Xanthoma

Other Names: Skin growths – fatty; Xanthelasma

Description:
A xanthoma, from Greek xanthos, “yellow”, is a deposition of yellowish cholesterol-rich material that can appear anywhere in the body in various disease states.It is a skin condition in which certain fats build up under the surface of the skin. They are cutaneous manifestations of lipidosis in which lipids accumulate in large foam cells within the skin. They are associated with hyperlipidemias, both primary and secondary types.

Tendon xanthomas are associated with type II hyperlipidemia, chronic biliary tract obstruction, and primary biliary cirrhosis. Palmar xanthomata and tuboeruptive xanthomata (over knees and elbows) occur in type III hyperlipidemia.

Types:
Xanthelasma:
A xanthelasma is a sharply demarcated yellowish collection of cholesterol underneath the skin, usually on or around the eyelids. Strictly, a xanthelasma is a distinct condition, only being called a xanthoma when becoming larger and nodular, assuming tumorous proportions. Still, it is often classified simply as a subtype of xanthoma.

Xanthoma tuberosum:
Xanthoma tuberosum (also known as tuberous xanthoma) is characterized by xanthomas located over the joints.

Xanthoma tendinosum:
Xanthoma tendinosum (also tendon xanthoma or tendinous xanthoma) is clinically characterized by papules and nodules found in the tendons of the hands, feet, and heel. Also associated with familial hypercholesterolemia (FH).

Eruptive xanthoma:
Eruptive xanthoma (ILDS E78.220) is clinically characterized by small, yellowish-orange to reddish-brown papules that appear all over the body. It tends to be associated with elevated triglycerides.

Xanthoma planum:
Xanthoma planum (ILDS D76.370), also known as plane xanthoma, is clinically characterized by macules and plaques spread diffusely over large areas of the body.

Palmar xanthoma:
Palmar xanthoma is clinically characterized by yellowish plaques that involve the palms and flexural surfaces of the fingers.[2]:531 Plane xanthomas are characterised by yellowish to orange, flat macules or slightly elevated plaques, often with a central white area which may be localised or generalised. They often arise in the skin folds, especially the palmar creases. They occur in hyperlipoproteinaemia type III and type IIA, and in association with biliary cirrhosis. The presence of palmar xanthomata, like the presence of tendinous xanthomata, is indicative of hypercholesterolaemia.

Tuberoeruptive xanthoma:
Tuberoeruptive xanthoma (ILDS E78.210) is clinically characterized by red papules and nodules that appear inflamed and tend to coalesce.[2]:532 Tuberous xanthomata are considered similar, and within the same disease spectrum as eruptive xanthomata.

Symptoms:
A xanthoma looks like a yellow to orange bump (papule) with defined borders.

Xanthomas are common, especially among older adults and people with high blood lipids.

Xanthomas vary in size. Some are very small. Others are bigger than 3 inches in diameter. They appear anywhere on the body, but are most often seen on the elbows, joints, tendons, knees, hands, feet, or buttocks.

Causes:
Xanthomas may be a sign of a medical condition that involves an increase in blood lipids. Such conditions include:

*Certain cancers
*Diabetes
*Hyperlipidemia
*Inherited metabolic disorders such as familial hypercholesterolemia
*Primary biliary cirrhosis
*Pancreatitis
*Hypothyroidism

Xanthelasma palpebra, a common type of xanthoma that appears on the eyelids and may occur without any underlying medical condition, is not necessarily associated with elevated cholesterol or lipids.

Diagnosis:
Your health care provider will examine the skin. Usually, a diagnosis of xanthoma can be made by looking at your skin. A biopsy of the growth will show a fatty deposit.

You may have blood tests done to check lipid levels, liver function, and for diabetes.

Treatment:
If you have a disease that causes increased blood lipids, treating the condition may help reduce the development of xanthomas.

If the growth bothers you, your doctor may remove it. But xanthomas may come back after surgery.

Prognosis:
The growth is non-cancerous and painless, but may be a sign of another medical condition.

Prevention:
Control of blood lipids, including triglycerides and cholesterol levels, may help reduce development of xanthomas.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://www.nlm.nih.gov/medlineplus/ency/article/001447.htm

http://en.wikipedia.org/wiki/Xanthoma

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Takotsubo cardiomyopathy

Other Names: Broken-heart syndrome, Transient apical ballooning syndrome, Apical ballooning cardiomyopathy,Stress-induced cardiomyopathy, Gebrochenes-Herz-Syndrom, and Stress cardiomyopathy.
Definition:
Takotsubo cardiomyopathy is a type of non-ischaemic cardiomyopathy in which there is a sudden temporary weakening of the myocardium. Because this weakening can be triggered by emotional stress, It occurs as the response of the heart to sudden, intense emotional stress such as the death of a spouse; rejection at the workplace; acute fear; or uncontrolled anger. These intense emotions can cause immediate breathlessness or strokes. The broken heart can occur simultaneously or a few minutes later. Stress cardiomyopathy is a well-recognized cause of acute heart failure, lethal ventricular arrhythmias, and ventricular rupture.

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Around ten years ago, there were a few high profile deaths in young people. They were diagnosed as having died from a “broken heart”. Now, a broken heart or stunned myocardium syndrome is a documented condition.
Symptoms:
Takotsubo cardiomyopathy or Broken heart syndrome symptoms can mimic a heart attack.The symptoms are similar to a heart attack – chest pain, sweating, giddiness or dizziness, nausea, vomiting, weakness and palpitations. Blood pressure may drop. Heart failure may develop.

Any long-lasting or persistent chest pain could be a sign of a heart attack, so it’s important to take it seriously and call your doctor if you experience chest pain.

Causes:
The exact cause of Takotsubo cardiomyopathy is not very clear. It is thought that a surge of stress hormones, such as adrenaline, might temporarily damage the hearts of some people. How these hormones might hurt the heart or whether something else is responsible isn’t completely clear. A temporary constriction of the large or small arteries of the heart may play a role.

Takotsubo cardiomyopathy is often preceded by an intense physical or emotional event. Some potential triggers are:

*News of an unexpected death of a loved one
*A frightening medical diagnosis
*Domestic abuse
*Losing a lot of money
*Natural disasters
*A surprise party
*Having to perform publicly
*Job loss
*Divorce
*Physical stressors, such as an asthma attack, a car accident or major surgery

It’s also possible that some drugs, rarely, may cause broken heart syndrome by causing a surge of stress hormones. Drugs that may contribute to broken heart syndrome include:

*Epinephrine (EpiPen, EpiPen Jr), which is used to treat severe allergic reactions or a severe asthma attack
*Duloxetine (Cymbalta), a medication given to treat nerve problems in people with diabetes, or as a treatment for depression
*Venlafaxine (Effexor XR), which is a treatment for depression
*Levothyroxine (Synthroid, Levoxyl), a drug given to people whose thyroid glands don’t work properly
Differances between Takotsubo cardiomyopathy and hear attack are:

Heart attacks are generally caused by a complete or near complete blockage of a heart artery. This blockage is due to a blood clot forming at the site of narrowing from fatty buildup (atherosclerosis) in the wall of the artery. In Takotsubo cardiomyopathy, the heart arteries are not blocked, although blood flow in the arteries of the heart may be reduced.
Diagnosis:
Takotsubo cardiomyopathy or Transient apical ballooning syndrome is found in 1.7–2.2% of patients presenting with acute coronary syndrome. While the original case studies reported on individuals in Japan, Takotsubo cardiomyopathy has been noted more recently in the United States and Western Europe. It is likely that the syndrome went previously undiagnosed before it was described in detail in the Japanese literature.

The diagnosis of Takotsubo cardiomyopathy may be difficult upon presentation. The ECG findings are often confused with those found during an acute anterior wall myocardial infarction. It classically mimics ST-segment elevation myocardial infarction, and is characterised by acute onset of transient ventricular apical wall motion abnormalities (ballooning) accompanied by chest pain, dyspnea, ST-segment elevation, T-wave inversion or QT-interval prolongation on ECG. Elevation of myocardial enzymes is moderate at worst and there is absence of significant coronary artery disease.

The diagnosis is made by the pathognomonic wall motion abnormalities, in which the base of the left ventricle is contracting normally or is hyperkinetic while the remainder of the left ventricle is akinetic or dyskinetic. This is accompanied by the lack of significant coronary artery disease that would explain the wall motion abnormalities. Although apical ballooning has been classically described as the angiographic manifestation of takotsubo, it has been shown that left ventricular dysfunction in this syndrome includes not only the classic apical ballooning, but also different angiographic morphologies such as mid-ventricular ballooning and rarely local ballooning of other segments.

The ballooning patterns were classified by Shimizu et al. as takotsubo type for apical akinesia and basal hyperkinesia, reverse takotsubo for basal akinesia and apical hyperkinesia, mid-ventricular type for mid-ventricular ballooning accompanied by basal and apical hyperkinesia and localised type for any other segmental left ventricular ballooning with clinical characteristics of takotsubo-like left ventricular dysfunction.

The ECG changes are atypical, with imprecise changes in the ST segment and T waves. They are “suspicious of but non conclusive” of myocardial infraction. Blood tests for the enzyme creatine kinase and proteins troponin should be done. These are elevated in a heart attack. In a stunned heart, these results too are inconclusive. The echocardiogram is the clincher. The heart is ballooned out. This change occurs typically at the apex of the heart. It is important to make a distinction between heart attack and takotsubo as the medication is different.

Treatment:
The treatment for takotsubo is mainly supportive. Medication is given to remove fluid from the lungs and prevent clots. Recovery occurs within a few days.

About two per cent of people who were thought to have a heart attack actually had broken hearts. In the case of women, this increases to seven per cent. Women, mainly menopausal ones (60-75 years), have “broken hearts” eight to nine times more often than men. Some people are genetically prone to “broken hearts.” Depression plays a role in susceptibility to this condition. Recurrences can occur in 10 per cent of people.

People who are in poor physical condition do not need severe emotional stress to suffer a broken heart. An episode may be precipitated by a minor event like rejection, or even a lecture or talk before an audience.

In order to never develop this condition; it is important to develop metal and physical toughness. Walking for 40-60 minutes a day at a brisk pace exposes the heart to small doses of adrenaline and nor adrenaline in a controlled manner. The heart gets conditioned and is immune to sudden chemical surges. Meditation and yoga provide calmness and the mental strength to cope with good days and bad.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://en.wikipedia.org/wiki/Takotsubo_cardiomyopathy

http://www.mayoclinic.org/diseases-conditions/broken-heart-syndrome/basics/causes/con-20034635

http://www.telegraphindia.com/1141208/jsp/knowhow/story_2612.jsp

Nicotiana benthamiana

Botanical Name: Nicotiana benthamiana
Family: Solanaceae
Genus: Nicotiana
Species:N. benthamiana
Kingdom:Plantae
Order: Solanales

Synonyms: Nicotiana suaveolens var. cordifolia

Common indigenous names: Tjuntiwari and Muntju. Tangungnu, Ngkwerlp-pweter, Pinapitilypa, Tjiknga, Munju, Pirnki-warnu, Turlkamula

Habitat :Nicotiana benthamiana is native to Australia.It is found amongst rocks on hills and cliffs throughout the northern regions of Australia.

Description:
Nicotiana benthamiana is an erect, sometimes sprawling, annual herbaceous plant. This short-lived herb will reach from 0.65-5 feet (0.2-1.5 m) tall. Grown in containers, the plants rarely reach over 18 inches (0.45 m) tall by about half as wide. The dark green, broadly ovate leaves will reach up to 4 inches (10 cm) wide by 5 inches (12.7 cm) long. We selected this plant to use for TMV research because it is very susceptible to all kinds of viruses. Plants are easy to grow and we always keep several different ages of plants available at all times.

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Blooming: In the greenhouse, plants flower all year round, but in nature, they normally bloom from May-September. The small, white flowers are 3/8 inch (1 cm) across by 1.5 inches (3.8 cm) long.

A vigorous plant with numerous erect leafy stems. Its alternate leaves are broadly egg-shaped, dull green and soft. Except at the top of the stems, where they are stalkless, its leaves have slender stalks. Flowers are whitish, with a long, slender tube and five blunt lobes; fruits are capsules containing many pitted seeds.

This plant is a close relative of tobacco and species of Nicotiana indigenous to Australia.The plant was used by peoples of Australia as a stimulant – it contains nicotine and other alkaloids – before the introduction of commercial tobacco (N.tabacum and N.rustica). It was first collected on the north coast of Australia by Benjamin Bynoe on a voyage of the H.M.S. Beagle in 1837.

Cultivation:
Nicotiana benthamiana need full sun to partial shade using a well-drained soil mix. In the greenhouse, we use a soil mix consisting of 2 parts peat moss to 1 part loam to 1 part coarse sand or perlite. Since we grow these plants for research, they are given water on a daily basis to keep them stress free. They are fertilized weekly with a balanced fertilizer diluted to 1/2 the strength recommended on the label. Since we have to have these plants for research, once they set seed, plants are discarded. During the winter months, we use supplemental lighting to keep the plants growing strong.

Propagation: Nicotiana benthamiana is best propagated from seed.
Medicinal Uses:
The scientists have shown that transgenic versions of a plant Nicotiana benthamiana, also known as ‘Tjuntiwari’ in the native language, may be able to produce large quantities of a protein griffithsin which can be used as an anti-HIV microbicide gel.The protein has shown capabilities of neutralizing HIV as it binds to the virus molecule in such a way that the virus could not disguise itself from the immune system of humans.

Anti-HIV microbicide gel directly targets entry of the virus and averts infection at the surfaces but at present they are being produced using biologicals like bacteria E.coli, an expensive process which is not cost-effective.

The researchers from USA and UK altered the genetic nature of the plant using a tobacco mosaic virus which produced the protein griffithsin.(Published in The Times Of India)

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

Resources:

http://en.wikipedia.org/wiki/Nicotiana_benthamiana

http://www.plantoftheweek.org/week425.shtml

http://biolinfo.org/cmkb/view.php?comname=cmkb_public&scid=412

Lupus Nephritis

Alternative Names: Nephritis – lupus; Lupus glomerular disease

Definition:
Lupus nephritis is an inflammation of the kidney caused by systemic lupus erythematosus (SLE), a disease of the immune system. Apart from the kidneys, SLE can also damage the skin, joints, nervous system and virtually any organ or system in the body.

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Symptoms:
General symptoms of lupus include malar rash, discoid rash, photosensitivity, oral ulcers, nonerosive arthritis, pleuropericarditis, renal disease, neurological manifestations, and haematological disorders.

Clinically, SLE usually presents with fever, weight loss (100%), arthralgias, synovitis, arthritis (95%), pleuritis, pericarditis (80%), malar facial rash, photodermatosis, alopecia (75%), anaemia, leukopaenia, thrombocytopaenia, and thromboses (50%).

About half of cases of SLE demonstrate signs of lupus nephritis at one time or another. Renal-specific signs include proteinuria (100%), nephrotic syndrome (55%), granular casts (30%), red cell casts (10%), microhematuria (80%), macrohematuria (2%), reduced renal function (60%), RPGN (30%), ARF (2%), hypertension (35%), hyperkalemia (15%) and tubular abnormalities (70%).

The World Health Organization (WHO) developed a system to classify the six different stages of lupus nephritis:

Stage 1: no evidence of lupus nephritis:
In histology, Stage I (minimal mesangial) disease has a normal appearance under light microscopy, but mesangial deposits are visible under electron microscopy. At this stage urinalysis is typically normal.
Stage 2: mildest form, easily treated with corticosteroids:
Stage 2 disease (mesangial proliferative) is noted by mesangial hypercellularity and matrix expansion. Microscopic haematuria with or without proteinuria may be seen. Hypertension, nephrotic syndrome, and acute renal insufficiency are rare at this stage.
Stage 3: earliest stage of advanced lupus. Treatment requires high amounts of corticosteroids. The outlook remains favorable.

Stage 3 disease (focal lupus nephritis) is indicated by sclerotic lesions involving less than 50% of the glomeruli, which can be segmental or global, and active or chronic, with endocapillary or extracapillary proliferative lesions. Under electron microscopy, subendothelial deposits are noted, and some mesangial changes may be present. Immunofluorescence reveals the so-called “Full House” stain, staining positively for IgG, IgA, IgM, C3, and C1q. Clinically, haematuria and proteinuria is present, with or without nephrotic syndrome, hypertension, and elevated serum creatinine.
Diffuse proliferative lupus nephritis; photo shows the classic “flea-bitten” appearance of the cortical surface in the diffuse proliferative glomerulonephritides

Stage 4: advanced stage of lupus.

Stage 4 lupus nephritis (diffuse proliferative) is both the most severe, and the most common subtype. More than 50% of glomeruli are involved. Lesions can be segmental or global, and active or chronic, with endocapillary or extracapillary proliferative lesions. Under electron microscopy, subendothelial deposits are noted, and some mesangial changes may be present. Immunofluorescence reveals the so-called “Full House” stain, staining positively for IgG, IgA, IgM, C3, and C1q. Clinically, haematuria and proteinuria are present, frequently with nephrotic syndrome, hypertension, hypocomplementemia, elevated anti-dsDNA titres and elevated serum creatinine. There is the risk of kidney failure. Patients require high amounts of corticosteroids and immune suppression medications.
A wire-loop lesion may be present in stage III and IV. This is a glomerular capillary loop with subendothelial immune complex deposition that is circumferential around the loop. Stage V is denoted by a uniformly thickened, eosinophilic basement membrane. Stage III and IV are differentiated only by the number of glomeruli involved (which is subject to inherent sample bias), but clinically the presentation and prognosis are both expected to be more severe in stage 4 versus stage 3.
Stage 5:
Stage 5 (membranous lupus nephritis) is characterized by diffuse thickening of the glomerular capillary wall (segmentally or globally), with diffuse membrane thickening, and subepithelial deposits seen under electron microscopy. Clinically, stage V presents with signs of nephrotic syndrome. Microscopic haematuria and hypertension may also been seen. Plasma creatinine is usually normal or slightly elevated, and stage V may not present with any other clinical/serological manifestations of SLE (complement levels may be normal; anti-DNA Ab may not be detectable). Stage 5 also predisposes the affected individual to thrombotic complications such as renal vein thromboses or pulmonary emboli.Excessive protein loss and swelling. Doctors will treat with high amounts of corticosteroids. Doctors may or may not give immune-suppressing drugs.
A final stage is usually included by most practitioners, stage VI, or advanced sclerosing lupus nephritis. It is represented by Global sclerosis involving more than 90% of glomeruli, and represents healing of prior inflammatory injury. Active glomerulonephritis is usually not present. This stage is characterised by slowly progressive renal dysfunction, with relatively bland urine sediment. Response to immunotherapy is usually poor.

A tubuloreticular inclusion is also characteristic of lupus nephritis, and can be seen under electron microscopy in all stages. It is not diagnostic however, as it exists in other conditions. It is thought to be due to chronic interferon exposure.
Causes:
Systemic lupus erythematosus (SLE, or lupus) is an autoimmune disease. This means there is a problem with the body’s immune system.

Normally, the immune system helps protect the body from infection or harmful substances. But in patients with an autoimmune disease, the immune system cannot tell the difference between harmful substances and healthy ones. As a result, the immune system attacks otherwise healthy cells and tissue.

SLE may damage different parts of the kidney, leading to interstitial nephritis, nephrotic syndrome, and membranous GN. It may rapidly worsen to kidney failure.

Lupus nephritis affects approximately 3 out of every 10,000 people. In children with SLE, about half will have some form or degree of kidney involvement.

More than half of patients have not had other symptoms of SLE when they are diagnosed with lupus nephritis.

SLE is most common in women ages 20 – 40.
Diagnosis:
The diagnosis of lupus nephritis depends on blood tests, urinalysis, X-rays, ultrasound scans of the kidneys, and a kidney biopsy. On urinalysis, a nephritic picture is found and RBC casts, RBCs and proteinuria is found.

The World Health Organization has divided lupus nephritis into five stages based on the biopsy. This classification was defined in 1982 and revised in 1995.

* Class I is minimal mesangial glomerulonephritis which is histologically normal on light microscopy but with mesangial deposits on electron microscopy. It constitutes about 5% of cases of lupus nephritis. Renal failure is very rare in this form.[2]

*Class II is based on a finding of mesangial proliferative lupus nephritis. This form typically responds completely to treatment with corticosteroids. It constitutes about 20% of cases.[2] Renal failure is rare in this form.[2]

* Class III is focal proliferative nephritis and often successfully responds to treatment with high doses of corticosteroids. It constitutes about 25% of cases. Renal failure is uncommon in this form.

*Class IV is diffuse proliferative nephritis. This form is mainly treated with corticosteroids and immunosuppressant drugs. It constitutes about 40% of cases. Renal failure is common in this form.

* Class V is membranous nephritis and is characterized by extreme edema and protein loss. It constitutes about 10% of cases.[2] Renal failure is uncommon in this form.

Medicines are prescribed that decrease swelling, lower blood pressure, and decrease inflammation by suppressing the immune system: Patients may need to monitor intake of protein, sodium, and potassium. Patients with severe disease should restrict their sodium intake to 2 grams per day and limit fluid as well. Depending on the histology, renal function and degree of proteinuria, patients may require steroid therapy or chemotherapy regimens such as cyclophosphamide, azathioprine, mycophenolate mofetil, or cyclosporine.
Possible Complications:

*Acute renal failure
*Chronic renal failure
*End-stage renal disease
*Nephrotic syndrome
Treatment:

There is no cure for lupus nephritis. The goal of treatment is to keep the problem from getting worse. Stopping kidney damage early can prevent the need for a kidney transplant.

Treatment can also provide relief from lupus symptoms.

Common treatments include:

*minimizing intake of protein and salt
*taking blood pressure medication
*using steroids to reduce swelling and inflammation
*taking immune-suppression medicines like prednisone to reduce immune system damage to the kidneys

Extensive kidney damage may require additional treatment.

Drug regimens prescribed for lupus nephritis include mycophenolate mofetil (MMF), intravenous cyclophosphamide with corticosteroids, and the immune suppressant azathioprine with corticosteroids. MMF and cyclophosphamide with corticosteroids are equally effective in achieving remission of the disease. MMF is safer than cyclophosphamide with corticosteroids, with less chance of causing ovarian failure, immune problems or hair loss. It also works better than azathioprine with corticosteroids for maintenance therapy.

Prognosis:  How well you do depends on the specific form of lupus nephritis. You may have flare-ups, and then times when you do not have any symptoms.

Some people with this condition develop chronic kidney failure.

Although lupus nephritis may return in a transplanted kidney, it rarely leads to end-stage kidney disease.
Prevention: There is no known prevention for lupus nephritis.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.
Resources:

http://en.wikipedia.org/wiki/Lupus_nephritis

http://www.nlm.nih.gov/medlineplus/ency/article/000481.htm

http://www.healthline.com/health/lupus-nephritis#Diagnosis3

Bone Broth Is A Most Nourishing Food And good For Any Ailment

Bone broth has a long history of medicinal use. It’s known to be warm, soothing, and nourishing for body, mind, and soul.

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Physicians harkening as far back as Hippocrates have associated bone broth with gut healing. And while the importance of gut health is just now starting to fill our medical journals, this knowledge is far from new.

In fact, you could say modern medicine is just now rediscovering how the gut influences health and disease.

Many of our modern diseases appear to be rooted in an unbalanced mix of microorganisms in your digestive system, courtesy of a diet that is too high in sugars and too low in healthful fats and beneficial bacteria.

Digestive problems and joint problems, in particular, can be successfully addressed using bone broth. But as noted by Dr. Kaayla Daniel, vice president of the Weston A. Price Foundation and coauthor (with Sally Fallon Morell) of the book, Nourishing Broth, bone broth is a foundational component of a healing diet regardless of what ails you.

BENEFITS OF BONE BROTH :

Leaky gut is the root of many health problems, especially allergies, autoimmune disorders, and many neurological disorders. The collagen found in bone broth acts like a soothing balm to heal and seal your gut lining, and broth is a foundational component of the Gut and Psychology Syndrome (GAPS) diet, developed by Russian neurologist Dr. Natasha Campbell-McBride.

The GAPS diet is often used to treat children with autism and other disorders rooted in gut dysfunction, but just about anyone with suboptimal gut health can benefit from it.

Bone broth is also a staple remedy for acute illnesses such as cold and flu. While there aren’t many studies done on soup, one study did find that chicken soup opened up the airways better than hot water.

Processed, canned soups  may not work as well as the homemade version made from slow-cooked bone broth. If combating a cold, make the soup hot and spicy with plenty of pepper.

The spices will trigger a sudden release of watery fluids in your mouth, throat, and lungs, which will help thin down the respiratory mucus so it’s easier to expel. Bone broth contains a variety of valuable nutrients in a form your body can easily absorb and use. And these are:

1. Calcium, phosphorus, and other minerals……Components of collagen and cartilage

2.Silicon and other trace minerals………….Components of bone and bone marrow

3.Glucosamine and chondroitin sulfate……….The “conditionally essential” amino acids proline, glycine, and glutamine

These nutrients account for many of the healing benefits of bone broth, which include the following:

1.Reduces joint pain and inflammation, courtesy of chondroitin sulfate, glucosamine, and other compounds extracted from the boiled down cartilage and collagen.

2.Inhibits infection caused by cold and flu viruses etc.
Indeed, Dr. Daniel reports2 chicken soup — known as “Jewish penicillin“—has been revered for its medicinal qualities at least since Moses Maimonides in the 12th century. Recent studies on cartilage, which is found abundantly in homemade broth, show it supports the immune system in a variety of ways; it’s a potent normalizer, true biological response modifier, activator of macrophages, activator of Natural Killer (NK) cells, rouser of B lymphocytes and releaser of Colony Stimulating Factor.

3.Fights inflammation: Amino acids such as glycine, proline, and arginine all have anti-inflammatory effects. Arginine, for example, has been found to be particularly beneficial for the treatment of sepsis3 (whole-body inflammation). Glycine also has calming effects, which may help you sleep better.

4.Promotes strong, healthy bones: Dr. Daniel reports bone broth contains surprisingly low amounts of calcium, magnesium and other trace minerals, but she says “it plays an important role in healthy bone formation because of its abundant collagen. Collagen fibrils provide the latticework for mineral deposition and are the keys to the building of strong and flexible bones.”

5.Promotes healthy hair and nail growth, thanks to the gelatin in the broth. Dr. Daniel reports that by feeding collagen fibrils, broth can even eliminate cellulite too.

In the conclution it can be said :Bone Broth—A Medicinal ‘Soul Food

Slow-simmering bones for a day will create one of the most nutritious and healing foods there is. You can use this broth for soups, stews, or drink it straight. The broth can also be frozen for future use. Making bone broth also allows you to make use of a wide variety of leftovers, making it very economical. Bone broth used to be a dietary staple, as were fermented foods, and the elimination of these foods from our modern diet is largely to blame for our increasingly poor health, and the need for dietary supplements.

“I would like to urge people to make as much broth as possible,” Dr. Daniel says in closing. “Keep that crockpot going; eat a variety of soups, and enjoy them thoroughly.”

Resources: Mercola.com

Lumbar Spondylosis

Definition:
Lumbar Spondylosis is a condition associated with degenerative changes in the intervertebral discs and facet joints. Spondylosis, also known as spinal osteoarthritis, can affect the lumbar, thoracic, and/or the cervical regions of the spine. Although aging is the primary cause, the location and rate of degeneration is individual. As the lumbar discs and associated ligaments undergo aging, the disc spaces frequently narrow. Thickening of the ligaments that surround the disc and those that surround the facet joints develops. These ligamentous thickening may eventually become calcified. Compromise of the spinal canal or of the openings through which the spinal nerves leave the spinal canal can occur.

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Lumbar spondylosis encompasses lumbar disc bulges, herniations, facet joint degeneration, and vertebral bony overgrowths (osteophytes). Degenerative changes, including osteophyte formation, increase with age but are often asymptomatic. Disc herniation is symptomatic when it causes nerve root compression and spinal stenosis. Common symptoms include low back pain, sciatica, and restriction in back movement. Treatment is usually conservative, although surgery is indicated for spinal cord compression or intractable pain. Relapse is common, with patients experiencing episodic back pain.

Symptoms:
Symptoms of lumbar spondylosis follow those associated with each of the various aspects of the disorder: disc herniation, sciatica, spinal stenosis, degenerative spondylolisthesis, and degenerative scoliosis. Pain associated with disc degeneration may be felt locally in the back or at a distance away. This is called referred pain, as the pain is not felt at its site of origin. Lower back arthritis may be felt as pain in the buttock, hips, groin, and thighs. As with spinal stenosis or disc herniation in the lumbar region, it is important to be aware of any bowel or bladder incontinence, or numbness in the perianal area. These signs and symptoms could represent an important massive nerve compression needing surgical intervention (cauda equina syndrome).

Causes:
Spondylosis is mainly caused by ageing. As people age, certain biological and chemical changes cause tissues throughout the body to degenerate. In the spine, the vertebrae (spinal bones) and intervertebral discs degenerate with ageing. the intervertebral discs are cushion like structures that act as shock absorbers between the vertebral bones.

One of the structures that form the discs is known as the annulus fibrosus. The annulus fibrosus is made up of the 60 or more tough circular bands of collagen fiber (called lamellae). Collagen is a type of inelastic fiber. Collagen fibers, along with water and proteoglycans (types of large molecules made of a protein and at least one carbohydrate chain) help to form the soft, gel-like center part of each disk. This soft, center part is known as the nucleus pulposus and is surrounded by the annulus fibrosus.

The degenerative effects of ageing can cause the fibers of the discs to weaken, causing wear and tear. Constant wear and tear and injury to the joints of the vertebrae causes inflammation in the joints. Degeneration of the discs leads to the formation of mineral deposits within the discs. The water content of the center of the disc decreases with age and as a result the discs become hard, stiff, and decreased in size. This, in turn, results in strain on all the surrounding joints and tissues, causing the sensation of stiffness. With less water in the center of the discs, they have decreased shock absorbing qualities. An increased risk of disc herniation also results, which is when the disc abnormally protrudes from its normal position.

Each vertebral body contains four joints that act as hinges. These hinges are known as facet joints or zygapophyseal joints. The job of the facet joins is to allow the spinal column to flex, extend, and rotate. The bones of the facet joints are covered with cartilage (a type of flexible tissue) known as end plates. The job of the end plates is to attach the disks to the vertebrae and to supply nutrients to the disc. When the facet joints degenerate, the size of the end plates can decrease and stiffen. Movement can stimulate pain fibers in the facet joints and annulus fibrosus. Furthermore, the vertebral bone underneath the end plates can become thick and hard.

Degenerative disease can cause ligaments to lose their strength. A ligament is a tough band of tissue that attaches to joint bones. In the spine, ligaments connect spinal structures such as vertebrae and prevent them from moving too much. In degenerative spondylosis, one of the main ligaments (known as the ligamentum flavum) can thicken or buckle, making it weaken.

Knobby, abnormal bone growths (known as bone spurs or osteophytes) can form in the vertebrae. These changes can also cause osteoarthritis. Osteoarthritis is a disease of the joints that is made worse by stress. In more severe cases, these bones spurs can compress nerves coming out of the spinal cord and/or decreased blood supply to the vertebrae. Areas of the body supplied by these nerves may become painful or develop loss of sensation and function.

Carrying around excessive weight can cause lumbar spondylosis. Spending much of the day seated can also be a contributing factor. An injury or trauma to the back can also contribute, as can genetic factors.

The main Risk Factors:
• Age: As a person ages the healing ability of the body decreases and developing arthritis at that time can make the disease progress much faster. Persons over 40 years of age are more prone to developing lumbar spondylosis.

• Obesity: Overweight puts excess load on the joints as the lumbar region carries most of the body’s weight, making a person prone to lumbar spondylosis.

• Sitting for prolonged periods: Sitting in one position for prolonged time which puts pressure on the lumbar vertebrae.

• Prior injury: Trauma makes a person more susceptible to developing lumbar spondylosis.

• Heredity or Family history
Diagnosis:
Physical Examination:
A thorough physical examination reveals much about the patient’s health and general fitness. The physical part of the exam includes a review of the patient’s medical and family history. Often laboratory tests such as complete blood count and urinalysis are ordered. The physical exam may include:

*Palpation (exam by touch) determines spinal abnormalities, areas of tenderness, and muscle spasm.

*Range of Motion measures the degree to which a patient can perform movement of flexion, extension, lateral bending, and spinal rotation.

*A neurologic evaluation assesses the patient’s symptoms including pain, numbness, paresthesias (e.g. tingling), extremity sensation and motor function, muscle spasm, weakness, and bowel/bladder changes. Particular attention may be given to the extremities. Either a CT Scan or MRI study may be required if there is evidence of neurologic dysfunction.

X-rays and Other Tests:
Radiographs (X-rays) may indicate loss of vertebral disc height and the presence of osteophytes, but is not as useful as a CT Scan or MRI. A CT Scan may help reveal bony changes sometimes associated with spondylosis. An MRI is a sensitive imaging tool capable of revealing disc, ligament, and nerve abnormalities. Discography seeks to reproduce the patient’s symptoms to identify the anatomical source of pain. Facet blocks work in a similar manner. Both are considered controversial.

The physician compares the patient’s symptoms to the findings to formulate a diagnosis and treatment plan. The results from the examination provide a baseline from which the physician can monitor and measure the patient’s progress.

Treatment:
Each patient is treated differently for arthritis depending on their individual condition. In the early stages lifestyle modifications or medicines are used for treatment and surgery is needed only if these measures are ineffective.

Yoga:
A few yoga poses and sequences can help lumbar spondylosis. Sun salutations, also known as Surya Namaskar A and B, are good for back strengthening and flexibility. The cobra pose, or Bhjangasana, stretches the lower back. The locust pose, or Shalabhasana, strengthens the lower back because it requires lifting one’s upper and lower body off the ground from a prone position on the floor. Meditation & pranayam 

Exercises:
Physical therapy is often prescribed to relieve problems caused by lumbar spondylosis. Back extensions are used on patients who can tolerate them. The patient lies face down on her stomach and then slowly lifts only her upper body off the floor. The arms may be placed palms down under her chest to take some strain off the back muscles. If lying down is too painful, this exercise can also be done against a wall. The patient puts her hands against a wall, standing about a foot away, and bends back, using a combination of lower back muscles and arms.

Stretches to Avoid:
Lying on the back and bringing the knees into the chest is an example of a common lower back stretch that flexes the spine. This is not recommended for people with lumbar spondylosis. Bending down to touch one’s toes from a standing position is also not recommended. Reaching for the toes while sitting can be problematic, too.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://www.ehow.com/about_5039006_lumbar-spondylosis-exercises.html

http://www.physiotherapy-treatment.com/lumbar-spondylosis.html

 

Preventing Kidney Stones May Be Simple

Today, the rates of kidney stones are rising like any other diseas.In most cases, kidney stones pass without causing lasting damage, but the pain during passing can be excruciating. Kidney stones are also sometimes associated with lower back pain, stomach pain, nausea or vomiting, fever, and chills.

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Generally, the larger the stone, the more pain and symptoms it will cause. Sometimes aggressive treatments are needed to clear the stones, and each year, more & more people are going to emergency rooms due to kidney stones.

Once you’ve had them, your risk of recurrence increases. About 35 percent to 50 percent of people will have another bout with kidney stones within five years unless changes are made.Now, What type of changes? According to new guidelines issued by the American College of Physicians (ACP), one of the simplest strategies you can take is to drink more water.
If you Stay Hydrated you Lower Your Risk of Recurrent Kidney Stones:

The number one risk factor for kidney stones is not drinking enough water. If you aren’t drinking enough, your urine will have higher concentrations of substances that can precipitate out and form stones.

Specifically, stone-forming chemicals include calcium, oxalate, urate, cysteine, xanthine, and phosphate. These chemicals should be eliminated in your urine via your kidney, but if too little liquid is present, they can join together to form a stone. According to the National Kidney Foundation:

Urine has various wastes dissolved in it. When there is too much waste in too little liquid, crystals begin to form. The crystals attract other elements and join together to form a solid that will get larger unless it is passed out of the body with the urine… In most people, having enough liquid washes them out or other chemicals in urine stop a stone from forming.”

The new ACP guidelines call for people who have had a kidney stone in the past to increase their fluid intake so they have at least two liters of urine per day, which they say could decrease stone recurrence by at least half.And to achieve this, they recommend increased fluid intake spread throughout the day, pointing out that both water and mineral water are beneficial.

The National Kidney Foundation recommends drinking more than 12 glasses of water a day, but a simpler way to know if you are drinking enough water is to check the color of your urine; you want your urine to be a very light, pale yellow (darker urine is more concentrated).

Every person’s water requirement is different, depending on your particular metabolic requirements and activity level, but simply keeping your urine light yellow will go a long way toward preventing kidney stones.

Remember to increase your water intake whenever you increase your activity and when you’re in a warmer climate. If you happen to be taking any multivitamins or B supplements that contain vitamin B2 (riboflavin), the color of your urine will be a very bright, nearly fluorescent yellow and this will not allow you to use the color of your urine as a guide to how well you are hydrated.

By increasing water intake you will get rid of discomfort like, constipation,prostrate problems etc.

But if it in mind that Water Reduces Risk of kidney stone, but Soda wate or any othar areated water Increases It:

One important point: not just any fluid will do to increase your urine output. While water and mineral water were protective, drinking soda is associated with kidney stones, possibly because the phosphorus acid it contains acidifies your urine, which promotes stone formation.

In addition, one South African study found that drinking soda exacerbates conditions in your urine that lead to formation of calcium oxalate kidney stone problems.6 The sugar, including fructose (and high fructose corn syrup in soda), is also problematic.

A diet high in sugar can set you up for kidney stones, since sugar upsets the mineral relationships in your body by interfering with calcium and magnesium absorption. The consumption of unhealthy sugars and soda by children is a large factor in why children as young as age 5 are now developing kidney stones.

Sugar can also increase kidney size and produce pathological changes in your kidney, such as the formation of kidney stones. According to The National Kidney Foundation, you should pay particular attention to keeping your fructose levels under control:

“Eating too much fructose correlates with increasing risk of developing a kidney stone. Fructose can be found in table sugar and high fructose corn syrup. In some individuals, fructose can be metabolized into oxalate.”

So if you’re a soda drinker, cutting back is an important strategy to remember. In one study, those with kidney stones who eliminated soda from their diet lowered their risk of recurrence by about 15 percent.
Kidney Stones Associated with Increased Risk of Broken Bones:

As mentioned, kidney stones usually pass without any lasting complications, however there are some long-term associated risks. Kidney stones increase your risk of developing chronic kidney disease, for instance, and new research also shows they might be associated with more brittle bones.

Past research has suggested that people with kidney stones have lower bone mineral density. The new study used data from more than 52,000 people and showed that those with kidney stones were at a significantly higher risk of bone fractures. Specifically:

*Men with kidney stones were 10 percent more likely to suffer broken bones than men without

*Male teens with kidney stones had a 55 percent higher fracture risk than those without

*Women with kidneys stones had a 17 percent to 52 percent increased fracture risk depending on age (from their 20s to 60s); those aged 30-39 had the highest risk
Fluoride Also Linked to Kidney Stones:

If you live in area with fluoridated drinking water (such as most of the US), you might be interested to know that high levels of fluoride in water are associated with kidney stones.11 The condition was nearly five times more common in an area with high fluoride (3.5 to 4.9 parts per million, or ppm) than a similar area without high fluoride levels in the water.

Overall, the prevalence of kidney stones in the high-fluoride area was nearly double in those with fluorosis than those without. Dental fluorosis – a condition in which your tooth enamel becomes progressively discolored and mottled – is one of the first signs of over-exposure to fluoride.

Eventually, it can result in badly damaged teeth, and worse… It’s important to realize that dental fluorosis is NOT “just cosmetic.” It can also be an indication that the rest of your body, such as your bones and internal organs, including your brain, has been overexposed to fluoride as well. In other words, if fluoride is having a visually detrimental effect on the surface of your teeth, you can be virtually guaranteed that it’s also damaging other parts of your body, such as your bones. A reverse osmosis water filtration system can remove fluoride from your drinking water.

Exercise, Avoiding Overeating Are Two More Powerful Tools for Preventing Kidney Stones:

You’re more prone to kidney stones if you’re bedridden or very sedentary for a long period of time, partly because limited activity can cause your bones to release more calcium. Exercise will also help you to resolve high blood pressure, a condition that doubles your risk for kidney stones. Even low amounts of exercise may be beneficial to reducing your risk. In a study involving more than 84,000 postmenopausal women, it was found that those who exercised had up to a 31 percent lower risk of kidney stones.13 The link persisted even with only small amounts of physical activity.

Specifically, the research showed a lower risk from three hours a week of walking, four hours of light gardening or just one hour of moderate jogging. You can find my comprehensive exercise recommendations, including how to perform highly recommended high-intensity interval training (HIIT), here. Diet wise, women who ate more than 2,200 calories per day increased their risk of kidney stones by up to 42 percent, while obesity also raised the risk. It should be noted that even though obesity increases kidney stone risk, weight loss surgery that alters your digestive tract actually makes them more common. After weight loss surgery, levels of oxalate are typically much higher (oxalate is the most common type of kidney stone crystal).
Dietary Approaches for Avoiding Kidney Stones:-

1. Make Sure You’re Getting Enough Magnesium

Magnesium is responsible for more than 300 biochemical reactions in your body, and deficiency of this mineral has been linked to kidney stones. An estimated 80 percent of Americans are deficient, so this could be a major factor. Magnesium plays an important role in your body’s absorption and assimilation of calcium, as if you consume too much calcium without adequate magnesium, the excess calcium can actually become toxic and contribute to health conditions like kidney stones.

Magnesium helps prevent calcium from combining with oxalate, which, as mentioned, is the most common type of kidney stone. Green leafy vegetables like spinach and Swiss chard are excellent sources of magnesium, and one of the simplest ways to make sure you’re consuming enough of these is by juicing your vegetables. Vegetable juice is an excellent source of magnesium, as are some beans, nuts like almonds, and seeds, pumpkin seeds, sunflower seeds, and sesame seeds. Avocadoes are also a good source.

2. Eat Calcium-Rich Foods (But Be Careful with Supplements)

In the past, kidney stone sufferers have been warned to avoid foods high in calcium, as calcium is a major component of the majority of kidney stones. However, there is now evidence that avoiding calcium may do more harm than good. The Harvard School of Public Health conducted a study of more than 45,000 men,14 and the men who had diets rich in calcium had a one-third lower risk of kidney stones than those with lower calcium diets. It turns out that a diet rich in calcium actually blocks a chemical action that causes the formation of the stones.

It binds with oxalates (from foods) in your intestine, which then prevents both from being absorbed into your blood and later transferred to your kidneys. So, urinary oxalates may be more important to formation of calcium-oxalate kidney stone crystals than is urinary calcium. It is important to note that it is the calcium from foods that is beneficial — not calcium supplements, which have actually been found to increase your risk of kidney stones by 20 percent.
3. Avoid Non-Fermented Soy:

Soybeans and soy-based foods may promote kidney stones in those prone to them, as they may contain high levels of oxalates, which can bind with calcium in your kidney to form kidney stones. This is just one reason why unfermented soy — the type found in soy milk, soy burgers, soy ice cream, and even tofu — is not a health food. If you were to carefully review the thousands of studies published on soy, I strongly believe you would reach the same conclusion as I have — which is, the risks of consuming unfermented soy products FAR outweigh any possible benefits.

If you’re interested in enjoying the health benefits of soy, choose fermented soy, as after a long fermentation process, the phytate (which blocks your body’s uptake of essential minerals) and anti-nutrient levels of soybeans (including oxalates) are reduced, and their beneficial properties become available to your digestive system.

In the conclution it can be said that the good news is  there’s plenty you can do to reduce your risk of kidney stones.

Sources:Mercola.com

Jute

Botanical Name:Corchorus capsularis
Family: Malvaceae
Subfamily: Grewioideae
Genus:     Corchorus
Kingdom: Plantae
Order:     Malvales

Common Name : Jute
Habitat :Jute is native to tropical and subtropical regions throughout the world.A tropical plant in essence, Jute thrives in hot, humid conditions and in soils that have high levels of sand and clay. It is little wonder then, that the Ganges River Delta is at the centre of global Jute production. This area also encounters heavy rainfall during the monsoon season that further benefits Jute growth and the reliability of a good crop.

Description:
Jute plants are tall, usually annual herbs, reaching a height of 2–4 m, unbranched or with only a few side branches. The leaves are alternate, simple, lanceolate, 5–15 cm long, with an acuminate tip and a finely serrated or lobed margin. The flowers are small (2–3 cm diameter) and yellow, with five petals; the fruit is a many-seeded capsule. It thrives almost anywhere, and can be grown year-round.

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Jute plant has about 40–100 species, including:
Corchorus aestuans
Corchorus capsularis
Corchorus carnarvonensis
Corchorus cunninghamii
Corchorus erodiodes
Corchorus junodi
Corchorus olitorius
Corchorus sidoides
Corchorus tridens
Corchorus walcottii

Cultivation:
Jute needs a plain alluvial soil and standing water. The suitable climate for growing jute (warm and wet) is offered by the monsoon climate, during the monsoon season. Temperatures from 20 degree cent. to 40degree cent. and relative humidity of 70%–80% are favourable for successful cultivation. Jute requires 5–8 cm of rainfall weekly, and more during the sowing time.

Edible Uses:
In Nigeria, leaves of Corchorus olitorius are prepared in sticky soup called ewedu together with ingredients such as sweet potato, dried small fish or shrimp. The leaves are rubbed until foamy or sticky before adding to the soup. The leaves of the Jute plant are widely used in Nigeria to prepare a sticky soup. Amongst the Yoruba of Nigeria, the leaves are called Ewedu, and in the Hausa-speaking northern Nigeria, the leaves are called turgunuwa or lallo. The jute leaves are cut into shreds and added to the soup which would normally contain other ingredients such as meat and/or fish, pepper, onions, and other spices. Likewise, the Lugbara of Northwestern Uganda eat the leaves as soup, locally called pala bi. Jute is also a totem for Ayivu, one of the Lugbara clans.

In the Philippines, especially in Ilocano-dominated areas, this vegetable, locally known as saluyot, can be mixed with either bitter gourd, bamboo shoots, loofah, or sometimes all of them. These have a slimy and slippery texture.

In Bengal the leaf is used and cooked as  jute vegetable called as pat shak.

Chemical Constituents:
Per 100 g, the leaves are reported to contain 43-58 calories, 80.4-84.1 g H2O, 4.5-5.6 g protein, 0.3 g fat, 7.6-12.4 g total carbohydrate, 1.7-2.0 g fiber, 2.4 g ash, 266-366 mg Ca, 97-122 mg P, 7.2-7.7 mg Fe, 12 mg Na, 444 mg K, 6,410-7,850 ug beta-carotene equivalent, 0.13-0.15 mg thiamine, 0.26- 0.53 mg riboflavin, 1.1-1.2 mg niacin, and 53-80 mg ascorbic acid. Leaves contain oxydase and chlorogenic acid. The folic acid content is substantially higher than that of other folacin-rich vegetables, ca 800 micrograins per 100 g (ca 75% moisture) or ca 3200 micrograms on a zero moisture basis (Chen and Saad, 1981).
The seeds contain 11.3-14.8% oil (Watt and Breyer-Brandwijk, 1962), reportedly estrogenic (Sharaf et al, 1979), which contains 16.9% palmitic-, 3.7% stearic-, 1.8% behenic-, 1.1% lignoceiic-, 9.1% oleic-, 62.5% linoleic-, and 0.9% linolenic- acids as well as large portions of B, Mn, Mo, and Zn.

Medicinal Uses:
While perhaps better known as a fiber crop, jute is also a medicinal “vegetable”, eaten from Tanganyika to Egypt. Dried leaves were given me by an Egyptian friend who had brought them with him to this country. They are used in soups under the Arabic name  “Molukhyia.” In India the leaves and tender shoots are eaten. The dried material is there  known as “nalita.” Injections of olitoriside markedly improve cardiac insufficiencies and  have no cumulative attributes; hence, it can serve as a substitute for strophanthin.

Reported to be demulcent, deobstruent, diuretic, lactagogue, purgative, and tonic, tussah  jute is a folk remedy for aches and pains, dysentery, enteritis, fever, dysentery, pectoral  pains, and tumors (Duke and Wain, 1981; List and Horhammer, 1969-1979). Ayurvedics.

The leaves are used for ascites, pain, piles, and tumors. Elsewhere the leaves are used for  cystitis, dysuria, fever, and gonorrhea. The cold infusion is said to restore the appetite and  strength (Source: James A. Duke. 1983. Handbook of Energy Crops.http://www.worldjute.com/jute_news/medijut.html).

Other Uses:
Jute is a long, soft, shiny vegetable fiber that can be spun into coarse, strong threads. It is produced from plants in the genus Corchorus, which was once classified with the family Tiliaceae, more recently with Malvaceae, and has now been reclassified as belonging to the family Sparrmanniaceae. “Jute” is the name of the plant or fiber that is used to make burlap, Hessian or gunny cloth…..click & see

Jute is one of the most affordable natural fibers and is second only to cotton in amount produced and variety of uses of vegetable fibers. Jute fibers are composed primarily of the plant materials cellulose and lignin. It falls into the bast fiber category (fiber collected from bast or skin of the plant) along with kenaf, industrial hemp, flax (linen), ramie, etc. The industrial term for jute fiber is raw jute. The fibers are off-white to brown, and 1–4 metres (3–13 feet) long. Jute is also called “the golden fiber” for its color and high cash value.

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Jute is used in the manufacture of a number of fabrics such as Hessian cloth, sacking, scrim, carpet backing cloth (CBC), and canvas. Hessian, lighter than sacking, is used for bags, wrappers, wall-coverings, upholstery, and home furnishings. Sacking, a fabric made of heavy jute fibers, has its use in the name. CBC made of jute comes in two types. Primary CBC provides a tufting surface, while secondary CBC is bonded onto the primary backing for an overlay. Jute packaging is used as an eco-friendly substitute.

Jute floor coverings consist of woven and tufted and piled carpets. Jute Mats and mattings with 5 / 6 mts width and of continuous length are easily being woven in Southern parts of India, in solid and fancy shades, and in different weaves like, Boucle, Panama, Herringbone, etc. Jute Mats & Rugs are made both through Powerloom & Handloom, in large volume from Kerala, India. The traditional Satranji mat is becoming very popular in home décor. Jute non-wovens and composites can be used for underlay, linoleum substrate, and more.

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Jute has many advantages as a home textile, either replacing cotton or blending with it. It is a strong, durable, color and light-fast fiber. Its UV protection, sound and heat insulation, low thermal conduction and anti-static properties make it a wise choice in home décor. Also, fabrics made of jute fibers are carbon-dioxide neutral and naturally decomposable. These properties are also why jute can be used in high performance technical textiles.

The dry  jute stem is used as fire wood.

As a diversified byproducts from jute can be used in cosmetics,  paints, and other products.

Toxicity:
Contains HCN and several cardiac glycosides. Negm et al (1980) report the LD50 of tissue extracts to mice. The “lethal dose” of Corchoroside A to cats is 0.053-0.0768 mg/kg and Corchoroside B 0.059-0.1413, but some authors say that Corchoroside A is twice as active as Corchoroside B.

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

Resources:

http://en.wikipedia.org/wiki/Jute

http://www.jute-rugs.co.uk/aboutjute.php

http://indianjute.blogspot.in/p/medicinal-use-herbal-use-of-jute-jute.html

http://www.worldjute.com/jute_news/medijut.html

BALANCE DISORDER

Definition:
A balance disorder is a disturbance that causes an individual to feel unsteady, for example when standing or walking. It may be accompanied by feelings of giddiness or wooziness, or having a sensation of movement, spinning, or floating. Balance is the result of several body systems working together: the visual system (eyes), vestibular system (ears) and proprioception (the body’s sense of where it is in space). Degeneration or loss of function in any of these systems can lead to balance deficits
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Balance disorders can be caused by certain health conditions, medications, or a problem in the inner ear or the brain.

Our sense of balance is primarily controlled by a maze-like structure in our inner ear called the labyrinth, which is made of bone and soft tissue. At one end of the labyrinth is an intricate system of loops and pouches called the semicircular canals and the otolithic organs, which help us maintain our balance. At the other end is a snail-shaped organ called the cochlea, which enables us to hear. The medical term for all of the parts of the inner ear involved with balance is the vestibular system.

Symptoms:
When balance is impaired, an individual has difficulty maintaining upright orientation. For example, an individual may not be able to walk without staggering, or may not even be able to stand. They may have falls or near-falls. The symptoms may be recurring or relatively constant. When symptoms exist, they may include:

*Dizziness or vertigo (a spinning sensation)
*Falling or feeling as if you are going to fall
*Lightheadedness, faintness, or a floating sensation
*Blurred vision
*Confusion or disorientation

Some individuals may also experience nausea and vomiting, diarrhea, faintness, changes in heart rate and blood pressure, fear, anxiety, or panic. Some reactions to the symptoms are fatigue, depression, and decreased concentration. The symptoms may appear and disappear over short time periods or may last for a longer period.

Cognitive dysfunction (disorientation) may occur with vestibular disorders. Cognitive deficits are not just spatial in nature, but also include non-spatial functions such as object recognition memory. Vestibular dysfunction has been shown to adversely affect processes of attention and increased demands of attention can worsen the postural sway associated with vestibular disorders. Recent MRI studies also show that humans with bilateral vestibular damage undergo atrophy of the hippocampus which correlates with their degree of impairment on spatial memory tasks

Causes:
Problems with balance can occur when there is a disruption in any of the vestibular, visual, or proprioceptive systems. Abnormalities in balance function may indicate a wide range of pathologies from causes like inner ear disorders, low blood pressure, brain tumors, and brain injury including stroke.

Many different terms are often used for dizziness, including lightheaded, floating, woozy, giddy, confused, helpless, or fuzzy. Vertigo, Disequilibrium and pre-syncope are the terms in use by most physicians and have more precise definitions.

*Vertigo: Vertigo is the sensation of spinning or having the room spin about you. Most people find vertigo very disturbing and report associated nausea and vomiting.

*Disequilibrium: Disequilibrium is the sensation of being off balance, and is most often characterized by frequent falls in a specific direction. This condition is not often associated with nausea or vomiting.

*Pre-syncope (links to syncope, which is different): Pre-syncope is a feeling of lightheadedness or simply feeling faint. Syncope, by contrast, is actually fainting. A circulatory system deficiency, such as low blood pressure, can contribute to a feeling of dizziness when one suddenly stands up.

Problems in the skeletal or visual systems, such as arthritis or eye muscle imbalance, may also cause balance problems.

Related to the ear:
Causes of dizziness related to the ear are often characterized by vertigo (spinning) and nausea. Nystagmus (flickering of the eye, related to the Vestibulo-ocular reflex [VOR]) is often seen in patients with an acute peripheral cause of dizziness.

*Benign Paroxysmal Positional Vertigo (BPPV) – The most common cause of vertigo. It is typically described as a brief, intense sensation of spinning that occurs when there are changes in the position of the head with respect to gravity. An individual may experience BPPV when rolling over to the left or right, upon getting out of bed in the morning, or when looking up for an object on a high shelf.  The cause of BPPV is the presence of normal but misplaced calcium crystals called otoconia, which are normally found in the utricle and saccule (the otolith organs) and are used to sense movement. If they fall from the utricle and become loose in the semicircular canals, they can distort the sense of movement and cause a mismatch between actual head movement and the information sent to the brain by the inner ear, causing a spinning sensation.

*Labyrinthitis - An inner ear infection or inflammation causing both dizziness (vertigo) and hearing loss.

*Vestibular neuronitis – an infection of the vestibular nerve, generally viral, causing vertigo

*Cochlear Neuronitis – an infection of the Cochlear nerve, generally viral, causing sudden deafness but no vertigo

*Trauma – Injury to the skull may cause either a fracture or a concussion to the organ of balance. In either case an acute head injury will often result in dizziness and a sudden loss of vestibular function.

*Surgical trauma to the lateral semicircular canal (LSC) is a rare complication which does not always result in cochlear damage. Vestibular symptoms are pronounced. Dizziness and instability usually persist for several months and sometimes for a year or more.

   *Ménière’s disease – an inner ear fluid balance disorder that causes lasting episodes of vertigo, fluctuating hearing loss, tinnitus (a ringing or roaring in the ears), and the sensation of fullness in the ear. The cause of Ménière’s disease is unknown.

    *Perilymph fistula - a leakage of inner ear fluid from the inner ear. It can occur after head injury, surgery, physical exertion or without a known cause.

    *Superior canal dehiscence syndrome - a balance and hearing disorder caused by a gap in the temporal bone, leading to the dysfunction of the superior canal.

  *Bilateral vestibulopathy - a condition involving loss of inner ear balance function in both ears. This may be caused by certain antibiotics, anti-cancer, and other drugs or by chemicals such as solvents, heavy metals, etc., which are ototoxic; or by diseases such as syphilis or autoimmune disease; or other causes. In addition, the function of the semicircular canal can be temporarily affected by a number of medications or combinations of medications.

Related to the brain and central nervous system:
Brain related causes are less commonly associated with isolated vertigo and nystagmus but can still produce signs and symptoms, which mimic peripheral causes. Disequilibrium is often a prominent feature.

*Degenerative: age related decline in balance function
*Infectious: meningitis, encephalitis, epidural abscess, syphilis
*Circulatory: cerebral or cerebellar ischemia or hypoperfusion, stroke, lateral medullary syndrome (Wallenberg’s syndrome)
*Autoimmune: Cogan syndrome
*Structural: Arnold-Chiari malformation, hydrocephalus
*Systemic: multiple sclerosis, Parkinson’s disease
*Vitamin deficiency: Vitamin B12 deficiency
*CNS or posterior neoplasms, benign or malignant
*Neurological: Vertiginous epilepsy
*Other – There are a host of other causes of dizziness not related to the ear.

*Mal de debarquement is rare disorder of imbalance caused by being on board a ship. Patients suffering from this condition experience disequilibrium          even when they get off the ship. Typically treatments for seasickness are ineffective for this syndrome.

*Motion sickness – a conflict between the input from the various systems involved in balance causes an unpleasant sensation. For this reason, looking          out of the window of a moving car is much more pleasant than looking inside the vehicle.

*Migraine-associated vertigo
*Toxins, drugs, medications

Pathophysiology:
The semicircular canals, found within the vestibular apparatus, let us know when we are in a rotary (circular) motion. The semicircular canals are fluid-filled. Motion of the fluid tells us if we are moving. The vestibule is the region of the inner ear where the semicircular canals converge, close to the cochlea (the hearing organ). The vestibular system works with the visual system to keep objects in focus when the head is moving. This is called the vestibulo-ocular reflex (VOR).
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Movement of fluid in the semicircular canals signals the brain about the direction and speed of rotation of the head – for example, whether we are nodding our head up and down or looking from right to left. Each semicircular canal has a bulbed end, or enlarged portion, that contains hair cells. Rotation of the head causes a flow of fluid, which in turn causes displacement of the top portion of the hair cells that are embedded in the jelly-like cupula. Two other organs that are part of the vestibular system are the utricle and saccule. These are called the otolithic organs and are responsible for detecting linear acceleration, or movement in a straight line. The hair cells of the otolithic organs are blanketed with a jelly-like layer studded with tiny calcium stones called otoconia. When the head is tilted or the body position is changed with respect to gravity, the displacement of the stones causes the hair cells to bend.

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The balance system works with the visual and skeletal systems (the muscles and joints and their sensors) to maintain orientation or balance. For example, visual signals are sent to the brain about the body’s position in relation to its surroundings. These signals are processed by the brain, and compared to information from the vestibular, visual and the skeletal systems.
Diagnosis:
Diagnosis of a balance disorder is complicated because there are many kinds of balance disorders and because other medical conditions — including ear infections, blood pressure changes, and some vision problems — and some medications may contribute to a balance disorder. A person experiencing dizziness should see a physiotherapist or physician for an evaluation. A physician can assess for a medical disorder, such as a stroke or infection, if indicated. A physiotherapist can assess balance or a dizziness disorder and provide specific treatment.

The primary physician may request the opinion of an otolaryngologist to help evaluate a balance problem. An otolaryngologist is a physician/surgeon who specializes in diseases and disorders of the ear, nose, throat, head, and neck, sometimes with expertise in balance disorders. He or she will usually obtain a detailed medical history and perform a physical examination to start to sort out possible causes of the balance disorder. The physician may require tests and make additional referrals to assess the cause and extent of the disruption of balance. The kinds of tests needed will vary based on the patient’s symptoms and health status. Because there are so many variables, not all patients will require every test.

Diagnostic testing:
Tests of vestibular system (balance) function include electronystagmography (ENG), Videonystagmograph (VNG), rotation tests, Computerized Dynamic Posturography (CDP), and Caloric reflex test.

Tests of auditory system (hearing) function include pure-tone audiometry, speech audiometry, acoustic-reflex, electrocochleography (ECoG), otoacoustic emissions (OAE), and auditory brainstem response test (ABR; also known as BER, BSER, or BAER).

Other diagnostic tests include magnetic resonance imaging (MRI) and computerized axial tomography (CAT, or CT).

Treatment and Prevention:
There are various options for treating balance disorders. One option includes treatment for a disease or disorder that may be contributing to the balance problem, such as ear infection, stroke, multiple sclerosis, spinal cord injury, Parkinson’s, neuromuscular conditions, acquired brain injury, cerebellar dysfunctions and/or ataxia. Individual treatment will vary and will be based upon assessment results including symptoms, medical history, general health, and the results of medical tests. Additionally, tai chi may be a cost-effective method to prevent falls in the elderly.

Many types of balance disorders will require balance training, prescribed by an occupational therapist or physiotherapist. Physiotherapists often administer standardized outcome measures as part of their assessment in order to gain useful information and data about a patient’s current status. Some standardized balance assessments or outcome measures include but are not limited to the Functional Reach Test, Clinical Test for Sensory Integration in Balance (CTSIB), Berg Balance Scale and/or Timed Up and Go The data and information collected can further help the physiotherapist develop an intervention program that is specific to the individual assessed. Intervention programs may include training activities that can be used to improve static and dynamic postural control, body alignment, weight distribution, ambulation, fall prevention and sensory function. Although treatment programs exist which seek to aid the brain in adapting to vestibular injuries, it is important to note that it is simply that – an adaptation to the injury. Although the patient’s balance is restored, the balance system injury still exists

Benign Paroxysmal Positional Vertigo (BPPV):
It is caused by misplaced crystals within the ear. Treatment, simply put, involves moving these crystals out of areas that cause vertigo and into areas where they do not. A number of exercises have been developed to shift these crystals. The following article explains with diagrams how these exercises can be performed at the office or at home with some help: The success of these exercises depends on their being performed correctly.

The two exercises explained in the above article are:

*The Brandt-Daroff Exercises, which can be done at home and have a very high success rate but are unpleasant and time consuming to perform.

*The Epley’s exercises are often performed by a doctor or other trained professionals and should not be performed at home. Various devices are available      for home BPPV treatment.

Ménière’s disease:
  *Diet:
Dietary changes such as reducing intake of sodium (salt) may help. For some people, reducing alcohol, caffeine, and/or avoiding nicotine may be               helpful. Stress has also been shown to make the symptoms associated with Ménière’s worse.

 *Drugs:
#Beta-histine (Serc) is available in some countries and is thought to reduce the frequency of symptoms
#Diuretics such as hydrochlorothiazide (Diazide) have also been shown to reduce the frequency of symptoms
#Aminoglycoside antibiotics (gentamicin) can be used to treat Ménière’s disease. Systemic streptomycin (given by injection) and topical gentamicin         (given directly to the inner ear) are useful for their ability to affect the hair cells of the balance system. Gentamicin also can affect the hair  cells of the cochlea, though, and cause hearing loss in about 10% of patients. In cases that do not respond to medical management, surgery may be indicated.

      *Surgery for Ménière’s disease is a last resort.
#Vestibular neuronectomy can cure Ménière’s disease but is very involved surgery and not widely available. It involves drilling into the skull and  cutting the balance nerve just as it is about to enter the brain.
#Labyrinthectomy (surgical removal of the whole balance organ) is more widely available as a treatment but causes total deafness in the affected ear.

Labyrinthitis:
Treatment includes balance retraining exercises (vestibular rehabilitation). The exercises include movements of the head and body specifically developed for the patient. This form of therapy is thought to promote habituation, adaptation of the vestibulo-ocular reflex, and/or sensory substitution. Vestibular retraining programs are administered by professionals with knowledge and understanding of the vestibular system and its relationship with other systems in the body.

Bilateral vestibular loss:
Dysequilibrium arising from bilateral loss of vestibular function – such as can occur from ototoxic drugs such as gentamicin – can also be treated with balance retraining exercises (vestibular rehabilitation) although the improvement is not likely to be full recovery

Medication:
Sedative drugs are often prescribed for vertigo and dizziness, but these usually treat the symptoms rather than the underlying cause. Lorazepam (Ativan) is often used and is a sedative which has no effect on the disease process rather helps patients cope with the sensation.

Anti-nauseants, like those prescribed for motion sickness, are also often prescribed but do not affect the prognosis of the disorder.

Specifically for Meniere’s disease a medication called Serc (Beta-histine) is available. There is some evidence to support it is effective to reduce the frequency of attacks. Also Diuretics, like Diazide (HCTZ/triamterene), are effective in many patients. Finally, ototoxic medications delivered either systemically or through the eardrum can eliminate the vertigo associated with Meniere’s in many cases, although there is about a 10% risk of further hearing loss when using ototoxic medications.

Treatment is specific for underlying disorder of balance disorder:

#anticholinergics
#antihistamines
#benzodiazepines
#calcium channel antagonists, specifically Verapamil and Nimodipine
#GABA modulators, specifically gabapentin and baclofen
#Neurotransmitter reuptake inhibitors such as SSRI’s, SNRI’s and Tricyclics

Research:
Scientists at the National Institute on Deafness and Other Communication Disorders (NIDCD) are working to understand the various balance disorders and the complex interactions between the labyrinth, other balance-sensing organs, and the brain. NIDCD scientists are studying eye movement to understand the changes that occur in aging, disease, and injury, as well as collecting data about eye movement and posture to improve diagnosis and treatment of balance disorders. They are also studying the effectiveness of certain exercises as a treatment option.

Other projects supported by the NIDCD include studies of the genes essential to normal development and function in the vestibular system. NIDCD scientists are also studying inherited syndromes of the brain that affect balance and coordination.

The NIDCD supports research to develop new tests and refine current tests of balance and vestibular function. For example, NIDCD scientists have developed computer-controlled systems to measure eye movement and body position by stimulating specific parts of the vestibular and nervous systems. Other tests to determine disability, as well as new physical rehabilitation strategies, are under investigation in clinical and research settings.

Scientists at the NIDCD hope that new data will help to develop strategies to prevent injury from falls, a common occurrence among people with balance disorders, particularly as they grow older.
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://en.wikipedia.org/wiki/Balance_disorder

http://www.medicinenet.com/vestibular_balance_disorders/article.htm#what_is_a_balance_disorder

Gestational Diabetes

Definition:
Gestational diabetes (or gestational diabetes mellitus, GDM) is a condition in which women without previously diagnosed diabetes exhibit high blood glucose levels during pregnancy (especially during their third trimester). Gestational diabetes is caused when insulin receptors do not function properly. This is likely due to pregnancy-related factors such as the presence of human placental lactogen that interferes with susceptible insulin receptors. This in turn causes inappropriately elevated blood sugar levels.

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Gestational diabetes generally has few symptoms and it is most commonly diagnosed by screening during pregnancy. Diagnostic tests detect inappropriately high levels of glucose in blood samples. Gestational diabetes affects 3-10% of pregnancies, depending on the population studied.

As with diabetes mellitus in pregnancy in general, babies born to mothers with untreated gestational diabetes are typically at increased risk of problems such as being large for gestational age (which may lead to delivery complications), low blood sugar, and jaundice. If untreated, it can also cause seizures or stillbirth. Gestational diabetes is a treatable condition and women who have adequate control of glucose levels can effectively decrease these risks. The food plan is often the first recommended target for strategic management of GDM.

Clasifications:
There are two subtypes of gestational diabetes:
Type A1: abnormal oral glucose tolerance test (OGTT), but normal blood glucose levels during fasting and two hours after meals; diet modification is sufficient to control glucose levels

Type A2: abnormal OGTT compounded by abnormal glucose levels during fasting and/or after meals; additional therapy with insulin or other medications is required

Approximately 7% of all pregnancies are complicated by GDM, resulting in more than 200,000 cases annually. The prevalence may range from 1 to 14% of all pregnancies, depending on the population studied and the diagnostic tests employed.

Symptoms:
Because gestational diabetes does not cause much symptoms, the patient need to be tested for the condition. This is usually done between the 24th and 28th weeks of pregnancy. It is surprised if your test shows a high blood sugar level and is important for the patient to be tested for gestational diabetes, because high blood sugar can cause problems for both the pregnent woman and the baby.Sometimes, a pregnant woman has been living with diabetes without knowing it. If she has the  symptoms of diabetes  and that may include:

*Increased thirst.
*Increased urination.
*Increased hunger.
*Blurred vision.

Pregnancy causes most women to urinate more often and to feel more hungry, so having these symptoms doesn’t always mean that a woman has diabetes.Doctor should be consulted wheather  these symptoms are for diabetes  and then he can suggest for the test of diabetes.

*Infections:
Since diabetes interferes with the body’s ability to fight infections, the pregnant woman may experience frequent infections in areas such as the bladder, vagina and skin. White blood cells defend the body against bacteria, but these cells aren’t able to function normally when a person has a high blood sugar. A woman with gestational diabetes may also complain of a yeast infection in the vagina or on the skin. Yeast cells are normally present in the vaginal area in small amounts. The vaginal secretions and urine contain more glucose when a woman has gestational diabetes. The yeast cells use the glucose as food, which causes the cells to multiply. With the body’s immune system compromised by the high level of glucose in the blood, this increase in yeast cells turns into a yeast infection.

*High Blood Sugar:
Since a woman may not have any noticeable symptoms of gestational diabetes and symptoms can mimic regular pregnancy symptoms, screening for this condition is part of prenatal care for at-risk women between weeks 24 and 28 of pregnancy. The doctor will initially order a blood test called a glucose challenge test. If the glucose challenge test indicates a high blood sugar level, the doctor may order a glucose tolerance test to confirm the diagnosis of gestational diabetes. Both tests involve drinking a sweet glucose solution and having your blood drawn after a prescribed amount of time.

Causes:
Almost all women have some degree of impaired glucose intolerance as a result of hormonal changes that occur during pregnancy. That means that their blood sugar may be higher than normal, but not high enough to have diabetes. During the later part of pregnancy (the third trimester), these hormonal changes place pregnant woman at risk for gestational diabetes.

During pregnancy, increased levels of certain hormones made in the placenta (the organ that connects the baby by the umbilical cord to the uterus) help shift nutrients from the mother to the developing fetus. Other hormones are produced by the placenta to help prevent the mother from developing low blood sugar.

They work by resisting the actions of insulin.
Over the course of the pregnancy, these hormones lead to progressive impaired glucose intolerance (higher blood sugar levels). To try to decrease blood sugar levels, the body makes more insulin to get glucose into cells to be used for energy.
Usually, the mother’s pancreas is able to produce more insulin (about three times the normal amount) to overcome the effect of the pregnancy hormones on blood sugar levels. If, however, the pancreas cannot produce enough insulin, blood sugar levels will rise, resulting in gestational diabetes.

Risk factors:
Any woman can develop gestational diabetes, but some women are at greater risk. Risk factors for gestational diabetes include:

*Age greater than 25. Women older than age 25 are more likely to develop gestational diabetes.
*Family or personal health history. the risk of developing gestational diabetes increases if the woman has prediabetes — slightly elevated blood sugar that may be a precursor to type 2 diabetes — or if a close family member, such as a parent or sibling, has type 2 diabetes.the woman is also more likely to develop gestational diabetes if she had it during a previous pregnancy, if the woman delivered a baby who weighed more than 9 pounds (4.1 kilograms), or if she had an unexplained stillbirth.
*Excess weight. You’re more likely to develop gestational diabetes if you’re significantly overweight with a body mass index (BMI) of 30 or higher.
*Race factor. For reasons that aren’t clear, women who are black, Hispanic, American Indian or Asian are more likely to develop gestational diabetes.

Complications:
Most women who have gestational diabetes deliver healthy babies. However, gestational diabetes that’s not carefully managed can lead to uncontrolled blood

sugar levels and cause problems for patient and the baby, including an increased likelihood of needing a C-section to deliver.

Complications that may affect the baby are:
1.Excessive birth weight. Extra glucose in your bloodstream crosses the placenta, which triggers your baby’s pancreas to make extra insulin. This can cause the baby to grow too large (macrosomia). Very large babies — those that weigh 9 pounds or more — are more likely to become wedged in the birth canal, sustain birth injuries or require a C-section birth.

2.Early (preterm) birth and respiratory distress syndrome. A mother’s high blood sugar may increase her risk of early labor and delivering her baby before its due date. Or her doctor may recommend early delivery because the baby is large.

3.Babies born early may experience respiratory distress syndrome — a condition that makes breathing difficult. Babies with this syndrome may need help breathing until their lungs mature and become stronger. Babies of mothers with gestational diabetes may experience respiratory distress syndrome even if they’re not born early.

4.Low blood sugar (hypoglycemia). Sometimes babies of mothers with gestational diabetes develop low blood sugar (hypoglycemia) shortly after birth because their own insulin production is high. Severe episodes of hypoglycemia may provoke seizures in the baby. Prompt feedings and sometimes an intravenous glucose solution can return the baby’s blood sugar level to normal.

5.Type 2 diabetes later in life. Babies of mothers who have gestational diabetes have a higher risk of developing obesity and type 2 diabetes later in life.
Untreated gestational diabetes can result in a baby’s death either before or shortly after birth.

Complications that may affect the patient are:
1.High blood pressure and preeclampsia. Gestational diabetes raises your risk of high blood pressure, as well as, preeclampsia — a serious complication of pregnancy that causes high blood pressure and other symptoms that can threaten the lives of both mother and baby.

2.Future diabetes. If the pregnent woman has gestational diabetes, she is more likely to get it again during a future pregnancy and also more likely to develop type 2 diabetes as she gets older. However, making healthy lifestyle choices such as eating healthy foods and exercising can help reduce the risk of future type 2 diabetes.Of those women with a history of gestational diabetes who reach their ideal body weight after delivery, fewer than 1 in 4 eventually develops type 2 diabetes.

Diagnosis:
Gestational diabetes usually starts halfway through the pregnancy. All pregnant women should receive an oral glucose tolerance test between the 24th and 28th week of pregnancy to screen for the condition. Women who have risk factors for gestational diabetes may have this test earlier in the pregnancy.

Once the pregnent woman is diagnosed with gestational diabetes, she can see how well she is doing by testing the glucose level at home. The most common way involves pricking her finger and putting a drop of the blood on a machine that will give her the glucose reading.

Treatment:
The goals of treatment are to keep blood sugar (glucose) levels within normal limits during the pregnancy, and to make sure that the growing baby is healthy.

Watching the baby:
1.The health care provider should closely check both the patient  and the baby throughout the pregnancy. Fetal monitoring will check the size and health of the fetus.

2.A nonstress test is a very simple, painless test for the patient and the baby.

3.A machine that hears and displays the baby’s heartbeat (electronic fetal monitor) is placed on the abdomen.
The health care provider can compare the pattern of the baby’s heartbeat to movements and find out whether the baby  is doing well.

Diet and exercise:
The best way to improve the pregnent woman’s diet is by eating a variety of healthy foods.She should learn how to read food labels, and check them when making food decisions.The doctor or dietitian  should advice the diet chart and that should be strictly followed  during pregnancy.

In general, when the pregnent woman has gestational diabetes the diet should:
*Be moderate in fat and protein.

#Provide  carbohydrates through foods that include fruits, vegetables, and complex carbohydrates (such as bread, cereal, pasta, and rice)
Be low in foods that contain a lot of sugar, such as soft drinks, fruit juices, and pastries.

#If managing the diet does not control blood sugar (glucose) levels, she may be prescribed diabetes medicine by mouth or insulin therapy.
Most women who develop gestational diabetes will not need diabetes medicines or insulin, but some will.

Prevention:
Theoretically, smoking cessation may decrease the risk of gestational diabetes among smokers.Physical exercise has not been found to have a significant effect of primary prevention of gestational diabetes in randomized controlled trials. It may be effective as tertiary prevention for women who have already developed the condition.
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://en.wikipedia.org/wiki/Gestational_diabetes

http://www.webmd.com/diabetes/guide/gestational-diabetes-symptoms

http://www.ehow.com/list_6080912_signs-symptoms-gestational-diabetes.html

http://www.webmd.com/diabetes/guide/gestational_diabetes

http://www.mayoclinic.org/diseases-conditions/gestational-diabetes/basics/risk-factors/CON-20014854

http://www.nytimes.com/health/guides/disease/gestational-diabetes/overview.html