AffectedForLife says…Watch out folks. Started using JFM last summer – once per month, and developed Vitilligo. JFM co. is paying for dermatologist treatments etc, so they know there is a problem. Their box now warns about Vitilligo. I don’t believe it did back when I started using it last summer. I could be wrong about that, but clearly they know about a connection now.
The Right Brain responds:
When I saw AFL’s comment I was immediately skeptical. I expected the reason they’re paying her doctor’s bills is that it was cheaper than going to court. So I searched the literature for a connection between this product and vitillgo but I didn’t really expect to find anything. Hoo boy was I wrong!
Until I checked it out I didn’t realize that JFM contains paraphenylenediamine (PPD) a chemical used in hair dyes that is known to cause sensitizing problems in some cases. In particular, PPD is known to cause skin depigmentation in some individuals. (The chemical affects the melanocytes which produce skin color.) Whether or not this is exactly the same condition as vitilligo I don’t know but the end result is the same: white patches on your skin that may or may not ever resume their natural color. As AFL pointed out, Just For Me includes the following warning statement on their package:
In rare cases, use of hair dye has been associated with skin depigmentation (skin lightening or loss of skin color), which may be temporary or permanent. If you notice any skin depigmentation or other allergic reaction such as discomfort or severe itching, discontinue use immediately.
Do not use this product at all if you have depigmentation problems such as white patches on your skin (a condition called vitiligo) or if you have a family history of skin depigmentation problems, as an allergic reaction may cause temporary or permanent loss of skin pigment.
Water, Coco Glucoside, Amino Methyl Propanol, Carbomer, Isopropyl Alcohol, Fragrance, Isopropyl Acetate, Trisodium EDTA, Erythorbic Acid, 2 Methyl 5 Hydroxyethylaminophenol, 1,2,4 Trihydroxybenzene, P Phenylenediamine, Sodium Sulfate, P Aminophenol, N,n Bis (2 Hydroxyethyl) P Phenylenediamine Sulfate, Sulfuric Acid, Cinnamidopropyl Trimethyl Ammonium Chloride
While there is cause for concern you shouldn’t freak out about this. MANY people use this product (and other hair dyes that contain PPD) without any problem . But for those individuals who are susceptible to this condition, PPD can cause a real problem. Always do a patch test as recommended by the manufacturer and discontinue using the product if you have any issues.
Image credit: Amazon.com
References:
http://www.ncbi.nlm.nih.gov/m/pubmed/17244086/
Taylor JS, Maibach HJ, Fisher AA, Bergfeld WF. Contact leucoderma associated with the use of hair colors. Cutis 1993;52:273-80.
http://www.e-ijd.org/article.asp?issn=0019-5154;year=2010;volume=55;issue=3;spage=250;epage=254;aulast=Bajaj
If your a.m. meal of choice is a high-fat breakfast sandwich, you may want to rethink your breakfast preference for the sake of your heart.
A new study presented at the Canadian Cardiovascular Congress shows that eating just two of those typical high-fat sandwiches -- you know, processed cheese and some kind of meat nestled inside two halves of a bun -- in a day can take a real toll on your blood flow and blood pressure.
It can make "your blood vessels become unhappy," study researcher Dr. Todd Anderson, the director of the Libin Cardiovascular Institute of Alberta, said in a statement.
For the study, Anderson examined college students to see how high-fat breakfast sandwiches affected their blood pressure, by seeing how much blood is able to flow in their arms -- a measurement called VTI, or velocity time integral. A VTI that is high is good, because that means the vessels are able to dilate as much as possible, allowing for the flow of blood through the vessels.
The participants had their VTI measured one day when they had no breakfast, and then on one day when they had two 900-calorie breakfast sandwiches that had 50 grams of fat.
Researchers found that the participants VTI were 15 to 20 percent lower -- which is a bad sign for blood flow -- two hours after they ate the breakfast sandwiches, compared with when they didn't eat breakfast.
Also on HuffPost:
For Immediate Release
Thursday, November 1, 2012
National Institutes of Health (NIH) researchers have discovered a significant new mechanism of action for a class of chemotherapy drugs known as poly (ADP-ribose) polymerase inhibitors, or PARP inhibitors. They have also identified differences in the toxic capabilities of three drugs in this class which are currently being tested in clinical trials. The study, by scientists at the National Cancer Institute (NCI), part of NIH, and their colleagues, appeared in Cancer Research, Nov 1, 2012.
In recent years, drugs classified as PARP inhibitors have been shown to be promising anticancer agents for breast and ovarian cancer. Members of the PARP family of proteins are involved in a number of critical cellular processes, including DNA damage repair and programmed cell death. Prior to this study, PARP inhibitors were thought to work primarily by blocking PARP enzyme activity, thus preventing the repair of DNA damage and ultimately causing cell death.
In this study, scientists established that PARP inhibitors have an additional mode of action: localizing PARP proteins at sites of DNA damage, which has relevance to their anti-tumor activity. The trapped PARP protein–DNA complexes are highly toxic to cells because they block DNA replication. When the researchers tested three PARP inhibitors for their differential ability to trap PARP proteins on damaged DNA, they found that the trapping potency of the inhibitors varied widely.
"Critical to our research is that, while PARP inhibitors had been assumed to be of equivalent potency based on the degree to which they elicit PARP inhibition, we now know that they are not equivalent with respect to their potency to trap PARP," said Yves Pommier, M.D., Ph.D., NCI Center for Cancer Research. "Our findings suggest that PARP inhibitors should be categorized according to their potency to trap PARP, in addition to their enzyme inhibition abilities."
The PARP family of proteins in humans includes PARP1 and PARP2, which are DNA binding and repair proteins. When activated by DNA damage, these proteins recruit other proteins that do the actual work of repairing DNA. Under normal conditions, PARP1 and PARP2 are released from DNA once the repair process is underway. However, as this study shows, when they are bound to PARP inhibitors, PARP1 and PARP2 become trapped on DNA. The researchers showed that trapped PARP–DNA complexes are more toxic to cells than the unrepaired single-strand DNA breaks that accumulate in the absence of PARP activity, indicating that PARP inhibitors act as PARP poisons.
In collaboration with James Doroshow, M.D., deputy director for clinical and translational research at NCI, the investigators used PARP assays (ways of measuring PARP activity in cells and tissues) to compare three PARP inhibitor compounds that are currently in clinical testing: MK-4827, olaparib, and veliparib.
The scientists found that the three PARP inhibitors differed in their ability to inhibit PARP enzyme activity, with olaparib being the most potent inhibitor, followed by veliparib and then MK-4827. However, in terms of toxicity, MK-4827 was the most potent, followed by olaparib and then veliparib. Moreover, PARP1 complexes with MK-4827 and olaparib were shown to be more tightly bound to DNA than complexes with veliparib.
These findings suggest that there may be two classes of PARP inhibitors, catalytic inhibitors that act mainly to inhibit PARP enzyme activity and do not trap PARP proteins on DNA, and dual inhibitors that both block PARP enzyme activity and act as PARP poison.
"Our findings suggest that clinicians who use PARP inhibitors in clinical trials should carefully choose their drug, because we now suspect results may differ, depending upon the PARP inhibitor used," said Junko Murai, M.D., Ph.D., NCI Center for Cancer Research. "As a next step, we are working to categorize other leading PARP inhibitors based upon both PARP trapping and PARP inhibition."
This work was supported by the Intramural Program of NCI and by the Japan Society for the Promotion of Science (JSPS) Core-to-Core Program. First author Junko Murai is a JSPS fellow working at NCI Center for Cancer Research. Funding was provided by NCI grant Z01 BC 006150-19LMP.
The National Cancer Institute (NCI) leads the National Cancer Program and the NIH effort to dramatically reduce the burden of cancer and improve the lives of cancer patients and their families, through research into prevention and cancer biology, the development of new interventions, and the training and mentoring of new researchers. For more information about cancer, please visit the NCI website at http://www.cancer.gov or call NCI's Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.
NIH...Turning Discovery Into Health ®
###
