Archive for September, 2013

Why Are You Not Dead Yet?

Wednesday, September 25, 2013 // Uncategorized

This is an interesting article from Laura Helmuth in Slate.com.

Why Are You Not Dead Yet?

 

Life expectancy doubled in the past 150 years. Here’s why.

        By

Fresh air was a part of the regimen to battle tuberculosis. Above, patients receive fresh air treatment on the sun porch at Waverly Tuberculosis Hospital in Louisville.  
Fresh air was a part of the regimen to battle tuberculosis. Above, patients receive fresh air treatment on the sun porch at Waverly Tuberculosis Hospital in Louisville, Ky., in the 1950s.

Photo courtesy of Kentucky Cabinet for Health and Family Services

The most important difference between the world today and 150 years ago isn’t airplane flight or nuclear weapons or the Internet. It’s lifespan. We used to live 35 or 40 years on average in the United States, but now we live almost 80. We used to get one life. Now we get two.

You may well be living your second life already. Have you ever had some health problem that could have killed you if you’d been born in an earlier era? Leave aside for a minute the probabilistic ways you would have died in the past—the smallpox that didn’t kill you because it was eradicated by a massive global vaccine drive, the cholera you never contracted because you drink filtered and chemically treated water. Did some specific medical treatment save your life? It’s a fun conversation starter: Why are you not dead yet? It turns out almost everybody has a story, but we rarely hear them; life-saving treatments have become routine. I asked around, and here is a small sample of what would have killed my friends and acquaintances:

  • Adrian’s lung spontaneously collapsed when he was 18.
  • Becky had an ectopic pregnancy that caused massive internal bleeding.
  • Carl had St. Anthony’s Fire, a strep infection of the skin that killed John Stuart Mill.*
  • Dahlia would have died delivering a child (twice) or later of a ruptured gall bladder.
  • David had an aortic valve replaced.
  • Hanna acquired Type 1 diabetes during a pregnancy and would die without insulin.
  • Julia had a burst appendix at age 14.
  • Katherine was diagnosed with pernicious anemia in her 20s. She treats it with supplements of vitamin B-12, but in the past she would have withered away.
  • Laura (that’s me) had scarlet fever when she was 2, which was once a leading cause of death among children but is now easily treatable with antibiotics.
  • Mitch was bitten by a cat (filthy animals) and had to have emergency surgery and a month of antibiotics or he would have died of cat scratch fever.

After a while, these not-dead-yet stories start to sound sort of absurd, like a giddy, hooray-for-modernity response to The Gashleycrumb Tinies. Edward Gorey’s delightfully dark poem is an alphabetical list of children (fictional!) who died gruesome deaths: “A is for Amy who fell down the stairs/ B is for Basil assaulted by bears.” Here’s how modern science, medicine, and public health would amend it:

M is for Maud who was swept out to sea … then brought back to shore by a lifeguard and resuscitated by emergency medical technicians.

O is for Olive run through with an awl … but saved during a four-hour emergency surgery to repair her collapsed lung.

S is for Susan, who perished of fits … or who would have, anyway, if her epilepsy hadn’t been diagnosed promptly and treated with powerful anticonvulsant drugs.


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Now we’d like to hear your stories. What would have killed you but didn’t? Which friend or relative is alive today thanks to some medical intervention, whether heroic or trivial? Please send your stories to [email protected] or share them on Twitter using the hashtag #NotDeadYet. We’ll collect the best stories and publish them in Slate next week, at the end of a series of articles about why life expectancy has increased. And congratulations on being alive!

* * *

When I first started looking into why average lifespan has increased so much so rapidly, I assumed there would be a few simple answers, a stepwise series of advances that each added a few years: clean water, sewage treatment, vaccines, various medical procedures. But it turns out the question of who or what gets credit for the doubling of life expectancy in the past few centuries is surprisingly contentious. The data are sparse before 1900, and there are rivalries between biomedicine and public health, obstetricians and midwives, people who say life expectancy will rise indefinitely and those who say it’s starting to plateau.

It’s important to assign the credit correctly. In much of the developing world, average lifespan hasn’t increased nearly as dramatically as in the United States and the rest of the developed world. (And the United States has a lousy life expectancy compared to other wealthy nations.) Even within the United States, there are huge differences among races, geographic regions, and social classes. Even neighborhoods. These discrepancies are among the greatest injustices of the 21st century. How can we prevent needless premature deaths? What interventions are mostly likely to grant people in poorer countries extra years? And what’s the best way to prolong life and health even further in rich countries?

Poster encouraging truck drivers to report to proper authorities cases of communicable diseases encountered on their routes, July 20 1940.  
A 1940s poster encourages truck drivers to report cases of communicable diseases encountered on their routes.

Courtesy of Work Projects Administration Poster Collection/Library of Congress

To understand why people live so long today, it helps to start with how people died in the past. (To take a step back in time, play our interactive game.) People died young, and they died painfully of consumption (tuberculosis), quinsy (tonsillitis), fever, childbirth, and worms. There’s nothing like looking back at the history of death and dying in the United States to dispel any romantic notions you may have that people used to live in harmony with the land or be more in touch with their bodies. Life was miserable—full of contagious disease, spoiled food, malnutrition, exposure, and injuries.

But disease was the worst. The vast majority of deaths before the mid-20th century were caused by microbes—bacteria, amoebas, protozoans, or viruses that ruled the Earth and to a lesser extent still do. It’s not always clear which microbes get the credit for which kills. Bills of mortality (lists of deaths by causes) were kept in London starting in the 1600s and in certain North American cities and parishes starting in the 1700s. At the time, people thought fevers were spread by miasmas (bad air) and the treatment of choice for pretty much everything was blood-letting. So we don’t necessarily know what caused “inflammatory fever” or what it meant to die of “dropsy” (swelling), or whether ague referred to typhoid fever, malaria, or some other disease. Interpreting these records has become a fascinating sub-field of history. But overall, death was mysterious, capricious, and ever-present.

The first European settlers to North America mostly died of starvation, with (according to some historians) a side order of stupidity. They picked unnecessary fights with Native Americans, sought gold and silver rather than planting food or fishing, and drank foul water. As Charles Mann points out in his fascinating book 1493: Uncovering the New World Columbus Created, one-third of the first three waves of colonists were gentlemen, meaning their status was defined by not having to perform manual labor. During the winter of 1609–10, aka “the starving time,” almost everyone died; those who survived engaged in cannibalism.

Deadly diseases infiltrated North America faster than Europeans did. Native Americans had no exposure and thus no resistance to the common European diseases of childhood, and unimaginable pandemics of smallpox, measles, typhus, and other diseases swept throughout the continent and ultimately reduced the population by as much as 95 percent.

The slave trade killed more than 1 million Africans who were kidnapped, shackled, and shipped across the Atlantic. Those who survived the journey were at risk of dying from European diseases, as well as starvation and abuse. The slave trade introduced African microbes to North America; malaria and yellow fever were the ones that killed the most.

Surviving colonists remove the bodies of the dead from their Virginia settlement, around 1610.  
Surviving settlers remove the bodies of the dead from their Virginia settlement around 1610.

Painting by Sidney King/National Park Service/MPI/Getty Images

Global trade introduced new diseases around the world and caused horrific epidemics until the 1700s or so, when pretty much every germ had made landfall on every continent. Within the United States, better transportation in the 1800s brought wave after wave of disease outbreaks to new cities and the interior. Urbanization brought people into ideal proximity from a germ’s point of view, as did factory work. Sadly, so did public schools: Children who might have toiled in relative epidemiological isolation on farms were suddenly coughing all over one another in enclosed schoolrooms.

One of the best tours of how people died in the past is The Deadly Truth: A History of Disease in America by Gerald Grob. It’s a great antidote to all the heroic pioneer narratives you learned in elementary school history class, and it makes the Little House on the Prairie books seem delusional in retrospect. Pioneers traveling west in wagon trains had barely enough food, and much of it spoiled; their water came from stagnant, larvae-infested ponds. They died in droves of dysentery. Did you ever play with Lincoln logs or dream about living in a log cabin? What a fun fort for grown-ups, right? Wrong. The poorly sealed, damp, unventilated houses were teeming with mosquitoes and vermin. Because of settlement patterns along waterways and the way people cleared the land, some of the most notorious places for malaria in the mid-1800s were Ohio and Michigan. Everybody in the Midwest had the ague!

* * *

How did we go from the miseries of the past to our current expectation of long and healthy lives? “Most people credit medical advances,” says David Jones, a medical historian at Harvard—“but most historians would not.” One problem is the timing. Most of the effective medical treatments we recognize as saving our lives today have been available only since World War II: antibiotics, chemotherapy, drugs to treat high blood pressure. But the steepest increase in life expectancy occurred from the late 1800s to the mid-1900s. Even some dramatically successful medical treatments such as insulin for diabetics have kept individual people alive—send in those #NotDeadYet stories!—but haven’t necessarily had a population-level impact on average lifespan. We’ll examine the second half of the 20th century in a later story, but for now let’s look at the bigger early drivers of the doubled lifespan.

The credit largely goes to a wide range of public health advances, broadly defined, some of which were explicitly aimed at preventing disease, others of which did so only incidentally. “There was a whole suite of things that occurred simultaneously,” says S. Jay Olshansky, a longevity researcher at the University of Illinois, Chicago. Mathematically, the interventions that saved infants and children from dying of communicable disease had the greatest impact on lifespan. (During a particularly awful plague in Europe, James Riley points out in Rising Life Expectancy: A Global History, the average life expectancy could temporarily drop by five years.) And until the early 20th century, the most common age of death was in infancy.

Clean water may be the biggest lifesaver in history. Some historians attribute one-half of the overall reduction in mortality, two-thirds of the reduction in child mortality, and three-fourths of the reduction in infant mortality to clean water. In 1854, John Snow traced a cholera outbreak in London to a water pump next to a leaky sewer, and some of the big public works projects of the late 1900s involved separating clean water from dirty. Cities ran water through sand and gravel to physically trap filth, and when that didn’t work (germs are awfully small) they started chlorinating water.

Closely related were technologies to move wastewater away from cities, but as Grob points out in The Deadly Truth, the first sewage systems made the transmission of fecal-borne diseases worse. Lacking an understanding of germs, people thought that dilution was the best solution and just piped their sewage into nearby waterways. Unfortunately, the sewage outlets were often near the water system inlets. Finally understanding that sewage and drinking water need to be completely separated, Chicago built a drainage canal that in 1900 reversed the flow of the Chicago River. The city thus sent its sewage into the greater Mississippi watershed and continued taking its drinking water from Lake Michigan.

"Guard Against Tuberculosis" poster from the Office for Emergency Management, Office of War Information, Domestic Operations Branch, Bureau of Special Services.  
“Guard Against Tuberculosis”

Courtesy of U.S. National Archives and Records Administration

The germ theory of disease didn’t catch on all that quickly, but once it did, people started washing their hands. Soap became cheaper and more widespread, and people suddenly had a logical reason to wash up before surgery, after defecating, before eating. Soap stops both deadly and lingering infections; even today, kids who don’t have access to soap and clean water have stunted growth.

Housing, especially in cities, was crowded, filthy, poorly ventilated, dank, stinky, hot in the summer, and cold in the winter. These were terrible conditions to live in as a human being, but a great place to be an infectious microbe. Pretty much everyone was infected with tuberculosis (the main cause of consumption), the leading killer for most of the 19th century. It still has a bit of a reputation as a disease of the young, beautiful, and poetic (it claimed Frederic Chopin and Henry David Thoreau, not to mention Mimì in La Bohème), but it was predominantly a disease of poverty, and there was nothing romantic about it. As economic conditions started improving in the 19th century, more housing was built, and it was airier, brighter (sunlight kills tuberculosis bacteria), more weather-resistant, and less hospitable to vermin and germs.

We live like kings today—we have upholstered chairs, clean beds, a feast’s worth of calories at any meal, all the nutmeg (people once killed for it) and salt we could ever want. But wealth and privilege didn’t save royalty from early deaths. Microbes do care about breeding—some people have evolved defenses against cholera, malaria, and possibly the plague—but microbes killed off people without regard to class distinctions through the 1600s in Europe. The longevity gap between the rich and the poor grew slowly with the introduction of effective health measures that only the rich could afford: Ipecac from the New World to stop bloody diarrhea, condoms made of animal intestines to prevent the transmission of syphilis, quinine from the bark of the cinchona tree to treat malaria. Once people realized citrus could prevent scurvy, the wealthy built orangeries—greenhouses where they grew the life-saving fruit.

Improving the standard of living is one important life-extending factor. The earliest European settlers in North America suffered from mass starvation initially, but once the Colonies were established, they had more food and better nutrition than people in England. During the Revolutionary War era, American soldiers were a few inches taller than their British foes. In Europe, the wealthy were taller than the poor, but there were no such class-related differences in America—which means most people had enough to eat. This changed during the 1800s, when the population expanded and immigrants moved to urban areas. Average height declined, but farmers were taller than laborers. People in rural areas outlived those in cities by about 10 years, largely due to less exposure to contagious disease but also because they had better nutrition. Diseases of malnutrition were common among the urban poor: scurvy (vitamin C deficiency), rickets (vitamin D deficiency), and pellagra (a niacin deficiency). Improved nutrition at the end of the 1800s made people taller, healthier, and longer lived; fortified foods reduced the incidence of vitamin-deficiency disorders.

Portrait of French scientist Louis Pasteur in mid-career.  
French scientist Louis Pasteur

Photo courtesy of New York Public Library Archives/Tucker Collection

Contaminated food was one of the greatest killers, especially of infants; once they stopped breast-feeding, their food could expose them to typhoid fever, botulism, salmonella, and any number of microbes that caused deadly diarrhea in young children. (Death rates for infants were highest in the summer, evidence that they were dying of food contaminated by microbes that thrive in warm conditions.) Refrigeration, public health drives for pure and pasteurized milk, and an understanding of germ theory helped people keep their food safe. The Pure Food and Drug Act of 1906 made it a crime to sell adulterated food, introduced labeling laws, and led to government meat inspection and the creation of the Food and Drug Administration.

People had started finding ways to fight disease epidemics in the early 1700s, mostly by isolating the sick and inoculating the healthy. The United States suffered fewer massive epidemics than Europe did, where bubonic plague (the Black Death) periodically burned through the continent and killed one-third of the population. Low population density prevented most epidemics from becoming widespread early in the United States history, but epidemics did cause mass deaths locally, especially as the population grew and more people lived in crowded cities. Yellow fever killed hundreds of people in Savannah in 1820 and 1854; the first devastating cholera epidemic hit the country in 1832. Port cities suffered some of the worst outbreaks because sailors brought new diseases and strains with them from all over the world. Port cities instituted quarantines starting in the 19th century, preventing sailors from disembarking if there was any evidence of disease, and on land, quarantines separated contagious people from the uninfected.


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A smallpox epidemic in Boston in 1721 led to a huge debate about variolation, a technique that involved transferring pus from an infected person to a healthy one to cause a minor reaction that confers immunity. Rev. Cotton Mather was for it—he said it was a gift from God. Those opposed said that disease was God’s will. People continued to fight about variolation, then inoculation (with the related cowpox virus, introduced in the late 1700s), and finally vaccination. The fight over God’s will and the dangers of vaccinations (real in the past, imaginary today) are still echoing.

In the early 1900s, antitoxins to treat diphtheria and vaccines against diphtheria, tetanus, and pertussis helped stop these deadly diseases, followed by vaccines for mumps, measles, polio, and rubella.

Anne Schuchat, assistant surgeon general and the acting director of CDC’s Center for Global Health, says it’s not just the scientific invention of vaccines that saved lives, but the “huge social effort to deliver them to people improved health, extended life, and kept children alive.” Vaccines have almost eliminated diseases that used to be common killers, but she points out that “they’re still circulating in other parts of the world, and if we don’t continue to vaccinate, they could come back.”

Estimated Annual Deaths Before Vaccine, and in 2004  
Historical comparisons of morbidity and mortality for vaccine-preventable diseases with vaccines licensed or recommended before 1980

Courtesy of Sandra W. Roush, Trudy V. Murphy, and the Vaccine-Preventable Disease Table Working Group/Journal of the American Medical Association

Vaccines have been so effective that most people in the developed world don’t know what it’s like to watch a child die of pertussis or measles, but parents whose children have contracted these diseases because of anti-vaccine paranoia can tell them. “The mistake that we made was that we underestimated the diseases and we totally overestimated the adverse reactions [to vaccines],” says a father in New Zealand whose child almost died of an agonizing bout of tetanus.

Schuchat says the HPV vaccine is a huge priority now; only one-third of teenage girls have received the full series of three shots required to protect them against viruses that cause cervical cancer. The vaccines “are highly effective and very safe, but our uptake is horrible. Thousands of cases of cervical cancer will occur in a few decades in people who are girls now.”

A baby is vaccinated against smallpox at an emergency clinic in Karachi during the worst epidemic of smallpox in Pakistan's history, January 1962.   
A baby is vaccinated against smallpox at an emergency clinic in Karachi, Pakistan, January 1962.

Photo by Keystone Features/Getty Images

Some credit for the historical decrease in deadly diseases may go to the disease agents themselves. The microbes that cause rheumatic fever, scarlet fever, and a few other diseases may have evolved to become less deadly. Evolutionarily, that makes sense—it’s no advantage to a parasite to kill its own host, and less-deadly strains may have spread more readily in the human population. Of course, sudden evolutionary change in microbes can go the other way, too: The pandemic influenza of 1918–19 was a new strain that killed more people than any disease outbreak in history—around 50 million. In any battle between microbes and mammals, the smart money is on the microbes.

Over the next week, we’ll take a closer look at deaths in childbirth and changes in life expectancy in adulthood. We’ll examine the evolution of old age and the social repercussions of having infants that survive and a robust population of old people, and we’ll list some of the oddball, underappreciated innovations that may have saved your life. In the meantime, please play the Wretched Fate game and send us your #NotDeadYet survival stories on Twitter or [email protected]

Please read the rest of Laura Helmuth’s series on longevity, and play our “Wretched Fate” interactive game to learn how you would have died in 1890.

 

Correction, Sept. 5, 2013: This article originally misspelled John Stuart Mill’s middle name.

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Laura Helmuth is Slate‘s science and health editor.

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Using the Practice Patient Portal

Monday, September 9, 2013 // Uncategorized

The following are the instructions for practice patients to access their test results via the secure patient portal.  When results are available I upload them to the portal.  On their initial uploading , a patient is sent an email with instructions on accessing the portal using a Super Pin (not sure why it has to be Super) that we give them.

About the Patient’s Activation Process

This is section contains some information about what your patients will do to activate their CGM LIFE eSERVICES account, once they have been registered. You can use this as a reference, if a patient calls asking for help with the process.

When you register a patient for CGM LIFE eSERVICES (via uploading a CCR), an instructional, “welcome” e-mail is generated and sent to the patient’s e-mail address that is recorded in his or her Demographic Information in Alteer Office. Also, the Print SuperPin button becomes enabled on the Facesheet toolbar so that you can print the patient’s SuperPin, which he or she will need to log on to the patient portal for the first time.

To activate his or her patient portal account, the patient will need the welcome e-mail and will do the following:

1

Access his or her e-mail account that is recorded in Alteer Office.

2

Look for an e-mail from your practice or CGM LIFE eSERVICES. By default, the e-mail will show the sender as [email protected], and the subject will be “Welcome to eServices!”

3

The patient will open the e-mail and click the link to navigate to the CGM LIFE eSERVICES patient portal.

4

The patient will then type his or herCGM Life Super-PIN number, (which was given to him or her by your practice), and then click Continue.

5

Next, the patient must create a password. On the second screen, the patient will create a password and then click Continue.

6

On the third screen, the patient will see a summary of his or her personal data as it is currently recorded in Alteer Office. On this screen, the patient must review the terms and conditions for using the portal, and select the Yes, I accept the terms and condition check box to acknowledge acceptance of the terms and be able to finish the activation process. Once the patient selects the check box, the Continue button is enabled for them to click.

After clicking Continue, the patient’s account is fully registered and activated, and the Welcome screen appears. The patient can start using the portal.

7

To view medical information that has been uploaded to the portal by the practice from within Alteer Office, the patient will click the Medical Data folder. [The medical information is in the form of a Continuity of Care Record (CCR), which includes basic demographic information, a list of the patient’s problems (diagnoses), (current) medications, (current) allergies, and any lab results.]

 

 

 

 

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Flu Vaccine Frenzy

Sunday, September 8, 2013 // Uncategorized

It’s that time of year when people should be vaccinated against seasonal influenza.  consumers are faced with three different types of injectable vaccine and one intranasal vaccine.

What kinds of flu vaccines are available?

There are two types of vaccines:

  • The “flu shot” — an inactivated vaccine (containing killed virus) that is given with a needle, usually in the arm. The flu shot is approved for use in people older than 6 months, including healthy people and people with chronic medical conditions.
    There are three different flu shots available:

    The regular seasonal flu shot is “intramuscular” which means it is injected into muscle (usually in the upper arm). It has been used for decades and is approved for use in people 6 months of age and older, including healthy people, people with chronic medical conditions and pregnant women. Regular flu shots make up the bulk of the vaccine supply produced for the United States.

    Fluzone High-Dose vaccine contains four times the amount of antigen (the part of the vaccine that prompts the body to make antibody) contained in regular flu shots. The additional antigen is intended to create a stronger immune response (more antibody) in the person getting the vaccine.

  • The intradermal flu vaccine is a shot that is injected into the skin instead of the muscle. The intradermal shot uses a much smaller needle than the regular flu shot, and it requires less antigen to be as effective as the regular flu shot. It may be used in adults 18-64 years of age.

The nasal-spray flu vaccine — a vaccine made with live, weakened flu viruses that is given as a nasal spray (sometimes called LAIV for “Live Attenuated Influenza Vaccine”). The viruses in the nasal spray vaccine do not cause the flu. LAIV is approved for use in healthy* people 2 through 49 years of age who are not pregnant. Unlike the flu shot, the nasal spray flu vaccine does contain live viruses. However, the viruses are attenuated (weakened) and cannot cause flu illness. The weakened viruses are cold-adapted, which means they are designed to only cause infection at the cooler temperatures found within the nose. The viruses cannot infect the lungs or other areas where warmer temperatures exist. Some children and young adults 2-17 years of age have reported experiencing mild reactions after receiving nasal spray flu vaccine, including runny nose, nasal congestion or cough, chills, tiredness/weakness, sore throat and headache. Some adults 18-49 years of age have reported runny nose or nasal congestion, cough, chills, tiredness/weakness, sore throat and headache. These side effects are mild and short-lasting, especially when compared to symptoms of influenza infection.

Seasonal flu vaccines protect against the three influenza viruses (trivalent) that research indicates will be most common during the upcoming season. The viruses in the vaccine can change each year based on international surveillance and scientists’ estimations about which types and strains of viruses will circulate in a given year. While some manufacturers are planning to produce a quadrivalent (four component) vaccine in the future, quadrivalent vaccines are not expected to be available for the 2012-2013 season.  It is not known whether the quadrivalent vaccine is more effective.

About 2 weeks after vaccination, antibodies that provide protection against the influenza viruses in the vaccine develop in the body.

Here is a Q and A on the high dose flu vaccine.  the key point is that while it may results in higher antibody levels, it remains to be seen whether it is more effective.  It is more expensive.

Why is a higher dose vaccine available for adults 65 and older?

Human immune defenses become weaker with age, which places older people at greater risk of severe illness from influenza. Also, ageing decreases the body’s ability to have a good immune response after getting influenza vaccine. A higher dose of antigen in the vaccine is supposed to give older people a better immune response, and therefore, better protection against flu.

Does the higher dose vaccine produce a better immune response in adults 65 years and older?

Data from clinical trials comparing Fluzone to Fluzone High-Dose among persons aged 65 years or older indicate that a stronger immune response (i.e., higher antibody levels) occurs after vaccination with Fluzone High-Dose. Whether or not the improved immune response leads to greater protection against influenza disease after vaccination is not yet known. An ongoing study designed to determine the effectiveness of Fluzone High-Dose in preventing illness from influenza compared to Fluzone is expected to be completed in 2014-2015.

Is Fluzone High-Dose safe?

The safety profile of Fluzone High-Dose vaccine is similar to that of regular flu vaccines, although some adverse events (which are also reported after regular flu vaccines) were reported more frequently after vaccination with Fluzone High-Dose. The most common adverse events experienced during clinical studies were mild and temporary, and included pain, redness and swelling at the injection site, headache, muscle aches, fever and malaise. Most people had minimal or no adverse events after receiving the Fluzone High-Dose vaccine.

Who can get this vaccine?

Fluzone High-Dose is approved for use in people 65 years of age and older. As with all flu vaccines, Fluzone High-Dose is not recommended for people who have had a severe reaction to the flu vaccine in the past.

Does CDC recommend one vaccine above another for people 65 and older?

CDC and the Advisory Committee on Immunization Practices (ACIP) recommends flu vaccination as the first and most important step in protecting against the flu; however, neither CDC nor ACIP has expressed a preference for one vaccine over another at this point.

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Treating Cholesterol in the Elderly

Monday, September 2, 2013 // Uncategorized

Treating elevated cholesterol in patients with cardiovascular disease is fairly standard, but there is less solid proof  that treating older patients without heart disease is effective.  The following is the abstract of a a meta- analysis published by the American College of Cardiology.  I am following it by a summary of the data from UpToDate.  The bottom line is that more older patients could benefit from taking statins.  Some people may be put of by the definition of elderly, 65 and older:

Clinical Research                         | August 2013

Benefits Of Statins In Elderly Subjects Without Established Cardiovascular Disease. A Meta-Analysis                                                 ONLINE FIRST

Gianluigi Savarese, MD; Antonio M. Gotto, MD, PhD; Stefania Paolillo, MD; Carmen D’Amore, MD; Teresa Losco, MD; Francesca Musella, MD; Oriana Scala, MD; Caterina Marciano, MD; Donatella Ruggiero, MD; Fabio Marsico, MD; Giuseppe De Luca, MD, PhD; Bruno Trimarco, MD, PhD; Pasquale Perrone-Filardi, MD, PhD
J Am Coll Cardiol. 2013;():.                               doi:10.1016/j.jacc.2013.07.069
                        Published online

Objectives      To assess whether statins reduce all-cause mortality and CV events in elderly people without established CV disease.

Background      Since ageing of the population is steadily raising, prevention of cardiovascular (CV) disease in the elderly is relevant. In elderly patients with previous CV events, use of statins is recommended by guidelines, whereas benefits of these drugs in elderly subjects without previous CV events are still debated.

Methods      Randomized trials comparing statins versus placebo and reporting all-cause and CV mortality, myocardial infarction (MI), stroke, and new cancer onset in elderly (>65 years old) subjects without established CV disease were included.

Results      Eight trials enrolling 24,674 subjects (42.7% females; mean age 73.0+2.9; mean follow-up 3.5+1.5 years) were included in analyses. Statins, compared to placebo, significantly reduced the risk of MI by 39.4% (relative risk [RR]: 0.606 [95% confidence interval (CI): 0.434 to 0.847]; p=0.003), as well as the risk of stroke by 23.8% (RR: 0.762 [CI: 0.626 to 0.926]; p=0.006). In contrast, the risk of all-cause death (RR: 0.941 [CI: 0.856 to 1.035]; p=0.210) and of CV death (RR: 0.907 [CI: 0.686 to 1.199]; p=0.493) were not significantly reduced. New cancer onset did not differ between statin- compared to placebo-treated subjects (RR: 0.989 [CI: 0.851 to 1.151]; p=0.890).

Conclusions      In elderly subjects at high CV risk without established CV disease, statins significantly reduce the incidence of MI and stroke, but do not significantly prolong survival in the short-term

BENEFITS OF LIPID LOWERING LIPID IN THE ELDERLY

Clinical trials — The secondary prevention trials of LDL-cholesterol lowering therapies have shown a reduction in cardiac events and all cause mortality (see “Clinical trials of cholesterol lowering in patients with coronary heart disease or coronary risk equivalents”). However, these studies had only limited data in older subjects. Nevertheless, subgroup analysis of trials that included elderly individuals suggests that they have a similar benefit from lipid lowering therapy as younger subjects [2,16-21].

  • The Scandinavian Simvastatin Survival Study (4S trial) included 1021 patients greater than 65 years of age with angina or a previous myocardial infarction and hypercholesterolemia (baseline plasma total cholesterol levels between 212 and 309 mg/dL [5.5 and 8.0 mmol/L]) [16]. Similar reductions in serum lipids were observed among elderly and younger individuals. In the older patients, treatment with simvastatin reduced all cause mortality (34 percent lower), mortality from coronary heart disease (43 percent), major coronary events (34 percent), and the number of revascularization procedures (41 percent).
  • The Cholesterol and Recurrent Events (CARE) trial included 1283 patients between the ages of 65 and 75 who had average levels of total, LDL and HDL cholesterol of 209 mg/dL, 139 mg/dL, and 39 mg/dL (5.4, 3.6, and 1.0 mmol/L) [18]. Reductions in coronary events were similar to the 4S trial (figure 4). It was estimated that for every 1000 older patients treated, 225 cardiovascular hospitalizations and 207 cardiovascular events would be prevented compared with 121 hospitalizations and 150 cardiovascular events in 1000 younger patients [18,19].
  • The LIPID trial included 3514 patients between the ages of 65 and 75 years who had a prior infarction or unstable angina in addition to a baseline serum cholesterol of 155 to 271 mg/dL (4 to 7 mmol/L) [20]. Although the risk of all cardiovascular events and all-cause mortality were reduced by pravastatin therapy to a similar degree in older and younger patients, the absolute benefit was greater in the elderly because of a greater risk for these events; fewer elderly patients needed to be treated to prevent one death from any cause (22 versus 46 for younger patients), one death from CHD (35 versus 71), one cardiovascular death (28 versus 61), one fatal or nonfatal MI (30 versus 36), or one stroke (79 versus 170).
  • The Heart Protection Study included over 20,000 patients with varying lipid profiles (33 percent had baseline LDL cholesterol <116 mg/dL [<3 mmol/L], 25 percent had a level of 116 to 135 mg/dL [3 to 3.5 mmol/L], and 42 percent had levels >135 mg/dL [>3.5 mmol/L]) who were randomly assigned to simvastatin or placebo [21]. Entry criteria were age 40 to 80 years, a history of cardiovascular disease (coronary cerebrovascular, or peripheral vascular disease), diabetes mellitus, or treated hypertension. Thus, most patients were treated for secondary prevention. Treatment with simvastatin was associated with a reduction in cardiovascular events that was similar in patients above and below age 65. (See “Clinical trials of cholesterol lowering in patients with coronary heart disease or coronary risk equivalents”, section on ‘Heart Protection Study’.)
  • Similarly, in the CARDS study in patients with type 2 diabetes without known CHD, atorvastatin 10 mg daily reduced first major cardiovascular events by 37 percent in patients younger than 65 and by 38 percent in patients 65 and older [22].
  • In the TNT (Treating to New Targets) study, atorvastatin 80 mg versus 10 mg in 10,001 patients with stable CHD significantly decreased the risk for major cardiovascular events in those both ages 65 and older (n = 3809) and in younger patients [23,24]. (See “Clinical trials of cholesterol lowering in patients with coronary heart disease or coronary risk equivalents”, section on ‘TNT trial’.)

 

Similar findings were noted in an analysis of pooled data from three randomized trials of pravastatin involving 19,768 patients (CARE, LIPID, and WOSCOPS) [25]; two of these are discussed individually above. The relative reduction in the risk of cardiac events was comparable for patients ages <55 years, 55 to 64 years, and 65 to 75 years (32, 21, and 26, respectively).

Subgroup analyses from primary prevention trials of statins, including AFCAPS/TexCAPS, and ASCOT-LLA found similar relative effects of therapy on clinical endpoints in younger and older individuals [26-28]. In JUPITER, a large trial of rosuvastatin in patients with low-to-average LDL-C levels and elevated c-reactive protein levels, although the relative risk reductions were similar in older and younger patients, the absolute reduction in the primary composite cardiovascular endpoint was 0.77 events per 100 patient-years in the 5695 patients ages 70 and older, which was greater than the reduction of 0.52 events per 100 patient-years seen in the 12,107 patients ages 50 to 69 [28].

Other studies that specifically included older adult patients add further evidence that treatment of hypercholesterolemia in older adults provides similar benefits to that of treatment in younger people [29,30]:

  • The PROSPER trial randomly assigned 5804 men and women ages 70 to 82 years with a history of or risk factors for vascular disease to pravastatin (40 mg per day) or placebo [30]. During a mean follow-up of only three years, pravastatin treatment was associated with both significantly lower LDL concentrations and a significantly reduced risk of the primary end point (coronary death, nonfatal myocardial infarction, and fatal or nonfatal stroke, hazard ratio [HR] 0.81, 95% CI 0.74-0.97). Stroke risk alone was unaffected by therapy, but pravastatin was associated with significantly lower risk of coronary death and nonfatal myocardial infarction. There was, however, no significant reduction in all-cause mortality (HR 0.97, CI 0.83-1.14), and there was a significant increase in new diagnoses of cancer (HR 1.25, CI 1.04-1.51). The authors performed a meta-analysis of statin trials including PROSPER and found no overall evidence of an increased risk of cancer with statins (HR 1.02, CI 0.96-1.09). (See “Statins: Actions, side effects, and administration”, section on ‘Side effects’.)
  • The SAGE trial compared intensive and moderate statin therapy in patients with known CHD ages 65 to 85 who had at least one episode of ischemia on baseline screening with 48-hour ambulatory monitoring [31]. Patients were randomly assigned to treatment with atorvastatin 80 mg daily or pravastatin 40 mg daily. There was no difference between the two groups in the primary endpoint of duration of ischemia on ambulatory monitoring at month 12. However, there was a trend toward a reduction in a composite endpoint of major cardiovascular events with intensive therapy (HR 0.71, CI 0.46-1.09), and a post-hoc analysis found a reduction in mortality (HR 0.33, CI 0.13-0.83). In contrast, no similar reduction in mortality was seen with intensive statin therapy in patients ages 65 and older (n = 3809) in the TNT trial (HR 1.08, CI 0.87-1.33) [24,32]. (See “Clinical trials of cholesterol lowering in patients with coronary heart disease or coronary risk equivalents”, section on ‘TNT trial’ and “Intensity of lipid lowering therapy in secondary prevention of coronary heart disease”.)

 

Despite these apparent benefits, compliance with statin therapy declines substantially with time in older adult patients [33,34]. This occurs even when cost is not an issue. The adherence rate is similar to that observed for treatment of hypertension, another asymptomatic condition.

Time course for CHD benefit — The prevention of CHD in elderly subjects has been hindered by the perception that LDL lowering therapy requires many years before the course of atherosclerosis can be altered. This concept has been challenged by the observation that clinical benefits are seen as early as six months to two years (figure 5), in many cases before atherosclerosis regression has occurred [35-37]. In addition, statin therapy can improve endothelial dysfunction within three days of initiating therapy [38]. (See “Mechanisms of benefit of lipid-lowering drugs in patients with coronary heart disease”.)

Side effects — The safety of lipid lowering agents in older subjects was evaluated in two double-blind, placebo-controlled trials that included 573 patients over the age of 64 [39,40]. Treatment with lovastatin or pravastatin was associated with a fall in cholesterol levels similar to that seen in younger subjects. There was no statistically significant difference in side effects between the treatment and placebo groups. Neither trial provided information regarding the effect of therapy on morbidity and mortality.

An analysis from the CARDS study of atorvastatin 10 mg daily in patients with type 2 diabetes without known CHD found similar rates of adverse events in patients younger than age 65 and in those ages 65 and older [22]. For both younger and older patients, the rates of adverse events were no different with atorvastatin or placebo.

Summary

The decision whether to treat high or high-normal serum cholesterol in an elderly individual needs to be individualized, being based upon both chronological and physiologic age. As an example, a patient with a limited life span from a concomitant illness is probably not a candidate for drug therapy. On the other hand, an otherwise healthy elderly individual should not be denied drug therapy simply on the basis of age alone [2].

The studies described above support the use of lipid lowering therapy for secondary prevention in older patients with established CHD who do not have life-limiting comorbid disease [16-18,20,21]. These patients should be treated similar to younger patients according to the guidelines established by the National Cholesterol Education Program (see “Treatment of lipids (including hypercholesterolemia) in secondary prevention”) [1,2]. There are limited data on the value of treating elderly patients with low HDL-cholesterol (<40 mg/dL [1.03 mmol/L]), but again, presumably the same principles would apply as in younger patients. (See “HDL metabolism and approach to the patient with abnormal HDL-cholesterol levels”.)

In comparison, there are more limited data concerning the use of lipid lowering for primary prevention of CHD in elderly hypercholesterolemic patients. Because of the progressive elevation in total and LDL cholesterol levels with aging (figure 2), it has been estimated 40 percent or more of those above age 65 meet the National Cholesterol Education Program guidelines for treating hypercholesterolemia (see “Treatment of lipids (including hypercholesterolemia) in primary prevention”) This would entail a large annual cost.

On the other hand, over 50 percent of older individuals will eventually die from cardiovascular disease and data from the Cardiovascular Health Study suggest significant benefit from primary prevention in patients ages 65 and older [41]. The Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III or ATP III), published before the results of the Cardiovascular Health Study were available, recommended that therapeutic lifestyle changes are the first line of primary prevention for older individuals, although LDL-cholesterol lowering drugs can be considered when older patients have multiple risk factors for CHD as shown in the table (table 1) [1].

Despite their proven benefit, lipid-lowering drugs are markedly underutilized in elderly patients. This was illustrated in a prospective study of 500 patients with a mean age of 81 years and a Q wave myocardial infarction [42]. Although 67 percent had a serum LDL-cholesterol concentration above 125 mg/dL (3.2 mmol/L); only 5 percent were treated with a lipid-lowering drug. A retrospective cohort study of 396,077 high-risk elderly patients found that prescription of statins decreased with increasing age and also with increasing cardiovascular risk and risk of death; thus, the elderly patients likely to get the greatest absolute benefit from statins appear least likely to receive them [43].

ADDITIONAL ISSUES IN OLDER ADULTS

Secondary causes — Older adult patients commonly have medical conditions that may contribute to dyslipidemia. Etiologies to consider include hypothyroidism, diabetes mellitus, and nephrotic syndrome. Therapies may also contribute to dyslipidemias. As examples, thiazide diuretics can affect lipid metabolism, and antipsychotics used for agitation in dementia can produce weight gain. (See “Secondary causes of dyslipidemia”.)

Dietary modifications — While therapeutic lifestyle changes involving exercise and diet are generally the first line of treatment for dyslipidemias, providers should avoid dietary restrictions in older patients who are at high risk of malnutrition. These include patients with dementia or physical disabilities that limit their access to adequate nutrition. (See “Treatment of dementia”, section on ‘Nutrition’.)

Drug interactions and side effects — Elderly patients are frequently treated with multiple medications and so are at increased risk for complications of drug interactions. As an example, macrolide antibiotics can raise statin levels and thus the risk of muscle toxicity (see “Statins: Actions, side effects, and administration”). Providers should be particularly cautious of such interactions in older patients.

Additionally, older adult patients may have greater susceptibility to medication side effects, such as bloating and constipation with bile acid sequestrants, and hyperglycemia and gout with niacin. (See “Lipid lowering with drugs other than statins and fibrates”, section on ‘Bile acid sequestrants’ and “Lipid lowering with drugs other than statins and fibrates”, section on ‘Nicotinic acid (Niacin)’.)

SUMMARY AND RECOMMENDATIONS

  • Coronary heart disease (CHD) is the most common cause of death in older patients, and, as in younger patients, dyslipidemia is associated with an increased risk of CHD. (See ‘Cardiovascular disease in older adults’ above.)
  • Although the relative risk of hypercholesterolemia is somewhat lower in older patients, the absolute risk is higher than in younger patients. (See ‘Relative risk versus attributable risk’ above.)
  • The relative benefit of lipid lowering therapy in older patients is similar to that in younger patients, and the absolute benefit is typically greater than in younger patients. Particularly in secondary prevention, the absolute benefits are large enough that many older patients with CHD would benefit from lipid-lowering therapy, and older patients with a reasonable life expectancy may also benefit in primary prevention. Side effects of lipid lowering therapy may also be similar in older and younger patients. (See ‘Benefits of lipid lowering lipid in the elderly’ above.)
  • Reductions in events with statin therapy can occur quickly (within weeks to months), and so even in older patients such therapy can be expected to reduce events during a patient’s expected lifespan. (See ‘Time course for CHD benefit’ above.)
  • Secondary causes of dyslipidemia such as hypothyroidism, diabetes, nephrotic syndrome, and drug effects should be considered, particularly in older patients. (See “Secondary causes of dyslipidemia”.)

 

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REFERENCES

 

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