FDA is notifying consumers and healthcare providers of its warning not to use ear candles – a hollow cone about 10 inches long made from a fabric tube soaked in beeswax, paraffin or a mixture of the two – because they can cause serious injuries, even when used according to the manufacturer’s directions. According to advertised claims, a burning ear candle draws ear wax and “impurities” or “toxins” out of the ear canal. Other claims for ear candles include relief from sinus and ear infections, headache and earache, as well as improved hearing, “blood purification,” improvements in brain function, and cure cancer. FDA has found no valid scientific evidence to support the safety or effectiveness of these devices for any medical claims or benefits.
FDA has received reports of burns, perforated eardrums and blockage of the ear canal which required outpatient surgery from the use of ear candles. FDA is especially concerned because some ear candles are being advertised for use in children. Children of any age, including babies, are likely at increased risk for injuries and complications if they are exposed to ear candles. Small children and infants may move during the use of the device, increasing the likelihood of wax burns and ear candle wax plugging up the ear canal. Also, their smaller ear canal size may make children more susceptible than adults to injuries.
Ear candles are sold and promoted in a variety of locations, including health food stores, flea markets, health spas and salons, as well as on commercial web sites.
Consumers and health care professionals are strongly encouraged to report injury related to the use of ear candles to the FDA’s MedWatch Safety Information and Adverse Event Reporting Program:
- Online: www.fda.gov/MedWatch/report.htm
- Phone: 1-800-332-1088
- Mail: return the postage-paid FDA form 3500, which may be downloaded from the MedWatch “Download Forms” page, to address on the pre-addressed form
- Fax: 1-800-FDA-0178
Read the complete MedWatch 2010 Safety summary, including a link to the FDA Advice for Patients, at:
This is good advice, endorsed by The Health Gazette.
Tags: ear candles
Trust the French. They do seem to have a penchant for doing their own thing or being different for the sake of being different. That probably is a quality the chemical industry can exploit.
In an update to its position on bisphenol A (BPA) last week, the French Food Safety Agency (AFSSA) said it did not accept the conclusions of dozens of studies carried out on animals that had found a link between exposure to BPA and a raft of serious health problems. After all, what would the rest of the world know?
Not surprisingly, a European plastics industry body has hailed the decision by the AFSSA to use “scientific” considerations to guide its ongoing evaluation of bisphenol A (BPA). Does this mean the European chemical industry has secured some “good scientists” who can be trusted to make “the right” findings in their “research”? Good question. Quite possibly, since that is how such marketing challenges are usually dealt with.
Interestingly, while AFSSA did not recommend any regulatory changes to restrict the use of BPA, it listed a number of measures that consumers should take to minimise their exposure to BPA, after highlighting there were indeed actually “warning signs” over the chemical. It also called for the rapid development of a methodology to detect potential toxicity in humans of very low doses of BPA and for more research to be carried out into replacement products and endocrine disruptors in general. It sounds like the French agency is not overwhelmingly confident that everyone else is wrong and that “their scientists” can find what the industry wants.
Read more in our earlier articles.
Bisphenol-A Dose-related Increase in Sexual Dysfunction Risk in Humans
Study Finds BPA Associated With Heart Disease
It is time to avoid exposure to bisphenol A.
Tags: bisphenol A, BPA
Consuming two or more soft drinks per week increased the risk of developing pancreatic cancer by nearly two-fold compared with individuals who did not consume soft drinks, according to a report in Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research.
Although relatively rare, pancreatic cancer remains one of the most deadly; only 5 percent of people who are diagnosed survive five years later.
Mark Pereira, Ph.D., senior author on the study and associate professor in the School of Public Health at the University of Minnesota, and first author Noel Mueller, M.P.H., said people who consume soft drinks on a regular basis, defined as primarily carbonated sugar-sweetened beverages, tend to have a poor behavioral profile overall.
However, the effect of these drinks on pancreatic cancer may be unique.
“The high levels of sugar in soft drinks may be increasing the level of insulin in the body, which we think contributes to pancreatic cancer cell growth,” said Pereira.
For the current study, Pereira and colleagues observed 60,524 men and women in the Singapore Chinese Health Study for 14 years. During that time, there were 140 pancreatic cancer cases. Those who consumed two or more soft drinks per week (averaging 5 per week) had an 87 percent increased risk compared with individuals who did not.
No association was seen between fruit juice consumption and pancreatic cancer.
Pereira said that these results from Singapore are likely applicable to the United States.
“Singapore is a wealthy country with excellent health care. Favorite pastimes are eating and shopping, so the findings should apply to other western countries,” said Pereira.
Susan Mayne, Ph.D., associate director of the Yale Cancer Center and professor of epidemiology at the Yale School of Public Health, said the study had some key limitations that should be considered in any interpretation.
“Although this study found a risk, it remains unclear whether it is a causal association or not. Soft drink consumption in Singapore was associated with several other adverse health behaviors such as smoking and red meat intake, which we can’t accurately control for,” said Mayne, an editorial board member of Cancer Epidemiology, Biomarkers and Prevention.
Yet Pereira points out that the findings are biologically plausible, held up in non-smokers, remained similar after taking other dietary habits into account, and are consistent with findings in Caucasian populations.
Source: University of Minnesota
Damage inflicted by amyloid protein implicated as shared disease mechanism
Nearly 20 years ago Huntington Potter kicked up a storm of controversy with the idea that Down syndrome and Alzheimer’s were the same disease. Now the evidence is in: He was right.
And that’s not all. Down syndrome, artery-clogging cardiovascular disease, and possibly even diabetes, appear to share a common disease mechanism with Alzheimer’s disease, Dr. Potter and colleagues at the Florida Alzheimer’s Disease Research Center, USF Health Byrd Alzheimer’s Institute, recently reported.
The researchers’ two papers – one in Molecular Biology of the Cell and the other in PLoS ONE — implicate the Alzheimer’s-associated protein beta amyloid (amyloid protein), which damages the microtubule transport system responsible for moving chromosomes, proteins and other cargo around inside cells. Both studies were done in mice and humans cell cultures modeling Alzheimer’s disease. Together, the laboratory discoveries suggest that protecting the microtubule network from this amyloid damage might be an effective way to prevent or even reverse Alzheimer’s disease and associated disorders.
The first paper, by Antoneta Granic and colleagues published online Dec. 23 in Molecular Biology of the Cell, provides the mechanism behind previous work by Dr. Potter’s laboratory showing that all Alzheimer’s disease patients harbor some cells with three copies of chromosome 21, known as trisomy 21, instead of the usual two. Trisomy 21 is a characteristic shared by all the cells in people with the birth defect Down syndrome as well. This earlier work demonstrated that Alzheimer’s disease could be considered a late onset form of Down syndrome.
By age 30 to 40, all people with Down syndrome develop the same brain pathology seen in Alzheimer’s disease, including a nerve-killing buildup of sticky amyloid protein clumps. This contributes to accelerated nerve cell loss and dementia.
With the study reported in MBC, Dr. Potter and his colleagues now show that the Alzheimer’s-associated amyloid protein is the culprit that interferes with the microtubule transport system inside cells. The microtubules are responsible for segregating newly duplicated chromosomes as cells divide.
“Beta amyloid basically creates potholes in the protein highways that move cargo, including chromosomes, around inside cells,” said Dr. Potter, who holds the Eric Pfeiffer Endowed Chair for Research on Alzheimer’s Disease.
When the microtubule network is disrupted, chromosomes can be incorrectly transported as cells divide and the result is new cells with the wrong number of chromosomes and an abnormal assortment of genes. For example, Down syndrome cells contain three copies of the beta amyloid gene on chromosome 21 – leading to more accumulation of the “bad” amyloid protein over a lifetime, Dr. Potter says. “Alzheimer’s disease probably is caused in part from the continuous development of new trisomy 21 nerve cells, which amplify the disease process by producing extra beta amyloid.”
The second paper by lead author Jose Abisambra and colleagues, published Dec. 31 in the online journal PLoS ONE, describes another consequence of the damaged microtubule network caused by the amyloid protein.
Many Alzheimer’s disease patients also commonly develop vascular diseases and diabetes. Whether this coincidence is bad luck or due to shared disease processes is intensely debated. Research teams have investigated the role that low-density lipoprotein (LDL), the bad cholesterol that causes atherosclerosis, cardiovascular disease and stroke, may play in the development of Alzheimer’s with mixed results. However, the USF group focused on the amyloid protein’s potential effects on LDL metabolism. The receptor needed to detect and use LDL is among the proteins transported by the microtubules.
As previously reported by their colleagues in the MBC paper, the second USF team found that the amyloid protein inflicts damage to the microtubule network. As a consequence, the receptor needed to pull LDL circulating throughout the bloodstream into the body’s cells has trouble getting to the cell surface to retrieve this bad cholesterol. This interference with LDL metabolism may allow bad cholesterol to build up in into plaques that choke off blood supply to the brain and heart in people with Alzheimer’s, Dr. Potter said.
Similarly, other key proteins – including insulin receptors and receptors for brain signaling molecules — are also likely locked inside cells when the transport system is damaged by amyloid or other factors. “The insulin receptors are needed to get blood sugar inside the cell where it can be used for energy. The nerve cell signaling receptors help promote memory and learning,” Dr. Potter said. “So, if these receptors are unable to function properly, it may lead to diabetes and problems with learning and memory.”
“We’re beginning to understand how conditions like cardiovascular disease and diabetes may manifest some of the same underlying disease processes as Alzheimer’s disease,” he said, “rather than being independent diseases that just happen to develop in the same patient.”
Journal articles cited:
1. “Alzheimer Ab Peptide Induces Chromosome Mis-segregation and Aneuploidy, including Trisomy 21; Requirement for Tau and APP,” Antoneta Granic, Jaya Padmanabhan, Michelle Norden, and Huntington Potter. Molecular Biology of the Cell, Dec. 23, 2009.
2. “LDLR Expression and Localization Are Altered in Mouse and Human Cell Culture Models of Alzheimer’s Disease,” Jose Abisambra, Tina Fiorella, Jaya Padmanabhan, Peter Neame, Inge Wefes, and Huntington Potter, PLoS ONE, Volume 5, Issue 1. (January 2010).
Source: University of South Florida Health
Tags: Alzheimer's disease, Down syndrome
A study by the University of Exeter and the Peninsula Medical School for the first time links thyroid disease with human exposure to perfluorooctanoic acid (PFOA). PFOA is a persistent organic chemical used in industrial and consumer goods including nonstick cookware and stain- and water-resistant coatings for carpets and fabrics.
Published in the journal Environmental Health Perspectives, The study revealed that people with higher concentrations of PFOA in their blood have higher rates of thyroid disease. The researchers analysed samples from the US Centers for Disease Control and Prevention’s nationally representative National Health and Nutrition Examination Survey (NHANES).
Tamara Galloway, a professor Ecotoxicology at the University of Exeter and the study’s senior author, says: “Our results highlight a real need for further research into the human health effects of low-level exposures to environmental chemicals like PFOA that are ubiquitous in the environment and in people’s homes. We need to know what they are doing.”
“There have long been suspicions that PFOA concentrations might be linked to changes in thyroid hormone levels,” adds study author, David Melzer, a professor of Epidemiology and Public Health at the Peninsula Medical School. “Our analysis shows that in the ‘ordinary’ adult population there is a solid statistical link between higher concentrations of PFOA in blood and thyroid disease.”
PFOA is a very stable man-made chemical that excels at repelling heat, water, grease, and stains. It is used during the process of making common household and industrial items including nonstick pots and pans, flame-resistant and waterproof clothing, wire coatings, and chemical-resistant tubing. PFOA can also be formed by the break-down of certain other highly fluorinated chemicals used in oil and grease-resistant coatings on fast-food containers and wrappers and in stain-resistant carpets, fabrics, and paints.
The study included 3966 adults aged 20 and older whose blood serum was sampled between 1999 and 2006 for PFOA and other perfluoroalkyl acid (PFAA) compounds, including perfluoroctane sulphonate (PFOS). The researchers found that the individuals with the highest 25% of PFOA concentrations (above 5.7ng/ml) were more than twice as likely to report current thyroid disease than individuals with the lowest 50% of PFOA concentrations (below 4.0ng/ml). The most specific analysis included 163 women and 46 men who reported having current thyroid disease and who were taking thyroid medication at the time the blood samples were taken. The models used in the analysis were adjusted for potential confounding factors, such as age, gender, ethnicity, smoking, and body mass index.
Previous animal studies carried out by other scientists have shown that the compounds can affect the function of the mammalian thyroid hormone system. This is essential for maintaining heart rate, regulating body temperature and supporting many other body functions, including metabolism, reproduction, digestion and mental health.
The findings are important because research has shown that PFAAs are found in water, air and soil throughout the world, even in remote polar regions. PFOA and PFOS have also been detected in the blood of people from across the globe, as well as in wildlife including birds, fish, and polar bears.
The main source of human exposure to PFOA and PFOS remains uncertain but is believed to be through diet. However, people may also be exposed through the PFAAs used in consumer goods such as textiles, footwear, furniture, and carpets, which can contaminate indoor air and dust.
Although more research is needed to understand the mechanism by which PFOA and PFOS may affect human thyroid functioning, it is plausible that the compounds could disrupt binding of thyroid hormones in the blood or alter their metabolism in the liver. However, this new evidence does not rule out the possibility that having thyroid disease changes the way the body handles PFOA and/or PFOS. The presence of the compounds might also prove to be simply a marker for some other factor associated with thyroid disease.
Thyroid diseases, particularly hypothyroidism, are much more common in women than men. However, in terms of the link between PFOA and thyroid disease, the researchers found no evidence of a statistically different effect between the sexes. The researchers also found a link between thyroid disease and higher concentrations of PFOS in men, but not in women.
Although previous studies of people living in communities near where PFOA and PFOS are manufactured did not find an association between exposure to these chemicals and thyroid hormone functioning, the largest study of such exposed communities is currently underway. (The ‘C8’ study of communities near DuPont’s Washington Works plant, including Marietta, OH, and Parkersburg, WV, both in the US).
In addition to Galloway and Melzer, the paper’s authors include Neil Rice of the Peninsula Medical School’s Epidemiology and Public Health Group; Michael H Depledge of the Peninsula Medical School’s European Centre for the Environment and Human Health; and William E Henley of the School of Mathematics and Statistics of the University of Plymouth . They used the U.S. NHANES dataset because it is the only large-scale data available on PFOA and PFOS in a ‘general’ population anywhere in the world.
Source: The Peninsula College of Medicine and Dentistry
Tags: environmental toxins, PFOA, thyroid disease, toxins