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Hemolytic Uremic Syndrome (HUS)

Alternative names:  Haemolytic-uraemic syndrome, HUS

Definition:
Hemolytic uremic syndrome, or HUS, is a kidney condition that happens when red blood cells are destroyed and block the kidneys‘ filtering system. Red blood cells contain hemoglobin—an iron-rich protein that gives blood its red color and carries oxygen from the lungs to all parts of the body.

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When the kidneys and glomeruli—the tiny units within the kidneys where blood is filtered—become clogged with the damaged red blood cells, they are unable to do their jobs. If the kidneys stop functioning, a child can develop acute kidney injury—the sudden and temporary loss of kidney function. Hemolytic uremic syndrome is the most common cause of acute kidney injury in children.

It is a disease characterized by hemolytic anemia (anemia caused by destruction of red blood cells), acute kidney failure (uremia), and a low platelet count (thrombocytopenia). It predominantly, but not exclusively, affects children. Most cases are preceded by an episode of infectious, sometimes bloody, diarrhea acquired as a foodborne illness or from a contaminated water supply and caused by E. coli O157:H7, although Shigella, Campylobacter and a variety of viruses have also been implicated. It is now the most common cause of acquired acute renal failure in childhood. It is a medical emergency and carries a 5–10% mortality; of the remainder, the majority recover without major consequences but a small proportion develop chronic kidney disease and become reliant on renal replacement therapy.

The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the two kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra fluid. Children produce less urine than adults and the amount produced depends on their age. The urine flows from the kidneys to the bladder through tubes called ureters. The bladder stores urine. When the bladder empties, urine flows out of the body through a tube called the urethra, located at the bottom of the bladder.

Symptoms:
STEC-HUS occurs after ingestion of a strain of bacteria, usually types of E. coli, that expresses verotoxin (also called Shiga-like toxin). Bloody diarrhea typically follows. HUS develops about 5–10 days after onset of diarrhea, with decreased urine output (oliguria), blood in the urine (hematuria), kidney failure, thrombocytopenia (low levels of platelets) and destruction of red blood cells (microangiopathic hemolytic anemia). Hypertension is common. In some cases, there are prominent neurologic changes.

A child with hemolytic uremic syndrome may develop signs and symptoms similar to those seen with gastroenteritis—an inflammation of the lining of the stomach, small intestine, and large intestine—such as

*vomiting
*bloody diarrhea
*abdominal pain
*fever and chills
*headache

As the infection progresses, the toxins released in the intestine begin to destroy red blood cells. When the red blood cells are destroyed, the child may experience the signs and symptoms of anemia—a condition in which red blood cells are fewer or smaller than normal, which prevents the body’s cells from getting enough oxygen.

Signs and symptoms of anemia may include:-

*fatigue, or feeling tired
*weakness
*fainting
*paleness

As the damaged red blood cells clog the glomeruli, the kidneys may become damaged and make less urine. When damaged, the kidneys work harder to remove wastes and extra fluid from the blood, sometimes leading to acute kidney injury.

Other signs and symptoms of hemolytic uremic syndrome may include bruising and seizures.

When hemolytic uremic syndrome causes acute kidney injury, a child may have the following signs and symptoms:

*edema—swelling, most often in the legs, feet, or ankles and less often in the hands or face
*albuminuria—when a child’s urine has high levels of albumin, the main protein in the blood
*decreased urine output
*hypoalbuminemia—when a child’s blood has low levels of albumin
*blood in the urine

Causes:
A number of things can cause hemolytic uremic syndrome, but the most common cause — particularly in children — is an infection with a specific strain of E. coli, usually the strain known as O157:H7. However, other strains of E. coli have been linked to hemolytic uremic syndrome, too.

Normally, harmless strains, or types, of E. coli are found in the intestines and are an important part of digestion. However, if a child becomes infected with the O157:H7 strain of E. coli, the bacteria will lodge in the digestive tract and produce toxins that can enter the bloodstream. The toxins travel through the bloodstream and can destroy the red blood cells. E. coli O157:H7 can be found in:

*Contaminated meat or produce
*Swimming pools or lakes contaminated with feces
*undercooked meat, most often ground beef
*unpasteurized, or raw, milk
*unwashed, contaminated raw fruits and vegetables
*contaminated juice

Less common causes, sometimes called atypical hemolytic uremic syndrome, can include:-

*taking certain medications, such as chemotherapy
*having other viral or bacterial infections
*inheriting a certain type of hemolytic uremicsyndrome that runs in families

Children who are more likely to develop hemolytic uremic syndrome include those who
are younger than age 5 and have been diagnosedwith an E. coli O157:H7 infection

*have a weakened immune system
*have a family history of inherited hemolyticuremic syndrome
*Hemolytic uremic syndrome occurs in about two out of every 100,000 children.

Most people who are infected with E. coli, even the more dangerous strains, won’t develop hemolytic uremic syndrome. It’s also possible for hemolytic uremic syndrome to follow infection with other types of bacteria.

In adults, hemolytic uremic syndrome is more commonly caused by other factors, including:

*The use of certain medications, such as quinine (an over-the-counter muscle cramp remedy), some chemotherapy drugs, the immunosuppressant medication cyclosporine (Neoral, Sandimmune) and anti-platelet medications

*Pregnancy

*Certain infections, such as HIV/AIDS or an infection with the pneumococcal bacteria

*Genes, which can be a factor because a certain type of HUS — atypical hemolytic uremic syndrome — may be passed down from your parents

The cause of hemolytic uremic syndrome in adults is often unknown

Diagnosis:
The Doctor diagnoses hemolytic uremic syndrome with

*a medical and family history
*a physical exam
*urine tests
*a blood test
*a stool test
*kidney biopsy

The similarities between HUS, aHUS, and TTP make differential diagnosis essential. All three of these systemic TMA-causing diseases are characterized by thrombocytopenia and microangiopathic hemolysis, plus one or more of the following: neurological symptoms (e.g., confusion, cerebral convulsions, seizures); renal impairment (e.g., elevated creatinine, decreased estimated glomerular filtration rate [eGFR], abnormal urinalysis ); and gastrointestinal (GI) symptoms (e.g., diarrhea, nausea/vomiting, abdominal pain, gastroenteritis).The presence of diarrhea does not exclude aHUS as the etiology of TMA, as 28% of patients with aHUS present with diarrhea and/or gastroenteritis. First diagnosis of aHUS is often made in the context of an initial, complement-triggering infection, and Shiga-toxin has also been implicated as a trigger that identifies patients with aHUS. Additionally, in one study, mutations of genes encoding several complement regulatory proteins were detected in 8 of 36 (22%) patients diagnosed with STEC-HUS. However, the absence of an identified complement regulatory gene mutation does not preclude aHUS as the etiology of the TMA, as approximately 50% of patients with aHUS lack an identifiable mutation in complement regulatory genes.

Diagnostic work-up supports the differential diagnosis of TMA-causing diseases. A positive Shiga-toxin/EHEC test confirms an etiological cause for STEC-HUS, and severe ADAMTS13 deficiency (i.e., ?5% of normal ADAMTS13 levels) confirms a diagnosis of TTP

Complications:
Most children who develop hemolytic uremic syndrome and its complications recover without permanent damage to their health.1
However, children with hemolytic uremic syndrome may have serious and sometimes life-threatening complications, including

*acute kidney injury
*high blood pressure
*blood-clotting problems that can lead to bleeding
*seizures
*heart problems
*chronic, or long lasting, kidney disease
*stroke
*coma

Treatment:
The Doctor will treat a child’s urgent symptoms and try to prevent complications by

*observing the child closely in the hospital
*replacing minerals, such as potassium and salt, and fluids through an intravenous (IV) tube
*giving the child red blood cells and platelets—cells in the blood that help with clotting—through an IV
*giving the child IV nutrition
*treating high blood pressure with medications

Treating Acute Kidney Injury:
If necessary,the Doctor will treat acute kidney injury with dialysis—the process of filtering wastes and extra fluid from the body with an artificial kidney. The two forms of dialysis are hemodialysis and peritoneal dialysis. Most children with acute kidney injury need dialysis for a short time only.

Treating Chronic Kidney Disease:
Some children may sustain significant kidney damage that slowly develops into CKD. Children who develop CKD must receive treatment to replace the work the kidneys do. The two types of treatment are dialysis and transplantation.

In most cases, The Doctor treat CKD with a kidney transplant. A kidney transplant is surgery to place a healthy kidney from someone who has just died or a living donor, most often a family member, into a person’s body to take over the job of the failing kidney. Though some children receive a kidney transplant before their kidneys fail completely, many children begin with dialysis to stay healthy until they can have a transplant. click to know more

Prevention:

Hemolytic uremic syndrome, or HUS, is a kidney condition that happens when red blood cells are destroyed and block the kidneys’ filtering system.
The most common cause of hemolytic uremic syndrome in children is an Escherichia coli (E. coli) infection of the digestive system.
Normally, harmless strains, or types, of E. coli are found in the intestines and are an important part of digestion. However, if a child becomes infected with the O157:H7 strain of E. coli, the bacteria will lodge in the digestive tract and produce toxins that can enter the bloodstream.
A child with hemolytic uremic syndrome may develop signs and symptoms similar to those seen with gastroenteritis, an inflammation of the lining of the stomach, small intestine, and large intestine.

Most children who develop hemolytic uremic syndrome and its complications recover without permanent damage to their health.
Some children may sustain significant kidney damage that slowly develops into chronic kidney disease (CKD).

Parents and caregivers can help prevent childhood hemolytic uremic syndrome due to E. coli O157:H7 by

*avoiding unclean swimming areas
*avoiding unpasteurized milk, juice, and cider
*cleaning utensils and food surfaces often
*cooking meat to an internal temperature of at least 160° F
*defrosting meat in the microwave or refrigerator
*keeping children out of pools if they have had diarrhea
*keeping raw foods separate
*washing hands before eating
*washing hands well after using the restroom and after changing diapers

When a child is taking medications that may cause hemolytic uremic syndrome, it is important that the parent or caretaker watch for symptoms and report any changes in the child’s condition to the Doctor as soon as possible.

Prognosis:
Acute renal failure occurs in 55-70% of patients with STEC-HUS, although up to 70-85% recover renal function. Patients with aHUS generally have poor outcomes, with up to 50% progressing to ESRD or irreversible brain damage; as many as 25% die during the acute phase. However, with aggressive treatment, more than 90% of patients survive the acute phase of HUS, and only about 9% may develop ESRD. Roughly one-third of persons with HUS have abnormal kidney function many years later, and a few require long-term dialysis. Another 8% of persons with HUS have other lifelong complications, such as high blood pressure, seizures, blindness, paralysis, and the effects of having part of their colon removed. The overall mortality rate from HUS is 5-15%. Children and the elderly have a worse prognosis.

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://kidney.niddk.nih.gov/KUDiseases/pubs/childkidneydiseases/hemolytic_uremic_syndrome/
http://en.wikipedia.org/wiki/Hemolytic-uremic_syndrome
http://www.mayoclinic.org/diseases-conditions/hemolytic-uremic-syndrome/basics/causes/con-20029487

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Haemochromatosis

Definition:
Haemochromatosis is a disease caused by excess iron in the body.

Iron is needed in the diet to maintain good health, particularly for making red blood cells that carry oxygen around the body. These red blood cells contain large amounts of iron.

Lack of iron can cause anaemia, but excessive iron is toxic. The body has few ways of disposing of unwanted iron, so it builds up in tissues causing damage and disease.

Haemochromatosis – or genetic haemochromatosis (GH) – is a disorder that causes the body to absorb an excessive amount of iron from the diet.

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We can only use a limited amount of iron and any excess is deposited around the body. This accumulates mainly in the liver, but can also affect the heart, pancreas and pituitary gland, damaging these vital body organs and resulting in a deterioration of their functional capacity.

Haemochromatosis is more common in Caucasian or white populations, with about 1 in 300 to 1 in 400 affected. About half that number are affected in black populations.

Men are more likely to have hereditary haemochromatosis and suffer from it at an earlier age, as women regularly lose iron in menstruation or use stores in pregnancy.

Symptoms:
Although haemochromatosis and the potential for the condition to cause problems is present from birth, symptoms don’t usually become apparent until middle age.

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Common symptoms that might be noticed then include:

•weakness, tiredness and lack of energy
•joint pain and stiffness – particularly in the hands and fingers
•a tanned or bronzed appearance of the skin
•impotence in men
•shrinking of testicles
•weight loss
•abdominal pain
.
Later, more serious symptoms may develop including:

•diabetes
•arthritis
•heart problems
•enlargement or damage to the liver

Clinical presentation:
Organs commonly affected by haemochromatosis are the liver, heart, and endocrine glands.

Haemochromatosis may present with the following clinical syndromes:

*Cirrhosis of the liver
*Diabetes due to pancreatic islet cell failure
*Cardiomyopathy
*Arthritis (iron deposition in joints)
*Testicular failure
*Tanning of the skin

Causes:
The causes can be distinguished between primary cases (hereditary or genetically determined) and less frequent secondary cases (acquired during life). People of Celtic (Irish, Scottish, Welsh) origin have a particularly high incidence of whom about 10% are carriers of the gene and 1% sufferers from the condition.

Primary haemochromatosis:
The fact that most cases of haemochromatosis were inherited was well known for most of the 20th century, though they were incorrectly assumed to depend on a single gene. The overwhelming majority actually depend on mutations of the HFE gene discovered in 1996, but since then others have been discovered and sometimes are grouped together as “non-classical hereditary haemochromatosis”, “non-HFE related hereditary haemochromatosis”, or “non-HFE haemochromatosis

It is thought to be mainly caused by a mutation of a gene called HFE, which probably allows excess iron to be absorbed from the diet. This mutation is known as C282Y and to develop haemochromatosis you usually need two genes (one from each parent) to be C282Y.

However, not everyone with the mutation may develop the disease, and it may occur if only one C282Y gene is present.

Confusingly, another mutation labelled H63D elsewhere on the HFE gene may occur alone or with C282Y and also influence iron levels.

Other rare mutations may give rise to haemochromatosis, especially in children.

Secondary haemochromatosis:
*Severe chronic haemolysis of any cause, including intravascular haemolysis and ineffective erythropoiesis (haemolysis within the bone marrow).
*Multiple frequent blood transfusions (either whole blood or just red blood cells), which are usually needed either by individuals with hereditary anaemias (such as beta-thalassaemia major, sickle cell anaemia, and Diamond–Blackfan anaemia) or by older patients with severe acquired anaemias such as in myelodysplastic syndromes.
*Excess parenteral iron supplements, such as can acutely happen in iron poisoning
*Excess dietary iron
*Some disorders do not normally cause haemochromatosis on their own, but may do so in the presence of other predisposing factors. These include cirrhosis (especially related to alcohol abuse), steatohepatitis of any cause, porphyria cutanea tarda, prolonged haemodialysis, post-portacaval shunting.

Risk Factors:
The onset of hereditary haemochromatosis usually occurs between the ages of 30 and 60 as the build up of iron takes years.

However, a rapid form of the disease does affect children. If left untreated excess iron builds up in the organs especially the liver, heart and pancreas. This may cause heart or liver failure, which can be fatal.

Diagnosis:
There are several methods available for diagnosing and monitoring iron loading including:

*Serum ferritin
*Liver biopsy
*HFE
*MRI

Serum ferritin is a low-cost, readily available, and minimally invasive method for assessing body iron stores. However, the major problem with using it as an indicator of iron overload is that it can be elevated in a range of other medical conditions unrelated to iron levels including infection, inflammation, fever, liver disease, renal disease, and cancer. Also, total iron binding capacity may be low, but can also be normal.

The standard of practice in diagnosis of hemochromatosis was recently reviewed by Pietrangelo. Positive HFE analysis confirms the clinical diagnosis of hemochromatosis in asymptomatic individuals with blood tests showing increased iron stores, or for predictive testing of individuals with a family history of hemochromatosis. The alleles evaluated by HFE gene analysis are evident in ~80% of patients with hemochromatosis; a negative report for HFE gene does not rule out hemochromatosis. In a patient with negative HFE gene testing, elevated iron status for no other obvious reason, and family history of liver disease, additional evaluation of liver iron concentration is indicated. In this case, diagnosis of hemochromatosis is based on biochemical analysis and histologic examination of a liver biopsy. Assessment of the hepatic iron index (HII) is considered the “gold standard” for diagnosis of hemochromatosis.

MRI is emerging as an alternative to liver biopsy for measuring liver iron loading. For measuring liver iron concentrations, R2-MRI (also known as FerriScan)  has been validated and is coming into use in medical centers. It is not recommended in practice guidelines at this time

Prognosis:
A third of those untreated develop hepatocellular carcinoma.

Treatment:
Routine treatment in an otherwise-healthy person consists of regularly scheduled phlebotomies (bloodletting). When first diagnosed, the phlebotomies may be fairly frequent, perhaps as often as once a week, until iron levels can be brought to within normal range. Once iron and other markers are within the normal range, phlebotomies may be scheduled every other month or every three months depending upon the patient’s rate of iron loading.

For those unable to tolerate routine blood draws, there is a chelating agent available for use. The drug Deferoxamine binds with iron in the bloodstream and enhances its elimination via urine and faeces. Typical treatment for chronic iron overload requires subcutaneous injection over a period of 8–12 hours daily. Two newer iron chelating drugs that are licensed for use in patients receiving regular blood transfusions to treat thalassemia (and, thus, who develop iron overload as a result) are deferasirox and deferiprone.

Haemochromatosis is treated by:

•Reducing the amount of iron absorbed by the body – patients are advised to avoid iron-rich foods and alcohol.
•Removing excess iron from the body by removing blood from the body (venesection therapy or phlebotomy). Initially this may involve removing a unit of blood a week (sometimes for many months) until iron levels in the blood are normal. Then most people can be kept stable by removing a unit of blood every 2-3 months.

If phlebotomy is started before liver damage occurs the outlook is good, and the affected person can expect to live an otherwise normal life.

Acquired haemochromatosis is normally treated by a drug that binds iron and allows it to be excreted from the body.

Associated problems such as heart failure and diabetes are treated as appropriate.

Good advice:-
*Limit the amount of iron in your diet.
*Eating red or organ meats (such as liver) is not recommended.
*Iron supplements should also be avoided, including iron combined with other multivitamins.
*Vitamin C increases iron absorption from the gut and intake should also be limited.
*Avoid excess alcohol as this may make liver disease worse

Future prospects:
Your prospects largely depend on the stage at which the disease was diagnosed. Symptoms of tiredness and general weakness often improve, but joint problems may not.

Abdominal pain and liver enlargement can also lessen or disappear, and heart function may also improve with treatment.

However, liver cirrhosis is irreversible and a liver transplant may be required.

Patients with liver disease are also usually monitored for liver cancer, which can be a long-term complication.

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.bbc.co.uk/health/physical_health/conditions/haemochromatosis1.shtml
http://en.wikipedia.org/wiki/Iron_overload
http://www.netdoctor.co.uk/diseases/facts/haemochromatosis.htm

https://runkle-science.wikispaces.com/Haemochromatosis

http://www.ironxs.com.au/the-symptoms-of-haemochromatosis.html

http://www.goldbamboo.com/topic-t1404-a1-6Haemochromatosis.html

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Dealing with Sexual Assault

We perceive India as a safe, tradition bound country that honours women and loves children. Yet, our cities are becoming famous, even internationally, for molestation and rape. The number of cases reported has increased 700 per cent since Independence. And this is probably only the tip of the iceberg.CLICK & SEE

Shame, family pressures, social stigma, economic vulnerability and lack of knowledge of legal procedures coerce a victim into silence. To make things worse, the victim is often regarded by our inadequately educated, underpaid and insensitive police personnel as the one at “fault”.

Rape is traditionally considered a crime against women. But times are changing. Horror stories abound about homosexual sexual predators targeting, kidnapping and victimising young boys. The victims range from six-month-olds to 80-year-olds. The perpetuators of rape, however, are almost always male.

Around 80 per cent of the crime is committed by someone known to the victim. Often, the abuser is a member of the victim’s family or belongs to his or her circle of acquaintances. In such cases, the crime is perpetuated in a known place, in either of their homes or that of a friend, relative or neighbour.

Today, children of both sexes are in danger, in exclusive neighbourhoods as well as the slums. Their lack of knowledge, inexperience and trusting nature make them ideal victims. Many of these attacks are not random but well planned by a predator known to the victim.

Police complaints are often followed by unwelcome media publicity. There are no “special victim units” in the police force yet, that may be trained to handle such cases with discretion and empathy. The guidelines provided deal mostly with the rape of women. The concept of male or child rape is new and the level of expertise in dealing with this is low.

Despite this, if a parent or the victim wishes to prosecute the assailant, a physical medical examination, documentation of the evidence and registration of an FIR (First Information Report) must be done.

Even otherwise, a thorough medical examination must be undertaken as soon as possible to treat and record lacerations and injuries, both external and internal.

The greatest fear about sexual assault is that of acquiring STDs. The number infected varies between 5 and 10 per cent. Infection depends upon several factors, such as the type of sexual contact, number of assailants, and whether or not they had an STD at the time of the assault.

The risk of contracting STDs can be reduced by taking medication as a preventive measure. Immediate and effective treatment options are available for some STDs such as hepatitis B, gonorrhea, syphilis, herpes, chlamydia and trichomonas vaginalis.

The regimen recommended is a single injection of ceftriaxone, plus an oral dose of azithromycin, plus either secnidazole, tinidazole or metronidazole. Herpes can be tackled with a five or seven-day course of acyclovir.

The risk of acquiring HIV infection is less than 1 per cent. However, it is important for medico-legal reasons to document the HIV status immediately. The test should be repeated after six months and then a year. A 28-day regimen of zidovudine and lamivudine provides post-exposure prophylaxis for HIV and should be started as soon as possible, preferably within 72 hours.

Injuries and lacerations require a single booster dose of tetanus toxoid. Hepatitis B can be sexually transmitted. Most children today have received three doses of the vaccine as part of their immunisation schedule and are thus protected against the infection. In that case, only a booster dose needs to be given. If the victim has not been immunised in childhood, immunoglobulin needs to be given. In addition, three doses of the vaccine must be given — immediately after the incident, after a month and after six months.

Prophylactic treatment against syphilis is not advised. Instead, a blood test can be done after three months to ascertain if infection has occurred.

Counselling, psychiatric evaluation and support are necessary for the victim as well as his or her family to overcome the trauma.

To protect children —

• Make them learn addresses and phone numbers by heart

• Teach them certain body parts are not to be touched

• Discourage them from talking to strangers

• Do not send them anywhere alone, especially after dark

• Escort them to and from school bus stops

• Encourage physical fitness and teach them martial arts

• Teach them to trust their survival instincts and, if needed, run in the opposite direction as fast as they can, shouting all the way.

For adults, the best bet is —

*To have peepholes in the front door

*Avoid dark and deserted areas

*Be physically fit and able to run fast.

Source: The Telegraph ( Kolkata, India)

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Eat Spinach for Better Health.

If you want bulging biceps like Popeye the sailor, then all you have to do is eat his favourite food – spinach.

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And, saying this are scientists from Rutgers University who have found that the green vegetable really does boost strength. The secret behind this, they reveal, is that spinach contains phytoecdysteroids, a type of steroid that increases the development of muscles.

As a part of their study the researchers used extracts of phytoecdysteriods on lab samples of human muscle, and found that it speeded up muscle growth by 20%. According to the New Scientist, on conducting trials on rats, the researchers found that spinach extracts made the rodents stronger within a month, the Daily Express reported on Thursday.

Researchers state that eating spinach is not only a good idea if you want strong muscles, but also if you want to keep eye disease, teeth, gum problems and anaemia at bay. But it does suggest the US creators of the famous nautical hero were ahead of their time.

It is said they toyed with the idea of making garlic Popeye’s strength enhancer when they devised the original comic strip in 1919 – but by 1932 he was eating spinach to give him almost superhuman powers.

Spinach was chosen because it was known to be extremely healthy. It was used as a cure for scurvy because it was rich in iron, although it actually contains less iron than many other vegetables. But since then more and more health-giving properties of spinach have been discovered.

Apart from this, it has also been found to have heart benefits. Research has shown that the vegetable can strengthen hearts, reduce the risk of a heart attack and boost survival rates by a third for attack victims.

However, getting biceps like Popeye will not be an easy task for the researchers also stated that to do so, you would need to eat at least a kilo of spinach a day.

Spinach became one of trendiest foods in Britain and sales soared by 30% in 2006 after TV chefs and health gurus backed it as something essential for health.

“Spinach is the broom of the stomach.” French Proverb

You may click to see also:->

Spinach Recipe

Spinach Can Reduce Ovarian Cancer Risks

Can Spinach save your eyesight?

Sources: The Times Of India

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Blood Group For Lower Malaria Risk

 

The most common blood type in Indians seems to provide better protection against the most deadly form of malaria. British scientists have found that people with blood group O – around 38% of the Indian population – are naturally protected from some of the most severe forms of the disease, which kills around two million people annually across the globe……....click  & see

A team from Edinburgh University, with researchers in the US, Mali and Kenya, studied African children and found that those with this blood type were two-thirds less likely to experience coma or life-threatening anaemia conditions synonymous with severe malaria.

This discovery now brings hope of developing drugs which mimic the properties of red cells. In fatal malaria, it is often found that red blood cells infected by parasites block blood vessels which supply oxygen to the brain.

The malarial parasites arm the blood cells  surface with proteins which stick to blood vessel walls. O and B are the commonest blood group among Indians. Nearly 32% of north Indians and 38% south Indians have O blood group.

“The finding that red cells present in O group blood play the major role in preventing malaria from worsening is a significant finding for India. Blood is made of antigens or proteins, some of which show protection against certain diseases. Why that occurs has not been scientifically proven yet but statistically, they have shown significant protection rates,” blood safety specialist Dr Debasish Gupta said.

Edinburgh University’s Dr Alex Rowe, whose finding was published in the journal ‘PNAS’ on Tuesday, said, “This explains why some people are less likely to suffer from life-threatening malaria than others and tells us that if we can develop a drug to reduce rosetting and mimic the effect of being blood group O, we may reduce the number of children dying from severe malaria.”

The scientists found that malaria parasites recruit healthy RBCs to stick to the parasite, encasing the infected RBC inside a so-called rosette. It makes the blockage, and the disease, worse.

However, the team’s findings suggest that group O RBCs do not easily join rosettes as the cells surface structure prevents it from sticking. The study suggests that reduced rosetting of malaria parasites is the reason why people with group O blood are less likely to suffer severe malaria.

ABO blood group types were assessed on 567 blood samples from Malian children. We found that blood group O was present in only 21% of the severe malaria cases compared to 45% of other blood groups. Rosetting was shown to be significantly lower in parasite isolates from patients with blood group O compared to non-O blood groups,” the study said.

Source: The Times Of India