The Dollars and Sense of Alzheimer’s

June 19, 2015 by

June 19, 2015

By Medical Discovery News

As people age, they begin to worry about developing dementia and its most common cause, Alzheimer’s. Alzheimer’s is a neurodegenerative disease that can affect your cognitive abilities, the ability to function in daily life, and orientation. If that’s not devastating enough, those with Alzheimer’s only live four to eight years on average after diagnosis.

In America, Alzheimer’s is the 6th leading cause of death. Today 5.1 million of those 65 or older are living with this disease, a number that is only expected to grow as the population ages – by 2050 it is projected to affect 13.5 million of those 65 or older. The few drugs readily available only moderate the symptoms, as there is no way to cure, slow, or prevent Alzheimer’s.

Recently, the Alzheimer’s Association published a report called “Changing the Trajectory of Alzheimer’s Disease: How a Treatment by 2025 Saves Lives and Dollars.” It focuses on the costs associated with a theoretical treatment that could delay the onset of Alzheimer’s for five years. If such a thing were discovered, it could have a huge impact on people’s lives and their financial.

Since Alzheimer’s is a disease of older Americans, treatments for it are mostly funded by Medicaid and Medicare. Currently, Medicare covers 80 percent of the total costs of Alzheimer’s care in America, which equates to $153 billion. By 2050, the total costs of caring for those with Alzheimer’s is expected to rise to $1.1 trillion, with Medicare allocating one-third of all its expenses to treating it.

Within the Alzheimer’s population, a higher proportion will be in severe stages of the disease by 2050, as opposed to early or moderate stages. In the early stage of the disease, people can continue everyday functions and may appear symptom-free. They do have deficits in their abilities to think and learn, but the financial impact and burden on family members are low. In the moderate stage, memory lapses, inability to express thoughts, and confusion become apparent. Finally, in the severe stage, people have trouble taking care of themselves and require extensive daily care. In 2050, almost half of those affected will be in the severe stage.

The Alzheimer’s Assocation presents a case for funding biomedical research now, before the human and economic costs can be realized. For the sake of argument, they describe a hypothetical new treatment that would delay the onset of Alzheimer’s symptoms by five years. If such a thing were available by 2025, it would save $220 billion in its first five years. By 2050, 6 million fewer people would be affected by Alzheimer’s, saving families $90 billion in healthcare costs and the federal government $367 billion. Even if such research costs $2 billion a year starting today, a way to delay Alzheimer’s by just five years would pay for itself within three years.

Research from very basic studies on the brain to translational research leading to new therapeutics and early diagnostics are desperately needed. There are many promising studies that suggest a delay in the progression or even cure for Alzheimer’s are possible.

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Gesundheit Again

June 12, 2015 by

By Medical Discovery News

June 12, 2015

Person sneezing

Have you ever noticed that many times sneezes come in threes? Repeated sneezes may be your body’s efforts to get rid of irritants in the nose when the initial sneeze is not strong enough to do so.

Sneezing has different meanings in cultures around the world. The Athenian General Xenophon gave an encouraging speech to his army that went on for an hour until a soldier sneezed. Taken as a favorable sign from the gods, the army proceeded to attack the Persians, but was ultimately defeated and the general killed. One of the Pagan beliefs is that sneezing opened one’s body to Satan or evil spirits, which is how the common response “Bless You” arose. In fact, Pope Gregory VII made the short prayer “May God Bless You” a required response to a sneeze as protection from the Black Plague. As you can see, the sneeze has often been misinterpreted in history.

The sneeze can be divided into two phases. The first phase, called the nasal or sensitive phase, results from a chemical or physical irritation of the tissue lining the nose called the nasal mucosa. This signal is transmitted through nerves to the sneezing center of the brain in the lateral medulla. The second phase begins once a sufficient number of nerves are stimulated. This is when the eyes shut, a deep breath is taken, and the opening between the vocal chords closes, increasing lung pressure to allow an explosive release of air through the mouth and nose. The purpose of the sneeze is to dislodge the irritant from the nose, since an estimated 40,000 microscopic particles are expelled by a sneeze. The speed of a sneeze is estimated to be between 135 and 950 feet per second, or up to 85 percent of the speed of sound.

Allergies, infections, and inflammation of the nose’s mucous membrane (rhinitis) can trigger fits of sneezing. Allergies are the result of an immune response to substances in the environment that do not bother most people, like pollen, pet dander, or bee venom. People with allergies mount an immune response to those substances including the inflammation, which again irritates the nasal passages and causes sneezing. When you have a virus like the cold or flu, the immune response also causes inflammation of the nasal passages, which irritates the nerve endings and leads to the familiar itching and sneezing.

The sneeze is also a way for the body to reboot the environment in the nose, so the nasal mucosa can once again trap particles we breathe in from the environment. Sneezing more than once in a row is often an attempt to eject whatever is irritating the nasal passages when the first sneeze was not successful. This explains why people suffering from allergies sneeze more often, since the allergen they are trying to expel is still around. Other people who routinely sneeze many times in a row may just not have forceful sneezes.

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Bad News for Smokers

June 12, 2015 by

By Medical Discovery News

June 5, 2015

Person smoking a cigarette

Smoking isn’t the only thing that raises your risk of lung cancer. As it turns out, your DNA can have that effect too.

A scientific study scanned the genomes, the entire genetic code, of 11,000 people of European descent in an effort to identify if there was any correlation between gene sequences and a common form of lung cancer, non-small cell carcinoma. They discovered that variants of certain genes increase a person’s susceptibility to developing lung cancer, especially in smokers.

One of the three gene variants they identified, named BRCA2, can double a smoker’s chance for developing lung cancer. BRCA2 is a tumor suppressor gene. It encodes a protein involved in the repair of damaged DNA, which is critical to ensure the stability of cell’s genetic material. When cellular DNA is damaged, there are several ways for the body to detect and repair that damage. If the damage to DNA cannot be repaired, then the cell is programmed to die by a process called apoptosis in order to prevent the damage being passed on to its daughter cells.

Like other tumor suppressor genes, the BRCA2 protein helps to repair breaks in DNA. It also prevents damaged cells from growing and dividing too rapidly. Variants of BRCA2 associated with breast, ovarian, and now lung cancers produce proteins that do not repair DNA damage properly. This causes cells to accumulate additional mutations, which can lead to cells that grow and divide uncontrollably. Such mutations lead to an increased risk of developing cancer.

Scientists have discovered over 800 mutations of BRCA2 that cause disease, including breast, ovarian, lung, prostate, pancreatic, fallopian, and melanoma cancers. Most of the mutations result from the insertion or deletion of a few letters of genetic code into the part of the gene that code for a protein. This disrupts the production of the BRCA2 protein and results in a shortened and nonfunctional form of the BRCA2 protein.

Lung cancer is a leading killer of Americans. Nearly 160,000 Americans will die from lung cancer this year, representing 27 percent of all cancer deaths. Active smoking causes close to 90 percent of lung cancers.

The good news from this discovery is that since scientists first linked BRCA2 to an increased risk of breast cancer, new therapies have been developed. Current treatments for breast and ovarian cancers could be effective with BRCA2-associated lung cancers, such as PARP inhibition.  PARP1 is another protein involved in repairing DNA damage. When one of two strands of DNA are broken or nicked, PARP1 moves to the region and recruits other proteins to the site to repair the damage. Many chemotherapy agents kill cancer cells by inducing DNA damage in the tumor and inhibiting PARP1. This doesn’t allow cancer cells to repair damage and makes them more susceptible to chemotherapy and radiation therapy. Now that we know this gene is linked to lung cancer, such therapies may be more effective in treating lung cancer and saving lives.

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A Close-Up Look at Metastasis

June 12, 2015 by

By Medical Discovery News

May 29, 2015

A Close-Up Look at Metastasis

One of the things that make cancer cells so deadly is metastasis, their ability to dislodge from their original location and migrate to other tissues. Most people who die of cancer are victims of this process. Even if a tumor is removed surgically, doctors can’t be certain that some of the tumor cells haven’t already metastasized, hence the need for treatments such as chemotherapy to target those cells. Unsurprisingly, metastasis is a subject of intense research, and luckily scientists now have a new tool to help them understand how tumor cells move.

While most tumors have the ability to metastasize to many different tissues, they prefer to spread to certain ones, like those in the bones, liver, and lungs. Cancer begins to spread by invading nearby tissue, then through a process called intravasation, tumor cells enter a blood or lymphatic vessel, allowing them to circulate to other parts of the body.

When tumor cells stop moving in a tiny blood vessel called a capillary, the can move out of the blood vessel and into the tissue, which is called extravasation. They will proliferate in this new location and release signals to stimulate the production of new blood vessels to satisfy the oxygen and nutrient demands of the tumor, a process called angiogenesis. Not all cells of the tumor are equally capable of metastasizing, and depending on the new environment they may not be able to grow in their new locations. In general, cells in metastatic tumors acquire additional genetic mutations that make them better able to relocate to other sites in the body. In some cancers, the metastatic cells have evolved to be remarkably different from the original tumor cells, which may contribute to the failure of treatments, the identity of the original cancer, and the recurrence of cancer.

Engineers and scientists at Johns Hopkins University have reproduced the 3-D extracellular matrix (ECM) that surrounds human cells. They also created an artificial blood vessel that runs through the matrix to simulate the flow of blood or lymph. They then added breast cancer cells either individually or in clumps.

Using fluorescent microscopy, they studied how the tumor cells interacted with the model to investigate how tumor cells get into and out of vessels, a key step in metastasis. They found that the tumor cells first dissolved some of the ECM to form a tunnel. The cells moved back and forth within this tunnel, occasionally coming into contact with the vessel. Then the cancer cells attached to the vessel through a long process, finally sitting on the surface of the blood vessel. They appear to change shape and move along the outer surface of the blood vessel. After a few days, the cancer cells force their way between the outer cells of the vessel and are swept away by the fluid moving through it.

About 60-70 percent of cancer patients are already at the stage of metastasis by the time they have been diagnosed. This new device will allow scientists to gain a better understanding of the processes and molecular players in metastasis, which will hopefully lead to new interventions or therapies that could interrupt or prevent this process.

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You’re More Like Your Mother Than You Know

May 24, 2015 by

May 22, 2015

By Medical Discovery News

Photo of mother and child

While the benefits of breast feeding have been well-documented, scientists were surprised to learn of another one: breast milk contains a mother’s stem cells that become a part of different organs of the baby’s body.

Breast feeding protects infants against infections early in life and reduces their risk of juvenile diabetes, heart disease, and cancer as children. It also helps mothers lose weight after giving birth and lowers their risk of osteoporosis and uterine and ovarian cancer.

In addition, seven years ago scientists discovered the presence of mammary stem cells in breast milk. The mammary gland is unique in its ability to go through different stages in anticipation of producing milk, then a period of milk secretion followed by a return to the non-lactating state. All of this can occur as many times as necessary. This massive restructuring of the breast suggested the presence of stem cells.

Human breast milk contains about 14,000 cells in each milliliter. Most of these are the epithelial cells that are abundant in the breast and cells of the immune system. Some of the cells in breast milk had a molecule called nestin on the surface, which in adults is a marker for multipotent stem cells that can develop into many different types of cells, like those in the brain, pancreas, liver, skin, and bone marrow. When scientists transplanted a single nestin-positive stem cells into the fat pad of a grown mouse, it reconstituted a functional mammary gland. Scientists wondered if such cells were serving the same function in humans.

However, further research revealed quite a surprise. First, they genetically modified mice to produce a protein that makes the cells glow red under fluorescent light. Mothers with this new feature were given normal pups to nurse. When they were examined as adult mice, they had cells that glowed red like the mice they had nursed from in their blood, brain, thymus, pancreas, spleen, and kidneys. These cells became functional cells within these organs, so the ones in the brain behaved like neurons and those in the liver made albumin. Based on this experiment, breast milk stem cells travel into the baby’s blood and become functional parts of various organs, at least in mice.

In the laboratory, these stem cells have also shown the ability to differentiate into breast cells that produce milk in a petri dish, as well as bone cells, joint cells, brain cells, heart cells, liver cells, and pancreatic cells that synthesize insulin. In addition, this study may have also discovered a non-invasive, ethical, and sustainable source of multipotent stems.

We don’t yet fully understand the role of these cells in offspring, whether they maintain a tolerance for the mother’s milk, play a role in normal growth and development, or both. Until then, know that your mother is more a part of you than you ever realized.

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Cigars Are No Better

May 15, 2015 by

May 15, 2015

By Medical Discovery News

Person smoking a cigarette

A common argument made by those who smoke cigars is that they are safer than cigarettes.  However, several studies argue that this is not true.

Cigar smoking has increased dramatically in the U.S. Between 2000 and 2011, small cigar sales rose 65 percent and large cigar sales increased 233 percent. Americans smoked more than 13 million cigars in 2010, twice the number from 2000. About 13.4 million people age 12 or older smoke cigars. A cigar culture has arisen, with cigar bars or clubs, shops with walk-in humidors, and magazines for those who consider themselves cigar connoisseurs. Their use among sports figures and celebrities has made them seem fashionable or sophisticated, a symbol of status or success.

The tobacco in cigars is cured and fermented to enhance the flavor, but this process also increases the amounts of harmful ingredients. Cigars come in three basic sizes, but the classic cigars are the large ones that contain more than half an ounce of tobacco, and some contain as much as an entire pack of cigarettes.

Just like cigarettes, cigars contain nicotine and can be very addictive. Most people who smoke cigars do not inhale, and therefore the nicotine is absorbed more slowly. However, cigar smoke dissolves more easily in saliva than cigarette smoke, enhancing the amount of nicotine absorbed.  Smokers absorb one to two milligrams of nicotine out of the eight total milligrams in cigarettes. The large cigars contain anywhere from 100 to over 400 milligrams of nicotine, and the amount a person absorbs varies greatly depending on how long the cigar is smoked, how many puffs are taken, and how much smoke is inhaled. Second- and third-hand cigar smoke is dangerous, just like it is with cigarettes.

In one study, scientists measured the levels of two biomarkers for tobacco as well as arsenic and lead in over 25,000 cigar smokers. Cigar smokers had higher levels of these carcinogens than nonsmokers and equal levels to cigarette smokers. Overall, the study found that cigars are not safer than cigarettes. Cigar smokers are less likely to develop lung cancer than cigarette smokers, but they are at higher risks of developing other cancers.

Those who inhale while smoking cigars are more likely to develop laryngeal cancer, lung cancer, bladder cancer, pancreatic cancer, and cancers of the tongue, mouth, or throat than nonsmokers. Even those who don’t inhale the smoke directly still inhale the secondhand smoke and are at an increased risk of lung cancer. Cigar smokers are four to 10 times more likely to die from cancers of the mouth, larynx, and esophagus than nonsmokers.

Cigar smoking also increases the risk of other diseases including emphysema, chronic bronchitis, heart attacks, gum disease, and erectile dysfunction. One long-term study determined that cigar or pipe smoking costs people 10 years on average – they spent an extra five years in bad health and died five years earlier.

So before you take up cigars in an attempt to look cool, ask yourself if your image is more important than your health.

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Sweet Stem Cells

May 11, 2015 by

May 8, 2015

By Medical Discovery News

Stem Cells

Diabetes may be common, but it’s serious business. Diabetes is repeatedly in the top 10 causes of death for Americans, killing or contributing to the deaths of 300,000 Americans in 2010. An estimated one in 10 people have it, but about one-third of them are undiagnosed. Diabetes costs the country $250 billion. But scientists are working on some good news for diabetics with the help of stem cells.

Type 1 diabetes is largely associated with children and represents about 5 percent of all diabetes cases. The more common form, type 2 diabetes, mostly affects adults and manifests when cells do not use insulin effectively so higher levels are needed (also called insulin resistance). Insulin is a molecule of protein, made and secreted by beta cells in the pancreas, an organ that regulates glucose levels in the blood.

Diabetes is a multifaceted disease that leads to a host of medical conditions and complications, such as high blood pressure, elevated cholesterol, blindness, cardiovascular disease, and kidney problems. Those with diabetes are two times more likely to die of a heart attack and one and half times more likely to die of a stroke. Diabetes is the leading cause of kidney failure, leading to transplants and dialysis. Almost 60 percent of lower extremity amputations are the result of diabetes.

Administering insulin is a common treatment for the disease and there are many different forms that can be used. Insulin can be injected by a syringe or delivered via an automated pump. There are also different pharmaceuticals used in oral treatments for diabetes. Biomedical scientists are developing other methods to treat diabetes, such as transferring insulin-producing beta cells from a donated pancreas into a diabetic patient. This works well, but the cells stop working over time. Transplanting a whole pancreas is also an option that relieves the need to administer insulin, but there is always a short supply of donated organs and the possibility that the new body will reject it.

However, recent stem cell experiments by multiple groups working independently show promise. These cells, called S7, produce insulin and regulate the level of glucose in the blood and successfully eliminated diabetes in an animal model in about 40 days. Unlike organ transplants, there is no limit to the supply of these stems cells, no long wait for a donation that’s a good fit, and no need for immunosuppressant drugs.

But the method is not perfect. First, S7 cells react slower to glucose than natural beta cells and do not make as much insulin. There are also questions as to whether this approach could be used to treat Type 1 diabetes, because the insulin-producing cells are destroyed in an autoimmune process, which might destroy the transplanted cells as well.

It’s premature to claim this innovation is a victory over diabetes, but its development will definitely be worth following.

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The Birth of Ebola

May 11, 2015 by

May 1, 2015

By Medical Discovery News

Colorized micrograph of Ebola by Dr. F.A. Murphy

For most Americans, the Ebola scare seems to have come and gone, but that doesn’t mean the outbreak is over in Africa or that we’ve seen the last of the virus, especially considering its history. Scientists believed that Ebola is relatively new as far as viruses go – only 10,000 years old. However, ancient animal bones show that Ebola appeared between 16 and 23 million years ago, perhaps even earlier.

The Ebola virus was discovered in 1976 during two outbreaks in what was then called Northern Zaire (now the Democratic Republic of the Congo) and Southern Sudan. The outbreaks were actually caused by two different strains of the Ebola virus named Zaire and Sudan, with 90 and 50 percent mortality rates respectively. Since then, three other strains have been identified: Tai Forest, Bundibugyo, and Reston, which is the only one that doesn’t affect people. Overall, there have been 27 outbreaks, but the current outbreak that started in March 2014 is by far the worst, infecting almost 25,000 people and killing over 10,000, thereby making it the world’s first Ebola epidemic.

Ebola is a member of the filovirus family, which also includes the Marburg virus discovered in 1967. Filoviruses are zoonotic, meaning they replicate in other animals, their natural reservoirs, before transmitting to humans. The Ebola virus’s natural reservoir is African fruit bats, so it can transfer to humans who come into contact with an infected bat or another species that has been infected, such as chimpanzees, antelope, and porcupine. Then the virus can spread from person to person.

New research into the origins of filoviruses shows that they have evolutionary ties that go back millions of years. Scientists tracked the viruses’ origins by looking for pieces of their genetic information in fossilized animal bones. While using the bones to study the genomes of ancient voles and hamsters, they found the same pieces of the viruses’ genetic material in the same locations in both rodent species. This suggests that the viruses have existed at least as long as the two species have.

Given the billions of bases each animal has in its genome, it is highly unlikely that these fragments of viral genetic information would have been inserted in exactly the same locations during different infections. Scientists therefore concluded that the virus had infected a common ancestor of these two rodents sometime before the Miocene Epoch, 5-23 million years ago, around the time the great apes arose. Furthermore, the viral genetic elements more closely resemble Ebola than Marburg, meaning the two viruses had already diverged from each other. Sometime before then, the two viruses shared a common ancestor that has not yet been identified.

This means that these viruses have been coevolving with mammals for millions and millions of years, much longer than previously believed. An understanding of the origins and evolution of filoviruses could help us better prevent outbreaks of them and hopefully even create a vaccine that would be effective against all of them.

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The Teen Brain on Weed

April 25, 2015 by

April 24, 2015

By Medical Discovery News

A brain

It is now legal to use marijuana (recreationally and/or medically) in more than 20 states and the District of Columbia, and as more places debate legalizing the substance, more people are asking about its consequences on human health. There are many myths and misconceptions out there, but this is what science has to say about the subject.

As with all substances, the health effects depend on the potency, amount, and a person’s age. An independent scientific committee in the United Kingdom evaluated how harmful various drugs were based on 16 criteria and ranked heroin, crack cocaine, and methamphetamine as the most harmful drugs to individuals using them, and ranked alcohol, heroin, and crack cocaine as the drugs that cause the most harm to others. Marijuana ranks eighth, with slightly more than one-quarter the harm of alcohol.

Short-term use is associated with impaired short-term memory, making it difficult to learn and retain information while under the influence. Short-term use can also impair motor coordination, interfering with tasks such as driving. The overall risk of an accident doubles if a person drives soon after using marijuana. In comparison, those with blood alcohol levels above the legal limit are five times more likely to have an accident, and the combination of alcohol and marijuana is higher than either one alone.

Long-term or heavy use is associated with diminished life satisfaction and achievement overall. At high doses, marijuana can cause paranoia and psychosis, and long-term marijuana use increases the risk of developing schizophrenia or other chronic psychotic illnesses. Nine percent of all marijuana users, or 2.7 million people, develop an addiction to it. That figure jumps to 25-50 percent for those who use marijuana daily, and 17 percent of people who begin using marijuana as adolescents become addicted. Cannabis withdrawal syndrome is real and includes symptoms of irritability, sleep disturbance, dysphoria, craving, and anxiety.

Adults who occasionally use marijuana do so with little to no risk, but adolescent brains are not fully developed, making them more vulnerable to the adverse effects of marijuana. Using marijuana during adolescence can alter brain development, causing impaired cognition and lower IQs. This is probably because the active ingredient in marijuana, tetrahydrocannabinol, affects the brain’s ability to make connections between neurons in certain regions of the brain. Adolescent marijuana users also have a smaller hippocampus, which is important in learning and memory, and a less active prefrontal cortex, which is important in cognitive tasks such as planning and problem-solving.

Since acute marijuana intoxication can impair cognitive functions for days, students who use marijuana may function well below their natural abilities, causing academic difficulties. High school dropouts do report higher marijuana usage than their peers. Some evidence suggests that these cognitive impairments could be long-lasting or permanent in long-term users who started at younger ages, which can impact their abilities to succeed academically and professionally.

There is no clear association between long-term marijuana use and any deadly disease, although chronic marijuana smokers have increased rates of respiratory infections and pneumonia and an increased risk of heart attack and stroke. The effects of marijuana on a developing embryo and the effects of second-hand or third-hand marijuana smoke have not been well-studied, but as marijuana legalization continues to be an issue the science behind it will as well.

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The Bright Side of Black Death

April 25, 2015 by

April 17, 2015

By Medical Discovery News

Bright Side of Black Death

It’s easy to think that nothing good could come from a disease that killed millions of people. But Dr. Pat Shipman, an anthropologist at Pennsylvania State University, disputed that notion in his recent article in “American Scientist,” where he suggested the Black Death that ravaged Europe in the Middle Ages may have resulted in some positive effects on the human population. Considering that we are in the midst another significant plague (the Ebola virus in West Africa), we could certainly use more information about the role of pandemics on human populations.

The Black Death or Bubonic plague started in the mid-1300s and was caused by a bacterium called Yersinia pestis, which typically enters the body through the bite of a flea. Once inside, the bacterium concentrates in our lymph glands, which swell as the bacteria grow and overwhelm the immune system, and the swollen glands, called buboes, turn black. The bacteria can make their way to the lungs and are then expelled by coughing, which infects others who breathe in the bacteria. The rapid spread of the infection and high mortality rates wiped out whole villages, causing not only death from disease but starvation as crops were not planted or harvested. It killed somewhere between 100 million to 200 million people in Europe alone, which was one-third to one-half of the entire continent’s population at the time. The plague originated in the Far East and spread due to improved trade routes between these two parts of the world.

Today, global travel is easier than ever thanks to extensive international airline networks. Just like with the Black Death, our transportation systems could enhance the spread of a modern plague. Of course, modern healthcare is also more sophisticated and effective, but as the latest Ebola outbreak has reminded us, a pandemic is a realistic possibility.

Dr. Sharon DeWitte, a biological anthropologist at the University of South Carolina, recently made several discoveries from comparing the skeletal remains of those who died from the Black Death and those who died from other causes during the same era. First, she found that older people, who were therefore already frail, died at higher rates. Killing this group at a higher rate created a strong source of natural selection, removing the weakest part of the population.

After the plague years, she found that in general people lived longer. In medieval times, living to 50 was considered old age. But the children and grandchildren of plague survivors lived longer, probably because their predecessors lived long enough to pass on advantageous genes. Today, a genetic variant in European people called the CCR5-D32 allele, which was favored during the natural selection initiated by the plague, is associated with a higher resistance to HIV/AIDS.

Microbes have an intimate relationship with human populations and have shaped human evolution through the ages. We may see survivors of the Ebola virus passing on similarly advantageous genes through natural selection as well.

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