Half a million tests and many mosquitoes later, new buzz about a malaria prevention drug

Most malaria drugs are designed to reduce symptoms after infection. They work by blocking replication of the disease-causing parasites in human blood, but they don’t prevent infection or transmission via mosquitoes. What’s worse, the malaria parasite is developing resistance to existing drugs.

“In many ways, the search for new malaria drugs has been a search for something akin to aspirin — it makes you feel better but doesn’t necessarily go after the root of the problem,” said Elizabeth Winzeler, PhD, professor of pharmacology and drug discovery at University of California San Diego School of Medicine.

In a study publishing December 7 in Science, Winzeler and her team took a different approach: targeting the malaria parasite at an earlier stage in its lifecycle, when it initially infects the human liver, rather than waiting until the parasite is replicating in blood and making a person ill.

The team spent two years extracting malaria parasites from hundreds of thousands of mosquitoes and using robotic technology to systematically test more than 500,000 chemical compounds for their ability to shut down the malaria parasite at the liver stage. After further testing, they narrowed the list to 631 promising compounds that could form the basis for new malaria prevention drugs.

To help speed this effort, the researchers made the findings open source, meaning the data are freely shared with the scientific community.

“It’s our hope that, since we’re not patenting these compounds, many other researchers around the world will take this information and use it in their own labs and countries to drive antimalarial drug development forward,” Winzeler said.

Most cases of malaria are caused by the mosquito-borne parasites Plasmodium falciparum or Plasmodium vivax. The parasites’ lifecycle begins when an infected mosquito transmits sporozoites into a person while taking a blood meal. A few of these sporozoites may establish an infection in the liver. After replicating there, the parasites burst out and infect red blood cells. That’s when the person begins to experience malarial symptoms, such as fever, chills and headaches. That’s also when the parasite can be sucked up by a new mosquito and transmitted to another person.

For safety’s sake, Winzeler and team used a related parasite called Plasmodium berghei in the study, which can only infect mice. Their collaborators in New York infected mosquitos with these parasites and every Tuesday, Winzeler’s team would receive a big orange box of mosquitoes by FedEx. On Tuesday afternoons, they would extract the sporozoites, transfer them to plates containing 1,536 tiny divots, or wells, and then carry the plates over to the drug screening facilities at Skaggs School of Pharmacy and Pharmaceutical Sciences at UC San Diego or across the street to the Genomics Institute of the Novartis Research Foundation.

“In a good week, we’d be able to test 20,000 compounds,” Winzeler said, “but of course many of the mosquitoes we received would be dried out, frozen or covered in fungus.”

These sporozoites were engineered to produce luciferase, the same enzyme that fireflies use to produce their telltale glow. Then, in the drug screening facilities, researchers used robotic technology and sound waves to add minute amounts of each chemical compound, one compound per sporozoite-containing well.

The researchers looked for the compounds that switch the glow “off,” meaning they had killed the parasites or blocked their ability to replicate. They took those compounds, confirmed their potency and weeded out the ones toxic to liver cells. They also tested the compounds for their ability to inhibit or kill other Plasmodium species and parasites at other lifecycle stages.

That left them with 631 promising chemical compounds — chemical starting points for the development of new drugs to block a malaria infection before symptoms begin, and prevent their transmission to the blood, mosquitoes and other people. Winzeler said she was surprised to find that many compounds (58) block the parasite’s electron transport chain, an energy-generating process in its mitochondria.

The team will next take a closer look at the 631 promising drug candidates to determine how many work against the liver stage of the Plasmodium species that affect humans. Winzeler and members of the Bill and Melinda Gates Foundation Malaria Drug Accelerator (MalDA), an international consortium focused on speeding drug development, are collaborating to unravel the mechanism by which many of the compounds work against the malaria parasite.

The team and others will also continue the work necessary to develop the compounds into drugs that are safe for human consumption and effective at preventing liver-stage parasites from replicating and bursting out into the bloodstream. The ideal new drug would also be affordable and practical for administration in parts of the world without refrigeration or an abundance of health care providers.

“It’s difficult for many people to consistently sleep under mosquito nets or take a daily pill,” Winzeler said. “We’ve developed many other options for things like birth control. Why not malaria? The malaria research community has always been particularly collaborative and willing to share data and resources, and that makes me optimistic that we’ll soon get there too.”

According to a new report from the World Health Organization (WHO), malaria cases are on the rise, particularly in 13 countries, including Madagascar, Nigeria and the Democratic Republic of the Congo. There were 219 million cases of malaria in 2017, compared to 217 million the previous year. In 2017, approximately 435,000 people died of malaria.

Mutations boost immunity: Toward a cancer vaccine

Despite significant advances in cancer research, the disease continues to exact a devastating toll. Because cancer is a disease of the body’s own cells, which mutate and develop under evolutionary pressure, conventional treatments like chemotherapy and radiation often leave behind a residue of resistant cells that go on to expand and wreak havoc.

The best weapon against this implacable foe would be prevention, though to date, this has been an elusive goal.

In a new study, Stephen Albert Johnston and his colleagues describe a method for pinpointing tumor-specific factors in blood that can elicit a protective immune response in the body and may one day be harnessed to produce an effective vaccine against the disease.

The new study outlines a means for rapidly identifying peptides produced by tumor-associated mutations, then screening these peptides to find those exhibiting a strong immune response.

A new vision

The work is part of a sea change in the field of oncology, where increasingly, the body’s immune system is induced to attack the disease. Immunotherapies have already shown startling effectiveness against certain previously intractable cancers and a pair of scientists were awarded this year’s Nobel Prize for their research into immune mechanisms known as checkpoint inhibitors.

The technique described in the new study relies on libraries of peptides printed on slides known as peptide arrays. When such arrays are exposed to cancer-linked antigens in samples of patient blood, specific peptides bind with antibodies, suggesting they are recognized by the immune system and may be used in a vaccine against that cancer.

Results of the study indicate that tumor-associated peptide mutations not only bind with immune antibodies, but can effectively provide cancer protection, (at least in animal models of the disease). The peptides generating a strong immune response could be incorporated into a vaccine or alternatively, used in conjunction with other forms of immunotherapy to treat existing cancers.

Johnston and his colleagues used peptide arrays to screen for tumor-linked peptides in blood samples from dogs, examining responses to 9 different forms of cancer. The antigens showing the greatest immune response in the array were then evaluated for their protective effect against two forms of cancer, in a mouse model.

The study confirmed that some of the peptides exhibiting a strong antibody response on the peptide arrays offered protection from cancer in mice, while non-immunogenic peptides did not.

“Our system has the advantages of not requiring tumor tissue to DNA sequence and not having to guess whether a mutation elicits an immune response,” Johnston says.

Johnston directs the Biodesign Institute Center for Innovations in Medicine. The new study appears in the journal Scientific Reports.

Hidden in plain sight

When viruses, bacteria or other pathogens attack the body, they often carry particular molecular signatures not present in normal cells. The immune system can recognize these foreign signatures, mounting a defense against the disease-causing invader.

Cancer is different. Because cancer is a disease involving the body’s own native cells, most telltale signs of an alien presence, capable of triggering the immune system, are lacking.

Fortunately, the body is not entirely defenseless against cancer. Certain signposts of illness produced by cancerous tumors can indeed provoke an immune response. Particular mutated peptides can act to alert the immune system, once they have been expressed, processed and presented on the cell surface, allowing the immune system warriors — the T cells — to recognize and attack the cancer.

Identifying and harnessing these factors — known as neoantigens — is the focus of the new study.

But while cancer produces a variety of mutations, whose traces may be registered by the immune system, Johnston notes that not all mutations are created equal. A specific form — known as frameshift mutations — have been shown to be more effective stimulators of immune response. They have been difficult to isolate and identify, until now.

If tumor-specific frameshift mutations can be recognized and applied in cancer therapy, the results are potentially dramatic, because T cells specific to cancer neoantigens can aggressively attack malignant cells without harming normal tissue.

Shifting frames of reference

Most efforts toward a cancer vaccine have focused on so-called point mutations. Such mutations occur when a single DNA nucleotide letter is replaced with a different nucleotide. For example, an original sequence of ACCTACA could mutate to form a sequence reading ACCTATA.

Point mutations therefore leave the sequence length unchanged, altering only the content of the DNA and resulting RNA transcripts. By contrast, frameshift mutations occur when sequence letters are inserted or deleted. (INDELS is the term for these insertion-deletion mutations.)

Currently, use of point mutations for experimental cancer vaccines have been largely based on algorithms that make predictions about which neoantigens will yield an effective immune response, which can only be tested for effectiveness once the vaccine has been manufactured. The process, which is estimated to take 1-3 months, is cumbersome, very expensive and inaccurate. Use of frameshift peptide arrays could provide immediate information on peptide vaccine candidates and assess their immune reactivity before the formulation of vaccines.

In addition to indels, frameshift mutations can occur through a process known as exon mis-splicing. Exon splicing occurs prior to translation from RNA to protein. Here, nucleotide sequences known as introns, which do not code for proteins, are cut from sequences and ends of the remaining coding regions, known as exons, are fused. This process can mis-splice — either omitting part of the exon or including part of the unwanted intron sequence. Like indel mutations, exon mis-splicing is a rich source of immunogenic mutations, explored in the current research.

The search

The new study describes a means of ferreting out tumor-specific peptides resulting from frame shift mutations by preparing peptide arrays containing libraries of frameshift peptides to probe for cancer-specific antibodies to them in dogs, then testing the capacity of the resulting antigens to protect against cancer in a mouse model.

Dogs are subject to a variety of cancers that also plague humans, making them attractive subjects for such a study. Johnston plans to explore both therapeutic and prophylactic vaccines in dogs in parallel to human trials.

As the authors note, there are a finite number of possible peptides displaying frameshift mutations, so it is possible to construct arrays capable of interrogating the entire sequence space of these mutations, eventually establishing the most immunogenic candidates. A group of 10-20 such frameshift peptides could be used for an anti-cancer vaccine.

In the present study, 830 peptides from 377 predicted frameshift antigens were synthesized and affixed to array slides. 116 samples of blood serum from 26 dog breeds, representing 9 types of dog cancer (carcinoma, fibrosarcoma, hemangiosarcoma, lymphoma, mast cell tumor, osteosarcoma, histiocytic sarcoma, synovial cell sarcoma and malignant histiocytosis) were screened on the dog frameshift peptide array. 52 age-matched, blood samples from healthy dogs were used as control. (Each frameshift antigen was represented with 1-4, frameshift peptides, 17 nucleotides in length on the array.)

Subsequent testing of the frameshift peptides demonstrated that reactive peptides provided T cell protection from melanoma and breast cancer in mice, whereas non-reactive peptides offered no such protection. Intriguingly, this tumor protection directly correlated to the degree of antibody response to frameshift peptides seen in the array results.

The research paves the way for the development of potent new weapons against cancer, leveraging the body’s own immune defenses to stop this leading killer in its tracks.

Implants ‘made of your own cells’ could end back pain

Back and neck pain are often the result of the progressive damage of the discs that separate the spinal vertebrae. Thanks to new multidisciplinary research, we may soon have a better solution to this problem: bioengineered discs grown out of a person’s own cells.

Intervertebral disc degeneration is a common problem that affects a large segment of the population.

Typically, healthy intervertebral discs function by absorbing stress placed on the spine as we move and adjust our posture in a similar way to a car suspension.

If those discs wear out, it can cause pain in various areas of a person’s back or neck.

So far, treatments for intervertebral disc degeneration include spinal fusion surgery and replacing the damaged discs with artificial ones.

However, these approaches bring limited benefits because they cannot restore full function of the intervertebral discs they replace.

Now, a multidisciplinary research team from the University of Pennsylvania’s Perelman School of Medicine, School of Engineering and Applied Science, and School of Veterinary Medicine is aiming to solve this issue by developing bioengineered intervertebral discs made out of an individual’s own stem cells.

Stem cells are undifferentiated cells that have the potential to “transform” into any specialized cells. That is why they have become the focus of multiple medical research studies, including the current one.

The researchers at the University of Pennsylvania have been working for the past 15 years on bioengineered disc models — first in laboratory studies, then in small animal studies, and most recently in large animal studies.

“This is a major step: to grow such a large disc in the lab, to get it into the disc space, and then to have it to start integrating with the surrounding native tissue. That’s very promising,” says Prof. Robert L. Mauck, co-senior author of the current study.

“The current standard of care does not actually restore the disc, so our hope with this engineered device is to replace it in a biological, functional way and regain full range of motion,” he adds.

Studies in animal successful so far
Previously, the researchers tested the new discs — called “disc-like angle ply structures” (DAPS) — in rat tails for 5 weeks.

In the new study, whose results appear in the journal Science Translational Medicine, the team developed the engineered discs even further. They then tested the new model — called ” endplate-modified DAPS” (eDAPS) — in rats again, but this time for up to 20 weeks.

The new structure of the bioengineered disc allows it to retain its shape better, and integrate more easily with the surrounding tissue.

Following several tests — MRI scans and several in-depth tissue and mechanical analyses — the researchers found that, in the rat model, eDAPS effectively restored original disc structure and function.

This initial success motivated the research team to study eDAPS in goats, and they implanted the device into the cervical spines of some of the animals. The scientists chose to work with goats because, as they explain, the cervical spinal discs of goats have similar dimensions to those of humans.

Moreover, goats have semi-upright stature, allowing the researchers to bring their study one step closer to human trials.

‘A very good reason to be optimistic’
The researchers’ tests on goats were also successful. They noticed that the eDAPS integrated well with the surrounding tissue, and the mechanic function of the discs at least matched, if not surpassed, that of the original cervical discs of the goats.

“I think it’s really exciting that we have come this far, from the rat tail all the way up to human-sized implants,” says Dr. Harvey E. Smith, co-senior author of the study.

“When you look at the success in the literature from mechanical devices, I think there is a very good reason to be optimistic that we could reach that same success, if not exceed it with the engineered discs.” – Dr. Harvey E. Smith

The researchers say that the next step will include conducting further, more extensive trials in goats, which will allow the scientists to understand better how well eDAPS works.

Moreover, the research team plans to test out eDAPS in models of human intervertebral disc degeneration, thus hopefully getting one step closer to clinical trials.

“There is a lot of desirability to implant a biological device that is made of your own cells,” notes Dr. Smith, adding that, “Using a true tissue-engineered motion-preserving replacement device in arthroplasty of this nature is not something we have yet done in orthopaedics.”

“I think it would be a paradigm shift for how we really treat these spinal diseases and how we approach motion sparing reconstruction of joints,” he continues.

New drug options, risk factors added to U.S. heart guidelines

The recommendations from the American Heart Association and the American College of Cardiology, last issued in 2013, acknowledge recent research showing the benefit of very low levels of “bad” LDL cholesterol, which contributes to fatty plaque buildup and narrowing of arteries.

The medical groups, which announced the guidelines on Saturday at the AHA’s annual meeting in Chicago, still emphasize a healthy diet and exercise as the first line of defense against heart disease, the No. 1 killer in the country.

When cholesterol is not controlled by lifestyle efforts, patients are typically prescribed statin drugs, available as low cost generic pills that have long been proven to safely and effectively lower LDL levels and heart disease risk.

For people who have had a heart attack or stroke, are at high risk for another and whose cholesterol levels are not adequately lowered by statins, the guidelines now recommend adding newer cholesterol drugs.

Higher risk patients are advised to first try statins in combination with ezetimibe, the generic version of Zetia, which lowers cholesterol by limiting its absorption from the intestine. If that does not work, the guidelines call for newer injected medications known as PCSK9 inhibitors, specifically for people who are at very high risk or who have a genetic condition that causes very high cholesterol levels.

Two PCSK9 drugs – Amgen Inc’s (AMGN.O) Repatha and Praluent from partners Regeneron Pharmaceuticals Inc (REGN.O) and Sanofi SA (SASY.PA) – were launched in 2015 at U.S. prices of over $14,000 a year.

Both have been shown to dramatically lower cholesterol levels, but uptake as been slow as the medical community and health insurers questioned their cost effectiveness.

To help spur usage, Amgen last month cut Repatha’s list price by 60 percent to $5,850 and Praluent’s annual net price was cut earlier this year to between $4,500 and $6,600.

The new guidelines are fairly “conservative” in recommending that the newer drugs be used only after other options, said Dr. Francisco Lopez-Jimenez, a cardiologist at the Mayo Clinic in Rochester, Minnesota, adding “I think that was the right approach.”

The guidelines continue to include a calculator introduced in 2013 to identify a patient’s 10-year risk for cardiovascular disease. In addition to traditional risk factors such as smoking and high blood pressure, doctors are now urged to discuss family history and ethnicity as well as health conditions such as chronic kidney disease and premature menopause.

They are also advised to test for cholesterol levels in children as young as two with a family history of heart disease or high cholesterol, while other children should have an initial test between the ages of nine and 11.

Coronary artery calcium measurements are advised for people whose risk level is not clear.

The guidelines update has more specific recommendations for certain age and ethnic groups, as well as for people with diabetes.

Long-lasting HIV injection is a step closer after second GSK study

LONDON (Reuters) – A once-monthly injection to control HIV proved as effective as daily pills in a second study by GlaxoSmithKline, paving the way for a new regimen that could be simpler for some patients to be filed with regulators.

The experimental two-drug injection of cabotegravir and rilpivirine was shown to suppress the HIV virus in a cohort of adults who had not been on a long-established daily three-drug oral regimen, GSK’s majority-owned HIV unit ViiV Healthcare said.

In the study, adults with HIV were first put on a 20-week three-drug program of daily tablets to suppress the virus before being switched to monthly injections. After 48 weeks, the injections maintained a similar rate of suppression as the pills, it said.

The results support an earlier major study, which involved adults who had been using a three-drug oral regimen to control the virus.

ViiV Healthcare’s chief medical officer John C. Pottage said the trial provided further evidence that a long-acting injection could offer an alternative to daily, oral therapy for people who had previously achieved viral suppression.

“This innovative dosing regimen could transform HIV therapy by reducing the number of days a person receives treatment from 365 to 12,” he said.

“Work on new methods of HIV treatment, including long-acting injectable therapies, supports our goal of making HIV a smaller part of the lives of people living with HIV.”

ViiV Healthcare, which is also owned by Pfizer and Shionogi, hopes that its work on developing two-drug therapies will help it compete against Gilead Sciences, the U.S. drugmaker that dominates the $26 billion-a-year HIV market.

The company said detailed results of the study would be presented at an upcoming scientific meeting.

Tech breakthrough offers early warning system for heart attacks

OXFORD, England (Reuters) – A new method of analyzing images from CT scans can predict which patients are at risk of a heart attack years before it occurs, researchers say.

The technology, developed by teams at Oxford University and institutions in Germany and the United States, uses algorithms to examine the fat surrounding coronary arteries as it shows up on computed tomography (CT) heart scans.

That fat gets altered when an artery becomes inflamed, serving as an early warning system for what one of the researchers believes could be up 30 percent of heart attacks.

“If you are able to identify inflammation in the arteries of the heart then you can say which arteries … will cause heart attacks,” Oxford Professor of Cardiovascular Medicine, Charalambos Antoniades, told Reuters.

“With the new technology that we have we can achieve this by analyzing simple CT scans.”

Most heart attacks are caused by a build-up of plaque – a fatty deposit – inside the artery, which interrupts the flow of blood.

Currently, CT scans tell a doctor when an artery has already become narrowed by plaque.

With the new technology, for which the researchers hope to gain regulatory approval on both sides of the Atlantic within a year, doctors will be able to say which arteries are at risk of narrowing.

“(We) can say …your arteries are inflamed and a narrowing will be developed five years down the line. So maybe you can start preventive measures to avoid this formation of the plaques,” Antoniades said.

Heart disease and stroke are the two biggest causes of death worldwide.

“Although we have not estimated the exact number of heart attacks that we can prevent, we could potentially identify at least 20 or 30 percent of the people before they have (one),” Antoniades said.

An Oxford University spin-off company is now developing a service to analyze CT scans from across the globe in around 24 hours.

The research was published in late August in medical journal The Lancet.

“Urgent Care Industry Hits $18 Billion As Big Players Drive Growth” According to a Report in FORBES

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According to a Feb. 23, 2018 Forbes report, “urgent care is becoming an increasingly popular form of healthcare delivery with even more players expected to enter the business.” The article cited figures from the Urgent Care Association of America showing growth in urgent care centers increasing nearly six percent consistently year over year for the past few years, and it’s expected to continue.

The Urgent Care Association of America said there has been a consumer-based move toward value-based payment of medical care providers as a reason for the growth. Read the full report: FORBES – Urgent Care Industry Growing

TheBattleContinues.org is Born: Affecting Change and Helping Improve Veterans’ Lives

By Dr. Sudip Bose, MD, FACEP, FAAEM

The creation of TheBattleContinues.org was a very important step for me that allowed me to transition from being a front line Army doctor treating all manner of battle wounds to an emergency room doctor to becoming an entrepreneur who can affect change and help improve veterans’ lives in a very direct way.

In the years leading up to the launch of TheBattleContinues.org, I frequently got involved in activities that would help raise funds for our nation’s veterans. I was happy to do that. But one of the things that struck me regarding these fund-raisers was that the amount of money that went to overhead and administration within these charities seemed too much – even among the best of them. And the best of them run at about a 25 percent overhead related to administrative and fundraising expenses relative to the amount of expenses that actually go to the programs and services a top charity delivers.

​Dr. Sudip Bose as a captain serving with the 1st Calvary Division in Iraq in 2004, creator of TheBattleContinues.org.

I thought I could do better than that.

TheBattleContinues.org is an organization founded on the idea that even after serving our country abroad, the battle for many veterans and their families continues at home. As a combat physician, Army war veteran and Bronze Star recipient, I wanted to establish TheBattleContinues.org to help alleviate many of the burdens veterans come home carrying while simultaneously promoting improved health and well-being. The Battle Continues Inc. is a 501(c)(3) nonprofit organization aimed to raise awareness and help veterans who have returned from war; 100 percent of money donated to the organization goes towards assisting and supporting veterans.

I joined the Army at the age of 21 and was an officer in the Army for 12 years. It was a great way to serve my country. I’m very thankful for the incredible opportunities that my parents have received, and I’ve received as a result, after they immigrated to America. I was fortunate enough to have done my undergraduate pre-med work at a top school in Chicago, Northwestern University, and went there for medical school as well to become a doctor. I was a practicing emergency medicine physician in the Army, and on Sept. 11, 2001, I joined an infantry unit, and I had the honor of serving on the front lines in Iraq during the Iraq War. And it’s that experience on the front lines of combat as well as the front lines of the emergency room that I hope to use to help others through TheBattleContinues.org.

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The Multiplier Effect & Medical Leadership: We All Can Play a Role and Multiply Ourselves

By Dr. Sudip Bose, MD, FACEP, FAAEM

I remember distinctly the day that changed the way I thought and changed my life’s mission into the direction I’ve taken over the past decade.

It was March 2, 2004 in Iraq – a day that was pivotal for me and really drove my mission in healthcare. I was in Bagdad; it was a hot day, and it was a religious holiday. It was Ashura, the most important holy day on the Shiite Muslim calendar. There were thousands of people marching on the road. They were the faithful, the hopeful, the committed – they’re marching on this religious holiday, and mingled in with that crowd were suicide bombers. They detonated themselves. All of a sudden, this peaceful, religious observance turned into a scene of complete chaos.

Dr. Sudip Bose and his team work on an injured soldier in Iraq.

Suddenly there were dozens and dozens of injured lying all over the place. Smoke and dust from the explosions drifted through the air. Screams rang out from all along the road. I was the only physician anywhere near the scene, somewhere around 800 meters away from the area of the detonations. Our team rushed into the middle of it all, and at that moment, immersed in the chaos, everything went into slow motion. I looked around, and I was wondering, how am I going to address all these patients? How am I going to get to everyone and see everyone and help everyone? It was an overwhelming thought.

But in slow motion, in my mind, I saw our medics moving into action. They were functioning autonomously. They were tying tourniquets, they were starting airway devices, they were patching up holes in chests, and at that moment, I was very grateful that we had taken the time to train those medics. Because by training those medics, I had multiplied myself. One physician can’t reach all these patients, but by training the medics, I had multiplied myself and we were able to address those casualties.

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The Single-Payer Healthcare System: Is it Right for America? Looking at How to Solve the Problems America is Having in Ironing Out a Healthcare System That Works for All the People


Dr. Sudip Bose (foreground, right) talks with a first-responder in the Emergency Department.

By Dr. Sudip Bose, MD, FACEP, FAAEM

You’ve likely heard the term “single-payer” used during the course of discussions of how to solve the problems America is having in ironing out a healthcare system that works for all the people.

I’ve had some experience in a single-payer system of healthcare – the US military. I trained and worked in single-payer for over a decade when I was an Army doctor. I was both patient and provider. And I’ve got one thing to say about it: Don’t be disillusioned. Single-payer is not something that will solve all our healthcare concerns. It’s one option being discussed, but it’s not the golden ticket, if you will. Nothing is, actually. It certainly has its advantages, but there also are disadvantages that the American public may not like. There are good things and bad things about almost any healthcare proposal. It seems to me that in America, we’re at a crossroads of looking for the lesser of evils when it comes to healthcare.

So let’s look at the good, the bad and the ugly as it relates to a single-payer system.

THE GOOD

Let’s start out by defining what single-payer healthcare is. This explanation that you can find on Wikipedia seems as good as any:

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