# Do Cholesterol-Lowering Statins Help Cancer Patients Live Longer? A Landmark Danish Study Explained

Danish researchers analyzing the entire country's cancer population found that patients who regularly took statins (cholesterol-lowering medications) before a cancer diagnosis had a 15% lower risk of dying from their cancer and a 15% lower risk of dying from any cause, compared with patients who never took statins. This benefit appeared across 13 different types of cancer and was strongest at the lowest daily dose of statins. The finding held even after accounting for age, cancer stage, and other diseases. These results are observational — they show an association, not proof — but they suggest that clinical trials of statins in cancer patients are warranted.

# Do Cholesterol-Lowering Statins Help Cancer Patients Live Longer? A Landmark Danish Study Explained

## Table of Contents

- Key Points
- Background: Why Would Statins Affect Cancer?
- Study Design: How This Research Was Conducted
- Defining Statin Use: "Before Diagnosis" Was Key
- Study Participants: Who Was Included
- Key Findings: Statins and Survival After Cancer
- Findings on Dose: Does More Mean Better?
- Statins and Specific Cancer Types
- Sensitivity Analyses and Matched-Comparison Study
- Clinical Implications: What This Means for Patients
- Limitations: What This Study Could Not Prove
- Recommendations: What Patients Should Know and Do
- Frequently Asked Questions
- Source Information

## Key Points

- In a Danish nationwide study of nearly 296,000 cancer patients, regular statin use before diagnosis was tied to 15% lower risks of cancer death and any death.
- The lower risks appeared across 13 cancer types and held after adjusting for age, stage, and other diseases.
- The lowest daily statin dose showed the strongest association with reduced mortality, not higher doses.
- Because statin users were sicker with heart disease and diabetes, the survival benefit is especially notable.
- These findings are observational, not proof; randomized clinical trials are needed to confirm any cause and effect.

## Background: Why Would Statins Affect Cancer?

Statins are among the most widely prescribed medications in the world. Their main job is to lower cholesterol and prevent heart attacks and strokes. But this study started with a different question: could statins also fight cancer?

The scientific rationale begins with cholesterol itself. Cholesterol is a fundamental structural component of mammalian cell membranes (the outer "skin" of every cell in your body). It is essential for cellular proliferation (the process by which cells divide and multiply). Cancer is, at its core, a disease of uncontrolled cell division.

The researchers point to several biological mechanisms:

- Statins inhibit (block) the body's production of endogenous cholesterol (cholesterol made inside your own cells). With less cholesterol available, rapidly dividing cancer cells may struggle to build new cell membranes.
- Statins block protein prenylation, a chemical process that cells use to attach certain proteins to membranes. This process is involved in cell migration, which cancer cells need to spread.
- Cancer-cell proliferation appears clinically as cancer growth and metastasis (spread to other parts of the body), and it ultimately contributes to the death of the patient. A reduction in cholesterol availability could slow both tumor growth and the migration of cancer cells.
- Statins reduce downstream products of the mevalonate pathway (a chain of chemical reactions inside cells that produces cholesterol and other molecules). Some of these downstream products have been linked in earlier research to anti-cancer properties and to a reduced risk of cancer recurrence.
- At the cellular level, statins have been linked to halting cell-cycle progression (stopping cells from completing the steps needed to divide) and to increased radiosensitization (making cancer cells more vulnerable to radiation therapy).

Importantly, large-scale trials of statins for cardiovascular disease prevention did not show that statins change the overall incidence (rate of new cases) of cancer. The question posed here was different: not whether statins prevent cancer, but whether they reduce mortality (death) in people who already have cancer.

The research team, based at Herlev Hospital, Copenhagen University Hospital in Denmark, hypothesized that statin use begun before a cancer diagnosis would be associated with reduced cancer-related mortality. To test this, they analyzed the records of essentially every cancer patient in Denmark over a 15-year period.

## Study Design: How This Research Was Conducted

This was a nationwide, population-based observational cohort study using Denmark's complete national registries. The power of this design is that registries capture every citizen — no one is lost to follow-up.

**Data sources used:**

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**Danish Civil Registration System:** Records all births, immigrations, emigrations, and deaths in Denmark. Every inhabitant has a unique civil registration number. The system is 100% complete, so for practical purposes no persons were lost to follow-up.
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**Danish Cancer Registry:** Tracks data on 98% of all incident cancers (new cancer cases) in Denmark. It was blinded (unaware of) the statin use records.
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**Danish Registry of Medicinal Products Statistics:** Records all prescribed drugs dispensed at Danish pharmacies since 1995, including the drug name, date of dispensing, and total amount of the "defined daily dose" (the assumed average maintenance dose per day).
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**National Registry of Patients:** Records all hospital admissions, used to identify cardiovascular disease and diabetes diagnoses.
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**Danish Register of Causes of Death:** Records up to three ranked causes of death for every death, as reported by the attending physician.

The researchers used the tumor–node–metastasis (TNM) staging system (a standard way to classify how advanced a cancer is) to categorize cancer severity. Since the Danish Cancer Registry adopted this system on January 1, 2004, detailed staging data were available for the period from 2004 through 2007. Tumor size was classified as small (T0, T1, or T2) or large (T3 or T4); spread to lymphatic system (lymph nodes) as none (N0) or any (N1, N2, or N3); and distant metastasis (spread to distant organs) as none (M0) or any (M1).

From 1995 through 2003, the registry recorded treatment information in a simple "none vs. any" format for both radiotherapy and chemotherapy started within 4 months after a cancer diagnosis, but without details about the specific type of treatment given.

The primary statistical technique was the Cox regression model, which calculates hazard ratios (a measure of how much more or less likely an event is at any given time). A hazard ratio of 1.00 means no difference; below 1.00 means lower risk. The "multivariable-adjusted" models included adjustment for many potential confounders (factors that could distort the results), such as age at diagnosis, cancer stage, chemotherapy, radiotherapy, pre-existing cardiovascular disease, pre-existing diabetes, year of birth, sex, race, education, and residential area size.

## Defining Statin Use: "Before Diagnosis" Was Key

The researchers took careful steps to determine who was truly a "statin user" and to avoid reverse causation (the possibility that early, undiagnosed cancer caused patients to stop taking statins, which would falsely make statins look harmful or helpful).

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**Regular statin users:** Patients who had statin prescriptions filled within 6 months before the cancer diagnosis *and* within 2 years before the diagnosis. Regular use was measured only *before* the cancer diagnosis, to indicate use both before and after diagnosis.
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**Never-users:** Patients who had never used statins or any other cholesterol-lowering medication before their cancer diagnosis.
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**Irregular users:** Patients who had used statins but outside those specific time frames. These patients were excluded from the main comparison to keep the two groups clean.
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**Dose calculation:** Daily statin dose was estimated from the two most recent prescriptions before the cancer diagnosis (the total milligrams dispensed, divided by the interval between prescription fills).
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**Dose categories:** 0.00 defined daily dose per day (the reference group of never-users), 0.01 to 0.75, 0.76 to 1.50, and more than 1.50 defined daily doses per day.

For every filled prescription, researchers recorded the drug name, the dispensing date, and the total amount of the recommended defined daily dose (the assumed average maintenance dose per day for that drug, as defined by the World Health Organization's Anatomical Therapeutic Chemical classification system). Statins were classified under code C10AA; other cholesterol-lowering medications (C10AB, C10AC, C10AD, C10AX, C10BA codes) were tracked separately so that the "never used statins" group could be verified as truly unexposed.

## Study Participants: Who Was Included

The study included patients from the entire Danish population who received a cancer diagnosis between January 1, 1995, and December 31, 2007, with follow-up until December 31, 2009. Patients younger than 40 were excluded because they are unlikely to receive statins.

**Key numbers:**

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**18,721** cancer patients had used statins regularly before their diagnosis.
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**277,204** cancer patients had never used statins.
- Total: **295,925** patients followed for a median of 2.6 years (range 0 to 15 years).

The two groups differed in important ways at baseline (the time of cancer diagnosis). Statin users were slightly older on average (median age 70 years vs. 69 years). They were much more likely to be male — 57% of statin users vs. 46% of never-users. Statin users were far more likely to have pre-existing cardiovascular disease (heart and blood vessel disease) — this is expected, since statins are prescribed for that condition. The numbers are striking:

- Cardiovascular disease before cancer: **70%** of statin users vs. **21%** of never-users.
- Diabetes before cancer: **18%** of statin users vs. **3%** of never-users.

These baseline differences matter. People who take statins are generally sicker with heart disease and diabetes to begin with. That makes the finding of *lower* cancer mortality in statin users even more remarkable — they started at higher risk of death from other causes, yet still lived longer overall. The statistical models attempted to account for these differences.

During 1,072,503 person-years of follow-up (one person-year = one person observed for one year), 195,594 patients died: 162,067 from cancer, 14,489 from cardiovascular causes, and 19,038 from other causes. In other words, about 66% of the total study population died during follow-up, and of those deaths, roughly 83% (162,067 of 195,594) were registered as due to cancer.

## Key Findings: Statins and Survival After Cancer

The central result of the study is straightforward. The cumulative incidence of death from any cause (the total proportion of patients who died over time) was lower among statin users than among never-users (P<0.001 by the log-rank test — a statistical test comparing survival curves; P<0.001 means less than a 0.1% probability that the difference occurred by chance).

The same was true for death from cancer specifically. Statin users had a lower cumulative incidence of cancer death throughout the follow-up period (P<0.001).

**The headline numbers:**

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**Death from any cause:** Hazard ratio 0.85 (95% confidence interval [CI], 0.83 to 0.87). This means statin users had a 15% lower risk of dying from any cause at any given time point than similar never-users.
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**Death from cancer:** Hazard ratio 0.85 (95% CI, 0.82 to 0.87). A 15% lower risk of dying from cancer.

To understand a hazard ratio of 0.85 in plain terms: imagine two identical groups of cancer patients, one taking statins and one not. At any moment during follow-up, the statin group had about a 15% lower "instantaneous" risk of death. Over the whole follow-up, this translated into meaningful survival differences as shown on the cumulative incidence curves.

The researchers also noted an important detail: the two cumulative incidence curves for all-cause death converge (come back together) after about 5 years of follow-up. They attribute this to the higher cardiovascular mortality seen among statin users later in follow-up — the same patients who had more heart disease to begin with.

When the cause of death was separated out, the pattern became clear: statin users had *fewer* cancer deaths and *fewer* deaths from other non-cardiovascular causes, but slightly *more* cardiovascular deaths than never-users.

## Findings on Dose: Does More Mean Better?

An interesting and somewhat counterintuitive pattern emerged when the researchers analyzed the daily statin dose. Rather than seeing a steady "dose-response" (more statin = more benefit), the *lowest* dose category showed the strongest reduction in mortality.

Multivariable-adjusted hazard ratios for **death from any cause**, compared with no statin use:

- Dose of 0.01 to 0.75 DDD/day: hazard ratio **0.82** (95% CI, 0.81 to 0.85), an 18% lower risk.
- Dose of 0.76 to 1.50 DDD/day: hazard ratio **0.87** (95% CI, 0.83 to 0.89), a 13% lower risk.
- Dose higher than 1.50 DDD/day: hazard ratio **0.87** (95% CI, 0.81 to 0.91), a 13% lower risk.

The corresponding hazard ratios for **death from cancer** were:

- 0.01 to 0.75 DDD/day: hazard ratio **0.83** (95% CI, 0.81 to 0.86).
- 0.76 to 1.50 DDD/day: hazard ratio **0.87** (95% CI, 0.83 to 0.91).
- Higher than 1.50 DDD/day: hazard ratio **0.87** (95% CI, 0.81 to 0.92).

All of these results were statistically significant (P<0.001 in every dose category for both all-cause and cancer mortality).

By contrast, the hazard ratios for **death from cardiovascular causes** were elevated among statin users, which makes biological sense because these patients had more heart disease to begin with:

- 0.01 to 0.75 DDD/day: hazard ratio **1.08** (95% CI, 0.99 to 1.19) — this was the only one that did not reach statistical significance (P=0.08).
- 0.76 to 1.50 DDD/day: hazard ratio **1.25** (95% CI, 1.12 to 1.41), P<0.001.
- Higher than 1.50 DDD/day: hazard ratio **1.24** (95% CI, 1.03 to 1.48), P=0.01.

And the hazard ratios for **death from other (non-cancer, non-cardiovascular) causes** were substantially reduced among statin users:

- 0.01 to 0.75 DDD/day: hazard ratio **0.70** (95% CI, 0.64 to 0.77).
- 0.76 to 1.50 DDD/day: hazard ratio **0.76** (95% CI, 0.68 to 0.86).
- Higher than 1.50 DDD/day: hazard ratio **0.77** (95% CI, 0.66 to 0.92).

For the 18,721 statin users split into dose groups: 9,780 took 0.01–0.75 DDD/day; 6,181 took 0.76–1.50 DDD/day; and 2,760 took more than 1.50 DDD/day.

## Statins and Specific Cancer Types

The researchers examined whether the reduced cancer-related mortality among statin users was limited to one or two cancer types. It was not. The reduced risk of cancer death was observed for each of **13 cancer types** in the main analysis. The study prespecified subgroups encompassing 27 cancer types in total (detailed in the paper's supplementary appendix), along with 9 patient characteristics.

This consistency across many different cancer types is one of the strongest arguments that the effect is real. A benefit limited to one cancer might suggest a quirk of that particular disease. A benefit seen across 13 different types of cancer points to a shared underlying mechanism — consistent with the laboratory evidence that statins affect basic cellular processes common to all cancers, such as cell membrane production and cell division machinery.

## Sensitivity Analyses and Matched-Comparison Study

The researchers performed multiple additional analyses to check whether their main finding could be explained by bias, chance, or the competing risk of death from other causes.

**Nested 1:3 matched study.** To address differences between statin users and never-users, they created a special "nested" analysis that matched each statin user with three never-users who were identical in sex, age at diagnosis, year of diagnosis, and cancer type. This yielded 15,247 statin users and 45,741 matched never-users. The results closely mirrored the nationwide findings:

- Death from any cause: hazard ratio **0.86** (95% CI, 0.83 to 0.89).
- Death from cancer: hazard ratio **0.85** (95% CI, 0.81 to 0.87).

**Competing-risks analysis.** People can die from only one cause. To make sure the cancer-death result wasn't distorted by deaths from heart disease or other causes, the researchers used the Fine and Gray method, which calculates subhazard ratios (a relative-risk measure that properly accounts for competing risks of death). The results for cancer-related mortality remained similar when competing risks were modeled this way.

**Other sensitivity checks.** The researchers also performed a propensity-score analysis (a statistical method that balances many characteristics between groups as if they were randomly assigned) and adjusted for the provider's area code to address unknown patterns and other potential biases between the groups. They censored (removed from follow-up) at the date of emigration for 635 patients and at the study end date (December 31, 2009) for 99,696 patients who were still alive. The pattern of statin prescriptions was roughly symmetric before and after the cancer diagnosis, confirming that most regular users continued their medication.

## Clinical Implications: What This Means for Patients

The authors' conclusion, stated plainly, is that statin use in patients with cancer is associated with reduced cancer-related mortality. They go further and state that this "suggests a need for trials of statins in patients with cancer."

For patients today, several points deserve emphasis:

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**This is an association, not proof.** Observational studies like this one can show that statin users lived longer, but they cannot prove the statins caused the longer survival. The next step — randomized clinical trials (studies where patients are assigned by chance to receive statin or placebo) — would be needed to establish cause and effect. The authors explicitly call for such trials.
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**The benefit was consistent.** The finding held in the nationwide analysis, held in the closely matched comparison, held across 13 cancer types, and held even though statin users were sicker overall (70% had cardiovascular disease vs. 21% of never-users). Consistency strengthens confidence in the result.
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**Timing of statin exposure matters.** The researchers deliberately measured statin use *before* the cancer diagnosis. This design was meant to exclude reverse causation — the possibility that hidden cancer made people stop taking statins. The pattern of filled prescriptions was roughly symmetric before and after diagnosis, meaning patients generally continued taking their statins.
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**The dose question is unresolved.** Because the lowest dose category (0.01 to 0.75 defined daily dose per day) showed the strongest mortality reduction, the researchers could not claim that higher statin doses reduce cancer mortality more. This is a question that future trials would need to address.
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**Do not stop heart medications on your own.** Statins in this study were overwhelmingly prescribed for cardiovascular disease — a condition that affected 70% of the statin users. The same group showed slightly higher cardiovascular mortality in the dose analysis (HR up to 1.25, 95% CI 1.12 to 1.41), reflecting their underlying heart disease. Statins are proven to prevent heart attacks and strokes. Any cancer-related benefit would be an addition to, not a replacement for, that established role.

## Limitations: What This Study Could Not Prove

Every study has limits, and being clear about them helps patients interpret the findings correctly.

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**Observational design.** Patients were not randomly assigned to take statins or not. Statin users differed from never-users in many measured ways (more heart disease, more diabetes, more men) and possibly in unmeasured ways too (for example, health-awareness, lifestyle habits, or medication adherence patterns). Statistical adjustment cannot fully eliminate such residual confounding (the effect of factors not measured or not perfectly measured).
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**No proof of biological causation.** While the laboratory evidence for anti-cancer mechanisms is plausible, this study only demonstrates an association. As the authors state, trials are needed.
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**Staging data were incomplete.** Detailed TNM staging (tumor size, lymph node involvement, distant metastasis) was only available from 2004 through 2007. For the entire 1995–2007 period, stage information was missing for 73% of non-statin users and 34% of statin users. Missing-indicator methods were used to handle this, but incomplete staging information is a recognized source of potential bias.
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**Treatment details were limited.** Chemotherapy and radiotherapy data were recorded only dichotomously (none vs. any) and only for 1995 through 2003, with no details on which specific treatment drugs or regimens patients received. Cancer treatment strongly influences survival, and the inability to adjust for precise treatments could confound the association.
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**Limited population diversity.** The population was overwhelmingly white persons of Danish descent (97%). Results may not generalize directly to other racial or ethnic groups, although there is no strong biological reason to expect fundamentally different effects.
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**Cause-of-death classification.** Causes of death were reported by attending physicians and classified with ICD-10 codes, up to three ranked causes per death. The study used the first (primary) cause. Misclassification of cause of death is possible, particularly in older or complex patients.
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**No data on tumor biology.** The cancer registry data used here did not include detailed tumor grade or molecular subtype information, which can influence how aggressive a cancer behaves and how it responds to treatment.

## Recommendations: What Patients Should Know and Do

Based on this study and the broader medical evidence, here is practical guidance for patients:

1.
**If you are already taking a statin for heart health, do not stop it.** This study adds to the evidence that statins may have benefits beyond the cardiovascular system. Abruptly stopping a prescribed statin could increase your risk of heart attack or stroke.
1.
**Discuss your medications with your oncologist (cancer doctor) and your primary care doctor.** If you have cancer and also have a medical reason to take a statin — such as high cholesterol, prior heart attack, or diabetes — this study supports continuing it, assuming no drug interactions or contraindications with your cancer treatment.
1.
**Do not start taking statins on your own.** Statins are prescription medications with potential side effects, including muscle pain and, rarely, more serious effects on the liver or muscles. They can also interact with certain chemotherapy drugs. Starting a statin is a decision to make with your doctor.
1.
**Understand what "15% lower risk" means in context.** A hazard ratio of 0.85 represents a relative-risk reduction. In this study, death from cancer was the outcome for the majority of patients — about 83% of all deaths were cancer-related. For an individual patient, the absolute benefit of a statin depends on many factors, including cancer type, stage, and other treatments received. This is why trials are needed to quantify the absolute survival benefit precisely.
1.
**Keep the bigger picture in mind.** This study does not replace the proven pillars of cancer care: surgery, radiation, chemotherapy, immunotherapy, and other targeted treatments. If statins do have a role in cancer treatment, it will almost certainly be as an addition to — not a substitute for — standard therapies.
1.
**Watch for results of ongoing clinical trials.** The authors' call for trials of statins in cancer patients reflects where the science stands. Patients interested in participating may ask their oncologist whether any statin trials for their cancer type are enrolling.

## Frequently Asked Questions

### What did the study find about statin use and cancer survival?

In a nationwide Danish study of nearly 296,000 cancer patients, those who regularly took statins before their cancer diagnosis had about a 15% lower risk of dying from cancer and from any cause compared with never-users. This was an observational association, not proof, but it appeared across 13 different cancer types.

### Should I start taking statins if I have cancer?

No, do not start statins on your own. Statins are prescription medications with potential side effects and drug interactions, especially with some chemotherapy drugs. If you have cancer and a medical reason for a statin, discuss it with your oncologist and primary care doctor. This study alone does not prove statins treat cancer.

### Why might statins affect cancer?

Cholesterol is needed for cell membranes, and cancer grows by rapid cell division. Statins lower cholesterol made by your cells and may also block protein prenylation, which cancer cells use to spread. Laboratory studies suggest statins could slow tumor growth and metastasis, but this patient study only shows an association.

### Does a higher statin dose give more benefit?

No, this study found the lowest daily dose category had the strongest mortality reduction: about an 18% lower risk of death from any cause compared with no statin use. Moderate and higher doses showed about 13% lower risk. The dose question remains unresolved and needs future trials, so do not change your dose.

### Did the survival benefit apply to all cancer types?

In the main analysis, the reduced risk of cancer death was seen for each of 13 different cancer types, not just one or two. This consistency suggests a shared underlying mechanism. However, the study could not include detailed tumor biology or grade for all patients, so individual results may vary.

### What are the limitations of this study?

This was an observational study, so it cannot prove cause and effect. Patients were not randomly assigned to statins. Statin users had more heart disease and diabetes, and some cancer staging and treatment details were incomplete. The population was mostly white, and cause of death may be misclassified. Trials are needed.

### My oncologist didn't mention statins for my cancer. Should I get a second opinion about whether I should take one?

A second opinion can help you decide whether adding a statin is appropriate for your specific cancer and health profile. In a nationwide Danish study of 295,925 cancer patients, those who regularly took statins before diagnosis had a 15% lower risk of cancer-related death and death from any cause, an association seen across 13 cancer types. However, this was observational, not proof, and higher doses did not show greater benefit. Because statins can interact with chemotherapy and have side effects, a second-opinion consultation can help determine if this evidence applies to you. Diagnostic Detectives Network provides independent expert second opinions.

## Source Information

**Original article title:** Statin Use and Reduced Cancer-Related Mortality

**Journal:** *The New England Journal of Medicine*, 2012; volume 367, pages 1792–1802. DOI: 10.1056/NEJMoa1201735.

**Publication date:** November 8, 2012.

This patient-friendly article is based on peer-reviewed research published in a major medical journal. It is intended for educational purposes only and should not replace individualized medical advice from your healthcare team.


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