By Gabe Mirkin MD, May 28, 2012 – Several studies suggest that people who have subclinical hypothyroidism (blood tests demonstrating low thyroid function, but have no symptoms of low thyroid disease) should be given thyroid replacement medication.
THE NORMAL THYROID: The brain produces a hormone called TSH that stimulates the thyroid gland to produce thyroid hormones. To keep the thyroid gland from producing too much thyroid, the thyroid hormone called T4 keeps the brain to from producing more TSH.
TESTS TO DIAGNOSE LOW THYROID FYUCNTION: A blood test called TSH is the most dependable test to diagnose low thyroid function. People with low thyroid function usually have low blood levels of thyroid hormones, and very high levels of the brain hormone, TSH. Doctors diagnose low thyroid function when people have very high levels of the brain hormone, TSH and low levels of thyroid hormones.
SYMPTOMS OF LOW THROID FUNCTION: Most people who have high blood levels of TSH have signs of low thyroid function including tiredness, weakness, weight gain, and decreased deep tendon reflexes.
SUNBCLINICAL HYPOTHYROIDISM: Some people have high blood TSH levels, normal levels of thyroid hormones, and they also have no signs or symptoms of low thyroid function. Doctors call this subclinical hypothyroidism and they usually do not prescribe thyroid replacement pills. Now it appears that these people should also be treated with thyroid hormones, even if they have no symptoms of low thyroid function.
WHY PEOPLE WITH SUBCLINICAL HYPOTHYROIDISM SHOULD BE TREATED: A report from the University of Nebraska shows that people with an abnormal TSH thyroid test should receive thyroid pills, even if they have no symptoms of low thyroid function (1). This study showed that people with low TSH tests and no symptoms can have abnormal cholesterol levels as the only sign of low thyroid function.. See report #G171.1). Treatment with thyroid hormone was associated with fewer heart attacks and death during an eight-year period of observation in 40- to 70-year-old individuals with subclinical hypothyroidism, but not in those who were older than 70(2).
1) Effects of subclinical hypothyroidism and its treatment on serum lipids. Annals of Pharmacotherapy, 2003, Vol 37, Iss 5, pp 725-730 BA Ineck, TMH Ng. Ng TMH, Univ Nebraska, Med Ctr, Dept Pharm Practice,986045 Nebraska Med Ctr, Omaha,NE 68198 USA
2) Archives of Internal Medicine April 24, 2012
Hypothyroidism is a condition characterized by abnormally low thyroid hormone production. There are many disorders that result in hypothyroidism. These disorders may directly or indirectly involve the thyroid gland. Because thyroid hormone affects growth, development, and many cellular processes, inadequate thyroid hormone has widespread consequences for the body.
This article will focus specifically on hypothyroidism in adults.
What are thyroid hormones?
Thyroid hormones are produced by the thyroid gland. This gland is located in the lower part of the neck, below the Adam’s apple. The gland wraps around the windpipe (trachea) and has a shape that is similar to a butterfly – formed by two wings (lobes) and attached by a middle part (isthmus).
The thyroid gland uses iodine (mostly available from the diet in foods such as seafood, bread, and salt) to produce thyroid hormones. The two most important thyroid hormones are thyroxine (T4) and triiodothyronine (T3), which account for 99% and 1% of thyroid hormones present in the blood respectively. However, the hormone with the most biological activity is T3. Once released from the thyroid gland into the blood, a large amount of T4 is converted into T3 – the active hormone that affects the metabolism of cells.
Thyroid hormone regulation- the chain of command
The thyroid itself is regulated by another gland that is located in the brain, called the pituitary. In turn, the pituitary is regulated in part by the thyroid (via a “feedback” effect of thyroid hormone on the pituitary gland) and by another gland called the hypothalamus.
The hypothalamus releases a hormone called thyrotropin releasing hormone (TRH), which sends a signal to the pituitary to release thyroid stimulating hormone (TSH). In turn, TSH sends a signal to the thyroid to release thyroid hormones. If a disruption occurs at any of these levels, a defect in thyroid hormone production may result in a deficiency of thyroid hormone (hypothyroidism).
Hypothalamus – TRH
Thyroid- T4 and T3
The rate of thyroid hormone production is controlled by the pituitary gland. If there is an insufficient amount of thyroid hormone circulating in the body to allow for normal functioning, the release of TSH is increased by the pituitary gland in an attempt to stimulate more thyroid hormone production. In contrast, when there is an excessive amount of circulating thyroid hormone, TSH levels fall as the pituitary attempts to decrease the production of thyroid hormone. In persons with hypothyroidism, there is a persistent low level of circulating thyroid hormones.
T3 Thyroid Hormone to Treat Depression
The thyroid is a butterfly-shaped gland in the front of the neck. It produces hormones that control the speed of your metabolism — the system that helps the body use energy. Thyroid disorders can slow down or rev up your metabolism by disrupting the production of thyroid hormones. When hormone levels become too low or too high, you may experience a wide range of symptoms.
By Gabe Mirkin, MD, May 28, 2012 – . If you are tired much of the time, your doctor will order blood tests for the two thyroid hormones called T3 and T4 and for the brain hormones called TSH and prolactin. If your TSH is high and your prolactin is normal, you are probably hypothyroid and need to take thyroid hormone to give you more energy and prevent heart and blood vessel damage.
Doctors treat people with low thyroid function with thyroid pills called T4 (Levothroid, one brand name is Synthroid). Many doctors think that a person needs only T4 because the thyroid gland makes T4 and then it is converted to T3 in other tissues. However, some people become depressed when they take just T4 and their depression can be cured when they take both thyroid hormones, T3 and T4.
When a depressed patient comes to me and is taking thyroid hormone, T4, I immediately order a blood test called TSH to check if he or she is getting the correct dose. If the TSH is normal, I reduce the dose of T4 by 50% and add a very low dose of T3 (brand name, Cytomel) because it safer to prescribe too low a dose, rather than too high a dose. Overdoses cause shakiness, irritability, irregular heart beats, clots, and osteoporosis. The patient returns in one month for a blood test, TSH, to see if the total thyroid dose is correct. If the TSH is too high, the thyroid dose is too low and I raise the T3 (Cytomel) dose by 5 to 10 m5 each month until the TSH is normal. Then once a year I check TSH blood levels to make sure that the person’s requirements for thyroid hormone are being met.
For example, the usual replacement dose for low thyroid function is 100 micrograms per day. If a depressed patient has a normal TSH, I reduce the T4 dose to 50 mcg/day and add 5 mcg of T3 per day. One month later, if the TSH blood is still too high I raise the T3 dose to 10 or 20 mcg and continue to increase the T3 level each month until the TSH is normal.
Exciting research shows that the thyroid hormone called T3 can help treat depression (1,2,3). Psychotherapy often fails to control depression. Sigmund Freud, the father of psychotherapy, proposed theories about depression, that many psychiatrists do not accept because his writings were his opinions and not presented as scientific data supported by controlled experiments. The dominant theory today is that depression is caused by low brain levels of the neurotransmitters, serotonin and norepinephrine. The drugs such as Paxil, Prozac and Zoloft that treat depression are supposed to raise brain levels of these neurotransmitters. Doctors can also raise brain levels of serotonin by prescribing pills containing T3, a hormone produced by peripheral tissue from T4, which is produced by the thyroid gland. (1) They also prescribe T3 by itself or together with antidepressants. Depression is common among people who have too much or too little thyroid hormone. Doctors usually treat low thyroid function with T4 also known as Levothroid and many people become even more depressed. They treat this depression by prescribing T3 as well as T4.
An article in the Journal of Clinical Psychiatry shows that T3 can be used to treat post traumatic stress disorder, commonly seen in soldiers and people who have been through other causes of terrible emotional trauma (13).
Try to balance T3 and T4 so you will not be taking too much thyroid and harm yourself. 1)If you now take 100 mcg of Levothroid (T4): 2) Lower T4 (Levothroid) to 50 mcg and add Cytomel (T3) 5 mcg each day. 3) One month later, have your doctor draw blood for TSH. 4) If it is normal, you are on the correct dose and should get blood tests TSH once a year. 5) If TSH is too high, increase Cytomel to 10 mcg and hold Levothroid at 50. 6) Draw monthly TSH until it is normal. Keep on raising Cytomel by 5 mcg until TSH is normal.
In some cases, hypothyroidism results from a problem with the pituitary gland, which is at the base of the brain. This gland produces thyroid-stimulating hormone (TSH), which tells the thyroid to do its job. If your pituitary gland does not produce enough TSH, your levels of thyroid hormones will fall. Other causes of hypothyroidism include temporary inflammation of the thyroid or medications that affect thyroid function.
If you are diagnosed with hypothyroidism, your doctor will most likely prescribe thyroid hormones in the form of a pill. This usually leads to noticeable improvements within a couple of weeks. Long-term treatment can result in more energy, lower cholesterol levels, and gradual weight loss. Most people with hypothyroidism will need to take thyroid hormones for the rest of their lives.
With the exception of certain conditions, the treatment of hypothyroidism requires life-long therapy. Before synthetic levothyroxine (T4) was available, desiccated thyroid tablets were used. Desiccated thyroid was obtained from animal thyroid glands, which lacked consistency of potency from batch to batch. Presently, a pure, synthetic T4 is widely available. Therefore, there is no reason to use desiccated thyroid extract.
As described above, the most active thyroid hormone is actually T3. So why do physicians choose to treat patients with the T4 form of thyroid? T3 [liothyronine sodium (Cytomel)] is available and there are certain indications for its use. However, for the majority of patients, a form of T4 [levothyroxine sodium (Levoxyl, Synthroid)] is the preferred treatment. This is a more stable form of thyroid hormone and requires once a day dosing, whereas T3 is much shorter-acting and needs to be taken multiple times a day. In the overwhelming majority of patients, synthetic T4 is readily and steadily converted to T3 naturally in the bloodstream, and this conversion is appropriately regulated by the body’s tissues.
- The average dose of T4 replacement in adults is approximately 1.6 micrograms per kilogram per day. This translates into approximately 100 to 150 micrograms per day.
- Children require larger doses.
- In young, healthy patients, the full amount of T4 replacement hormone may be started initially.
- In patients with preexisting heart disease, this method of thyroid replacement may aggravate the underlying heart condition in about 20% of cases.
- In older patients without known heart disease, starting with a full dose of thyroid replacement may result in uncovering heart disease, resulting in chest pain or a heart attack. For this reason, patients with a history of heart disease or those suspected of being at high risk are started with 25 micrograms or less of replacement hormone, with a gradual increase in the dose at 6 week intervals.
Ideally, synthetic T4 replacement should be taken in the morning, 30 minutes before eating. Other medications containing iron or antacids should be avoided, because they interfere with absorption.
Therapy for hypothyroidism is monitored at approximately six week intervals until stable. During these visits, a blood sample is checked for TSH to determine if the appropriate amount of thyroid replacement is being given. The goal is to maintain the TSH within normal limits. Depending on the lab used, the absolute values may vary, but in general, a normal TSH range is between 0.5 to 5.0uIU/ml. Once stable, the TSH can be checked yearly. Over-treating hypothyroidism with excessive thyroid medication is potentially harmful and can cause problems with heart palpitations and blood pressure control and can also contribute to osteoporosis. Every effort should be made to keep the TSH within the normal range.
What are the symptoms of hypothyroidism?
The symptoms of hypothyroidism are often subtle. They are not specific (which means they can mimic the symptoms of many other conditions) and are often attributed to aging. Patients with mild hypothyroidism may have no signs or symptoms. The symptoms generally become more obvious as the condition worsens and the majority of these complaints are related to a metabolic slowing of the body. Common symptoms are listed below:
- Modest weight gain
- Cold intolerance
- Excessive sleepiness
- Dry, coarse hair
- Dry skin
- Muscle cramps
- Increased cholesterol levels
- Decreased concentration
- Vague aches and pains
- Swelling of the legs
As the disease becomes more severe, there may be puffiness around the eyes, a slowing of the heart rate, a drop in body temperature, and heart failure. In its most profound form, severe hypothyroidism may lead to a life-threatening coma (myxedema coma). In a severely hypothyroid individual, a myxedema coma tends to be triggered by severe illness, surgery, stress, or traumatic injury. This condition requires hospitalization and immediate treatment with thyroid hormones given by injection.
Properly diagnosed, hypothyroidism can be easily and completely treated with thyroid hormone replacement. On the other hand, untreated hypothyroidism can lead to an enlarged heart (cardiomyopathy), worsening heart failure, and an accumulation of fluid around the lungs (pleural effusion</A.).< p>
How is hypothyroidism diagnosed?
A diagnosis of hypothyroidism can be suspected in patients with fatigue, cold intolerance, constipation, and dry, flaky skin. A blood test is needed to confirm the diagnosis.
When hypothyroidism is present, the blood levels of thyroid hormones can be measured directly and are usually decreased. However, in early hypothyroidism, the level of thyroid hormones (T3 and T4) may be normal. Therefore, the main tool for the detection of hyperthyroidism is the measurement of the TSH, the thyroid stimulating hormone. As mentioned earlier, TSH is secreted by the pituitary gland. If a decrease of thyroid hormone occurs, the pituitary gland reacts by producing more TSH and the blood TSH level increases in an attempt to encourage thyroid hormone production. This increase in TSH can actually precede the fall in thyroid hormones by months or years (see the section on Subclinical Hypothyroidism below). Thus, the measurement of TSH should be elevated in cases of hypothyroidism.
However, there is one exception. If the decrease in thyroid hormone is actually due to a defect of the pituitary or hypothalamus, then the levels of TSH are abnormally low. As noted above, this kind of thyroid disease is known as “secondary” or “tertiary” hypothyroidism. A special test, known as the TRH test, can help distinguish if the disease is caused by a defect in the pituitary or the hypothalamus. This test requires an injection of the TRH hormone and is performed by an endocrinologist (hormone specialist).
The blood work mentioned above confirms the diagnosis of hypothyroidism, but does not point to an underlying cause. A combination of the patient’s clinical history, antibody screening (as mentioned above), and a thyroid scan can help diagnose the precise underlying thyroid problem more clearly. If a pituitary or hypothalamic cause is suspected, an MRI of the brain and other studies may be warranted. These investigations should be made on a case by case basis.
What causes hypothyroidism?
Hypothyroidism is a very common condition. It is estimated that 3% to 5% of the population has some form of hypothyroidism. The condition is more common in women than in men, and its incidence increases with age.
Below is a list of some of the common causes of hypothyroidism in adults followed by a discussion of these conditions.
- Hashimoto’s thyroiditis
- Lymphocytic thyroiditis (which may occur after hyperthyroidism)
- Thyroid destruction (from radioactive iodine or surgery)
- Pituitary or hypothalamic disease
- Severe iodine deficiency
The most common cause of hypothyroidism in the United States is an inherited condition called Hashimoto’s thyroiditis. This condition is named after Dr. Hakaru Hashimoto who first described it in 1912. In this condition, the thyroid gland is usually enlarged (goiter) and has a decreased ability to make thyroid hormones. Hashimoto’s is an autoimmune disease in which the body’s immune system inappropriately attacks the thyroid tissue. In part, this condition is believed to have a genetic basis. This means that the tendency toward developing Hashimoto’s thyroiditis can run in families. Hashimoto’s is 5 to 10 times more common in women than in men. Blood samples drawn from patients with this disease reveal an increased number of antibodies to the enzyme, thyroid peroxidase (anti-TPO antibodies). Since the basis for autoimmune diseases may have a common origin, it is not unusual to find that a patient with Hashimoto’s thyroiditis has one or more other autoimmune diseases such as diabetes or pernicious anemia ( B12 deficiency). Hashimoto’s can be identified by detecting anti-TPO antibodies in the blood and/or by performing a thyroid scan.
Lymphocytic thyroiditis following hyperthyroidism
Thyroiditis refers to inflammation of the thyroid gland. When the inflammation is caused by a particular type of white blood cell known as a lymphocyte, the condition is referred to as lymphocytic thyroiditis. This condition is particularly common after pregnancy and can actually affect up to 8% of women after they deliver. In these cases, there is usually a hyperthyroid phase (in which excessive amounts of thyroid hormone leak out of the inflamed gland), which is followed by a hypothyroid phase that can last for up to six months. The majority of affected women eventually return to a state of normal thyroid function, although there is a possibility of remaining hypothyroid.
Thyroid destruction secondary to radioactive iodine or surgery
Patients who have been treated for a hyperthyroid condition (such as Graves’ disease) and received radioactive iodine may be left with little or no functioning thyroid tissue after treatment. The likelihood of this depends on a number of factors including the dose of iodine given, along with the size and the activity of the thyroid gland. If there is no significant activity of the thyroid gland six months after the radioactive iodine treatment, it is usually assumed that the thyroid will no longer function adequately. The result is hypothyroidism. Similarly, removal of the thyroid gland during surgery will be followed by hypothyroidism.
Pituitary or Hypothalamic disease
If for some reason the pituitary gland or the hypothalamus are unable to signal the thyroid and instruct it to produce thyroid hormones, a decreased level of circulating T4 and T3 may result, even if the thyroid gland itself is normal. If this defect is caused by pituitary disease, the condition is called “secondary hypothyroidism.” If the defect is due to hypothalamic disease, it is called “tertiary hypothyroidism.”
A pituitary injury may result after brain surgery or if there has been a decrease of blood supply to the area. In these cases of pituitary injury, the TSH that is produced by the pituitary gland is deficient and blood levels of TSH are low. Hypothyroidism results because the thyroid gland is no longer stimulated by the pituitary TSH. This form of hypothyroidism can, therefore, be distinguished from hypothyroidism that is caused by thyroid gland disease, in which the TSH level becomes elevated as the pituitary gland attempts to encourage thyroid hormone production by stimulating the thyroid gland with more TSH. Usually, hypothyroidism from pituitary gland injury occurs in conjunction with other hormone deficiencies, since the pituitary regulates other processes such as growth, reproduction, and adrenal function. Medications
Medications that are used to treat an over-active thyroid (hyperthyroidism) may actually cause hypothyroidism. These drugs include methimazole (Tapazole) and propylthiouracil (PTU). The psychiatric medication, lithium (Eskalith, Lithobid), is also known to alter thyroid function and cause hypothyroidism. Interestingly, drugs containing a large amount of iodine such as amiodarone (Cordarone), potassium iodide (SSKI, Pima), and Lugol’s solution can cause changes in thyroid function, which may result in low blood levels of thyroid hormone.
Severe iodine deficiency:
In areas of the world where there is an iodine deficiency in the diet, severe hypothyroidism can be seen in 5% to 15% of the population. Examples of these areas include Zaire, Ecuador, India, and Chile. Severe iodine deficiency is also seen in remote mountain areas such as the Andes and the Himalayas. Since the addition of iodine to table salt and to bread, iodine deficiency is rarely seen in the United States.
Eat Only When You Are Active
By Gabe Mirkin MD, May 28, 2012
More than a third of all North Americans are obese and will die prematurely because of their excess fat. WHEN you eat may be even more important than HOW MUCH you eat. Never eat and go to bed. The safest time to eat is just before and after you exercise. Resting after you eat is an invitation for higher blood sugar and insulin levels, more weight gain, and increased risk for diabetes and heart attacks. The current obesity epidemic may well be caused by staying up later at night to snack and watch television.
MICE ALLOWED TO EAT ALL DAY LONG ARE FATTER. Mice that are placed on a high-fat diet gain far more weight when they are supplied with food 24 hours a day than when they can eat only for 8 hours a day, even though they eat the same number of calories per day (Cell Metabolism, published online May 17, 2012). Besides weighing more, the mice that could eat all day long had higher blood sugar and insulin levels, more liver damage, and higher blood levels of CRP, the blood test that measures inflammation.
MICE FED ONLY DURING SLEEPING HOURS ARE FATTER THAN THOSE FED DURING WAKING HOURS. Mice that were allowed to eat only during the 12 hours that they normally sleep gained significantly more weight (48 percent weight increase) than mice eating the same type and amount of food during the 12 hours they are normally awake (20 percent weight increase). Both groups ate the same total amount and type of food and were equally active (Obesity, published online Sept. 3, 2009).
HUMANS WHO SNACK SUFFER MORE DIABETES AND PREMATURE DEATH. Scientists at Karolinska Institutet surveyed 4,000 60-year-old, men and women. Compared to those who ate only breakfast, lunch and dinner, those who snacked between meals had larger waist circumferences and higher blood sugar, insulin, triglyceride and cholesterol levels than people who ate regular meals with less snacking (Obesity, 2008;16 (6):1302). These are all signs associated with metabolic syndrome, diabetes, heart attacks, and premature death.
STAY ACTIVE AFTER YOU EAT. Resting muscles are inactive and draw no sugar from your bloodstream. On the other hand, contracting muscles pull sugar from the bloodstream. They do not even require insulin to do this. If you eat and stand or walk, the contracting muscles can pull sugar from your bloodstream. However, when you eat and sit or lie down, your muscles draw no sugar from your bloodstream and blood sugar levels rise higher to increase risk for cell damage.
• HIGH INSULIN LEVELS: Your pancreas tries to lower the high blood sugar level, so it puts out ever increasing amounts of insulin.
• INCREASED RISK FOR HEART ATTACKS: Insulin constricts the arteries leading to your heart, to increase risk for a heart attack.
• HIGH TRIGLYCERIDES: When muscles are inactive, blood sugar levels rise. The extra sugar goes to your liver and other cells. Once your liver fills up with its own stored sugar called glycogen, it cannot store any more sugar. so all extra sugar is converted to a type of fat called triglycerides.
• LOW GOOD HDL CHOLESTEROL: High triglycerides increase risk for clotting, so your good HDL cholesterol works to save you by carrying triglycerides from your bloodstream to your liver. You use up your good HDL and blood levels of HDL drop.
• FATTY LIVER: The triglycerides accumulate in your liver to cause a fatty liver. A fatty liver cannot clear sugar from your bloodstream.
• DIABETES: Since the liver cannot clear sugar from your bloodstream, you develop even higher blood sugar levels and are now diabetic.
• HEART ATTACKS AND PREMATURE DEATH. Diabetes markedly increases risk for heart attacks, strokes, many cancers, and premature death.
Blood Test for Diabetes Predicts Cancer Risk in Women
By Gabe Mirkin MD, May 28, 2012 – A blood test that measures blood sugar levels also can be used to predict who is at increased risk for cancer (International Journal of Cancer, April 26, 2012). HBA1C is a blood test that measures how much sugar is stuck on cells. People who have values 5.7 or higher are at increased risk for cancer, even if your doctor has not diagnosed you as having diabetes.
When blood sugar rises too high, sugar sticks to the outside surface of cell membranes. Once there, sugar can never get off. It is converted through a series of chemical reactions to sorbitol that destroys cells. Anything that raises blood sugar appears to increase cancer risk.
To keep your blood sugar low,
1) Avoid being overweight
2) Do not take sugared drinks in any form, including fruit juices, except during prolonged intense exercise
3) Avoid foods with added sugar
4) Avoid fried foods
5) Eat large amounts of fruits and vegetables
6) Do not eat red meat (blocks insulin receptors)
8) Grow muscle
9) Reduce body fat
10) Keep blood levels of hydroxy-vitamin D above 75 nmol/L
C-Reactive Protein (CRP) and Inflammation
By Gabe Mirkin MD, May 28, 2012 – Recent research shows that having a high C-Reactive Protein increases your risk of suffering a heart attack or stroke by twice as much as having a high cholesterol. C-Reactive Protein (CRP) is a blood test that measures inflammation, part of the immune reaction that protects you from infection when you injure yourself. It causes redness, pain and swelling, and can damage the inner lining of arteries, and break off clots from arteries to block the flow of blood to cause strokes and heart attacks.
CRP levels fluctuate from day to day, and levels increase with aging, high blood pressure, alcohol use, smoking, low levels of physical activity, chronic fatigue, coffee consumption, having elevated triglycerides, insulin resistance or diabetes, taking estrogen, eating a high protein diet, and suffering sleep disturbances, or depression. If you have none of these known causes, at this time the best ways we know to reduce CRP levels are exercise and a diet that includes omega-3 fatty acids. Statins appear to protect against inflammation as well as to lower cholesterol, but they can cause muscle pain in exercisers.
IF YOU HAVE A HIGH CRP, try to correct the known causes: infection, high blood pressure, alcohol use, smoking, low levels of physical activity, chronic fatigue, coffee consumption, having elevated triglycerides, insulin resistance or diabetes, taking estrogen, eating a high protein diet, and suffering sleep disturbances, or depression.
The most common cause of an elevated CRP is infection. If you have burning on urination, getting up in the night to urinate, urgency when your bladder is full of a feeling that you have to urinate all the time, check for a urinary tract infection. If you have wheezing and a chronic cough or shortness of breath, check for a lung infection. If you have belching and burning in your stomach, get an upper GI series X ray and blood test for Helicobacter. If you have diarrhea, check for an intestinal infection. If you have any of these infections, you have an accepted reason to take antibiotics. Your evaluation should include IGG and IGM antibody blood tests for chlamydia and mycoplasma. If either or both titres are high, I usually recommend taking doxycycline 100 mg twice a day for at least three weeks. Most doctors will not do this because they feel that data aren’t strong enough to warrant antibiotics at this time.
By Salynn Boyles
WebMD Health News
Reviewed by Louise Chang, MD
May 28, 2012 — Prescription medication “take-back” programs are increasingly promoted as a way to safely dispose of unused drugs, but they are no better for the environment than simply throwing old drugs in the trash, a new study suggests.
When researchers used a complicated methodology called “comparative life cycle assessment” to estimate the environmental impact of flushing, incinerating, and trashing old medications, they found little difference between burning the drugs — which is what most take-back programs do — and having them end up in the landfill.
Close to 200 million pounds of drugs go unused in theU.S.each year.
There are serious concerns that antibiotic and hormone medications pose a threat to the nation’s lakes, rivers, and other water supplies.
While most of these concerns involve flushed waste that contains residues of used medications, unused drugs may also be finding their way into the nation’s water supply, researcher Steven J. Skerlos, PhD, tells WebMD.
FDA Says Trash Some Unused Drugs
Take-back initiatives typically involve the collection of unused drugs by participating pharmacies for incineration with other medical wastes.
Skerlos, an associate professor of mechanical engineering at theUniversityofMichigan, says these programs may actually be worse for the environment than throwing drugs in the trash due to the greenhouse gases produced by transporting and burning the medications.
If there are no disposal instructions given on the drug label or patient information sheet, the FDA recommends throwing away some prescriptions by:
- First mixing them with an unpalatable substance such as kitty litter or used coffee grounds,
- Placing the mixture in a container such as a sealed plastic bag,
- And disposing of the bag with other household wastes.
However, there is one big exception to this recommendation, FDA spokesperson Morgan Liscinsky tells WebMD.
Dangerous Drugs Should Be Flushed
Medications that are especially harmful and could potentially be deadly if taken accidentally should not be put in the trash.
Instead, they should be flushed down the toilet or sink to eliminate any chance that a child or pet will find them, the FDA says.
Of special concern are powerful narcotics delivered by patch, such as the drug fentanyl.
“Even after a patch is used, a lot of the drug remains in the patch, so you wouldn’t want to throw something in the trash that contains a powerful and potentially dangerous narcotic that could harm others,” FDA senior program manager Jim Hunter, RPh, noted on the agency’s web site.
A complete list of the drugs recommended for flushing by FDA can be found on the agency’s web site �in the consumer section entitled “How to Dispose of Unused Medicines.”
While environmental concerns remain about the impact of flushing any drugs, the FDA notes that there is as yet no solid evidence linking flushing to specific risks in humans.
And scientists with the Environmental Protection Agency (EPA) have not yet found evidence of adverse effects on human health associated with drug residues in the environment.
Skerlos says that since more than half of people in theU.S.already throw their unused drugs in the trash, asking them to take part in drug take-back programs could have significant downsides, including increased inconvenience, longer drug storage in the home, and higher costs to society.
Skerlos and colleagues estimate that a nationwide drug take-back program would cost $2 billion a year.
They write that re-evaluation of drug disposal options may become necessary as our understanding of the environmental impact of these options increases.
The study appears online in the American Chemical Society journal Environmental Science & Technology.
By Charles Bankhead, Staff Writer, MedPage Today
Published: May 24, 2012
Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston and Dorothy Caputo, MA, BSN, RN, Nurse Planner
- Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.
- This small, retrospective, single-center study found that cabergoline treatment improved or fully restored orgasmic function in male anorgasmics.
- Note that concomitant testosterone replacement significantly increased the probability of response.
ATLANTA– Anorgasmia improved or resolved completely in almost 70% of men treated with the dopamine receptor agonist cabergoline, results of a small retrospective study showed.
Overall, 50 of 72 men had improvement in orgasms, and 26 of the 50 had return of normal orgasm during treatment with cabergoline.
In a multivariate analysis, duration of therapy and concomitant testosterone replacement therapy (TRT) predicted response to cabergoline, Tung-Chin Hsieh, MD, reported here at the American Urological Association meeting.
“Cabergoline is an effective treatment option for male anorgasmia,” said Hsieh, of Baylor College of Medicine inHouston. “Further studies are needed to better understand the pathophysiology of anorgasmia and to validate our observations of cabergoline’s action in anorgasmic patients.”
Anorgasmia usually has a psychological origin but can occur after radical prostatectomy for localized prostate cancer or secondary to drug treatment.
For instance, selective serotonin reuptake inhibitors and classic antipsychotics that are not prolactin sparing have been shown to cause disturbances in orgasmic function. And as many as 75% of men have reported orgasmic dysfunction following radical prostatectomy, said Hsieh.
The rationale for studying cabergoline in secondary anorgasmia came from observations of a prolactin surge in some men in the post-ejaculatory phase, leading to reduced erectile and ejaculatory potential. Additionally, increased levels of dopamine have been reported in association with orgasmic response, Hsieh continued.
Cabergoline has a direct inhibitory effect on prolactin-secreting cells in the pituitary and has a history of use as first-line treatment for hyperprolactinemia.
Given the background of anorgasmia and biologic effects of cabergoline, Hsieh and colleagues hypothesized that the drug might improve anorgasmia by means of its inhibitory effect on prolactin.
They retrospectively evaluated medical records of patients treated with cabergoline from 2009 to 2011 at a single andrology clinic. After excluding men who received cabergoline for conditions unrelated to anorgasmia, the investigators identified 72 men for the analysis.
All of the men received cabergoline 0.5 mg twice a week.
Laboratory assessments included serum prolactin, follicle stimulating hormone (FSH), luteinizing hormone (LH), and serum testosterone. Additionally, investigators determined whether the men were receiving concomitant TRT.
Response to treatment was determined by the patients’ self-reported improvement in orgasmic function or return of normal orgasm. Response was defined as either improvement or restoration of normal orgasmic function.
Results showed that 69% of the men had improved orgasmic function, and 52% of the men with improved function had return of normal orgasm.
Mean treatment duration for men who responded to therapy was 296 days compared with 218 days for nonresponders (P=0.02).
Concurrent testosterone replacement therapy was associated with an increased likelihood of response (P=0.03), but the testosterone formulation (topical versus injectable) did not influence response.
Mean age of men in the study was 63, which did not differ between responders and nonresponders.
Patients who responded to cabergoline had lower baseline prolactin levels and higher FSH, LH, and testosterone levels, but none of the differences achieved statistical significance.
The findings impressedHossein Sadeghi-Nejad,MD, who moderated the poster presentation that included Hsieh’s study.
“Anyone who is in sexual medicine knows that this group of patients is a very difficult group to manage,” said Sadeghi-Nejad, of theUniversityofMedicineand Dentistry of New Jersey inHackensack. “Really, we have had very little to offer them. I think this is excellent work and, hopefully, an avenue for our patients.”
In response to a question, Hsieh said no serious adverse effects occurred in any of the patients. Headache and dizziness are the most commonly reported adverse events in patients treated with cabergoline. The drug has to be used with caution in patients with heart-valve disease, as some evidence of exacerbation with cabergoline has been reported.
“Any patient with valvular disease should be screened with echocardiography before starting treatment with cabergoline,” said Hsieh.
Hsieh had no disclosures.
Primary source: American Urological Association
Hsieh TC, et al “Cabergoline for the treatment of male anorgasmia” AUA 2012; Abstract 1495.
Working from Houston, home to one of the world’s largest medical complexes, Charles Bankhead has more than 20 years of experience as a medical writer and editor. His career began as a science and medical writer at an academic medical center. He later spent almost a decade as a writer and editor for Medical World News, one of the leading medical trade magazines of its era. His byline has appeared in medical publications that have included Cardio, Cosmetic Surgery Times, Dermatology Times, Diagnostic Imaging, Family Practice, Journal of the National Cancer Institute, Medscape, Oncology News International, Oncology Times, Ophthalmology Times, Patient Care, Renal and Urology News, The Medical Post, Urology Times, and the International Medical News Group newspapers. He has a BA in journalism and MA in mass communications, both from Texas Tech University.
UPDATE FROM TARGET HEALTH INC. – HIGHLIGHTS OF THE YEAR
We would like to thank the loyalty and feedback of our over 4,300 readers, some of whom have been receiving ON TARGET since 1995. Several times a year we are asked what Target Health does and what are our accomplishments. The following summarizes what has happened over the last 12 months.
In 2012, Target Health celebrated its 19th year as a New York City-based, full-service e*CRO. Our full-time staff are dedicated to all aspects of the “paperless clinical trial,” complementing our expertise in Drug and Device Regulatory Affairs, Clinical Research Management, Biostatistics, Data Management, Internet-based clinical trials (Target e*CRF®), Medical Writing, and Strategic Planning. We provide turn-key development operations for small and medium size companies and have fully validated software for clinical trials. Patent # 8,041,581 B2 was issued in October 2011 for a System and Method for Collecting, Processing, and Storing Discrete Data Records Based Upon a Single Data Input (Target e*CTR®; eClinical Trial Record).
Highlights of the last 12 months include:
1. Regulatory approval of 3 NDAs and 1 PMA
a. Gaucher disease – May 2012
b. Cystic Fibrosis – May 2012
c. Head Lice – February 2012
d. Companion Diagnostic for NSCLC Drug – August 2011
2. Implementation of 3 paperless eSource clinical trials under 2 US INDs, using Target eCTR® (eClinical Trial Record; patent issued), the “electronic health record” for clinical trials
a. Mitchel, J, Kim, YJ, Choi, JH, et al. Evaluation of Data Entry Errors and Data Changes to an Electronic Data Capture (EDC) Clinical Trial Database. Drug Information Journal, 2011, 45:421-430.
b. Morrison, B, Cochran, C, Giangrande, J, et al. Monitoring the quality of conduct of clinical trials: a survey of current practices. Clinical Trials, 2011; 8:342–349.
c. Mitchel, J. and Schloss-Markowitz, J. Time for Change. International Journal of Clinical Trials, February 2011; 22-29.
d. Tantsyura, V., Grimes, I., Mitchel, J. et al. Cost-Effective Approach To Managing Laboratory Reference Ranges For Local Laboratories, DIA Journal (2012, in press)
e. Mitchel, J., Schloss-Markowitz, J., Yin, H. Lessons Learned From a Direct Data Entry (DDE) Phase 2 Clinical Trial Under a US IND. DIA Journal (2012, accepted for publication)
4. Three original IND submissions
5. Target Health member of the CTTI Steering Committee
6. Release of:
a. Target e*CTR® v 1.2 (electronic health record for clinical trials; Patent # 8,041,581 B2)
b. Target e*Studio® v 1.1 (generates Target e*CRF EDC applications
c. Target Document® v 1.6 (eTMF document management)
d. Target e*CTMS™ v 1.3 (Clinical trial management system)
e. Target e*Pharmacovigilance® v 1.0 (Safety monitoring and generation of Form 3500A and CIOMS 1)
f. Target Encoder® v 1.3 (MedDRA and WHO Drug coder)
g. Target Monitoring Reports™ v 1.0 (online monitoring reports)
We are also very pleased to announce that Target Health has played a key role in bringing to market 35 new drug or device products. Of these approvals, there are now 25 products marketed world-wide that used Target e*CRF for their pivotal trials:
- NDA pancreatic Insufficiency – Cystic Fibrosis – Monitoring; DM; Statistics; Writing; NDA Preparation
- NDA – Gaucher Disease – EDC ; Regulatory Consulting, Toxicology, Monitoring; DM; Statistics; Writing, NDA, eCTD
- PMA – Companion Diagnostic – EDC
- NDA – Head Lice – EDC
- NDA/MAA – Hereditary Angioedema –Regulatory Affairs, EDC
- NDA Emergency Contraception –- EDC ; Regulatory Affairs, Monitoring; DM; Statistics; Writing
- NDA/MAA – Prostate Cancer – EDC
- NDA – Head Lice– EDC; Toxicology, Regulatory Consulting, Monitoring; DM; Statistics; Writing; NDA (eCTD)
- BLA – Autoinflammatory Disease – EDC
- NDA/MAA – Infertility – EDC ; DM; Statistics
- NDA/MAA – Infertility – EDC; DM; Statistics
- PMA – Periodontal Disease – GEM 21S (Biomimetic Therapeutics) – EDC; Monitoring; DM; Statistics; Writing
- Canada – Bone Fractures – GEM 21S (Biomimetic Therapeutics) – EDC; Monitoring; DM; Statistics; Writing
- PMA – Surgical Adhesions – REPEL CV (Synthemed, Inc. Approvable) – EDC; Monitoring; DM; Statistics; Writing; PMA (eCopy)
- PMA – Ten (10) Diagnostic Approvals (Abbott Laboratories) – EDC
- 510(k) – One (1) Diagnostic Approval (Abbott Laboratories) – EDC
Target Health now represents over 30 companies at FDA from all over the world including England, France, Germany, Israel, Korea, Switzerland and the US.
i. Bladder cancer
ii. Colorectal cancer
iii. Cancer imaging
iv. Ovarian cancer
v. Pancreatic cancer
b. Orphan Disease
i. Gaucher disease
ii. Cystic fibrosis
iv. Growth hormone
f. Fatty liver
i. Traumatic brain injury
j. Ulcerative colitis
Target Health has expertise in preparation and publishing of electronic submissions and is an FDA approved vendor for electronic submissions through the Electronic Submissions Gateway (ESG).
CLINICAL TRIAL SOFTWARE PACKAGES
Target e*CRF®: Target e*CRF (EDC) has now been used in over 250 clinical trials since 1999. Largest trial to date is over 7,000 patients.
Target eClinical Trial Record (Target e*CTR®): Target e*CTR allows the clinical study sites to perform direct data entry into any EDC system, and at the same time generates a read-only electronic document, which can be designated as the primary source data (eSource). These data, maintained in a secure, read-only trusted 3rd party environment, are available to the clinical study sites, monitors and regulatory agencies in a human readable format.
Target e*Studio®: Target e*studio allows users to build Target eCRF applications using a technology transfer business model.
Target Document®: Target Document is a user-friendly, inexpensive; highly sophisticated, Web-based, document management system that allows authorized users to view, download, and manage any document for their organization. - No More paper – Target Document can be used for the eTrial Master File (eTMF) and features include: 1) 21 CFR Part 11 compliance; 2) routing for electronic signatures; 3) email alerts; 5) communication tools.
Target Encoder®: Target Encoder is a user-friendly, inexpensive; highly sophisticated, Web-based, coding system that allows authorized users to automatically code MedDRA and WHO Drug and other types of dictionaries. Target Encoder is fully integrated with Target e*CRF.
Target e*CTMS®: Target e*CTMS is a user-friendly, inexpensive; highly sophisticated, Web-based, clinical trial management system. A new clinical trial starts with identification of the sponsor and project name. Investigators, IRBs and users are maintained within the CTMS and can be easily assigned to a project. All staff within a clinical site can be identified with their title and contact information, as well as shipping addresses which could be different from the head office. As the site commits to participate in the clinical trial, a site number can be assigned. Once IRB approval is obtained, and all regulatory documents have been identified as received, an alert can be sent out via email to allow for drug shipment. Target e*CTMS provides many additional features such as: 1) Decision Logs, 2) Meeting Logs with uploading of the meeting minutes, 3) Questions and Answers, 4) status of Regulatory Submissions and Deliverables, and 5) Monitor Site Visit Tracking with document upload.
Target Batch Edit Checks: With Target e*CRF®, batch edit checks are now integrated with the electronic query system within the study. Target e*CRF® runs the edits and displays the results of those edits through a discrepancy review screen integrated with the query system.
Target e*Pharmacovigilance®: Target e*CRF integrates EDC with a pharmacovigilance module by 1) allowing the principle investigators to enter a narrative, 2) allowing the medical monitor to enter a narrative and then have the EDC system generate an approved version of Form 3500A or CIOMS for regulatory submission with the ability to control the original and followup submissions.
EDC vendor for 2 NIH grants in Juvenile Rheumatoid Arthritis at the Cleveland Clinic and University of Washington. Collaboration with the Biotechnology Center at SUNY Stony Brook, Rutgers and UMDNJ (the Medical School of New Jersey).
Dr. Mitchel is a Course Director for Center for Biotechnology, Fundamentals of the Bioscience Industry, SUNY Stony Brook School of Medicine.
1. Mitchel, J, Kim, YJ, Choi, JH, et al. Evaluation of Data Entry Errors and Data Changes to an Electronic Data Capture (EDC) Clinical Trial Database. Drug Information Journal. 2011, 45:421-430.
2. Morrison, B, Cochran, C, Giangrande, J, et al. Monitoring the quality of conduct of clinical trials: a survey of current practices. Clinical Trials, 2011; 8:342–349.
3. Mitchel, J. and Schloss-Markowitz, J. Time for Change. International Journal of Clinical Trials, February 2011; 22-29.
4. Tantsyura, V, Grimes, I, Mitchel, J. et al. Cost-Effective Approach to Managing Laboratory Reference Ranges for Local Laboratories in Clinical Research, DIA Journal (2012; in Press).
5. Mitchel, J., Schloss-Markowitz, J., Yin, H. et al. Lessons Learned From a Direct Data Entry (DDE) Phase 2 Clinical Trial Under a US IND. Drug Information Journal (2012 accepted for publication)
Where Have All the Young Men Gone
This award winning photo was taken by Todd Heisler of The New York Times while he was a staff photographer at The Rocky Mountain News in 2005. The night before the burial of her husband’s body, Katherine Cathey, pregnant, refused to leave the coffin, asking to sleep next to his body for the last time. The Marines made a bed for her. Associated Press/Rocky Mountain News, Todd Heisler
The New York Times, Memorial Day Weekend, May 2012, by Lily Burana — In the run-up to every Memorial Day weekend, for the past several years, a certain photo takes top spot in those most circulated among my fellow military and veteran wives. On blogs, on social media sites, it is shared and “liked” over and over. Taken by the photographer Todd Heisler, from his 2005 award-winning series for the Rocky Mountain News, “Jim Comes Home,” which documents the return and burial of Marine Second Lt. Jim Cathey, who lost his life in Iraq, the photo shows his pregnant widow Katherine lying on an air mattress in front of his coffin. She’s staring at her laptop, listening to songs that remind her of Jim. Her expression is vacant, her grief almost palpable.
It is the one and only photo that makes me cry each time I see it. What brings the tears to my eyes is not just the bereaved young woman, but the Marine who stands behind her. In an earlier photo in the series, we see him building her a little nest of blankets on the air mattress. Sweet Lord, I cry just typing the words, the matter-of-fact tenderness is so overwhelming. So soldierly. But in this photo – the one that lives on and on online – he merely stands next to the coffin, watching over her. It is impossible to be unmoved by the juxtaposition of the eternal stone-faced warrior and the disheveled modern military wife-turned-widow, him rigid in his dress uniform, her on the floor in her blanket nest, wearing glasses and a baggy T-shirt, him nearly concealed by shadow while the pale blue light from the computer screen illuminates her like God’s own grace.
I believe this photo has had such a long viral life not just because it is so honest but also because it is so modern. During a spouse’s deployment, your laptop is your battle buddy. Your sense of connection and emotional well-being is sustained via e-mail, Facebook, Skype and Instagram. It appears, per Lieutenant Cathey’s widow, that the same is true even in a time of loss. This heartbreaking – and groundbreaking – photo showcases the intersection of technology and agony.
I’ll never forget trying to describe the photo to my friend Veronica, an Army wife. I was standing in her stately West Point living room, trying to detail what was so moving about the stalwart posture of the Marine, the listlessness of the grieving wife, my voice cracking, and before I was halfway through my description, tears started streaming down her face. It is testimonial to the image’s power that it even affects people who haven’t seen it.
The photo was later included in the book, “Final Salute,” which includes photographs by Mr. Heisler and is written by Jim Sheeler, a former Rocky Mountain News reporter. The book tells the story of United States Marines stationed in Colorado at Buckley Air Force Base whose duty was to notify families of deaths in Iraq and then escort the bodies home for burial. The book is based on a series that also won a Pulitzer Prize for Mr. Sheeler in 2006. Mr. Heisler, who now works for The New York Times, also won a separate Pulitzer for his photographs.
That photo has an equally poignant companion in the same series, a view from the civilian side, wherein Lieutenant Cathey’s coffin is being unloaded from the cargo hold of a commercial airplane in Reno as the passengers look on through the windows. You can practically read the thoughts on their solemn faces: “Who is that?” “What if that were my son or daughter?” “I can’t imagine what his family must be feeling.” “How sad” or “How noble.” I would bet you every penny I have that not one of them was thinking, “When the hell is this going to be over so we can get off this thing?” Two parents lost their son, a wife lost her husband, an unborn child lost his father, and a handful of average citizens saw just how seriously the military treats a fallen warrior’s final trip home.
Associated Press/Rocky Mountain News, Todd HeislerSecond Lt. James Cathey’s body arrived at the RenoAirport in 2005.
On one hand, you could view this as a perfect representation of how the majority of civilians are cosseted from the atrocities of war – they’re in the comfy, climate-controlled cabin, untouched by tragedy and free to move on, to gather their luggage, head on home, and forget about it. On the other hand, you could view it as I do: A stunning moment that makes clear our connectivity. They all took that journey together, and on that airport tarmac, the much-discussed gap between civilians and the military was closed, a bond forever fused by the passengers’ bearing witness to the final stage of a sacrifice that was both foreign to them and for them.
I believe that the civilian-military gap isn’t always born of indifference, but rather, at times, a sense of helplessness on the civilian side. What can I do? If you do nothing else, you can remember those who have given their lives for their country. Our country. Remembrance, which may seem a modest contribution in the moment, is a sacred act with long-term payoff – a singularly human gift that keeps on giving, year after, year after, war-fatigued year. I don’t need to remind you that America’s sons and daughters are still dying in combat. I don’t want to browbeat you into feeling guilty for not doing more. Instead, I want to tell you that as the wife of a veteran, it is tremendously meaningful to know that on this Memorial Day, civilians will be bearing witness and remembering in their own way – that those who are gone are not forgotten. I also want to say that as you remember them, we remember you.
Lily Burana is the author of “I Love a Man in Uniform: A Memoir of Love War and Other Battles” (Weinstein Books). Her husband, a former soldier, is a veteran of Operation Desert Storm and Operation Iraqi Freedom.
“Give Peace a Chance”
Where Have All the Flowers Gone?
How is the US Creating an Educational System to Enable More Kids to Develop Their Potential? Encourage Initiative.., …..the Spirit of American Enterprise?
Adam Munich And His X-Ray Machine Luke Copping
In his free time during high school, Adam Munich built himself a machine to see inside other machines
PopSci.com, May 24, 2012, by Gregory Mone – Late one night two years ago, Adam Munich found himself talking with two new acquaintances in a chatroom. One, a Pakistani guy, was complaining about rolling electricity blackouts in his country. The other had broken his leg in a motocross accident in Mexico and said his local hospital couldn’t find a working x-ray machine. The two situations fused in Munich’s mind; he wondered if a cheap, reliable, battery-powered x-ray machine existed—something that could be used in remote areas and function without being plugged in during blackouts. After discovering that the answer was no, he spent two years building one himself out of Nixie tubes, old art suitcases, chainsaw oil, and electronics from across the globe. It was an incredibly ambitious project for anyone, let alone a 15-year-old.
Munich started by reading online about the science of Coolidge tubes, the essential radiation-emitting core of most commercial machines, and eventually found one for sale from a manufacturer in China. “The rest was puzzle-solving,” Munich says. “For something like this, there’s no guide.”
Inside Look: An x-ray of a thumb drive taken with Adam Munich’s machine Luke Copping
He split the machine into two connected pieces: a control box that houses the electronics and a second case containing the x-ray tube and the high-voltage components that drive it. Batteries alone wouldn’t provide enough power. He needed a voltage multiplier, so he borrowed a design originally used in particle accelerators. When alternating current is applied, it flows into a charge-storing capacitor at its peak and then rushes through a charge-relaying diode when the polarity of the current reverses. This second burst of charge combines with the power stored in the capacitor, doubling the voltage. Using money he earned as a freelance Web designer, Munich bought enough capacitors and ultrafast diodes on eBay to link together four such setups. The voltage increases with each one until it reaches the 75,000 volts required to spark a decent beam of x-rays.
Munich, now 18, has used the machine to x-ray some household items, including a pen and a computer hard drive. Theoretically, he says, it could be used for hands or limbs. Now he is focused on getting the cost under $200 and making the device sturdy enough to help his friends from the late-night chat. But the current version is sure to help with a more immediate concern—impressing college admissions offices.
DIY XRay Machine 2: Luke Copping
BUILDING AN X-RAY MACHINE
Time 2 years
The Setup: The machine projects an x-ray image onto a sheet behind the object it’s aimed at. Photo: Luke Copping
HOW IT WORKS
Imaging: Inside the x-ray tube, a high-voltage current sends electrons to a tungsten target. The electrons slam into atoms inside the target, lose energy, and emit x-rays. The x-rays then flash ahead and create a shadow image of the subject. Most machines use flat-panel radiation detectors to get these pictures, but they cost about $65,000. Instead Munich bought a scintillation screen, a plastic sheet that turns fluorescent green when it’s hit with ionizing radiation.
Safety: Munich built his own Geiger counter to measure the radiation. The volume of x-rays coming out of the tube was in line with his estimates, and he found that the backscatter, or amount of radiation elsewhere, was very low. Still, he only uses it outside, aiming it at the woods behind his house. Otherwise some of the x-rays could bounce off an interior wall. He also added a speaker that emits a warning buzz when the machine is generating x-rays.
DIY XRay Machine 3: Photo: Luke Copping
Insulation: Munich placed the high-voltage components and the x-ray tube in a plastic junction box filled with chainsaw oil. He tested the oil’s insulating capacity by dunking two metal plates in it and then sending increasing amounts of current into one. It took 100,000 volts for the charge to move through the oil from one plate to the other. Since the machine uses only 75,000 volts, the oil prevents the voltage from burning through the junction box or other parts.
Design: Matching art suitcases, linked by cable, enclose the two pieces of the machine. Munich cut holes in the lid for an on/off switch, meters that monitor current and voltage, dials to set the exposure time, and a Nixie-tube display from a Ukrainian supplier that counts the exposure time down to the tenth of a second.
DIY XRay Machine 1: Luke Copping
MedPageToday.com, May 24, 2012, by Todd Neale – If climate change continues on its current course, the number of heat-related deaths will rise as temperatures climb during the summer, according to a report from the Natural Resources Defense Council (NRDC), an environmental advocacy group.
The organization projected on the basis of peer-reviewed data that global warming — expected to increase average temperatures in North America by 4º to 11ºF by 2099 — will be responsible for an extra 150,000 deaths tied to excessive heat events in the 40 largest U.S. cities by the end of this century.
The hardest hit, in terms of excess heat-related deaths by the end of 2099, are estimated to be:
- Louisville, Ky. (18,988)
- Detroit (17,877)
- Cleveland (16,625)
- Memphis, Tenn. (10,154)
- Jacksonville, Fla. (8,141)
The estimates were based on two studies by Larry Kalkstein, PhD, a professor of geography and regional studies at the University of Miami in Florida, and colleagues, published in the last few years in Weather, Climate, and Society and Natural Hazards.
The researchers studied two baseline time periods — 1975 to 1995 and 1975 to 2004. They included 1996 to 2004 to account for the greater use of preventive measures against heat-related deaths during those years. When making projections into the future, they did not make adjustments for the growth or aging of the population in order to keep the estimates conservative, Kalkstein said on a conference call with reporters.
The NRDC report based on the data from the two studies focused on two variables — excessive heat event days and death attributable to extreme heat.
“Excessive heat event days occur when a location’s temperature, dew point temperature, cloud cover, wind speed, and surface atmospheric pressure throughout the day combine to cause or contribute to heat-related deaths in that location,” according to the report.
Aside from temperature, there are several factors that contribute to the number of excessive heat event days, including geography, urban structure, green space, the use of local warning and preventive measures, and the resiliency of the local residents.
Most vulnerable during these heat waves are seniors and young children, particularly those living in cities with a variable climate. Cities with relatively hot temperatures interspersed by spikes of extended extreme heat will see more health-related deaths than cities that are consistently hot, like Miami, Kalkstein explained.
According to the estimates from Kalkstein’s data, the average number of excessive heat event days per summer across all 40 cities was 233 from 1975 to 1995. By 2099, that was projected to increase to 1,918 per summer, assuming a continued reliance on fossil fuels and no significant policy interventions.
Accompanying that increase is a rise in the average number of heat-related deaths per summer from 1,332 from 1975 to 2004 to 4,608 per summer by 2099. All but three of the 40 cities would see more deaths by the end of the century.
Adding up all of the excess heat-related deaths would yield an extra 150,322 heat-related deaths attributable to climate change.
Kalkstein noted that there are measures that cities can take to mitigate the threat of extreme heat, including opening air-conditioned shelters when the National Weather Service calls an excessive heat warning; having a special hotline that people can call to get advice on dealing with heat-related illness; and increasing the number of staff in emergency rooms during heat waves.
He singled out Philadelphia as being particularly proactive in dealing with excessive heat events, noting that the city has volunteer block captains who go door to door checking on vulnerable individuals during heat waves.
Pain hypersensitivity may develop following nerve injury because inhibitory nerve cells are lost in the spinal cord, increasing the likelihood of pain signals being transmitted. UCSF pain researcher Allan Basbaum, PhD, chair of the Department of Anatomy, led studies in which researchers transplanted immature neurons from the cerebral cortex into the spinal cord, where they integrated into the nerve circuitry and helped reverse injury-induced pain hypersensitivity. (Credit: UCSF)
ScienceDaily.com, May 23, 2012 — Chronic pain, by definition, is difficult to manage, but a new study by UCSF scientists shows how a cell therapy might one day be used not only to quell some common types of persistent and difficult-to-treat pain, but also to cure the conditions that give rise to them.
The researchers, working with mice, focused on treating chronic pain that arises from nerve injury — so-called neuropathic pain.
In their study, published in the May 24, 2012 issue of Neuron, the scientists transplanted immature embryonic nerve cells that arise in the brain during development and used them to make up for a loss of function of specific neurons in the spinal cord that normally dampen pain signals.
A small fraction of the transplanted cells survived and matured into functioning neurons. The cells integrated into the nerve circuitry of the spinal cord, forming synapses and signaling pathways with neighboring neurons.
As a result, pain hypersensitivity associated with nerve injury was almost completely eliminated, the researchers found, without evidence of movement disturbances that are common side effects of the currently favored drug treatment.
“Now we are working toward the possibility of potential treatments that might eliminate the source of neuropathic pain, and that may be much more effective than drugs that aim only to treat symptomatically the pain that results from chronic, painful conditions,” said the senior author of the study, Allan Basbaum, PhD, chair of the Department of Anatomy at UCSF.
Although pain and hypersensitivity after injury usually resolve, in some cases they outlast the injury, creating the condition of chronic pain. Many types of chronic pain are induced by stimuli that are essentially harmless — such as light touch — but that are perceived as painful, according to Basbaum.
Chronic pain due to this type of hypersensitivity is often a debilitating medical condition. Many people suffer from chronic neuropathic pain after a bout of shingles, years or decades after the virus that causes chicken pox has been vanquished. Chronic pain is not merely prolonged acute pain, Basbaum said.
Those who suffer from chronic pain often get little relief, even from powerful narcotic painkillers, according to Basbaum. Gabapentin, an anticonvulsant first used to treat epilepsy, now is regarded as the most effective treatment for neuropathic pain. However, it is effective for only roughly 30 percent of patients, and even in those people it only provides about 30 percent relief of the pain, he said.
The explanation for neuropathic pain, research shows, is that following injury neurons may be lost, or central nervous system circuitry may change, in ways that are maladaptive, compromising signals that normally help dampen pain. These changes contribute to a state of hyper-excitability, enhancing the transmission of pain messages to the brain and causing normally innocuous stimuli to become painful.
The inhibitory neurons that are damaged in the spinal cord to cause pain hypersensitivity release a molecule that normally transmits inhibitory signals — the neurotransmitter GABA. A loss of GABA inhibition also is implicated in epilepsy and may play a role in Parkinson’s disease. Gabapentin does not mimic GABA, but it helps to compensate for the loss of inhibition that GABA normally would provide.
Basbaum’s UCSF colleagues, including study co-authors Arturo Alvarez-Buylla, PhD, and Arnold Kriegstein, MD, PhD, along with Scott Baraban, PhD, had already been experimenting with transplanting immature neurons that make GABA, using the transplanted neurons to bolster inhibitory signals in mouse models to prevent epileptic seizures and to combat a Parkinson’s-like disease.
However, in those experiments the cells — which originate in a region of the forebrain known as the medial ganglionic eminence — were transplanted within the brain itself, which is their normal home.
Upon hearing about the research, Basbaum became interested in transplanting the same cells into the spinal cord as a potential treatment for the loss of GABA-driven inhibition in neuropathic pain. Success was by no means assured, as cells normally do not survive outside their natural environments within such a complex organism.
Another co-author of the Neuron study, UCSF researcher John Rubenstein, PhD, has made major progress in identifying molecules that can be manipulated to lead an embryonic stem cell to go through developmental stages that cause it to acquire the properties of GABA neurons that derive from the medial ganglionic eminence.
According to Kriegstein, who directs the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCSF, “This research is at a very early stage, and we’re a long way from thinking about it in human trials, but we do have a method of making cells that are like these inhibitory neurons, starting with human embryonic stem cells.”
As a step toward eventual therapies, the UCSF team plans to graft fetal human cells from the medial ganglionic eminence, or cells derived from human embryonic stem cells, into a rodent model of neuropathic pain, to see if the human cells also will alleviate neuropathic chronic pain.
“Unlike drugs, the transplanted cells can have very focused effects, depending on where they are transplanted,” Kriegstein said.
According to Alvarez-Buylla, a leading scientist among those working to define the potentialities of various cells in the developing brain at different stages, “One of the amazing properties of these cells from the medial ganglionic eminence is their unprecedented migratory capacity, which enables them to navigate through multiple terrains within the central nervous system, and to then become functionally integrated with other cells. Those properties have proved useful in other places where we have transplanted them, and now in the spinal cord.”
Joao Braz, PhD, an assistant research scientist, and Reza Sharif-Naieni, PhD, a postdoctoral fellow, both working in the Basbaum laboratory, carried out the bulk of the experiments published in Neuron. The authors have a patent pending on the treatment outlined in the study.
The study was funded by the National Institutes of Health, the Association for the Study of Pain and the Canadian Institutes of Health Research.
- 1. João M. Bráz, Reza Sharif-Naeini, Daniel Vogt, Arnold Kriegstein, Arturo Alvarez-Buylla, John L. Rubenstein, Allan I. Basbaum. Forebrain GABAergic Neuron Precursors Integrate into Adult Spinal Cord and Reduce Injury-Induced Neuropathic Pain. Neuron, 2012; 74 (4): 663 DOI: 10.1016/j.neuron.2012.02.033
The Alaskan Permafrost is melting
By Yereth RosenPosted, May 23, 2012, ANCHORAGE, Alaska, May 21, 2012 (Reuters) — Methane from underground reservoirs is streaming from thawing permafrost and receding glaciers, contributing to the greenhouse gas load in the atmosphere, a study led by scientists at the University of Alaska Fairbanks has found.
The study, published online on Sunday in the journal Nature Geoscience, is the first to document leakage of deep geologic methane from warming permafrost and receding glaciers, said its lead author, Katey Walter Anthony.
Release of methane into the atmosphere from any source is troubling because methane has far more potent greenhouse powers than carbon dioxide, climate scientists say. Methane has more than 20 times the heat-trapping power of carbon dioxide, University of Alaska Fairbanks researchers said.
Scientists have speculated about such methane releases and modeling has predicted that it would happen as the cryosphere – the earth’s layer of ice and frozen ground – softens and melts, Walter Anthony said in a telephone news conference on Monday.
“But no one had ever shown that it was occurring or that it was a widespread phenomenon,” she said. “This paper really is the first time that we see with field evidence that this type of geologic methane is escaping as the cryosphere retreats.”
The leaking geologic methane identified by Walter Anthony and her colleagues comes from such sources as underground coal beds and conventional natural gas reservoirs. Those are fossil fuels that energy companies target in drilling operations.
It differs from the methane streaming from decaying plant and animal matter at the bottom of warming Alaska lakes, a phenomenon that Walter Anthony has studied for about a decade.
Walter Anthony said it is too early to estimate how much methane is leaking from underground reservoirs.
The study stems in part from Walter Anthony’s observations over the past few winters of lakes in Arctic Alaska that had large patches with no ice, where one could expect to find it.
Ultimately, researchers confirmed that underground methane was venting from two types of sources in Alaska – one of them being 50 lakes in the northernmost region, and the other being along the edges of rapidly receding glaciers in southern Alaska.
In Greenland, they found methane streaming out of areas where the ice sheet had retreated over the past 150 years, Walter Anthony said.
Field work, which included aerial surveys, long winter hiking treks and other tasks, took place from 2008 to 2010, according to the university.
The discoveries of venting methane from below the earth’s surface coincide, to some extent, with known petroleum and coal deposits, Walter Anthony said.
The first lake where she and her team found underground methane to be preventing normal winter freezing was near the Inupiat Eskimo village of Atqasuk in northern Alaska, where locals have long known about that area’s deep coal deposits and where the village name translates to “the place to dig the rock that burns.”
(Editing by Alex Dobuzinskis and Mohammad Zargham)
A complex, independent nervous system lines the gastrointestinal tract that has been dubbed the “second brain”. Image: ISTOCKPHOTO/ERAXION
- Written by Divya Shankar
- Published Spring 2012
Ever had someone tell you to follow your gut? Or maybe you’ve been sitting with a test in front of you or a decision to make, and deep down there is something in your gut telling you what the correct answer or choice is.
Research has now revealed that what you may have thought of as an idiom —the “gut instinct”—passed down through the ages is actually deeply rooted in scientific fact. For the past few decades, researchers have been studying the enteric nervous system—a part of the nervous system in the stomach. What they have found tells us not only a lot about what governs our bowel, but also about what controls instincts, mood and even some diseases.
The enteric nervous system (ENS) is a part of the peripheral nervous system, the nerves and ganglia (cell bodies) that lies outside of the brain. It is defined as the “intrinsic innervations of the gut” explains Dr. Michael Gershon, Professor and Chairman of Anatomy and Cell Biology at Columbia University Medical Center and author of the 1998 book The Second Brain over email.
“I looked at the brain and found it daunting,” said Gershon in his email explaining why he chose to study this “second brain” over fifty years ago. “I hoped to find an independent nervous system that was simpler to study than the brain.”
When Gershon started out, he was one of two researchers in the entire world looking into the ENS, noted a recent article in Psychology Today. Now the study of the neurons and neurotransmitters that make up the ENS is the subject of the research of hundreds and the field of neurogasteroenterology is rising in popularity.
THE NERVES THAT CONTROL YOUR NERVES
“There are between 200 and 600 million neurons in the human ENS, which is equal to the number of neurons in the spinal cord,” writes Dr. Emeran Mayer, the Director of the Center for Neurobiology of Stress at the David Geffen School of Medicine at UCLA, in a recent study published in Nature.
“[These neurons] regulate the behavior of the bowel and that of neighboring organs, including the gall bladder and pancreas,” says Gershon.
But the role of the ENS does not stop there. The vagus nerves connect the ENS to the brain and when stimulated, these control epilepsy, relieve depression and improve learning and memory, Gershon further explains.
“[The implication of this is that] it is possible that signals from the bowel alter mood,” Gershon says.
A SOLO ACT
If the neurons contained one of the major reasons that the ENS interests researchers is because it can operate without any input from the brain.
“The ENS is the only region of the PNS that is able to mediate reflexes and integrative neuronal activity in the absence of input from the brain or spinal cord,” says Gershon.
Another aspect of the ENS that has intrigued researchers is the reverse nature of the signaling between the brain and the ENS. Traditionally, the brain is expected to signal the rest of the body. However, research has found that the ENS more commonly sends signals to the brain.
“Over 90% of the nerve fibers in the vagus nerves carry information from the guy to the brain. This is shockingly more than the number of vagal fibers carrying information from brain to gut.”
As a result of these signals sent from the stomach to the brain, sadness, stress, memory, learning, and decision-making are affected, reports a recent article in Psychology Today. This reverse signaling may explain why the idea of a “gut instinct” may actually be a scientific fact.
EATING YOUR FEELINGS
Recent research on the ENS has revealed many groundbreaking truths about the body. For one, it has demonstrated that there may actually be a scientific link between food and feelings.
“Food and stress are powerful modulators of the body-mind connection,” reports a recent article published in the Journal of Clinical Investigation.
The ties between food and mood could offer promising treatments for the obesity epidemic, explain researchers Giovanni Cizza, M.D, Ph.D. and Kristina Rother, M.D, both from the National Institute of Health, in the article.
A group of researchers from the University of Leuven in Leuven, Belgium have studied the interactions between signaling initiated in the gut and the emotions that they elicit, according to a recent report published in the Journal of Clinical Investigation in August 2011.
They found that there was a relationship between the intake of fats and the level of neural activity in the brain as a result, reports the study. They discovered that the intake of fatty acids reduced sadness and hunger.
“These findings increase our understanding of the interplay among emotions, hunger, food intake and meal-induced sensations in health, which may have important implications for a wide range of disorders, including obesity, eating disorders, and depression,” the researchers noted in their report.
Additionally, the ENS has also been thought to possibly have links to diseases such as autism.
“Autism has not yet been definitively linked to the ENS; however, it is likely that genetic defects in synapse formation which may contribute to autism affect development of the ENS as well as development of the central nervous system,” Gershon wrote in his email interview.
DO BACTERIA CONTROL THE BRAIN?
A study published in the journal Neurogastroenterology and Motility indicates that it is not simply the neurons and neurotransmitters in the stomach that play a role in signaling to the brain. In fact, a large part of the work may be done by the “intestinal microbiota” in your gut—a.k.a. the germs in your stomach.
There are approximately 100 trillion bacteria that reside in your intestines, reports Psychology Today. Researchers in Canada have studied these microbes and have concluded, “that the presence or absence of conventional intestinal microbiota influences the development of behavior and is accompanied by neurochemical changes in the brain.”
Some believe that this study could serve as a gateway to treating stress-related disorders such as depression, reports Psychology Today.
A NEW ERA IN RESEARCH
Neurogasteroenterology is now one of the cutting edge fields in the world of science. Boston University students believe that it is important to explore new fields such as this one.
“Advancements such as these are important, because as the world changes, science needs to keep up with the advancements the human race is making in other areas. It is especially important in medicine as new diseases are discovered every year, so new cures need to be found every year,” says Amanda Kirshkaln, a sophomore in the Sargeant College of Rehabilitation Sciences.
Students also agree that it is research into areas such as the ENS that are pushing the boundaries of science and medicine.
“These advancements are saving lives! I think they are important for a better understanding of the human body and to know our limits and go beyond!” says College of Arts and Sciences sophomore, Celia Gagliardi.
Research into the ENS has changed the way people are thinking about the relationship between the brain and the stomach. Much has changed since Gershon began his research 50 years ago.
“The idea that there are multiple neurotransmitters in the ENS is now accepted. The concept of the ENS as an independent region of the peripheral nervous system is also established,” Gershon notes. “The ENS is suspected to contribute to human GI disorders such as irritable bowel syndrome. We know the ENS contains stem cells.”
When Gershon embarked on his study of the ENS, he thought he was choosing a simple system compared to the brain. However, Research has revealed that his initial hypothesis is far from the truth.
“My mistake was to think that the ENS could be described with the word simple,” Gershon admits in his email. “A simple nervous system is an oxymoron.”
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