable of reversing ulcers along the entire human digestive tract before it is cooked. Oatmeal is also commonly prescribed.
Fish oil, and eicosapentaenoic acid (EPA) derived from fish oil, inhibits leukotriene activity, the latter which may be a key factor of inflammation. As an IBD therapy, there are no conclusive studies in support and no recommended dosage. But dosages of EPA between 180 to 1500 mg/day are recommended for other conditions, most commonly cardiac.
Short chain fatty acid (butyrate) enema. The colon utilizes butyrate from the contents of the intestine as an energy source. The amount of butyrate available decreases toward the rectum. Inadequate butyrate levels in the lower intestine have been suggested as a contributing factor for the disease. This might be addressed through butyrate enemas. The results however are not conclusive.
Herbal medications are used by patients with ulcerative colitis. Compounds that contain sulfhydryl may have an effect in ulcerative colitis (under a similar hypothesis that the sulfa moiety of sulfasalazine may have activity in addition to the active 5-ASA component). One randomized control trial evaluated the over-the-counter medication S-methylmethionine and found a significant decreased rate of relapse when the medication was used in conjunction with oral sulfasalazine.
Boswellia is an Ayurvedic (Indian traditional medicine) herb. One study has found its effectiveness similar to sulfasalazine.
helminthic therapy is the use of intestinal parasitic nematodes to treat ulcerative colitis, and is based on the premises of the hygiene hypothesis. Studies have shown that helminths ameliorate and are more effective than daily corticosteroids at blocking chemically induced colitis in mice, and a trial of intentional helminth infection of rhesus monkeys with idiopathic chronic diarrhea (a condition similar to ulcerative colitis in humans) resulted in remission of symptoms in 4 out of 5 of the animals treated. A randomised controlled trial of Trichuris suis ova in humans found the therapy to be safe and effective, and further human trials are currently on going. Yoga and meditation may help a lot.
Helminthic therapy using the whipworm Trichuris suis has been shown in a randomized control trial from Iowa to show benefit in patients with ulcerative colitis. The therapy tests the hygiene hypothesis which argues that the absence of helminths in the colons of patients in the developed world may lead to inflammation. Both helminthic therapy and fecal bacteriotherapy induce a characteristic Th2 white cell response in the diseased areas, which was unexpected given that ulcerative colitis was thought to involve Th2 overproduction.
Alicaforsen is a first generation antisense oligodeoxynucleotide designed to bind specifically to the human ICAM-1 messenger RNA through Watson-Crick base pair interactions in order to subdue expression of ICAM-1. ICAM-1 propagates an inflammatory response promoting the extravasation and activation of leukocytes (white blood cells) into inflamed tissue. Increased expression of ICAM-1 has been observed within the inflamed intestinal mucosa of ulcerative colitis sufferers, where ICAM-1 over production correlated with disease activity. This suggests that ICAM-1 is a potential therapeutic target in the treatment of ulcerative colitis
Ulcerative colitis is a form of inflammatory bowel disease for which there is no cure. For the first 10 years after diagnosis, the prognosis for most people with ulcerative colitis is good — the rate of colectomy is low, and most patients achieve remission.
Patients with ulcerative colitis usually have an intermittent course, with periods of disease inactivity alternating with “flares” of disease. Patients with proctitis or left-sided colitis usually have a more benign course: only 15% progress proximally with their disease, and up to 20% can have sustained remission in the absence of any therapy. Patients with more extensive disease are less likely to sustain remission, but the rate of remission is independent of the severity of disease.
Other long-term features and Mortality:
Changes that can be seen in chronic ulcerative colitis include granularity, loss of the vascular pattern of the mucosa, loss of haustra, effacement of the ileocecal valve, mucosal bridging, strictures and pseudopolyps.
Research has not revealed any difference in overall risk of dying in patients with Ulcerative colitis from that of the background population. The cause-of-death distribution may be different from that of the background population. It is thought that the disease primarily affects quality of life, and not lifespan.
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.
Seedlings: Cotyledons are narrow, linear in outline, often resembling and being mistaken for a grass. The stem below the cotyledons (hypocotyl) is often reddish in color.
Roots: A taproot.
Leaves: Arranged alternately along the stem, lanceolate in outline, approximately 1/2 to 1 1/4 inches long and 1 to 8 mm wide. Leaves have short petioles and a distinctive thin membranous sheath (ocrea) that encircles the stem at the leaf base.
Fruit: A dark red to brown achene.
Stems: Branching, growing prostrate along the ground, ranging from 4 to 24 inches in length. Stems are swollen at the nodes with a thin membranous sheath (ocrea) encircling the stem at each leaf base.
Flowers: Occur in the area between the stems and leaves (leaf axils). From 1 to 5 flowers occur in clusters and are very small and inconspicuous, white to pinkish-white in color. Edible Uses: Young leaves and plants are eaten raw or cooked. Used as a potherb, they are very rich in zinc. A nutritional analysis is available. Seeds are also eaten raw or cooked. Rather small and fiddly to utilize, they can be used in all the ways that buckwheat (Fagopyrum esculentum) is used, either whole or dried and ground into a powder for use in pancakes, biscuits and piñole. The leaves are a tea substitute.
Succeeds in an ordinary garden soil but prefers a moisture retentive not too fertile soil in sun or part shade. Repays generous treatment, in good soils the plant will cover an area up to a metre in diameter. Prefers an acid soil. Dislikes shade. Knotweed is a common and invasive weed of cultivated ground. It is an important food plant for the caterpillars of many species of butterflies[. It also produces an abundance of seeds and these are a favourite food for many species of birds. Plants seem to be immune to the predations of rabbits. The flowers have little or no scent or honey and are rarely visited by pollinating insects. Self-fertilization is the usual method of reproduction, though cross-fertilization by insects does sometimes occur. The plant also produces cleistogomous flowers – these never open and therefore are always self-fertilized. The plant is very variable and is seen by most botanists as an aggregate species of 4 very variable species, viz. – P. aviculare. L.; P. boreale. (Lange.)Small.; P. rurivacum. Jord. ex Box.; and P. arenastrum. Box.
Seed – sow spring in a cold frame. Germination is usually free and easy. When they are large enough to handle, prick the seedlings out into individual pots and plant them out in the summer if they have reached sufficient size. If not, overwinter them in a cold frame and plant them out the following spring after the last expected frosts. Division in spring or autumn. Very easy, larger divisions can be planted out direct into their permanent positions. We have found that it is better to pot up the smaller divisions and grow them on in light shade in a cold frame until they are well established before planting them out in late spring or early summer.
Figures in grams (g) or miligrams (mg) per 100g of food.
Leaves (Fresh weight)
The plant is an astringent, coagulant, diuretic and expectorant.
It has been used in the treatment of chronic urinary tract infections. It is claimed to be useful in the prevention of the formation of renal calculi. It stops bleeding and alleviates colics and catarrhs (usually combined with silverweed and ribwort plantain). It is an ingredient in many herbal teas. It operates in the basal metabolism as an adjuvant in diabetic, expectorant and antidiarrheic preparations. It is used to treat bronchitis with bleeding. It is used for pulmonary complaints since its silicic acid content helps strengthen connective tissue within the lungs. It is also used in combination with other herbs to treat rheumatic conditions, gout, and skin disease. It is regarded as a “blood purifying’ remedy. Knotgrass has also been used to treat inflammations of the mucous membranes of the intestinal tract and has been useful in cases of flatulence and biliary insufficiency. Externally it has been used to treat sore throats and vaginal inflammation. Dosage is a decoction of the root from 10-20g to 2 glasses of water, half a glass 3 times a day. Can be used for douches, compresses, rinses. Alcoholic extracts prevent the crystallization of mineral substances in the urine and are antiphlogistic, bacteriostatic and diuretic. Research is being done on the efficacy of the plant in reducing the fragility of blood capillaries, especially in the alimentary canal.
In the Chinese tradition, knotgrass is given for intestinal worms, to treat diarrhea and dysentery, and as a diuretic, particularly in cases of painful urination. Chinese research indicates that the plant is a useful medicine for bacillary dysentery.
Other Uses :……Dye…….Yields a blue dye that is not much inferior to indigo. The part used is not specified, but it is likely to be the leaves. Yellow and green dyes are obtained from the whole plant. The roots contain tannins, but the quantity was not given.
Known Hazards: Although no specific mention has been made for this species, there have been reports that some members of this genus can cause photosensitivity in susceptible people. Many species also contain oxalic acid (the distinctive lemony flavour of sorrel) – whilst not toxic this substance can bind up other minerals making them unavailable to the body and leading to mineral deficiency. Having said that, a number of common foods such as sorrel and rhubarb contain oxalic acid and the leaves of most members of this genus are nutritious and beneficial to eat in moderate quantities. Cooking the leaves will reduce their content of oxalic acid. People with a tendency to rheumatism, arthritis, gout, kidney stones or hyperacidity should take especial caution if including this plant in their diet since it can aggravate their condition.
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.
Since ancient times has been used medicinally mainly to relieve stomach problems, but they have also discovered other properties for this, as for example that may help improve cold, flu, pneumonia, other property is that it helps digestion of fats and proteins, is used as an aphrodisiac and antiseptic, it also has an effect antiflatulent and purifying properties, this not only used but also the leaves and stems of the flowers.
The medicinal properties lie principally in its resin and volatile oil, the resin acting chiefly on the bowels and urinary passages, and the volatile oil on the lungs. It does not cause disorder to the stomach and bowels, it is a valuable remedy in dysentery, chronic diarrhea specially of tuberculous nature and in chronic cystitis. Internally is it used as a tea for loss of appetite and non-ulcer dyspepsia with fullness, flatulence, change of bowel habits, etc. associated with minor disorders of the hepatobiliary tract (chronic cholecycstitis, nonobstructive gallstones, chronic hepatitis and for inflammations of the upper respiratory tract. Also as a diaphoretic hot tea for the common cold and to enhance the effects in problems of the genitourinary tract, the fluid intake should be more than 2 liters per day. Externally it is used as a wet compress or poultice for minor skin inflammations and wounds.
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.