Obesity and Diabetes – Is Your Gut in Control?

August 28, 2015 by

Aug. 21, 2015

By Medical Discovery News

Your body is like a forest, providing a home to microscopic flora and fauna. In fact, your body is home to up to 100 times more microbes than your own cells, which make up your microbiome. While we provide them residence, these microbes help us out by providing a first line of defense against disease trying to invade our bodies, even breaking down food during digestion and producing vitamins. Now, the microbes that live in the digestive tract are helping us understand diabetes better.

According to the Human Microbiome Project sponsored by the National Institutes of Health, the microbiome plays a huge role in human health. When the microbiome is altered or imbalanced, it can cause conditions like obesity, irritable bowel syndrome, skin disease, urogenital infection, allergy, and can even affect emotion and behavior.

Recently, scientists from Israel discovered another surprising effect of the microbiome while investigating the use of artificial sweeteners in relation to glucose intolerance and diabetes. Artificial sweeteners such as saccharin, sucralose, and aspartame are commonly used in weight loss strategies because they do not add calories while still satisfying sweet cravings. However, artificial sweeteners are not always effective in managing weight and glucose, and scientists at the Weizmann Institute of Science may have figured out why.

Through experimentation they observed that adding artificial sweeteners to the diets of mice caused significant metabolic changes, including increasing blood sugar levels more than mice fed regular sugar. It didn’t matter whether the mouse was obese or at a normal weight, they all reacted the same. Dietary changes can alter the populations of bacteria in our guts, so the study addressed whether those changes affected blood glucose levels as well. After being treated with saccharin for nine days, the populations of gut bacteria in the mice shifted dramatically and corresponded with an increase in their glycemic index. Specifically, the bacterial group Bacteroidetes increased while the group Clostridiales decreased. These changes in bacterial populations is associated with obesity in mice and people.

When they administered antibiotics to reverse this and return the bacterial populations to a healthy state, it also countered the effects of saccharin, returning glucose levels to normal. To take it a step further, researchers took feces from saccharin-consuming mice showing glucose intolerance and transplanted them into other mice that had never consumed saccharin. Remarkably, those mice started showing signs of glucose intolerance.

In a study of 400 people, those who consumed artificial sweeteners had a gut microbiome that was vastly different from those who did not. They had a group of people consume high levels of artificial sweeteners for seven days, and like the rats their glucose levels increased and their microbiomes changed.

Overall, these studies show that artificial sweeteners may induce glucose intolerance instead of preventing it due to the intimate connection between the bacteria that live in our digestive systems and our metabolic state. In the future, expect to see diagnostic and therapeutic procedures that utilize our microbial friends.

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The Plague: It was the Gerbils

August 28, 2015 by

Aug. 7, 2015

By Medical Discovery News

In the past 800 years, many things have been blamed for the plague that swept through Europe in the Middle Ages: the alignment of the planets, bad air, lack of proper hygiene, black rats, and their fleas. Now scientists have data that suggests the climate in Central Asia at that time influenced the size of the great gerbil population, which triggered cycles of plague in Europe. These furry little rodents carried the plague bacterium, as did the fleas that fed on them. When the gerbil population shrank, the fleas found alternate hosts like horses, humans, and eventually rats, which then made their way to Europe and triggered the plague pandemics.

The plague was caused by the bacterium Yersinia pestis. It is transmitted to humans through the bite of a flea that has fed on an infected rodent. Plague outbreaks have afflicted humans for thousands of years and changed the course of history. The first recorded plague pandemic began in 541 and was named the Justinian Plague after the 6th century Byzantine emperor. Frequent outbreaks for the next 200 years are likely to have killed over 25 million people. The second pandemic, called the Great Plague or the Black Death, began in China and spread westward along trade routes to Constantinople and into Europe. About 60 percent of Europeans died, eliminating entire towns.

The third pandemic, or Modern Plague, also began in China and spread to Hong Kong by 1894. Rats hitching rides on steamships spread the plague to port cities around the world for the next 20 years, killing about 10 million people. By then scientists were able to identify the bacterium responsible and how it spread. Efforts to control the rat population eventually ended the pandemic. It continued to infect people (although in much smaller numbers than before) during the 20th century, such as in Vietnam during the war. The bacterium is still in the reservoir of wild rodents, and today most cases of plague are in sub-Saharan Africa and Madagascar. The plague can be effectively treated with common antibiotics, but if left untreated it has a high mortality rate.

Since there are still lots of rats in Europe, some wonder, why is there no plague? Researchers proposed that each time, the plague actually started in Asia. To test their theory, they examined climate records using the rings of trees. The incidence of plague did not correlate with climate changes in Europe, but it did with changes in Asia. It was already known that the Asian great gerbil carries Yersinia pestis, and when the weather in Asia was good, gerbils thrived, but when it turned bad, their population would crash. Then their fleas would seek another host such as human traders and their pack animals, who spread the plague to other parts of the world. They found no evidence that rodents in Europe carried Yersinia pestis, so that would explain why cases of the plague disappeared between pandemics.

So don’t worry about the little gerbils in the pet store – they are not carrying the plague.

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A Way Our of Our Antibiotic Crisis

August 28, 2015 by

July 24, 2015

By Medical Discovery News

A petri dish

Antibiotic resistance occurs when strains of bacteria that infect people – such as staph, tuberculosis, and gonorrhea – do not respond to antibiotic treatments. In America, 2 million people become infected with resistant bacteria every year and at least 23,000 die each year because of those infections. If nothing is done to stop or slow the resistance of bacteria to antibiotics, the World Health Organization (WHO) warns that we will find ourselves in a post-antibiotic world, in which minor injuries and common infections will be life-threatening once again.

The crisis arose primarily from three conditions. First, when people are given a weeks’ worth of antibiotics and stop taking them as soon as symptoms improve, they often expose the bacteria causing their infection to the medicine without killing it. This allows the bacteria to quickly mutate to further avoid the effects of the antibiotic. Second, antibiotics are over-prescribed. Most common illnesses like the cold, flu, sore throat, bronchitis, and ear infection are caused by viruses, not bacteria, so antibiotics are essentially useless against them. Yet they are prescribed 60-70 percent of the time for these infections. This once again provides bacteria in the body unnecessary contact with antibiotics. Third, tons of antibiotics are used every year in the agriculture industry. They are fed to livestock on a regular basis with feed to promote growth and theoretically for good health. But animals are also prone to bacterial infections, and now, to antibiotic-resistant bacteria, which spreads to humans who eat their meat or who eat crops that have been fertilized by the livestock. The good news is that the Food and Drug Administration (FDA) is working to focus antibiotic use on bacterial infections and regulate its use in livestock.

An easy solution to this problem might be to create new antibiotics, but it’s not that simple. It takes an average of 12 years and millions of dollars to research new antibiotics and make them available on the market, which is a huge investment considering they are normally only taken for up to 10 days. But there’s an even bigger challenge: microbiologists can only cultivate about 1 percent of all bacteria in the lab, including specimens that live in and on the human body. The ability to grow diverse bacteria is important because most antibiotics actually come from bacteria, produced as a defense against other microbes.

Slava Epstein, a professor of microbial ecology at Northeastern University, came up with an ingenious approach to solving this problem. He speculated that we are unable to grow these bacteria in the lab because we were not providing the essential nutrients they needed to grow. Working with soil bacteria, which are a huge source for developing antibiotics, he created the iChip. The iChip allows bacteria to grow directly in soil, which is their natural environment, while being monitored.

To date, about 24 potential antimicrobials have been identified from 50,000 bacteria that remain unable to grow in the lab. With possibly billions of bacteria left to grow and examine, the number of new drugs awaiting discovery is seemingly endless.

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The Catastrophe of Antibiotic Resistance

March 17, 2015 by

March 6, 2015

By Medical Discovery News

The Catastrophe of Antibiotic Resistance

The World Health Organization has categorized antibiotic resistance as “a major global threat” and multidisciplinary research teams estimate it could lead to 10 million deaths each year by 2050. Bacteria that cause disease in humans can become resistant to the drugs used to treat them, and this poses a growing problem to public health.

Antibiotics were first introduced in the 1940s with the discovery and development of penicillin and saved many people from otherwise life-threatening infections. This one class of drugs has had an incredible impact on decreasing the severity of infections and saving lives.

Lately antibiotics have become overused and misused, which has allowed bacteria to mutate in ways that render antibiotics relatively powerless. Bacteria were one of the earliest life forms on Earth and remain one of the most successful, present everywhere from Arctic glaciers to geothermal springs. Because they are masters of adaptation, exposure to antibiotics causes the bacteria to accumulate mutations that will allow them to ignore the action of the antibiotics. That’s why doctors should only prescribe an antibiotic in the likelihood of a bacterial infection, and why it’s important to take all of the prescribed doses of an antibiotic. Otherwise, you can give the bacteria enough contact with the antibiotic to mutate but not enough to kill them, and they can come back stronger.

Half the use of antibiotics does not come from a doctor’s office or hospital, but a farm. Chickens, pigs, cows, and other livestock raised for food production are fed antibiotics to prevent infections and for faster weight gain. Many countries now ban this practice, and in 2013 the U.S. Food and Drug Administration (FDA) asked pharmaceutical companies to voluntarily curtail the sale of antibiotics directly to famers. Today, 26 pharmaceutical companies will only issue antibiotics for animals with a veterinarian’s prescription.

Infections by drug-resistant bacteria can be twice as likely to result in hospitalization and death. And while some bacteria are resistant to a single antibiotic, others are resistant to many. Methicillin-resistant Staphylococcus aureus (MRSA), multi-drug-resistant Neisseria gonorrhea, and multi-drug-resistant Clostridium difficile are superbugs taking a devastating toll worldwide. Some bacteria have mutated against all forms of antibiotics normally used to treat them, leaving no effective treatment options. Such infections are occurring around the globe in both rich and developing countries.

Legislation in the U.S. Congress proposes to permanently ban antibiotics that are used in humans from being used in livestock as well.  However, some argue that there is not a clear link between the antibiotic-resistant bacterial strains generated in livestock practices and those seen in human disease, which requires more intense research to answer. Whatever the outcome, the emergence and spread of antibiotic-resistant bacteria must be stopped. We also desperately need to develop new antimicrobials human use.

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Semi-Precious Pathogens

October 17, 2014 by

Oct. 17, 2014

By Medical Discovery News

Bug in amber

Some diseases are older than others. AIDS, for instance, is a recent phenomenon, while malaria has plagued humans for millennia. Recently, scientists examining ticks fossilized in amber found they were infected with bacteria similar to those that cause Lyme disease, a spirochete named Borrelia burgdorferi. Lyme disease is a bacterial infection caused by the bite of an infected tick. The discovery of an ancient Borrelia-like bacterium, now named Palaeoborrelia dominicana, shows that tick-borne diseases have been around for millions of years.

Lyme disease was identified in the early 1970s when mysterious cases of rheumatoid arthritis struck children in Lyme, Conn., and two other nearby towns. The first symptom is a rash called erythema migrans, which begins with a small red spot where the tick bite occurred. Over the next few days or weeks, the rash gets larger, forming a circular or oval red rash much like a bull’s eye. This rash can stay small or can cover the entire back. But not everyone with Lyme disease gets this rash, and the other symptoms, including fever, headaches, stiff neck, body aches, and fatigue, are common to many other ailments. Some people develop symptoms of arthritis, nervous system problems, or even cardiac issues.

Lyme disease can be difficult to diagnose. Sometimes, people write off their initial symptoms as the flu or another common illness, and experience symptoms for months or even years before finding the true cause. To diagnose Lyme disease, doctors measure the levels of antibodies the body produces in response to Borrelia infection. Lyme patients are treated with antibiotics, but if the bacteria have been in the body for a long period of time, it can take a long time to cure. The sooner diagnosis and treatment begin, the more quickly and completely patients will recover. Even after treatment for Lyme disease, people can still experience muscle or joint aches and nervous system symptoms.

Scientists from Oregon State University have studied 15- to 20-million-year-old amber found in the Dominican Republic. Despite existing for millions of years, bacteria are rarely found in fossils. However, free-flowing tree resin traps and preserves material such as seeds, leaves, feathers, and insects in great detail. Amber is then formed from the fossilization of the resin over millions of years as it turns into a semi-precious stone. This is the oldest fossil evidence of ticks containing such bacteria.

Four ticks from the Dominican amber were examined and found to have large populations of spirochetes that resemble the Borrelia bacteria, such as those that cause Lyme disease today. The oldest reported case of Lyme disease was Oetzi, a well-preserved natural mummy who lived 5,000 years ago and was discovered by hikers in the Alps. In other studies, fossils have revealed bacteria such as Rickettsia, which cause modern diseases like Spotted Fevers and Typhus, found in ticks from about 100 million years ago. Evidence suggests that even dinosaurs may have been infected with Rickettsia, showing these microbes likely infected other creatures before humans were added to the mix. Millions of years of co-evolution resulted in highly adapted pathogens that scientists and physicians still struggle to understand and treat.

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Hope for Sickle Cell

September 20, 2014 by

Sept. 19, 2014

By Medical Discovery News

While sickle cell disease has long been studied, a recent discovery revealed that the disease significantly increases the levels of a molecule called sphingosine-1-phosphate (S1P), which is generated by an enzyme called sphingosine kinase 1 (SphK1). Inhibiting the enzyme SphK1 was found to reduce the severity of sickle cell disease in mice, which will hopefully lead to new drugs that target SphK1in order to treat sickle cell disease in humans.

Sickle cell disease is caused by a change in the gene that is responsible for a type of hemoglobin, the protein molecule in red blood cells that carries oxygen. This tiny change results in hemoglobin clumping together, changing the shape of red blood cells.

The name for sickle cell disease actually comes from misshapen red blood cells. Rather than being shaped like a disk, or a donut without a whole, sickle cells are shaped like a crescent, sort of bending over on themselves. The normal shape is critical to red blood cells’ ability to easily travel through blood vessels and deliver oxygen to cells and tissues. Sickle cells become inflexible and stick to each other, blocking the flow of blood through blood vessels.

Symptoms of the disease begin to appear at about four months of age. Normally, red blood cells live for about 120 days. Sickle cells only survive 10-20 days. Although the bone marrow tries to compensate for the rapid loss of red blood cells, it cannot keep up. The disease causes pain, anemia, organ damage, and possibly infections.

Although the symptoms and their severity vary, most people with sickle cell disease will have periodic crises lasting hours or days. Symptoms include fatigue, paleness, shortness of breath, increased heart rate, jaundice, and pain. Long-term damage can occur in the spleen, eyes, and other organs, and sickle cell disease increases the risk of stroke. People who only inherit one copy of the sickle cell hemoglobin gene have a milder case of the disease than those who inherit two copies, one from each parent.

Current treatments only reduce the number and the severity of crises using hydroxyrurea, blood transfusions, pain medications, and antibiotics. As the disease advances, dialysis, kidney transplants, eye surgeries, gall bladder removal, and other treatments may be necessary. The only cure for the disease is a bone marrow transplant, which is not an option for everyone.

So it’s pretty exciting that when scientists found that levels of S1P were elevated in mice with sickle cell disease, they inhibited the enzyme SphK1 to reduce the levels of S1P. As a result, red blood cells lived longer and had less sickling. The mice also had less inflammation and tissue damage, which would reduce damage to red blood cells and prevent symptoms of the disease. When they engineered sickle cell disease mice without the gene for the enzyme SphK1 that makes S1P, again the mice had less sickling and symptoms.

How does S1P influence sickling? Apparently, it binds directly to hemoglobin and reduces its ability to collect and carry oxygen, which causes the characteristic folding of cells. S1P has other roles in the body, so it is unknown whether inhibitors to SphK1 can safely and effectively be used in humans to treat sickle cell disease.

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First in the No. 2 Business

June 13, 2014 by

June 13, 2014

By Medical Discovery News

Antibiotic resistance among disease-causing bacteria is a growing and dangerous problem. Bacteria resistant to one or antibiotics, like Staph and Strep, are approaching catastrophic levels. Bacteria so resistant to common antibiotics that few if any drugs are available to treat them have been dubbed superbugs. One widely feared bacterium, called Clostridium difficle or C. diff for short, causes intestinal disease so severe that it can become life-threatening. It kills almost 15,000 Americans every year, mostly the elderly. Super-resistant forms of this microbe are almost impossible to treat with antibiotics. 

This bacterium produces a powerful toxin that destroys intestinal cells and can rupture small blood vessels. It also causes abnormal intestinal behavior, mainly excess water that produces diarrhea. It’s an unpleasant and painful prospect for those infected with C. diff. 

Roughly 5-15 percent of the population carries this bacterium in their digestive system naturally, but it is kept in check by the rest of the bacterial population. But an underlying disease, antibiotics, another infection, or chemotherapy can weaken bacterial systems, allowing C. diff to expand into an infection. And a super-resistant version of C. diff can be a real problem.

As gross as it may sound, fecal transplants are getting lots of attention as an option for C. diff infections. First tried in the late 1950s, the rationale for this approach is that the disease occurs because the bacterial populations are disrupted, so providing a source of normal bacteria restores the ecology of the intestine and prevents C. diff from growing. 

Where exactly does one find fecal matter for such a transplant? It’s not as if anyone wants to ask family or friends to share their poop. Actually, there are major regulatory obstacles for fecal transplants. For instance, the fecal source must test negative for disease-causing bacteria, viruses, and parasites. Basically, it’s not something anyone can find at Whole Foods or on Amazon.

So a group of enterprising graduate students at the Massachusetts Institute of Technology (MIT) who observed a friend’s struggle with C. diff formed a company to distribute safe, certified fecal matter for transplant. OpenBiome collects, tests, and distributes fecal matter like a blood bank distributes blood. Samples are certified by Food and Drug Administration (FDA) procedures, which cost about $3,000. Then they are frozen at super-cold temperatures (-112 degrees) and shipped to hospitals and physicians. Currently, the company operates as a nonprofit and only collects a shipping and processing fee for transplant material.

We already know that our normal bacterial systems, which together make up our microbiome, help protect us from skin, urogenital, and oral diseases. Changes in our microbiome may also contribute to an underlying disease like diabetes. There is still much to be discovered about these organisms that call our bodies home, especially since we house 10 times more microbes than our own cells!

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New Weapons Against TB

January 19, 2013 by

Jan. 18, 2013

By Medical Discovery News

Tuberculosis (TB), the world’s No. 2 killer from a single infectious agent, has a knack for resisting antibiotics. Doctors discovered combining antibiotics had better results, until recent years when TB evolved beyond existing antibiotic cocktails. That may change with a new drug combination that seems to work. 

The new therapy couldn’t come at a better time. Even though TB had been well controlled, it began to make a dramatic comeback in the 1980s. TB, caused by a bacterium called Mycobacterium tuberculosis, infects one person in the world every second. It’s among the top three killers of women and left 10 million children orphaned in 2009.

TB is also the leading cause of death for people with HIV because their weaker immune systems make them vulnerable to the disease. The rise of global HIV infections is largely to blame for the reemergence of TB. Currently, an estimated 14 million people worldwide are co-infected with HIV and TB, and most of them will die without treatment.

TB’s resurgence is also due to drug resistance. To treat people with active, extensively drug resistant strains of TB, doctors prescribe a combination of four drugs: isoniazid, rifampin, pyrazinamide, and ethambutol. Yet in recent years completely drug resistant strains of TB have developed and pose a global threat.

TB is transmitted by inhaling the droplets of an infected person’s sneeze or cough, but also through ingestion. Most infections start in the lungs and initially have no symptoms or at worst feel like the flu. The immune system can wall off the bacteria in what is called a granuloma, a round structure with a core that encases the bacteria and infected cells. Nine out of 10 infections stop at this stage, but some people live with a latent infection for years.

In about 5 percent of cases, the latent TB bacteria reactivate after one to two years. The bacteria replicate rapidly and spread throughout the body. Signs and symptoms of active TB include long-lasting cough bringing up sputum and blood, unexplained weight loss, fatigue, fever, night sweats, chills, loss of appetite, pain with breathing or coughing, and chest pain. Though TB most often affects the lungs, it can also involve the genitourinary system, bones, joints, lymph nodes, and peritoneum.

If TB bacteria’s proliferation is not controlled by the immune system, a severe form of the disease called miliary TB develops. The bacteria eventually cause extensive and progressive damage to the structure of the lungs and ultimately death.

With the new drug combination, fewer people will suffer these ravaging consequences. One new cocktail is called PA-824 and consists of moxifloxacin, a relatively new antibiotic, and pyrazinamide, an older TB drug. The combination works faster than current therapies, and doesn’t seem to interact with HIV drugs.

At least three other drugs or combinations are in the testing phase, just in time to treat multiple-drug-resistant forms of this deadly disease. If effective, the drugs will help a global initiative to reverse the spread of TB by 2015.

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Overuse of Antibiotics on Farms

August 2, 2012 by

By Medical Discovery News

July 21, 2012

 

 

 

Resistance to antibiotics has become a crisis that is overall alarmingly ignored. Some scientists believe without new antibiotics, medicine as practiced now will have to fundamentally change. Doctors struggle to control bacterial infections that continually evolve into lethal killers because current antibiotics are useless against them.

Bacteria have grown resistant because antibiotics have been overprescribed for the past 50 years and patients often quit taking antibiotics as soon as symptoms go away, giving bacteria an introduction to the antibiotic without killing them. Several bacteria are now considered super bugs, meaning they’re resistant to multiple antibiotics. Recent numbers show these super bacteria killed nearly 100,000 Americans in one year alone.

While doctors in the U.S. are becoming more aware and restrained in prescribing antibiotics, they account for less than 20 percent of the antibiotics used. The rest, more than 80 percent (28 million pounds), go to agriculture. But this massive amount of antibiotics is not being used to treat sick animals. Instead, subtherapeutic levels are routinely injected or added to animal water and feed to boost livestock weight and compensate for the unsanitary, packed conditions of commercial American farms.

These conditions create the perfect petri dish to produce resistant bacteria. As bacteria multiply in these tight, unsanitary conditions, the animals such as chickens, turkeys, pigs and cattle are treated with common human antibiotics that include streptomycin, kanamycin, and millions of pounds of penicillin. Studies show long-term subtherapeutic levels of antibiotics may be more conducive to producing resistant bacterial strains than the short-term, high-level antibiotic treatments of humans.

These bacteria, which thrive in the intestinal tract of animal, can contaminate human food  during slaughter, processing, and food preparation. The result is that more people die from foodborne illnesses. Looking at outbreaks caused by antibiotic-resistant bacteria over the past several decades, the Center for Science in the Public Interest concluded the responsible bacteria were resistant to 14 different antibiotics. Of those, seven are classified by the World Health Organization as critically important to human medicine and eight as highly important.

The issue has become critical enough that the EU banned the use of penicillin for animal growth, then in 2006 banned the use of all antibiotics for animal growth on farms. Though the Food and Drug Administration tried at one time to follow the EU’s move by banning penicillin use, farm lobbyists prevailed. Now the FDA is asking pharmaceutical companies to voluntarily limit the sale of antibiotics to farms to just medical treatments and only through a veterinarian (they are now available through retail stores open to the public).

This pits the FDA against the powerful agriculture industry, which defends the practice as a proven way to produce economical animal-based food products. They argue that banning antibiotics will raise food costs astronomically.

But follow-up studies in countries such as Sweden and Denmark show better handling of farm animals led to a decrease in the need for antibiotics, and retail prices on meat did not rise dramatically. Denmark cited just a one percent rise in pork prices.

Ignoring the problem is not an option as people continue to die from bacterial infections that can’t be treated by existing antibiotics, especially since many drug companies have stopped developing new, more powerful antibiotics.

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