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Insomnia Cures Are Here!

Written by Dave Turo-Shields, ACSW, LCSW

I yawn, stretch my arms behind my head and stare at the ceiling. I’ve been in bed for a few minutes. Ahhh, the peaceful quiet all around. The room is dark. The kids are asleep. It’s an expansive moment for my mind. My mind seems to fill the entire room.

Okay, it’s been 20 minutes now. The novel meditative moment has passed. Now my mind seems to be filling up like a bowl that’s been left outside in a torrential downpour. I can’t seem to slow down or empty out my mind. So many things to think about, not the least of which is why in tarnation can’t I fall asleep?

I am tired, but cannot sleep. I begin to feel agitated and become physically restless. I turn this way… I turn that way. I cross and uncross my legs. I lay on my stomach, side and back. Each passing moment lends itself to increased anger and frustration. Now my mind has jumped ahead to tomorrow, lining up all those things I have to accomplish knowing that I’ll only do so by dragging this haggard, exhausted and fatigued body around for the entire day. This process goes deeply into the night.

Any of that sound familiar?

Recent estimates indicate that approximately 25 million Americans suffer from chronic insomnia. Some reasons for insomnia include:

Restless Leg Syndrome

Circadian Rhythm Disorders

Depression

Alcohol and other drug abuse

Life changes and/or accumulation of life stressors

Anxiety

Sleep Apnea

You should consult with your physician in order to determine the exact cause of your sleep problems. He/she may order a sleep study, give you a depression screen, check social stressors, order a blood panel to check for vitamin and mineral deficiencies, suggest you stop drinking, give an anxiety scale or any number of interventions to identify a cause and get you focused on appropriate solutions. In the meantime here are a few “Do’s and Don’ts” on how to reclaim your beauty sleep.

When you lay down to sleep, deepen and lengthen your breathing patterns — shoot for five second inhales and five second exhales. You’ll be taking 6 breathes per minute. This takes some practice but works nicely.

Take a deep breath and hold it. While holding your breathe, tense up the muscles throughout your entire body and hold both for 30 seconds. Exhale completely and relax. Take several relaxed breathes and repeat three times.

Choose any relaxing color (blue, green, yellow, etc). Place your hands on your stomach and imagine that you are expanding a colored balloon in your stomach. Exhale an insomnia/anxiety color (red, black, etc) through your mouth. Continue this for 5-10-50 times, whatever it takes. It is impossible to focus on your body/breath while entertaining thoughts.

Take a hot shower or bath before bed, or get up and do so if you are unable to fall asleep within 15 minutes.

Take some sleep food for the brain. Before going to bed eat 1 ounce of protein, 1 ounce of cheese and 5 grapes or the equivalent.

Get out of bed if you have not fallen asleep within 15 minutes. The brain is quite easily programmed. I don’t want your brain to associate “bed” with “awake.”

Once you’re out of bed do not watch TV, get on the computer, listen to stimulating music, turn on a bunch of lights or do anything else that stimulates your brain into high gear.

Once out of bed do sit quietly, meditate on emptying the mind, listen to quiet, soothing music or do some “light” reading. The research shows that deep meditation is as restorative as sleep and takes less time than sleeping for 8 hours.

Purchase a Brain Entrainment CD and some ear buds (they are the most comfortable to sleep on). Make sure the CD is designed for sleep. I won’t go into all the scientific details here. Just know that the brain needs to be in delta wave state 60 minutes for you to wake up feeling fresh. My favorite is “Sleeping Through The Rain” by a company you can find at www.hemi-sync.com. Don’t try this on just a boom box. The ear buds are very important to make this work.

Make sure your bedroom is dark. Lights out!

Exercise regularly. Exercise does a fantastic job of regulating sleep cycles. The only catch here is do not exercise within two hours of bedtime, as this can activate mind and body systems that will keep you awake.

Drink Chamomile Tea an hour before bedtime and take Valerian root with it. If you open up your first bottle of Valerian root and it smells like rotten socks, don’t throw it away, it’s supposed to smell like that! Can you believe it!? 😉

If worse comes to worst, consult a doctor. There are many effective medications used for sleep which can be prescribed by your doctor. Some of these include Ambien, Temazepam, Sonata, Remeron, Benadryl (non-prescription), Melatonin (Don’t take this if you have Seasonal Affective Disorder) Trazadone and others.

Stay away from alcohol as a sleep aid. Many will argue that alcohol gets them to sleep, but brain wave studies show that once asleep, an individual does not reach the restorative level of sleep that results in feeling well rested in the morning.

Too many sleepless nights can lead to what feels like a psychotic break, so don’t push yourself over the edge. Good self care is so important. After just 2 nights without sleep, intervention is necessary! Please take care of yourself. A great night’s sleep after not sleeping well for a long time can be an absolutely wonderful gift to give yourself.

I welcome you to more restful nights!

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Introduction to Anxiety

Generalized anxiety disorder (or GAD) is characterized by excessive, exaggerated anxiety and worry about everyday life events with no obvious reasons for worry. People with symptoms of generalized anxiety disorder tend to always expect disaster and can’t stop worrying about health, money, family, work, or school. In people with GAD, the worry often is unrealistic or out of proportion for the situation. Daily life becomes a constant state of worry, fear, and dread. Eventually, the anxiety so dominates the person’s thinking that it interferes with daily functioning, including work, school, social activities, and relationships.

What Are the Symptoms of GAD?

GAD affects the way a person thinks, but the anxiety can lead to physical symptoms, as well. Symptoms of GAD can include:

  • Excessive, ongoing worry and tension
  • An unrealistic view of problems
  • Restlessness or a feeling of being “edgy”
  • Irritability
  • Muscle tension
  • Headaches
  • Sweating
  • Difficulty concentrating
  • Nausea
  • The need to go to the bathroom frequently
  • Tiredness
  • Trouble falling or staying asleep
  • Trembling
  • Being easily startled

In addition, people with GAD often have other anxiety disorders (such as panic disorder, obsessive-compulsive disorder, and phobias), suffer from depression, and/or abuse drugs or alcohol.

What Causes GAD?

The exact cause of GAD is not fully known, but a number of factors — including genetics, brain chemistry and environmental stresses — appear to contribute to its development.

  • Genetics: Some research suggests that family history plays a part in increasing the likelihood that a person will develop GAD. This means that the tendency to develop GAD may be passed on in families.
  • Brain chemistry: GAD has been associated with abnormal levels of certain neurotransmitters in the brain. Neurotransmitters are special chemical messengers that help move information from nerve cell to nerve cell. If the neurotransmitters are out of balance, messages cannot get through the brain properly. This can alter the way the brain reacts in certain situations, leading to anxiety.
  • Environmental factors: Trauma and stressful events, such as abuse, the death of a loved one, divorce, changing jobs or schools, may lead to GAD. GAD also may become worse during periods of stress. The use of and withdrawal from addictive substances, including alcohol, caffeine, and nicotine, can also worsen anxiety.

How Common Is GAD?

About 4 million adult Americans suffer from GAD during the course of a year. It most often begins in childhood or adolescence, but can begin in adulthood. It is more common in women than in men.

How Is GAD Diagnosed?

If symptoms of GAD are present, the doctor will begin an evaluation by asking questions about your medical history and performing a physical examination. Although there are no laboratory tests to specifically diagnose anxiety disorders, the doctor may use various tests to look for physical illness as the cause of the symptoms.

The doctor bases his or her diagnosis of GAD on reports of the intensity and duration of symptoms — including any problems with functioning caused by the symptoms. The doctor then determines if the symptoms and degree of dysfunction indicate a specific anxiety disorder. GAD is diagnosed if symptoms are present for more days than not during a period of at least six months. The symptoms also must interfere with daily living, such as causing you to miss work or school.

How Is GAD Treated?

If no physical illness is found, you may be referred to a psychiatrist or psychologist, mental health professionals who are specially trained to diagnose and treat mental illnesses like GAD. Treatment for GAD most often includes a combination of medication and cognitive-behavioral therapy.

  • Medication: Drugs are available to treat GAD and may be especially helpful for people whose anxiety is interfering with daily functioning. The medications most often used to treat GAD in the short-term are from a class of drugs called benzodiazepines. These medications are sometimes referred to as “tranquilizers,” because they leave you feeling calm and relaxed. They work by decreasing the physical symptoms of GAD, such as muscle tension and restlessness. Common benzodiazepines include Xanax, Librium, Valium and Ativan. Antidepressants, such as Paxil, Effexor, Prozac, Lexapro, and Zoloft, are also being used to treat GAD. These antidepressants may take a few weeks to start working but they’re more appropriate for long-term treatment of GAD.
  • Cognitive-behavioral therapy: People suffering from anxiety disorders often participate in this type of therapy, in which you learn to recognize and change thought patterns and behaviors that lead to anxious feelings. This type of therapy helps limit distorted thinking by looking at worries more realistically.

In addition, relaxation techniques, such as deep breathing and biofeedback, may help to control the muscle tension that often accompanies GAD.

Are There Side Effects of GAD Treatment?

Dependency on anti-anxiety medications (benzodiazepines) is a potential complication of treatment. Side effects of antidepressants vary by specific drug and the person taking them. Common side effects can include sleepiness, weight gain, and sexual problems.

What Is the Outlook for People With GAD?

Although many people with GAD cannot be cured and symptoms can return from time to time, most people gain substantial relief from their symptoms with proper treatment.

Can GAD Be Prevented?

Anxiety disorders like GAD cannot be prevented. However, there are some things that you can do to control or lessen symptoms, including:

  • Stop or reduce your consumption of products that contain caffeine, such as coffee, tea, cola and chocolate.
  • Ask your doctor or pharmacist before taking any over-the-counter medicines or herbal remedies. Many contain chemicals that can increase anxiety symptoms.
  • Exercise daily and eat a healthy, balanced diet.
  • Seek counseling and support after a traumatic or disturbing experience.
  • Practice stress management techniques like yoga or meditation
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What is Lung Cancer?

by: Peter Crosta

Cancer is a class of diseases characterized by out-of-control cell growth, and lung cancer occurs when this uncontrolled cell growth begins in one or both lungs. Rather than developing into healthy, normal lung tissue, these abnormal cells continue dividing and form lumps or masses of tissue called tumors. Tumors interfere with the main function of the lung, which is to provide the bloodstream with oxygen to be carried to the entire body. If a tumor stays in one spot and demonstrates limited growth, it is generally considered to be benign.

More dangerous, or malignant, tumors form when the cancer cells migrate to other parts of the body through the blood or lymph system. When a tumor successfully spreads to other parts of the body and grows, invading and destroying other healthy tissues, it is said to have metastasized. This process itself is called metastasis, and the result is a more serious condition that is very difficult to treat.

Lung cancer is called “primary” if the cancer originates in the lungs and “secondary” if it originates elsewhere in the body but has metastasized to the lungs. These two types are considered different cancers from diagnostic and treatment perspectives.

In 2007, about 15% of all cancer diagnoses and 29% of all cancer deaths were due to lung cancer. It is the number one cause of death from cancer every year and the second most diagnosed after breast and prostate cancers (for women and men, respectively). Lung cancer is usually found in older persons because it develops over a long period of time.

How is lung cancer classified?
Lung cancer can be broadly classified into two main types based on the cancer’s appearance under a microscope: non-small cell lung cancer and small cell lung cancer. Non-small cell lung cancer (NSCLC) accounts for 80% of lung cancers, while small cell lung cancer accounts for the remaining 20%.

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NSCLC can be further divided into four different types, each with different treatment options:

• Squamous cell carcinoma or epidermoid carcinoma. As the most common type of NSCLC and the most common type of lung cancer in men, squamous cell carcinoma forms in the lining of the bronchial tubes.

• Adenocarcinoma. As the most common type of lung cancer in women and in nonsmokers, adenocarcinoma forms in the mucus-producing glands of the lungs.

• Bronchioalveolar carcinoma. This type of lung cancer is a rare type of adenocarcinoma that forms near the lungs’ air sacs.

• Large-cell undifferentiated carcinoma. A rapidly growing cancer, large-cell undifferentiated carcinomas form near the outer edges or surface of the lungs.

Small cell lung cancer (SCLC) is characterized by small cells that multiply quickly and form large tumors that travel throughout the body. Almost all cases of SCLC are due to smoking.

What causes cancer?

Cancer is ultimately the result of cells that uncontrollably grow and do not die. Normal cells in the body follow an orderly path of growth, division, and death. Programmed cell death is called apoptosis, and when this process breaks down, cancer begins to form. Unlike regular cells, cancer cells do not experience programmatic death and instead continue to grow and divide. This leads to a mass of abnormal cells that grows out of control.

Lung cancer occurs when a lung cell’s gene mutation makes the cell unable to correct DNA damage and unable to commit suicide. Mutations can occur for a variety of reasons. Most lung cancers are the result of inhaling carcinogenic substances.

Carcinogens
Carcinogens are a class of substances that are directly responsible for damaging DNA, promoting or aiding cancer. Tobacco, asbestos, arsenic, radiation such as gamma and x-rays, the sun, and compounds in car exhaust fumes are all examples of carcinogens. When our bodies are exposed to carcinogens, free radicals are formed that try to steal electrons from other molecules in the body. These free radicals damage cells and affect their ability to function and divide normally.

About 87% of lung cancers are related to smoking and inhaling the carcinogens in tobacco smoke. Even exposure to second-hand smoke can damage cells so that cancer forms.

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Genes
Cancer can be the result of a genetic predisposition that is inherited from family members. It is possible to be born with certain genetic mutations or a fault in a gene that makes one statistically more likely to develop cancer later in life. Genetic predispositions are thought to either directly cause lung cancer or greatly increase one’s chances of developing lung cancer from exposure to certain environmental factors.

What are the symptoms of lung cancer?

Cancer symptoms are quite varied and depend on where the cancer is located, where it has spread, and how big the tumor is. Lung cancer symptoms may take years before appearing, usually after the disease is in an advanced stage.

Many symptoms of lung cancer affect the chest and air passages. These include:

• Persistent or intense coughing

• Pain in the chest shoulder, or back from coughing

• Changes in color of the mucus that is coughed up from the lower airways (sputum)

• Difficulty breathing and swallowing

• Hoarseness of the voice

• Harsh sounds while breathing (stridor)

• Chronic bronchitis or pneumonia

• Coughing up blood, or blood in the sputum

If the lung cancer spreads, or metastasizes, additional symptoms can present themselves in the newly affected area. Swollen or enlarged lymph nodes are common and likely to be present early. If cancer spreads to the brain, patients may experience vertigo, headaches, or seizures. In addition, the liver may become enlarged and cause jaundice and bones can become painful, brittle, and broken. It is also possible for the cancer to infect the adrenal glands resulting in hormone level changes.

As lung cancer cells spread and use more of the body’s energy, it is possible to present symptoms that may also be associated with many other ailments. These include:

• Fever

• Fatigue

• Unexplained weight loss

• Pain in joints or bones

• Problems with brain function and memory

• Swelling in the neck or face

• General weakness

• Bleeding and blood clots

How is lung cancer diagnosed and staged?
Physicians use information revealed by symptoms as well as several other procedures in order to diagnose lung cancer. Common imaging techniques include chest X-rays, bronchoscopy (a thin tube with a camera on one end), CT scans, MRI scans, and PET scans. Physicians will also conduct a physical examination, a chest examination, and an analysis of blood in the sputum. All of these procedures are designed to detect where the tumor is located and what additional organs may be affected by it.

Although the above diagnostic techniques provided important information, extracting cancer cells and looking at them under a microscope is the only absolute way to diagnose lung cancer. This procedure is called a biopsy. If the biopsy confirms lung cancer, a pathologist will determine whether it is non-small cell lung cancer or small cell lung cancer.

After a diagnosis is made, an oncologist will determine the stage of the cancer by finding out how far the cancer has spread. The stage determines which choices will be available for treatment and informs prognosis. The most common cancer staging method is called the TNM system. T (1-4) indicates the size and direct extent of the primary tumor, N (0-3) indicates the degree to which the cancer has spread to nearby lymph nodes, and M (0-1) indicates whether the cancer has metastasized to other organs in the body. A small tumor that has not spread to lymph nodes or distant organs may be staged as (T1, N0, M0), for example.

For non-small cell lung cancer, TNM descriptions lead to a simpler categorization of stages. These stages are labeled from I to IV, where lower numbers indicate earlier stages where the cancer has spread less. More specifically:

• Stage I is when the tumor is found only in one lung and in no lymph nodes.

• Stage II is when the cancer has spread to the lymph nodes surrounding the infected lung.

• Stage IIIa is when the cancer has spread to lymph nodes around the trachea, chest wall, and diaphragm, on the same side as the infected lung.

• Stage IIIb is when the cancer has spread to lymph nodes on the other lung or in the neck.

• Stage IV is when the cancer has spread throughout the rest of the body and other parts of the lungs.

Small cell lung cancer has two stages: limited or extensive. In the limited stage, the tumor exists in one lung and in nearby lymph nodes. In the extensive stage, the tumor has infected the other lung as well as other organs in the body.

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How is lung cancer treated?
Lung cancer treatments depend on the type of cancer, the stage of the cancer (how much it has spread), age, health status, and additional personal characteristics. As there is usually no single treatment for cancer, patients often receive a combination of therapies and palliative care. The main lung cancer treatments are surgery, chemotherapy, and/or radiation. However, there also have been recent developments in the fields of immunotherapy, hormone therapy, and gene therapy.

Surgery
Surgery is the oldest known treatment for cancer. If a cancer is in stage I or II and has not metastasized, it is possible to completely cure a patient by surgically removing the tumor and the nearby lymph nodes. After the disease has spread, however, it is nearly impossible to remove all of the cancer cells.

Lung cancer surgery is performed by a specially trained thoracic surgeon. After removing the tumor and the surrounding margin of tissue, the margin is further studied to see if cancer cells are present. If no cancer is found in the tissue surrounding the tumor, it is considered a “negative margin.” A “positive margin” may require the surgeon to remove more of the lung tissue.

Lung cancer surgery can be curative or palliative. Curative surgery aims to cure a patient with early stage lung cancer by removing all of the cancerous tissue. Palliative surgery aims to remove an obstruction or open an airway, making the patient more comfortable but not necessarily removing the cancer.

Surgery carries side effects – most notably pain and infection. Lung cancer surgery is an invasive procedure that can cause harm to the surrounding body parts. Doctors will usually provide several options for alleviating any pain from surgery. Antibiotics are commonly used to prevent infections that may occur at the site of the wound or elsewhere inside the body.

Radiation
Radiation treatment, also known as radiotherapy, destroys or shrinks lung cancer tumors by focusing high-energy rays on the cancer cells. This causes damage to the molecules that make up the cancer cells and leads them to commit suicide. Radiotherapy utilizes high-energy gamma-rays that are emitted from metals such as radium or high-energy x-rays that are created in a special machine. Radiation can be used as the main treatment for lung cancer, to kill remaining cells after surgery, or to kill cancer cells that have metastasized.

Early radiation treatments caused severe side-effects because the energy beams would damage normal, healthy tissue, but technologies have improved so that beams can be more accurately targeted. Radiation oncologists can focus the radiation in precise locations in the body for certain lengths of time, reducing the risk of damage to surrounding healthy tissue. Treatments occur intermittently over weeks or months depending on the size and extent of the tumor, the dosage of radiation, and how much damage is being done to noncancerous tissue.

Common side effects of radiation therapy include fatigue, nausea, loss of appetite, hair loss, and skin affectations that cause skin to become dry, irritated, and sensitive.

Chemotherapy
Chemotherapy utilizes strong chemicals that interfere with the cell division process – damaging proteins or DNA – so that cancer cells will commit suicide. These treatments target any rapidly dividing cells (not just cancer cells), but normal cells usually can recover from any chemical-induced damage while cancer cells cannot. Chemotherapy is considered systemic because its medicines travel throughout the entire body, killing the original tumor cells as well as cancer cells that have spread throughout the body.

A medical oncologist will usually prescribe chemotherapy drugs for lung cancer to be taken intravenously, but there are also drugs available in tablet, capsule, and liquid form. Chemotherapy treatment occurs in cycles so the body has time to heal between doses, and dosages are determined by the type of lung cancer, the type of drug, and how the person responds to treatment. Medicines may be administered daily, weekly, or monthly, and can continue for months or even years.

Combination therapies often include multiple types of chemotherapy, and chemotherapy is also given as adjuvant therapy as a complement to surgery and radiation. Adjuvant therapy is designed to reduce the risk of cancer recurrence after surgery and killing any cancer cells that exist after surgery. Chemotherapy can be given before surgery, called neo-adjuvant therapy, to shrink tumors and to make surgery more successful.

Chemotherapy carries several common side effects, but they depend on the type of chemotherapy and the health of the patient. These include nausea and vomiting, appetite loss, diarrhea, hair loss, fatigue from anemia, infections, bleeding, and mouth sores. Many of these side effects are only temporarily felt during treatment, and several drugs exist to help patients cope with the symptoms.

Other Treatments
Researchers continue to search for ways to improve lung cancer treatments and find new methods of treating the disease. Targeted therapies are designed to only treat cancer cells while leaving alone normal and healthy lung cells. These include monoclonal antibodies that travel directly to the cancer cells and release drugs or radiation, anti-angiogenesis agents that interfere with the blood supply creation mechanism of cancer cells, and growth factor inhibitors that block the effects of growth factors and disallow the cancerous cells to grow. There is also some research in the area of lung cancer vaccines that first transform cancer cells so they are no longer cancerous. However, the cells will exist such that the body’s immune system can recognize the cancerous cells as foreign and attack them. These targeted therapies are also called immunotherapies because the treatment tweaks the body’s natural immune responses.

How can lung cancer be prevented?
Cancers that are closely linked to certain behaviors are the easiest to prevent. For example, choosing not to smoke tobacco or drink alcohol significantly lowers the risk of several types of cancer – most notably lung, throat, mouth, and liver cancer. Even if you are a current tobacco user, quitting can still greatly reduce your chances of getting cancer. The most important preventive measure you can take to avoid lung cancer is to quit smoking.

Quitting smoking will also reduce your risk of several other types of cancer including esophagus, pancreas, larynx, and bladder cancer. If you quit smoking, you will usually reap additional benefits such as lower blood pressure, enhanced blood circulation, and increased lung capacity.

Exposure to tobacco smoke is not the only risk factor for lung cancer though. Those who have come into contact with asbestos, radon, and secondhand smoke also have an increased risk of developing lung cancer. In addition, having a family member who developed lung cancer without being exposed to carcinogens could mean that you have a genetic predisposition for developing the disease, increasing your overall risk.

Screening techniques are designed to find cancer at the earliest stage so that the most treatment options are available, increasing survival rates and avoiding highly invasive procedures. Most lung cancers are detected in the late stages of the disease after they have spread and are harder to treat. Although there currently do not exist approved screening tests for lung cancer that improve survival or detect localized disease, there is promising research underway. Advocates of screening recommend that certain high risk groups be screened. This includes persons age 60 or older with a history of smoking, previous lung tumors, or chronic obstructive pulmonary disease (COPD). Possible lung cancer screening tests include analysis of sputum cells, fiberoptic examination of bronchial passages (bronchoscopy), and low-dose spiral CT scans.

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Breast Cancer Research

breast_cancerOver 1.1 million women are diagnosed worldwide each year with breast cancer,1 and this number has almost doubled since 1975.2 In addition, breast cancer is the most prevalent cancer in the world, with 4.4 million survivors up to 5 years following diagnosis,1 and millions more surviving longer than 5 years.

In the United States, the American Cancer Society reports that approximately 250,000 women are diagnosed each year with breast cancer.3 And while 40,000 women die annually in this country from breast cancer, there are, at any point in time, an estimated 2.3 million breast cancer survivors in the U.S.3

Although the overall incidence of breast cancer has been increasing for more than two decades, there has been a gradual reduction in mortality beginning in 1990 when the rate began to decline by 2.3% annually.3 This improvement in survival has been attributed to two factors, roughly equal in effect: 1) early detection through mammography screening programs, and 2) the increased utilization of adjuvant systemic therapies (antihormonal drugs and chemotherapy).4 Improving the former – the impact of early detection – is the focus herein.

Assessing the Impact of Early Detection Through Screening Mammography

Although early diagnosis has been a pervasive theme for improving survival rates with many types of cancer, the scientific evidence that mass screening improves survival is remarkably sparse. Even today, there is no evidence to support mass screening for common cancers such as lung5 and prostate6 in spite of available testing for early detection. Undaunted, health care professionals and the public have consistently demonstrated enthusiasm for cancer screening,7 and it is still possible that screening studies underway will validate early diagnosis as a principle to be applied to most types of cancer.

Currently, however, breast cancer is one of the few types of malignancy where mass screening has already been validated as reducing mortality, in this case through the use of mammography. (Self-exam, although recommended in all guidelines, remains controversial as to its impact on mortality reduction.) No method of cancer screening has been studied with such scrutiny for so many years, as has mammography; yet, the proof of mortality reduction did not come easy.

In fact, at the same time that the clinical trials for screening mammography were being launched, a new theory of breast cancer biology emerged indicating that breast cancer was a systemic disease at its inception, implying that early diagnosis would have little or no impact. This so-called Fisher theory8 of breast cancer biology was supported by findings in the clinical trials that confirmed the equivalency of breast conservation (lumpectomy) to mastectomy.9 Yet, after multiple mammography screening studies and many years of controversy, it is now generally accepted that mammography reduces breast cancer mortality in screened populations.10 Thus, the concept of breast cancer being systemic at its inception had to be modified in order to explain how early detection could make such an impact. This resulted in the Spectrum Theory11 that dominates today, a theory which suggests a spectrum of biologies such that many, but not all, breast cancers are vulnerable to early detection, supporting efforts to improve mammography as well as other diagnostic measures.

The benefit of screening mammography has now been reflected in mortality reductions seen outside the confines of clinical trials in countries where mammography is standard screening practice.12 Trying to quantify the benefit, though, is a challenge. Certainly, the benefit of screening only applies to women who comply with guidelines. Even then, however, some patients adhering closely to screening guidelines will die from breast cancer.

For instance, when prospective randomized studies indicate a “30% reduction in breast cancer mortality” for women in mammography screening programs, this is based on a comparison to the mortality rate demonstrated in a control group where women did not have regular mammograms. If such a study included, for instance, 10,000 patients, and of those in the control group who developed breast cancer, 100 women died of their disease, then a “30% reduction” means that in the mammography screening group, only 70 women died from breast cancer. The obvious question is, “Why did the 70 women who were compliant with mammography still die?”

This brings us back to the issue of breast cancer biology. Perhaps, these deaths occur in women with more aggressive breast cancers in whom early diagnosis makes no difference. However, biology is not the only determinant regarding the efficacy of cancer screening. The other powerful factor is the sensitivity of the screening tool. Stated alternatively as a question: What percentage of detectable breast cancers are actually detected by mammography? Although it is often stated as a truism that breast cancer is present 5-10 years prior to detection by mammography, this concept is loaded with caveats and, even if valid, does not become clinically relevant unless the cancer is large enough to be detected through current technology, thus allowing therapeutic intervention. Thus, the question of mammographic sensitivity relates to occult cancers that are missed, yet clinically detectable and treatable.

Sensitivity of Mammography

While the controversies about breast cancer screening lasted for decades and focused almost entirely on mortality reduction in the prospective, randomized mammography screening trials, a critical parameter went virtually unnoticed in both the radiologic community and physicians in general – mammographic sensitivity.

Popular media continue to propagate the myth that mammography can find “90% of breast cancers in women who have no symptoms of the disease.” 13 Even the American Cancer Society makes the position statement that “mammography will detect about 80-90%” of asymptomatic cancers,14 though the origin of this sensitivity level is not referenced. In fact, the origin of the “mythical 90%” is difficult to find, perhaps derived from those early studies of mammography that measured sensitivity of the new tool in women with palpable cancers. If cancers are palpable, of course, this is no longer “screening asymptomatic patients,” yet it appears that the medical community then applied this “90% sensitivity” to non-palpable cancers as well (at the time, there were no other proven modalities to detect breast cancer).

While certain subsets of patients, based on advanced age or low density mammograms, will demonstrate 90% sensitivity with mammography, there is no support in the published literature for such an optimistic value when addressing the general screening population. Mammographic sensitivity is, in fact, highly variable among individuals and should be a customized number for the informed patient; however, for general population screening, mammographic sensitivity doesn’t come close to 90%.

In a rare review of the historical mammography screening trials,15 sensitivity for mammograms alone ranged from 39% in the Health Insurance Plan to the highest figure of 92% in a subset (ages 70-74 in the Swedish Two-County study); however, most sensitivity determinations were in the range of 60-66% overall, with Malmo at 61%, Edinburgh 63%, CNBSS-1 (ages 40-49) 61%, and CNBSS-2 (ages 50-59) 66%.

These low sensitivity values have been attributed to the fact that these trials began three decades ago and that mammographic quality has been vastly improved in the years since. However, using the most advanced technology in the recent Digital Mammographic Imaging Screening Trial (DMIST) coordinated by the American College of Radiology,16 the overall sensitivity as defined by a 12-month follow-up period revealed only 70% sensitivity with digital technology and 66% for state-of-the-art film screen technology, comparable to the sensitivities in the historical trials.

But these remarkably low sensitivity values may, in fact, be optimistic. One of the many problems plaguing the quantification of mammographic sensitivity has been the definition of a “missed cancer.” How does one discover an undiscovered cancer? And how does one define such a discovery? Historically, the accepted definition comes through long-term follow-up data, with any cancer discovered within 12 months following a negative mammogram considered to be a “missed cancer” on the previous study.

Nothing is magical about 12 months of follow-up, of course, and in the DMIST study noted above,16 investigators took the unconventional approach of calculating sensitivity based on 15-month follow-up as well, under the assumption that a cancer discovered within a 15-month time frame following a negative mammogram was likely to have been present on the prior study. Remarkably, mammographic sensitivity under this definition turned out to be 41%, and the difference between digital technology and film screen disappeared entirely.

It has to be considered that long-term follow-up is a harsh definition, given the fact that aggressive interval cancers (those cancers with rapid doubling times that emerge between screening studies on self exam or clinical exam) may not have been clinically detectable on the prior study. Also, cancers are sometimes detectable on the prior mammogram, but are missed due to radiologist error; or, changes on X-ray might have been so subtle that the threshold for biopsy was not met. These issues point out the difficulty in trying to assess true mammographic sensitivity using the historical standard of long-term follow-up. More recently, with the introduction of breast ultrasound and breast MRI, the ability to determine true mammographic sensitivity through multi-modality imaging is vastly improved. As it turns out, the 70% sensitivity using the standard definition in the DMIST study may be too high.

Mammographic Sensitivity as Defined by Breast MRI

Multiple prospective trials have now addressed multi-modality imaging for the detection of breast cancer in high-risk women. While breast ultrasound can routinely identify breast cancers missed by mammography, especially in women with dense breasts, its sensitivity is overshadowed by MRI. Thus, breast MRI has recently been recommended as an adjunct to mammography in the new American Cancer Society screening guidelines for high-risk women that emerged from the prospective multi-modality studies.17

In spite of many differences among the prospective, non-randomized trials of multi-modality imaging in asymptomatic women, a consistent feature is noted in that MRI demonstrates twice the sensitivity of mammography. In a recent analysis combining the five largest studies, the sensitivity of mammography alone was 40% while the sensitivity of breast MRI alone was 81%.18 It is largely because of this large improvement in sensitivity in all studies that the American Cancer Society has endorsed breast MRI for screening even in the absence of corresponding mortality reduction data. It is noteworthy that the only way to achieve the oft-quoted “90%” sensitivity in these studies was to perform both mammography and breast MRI. Mammograms continue to be valuable in the detection of microcalcifications (not well seen on MRI), which can be the earliest indicator of malignancy. Then, MRI can detect the non-calcifying cancers that are lost in the background density of the normal breast tissue on X-ray.

A general misconception exists, again in the popular media, that these prospective MRI trials validated the use of MRI only for women with mutations in one of the BRCA genes. In fact, only one of seven trials was limited to BRCA-positive patients,19 and it was possible to enter one of the trials when lifetime risk of breast cancer was only 15%,20 barely above the risk seen in the general population. Overall, family histories predominated as the entry criteria in these trials, and this is reflected in the new American Cancer Society guidelines, which recommend using mathematical models that focus on family history to identify patients at “20-25% lifetime risk” for the development of breast cancer. For these women, the addition of annual breast MRI to annual mammography is recommended. 17

In addressing the poor mammographic sensitivity in these trials, it is often pointed out that all published studies have been limited to high-risk women, and that these trials are skewed toward younger women with higher-density mammograms. The implication here is that the sensitivity of mammography in the general population is better; however, it is interesting to note that the 40% sensitivity for mammography in high-risk patients in these MRI trials is virtually identical to the 41% sensitivity for mammography in the general population in the DMIST trial when using the 15-month follow-up definition.

In addition, subset analysis in the aforementioned Toronto study,19 where all the participants were BRCA-positive, revealed that the difference in sensitivity between MRI and mammography was no greater for women under 50 than for women ages 50 and older.21 Then, another subset analysis by the same researchers revealed that even in the low-density group, the sensitivity of mammography was less than 50%.22 The findings in both of these subset analyses were contrary to the expectations of the investigators,23 and it emphasizes the importance of close scrutiny in these trials before attributing the poor performance of mammography to a skewed study population.

Regardless of the measure used, mammographic sensitivity does not come close to the “90%” figure that is so prevalent, still conspicuous today as a disclaimer found at the bottom of many radiology reports. At best, using the more lenient definition of the DMIST study, mammographic sensitivity is 70% while it may be as low as 40% overall as evidenced by the high-risk multi-modality studies or, alternatively, the 15-month definition of the DMIST study. For individuals, the range of sensitivity with mammography extends from near-zero in patients with extreme density to near-100% in women with complete fatty replacement. But for the general population, one way to consider the sensitivity of mammography is as follows: For every mammographic discovery of a breast cancer in a screening program, there is another asymptomatic woman sent out the door with a detectable breast cancer and a “negative” mammogram report.

Upcoming Improvements in Mammographic Sensitivity

To date, minimal improvement in mammographic sensitivity has come through technologic advances. Certainly, the quality of the images today is far superior to what was seen decades ago, but if a cancer, being white on X-ray, is buried in the comparable “whiteness” of dense breast tissue, it is likely to be invisible no matter how sharp the images.

Witness the minimal improvement in cancer detection seen with the advent of digital mammography as noted in the DMIST study above,16 and the continued controversy as to whether or not CAD (computer-assisted diagnosis) improves sensitivity, or if it is helpful only for less experienced radiologists.24

The great weakness of mammography is its dependence on anatomic contrasts, when, in dense breast tissue, such contrasts may be absent. Thus, there is an inverse correlation between mammographic sensitivity and mammographic density. MRI is impacted only slightly by breast density, as it relies on the physiologic identification of cancers using a contrast-enhancing agent (gadolinium) that is infused as part of the procedure, not to mention the very thin slices (1-2 mm) of the images. Similar to the principles of MRI, upcoming improvements in mammography include using intravenous infusions as part of contrast enhanced mammography,25 as well as tomosynthesis26 wherein the images of the breast are made in slices (albeit much thicker than MRI). Preliminary evidence suggests there will be improvements in mammographic sensitivity, and perhaps the greatest improvement will come when both contrast-enhancement and tomosynthesis are used together. However, many limitations with mammographic screening will continue, most notably the extraordinary costs for this added technology when, in fact, it is critical for mass screening programs to keep costs controlled.

Persistent Limitations with Screening Mammography in Spite of Improvements

The purpose of screening is to save lives, not money. Many are surprised to learn that screening mammography as a public health policy does not decrease health care expenditures. It adds. While it may be intuitive to think otherwise, it was well known even in the days of sub-$100 mammograms that asymptomatic screening adds to the cost of finding and treating breast cancer. Even with a disease as common as breast cancer, the vast majority of women who undergo mammography do not have cancer, yet mammographic screening prompts false-positives with the attendant call-backs for special views, additional ultrasound studies, diagnostic MRI, image-guided biopsies, and surgical biopsies.

And, simply finding a cancer on mammography does not translate into a “saved life.” Some cancers will be cured even if discovered later on exam, while other cancers will already have metastasized when discovered on mammography. In fact, one estimate by a noted mammography advocate/radiologist is that a single life is saved for every 7.4 breast cancers detected by mammography, requiring 1,460 mammographic examinations.27 Opponents of screening mammography would likely quote statistics even more inefficient.

Much of the cost-effectiveness literature is therefore based on parameters that acknowledge the fact that screening “costs” rather than “saves,” with a typical example being “marginal cost per year of life saved” or MCYLS (note: this is “life saved,” not cost savings). Thus, when one study,28 for example, claims that screening all women from ages 40 to 79 is “cost effective” because the MCYLS of $18,800 is comparable to less frequent imaging after age 50 where MCYLS is $16,100, we are learning that “cost effectiveness” is a relative term used for comparisons, as well as deeming various approaches “acceptable.” Yet, these are costs just the same. Remembering that MCYLS is a “per year” value, one can readily calculate the cost of saving the life of one 40-year-old woman to be well in excess of a half million dollars given her normal life expectancy.

And when computer-assisted detection (CAD) is added to mammography, we find a study revealing that the MCYLS is 19% greater, again within the “acceptable” range of cost-effectiveness.29 But what will be the additional increases in MCYLS when tomosynthesis becomes part of routine screening? And when contrast-enhanced mammography is added? With gradual cost elevations, we can easily lose sight of the fact that asymptomatic screening is extraordinarily expensive. As we enter this era of explosive growth in technology with regard to breast imaging, we have to consider the possibility that we could greatly exceed our resources for asymptomatic screening, and that sophisticated imaging might best be considered as the second line of defense for localization of disease, subsequent to a low-cost general screen.

But rising costs are not the only limitation of mammography. Compliance has been variously reported using different criteria, with estimates greater than 50% since 19903 when simply having a mammogram within the past 2 years is considered “compliant.” However, when stricter criteria are utilized, more likely in line with utilization that translates to saved lives, one study revealed a mere 6% of women who received a mammogram in 1992 were compliant with annual mammograms over the next 10 years.30 Multiple reasons have been identified for the lack of higher compliance, but fear of radiation exposure, cost, pain with breast compression, and general fear of negative outcomes are among the many listed reasons.

Then, additional limitations in mammography exist in that women under the age of 40 are not advised to undergo mammograms unless risk factors are present. Thus, an estimated 11,000 women in the U.S. who will develop breast cancer each year prior to the age of 403 are disenfranchised from mammographic screening. The situation is far worse in many countries where access to mammograms are limited or completely non-existent. Clearly, the benefits of mammographic screening are limited by geography, age, economics, social, and psychological issues.

Mortality Reduction Re-visited in Light of Poor Mammographic Sensitivity

Simply because a screening tool can detect cancer does not automatically translate to a reduction in mortality. As noted above, breast cancer screening with mammography is actually the exception rather than the rule, as a mortality reduction has indeed been confirmed with mammographic screening as opposed to most other cancers where the evidence is still lacking for screening efficacy.

Proving a mortality reduction can only be accomplished through prospective randomized trials, where one group is screened and the other group is not screened. This approach is mandatory to nullify powerful biases that otherwise cloud non-randomized study results: lead time bias, length time bias, overdiagnosis bias, and selection bias. With these biases negated through prospective randomization, only two variables remain that determine efficacy: 1) the natural history (biology) of the disease as it pertains to its interruption through diagnosis/treatment, and 2) the sensitivity of the screening tool. Issues such as disease prevalence and incidence, patient compliance, and the specificity of the screening tool, pertain more to the socioeconomic realities of screening, rather than effectiveness as defined by a reduction in mortality.

The importance of the mammographic screening trials that proved a reduction in mortality cannot be overstated, not necessarily as a testimony to X-ray technology, but rather in demonstrating the validity of early detection as a principle in the fight against breast cancer. The more recent realization that this effective early detection was accomplished with a tool that has only modest sensitivity opens a door to huge potential. Simply stated, if a tool with only 40 to 70% sensitivity can reduce breast cancer mortality, then not only is early detection valid, but it is also a more powerful approach than ever imagined. What might be accomplished with an approach that has 80% sensitivity? Or 90% sensitivity?

When it comes to breast MRI, critics have charged that we need the same prospective, randomized trials to prove a reduction in mortality. But that may not be the case at all. In the mammography trials, where it was unknown if early detection was valid or not from a biologic standpoint, such trials were mandatory. Now that the concept of early detection has been validated, the only remaining variable is the sensitivity of the screening tool. The natural history of breast cancer and the epidemiologic biases have already been accounted for.

It is reasonable to theorize that a doubling of sensitivity as seen with breast MRI will result in a doubling of the reduction in breast cancer mortality. Whether or not finding cancers “earlier” than mammography with MRI has a measurable benefit is unknown; however, the obvious benefit is simply finding the “other 50%” of detectable cancers being missed by mammograms, those tumors large enough to be seen by mammography, but are simply hidden by dense breast tissue.

Clearly, the American Cancer Society did not wait for a mortality reduction with breast MRI before endorsing its use. The sensitivity data alone was so powerful with MRI, along with a dramatic plunge in the incidence of interval cancers, that this highly sensitive modality is now part of the screening regimen for high-risk women.

Although it is impractical to consider breast MRI screening for the general population, to the point that the American Cancer Society actually advises against this practice, there is no reason to believe that the wide disparity in sensitivity between mammography and breast MRI will be any different for the average risk patient. A woman without known risk factors is facing a 13% lifetime risk for breast cancer,3 a figure that is already high, and not that much different than so-called high-risk patients who qualify for MRI screening at 20% lifetime risk, especially when considering that the risk differential is spread out over a 40-year period, or an increased risk of less than 2/10ths of 1% per year.

The hesitancy to recommend widespread screening with MRI is based not only on the limitations imposed by the available published data being limited to high-risk women, but also on the lack of breast MRI expertise, the lack of available facilities, and staggering cost implications with MRI costing 5 to 10 times as much as a mammogram.

In short, we have all the ingredients for creating a massive reduction in breast cancer mortality: 1) the impact of early detection and interrupting the natural history of breast cancer has been proven, 2) the epidemiologic biases that interfere with this proof have been controlled through prospective, randomized trials, and 3) a greater than 90% sensitivity can be accomplished by combining mammography and breast MRI. Yet, this is where the aforementioned socio-economic realities of screening come into play. Given the false-positives of mammography and MRI, the overall costs of dual-modality screening, disease prevalence and incidence, and patient compliance, the prospects of screening the general population with both mammography and MRI are dim. In an era of health care cost containment, one cannot reasonably propose multi-modality screening for the general population. Thus, most investigators have been focused on limiting multi-modality screening to high-risk patients.

Strategies to Improve Screening Efficiency Based on Risk Assessment and BRCA Genetic Testing

The profound improvement in breast cancer detection with breast MRI is countered by the socioeconomic realities noted above. Thus, clinical trials using breast MRI focused exclusively on high-risk patients in an effort to have the highest possible yields that would allow reasonable cost-effectiveness. To date, cost-effectiveness studies (usually rather crude measures based on thought experiments) have been limited to breast MRI applied only to BRCA-mutation carriers,31 and there is little information regarding the costs for other high-risk groups. But with MRI costing 5 to 10 times that of mammography, there is little doubt that screening women at lower levels of risk than gene-carriers is going to have enormous financial consequences.

Women who test positive for the BRCA genes were originally considered to be at an 85% lifetime risk for the development of breast cancer, though these estimates were derived from families with a high degree of penetrance; so, for women unselected for family history, the lifetime risk appears to be 65% for BRCA1 mutation carriers and 45% for BRCA-2.32 These lower values are still remarkably elevated above baseline risk and a sharp contrast to women at a 20% lifetime risk who are also called “high-risk” in the ACS screening guidelines. Still, the point of focusing on these patients in the MRI screening studies was to highlight yields in the context of cost-effectiveness.

All prospective clinical trials with breast MRI to date have utilized a positive family history for the entry criteria, thus forming the basis of the new American Cancer Society recommendations for MRI screening. However, this has been followed by circular reasoning that suggests MRI is effective only in these high-risk populations. In fact, the American Cancer Society has specifically advised against screening in the so-called “normal risk” population. And this is where the lines have blurred between cost-effectiveness and straightforward effectiveness.

There is no biologic or radiologic reason to suggest that MRI only works in the high-risk population; in fact, it would be ludicrous to suggest this as the case. The high sensitivity of MRI has been demonstrated in many non-screening studies that address its usefulness in diagnostic situations and pre-operative staging for newly diagnosed patients. MRI should have twice the sensitivity of mammography in all situations, no matter what its indication and no matter what the lifetime risk of the patient may be.

In fact, one of the prospective screening trials for MRI33 reported sensitivity as a function of risk level. In this study, only 8% of the participants were BRCA-positive (n=43), and for this group, mammographic sensitivity was 25% (2 of 8 cancers discovered by mammography) and MRI sensitivity was 100% (8/8). However, similar differences were seen at all levels of risk. Patients at a 21-40% lifetime risk (n=241) had a mammographic sensitivity of 25% (5/20) and a MRI sensitivity of 100% (20/20). Then, in the lowest risk group where women had only a 20% lifetime risk (n=110), as compared to the general population risk of 13%, mammographic sensitivity was 50% (3/6), while MRI sensitivity was again 100% (6/6). These results support the common sense concept that improved cancer detection with MRI is not a function of risk levels, but due to the inherent attribute of the screening tool.

Nevertheless, using a variety of mathematical models to establish lifetime risk, or through BRCA genetic testing, are the approved approaches today for selecting patients for high-risk screening with MRI. Yet, the inherent weakness of this approach has to be considered – whenever levels of risk are utilized as the sole criteria, the majority of women who will develop breast cancer are excluded. And, the higher the risk level required for MRI screening, the greater the number of women that will be excluded. This is a simple function of the fact that only the minority of women who develop breast cancer have a positive family history for the disease.

The American Cancer Society guidelines acknowledge the need for “more research” when it comes to other risk factors such as atypical hyperplasia, a prior history of breast cancer, or breast density, addressing the population where lifetime risk is between 15 and 20%. The lower end of this controversial group (at 15% lifetime risk) is virtually identical to the 13% lifetime risk of the general population, and becomes a meaningless difference when one considers that these risks are spread out over decades. Thus, many problems exist in the attempts to justify current guidelines for MRI screening that are remarkably aggressive for women above 20% (annual MRI in addition to annual mammography, beginning at age 30), while all others are to simply begin mammography alone at age 40.

Risk is, in fact, only half the story. Theoretically, lifetime risk is intended to translate into the probability that a MRI study, or sequential MRIs, will be positive. But there is another factor present that may be as important as risk, and this is the probability that a cancer will be missed on mammography. And the primary determinant as to whether or not a cancer will be missed is the degree of breast density on mammography. In the American Cancer Society guidelines, breast density is singled out as one of the risk factors that requires “more research.” But it is unclear whether or not the ACS is referring to breast density as a risk factor (where it has unappreciated power), or whether it is referring to its influence on mammographic invisibility. Nevertheless, the case has been made that if one used breast density alone to determine the appropriateness of adding MRI to mammograms, more occult cancers would be discovered in the screening population than by relying on risk.34

In summary, centers of excellence have adopted an approach for utilizing screening breast MRI that rely on complex mathematical models and/or genetic testing that are predicting the likelihood of future disease, but only slightly impact the likelihood of disease at the time of the MRI study. Breast density would, perhaps, yield more cancers discovered through MRI by focusing on those women where mammography is at its worst. And the most efficient approach, in both yield and cost-effectiveness, would likely be a combination of lifetime risk and breast density.

But what would be ideal, going beyond risk and beyond density, would be if a screening tool – a blood test – could identify patients with mammographically occult breast cancer, such that the probability of MRI discovery would be dramatically heightened. Such an approach would address the current risk of occult disease as distinct from the future probability that a disease might occur.

Blood Testing as a Screening Tool

Currently, if a 30 year-old woman has been calculated to be at a 40% lifetime risk for breast cancer, a level where general agreement would dictate the need for MRI screening, she has nearly a 1% probability that a cancer will develop each year. Using the assumption that this cancer will be missed on mammography due to high density, there is a 1% chance that a single screen with MRI will identify a cancer. In fact, this is a respectable yield, given our acceptance of comparable yields with screening mammography in the general population. Thus, 100 women at comparable risk would need to be studied with MRI to find one cancer. However, the screening cost to find this one cancer will approximate $100,000 for the 100 MRIs, not to mention the extra costs related to call-back studies and false-positive biopsies. Then, remembering that only 1 in 7 image-discovered cancers actually results in a life saved, it is likely that costs will prove to be several million dollars to save one life with breast MRI screening – and this is when MRI is used selectively, at risk levels far above the minimum risk elevation suggested by the American Cancer Society guidelines.

Needless to say, if that one individual could be singled out from the 100 as having occult breast cancer through a blood test, then MRI could be recommended and the cancer discovered with remarkable efficiency. Such a test would be highly valuable if it simply reduced the number of women that had to be screened with MRI from 100 down to 5 women. Even reducing the number down to 10 or 20 would be a major advance with regard to efficient utilization of breast MRI.

Applied thusly, the standard for breast screening would become annual mammography and annual blood testing. If mammograms were negative, but blood test positive, the patient would then undergo diagnostic MRI for confirmation and localization of the cancer. Such an approach would revolutionize breast cancer screening, making the potential for MRI available to all women, with no exclusions based on “normal risk.” Remembering that mammography is only identifying approximately one-half of detectable cancers, this approach would, in theory, double the number of early detections, and thus double the mortality reduction seen with mammography alone.

Other benefits of a screening blood test would be the utilization in women considered “too young” for mammography, the disenfranchised 11,000 women each year who develop breast cancer prior to the age of 40.3 Annual blood testing could begin at age 25 without breast imaging of any type, then if the blood test is positive, young women could undergo any combination of ultrasound, MRI, or mammography for disease confirmation and localization. Similarly, older women who currently refuse mammography could undergo blood testing as a single screening tool, with the understanding that they would consent to breast imaging if positive.

Lastly, such blood testing could be considered as the sole modality for those countries where breast imaging equipment is sparse or non-existent. The impact on mortality reduction through blood testing in these locations would vastly exceed what can be anticipated in those countries accustomed to mammographic screening where a modest reduction in mortality is already being accomplished.

What would the sensitivity of screening blood test need to be for breast cancer? When this concept is introduced, it is easy to make the analogy to PSA blood screening for prostate cancer, and this is a valid comparison to explain the rationale. But surprisingly, the sensitivity of PSA is controversial, largely because the natural history of prostate cancer discovered by PSA testing is unknown. And, the impact of PSA screening is also unknown since a mortality reduction through early detection has not yet been demonstrated. So, while the comparison is fair for illustrative purposes, there is no measure available regarding an acceptable sensitivity for a cancer-screening blood test.

On the other hand, for breast cancer, we do have a non-blood-based measure by comparing to the sensitivity already provided by mammography. For those radiologists and clinicians who believe that mammograms alone are providing 90% sensitivity, a blood test will make little sense. But for those who realize it takes both mammography and MRI to achieve such a high sensitivity, and that mammograms alone are only 40%-70% sensitive (depending on the definition), the benefits of a blood test become readily apparent.

Even if a blood test only has sensitivity equivalent to mammography, it is likely that such a test will be helpful, as it may be picking up a “different” 40-70%. There should be no variance in sensitivity based on breast density with a blood test, as occurs with mammography. A blood test would be “blind” to breast density, so it is likely that even modest sensitivity would identify cancers missed by mammography. Certainly, though, the greater the sensitivity of a blood test, the more useful it will be. And while 90% sensitivity and 90% specificity is always a nice goal, sensitivity levels below 90%, perhaps below 80%, could still revolutionize breast cancer screening when it is realized that the “gold standard” of mammography has lowered breast cancer mortality in spite of its remarkably low sensitivity.

The caveat here is actually “specificity” because, when it comes to screening, false-positives cause considerable problems. What happens after a positive blood test, but a negative MRI? Certainly, short-interval follow-ups with MRIs would be recommended, but for how long? And, what is going to be the impact on patients wherein considerable anxiety will be transmitted to women with false-positive results?

False-positives with a blood test would also add to the burden of false-positives already being seen in breast imaging where such results are an inherent part of mammography, ultrasound, and MRI. And when screening large numbers of women, a relatively low false-positive rate can still translate into a large number of patients who must deal with the uncertainties imparted, including the realization that an alleged false-positive might actually be pre-dating the clinical appearance of a breast cancer. It is conceivable that 5 to 7 years of aggressive follow-up might be needed to confirm that a positive result is, indeed, false.

Although this scenario is problematic, if it turns out that a blood test is actually pre-dating the clinical appearance of cancer, then such patients might be ideal candidates for the antihormonal measures that are currently FDA-approved to prevent breast cancer. For instance, if 20% of women who are called “false-positive” end up getting breast cancer over the next 5 years following blood testing, when only 1% would have been anticipated, the blood test would clearly be identifying the development of breast cancer well before MRI. And such subclinical disease could prove susceptible to the anti-hormonal agents that are known to prevent the emergence of clinical breast cancer.

Although this “earlier than MRI detection” would introduce a new set of controversies – as to whether or not MRI follow-up would still provide detection early enough, or if antihormonal drugs are indicated for suppression of emerging disease, or if some women might leap to preventive mastectomy – such information would still be of great help in the long run after the necessary clinical information emerged to guide patient options.

In summary, given the ever-present balance between sensitivity and specificity, when it comes to screening, the focus will be on specificity, while only a modest sensitivity would still be helpful in light of the relatively poor sensitivity of mammography.

Blood Testing as a Diagnostic Tool

Up to this point, the foregoing discussion has focused entirely on screening, first with the weakness of mammography, then the vast improvement but inefficiency of MRI, and finally on a blood test that would efficiently select patients for MRI. However, given a blood test that can detect early cancer, such a test would also be useful in the diagnostic setting for the radiologist.

In spite of the BI-RADS® system for breast imaging interpretations as outlined by the American College of Radiology,35 which guides radiologists in their decision as to whether or not to perform a biopsy, the interpreter of breast images is often faced with ambiguous findings wherein the decision for biopsy is subjective. This invites circular reasoning in the interpretation, wherein the radiologist decides not to biopsy, and thus issues a “BI-RADS 3” level on the official report to support the position. Or, the radiologist might be uncomfortable with observation for a particular finding, and could issue a “BI-RADS 4” level on imaging to support the need for a biopsy. Yet, a different radiologist might issue different BI-RADS levels in both situations. Subjectivity cannot be eradicated in diagnostic imaging, no matter how elaborate the protocol.

The use of a blood test in the diagnostic work-up could then be helpful in either of two ways: 1) With strong sensitivity and thus strong Negative Predictive Value (NPV), a negative blood test would give the radiologist support not to perform a biopsy; or, 2) With strong specificity and thus strong Positive Predictive Value (PPV), a positive blood test would offer support to go ahead with the biopsy. Unlike screening wherein a difficult balance exists between sensitivity and specificity, a blood test with great strength in one or the other could still play a key role in diagnosis when used appropriately.

Currently, the vast majority of breast biopsies based on imaging are negative, and the BI-RADS system has had little impact in this regard. While BI-RADS 5 findings are almost always cancers and radiologists need little help here, only 15-25% of BI-RADS 4 findings will be positive, and many breast centers have positive yields lower than this. This low PPV, even after 30 years to improve mammography, is a major contributor to the inefficiency of screening, not to mention the additional patient anxiety associated with screening. A blood test that could refine the decision-making process for the radiologist would have an enormous benefit.

Many diagnostic situations arise wherein blood testing might help. It is common for findings on breast imaging to be not only ambiguous, but multiple. A breast radiologist is confronted almost daily with mammograms that are dense with multiple “probably benign” calcium clusters, various densities, and perhaps ambiguous findings on ultrasound as well. A blood test could help steer these patients toward (or away from) MRI or biopsy, depending on the specific strengths of the blood test.

Radiologists are not the only specialists who need help. Surgeons and primary care physicians often deal with findings on physical exam that are quite concerning, yet conventional breast imaging, sometimes including breast MRI, are negative. There are some cancers, most notoriously invasive lobular carcinoma, that simply do not appear on any form of breast imaging. A blood test would be helpful, once again, in determining the need to proceed with biopsy or observation. Other symptoms, such as breast pain, nipple discharge, skin changes, etc., can sometimes be the presenting complaint in breast cancer, yet imaging can be negative, so the diagnostic applications of a blood test are many.

Blood Testing as a Tool for Cancer Follow-up

A blood test that is capable of detecting early breast cancer, still contained in the breast, is likely to be an effective tool as part of cancer follow-up as well. This is especially true for women whose abnormal results pre-operatively return to normal post-operatively. A subsequent abnormal test is likely a signal of recurrence disease.

In fact, it is here that most of the blood testing research has concentrated in the past, with “serum tumor markers” in current use by many medical oncologists. CEA, CA15-3, CA27.29 have all been found helpful in the identification of recurrent cancer, but with sensitivity and specificity issues that limit usefulness, even in the metastatic setting where there is questionable benefit when preclinical lead times with positive results are only 2 to 9 months.36 None of these common serum markers has been found to be sensitive enough to use for identifying early breast cancer, however.

If there is little impact in diagnosing metastatic cancer 2 to 9 months earlier than when the disease would become obvious anyway, then a blood test for early breast cancer may not have a great deal of benefit over the currently utilized serum markers – at least, not until curative measures are developed for metastatic disease. However, for those women undergoing breast conservation, detection of recurrence within the breast is quite important as a salvage mastectomy can still result in a cure in many cases. Thus, an accurate blood test for breast-only disease would play a major role in the follow-up of breast cancer patients who have elected breast conservation as their initial locoregional treatment strategy.

History of BC-SeraPro® Blood Testing by Power3 Medical Products, Inc.

In March 2007, Power3 Medical Products received CLIA Certification (Clinical Laboratory Improvement Amendment) for the BC-SeraPro® test to be used in the early detection of breast cancer. This achievement began when Power3, focusing on proteomics, acquired a set of ductal fluid biomarkers developed at M.D. Anderson Cancer Center in Houston, prompting a multi-site clinical trial to determine if these biomarkers could aid in the diagnosis of breast cancer via nipple aspirate fluid (NAF).

The leadership for this study was provided by Essam Sheta, PhD, Director of Biochemistry and the Power3 CLIA (Clinical Laboratory Improvement Amendment) Laboratory Director. He was awarded the prestigious Fulbright Scholarship at The University of Texas at San Antonio where he provided the first bidomain structural proof of nitric oxide synthase, the most complex human enzyme known. This was followed by his unique methodology in the first commercial production of the enzyme by overexpression in E. coli. As an Associate Professor of the Department of Biochemistry at Alexandria University, he supervised several graduate students for Master and Ph.D. degrees in biochemistry and served on the Fulbright Committee Review Board in Cairo. Dr. Sheta is assisted by Ira L. Goldknopf, PhD, Director of Proteomics at Power3 Medical Products and a pioneer in the field. Dr. Goldknopf was the discoverer of a central protein system involved in cell proliferation, apoptosis, and most major cellular regulatory functions. This “ubiquitin system” was cited in the 2004 Nobel Prize for Chemistry.

While the premise of the ductal fluid test was valid, an enormous obstacle with this approach to improve breast cancer diagnosis was the difficulty encountered in the retrieval of bilateral NAF from patients through a laborious process of breast compressions. However, as part of this clinical trial, serum samples had been obtained as well, yielding a number of unique biomarkers signaling the presence of breast cancer.

This finding led to a collaborative research agreement with Mercy Women’s Center in Oklahoma City, a multidisciplinary breast screening and diagnostic facility that is part of Mercy Health Center. Mercy hospital is the busiest location in the state of Oklahoma for the diagnosis and treatment of breast cancer, and the Women’s Center is one of the most experienced sites in the nation with breast MRI. Mercy also has an active risk assessment and genetic testing program, and the director of that program, Dr. Alan Hollingsworth, had been collecting and storing serum samples on breast cancer patients and controls for a number of years.

Figure 1:

From 775 of these samples, 22 protein markers were identified (patents pending) that were differentially expressed in the serum of breast cancer patients. Using 2-D gel electrophoresis and gel image analysis (see Figure 1), the effects of individual and combined markers were used to differentiate breast cancer patients from controls (see Figures 2 & 3). When the test had evolved to the point of potential clinical utility, a blinded study was performed, with results presented at the 30th Annual San Antonio Breast Cancer Symposium held in December 2007.

Figure II:

Figure III:

Presentation at the San Antonio Breast Cancer Symposium

Using 98 samples obtained from two clinical sites – Mercy Women’s Center in Oklahoma City and Obstetrical & Gynecological Associates, PA in Houston – BC- SeraPro® was performed. Samples were obtained from 21 healthy controls, 38 women with confirmed benign breast disease, and 39 breast cancer patients at various stages. The 39 breast cancer patients had various histologies as well, with 7 patients having Stage 0 DCIS, 4 patients with invasive lobular carcinoma, and 28 patients with invasive ductal carcinoma.

For the entire group of samples, the sensitivity and specificity were both 90%, with 35 of the 39 breast cancer patients correctly identified, and 53 of 59 controls/benign disease correctly identified. (see Table I – Healthy controls and women with confirmed benign disease were combined for linear discriminant analysis in a two-way comparison.)

Table I:

Table II:

Although 98 samples were included in the formal study, additional outcomes were analyzed for 60 previously untested samples (of the original 98) that had been blinded to the researchers with regard to clinical information. For these 60 patients, sensitivity was 80% and specificity 87% (see Table II). Breakdown of the 30 cancer patients within this grouping revealed predominantly early-stage disease, with 24 patients having Stage 0 & I breast cancer, 5 patients with Stage II disease, and only 1 patient with Stage III. Later analysis was performed as to histologic grade, ER/PR positivity, and HER2/neu status, and though sub-groups were too small for statistical differences, no trends could be noted. The accuracy of BC-SeraPro® appeared to be the same across all groupings.

Prospective Clinical Trial for BC-SeraPro® Validation

Subsequent to the study of the blinded samples above, a prospective clinical trial was begun to confirm the utility of BC-SeraPro® in the clinical setting. Under an IRB-approved protocol, patients at Mercy Women’s Center in Oklahoma City who have suspicious mammograms, undergo drawing of blood samples prior to breast biopsy. In addition, samples are drawn in healthy controls from asymptomatic women who are part of the MRI screening program and who have both negative mammograms and MRI at the time of the blood draw.

Because some women, especially those with benign breast disease, end up with BC-SeraPro® values in an intermediate range, this trial is utilizing an “indeterminate” category in order to offer helpful clinical information, minimizing the confusion caused by false-positives and false-negatives. A “positive” result is thus intended to indicate the presence of breast cancer, a “negative” result is intended to denote the absence of cancer, and an “indeterminate” result prompts the need for follow-up blood testing to see if there is a worsening proteomic pattern over time.

This approach is analogous to the system currently in widespread clinical use for OncotypeDX, a genomic-based study of breast cancers where an attempt is made to predict the likelihood of systemic cancer recurrence. Breast cancers submitted for OncotypeDX analysis are given a “low” recurrence score, which indicates no need for adjuvant systemic chemotherapy, or a “high recurrence score,” which indicates the need for adjuvant chemotherapy. However, a “mid-range recurrence score” is an open-ended result where clinical judgment is utilized, while a prospective, randomized clinical trial is in progress (TAILORx) to determine whether or not chemotherapy should be utilized for this group.

In the same fashion, Power3 plans the “indeterminate” score for BC-SeraPro® to be modified with additional experience, hoping to minimize this category over time. The balance between sensitivity and specificity is always a challenge, since gains in one parameter almost always impart losses in the other. Setting a single score for dichotomous reporting of positivity vs. negativity would limit clinical use at this early point in the clinical introduction of a new modality. Thus, the “indeterminate” category is planned for the initial launch and will likely continue as part of the assay until the database is so deep that the category can be used infrequently or dropped entirely.

The intended use for the blood test is as stated above – screening, diagnostic work-ups, and cancer follow-up. To date, however, testing has been limited to this pre-clinical prospective, blinded trial in order to provide meaningful sensitivity and specificity data for clinicians.

Competition

While it is not believed that there is another breast cancer blood test at the threshold for commercial launch, research in this area is ongoing at major biotech and pharmaceutical companies as well as smaller biotech companies using a variety of approaches such as SELDI-TOF and mass spectroscopy. The complexity and heterogeneity of breast cancer has made the development of such a test quite difficult. Unlike prostate cancer where a single antigen – prostate specific antigen (PSA) – is manufactured almost exclusively by the prostate gland, and to an elevated degree by most prostate cancer cells, breast cancer has no known common or unique antigen. Use of other solitary markers for breast cancer, such as the nuclear matrix protein NMP-66 (Matritech, Inc.) proved unsuccessful, leaving the vast majority of research focused on the identification of multiple markers followed by the integration of these markers into meaningful patterns.

Future Directions

Breast cancer is not unique in its complexity with regard to blood testing research. It appears, in fact, that most cancers under study will require an array of markers in order to arrive at a clinically useful test. For instance, the currently available CA-125 blood test for ovarian cancer has been in use for over 20 years, but is recommended sparingly for screening due to its modest accuracy. Thus, several investigators are using a multiple marker approach for ovarian cancer to replace the CA-125. The “simplicity” of tests like PSA for prostate cancer is unlikely to be found in most cancer types, so it is anticipated that the multiple marker approach will become the standard.

At the same time, imaging technology has progressed to the point where virtually any malignancy in the body can be identified by the time it reaches 1.0cm in size, using MRI, CT, PET scanning, endoscopy, as well as various combinations of these modalities. However, for the same principles as noted earlier in this document, the more complex and expensive these procedures become, the more inaccessible is their use for general population screening. The sequence of a low-cost screening blood test will very likely be the standard eventually for cancer of all types, reserving the expensive diagnostic procedures as a second-line approach for diagnostic confirmation as well as localization of the cancer to allow treatment.

The more futuristic step will be linking therapeutics to the blood test, such that abnormalities in the body might be treated according the proteomic or genomic profile of the individual cancer. Furthermore, it is not unreasonable to predict that the next generation of scientists will be able to intimately link blood testing to both cancer detection and therapy, such that all is accomplished as a single step. To assist in this goal, blood samples from patients with all types of cancer are being collected to allow biomarker discoveries that will apply broadly in the field of oncology.

The development of BC-SeraPro® is the first step toward this goal in breast cancer. After the prospective blinded trial currently underway, the blood test will need to be implemented into actual clinical scenarios at multiple sites and data collected through a registry and formal clinical trials in order to allow its role to be defined in screening, diagnosis, and cancer follow-up.

At this point, it is currently unknown where, in the clinical “life” of a breast cancer, BC-SeraPro® is detecting the malignancy – before mammography?…at the same time as MRI?…or, before MRI? The distinction may not be necessary given that the primary purpose of the blood test is to detect cancers being missed by mammography. However, the most challenging development will occur if BC-SeraPro® is actually detecting cancer earlier than MRI. This would result in the unusual situation in which clinical imaging would need to “catch up” to blood testing. Such advancements are in progress as breast MRI technology continues to improve with thinner and thinner slices (currently at 1mm with some units), as well as improved accuracy through the addition of MRI spectroscopy.37 PET mammography is also making an entry into the clinical arena, bringing with it the possibility of receptor-targeted therapies in addition to improved breast cancer detection.38

The early diagnosis of breast cancer appears to be on the eve of a revolution – a new approach to cancer detection through blood testing, first as an adjunct to mammography, indicating the need for further study, such as MRI. Then, over time, if adequate sensitivity can be reached, blood testing alone could serve as the initial sole screening methodology, not only for breast cancer but also other types of cancer, guiding the efficient use of expensive imaging technologies for disease confirmation, localization, and treatment.

1 Parkin DM, Bray F, Ferlay J, Pisani P. Global cancer statistics, 2002. CA Cancer J Clin 2005; 55:74-108.

2 Parkin DM, Stjernsward J, Muir CS. Estimates of the worldwide frequency of twelve major cancers. Bull World Health Organ 1984; 62:163-182.

3 American Cancer Society. Breast Cancer Facts and Figures 2005-2006. Atlanta:American Cancer Society, Inc.

4 Berry DA, Cronin KA, Plevritis SK, et al. Effect of screening and adjuvant therapy on mortality from breast cancer. N Engl J Med 2005; 353:1784-1792.

5 Black WC. Computed tomography screening for lung cancer: review of screening principles and update on current status. Cancer 2007; 110:2370-2384.

6 Concato J, Wells CK, Horwitz RI, et al. The effectiveness of screening for prostate cancer: a nested case-control study. Arch Intern Med 2006; 166:38-43.

7 Schwartz LM, Woloshin S, Fowler FJ Jr, Welch HG. Enthusiasm for cancer screening in the United States. JAMA 2004; 291:71-78.

8 Fisher B, Montague E, Redmond C, et al. Comparison of radical mastectomy with alternative treatments for primary breast cancer. Cancer 1977; 39:2827-2839.

9 Fisher B, Anderson S. Bryant J, et al. Twenty-year follow-up of a randomized trial comparing total mastectomy, lumpectomy, and lumpectomy plus irradiation for the treatment of invasive breast cancer. N Engl J Med 2002; 347:1233-1241.

10 Smith RA, Saslow D, Sawyer KA, et al. American Cancer Society guidelines for breast cancer screening: Update 2003. CA Cancer J Clin 2003; 53:141-169.

11 Hellman S. Karnofsky memorial lecture: Natural history of small breast cancers. J Clin Oncol 1994; 12:2229-2234.

12 Feig SA. Effect of service screening mammography on population mortality from breast carcinoma. Cancer 2002; 95:451-457.

13 Park A. Breast-Cancer Basics: mammogram vs. MRI. TIME Magazine, October 15, 2007. Time, Inc., New York, NY.

14 American Cancer Society. Cancer Facts & Figures 2007, page 9. Atlanta: American Cancer Society; 2007.

15 Shen Y, Zelen M. Screening sensitivity and sojourn time from breast cancer early detection trials: mammograms and physical examinations. J Clin Oncol 2001; 19:3490-3499.

16 Pisano ED, Gatsonis C, Hendrick E, et al. Diagnostic performance of digital versus film screen mammography for breast-cancer screening. N Engl J Med 2005; 353:1773-1783.

17 Saslow D, Boetes C, Burke W, et al. American Cancer Society guidelines for breast screening with MRI as an adjunct to mammography. CA Cancer J Clin 2007; 57:75-89.

18 Sardanelli F, Podo F. Breast MR imaging in women at high risk of breast cancer. Is something changing in early breast cancer detection? Eur Radiol 2007; 17:873-887.

19 Warner E, Plewes D, Hill K, et al. Surveillance of BRCA1 and BRCA2 mutation carriers with magnetic resonance imaging, ultrasound, mammography, and clinical breast exam. JAMA 2004; 292:1317-1325.

20 Kriege M, Brekelmans CTM, Boetes C, et al. Efficacy of MRI and mammography for breast-cancer screening in women with a familial or genetic predisposition. N Engl J Med 2004; 351:427-437.

21 Warner E, Plewes D, Hill K, et al. Effect of age and temporal patterns over 5 years in a magnetic resonance imaging-based breast surveillance study for BRCA mutation carriers. Proc Am Soc Clin Oncol 2004; 23:831 (abstr).

22 Bigenwald R, Warner E, Gunasekara K, et al. Is mammography adequate for screening BRCA mutation carriers with low breast density? Proc Am Soc Clin Oncol 2006; 24:544s (abstr).

23 Dent R, Warner E. Screening for hereditary breast cancer. Semin Oncol 2007; 34:392-400.

24 Hukkinen K, Pamilo M. Does computer-aided detection assist in the early detection of breast cancer? Acta Radiol 2005; 46:135-139.

25 Jong RA, Yaffe MJ, Skarpathiotakis M, et al. Contrast-enhanced digital mammography: initial clinical experience. Radiology 2003; 228:842-850.

26 Chan HP, Wei J, Sahiner B, et al. Computer-aided detection system for breast masses on digital tomosynthesis mammograms: preliminary experience. Radiology 2005; 237:1075-1080.

27 Tabar L, Fagerberg G, Duffy SW, Day NE. The Swedish two county trial of mammographic screening for breast cancer: recent results and calculation of benefit. J Epidemiol Community Health 1989; 43:107-114.

28 Rosenquist CJ, Lindfors KK. Screening mammography beginning at age 40 years: a reappraisal of cost-effectiveness. Cancer 1998; 82:2235-2240.

29 Lindfors KK, McGahan MC, Rosenquist CJ, Hurlock GS. Computer-aided detection of breast cancer: a cost-effectiveness study. Radiology 2006; 239:710-717.

30 Blanchard K, Colbert JA, Puri D, et al. Mammographic screening: patterns of use and estimated impact on breast carcinoma survival. Cancer 2004; 101:495-507.

31 Plevritis SK, Kurian AW, Sigal BM, et al. Cost-effectiveness of screening BRCA 1/2 mutation carriers with breast magnetic resonance imaging. JAMA 2006; 295:2374-2384.

32 Antoniou A, Pharoah PD, Narod S, et al. Average risks of breast and ovarian cancer associated with BRCA1 or BRCA2 mutations detected in case series unselected for family history: a combined analysis of 22 studies. Am J Hum Genet 2003:72:1117-1130.

33 Kuhl CK, Schrading S, Leutner CC, et al. Mammography, breast ultrasound, and magnetic resonance imaging for surveillance of women at high familial risk for breast cancer. J Clin Oncol 2005; 23:8469-8476.

34 Hollingsworth AB, Stough RG. Breast MRI screening for high-risk patients. Sem Breast Dis (accepted for publication in 2008).

35 ACR BI-RADS®-Mammography, 4th Edition. In: ACR Breast Imaging Reporting and Data System, Breast Imaging Atlas. Reston, VA. American College of Radiology; 2003.

36 Duffy M. Serum tumor markers in breast cancer: are they of clinical value? Clin Chem 2006; 52:345-351.

37 Bolan PJ, Nelson MT, Yee D, Garwood M. Imaging in breast cancer: magnetic resonance spectroscopy. Breast Cancer Res 2005; 7:149-152.

38 Hofmann M. From scinti-mammography and metabolic imaging to receptor targeted PET – new principles of breast cancer detection. Phys Med 2006; 21 Suppl 1:11.

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Blood Clots/Stroke – They Now Have a Fourth Indicator

strokeSTROKE:Remember the 1st Three Letters….S.T..R.

My nurse friend sent this and encouraged me to post it and spread the word.  I agree.

If everyone can remember something this simple, we could save some folks.
Seriously…

Please read:

STROKE IDENTIFICATION:

During a BBQ, a friend stumbled and took a little fall.  She assured everyone that she was fine (They offered to call paramedics).  She said she had just tripped over a brick because of her new shoes.

They got her cleaned up and got her a new plate of food. While she appeared a bit shaken up, Ingrid went about enjoying herself the rest of the evening.

Ingrid’s husband called later telling everyone that his wife had been taken to the hospital.  At 6:00 pm Ingrid passed away… She had suffered a stroke at the BBQ.. Had they known how to identify the signs of a stroke, perhaps Ingrid would be with us today. Some don’t die.  They end up in a helpless, hopeless condition instead.

It only takes a minute to read this…

A neurologist says that if he can get to a stroke victim within 3 hours he can totally reverse the effects of a stroke…totally. He said the trick was getting a stroke recognized, diagnosed, and then getting the patient medically cared for within 3 hours, which is tough.

RECOGNIZING A STROKE:

Thank God for the sense to remember the ‘3’ steps, STR . Read and Learn!

Sometimes symptoms of a stroke are difficult to identify.    Unfortunately, the lack of awareness spells disaster. The stroke victim may suffer severe brain damage when people nearby fail to recognize the symptoms of a stroke.

Now doctors say a bystander can recognize a stroke by asking three simple questions:

S *Ask the individual to SMILE.
T *
Ask the person to TALK and SPEAK A SIMPLE SENTENCE, coherently.  (i.e. It is sunny out today.)
R
*Ask him or her to RAISE BOTH ARMS.

If he or she has trouble with ANY ONE of these tasks, call emergency number immediately and describe the symptoms to the dispatcher.

New Sign of a Stroke ——– Stick out Your Tongue

NOTE: Another ‘sign’ of a stroke is this: Ask the person to ‘stick’ out his tongue….. If the tongue is ‘crooked’, if it goes to one side or the other, that is also an indication of a stroke.

A cardiologist says if everyone who gets this e-mail sends it to 10 people; you can bet that at least one life will be saved…also remember you don’t have to be a senior citizen to have a stroke.

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Health and Habits of College Students

Report on Health and Habits of College Students Released
Dr. Ed Ehlinger, the director and chief health officer of the University’s Boynton Health Service

ParentsOfCollegeBoundKidsA report released by the University of Minnesota Boynton Health Service is the first of its kind in the nation to conduct a comprehensive survey on the health of college students. About 10,000 college students completed the survey. Although the study is focused on students from 14 campuses in Minnesota, the health findings here reflect national health trends for college students, says Dr. Ed Ehlinger, the director and chief health officer of the university’s Boynton Health Service.

The report examines everything from mental health and obesity to financial health and sexual health. It also looks at alcohol use, smoking, personal safety, physical activity and how many students do not have health insurance. One key finding is beginning to show how today’s technology is impacting students’ health and their academics. In fact, 28.7 percent of students surveyed report excessive computer/Internet/TV use and 41.8 percent indicate the activity affected their academic performance.

Ehlinger said members of the public, higher education leaders and policymakers should pay attention to the findings and make the health of college students a priority.

“The health of college students is important not only to the institutions they attend but also to the health of the state of Minnesota. Good health helps students remain in school, and a college degree or certificate is an excellent predictor of better health and economic status throughout one’s lifetime,” Ehlinger said.

Education is one of the strongest influences on economic and health status, Ehlinger said. “College students are a large and growing population and are establishing lifestyles and behavior patterns, they are the trendsetters and the role models for younger people and they are the future leaders of our society. That is why we need to make them a priority,” Ehlinger said.

“There is a shortage of information about these students particularly in areas that go beyond alcohol, tobacco and other drug use,” Ehlinger said. A survey like this one is beginning the shift to a more comprehensive examination of college student health. Along with Boynton, the study was funded Blue Cross/Blue Shield of Minnesota.

About 24,000 students from 14 Minnesota colleges and universities were randomly selected to participate in this study and 9,931 completed and returned the College Student Health Survey Report which tracks a wide range of student health issues from mental health and financial health to tobacco, nutrition/obesity and alcohol use.

Survey results will help schools determine what programs they need in place in order to improve the health of students. All five University of Minnesota campuses were included in the survey along with the following schools: Alexandria Technical College; Anoka-Ramsey Community College; Lake Superior College; Minnesota State Community and Technical College; North Hennepin Community College; Northwest Technical College; Bemidji State University; Concordia College; Minnesota State University Moorhead. Ehlinger will outline the report’s overall findings.

“The reason we’re studying students from 14 schools is because these health issues are community and state issues. We really need to address college student health issues on a statewide basis and not just on an individual school basis,” Ehlinger said. The survey was designed to look at students in a more holistic way, he said.

“College students face multiple risks to their health and their behavior affects all parts of their existence. We need to look at a student as a complex and complete person,” Ehlinger said.

In addition to the comprehensive 14 school report each participating institution will receive its own school-specific report. Some details on the University of Minnesota, Twin Cities report are available at this point — 2,920 U of M, Twin Cities students completed the survey out of 6,000 who were randomly selected to participate.

Report findings:

Mental health

Results show that 27.1 percent of students surveyed have been diagnosed with a mental health illness within their lifetime and 15.7 percent were diagnosed with a mental health illness in the last 12 months. At the U of M, Twin Cities, 25.1 percent report being diagnosed with at least one mental health condition in their lifetime. Throughout the schools surveyed and on the U of M, Twin Cities campus, depression and anxiety are the two most frequently reported mental health diagnoses of students for both their lifetime and the last 12 months. Of all the surveyed students, 18.5 percent reported being diagnosed during their lifetime with depression and 13.3 percent were diagnosed with anxiety.

Physical activity, nutrition, obesity

Nearly two-fifths or 38.5 percent of all students surveyed fall within the overweight or obese/extremely obese categories. At the University of Minnesota, Twin Cities, 29.1 percent of those surveyed fall within the overweight or obese/extremely obese categories. A new issue is surfacing when it comes to student physical health, 28.7 percent of students surveyed report excessive computer/Internet use and 41.8 percent indicate the activity affected their academic performance. On the U of M, Twin Cities campus, 32.2 percent of students surveyed reported excessive computer/Internet use and among this group, 41.9 percent indicate this activity impacted their academic performance.

Health insurance, uninsured

One key finding of the report is that 9.4 percent of all undergraduate students surveyed don’t have health insurance. For students in the University of Minnesota system, that rate is only 5.6 without health insurance compared with the 13.7 percent uninsured in non-U of M schools. At the U of M, Twin Cities, the uninsured rate for undergraduate students is 6.5 percent. Students in the 18- to-24-year-old range tend to have insurance, but students who are 25 to 29-years-old are less likely to have insurance.

“We have a fairly low uninsured rate here in the University of Minnesota system where students are required to carry insurance. The higher uninsured rate throughout the rest of the schools makes the argument that a requirement for insurance coverage is a good thing for schools and for students,” Ehlinger said.

The students who have insurance are more likely to go in for preventive health services and have fewer sick days.

“College students use health services on campus and in communities and when it comes to mental health services, students seek out assistance on campus.”That tells us that colleges really do need to invest in on campus support services.”

Financial health

Of students surveyed, 33.4 percent of them report carrying some level of credit card debt over the past month and 57.8 percent report the debt as $1,000 or more. On the U of M, Twin Cities campus, 29 percent of students report carrying some level of credit card debt and 59.9 percent report the debt as $1,000 per month or more.

“Students with greater than $1,000 of credit card debt tend to have higher rates of depression and have lower grade point averages,” Ehlinger said.

Alcohol

Alcohol use continues to be a concern for universities and colleges. Among students surveyed, 70.5 percent report using alcohol in the last 30 days and 37.1 percent report engaging in high-risk drinking within the past two weeks. At the U of M, Twin Cities, 74.3 percent report using alcohol in the last 30 days and 36.5 percent report engaging in high-risk drinking. Illicit drug use among those surveyed is low with 6.8 percent reporting they had used illicit drugs. On the Twin Cities campus, 7.1 percent report using illicit drugs.

Sexual violence

More than one in five or 22.4 percent of female students report experiencing a sexual assault in their lifetime with 6.8 percent reporting having been assaulted in the last 12 months. For male students, only 4.9 percent report being sexually assaulted in their lifetime with 1.9 percent reporting an assault within the past 12 months. Such assaults have lingering impact on students and their academic performance, Ehlinger said. Students who have been victims of sexual assault report higher rates of depression.

Sexual health

Of students surveyed, 77.6 percent report having been sexually active in their lifetime and 72.1 percent having been sexually active within the past 12 months. On the U of M, Twin Cities campus, 77.1 percent report having been sexually active in their lifetime and 71.7 percent report having been sexually active within the past 12 months. Nearly four out of five or 78.5 percent of students report having had zero or one sexual partner within the last 12 months. On the U of M, Twin Cities campus, 77.8 students reported having zero or one partner within the last 12 months. “Students are pretty monogamous according to the results, which contradicts the commonly held stereotype of students being promiscuous,” Ehlinger said.

Tobacco use

The current tobacco use rate in the last 30 days for all students at the 14 schools is 25 percent. On the U of M, Twin Cities campus, the current tobacco use rate is 20.9 percent for students ages 18 to 24 and their daily use rate at 3.7 percent, which are the lowest reported use rates among U of M, Twin Cities students since the tobacco data was first collected in 1992. Tobacco use is defined as both smoke and smokeless tobacco.

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What is ADHD?

What is ADHD (Attention Deficit Hyperactivity Disorder)?

adhdHealth experts say that ADHD (attention deficit hyperactivity disorder) is the most common behavioral disorder that starts during childhood. However, it does not only affect children – people of all ages can suffer from ADHD. Psychiatrists say ADHD is a neurobehavioral developmental disorder.

An individual with ADHD finds it much more difficult to focus on something without being distracted. He has greater difficulty in controlling what he is doing or saying and is less able to control how much physical activity is appropriate for a particular situation compared to somebody without ADHD. In other words, a person with ADHD is much more impulsive and restless.

Health care professionals may use any of the following terms when describing a child (or an older person) who is overactive and has difficulty concentrating – attention deficit, attention deficit hyperactivity disorder, hyperkinetic disorder, hyperactivity.

North Americans commonly use the terms ADD (attention deficit disorder) or ADHD (attention deficit hyperactivity disorder). In the UK hyperkinetic disorder is the official term – however, ADD and ADHD have become widely used.

ADHD in children is completely different from normal childhood excited and boisterous behavior. Many children, especially very young ones, are inattentive and restless without necessarily being affected by ADHD.

The Centers for Disease Control and Prevention (CDC) estimates that approximately 4.4 million children aged 4 to 17 have been diagnosed with ADHD in the USA by a healthcare professional. As of 2003 two-and-a-half million American children aged 4 to 17 are being treated for ADHD with medicines. The CDC adds that in 2003 7.8% of all school-aged American children were reported to have an ADHD diagnosis by their parent.

Three types of ADHD

According to the CDC, there are three types of ADHD. They are defined according to which symptoms stand out the most.

  1. Predominantly Inattentive Type
    The person finds it very difficult to organize or finish a task. They find it hard to pay attention to details and find it difficult to follow instructions or conversations.
  2. Predominantly Hyperactive-Impulsive Type
    The person finds it hard to keep still – they fidget and talk a lot. A smaller child may be continually jumping, running or climbing. They are restless and impulsive – interrupting others, a grabbing things and speaking at inappropriate times. They have difficulty waiting their turn and find it hard to listen to directions. A person with this type of ADHD will have more injuries and/or accidents than others.
  3. Combined Type
    A person whose symptoms include all those of 1 and 2, and whose symptoms are equally predominant. In other words, all the symptoms in 1 and 2 stand out equally.

What are the general signs of ADHD in children?

  • the child is restless, overactive, fidgety
  • the child is constantly chattering
  • the child is continuously interrupting people
  • the child cannot concentrate for long on specific tasks
  • the child is inattentive
  • the child finds it hard to wait his/her turn in play, conversations or standing in line (queue)

The above signs may be observed in children frequently and usually do not mean the child has ADHD. It is when these signs become significantly more pronounced in one child, compared to other children of the same age, and when his/her behavior undermines his/her school and social life, that the child may have ADHD.

What causes ADHD?

We are not sure. Studies reveal that a person’s risk of developing ADHD is higher if a close relative also has/had it. Twin studies have indicated that ADHD is highly heritable. We also know that ADHD is much more common in boys than girls. The scientific community generally agrees that ADHD is biological in nature. Many reputable scientists believe ADHD is the result of chemical imbalances in the brain.

Some studies have indicated that food additives, specifically some colorings, may have an impact on ADHD behaviors. In July 2008, the European Union ruled that synthetic food colorings (called azo dyes) must be labeled not only with the relevant E number, but also with the words “may have an adverse effect on activity and attention in children”.

A 1984 study by Benton and team, demonstrated that sugar has no effect on behavior. A study in 1986 by Milich and Pelham, and another by Wolraich and team in 1985 also found no link between sucrose (sugar) and behavior impact on children with ADHD. However, most sugars found in sugary foods and sweets (candy) consumed by children are corn syrup and high fructose corn syrup – these sugars were not used in any of the above-mentioned studies.

Interesting link
Possible causes of ADHD (New Zealand’s ADHD Online Support Group)

How do I know if I, my child, spouse or relative has ADHD?

ADHD cannot be diagnosed physically, i.e. with a blood test, urine test, brain scan or a physical check up. As most children have problems with self-control anyway, a proper diagnosis can be quite challenging.

An ADHD diagnosis has to be carried out by a specialist – usually a psychiatrist, psychologist or pediatrician. The specialist will observe the child and recognize behavior patterns. Data regarding the child’s behavior at home and at school will also be studied. Only a specialist will be able to accurately detect whether other problems and/or conditions are resulting in ADHD-like behavioral characteristics.

Interesting links
Diagnostic Criteria for ADHD (ADHD Information Services)

If you do not know how to find a specialist, ask your GP.

Recognizing ADD and ADHD in Children – Video

A video about attention deficit hyperactivity disorder (ADHD or ADD) in children. Includes information on symptoms and diagnosis. Video by SaberHacer.com.

When does ADHD start? How long does ADHD last?

According to New Zealand’s ADHD Online Support Group, the onset of ADHD usually occurs before the person is 7 years old. For about 75% of ADHD sufferers, symptoms continue into adulthood. However, levels of hyperactivity tend to decrease as the person gets older.

Adult ADHD

It was not until the 1970s that researchers began to realize that what we today know as ADHD did not always go away during a person’s teen years. It was during that decade that it was also noticed that some ADHD symptoms were identified in the parents of children undergoing ADHD treatment. In 1978 ADHD was formally recognized as a condition that also afflicts adults, and the term Adult ADD began – the ‘H’ of ADHD was dropped because it seemed the adults were not as hyperactive as children.

According to uspharmacist.com, approximately 8 million adults in the USA have ADHD. An adult with ADHD who is untreated will tend to have a chaotic lifestyle – they may seem more disorganized compared to people who are not afflicted with ADHD. Healthcare professionals believe there are millions of adults who have ADHD but do not know and remain untreated. Studies indicate that adults with ADHD benefit enormously from a combination of medication and behavior therapy.

What is ADHD? Adult ADHD – Video

A series of videos on living with adult ADHD. Watch this introduction, then click on the next associated video in the series, at the end of the video. Videos produced for Experts Village.

A list of some of the more common ADHD medications

Amphetamines

Adderal (two strengths, one for short period, one for longer periods)
Dexedrine (lower dosage – taken several times a day)

Methylphenidate

Ritalin
Ritalin LA (will last up to 12 hours). Methylin
Focalin
Focalin XR (will last up to 12 hours)
Metadate CD

Others

Atomoxetine HCI (Strattera)
Bupropion (Wellbutrin XL)
Benzphetamine
Clonidine
Provigil

What is ADHD? – Video

A closer look at HD, ADD and ADHD with Dr. Matthew H. Erdelyi Ph.D, Professor of Psychology at Brooklyn College. Video by illumistream Health.

Further information

ADHD news

Medical News Today is a leading resource for the latest headlines on ADHD. So, check out our ADHD news section. You can also sign up to daily ADHD news alerts or our weekly digest newsletters to ensure that you stay up-to-date with the latest news.


This what is ADHD? Information section was written by Christian Nordqvist and may not be re-produced in any way without the permission of Medical News Today.

Sources


Disclaimer: This guide is provided for general information purposes only. The materials contained within this guide do not constitute medical or pharmaceutical advice, which should be sought from qualified medical and pharmaceutical advisers. Full disclaimer.

© MediLexicon International Ltd

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What are Stem Cells?

cell

Stem cells are a class of undifferentiated cells that are able to differentiate into specialized cell types. Commonly, stem cells come from two main sources:

Embryos formed during the blastocyst phase of embryological development (embryonic stem cells) and
Adult tissue (adult stem cells).

    Both types are generally characterized by their potency, or potential to differentiate into different cell types (such as skin, muscle, bone, etc.).

    Adult stem cells

    Adult or somatic stem cells exist throughout the body after embryonic development and are found inside of different types of tissue. These stem cells have been found in tissues such as the brain, bone marrow, blood, blood vessels, skeletal muscles, skin, and the liver. They remain in a quiescent or non-dividing state for years until activated by disease or tissue injury.

    Adult stem cells can divide or self-renew indefinitely, enabling them to generate a range of cell types from the originating organ or even regenerate the entire original organ. It is generally thought that adult stem cells are limited in their ability to differentiate based on their tissue of origin, but there is some evidence to suggest that they can differentiate to become other cell types.

    Embryonic stem cells

    Embryonic stem cells are derived from a four- or five-day-old human embryo that is in the blastocyst phase of development. The embryos are usually extras that have been created in IVF (in vitro fertilization) clinics where several eggs are fertilized in a test tube, but only one is implanted into a woman.

    Sexual reproduction begins when a male’s sperm fertilizes a female’s ovum (egg) to form a single cell called a zygote. The single zygote cell then begins a series of divisions, forming 2, 4, 8, 16 cells, etc. After four to six days – before implantation in the uterus – this mass of cells is called a blastocyst. The blastocyst consists of an inner cell mass (embryoblast) and an outer cell mass (trophoblast). The outer cell mass becomes part of the placenta, and the inner cell mass is the group of cells that will differentiate to become all the structures of an adult organism. This latter mass is the source of embryonic stem cells – totipotent cells (cells with total potential to develop into any cell in the body).

    In a normal pregnancy, the blastocyst stage continues until implantation of the embryo in the uterus, at which point the embryo is referred to as a fetus. This usually occurs by the end of the 10th week of gestation after all major organs of the body have been created.

    However, when extracting embryonic stem cells, the blastocyst stage signals when to isolate stem cells by placing the “inner cell mass” of the blastocyst into a culture dish containing a nutrient-rich broth. Lacking the necessary stimulation to differentiate, they begin to divide and replicate while maintaining their ability to become any cell type in the human body. Eventually, these undifferentiated cells can be stimulated to create specialized cells.

    Stem cell cultures

    Stem cells are either extracted from adult tissue or from a dividing zygote in a culture dish. Once extracted, scientists place the cells in a controlled culture that prohibits them from further specializing or differentiating but usually allows them to divide and replicate. The process of growing large numbers of embryonic stem cells has been easier than growing large numbers of adult stem cells, but progress is being made for both cell types.

    Stem cell lines

    Once stem cells have been allowed to divide and propagate in a controlled culture, the collection of healthy, dividing, and undifferentiated cells is called a stem cell line. These stem cell lines are subsequently managed and shared among researchers. Once under control, the stem cells can be stimulated to specialize as directed by a researcher – a process known as directed differentiation. Embryonic stem cells are able to differentiate into more cell types than adult stem cells.

    Potency

    Stem cells are categorized by their potential to differentiate into other types of cells. Embryonic stem cells are the most potent since they must become every type of cell in the body. The full classification includes:

    • Totipotent – the ability to differentiate into all possible cell types. Examples are the zygote formed at egg fertilization and the first few cells that result from the division of the zygote.
    • Pluripotent – the ability to differentiate into almost all cell types. Examples include embryonic stem cells and cells that are derived from the mesoderm, endoderm, and ectoderm germ layers that are formed in the beginning stages of embryonic stem cell differentiation.
    • Multipotent – the ability to differentiate into a closely related family of cells. Examples include hematopoietic (adult) stem cells that can become red and white blood cells or platelets.
    • Oligopotent – the ability to differentiate into a few cells. Examples include (adult) lymphoid or myeloid stem cells.
    • Unipotent – the ability to only produce cells of their own type, but have the property of self-renewal required to be labeled a stem cell. Examples include (adult) muscle stem cells.

    Embryonic stem cells are considered pluripotent instead of totipotent because they do not have the ability to become part of the extra-embryonic membranes or the placenta.

    What are stem cells – Video

    A video on how stem cells work and develop.

    Identification of stem cells

    Although there is not complete agreement among scientists of how to identify stem cells, most tests are based on making sure that stem cells are undifferentiated and capable of self-renewal. Tests are often conducted in the laboratory to check for these properties.

    One way to identify stem cells in a lab, and the standard procedure for testing bone marrow or hematopoietic stem cell (HSC), is by transplanting one cell to save an individual without HSCs. If the stem cell produces new blood and immune cells, it demonstrates its potency.

    Clonogenic assays (a laboratory procedure) can also be employed in vitro to test whether single cells can differentiate and self-renew. Researchers may also inspect cells under a microscope to see if they are healthy and undifferentiated or they may examine chromosomes.

    To test whether human embryonic stem cells are pluripotent, scientists allow the cells to differentiate spontaneously in cell culture, manipulate the cells so they will differentiate to form specific cell types, or inject the cells into an immunosuppressed mouse to test for the formation of a teratoma (a benign tumor containing a mixture of differentiated cells).

    Research with stem cells

    Scientists and researchers are interested in stem cells for several reasons. Although stem cells do not serve any one function, many have the capacity to serve any function after they are instructed to specialize. Every cell in the body, for example, is derived from first few stem cells formed in the early stages of embryological development. Therefore, stem cells extracted from embryos can be induced to become any desired cell type. This property makes stem cells powerful enough to regenerate damaged tissue under the right conditions.

    Organ and tissue regeneration

    Tissue regeneration is probably the most important possible application of stem cell research. Currently, organs must be donated and transplanted, but the demand for organs far exceeds supply. Stem cells could potentially be used to grow a particular type of tissue or organ if directed to differentiate in a certain way. Stem cells that lie just beneath the skin, for example, have been used to engineer new skin tissue that can be grafted on to burn victims.

    Brain disease treatment

    Additionally, replacement cells and tissues may be used to treat brain disease such as Parkinson’s and Alzheimer’s by replenishing damaged tissue, bringing back the specialized brain cells that keep unneeded muscles from moving. Embryonic stem cells have recently been directed to differentiate into these types of cells, and so treatments are promising.

    Cell deficiency therapy

    Healthy heart cells developed in a laboratory may one day be transplanted into patients with heart disease, repopulating the heart with healthy tissue. Similarly, people with type I diabetes may receive pancreatic cells to replace the insulin-producing cells that have been lost or destroyed by the patient’s own immune system. The only current therapy is a pancreatic transplant, and it is unlikely to occur due to a small supply of pancreases available for transplant.

    Blood disease treatments

    Adult hematopoietic stem cells found in blood and bone marrow have been used for years to treat diseases such as leukemia, sickle cell anemia, and other immunodeficiencies. These cells are capable of producing all blood cell types, such as red blood cells that carry oxygen to white blood cells that fight disease. Difficulties arise in the extraction of these cells through the use of invasive bone marrow transplants. However hematopoietic stem cells have also been found in the umbilical cord and placenta. This has led some scientists to call for an umbilical cord blood bank to make these powerful cells more easily obtainable and to decrease the chances of a body’s rejecting therapy.

    General scientific discovery

    Stem cell research is also useful for learning about human development. Undifferentiated stem cells eventually differentiate partly because a particular gene is turned on or off. Stem cell researchers may help to clarify the role that genes play in determining what genetic traits or mutations we receive. Cancer and other birth defects are also affected by abnormal cell division and differentiation. New therapies for diseases may be developed if we better understand how these agents attack the human body.

    Another reason why stem cell research is being pursued is to develop new drugs. Scientists could measure a drug’s effect on healthy, normal tissue by testing the drug on tissue grown from stem cells rather than testing the drug on human volunteers.

    Stem cell controversy

    The debates surrounding stem cell research primarily are driven by methods concerning embryonic stem cell research. It was only in 1998 that researchers from the University of Wisconsin-Madison extracted the first human embryonic stem cells that were able to be kept alive in the laboratory. The main critique of this research is that it required the destruction of a human blastocyst. That is, a fertilized egg was not given the chance to develop into a fully-developed human.

    When does life begin?

    The core of this debate – similar to debates about abortion, for example – centers on the question, “When does life begin?” Many assert that life begins at conception, when the egg is fertilized. It is often argued that the embryo deserves the same status as any other full grown human. Therefore, destroying it (removing the blastocyst to extract stem cells) is akin to murder. Others, in contrast, have identified different points in gestational development that mark the beginning of life – after the development of certain organs or after a certain time period.

    Chimeras

    People also take issue with the creation of chimeras. A chimera is an organism that has both human and animal cells or tissues. Often in stem cell research, human cells are inserted into animals (like mice or rats) and allowed to develop. This creates the opportunity for researchers to see what happens when stem cells are implanted. Many people, however, object to the creation of an organism that is “part human”.

    Legal issues

    The stem cell debate has risen to the highest level of courts in several countries. Production of embryonic stem cell lines is illegal in Austria, Denmark, France, Germany, and Ireland, but permitted in Finland, Greece, the Netherlands, Sweden, and the UK. In the United States, it is not illegal to work with or create embryonic stem cell lines. However, the debate in the US is about funding, and it is in fact illegal for federal funds to be used to research stem cell lines that were created after August 2001.

    Everything you’ve wanted to know about stem cells – Video

    A video by Daniel Kraft, MD (Stanford University School of Medicine) for Google Tech Talks.

    Stem cell research news

    Medical News Today is a leading resource for the latest headlines on stem cell research. So, check out our stem cell research news section. You can also sign up to daily stem cell news alerts or our weekly digest newsletters to ensure that you stay up-to-date with the latest news.

    This what are stem cells? information section was written by Peter Crosta

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    Smoking Health Risks

    Smoking Health Risks:

    Health Risks

    doctorEffects on the Lungs

    According to the American Lung Association, smoking is directly responsible for about 90 percent of the deaths due to lung cancer. Smoking is also responsible for the majority of deaths due to chronic obstructive pulmonary disease (COPD), which includes emphysema and chronic bronchitis.

    A study in the July 2006 American Journal of Respiratory and Critical Care Medicine showed that smokers with asthma who give up smoking can improve their lung function in as little as 1 week. The small study involved 21 smokers with asthma. Ten of them quit smoking for 10 weeks, while the others continued to smoke. After just a week, lung function test scores in those who stopped smoking improved considerably. In less than 2 months, lung function scores among those who stopped smoking improved by more than 15%.

    Study authors say their findings show that there is a “reversible component to the harmful effects of smoking on the airways in asthma.”

    Secondhand Smoke

    Secondhand smoke is produced by a burning cigarette or other tobacco product. An estimated 4 million children a year get sick from being around secondhand smoke. Parental smoking has been shown to affect the lungs of infants as early as the first 2 – 10 weeks of life, and such abnormal lung function could persist throughout life.

    Exposure to secondhand smoke in the home increases the risk for asthma and asthma-related emergency room visits in children who have existing asthma.

    Parental smoking is believed to increase the risk for lower respiratory tract infections (such as bronchitis or pneumonia) by 50%. Environmental exposure to smoke is thought to be responsible for 150,000 – 300,000 such cases of such every year.

    Effects on the Heart and Blood Vessels

    All forms of tobacco raise one’s heart attack risk. Smoking, chewing tobacco, and being exposed to secondhand smoke greatly increase one’s risk of a heart attack. In some cases, the risk of heart problems in people who smoke or are epoxies to smoke may be three times greater, according to a study published in the Lancet. However, the study also found that the risk of a heart attack among those who stopped smoking slowly decreased over time.

    Effects on Male Fertility and Impotence

    Smoking has a negative affect on a man’s sexuality and fertility. Heavy smoking is frequently cited as a contributory factor in impotence because it decreases the amount of blood flowing into the penis. One study noted that among men with high blood pressure, smoking caused a 26-fold increase in impotence.

    Smoking impairs sperm motility, reduces sperm lifespan, and may cause genetic changes that can affect a man’s offspring. One 2002 trial found that men or women who smoke have lower success rates with fertility treatments. An earlier study reported that men who smoke also have lower sex drives and less frequent sex.

    Effects on Pregnancy and Female Infertility

    Studies have linked cigarette smoking to many reproductive problems. Continuing to smoke during pregnancy may also cause health problems in the baby.

    Negative effects of smoking on female fertility include:

    • Greater risk for infertility. Women at greatest risk for fertility problems are those who smoke one or more packs a day and who started smoking before age 18.
    • Earlier menopause. Women who smoke tend to start menopause at an earlier age than nonsmokers, perhaps because toxins in cigarette smoke damage eggs.
    • Pregnancy complications. Women who smoke have a greater risk for ectopic pregnancy and miscarriage.

    Effects on Unborn Child. Smoking during pregnancy is harmful to an unborn child in many ways. Smoking reduces the mother’s folate levels, a B vitamin that is important for preventing birth defects. Pregnant women who smoke increase the risk for stillbirth, prematurity and low birth weight in their babies. Infant mortality rates in pregnant smokers are increased by 33%, mostly because of low birth rate.

    Some women carry particular genes that may make it especially likely that they will deliver low birth weight infants if they smoke, although newborns of all female smokers have a greater risk for low weight.

    The good news is that women who quit before becoming pregnant or even during the first trimester reduce the risk for a low birth weight baby to that of women who never smoked.

    Children of mothers who smoke during pregnancy may also be at increased risk for obesity and diabetes.

    Women who want to become pregnant should try smoking cessation aids before they try to conceive and make all attempts to quit. If new mothers cannot quit, they should be sure not to smoke in the same room as their infant. This simple behavior can considerably reduce the risks to the child.

    Effects on Bones and Joints

    Smoking has many harmful effects on bones and joints:

    • Smoking can keep new bone from forming. Women who smoke are at high risk for loss of bone density and osteoporosis.
    • Postmenopausal women who smoke have a significantly greater risk for hip fracture than those who do not.
    • Smokers are more apt to develop degenerative disorders and injuries in the spine.
    • Smokers have more trouble recovering from surgeries, including knee or hip replacements.
    • Smokers whose jobs involve lifting heavy objects are more likely to develop low back pain than nonsmokers.
    • Smoking may increase the risk of rheumatoid arthritis in some older women. A 2006 study in Annals of the Rheumatic Diseases showed that smoking nearly doubled the risk of rheumatoid arthritis in postmenopausal women who did not have the most established genetic risk factor for the disease, a genotype called HLA-DRB1 SE.

    Smoking and Diabetes

    Smoking may increase the risk of developing diabetes. Researchers involved in the Insulin Resistance Atherosclerosis Study (IRAS) looked at the relationship between smoking and diabetes and found that 25% of smokers who started the trial with normal blood sugar had diabetes 5 years later compared to 14% of non-smokers. The results were published in Diabetes Care.

    A study released in 2006 supports earlier beliefs that smokers have a higher risk of developing glucose intolerance, a condition that precedes diabetes. The study, published in the British Medical Journal, involved 4,572 people. The findings suggest that chemicals in smoke could affect the pancreas. The pancreas is the organ that produces insulin, which helps control blood sugar (glucose) levels.

    Smoking and the Gastrointestinal Tract

    Smoking increases acid production in the stomach. It also reduces blood flow and production of compounds that protect the stomach lining.

    Diverticulitis. A 2000 study suggested that smoking was a major risk factor in diverticulitis, a condition in which small bumps develop in the wall of the colon. In addition, smokers were at risk for complications from diverticulitis, including bleeding and abscess. Diverticulitis mostly affects people over age 50.

    Reviewed By: Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital

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    Smoking Kills

    smokingSmoking Kills

    (This is how people who are addicted to using/ smoking Tobacco products rationalize using/smoking Tobacco products.)

    Tobacco smoking has been fingered (e.g., U.S. Department of Health, Education, and Welfare [U.S. DHEW], 1964) as a major cause of mortality and morbidity, responsible for an estimated 434,000 deaths per year in the United States (Centers for Disease Control [CDC], 1991a).

    But, did you know that the so much publicized 400,000+ “smoking-related’ deaths in the US simply does not exist?

    That number is a guess… a heavily slanted, politically manipulated estimate using a computer model programmed with the assumptions of causality in synergy with the current political agenda against tobacco.

    It DOES NOT represent an actual body count.

    Some claim that about 10 million people in the United States have died from causes attributed to smoking (including heart disease, emphysema, and other respiratory diseases) since the first Surgeon General’s report on smoking and health in 1964 with 2 million of these deaths the result of lung cancer alone.

    In fact, they like to say that “Cigarette smoking is the single most preventable cause of premature death in the United States.

    They declare one in every five deaths in the United States is smoking related. Every year, smoking kills more than 276,000 men and 142,000 women. (Centers for Disease Control and Prevention. Smoking-attributable mortality and years of potential life lost–United States, 1990. Morbidity and Mortality Weekly Report 1993;42(33):645-8.)

    How do they explain why non-smokers (75% of heart disease deaths) die from heart disease?

    Smoking Causes Cancer

    “Ninety-five per cent of lung cancer deaths are due directly to cigarette smoking”, according to Dr Desmond Carney, oncologist at University College, Dublin, and secretary general of the International Association for the Study of Lung Cancer.

    Women who smoke increase their risk of dying from lung cancer by nearly 12 times and the risk of dying from bronchitis and emphysema by more than 10 times. Between 1960 and 1990, deaths from lung cancer among women have increased by more than 400%–exceeding breast cancer deaths in the mid-1980s.(Morbidity and Mortality Weekly Report 1993;42(44)) The American Cancer Society predicts that 80,000 women will develop lung cancer this year and 67,000 will die from it, as compared to 43,500 deaths from breast cancer.

    Men who smoke increase their risk of death from lung cancer by more than 22 times and from bronchitis and emphysema by nearly 10 times. Smoking triples the risk of dying from heart disease among middle-aged men and women. (CDC Smoking-attributable mortality and years of potential life lost–United States, 1990. Morbidity and Mortality Weekly Report 1993; 42(33):645-8.)

    Now that you’re totally terrified,
    take a look at it another way…

    70%of all cancers occur in non-smokers.

    The National Cancer Institute, National Institutes of Health report in the 1995 Information Please Almanac states that only 30% of all cancers are caused by smoking.

    Did you know that United Nations statistics have listed Japan and South Korea respectively as first and second in both life expectancy and tobacco consumption? If smoking were really as dreadful, harmful, and dangerous as the Anti-Smoking propaganda blitz claims it to be . . . how can this be true?!

    The Japanese smoke twice as much as Americans and yet have half the number of lung cancers per 100,000 people.

    cartoon

    Why do some people get lung cancer — even if they never smoke?
    According to the Centers for Disease Control (CDC), lung cancer is the number one cause of cancer deaths worldwide. The American Thoracic Society points out that over 75 percent of lung cancers are small cell lung cancers (NSCLC) and have an average overall 35-year survival rate of only 14 percent. Previous research has shown that about 90 percent of NSCLC appear to be activated by specific signaling pathways in lung tissue. The new study by Dr. Cho and his research team found that high amounts of dietary inorganic phosphates actually stimulate those same cancer-triggering pathways.

    New research suggests eating a lot of processed foods containing inorganic phosphates could be the explanation. In research published in the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society, scientists from Seoul National University conclude that a diet high in inorganic phosphates, which are found in a host of processed foods including meats, cheeses, beverages, and bakery products, might spur the growth of lung cancer. The researchers also suggest the food additive may contribute to the development of malignancies in people predisposed to lung cancer.

    While living organisms need a moderate level of phosphate, the use of inorganic phosphates as a food additive to increase water retention and improve food texture artificially has soared over the past decade. That means the average American diet is loaded with excess amounts of phosphates. “In the 1990s, phosphorous-containing food additives contributed an estimated 470 mg per day to the average daily adult diet. However, phosphates are currently being added much more frequently to a large number of processed foods, including meats, cheeses, beverages, and bakery products. As a result, depending on individual food choices, phosphorous intake could be increased by as much as 1000 mg per day,” Dr. Cho explained in the media statement.

    In truth, smoking is not a leading cause of cancer.

    Lung cancer is primarily a condition developed in old age, with average age of onset age 65, according to American Cancer Society literature. It’s estimated more people will die of lung cancer in populations of older Americans, and where older Americans live, there more lung cancer deaths will be estimated. More incidences of lung cancer and deaths from lung cancer are likely to occur in Florida than in any other state. That’s where the highest percentage of retirees lives. And that’s where ACS estimates more lung cancers will occur. Lung cancer is a disease of old age, not smoking.

    Research has now firmly linked many of today’s cancers with tainted virus vaccinations given in the early 1950s. In 1960, researchers discovered that the polio vaccine distributed to certain states was infected with another virus called “Simian Virus 40.” SV-40 is a monkey virus that is not normally found in humans. Unknown at the time, it was present in hundreds of rhesus monkeys that were used to grow and harvest the polio vaccine. Injected into research animals, the SV-40 virus causes brain and lung cancers. Now, some forty years later, its effect on humans is just being investigated.

    • Michele Carbone, Assistant Professor of Pathology at Loyola University in Chicago, has recently isolated fragments of the SV-40 virus in human bone cancers and in a lethal form of lung cancer called mesothelioma. He found SV-40 in 33% of the osteosarcoma bone cancers studied, in 40% of other bone cancers, and in 60% of the mesotheliomas lung cancers.
    • Researchers from the Institute of Histology and General Embryology of the University of Ferrara, lead by Dr. Fernanda Martini, discovered SV-40’s presence in a variety other tumors. They found the rhesus monkey virus in 83% of choriod plexus papillomas, in 73% of ependymomas, in 47% of astrocytomas, in 50% of glioblastomas, and in 14% of meningiomas.
    • Even more shocking, SV-40 has appeared in 61% of all new cancer patients — patients even too young to have received the contaminated vaccine being administered forty years ago!
    • Instead of getting the “dead” virus in an injection, the Federal vaccination policy was changed mandating that children should be given the new live “oral polio vaccine” (OPV). This decision was based upon the belief that the OPV recipient would “shed” the virus through body contact with other non-vaccinated children and adults, thereby spreading the “live” virus throughout the population. The SV-40 virus that contaminated the oral polio vaccine quickly spread from child to child and from child to adult, crossing state lines and national boundaries. By 1960, when the virus was first detected, it was already too late to prevent its dissemination throughout the population. The FDA quietly and gradually instituted a program to eliminate rhesus monkeys, which harbor the SV-40, and replace them with African Green monkeys that are free of the virus.

    A number of public statements have been made by the National Cancer Institute, attempting to put their spin on these disturbing revelations. In a statement published in the January (1999) New England Journal of Medicine, the institute states that there is no evidence of an increase in humans of the types of cancers found in laboratory animals that have been injected with SV-40. But other researchers remind us that SV-40 has already been found in a wide variety of other tumors. It has been shown that individuals who received the tainted oral vaccine demonstrate a higher occurrence of these cancers.

    Not surprisingly, the US government and its agencies are reluctant to pursue this matter. In fact, requests to the National Institute for Health for grants to study the SIV and simian cytomegalovirus (SCMV) were recently denied. Microbiologist Howard Urnovitz, Ph.D., may have an explanation as he stated in the Boston Globe: “that almost 100 million Americans were exposed (to SV-40) through a government sponsored program, but for over 30 years, there has been virtually no government effort to see if anyone’s been harmed by the exposure.” He added, “The government will not fund science that makes it look culpable.”

    Philip Wiley sought at least $13.3 million in compensatory damages from six tobacco companies and two industry groups for the 1991 death of his wife. A jury in Muncie, Indiana agreed there is no proven connection between second hand smoke and cancer and said cigarettes were not a defective product that their makers were not negligent and the tobacco industry was not liable in the cancer death of a nonsmoking nurse exposed to secondhand smoke at a veteran’s hospital. Industry attorneys pointed out that Mrs. Wiley’s cancer may have had other causes and could have started in her pancreas, then spread to her lung.

    Smoking May Actually Be Healthy For You

    Smoking may actually help reduce the risk of breast cancer in some women, according to a study, published in the Journal of the National Cancer Institute. The study found that smoking reduces by 50 percent the risk of developing breast cancer in women who have a rare genetic mutation that can lead to the disease.

    Studies have shown evidence of an inverse relationship between smoking and the risk of contracting Alzheimer’s disease or Parkinson’s disease. In fact, most studies show that the more one smokes, the lower the risk level.

    Scientists reported at the Society for Neuroscience annual meeting that they’re encouraged they can design medications to capitalize on the benefits of nicotine without cardiovascular and other side effects. Apparently, they found that Nicotine-like compounds can improve memory and might one day be used in pills to treat disorders like Alzheimer’s disease. [CBS Market watch, Nov 8, 1998]

    What Is the Leading Cause of Death in America?

    Is cigarette smoking the single most preventable cause of premature death in the United States?

    • The CDC estimates 434,000 smoking related deaths per year in the U.S.
    • The number of babies that die from abortion in the United States is 1.2 million a year.

    A definitive review and close reading of medical peer-review journals, and government health statistics shows that American medicine frequently causes more harm than good. The number of people having in-hospital, adverse drug reactions (ADR) to prescribed medicine is 2.2 million. Dr. Richard Besser, of the CDC, in 1995, said the number of unnecessary antibiotics prescribed annually for viral infections was 20 million. Dr. Besser, in 2003, now refers to tens of millions of unnecessary antibiotics.

    The number of unnecessary medical and surgical procedures performed annually is 7.5 million. The number of people exposed to unnecessary hospitalization annually is 8.9 million. The total number of iatrogenic deaths is 783,936. It is evident that the American medical system is the leading cause of death and injury in the United States. The 2001 heart disease annual death rate is 699,697; the annual cancer death rate, 553,251. [Death by Medicine]

    Quitting Can be Dangerous

    According to three medical doctors writing in the journal Medical Hypotheses, giving up smoking can kill you. The doctors were “struck by the more than casual relationship between the appearance of lung cancer and an abrupt and recent cessation of the smoking.” In 182 of the 312 cases they treated, habitual smokers of at least a pack a day for at least a quarter-century developed lung cancer shortly after they gave up smoking.

    In a rush to cover their tracks and bad statistics, anti-smoking advocates are quickly revising their numbers to be more in line with their political ambitions. In the 1960’s epidemiologists estimated that smoking killed one fourth of all regular smokers. That estimate was later raised to one third. More recently they suggest that both estimates are too low. According to scientist Richard Peto, lifelong cigarette use, particularly if begun before age 20, kills at least half of all smokers.

    CDC Regularly Misrepresents the Facts

    Americans are not experiencing the “epidemic of tobacco related disease and death” the anti-smokers claim. If that were true, why would annual death rates decrease in the U.S. as cigarette sales rates increase?

    Cigarette

    Census             Death by    Death    Sales per

    Year   Population  All Cause  Rate%    Billion

    1900   75,994,600  1,307,107  1.72    2.5

    1910   91,972,260  1,351,992  1.47    8.6

    1920  105,710,600  1,374,358  1.30   44.6

    1930  122,775,100  1,387,358  1.13  119.3

    1940  131,669,300  1,422,028  1.08  181.9

    1950  150,697,400  1,446,695  0.96  369.8

    1960  179,323,200  1,703,570  0.95  484.4

    1970  203,302,000  1,921,031  0.94  536.5

    1980  226,545,800  1,989,841  0.88  631.5

    1990  248,709,900  2,162,000  0.87  525.0

    Smokers represented nearly 50% of the adult male/female population for several decades in the United States according to the Centers for Disease Control and Prevention. Smoking among adults decreased dramatically from 42% in 1965 to 26% in 1994. During this period, smoking among the adult male population declined from 52% to 28%; adult female smoking declined from 34% to 23%. In 1994, 48 million adults 18 years of age and older (25.3 million men, 22.7 million women) were current smokers in the United States.

    If nearly 50% of the population smoked, you would expect at least nearly 50% of the people who die would be smokers, if smoke has nothing to do with dying. It stands to reason we should start suspecting that smoke kills smokers only when over 50% of those who die in a given year are smokers. By their own statistics, only about 20% of the deaths are smokers.

    At the end of World War II, about 90 per cent of the adult male population of Britain smoked. If lung cancer takes about 20-25 years to show, as some claim, then by 1965, or 1970 at the latest, we would have seen an epidemic of truly catastrophic proportions. One in every eleven British men would have been dying of lung cancer. This simply did not happen.

    There hardly appears to be the profound danger anti-smoking advocates would have us believe. As a matter of fact, it would appear you have a greater chance of dying if you’re a non-smoker!

    In another look at the numbers, 38% of the people who smoke live beyond 80 years old, 50% live beyond 75 and 85% live beyond 65. This compares to 43% of non-smokers living beyond 80 years old, 50% of non-smokers live beyond 75, and 85% of non-smokers live beyond 65. The government and anti-smoking lobby can’t explain this disparity, so they lie.

    Fewer Cigarettes Equals MORE Cancer?

    U.S. historical statistics show that, in the period 1973-1994, annual per capita consumption of cigarettes FELL from 4,148 to 2,493. But in the same period, the incidence of lung and bronchial cancer ROSE from 42.5 to 57.1 cases per 100,000 population. How can this be if the propaganda of the Anti-Tobacco Pharmaceutical Cartel is correct?

    The deluge of anti-smoking hysteria is actually a very recent thing. And it’s quite sudden too. Look at a film from only 10 or 15 years ago and you’ll see everyone smoking away merrily and without a worry. They’re smoking in the elevator, in the office and, of course, in every decent bar!

    How can it be that we’ve been so suddenly immersed in this tidal wave of warnings and fear and – let’s be clear – propaganda? Doesn’t it seem a bit too orchestrated?

    At the risk of repeating myself again…
    It’s because of money, control, and jurisdiction.

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    Stair Design Could Help Fight Obesity

    Untitled-1Changes In Stair Design Could Help Fight Obesity
    The fight against obesity, according to an article in the June Southern Medical Journal, official journal of the Southern Medical Association. The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health, a leading provider of information and business intelligence for students, professionals, and institutions in medicine, nursing, allied health, pharmacy and the pharmaceutical industry.

    “Changing stair design to encourage their use requires a set of interventions on both architectural and legislative levels to create physical environments that support active living,” write the authors, led by Dr. Ishak A. Mansi of Louisiana State University Health Sciences Center, Shreveport. His wife, architect Nardine M. Mansi, is one of the co-authors.

    Current Design Discourages Staircase Use

    Encouraging people to take the stairs instead of the elevator or escalator is a promising approach to increasing moderate physical activity, the Mansis and their co-authors believe. “It involves a lifestyle choice that must be made (people must get to their destination) and it requires no personal financial cost.”

    But would climbing the stairs a few times a day really have that much of an impact on overweight and obesity? The authors point out that ordinary day-to-day physical activities contribute the most to total energy expenditure the key factor in maintaining a healthy body weight. Some simple changes in the design and location of staircases could help to make buildings more “physical activity friendly” and contribute to Research suggests that light to moderate physical activity is most effective in motivating people who are currently inactive and obese.

    But current approaches to stair design pose a problem. “Stairs are frequently hidden from entrances, with only small signs denoting their locations, typically in connection to the fire exit,” according to the article. Fire exits are usually guarded by heavy doors, not carpeted, and not air-conditioned. Architects find it challenging enough to comply with current building codes emphasizing fire safety and accessibility. “As a result, a conscious focus on health does not enter the design process.”

    Suggestions for Improving Stair Design

    Some simple interventions can do much toward encouraging people to take the stairs, research suggests. For example, a study performed at a Centers for Disease Control and Prevention building found that playing music in stairwells and displaying motivational signs significantly increased the use of stairs.

    These and other measures to make stairs attractive, safe, and readily accessible could help to make buildings more “physical activity-friendly,” the authors write. They suggest several ways to make stairs more comfortable and inviting for example, making staircases wider with less height per step and adding music, lighting, and air-conditioning.

    Such efforts would readily fit in with recommended policy and environmental changes to increase physical activity. “State and local agencies are being encouraged by federal and nongovernmental organizations to use policy interventions to address the public health problem of physical activity,” according to the Mansis and their co-authors. They call for physicians, architects, and other professionals to work together to promote change in such policies. They conclude, “Perhaps now is the time to address the need for standard national building codes that incorporate health concerns and support active living.”

    About the Southern Medical Journal

    The Southern Medical Journal is published monthly by the Southern Medical Association and Lippincott Williams & Wilkins. Devoted solely to continuing education, the Journal publishes annually more than 200 original clinical articles directed to the practicing physician and surgeon on topics such as hypertension, osteoporosis, alcoholism, obesity, dementia, asthma, and diabetes and includes monthly CME features.

    About the Southern Medical Association

    The Southern Medical Association (SMA) has been serving physicians’ needs since its inception in 1906. SMA’s mission is to promote the health of patients through advocacy, leadership, education, and service. Mark your calendars to attend the Annual Scientific Assembly of Southern Medical Association, December 3-5, 2009 at the Gaylord Texan Resort and Convention Center in Dallas, Texas.

    About Lippincott Williams & Wilkins

    Lippincott Williams & Wilkins (LWW) is a leading international publisher for healthcare professionals and students with nearly 300 periodicals and 1,500 books in more than 100 disciplines publishing under the LWW brand, as well as content-based sites and online corporate and customer services. LWW is part of Wolters Kluwer Health, a leading provider of information and business intelligence for students, professionals and institutions in medicine, nursing, allied health, pharmacy and the pharmaceutical industry.

    Wolters Kluwer Health is a division of Wolters Kluwer, a leading global information services and publishing company. The company provides products and services for professionals in the health, tax, accounting, corporate, financial services, legal, and regulatory sectors. Wolters Kluwer had 2008 annual revenues of €3.4 billion ($4.9 billion), employs approximately 20,000 people worldwide, and maintains operations in over 35 countries across Europe, North America, Asia Pacific, and Latin America. Wolters Kluwer is headquartered in Amsterdam, the Netherlands. Its shares are quoted on Euronext Amsterdam (WKL) and are included in the AEX and Euronext 100 indices

    Source: Lippincott Williams & Wilkins

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    REM Sleep Helps Solve Problems

    rem
    REM Sleep Helps Solve Problems

    Grabbing a quick nap may not only be refreshing but may also increase your ability to solve problems creatively, according to US researchers who suggest that REM (rapid eye movement) sleep directly enhances creative processes more than any other sleep or wakeful state.

    The study was the work of a leading expert on the positive effects of napping, Dr Sara Mednick, assistant professor of psychiatry at the University of California San Diego and the VA San Diego Healthcare System, and colleagues, and is published online in the 8th June issue of the Proceedings of the National Academy of Sciences (PNAS).

    The researchers said their findings are important because they show that sleep, and REM sleep in particular, helps the brain to form “associative networks”.

    Mednick said:

    “For creative problems that you’ve already been working on — the passage of time is enough to find solutions.”

    “However,” she added, “for new problems, only REM sleep enhances creativity.”

    The researchers discovered that it looks as if REM sleep stimulates associative networks helping the brain to make new and useful connections between unrelated ideas, the key to creativity.

    Previous studies have shown that sleep enhances problem solving, but they have not properly explored the effect of types of sleep, such as that with and without REM.

    Also scientists don’t really know whether creative thinking improves after sleep because of the effect of the sleep itself or because going to sleep removes distractions and interference that can disrupt the consolidation of memory; so this study included a comparison group that did not sleep but just had quiet rest.

    Mednick and colleagues used a creativity task called Remote Associates Test (RAT) where participants were shown groups of three words (for example “cookie”, “heart”, “sixteen”) and asked to find a fourth word that linked them all together (eg the word “sweet” in the example).

    The participants did the test in the morning and then again in the afternoon after they had either had a nap with REM sleep, a nap without REM sleep, or spent some quiet time resting with no verbal inputs.

    The results showed that the three groups performed the same on memory tests, but although the quiet rest and non-REM nap group had the same exposure to the task, their performance on the RAT test was the same in the morning and the afternoon.

    But what was striking was that the nap with REM group improved their performance by 40 per cent in the afternoon compared to the morning.

    “Compared with quiet rest and non-REM sleep, REM enhanced the formation of associative networks and the integration of unassociated information,” wrote the authors.

    They suggested that REM sleep causes changes in the levels of neurotransmitters, or more specifically “changes in cholinergic and noradrenergic neuromodulation” in the brain and this makes new linkages between previously unlinked networks which enhances “the integration of unassociated information for creative problem solving”.

    “REM, not incubation, improves creativity by priming associative networks.”
    Denise J Cai, Sarnoff A Mednick, Elizabeth M Harrison, Jennifer C Kanady, and Sara C Mednick
    PNAS published online before print June 8, 2009
    doi:10.1073/pnas.0900271106

    Sources: American Diabetes Association, WebMD, National Diabetes Information Clearing House (NDIC).

    Written by: Catharine Paddock, PhD

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    What Is Dialysis? What Is Kidney Dialysis?

    dialysis-machine1Dialysis is the artificial process of getting rid of waste (diffusion) and unwanted water (ultrafiltration) from the blood. This process is naturally done by our kidneys. Some people, however, may have failed or damaged kidneys which cannot carry out the function properly – they may need dialysis. In other words, dialysis is the artificial replacement for lost kidney function (renal replacement therapy). Dialysis may be used for people who have become ill and have acute kidney failure (temporary loss of kidney function), or for fairly stable patients who have permanently lost kidney function (stage 5 chronic kidney disease).

    When we are healthy our kidneys regulate our body levels of water and minerals, and remove waste. The kidneys also produce erythropoietin and 1,25-dihydroxycholecalciferol (calcitriol) as part of the endocrine system. Dialysis does not correct the endocrine functions of failed kidneys – it only replaces some kidney functions, such as waste removal and fluid removal.

    Dialysis and altitude – A study found that death rates for dialysis patients are 10%-15% lower for those whose homes are higher than 4,000 feet, compared to those who live at sea level.

    Some countries, such as the UK, are predicting a doubling of the number of patients on dialysis machine.

    Urology / Nephrology News

    The latest Urology News & Nephrology News articles published daily. Includes news on kidney failure, dialysis, urinary tract diseases, urologic oncology, incontinence, kidney stones, cancers of the bladder, kidney, ureter, testicles, penis and urethra.

    Why is dialysis necessary?

    Approximately 1,500 liters of blood are filtered by a healthy person’s kidneys each day. We could not live if waste products were not removed from our kidneys. People whose kidneys either do not work properly or not at all experience a buildup of waste in their blood. Without dialysis the amount of waste products in the blood would increase and eventually reach levels that would cause coma and death.

    Dialysis is also used to rapidly remove toxins or drugs from the blood.

    There are two main types of dialysis – hemodialysis and peritoneal dialysis

    What type of dialysis a patient should have really does depend on each individual case. Studies have indicated clearly that for kidney disease patients who need to undergo dialysis, one type of treatment is not best for all.

    What is hemodialysis?

    The blood circulates outside the body of the patient – it goes through a machine that has special filters. The blood comes out of the patient through a catheter (a flexible tube) that is inserted into the vein. The filters do what the kidney’s do; they filter out the waste products from the blood. The filtered blood then returns to the patient via another catheter. The patient is, in effect, connected to a kind of artificial kidney.

    Patients need to be prepared for hemodialysis. A blood vessel, usually in the arm, needs to be enlarged. Surgery is required for this. The enlarged vein makes the insertion of the catheters possible. US researchers have developed a new way of growing blood vessels using patients’ own skin cells to seed the growth of tissue and have tested it in dialysis patients with end stage kidney disease.

    Hemodialysis usually lasts about 3 to 4 hours each week. The duration of each session depends on how well the patient’s kidneys work, and how much fluid weight the patient has gained between treatments.

    In the UK hemodialysis is either done in a special dialysis center in a hospital, or at home. When it is carried out at home it is important that the patient, and/or his/her caregiver knows what to do. A study revealed that kidney disease patients who are educated about dialysis are more likely to undergo a standard but under-utilized dialysis-related procedure than less knowledgeable patients The following people may have hemodialysis done at home:

    • People who can and want to learn how to do it at home.
    • People who are willing to carry on doing it at home.
    • People whose condition has been stable while on dialysis.
    • People who do not suffer from other diseases which would make home hemodialysis unsafe.
    • People who have suitable blood vessels for the insertion of the catheters.
    • People who have a caregiver, and that caregiver is willing to help with hemodialysis. People whose homes can be adapted for hemodialysis equipment.

    In the UK, the National Institutes of Health and Clinical Excellence (NICE) recommends that every patient deemed suitable for home dialysis should have both home dialysis and hospital offered.

    What is peritoneal dialysis?

    A sterile (dialysate) solution rich in minerals and glucose is run through a tube into the peritoneal cavity, the abdominal body cavity around the intestine, where the peritoneal membrane acts as a semi-permeable membrane.

    The abdomen is the area between the chest and hips – it contains the stomach, small intestine, large intestine, liver, gallbladder, pancreas and spleen. Peritoneal dialysis uses the natural filtering ability of the peritoneum – the internal lining of the abdomen. In other words, peritoneal dialysis uses the lining of the abdomen as a filter of waste products from the blood.

    The dialysate is left there for some time so that it can absorb waste products. Then it is drained out through a tube and discarded. This exchange, or cycle, is generally repeated several times during the day – with an automated system it is often done overnight. The elimination of unwanted water (ultrafiltration) occurs through osmosis – as the dialysis solution has a high concentration of glucose, it results in osmotic pressure which causes the fluid to move from the blood into the dialysate. Consequently, a larger quantity of fluid is drained than introduced.

    Although peritoneal dialysis is not as efficient as hemodialysis, it is carried out for longer periods. The net effect in terms of total waste product and salt and water removal is about the same as hemodialysis.

    Peritoneal dialysis is done at home by the patient; by a willing and motivated patient. It gives the patient a greater amount of freedom and independence because he/she does not have to come in to the clinic at multiple times each week. It can also be done while traveling with a minimum of specialized equipment. Peritoneal dialysis is said to ‘save lives and save money’.

    Before having peritoneal dialysis, the patient needs to have a small surgical procedure to insert a catheter into the abdomen. This is kept closed off, except when fluid is being introduced or taken out of the abdomen.

    There are two principal types of peritoneal dialysis:

    • Continuous ambulatory peritoneal dialysis (CAPD) – this requires no machinery and can be done by the patient or a caregiver. The dialysate is left in the abdomen for up to eight hours. It is then replaced with a fresh solution straight away. This happens every day, about four to five times per day.
    • Continuous cyclic peritoneal dialysis (CCPD) – a machine does the dialysis fluid exchanges. It is generally done during the night while the patient sleeps. This needs to be done every night. Each session lasts from ten to twelve hours. After spending the night attached to the machine, the majority of people keep fluid inside their abdomen during the day. Some patients may require another exchange during the day. A study found that a significant number of patients prefer “dialysis while you sleep” treatment. Another study found that nocturnal dialysis improves heart disease in patients with end-stage kidney failure.

    Peritoneal is ideal for patients who may find hemodialysis too exhausting, such as elderly people, babies and children. As it can be done while the patient is traveling it is more convenient for those who have to go to school or to work.

    A study found that a combination of aspirin and the anti-platelet drug dipyridamole significantly reduce blockages and extend the useful life of new artery-vein access grafts used for hemodialysis.

    Dialysis helps, but is not as efficient as the kidneys

    Although dialysis helps patients whose kidneys have failed, it is not as efficient as a normal kidney. Consequently, patients on dialysis need to be careful about what and how much they drink and eat. They will also need medications.

    A significant number of patients on dialysis can work and lead normal lives. It is possible to go away on vacation as long as dialysis treatment is possible at their destination.

    Women on dialysis will probably not be able to get pregnant. There will be a higher level of waste products in the body compared to a woman with normal kidneys – this interferes with fertility. Women who do become pregnant while on dialysis will probably need increased dialysis during the pregnancy. If a woman has a successful kidney transplant her fertility should return to normal. Dialysis has some effect on male fertility, but much less than on female fertility.

    What are the symptoms of kidney failure?

    Kidney failure tends to happen gradually. Even if just one kidney works, or both work partially, normal kidney function is still possible. So, it can be a very long time before any symptoms are noticed by the patient. When symptoms do occur they tend to be different from person-to-person, making it harder for doctors to diagnose kidney failure quickly. The following symptoms may be present:

    • Fatigue (tiredness)
    • Frequent need to urinate, especially at night. Frequency grows with time
    • Itchy skin
    • Erectile dysfunction (men have difficulty getting and/or sustaining an erection)
    • Nausea
    • Shortness of breath
    • Water retention (swollen feet, hands, ankles)
    • Blood in urine
    • Protein in urine

    A sudden injury can cause kidney failure. When it does, symptoms tend to appear faster, and progress more rapidly as well.

    Anemia – People with chronic kidney disease are usually affected by anemia (90% of them). When levels of EPO (erythropoietin), which is produced by the kidneys, are low, anemia can develop. EPO makes the body produce red blood cells. When your red blood cell count is low you have anemia. Chronic kidney failure patients who have anemia are usually given an ESA (erythropoiesis-stimulating agent) injection. A study found that Ferumoxytol, a novel intravenous form of iron that permits rapid administration of large doses, is effective for treating iron deficiency in chronic kidney disease (CKD) patients on dialysis.

    What are the causes of kidney disease?

    • Diabetes – thought to cause about half of all cases
    • Hypertension (high blood pressure) – thought to cause about one quarter of all cases
    • Inflammation of the kidney (glomerulonephritis)
    • Malaria
    • Long-term exposure to lead, solvents and fuels
    • Systemic lupus erythematosus – body’s own immune system attacks the kidneys
    • Polycystic kidney disease – inherited
    • Physical injury, such as a heavy blow to the kidney
    • Kidney infection (pyelonephritis)
    • Jaundice
    • Over consumption of some medications
    • Unborn baby does not normally developing kidneys
    • Yellow fever

    Written by Christian Nordqvist
    Copyright: Medical News Today

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    New Drug Delivers “Fitness”

    pillsfitnessA New Drug Delivers “Fitness” Without the Workout

    Take a pill and simulate the effects of exercise. By Nicholas Bakalar

    It sounds too good to be true, but scientists announced in August that they have found drugs that simulate the effects of exercise.

    Endurance training alters metabolic processes in muscle fiber, increasing the expression of the genes that control the muscles’ ability to contract, recover, and grow. It does this by activating two proteins, AMPK and PGC1-alpha. The scientists, writing in the journal Cell [subscription required], theorized that AICAR and GW1516, drugs that increase production of these proteins, might mimic the biochemical changes associated with exercise, and they seem to be right. “The drugs activate the endurance gene network, which promotes energy metabolism and revs the muscle up to be able to burn fats,” says Ronald Evans of the Salk Institute in La Jolla, where the work was done.

    These drugs have been tested in mice with impressive results: a 44 percent increase in endurance in sedentary animals after four weeks of treatment with AICAR, and a 70 percent increase when GW1516 is combined with exercise. Both drugs are currently in clinical trials. AICAR is in trials for use in treating a heart condition and has been tested with other diseases over the past decade. GW1516 is being explored for controlling cholesterol. But neither compound has yet been tested for improving strength or endurance in humans.

    What about athletes who want to use them for performance enhancement? “You can’t keep a drug that has obvious potential benefits to individuals away from them,” Evans says. “Athletes will definitely want to go for these drugs, as will other people.”

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    Myofascial Pain in Athletes

    myoMyofascial Pain in Athletes

    Voluntary, or skeletal, muscle is the largest single organ of the human body and accounts for nearly 50% of the body’s weight. The number of muscles in the body depends on the degree of subdivision that is considered and on the number of variable muscles that are included. Not counting heads, bellies, and other divisions of muscles, the Nomina Anatomica reported by the International Anatomical Nomenclature Committee under the Berne Convention lists 200 paired muscles, or a total of 400 muscles. Any one of these muscles can develop myofascial trigger points (MTrPs). MTrPs are hyperirritable tender spots in palpable tense bands of skeletal muscle that refer pain and motor dysfunction, often to another location.

    The myofascial pain syndromes (MPS) owe their ever-widening acceptance to the pioneering work of Travell and her later collaboration with Simons. In 1983, they combined their clinical experience in a detailed description of the multiple pain syndromes attributed to this disorder. In doing so, they further defined the major clinical components that are characteristic of myofascial pain, the most important being the TrP, the taut band, and the local twitch response.

    Frequency

    United States

    MTrPs are extremely common and become a painful part of nearly everyone’s life at one time or another. Latent TrPs, which often cause motor dysfunction (eg, stiffness, restricted range of motion) without pain, are far more common than active TrPs that cause pain.

    Active TrPs are commonly found in postural muscles of the neck, shoulder, and pelvic girdles and in the masticatory muscles. In addition, the upper trapezius, scalene, sternocleidomastoid, levator scapulae, and quadratus lumborum muscles are commonly involved.

    Reports of the prevalence of MTrPs in specific patient populations are available. The data indicate a high prevalence of this condition among individuals with a regional pain complaint, as shown in Table 1.

    Table 1. Prevalence of Myofascial Pain

    Table

    Region Practice Number Studied Prevalence of Myofascial Pain, %
    General Medical 172 30
    General Pain medical center 96 93
    General Comprehensive pain center 283 85
    Craniofacial Head and neck pain clinic 164 55
    Lumbogluteal Orthopedic clinic 97 21
    Region Practice Number Studied Prevalence of Myofascial Pain, %
    General Medical 172 30
    General Pain medical center 96 93
    General Comprehensive pain center 283 85
    Craniofacial Head and neck pain clinic 164 55
    Lumbogluteal Orthopedic clinic 97 21

    The wide range in the prevalences of myofascial pain caused by TrPs is likely due to differences in the patient populations examined and in the degree of chronicity, at least in part. Probably even more important are differences in the criteria used to diagnose MTrPs and, most important, differences in the training and skill of the examiners.

    Functional Anatomy

    Some isolated large round muscle fibers and some groups of these darkly staining, enlarged; round muscle fibers appear in cross-sections. In longitudinal sections, the corresponding feature is a number of contraction knots. An individual knot appears as a segment of muscle fiber with extremely contracted sarcomeres. This contractured segment has a corresponding increase in diameter of the muscle fiber.

    The structural features of contraction knots presents a likely explanation for the palpable nodules and the taut bands associated with TrPs. Three single contraction knots can be seen scattered among normal muscle fibers. Beyond the thickened segment of the contracture muscle fiber at the contraction knot, the muscle fiber becomes markedly thinned and consists of stretched sarcomeres to compensate for the contracture ones in the knot segment. In addition, a pair of contraction knots separated by empty sarcolemma may represent one of the first irreversible complications that result from the continued presence of the contraction knot.

    Sport Specific Biomechanics

    The activation of a TrP is usually associated with some degree of mechanical abuse of the muscle in the form of muscle overload, which may be acute, sustained, and/or repetitive. In addition, leaving the muscle in a shortened position can convert a latent TrP to an active TrP; this process is greatly aggravated if the muscle is contracted while in the shortened position.

    In paraspinal muscles (and likely other muscles, too), a degree of nerve compression that causes identifiable neuropathic electromyographic (EMG) changes is associated with an increase in the numbers of active TrPs. These TrPs may be activated by disturbed microtubular communication between the neuron and the endplate because the motor endplate is involved in the path physiologic process of the peripheral core TrP.

    The histopathologic complications that could contribute to the chronicity of the condition and make treatment more difficult include the following:

    • Distortion of the striations (sarcomere arrangement) in adjacent muscle fibers for some distance beyond the contraction knot (see Image 1). This produces unnatural shear forces between fibers that could seriously and chronically stress the sarcolemma of the adjacent muscle fibers. If the membrane were stressed to the point at which it became pervious to the relatively high concentration of calcium in the extracellular space, it could induce massive contracture that could compound the shear forces.
    • The occasional finding of a segment of an empty sarcolemmal tube between 2 contractions knots may represent an additional irreversible complication of a contraction knot.

    Latent TrPs can produce other effects characteristic of a TrP, including increased muscle tension and muscle shortening; but these do not produce spontaneous pain. Both active and latent TrPs can cause significant motor dysfunction. The same factors that are responsible for the development of an active TrP can, to a lesser extent, cause a latent TrP. An active key TrP in one muscle can induce an active satellite TrP in another. Inactivation of the key TrP often inactivates its satellite TrP without treatment of the satellite TrP itself.

    The intensity and extent of the pattern of referred pain depends on the degree of irritability in the TrP, not on the size of the muscle. MTrPs in small, obscure, or variable muscles can be as troublesome to the patient as TrPs in large familiar muscles.

    TrPs are activated directly by acute overload, overwork fatigue, direct impact trauma, and radiculopathy. TrPs can be activated indirectly by other existing TrPs, visceral disease, arthritic joints, joint dysfunctions, and emotional distress. Satellite TrPs are prone to develop in muscles that lie within the pain reference zone of key MTrPs or within the zone of pain referred from a diseased viscus, such as the pain due to myocardial infarction, gastric ulcer, cholelithiasis, or renal colic. A perpetuating factor increases the likelihood of overload stress that can convert a latent TrP to an active TrP.

    With adequate rest and in the absence of perpetuating factors, an active TrP may spontaneously revert to a latent state. Pain symptoms disappear; however, occasional reactivation of the TrP by exceeding that muscle’s stress tolerance can account for a history of recurrent episodes of the same pain over a period of years.

    Clinical

    History

    • Symptoms
      • Active TrPs produce a clinical complaint, usually pain, that the patient recognizes when the TrP is compressed digitally. The patient is aware of the pain caused by an active TrP, but he or she may or may not be aware of the dysfunction it causes.
      • Latent TrPs characteristically cause increased muscle tension and limit the stretch range of motion, which often escapes the patient’s attention or is simply accepted. The patient becomes aware of pain originating from a latent TrP only when pressure is applied to it. Spontaneous referred pain appears with increased irritability of the TrP; then, the TrP is identified as active.
      • The patient usually presents with complaints due to the most recently activated TrP. When this TrP is successfully eliminated, the pain pattern may shift to that of an earlier key TrP that must also be inactivated. If the key TrP is inactivated first, the patient may recover without further treatment.
      • Patients with active MTrPs usually complain of poorly localized, regional, aching pain in subcutaneous tissues, including muscles and joints. They rarely complain of sharp, clearly localized coetaneous-type pain. The myofascial pain is often referred away from the TrP in a pattern that is characteristic for each muscle. Sometimes, the patient is aware of numbness or paresthesia rather than pain.
    • Dysfunction
      • In addition to the clinical symptoms produced by the sensory disturbances of referred pain, dysesthesias, and hypoesthesia’s, patients can also have clinically important disturbances of autonomic and motor functions.
      • Disturbances of autonomic functions
        • Disturbances of autonomic functions caused by TrPs include abnormal sweating, persistent lacrimation, persistent coryza, excessive salivation, and pilomotor activities.
        • Related proprioceptive disturbances caused by TrPs include imbalance, dizziness, tinnitus, and distorted perception of the weight of lifted objects.
      • Disturbances of motor functions
        • Disturbances of motor functions caused by TrPs include spasm of other muscles, weakness of the involved muscle function, and loss of coordination by the involved muscle, and decreased work tolerance of the involved muscle.
        • The weakness and loss of work tolerance are often interpreted as an indication for increased exercise, but if this is attempted without inactivating the responsible TrPs, the exercise is likely to encourage and further ingrain substitution by other muscles, with further weakening and deconditioning of the involved muscle.
        • The combination of weakness in the hands and loss of forearm muscle coordination makes the grasp unreliable. Objects sometimes slip unexpectedly from the patient’s grasp. The weakness results from reflex motor inhibition and characteristically occurs without atrophy of the affected muscle. Patients are prone to intuitively substitute muscles without realizing that, for instance, they are carrying the grocery bag in the nondominant but now stronger arm.
      • The motor effects of TrPs on the muscle in which they are located are considered in detail under Surface electromyography in Other Tests.
    • Sleep disturbances
      • Disturbance of sleep can be a problem for patients with a painful TrP syndrome. Authors of a series of studies have shown that many sensory disturbances, including pain, can seriously disturb the patient’s sleep.
      • This sleep disturbance can, in turn, increase pain sensitivity the next day. Active MTrPs become more painful when the muscle is held in the shortened position for long periods and if body weight compresses the TrP. Thus, for patients with active TrPs, sleep positioning can be critical to prevent unnecessary disturbances of their sleep.

    Physical

    Each muscle has a characteristic elicited referred pain pattern that, for active MTrPs, is familiar to the patient. Without a laboratory test or imaging method, diagnosis of MTrPs depends entirely on history and physical examination. MTrP symptoms follow muscle overload, are activated acutely by sudden overload, or develop gradually with prolonged contractions or repetitive activity. The diagnostic skill required depends on considerable innate palpation ability, authoritative training, and extensive clinical experience.

    Pain prevents a muscle with a MTrP from reaching its full stretch range of motion and also restricts its strength and/or endurance. Clinically, the lip is a localized spot of tenderness in a nodule within a palpable taut band of muscle fibers. Restricted stretch range of motion and a palpable increase in muscle tenseness (ie, decreased compliance) are more severe in more active MTrPs.

    Active MTrPs are identified when patients recognize the pain induced by applying pressure to a MTrP. The taut band fibers usually respond with an MTrP when the taut band is accessible and when the TrP is stimulated by properly applied snapping palpation. The taut band fibers have a consistent twitch response when a needle penetrates the MTrP.

    • Taut band
      • By gently rubbing across the direction of the muscle fibers in a superficial muscle, the examiner can feel a nodule at the MTrP and ropelike indurations that extends from this nodule to the attachment of the taut muscle fibers at each end of the muscle.
      • The taut band can be snapped or rolled under the finger in accessible muscles. With effective inactivation of the TrP, this palpable sign becomes less tense and often (but not always) disappears, sometimes immediately. See Image 2.
    • Tender nodule
      • Palpation along the taut band reveals a nodule exhibiting a highly localized and exquisitely tender spot that is characteristic of an MTrP. When the spot is tested for tenderness, displacement of the algometer by 2 cm produces a statistically significant decrement in pain threshold algometer readings. Clinically, displacement of the application of pressure by 1-2 mm at an MTrP can result in a markedly reduced pain response.
      • This strong localization of tenderness in the vicinity of an MTrP corresponds to the localized sensitivity of the experimental muscle for eliciting TrPs as demonstrated in rabbit experiments. A 5-mm displacement to either side of the trigger spot (at right angles to the taut band) results in almost total loss of response. However, the response fades out more slowly when stimulated over a range of several centimeters from the trigger spot along the taut band.
    • Recognition: Application of digital pressure on either an active or latent MTrP can elicit a referred pain pattern characteristic of that muscle. However, if the patient recognizes the elicited sensation as a familiar experience, this establishes the MTrP as being active and is one of the most important diagnostic criteria available when the palpable findings also are present. Similar recognition is observed frequently when a needle penetrates the MTrP and encounters an active locus.
    • Referred sensory signs: In addition to referring pain to the reference zone, MTrPs may refer other sensory changes such as tenderness and dysesthesias.
    • Local twitch response: Snapping palpation of the TrP frequently evokes a transient twitch response of the taut band fibers. Twitch responses can be elicited both from active and latent TrPs. Hubbard at al showed that no difference was noted in twitch responses whether elicited by snapping palpation or by needle penetration. See Image 3.
    • Limited range of motion
      • Muscles with active MTrPs have a restricted passive (stretch) range of motion because of pain. An attempt to passively stretch the muscle beyond this limit produces increasingly severe pain because the involved muscle fibers are already under substantially increased tension at rest length.
      • The limitation of stretch due to pain is not as great with active movement as with passive lengthening of the muscle; this finding at least partly due to reciprocal inhibition. When the TrP is inactivated and the taut band is released, range of motion returns to normal.
      • The degree of limitation produced by MTrPs is much more marked in some muscles (eg, subscapularis) than in other muscles (eg, latissimus dorsi).
    • Painful contraction: When a muscle with an active TrP is strongly contracted against fixed resistance, the patient feels pain. This effect is most marked when the patient attempts to contract the muscle when it is in a shortened position.
    • Weakness
      • Although weakness is generally characteristic of a muscle with active myofascial MTrPs, the magnitude is varied from muscle to muscle and from subject to subject.
      • EMG studies indicate that, in muscles with active MTrPs, the muscle starts out fatigued, it fatigues more rapidly, and it becomes exhausted sooner than normal muscles. The weakness may reflect reflex inhibition of the muscle by the MTrPs.

    Causes

    Causes of myofascial pain include or are related to the following:

    • The lack of motor unit action potentials due to the endogenous contracture of the contractile elements, rather than a nerve-initiated contraction of the muscle fibers
    • The frequency with which muscle overload activates TrPs, which may reflect the marked mechanical vulnerability of the synaptic cleft region of an endplate
    • The release of substances that could sensitize nociceptors in the region of the dysfunctional endplate of the TrP as a result of tissue distress caused by the energy crisis
    • The effectiveness of essentially any technique that elongates the TrP portion of the muscle to its full stretch length even briefly, which could break the cycle that includes energy-consuming contractile activity
    • Laborers who exercise their muscles heavily every day are less likely to develop active TrPs than sedentary workers who are prone to intermittent episodes of vigorous physical activity. This author’s clinical experience supports this observation.

    Author: Auri Bruno-Petrina, MD, PhD, Clinical Trainee, Pemberton Marine Medical Clinic, N Vancouver

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