Day: 05/02/2015

FDA Finally Admits Chicken Meat Contains Cancer-Causing Arsenic

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The FDA spent years trying to hide the issue, hoping that no one would go further with the subject. However, they finally admitted that the chicken sold all over the United States contains a toxic chemical called arsenic, known to cause cancer, and in high doses it is fatal.

What is even more horrible is the story explaining how does the chemical get in the chicken: It is added to their feed.Actually chickens are fed with it purposely!

The FDA confirmed that in their own research they found that the arsenic in the chicken feed really finishes in the meat that is later consumed by people. More precisely, in the last 60 years all the Americans that consumed conventional chicken have actually been consuming this cancer-causing chemical called arsenic!

After all those dark years of denial,the latest study brought light that arsenic actually ends up in the meat because it is being added to the chicken feed. We have to mention that both the FDA and the poultry industry denied this fact.FDA

For sixty years we have been believing in the fairy tale that “the arsenic is excreted in the chicken feces.” It is just a vain story presented by the poultry industry, and it was never backed up with scientific evidence. And we had to believe in it.

Some manufacturers, including the manufacturer of the chicken feed product known as Roxarsone,now that the world knows this undeniable evidence, has decided to withdraw all of their products off the supermarket shelves.

Interesting fact is that, the manufacturer that is adding the arsenic into the chicken feed is Pfizer. This is the same company that produces vaccines containing chemical adjuvants that are later used to inject children.

The company producing the Roxarsone chicken feed is called Alpharma LLC, and it is actually a subsidiary of Pfizer. Alpharma now decided to withdraw their products from the shelves all over the US, and they also saidthat there is no need to necessarily withdrawtheir products in other countries unless the regulators say otherwise. AP reported that:

“Pfizer Animal Health’s Veterinary Medicine Research and Development division, Scott Brown said that the company is also selling the ingredient in many other countries. He also said that Pfizer is contactingthe regulatory authorities in those countries and will decide if they are going to sell it on an individual basis.”

The FDA still denies these facts,even though the arsenic-containing products are pulled off the shelves, they claim that the chicken is safe for consumption as the arsenic in the meat is at a low level. It seems like thereis not going to be any changes regarding this subject, even though the FDA stated that the arsenic is a carcinogenous substance, which means that it increases the risk of cancer.

Even the National Chicken Council agrees with the FDA. As a response to the decision that Roxarsone’s products must be withdrawn from the shelves,in a statement they said, “The chicken is safe for consumption,” despite admitting the fact that the chemical is added in the chicken feed and the meat is later sold all over the United States.

We are shocked that the FDA still tells the consumers that it is safe to eat the arsenic-loaded chicken but it is dangerous to drink elderberry juice! The FDA recently conducted an armed raid and accused an elderberry juice manufacturer of the “crime” of selling “unapproved drugs”.

And what kind of drug would that be? The elderberry juice, explained the agency. The elderberry juice is considered as a “drug”, as you can see, at the very moment you tell people how it can improve their overall health.

Dozens of other manufacturers were also attacked by the FDA,for selling natural nutritional products or herbal products with a scientific back up that proves their ability to support and enhance health. The agency goes that far to say that even raw milk is dangerous. In other words, the food and drug regulatory agency in America says that it is dangerous to drink elderberry juice or raw milk, but approves the consumption of arsenic.

Common Running Injuries and How to Prevent Them

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Running can be an amazingly effective way to lose weight, torch calories, tone muscles and improve cardiovascular health. Not to mention it can also be a great way to clear your mind, relieve stress and discover your inner strength.

However, it isn’t as simple as just lacing up your sneakers and hitting the trail. If you want running to be a healthy and rewarding part of your lifestyle, you have to make sure that you protect your joints and your feet. Otherwise, you’ll end up throwing in the towel and missing out on all the wonderful benefits running can provide.

Running injuries

Here are the top five running injuries and how to prevent them:

1.Runner’s knee. Runner’s knee presents as pain just below the kneecap. The pain starts when you begin running and then gradually worsens. It may also flare up as you walk up and down stairs or even while you are sitting. It might possibly be caused by incorrect tracking of the kneecap as you run.

The solution: 80 percent of cases of runner’s knee can be cured by the use of orthotics for Iliotibial band (ITB) friction syndrome. Pain can also be alleviated by stretching the ITB, ice and deep-friction massage. Runner’s knee may require a reduction in training mileage and intensity or even a complete rest while the underlying causes are addressed.

2.Achilles tendonitis. This condition causes pain in the tendon that connects the back of your leg to the heel of your foot. It can be caused by excessively tight calf muscles, overpronation, wearing high heels, worn-out shoes and overtraining. Symptoms generally disappear while running.

The solution: Achilles tendonitis can be relieved with ice after each run. Reduction in training or complete rest may be needed. It’s a good idea to avoid hills and speed work while you have Achilles tendonitis.

3.Shin splints. Also known as medial tibial stress syndrome, shin splints occur when there is an irritation of the muscles and tendons at the point where they attach to the shin.

The solution: Treat the area with regular ice and consider reducing or even stopping your running for the time being. Next, figure out the cause and assess shoes, inserts and foot structure. Then rebuild training mileage slowly.

4.Stress fractures and reactions. These are periosteal reactions or hairline fractures of bones in the lower leg. They generally occur in the tibia, fibula or a bone in the foot (e.g., a metatarsal), thighbone and pelvis. Pain intensifies very rapidly and can be identified by highly localized pain under gentle pressure. These fractures are usually caused by excessive increases in training or low bone density possibly related to poor diet. They are more common in females, and women with irregular menstrual cycles are especially at risk.

The solution: Scale back on your running and set more moderate fitness goals. Eat a healthy diet and make sure you are getting the vitamins you need for healthy bones. Consider weight training to rebuild your strength and flexibility. Work out with a professional so that you can be sure you are not overdoing it or performing exercises incorrectly.

5.Plantar fasciitis. This presents as pain directly at the heel, which can radiate down the arch or up the back of the heel. Pain is often worse when you first get out of bed.

The solution: Proper stretching of the tight plantar fascia and calf muscles is key. You can also decrease inflammation with ice or anti-inflammatory drugs. Orthotics might also be required.

Remember, running offers amazing physical and mental benefits, but it must be undergone with moderation and caution, especially at first. Build up your endurance and speed slowly, and cross-train to help ensure that your body is as strong and fit as possible.

Talk to your doctor before beginning any exercise regimen, and make sure that you’re eating a healthy diet and drinking plenty of water to complement your new active lifestyle.

 

Emerging biomarkers for sarcopenia

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Identifying novel biomarkers of pathological sarcopenia could facilitate diagnosis and treatment among the elderly. However “researchers need to ensure that emerging biomarkers undergo a thorough analytical validation by laboratory specialists before they are used in prospective clinical studies,” said Dr. Etienne Cavalier from The University of Liège, in Liege, Belgium, at the recent WCO-IOF-ESCEO World Congress on Osteoporosis, Osteoarthritis, and Musculoskeletal Diseases held in Milan, Italy.

To illustrate the importance of this directive, Cavalier and colleagues performed a laboratory analysis of six established biomarkers for sarcopenia: myostatin, procollagen III N-terminal propeptide (PIIINP), activin A, irisin, osteoglycin, and transmembrane protein 19 (Tmem-19). Only myostatin and activin A were validated for use in prospective clinical studies.

Tmem-19 and osteoglycin were excluded from further study when it became clear that it was not possible to establish calibration curves for these markers. Irisin was excluded because of its high reproducibility coefficient of variation (20-45 percent vs approximately 10 percent for PIIINP, activin A, and myostatin).

Stability experiments revealed that although all three of the remaining markers were stable for 1 day at 4°C, only activin A and myostatin remained stable in both ethylenediaminetetraacetic acid (EDTA)-plasma and serum after 1 and 3 months at -20°C and -80°C.

Renal clearance of activin A, myostatin, and PIIINP was assessed in 10 patients with chronic kidney disease, and significant accumulation of both activin A and PIIINP was observed relative to the normal population.

The reference ranges for myostatin and activin A were established in 60 healthy men and 58 to 60 non-menopausal women with a mean age of 36.2±9.7 years and 30.1±5.5 years, respectively. The reference range for myostatin was 845 (437–1,312) to 6,067 (5,524–6,552) pg/mL for men or 600 (268–1,027) to 4,438 (4,026–4,837) pg/mL for women. The reference range for activin A was 177 (132–210) to 622 (580–661) pg/mL (men) or 98 (49–147) to 480 (430–525) pg/mL (women).

“Always perform a stability study [short- and long-term] in EDTA-plasma and serum before starting to collect relevant clinical samples for blood banks,” concluded Cavalier.

Novel radiation-free test to aid diagnosis of gastroparesis

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The US Food and Drug Administration (FDA) has approved gastric emptying breath test (GEBT) to aid the diagnosis of gastroparesis.

GEBT measures carbon-13, a naturally existing non-radioactive form of carbon-12, in a patient’s breath. Gastric scintingraphy, the standard diagnostic test for gastroparesis, uses radioactive material and requires specialist training. “[GEBT] can be performed in any clinical setting since it does not require the health care professionals administering the test to undergo special training or to take special precautions related to radiation emitting compounds,” as no radioactive materials are used said Dr. Alberto Gutierrez, director of the Office of In Vitro Diagnostics and Radiological Health in the FDA’s Center for Devices and Radiological Health.

The approval is based on study data of 115 participants who underwent both GEBT and gastric scintigraphy. Performed over a 4-hour period following an overnight fast, GEBT measured the ratio of carbon-13 to carbon-12 in breath samples at multiple points, which is then compared to the baseline measure. Participants consumed a carbon-13 enriched meal containing scrambled egg-mix and Spirulina platensis. GEBT and scintigraphy results agreed 73-97 percent of the time.

Gastroparesis interferes with normal digestion causing severe nausea and vomiting, dehydration, and malnutrition. Diabetes is the most common cause of gastroparesis. Other causes include infections, internal surgery, neurological disease like Parkinson’s disease, and endocrine disorders like hypothyroidism.

GEBT is not advisable for patients with an allergy to Spirulina, egg, milk or wheat, or certain lung diseases or conditions that cause small bowel malabsorption.

Tabalumab no better than placebo for RA

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An investigational anti-B-cell activating factor (BAFF) monoclonal antibody is no better than placebo in achieving clinical response in patients with rheumatoid arthritis (RA) who had not responded to methotrexate (MTX), a phase III study has shown.

 

There was no difference in ACR20 (American College of Cardiology 20 percent) response score at week 24 – the primary endpoint of the study – or change in mTSS (modified Total Sharp Score) from baseline at week 52 between patients treated with tabalumab and placebo. Nearly 30 percent of patients treated with tabalumab 120 mg every 4 weeks and 32.8 percent of those assigned to tabalumab 90 mg every 2 weeks achieved ACR20 compared with 25.1 percent for placebo. There were also no significant differences between the tabalumab and placebo groups in the percentage of patients achieving ACR50 and ACR70 responses at the end of treatment. [Ann Rheum Dis 2015; doi:10.1136/annrheumdis-2014-207090]

“Despite changes in CD20+ B cells, RF rheumatoid factor, and immunoglobulins following tabalumab treatment, BAFF inhibition with tabalumab was not clinically, functionally, or structurally efficacious in patients with moderate-to-severe RA taking MTX,” said lead investigator Professor Josef Smolen of the Medical University of Vienna in Vienna, Austria.

The study included 1,041 patients with moderate-to-severe RA (≥6 months duration) who had inadequate responses to MTX therapy, randomized to tabalumab 120 mg every 4 weeks or 90 mg every 2 weeks or placebo. Median CD20+ B-cell counts increased at week 1 in the tabalumab groups, but decreased from week 4 to 52. The differences in absolute and relative CD20+ B-cell-level changes from baseline to week 52 were significant in both tabalumab groups compared with the placebo group (p<0.001). Numerically more serious infections were seen with tabalumab groups (1.7 and 0.6 percent vs 0.3 percent for placebo).

The study was terminated early due to insufficient efficacy.

“BAFF blockade alone does not appear to provide sufficient interference with the immunopathogenesis of RA,” said the researchers.

Tabalumab is the third anti-BAFF monoclonal antibody to fail in RA studies. Earlier, belimumab and atacicept also failed to achieve significant responses in RA patients on background MTX.

Sustained weight loss reduces AF burden in obese patients

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Sustained weight loss in obese patients with atrial fibrillation (AF) reduces AF burden and symptom severity, the 5-year LEGACY* trial has shown. The benefits appeared to be dose dependent.

Patients who lost >10 percent of their body weight and kept it off for 4 years were six times more likely to achieve long-term freedom from arrhythmia without the help of medication or ablation compared with patients who lost less weight (p<0.001). Conversely, significant weight fluctuation over 4 years attenuated the positive impact of weight loss. Weight fluctuation of >5 percent was associated with a two-fold increased risk of arrhythmia recurrence (95% CI, 1.0-4.3; p=0.02). [J Am Coll Cardiol  2015;doi:10.1016/j.jacc.2015.03.002]

“LEGACY demonstrated that sustained weight loss is associated with dose dependent reduction in AF burden and maintenance of sinus rhythm,” said study author Dr. Rajeev Pathak, a cardiologist and electrophysiologist at the University of Adelaide in Adelaide, Australia. “Weight loss and avoidance of weight fluctuation are important strategies for reducing AF burden.”

The study enrolled 355 obese adults (body mass index ≥27 kg/m2) with AF, participating in a weight management program. Yearly weight trend and fluctuation were recorded.

After a median of 4 years, 135 patients lost >10 percent of their body weight, 103 patients lost 3-9 percent, and 117 lost ❤ percent. Arrhythmia-free survival rates were 86.2 percent, 66 percent and 40 percent, respectively.

“Weight loss also led to favourable changes in cardiovascular risk factors such as high blood pressure, obstructive sleep apnoea, and diabetes, along with improvements in the structure and function of the heart,” said Pathak.

Obesity and AF often co-exist. Weight loss in the short term reduces AF burden, but until this research, it is not known whether this benefit can be sustained in the long term, the authors said. LEGACY also addresses the impact of weight fluctuation and the role of weight loss clinics on arrhythmia control.

“A dedicated [weight loss] clinic improves patient engagement and promotes treatment adherence, thus preventing weight regain and fluctuation in AF patients.”

Diuretics, ACEIs, ARBs, and NSAIDs: A Nephrotoxic Combination.

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This triple therapy can increase the risk of acute renal failure.

Diuretics, angiotensin-converting enzyme inhibitors (ACEIs), and angiotensin receptor blockers (ARBs) represent 3 classes of drugs widely used in the treatment of hypertension and heart failure, often in combination. We previously reviewed the effect of nonsteroidal anti-inflammatory drugs (NASIDs) on the hypotensive response of various antihypertensive agents.1 In addition to blunting the hypotensive effects of diuretics, ACEIs, and ARBs, there is an increased risk of patients developing acute renal failure when an NSAID is co-administered. As hypertension, heart failure, and conditions causing chronic pain are common in the elderly, the risk of exposure to potential interactions between these drugs increases over time.

Mechanism of the Interaction

Diuretics can reduce plasma volume leading to reduced renal blood flow. This may lead to increased serum creatinine concentrations. The kidney can compensate via the renin-angiotensin system by constricting the efferent renal arteriole to increase glomerular filtration pressure and favor water and sodium retention. ACEIs and ARBs inhibit efferent renal arteriolar vasoconstriction that lowers glomerular filtration pressure. NSAIDs, by inhibition of prostaglandins and bradykinin, produce vasoconstriction of the afferent renal arteriole and reduce the ability of the kidney to regulate (increase) glomerular blood flow. The administration of an NSAID plus diuretic or ACEI or ARB may reduce the hypotensive effect of the antihypertensive agent but does not commonly lead to acute renal failure. When triple therapy with an NSAID plus diuretic and an ACEI or ARB is administered, the kidney is unable to use its normal compensatory mechanisms and may suffer an acute reduction in glomerular filtration that is marked by a rising serum creatinine.

Clinical Outcome

Several studies have noted the tendency for patients receiving triple therapy to have elevated serum creatines.2,3 Recently a large case-control study examined the risk of acute renal disease in patients receiving a) double therapy consisting of an NSAID combined with a diuretic or an NSAID with an ACEI or ARB, or b) triple therapy with both a diuretic and ACEI or ARB plus an NSAID.4 Patients were included only if kidney disease was their primary diagnosis upon admission to the hospital. The investigators were careful to control for confounders such as other diseases and drug usage. The study population included nearly 500,000 patients followed for a mean of about 6 years. Acute kidney injury was identified in 2215 patients who were compared with about 22,000 control patients. The overall incidence of acute kidney injury was 7 per 10,000 person-years. The risk of kidney disease in the patients was compared with matched control patients not exposed to the double or triple therapy. The use of double therapy was not associated with an increased risk of kidney injury.

Triple therapy was associated with a 31% increase in risk of injury. The greatest risk was noted within the first 30 days of concurrent therapy, when it was nearly twice as high in patients compared with the controls. Due to the study’s conservative entry criteria, it is possible that the study actually underestimates the risk. For example, increased serum creatinine levels may have caused prescribers to discontinue the combination therapy before kidney injury was severe enough to require hospitalization.

Management

Patients receiving NSAIDs chronically in combination with diuretics, ACEIs, or ARB, are at risk for diminished hypotensive response, elevated serum creatinine, and acute kidney injury. They should be monitored for altered blood pressure and serum creatinine, particularly during the first few months of combination therapy. While it appears that alternative hypotensive agents (eg, calcium channel blockers, centrally acting agents) are less affected by NSAIDs, similar data are not available for the risk of renal injury.

Drs. Horn and Hansten are both professors of pharmacy at the University of Washington School of Pharmacy. For an electronic version of this article, including references if any, visit http://www.hanstenandhorn.com.

References:

  1. Horn J et al. Coadministration of NSAIDs and antihypertensive agents. Pharmacy Times. 2006;72;54.
  2. Thomas MC. Diuretics, ACE inhibitors and NSAIDs – the triple whammy. Med J Aust. 2000;172:184-185.
  3. Loboz KK, Shenfield GM. Drug combinations and impaired renal function – the ‘triple whammy’. Br J Clin Pharmacol. 2004;59:239-243.
  4. Lapi F, Azoulay L, Yin H, Nessim SJ, Suissa S. Concurrent use of diuretics, angiotensin converting enzyme inhibitors, and angiotensin receptor blockers with non-steroidal anti-inflammatory drugs and risk of acute kidney injury: nested case-control study. BMJ. 2013;346:e8525.

– See more at: http://www.pharmacytimes.com/publications/issue/2013/April2013/Diuretics-ACEIs-ARBs-and-NSAIDs-A-Nephrotoxic-Combination#sthash.abgaOg2u.dpuf

How Our Thoughts Control Our DNA

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The common idea that DNA determines so much of who we are — not only our eye or hair color, for example, but also our addictions, disorders, or susceptibility to cancer — is a misconception. This concept “says you are less powerful than your genes.”

The problem with that belief system is that it extends to another level …  You find yourself to be more or less a victim of your heredity. You become irresponsible. You say, “I can’t do anything about it, so why try?”

How Our Thoughts Control Our DNA

In reality, a person’s perception, not genetic programming, is what spurs all action in the body. It is actually our beliefs that select our genes, that select our behavior.

The human body is comprised of 50 to 65 trillion cells. Cell functions independent of DNA and its perceptions of environmental stimuli affect DNA. This also applies the same principles to the human body as a whole, showing the power our perceptions, our beliefs, have over DNA.

5-Step Explanation
1.The cell is like a human body and it functions without DNA

The cell is like a human body. It is capable of respiration, digestion, reproduction, and other life functions. The nucleus, which contains the genes, has traditionally been viewed as the control center — the brain of the cell.

Yet, when the nucleus is removed, the cell continues with all of its life functions and it can still recognize toxins and nutrients. It appears the nucleus — and the DNA it contains — does not control the cell.

Scientists assumed some 50 years ago that genes control biology. It just seemed so correct, we bought the story. We don’t have the right assumptions.

2. DNA is controlled by the environment

Proteins carry out the functions in cells and they are building blocks of life. It has long been thought that DNA controls or determines the actions of proteins.

Here I propose a different model. Environmental stimuli that come into contact with the cell membrane are perceived by receptor proteins in the membrane. This sets off a chain reaction of proteins passing on what could be described as messages to other proteins, motivating action in the cell.

DNA is coated in a protective sleeve of protein. The environmental signals act on that protein, causing it to open up and to select certain genes for use — genes specifically needed to react to the current environment.

Basically, DNA is not the beginning of the chain reaction. Instead, the cell membrane’s perception of the environment is the first step.

If there are no perceptions, the DNA is inactive.

Genes can’t turn themselves on or off … they can’t control themselves. If a cell is cut off from any environmental stimuli, it doesn’t do anything. Life is due to how the cell responds to the environment.

3. Perception of the environment is not necessarily the reality of the environment

In a 1988 study done by John Cairns, published in the journal Nature titled “The Origin of Mutants,” heshowed that mutations in DNA were not random, but happened in a predetermined way in response to environmental stresses.

In every one of your cells, you have genes whose function it is to rewrite and adapt genes as necessary. In a chart illustrating Cairns findings in the journal, environmental signals were shown to be separate from the organism’s perception of environmental signals.

A being’s perception of the environment acts as a filter between the reality of the environment and the biological reaction to it.

Perception rewrites genes!

4. Human beliefs, choosing to perceive a positive or negative environment

Just as a cell has receptor proteins to perceive the environment outside the cell membrane, humans have the five senses.

These are what help a person determine which genes need to be activated for a given situation.

The genes are like programs on a computer disk. These programs can be divided into two classes: the first relates to growth, or reproduction; the second relates to protection.

When a cell encounters nutrients, the growth genes are activated and used. When a cell encounters toxins, the protection genes are activated and used.

When a human being encounters love, the growth genes are activated. When a human being encounters fear, the protection genes are activated.

A person may perceive a negative environment where there is actually a supportive or positive environment. When this negative perception activates the protection genes, the body’s response is the programmed “fight or flight.”

5. ‘Fight or Flight’

Blood flow is directed away from the vital organs to the limbs, which are used for fighting and running. The immune system becomes of lesser importance. If you picture the responses we once needed for running from a lion, for example, the legs would have been infinitely more important in that immediate situation than the immune system. Thus, the body favors the legs and neglects the immune system.

So, when a person perceives a negative environment, the body tends to neglect the immune system and vital organs. Stress also makes us less intelligent, less clear-minded. The part of the brain related to reflexes is given more prominence in fight or flight mode than the part related to memory and other mental functions.

When a person perceives a loving environment, the body activates growth genes and nurtures the body.

For example, in Eastern European orphanages where children are given lots of nutrients, but little love these types of institutions have found to have stunted development in terms of height, learning, and other areas. There is also a high incidence of autism. Autism in this case is a symptom of protection genes being activated, like walls being put up.

Beliefs act as a filter between the real environment and your biology. Thus, people have the power to change their biology. It is important to keep a clear perception because otherwise you won’t develop the right things biologically for the real environment around you.

You are not victims of genes. What beliefs are you choosing for your genes to be expressed?

Incidental Thyroid Nodules and Thyroid Cancer Considerations Before Determining Management

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The worldwide incidence of thyroid cancer is increasing substantially, almost exclusively attributable to small papillary thyroid cancers. Increased use of diagnostic imaging is considered the most likely explanation for this reported rise, but other factors may also be contributing. The increase in health care expenditures related to managing these presumably low-risk cancers, without a clear patient benefit, has resulted in a backlash against the early detection of thyroid cancer. Currently, there is no way to confidently predict which incidentally detected thyroid nodule may be the precursor to a more aggressive process. Predictions such as these would require more accurate characterization of the biology of individual thyroid cancers than is currently possible. With time, we might prove our ability to confidently differentiate low-risk from high-risk thyroid cancers, but until that happens, routine screening for thyroid cancer by imaging billed as a “health checkup” should not be performed. However, incidentally detected thyroid nodules should be reported, and a clear medical team management plan should be developed. Our ethical responsibility is to provide patients with objective, evidence-based information about their disease status, not to assume that we know what is best for them by selectively withholding information. In addition, providing patients with psychosocial assistance will help them process the information necessary to make informed decisions that will provide them with the most value when a small thyroid nodule or cancer is incidentally identified. Herein, we summarize the epidemiological data for disease incidence, discuss some controversies in disease management, and outline the key elements and ethical considerations of informed decision making as they apply to managing incidentally detected thyroid nodules and thyroid cancer.

Six ways mushroom can save the world.

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Mycologist Paul Stamets lists 6 ways the mycelium fungus can help save the universe: cleaning polluted soil, making insecticides, treating smallpox and even flu viruses.