Monday, December 17, 2007

Diabetic Nephropathy

Diabetic Nephropathy is a complication in which kidneys are damaged due to persistent high blood sugar level in the blood. It is one of the common causes of kidney failure world wide, especially seen in adults.

Kidney functions as a filtering machine for human body by throwing waste out of the body in the form of urine. It maintains electrolyte balance, blood pH level and regulates blood pressure, and also releases some of the hormones. When the kidneys start damaging, they fail to carry out these functions with proficiency. Protein molecules, along with other bodies which are present in the blood, start appearing in the urine. In the initial phase of nephropathy where damage is not too severe, drugs and diet can control the condition. When protein starts leaking in the urine it is called as microalbuminuria, as the condition starts worsening, large amount of protein is thrown in the urine with heavy losses of protein in the body, its macroalbuminiuria. Few easily noticed symptoms of kidney failure are fatigue, decreased appetite, nausea and vomiting. It had been observed that about 30 to 40 % of Type I diabetics, and 20 to 30 % of those with Type 2 diabetes, develop moderate to severe kidney failure.

Diabetic Nephropathy can be screened in simple urine test at any diagnostic laboratories. Type 1 diabetic must check nephropathy test in fourth year of diagnosis, and Type 2 at the time of diagnosis. It is always better to go for routine tests in further years. When it shows albuminiuria, modification of diet, regular exercise, with some medication for blood pressure (an ACE inhibitor or angiotension receptor blocker [ARB]) is generally recommended, even if blood pressure is normal. Patients with elevated blood pressures and albuminuria are treated with an ACE inhibitor or ARB. These medications can reduce the percent of protein extraction in the urine and can slow down the progression of diabetes, nephropathy and related kidney diseases.

Diabetes myonecrosis may develop before or at the time of diagnosis of diabetes, generally it is a type of gangrene caused by Clostridium bacteria. This bacteria produces toxins, which leads to tissue diabetic mastopathy, a condition usually seen in pre-menopausal women, suffering from Type 1 diabetes since many years with insulin therapy. Although very rare, it can be seen in men with diabetes as diabetic mastopathy, which is associated with micro-vascular complications such as damage to the eyes, kidneys and heart, or other disorders such as thyroid problem.

Suggestions for preventing Diabetic Nephropathy

** Maintain blood sugar level within normal range.
** Control blood pressure with modifying diet, relaxation techniques, and medication.
** Decrease intake of salt, fast foods, preserved and baked items to maintain blood pressure.
** Decrease animal protein, simple sugars and animal fats in the diet.
** Check urine regularly for microalbumin.
** Take care of bladder or urinary tract infections and treat them early.

Diabetes Skin Care

Diabetes affects different body parts of a person including skin. The skin disorders can be seen in normal individual too, but diabetics are more frequently prone to it. Fortunately, most of the skin infections can easily be controlled if detected in early stages. Infection can be bacterial, fungal or simple itching. Some of the specific skin infections frequently seen in the diabetes patients are Dermopathy, Necrobiosis lipoidica, Diabeticorum, Xanthomatosis and Blisters.

Diabetes Skin Infections:

Bacterial infections :- Bacterial infections are more commonly seen in the people with diabetes than in a normal individuals. Styes - Infection of glands and eyelids, Boils and hair follicles infections, skin and tissue are affected by carbuncles. These infections are spread by few bacterial germs but the most common out of them is Staphylococcus bacteria.

Fungal infections :- Candida-albicans is the yeast-like fungus, responsible for red sore skin with frequent sense of itching and developing into blisters and scales. These patchy infections usually appears where skin folding with moisture is persisting for long period, like armpits and groin, under the foreskin, under breast, finger and toes-nail (onychomycosis), in the mouth (thrush), in the vagina etc. Some of the known names in fungal infections are athlete's foot, ring worms and jock itch.

Itching :- Itching may result from poor blood circulation, dry skin, or any kind of bacterial and viral infection, mostly observed in lower extremities. Wiping your body till completely dry and using good moisturizing agent are the suggestive steps to manage with simple itching.

Diabetic Dermopathy :- Dermopathy shows skin changes occurring in the people with diabetes due to affected blood vessels (i.e. oval to circular), slightly indented dry brown to purple and scaly patches. When zinc doses are administered for several weeks it appears to help the lesions resolve over several months, especially when combined with near normal blood sugars.

Necrobiosis Lipoidica Diabeticorum :- Necrobiosis Lipodica Diabecicorum (NLD) seems similar to dermopathy, but it is more worst than the later, as it penetrates deeply into the skin, making the spots red with a well defined purple line. See your doctor at right time or else it may crack or break.

Xanthomatosis, Sclerosis and Diabetic blisters :- High blood sugar aggravates these conditions; xanthomatosis is slight yellowish pea like pigmentation in feet, arms, legs, hands, buttocks etc. In sclerosis, skin of toe, forehead, hands becomes thick and waxy, and stiffness in the joints are been observed. Sometimes painless diabetic blisters erupt in the fingers, toes, hands, forehands and feet look like burned sores. These are commonly seen in overweight, type 1 diabetic, and revert back to normal as soon as blood sugar is controlled out.

Disseminated Granuloma Annulare :- Sharp well define ring or arc shape raised area of skin is seen, then it is nothing but disseminated granuloma annulare. The common body parts where it can be seen are on the fingers or ears.

Acanthosis nigricans :- This is the condition, in which brown tanned patches appear in different parts of the body like neck, armpits and groin, hands, elbow and knees. This is usually seen in the people with overweight, especially women are more likely to be caught with this.

Allergic Reactions :- Visible allergic reaction in the area of skin is examined when insulin is injected and, it may develop rashes.

Sunday, December 16, 2007

Diabetic Neuropathy

Diabetic Neuropathy

Nerves depend on multiple tiny vessels that carry nutrients and oxygen to keep each and every segment of these very long nerves intact. Damage to one small segment can result in loss of feeling, pain or burning sensations that bother the foot and leg.

Feet:- Diabetes can decrease blood supply to the foot and gradually damages the nerves which carry sensation. A second micro vascular disease is diabetic foot or diabetic peripheral neuropathy or distal symmetric neuropathy. Neuropathy is the common complication of diabetes, due to high blood sugar, chemical changes occur in the nerves. It always starts in the feet as they are the longest nerves and fed with longest blood vessels of the body. Generally it is seen in the obese people, with high blood sugar levels and age more than 40 years. Neuropathy can develop within a span of first few years and it affects approximately 60% of diabetics.

Signs and symptoms of Diabetic Neuropathy

* Decrease or no sweating i.e. dry scaly skin with callus formation.
* Numbness, tingling, and some sort of burning sensation.
* Weakness and loss of reflexes.
* Decrease sensation to the slight change in temperature.


physical examination. The clinical examination will show the sensation in the feet and determine if it is normal or diminished.

Blood flow may be improved with good sources of vitamin E intake along with blood pressure medicine (ACE inhibitors). Although amputations are common with diabetes, about half can be prevented with simple steps that protect the feet.

Diabetic Retinopathy

Diabetic Retinopathy

The diabetic retinopathy is a type of micro vascular disease in which the micro vessel, supplying blood to the retina of our eye is affected. Retinopathy is related to high blood sugar level and obstructs the flow of oxygen to the cells of the retina. Retina is an ultra thin layer of blood vessel made up of rods and cones. As soon as the retina receives signals of light, it is sent to the brain, and a three dimensional figure is formed and identified, this is sent back to the eye by which we can recognize the things around us. The high blood glucose level hinders its working, and leaves obstacles in passing light through the retina, thus, leading to improper vision.

The early stage of this disease is called non proliferate diabetic retinopathy. The blurred and distorted vision is because of macular edema. Proliferative diabetic retinopathy is the advanced form of diabetic retinopathy; the new blood vessels break, as they are weak and leak blood into vitreous of the eye, which will lead to floating spots in the eye. The pace of damage is not similar in both the eyes; but both the eyes are affected by this disease. Some times one eye is affected more easily than the other. After some period, the swollen and scar nerve tissue of the retina is totally destroyed, and pulls up the entire layer of retina and detaches it from the back of the eye. Retinal detachment is the cause behind blindness among diabetics in middle age. The other two types of eye problems usually seen earlier in the people suffering from diabetes are:

** Cataract :- A thin cloudy layer appears in front of your eye leading to unclear vision. In cataract surgery this thin layer is removed and setting of a plastic layer in front of the lense is done, thus gives you a clear vision again.
** Glaucoma :- Due to high pressure on the optic nerve, it gets damaged. The damaged optic nerve creates disturbance in clear vision. Laser surgery or simple eye drops may help in regaining the normal vision.

A diabetic must regularly go for the regular eye checkup so that the early stages of diabetic retinopathy can be detected and, treated in initial stages itself, with less harm to the eyes. Blood sugar levels should also be monitored and maintained to prevent blood vessel damage.

Diabetes Complications

Complications
Once we have crossed the reversible stage of prediabetes and enter diabetes stage certain changes start developing in our body. These changes occur due to high blood sugar with instability in the hormones as well as blood vessels and nerves. When these changes become permanent in the body it develops into serious Diabetes Complications and body indicates these changes by steady symptoms.

Symptoms of the Diabetes Complications

* Diabetic retinopathy shows symptoms of pain in your eyes and may even result in loss of vision.
* Renal (kidney) disease shows symptoms of swelling (edema) in the feet and legs. It then passes over total body and as the disease progresses, blood pressure also increases.
* Tingling, burning, numbness, tightness, shooting or stabbing pain in the hands, feet or other parts of your body, especially at night. Digestive problems also occur if, the nerves controlling internal organs gets damaged (autonomic neuropathy).
* You may have scanty or profuse sweating, difficulty of sensing when your bladder is full, when there is a low blood sugar, increased sexual problems, weakness, dizziness, and fainting.
* Chest pain (angina) or shortness of breath dizziness or light headache, shoulder or stomach pain, fast heartbeat. You might not show any symptoms until having a heart attack or stroke.


When alarming symptoms given by the body are ignored and the same status is maintained, it starts damaging body organs, such as heart, kidney, eye, feet, and skin. The physiology for each and every affected organ is explained one by one.

Treatment
Women with gestational diabetes have healthy pregnancies and healthy babies if they follow a treatment plan from their health care provider. It needs to keep your blood glucose levels in a target range. Each woman should have a specific plan designed just for her needs, so one can follow these general tips to stay healthy with gestational diabetes:
* Know your blood sugar and keep it under control
* Eat a healthy diet
* Get regular, moderate physical activity
* Keep a healthy weight

Women with gestational diabetes should note down their blood sugar level, physical activity, and everything she eats and drinks, in a daily record book. This can help track how well the treatment is working and what is to be done further to maintain the normal blood sugar level. Some women with gestational diabetes will also need to take insulin, to help manage their diabetes if blood sugar is shooting up in spite of all this. The extra insulin can help lower their blood sugar level.

Gestational Diabetes Test

Gestational Diabetes Test
Depending on your risk factors, your doctor will decide when you need to be checked for diabetes. If you are at high risk, your blood glucose level may be checked at your first prenatal visit. If your test results are normal, you will be checked again sometime between weeks 24 and 28 of your pregnancy.
Depending on your risk and your test results, you may have one or more of the following tests:

Fasting blood glucose or random blood glucose test: When plasma glucose level is >126 mg/dl or when random plasma glucose >200 mg/dl is confirmed on a subsequent day then the woman is at risk to develop GDM. Hence you will be suggested by your doctor to go for some confirmatory tests.

Screening glucose challenge test: It is a preliminary screening test, which is performed between 26-28 weeks. This test will diagnose whether diabetes exists or not by indicating whether or not the body is using glucose. The Glucose Challenge Screening is now considered to be a standard test performed during the second trimester of pregnancy.

Oral glucose tolerance test (OGTT): Women who are considered at risk for gestational diabetes are being asked to go for this test. The glucose challenge is performed by giving 50 grams of glucose drink and then drawing a blood sample one hour later and measuring the level of blood glucose present. Women with a blood sugar level greater than 140 mg/dl may have gestational diabetes, and require a follow up test called a 3-hour oral glucose tolerance test (OGTT).

According to ADA following values are considered to be abnormal for the OGTT:

* Fasting Blood Glucose Level≥95 mg/dl
* 1 Hour Blood Glucose Level≥180 mg/dl
* 2 Hour Blood Glucose Level≥155 mg/dl
* 3 Hour Blood Glucose Level≥140 mg/dl

SYMPTOMS
Often women with gestational diabetes exhibit no symptoms. Screening glucose challenge test is a preliminary screening test performed between 26-28 weeks. However, symptoms of gestational diabetes are similar as Type II diabetes. It includes increased thirst, increased urination, fatigue, nausea and vomiting, bladder and yeast infection, and blurred vision.

Gestational Diabetes – Risk of diabetes in Future:

Gestational diabetes is only temporary phase, it disappears after pregnancy. But once you've had gestational diabetes, your chances are 2 in 3 that it will return in future. It is hard to tell whether the particular woman has diabetes due to gestational diabetes or type 2 diabetes. There seems to be a link between the tendency to have gestational diabetes and type 2 diabetes. Gestational diabetes and type 2 diabetes both involve insulin resistance.

Risk factors for gestational diabetes include:

* Strong family history of type 2 diabetes
* Mother’s age - a woman is at high risk if she is old at the time of pregnancy
* Obesity
* Fallen prey to gestational diabetes in previous pregnancy
* A previous pregnancy that resulted in a child with a birth weight of 9 pounds or more
If you have been diagnosed with prediabetes, impaired glucose tolerance, or impaired fasting glucose

Types

There are 2 types of gestational diabetes:

Type A1: Only diet modification is sufficient to maintain normal glucose levels.
Type A2: Insulin or other medications along with diet are required to maintain normal range of blood glucose.

Gestational diabetes is also classified into different forms of diabetes which existed prior to pregnancy:
* Type B: onset at age 20 or older or with duration of less than 10 years.
* Type C: onset at age 10-19 or duration of 1-19 years.
* Type D: onset before age 10 or duration greater than 20 years.
* Type F: diabetic nephropathy.
* Type R: diabetic retinopathy.
* Type H: diabetes with ischemic heart disease.
* Type T: diabetes requiring kidney transplant
.

Gestational Diabetes

Gestational diabetes is a form of diabetes which affects pregnant women. It is believed that the hormones produced during pregnancy reduce a woman's receptivity to insulin, leading to high blood sugar levels. Gestational diabetes affects about 4% of all pregnant women. It is estimated that about 135,000 cases of gestational diabetes arise in the United States each year.

Hormones involved in development of placenta, which helps the baby to develop also blocks, the action of the mother's insulin in her body. This problem is called insulin resistance. During pregnancy a mother may need up to three times more insulin for glucose to leave the blood and transform to energy. When body is not able to use insulin due to insulin resistance it develops into Gestational Diabetes. Glucose builds up in the blood to high level, it is called hyperglycemia.

Gestational diabetes affects the mother in late pregnancy and the baby too. Insulin does not cross the placenta, as glucose and other nutrients do. Extra blood glucose passes through the placenta that gives the baby a high blood glucose level. It results the baby's pancreas to make extra insulin to get rid of the blood glucose. Since the baby is getting more energy than it needs to develop and grow, the extra energy is stored as fat. It can lead to Macrosomia i.e. “Fat” baby. At birth this fat baby develops problem in breathing or may develop hypoglycemia due to over production of insulin.

Why there is a need to take care of gestational diabetes?

Gestational diabetes can harm you and your baby, so you need to consider about it seriously and start caring at once. The main aim of gestational diabetes treatment is to keep blood glucose levels equal to those of normal pregnant women. It needs a planned meal and scheduled physical activity, even blood glucose testing and insulin injections if required. If gestational diabetes is taken care off properly, reduces the risk of a cesarean section birth that high weight babies may require.

Diabetic Diet Don'ts

Diabetic Diet Don'ts

* Don't fry foods instead bake, broil, poach or saute in nonstick pans. Steam or microwave vegetables. Buy tuna packed in water, not oil
* Eat less high-fat red meat and more low-fat turkey and fish. Avoid organ meats
* Limit the use of condiments such as ketchup, mustard and salad dress ion--they're high in salt and can be high in sugar, too
* Rinse processed foods in water and, wherever possible, choose fresh foods over canned
* Limit your salt (sodium content)
* Read labels carefully. Soy sauce, brine and MSG, for example, contain a lot of sodium
* Don't select ready to eat and junk foods items available to you
* Don't smoke and stop alcohol consumption
* Don't skip meals and medicine times

Diabetic Diet Dos

Diabetic Diet Dos

* For breakfast, take cholesterol-lowering oatmeal
* Have nuts rich in mono unsaturated fat, such as pecans, walnuts, and almonds
* Eat pasta, stews and leafy salads along with beans-- kidney beans, chick peas, and dry beans, navy beans and peas which can reduce LDL "bad"; cholesterol
* Fat free milk, yogurt, and cheese to be taken
* Eggs whites to be included
* White meat chicken and Fish and shellfish (not battered) are good
* Increase intake of dry beans and peas
* Have at least 20 to 25 grams of raw onion daily
* Add wheat bran to your wheat flour (50% wheat flour + 50% wheat bran). This helps increase fiber in your diet
* You can also add flaxseed and methi seeds into the wheat flour
* Increase fiber intake in the form of raw fruits, vegetables, whole cereals etc
* Intake of cinnamon, garlic, onion, karela( bitter gaurd), guar beans is known to considerably reduce blood glucose level

Diabetes Care

Diabetes Care

*Eat food at fixed hours
*Do not overeat
*Do not eat immediately after a workout
*Make sure you have three proper meals & light snacks in between
*Eat about the same amounts of food each day
*Eat your meals and snacks at about the same times each day
*Make sure the gaps between your meals are short
*Do not eat fast; masticate and munch your food well before you swallow
*Drink a lot of water that will help flush the toxins off your system
*Avoid fried foods and sweetmeats
*Include fresh vegetable salad in every meal
*Include sprouts in the diet
*Take your medicines at the same times each day
*Exercise at about the same times each day
*Avoid smoking. Smoking leads to heart disease and poor circulation
*Check your feet for cuts, blisters, and swelling which are likely to result from diabetes-related nerve damage
*Take good sleep daily
*Check your blood sugar level regularly
*Try to stick up to the plan made up for sugar control
*Check the other tests such as kidney function, liver function, heart function, ketone level etc
*Check your weight periodically and maintain ideal body weight

Diet Management During Diabetes

Most items of food contain carbohydrate, protein and fat. Cereals are rich in carbohydrate, lentils, lean meat, chicken and fish are rich in protein, while oils, nuts and milk creams are rich in fat. Fat is rich in calorie, 1g of it provides 9 calories, while 1g carbohydrate or 1g protein give only 4 calories.

Carbohydrate is easily digested than fat and protein. The rise in blood glucose after a meal is due to absorption of glucose form a carbohydrate digestion and increase in production of glucose by liver. Sucrose (can sugar), sweets and syrups cause a rapid rise in blood glucose than whole cereals like ragi and wheat products.

In people with no diabetes, the rise in blood glucose after a meal comes down to the pre-meal level with in 2 hrs. In diabetes, the rise in blood glucose after a meal is not only higher but the fall to pre-meal level is slower (3-4 hrs). Therefore, snacks in between meals or frequent meals at short intervals tend to cause progressive increase in blood glucose in people with diabetes.

Glucose is constantly needed to provide ready energy for the functions of the brain, heart, kidneys, liver and blood cells. When glucose is not available from ingested food, our liver produces from its store of carbohydrate (glycocen) and body stores of fats and proteins. The liver produces about 3 gm of glucose/kg body weight in a day. For example the liver of a man or woman weighing 70 kg produces 200 gm of glucose in a day. The production of glucose by the liver is kept in a check by small amounts of insulin secreted by the pancreas.

These considerations and the modality of your treatment (tablets/insulin) are taken into account for formulating your diet management during diabetes and meal timings. The dietician would give your information on your diet.
The general guidelines on diet are:

In a typical day’s meals and snacks, you should have 1500-1800 calories with – 60% contribution from the carbohydrate, 20% from fat and 20% from proteins. You may need extra weight reduction. If you are on calorie-restricted diet, make sure to take 50-60% of calories as complex carbohydrate (whole cereals) to prevent any feeling of weakness.
You should eat a variety of items of food everyday. Do not skip meals. Avoid snacks, unless you are advised to (example during insulin treatment). Don’t over eat.

* Eat fruits and vegetables. Use less oil in cooking. Eat less, or avoid fried foods, milk cream or food cooked in coconut milk.

* Avoid ready to eat food preparations, sweets and sugary drinks (canned beverages) that provide empty calories (no vitamin or essential minerals).

* Keep a regular check on your weight – maintain this with in the estimated limit.

* Check your hemoglobin and proteins in blood samples at 6 months or 1 year’s interval, Suitable correction in diet format or supplementation may become necessary.

* Despite a good control of blood glucose, if your blood lipids are high, you will need lipid lowering drugs regularly. Some times your doctor may advice you lipid-lowering drugs from the beginning of your diabetes treatment.

* Match your mealtime to the form of insulin and insulin injection schedules as explained by your doctor or the diabetes nurse educated.

Diabetes Diet

Diet Plan For Diabetics

Diet plays a significant role in controlling the diabetes. The diabetic diet may be used alone or else in combination with insulin doses or with oral hypoglycemic drugs. Main objective of diabetic diet is to maintain ideal body weight, by providing adequate nutrition along with normal blood sugar levels in blood. The diet plan for a diabetic is based on height, weight, age, sex, physical activity and nature of diabetes. While planning diet, the dietician has to consider complications such as high blood pressure, high cholesterol levels.

With respect to the above factors, a dietician will assess calories to be given, like scheming the carbohydrates, proteins, fats, type of carbohydrate, amount of fiber and so on.

Exchange meal plan is a diet program which balances the amount of carbohydrate that we intake per day. Glucose is a sugar released from carbohydrate so if we want to control blood sugar we have to limit the consumption of simple carbohydrate. Carbohydrate foods are given as value per portion, known as the exchange. This plan helps us to decide on the type of food to be taken, the amount of food and also the time to eat. You can plan for more flexible meal as you get more knowledge about the diet of a diabetic, may be like the counting carbohydrate meal plan or constant carbohydrate. But there is no common diet that works for everyone. Nor is there any particular diet that works perfectly for any diabetic over a long period. While planning diabetes diet we should adhere to certain important factors, they are as follows:

  • Fiber should be at least 40 gm / day
  • Instead of 3 heavy meals, we should go for 4-5 small mid intervals
  • Replace bakery products and fast foods by simple whole cooked cereals, and don't eat carbohydrates 2 hours before bedtime
  • Consume fresh fruit and vegetables at least 5 exchange/ day

Diabetics must always need to take care of thier diet and also about the food they eat. Care has to be taken because all foods contain not only carbohydrate, but also some energy value. Protein and fat available in the food are converted to glucose in the body. This glucose has some effect on the blood sugar level which has to be taken care. Furthermore there is no need that you have to eat only bland boring diet. Instead you have to eat more fruits, vegetables and whole grains. It means that to select foods that are high in nutrition and low in calories and fat

Read More
What Causes Diabetics
Symptoms

What Causes Diabetes

What Causes Diabetes


The precise Etiology of most cases of diabetes is uncertain, although certain contributing factors are as follows :

Type 1 diabetes

Type 1 Diabetes is autoimmune disease that affects 0.3% on average. It is result of distruction of beta cells due to aggresive nature of cells present in the body. Researchers belive thats some of the Etiology and Risk factors which may trigger type 1 diabetes may be genetic, poor diet (malnutrition) and environment (virus affecting pancreas). Secondly, in most of the cases diabetes occurs because there is abnormal secretion of some hormones in blood which act as antagonists to insulin. Example- Adrenocortical hormone, Adrenaline hormone and Thyroid hormone.

Type 2 diabetes

Type 2 Diabetes, is also called non insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes. It occurs when the body produces enough insulin but cannot utilize it effectively. This type of diabetes usually develops in middle age. A general observation says that about 90-95 % of people with suffering with diabetes are type 2; about 80 percent are overweight. It is more common among people who are older; obese; have a family history of diabetes; have had gestational diabetes. There are number of risk factors found to be responsible for type 2 diabetes, the more the Etiology and Risk factors carried by an individual the higher the risk for developing the diabetes.

Following are the Causes of Diabetes


  • Hereditary or Inherited Traits : It is strongly believed that is due to some genes which passes from one generation to another. It depends upon closeness of blood relationship as mother is diabetes risk is 2 to 3%, father is diabetic risk is more than the previous case and if both the parents are diabetic, it has much greater risk for diabetes.
  • Age : Increased age is a factor which gives more possibility than in younger age. This disease may occur at any age, but 80% of cases occur after 50 year, incidences increase as age do in this group.
  • Poor Diet (Malnutrition Related Diabetes) : Improper nutrition, low protein and fibre intake, high intake of refined products are the expected reasons for developing diabetes.
  • Obesity and Fat Distribution : Being overweight means increased insulin resistance, that is if body fat is more than 30%, BMI 25+, waist grith 35 inches in women or 40 inches in males.
  • Sedentary Lifestyle : People with sedentary lifestyle are more prone to diabetes, when compare to those who exercise thrice a week, are at lesser risk of falling prey to diabetes.
  • Stress : Either physical injury or emotional disturbance is frequently blamed as the initial cause of the disease. Any disturbance in Cortiosteroid or ACTH therapy may lead to clinical signs of the diseases.
  • Drug Induced: Clozapine (Clozaril), olanzapine (Zyprexa), risperidone (Risperdal), quetiapine (Seroquel) and ziprasidone (Geodon) are known to induce this lethal disease.
  • Infection : Some of the strephylococci are suppose to be responsible factor for infection in pancreas.
  • Sex : It is commonly seen in elderly especially males but strong evidence of developing diabetes in females with multiple pregnancy has been observed or in females suffering from (PCOS) Polycystic Ovarian Syndrome.
  • Hypertension : It had been reported in many studies that there is direct relation between high systolic pressure and diabetes.
  • Serum lipids and lipoproteins : High triglyceride and cholesterol level in the blood are related to high blood sugars, in some cases it had been studied that risk are involved even with low HDL levels in circulating blood.

Symptoms of Diabetes

Symptoms of Diabetes
In both the types of diabetes, signs and symptoms are more likely to be similar as the blood sugar is high, either due to less production of insulin, or no production or insulin resistance. In any of the case if there is inadequate glucose in the cells, it can be identified through certain signs and symptoms. These symptoms are quickly relieved once the Diabetes is treated and also reduce the chances of developing serious health problems.

Diabetes Type 1:

In type 1, the pancreas stop producing insulin, due to autuimmune response or possibly viral attack on pancreas. In absence of insulin, body cells does not get glucose for producing ATP (Adenosin Triphosphate) units which results into primary symptom in the form of nausea and vomiting. In latter stage which leads to ketoacidosis in which body starts breaking down muscle tissue and fat for energy, there is consequently fast weight loss. Dehydration is also usually observed due to electrolyte disturbance. In advance stages even coma and death, are being witnessed.

Diabetes Type 2:



  • Increased fatigue : Due to inefficiency of cell to metabolise glucose, reserve fat of body is metabolised to gain energy. When fat is broken down in the body, it uses more energy as compared to glucose, hence body goes in negative calorie effect, which results in fatigue.
  • Polydipsia : As the concentration of glucose increases in the blood, brain receives signal for diluting it and in its counteraction we feel thirsty.
  • Polyuria: Increase in urine production is the result seen when excess of glucose is present in body. Body tries to get rid of the extra sugar in the blood by excreting it through the urine. This can also lead to dehydration because excreting the sugar which carries a large amount of water out of the body along with it.
  • Polyphegia : The hormone insulin is also responsible for stimulating hunger. In order to cope up with high sugar levels in blood, body produces insulin which leads to increased hunger.
  • Weight flactuation : Factors like loss of water (polyuria), glucosuria , metabolism of body fat and protein may lead to loss of weight. Few cases may show weight gain due to increased appetite.
  • Blurry vision : Hyperosmolar hyperglycemia nonketotic syndrome is the condition when body fluid is pulled out of tissues including lenses of eye, which affects the ability of lenses to focus resulting in blurry vision.
    Irritability : It is one of the sign of high blood sugar because of the inefficient supply of glucose to brain and other body organs, which makes us feel tired and uneasy.
  • Infections : Certain signals from the body is given whenever there is fluctuation of blood sugar (due to suppression of immune system) by frequent infections of fungal or bacterial like skin infection or UTI (urinary tract infection).
  • Poor wound healing : High blood sugar resists the flourishing of WBC, (white blood cell) which are responsible for body immune system. When these cells do not function accordingly, wound healing is not at good pace. Secondly, long standing diabetes leads to thickening of blood vessels which may affect proper circulation of blood in different body parts.

General Information

DIABETES MELLITUS

Diabetes mellitus is the common disease seen in the United States n many countries like India. It is estimated that 16 million Americans are already caught with diabetes, and 5.4 million diabetics are not aware of the existing disease. Diabetes prevalence has increased steadily in the last half of this century and will continue rising among U.S. population. It believed to be one of the main criterions for deaths in United States every year. This diabetes information hub tries to project the necessary steps and precautions to be taken, to control and eradicate diabetes completely.

Diabetes is a metabolic disorder where in human body does not produce or properly uses insulin, a hormone that is required to convert sugar, starches, and other food into energy. Diabetes mellitus is characterized by constant high levels of blood glucose (sugar). Human body has to maintain the blood glucose level at a very narrow range, which is done with insulin and glucagon. The function of glucagon is to release glucose from the liver to the blood stream so that, it can be transported to body tissues and cells for the production of energy.

There are three main types of diabetes:



  • Type 1 diabetes
  • Type 2 diabetes
  • Gestational diabetes

Type 1 and Type 2 diabetes impede a person’s carefree life. When breakdown of glucose is stopped completely, body uses fat and protein for producing the energy. Due to this mechanism symptoms like polydipsia, polyuria, polyphegia, and excessive weightloss can be observed in a diabetic. Desired blood sugar of human body should be maintained between 70 mg/dl -110 mg/dl at fasting state. If blood sugar is less than 70 mg/dl, it is termed as hypoglycemia and if more than 110 mg /dl, it’s hyperglycemia.

Diabetes is the primary reason for adult blindness, end-stage renal disease (ESRD), gangrene and amputations. Overweight, lack of exercise, family history and stress increases the likelihood of developing diabetes. When blood sugar level is constantly high it leads to kidney failure, cardiovascular problems and neuropathy. Patients with diabetes are 4 times more likely to have coronary heart disease and stroke. In addition, Gestational diabetes is more dangerous for pregnant women and their fetus.

Having complete diabetes information is very essential as, Diabetes mellitus is not completely curable but can be managed successfully. The control of diabetes mostly depends on the patient and it is his/her responsibility to take care of their diet, exercise and medication. Advances in diabetes research have led to better ways of controlling diabetes and treating its complications. Hence it includes:-

  • New improved Insulin and its therapy, (external and implantable insulin pumps) have advanced well to manage elevated blood sugars without any allergic reactions.

  • Oral hypoglycemic drugs, controls diabetes type 2.

  • New improved blood glucose monitors (new device for self blood glucose monitoring), and hemoglobin A1c laboratory test to measure blood glucose control during previous 3 months.

  • Effective availability of the treatments for affected body organs due to diabetes.

  • Better ways to manage health of the mother and the fetus during the gestational diabetes phase.

Wednesday, December 12, 2007

Prevention

Cancer prevention is defined as active measures to decrease the incidence of cancer. This can be accomplished by avoiding carcinogens or altering their metabolism, pursuing a lifestyle or diet that modifies cancer-causing factors and/or medical intervention (chemoprevention, treatment of pre-malignant lesions). The epidemiological concept of "prevention" is usually defined as either primary prevention, for people who have not been diagnosed with a particular disease, or secondary prevention, aimed at reducing recurrence or complications of a previously diagnosed illness.

Observational epidemiological studies that show associations between risk factors and specific cancers mostly serve to generate hypotheses about potential interventions that could reduce cancer incidence or morbidity. Randomized controlled trials then test whether hypotheses generated by epidemiological trials and laboratory research actually result in reduced cancer incidence and mortality. In many cases, findings from observational epidemiological studies are not confirmed by randomized controlled trials.

Modifiable ("lifestyle") risk factors

Examples of modifiable cancer risk factors include alcohol consumption (associated with increased risk of oral, esophageal, breast, and other cancers), smoking (although 20% of women with lung cancer have never smoked, versus 10% of men[21]), physical inactivity (associated with increased risk of colon, breast, and possibly other cancers), and being overweight (associated with colon, breast, endometrial, and possibly other cancers). Based on epidemiologic evidence, it is now thought that avoiding excessive alcohol consumption may contribute to reductions in risk of certain cancers; however, compared with tobacco exposure, the magnitude of effect is modest or small and the strength of evidence is often weaker. Other lifestyle and environmental factors known to affect cancer risk (either beneficially or detrimentally) include certain sexually transmitted diseases, the use of exogenous hormones, exposure to ionizing radiation and ultraviolet radiation, and certain occupational and chemical exposures.

Every year, at least 200,000 people die worldwide from cancer related to their workplace. [22] Millions of workers run the risk of developing cancers such as lung cancer and mesothelioma from inhaling asbestos fibers and tobacco smoke, or leukemia from exposure to benzene at their workplaces.[22] Currently, most cancer deaths caused by occupational risk factors occur in the developed world.[22] It is estimated that approximately 20,000 cancer deaths and 40,000 new cases of cancer each year in the U.S. are attributable to occupation.[23]

See alcohol and cancer for more on that topic.

Diet

The consensus on diet and cancer is that obesity increases the risk of developing cancer. Particular dietary practices often explain differences in cancer incidence in different countries (e.g. gastric cancer is more common in Japan, while colon cancer is more common in the United States). Studies have shown that immigrants develop the risk of their new country, often within one generation, suggesting a substantial link between diet and cancer.[24] Whether reducing obesity in a population also reduces cancer incidence is unknown.

Despite frequent reports of particular substances (including foods) having a beneficial or detrimental effect on cancer risk, few of these have an established link to cancer. These reports are often based on studies in cultured cell media or animals. Public health recommendations cannot be made on the basis of these studies until they have been validated in an observational (or occasionally a prospective interventional) trial in humans.

Proposed dietary interventions for primary cancer risk reduction generally gain support from epidemiological association studies. Examples of such studies include reports that reduced meat consumption is associated with decreased risk of colon cancer,[25] and reports that consumption of coffee is associated with a reduced risk of liver cancer.[26] Studies have linked consumption of grilled meat to an increased risk of stomach cancer,[27] colon cancer,[28] breast cancer,[29] and pancreatic cancer,[30] a phenomenon which could be due to the presence of carcinogens such as benzopyrene in foods cooked at high temperatures.

A 2005 secondary prevention study showed that consumption of a plant-based diet and lifestyle changes resulted in a reduction in cancer markers in a group of men with prostate cancer who were using no conventional treatments at the time.[31] These results were amplified by a 2006 study in which over 2,400 women were studied, half randomly assigned to a normal diet, the other half assigned to a diet containing less than 20% calories from fat. The women on the low fat diet were found to have a markedly lower risk of breast cancer recurrence, in the interim report of December, 2006.[32]

Vitamins

The concept that cancer can be prevented through vitamin supplementation stems from early observations correlating human disease with vitamin deficiency, such as pernicious anemia with vitamin B12 deficiency, and scurvy with Vitamin C deficiency. This has largely not been proven to be the case with cancer, and vitamin supplementation is largely not proving effective in preventing cancer. The cancer-fighting components of food are also proving to be more numerous and varied than previously understood, so patients are increasingly being advised to consume fresh, unprocessed fruits and vegetables for maximal health benefits.[33]

The Canadian Cancer Society has advised Canadians that the intake of vitamin D has shown a reduction of cancers by close to 60%,[34] and at least one study has shown a specific benefit for this vitamin in preventing colon cancer.[35]

Vitamin D and its protective effect against cancer has been contrasted with the risk of malignancy from sun exposure. Since exposure to the sun enhances natural human production of vitamin D, some cancer researchers have argued that the potential deleterious malignant effects of sun exposure are far outweighed by the cancer-preventing effects of extra vitamin D synthesis in sun-exposed skin. In 2002, Dr. William B. Grant claimed that 23,800 premature cancer deaths occur in the US annually due to insufficient UVB exposure (apparently via vitamin D deficiency).[36] This is higher than 8,800 deaths occurred from melanoma or squamous cell carcinoma, so the overall effect of sun exposure might be beneficial. Another research group[37][38] estimates that 50,000–63,000 individuals in the United States and 19,000 - 25,000 in the UK die prematurely from cancer annually due to insufficient vitamin D.

The case of beta-carotene provides an example of the importance of randomized clinical trials. Epidemiologists studying both diet and serum levels observed that high levels of beta-carotene, a precursor to vitamin A, were associated with a protective effect, reducing the risk of cancer. This effect was particularly strong in lung cancer. This hypothesis led to a series of large randomized clinical trials conducted in both Finland and the United States (CARET study) during the 1980s and 1990s. This study provided about 80,000 smokers or former smokers with daily supplements of beta-carotene or placebos. Contrary to expectation, these tests found no benefit of beta-carotene supplementation in reducing lung cancer incidence and mortality. In fact, the risk of lung cancer was slightly, but not significantly, increased by beta-carotene, leading to an early termination of the study.[39]

Results reported in the Journal of the American Medical Association (JAMA) in 2007 indicate that folic acid supplementation is not effective in preventing colon cancer, and folate consumers may be more likely to form colon polyps.[40]

Chemoprevention

The concept that medications could be used to prevent cancer is an attractive one, and many high-quality clinical trials support the use of such chemoprevention in defined circumstances.

Daily use of tamoxifen, a selective estrogen receptor modulator (SERM), typically for 5 years, has been demonstrated to reduce the risk of developing breast cancer in high-risk women by about 50%. A recent study reported that the selective estrogen receptor modulator raloxifene has similar benefits to tamoxifen in preventing breast cancer in high-risk women, with a more favorable side effect profile.[41]

Raloxifene is a SERM like tamoxifen; it has been shown (in the STAR trial) to reduce the risk of breast cancer in high-risk women equally as well as tamoxifen. In this trial, which studied almost 20,000 women, raloxifene had fewer side effects than tamoxifen, though it did permit more DCIS to form.[41]

Finasteride, a 5-alpha-reductase inhibitor, has been shown to lower the risk of prostate cancer, though it seems to mostly prevent low-grade tumors.[42] The effect of COX-2 inhibitors such as rofecoxib and celecoxib upon the risk of colon polyps have been studied in familial adenomatous polyposis patients[43] and in the general population.[44][45] In both groups, there were significant reductions in colon polyp incidence, but this came at the price of increased cardiovascular toxicity.

Genetic testing

Genetic testing for high-risk individuals is already available for certain cancer-related genetic mutations. Carriers of genetic mutations that increase risk for cancer incidence can undergo enhanced surveillance, chemoprevention, or risk-reducing surgery. Early identification of inherited genetic risk for cancer, along with cancer-preventing interventions such as surgery or enhanced surveillance, can be lifesaving for high-risk individuals.

Vaccination

Considerable research effort is now devoted to the development of vaccines to prevent infection by oncogenic infectious agents, as well as to mount an immune response against cancer-specific epitopes) and to potential venues for gene therapy for individuals with genetic mutations or polymorphisms that put them at high risk of cancer.

As reported above, a preventive human papillomavirus vaccine exists that targets certain sexually transmitted strains of human papillomavirus that are associated with the development of cervical cancer and genital warts. The only two HPV vaccines on the market as of October 2007 are Gardasil and Cervarix.

Screening

Cancer screening is an attempt to detect unsuspected cancers in an asymptomatic population. Screening tests suitable for large numbers of healthy people must be relatively affordable, safe, noninvasive procedures with acceptably low rates of false positive results. If signs of cancer are detected, more definitive and invasive follow up tests are performed to confirm the diagnosis.

Screening for cancer can lead to earlier diagnosis in specific cases. Early diagnosis may lead to extended life, but may also falsely prolong the lead time to death through lead time bias or length time bias.

A number of different screening tests have been developed for different malignancies. Breast cancer screening can be done by breast self-examination, though this approach was discredited by a 2005 study in over 300,000 Chinese women. Screening for breast cancer with mammograms has been shown to reduce the average stage of diagnosis of breast cancer in a population. Stage of diagnosis in a country has been shown to decrease within ten years of introduction of mammographic screening programs. Colorectal cancer can be detected through fecal occult blood testing and colonoscopy, which reduces both colon cancer incidence and mortality, presumably through the detection and removal of pre-malignant polyps. Similarly, cervical cytology testing (using the Pap smear) leads to the identification and excision of precancerous lesions. Over time, such testing has been followed by a dramatic reduction of cervical cancer incidence and mortality. Testicular self-examination is recommended for men beginning at the age of 15 years to detect testicular cancer. Prostate cancer can be screened using a digital rectal exam along with prostate specific antigen (PSA) blood testing, though some authorities (such as the US Preventive Services Task Force) recommend against routinely screening all men.

Screening for cancer is controversial in cases when it is not yet known if the test actually saves lives. The controversy arises when it is not clear if the benefits of screening outweigh the risks of follow-up diagnostic tests and cancer treatments. For example: when screening for prostate cancer, the PSA test may detect small cancers that would never become life threatening, but once detected will lead to treatment. This situation, called overdiagnosis, puts men at risk for complications from unnecessary treatment such as surgery or radiation. Follow up procedures used to diagnose prostate cancer (prostate biopsy) may cause side effects, including bleeding and infection. Prostate cancer treatment may cause incontinence (inability to control urine flow) and erectile dysfunction (erections inadequate for intercourse). Similarly, for breast cancer, there have recently been criticisms that breast screening programs in some countries cause more problems than they solve. This is because screening of women in the general population will result in a large number of women with false positive results which require extensive follow-up investigations to exclude cancer, leading to having a high number-to-treat (or number-to-screen) to prevent or catch a single case of breast cancer early.

Cervical cancer screening via the Pap smear has the best cost-benefit profile of all the forms of cancer screening from a public health perspective as, being largely caused by a virus, it has clear risk factors (sexual contact), and the natural progression of cervical cancer is that it normally spreads slowly over a number of years therefore giving more time for the screening program to catch it early. Moreover, the test itself is easy to perform and relatively cheap.

For these reasons, it is important that the benefits and risks of diagnostic procedures and treatment be taken into account when considering whether to undertake cancer screening.

Use of medical imaging to search for cancer in people without clear symptoms is similarly marred with problems. There is a significant risk of detection of what has been recently called an incidentaloma - a benign lesion that may be interpreted as a malignancy and be subjected to potentially dangerous investigations. Recent studies of CT scan-based screening for lung cancer in smokers have had equivocal results, and systematic screening is not recommended as of July 2007. Randomized clinical trials of plain-film chest X-rays to screen for lung cancer in smokers have shown no benefit for this approach.

Canine cancer detection has shown promise, but is still in the early stages of research.

Epidemiology

The risk of cancer rises with age

Cancer epidemiology is the study of the incidence of cancer as a way to infer possible trends and causes. The first such cause of cancer was identified by British surgeon Percivall Pott, who discovered in 1775 that cancer of the scrotum was a common disease among chimney sweeps. The work of other individual physicians led to various insights, but when physicians started working together they could make firmer conclusions.

A founding paper of this discipline was the work of Janet Lane-Claypon, who published a comparative study in 1926 of 500 breast cancer cases and 500 control patients of the same background and lifestyle for the British Ministry of Health. Her ground-breaking work on cancer epidemiology was carried on by Richard Doll and Austin Bradford Hill, who published "Lung Cancer and Other Causes of Death In Relation to Smoking. A Second Report on the Mortality of British Doctors" followed in 1956 (otherwise known as the British doctors study). Richard Doll left the London Medical Research Center (MRC), to start the Oxford unit for Cancer epidemiology in 1968. With the use of computers, the unit was the first to compile large amounts of cancer data. Modern epidemiological methods are closely linked to current concepts of disease and public health policy. Over the past 50 years, great efforts have been spent on gathering data across medical practise, hospital, provincial, state, and even country boundaries, as a way to study the interdependence of environmental and cultural factors on cancer incidence.

Cancer epidemiology must contend with problems of lead time bias and length time bias. Lead time bias is the concept that early diagnosis may artificially inflate the survival statistics of a cancer, without really improving the natural history of the disease. Length time bias is the concept that slower growing, more indolent tumors are more likely to be diagnosed by screening tests, but improvements in diagnosing more cases of indolent cancer may not translate into better patient outcomes after the implementation of screening programs. A similar epidemiological concern is overdiagnosis, the tendency of screening tests to diagnose diseases that may not actually impact the patient's longevity. This problem especially applies to prostate cancer and PSA screening.[46]

Some cancer researchers have argued that negative cancer clinical trials lack sufficient statistical power to discover a benefit to treatment. This may be due to fewer patients enrolled in the study than originally planned.[47]

State and regional cancer registries are organizations that abstract clinical data about cancer from patient medical records. These institutions provide information to state and national public health groups to help track trends in cancer diagnosis and treatment. One of the largest and most important cancer registries is SEER, administered by the US Federal government.[48] Health information privacy concerns have led to the restricted use of cancer registry data in the United States Department of Veterans Affairs[49][50][51] and other institutions.[52]

In some Western countries, such as the USA,[3] and the UK[53] cancer is overtaking cardiovascular disease as the leading cause of death. In many Third World countries cancer incidence (insofar as this can be measured) appears much lower, most likely because of the higher death rates due to infectious disease or injury. With the increased control over malaria and tuberculosis in some Third World countries, incidence of cancer is expected to rise; this is termed the epidemiologic transition in epidemiological terminology.

Cancer epidemiology closely mirrors risk factor spread in various countries. Hepatocellular carcinoma (liver cancer) is rare in the West but is the main cancer in China and neighbouring countries, most likely due to the endemic presence of hepatitis B and aflatoxin in that population. Similarly, with tobacco smoking becoming more common in various Third World countries, lung cancer incidence has increased in a parallel fashion.

Pathophysiology


Pathophysiology

Cancers are caused by a series of mutations. Each mutation alters the behavior of the cell somewhat.

Cancer is fundamentally a disease of regulation of tissue growth. In order for a normal cell to transform into a cancer cell, genes which regulate cell growth and differentiation must be altered. Genetic changes can occur at many levels, from gain or loss of entire chromosomes to a mutation affecting a single DNA nucleotide. There are two broad categories of genes which are affected by these changes. Oncogenes may be normal genes which are expressed at inappropriately high levels, or altered genes which have novel properties. In either case, expression of these genes promotes the malignant phenotype of cancer cells. Tumor suppressor genes are genes which inhibit cell division, survival, or other properties of cancer cells. Tumor suppressor genes are often disabled by cancer-promoting genetic changes. Typically, changes in many genes are required to transform a normal cell into a cancer cell.

There is a diverse classification scheme for the various genomic changes which may contribute to the generation of cancer cells. Most of these changes are mutations, or changes in the nucleotide sequence of genomic DNA. Aneuploidy, the presence of an abnormal number of chromosomes, is one genomic change which is not a mutation, and may involve either gain or loss of one or more chromosomes through errors in mitosis.

Large-scale mutations involve the deletion or gain of a portion of a chromosome. Genomic amplification occurs when a cell gains many copies (often 20 or more) of a small chromosomal locus, usually containing one or more oncogenes and adjacent genetic material. Translocation occurs when two separate chromosomal regions become abnormally fused, often at a characteristic location. A well-known example of this is the Philadelphia chromosome, or translocation of chromosomes 9 and 22, which occurs in chronic myelogenous leukemia, and results in production of the BCR-abl fusion protein, an oncogenic tyrosine kinase.

Small-scale mutations include point mutations, deletions, and insertions, which may occur in the promoter of a gene and affect its expression, or may occur in the gene's coding sequence and alter the function or stability of its protein product. Disruption of a single gene may also result from integration of genomic material from a DNA virus or retrovirus, and such an event may also result in the expression of viral oncogenes in the affected cell and its descendants.

Epigenetics

Epigenetics is the study of the regulation of gene expression through chemical, non-mutational changes in DNA structure. The theory of epigenetics in cancer pathogenesis is that non-mutational changes to DNA can lead to alterations in gene expression. Normally, oncogenes are silent, for example, because of DNA methylation. Loss of that methylation can induce the aberrant expression of oncogenes, leading to cancer pathogenesis. Known mechanisms of epigenetic change include DNA methylation, and methylation or acetylation of histone proteins bound to chromosomal DNA at specific locations. Classes of medications, known as HDAC inhibitors and DNA methyltransferase inhibitors, can re-regulate the epigenetic signaling in the cancer cell.

Oncogenes

Oncogenes promote cell growth through a variety of ways. Many can produce hormones, a "chemical messenger" between cells which encourage mitosis, the effect of which depends on the signal transduction of the receiving tissue or cells. In other words, when a hormone receptor on a recipient cell is stimulated, the signal is conducted from the surface of the cell to the cell nucleus to effect some change in gene transcription regulation at the nuclear level. Some oncogenes are part of the signal transduction system itself, or the signal receptors in cells and tissues themselves, thus controlling the sensitivity to such hormones. Oncogenes often produce mitogens, or are involved in transcription of DNA in protein synthesis, which creates the proteins and enzymes responsible for producing the products and biochemicals cells use and interact with.

Mutations in proto-oncogenes, which are the normally quiescent counterparts of oncogenes, can modify their expression and function, increasing the amount or activity of the product protein. When this happens, the proto-oncogenes become oncogenes, and this transition upsets the normal balance of cell cycle regulation in the cell, making uncontrolled growth possible. The chance of cancer cannot be reduced by removing proto-oncogenes from the genome, even if this were possible, as they are critical for growth, repair and homeostasis of the organism. It is only when they become mutated that the signals for growth become excessive.

One of the first oncogenes to be defined in cancer research is the ras oncogene. Mutations in the Ras family of proto-oncogenes (comprising H-Ras, N-Ras and K-Ras) are very common, being found in 20% to 30% of all human tumours.[15] Ras was originally identified in the Harvey sarcoma virus genome, and researchers were surprised that not only was this gene present in the human genome but that, when ligated to a stimulating control element, could induce cancers in cell line cultures.[16]

Tumor suppressor genes

Tumor suppressor genes code for anti-proliferation signals and proteins that suppress mitosis and cell growth. Generally, tumor suppressors are transcription factors that are activated by cellular stress or DNA damage. Often DNA damage will cause the presence of free-floating genetic material as well as other signs, and will trigger enzymes and pathways which lead to the activation of tumor suppressor genes. The functions of such genes is to arrest the progression of the cell cycle in order to carry out DNA repair, preventing mutations from being passed on to daughter cells. The p53 protein, one of the most important studied tumor suppressor gene, is a transcription factor activated by many cellular stressors including hypoxia and ultraviolet radiation damage.

Despite nearly half of all cancers possibly involving alterations in p53, its tumor suppressor function is poorly understood. p53 clearly has two functions: one a nuclear role as a transcription factor, and the other a cytoplasmic role in regulating the cell cycle, cell division, and apoptosis.

The Warburg hypothesis is the preferential use of glycolysis for energy to sustain cancer growth. p53 has been shown to regulate the shift from the respiratory to the glycolytic pathway.[17]

However, a mutation can damage the tumor suppressor gene itself, or the signal pathway which activates it, "switching it off". The invariable consequence of this is that DNA repair is hindered or inhibited: DNA damage accumulates without repair, inevitably leading to cancer.

Mutations of tumor suppressor genes that occur in germline cells are passed along to offspring, and increase the likelihood for cancer diagnoses in subsequent generations. Members of these families have increased incidence and decreased latency of multiple tumors. The tumor types are typical for each type of tumor suppressor gene mutation, with some mutations causing particular cancers, and other mutations causing others. The mode of inheritance of mutant tumor suppressors is that an affected member inherits a defective copy from one parent, and a normal copy from the other. For instance, individuals who inherit one mutant p53 allele (and are therefore heterozygous for mutated p53) can develop melanomas and pancreatic cancer, known as Li-Fraumeni syndrome. Other inherited tumor suppressor gene syndromes include Rb mutations, linked to retinoblastoma, and APC gene mutations, linked to adenopolyposis colon cancer. Adenopolyposis colon cancer is associated with thousands of polyps in colon while young, leading to colon cancer at a relatively early age. Finally, inherited mutations in BRCA1 and BRCA2 lead to early onset of breast cancer.

Development of cancer was proposed in 1971 to depend on at least two mutational events. In what became known as the Knudson two-hit hypothesis, an inherited, germ-line mutation in a tumor suppressor gene would only cause cancer if another mutation event occurred later in the organism's life, inactivating the other allele of that tumor suppressor gene.[18]

Usually, oncogenes are dominant, as they contain gain-of-function mutations, while mutated tumor suppressors are recessive, as they contain loss-of-function mutations. Each cell has two copies of the same gene, one from each parent, and under most cases gain of function mutations in just one copy of a particular proto-oncogene is enough to make that gene a true oncogene. On the other hand, loss of function mutations need to happen in both copies of a tumor suppressor gene to render that gene completely non-functional. However, cases exist in which one mutated copy of a tumor suppressor gene can render the other, wild-type copy non-functional. This phenomenon is called the dominant negative effect and is observed in many p53 mutations.

Knudson’s two hit model has recently been challenged by several investigators. Inactivation of one allele of some tumor suppressor genes is sufficient to cause tumors. This phenomenon is called haploinsufficiency and has been demonstrated by a number of experimental approaches. Tumors caused by haploinsufficiency usually have a later age of onset when compared with those by a two hit process.[19]

Cancer cell biology

Tissue can be organized in a continuous spectrum from normal to cancer.

Often, the multiple genetic changes which result in cancer may take many years to accumulate. During this time, the biological behavior of the pre-malignant cells slowly change from the properties of normal cells to cancer-like properties. Pre-malignant tissue can have a distinctive appearance under the microscope. Among the distinguishing traits are an increased number of dividing cells, variation in nuclear size and shape, variation in cell size and shape, loss of specialized cell features, and loss of normal tissue organization. Dysplasia is an abnormal type of excessive cell proliferation characterized by loss of normal tissue arrangement and cell structure in pre-malignant cells. These early neoplastic changes must be distinguished from hyperplasia, a reversible increase in cell division caused by an external stimulus, such as a hormonal imbalance or chronic irritation.

The most severe cases of dysplasia are referred to as "carcinoma in situ." In Latin, the term "in situ" means "in place", so carcinoma in situ refers to an uncontrolled growth of cells that remains in the original location and has not shown invasion into other tissues. Nevertheless, carcinoma in situ may develop into an invasive malignancy and is usually removed surgically, if possible.

Clonal evolution

The process of malignancy can be explained from an evolutionary perspective. Millions of years of biological evolution insure that the cellular metabolic changes that enable cancer to grow occur only very rarely. Most changes in cellular metabolism that allow cells to grow in a disorderly fashion lead to cell death. Cancer cells undergo a process analogous to natural selection, in that the few cells with new genetic changes that enhance their survival continue to multiply, and soon come to dominate the growing tumor, as cells with less favorable genetic change are outcompeted. This process is called clonal evolution. Tumors often continue to evolve in response to chemotherapy treatments, and on occasion aberrant cells may acquire resistance to particular anti-cancer pharmaceuticals.

Biological properties of cancer cells

In a 2000 article by Hanahan and Weinberg, the biological properties of malignant tumor cells were summarized as follows:[20]
Acquisition of self-sufficiency in growth signals, leading to unchecked growth.
Loss of sensitivity to anti-growth signals, also leading to unchecked growth.
Loss of capacity for apoptosis, in order to allow growth despite genetic errors and external anti-growth signals.
Loss of capacity for senescence, leading to limitless replicative potential (immortality)
Acquisition of sustained angiogenesis, allowing the tumor to grow beyond the limitations of passive nutrient diffusion.
Acquisition of ability to invade neighbouring tissues, the defining property of invasive carcinoma.
Acquisition of ability to build metastases at distant sites, the classical property of malignant tumors (carcinomas or others).

The completion of these multiple steps would be a very rare event without :
Loss of capacity to repair genetic errors, leading to an increased mutation rate (genomic instability), thus accelerating all the other changes.

These biological changes are classical in carcinomas; other malignant tumor may not need all to achieve them all. For example, tissue invasion and displacement to distant sites are normal properties of leukocytes; these steps are not needed in the development of Leukemia. The different steps do not necessarily represent individual mutations. For example, inactivation of a single gene, coding for the P53 protein, will cause genomic instability, evasion of apoptosis and increased angiogenesis.

Causes

Causes



Cancer is a diverse class of diseases which differ widely in their causes and biology. The common thread in all known cancers is the acquisition of abnormalities in the genetic material of the cancer cell and its progeny. Research into the pathogenesis of cancer can be divided into three broad areas of focus. The first area of research focuses on the agents and events which cause or facilitate genetic changes in cells destined to become cancer. Second, it is important to uncover the precise nature of the genetic damage, and the genes which are affected by it. The third focus is on the consequences of those genetic changes on the biology of the cell, both in generating the defining properties of a cancer cell, and in facilitating additional genetic events, leading to further progression of the cancer.

The Main Causes

  • Chemical carcinogens
  • Ionizing radiation
  • Infectious diseases
  • Hormonal imbalances
  • Immune system dysfunction
  • Heredity
  • Other causes.


Chemical carcinogens

Cancer pathogenesis is traceable back to DNA mutations that impact cell growth and metastasis. Substances that cause DNA mutations are known as mutagens, and mutagens that cause cancers are known as carcinogens. Particular substances have been linked to specific types of cancer. Tobacco smoking is associated with lung cancer and bladder cancer. Prolonged exposure to asbestos fibers is associated with mesothelioma.

Many mutagens are also carcinogens, but some carcinogens are not mutagens. Alcohol is an example of a chemical carcinogen that is not a mutagen. Such chemicals are thought to promote cancers through their stimulating effect on the rate of cell mitosis. Faster rates of mitosis leaves less time for repair enzymes to repair damaged DNA during DNA replication, increasing the likelihood of a genetic mistake. A mistake made during mitosis can lead to the daughter cells receiving the wrong number of chromosomes (see aneuploidy above).

The incidence of lung cancer is highly correlated with smoking. Source:NIH.

Decades of research have demonstrated the strong association between tobacco use and cancers of many sites, making it perhaps the most important human carcinogen. Hundreds of epidemiological studies have confirmed this association. Further support comes from the fact that lung cancer death rates in the United States have mirrored smoking patterns, with increases in smoking followed by dramatic increases in lung cancer death rates and, more recently, decreases in smoking followed by decreases in lung cancer death rates in men.

Ionizing radiation

Sources of ionizing radiation, such as radon gas, can cause cancer. Prolonged exposure to ultraviolet radiation from the sun can lead to melanoma and other skin malignancies.

Infectious diseases

Furthermore, many cancers originate from a viral infection; this is especially true in animals such as birds, but also in humans, as viruses are responsible for 15% of human cancers worldwide. The main viruses associated with human cancers are human papillomavirus, hepatitis B and hepatitis C virus, Epstein-Barr virus, and human T-lymphotropic virus. Experimental and epidemiological data imply a causative role for viruses and they appear to be the second most important risk factor for cancer development in humans, exceeded only by tobacco usage.[10] The mode of virally-induced tumors can be divided into two, acutely-transforming or slowly-transforming. In acutely transforming viruses, the viral particles carry a gene that encodes for an overactive oncogene called viral-oncogene (v-onc), and the infected cell is transformed as soon as v-onc is expressed. In contrast, in slowly-transforming viruses, the virus genome is inserted, especially as viral genome insertion is an obligatory part of retroviruses, near a proto-oncogene in the host genome. The viral promoter or other transcription regulation elements in turn cause overexpression of that proto-oncogene, which in turn induces uncontrolled cellular proliferation. Because viral genome insertion is not specific to proto-oncogenes and the chance of insertion near that proto-oncogene is low, slowly-transforming viruses have very long tumor latency compared to acutely-transforming viruses, which already carry the viral oncogene.

Hepatitis viruses, including hepatitis B and hepatitis C, can induce a chronic viral infection that leads to liver cancer in 0.47% of hepatitis B patients per year (especially in Asia, less so in North America), and in 1.4% of hepatitis C carriers per year. Liver cirrhosis, whether from chronic viral hepatitis infection or alcoholism, is associated with the development of liver cancer, and the combination of cirrhosis and viral hepatitis presents the highest risk of liver cancer development. Worldwide, liver cancer is one of the most common, and most deadly, cancers due to a huge burden of viral hepatitis transmission and disease.

Advances in cancer research have made a vaccine designed to prevent cancer available. In 2006, the US FDA approved a human papilloma virus vaccine, called Gardasil®. The vaccine protects against four HPV types, which together cause 70% of cervical cancers and 90% of genital warts. In March 2007, the US CDC Advisory Committee on Immunization Practices (ACIP) officially recommended that females aged 11-12 receive the vaccine, and indicated that females as young as age 9 and as old as age 26 are also candidates for immunization.

In addition to viruses, researchers have noted a connection between bacteria and certain cancers. The most prominent example is the link between chronic infection of the wall of the stomach with Helicobacter pylori and gastric cancer.[11]

Hormonal imbalances

Some hormones can act in a similar manner to non-mutagenic carcinogens in that they may stimulate excessive cell growth. A well-established example is the role of hyperestrogenic states in promoting endometrial cancer.

Immune system dysfunction

HIV is associated with a number of malignancies, including Kaposi's sarcoma, non-Hodgkin's lymphoma, and HPV-associated malignancies such as anal cancer and cervical cancer. AIDS-defining illnesses have long included these diagnoses. The increased incidence of malignancies in HIV patients points to the breakdown of immune surveillance as a possible etiology of cancer.[12] Certain other immune deficiency states (e.g. common variable immunodeficiency and IgA deficiency) are also associated with increased risk of malignancy.[13]

Heredity

Most forms of cancer are "sporadic", and have no basis in heredity. There are, however, a number of recognised syndromes of cancer with a hereditary component, often a defective tumor suppressor allele. Famous examples are:
certain inherited mutations in the genes BRCA1 and BRCA2 are associated with an elevated risk of breast cancer and ovarian cancer
tumors of various endocrine organs in multiple endocrine neoplasia (MEN types 1, 2a, 2b)
Li-Fraumeni syndrome (various tumors such as osteosarcoma, breast cancer, soft tissue sarcoma, brain tumors) due to mutations of p53
Turcot syndrome (brain tumors and colonic polyposis)
Familial adenomatous polyposis an inherited mutation of the APC gene that leads to early onset of colon carcinoma.
Hereditary nonpolyposis colorectal cancer (HNPCC, also known as Lynch syndrome) can include familial cases of colon cancer, uterine cancer, gastric cancer, and ovarian cancer, without a preponderance of colon polyps.
Retinoblastoma, when occurring in young children, is due to a hereditary mutation in the retinoblastoma gene.
Down syndrome patients, who have an extra chromosome 21, are known to develop malignancies such as leukemia and testicular cancer, though the reasons for this difference are not well understood.

Other causes

A few types of cancer in non-humans have been found to be caused by the tumor cells themselves. This phenomenon is seen in Sticker's sarcoma, also known as canine transmissible venereal tumor.[14] The closest known analogue to this in humans is individuals who have developed cancer from tumors hiding inside organ transplants

Treatment

Treatment


Cancer can be treated by surgery, chemotherapy, radiation therapy, immunotherapy, monoclonal antibody therapy or other methods. The choice of therapy depends upon the location and grade of the tumor and the stage of the disease, as well as the general state of the patient (performance status). A number of experimental cancer treatments are also under development.

Complete removal of the cancer without damage to the rest of the body is the goal of treatment. Sometimes this can be accomplished by surgery, but the propensity of cancers to invade adjacent tissue or to spread to distant sites by microscopic metastasis often limits its effectiveness. The effectiveness of chemotherapy is often limited by toxicity to other tissues in the body. Radiation can also cause damage to normal tissue.

Because "cancer" refers to a class of diseases, it is unlikely that there will ever be a single "cure for cancer" any more than there will be a single treatment for all infectious diseases.

Main Treatment Strategies are

  • Surgery
  • Radiation Therapy
  • Chemotherapy
  • Targeted Therapies
  • Immuno Therapy
  • Hormonal Therapy


Surgery

In theory, cancers can be cured if entirely removed by surgery, but this is not always possible. When the cancer has metastasized to other sites in the body prior to surgery, complete surgical excision is usually impossible. In the Halstedian model of cancer progression, tumors grow locally, then spread to the lymph nodes, then to the rest of the body. This has given rise to the popularity of local-only treatments such as surgery for small cancers. Even small localized tumors are increasingly recognized as possessing metastatic potential.

Examples of surgical procedures for cancer include mastectomy for breast cancer and prostatectomy for prostate cancer. The goal of the surgery can be either the removal of only the tumor, or the entire organ. A single cancer cell is invisible to the naked eye but can regrow into a new tumor, a process called recurrence. For this reason, the pathologist will examine the surgical specimen to determine if a margin of healthy tissue is present, thus decreasing the chance that microscopic cancer cells are left in the patient.

In addition to removal of the primary tumor, surgery is often necessary for staging, e.g. determining the extent of the disease and whether it has metastasized to regional lymph nodes. Staging is a major determinant of prognosis and of the need for adjuvant therapy.

Occasionally, surgery is necessary to control symptoms, such as spinal cord compression or bowel obstruction. This is referred to as palliative treatment.

Radiation therapy


Radiation therapy (also called radiotherapy, X-ray therapy, or irradiation) is the use of ionizing radiation to kill cancer cells and shrink tumors. Radiation therapy can be administered externally via external beam radiotherapy (EBRT) or internally via brachytherapy. The effects of radiation therapy are localised and confined to the region being treated. Radiation therapy injures or destroys cells in the area being treated (the "target tissue") by damaging their genetic material, making it impossible for these cells to continue to grow and divide. Although radiation damages both cancer cells and normal cells, most normal cells can recover from the effects of radiation and function properly. The goal of radiation therapy is to damage as many cancer cells as possible, while limiting harm to nearby healthy tissue. Hence, it is given in many fractions, allowing healthy tissue to recover between fractions.

Radiation therapy may be used to treat almost every type of solid tumor, including cancers of the brain, breast, cervix, larynx, lung, pancreas, prostate, skin, stomach, uterus, or soft tissue sarcomas. Radiation is also used to treat leukemia and lymphoma. Radiation dose to each site depends on a number of factors, including the radiosensitivity of each cancer type and whether there are tissues and organs nearby that may be damaged by radiation. Thus, as with every form of treatment, radiation therapy is not without its side effects.

Chemotherapy


Chemotherapy is the treatment of cancer with drugs ("anticancer drugs") that can destroy cancer cells. In current usage, the term "chemotherapy" usually refers to cytotoxic drugs which affect rapidly dividing cells in general, in contrast with targeted therapy (see below). Chemotherapy drugs interfere with cell division in various possible ways, e.g. with the duplication of DNA or the separation of newly formed chromosomes. Most forms of chemotherapy target all rapidly dividing cells and are not specific for cancer cells, although some degree of specificity may come from the inability of many cancer cells to repair DNA damage, while normal cells generally can. Hence, chemotherapy has the potential to harm healthy tissue, especially those tissues that have a high replacement rate (e.g. intestinal lining). These cells usually repair themselves after chemotherapy.

Because some drugs work better together than alone, two or more drugs are often given at the same time. This is called "combination chemotherapy"; most chemotherapy regimens are given in a combination.

The treatment of some leukaemias and lymphomas requires the use of high-dose chemotherapy, and total body irradiation (TBI). This treatment ablates the bone marrow, and hence the body's ability to recover and repopulate the blood. For this reason, bone marrow, or peripheral blood stem cell harvesting is carried out before the ablative part of the therapy, to enable "rescue" after the treatment has been given. This is known as autologous stem cell transplantation. Alternatively, hematopoietic stem cells may be transplanted from a matched unrelated donor (MUD).

Targeted therapies


Targeted therapy, which first became available in the late 1990s, has had a significant impact in the treatment of some types of cancer, and is currently a very active research area. This constitutes the use of agents specific for the deregulated proteins of cancer cells. Small molecule targeted therapy drugs are generally inhibitors of enzymatic domains on mutated, overexpressed, or otherwise critical proteins within the cancer cell. Prominent examples are the tyrosine kinase inhibitors imatinib and gefitinib.

Monoclonal antibody therapy is another strategy in which the therapeutic agent is an antibody which specifically binds to a protein on the surface of the cancer cells. Examples include the anti-HER2/neu antibody trastuzumab (Herceptin®) used in breast cancer, and the anti-CD20 antibody rituximab, used in a variety of B-cell malignancies.

Targeted therapy can also involve small peptides as "homing devices" which can bind to cell surface receptors or affected extracellular matrix surrounding the tumor. Radionuclides which are attached to this peptides (e.g. RGDs) eventually kill the cancer cell if the nuclide decays in the vicinity of the cell. Especially oligo- or multimers of these binding motifs are of great interest, since this can lead to enhanced tumor specificity and avidity.

Photodynamic therapy (PDT) is a ternary treatment for cancer involving a photosensitizer, tissue oxygen, and light (often using lasers). PDT can be used as treatment for basal cell carcinoma (BCC) or lung cancer; PDT can also be useful in removing traces of malignant tissue after surgical removal of large tumors.[5]

Immunotherapy


Cancer immunotherapy refers to a diverse set of therapeutic strategies designed to induce the patient's own immune system to fight the tumor. Contemporary methods for generating an immune response against tumours include intravesical BCG immunotherapy for superficial bladder cancer, and use of interferons and other cytokines to induce an immune response in renal cell carcinoma and melanoma patients. Vaccines to generate specific immune responses are the subject of intensive research for a number of tumours, notably malignant melanoma and renal cell carcinoma. Sipuleucel-T is a vaccine-like strategy in late clinical trials for prostate cancer in which dendritic cells from the patient are loaded with prostatic acid phosphatase peptides to induce a specific immune response against prostate-derived cells.

Allogeneic hematopoietic stem cell transplantation ("bone marrow transplantation" from a genetically non-identical donor) can be considered a form of immunotherapy, since the donor's immune cells will often attack the tumor in a phenomenon known as graft-versus-tumor effect. For this reason, allogeneic HSCT leads to a higher cure rate than autologous transplantation for several cancer types, although the side effects are also more severe.

Hormonal therapy

The growth of some cancers can be inhibited by providing or blocking certain hormones. Common examples of hormone-sensitive tumors include certain types of breast and prostate cancers. Removing or blocking estrogen or testosterone is often an important additional treatment. In certain cancers, administration of hormone agonists, such as progestogens may be therapeutically beneficial.

Symptom control

Although the control of the symptoms of cancer is not typically thought of as a treatment directed at the cancer, it is an important determinant of the quality of life of cancer patients, and plays an important role in the decision whether the patient is able to undergo other treatments. Although all practicing doctors have the therapeutic skills to control pain, nausea, vomiting, diarrhea, hemorrhage and other common problems in cancer patients, the multidisciplinary specialty of palliative care has arisen specifically in response to the symptom control needs of this group of patients.

Pain medication, such as morphine and oxycodone, and antiemetics, drugs to suppress nausea and vomiting, are very commonly used in patients with cancer-related symptoms. Improved antiemetics such as ondansetron and analogues, as well as aprepitant have made aggressive treatments much more feasible in cancer patients.

Chronic pain due to cancer is almost always associated with continuing tissue damage due to the disease process or the treatment (i.e. surgery, radiation, chemotherapy). Although there is always a role for environmental factors and affective disturbances in the genesis of pain behaviors, these are not usually the predominant etiologic factors in patients with cancer pain. Furthermore, many patients with severe pain associated with cancer are nearing the end of their lives and palliative therapies are required. Issues such as social stigma of using opioids, work and functional status, and health care consumption are not likely to be important in the overall case management. Hence, the typical strategy for cancer pain management is to get the patient as comfortable as possible using opioids and other medications, surgery, and physical measures. Doctors have been reluctant to prescribe narcotics for pain in terminal cancer patients, for fear of contributing to addiction or suppressing respiratory function. The palliative care movement, a more recent offshoot of the hospice movement, has engendered more widespread support for preemptive pain treatment for cancer patients.

Complementary and alternative

Complementary and alternative medicine (CAM) treatments are the diverse group of medical and health care systems, practices, and products that are not part of conventional medicine.[6] Oncology, the study of human cancer, has a long history of incorporating unconventional or botanical treatments into mainstream cancer therapy. Some examples of this phenomenon include the chemotherapy agent paclitaxel, which is derived from the bark of the Pacific Yew tree, and ATRA, all-trans retinoic acid, a derivative of Vitamin A that induces cures in an aggressive leukemia known as acute promyelocytic leukemia. Many "complementary" and "alternative" medicines for cancer have not been studied using the scientific method, such as in well-designed clinical trials, or they have only been studied in preclinical (animal or in-vitro) laboratory studies. Many times, "complementary" and "alternative" medicines are supported by marketing materials and "testimonials" from users of the substances. Frequently, when these treatments are subjected to rigorous scientific testing, they are found not to work. A recent example was reported at the 2007 annual meeting of the American Society of Clinical Oncology: a Phase III clinical trial comparing shark cartilage extract to placebo in non-small cell lung cancer demonstrated no benefit of the shark cartilage extract, AE-491.[7]

"Complementary medicine" refers to methods and substances used along with conventional medicine, while "alternative medicine" refers to compounds used instead of conventional medicine. A study of CAM use in patients with cancer in the July 2000 issue of the Journal of Clinical Oncology found that 69% of 453 cancer patients had used at least one CAM therapy as part of their cancer treatment.[8]

Some complementary measures include botanical medicine, such as an NIH trial currently underway testing mistletoe extract combined with chemotherapy for the treatment of solid tumors, acupuncture for managing chemotherapy-associated nausea and vomiting and in controlling pain associated with surgery, psychological approaches such as "imaging" or meditation to aid in pain relief or improve mood.[8]

A wide range of alternative treatments have been offered for cancer over the last century. The appeal of alternative cures arises from the daunting risks, costs, or potential side effects of many conventional treatments, or in the limited prospect for cure. Some people resort to these so-called "alternative" forms of treatment in desperation or as a last resort. However, no alternative therapies have been shown in any scientific study to effectively treat cancer. Some express the view that the promotion and sale of certain alternative modalities known to be ineffective constitute quackery.[9]

Treatment trials

Clinical trials, also called research studies, test new treatments in people with cancer. The goal of this research is to find better ways to treat cancer and help cancer patients. Clinical trials test many types of treatment such as new drugs, new approaches to surgery or radiation therapy, new combinations of treatments, or new methods such as gene therapy.

A clinical trial is one of the final stages of a long and careful cancer research process. The search for new treatments begins in the laboratory, where scientists first develop and test new ideas. If an approach seems promising, the next step may be testing a treatment in animals to see how it affects cancer in a living being and whether it has harmful effects. Of course, treatments that work well in the lab or in animals do not always work well in people. Studies are done with cancer patients to find out whether promising treatments are safe and effective.

Patients who take part may be helped personally by the treatment(s) they receive. They get up-to-date care from cancer experts, and they receive either a new treatment being tested or the best available standard treatment for their cancer. Of course, there is no guarantee that a new treatment being tested or a standard treatment will produce good results. New treatments also may have unknown risks, but if a new treatment proves effective or more effective than standard treatment, study patients who receive it may be among the first to benefit.

Prognosis

Cancer has a reputation for being a deadly disease. While this certainly applies to certain particular types, the truths behind the historical connotations of cancer are increasingly being overturned by advances in medical care. Some types of cancer have a prognosis that is substantially better than nonmalignant diseases such as heart failure and stroke.

Progressive and disseminated malignant disease has a substantial impact on a cancer patient's quality of life, and many cancer treatments (such as chemotherapy) may have severe side-effects. In the advanced stages of cancer, many patients need extensive care, affecting family members and friends. Palliative care solutions may include permanent or "respite" hospice nursing.

Cancer patients, for the first time in the history of oncology, are visibly returning to the athletic arena and workplace. Patients are living longer with either quiescent persistent disease or even complete, durable remissions. The stories of Lance Armstrong, who won the Tour de France after treatment for metastatic testicular cancer, or Tony Snow, who was working as the White House Press Secretary as of June, 2007 despite relapsed colon cancer, continue to be an inspiration to cancer patients everywhere.

Emotional impact

Many local organizations offer a variety of practical and support services to people with cancer. Support can take the form of support groups, counseling, advice, financial assistance, transportation to and from treatment, films or information about cancer. Neighborhood organizations, local health care providers, or area hospitals may have resources or services available.

While some people are reluctant to seek counseling, studies show[citation needed] that having someone to talk to reduces stress and helps people both mentally and physically. Counseling can also provide emotional support to cancer patients and help them better understand their illness. Different types of counseling include individual, group, family, peer counseling, bereavement, patient-to-patient, and sexuality.

Many governmental and charitable organizations have been established to help patients cope with cancer. These organizations often are involved in cancer prevention, cancer treatment, and cancer research.

 

Forex | Make Money Online