A study conducted by Saudi Arabian researchers has confirmed that a herb called Rocket “Eruca sativa L.” (EER), a member of the Brassicacae family, has potential anti-ulcer medicinal properties.
Led by Dr. Syed Rafatullah, the research team validated the gastric anti-ulcer properties of EER on experimentally-induced gastric secretion and ulceration in albino rats.
For their research, the group undertook gastric acid secretion studies using pylorus-ligated rats.
They revealed that gastric lesions in the rats were induced by noxious chemicals including ethanol, strong alkalis, indomethacin and hypothermic restraint stress.
The levels of gastric wall mucus, nonprotein sulfhydryls and malondialdehyde were also measured in the glandular stomach of rats following ethanol administration. The gastric tissue was also examined histologically. The extract was used in two doses (250 and 500 mg/kg body weight) in all experiments.
The researchers observed that the ethanolic extract of EER significantly and dose-dependently reduced the basal gastric acid secretion, titratable acidity and ruminal ulceration.
Rocket extract significantly attenuated gastric ulceration induced by necrotizing agents, indomethacin and hypothermic restraint stress. The anti-ulcer effect was further confirmed histologically.
On the other hand, the extract significantly replenished gastric wall mucus and nonprotein sulfhydryls levels, as well as the malondialdehyde level significantly reduced by extract pretreatment.
They concluded that EER extract possesses antisecretory, cytoprotective, and anti-ulcer activities against experimentally-induced gastric lesions. The anti-ulcer effect is possibly through prostaglandinmediated activity and/or through its anti-secretory and antioxidant properties.
Other Names:
Okra, Okro, Ochro, Okoro, Quimgombo (Cuba), Quingumbo, Ladies Fingers,gombo, quingombo, Gombo, Kopi Arab, Kacang Bendi, Bhindi (S. Asia), Bendi (Malaysia), Bamia, Bamya or Bamieh (middle east), Gumbo (Southern USA), Quiabo, Quiabos (Portugal and Angola), okura (Japan), qiu kui (Taiwan),in India it is bhindi,eastern Mediterranean and Arab countries bamies.
Parts Used: Immature pods
Etymology, origin and distribution
The name “okra” is of West African origin . In various Bantu languages, okra is called “kingombo” or a variant thereof, and this is the origin of its name in Portuguese, Spanish, Dutch and French. The Arabic “bemyah” is the basis of the names in the Middle East, the Balkans, Turkey, Greece, North Africa and Russia. In Southern Asia, its name is usually a variant of “bhindi” or “vendi.”
The species apparently originated in the Ethiopian Highlands, though the manner of distribution from there is undocumented. The Egyptians and Moors of the 12th and 13th centuries used the Arab word for the plant, suggesting that it had come from the east. The plant may thus have been taken across the Red Sea or the Bab-el-Mandeb strait to the Arabian Peninsula, rather than north across the Sahara. One of the earliest accounts is by a Spanish Moor who visited Egypt in 1216, who described the plant under cultivation by the locals who ate the tender, young pods with meal.
From Arabia, the plant spread around the shores of the Mediterranean Sea and eastward. The lack of a word for okra in the ancient languages of India suggests that it arrived there in the Common Era. The plant was introduced to the Americas by ships plying the Atlantic slave trade by 1658, when its presence was recorded in Brazil. It was further documented in Suriname in 1686. Okra may have been introduced to the southeastern North America in the early 18th century and gradually spread. It was being grown as far north as Philadelphia by 1748, while Thomas Jefferson noted that it was well established in Virginia by 1781. It was commonplace throughout the southern United States by 1800 and the first mention of different cultivars was in 1806
Description:
Okra is a member of the Mallow family, related to cotton, hibiscus and hollyhock. It has heart shaped leaves (one species is cultivated for its edible leaves), and large, yellow, hibiscus-like flowers.
The species is an annual or perennial, growing to 2 m tall. The leaves are 10–20 cm long and broad, palmately lobed with 5–7 lobes. The flowers are 4–8 cm diameter, with five white to yellow petals, often with a red or purple spot at the base of each petal. The fruit is a capsule up to 18 cm long, containing numerous seeds.
It is a tall-growing, warm-season, annual vegetable from the same family as hollyhock, rose of Sharon and hibiscus. The pods, when cut, exude a mucilaginous juice that is used to thicken stews (gumbo), and have a flavor somewhat like a cross between asparagus and eggplant.
Cultivation:
Abelmoschus esculentus is among the most heat- and drought-tolerant vegetable species in the world. It will tolerate poor soils with heavy clay and intermittent moisture. Severe frost can damage the pods.
It is an annual crop in the southern United States.
Recommended Varieties :
Annie Oakley (hybrid; 52 days to harvest; compact plant; extra tender pods)
Dwarf Green Long Pod (52 days; ribbed pods)
Clemson Spineless (56 days; AAS winner)
In cultivation, the seeds are soaked overnight prior to planting to a depth of 1-2 cm. Germination occurs between six days (soaked seeds) and three weeks. Seedlings require ample water. The seed pods rapidly become fibrous and woody and must be harvested within a week of the fruit being pollinated to be edible.
The products of the plant are mucilaginous, resulting in the characteristic “goo” when the seed pods are cooked. In order to avoid this effect, okra pods are often stir fried, so the moisture is cooked away, or paired with slightly acidic ingredients, such as citrus or tomatoes. The cooked leaves are also a powerful soup thickener.
Based on the rising experiences with its country cousin, kenaf (Hibiscus cannabinus), okra could, at least in principle, have a future producing yet more things that are strange for a vegetable crop, including:
*Construction materials: Kenaf-blend panels are said to perform better than the present particleboard.
*Handicrafts: Kenaf fiber makes excellent mats, hats, baskets, and more.
*Forage: Chopping up the whole kenaf plant and feeding it to animals has proven successful.
*Fuel: Kenaf roots and stems burn fiercely.
Uses:
Abelmoschus esculentus is cultivated throughout the tropical and warm temperate regions of the world for its fibrous fruits or pods containing round, white seeds. The fruits are harvested when immature and eaten as a vegetable.
The immature pods are used for soups, canning and stews or as a fried or boiled vegetable. The hibiscus like flowers and upright plant (3 to 6 feet or more in height) have ornamental value for backyard gardens.
A traditional food plant in Africa, this little-known vegetable has potential to improve nutrition, boost food security, foster rural development and support sustainable landcare.
In Egypt, Greece, Iran, Iraq, Jordan, Lebanon, Turkey and Yemen, and other parts of the eastern Mediterranean, okra is widely used in a thick stew made with vegetables and meat. In Indian cooking, it is sauteed or added to gravy-based preparations and is very popular in South India. In Caribbean islands okra is cooked up and eaten as soup, often with fish. In Haiti, it is cooked with rice and maize; it is also used as a sauce for meat. It became a popular vegetable in Japanese cuisine toward the end of the 20th century, served with soy sauce and katsuobushi or as tempura. It is used as a thickening agent in gumbo. Breaded, deep fried okra is served in the southern United States. The immature pods may also be pickled.
Okra leaves may be cooked in a similar manner as the greens of beets or dandelions. The leaves are also eaten raw in salads. Okra seeds may be roasted and ground to form a non-caffeinated substitute for coffee. As imports were disrupted by the American Civil War in 1861, the Austin State Gazette noted, “An acre of okra will produce seed enough to furnish a plantation of fifty negroes with coffee in every way equal to that imported from Rio.
Okra forms part of several regional “signature” dishes. Frango com quiabo (chicken with okra) is a Brazilian dish that is especially famous in the region of Minas Gerais. Gumbo, a hearty stew whose key ingredient is okra, is found throughout the Gulf Coast of the United States and in the South Carolina Lowcountry. The word “gumbo” is based on the Central Bantu word for okra, “kigombo”, via the Caribbean Spanish “guingambó” or “quimbombó”. It is also an expected ingredient in callaloo, a Caribbean dish and the national dish of Trinidad & Tobago. Okra is also enjoyed in Nigeria where okra soup (Draw soup) is a special delicacy with Garri(eba) or akpu.
In Vietnam, okra is the important ingredient in the dish canh chua.
Mature okra is used to make rope and paper! (Avoid those old woody pods!).
Medicinal Uses: Nutrition:
Okra is a good source of vitamin C and A, also B complex vitamins, iron and calcium. It is low in calories, a good source of dietary fiber, and is fat-free.
Okra oil is a pressed seed oil, extracted from the seeds of the okra. The greenish yellow edible oil has a pleasant taste and odor, and is high in unsaturated fats such as oleic acid and linoleic acid. The oil content of the seed is quite high at about 40%. Oil yields from okra crops are also high. At 794 kg/ha, the yield was exceeded only by that of sunflower oil in one trial.
Unspecified parts of the plant reportedly possess diuretic properties.
Contains male contraceptive gossypol.
According to Sylvia W. Zook, Ph.D. (nutritionist) Okra has several benefits.
1. The superior fiber found in okra helps to stabilize blood sugar by curbing the rate at which sugar is absorbed from the intestinal tract.
2. Okra’s mucilage binds cholesterol and bile acid carrying toxins dumped into it by the filtering liver.
3. Okra helps lubricate the large intestines due to its bulk laxative qualities. The okra fiber absorbs water and ensures bulk in stools. This helps prevent and improve constipation. Unlike harsh wheat bran, which can irritate or injure the intestinal tract, okra’s mucilage soothes, and okra facilitates elimination more comfortably by its slippery characteristic. Okra binds excess cholesterol and toxins (in bile acids). These, if not evacuated, will cause numerous health problems. Okra also assures easy passage out of waste from the body. Okra is completely non-toxic, non-habit forming, has no adverse side effects, is full of nutrients, and is economically within reach of most unlike the OTC drugs.
4. Okra fiber is excellent for feeding the good bacteria (probiotics). This contributes to the health of the intestinal tract.
5. Okra is a supreme vegetable for those feeling weak, exhausted, and suffering from depression.
6. Okra is used for healing ulcers and to keep joints limber. It helps to neutralize acids, being very alkaline, and provides a temporary protective coating for the digestive tract.
7. Okra treats lung inflammation, sore throat, and irritable bowel.
8. In India, okra has been used successfully in experimental blood plasma replacements.
To retain most of okra’s nutrients and self-digesting enzymes, it should be cooked as little as possible, e.g. with low heat or lightly steamed. Some eat it raw.
Specific Ailments:-
Acid Reflux and Constipation
A person, suffering from constipation for the past 20 years and recently from acid reflux, started eating 6 pieces of Okra. Since then, has not taken any other medication. Now, his blood sugar has dropped from 135 to 98 and his cholesterol and acid reflux are also under control.
Asthma
Vitamin C is a powerful antioxidant and anti-inflammatory. This anti-inflammatory activity may curtail the development of asthma symptoms. A large preliminary study has shown that young children with asthma experience significantly less wheezing if they eat a diet high in fruits rich in vitamin C. 1/2 cup of cooked Okra contains over 13 mg of vitamin C.
Atherosclerosis
Diets high in insoluble fiber, such as those containing okra, are associated with protection against heart disease in both men and women.
Cancer
The insoluble fiber found in Okra helps to keep the intestinal tract healthy, decreasing the risk of some forms of cancer, especially colo-rectal cancer.
Capillary fragility
Eating plenty of flavonoid and vitamin C-rich fruits and vegetables such as okra helps to support the structure of capillaries.
Cataracts
1/2 cup of cooked okra contains 460 IU of vitamin A. Some studies have reported that eating more foods rich in beta-carotene or vitamin A was associated with a lower risk of cataracts.
Cholesterol
A study (JAMA July 23, 2003) showed that consuming a “dietary portfolio” of vegetarian foods lowered cholesterol nearly as well as the prescription drug lovastatin (Mevacor). The diet was rich in soluble fiber from oats, barley, psyllium, eggplant and okra. It used soy substitutes instead of meat and milk and included almonds and cholesterol-lowering margarine (such as Take Control) every day.
Depression and Lack of Energy
Okra is a supreme vegetable for those feeling weak, exhausted, and suffering from depression.
High homocysteine
A controlled trial showed that eating a diet high in fruits and vegetables containing folic acid, beta-carotene, and vitamin C effectively lowered homocysteine levels. Healthy people were assigned to either a diet containing a pound of fruits and vegetables per day, or to a diet containing 3 1/2 ounces (99g) of fruits and vegetables per day. After four weeks, those eating the higher amount of fruits and vegetables had an 11 percent lower homocysteine level compared to those eating the lower amount of fruits and vegetables. Okra is a storehouse of vitamins and folic acid.
Multiple sclerosis (MS)
In one survey, researchers gathered information from nearly 400 people (half with MS) over three years. They found that consumption of vegetable protein, fruit juice, and foods rich in vitamin C, thiamine, riboflavin, calcium, and potassium correlated with a decreased MS risk.
Known Hazards : The hairs on the seed pods can be an irritant to some people and gloves should be worn when harvesting. These hairs can be easily removed by washing.
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.
Defibition: Rift Valley Fever (RVF) is a viral zoonosis (affects primarily domestic livestock, but can be passed to humans) causing fever. It is spread by the bite of infected mosquitoes, typically the Aedes or Culex genera.
The disease is caused by the RVF virus, a member of the genus Phlebovirus (family Bunyaviridae). The disease was first reported among livestock in Kenya around 1915, but the virus was not isolated until 1931. RVF outbreaks occur across sub-Saharan Africa, with outbreaks occurring elsewhere infrequently (but sometimes severely – in Egypt in 1977-78, several million people were infected and thousands died during a violent epidemic. In Kenya in 1998, the virus claimed the lives of over 400 Kenyans. In September 2000 an outbreak was confirmed in Saudi Arabia and Yemen).
In humans the virus can cause several different syndromes. Usually sufferers have either no symptoms or only a mild illness with fever, headache, myalgia and liver abnormalities. In a small percentage of cases (< 2%) the illness can progress to hemorrhagic fever syndrome, meningoencephalitis (inflammation of the brain), or affecting the eye. Patients who become ill usually experience fever, generalized weakness, back pain, dizziness, and weight loss at the onset of the illness. Typically, patients recover within 2-7 days after onset.
RVF virus is a member of the Phlebovirus genus, one of the five genera in the family Bunyaviridae. The virus was first identified in 1931 during an investigation into an epidemic among sheep on a farm in the Rift Valley of Kenya. Since then, outbreaks have been reported in sub-Saharan and North Africa. In 1997-98, a major outbreak occurred in Kenya, Somalia and Tanzania and in September 2000, RVF cases were confirmed in Saudi Arabia and Yemen, marking the first reported occurrence of the disease outside the African continent and raising concerns that it could extend to other parts of Asia and Europe.
Approximately 1% of human sufferers die of the disease. Amongst livestock the fatality level is significantly higher. In pregnant livestock infected with RVF there is the abortion of virtually 100% of fetuses. An epizootic (animal disease epidemic) of RVF is usually first indicated by a wave of unexplained abortions.
TRANSMISSION TO HUMANS:
*The vast majority of human infections result from direct or indirect contact with the blood or organs of infected animals. The virus can be transmitted to humans through the handling of animal tissue during slaughtering or butchering, assisting with animal births, conducting veterinary procedures, or from the disposal of carcasses or fetuses. Certain occupational groups such as herders, farmers, slaughterhouse workers and veterinarians are therefore at higher risk of infection. The virus infects humans through inoculation, for example via a wound from an infected knife or through contact with broken skin, or through inhalation of aerosols produced during the slaughter of infected animals. The aerosol mode of transmission has also led to infection in laboratory workers.
*There is some evidence that humans may also become infected with RVF by ingesting the unpasteurized or uncooked milk of infected animals.
*Human infections have also resulted from the bites of infected mosquitoes, most commonly the Aedes mosquito.
*Transmission of RVF virus by hematophagous (blood-feeding) flies is also possible.
*To date, no human-to-human transmission of RVF has been documented, and no transmission of RVF to health care workers has been reported when standard infection control precautions have been put in place.
*There has been no evidence of outbreaks of RVF in urban areas.
CLINICAL FEATURES IN HUMANS Mild form of RVF in humans
*The incubation period (interval from infection to onset of symptoms) for RVF varies from two to six days.
*Those infected either experience no detectable symptoms or develop a mild form of the disease characterized by a feverish syndrome with sudden onset of flu-like fever, muscle pain, joint pain and headache.
*Some patients develop neck stiffness, sensitivity to light, loss of appetite and vomiting; in these patients the disease, in its early stages, may be mistaken for meningitis.
*The symptoms of RVF usually last from four to seven days, after which time the immune response becomes detectable with the appearance of antibodies and the virus gradually disappears from the blood.
Severe form of RVF in humans:
*While most human cases are relatively mild, a small percentage of patients develop a much more severe form of the disease. This usually appears as one or more of three distinct syndromes: ocular (eye) disease (0.5-2% of patients), meningoencephalitis (less than 1%) or haemorrhagic fever (less than 1%).
*Ocular form: In this form of the disease, the usual symptoms associated with the mild form of the disease are accompanied by retinal lesions. The onset of the lesions in the eyes is usually one to three weeks after appearance of the first symptoms. Patients usually report blurred or decreased vision. The disease may resolve itself with no lasting effects within 10 to 12 weeks. However, when the lesions occur in the macula, 50% of patients will experience a permanent loss of vision. Death in patients with only the ocular form of the disease is uncommon.
*Meningoencephalitis form: The onset of the meningoencephalitis form of the disease usually occurs one to four weeks after the first symptoms of RVF appear. Clinical features include intense headache, loss of memory, hallucinations, confusion, disorientation, vertigo, convulsions, lethargy and coma. Neurological complications can appear later (> 60 days). The death rate in patients who experience only this form of the disease is low, although residual neurological deficit, which may be severe, is common.
*Haemorrhagic fever form: The symptoms of this form of the disease appear two to four days after the onset of illness, and begin with evidence of severe liver impairment, such as jaundice. Subsequently signs of haemorrhage then appear such as vomiting blood, passing blood in the faeces, a purpuric rash or ecchymoses (caused by bleeding in the skin), bleeding from the nose or gums, menorrhagia and bleeding from venepuncture sites. The case-fatality ratio for patients developing the haemorrhagic form of the disease is high at approximately 50%. Death usually occurs three to six days after the onset of symptoms. The virus may be detectable in the blood for up to 10 days, in patients with the hemorrhagic icterus form of RVF.
The total case fatality rate has varied widely between different epidemics but, overall, has been less than 1% in those documented. Most fatalities occur in patients who develop the haemorrhagic icterus form.
DIAGNOSIS
Acute RVF can be diagnosed using several different methods. Serological tests such as enzyme-linked immunoassay (the “ELISA” or “EIA” methods) may confirm the presence of specific IgM antibodies to the virus. The virus itself may be detected in blood during the early phase of illness or in post-mortem tissue using a variety of techniques including virus propagation (in cell cultures or inoculated animals), antigen detection tests and RT-PCR.
TREATMENT AND VACCINE
*As most human cases of RVF are relatively mild and of short duration, no specific treatment is required for these patients. For the more severe cases, the predominant treatment is general supportive therapy.
*An inactivated vaccine has been developed for human use. However, this vaccine is not licensed and is not commercially available. It has been used experimentally to protect veterinary and laboratory personnel at high risk of exposure to RVF. Other candidate vaccines are under investigation.
RVF VIRUS IN ANIMAL HOSTS
*RVF is able to infect many species of animals causing severe disease in domesticated animals including cattle, sheep, camels and goats. Sheep appear to be more susceptible than cattle or camels.
*Age has also been shown to be a significant factor in the animal’s susceptibility to the severe form of the disease: over 90% of lambs infected with RVF die, whereas mortality among adult sheep can be as low as 10%.
*The rate of abortion among pregnant infected ewes is almost 100%. An outbreak of RVF in animals frequently manifests itself as a wave of unexplained abortions among livestock and may signal the start of an epidemic.
RVF VECTORS
*Several different species of mosquito are able to act as vectors for transmission of the RVF virus. The dominant vector species varies between different regions and different species can play different roles in sustaining the transmission of the virus.
*Among animals, the RVF virus is spread primarily by the bite of infected mosquitoes, mainly the Aedes species, which can acquire the virus from feeding on infected animals. The female mosquito is also capable of transmitting the virus directly to her offspring via eggs leading to new generations of infected mosquitoes hatching from eggs. This accounts for the continued presence of the RVF virus in enzootic foci and provides the virus with a sustainable mechanism of existence as the eggs of these mosquitoes can survive for several years in dry conditions. During periods of heavy rainfall, larval habitats frequently become flooded enabling the eggs to hatch and the mosquito population to rapidly increase, spreading the virus to the animals on which they feed.
*There is also a potential for epizootics and associated human epidemics to spread to areas that were previously unaffected. This has occurred when infected animals have introduced the virus into areas where vectors were present and is a particular concern. When uninfected Aedes and other species of mosquitoes feed on infected animals, a small outbreak can quickly be amplified through the transmission of the virus to other animals on which they subsequently feed.
PREVENTION AND CONTROL Controlling RVF in animals
*Outbreaks of RVF in animals can be prevented by a sustained programme of animal vaccination. Both modified live attenuated virus and inactivated virus vaccines have been developed for veterinary use. Only one dose of the live vaccine is required to provide long-term immunity but the vaccine that is currently in use may result in spontaneous abortion if given to pregnant animals. The inactivated virus vaccine does not have this side effect, but multiple doses are required in order to provide protection which may prove problematic in endemic areas.
*Animal immunization must be implemented prior to an outbreak if an epizootic is to be prevented. Once an outbreak has occurred animal vaccination should NOT be implemented because there is a high risk of intensifying the outbreak. During mass animal vaccination campaigns, animal health workers may, inadvertently, transmit the virus through the use of multi-dose vials and the re-use of needles and syringes. If some of the animals in the herd are already infected and viraemic (although not yet displaying obvious signs of illness), the virus will be transmitted among the herd, and the outbreak will be amplified.
*Restricting or banning the movement of livestock may be effective in slowing the expansion of the virus from infected to uninfected areas.
*As outbreaks of RVF in animals precede human cases, the establishment of an active animal health surveillance system to detect new cases is essential in providing early warning for veterinary and human public health authorities.
Public health education and risk reduction:
*During an outbreak of RVF, close contact with animals, particularly with their body fluids, either directly or via aerosols, has been identified as the most significant risk factor for RVF virus infection. In the absence of specific treatment and an effective human vaccine, raising awareness of the risk factors of RVF infection as well as the protective measures individuals can take to prevent mosquito bites, is the only way to reduce human infection and deaths. Public health messages for risk reduction should focus on:
*reducing the risk of animal-to-human transmission as a result of unsafe animal husbandry and slaughtering practices. Gloves and other appropriate protective clothing should be worn and care taken when handling sick animals or their tissues or when slaughtering animals.
*reducing the risk of animal-to-human transmission arising from the unsafe consumption of fresh blood, raw milk or animal tissue. In the epizootic regions, all animal products (blood, meat and milk) should be thoroughly cooked before eating.
*the importance of personal and community protection against mosquito bites through the use of impregnated mosquito nets, personal insect repellent if available, by wearing light coloured clothing (long-sleeved shirts and trousers) and by avoiding outdoor activity at peak biting times of the vector species. Infection control in health care settings
*Although no human-to-human transmission of RVF has been demonstrated, there is still a theoretical risk of transmission of the virus from infected patients to healthcare workers through contact with infected blood or tissues. Healthcare workers caring for patients with suspected or confirmed RVF should implement Standard Precautions when handling specimens from patients.
*Standard Precautions define the work practices that are required to ensure a basic level of infection control. Standard Precautions are recommended in the care and treatment of all patients regardless of their perceived or confirmed infectious status. They cover the handling of blood (including dried blood), all other body fluids, secretions and excretions (excluding sweat), regardless of whether they contain visible blood, and contact with non-intact skin and mucous membranes. A WHO Aide–memoire on Standard Precautions in health care is available at: http://www.who.int/csr/resources/publications/standardprecautions/en/index.html
*As noted above, laboratory workers are also at risk. Samples taken from suspected human and animal cases of RVF for diagnosis should be handled by trained staff and processed in suitably equipped laboratories.
. Vector control
*Other ways in which to control the spread of RVF involve control of the vector and protection against their bites.
*Larviciding measures at mosquito breeding sites are the most effective form of vector control if breeding sites can be clearly identified and are limited in size and extent. During periods of flooding, however, the number and extent of breeding sites is usually too high for larviciding measures to be feasible.
. RVF FORESCASTING AND CLIMATIC MODELS
Forecasting can predict climatic conditions that are frequently associated with an increased risk of outbreaks, and may improve disease control. In Africa, Saudi Arabia and Yemen RVF outbreaks are closely associated with periods of above-average rainfall. The response of vegetation to increased levels of rainfall can be easily measured and monitored by Remote Sensing Satellite Imagery. In addition RVF outbreaks in East Africa are closely associated with the heavy rainfall that occurs during the warm phase of the El Niño/Southern Oscillation (ENSO) phenomenon.
These findings have enabled the successful development of forecasting models and early warning systems for RVF using satellite images and weather/climate forecasting data. Early warning systems, such as these, could be used to detect animal cases at an early stage of an outbreak enabling authorities to implement measures to avert impending epidemics.
Within the framework of the new International Health Regulations (2005), the forecasting and early detection of RVF outbreaks, together with a comprehensive assessment of the risk of diffusion to new areas, are essential to enable effective and timely control measures to be implemented.
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.
Definition: Angina pain develops when the muscles of the heart are not getting enough oxygen. This is usually caused by narrowing or blockages of the coronary arteries which deliver oxygen-rich blood to the heart muscle (known as coronary artery disease). So angina is a sign of heart disease……….click & see
If the blockage of a coronary artery progresses and becomes complete, then the blood supply to part of the muscles of the heart is lost, causing a heart attack. Angina is a warning sign that the heart is at risk of a heart attack, and should be taken very seriously. One patient in every ten will go on to have a heart attack within a year of diagnosis of angina.
When your heart isn’t getting enough blood and oxygen, the crushing, squeezing pain of angina is typically the result. Usually the pain begins below the breastbone and radiates to the shoulder, arm, or jaw, increasing in intensity until it reaches a plateau and then diminishes. The attack can last up to 15 minutes.
Angina may be an occasional problem or may rapidly increase in severity and duration until a heart attack occurs.
Although conventional medications for angina may help relieve the intense chest pain of this heart disorder, they do very little to halt the physiological mechanisms behind it. Vitamins, minerals, and natural remedies may actually improve the condition — or at least keep it from.
Symptoms:…….
Symptoms include:
*Crushing or squeezing chest pain.
*Weakness.
*Sweating.
*Shortness of breath.
*Palpitations.
*Nausea.
*Light-headedness.
When to Call Your Doctor
If you have any of the above symptoms for the first time.
If there is any change in the normal pattern of your angina attacks — for example, if they increase in frequency, intensity, or duration, or if they are brought on by new activities.
If an angina attack lasts more than 15 minutes, which may be a heart attack — call for an ambulance immediately. Reminder: If you have a medical condition, talk to your doctor before taking supplements.
Causes and risk factors:
Angina is common – about eight per cent of men and three per cent of women aged between 55 and 64 have experienced it, and it becomes more common with age.
It’s most commonly caused by narrowing of the arteries which carry oxygen to the heart muscle by a process called atherosclerosis (sometimes known as hardening of the arteries). This is a common condition where fatty deposits or plaques build up in the coronary arteries. Symptoms don’t usually develop until there is at least a 50 per cent blockage of the artery.
Most people in the developed world will have some atherosclerosis by the time they reach mid-life (and often much earlier), but some conditions can make it worse including:
•High cholesterol levels in the blood (especially if there is an inherited tendency to high cholesterol or a strong family history of heart disease).
•Cigarette smoking.
•Diabetes mellitus.
•High blood pressure. Other conditions can also interfere with the blood supply to the heart muscle and lead to angina. These include:
•Abnormal heart rhythms (for example when the heart beats so fast that it isn’t pumping blood efficiently around the body).
•Heart valve disease.
•Inherited structural abnormalities of the coronary arteries.
•Severe anaemia (where the blood count is so low that it cannot carry much oxygen to the tissues).
Other important risk factors for angina include obesity, and raised levels of chemical in the blood called homocysteine, or other chemicals involved with clotting.
In another condition, known as Prinzmetal’s angina or coronary artery spasm, the coronary arteries aren’t permanently blocked but intermittently narrowed by spasm. This often develops in the early hours of the morning and may last up to 30 minutes. Those affected may also complain of palpitations and abnormal heart rhythms, or have similar conditions linked to spasm of the arteries such as migraine or Raynaud’s phenomenon.
Events which put extra strain on the heart can make angina worse, such as:
•Fever.
•Infection and serious illness.
•Emotional stress.
•An overactive thyroid gland.
•Sudden extreme exertion.
But angina can come on at rest, even when a person is lying down in bed.
Diagnosis and modern treatment :
There are many problems which can be confused with angina, especially simply indigestion or gastro-oesophageal reflux. There may be no visible signs of angina so it’s important that tests are done to establish the diagnosis, to ensure the affected person gets the right treatment.
An electrocardiogram (ECG) is essential and may show typical changes but can be normal in angina. Blood tests can be done to check for causes such as anaemia and look for chemical enzymes (called Troponins) released from the heart if a heart attack has occurred. Other checks for cholesterol levels, blood fats, diabetes and thyroid disease may be done. In most areas of the UK these tests will be done at the local Rapid Access Chest Pain Clinic.
More complex tests such as an ECG during exercise, echocardiogram or other sophisticated x-ray tests may be recommended. However, NICE has recently produced guidelines which direct which tests should be done based on a statistical calculation of how likely to patient is to have angina. For example, invasive coronary angiography (where a tube is inserted into the coronary arteries and dye injected to produce x-rays pictures of the coronary arteries) is usually offered when there is a greater than 61 per cent chance of coronary artery disease.
Treatment of angina includes:
•Lifestyle advice to manage risk factors, such as weight loss, exercise, quitting smoking and a healthy diet.
•Medical treatment, including a drug called glyceryl trinitrate or GTN which can be taken repeatedly as a tablet put under the tongue or as a spray, and medical advice on what to do if pain persists (ie. if there is a risk of a heart attack).
•Assessment and treatment for coronary artery disease, including a variety of drug treatments to help open the arteries or treatments such as aspirin and a statin type drug which help to reduce the risk of a heart attack. More invasive treatments to open up the coronary arteries may be recommended especially when there is severe blockage. These are known as coronary revascularisation. The main two types are either coronary artery bypass grafting, or percutaneous transluminal angioplasty.
How Supplements Can Help
The supplements listed in the chart can all be used together or alone. They can also complement your prescription angina medications; never stop your heart medication without first consulting your doctor, however.
The antioxidant effect of vitamins C and E can help prevent cell damage: Vitamin C aids in the repair of the arteries injured by plaque, and vitamin E blocks the oxidation of LDL (“bad”) cholesterol, the initial step in the formation of plaque. In addition, some people with heart disease have low levels of vitamin E as well as the mineral magnesium, which may inhibit spasms of the coronary arteries.
Amino acids can benefit the heart in several ways. Arginine plays a role in forming nitric oxide, which relaxes artery walls. One study found that taking this amino acid three times a day increased the amount of time individuals with angina could exercise at moderate intensity without having to stop because of chest pain. Carnitine, an amino acid-like substance, allows heart muscle cells to use energy more efficiently, and another amino acid, taurine, may temper heart rhythm abnormalities.
Like carnitine, the nutritional supplement coenzyme Q10 enhances the heart muscle, reducing its workload, and the herb hawthorn improves blood flow to the heart. Essential fatty acids may be effective in lowering triglyceride levels and keeping arteries flexible.
What Else You Can Do
Eat a low-fat, fiber-rich diet; use canola or olive oil instead of butter.
Don’t smoke and avoid smoky places.
Learn to relax. Meditation, t’ai chi, and yoga may reduce angina attacks.
Join a support group. Determine what brought you to this point in your life and what you can do to begin reversing the disease.
Supplement Recommendations
Vitamin C
Vitamin E
Magnesium
Arginine
Carnitine
Taurine
Coenzyme Q10
Hawthorn
Essential Fatty Acids
Vitamin C
Dosage: 1,000 mg 3 times a day.
Comments: Reduce dose if diarrhea develops.
Vitamin E
Dosage: 400 IU twice a day.
Comments: Check with your doctor if taking anticoagulant drugs.
Magnesium
Dosage: 200 mg twice a day.
Comments: Do not take if you have kidney disease.
Arginine
Dosage: 500 mg L-arginine 3 times a day on an empty stomach.
Comments: If using longer than 1 month, add mixed amino acids.
Carnitine
Dosage: 500 mg L-carnitine 3 times a day on an empty stomach.
Comments: If using longer than 1 month, add mixed amino acids.
Taurine
Dosage: 500 mg L-taurine 3 times a day on an empty stomach.
Comments: If using longer than 1 month, add mixed amino acids.
Coenzyme Q10
Dosage: 100 mg twice a day.
Comments: For best absorption, take with food.
Hawthorn
Dosage: 100-150 mg 3 times a day.
Comments: Standardized to contain at least 1.8% vitexin.
Essential Fatty Acids
Dosage: 1 tbsp. flaxseed oil a day; 2,000 mg fish oils 3 times a day.
Comments: Take fish oils if you don’t eat fish at least twice a week.
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.
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