The Future of Primary Care: Perspectives in the New England Journal of Medicine

Our readers may be interested in several perspectives on the state of primary care in the U.S. that appear in the current New England Journal of Medicine.

Six experts approach the topic from various angles, including the need to refocus on the physician-patient relationship and a call for reform of payment systems. Several of the commentators also took part in a roundtable discussion, which was videotaped and is available on the journal’s website.

Barbara Starfield, M.D., M.P.H.

The editors asked several experts to share their perspectives on the crisis in U.S. primary care. Their articles, which address this crisis from six different angles, follow. We also brought the five U.S. contributors together for a roundtable discussion of the problems and potential solutions for training, practice, compensation, and systemic change. A video of the discussion and reader comments can be seen at

Robust evidence shows that patient care delivered with a primary care orientation is associated with more effective, equitable, and efficient health services. Countries more oriented to primary care have residents in better health at lower costs. Health is better in U.S. regions that have more primary care physicians, whereas several aspects of health are worse in areas with the greatest supply of specialists. People report better health when their regular source of care performs primary care functions well. In addition to features promoting effectiveness and efficiency, there are fewer disparities in health across population subgroups in primary care–oriented health systems.

Important functions of primary care include serving as the first point of contact for all new health needs and problems; delivering long-term, person-focused care; comprehensively meeting all health needs except those whose rarity renders it impossible for a generalist to maintain competence in them; and coordinating care that must be received elsewhere. The appropriateness of primary care–based health systems has been endorsed by the Pan American Health Organization and the World Health Organization.

The United States now ranks 15th to 40th worldwide on various key health measures, such as life expectancy or years of life lost owing to preventable causes. And our rank has been falling steadily, indicating a need to reassess the delivery of services and the balance between primary care and specialty services. Today, more than half of specialist visits are for routine follow-up — a misuse of expensive resources. There are large interregional variations in referral rates and use of specialist services that cannot be explained by differences in patients’ needs. Primary care services in most industrialized countries are more comprehensive than those in the United States, where patients are often referred to specialists for problems — such as conditions requiring minor surgery or joint aspirations — that are common in the population and should therefore be addressed in primary care.

There are a number of policy options for improving U.S. primary care. The first imperative is to recognize that the health services system is dysfunctional. Most approaches to reform do not distinguish the use of primary care services from that of specialty services, despite the underuse of the former and overuse of the latter.

Second, perverse financing incentives must be eliminated. Federal subsidies for specialists’ training programs now greatly exceed those for primary care physicians — a situation that needs redressing. Encouraging the use of primary care physicians for common health needs instead of specialists in diseases, organ systems, or procedures requires increasing earnings of the former to levels commensurate with those of the latter. In many countries, specialists are paid by salary. In other places, specialist-visit reimbursements are lower when patients are not referred by a primary care physician.

Relatedly, better use of information on the frequency of various illnesses and complications could provide a much-needed basis for understanding when specialist services are warranted. These criteria should focus on the likelihood that patients have uncommon conditions or unusual complications. Primary care management for the vast majority of health problems should be the rule for most diagnosis and care, with specialist intervention when diagnosis requires confirmation with the use of special technology that is impractical to provide in primary care settings. For management dilemmas, primary care physicians can often seek advice from a specialist themselves, obviating the need for direct contact between patient and specialist.

In addition, evidence regarding the benefits of health services interventions in primary care would be more useful if interventions were tested in community-based primary care settings. Primary care practitioners should be the main decision makers about the applicability of clinical-trial results in primary care populations.

Since it will be a long time before U.S. primary care services are equitably distributed, the network of federally funded community health centers should be expanded in areas of shortage. At the same time, we urgently need to standardize insurance benefits to ensure that the benefits of health services are equally available to everyone.

Health challenges are changing. States of increased risk, such as elevated blood sugar level or elevated blood pressure, are now treated as diseases. With conditions being diagnosed earlier and populations aging, the prevalence of various illnesses has increased, their character has changed, and patients with multiple coexisting conditions are common. Still, much of primary care consists of dealing with problems that are never attributed to a specific diagnosis.5

Better patient-level measures, such as physical and emotional signs and symptoms, rather than disease-oriented measures, such as laboratory values, will be necessary to more adequately assess outcomes and the quality of care.

Finally, new approaches to information technology will be needed to facilitate the recording of patients’ problems and assessment of their responsiveness to interventions, encourage practice-based learning about interventions’ effects, eliminate duplicate and conflicting services through care coordination, and provide for ongoing upgrading of an information base for assessing community health needs and detecting adverse effects, incipient epidemics, and health-compromising exposures.

A stronger primary care infrastructure — with more appropriate, evidence-based specialty care as backup — demands policy consideration if the United States is to improve its international standing in health.

No potential conflict of interest relevant to this article was reported.

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Dr. Starfield is a professor of health policy and management at the Bloomberg School of Public Health, Johns Hopkins University, Baltimore.

Lessons from the U.K.

Martin Roland, D.M.

The editors asked several experts to share their perspectives on the crisis in U.S. primary care. Their articles, which address this crisis from six different angles, follow. We also brought the five U.S. contributors together for a roundtable discussion of the problems and potential solutions for training, practice, compensation, and systemic change. A video of the discussion and reader comments can be seen at

The United Kingdom takes the importance of primary care for granted. The U.K. government is effectively the country’s single payer, and successive administrations have been convinced by mounting evidence that primary care promotes high-quality, cost-effective, and equitable health care.1

If anything, the U.K. government has become more convinced over the past 15 years that strong primary care needs to be at the heart of the country’s health care system — quite the reverse of the situation in the United States. U.K. primary care physicians now have average earnings of $220,000 (in U.S. dollars), which is more than many specialists earn. The payment system is a mixture of risk-adjusted capitation and 25% additional pay for performance.

Having a single-payer system helps a great deal in terms of organizing quality-improvement activities. Over the past decade, the U.K. government has been able to introduce myriad nationwide quality-improvement initiatives, ranging from annual performance reviews of all physicians by local peers and national standards for the care of major diseases to coordinated local programs of clinical auditing. These activities have resulted in substantial quality gains2 so that the additional introduction of a major pay-for-performance scheme in 2004 resulted in only modest further improvement.

Redesigning Primary Care

In a video roundtable discussion moderated by Dr. Thomas Lee, four experts in primary care and related policy explore the crisis, as well as possible solutions for training, practice, compensation, and systemic change.

U.K. primary care physicians increasingly work in multidisciplinary teams, with nurses taking on an increasing proportion of the work. Nurses see patients with minor illnesses and assume responsibility for the routine management of chronic diseases. Physicians generally agree that it makes sense to hire nurses to provide protocol-driven care for chronic diseases. This model has now become universal for primary care in Britain, although there is some concern that the increasing use of nurses in specialized roles may result in physicians’ becoming “deskilled.”4

Having a single-payer system also means that U.K. primary care physicians hold each patient’s lifelong record, which includes a letter regarding every visit to a specialist. Virtually all primary care physicians use electronic medical records, and laboratories now generally download lab results directly into family practitioners’ computer systems. Again, the government took advantage of having a single-payer system to define common standards to which all suppliers of electronic medical records must adhere.

Some U.K. primary care physicians are concerned that they are losing the personal contact they used to have with patients. Many recognize that the very personal care long associated with the “family doctor” is becoming less common. To some extent this is because primary care physicians have increasingly focused on clinical quality indicators for major chronic diseases and work in larger teams with other physicians and nurses in an effort to perform well on those measures.4

If such a team becomes too large and the physician becomes too remote from the patient, however, other aspects of care may suffer. To redress this balance, the U.K. government is now starting to survey patients, and it plans to use the results to report publicly on continuity of care and the interpersonal qualities of physicians in all 8500 primary care practices in England.

U.K. primary care physicians gave up contractual responsibility for providing 24-hour care in 2004. Although this move was very popular with physicians, it may turn out to have done long-term harm to both physicians and patients. Most physicians were already organized into large groups for the provision of off-hours care, so the actual additional workload was small. Since the change, off-hours care has become much more fragmented. Patients sometimes receive poor service, and they have lost the sense they once had that their primary care physician was “always there for them” (even if, in reality, he or she rarely was).

It is hard to discuss U.K. medical care without mentioning universal coverage. Although it may not be politically achievable in the United States, universal access to care is probably the key factor behind findings that U.K. citizens have better health outcomes than their U.S. counterparts despite having health care costs that are a fraction of those in the United States.5

Although some features of U.K. health care would be hard to transplant to the United States, some that seem to work well in Britain have been advocated by U.S. experts on primary care — for example, registration with a primary care physician, payment involving a mix of risk-adjusted capitation and pay for performance, electronic medical records, and the use of extended teams to improve quality. Are these approaches beyond the realm of political possibility for U.S. health care?

No potential conflict of interest relevant to this article was reported.

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Dr. Roland is a professor of general practice and director of the National Primary Care Research and Development Centre, University of Manchester, Manchester, United Kingdom.

The Healthy Skinny Pill

Marathon mice: Last year, scientists tested the health effects of resveratrol, a compound found in red wine, that targets the same pathway as the synthetic compound SRT1720. In both instances, mice fed these compounds have increased running endurance. The mouse on the right (fed resveratrol) runs for longer than the untreated mouse on the left.
Credit: Institut Clinique de la Souris, Illkirch, France

MIT Technology Review, November 13, 2008, by Brittany Sauser — A pill that delivers the health benefits of diet and exercise without any of the effort is one step closer to becoming a reality. European scientists have found that mice fed a high-fat, high-calorie diet and prevented from exercising regularly can be protected from weight gain and metabolic disorders when given a drug that targets a gene linked to longevity. The treatment even increases the animals’ running endurance.

The drug was developed last year by Sirtris Pharmaceuticals, based in Cambridge, MA, and preliminary studies of the compound showed it to be effective in treating mice models of type 2 diabetes, a disease that results in an impaired ability to produce or process insulin, the risk of which increases with age. Now scientists led by professor Johan Auwerx at Ecole Polytechnique Federale de Lausanne (EPFL), in Switzerland, have shown that the compound involved, known as SRT1720, also blocks weight gain and obesity-related disorders and increases muscle stamina.

In the study, scientists fed the mice a high-fat, high-calorie diet mixed with doses of SRT1720 for approximately 10 weeks. The mice were given 100 or 500 milligrams of fat per kilogram of body weight each day (a high dose even for humans). The mice did not exercise regularly, although the scientists tested the animals’ exercise capacity, or endurance, by making them run on a treadmill. “The mice treated with the compound ran significantly longer,” says Auwerx. The drug also protected the animals from the negative effects of high-calorie diets: metabolic disorders, obesity-related diseases, and insulin resistance. It even improved the mice’s cholesterol.

It is significant that the drug mimics the effects of a calorie-restricted diet, since this has previously been tied to increased life expectancy, says William Evans, a professor of geriatric medicine, nutrition, and physiology at the University of Arkansas for Medical Sciences.

It’s as if the couch-potato mice underwent a strict diet and exercise regime, says David Sinclair, a biologist at Harvard Medical School, in Boston, who is one of the cofounders of Sirtris but was not involved in the current study. The new study “is a major step forward, showing that we can design and synthesize potent, druglike molecules that could slow down the aging process,” says Sinclair.

The effects of the compound are similar to those of resveratrol, a molecule found in red wine that has previously been shown to extend life span and have health benefits in mice. But SRT1720 is a thousand times more potent than resveratrol, meaning that it could be taken in smaller doses. A person would have to drink hundreds of glasses of wine to get the same health benefits from resveratrol, and, while supplements are available, it is unclear whether they are as effective. “Resveratrol will pretty soon look like ancient technology,” says Sinclair.

The findings in the new study, which is published in the November issue of the journal Cell Metabolism, also answer a big scientific question: whether scientists searching for ways to combat aging have been targeting the right gene.

SRT1720, like resveratrol, works by targeting a gene known as sirtuin 1, or SIRT1, which many scientists believe plays a fundamental role in regulating life span. SIRT1 encodes for a class of proteins known as sirtuins, and it is a central controller of mitochondrial activity (mitochondria are the powerhouse energy providers to the cells). “Firing up mitochondria is one of the best treatments against diabetes and obesity because you burn off extra energy instead of storing it,” notes Auwerx.

However, unlike the new compound, resveratrol is not specific to SIRT1, and thus many experts have questioned whether the effects of resveratrol in mice were mediated by SIRT1 activation or by some other pathway.

The fact that another chemical activates the same gene and produces similar effects strongly suggests that the metabolic benefits can be attributed to SIRT1, says Leonard Guarente, an MIT biologist whose lab first discovered the sirtuin 1 gene. He is on Sirtris’s advisory board but wasn’t involved in the study. “This is a very important finding, and [it] means that [SIRT1 activators] are good candidates for lead compounds [in] antidiabetic drugs in humans,” Guarente says. SIRT1 could also be a target for other diseases related to aging, he adds, “which would be a silver bullet.”

“The scientific community is focusing on mitochondria as the most important organelle in muscle that affects the risk of diabetes, hypertension, and the loss of physical function in elderly people,” says Evans. “The compound may be one additional help or aid that we could use to treat these conditions. It is an exciting, new development.”

Sinclair says that a cousin molecule of SRT1720, which is even more potent, is currently in human trials and will enter clinical studies for the treatment of diseases like type 2 diabetes in 2009. “We could know as early as next year if the same types of benefits we see in mice, we see in humans,” he says.

Synthetic biology could yield microbes that fight cavities and produce vitamins

Engineering Edible Bacteria

Plaque-busting bugs: Students from MIT are engineering the bacterium Lactobacillus bulgaricus (shown here in brown), found in yogurt, to prevent cavities.
Credit: Utah State University

MIT Technology Review, November 13, 2008, by Emily Singer — Probiotics, a field that seeks to use edible bacteria to improve human health, may soon undergo a metamorphosis. Students at MIT and Caltech are using the techniques of synthetic biology to create bacteria that fight cavities, produce vitamins, and treat lactose intolerance, as part of the International Genetically Engineered Machines (iGEM) competition at MIT. The new research might lead to a cheaper way to produce medicines or improve diets in the developing world.

Synthetic biology is the quest to design and build novel organisms that perform useful functions. Much research in the field has concentrated on using bacteria as a factory: one of its early successes was the development of microbes that produce malaria medicine. Other research has investigated targeted delivery vehicles, such as microbes engineered to bring medicine to a specific part of the body. But the new projects are attempts to enhance the health benefits of edible bacteria.

These projects capitalize on the fact that our bodies are already colonized by billions of bacteria. “If you really want to apply a bacterium to a person, think about where they naturally exist and survive in a human while still trying to engineer new functions,” says Christina Smolke, a synthetic biologist at Caltech who advises the university’s team.

Our mouths, for example, are a haven to bacteria, both good and bad. Bacteria that live in the dental plaque, called Streptococcus mutans, feed off of sugar on our teeth and then excrete acids, which wear away dental enamel and cause cavities. To create cavity-fighting microbes, the MIT team started with a peptide–a short protein segment–that has been previously shown to prevent the bad bacteria from sticking to the teeth. The team built a piece of DNA containing both the gene that makes the peptide and a gene for a molecular signal that causes the bacterium to excrete it.

The next step will be to insert this piece of DNA into Lactobacillus bulgaricus, a microbe common in yogurt. The students haven’t done that yet, but they have successfully introduced foreign DNA into the microbe, which primes the microbe for further genetic engineering. That in itself is an impressive feat, given that Lactobacillus bulgaricus is not commonly used in the lab and thus requires development of new experimental techniques.

If the microbe can be successfully engineered, eating yogurt would deposit it on the teeth, where it would produce the protective peptide. “This would probably be more effective than an antibacterial that kills everything,” says Chia-Yung Wu, a biology graduate student at MIT who advises the team. “It just targets the harmful stuff.” (A common problem with antibiotics is that they kill both harmful and helpful bacteria in the mouth and gut, leaving an open landscape for bad bacteria to colonize.)

One central project in synthetic biology is the attempt to create a huge, publicly accessible “parts list,” a catalogue of gene sequences and the functions of the resulting proteins. The MIT team doesn’t intend to develop a product for commercial use, but the biological parts that it creates might one day be used in other applications–enhancing the nutritional value of yogurt, for example, with bacteria that produce a specific type of vitamin. The team, which includes undergrads Sara Mouradian and Derek Ju, has already deposited the parts that it’s created in a central repository at MIT called the Registry of Standard Biological Parts. Expanding the registry is one of the most important aspects of the competition. “This year, we sent out 2,000 DNA parts to each team, and we’re getting back 1,500 new parts,” says Randy Rettberg, iGEM director and a principal research scientist at MIT.

The Caltech team focused on microbes in the gut, aiming to create a microbial solution to lactose intolerance. “Rather than taking a daily vitamin, you could drink some gut microbes and be set for a week or month or however long the microbes last,” says Josh Michener, a Caltech graduate student who advises the team.

People who can tolerate dairy naturally secrete lactase, an enzyme that breaks down lactose, a sugar in milk. The breakdown products, which include glucose, are then absorbed into the blood from the small intestine. In people who are lactose intolerant, the sugar is passed to the large intestine, where it is eventually metabolized by a chain of bacteria. In the process, the microbes produce hydrogen and methane gas, the culprits behind the troublesome symptoms–nausea, bloating, gas, and diarrhea–of the disorder.

Lactase pills are available to help people digest milk products, but the Caltech students wanted a more permanent solution. They started with a strain of E. coli often used as a probiotic in Germany. The strain, called Nissle 1917, was originally extracted from soldiers in World War I who were immune to an extreme gastrointestinal virus that swept through an army camp, says Michener.

The students added three biological parts to the Nissle bacterium: a gene that produces the lactase enzyme, a receptor that recognizes lactose, and a sensor that causes the cell to break open at a certain concentration of lactose. With this system, bacteria in the gut would constantly produce lactase. When the receptors on a bacterium’s outer surface bound to a sufficient amount of lactose, they would trigger the explosion of the cell, releasing lactase into the intestine to break down the sugar. The students have so far created the first two components but are having trouble designing the microbes to self-destruct in the proper manner. The team is also working on an edible microbe that would produce folate, a vitamin important for preventing birth defects.

Both teams presented their research at the iGEM competition at MIT this weekend, along with more than 70 other teams from universities around the globe. In past years, students have created everything from bacterial photographic film to banana-scented bacteria and tiny boxes made of DNA.

Geared up: Two immune cells (gray) wear polymer “backpacks” (green). The attached backpacks have two layers: a cell adhesion layer that grabs on to the cell surface, and a payload layer that carries some chemical cargo–in this case, green fluorescent dye. Researchers hope that the backpacks can one day be adapted to deliver drugs or imaging agents to specific regions in the body.
Credit: Nano Letters

Polymer patches hitched to the surfaces of immune cells can transport a variety of cargo

MIT Technology Review, November 13, 2008, by Jocelyn Rice — Living cells wearing microscopic “backpacks”–nanostructured polymer patches loaded with chemical cargo–might one day be able to ferry drugs or imaging agents to diseased tissue. MIT researchers say that they have successfully constructed such backpacks, filled them with magnetic particles, and tethered them to the surfaces of immune cells without disrupting the cells’ ability to interact with their environment. The work is described in a recent issue of Nano Letters.

“Overall, this is a very significant piece of work,” says Michael Sailor, a professor of chemistry and biochemistry at the University of California, San Diego, who was not involved in the study. “There are many possible variations on this theme for a host of different diseases. I think it could start an entirely new subdiscipline.”

The backpacks are built from three thin layers of polymer film. The bottom layer anchors the backpack to a surface during construction and loading. The middle layer carries the backpack’s cargo. And the top layer acts as a hook that latches on to a cell’s surface.

Once they had synthesized the backpacks, the researchers added a solution containing living immune cells, which were immediately hooked by the backpacks’ top layers. Then, by lowering the temperature, they triggered the bottom polymer layers to dissolve, releasing the backpack-wearing cells from the surface.

This process allows for incredible versatility in the backpacks’ cargo, says Michael Rubner, director of MIT’s Center for Materials Science and Engineering and senior author of the paper. Because the cells aren’t added until the very end, there’s no danger in using toxic chemicals and harsh conditions to build and load the backpacks. “You can use all the harsh chemistry you want, because the cell isn’t there to be killed,” says Rubner. “It’s only in the last step of the process that the cell attaches to the surface, grabs its backpack, and lifts it off.”

To test how tightly the backpacks attached, the researchers filled them with magnetic nanoparticles, loaded them onto immune cells, and placed the cells near a magnet. Under a microscope, the cells could be seen migrating toward the magnet–tugged along by their backpacks, which stayed firmly anchored in place.

Usually, particles incorporated into a cell’s surface are internalized in a matter of seconds, says Mauro Ferrari, director of the division of nanomedicine at the University of Texas, who was not involved in the work. “The fact that this thing stays there for longer than seconds is remarkable,” he says.

Sailor cautions that while the technology is promising, the real challenge will be getting it to work inside the body. There’s no way of knowing at this stage how the backpack-wearing cells would fare as they circulated in the bloodstream. They might engulf or shed their packs, or lodge in tight spaces. Initial studies suggest that the backpacks don’t pose any danger to the immune cells’ health, but much more work is needed before the system can be tested inside a living animal, says Rubner.

When they do reach the point of animal testing, the researchers plan to start by loading the backpacks with a trackable substance–perhaps the magnetic nanoparticles, which can be imaged by MRI, or perhaps fluorescent molecules. That will allow the team to determine how the cells migrate, and whether they reach the desired targets.

Eventually, Rubner and his colleagues envision using the backpacks for therapies that retool the body’s own immune system to attack diseased or cancerous tissue. For example, immune cells could be removed from the bloodstream, equipped with backpacks, activated to home in on a tumor, and returned to the body. There, they would deliver their cargo–be it an imaging agent or a chemotherapeutic drug–directly to the tumor, sparing healthy tissues from exposure to the toxic payload.

The researchers initially expected that each backpack would adhere uniformly to its carrier cell’s surface, much like a Band-Aid. Instead, the patches seemed to stick firmly at one spot, with the rest dangling off–sort of like a real backpack, which anchors only at the shoulders, says Rubner. This unexpected phenomenon might actually come in handy, he says. Immune cells need to squeeze through narrow openings in the body; a plastered-on pack might make cells less pliable, while a dangling pack could be pulled through.

For the most part, the cells and backpacks hooked up in a one-to-one ratio. But occasionally, under certain conditions, giant clumps of aggregated cells and backpacks formed. Because the backpacks didn’t lie flat against the cells, more than one cell could latch on to a single patch, or more than one patch could attach to a cell. Rubner hopes that his team can learn how to manipulate this process, perhaps serving as a basis for bottom-up tissue engineering.

“This is a new approach,” says Rubner. “There’s a lot of flexibility in what you can do with it, and we’re hopeful that flexibility is going to turn into something that’s going to have great value for society.”

“But that’s going to take a while,” he adds.

Vive la différence. Extra (green) or missing (red) copies of genes can drive evolution.
Credit: Adapted from G. Perry et al., Genome Research (2008)

ScienceNOW/Daily News, November 2008, by Jon Cohen — As close as humans are to chimpanzees, why do they dodge some diseases that afflict us? And why are we different on so many other levels? A new study that compares genomes from more humans and chimps than ever before suggests that these and other variations might stem from extra or missing copies of key genes.

Although small genetic mutations often receive top billing as the drivers of evolution, the new study focuses on entire genes that are deleted or duplicated, so-called copy number variants (CNVs). Humans and chimps carry two copies of most genes, but different individuals can be missing a gene altogether or have a dozen extra copies. Studies in humans have connected CNVs to myriad diseases, to how we metabolize food, and even to how much testosterone men make. These results led a group headed by molecular cytogeneticist Richard Redon of the Wellcome Trust Sanger Institute near Cambridge, U.K., to collect DNA from 30 chimps and 30 humans and compare regions in which stretches were deleted or copied. (For technical reasons, CNV regions, or CNVRs, are easier to identify than CNVs themselves.)

Earlier studies, like this one, included far fewer individuals, which made it difficult to draw firm conclusions, such as whether an extra gene in a human had evolutionary significance or was just a personal peculiarity, says Redon.

The researchers found several hundred CNVRs in each species, but a big evolutionary question loomed: How many of these are in all humans and all chimps and are thus “fixed” differences that denote evolutionary changes between the two species?

To answer this question, they compared CNVRs in a “reference” human to a reference chimp, which revealed more than 300 copy-number differences. With their data from the 60 other chimps and humans, they determined that 92 copy-number differences between the species were fixed. The team publishes its findings in this month’s issue of Genome Research.

First author George Perry, a molecular anthropologist who recently moved from the University of Arizona, Tempe, to the University of Chicago, says some of these variants may help explain phenotypic differences between the species. “There are lots of examples from other species where there’s gene duplication, and then one of the copied genes changes slightly and it results in physical innovations,” he explains. Similarly, gene deletions can have profound effects.

As an example, Perry points to a gene involved in cholesterol metabolism called APOL1 that has been deleted in chimpanzees; in humans, it confers resistance to a parasite that causes sleeping sickness. Other fixed differences the team uncovered include genes for inflammatory responses and cell growth. The researchers also found evidence that questions whether a CNV that became famous for influencing human susceptibility to HIV, CCL3L1, evolved because of AIDS, as earlier studies asserted.

Geneticist Chris Ponting, who studies comparative genomics at the University of Oxford in the U.K., says the study provides “tantalizing clues.” Yet Ponting and the authors caution that many more genomic comparisons of chimpanzees and humans–and finer tools than this study used–will be necessary to identify which CNVs evolved because of natural selection and truly have an impact. Still, Ponting says the study “has shown the way forward in how to approach this issue under an overarching evolutionary framework.”

Harvard Medical School — Heart failure — which means the heart can’t pump as well as it should — is a serious but manageable condition. It’s more common than you might guess: an estimated 5.2 million adults in the United States have heart failure, and 550,000 new cases are revealed each year. Most cases stem from heart muscle damage after a heart attack. The information in this report will help you understand heart failure so that you can actively participate in your care.

Are there different kinds of heart failure?

Q: Several years ago, a friend in my sewing circle was diagnosed with congestive heart failure. My doctor just told me I have heart failure. Are these the same condition or different ones?

A. You and your friend have the same problem: your hearts are having trouble pumping blood effectively. Doctors used to call it congestive heart failure, because many people with it had fluid buildup in the lungs (hence the “congestive”) and legs. But others don’t. That’s why we now call it just heart failure.

This isn’t to say that all heart failure is the same. There are two important types. In people with systolic heart failure, the heart muscle becomes stretchy and weak. People with diastolic heart failure have the opposite problem — the heart muscle becomes too stiff and can’t relax enough to completely fill with blood. The end result in both is a reduction in the amount of blood that each heartbeat pumps into circulation. An echocardiogram can reveal which type a person has.

It’s important to know the difference, because systolic and diastolic heart failure require different treatments. Although many of the same drugs are used for both conditions, the focus of management and the doses of medication vary.

Another common name, chronic heart failure, is also falling by the wayside. Although most heart failure is, indeed, chronic, meaning long-lasting, some episodes occur suddenly, and can go away almost as quickly.

— Thomas Lee, M.D.

Editor in Chief, Harvard Heart Letter