Archive for October, 2012

Lethal Monster Drinks? More Tricks than Treats

Wednesday, October 31, 2012 // Uncategorized

I have read drinkd. several articles about the cardiovascular effects of energy drinks which are high in caffeine.  The short version is that the effects may be toxic.  My best friend was “hooked” on energy drinks.  He died of an intracerebral hemorrhage.   Here is the latest calling their safety into question.  The following is a summary from Journal Watch.  The New York Times article follows.   Another problem is that young people use them as mixers with alcohol combining an” uppers: and “downers” in a potentially lethal poor man’s “speedball”.

FDA Investigating 5 Deaths Linked to Monster Energy Drink

The FDA has received reports of five people who died after consuming Monster Energy — a high-caffeine energy drink — in the past 3 years, the New York Times reports.

Other adverse events reported to the agency include one nonfatal MI, abdominal pain, vomiting, tremors, and abnormal heart rate. It is unclear whether patients who experienced adverse events also took alcohol or drugs.

In a statement, an FDA spokesperson said that it is the manufacturer’s responsibility to investigate adverse events associated with the beverage, according to the Times. She added that the FDA had not yet established a causal link between the energy drink and the deaths.

A 24-oz. can of Monster Energy contains 240 mg of caffeine, roughly equivalent to two cups of brewed coffee.

Monster Energy Drink Cited in Deaths

By
Published: October 22, 2012
 

Five people may have died over the past three years after drinking Monster Energy, a popular energy drink that is high in caffeine, according to incident reports recently released by the Food and Drug Administration.

Marty Katz for The New York Times

Wendy Crossland of Hagerstown, Md., with a picture of her daughter, Anais Fournier, who died last year of cardiac arrest.

The reports, like similar filings with the F.D.A. in cases involving drugs or medical devices, do not prove a link between Monster Energy and the deaths or other health problems. The records were recently obtained under the Freedom of Information Act by the mother of a 14-year-old Maryland girl who died in December from a heart arrhythmia after drinking large cans of Monster Energy on two consecutive days.

Last week, Wendy Crossland, the mother of that teenager, filed a lawsuit against Monster Beverage, a publicly traded company in Corona, Calif., that used to be known as Hansen Natural. The lawsuit charges that Monster failed to warn about the risks of its energy drinks; a spokeswoman for the company said last week that its products were safe and not the cause of the teenager’s death.

That spokeswoman, Judy Lin Sfetcu, added that Monster was “unaware of any fatality anywhere that has been caused by its drinks.”

Monster Beverage’s stock ended down Monday more than 14 percent, sliding sharply after The New York Times reported about the F.D.A. filings.

In an interview, an F.D.A. spokeswoman, Shelly Burgess, said the agency had received reports of five deaths with possible links to the drink as well as a report of a nonfatal heart attack. Additional incident reports referred to other adverse events such as abdominal pain, vomiting, tremors and abnormal heart rate. The reports disclosed cover a period of 2004 to June of this year, but all the deaths occurred in 2009 or later.

The filings do not make clear whether the incidents involved other factors, like alcohol or drugs. However, the number of reports that the F.D.A. receives about any product it regulates usually understates by a large degree the actual number of problems.

The release of the filings about Monster Energy may increase Congressional calls for greater regulation of the energy products industry. Monster Energy is among scores of energy drinks like Red Bull and Rock Star, and energy “shots” like 5-hour Energy, that companies are aggressively marketing to teenagers and young people.

In a statement, Ms. Burgess, the F.D.A. spokeswoman, said that it was the responsibility of energy drink manufacturers to investigate accusations of death or injuries associated with them. She said that the agency was still looking into the cases but had yet to establish a causal link between the deaths and the drink.

But the release of the F.D.A. reports may also raise questions about how closely producers of energy products monitor their safety or whether the F.D.A. reviews those activities.

Late Monday, Ms. Sfetcu, the Monster Beverage spokesman, said that the company had not received copies of the F.D.A. incident filings about possible fatalities associated with its products apart from the one filed in connection with the December death of the Maryland teenager, Anais Fournier. She said she did not know whether the company actively monitored the F.D.A. database that collects reports about such incidents.

Monster Beverage makes a variety of energy drinks with names like Monster Rehab, Monster Assault and Monster Heavy Metal. Labels on the containers state that they are “not recommended” for some consumers, including children — a group that beverage producers define as those under 12 years — and people “sensitive” to caffeine.

Under current F.D.A. rules, companies are not required to disclose caffeine levels in their beverages and can choose to market them as drinks or as dietary supplements. Those regulatory categories have differing labeling and ingredient rules.

While healthy adults can safely consume large quantities of caffeine from sources like coffee, tea and energy drinks, the drug, which acts as a stimulant, can pose risks to those with underlying conditions like heart disorders.

The type of 24-ounce can of Monster Energy that the Maryland teenager, Anais Fournier, drank contains 240 milligrams of caffeine.

The lawsuit filed last week on behalf of the teenager referred to autopsy and medical examiner reports that said she had died of “cardiac arrhythmia due to caffeine toxicity” that had exacerbated an existing heart problem. The report also showed that the teenager had Ehlers-Danlos syndrome, which can affect the body’s connective tissue, including blood vessels. A lawyer for her family, Kevin Goldberg, said that the 14-year-old had been aware she had an underlying heart condition but added that her doctors had not told her to restrict her physical activities or her caffeine use.

In an April letter citing the teenager’s death, Senator Richard J. Durbin, Democrat of Illinois, urged the F.D.A. to enforce caffeine levels in energy drinks.

In August, F.D.A. officials responded by saying that there was insufficient evidence to take action on caffeine levels in energy drinks. However, the agency also noted then that it had not yet received medical reports related to the Maryland teenager’s death.

This article has been revised to reflect the following correction:

Correction: October 22, 2012

Because of an editing error, an earlier version of this article described Ehlers-Danlos syndrome incorrectly. It is a genetic disorder, not an autoimmune disease.

A version of this article appeared in print on October 23, 2012, on page B1 of the New York edition with the headline: F.D.A. Is Told of Deaths After Using Energy Drink.
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Do Multivitamins Prevent Cancer?

Sunday, October 28, 2012 // Uncategorized

Maybe, according to an industry sponsored trial. 

I quit taking a multivitamin years ago when the preponderance of evidence showed that there was no benefit.  You must understand.  Medical knowledge ebbs and flows throughout the years.  Opinions go back and forth until an issue is settled.  This may take years.

The following is a summary from Journal Watch followed by the article from JAMA.

Multivitamins May Confer a Small, but Significant, Cancer Risk Reduction in Men

 

Middle-aged and older men who take multivitamins have a modestly reduced risk for cancer, according to an industry-supported study in JAMA.

Nearly 15,000 male U.S. physicians aged 50 and older were randomized to a daily multivitamin or placebo and then followed for roughly 11 years. Multivitamin recipients had a small but significant reduction in total cancer diagnoses (17.0 vs. 18.3 cancers per 1000 person-years). There were, however, no reductions in site-specific cancers — including prostate cancer, the most frequently diagnosed.

 The authors conclude: “Although the main reason to take multivitamins is to prevent nutritional deficiency, these data provide support for the potential use of multivitamin supplements in the prevention of cancer in middle-aged and older men.”

 THERE WAS NO EFFECT ON MORTALITY.  I MAY WAIT AWHILE BEFORE STARTING BACK ON THAT MULTIVITAMIN.

Original Contribution | ONLINE FIRST
J. Michael Gaziano, MD, MPH; Howard D. Sesso, ScD, MPH; William G. Christen, ScD; Vadim Bubes, PhD; Joanne P. Smith, BA; Jean MacFadyen, BA; Miriam Schvartz, MD; JoAnn E. Manson, MD, DrPH; Robert J. Glynn, ScD; Julie E. Buring, ScD

Author Affiliations: Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts (Drs Gaziano, Sesso, Christen, Bubes, Schvartz, Manson, Glynn, and Buring and Mss Smith and MacFadyen); VA Boston Healthcare System, Boston, Massachusetts (Dr Gaziano); and Departments of Epidemiology (Drs Sesso, Manson, and Buring) and Biostatistics (Dr Glynn), Harvard School of Public Health, Boston, Massachusetts. Dr Gaziano is also Contributing Editor, JAMA.

ABSTRACT

 

Context  Multivitamin preparations are the most common dietary supplement, taken by at least one-third of all US adults. Observational studies have not provided evidence regarding associations of multivitamin use with total and site-specific cancer incidence or mortality.

Objective  To determine whether long-term multivitamin supplementation decreases the risk of total and site-specific cancer events among men.

Design, Setting, and Participants  A large-scale, randomized, double-blind, placebo-controlled trial (Physicians’ Health Study II) of 14 641 male US physicians initially aged 50 years or older (mean [SD] age, 64.3 [9.2] years), including 1312 men with a history of cancer at randomization, enrolled in a common multivitamin study that began in 1997 with treatment and follow-up through June 1, 2011.

Intervention  Daily multivitamin or placebo.

Main Outcome Measures  Total cancer (excluding nonmelanoma skin cancer), with prostate, colorectal, and other site-specific cancers among the secondary end points.

Results  During a median (interquartile range) follow-up of 11.2 (10.7-13.3) years, there were 2669 men with confirmed cancer, including 1373 cases of prostate cancer and 210 cases of colorectal cancer. Compared with placebo, men taking a daily multivitamin had a statistically significant reduction in the incidence of total cancer (multivitamin and placebo groups, 17.0 and 18.3 events, respectively, per 1000 person-years; hazard ratio [HR], 0.92; 95% CI, 0.86-0.998; P = .04). There was no significant effect of a daily multivitamin on prostate cancer (multivitamin and placebo groups, 9.1 and 9.2 events, respectively, per 1000 person-years; HR, 0.98; 95% CI, 0.88-1.09; P = .76), colorectal cancer (multivitamin and placebo groups, 1.2 and 1.4 events, respectively, per 1000 person-years; HR, 0.89; 95% CI, 0.68-1.17; P = .39), or other site-specific cancers. There was no significant difference in the risk of cancer mortality (multivitamin and placebo groups, 4.9 and 5.6 events, respectively, per 1000 person-years; HR, 0.88; 95% CI, 0.77-1.01; P = .07). Daily multivitamin use was associated with a reduction in total cancer among 1312 men with a baseline history of cancer (HR, 0.73; 95% CI, 0.56-0.96; P = .02), but this did not differ significantly from that among 13 329 men initially without cancer (HR, 0.94; 95% CI, 0.87-1.02; P = .15; P for interaction = .07).

Conclusion  In this large prevention trial of male physicians, daily multivitamin supplementation modestly but significantly reduced the risk of total cancer.

Trial Registration  clinicaltrials.gov Identifier: NCT00270647.

 

Multivitamins are the most common dietary supplement, regularly taken by at least one-third of US adults.1 – 2 The traditional role of a daily multivitamin is to prevent nutritional deficiency. The combination of essential vitamins and minerals contained in multivitamins may mirror healthier dietary patterns such as fruit and vegetable intake, which have been modestly and inversely associated with cancer risk in some,3 but not all,4 – 5 epidemiologic studies. Observational studies of long-term multivitamin use and cancer end points have been inconsistent.6 – 12 To date, large-scale randomized trials testing single or small numbers of higher-dose individual vitamins and minerals for cancer have generally found a lack of effect.13 – 18

 

According to the 2010 Dietary Guidelines for Americans, “For the general, healthy population, there is no evidence to support a recommendation for the use of multivitamin/mineral supplements in the primary prevention of chronic disease.”19 A National Institutes of Health–sponsored State-of-the-Science Conference also concluded that the present evidence is insufficient to recommend either for or against the use of [multivitamins] to prevent chronic disease.20 Despite the lack of definitive trial data regarding the benefits of multivitamins in the prevention of chronic disease, including cancer, many men and women take them for precisely this reason.21

 

Thus, definitive information on the potential benefits, risks, or lack thereof, related to taking a daily multivitamin may have substantial effects on personal and clinical decision making and policy making. The Physicians’ Health Study II (PHS II) represents the only large-scale, randomized, double-blind, placebo-controlled trial testing the long-term effects of a common multivitamin in the prevention of chronic disease. We present the findings for multivitamin use on total and other common site-specific cancers; the effects of a multivitamin on cardiovascular events, eye disease, and cognitive decline are being published separately.

METHODS

 

The PHS II was a randomized, double-blind, placebo-controlled, 2×2×2×2 factorial trial evaluating the balance of risks and benefits of a multivitamin (Centrum Silver or its placebo daily; Pfizer [formerly Wyeth, American Home Products, and Lederle]), vitamin E (400-IU synthetic α-tocopherol or its placebo on alternate days; BASF Corporation), vitamin C (500-mg synthetic ascorbic acid or its placebo daily; BASF Corporation), and beta carotene (50-mg Lurotin or placebo on alternate days; BASF Corporation) in the prevention of cancer, cardiovascular disease, eye disease, and cognitive function among 14 641 male physicians aged 50 years or older.22 The beta carotene component was terminated on schedule in March 2003. Treatment and follow-up of the vitamin E and vitamin C components continued through August 31, 2007, their scheduled end, with findings of no overall association reported for cancer18 and cardiovascular disease.23

 

The study design of PHS II has been previously described in detail.18 ,22 – 23 The recruitment, enrollment, and randomization of men into PHS II occurred in 2 phases (Figure 1). Beginning in July 1997, during phase 1, we invited 18 763 living participants from PHS I, a randomized trial of low-dose aspirin and beta carotene among 22 071 male physicians,14 ,24 to participate in PHS II. Men were ineligible if they reported a history of cirrhosis, active liver disease, were taking anticoagulants, or reported a serious illness that might preclude participation. Men also must have been willing to forego the use of multivitamins or individual supplements containing more than 100% of the recommended dietary allowance of vitamin E, vitamin C, beta carotene, or vitamin A. Those men with a history of cancer, as well as myocardial infarction or stroke, remained eligible to enroll into PHS II. We randomized 7641 willing participants (41%) from PHS I into PHS II and retained their original PHS I beta carotene treatment assignment.

 

 

 

Image not available.

 

Beginning in July 1999, during phase 2, invitational letters and baseline questionnaires were mailed to 254 597 US male physicians aged 50 years or older identified from a list provided by the American Medical Association. Through July 2001, 42 165 men responded, of whom 11 128 were willing and eligible. A 12-week placebo, run-in period excluded men who were nonadherent.25 Of 11 128 physicians who entered the run-in phase, 7000 (63%) willing and eligible men took at least two-thirds of their pills and were randomized into PHS II, resulting in a total of 14 641 participants.

 

Men were randomized in blocks of 16, stratified by age (in 5-year age groups), prior cancer, prior cardiovascular disease, and, for the 7641 participants in PHS I, their original beta carotene treatment assignment. There were 1312 men (9.0%) with a history of cancer (excluding nonmelanoma skin cancer) before randomization into PHS II through either confirmed events among PHS I participants or self-reports among new PHS II participants. All participants provided written informed consent and the institutional review board at Brigham and Women’s Hospital, Boston, Massachusetts, approved the PHS II research protocol.

 

Participants were sent monthly calendar packs containing a multivitamin or placebo (taken daily) every 6 months for the first year, then annually thereafter. We also sent participants annual questionnaires asking about adherence, adverse events, new end points, and risk factors. A National Death Index search was performed for any participants with unknown vital status. Blinded treatment and follow-up continued through June 1, 2011, the scheduled end of the multivitamin component of PHS II, for a median (interquartile range) follow-up of 11.2 (10.7-13.3) years. Data analyses included validated end points that occurred during randomized treatment and were reported by August 2012. Morbidity and mortality follow-up in PHS II were extremely high, at 98.2% and 99.9%, respectively. Furthermore, morbidity and mortality follow-up as a percentage of person-time each exceeded 99.9%, with only 2991 and 79 person-years of morbidity and mortality follow-up lost out of 164 320 person-years of follow-up through June 1, 2011.

 

For the multivitamin component, the primary end points were total cancer (excluding nonmelanoma skin cancer) and major cardiovascular events. Prespecified secondary cancer end points included prostate, colorectal, and other site-specific cancers. Epithelial cell cancer, total and cancer mortality, and cancer-specific death were other end points examined in the analysis. Epithelial cell cancer was limited to carcinomas, which included all cancers except for lymphoma and leukemia. Because prostate cancer comprised more than half of all confirmed cancers in PHS II most likely due to increases in screening for prostate-specific antigen levels and detection of less aggressive cancer, we also evaluated the end point of total minus prostate cancer.

 

All cancer and mortality end points were assessed and validated by medical record review by the PHS II Endpoints Committee composed of physicians blinded to treatment assignment; 96.9% of confirmed total cancers were based on pathology or cytology reports. Cases of cancer were otherwise confirmed based on strong clinical and radiological or laboratory marker evidence. Total mortality was confirmed by the PHS II Endpoints Committee or by obtaining a death certificate. Only confirmed cancer and mortality end points are included herein.

 

All primary analyses classified study participants based on the intention-to-treat principle, in which all 14 641 randomized participants were classified according to their randomized multivitamin treatment assignment and followed up until the occurrence of cancer, death, loss to follow-up, or the end of the multivitamin component of PHS II on June 1, 2011, whichever came first. We used SAS version 9.2 (SAS Institute Inc) and S-Plus (Insightful Corporation), with statistical significance set at P < .05 using 2-sided tests. The PHS II was estimated to have 80% power to detect a 10% reduction of the multivitamin on the primary end point of total cancer based on event rates among trial participants, with an average adherence of 75% during the entire treatment period and no interaction with other randomized components.

 

Initial analyses displayed distributions of baseline characteristics by multivitamin treatment assignment. Consistent with previous PHS II trial analyses,18 ,23 we used Cox proportional hazards regression models to estimate the hazard ratios (HRs) and 95% CIs comparing event rates in the multivitamin and placebo groups. For each prespecified end point, Cox proportional hazards regression models were stratified on the presence of cancer at randomization and adjusted for PHS II study design variables for age (in years), PHS cohort (original PHS I participant, new PHS II participant), and randomized vitamin E, vitamin C, and beta carotene assignments.

 

Only first cancer events after randomization were considered for analyses of total cancer, epithelial cell cancer, and total minus prostate cancer. For analyses of total cancer, all new cancers were included, regardless of whether the participant had a baseline history of cancer. For analyses of each site-specific cancer, we excluded participants if they had a baseline history of cancer of that site. Thus, these analyses included 13 980 men initially without prostate cancer, 14 519 initially without colorectal cancer, and 14 610 initially without lung cancer. Analyses of each site-specific cancer did not censor men on occurrence of cancer at another site. In addition, for analyses of site-specific cancer deaths, total cancer mortality, and total mortality, we included all 14 641 participants, and for total mortality, we additionally stratified on the presence of cardiovascular disease at randomization.

 

We tested the Cox proportional hazards regression assumptions by including an interaction term for treatment with the logarithm of time; this assumption was not violated for total cancer, prostate cancer, colorectal cancer, or other site-specific cancers (each P > .05). Cumulative incidence curves compared the overall effect of the multivitamin intervention on total and major site-specific cancers over time using a crude log-rank test. We then investigated whether multivitamin adherence affected our primary results through sensitivity analyses.

 

Additional exploratory analyses examined the effect of the multivitamin intervention on total cancer excluding the first 2 or 5 years of follow-up to explore a possible early vs late benefit associated with long-term multivitamin use. In addition, we conducted subgroup analyses stratified by major cancer risk factors, parental history of cancer, selected dietary factors, and other PHS II interventions. We also evaluated treatment effects within the prespecified subgroups of 1312 men with and 13 329 men without a baseline history of cancer. Effect modification was assessed by using interaction terms between subgroup indicators and multivitamin assignment.

RESULTS

 

A total of 14 641 male physicians were randomized with a mean (SD) age of 64.3 (9.2) years. All baseline characteristics had comparable distributions between the multivitamin and placebo groups (Table 1). Participants had a mean (SD) body mass index (BMI, calculated as weight in kilograms divided by height in meters squared) of 26.0 (3.6), with a large proportion of former smokers (40.0%) and a very low proportion of current smokers (3.6%). Current aspirin use at baseline was high (77.4%) in this population of physicians, in part reflective of their previous participation and results of the PHS I randomized trial testing aspirin and cardiovascular disease.24 There were 1312 men (9.0%) with a baseline history of cancer and 754 men (5.1%) with a baseline history of cardiovascular disease.

COMMENT

 

In this large-scale, randomized, placebo-controlled trial among middle-aged and older men, long-term daily multivitamin use had a modest but statistically significant reduction in the primary end point of total cancer after more than a decade of treatment and follow-up. We found no evidence that this effect was driven by any individual site-specific cancers. In prespecified analyses, we found that the effect of a daily multivitamin in reducing cancer appeared stronger among men for secondary vs primary prevention of cancer in PHS II, although this difference was not significant for total cancer but was for total epithelial cell cancer. Approximately half of those men with baseline cancer in PHS II were last diagnosed 5 years or more ago, and we found no suggestion that more remote vs proximate diagnoses affected cancer risk.

 

Total cancer rates in our trial were likely influenced by the increased surveillance for prostate-specific antigen and subsequent diagnoses of prostate cancer during PHS II follow-up starting in the late 1990s.26 Approximately half of all confirmed cancers in PHS II were prostate cancer, of which the majority were earlier stage, lower-grade prostate cancer with high survival rates. The significant reduction in total cancer minus prostate cancer suggests that daily multivitamin use may have a greater benefit on more clinically relevant cancer diagnoses.

 

In the Cancer Prevention Study II, which followed up more than 1 million US adults beginning in the early 1980s, multivitamin use was not associated with cancer mortality.27 The Women’s Health Initiative found that multivitamins had little or no relationship with the risk of breast, colon, or other cancers in more than 160 000 women followed up for a mean of 8 years.9 Among 35 000 Swedish women, however, multivitamin use was associated with a 19% increased risk of breast cancer (95% CI, 1.04-1.37) during a 10-year period compared with women not using these vitamins.8 How these results for breast and other cancers in women extend to our trial of men in PHS II remains unclear.

 

Other observational studies suggest protective relationships of multivitamins with various cancers,28 – 29 no association,30 – 31 and possible harm.32 Studies with an association between multivitamins and specific cancers are typically of long duration, allowing for either a long latent period11 – 12 ,33 – 34 or increased statistical power. For example, increasing duration of multivitamin use was strongly associated with a reduced risk of colon cancer in 88 756 participants in the Nurses’ Health Study followed up for 15 years.12 A long latency period was also noted in the Cancer Prevention Study II, with an inverse association between multivitamin use with both colon cancer incidence34 and mortality11 after more than a decade of multivitamin use; however, these findings were not supported in PHS II.

 

Only a few large-scale, long-term chemoprevention trials have considered combinations of selected vitamins or minerals, although not with the typical diversity of common multivitamin formulations with recommended dietary allowance levels of vitamins and minerals such as that tested in PHS II. The Linxian Chinese Cancer Prevention Trial,35 targeting 29 584 adults with low baseline nutrient status, tested a combination of beta carotene, vitamin E, and selenium for 6 years and found significant reductions of 9% in total mortality, 13% in cancer mortality, and 21% in gastric cancer mortality. After 10 years of posttrial follow-up, the beneficial effects on total and cancer mortality remained.36 The Heart Protection Study37 tested higher doses of those 3 nutrients among individuals with adequate dietary intake and found no reductions in total or site-specific cancers. A meta-analysis38 of 8 large randomized trials of folic acid and vitamin B supplementation found no effect on total cancer. In addition, the Supplementation en Vitamines et Mineraux Antioxydants (SU.VI.MAX) primary prevention trial39 of 13 017 participants randomized to a low-dose combination of vitamin C, vitamin E, beta carotene, selenium, and zinc found no overall effect on total cancer, but there was a significant interaction with sex with a reduction in risk of total cancer in women only (relative risk, 0.69; 95% CI, 0.53-0.91).

 

Although numerous individual vitamins and minerals contained in the PHS II multivitamin study have postulated chemopreventive roles, it is difficult to definitively identify any single mechanism of effect through which individual or multiple components of our tested multivitamin may have reduced cancer risk. The reduction in total cancer risk in PHS II argues that the broader combination of low-dose vitamins and minerals contained in the PHS II multivitamin (eTable 2), rather than an emphasis on previously tested high-dose vitamins and mineral trials, may be paramount for cancer prevention. For example, in the Women’s Health Initiative calcium and vitamin D trial, women not taking personal supplements randomized to vitamin D (400 IU/d) and calcium (1000 mg/d) had a reduction in total cancer similar to that observed in PHS II.40 The role of a food-focused cancer prevention strategy such as targeted fruit and vegetable intake remains promising41 but unproven given the inconsistent epidemiologic evidence42 and lack of definitive trial data.

 

One explanation for results of some previous trials of supplements has been that the trial populations are already well-nourished.43 This may also be particularly true in PHS II, composed of male physicians, although population-based clinical trials also recruit healthier individuals.44 – 46 Participants in PHS II represent on average a well-nourished population for whom the effect of a daily multivitamin on cancer outcomes may be less applicable to those of poorer nutritional status. Additional studies need to evaluate how the range of baseline nutritional status modifies the effect of a daily multivitamin on cancer.

 

Strengths of PHS II include the long duration of treatment and follow-up and consistently good adherence to taking a daily multivitamin. The inclusion of physician participants provided high-quality reporting of health information. We are unaware of other long-term clinical trials testing a common multivitamin in the prevention of cancer and chronic disease. We selected a commonly used multivitamin formulation, Centrum Silver, at the time we initiated PHS II in 1997 to increase the potential generalizability of our findings.

 

Several limitations should also be considered. The formulations of the multivitamin preparation used in our trial and other multivitamin preparations have changed over time, reflecting evolving perspectives and priorities in nutrition. For example, since PHS II was initiated, in the commercial form of this multivitamin, vitamin D increased from 400 to 500 IU, vitamin A (% as beta carotene) decreased from 5000 IU (50%) to 2500 IU (40%), and 250 μg of lutein and 300 μg of lycopene were added. However, the formulation of the multivitamin used throughout PHS II (eTable 2) remained the same, resulting in a consistent intervention in our trial. An improved understanding of the effects of single vs combined nutrients—at usual levels of dietary intake—on intermediate mechanisms leading to cancer is critically needed.

 

It is unclear how easily our trial results for cancer outcomes may be replicated given the high prevalence of multivitamin use in adults and difficulty of conducting a long-term, blinded clinical trial. This is especially important given the potential challenge of generalizing to younger men and women and racial and ethnic groups not included in PHS II. It remains possible that more effective chemoprevention via multivitamins may occur with longer treatment or follow-up than conducted to date in PHS II, given the apparent latent results on colon cancer and mortality in some cohorts.11 – 12 ,34 This is particularly salient in our analyses of site-specific cancers, for which continued PHS II follow-up would increase statistical power and detect any emergent latent effects. Adherence remains of concern as in any long-term trial, but adherence with the multivitamin component of PHS II remained consistently good during a mean follow-up of 11 years. Drop-in rates of outside multivitamin use did increase during follow-up, paralleling general population trends of increased vitamin supplement use in the United States,2 ,47 but there were no differences in rates in active vs placebo multivitamin groups and analyses accounting for adherence did not greatly affect the HRs of total and site-specific cancers.

 

As in any trial, the role of chance must be considered. This is particularly important when multiple hypotheses are being addressed. In PHS II, we had only 2 primary outcomes—total cancer and major cardiovascular events. However, there are additional secondary outcomes that include eye disease, cognitive function, and a number of prespecified secondary analyses. Caution must be applied in the interpretation of these analyses.

 

In this large-scale randomized trial of 14 641 middle-aged and older men, a daily multivitamin supplement significantly but modestly reduced the risk of total cancer during a mean of 11 years of treatment and follow-up. Although the main reason to take multivitamins is to prevent nutritional deficiency, these data provide support for the potential use of multivitamin supplements in the prevention of cancer in middle-aged and older men.

AUTHOR INFORMATION

 

Corresponding Author: J. Michael Gaziano, MD, MPH, Department of Medicine, Brigham and Women’s Hospital, 1620 Tremont St, Boston, MA 02120 ([email protected]).

Published Online: October 17, 2012. doi:10.1001/jama.2012.14641

Author Contributions: Drs Gaziano and Sesso had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analyses. Drs Gaziano and Sesso contributed equally to this manuscript.

Study concept and design: Gaziano, Sesso, Christen, Manson, Glynn, Buring.

Acquisition of data: Gaziano, Sesso, Christen, Bubes, Smith, MacFadyen, Schvartz, Manson, Glynn, Buring.

Analysis and interpretation of data: Gaziano, Sesso, Christen, Bubes, Manson, Glynn, Buring.

Drafting of the manuscript: Gaziano, Sesso.

Critical revision of the manuscript for important intellectual content: Gaziano, Sesso, Christen, Bubes, Smith, MacFadyen, Schvartz, Manson, Glynn, Buring.

Statistical analysis: Gaziano, Sesso, Bubes, Glynn.

Obtained funding: Gaziano, Sesso, Buring.

Administrative, technical, or material support: Gaziano, Sesso, Bubes, Smith, MacFadyen, Schvartz, Manson, Glynn.

Study supervision: Gaziano, Sesso, Bubes, Smith, MacFadyen, Glynn.

Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Gaziano reported receiving investigator-initiated research funding from the National Institutes of Health (NIH), the Veterans Administration, and the BASF Corporation; assistance with study agents and packaging from BASF Corporation and Pfizer (formerly Wyeth, American Home Products, and Lederle); and assistance with study packaging provided by DSM Nutritional Products Inc (formerly Roche Vitamins). Dr Sesso reported receiving investigator-initiated research funding from the NIH, the Tomato Products Wellness Council, and Cambridge Theranostics Ltd. Dr Christen reported receiving research funding support from the NIH, Harvard University (Clinical Nutrition Research Center), and DSM Nutritional Products Inc (formerly Roche Vitamins). Dr Manson reported receiving investigator-initiated research funding from the NIH, and assistance with study pills and packaging from BASF and Cognis Corporations for the Women’s Antioxidant and Folic Acid Cardiovascular Study and from Pronova BioPharma and Pharmavite for the VIT amin D and Omeg A-3 Tria L, and funding from the nonprofit Aurora Foundation. Dr Glynn reported receiving investigator-initiated research funding from the NIH, Bristol-Meyers Squibb, AstraZeneca, and Novartis; and signed a consulting agreement with Merck to give an invited talk. Dr Buring reported receiving investigator-initiated research funding from the NIH, and assistance with study pills and packaging from Natural Source Vitamin E Association and Bayer Healthcare for the Women’s Health Study. No other authors reported any financial disclosures.

Funding/Support: This work was supported by grants CA 097193, CA 34944, CA 40360, HL 26490, and HL 34595 from the NIH and an investigator-initiated grant from BASF Corporation. Study agents and packaging were provided by BASF Corporation and Pfizer (formerly Wyeth, American Home Products, and Lederle) and study packaging was provided by DSM Nutritional Products Inc (formerly Roche Vitamins).

Role of the Sponsors: The NIH, BASF Corporation, Pfizer, and DSM Nutritional Products Inc had no role in the study design and conduct of the study; in the collection, management, analysis, and interpretation of the data; or in the preparation, review, or approval of the manuscript.

Data and Safety Monitoring Board: Voting members over the course of the PHS II trial included Lawrence Cohen, Rory Collins, Theodore Colton, I. Craig Henderson, Andrea LaCroix, Ross Prentice, and Nanette Wenger (chair); ex-officio members included Mary Francis Cotch, Jeffrey Cutler, Frederick Ferris, Jerome Fleg, Peter Greenwald, Natalie Kurinij, Howard Parnes, Marjorie Perloff, Eleanor Schron, and Alan Zonderman.

Disclaimer: Dr Gaziano, a contributing editor for JAMA, was not involved in the editorial review of or decision to publish this article.

Additional Contributions: We thank the 14 641 physician participants for their long-standing dedication and conscientious collaboration. We also thank Charles Hennekens, MD, DrPH (Florida Atlantic University), for the long-term contributions to the PHS, and the exemplary contributions of the staff of the PHS at Brigham and Women’s Hospital, under the leadership of Joanne Smith: Charlene Belanger, Eileen Bowes, Kenneth Breen, Mary Breen, Mary G. Breen, Jose Carrion, Shamikhah Curry, Colleen Evans, Ivan Fitchorov, Natalya Gomelskaya, Cindy Guo, Delia Guo, Jasmah Hanna, Beth Holman, Andrea Hrbek, Gregory Kotler, Tony Laurinaitis, Hannah Mandel, Chandra McCarthy, Geneva McNair, Annie Murray, Leslie Power, Philomena Quinn, Harriet Samuelson, Fred Schwerin, Andromache Sheehey, Sara Tower, Martin Van Denburgh, Diana Walrond, Phyllis Johnson Wojciechowski, and Angela Zhang. In addition, we thank the PHS Endpoints Committee, including Samuel Goldhaber, Carlos Kase, Meir Stampfer, and James Taylor, over the course of PHS II. Each named individual was compensated for his or her contribution as part of the grant support.

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New SARS Like Virus Discovered Before It Causes An Outbreak

Sunday, October 21, 2012 // Uncategorized

Here is a fascinating behind the scene look at the discovery of a novel corona virus, the same family of viruses that caused SARS a few years ago, before it caused an outbreak.  It gives an insight into the networks of scientists that study infectious diseases and how they communicate.

From ProMed Digest:

Date: Sun, 21 Oct 2012 20:45:49 -0400 (EDT)
From: ProMED-mail <[email protected]>
Subject: PRO/AH/EDR> Novel coronavirus – Saudi Arabia (13): history, collateral damage

NOVEL CORONAVIRUS – SAUDI ARABIA (13): HISTORY, COLLATERAL DAMAGE
*****************************************************************
A ProMED-mail post
<http://www.promedmail.org>
ProMED-mail is a program of the
International Society for Infectious Diseases
<http://www.isid.org>

Date: 21 Oct 2012
Source: Toronto Star [edited]
<http://www.thestar.com/news/gta/crime/article/1274934–new-sars-like-virus-discovered-before-it-causes-outbreak>

Four months ago, a mucus sample arrived in Dr. Ali Mohamed Zaki’s
laboratory in Saudi Arabia. The mucus had been coughed up by a
60-year-old Saudi Arabian man with a strange case of pneumonia. He had
been admitted to the Dr. Soliman Fakeeh hospital in Jeddah on [13 Jun
2012]; soon after, his kidneys began to fail. Eleven days after being
hospitalized, the man was dead.

When the patient was admitted, Zaki was working in the hospital’s
virology lab, which he helped establish in 1994. He was sent samples
of the patient’s sputum, mucus coughed up from his lungs.

Eventually, this spot of sputum would lead Zaki to the discovery of a
virus never before seen in humans: a novel coronavirus, the same type
of virus behind the SARS outbreak in 2003 that swept across 30
countries and killed approximately 800 people, including 44
Torontonians.

Zaki’s discovery — and his decision to post it online — touched off
a chain of events that quickly unearthed a 2nd patient in another
country and enabled the global health community to gain an upper hand
in the face of a potentially deadly new virus.

Scientists have now learned the virus’s genetic code, discovered its
likely link to bats, and equipped labs around the world with the means
to diagnose it. Virologist buddies from the “old SARS club” have
reunited, collaborating once again across borders, and teams of
experts have been deployed to the Middle East to aggressively
investigate the virus and its origins.

And the World Health Organization currently feels reassured enough to
give its blessing for travel to Saudi Arabia, where millions of
pilgrims are descending this week for the hajj, one of the world’s
largest mass gatherings.

For Zaki, his discovery was fortunate, “a favour for the globe.” Yet,
as of last week, it seems to have cost him his job.

But on [13 Jun 2012], Zaki was still faced with that basic medical
question: What mysterious thing was making this patient so sick?

Zaki 1st ran a battery of tests on the sputum and blood samples.
Initially, he looked for influenza, the usual suspect in a respiratory
ailment. All initial results came back negative.

Zaki decided to culture the samples to see what grew. In late June
[2012], viruses began replicating in the sputum culture, but by this
point, the patient was already dead.

Yet Zaki continued his sleuthing. He had a sense that this was
something bigger than just one patient. So Zaki turned his mind to the
possibility of a paramyxovirus, a class of virus responsible for some
acute respiratory diseases. It was a path that took him to Dr. Ron
Fouchier, a professor of molecular virology at the Erasmus Medical
Centre in the Netherlands.

Zaki has never met Fouchier but knew his reputation as one of the
world’s leading influenza researchers. He also knew Fouchier had
recently developed a test for paramyxoviruses and called him.

Fouchier listened to Zaki and could not help thinking about SARS; the
clinical picture just sounded so similar. Had Zaki tested for
coronaviruses yet?

This was certainly going to be Zaki’s next step. He mailed the virus
to Fouchier in Rotterdam. While he waited for a response, Zaki tested
his virus sample to identify whether it was in the coronavirus family.
It was.

Coronaviruses can infect many animals and humans and are named for
their distinctive crown-like appearance under a microscope. Before
2003, there were only 2 coronaviruses known to infect humans, and both
were associated with the common cold. The discovery of SARS 9 years
ago [2003] changed everything and opened the world’s eyes to the
coronavirus’s deadly potential and the ominous possibility that new
strains were lurking undiscovered.

Zaki did not have the equipment to sequence the genome, in other
words, to determine its genetic code and identify it specifically. But
Fouchier did.

In 2003, Fouchier had played a major role in identifying the SARS
genetic sequence, a process that took 3 or 4 weeks. Sequencing the
virus’s genome allows scientists to perform their life-saving work —
developing antivirals, vaccines and diagnostic tests — more easily
and quickly.

This time, with advanced technologies and resources, it only took
Fouchier a few days to sequence Zaki’s virus. He found it was closely
related to a coronavirus found in bats, the same animal from which
SARS is believed to have sprung. But this was not the SARS
coronavirus.

“It was a new kind,” Zaki said, admitting that at this point he began
to worry about his own exposure to the virus. “I became afraid it
could (spread) like SARS, and I listed it on ProMED-mail.”

ProMED-mail is an infectious disease reporting website that had been
used during the SARS outbreak. Designed to quickly disseminate
information, every message is vetted by a panel of experts before
being posted online and sent to more than 60 000 subscribers
worldwide.

Zaki’s email, which described his and Fouchier’s findings in 3 short
paragraphs, went online on [20 Sep 2012].

“NOVEL CORONAVIRUS — SAUDI ARABIA,” the summary read in capital
letters. “HUMAN ISOLATE.”

Zaki’s inbox was immediately flooded. Some congratulated him on his
discovery but most were anxious queries.

“The coronavirus is really not like any other virus,” said Dr.
Christian Drosten, who runs the virology department at the University
of Bonn in Germany. “This is not a thing that you see every day,
popping up new. If it’s a new coronavirus that has never been seen
before in humans, that is ringing the bell.”

The ringing of this bell was heard in every corner of the globe. Most
importantly, it reached a north London lab in England, where doctors
and scientists were scratching their heads over a puzzling case.

On [12 Sep 2012], 8 days before Zaki’s email went live on ProMED-mail,
a 49-year-old Qatari man with “atypical pneumonia” was airlifted to a
London hospital. The patient had fallen sick in Qatar but had visited
Saudi Arabia in August [2012].

Within days, the United Kingdom’s public health organization, the
Health Protection Agency (HPA), was notified of the case.

Initially, as had Zaki, they figured this could be influenza. The HPA
began conducting tests on [20 Sep 2012], the same day Zaki’s
ProMED-mail email went online.

That same night, 2 HPA employees working on this case — a clinician
and a scientist — independently noticed Zaki’s post. “They both had a
sort of light-bulb moment,” said Maria Zambon, the HPA’s director of
reference microbiology. “Should we test for this new virus?” The next
day, Friday [21 Sep 2012], the HPA clinicians tested for
coronaviruses. The test was positive. But they needed to figure out
which coronavirus. The team quickly began sequencing a tiny snippet of
the virus’s RNA, working through the night.

Early Saturday morning [22 Sep 2012], Zambon decided to contact Dr.
Albert Osterhaus, a long-time colleague with whom she had worked
during the SARS outbreak. Osterhaus is a flu expert and one of the
world’s leading virologists, but that is not why Zambon contacted him
exactly. Osterhaus works at the same Rotterdam laboratory as Fouchier,
the doctor contacted by Zaki who now had a sample of the new
coronavirus. Zambon emailed Osterhaus and asked him to call her. About
20 minutes later, her phone rang. “So, that tells you 2 things. One,
that he reads his emails at 7 o’clock in the morning,” Zambon said,
chuckling. “And secondly, that he takes messages from me quite
seriously.”

Osterhaus hung up the phone with Zambon and called Fouchier, who was
actually in Canada at the time, attending a flu conference in Bromont,
Quebec, with post-doctoral students. “That is the moment where you’re
really shocked,” Fouchier said. “Once you hear about a 2nd case you
think, ‘Whoa. We’re not going to get another SARS.'”

By 2 p.m. London time, Zambon’s team had a genetic sequence for the
virus from the Qatari patient. It was indeed a new coronavirus. But
was it the same that had sickened the Saudi patient? She sent the
sequence to Fouchier.

As Fouchier’s post-doctoral students spoke at the conference, he
hovered over his laptop at the back of his room, analyzing the 2
viruses. He remembers a crowd gathering around him as the sequences
began to align.

“We were with quite a lot of people in Canada. They were all sitting
very excited up on my table as we were analyzing the sequences,” he
recalled.

At about 4 p.m. London time, Fouchier reported his result: a 99.5 per
cent match. It was the same virus. And with that revelation, the
situation took on a new level of urgency. “There was this kind of
concern that you may be looking at the tip of an iceberg,” Zambon
said.

That night, Zambon had a meeting with the HPA’s incident control team.
Fouchier also participated via teleconference, calling from a bus
taking him to the Montreal airport, where he caught his flight back to
Rotterdam.

The HPA declared a Level 3 incident, indicating a public health event
with potential national impact, and the news began to make its way
around the world (the HPA has 5 levels of alert for public health
threats, with 5 being the most serious). The World Health Organization
was also notified.

“At that point, the machinery started,” said Dr. Maurizio Barbeschi,
with the WHO’s global capacity, alert and response department.

One of the cogs in the machine was Drosten, the energetic 40-year-old
University of Bonn virologist. Drosten had shot to international
recognition in 2003 when he worked furiously (and mostly without
sleep) to develop the 1st diagnostic test for SARS just 11 days after
the WHO had issued a global alert, thus beating several other
high-performance labs racing toward the same goal.

Drosten, by this point, was well aware of the new coronavirus; about a
week before Zambon was emailing Osterhaus about the Qatari patient,
Fouchier and Drosten were discussing the virus from the Saudi.

Fouchier knew that Drosten, a friend and colleague, had done a lot of
work with bat coronaviruses. They are also both members of EMPERIE, a
European Commission-funded project coordinated by Osterhaus and
created post-SARS to establish a network of experts and medical labs
capable of mobilizing quickly in the face of a new virus.

The new coronavirus was reuniting scientists who were in the trenches
together during SARS. “This is the old SARS club,” Drosten commented
to Nature earlier this month [October 2012].

Two days after the 2nd confirmed case was announced, Fouchier sent
Drosten the virus so he could begin developing a diagnostic test. If
this virus were to spread, labs around the world would need tools for
diagnosing it.

Drosten’s capacity has also been hugely improved since SARS. In 2003,
it took him about 5 days to develop a diagnostic test; this time, it
took just over 2.

Drosten actually developed 3 diagnostic tests and shipped them to
Zambon, who tested them on the Qatari patient to confirm which ones
worked (2 did, one failed).

On [27 Sep 2012], the team published a paper — a detailed description
of how they developed a diagnostic test for identifying the new
coronavirus — in Eurosurveillance, a scientific journal that
emphasizes the rapid publication of papers on ongoing outbreaks.

“We sent the paper in the morning. I wrote it overnight, and it was
reviewed during the day by 2 proper reviewers, and it was out at
midnight,” Drosten said. “We published a complete scientific paper —
I think about 2800 words or something — showing all of this
validation data.”

For Zambon, she believes this “must be a world record” of some sort
(she notes, however, that the team barely slept that week). “That’s
e-publishing,” Drosten said. “This speeds up everything.”

In their paper, the team included information on how laboratories can
order materials for diagnosing the virus. Shipments have now been made
to approximately 150 labs around the world, according to Drosten.

On [4 Oct 2012], exactly 2 weeks after Zaki’s ProMED-mail post, public
health officials in the United Kingdom had tracked down 64 people who
had come into contact with the Qatari patient. Their finding likely
unleashed sighs of relief: nobody had developed serious symptoms.

The novel coronavirus, it would seem, is not easily transmitted
between humans. There have been multiple reports of suspected new
cases in recent weeks, everywhere from Hong Kong to Denmark, but none
has ultimately tested positive for the novel coronavirus. As for the
Qatari patient, he is still alive.

Investigations continue at a furious pace, both in laboratories and on
the ground in Qatar and Saudi Arabia, where international experts have
descended in recent weeks. They are searching for more signs of the
virus, both in humans (have other people been exposed?) and the

environment (could bats have passed the virus to other animals who are
now transmitting it to humans?). Fouchier and Osterhaus are also
working to prove the novel coronavirus ultimately killed the Saudi
Arabian victim, who also had bacterial infections that could have
caused the respiratory disease.

For Drosten, the discovery of this new coronavirus reinforces that
mysterious viruses lurk undetected in animal reservoirs, waiting to
spill over into human populations.

“You don’t hear about them for years, and then suddenly they pop up,”
Drosten said. “Chances are, there’s close human-animal contact, and
there’s been a jump.”

As for Zaki, he will also continue work on the novel coronavirus. But
not in Saudi Arabia.

This is not the 1st time Zaki had discovered a new virus in Saudi
Arabia, and, in 1994, he was the 1st scientist to isolate dengue fever
in the country. He found another virus, a tick-borne virus that killed
2 young butchers, in 1995.

But this time around, Zaki said his discovery has made the Saudi
Arabian ministry of health “very angry.”

“They were very aggressive with me. They sent a team to investigate
me,” he said. “And now they force the hospital administration to force
me to resign.”

A spokesperson for the hospital, however, said in an email that Dr.
Zaki is still employed there. She did not respond to follow-up
questions seeking clarification.

Zaki is back in his homeland, Egypt. He said he will now help the
Egyptian government test sick people returning from the hajj, the
annual Islamic pilgrimage to the holy city of Mecca in Saudi Arabia,
which begins Thursday [25 Oct 2012].

The hajj attracts millions of pilgrims every year. In other words,
Mecca will soon become the perfect breeding ground for a virus looking
to cause maximum damage. But so far, this virus is not easily
transmitted, and the WHO has not recommended any travel restrictions
to Saudi Arabia. But rest assured, they will be monitoring the
situation closely.

With this new coronavirus, the world has been much more prepared than
in 2003. But sheer luck has also been on our side.

With SARS, it was the outbreak that came 1st. The virus was only
discovered later. “Now, it’s really the reverse situation,” Drosten
said. “We already have the virus, and we’re waiting for an epidemic to
show up or not show up. It’s a much better scenario.”

[Byline: Jennifer Yang]

– —
Communicated by:
ProMED-mail from HealthMap alerts
<[email protected]>

[The above newswire presents a very interesting “behind the scenes”
account of events to date related to the identification of a novel
coronavirus identified in a fatal severe respiratory disease with
renal failure patient in Saudi Arabia, and a similar clinical syndrome
in a patient with probable exposure in Qatar, presently hospitalized
in the United Kingdom for intensive therapy.

If the information given in the above article is valid, that the
identifying scientist has had negative professional consequences as a
result of releasing this information to the scientific community
through a post on ProMED-mail, it is an unfortunate situation. As a
result of the dissemination of information through ProMED-mail, a 2nd
case was identified. This led to the activation of an international
public health alert and response network, and investigations are
underway to identify the extent of possible background infection rates
with this novel coronavirus in the region. Given the upcoming mass
gathering that will involve approximately 2-3 million people from all
over the world, the possibility of an outbreak of disease caused by a
novel coronavirus is a serious concern. The need for the international
community to be aware of this novel coronavirus — on a laboratory,
epidemiologic, and clinical level — is obvious, and not reporting on
this could potentially have led to a repeat of 2003’s experience with
SARS. – Mod.MPP

A HealthMap/ProMED-mail map can be accessed at:
<http://healthmap.org/r/1HAJ>.]

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Women’s Health

Tuesday, October 9, 2012 // Uncategorized

Here are a couple of recent articles on women’s health.  The first is from the New England Journal of Medicine and summarizes the cuts to family planning in Texas,  The second is reported by WebMD.  It has to do with an article in the journal Obstetrics and Gynecology to which I do not subscribe.  It relates the decline in abortion rate to access to contraception.

Perspective

Cutting Family Planning in Texas

Kari White, Ph.D., Daniel Grossman, M.D., Kristine Hopkins, Ph.D., and Joseph E. Potter, Ph.D.

N Engl J Med 2012; 367:1179-1181September 27, 2012DOI: 10.1056/NEJMp1207920

Article

 

Four fundamental principles drive public funding for family planning. First, unintended pregnancy is associated with negative health consequences, including reduced use of prenatal care, lower breast-feeding rates, and poor maternal and neonatal outcomes.1,2 Second, governments realize substantial cost savings by investing in family planning, which reduces the rate of unintended pregnancies and the costs of prenatal, delivery, postpartum, and infant care.3 Third, all Americans have the right to choose the timing and number of their children. And fourth, family planning enables women to attain their educational and career goals and families to provide for their children. These principles led to the bipartisan passage of Title X in 1970 and later to other federal- and state-funded programs supporting family planning services for low-income women.

Despite the demonstrated positive effects of these programs, political support and funding for them have begun to erode. Recently, efforts to expand access to contraception through the Affordable Care Act ignited a broad debate regarding the proper role of government in this sphere, and proposals have been put forth to eliminate Title X.

Several states have already taken substantial steps to reduce public funding for family planning and other reproductive health services. In 2011, Texas enacted the most radical legislation to date, cutting funding for family planning services by two thirds — from $111 million to $37.9 million for the 2-year period. The remaining funds were allocated through a three-tiered priority system, with organizations that provide comprehensive primary care taking precedence over those providing only family planning services (see pie chartsEffects on Clinics in Texas of Cuts in Family Planning Funding.). The Texas legislature also imposed new restrictions on abortion care and reauthorized the exclusion of organizations affiliated with abortion providers from participation in the state Medicaid waiver program, the Women’s Health Program (WHP), which was due for renewal in January 2012. Although the exclusion had not previously been enforced by the state Health and Human Services Commission, it runs contrary to federal policy, and the renewal of the WHP was declined by the Centers for Medicare and Medicaid Services. In 2010, the WHP provided services to nearly 106,000 women 18 years of age or older with incomes below 185% of the federal poverty level who had been legal residents of Texas for at least 5 years. Almost half of these women were served at Planned Parenthood clinics.

To implement the legislation and funding cuts, the Texas Department of State Health Services reduced the number of funded family planning organizations from 76 to 41. Some of the largest organizations that continue to receive funding lost up to 75% of their budgets. The WHP remains in place as of mid-September 2012, because Planned Parenthood providers obtained a preliminary injunction order on April 30, 2012, against enforcement of the rule banning abortion provider affiliates. The U.S. Court of Appeals for the Fifth Circuit held that the order should be vacated, but it remains in effect pending the ruling on a petition for rehearing.

Texas has a very high teen birth rate, many undocumented migrants, and the second-largest number of Medicaid births (after California). For demographically and socioeconomically similar states, Texas’s experience may be a harbinger of the broader impact of eliminating public funding for family planning.

As part of a comprehensive 3-year evaluation of the legislative changes to family planning policy in Texas, we have interviewed 56 leaders of organizations throughout the state that provided reproductive health services using Title X and other public funding before the cuts went into effect. From these interviews, we have identified the likely channels through which the legislation will influence reproductive outcomes and the women who are most likely to be affected.

Facing severe budget cuts, most clinics have restricted access to the most effective contraceptive methods because of their higher up-front costs.4 Even with the 340B drug-pricing program, which offers discounts of 50 to 80%, a clinic may pay $250 or more for an intrauterine device (IUD) or subdermal implant, whereas a pack of pills costs about $5. To continue serving as many clients as possible, clinics now rarely offer IUDs or implants, reserving these methods for women with medical contraindications to other contraceptives. Some providers have started waiting lists for IUDs and implants in the unlikely event that they can purchase them with money left over at the end of a funding period. In addition, as more women are steered toward contraceptive pills, they are being provided with fewer pill packs per visit, a practice that has been shown to result in lower rates of continuation with the method and that may increase the likelihood of unintended pregnancy — and therefore that of abortion.5

Many organizations have also implemented or expanded systems that require clients to pay for services if they don’t qualify for the WHP. Though the fees for well-woman exams and a pack of pills are lower than in the private sector, they vary widely among clinics and within communities and remain out of reach for some of the poorest women. Those who cannot pay are turned away, whereas previously their visit would have been covered by public funds. The organizational leaders we spoke to reported that women who can pay the newly instated fees are choosing less-effective methods, purchasing fewer pill packs, and opting out of testing for sexually transmitted infections to save money.

The 35 organizations that lost all funding are facing two additional repercussions. They are no longer eligible to buy contraceptives through the 340B discount program and must pay higher prices, which are passed on to patients. And they are no longer exempt from Texas’s law requiring parental consent for teens younger than 18 years of age who seek contraceptive services. Under a federal exemption to such state laws, providers receiving Title X funds are required to provide services to teens without parental consent. As a result of the cuts, teens seeking confidential services are already having to travel farther to obtain them.

Finally, there is considerable variation across Texas in terms of the willingness and ability of communities to cover the shortfall in public funding for family planning. In one community, the hospital-donated office space is a critical lifeline to a family planning clinic serving more clients with less public funding. In another community, the main public hospital is increasingly relying on the county’s indigent care program and accumulating a deficit as it continues to provide care for all women in need. Planned Parenthood affiliates in more affluent communities have offset funding cuts with private donations, but that hasn’t been possible for affiliates in impoverished or politically conservative areas — and it’s unclear how sustainable the fundraising will be even in the more affluent communities. In communities with a large population of migrants who are ineligible for the WHP, the challenge is even greater.

Ostensibly, the purpose of the law was to defund Planned Parenthood in an attempt to limit access to abortion, even though federal and state funding cannot be used for abortion care anyway. Instead, these policies are limiting women’s access to a range of preventive reproductive health services and screenings. Disadvantaged women must choose between obtaining contraception and meeting other immediate economic needs. And, as one of our interviewees pointed out, providers are put in the position of “trying to decide, out of the most vulnerable, who is the most, most vulnerable.” Moreover, the impact of these policies is not limited to Planned Parenthood; other organizations have had to close clinics, reduce hours, and lay off dedicated, experienced staff members. We are witnessing the dismantling of a safety net that took decades to build and could not easily be recreated even if funding were restored soon.

Time will reveal the full effects of these budget cuts on the rates of unintended pregnancies and induced abortions and on state and federal health care costs. Already, the legislation has created circumstances that force clinics and women in Texas to make sacrifices that jeopardize reproductive health and well-being. This unfortunate situation does offer an opportunity to compare outcomes such as contraceptive use, unintended pregnancy, and abortion in Texas and other states, such as California, that have less restrictive family planning policies. Such comparisons could provide important information about the impact of these policies. Debates about funding in Congress and in other states should consider the results of such research and take a hard look at the implications for women, families, and communities of restricting access to contraception.

 
 

Disclosure forms provided by the authors are available with the full text of this article at NEJM.org.

This article was updated on September 27, 2012, at NEJM.org.

Source Information

From the Department of Health Care Organization and Policy, School of Public Health, University of Alabama, Birmingham (K.W.); Ibis Reproductive Health, Oakland, CA (D.G.); the Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, San Francisco (D.G.); and the Department of Sociology and the Population Research Center, University of Texas, Austin (K.H., J.E.P).

Abortion Rates Fall When Birth Control Is Free

 
 
By
WebMD Health News
Reviewed by Louise Chang, MD
 

 

woman holding birth control pills

Oct. 4, 2012 — Abortions and unplanned pregnancies dropped dramatically in a new study when women and teenaged girls were provided birth control at no cost.

The women and girls were also more likely to choose IUDs or contraceptive implants when cost was not an issue.

Family planning advocates say the study shows the potential of the health reform law (now known by both supporters and opponents as Obamacare) to reduce unplanned pregnancies nationwide.

 

‘Cost Has Been Barrier to IUD, Implant Use’

The law requires health insurers to provide all FDA-approved forms of contraception without charging a co-pay.

They say cost has been a big barrier to the use of IUDs and implants, which have a much lower rate of failure than other reversible birth control methods.

“This study reinforces what I have seen in my own practice,” says Yale School of Medicine ob-gyn Nancy Stanwood, MD, who is chair-elect of the group Physicians for Reproductive Choice and Health.

“When women have access to all methods of birth control and cost is not a barrier, they prefer the highly effective methods.”

Half of Pregnancies in U.S. Unplanned

About half of all pregnancies in the U.S. are unplanned, and about half of these pregnancies happen when birth control is not used.

The rest happen when contraception is used only some of the time or is used incorrectly.

The new study, published online today in the journal Obstetrics & Gynecology, included close to 9,300 sexually active women and teen girls at risk for having an unplanned pregnancy.

While the women were offered any FDA-approved method of contraception at no cost, the researchers made sure they knew that IUDs and implants were the most effective.

Researcher Jeff Peipert, MD, of Washington University in St. Louis, says around 3 out of 4 study participants opted for the long-acting methods.

“That was a shocker,” he says. “We had hoped to get maybe 15% of the women to choose IUDs or implants, but it was closer to 75%. That made all the difference.”

Abortion rates among the women and teens ranged from 4.4 to 7.5 per 1,000 during the time they were enrolled in the study — far lower than the national rate of close to 20 abortions for every 1,000 women.

And the birth rate among the teen girls in the study was almost six times lower than the national average.

The researchers estimated that providing no-cost contraception and promoting long-acting birth control methods nationwide could reduce abortions by 41% to 71% annually.

That’s because the failure rate for IUDs and implants is less than 1% per year, compared to closer to 8% with typical pill use.

IUDs, Implants, and Teens

While cost has been a significant barrier to the use of IUDs and implants, it is not the only one, says Adam Sonfield, of the nonprofit reproductive health advocacy group Guttmacher Institute.

He says many health providers have not offered long-acting reversible birth control methods to teenagers in the past, but this is changing.

Just this month, the nation’s largest group of obstetricians and gynecologists published an opinion on the subject, concluding that IUDs and implants are both safe and appropriate methods of contraception for teens.

Sonfield points out that the average age for starting sexual activity is about 17, and many women now want to delay having children until their late 20s or early 30s.

“The gap is close to 10 years, so it makes sense that women would want a long-acting birth control method that they don’t have to think about every day,” he says

 
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