February 7, 2017

Anemia is a condition in which the body does not have enough healthy red blood cells. Red blood cells provide oxygen to body tissues. There are many types of anemia. Iron deficiency anemia occurs when the body does not have enough iron. Iron helps make red blood cells.

Iron is very important in maintaining many body functions, including the production of hemoglobin, the molecule in the blood that carries oxygen. Iron is also necessary to maintain healthy cells, skin, hair, and nails.

Iron from the food that people eat is absorbed into the body by the cells that line the gastrointestinal tract; the body only absorbs a small fraction of the iron the ingest. The iron is then released into the blood stream, where a protein called transferrin attaches to it and delivers the iron to the liver. Iron is stored in the liver as ferritin and released as needed to make new red blood cells in the bone marrow. When red blood cells are no longer able to function (after about 120 days in circulation), they are re-absorbed by the spleen. Iron from these old cells can also be recycled by the body.


Iron-deficiency anemia may be caused by the following –

  • Diets low in iron – Iron is obtained from foods in our diet; however, only 1 mg of iron is absorbed for every 10 to 20 mg of iron ingested. A person unable to have a balanced iron-rich diet may suffer from some degree of iron-deficiency anemia.
  • Body changes – An increased iron requirement and increased red blood cell production is required when the body is going through changes, such as growth spurts in children and adolescents, or during pregnancy and lactation.
  • Gastrointestinal tract abnormalities – Malabsorption of iron is common after some forms of gastrointestinal surgeries. Most of the iron taken in by foods is absorbed in the upper small intestine. Any abnormalities in the gastrointestinal (GI) tract could alter iron absorption and result in iron-deficiency anemia. Surgery or medications that stop stomach acid production will also decrease iron absorption.
  • Blood loss – Loss of blood can cause a decrease of iron and result in iron-deficiency anemia. Sources of blood loss may include GI bleeding, menstrual bleeding, or injury.
  • Intravascular hemolysis, a condition in which red blood cells break down in the blood stream, releasing iron that is then lost in the urine. This sometimes occurs in people who engage in vigorous exercise, particularly jogging. This can cause trauma to small blood vessels in the feet, so called “march hematuria.” Intravascular hemolysis can also be seen in other conditions including damaged heart valves or rare disorders such as thrombotic thrombocytopenia purpura (TTP) or diffuse intravascular hemolysis (DIC).

Risk Factors

  • Women who menstruate, particularly if menstrual periods are heavy
  • Women who are pregnant or breastfeeding or those who have recently given birth
  • People who have undergone major surgery or physical trauma
  • People with gastrointestinal diseases such as celiac disease (sprue), inflammatory bowel diseases such as ulcerative colitis, or Crohn disease
  • People with peptic ulcer disease
  • People who have undergone bariatric procedures, especially gastric bypass operations
  • Vegetarians, vegans, and other people whose diets do not include iron-rich foods (Iron from vegetables, even those that are iron-rich, is not absorbed as well as iron from meat, poultry, and fish.)
  • Children who drink more than 16 to 24 ounces a day of cow’s milk (Cow’s milk not only contains little iron, but it can also decrease absorption of iron and irritate the intestinal lining causing chronic blood loss.)


Most of the time, symptoms are mild at first and develop slowly. Symptoms may include:

  • Feeling grumpy
  • Feeling weak or tired more often than usual, or with exercise
  • Headaches
  • Problems concentrating or thinking

As the anemia gets worse, symptoms may include –

  • Blue color to the whites of the eyes
  • Brittle nails
  • Desire to eat ice or other non-food things (pica)
  • Feeling lightheaded when you stand up
  • Pale skin color
  • Shortness of breath
  • Sore tongue

Symptoms of the conditions that cause iron deficiency anemia include –

  • Dark, tar-colored stools or blood in the stool
  • Heavy menstrual bleeding (women)
  • Pain in the upper belly (from ulcers)
  • Weight loss (in people with cancer)


  • Heart problems – Iron deficiency anemia may lead to a rapid or irregular heartbeat
  • Problems during pregnancy – In pregnant women, severe iron deficiency anemia has been linked to premature births and low birth weight babies.
  • Growth problems – In infants and children, severe iron deficiency can lead to anemia as well as delayed growth and development.


Iron supplements – Iron supplements can be taken over several months to increase iron levels in the blood. Iron supplements can cause irritation of the stomach and discoloration of bowel movements. They should be taken on an empty stomach, or with orange juice, to increase absorption. They are much more effective than dietary interventions alone. In cases of malabsorption or intolerance, IV iron may be needed.

Evaluation for a source of blood loss – This may include upper endoscopy or colonoscopy.

Intravenous Iron – In some cases the doctor may recommend intravenous (IV) iron. IV iron may be necessary to treat iron deficiency in patients who do not absorb iron well in the gastrointestinal tract, patients with severe iron deficiency or chronic blood loss, patients who are receiving supplemental erythropoietin, a hormone that stimulates blood production, or patients who cannot tolerate oral iron. IV iron comes in different preparations:

  • Iron dextran
  • Iron sucrose
  • Ferric gluconate

Blood Transfusions – Red blood cell transfusions may be given to patients with severe iron-deficiency anemia who are actively bleeding or have significant symptoms such as chest pain, shortness of breath, or weakness. Transfusions are given to replace deficient red blood cells and will not completely correct the iron deficiency. Red blood cell transfusions will only provide temporary improvement.

Iron-rich diet – Eating a diet with iron-rich foods can help treat iron-deficiency anemia. Good sources of iron include the following –

  • Meats, such as beef, pork, lamb, liver, and other organ meats
  • Poultry, such as chicken, duck, turkey, (especially dark meat), liver
  • Fish, such as shellfish, including clams, mussels, and oysters, sardines, anchovies
  • Leafy greens of the cabbage family, such as broccoli, kale, turnip greens, and collards
  • Legumes, such as lima beans and green peas; dry beans and peas, such as pinto beans, black-eyed peas, and canned baked beans
  • Yeast-leavened whole-wheat bread and rolls
  • Iron-enriched white bread, pasta, rice, and cereals

Digestive Enzymes – Take digestive enzymes. To maximize the benefit of an iron supplement, you may need a digestive enzyme.

Supplements – Folic acid, Vitamin B-12, Extra pantothenic acid (vitamin B-5), Copper, Zinc, Raw spleen glandular, Vitamin A, Natural Beta Carotene and Vitamin E.

Chlorophyll is almost an exact match of the red blood cells or hemoglobin in the human body. With such a unique composition, chlorophyll can serve as a substitute for red blood cells until the body is able to replenish the healthy red blood cell count.

Dong quai – This herb is rich in vitamins and minerals.

Chive – This vegetable is rich in vitamin C and iron – eat fresh chives.

Quinoa – This is a grain rich in all eight essential amino acids that form a complete protein.

Gentian – The bitter herb gentian is popular in England for the treatment of anemia. Gentian can be brewed into a tea or you can take a commercially available extract.

Dandelion is also believed to help people with anemia. It is very rich in vitamins and minerals.

Other herbs that are of interest to those suffering from anemia include alfalfa, bilberry, burdock root, cherry, goldenseal, grape skins, hawthorn berry, horsetail, mullein, parsley, nettle, Oregon grape root, pau d’arco, red raspberry, shepherd’s purse, watercress, and yellow dock root.


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February 7, 2017

Hemolytic Uremic Syndrome (HUS), commonly referred to as “Hamburger Disease”, is a disease that affects the kidneys and other organs. It poses a substantial threat to Canadian children as one of the leading causes of both acute and chronic kidney failure.

HUS is considered a syndrome because it is a combination of findings that may have different causes. In most cases, HUS occurs after a severe bowel infection with certain toxic strains of the bacteria called E. coli. It may also occur in response to certain medicines, but this is rare. Even more rarely, HUS occurs for unknown reasons. This fact sheet primarily focuses on the type of HUS that occurs in infants and children as a result of an E. coli infection.

It is a condition that affects the blood and blood vessels. It results in the destruction of blood platelets (cells involved in clotting), a low red blood cell count (anemia) and kidney failure due to damage to the very small blood vessels of the kidneys. Other organs, such as the brain or heart, may also be affected by damage to very small blood vessels.

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. 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.

Though hemolytic uremic syndrome is a serious condition, getting timely and appropriate treatment leads to a full recovery for most people, especially young children.


HUS develops when Escherichia coli (E. coli) bacteria lodged in the digestive tract make toxins that enter the bloodstream and start to destroy red blood cells. Most cases of HUS occur after an infection of the digestive tract by the E. coli bacterium, which is found in foods like meat, dairy products, and juice when they are contaminated. Some people have contracted HUS after swimming in pools or lakes contaminated with feces.

Infection of the digestive tract is called gastroenteritis and may cause a child to vomit and have stomach cramps and bloody diarrhea. Most children who have gastroenteritis recover fully in 2 or 3 days and do not develop HUS.

E.coli O157:H7 can be found in –

  • Undercooked meat, most often ground beef
  • Unpasteurized, or raw, milk
  • Unwashed, contaminated raw fruits and vegetables
  • Contaminated juice
  • Contaminated swimming pools or lakes

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

More information about foodborne illnesses and the digestive system is provided in the NIDDK health topic, foodborne illnesses.

Risk Factors

Those most at risk of developing hemolytic uremic syndrome are –

  • Children under 5 years of age
  • People who have certain genetic changes that make them more susceptible

Young children and elderly adults are the most likely to be seriously ill from hemolytic uremic syndrome.


HUS often begins with vomiting and diarrhea, which may be bloody. Within a week, the person may become weak and irritable. Persons with this condition may urinate less than normal. Urine output may almost stop.

Red blood cell destruction leads to symptoms of anemia.

Early symptoms –

  • Blood in the stools
  • Irritability
  • Fever
  • Lethargy
  • Vomiting
  • diarrhea
  • Weakness

Later symptoms –

  • Bruising
  • Decreased consciousness
  • Low urine output
  • No urine output
  • Pallor
  • Seizures — rare
  • Skin rash that looks like fine red spots (petechiae)
  • Yellow skin (jaundice)


  • Blood clotting problems
  • Hemolytic anemia
  • Kidney failure
  • Nervous system problems
  • Too few platelets (thrombocytopenia)
  • Uremia


  • Fluid replacement – Lost fluid and electrolytes need to be carefully replaced because the kidneys aren’t removing fluids and waste as efficiently as normal.
  • Red blood cell transfusions – If patients don’t have enough red blood cells, they may feel chilled, fatigued and short of breath. They may have a rapid heart rate, yellow skin and dark urine. Red blood cell transfusions, given through an intravenous (IV) needle, may help reverse these signs and symptoms.
  • Platelet transfusions – If the patient is bleeding or bruising easily, platelet transfusions can help your blood clot more normally. Like red blood cell transfusions, platelet transfusions are given through an IV needle.
  • Plasma exchange – Plasma is the part of blood that supports the circulation of blood cells and platelets. Sometimes a machine is used to clear the blood of its own plasma and replace it with fresh or frozen donor plasma. This process is called plasmapheresis.
  • Kidney dialysis – Sometimes dialysis is needed to filter waste and excess fluid from the blood. Dialysis is usually a temporary treatment until the kidneys begin functioning adequately again. If the kidney damage is significant, however, permanent kidney failure — requiring long-term dialysis or a kidney transplant — is possible.

Alternative Treatment


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February 7, 2017

Hemochromatosis (HH) is a disease that results from excessive amounts of iron in the body (iron overload).

Hereditary (genetic) hemochromatosis (HHC) an inherited disorder of abnormal iron metabolism. Individuals with hereditary hemochromatosis absorb too much dietary iron. Once absorbed, the body does not have an efficient way of excreting iron excesses.  Over time, these excesses build to a condition of iron overload, which is a toxic to cells. Glands and organs, including the liver, heart, pituitary, thyroid, pancreas, synovium (joints) and bone marrow burdened with excess iron cannot function properly.  Symptoms develop and disease progresses.

As many as 1 in 200 Americans are believed to carry both copies of the gene for hemochromatosis, and it is estimated that about half of them will eventually develop complications. That puts it roughly on a par with type 1 diabetes for prevalence. Like type 2 diabetes, it is severely underdiagnosed.

Types of Hemochromatosis

Hemochromatosis is classified by type depending on the age of onset and other factors such as genetic cause and mode of inheritance.

Hemochromatosis type 1, the most common form of the disorder, and type 4 (also called ferroportin disease) are adult-onset disorders. Men with type 1 or type 4 hemochromatosis typically develop symptoms between the ages of 40 and 60, and women usually develop symptoms after menopause

Type 2 hemochromatosis is a juvenile-onset disorder. Iron accumulation begins early in life, and symptoms may begin to appear in childhood. By age 20, decreased or absent secretion of sex hormones is evident. Females usually begin menstruation in a normal manner, but menses stop after a few years. Males may experience delayed puberty or sex hormone deficiency symptoms such as impotence. If the disorder is untreated, heart disease is evident by age 30.

Onset of type 3 hemochromatosis is usually intermediate between types 1 and 2. Symptoms generally begin before age 30.generally begin before age 30.

In rare cases, iron overload begins before birth. These cases are called neonatal hemochromatosis. This type of hemochromatosis progresses rapidly and is characterized by liver damage that is apparent at birth or in the first day of life. The neonatal form causes rapid iron buildup in a baby’s liver that can lead to death.


Hemochromatosis is a hereditary disorder, which means it is passed down from parents to children through their genes. Hemochromatosis is mainly caused by a defect in the HFE gene. It is also known as primary hemochromatosis.

Some people get a copy of the HFE gene defect from just one parent. They are called “carriers” because they carry the defective gene and can pass it on to their children. Carriers usually do not get sick. People who get the HFE gene defect from both parents have a greater chance of getting the disease.

There are other types of hemochromatosis that are not caused by the HFE gene defect — including secondary, juvenile, and neonatal hemochromatosis – but they are less common than the primary form. Secondary hemochromatosis can be caused by disorders such as thalassemia, anemia, chronic alcoholism, and other conditions. Juvenile and neonatal hemochromatosis are caused by other types of gene defects.

Risk Factors

The known risk factors for hemochromatosis are:

Possessing two copies of a mutated HFE gene – the greatest risk factor for hereditary hemochromatosis. The person inherits one copy of the mutated HFE gene from each parent.

Family history – anybody who has a close relative (parent, offspring, brother or sister) with hemochromatosis is significantly more likely to develop it compared to other people.

Ancestry – people of British, Scandinavian Dutch, German, Irish and French ancestry have a higher risk of developing hemochromatosis compared to others. Their risk of having the HFE gene mutation is greater.

Gender – men are significantly more likely to develop hemochromatosis compared to women. Signs and symptoms tend to appear earlier on in life in males than females. This is because women lose iron during menstruation and pregnancy. A woman’s risk increases after the menopause or a hysterectomy. The male-to-female ratio is 1.8:1 (out of every 28 people with hemochromatosis, 18 are male and 10 are female).


A symptom is something the patient feels or reports, while a sign is something other people, including a doctor, may detect. For example, a headache may be a symptom while a rash may be a sign.

As signs and symptoms may be mild and could also be indications of other illnesses and conditions, identifying hemochromatosis is often not straightforward.

  • The main symptoms include:
  • Abdominal pain
  • Females may stop menstruating
  • High blood sugar levels
  • Hypothyroidism (low thyroid function)
  • Loss of libido (sex drive) and male impotence
  • Pain in the joints
  • Reduction in size of testicles
  • Skin becomes bronzed (has a tanned look)
  • Tiredness (fatigue)
  • Weakness
  • Weight loss


As the disorder progresses, the following conditions may develop:

  • Enlarged liver
  • Cirrhosis (scarring of the liver)
  • Liver cancer
  • Liver failure
  • Arthritis
  • Osteoporosis
  • Diabetes (from damage to the pancreas)
  • Irregular heartbeat
  • Enlarged heart
  • Congestive heart failure
  • Impotence
  • Early menopause
  • Hypothyroidism
  • Damage to adrenal glands
  • Enlarged spleen


  • Venesection (phlebotomy) – iron-rich blood is removed from the body regularly, just as if the patient were donating blood. In this case the aim is to bring iron levels down to normal. How much blood is taken and how often depends on the patient’s age, overall health and the severity of the iron overload. In most cases blood is removed weekly until levels are back to normal. When iron levels build up again the patient will need venesection treatment again.

Although venesection cannot reverse the symptoms of cirrhosis, it can improve symptoms such as nausea, abdominal pain and fatigue.

  • Medication – the patient may be given a drug that binds iron, which is then excreted from the body.

If hemochromatosis is diagnosed and treated early, before too much excessive iron accumulates, the patient should have a normal lifespan, experts say.

Alternative Treatment

Excess iron and treatment – Getting iron levels down is very important to the outcome of hemochromatosis. A therapeutic phlebotomy or blood transfusion are usually accomplished this. Blood donations are done every eight weeks; sever conditions may require up to eight donations per month. Some medications may help also. The goal is to get iron levels down.

Herbal Therapy – Here are some herbal therapies that have been known to be useful in treating iron overload.

  • Dandelion—reduces constipation caused by excess iron conditions.
  • Wild Hyssop—regulates blood sugar, reduces pain and inflammation surrounding nerve tissues needing iron supply to vital organs needing nutrients.
  • Milk Thistle—reduces the iron storage in the body and lowers blood sugar levels.

Chelation Therapy – Chelating therapy removes excess minerals, and toxic materials from the body through the use of drugs; making it easier for them to tolerate phlebotomy.

EDTA Chelation Therapy – EDTA is used to remove heavy metals from the body, with IV therapy; given under supervision of medical supervision.

Calcium – Taking 300 mg of calcium per day with a meal is a simple way to block the absorbed iron, and reduce it about 40%. Some people do build up a tolerance to calcium, so regular blood tests are needed.

Vitamins and minerals

  • Vitamin B6—blocks absorption of iron, especially when taking vitamin C.
  • Avoid Vitamin C—limit taking vitamin c supplements over 500mg, eat more fresh vegetables and fruit containing vitamin C instead.
  • Vitamin E—antioxidant used as a blood thinner (400-800IU)
  • Manganese—protects against damage from excess iron.

Black Tea – Drinking black tea may reduce iron absorption, and reduces amount of frequent phlebotomies patients may have. Green tea is also powerful as a chelator to remove iron.


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February 7, 2017

Gallstones are lumps of solid material that form in the gallbladder. They usually look like small stones or gravel, but can be as small as sand or as large as pebbles, sometimes filling the gallbladder.

The gallbladder is a small, pear-shaped pouch about three to six inches long. It is tucked just under the liver, below the right rib cage and is connected to the intestine and liver by small tubes called bile ducts. Bile ducts carry bile, a yellow-green fluid produced by your liver. Bile contains water, cholesterol, phospholipids and chemicals to aid digestion (bile acids), as well as waste products for excretion via the bowel, such as bilirubin.

Bile is collected and stored in the gallbladder, and released along the bile ducts into the intestine when we eat food. It plays a central role in helping the body digest fat. Bile acts as a detergent, breaking up the fat from food in the gut into very small droplets, so that it can be absorbed. It also makes it possible for the body to take up the fat-soluble vitamins A, D, E and K from the food passing through the gut.

Gallstones develop when cholesterol levels in the bile are too high and excess cholesterol turns into stones. Most gallstones are mixed stones or cholesterol stones, mostly made up of cholesterol. They are usually yellow or green. Another type of gallstones are pigment stones, which are mostly made up of bilirubin and are smaller and darker.

  • Pure Cholesterol Stones – these are the most common type of stone and are made up of cholesterol, which is a type of fat
  • Pure Pigment Stones – these consist of calcium and bilirubin (a pigment from broken down red blood cells) which have solidified
  • Mixed Stones – these are a combination of cholesterol and pigment stones

Gallstones vary greatly in size.  Some people may form one large stone, whereas others may have hundreds of tiny stones. Most commonly, gallstones are 5-10 mm in diameter.

About 70 per cent of people who have gallstones do not have noticeable symptoms and are often unaware that they have them. Gallstones may be discovered only during investigations for other problems. For this reason, they are sometimes called ‘silent’ gallstones.


Gallstones are formed when the different elements which make up the bile become imbalanced. Cholesterol stones form when cholesterol levels in the bile are much greater than the bile acid levels, this causes the cholesterol in the bile to solidify.

There is evidence that dietary factors, such as diets high in cholesterol, saturated fat, refined sugar and low in fibre, increase the risk of developing cholesterol gallstones.

Gallstones are more common in women than in men, especially during women’s fertile years and during pregnancy. This is because cholesterol is a component of oestrogen, and at these times fluctuating levels of oestrogen need to be broken down to cholesterol and excreted in bile.

Pigment stones may form when the amount of bilirubin in bile is excessive. This can occur in conditions such as sickle cell disease.

Gallstones can also form when the flow of bile is reduced. This may occur due to –

  • damage to the liver (cirrhosis) or damage to the biliary tract which affects the secretion and flow of bile
  • long periods of fasting during which there is less requirement for bile, leading to bile stasis (decreased flow of bile).

Genetics – Having a family member or close relative with gallstones may increase the risk. Up to one-third of cases of painful gallstones may be related to genetic factors. A mutation in the gene ABCG8 significantly increases a person’s risk of gallstones. This gene controls a cholesterol pump that transports cholesterol from the liver to the bile duct. It appears this mutation may cause the pump to continuously work at a high rate. A single gene, however, does not explain the majority of cases, so multiple genes and environmental factors play a complex role.

Risk Factors

Risk factors for developing gallstones include –

  • Being overweight or obese
  • Being female
  • Being over 40
  • A woman who’s had more than one pregnancy
  • Having cirrhosis of the liver
  • Having Crohn’s disease or IBS ( irritable bowel syndrome)
  • A family history of gallstones
  • Having weight loss surgery or recently having lost weight
  • Being treated with the antibiotic ceftriaxone
  • Being on the Pill
  • Women taking high-dose oestrogen therapy
  • Having type 2 diabetes is suspected of being a risk factor
  • A lack of exercise is also thought to increase the risk of gallstones


Gallstones vary in chemical structure. The two main types of gallstones are:

Cholesterol gallstones

The amount of cholesterol that can dissolve in bile depends on how much bile salt it contains.  Too much cholesterol, or too little bile salt, tends to cause gallstones to form in the gallbladder. Approximately 80% of all gallstones are cholesterol stones.

Pigment gallstones

These are formed by calcium and bilirubin and account for approximately 20% of all gallstones.   Pigment stones tend to form in patients with haemolytic anaemias (fragile red blood cells), including sickle-cell disease and thalassaemia.

Most people with gallstones do not experience any symptoms. If symptoms are present, the most common early sign of gallstones is upper abdominal pain.  This pain usually occurs in the upper right side of the abdomen, is often severe, and may radiate to the chest, back or the area between the shoulders.  Other symptoms that may occur include –

  • Indigestion
  • Nausea or vomiting
  • Jaundice (the yellow appearance of skin and the whites of eyes caused by bilirubin build-up in the blood) when gallstones block the passage of bile
  • Light coloured stools

Symptoms can occur suddenly and may be referred to as biliary colic. This type of pain is commonly set off by eating fatty foods and often occurs in the middle of the night. The symptoms experienced may be so severe that people need to seek immediate medical attention.


Biliary colic – Sometimes the gallstones may pass down through the bile duct into the duodenum. When this happens the patient may experience biliary colic – a painful condition. The pain is felt in the upper part of the abdomen, but can also exist in the center of the abdomen, or a little to the right of it. Pain is more common about an hour after eating, especially if the patient has had a high-fat meal. The pain will be constant and will last a few hours, and then subside. Some patients will have non-stop pain for 24 hours, while others may experiences waves of pain.

Infection – If the gallstones have caused a gallbladder infection the patient may have a fever and experience shivering. In the majority of gallstone infection cases the patient will be hospitalized and have the gallstone surgically removed.

Jaundice – If the gallstone leaves the gallbladder and gets stuck in the bile duct it may block the passage of bile into the intestine. The bile will then seep into the bloodstream and the patient will show signs of jaundice – the skin and the whites of the eyes will be yellow. In most cases this complication will require the surgical removal of the gallstone. Some patients are lucky and the gallstone eventually passes into the intestine.

Pancreatitis – If a small gallstone passes through the bile duct and blocks the pancreatic duct, or causes a reflux of liquids and bile into the duct, the patient may develop pancreatitis.


Surgery – Surgery to remove the gallbladder, called cholecystectomy, is one of the most common operations performed on adults in the United States. Surgeons perform two types of cholecystectomy.

  • Laparoscopic cholecystectomy – In a laparoscopic cholecystectomy, the surgeon makes several tiny incisions in the abdomen and inserts a laparoscope—a thin tube with a tiny video camera attached. The camera sends a magni­fied image from inside the body to a video monitor, giving the surgeon a close-up view of organs and tissues. While watching the monitor, the surgeon uses instruments to carefully separate the gallbladder from the liver, bile ducts, and other structures. Then the surgeon removes the gallbladder through one of the small incisions. Patients usually receive general anesthesia.
  • Open cholecystectomy – An open cholecystectomy is performed when the gallbladder is severely infl‑amed, infected, or scarred from other operations. In most of these cases, open cholecystectomy is planned from the start. However, a surgeon may perform an open cholecystectomy when problems occur during a laparoscopic cholecystectomy. In these cases, the surgeon must switch to open cholecystectomy as a safety measure for the patient.

Medication – Ursodiol (Actigall) and chenodiol (Chenix) are medications that contain bile acids that can dissolve gallstones. These medications are most effective in dissolving small cholesterol stones. Months or years of treatment may be needed to dissolve all stones.

Shock wave lithotripsy – A machine called a lithotripter is used to crush the gallstone. The lithotripter generates shock waves that pass through the person’s body to break the gallstone into smaller pieces. This procedure is used only rarely and may be used along with ursodiol.

Lifestyle Changes – Although lifestyle changes cannot eliminate the risk of developing gallstones for everyone, avoiding fatty food and cutting cholesterol and consuming a healthy balanced diet may be recommended.

Losing weight can help reduce the risk of gallstones. However, a gradual approach is better as rapid weight loss can increase the risk of gallstones.

Alternative Treatment

Multivitamins – A daily multivitamin, containing the antioxidant vitamins A, C, E, the B-complex vitamins, and trace minerals, such as magnesium, calcium, zinc, and selenium.

Vitamin C acts as an antioxidant and for immune support.

Phosphatidylcholine, may help dissolve gallstones. It may interfere with some medications, including anticholinergic medications used in the treatment of Alzheimer’s disease and glaucoma, among others.

Magnesium, for nutrient support. Magnesium can potentially react with a variety of medications, including some antibiotics, blood pressure medicines, diuretics, muscle relaxers, and others.

Taurine, for nutrient support. Taurine can potentially interact with lithium.

Globe artichoke, for support of gallbladder and liver function. Due to its ability to increase bile production, globe artichoke could trigger a gallbladder attack if there is bile duct obstruction.

Milk thistle or liver and gallbladder detoxification support.

Dandelion root is another liver tonic.

Acupuncture – Acupuncture may be especially helpful in pain relief, reducing spasm, easing bile flow, and restoring proper liver and gallbladder function.


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February 7, 2017
February 7, 2017

Insert Diet and Nutrition Videos:

Diet and Nutrition Intro https://youtu.be/5FEy1M-kwyc

Diet and Nutrition #1 https://youtu.be/oj2b79d4OGY

Diet and Nutrition #2 https://youtu.be/ZJlAaEe8ayQ

Diet and Nutrition #3 https://youtu.be/7VNumPW7FPo

Diet and Nutrition #4 https://youtu.be/tHr6THTsQjE

Diet and Nutrition #5 https://youtu.be/AM3s9dCGKdQ

Diet and Nutrition #6 https://youtu.be/RZChMZk4iqU


February 7, 2017

Diabetic neuropathies are a family of nerve disorders caused by diabetes. It has been defined as presence of symptoms and/or signs of peripheral nerve dysfunction in diabetics after exclusion of other causes, which may range from hereditary, traumatic, compressive, metabolic, toxic, nutritional, infectious, immune mediated, neoplastic, and secondary to other systemic illnesses.

About 60 to 70 percent of people with diabetes have some form of neuropathy. People with diabetes can develop nerve problems at any time, but risk rises with age and longer duration of diabetes. The highest rates of neuropathy are among people who have had diabetes for at least 25 years. Diabetic neuropathies also appear to be more common in people who have problems controlling their blood glucose, also called blood sugar, as well as those with high levels of blood fat and blood pressure and those who are overweight.

Types of Diabetic Neuropathy

There are different types of diabetic neuropathy. The distinction depends upon which types and location of nerves are affected.

  • Diabetic peripheral neuropathy refers to damage to peripheral nerves, most commonly the nerves of the feet and legs.
  • Diabetic proximal neuropathy affects nerves in the thighs, hips, or buttocks.
  • Diabetic autonomic neuropathy affects the autonomic nervous system, the nerves that control body functions. For example, it can affect nerves of the gastrointestinal, urinary, genital, or vascular systems.
  • Diabetic focal neuropathy affects a specific nerve or area at any site in the body.

Neuropathy is damage to nerves, and diabetic neuropathy is damage to nerves that occurs as a result of diabetes. Diabetes is thought to damage nerves as a result of prolonged elevated levels of blood glucose. Diabetic neuropathy can affect different parts of the body, and symptoms can range from mild to severe. Diabetic neuropathy is the most common complication of diabetes.


High glucose and lipid (fat) levels in the blood, and the toxic byproducts they generate through their metabolism, are thought to be the major causes of neuropathy associated with diabetes. However, good glucose control in people with type 1 diabetes can reduce neuropathy by 60 per cent.

It’s possible that elevated blood glucose levels damage the tiny blood vessels that lead to the nerves. If the blood vessels are damaged, they don’t bring oxygen and nutrients to the nerves as they should, which eventually can cause nerve damage.

Other factors may include –

  • Age – Diabetic neuropathy takes time to develop, so it’s much more common in older people who have had diabetes for 25 years or more.
  • Genetic factors – Unrelated to diabetes that make some people more susceptible to nerve damage.
  • Lifestyle choices – It seems that alcohol and smoking make the symptoms of neuropathy worse.
  • Nerve injury – Whether the nerves have been damaged through inflammation or through a mechanical injury (such as nerve compression associated with carpal tunnel syndrome), it’s possible the previously-damaged nerves are more susceptible to developing diabetic neuropathy.

Risk Factors

The longer a person has diabetes and the worse the control of their diabetes, the more likely they will develop diabetic neuropathy.

Those people experiencing complications of their diabetes elsewhere in their body (such as in the kidneys, heart or eyes) are also more likely to have or develop neuropathy, as the same factors that cause these problems also contribute to neuropathy. Smoking, high blood pressure and being overweight also make it more likely that people with diabetes will get nerve damage.


The symptoms of diabetic neuropathy depend on what type of neuropathy  the  person has. Symptoms are dependent on which nerves have been damaged. In general, diabetic neuropathy symptoms develop gradually; they may seem like minor and infrequent pains at first, but as the nerves become more damaged, symptoms may grow.

As mild symptoms can indicate the beginning of neuropathy, the following should be noted – pain, numbness, weakness, or tingling—even if it seems insignificant.

Peripheral Neuropathy Symptoms – Peripheral neuropathy affects nerves leading to the extremities—the feet, legs, hands, and arms. The nerves leading to the feet are the longest in the body, so they are the most often affected nerves (simply because there’s more of them to be affected). Peripheral neuropathy is the most common form of diabetic neuropathy. The symptoms include –

  • Pain
  • Numbness (loss of feeling)
  • Tingling
  • Muscle weakness
  • Muscle cramping and/or twitching
  • Insensitivity to pain and/or temperature
  • Extreme sensitivity to even the lightest touch

Symptoms get worse at night.

Proximal Neuropathy Symptoms – Proximal neuropathy affects the buttocks, hips, thighs, and legs. Its symptoms aren’t usually long-term; they may go away after several weeks or months.

Symptoms include –

  • Weakness in the legs
  • Trouble standing up from a seated position without help.

Autonomic Neuropathy Symptoms – The autonomic nervous system is in charge of the “involuntary” functions of the body. It keeps the heart pumping and keeps the digestion healthy.

  • Cardiovascular System
    • Dizziness just after standing
    • Fainting just after standing
    • Irregular heart rate
  • Digestive System
    • Bloating
    • Constipation
    • Diarrhea
    • Nausea
    • Vomiting
  • Eyes
    • Vision trouble at night or during sudden light changes (e.g., when stepping into a dark building from the sunlight)
  • Reproductive System
    • Sexual problems—erectile dysfunction in men; vaginal dryness in women
  • Sweat Glands
    • Profuse sweating, especially at night or when eating particular foods (cheese commonly causes excessive sweating, for example, although that’s not true for every person with diabetic neuropathy)
    • Reduced sweating, especially in the legs and feet
    • Urinary System
    • Bladder dysfunction

Focal Neuropathy Symptoms – This affects the head, torso, or legs. Symptoms include –

  • Head
    • Vision trouble—double vision, ache behind an eye, difficulty focusing
    • Sudden paralysis of one side of the face (Bell’s palsy)
  • Torso
    • Pain in the chest
    • Pain in the stomach
    • Pain on the side
    • Pain in the low back
  • Legs
    • Pain in the front of the thigh
    • Pain on the outside of the shin
    • Pain on the inside of the foot


he first treatment step is to bring blood glucose levels within the normal range to help prevent further nerve damage. Blood glucose monitoring, meal planning, physical activity, and diabetes medicines or insulin will help control blood glucose levels. Symptoms may get worse when blood glucose is first brought under control, but over time, maintaining lower blood glucose levels helps lessen symptoms. Good blood glucose control may also help prevent or delay the onset of further problems. As scientists learn more about the underlying causes of neuropathy, new treatments may become available to help slow, prevent, or even reverse nerve damage.x`

Medications – People with severe nerve pain may benefit from a combination of medications or treatments and should consider talking with a health care provider about treatment options.

Medications used to help relieve diabetic nerve pain include – Tricyclic antidepressants, such as amitriptyline, imipramine, and desipramine (Norpramin, Pertofrane) and other types of antidepressants, such as duloxetine (Cymbalta), venlafaxine, bupropion (Wellbutrin), paroxetine (Paxil), and citalopram (Celexa) Anticonvulsants, such as pregabalin (Lyrica), gabapentin (Gabarone, Neurontin), carbamazepine, and lamotrigine (Lamictal), Opioids and opioidlike drugs, such as controlled-release oxycodone, an opioid; and tramadol (Ultram), an opioid that also acts as an antidepressant.

Treatments that are applied to the skin—typically to the feet—include capsaicin cream and lidocaine patches (Lidoderm, Lidopain). Studies suggest that nitrate sprays or patches for the feet may relieve pain. Studies of alpha-lipoic acid, an antioxidant, and evening primrose oil suggest they may help relieve symptoms and improve nerve function in some patients.

A device called a bed cradle can keep sheets and blankets from touching sensitive feet and legs. Acupuncture, biofeedback, or physical therapy may help relieve pain in some people. Treatments that involve electrical nerve stimulation, magnetic therapy, and laser or light therapy may be helpful but need further study. Researchers are also studying several new therapies in clinical trials.

Treating gastroparesis – For gastroparesis, in which the stomach is not emptying properly, physicians at Joslin may prescribe metoclopramide (Reglan®), which will help the stomach push food and get it through the rest of the digestive process. These may be used in conjunction with sucralfate (Carafate®), which “helps to sop up extra acid that may be sitting in the stomach,” Dr. Gibbons says.

Treating bladder neuropathy – For those experiencing bladder neuropathy, which results in the bladder never completely emptying, bethanechol (Urecholine®) may be prescribed. “This is a urine propellant that helps to keep the bladder clear,” says Dr. Gibbons. “Because patients with this problem will be more likely to develop frequent urinary tract infections, the physician may also prescribe chronic antibiotic therapy to try and keep the bacterial count in the bladder and urinary tract at a manageable level.”

Treating impotence – Impotence in men that is a result neuropathy or blood vessel damage (versus psychological causes or due to medications such as anti-depressants or blood pressure medication) can be treated using certain drugs that are either inserted into the end of the penis or injected to cause an erection before intercourse. Vacuum devices that enable an erection to be achieved or a surgically implanted prosthesis are also options to be explored with a physician.

Alternative Treatment

  • Alpha lipoic acid is one if the most important nutrients to consider for diabetes. Alpha Lipoic acid has been evaluated for blood sugar control, and it may also be considered in diabetic neuropathy and kidney disease. Alpha-lipoic acid may improve symptomatic diabetic polyneuropathy.
  • Acetyl-L-carnitine is helpful in the treatment of diabetic neuropathy. It improves pain, nerve regeneration, and vibratory perception in patients with chronic diabetic neuropathy.
  • Benfotiamine has been evaluated in diabetic neuropathy with positive results
  • B vitamins could be helpful, perhaps combined with gabapentin (Neurotin). Vitamin B12 is a possible supplement to take for diabetic neuropathy. Vitamin B12 may be more effective than nortriptyline in improving painful diabetic neuropathy. It is more effective than nortriptyline for the treatment of symptomatic painful diabetic neuropathy.
  • Ginkgo biloba herbal extract has the best effect with the combination of folate for diabetic neuropathy.
  • Capsaicin applied to the skin, capsaicin cream can reduce pain sensations in some people. Side effects may include a burning feeling and skin irritation.
  • Vitamin B6 deficiency may be associated with the development of peripheral neuropathy. In addition, in the form of pyridoxine HCl, high doses of B6 have been implicated as a cause of PN.
  • Chromium is an essential mineral, chromium plays an important role in facilitating glucose metabolism.
  • Coenzyme Q10 is a cofactor used in oxidative respiration and is produced endogenously. Supplementation of coenzyme Q10 is especially popular for cardiovascular diseases.
  • Magnesium is an abundant mineral in the human body involved in numerous biochemical processes, including glucose metabolism. It Increases insulin sensitivity.
  • Omega-3 polyunsaturated fatty acids (PUFAs) are one of the most common dietary supplements taken in the United States. Studies indicate reductions in coronary artery disease and sudden cardiac death based on omega-3 PUFA intake. In patients with type 2 diabetes, a meta-analysis of omega-3 PUFA supplementation set of type 2 diabetes.60
  • Vanadium is a mineral with no known biological importance or deficiency-associated disease.
February 7, 2017

Diabetes or Diabetes mellitus is defined as a metabolic disorder of multiple etiologies characterized by chronic hyperglycemia with disturbances of carbohydrate, protein and fat metabolism resulting from defects in insulin secretion, insulin action, or both. is a defect in the body’s ability to convert glucose (sugar) to energy. Glucose is the main source of fuel for the body.

Foods that affect blood sugars are called carbohydrates. Carbohydrates, when digested, change to glucose. Examples of some carbohydrates are: bread, rice, pasta, potatoes, corn, fruit, and milk products. Individuals with diabetes should eat carbohydrates but must do so in moderation. Glucose is then transferred to the blood and is used by the cells for energy. In order for glucose to be transferred from the blood into the cells, the hormone – insulin is needed. Pancreas—an organ, located between the stomach and spine, that helps with digestion—releases a hormone it makes, called insulin, into the blood. Insulin helps the blood to carry glucose to all the body’s cells. Sometimes the body doesn’t make enough insulin or the insulin doesn’t work the way it should. The blood glucose levels get too high and can cause diabetes or prediabetes.

What is prediabetes?

Prediabetes is when the amount of glucose in the blood is above normal yet not high enough to be called diabetes. With prediabetes, the chances of getting type 2 diabetes, heart disease, and stroke are higher. With some weight loss and moderate physical activity, it can be delayed or prevented.

Over time, diabetes can lead to blindness, kidney failure, and nerve damage. These types of damage are the result of damage to small vessels, referred to as microvascular disease. Diabetes is also an important factor in accelerating the hardening and narrowing of the arteries (atherosclerosis), leading to strokes, coronary heart disease, and other large blood vessel diseases. This is referred to as macrovascular disease. Diabetes affects approximately 26 million people in the United States, while another 79 million have prediabetes. An estimated 7 million people in the United States have diabetes and don’t even know it. Diabetes is the seventh leading cause of death in the United States.

Types of Diabetes

Type 1 diabetes occurs most frequently in children and young adults, although it can occur at any age. Type 1 diabetes accounts for 5-10% of all diabetes in the United States. There does appear to be a genetic component to Type 1 diabetes, but the cause has yet to be identified. In type 1 diabetes, the body no longer makes insulin or enough insulin because the body’s immune system, which normally protects the body from infection by getting rid of bacteria, viruses, and other harmful substances, has attacked and destroyed the cells that make insulin.

Type 2 diabetes is much more common and accounts for 90-95% of all diabetes. Type 2 diabetes primarily affects adults, however recently Type 2 has begun developing in children. There is a strong correlation between Type 2 diabetes, physical inactivity and obesity. Type 2 diabetes usually begins with insulin resistance—a condition that occurs when fat, muscle, and liver cells do not use insulin to carry glucose into the body’s cells to use for energy. As a result, the body needs more insulin to help glucose enter cells. At first, the pancreas keeps up with the added demand by making more insulin. Over time, the pancreas doesn’t make enough insulin when blood sugar levels increase, such as after meals.

Gestational diabetes affects females during pregnancy. Some women have very high levels of glucose in their blood, and their bodies are unable to produce enough insulin to transport all of the glucose into their cells, resulting in progressively rising levels of glucose. Overweight or obese women have a higher chance of gestational diabetes. Also, gaining too much weight during pregnancy may increase the likelihood of developing gestational diabetes. Gestational diabetes most often goes away after the baby is born. However, a woman who has had gestational diabetes is more likely to develop type 2 diabetes later in life. Babies born to mothers who had gestational diabetes are also more likely to develop obesity and type 2 diabetes.


Diabetes causes vary depending on your genetic makeup, family history, ethnicity, health and environmental factors. There is no common diabetes cause that fits every type of diabetes.

Type 1

Type 1 diabetes is caused by the immune system destroying the cells in the pancreas that make insulin. This causes diabetes by leaving the body without enough insulin to function normally. This is called an autoimmune reaction, or autoimmune cause, because the body is attacking itself. There is no specific diabetes causes, but the following triggers may be involved:

  • Viral or bacterial infection
  • Chemical toxins within food
  • Unidentified component causing autoimmune reaction

Underlying genetic disposition may also be a type 1 diabetes cause.

Type 2

Type 2 diabetes causes are usually multifactorial – more than one diabetes cause is involved. Often, the most overwhelming factor is a family history of type 2 diabetes. This is the most likely type 2 diabetes cause. There are a variety of risk factors for type 2 diabetes, any or all of which increase the chances of developing the condition. These include:

  • Obesity
  • Living a sedentary lifestyle
  • Increasing age
  • Bad diet

Other type 2 diabetes causes such as pregnancy or illness can be type 2 diabetes risk factors.

Gestational Diabetes

The causes of diabetes in pregnancy also known as gestational diabetes remain unknown. However, there are a number of risk factors that increase the chances of developing this condition –

  • Family history of gestational diabetes
  • Overweight or obese
  • Suffer from polycystic ovary syndrome
  • Have had a large baby weighing over 9lb

Causes of gestational diabetes may also be related to ethnicity – some ethnic groups have a higher risk of gestational diabetes.

Other Causes

  • Pancreatitis or pancreatectomy as a cause of diabetes. Pancreatitis is known to increase the risk of developing diabetes, as is a pancreatectomy.
  • Polycystic Ovary Syndrome (PCOS). One of the root causes of PCOS is obesity-linked insulin resistance, which may also increase the risk of pre-diabetes and type 2 diabetes.
  • Cushing’s syndrome. This syndrome increases production of the cortisol hormone, which serves to increased blood glucose levels. An over-abundance of cortisol can cause diabetes.
  • Patients with glucagonoma may experience diabetes because of a lack of equilibrium between levels of insulin production and glucagon production.
  • Steroid induced diabetes (steroid diabetes) is a rare form of diabetes that occurs due to prolonged use of glucocorticoid therapy.

Medications and Chemical Toxins – Some medications, such as nicotinic acid and certain types of diuretics, anti-seizure drugs, psychiatric drugs, and drugs to treat human immunodeficiency virus (HIV), can impair beta cells or disrupt insulin action. These drugs can increase the risk of pancreatitis, beta cell damage, and diabetes. Also, glucocorticoids—steroid hormones that are chemically similar to naturally produced cortisol—may impair insulin action. Glucocorticoids are used to treat inflammatory illnesses such as rheumatoid arthritis, asthma, lupus, and ulcerative colitis.

Many chemical toxins can damage or destroy beta cells in animals, but only a few have been linked to diabetes in humans. For example, dioxin—a contaminant of the herbicide Agent Orange, used during the Vietnam War—may be linked to the development of type 2 diabetes.


Diabetes often goes undiagnosed because many of its symptoms seem harmless or don’t always appear right away. Recent studies show that early detection of diabetes symptoms and treatment can decrease the chance of developing the complications of diabetes.

Symptoms of diabetes include:

  • Increased thirst
  • Increased hunger
  • Having to urinate more often – especially at night
  • Feeling very tired
  • Weight loss
  • Blurry vision
  • Sores that do not heal
  • Tingling/numbness in the hands and feet

People who are concerned that they might have diabetes should talk to their doctor or health care provider to find out how to get tested for diabetes.

If blood sugar is consistently high, over time it can affect the heart, eyes, kidneys, nerves, and other parts of the body. These problems are called complications. Sometimes people with diabetes don’t realize that they have the disease until they begin to have other health problems. For example, a doctor or health care provider may detect signs of diabetes damage even though the patient does not know that he/she has the disease.

Other Complications

  • Heart Disease – People with diabetes have a higher risk for heart attack and stroke.
  • Eye Complications – People with diabetes have a higher risk of blindness and other vision problems.
  • Kidney Disease – Diabetes can damage the kidneys and may lead to kidney failure.
  • Nerve Damage (neuropathy) – Diabetes can cause damage to the nerves that run through the body.
  • Foot Problems – Nerve damage, infections of the feet, and problems with blood flow to the feet can be caused by diabetes.
  • Skin Complications – Diabetes can cause skin problems, such as infections, sores, and itching. Skin problems are sometimes a first sign that someone has diabetes.
  • Dental Disease – Diabetes can lead to problems with teeth and gums, called gingivitis and periodontitis.
  • Erectile dysfunction– Male impotence.
  • HHNS (Hyperosmolar Hyperglycemic Nonketotic Syndrome)– Blood glucose levels shoot up too high, and there are no ketones present in the blood or urine. It is an emergency condition.


Insulin Shots

  • Insulin shot – The patients use a needle attached to a syringe—a hollow tube with a plunger—that is filled with a dose of insulin. Some people use an insulin pen, a penlike device with a needle and a cartridge of insulin. Never share insulin needles or insulin pens, even with family.
  • Insulin pump – An insulin pump is a small device filled with insulin that you wear on your belt or keep in your pocket. The pump connects to a small, plastic tube and a small needle.
  • Insulin jet injector – This device sends a fine spray of insulin through the skin with high-pressure air instead of a needle.
  • Insulin injection port – The patient or the doctor inserts a small tube just beneath your skin, where it remains in place for several days.


  • Metformin is usually the first treatment offered, however, and it is the most widely used oral antihyperglycemic. Metformin is a sensitizer in the class known as biguanides; it works by reducing the amount of glucose released by the liver into the bloodstream and increasing cellular response to insulin.
  • Sulphonylureas are secretagogues that increase pancreatic insulin secretion. There are several drug names in this class, including – Chlorpropamide, Glimepiride, Glipizide, Glyburide.
  • Glitazones (also known as thiazolidinediones) are sensitizers – they increase the effect of insulin in the muscle and fat and reduce glucose production by the liver.
  • Alpha-glucosidase inhibitors are intestinal enzyme inhibitors that block the breakdown of carbohydrates into glucose, reducing the amount absorbed in the gut.
  • Dipeptidyl peptidase-4 (DPP4) inhibitors include alogliptin, linagliptin, saxagliptin and sitagliptin. Also known as gliptins, DPP4 inhibitors have a number of effects, including stimulating pancreatic insulin (by preventing the breakdown of the hormone GLP-1). They may also help with weight loss through an effect on appetite.
  • Sodium-glucose co-transporter 2 (SGLT2) inhibitors include canagliflozin and dapagliflozin. They work by inhibiting the reabsorption of glucose in the kidneys, causing glucose to be excreted in the urine (glycosuria).
  • Meglitinides include repaglinide and nateglinide. They stimulate the release of insulin by the pancreas. Meglitinides are associated with a higher chance of hypoglycemia and must be taken with meals three times a day.

The side effects of above drugs include – flatulence, diarrhea and bloating, urinary infection, nausea and vomiting, weight gain or swelling etc.

Alternative Treatment

Alpha-lipoic acid (ALA) – ALA is a chemical compound that is found in food (especially high in spinach, broccoli, and tomatoes), produced endogenously, and sold as a nutritional supplement. As an antioxidant, ALA may mitigate high levels of oxidative stress, which in patients with diabetes contributes to insulin resistance and secondary complications such as diabetic neuropathy.

Chromium – As an essential mineral, chromium plays an important role in facilitating glucose metabolism.

Coenzyme Q10 – Coenzyme Q10 is a cofactor used in oxidative respiration and is produced endogenously. Supplementation of coenzyme Q10 is especially popular for cardiovascular diseases.

Magnesium – Magnesium is an abundant mineral in the human body involved in numerous biochemical processes, including glucose metabolism.

Omega-3 fatty acid – Omega-3 polyunsaturated fatty acids (PUFAs) are one of the most common dietary supplements taken in the United States.3 Major sources of omega-3 PUFAs include fish, marine-derived supplements, and prescription formulations. Based on multiple studies, high omega-3 PUFA intake does not prevent the onset of type 2 diabetes.

Vanadium – Vanadium is a mineral with no known biological importance or deficiency-associated disease. Although three controlled studies of vanadium for type 2 diabetes reported significant decreases in fasting blood glucose levels, small sample sizes and lack of randomization limit these results.

Ginseng –  The panex genus contains multiple species described as ginseng, with two varieties most frequently used and studied: panex ginseng (Asian ginseng, Chinese ginseng, Korean ginseng) and panex quinquefolius (American ginseng). The root of this herb traditionally has been used in Asia and is one of the most popular botanicals in the United States.

Botanical products and Herbs like Allium sativum (garlic), Aloe vera, Coccinia indica (ivy gourd), Gymnema sylvestre (gymnema), Momordica charantia (bitter melon), Opuntia streptacantha (prickly pear cactus, nopal), Trigonella foenum graecum (fenugreek) are very essential for Diabetes.















February 7, 2017

Cushing syndrome is a rare endocrine disorder caused by the body’s exposure to an excess of the hormone cortisol. Cortisol affects all tissues and organs in the body. These effects together are known as Cushing’s syndrome.

The disorder, which leads to a variety of symptoms and physical abnormalities, is most commonly caused by taking medications containing the hormone over a long period of time. A more rare form of the disorder occurs when the body itself produces an excessive amount of cortisol.

In 1932, a physician named Harvey Cushing described 8 patients with central body obesity, glucose intolerance, hypertension, excess hair growth, osteoporosis, kidney stones, menstrual irregularity, and emotional liability. Hence, the name Cushing’s syndrome.

What leads to Cushing’s Syndrome?

Cortisol is a powerful steroid hormone, and excess cortisol has detrimental effects on many cells throughout the body.  Keep in mind that Cushing’s syndrome is rare, occurring in only about 10 patients per one million. On the other hand, simple obesity can be associated with some of these symptoms in the absence of an adrenal tumor; this is related to the slightly different mechanism by which normally-produced steroids are metabolized by individuals who are obese. Since cortisol production by the adrenal glands is normally under the control of the pituitary, overproduction can be caused by a tumor in the pituitary or within the adrenal glands themselves.

When the adrenal glands develop a tumor, like any other endocrine gland, they usually produce excess amounts of the hormone normally produced by these cells. If the adrenal tumor is composed of cortisol-producing cells, excess cortisol will be produced. Under these conditions, the normal pituitary will sense the excess cortisol and will stop making ACTH in an attempt to slow the adrenal down. In this manner, physicians can readily distinguish whether excess cortisol is the result of a pituitary tumor or an adrenal tumor.

An estimated 10-15 per million people are affected every year.  Pituitary adenomas (Cushing’s disease) account for more than 70 percent of cases in adults and about 60-70 percent of cases in children and adolescents.  Cushing’s syndrome most commonly affects adults ages 20-50 and is more prevalent in females, accounting for about 70 percent of all cases.


Cushing’s syndrome can be caused by overuse of cortisol medication, as seen in the treatment of chronic asthma or rheumatoid arthritis (iatrogenic Cushing’s syndrome), excess production of cortisol from a tumor in the adrenal gland or elsewhere in the body (ectopic Cushing’s syndrome) or a tumor of the pituitary gland secreting adrenocorticotropic hormone (ACTH) which stimulates the over-production of cortisol from the adrenal gland (Cushing’s disease).

Other causes may include –

Pituitary Adenomas – When the cause of excess cortisol is a pituitary adenoma, this is called “Cushing’s disease”. The excess ACTH produced by the pituitary tumor stimulates the adrenal to secrete excess cortisol. Adenomas are benign, or non-cancerous, tumors of the pituitary gland which can secrete increased amounts of ACTH. Women are affected 5 times as often as men.

Adrenal Tumors – Sometimes, an abnormality of the adrenal glands, most often an adrenal tumor, causes Cushing’s syndrome. The average age of onset is about 40 years. Most of these cases involve non-cancerous tumors of adrenal tissue, called adrenal adenomas, which release excess cortisol into the blood.

Ectopic ACTH Syndrome – Some benign or malignant (cancerous) tumors that arise outside the pituitary can produce ACTH, which leads to excess cortisol production by the adrenal glands. This condition is known as ectopic ACTH syndrome. The most common forms of ACTH-producing tumors are carcinoid tumors, which can be benign or malignant and small cell lung cancer, which accounts for about 25 percent of all lung cancer cases.

Adrenocortical carcinomas, or adrenal cancers, are the least common cause of Cushing’s syndrome. Cancer cells can secrete excess levels of several adrenal cortical hormones, including cortisol and adrenal androgens.

Familial Cushing’s Syndrome – Most cases of Cushing’s syndrome are not inherited. Rarely, however, some individuals have special causes of Cushing’s syndrome due to an inherited tendency to develop tumors of one or more endocrine glands. In Primary Pigmented Micronodular Adrenal Disease, children or young adults develop small cortisol-producing tumors of the adrenal glands.


  • Weight gain – particularly around the gut or mid-section
  • “Moon face” – a rounded shape of the face that develops from a specific pattern of fat distribution.
  • Easy bruising – the arms and legs are frequently covered with multiple bruises.
  • “Buffalo hump” – a mound of fat at the base of the back of the neck.
  • Abnormal hair growth – women with Cushing’s syndrome may develop more hair growth on the face or near the belly button.
  • Edema (leg swelling) – due to excess fluid buildup in the lower legs and feet.
  • Stretch marks (purple striae) – most common around the sides and lower abdomen, these may have a pink, red, or purple color.
  • Hypertension (high blood pressure)
  • Diabetes (high blood sugar levels)
  • Mood changes – many patients feel “hyper”, others may experience sudden emotional ups and downs or be quick to anger.
  • Thinning of the skin – the skin may develop a shiny, paper-thin quality and may rip or tear easily.
  • Ruddy complexion (plethora) – a reddening of the face or cheeks.
  • Muscle weakness – the arms and legs may become skinny like twigs from muscle wasting.
  • Menstrual disturbances – a woman’s period may be irregular or stop altogether.

Patients who have too much cortisol but do not have any clear signs or symptoms of hypercortisolism are said to have “subclinical Cushing’s.”


  • Bone loss (osteoporosis), which can result in unusual bone fractures, such as rib fractures and fractures of the bones in the feet
  • High blood pressure (hypertension)
  • Diabetes
  • Frequent or unusual infections
  • Loss of muscle mass and strength


Tumour of the pituitary gland – The tumour is surgically removed. Other options include radiation therapy and drug therapy to shrink the tumour and stop it from producing hormones. Various hormone replacements may be required after pituitary surgery.

Tumour of the adrenal gland – The tumour is surgically removed. Replacement hormone therapy may be necessary for a short while.

ACTHproducing tumours – Treatment includes surgery to remove the tumour, followed possibly by chemotherapy, immunotherapy and radiation therapy. Medication can reduce the ability of the adrenal glands to make cortisol.

MEN1 – Radiation therapy and surgery are used to remove the tumours and associated glands. Ongoing hormone replacement therapy is needed after surgery.

Glucocorticoid hormone therapy – Induced Iatrogenic Cushing’s syndrome – symptoms will gradually resolve if treatment can be reduced or stopped, which depends on the activity of the disorder. Treatment should never be stopped suddenly because of the possibility of adrenal suppression.

Alternative Treatment

Stop exposing the brain and head to strong magnetic or sound vibrations.

DHEA – DHEA may help to protect against the overproduction of cortisol from the adrenal glands and enhance the immune system. This is an important factor since too much cortisol accelerates aging and causes immune system disorders. Studies show that DHEA deficiency may actually debilitate immune status

Vitamin C – Studies show that vitamin C and aspirin can attenuate and influence cortisol, inducing an anti-inflammatory response to prolonged exercise and stress. Vitamin C has been shown to reduce the elevation of cortisol in response to heavy exercise.

Melatonin – Melatonin is secreted by the pineal gland and functions to regulate circadian rhythm and induce sleep. Melatonin circadian secretion in patients with pituitary- or adrenal-dependent Cushing’s syndrome was shown to be significantly lower compared to healthy control groups.

Phosphatidylserine (PS) – Phosphatidylserine is a phospholipid that is a structural component of the biological membranes in animals and plants. In studies, supplemental PS has been shown to improve mood and blunt the release of cortisol in response to physical stress.

Antioxidants – Antioxidants may improve immune functioning. Choosing a wide variety of low-potassium fruits and vegetables may help.

Fiber – A high-fiber diet can help maintain normal blood glucose levels.

Refined starches – Eliminating refined starches, following a consistent carbohydrate diet, and eating five or six small meals a day may help decrease carbohydrate cravings that typically occur with Cushing’s syndrome.

Dandelion – Helps normalize adrenal function. It is also an excellent tonic for the liver and kidneys. Dandelion reduces inflammation in the body and also contains vitamins and minerals necessary for hair growth.


Reference –














February 7, 2017

Coronary artery disease (CHD), also called coronary heart disease, is the leading cause of death in the United States for both men and women.

The heart is a strong muscular pump that is responsible for moving about 3,000 gallons of blood through the body every day. Like other muscles, the heart requires a continuous supply of blood to function properly. The heart muscle gets the blood it needs to do its job from the coronary arteries. CAD is caused by a thickening of the inside walls of the coronary arteries. This thickening is called atherosclerosis. A fatty substance called plaque builds up inside the thickened walls of the arteries, blocking or slowing the flow of blood. Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. Over time, plaque hardens and narrows the arteries, reducing blood flow to your heart muscle. If the heart muscle doesn’t get enough blood to work properly, the person may have angina or a heart attack.

Atherosclerosis is a process that can involve many of the body’s blood vessels with a variety of presentations. When it involves the coronary arteries it results in coronary artery disease, the cerebral arteries; cerebrovascular disease (transient ischemic attack, stroke), the aorta; aortic aneurysms, the ileo-femoral and popliteal arteries; peripheral vascular disease, the mesenteric arteries; intestinal ischemia. Half of all deaths in the developed world and a quarter of deaths in the developing world are due to Cardiovascular Disease which are comprised of hypertension and the diseases caused by atherosclerosis.

Over time, CHD can weaken the heart muscle and lead to heart failure and arrhythmias. Heart failure is a condition in which the heart can’t pump enough blood throughout the body. Arrhythmias are problems with the rate or rhythm of your heartbeat.


Research suggests that CHD starts when certain factors damage the inner layers of the coronary arteries. These factors include smoking, high amounts of certain fats and cholesterol in the blood, high blood pressure, and high amounts of sugar in the blood due to insulin resistance or diabetes.

When damage occurs, the body starts a healing process. This process causes plaque to build up where the arteries are damaged. The buildup of plaque in the coronary arteries may start in childhood. Certain traits, conditions, or habits raise your risk for CHD. These conditions are known as risk factors.

The major risk factors for CHD include:

  • Unhealthy blood cholesterol levels
  • High blood pressure
  • Smoking
  • Insulin resistance
  • Diabetes
  • Overweight or obesity
  • Metabolic syndrome
  • Lack of physical activity
  • Age (as you get older, your risk for CHD increases)
  • Family history of early heart disease Lifestyle changes, medicines, and/or medical procedures can prevent or treat CHD in most people.

African Americans have more severe high blood pressure than Caucasians and therefore have a higher risk of heart disease. Heart disease risk is also higher among Mexican Americans, American Indians, native Hawaiians and some Asian Americans. This is partly due to higher rates of obesity and diabetes in these populations.


The most common symptom of coronary artery disease is angina (also called angina pectoris). Angina is often referred to as chest pain. It is also described as chest discomfort, heaviness, tightness, pressure, aching, burning, numbness, fullness, or squeezing. It can be mistaken for indigestion or heartburn. Angina is usually felt in the chest, but may also be felt in the left shoulder, arms, neck, back or jaw.

Other symptoms that may occur with Coronary Artery disease include –

  • Shortness of breath
  • Palpitations (irregular heartbeats, skipped
  • beats or a “flip-flop” feeling in your chest)
  • A faster heartbeat
  • Dizziness
  • Nausea
  • Extreme weakness
  • Sweating


MedicationsMost people who have CAD take medicine to help control their condition. Medicines called beta-blockers, calcium channel blockers and nitrates can help relieve angina. Taking low-dose aspirin every day can reduce the chance of a second heart attack in people who have already had one. All medicines may have side effects. Aspirin may cause upset stomach. Nitrates may cause a flush (redness in the face) and headaches. Beta-blockers cause tiredness and sexual problems in some patients. Calcium channel blockers may cause constipation and leg swelling.

Surgeries – Angioplasty is a surgical treatment for CAD. Angioplasty uses a tiny balloon to push open blocked arteries around the heart. The balloon is inserted in an artery in the arm or leg. A small metal rod called a stent might be put into the artery where the blockage was to hold the artery open.

Another surgical treatment for CAD is bypass surgery. Pieces of veins or arteries are taken from the legs and sewn into the arteries of the heart to bring blood past a blockage and increase the blood flow to the heart. Bypass surgery is usually done when angioplasty isn’t possible.

Surgery, such as angioplasty or bypass surgery, also has potential risks. The major risks can include heart attack, stroke or even death. These are rare and most patients do well. After angioplasty, you can usually expect to return to your previous activity level, or even a better activity level, within a few days. It takes longer (a few weeks or months) to recover from bypass surgery.

Alternative Treatment

Chelation Therapy – Chelation therapy is a medical treatment commonly used to rid the body of heavy metals, like treating lead or mercury poisoning. Its use in treating heart disease is controversial and questionable. During chelation treatments, an amino acid called EDTA (ethylenediamine tetraacetic acid) is injected. It binds to heavy metals and minerals and leaves through the urine.

Niacin – This B vitamin works in the liver to reduce the fatty acids that form cholesterol. Niacin can help lower low-density lipoprotein (LDL) and triglyceride levels while boosting HDL. Potential side effects include nausea, intense flushing, and liver problems. Niacin should only be taken under a doctor’s supervision since special blood tests are necessary to monitor for liver damage.

Red yeast rice – Researchers have found that this Chinese supplement can lower LDL and triglycerides. Red yeast rice contains monacolin K, which is a statin — a chemical compound that lowers cholesterol. In fact, monacolin K is the principal ingredient in the prescription cholesterol drug lovastatin (Mevacor).

R-Lipoic Acid – R-lipoic acid improves endothelial function by, and the antioxidant also enhanced the benefits of a drug used to treat heart disease.

Curcumin – Curcumin is world-renowned for reducing inflammation and pain. Curcumin is the active ingredient in Turmeric.

Multivitamin – Vitamins help to prevent unnecessary blood clots that can block arteries. It is also necessary to control the amino acid homocysteine which appears to damage artery linings and encourage heart disease. itamin B12 deficiency has been associated with elevated levels of the dangerous homocysteine. Elevated levels of homocysteine, an amino acid produced by the body, can damage the inner surface of arteries. This can be treated and/or prevented with vitamin B12, vitamin B6 and folic acid. Many cardiologists are now using B-vitamins to help prevent coronary artery diseaseFolic Acid – Folic acid helps to control homocysteine, an amino acid that seems to play a major role in clogging the arteries.

Calcium – Calcium is believed to help keep cholesterol under control and may prevent dangerous blood clots. Too much calcium may increase the risk of heart disease, especially if there is much too much calcium in relation to magnesium.

Magnesium – Magnesium deficiency has been linked to an increased risk of CAD, heart attacks and improper heartbeats (ventricular tachyarrhythmias).

Phytosterols – These are found in unrefined vegetable oils, whole grains, nuts, and legumes. Eating foods enriched with at least 0.8 grams of plant sterols or stanols daily can reduce your LDL (bad) cholesterol.

Omega-3 fatty acids, derived from fatty fish, are thought to reduce inflammation in your body. Inflammation is a contributing factor in heart disease. Omega-3 fatty acids may also decrease triglycerides, lower blood pressure, and boost immunity.

Flax and flaxseed oil also contain beneficial omega-3 fatty acids, though studies have not found these sources to be as effective as fish. The shell on raw flaxseeds also contains soluble fiber, which can help lower blood cholesterol.

Selenium – The amount of selenium in the blood and red blood cells may be related to the risk of CHD and heart attacks. Lower the level of selenium, the more the risk. Selenium is an antioxidant that helps to prevent the conversion of LDL into its more artery-damaging, oxidized form. It may also help to “thin” the blood,” minimizing the blood clots and the heart attack.

Co-enzymes – Adequate levels of CoQ10 is necessary for a well functioning system. When the levels of CoQ10 drops below optimum levels, the disease takes over or already had done so. Heart muscle biopsies in patients with various cardiac diseases showed a CoQ10 deficiency in 50-75 percent of the cases. On the corollary, all the well functioning hearts had an adequate amount of CoQ10 in the tissue. When supplemental CoQ10 was introduced into the ailing hearts, they started getting signs of new life. CoQ10 increases oxygenation of heart tissue.


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February 7, 2017

Chelation therapy is a chemical process in which a synthetic solution-EDTA (ethylenediaminetetraacetic acid)-is injected into the bloodstream to remove heavy metals and/or minerals from the body. Chelation means “to grab” or “to bind.” When EDTA is injected into the veins, it “grabs” heavy metals and minerals such as lead, mercury, copper, iron, arsenic, aluminum, and calcium and removes them from the body. Except as a treatment for lead poisoning, chelation therapy is controversial and unproved.

Chelation Therapy is used for following –

  • Memory problems or “brain fog”
  • Heart disease: Angina & chest pains; arrhythmias; heart attack; stroke
  • Hypertension (high blood pressure)
  • Diabetes
  • Heavy metal toxicity
  • Chronic fatigue
  • Fibromyalgia & autoimmune disorders
  • Kidney disease
  • Leg cramps / walking problems
  • Hearing / vision loss
  • Shortness of breath
  • Hormone dysfunction
  • Erectile dysfunction
  • Poor circulation / cold feet and/or hands
  • Slow-healing sores

The word “chelate” is derived from the Greek word for claw and apparently refers to the alleged removal of plaque and calcium deposits from arteries and veins by EDTA. The therapy involves a series of intravenous infusions of the organic chemical ethylenediamine tetra acetic acid (EDTA) and various other substances to cure ailments. These medicines bind to the metals in the blood stream; this metal-chelator compound is then eliminated in the urine. While chelators are valuable drugs, they have side effects which limit their use to only a few medical conditions involving heavy metal toxicity, especially those due to lead, mercury, arsenic, and iron.

Chelation Therapy is used for –

  • Heavy metals such as Lead, Mercury, Cadmium, Arsenic, Nickel, and Antimony have been shown to relentlessly accumulate in human tissue over a lifetime. Aluminum has been implicated as a possible factor in the causation of Alzheimer’s disease. These poisonous metals disrupt the normal biochemical processes. They insinuate themselves into the active sites of enzymes thereby altering such enzymes’ activities, and they initiate “free radical reactions,” which produce noxious chemicals that damage cellular structures such as proteins, cell membranes and DNA. The results at the level of the whole organism are the development of degenerative diseases-arteriosclerosis, arthritis and cancers. The removal of these poison metals with Chelation Therapy is probably a major mechanism by which Chelation normalizes biochemical activity thereby improving circulation and energy.
  • Essential metals such as iron, copper, manganese, and zinc are rearranged in the various body compartments resulting in improved enzyme activity at the cellular level.
  • Calcium deposits are removed from vessels and intracellular membranes leading to increased blood flow and better functioning of the enzyme systems imbedded in those membranes. The result is, again, improved organ function, vitality and energy level.
  • The blood clotting elements known as platelets are made less sticky, reducing clots in the vessels and leading to improved circulation and reduction in the thromboses that occur during heart attacks and strokes.
  • D.T.A. binds trace elements like iron, which are known initiators of “free radical reactions”. These free radical reactions are thought to be the chemical origin of arteriosclerosis, cancer, and inflammations. In general, they are thought to be the cause of aging and its concomitant degenerative processes. With respect to #3 above, realize that a slight increase in the internal diameter of an occluded vessel results in a large increase in blood flow through that artery.

What does it include?

The Chelation agent, E.D.T.A. is administered intravenously in a solution of dilute salt water or in sterile water. Besides the E.D.T.A., the following substances are added to the bottle:

  • Vitamin C — This vitamin acts as an antioxidant and is needed to activate enzymes and assist in connective tissue synthesis and turnover.
  • Magnesium Sulfate — This mineral is added to counteract the effects of low calcium induced by E.D.T.A. and to replace magnesium, which is almost always deficient in the diet and in total body stores. Magnesium is needed to operate most enzyme systems and in particular, to improve heart function.
  • B-Complex Vitamins — These vitamins act as cofactors in all energy transformations in the body.
  • Pyridoxine (Vitamin B6) — This vitamin is needed for most biochemical steps in amino acid metabolism, especially in the processing of the cardiotoxic substance known as homocysteine. Some theories of atherosclerosis hold that abnormal elevations of homocysteine initiate vascular disorders.
  • Hydroxycobalamin (Vitamin B12 — Cyanocobalamin) — This vitamin is needed for brain function, blood formation and in the synthesis of genetic material.
  • Procaine — This substance is added to inhibit burning at the site of infusion.
  • Heparin — This substance is added to prevent vein inflammation.