Hi, I'm Howard Weintraub. I'm a cardiologist
from New York University (NYU) Medical Center, where I'm the Clinical
Director for the NYU Center for the Prevention of Cardiovascular
Disease, and a clinical associate professor of medicine.
I'm here to discuss an interesting alert that
the Us Food and Drug Administration (FDA) just came out with last week,
where they advised against the utilization of 80 mg of simvastatin
except in select groups of patients. Simvastatin, for those of you not
familiar, used to be called Zocor®.
It was a very popular medication
when it was branded, and even now that it's generic it has become the
most widely utilized statin.
There are some very, very good efficacy
studies that have been associated with this drug. Most notably, the
Heart Protection study, which proved that almost regardless of your LDL level, the use of the
statin, here it was 40 mg of simvastatin -- this is important to
remember -- 40 mg of simvastatin was associated with safe, effective,
lowering of cardiovascular events in a wide group of patients.
However, in 2 other studies that were done, one called A TO Z, which was an acute coronary syndrome study, and another that was more recently done called SEARCH, which was kind of a convoluted study that also involved looked at
homocystine, there were disturbing data about the development of
myopathy when 80 mg of simvastatin was used.
For this reason, the FDA, about a year ago,
hinted that maybe it wouldn't be such a good idea if we continued to use
80 of simvastatin. And now, they came out and said, "Yeah, we made our
mind up; you should not be using 80 mg of simvastatin."
The only place
where they think it might be okay is in those patients who have already
been taking the drug for over a year and have been obviously tolerating
it.
So, what does this mean? Well, it means that
the FDA doesn't think we should be prescribing 80 mg of simvastatin out
of the shoot. Now, that's not a recognized starting dose, but certainly
we're even talking about people who are not controlled on 40 mg of
simvastatin. What do you do? Clearly the answer here is that you should
not be graduating to 80 mg of simvastatin. So now, what can happen?
Well, my great concern is that physicians may
not be comfortable in escalating to branded statins because of the
resistance that they get from managed care, and sometimes the necessity
for this widely loved thing called a prior authorization.
And then, the
other problem comes when patients may vocalize their distaste for this
because of the added cost that they have to spend. But, I think that
physicians need to be aware that there are very, very good branded
alternatives that are safer and have had very good efficacy data in
their highest dose when used for long periods.
And, ultimately I think the cost of the drug
is one thing, but we need to recognize that using the drug to get the
event reduction that is desired in the kind of patient that you're
treating is ultimately our goal.
So, I think it's important for physicians to
recognize that if a patient is on 40 mg simvastatin, and they need
considerably more low-density lipoprotein (LDL) reduction, then their
choices are now limited to doing one of several things. One is to add a
drug to [simvastatin], which may be even more distasteful to some
patients, because both of [these additional drugs] are branded, and one
of them would be ezetimibe (Zetia®). I don't think I need to tell you
about some of the controversy that swirls around ezetimibe. And, the
other is to add a drug like colesevelam (Welchol®), which really has
some quite good data associated with it,.
Although there are some other
issues that patients sometimes find distasteful, actually I think this
drug is underutilized.
The alternative is to keep it at only 1 pill a
day, and that would be switching to either atorvastatin (Lipitor®) or
rosuvastatin (Crestor®).
These drugs have been shown to be very well
tolerated and highly effective in their maximal doses.
And, I think that
you can get considerably greater LDL reduction in the range of about
another relative 20%. So, instead of getting about 45% [reduction] with
80 mg with simvastatin, you can get a little over 50%, particularly when
you're using a drug like rosuvastatin, where you can get in the low
50th on 40 mg of rosuvastatin a day.
So, it's important for physicians to
recognize this new warning.
It's important that they try to avoid
harming their patients by utilizing the 80 mg of simvastatin.
It also
has more drug-drug interactions posted in their product insert than the
other prominent branded statins, such as atorvastatin and rosuvastatin.
And, I think it's important that ultimately
we think of the one thing, which is getting LDLs, triglycerides, and
high-density lipoprotein to the appropriate goal, so that our patients
experience the lowest possible cardiovascular risk.
Thursday, June 30, 2011
Preventive Efforts in Type 2 Diabetes Are Cost Effective
Medscape Medical News from the:American Diabetes Association (ADA) 71st Scientific Session
June 29, 2011 (San Diego, California) — Preventive treatment with metformin or lifestyle intervention in patients with type 2 diabetes reduced the cost of medical care, including costs for inpatient and outpatient care and prescriptions, compared with placebo, according to data from a 10-year cost-effectiveness analysis from the Diabetes Prevention Program (DPP).
William H. Herman, MD, MPH, professor of medicine and epidemiology at the University of Michigan, Ann Arbor, and coinvestigator of the DPP Research Group, and colleagues presented the findings in the late-breaking session here at the American Diabetes Association (ADA) 71st Scientific Sessions.
In the DPP, overweight and obese participants with impaired glucose tolerance were randomly assigned to lifestyle intervention, metformin, or placebo.
Previous results, reported in 2002, indicated that lifestyle intervention led to a 58% reduction in the development of diabetes, from about 11% per year to about 5% per year.
By comparison, metformin resulted in a 31% reduction in the development of diabetes.
These findings indicate that treatment with metformin or lifestyle intervention reduced the cost of medical care by $1700 and $2600 per person, respectively, over 10 years, compared with placebo. However, lifestyle intervention cost more to administer than metformin or placebo, so when the reductions in the cost of medical care were balanced against the cost of the interventions, metformin saved $30 per person, whereas the lifestyle intervention cost $1500 per person over the 10-year period.
The lifestyle intervention aimed for a 7% reduction in body weight and the goal of 150 minutes per week of moderate-intensity activity.
The lifestyle intervention was found to halve the number of people who progressed to diabetes, compared with the metformin intervention.
The lifestyle intervention also improved quality of life, compared with metformin or placebo.
When cost of care and measures of health and quality of life were considered simultaneously, both interventions were found to be highly cost effective.
These study findings put "diabetes prevention in the category of prenatal care or pediatric immunizations," noted Dr. Herman in an ADA release. "It's dramatic when an intervention can improve the health of the population and potentially save money at the same time," he added.
"The DPP has shown that lifestyle intervention and metformin can decrease the epidemic of diabetes that is currently affecting the United States and much of the world and, in doing so, may save money," noted David M. Nathan, MD, DPP chair and professor of medicine at Harvard Medical School, Boston, Massachusetts. "The cost savings may seem modest now, but any decrease in medical costs is welcome, and the savings may very well increase in the future."
According to the researchers, healthcare and societal policies should support the use of lifestyle intervention and metformin to prevent or delay diabetes.
The study was not commercially funded. Dr. Herman and Dr. Nathan have disclosed no relevant financial relationships.
American Diabetes Association (ADA) 71st Scientific Sessions: Abstract 0136-LBOR. Presented June 28, 2011.
Ambulatory vs In-Office BP Better for Predicting CKD
June 29, 2011 — In patients with chronic kidney disease (CKD),
ambulatory blood pressure (BP) monitoring, especially at night, appears
to be more accurate than office BP measurement in predicting risk for
renal and cardiovascular events, according to new research.
Roberto Minutolo, MD, PhD, from the Division of Nephrology, Second University of Naples, Italy, and colleagues reported their findings in the June 27 issue of the Archives of Internal Medicine.
According to the researchers, ambulatory BP measurement "allows a better risk stratification in essential hypertension compared with office blood pressure measurement, but its prognostic role in nondialysis [CKD] has been poorly investigated."
They also point out that office BP readings may be influenced by white coat hypertension in this setting.
To investigate the accuracy of ambulatory BP in predicting risk in patients with CKD, Dr. Minutolo and colleagues compared daytime and nighttime systolic and diastolic BP with office BP measurements in 436 consecutive patients with CKD.
The average age of the patients was approximately 65 years, and their mean glomerular filtration rate was 42.9 mL/minute/1.73 m2. About one third of the patients had diabetes and/or cardiovascular disease, and 41.7% were women.
Researchers measured the patient's BP 3 times during a morning office visit and outfitted the patient with an ambulatory BP monitor that took readings every 15 minutes during the day and every half hour at night. They also obtained 3 more in-office BP readings the next day, when patients returned. Participants also recorded their activities in a diary.
Mean systolic over diastolic blood pressure measured in-office was 146/82 mm Hg; daytime ambulatory measurement was 131/75 mm Hg, and nighttime measurement was 122/66 mm Hg.
During a median 4.2 years of follow-up, 155 patients had a renal endpoint (end-stage renal disease or renal death), and 103 patients had a cardiovascular endpoint (fatal or nonfatal cardiovascular events).
Compared with patients with a lower ambulatory daytime systolic BP of between 126 and 135 mm Hg, those with higher values were 2 to 3 times more likely to have a cardiovascular endpoint, and nearly twice as likely to have a renal endpoint.
In patients with higher nighttime ambulatory systolic BP, the risk for a cardiovascular endpoint was increased 2.5- to 4-fold, and the risk for a renal endpoint was increased by about 2-fold compared with the patients with the reference systolic BP value of 106 to 114 mm Hg.
In contrast, office measurement of BP did not predict risk for a renal or cardiovascular endpoint, the researchers found.
Patients who were "nondippers" and those who were "reverse dippers" had an increased risk for renal death and cardiovascular events. There was a 2-fold greater risk for cardiovascular events in nondipper and reverse-dipper subgroups, and their risk for renal death increased by 62% and 72%, respectively, in comparison with dippers.
"This study demonstrates that ambulatory BP monitoring is a better predictor of renal and cardiovascular end points compared with office BP measurement in patients with CKD," the researchers conclude.
"Given the importance of detecting BP elevation and of dealing with it efficiently and promptly, it is both exciting and challenging to see a report like the one by Minutolo and colleagues," state David Goldsmith, FRCP, from Guy's Hospital in London, United Kingdom, and Adrian Covic, MD, PhD, from the C. I. Parhon University Hospital in Iasi, Romania, in a related invited commentary.
According to the commentators, "there will be those who will question the time, effort, and expense of running an ambulatory BP service." However, selected cohorts of patients may benefit from ambulatory BP monitoring, the authors add.
"This new study by Minutolo and colleagues makes that case stronger for our patients with CKD," they write. "It is now harder to defend reliance on clinic BP measurement alone if we nephrologists are serious about targeted BP intervention."
This study was not commercially supported. The authors and editorialists have disclosed no relevant financial relationships.
Arch Intern Med. 2011;171:1090-1098, 1098-1099. Article Abstract Commentary Extract
According to the researchers, ambulatory BP measurement "allows a better risk stratification in essential hypertension compared with office blood pressure measurement, but its prognostic role in nondialysis [CKD] has been poorly investigated."
They also point out that office BP readings may be influenced by white coat hypertension in this setting.
To investigate the accuracy of ambulatory BP in predicting risk in patients with CKD, Dr. Minutolo and colleagues compared daytime and nighttime systolic and diastolic BP with office BP measurements in 436 consecutive patients with CKD.
The average age of the patients was approximately 65 years, and their mean glomerular filtration rate was 42.9 mL/minute/1.73 m2. About one third of the patients had diabetes and/or cardiovascular disease, and 41.7% were women.
Researchers measured the patient's BP 3 times during a morning office visit and outfitted the patient with an ambulatory BP monitor that took readings every 15 minutes during the day and every half hour at night. They also obtained 3 more in-office BP readings the next day, when patients returned. Participants also recorded their activities in a diary.
Mean systolic over diastolic blood pressure measured in-office was 146/82 mm Hg; daytime ambulatory measurement was 131/75 mm Hg, and nighttime measurement was 122/66 mm Hg.
During a median 4.2 years of follow-up, 155 patients had a renal endpoint (end-stage renal disease or renal death), and 103 patients had a cardiovascular endpoint (fatal or nonfatal cardiovascular events).
Compared with patients with a lower ambulatory daytime systolic BP of between 126 and 135 mm Hg, those with higher values were 2 to 3 times more likely to have a cardiovascular endpoint, and nearly twice as likely to have a renal endpoint.
In patients with higher nighttime ambulatory systolic BP, the risk for a cardiovascular endpoint was increased 2.5- to 4-fold, and the risk for a renal endpoint was increased by about 2-fold compared with the patients with the reference systolic BP value of 106 to 114 mm Hg.
In contrast, office measurement of BP did not predict risk for a renal or cardiovascular endpoint, the researchers found.
Patients who were "nondippers" and those who were "reverse dippers" had an increased risk for renal death and cardiovascular events. There was a 2-fold greater risk for cardiovascular events in nondipper and reverse-dipper subgroups, and their risk for renal death increased by 62% and 72%, respectively, in comparison with dippers.
"This study demonstrates that ambulatory BP monitoring is a better predictor of renal and cardiovascular end points compared with office BP measurement in patients with CKD," the researchers conclude.
"Given the importance of detecting BP elevation and of dealing with it efficiently and promptly, it is both exciting and challenging to see a report like the one by Minutolo and colleagues," state David Goldsmith, FRCP, from Guy's Hospital in London, United Kingdom, and Adrian Covic, MD, PhD, from the C. I. Parhon University Hospital in Iasi, Romania, in a related invited commentary.
According to the commentators, "there will be those who will question the time, effort, and expense of running an ambulatory BP service." However, selected cohorts of patients may benefit from ambulatory BP monitoring, the authors add.
"This new study by Minutolo and colleagues makes that case stronger for our patients with CKD," they write. "It is now harder to defend reliance on clinic BP measurement alone if we nephrologists are serious about targeted BP intervention."
This study was not commercially supported. The authors and editorialists have disclosed no relevant financial relationships.
Arch Intern Med. 2011;171:1090-1098, 1098-1099. Article Abstract Commentary Extract
Tuesday, June 28, 2011
New EAS Statement on High Triglycerides, Low HDL Cholesterol
Medscape Medical News from:
June 27, 2011 (Gothenburg, Sweden) — An expert consensus panel from the European Atherosclerosis Society (EAS) has issued new recommendations for the management of patients with elevated triglycerides and low HDL-cholesterol levels.
For patients with high triglycerides or low HDL-cholesterol levels, the first task is lifestyle modification, but barring that, fibrates, niacin, or even the intensification of statin therapy is recommended.
Interestingly, the recommendations are published on the heels of the discontinuation of the Atherothrombosis Intervention in Metabolic Syndrome with Low HDL Cholesterol/High Triglyceride and Impact on Global Health Outcomes (AIM-HIGH) study.
As reported by heartwire , the National Heart, Lung, and Blood Institute–sponsored study of high-dose extended-release niacin (Niaspan, Abbott), given in addition to statin therapy in patients with a history of cardiovascular disease, high triglycerides, and low levels of HDL cholesterol was halted 18 months ahead of schedule because niacin offered no additional benefits in this patient population.
The new EAS recommendations, which were presented this week here at the European Atherosclerosis Society 2011 Congress, state that the focus of treatment should be patients at high risk for cardiovascular disease who have triglyceride levels >150 mg/dL and/or HDL-cholesterol levels <40 mg/dL.
In the review, the panel assesses the evidence supporting the link between triglyceride-rich lipoproteins, HDL cholesterol, and cardiovascular disease, recommending that after insufficient improvement following intensive lifestyle management, physicians should consider adding niacin or a fibrate or even intensifying LDL therapy for further reductions.
The purpose of the new consensus statement is to also remind the clinical community that targeting triglyceride-rich lipoproteins and low HDL cholesterol can provide a further reduction in cardiovascular risk for patients with metabolic abnormalities who are already at LDL-cholesterol goal
.
"Possibly the most successful medication of the past 30 years, in terms of the impact on outcomes, has been the statins," Dr M John Chapman (Pitié-Salpetriere University Hospital, Paris, France), lead author of the consensus statement, told heartwire .
"Of course, statins have their primary effect on LDL cholesterol and small effects on HDL cholesterol and triglyceride levels, and we've drilled into clinicians' minds that you get lot of benefit in reducing cardiovascular events with statins." The new report is a reorientation, he suggested, getting physicians to think about other residual risk factors for cardiovascular disease in statin-treated patients.
What About the AIM-HIGH Study?
In an interview with heartwire about the recommendations, Chapman said that the antiatherosclerotic effects of niacin when used with a statin have been noted in plaque imaging studies, and a meta-analysis of niacin trials also indicates a clinical benefit in patients with cardiometabolic disease.
Chapman said it is too early to comment fully on the results of AIM-HIGH because all the data have not yet been published. That said, he notes that patients in the trial had the same dyslipidemic phenotype the new consensus statement is highlighting, but these patients were very well treated with intensive lifestyle modification and statin therapy.
"This means that the plaques in these individuals had benefited from intensive statin therapy, and we know that intensive therapy to very low LDL-cholesterol levels results in a significant reduction in clinical events," said Chapman. "At this point, we don't know the status of the plaques in AIM-HIGH, and one of the weaknesses of the trial was that there was no imaging performed. In other words, this could be shades of the ENHANCE study."
As reported by heartwire , ENHANCE was a controversial clinical trial that tested the effectiveness of combined therapy with ezetimibe (Merck) and simvastatin in patients with familial hypercholesterolemia (FH) and found that the combination did no better than simvastatin monotherapy on several surrogate end points.
The combination, known as Vytorin, did not result in a significant difference in changes in intima-media thickness (IMT) compared with simvastatin alone, despite significantly greater reductions in LDL cholesterol and C-reactive protein. Some speculated, including the investigators, that intensive statin therapy in this FH population limited ezetimibe's benefit. Others were less charitable, however, questioning whether the drug had any clinical benefit beyond LDL lowering.
Regarding the AIM-HIGH trial, Chapman suspects that increases in HDL of 10% to 15% would likely not have been enough to result in a significant reduction in cardiovascular events.
Instead, his "back-of-the-envelope" calculation based on patients' background therapy and baseline cardiovascular risks suggests that AIM-HIGH investigators would have needed to raise HDL cholesterol 25% to 30% to reduce cardiovascular events.
Chapman also suggested that blanket HDL raising might not be the right approach, pointing to other data suggesting that HDL raising is more beneficial in some clinical situations, particularly in the early course of the disease.
"The whole importance of identifying individuals with low HDL-cholesterol levels should be done far earlier for primary-prevention purposes," he told heartwire .
"Lifestyle and diet are the way go here.
Weight loss raises HDL cholesterol and quitting smoking raises HDL cholesterol. So basically, with AIM-HIGH, we don't want to throw the baby out with the bathwater."
In a report to investors, Larry Biegelsen, an analyst with Wells Fargo Securities, notes that in this third week since AIM-HIGH was stopped, total Niaspan prescriptions are down 5.3% and new prescriptions are down 9.5%. With annual sales of $1.1 billion in 2011, he anticipates a further 20% reduction in 2012, taking the total US sales down to $902 million.
Fibrates Also an Issue for the FDA
Regarding fibrates, Chapman acknowledged that the data are mixed and somewhat controversial.
Fenofibrate (Trilipix, Abbott Laboratories) was approved in 2008 to be used with a statin to reduce triglycerides and increase HDL cholesterol in diabetic patients with mixed dyslipidemia/coronary disease or those who were at risk of coronary disease but already on optimal statin therapy.
In ACCORD-Lipid, a study of combination fenofibrate and simvastatin vs simvastatin alone, there was no benefit on the primary outcome.
The FIELD trial also showed no significant difference in cardiovascular morbidity and mortality in diabetics with fenofibrate vs placebo.
However, subgroup analyses suggest that there was a benefit in patients with very low HDL cholesterol and very high triglyceride levels (baseline levels of triglycerides >204 mg/dL and HDL cholesterol <34 mg/dL). "We critically need a trial designed to test the hypothesis that the efficacy of fibrates is there in this subgroup," said Chapman. "We don't know that yet."
In late May, the Food and Drug Administration advisory panel came to the same decision.
They voted 13 to 0 to recommend that Abbott launch a new trial of fenofibrate in diabetic patients who have met their LDL-cholesterol goal on a statin but still have high triglycerides and low HDL cholesterol.
Patients in the trial should be randomized to fenofibrate plus a statin or placebo plus a statin, and the trial's primary end point should be based on clinical outcomes and not just changes in triglycerides or HDL-cholesterol levels, the panel agreed.
Thursday, June 23, 2011
Long-Term Complications Likely With Silicone Breast Implants
Medscape Medical News > Alerts, Approvals and Safety Changes > Medscape Alerts
At Least 1 in 5 Patients Will Need Implant Removal Within 10 Years, FDA Warns
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"Breast implants are not lifetime devices," Jeffrey Shuren, MD, JD, director of the FDA's Center for Devices and Radiological Health, said during a telephone news conference.
"One in 5 patients who received implants for breast augmentation will need them removed within 10 years of implantation. For patients who received implants for breast reconstruction, as many as half will require removal 10 years after implantation."
Women with silicone breast implants will need to monitor their breasts for the rest of their lives.
To screen for silent ruptures, women should undergo magnetic resonance imaging 3 years after implantation, and then every 2 years thereafter, Dr. Shuren said. Women with saline implants do not need regular imaging.
When the FDA allowed silicone breast implants back on the market in November 2006, it required manufacturers to conduct follow-up studies to learn more about the long-term performance and safety of the devices. The FDA's report is based on preliminary safety data from these studies, as well as other safety information from recent scientific publications and adverse events reported to the agency.
The most frequently observed complications and adverse outcomes are tightening of the area around the implant (capsular contracture), additional surgeries, and implant removal.
Other complications include a tear or hole in the outer shell (implant rupture), wrinkling, uneven appearance (asymmetry), scarring, pain, and infection.
Studies to date do not indicate that silicone breast implants cause breast cancer, reproductive problems, or connective tissue disease, such as rheumatoid arthritis, the FDA said. However, no study has been large enough or lasted long enough to completely rule out these and other rare complications.
"Most women report high levels of satisfaction" with their implants, Dr. Shuren said.
The FDA is working with the 2 manufacturers who make silicone breast implants, Allergan and Mentor, to address the challenges in collecting follow-up data on the women who have received these implants.
Approximately 5 to 10 million women worldwide have breast implants. In the United States, 296,203 breast augmentation procedures and 93,083 breast reconstruction procedures were performed last year, according to the American Society of Plastic Surgeons. About half the procedures used saline implants, and half used silicone implants.
Patients with either saline or silicone implants may have a very small risk for a rare cancer called anaplastic large-cell lymphoma (ALCL) adjacent to the implant. However, the risk is "profoundly small," said Dr. Shuren. "Since 1997, there are only 34 cases in the published literature, and at most 60 cases out of the 5 to 10 million women with implants worldwide," he said. "We don't yet know if there is a causal link."
When the FDA first released information about the risk in January, William Maisel, MD, MPH, chief scientist and deputy director for science in the FDA's Center for Devices and Radiologic Health, said the evidence suggests that the kind of ALCL found in conjunction with breast implants is less aggressive and is sometimes treatable by simply removing the implant, the capsule, and the collected fluid.
"The FDA will continue to monitor and collect safety and performance information on silicone gel–filled breast implants, but it is important that women with breast implants see their healthcare providers if they experience any symptoms," Dr. Shuren said. "Women who have enrolled in studies should continue to participate so that we may better understand the long-term performance of these implants and identify any potential problems."
The FDA is holding an expert advisory panel in the next few months to discuss how postapproval studies on breast implants can be more effective.
The FDA will issue an update at a future date on saline implants, Dr. Maisel said.
All serious adverse effects should be reported to the breast implant manufacturer and Medwatch, the FDA's safety information and adverse event reporting program, by telephone at 1-800-FDA-1088, by fax at 1-800-FDA-0178, online at https://www.accessdata.fda.gov/scripts/medwatch/medwatch-online.htm, or by mail to MedWatch, FDA, 5600 Fishers Lane, Rockville, Maryland 20852-9787.
Sun Protection Products (in children)
Posted: 06/20/2011
http://www.medscape.org/viewarticle/743531There’s no “may” about it. Neither is there any “may” about sunlight causing “photo-aging,” the development of leathery, wrinkled skin with long-term sun exposure. And the damaging effects of sunlight are not restricted to farmers toiling in the fields or to sun-worshipping yuppies in quest of that alluring tan. Children and infants are also vulnerable. Luckily, chemical protection is readily available. Uncertainties do, however, emerge when it comes to deciding on which specific chemicals to use. There is also the question of whether children, because of their more sensitive skin, need special products.
Some activist organizations claim that certain sunscreen ingredients are unsafe and blame regulatory agencies for not looking after the welfare of the public,while manufacturers profess that their products have been thoroughly tested for safety and efficacy. As usual, the public is left confused. Actually, when you blow away the superfluous blather emanating both from the alarmists and from industry, there is some simple advice to offer.
The challenge is clear. Find a chemical or mixture of chemicals that can be applied to the skin to reduce exposure to the full spectrum of UV light. Then make sure these chemicals do not degrade upon exposure to light, have no topical or systemic toxicity, are minimally absorbed into the body, are resistant to water, do not have a greasy feel, are cosmetically acceptable, do not stain clothing, and can be incorporated into a “vehicle” that allows for easy spreading. Secure Food and Drug Administration (FDA) approval, which is required unlike for other cosmetics. Quite a list of demands.
The first commercial “sunscreens” appeared in the 1960s and were designed to filter out “UVB,” the shorter wavelengths of UV light (290–320 nm). These are the rays that cause sunburn, which was the main concern at the time. Slightly longer waves, those responsible for tanning, were deemed safe. Finding chemicals that absorb the nasty UVB rays was not particularly difficult, with PABA, octocrylene, phenylbenzimidazole sulfonic acid, and various cinnamates and salicylates being up to the task.
Products with different concentrations of these ingredients were introduced for different skin types, each prominently featuring a “sun protection factor (SPF),” basically a measure of the time it takes for skin to redden compared with having no protection.
The SPF value is determined in the laboratory by applying 2 mg/cm2 of product to the skin of volunteers. Using a product with an SPF of 15 means that a person who normally begins to burn in 10 minutes can in theory stay in the sun for 150 minutes before experiencing any visible effect on the skin.
It didn’t take long for this scenario to prove to be too simplistic. As a clear link between skin cancer and UVB emerged, the focus shifted from preventing sunburn to preventing skin cancer, resulting in an industry frenzy of products with higher and higher SPF values. In truth, an SPF of 15 already blocks 94% of UVB, only 3% less than one labeled as SPF 30. In any case, these numbers are only meaningful if the product is applied the same way as in the lab studies, which turns out not to be the case. Most people were applying far less than 2 mg/cm2and were not getting the protection they thought they were getting. What many were getting, though, were various skin reactions. And something else became apparent as well.
The longer wavelengths of UV light, 320–400 nm, known as UVA, previously thought to be innocuous, were found to be more deeply penetrating than UVB and responsible for premature wrinkling and aging of the skin (“photo-aging”).
Unlike UVB, they can even pass through glass.
Furthermore, UVA also was found to be potentially carcinogenic.
This created a need for a novel class of products that would protect the skin both from UVB and UVA. Ideally, not one that would just absorb some wavelengths, but one that would reflect all UV light. Titanium dioxide and zinc oxide, both mineral pigments, fit the bill but left a white residue on the skin. That was all right for lifeguards’ noses, but not for vain sunbathers. The search was on for cosmetically acceptable molecules capable of absorbing UVA. Oxybenzone and avobenzone (Parsol 1789) were up to this task, but as usual, there are some “buts.”
When oxybenzone absorbs UV light, it becomes energized and some of this energy is dissipated through the production of free radicals. These are very active molecular species that have been linked to cancer. Oxybenzone also undergoes a reaction in the presence of UV light to form a compound called a semiquinone, which in turn can inactivate some of the naturally occurring antioxidants in the skin such as reduced glutathione.
This is not a good thing since antioxidants offer protection against free radicals.
And if that weren't enough, it turns out that oxybenzone can also mimic the behavior of estrogens, at least in fish exposed to high doses. It has therefore been labeled a potential "endocrine disruptor."
Concern has been raised, mostly by the EWG, an American activist organization, because surveys have shown that oxybenzone can be found in the blood of 97% of the population.
But, and a big “but” it is, there is no evidence reported in the scientific literature of oxybenzone being linked to any human health problem, except for photodermatitis, a skin reaction triggered by exposure to sunlight. There are hundreds and hundreds of compounds, both natural and synthetic that, if scrutinized the same way as oxybenzone, could be linked to problems. Phthalates, bisphenol A, soy extracts, and various pesticides are estrogenic. We live in a world full of hormone-like substances, and a complete analysis of our blood would reveal hundreds of these. All of this goes to say that the risks of oxybenzone as implied by the EWG are overstated.
Avobenzone is cosmetically elegant and nonirritating but becomes unstable after a couple of hours of exposure to UV light. However, its stability is increased when combined with oxybenzone, especially if another stabilizing agent known as diethylhexyl-2,6-napthalene (DEHN) is added. This combination, developed by Neutrogena, is known as Helioplex. An important question arises here: what happens to the UV energy that these chemicals absorb? The energy has to go somewhere. Might it not have a damaging effect? The answer: DEHN takes the energy absorbed by avobenzone and transfers it to oxybenzone that then fluoresces it as harmless red light.
Another effective broad-spectrum sunscreen is tetraphalydine dicamphor sulfonic acid, which goes by the trade name Mexoryl. It is stable, absorbs UV light, and dissipates the energy as harmless heat. Mexoryl isn’t absorbed through the skin and so far there are no safety issues. And recently, excellent products using “micronized” titanium dioxide and zinc oxide have been developed, which do not leave a tell-tale white residue. Presently it is difficult to judge exactly how much protection a product affords against UVA, because no SPF-like system has yet been devised. But regulatory agencies are working on it.
Sun protection products also contain ingredients beyond the ones that reduce UV light exposure. However, the EWG has also taken aim at some of these, particularly retinyl palmitate, added to some sunscreens with the aim of reducing “photo-aging,” is a potential carcinogen. The criticism is based on an inconclusive study on rodents that has not been published in the peer-reviewed literature. Furthermore, the comparison was not between sunscreens that contained retinyl palmitate and ones that didn’t. A cream that contains only retinyl palmitate is not an appropriate model for a sunscreen preparation. And why not mention a recent 2009 study that examined the combined effect of UV light and retinyl palmitate on hamster ovary cells, a protocol that is consistent with the current recommendations for effective testing of photogenotoxicity? This published peer-reviewed study concluded that retinyl palmitate had no photogenotoxic potential! Admittedly, though, the evidence that retinyl palmitate actually prevents skin damage is pretty thin, so there is really no need to include it.
There is 1 more “may” about sunscreens that has been converted to fact. We no longer have to say that sunscreens may prevent skin cancer, we can say with authority that they do. A study in Australia, where skin cancer is a huge concern, involved 1600 subjects who were given sunscreen to use every day for 4.5 years. They developed 40% fewer squamous cell cancers than a control group who just maintained normal skin care without being given specific instructions about the use of sunscreens.
Sunscreens can prevent skin cancer, which is not a rare disease. The World Health Organization estimates 48,000 deaths a year from melanoma (likely sun related but not conclusively proven) and 12,000 from other forms of skin cancer. What’s next?
The general recommendation is to look for a product with SPF 30 containing avobenzone, Mexoryl, titanium oxide, or zinc oxide. Since titanium dioxide (5%) and zinc oxide (10%) are the least irritating to the skin, products that use only these ingredients are the most appropriate for children.
Infants should be protected with clothing, but there is no evidence to suggest that sunscreens cannot be used on exposed parts. Fragrance-free products are also available if there is a concern about allergies and sensitivities.
The sun protection products should be applied about 15 minutes before going out in the sun.
As a general guideline, a shot glass full is needed for the body and half a teaspoon for the face.
Reapply frequently. Forget terms like “waterproof,” “all day protection,” and “sweat-proof.” They don’t mean much. And if you are buying something that is “chemical-free,” you are not getting a good deal because you’re buying a vacuum.
Sunscreens should not be used to prolong sun exposure, but rather to protect the skin when exposure is unavoidable.
Above all, it is important to remember that unfortunately there is no such thing as a healthy tan.
Wednesday, June 15, 2011
How Much Caffeine Is In Your Drink?
A lot of a good thing is not necessarily better; one of those things is caffeine, and the amount can vary widely depending on the source.
- A 6-oz cup of homemade coffee has about 75-100 mg of caffeine;
- A 6-oz cup of coffee from a coffeehouse can be as high as 150 mg (although no more than 25 mg caffeine per oz);
- A 12-oz can of soda contains about 35-50 mg of caffeine;
- The caffeine in energy drinks can be as high as 500 mg per serving; and
- So-called energy shots contain 100-350 mg/oz of caffeine.
Excess caffeine, especially from energy drinks, can have the following effects: anxiety, nervousness, sleep problems, elevated blood pressure, and heart palpitations.
Caffeine Plus Alcohol: Wide-Awake Drunkenness
There is a trend among college students and some adults of mixing energy drinks with alcohol in order to drink more and drink longer. The consequences can be dangerous and deadly. Caffeine does not counteract alcohol. The high caffeine content stimulant effect can prevent a person from becoming sleepy and experiencing drunkenness, but it does not prevent impairment, including in judgment, reaction time, and motor skills. The general report calls this "wide awake drunkenness," and it can lead to bad choices, risky behaviors, and worse.
The FDA Response
In 2006, 4 billion dollars worth of energy drinks were sold in the United States alone. Fortunately, on November 17, 2010, the US Food and Drug Administration (FDA) sent warning letters to 4 companies that caffeine added to malt alcohols is an unsafe food additive.[2] The companies included the following:
- Charge Beverages Corporations (maker of Core High Gravity);
- New Century Brewing Company (maker of Moonshot);
- Fusion Products (maker of 4Loko); and
- United Brands Company (maker of Joose and Max).
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