BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: medicine (Page 1 of 2)

How “Last-Resort” Antibiotics Kill Bacteria

Polymyxin antibiotics are considered to be “last-resort” antibiotics due to their incredible efficacy, even against otherwise antibiotic-resistant bacteria. However, little was known about exactly how they work – until now. Doxycycline 100mg capsulesResearchers at the University of Basel, Switzerland, have discovered that these antibiotics crystallize the plasma membranes of bacteria.

This crystallization causes the fatty part of a lipopolysaccharide to form a hexagonal structure, which decreases the thickness of the plasma membrane, weakens it, and eventually makes it burst, causing the death of the cell. The lipopolysaccharide normally contributes to the structure and stability of the plasma membrane; if a bacteria is coded without these genes, it will die quickly due to the plasma membrane bursting due to lack of stability. Similarly, the membrane loses much of its structural integrity and collapses when the antibiotic crystallizes it.

This breakthrough is important due to the growing problem of antibiotic resistance: antibiotics are simply less effective than they used to be, as bacteria evolve so that antibiotics no longer kill them. As a result, new antibiotics must be found to maintain efficacy. Now that we know more about why polymyxin antibiotics work, new derivatives can be found to improve public health.

A New Hope? Promising new research finds a way to treat COVID-19

Despite the recent decline in COVID-19 cases, researchers and public health officials struggle to treat and prevent new cases of the disease.  A 2022 article in the Washington post outlined the recent efforts by researchers to treat and prevent COVID-19, particularly examining monoclonal antibody treatment, a treatment that utilizes human-made antibodies to aid in the Body’s natural response.

However, according to researchers, new mutations are quickly arising which undermine the effectiveness of these treatments, making it difficult for the medical world to keep up with the virus, so biologists are turning to more novel methods.  One Quebec-based company, Sherbrooke, thinks they’ve found the solution, “We saw a sharp decline in viral loads,” says the company’s chief medical officer Bruno Maranda.

Traditional monoclonal antibody treatment has had trouble inhibiting the binding between the spike protein of the virus SARS-CoV-2 and human cells because the binding location of the spike protein is mutating quicker than researchers can adjust antibody treatment.  According to Andrés Finzi, associate professor at the University of Montréal, “there is a huge immune pressure on the virus,” indicating that it will likely continue to mutate in this way.  

 

Novel Coronavirus SARS-CoV-2 Spike Protein (49583626473)

 

 

However, scientists have noticed that certain areas of spike protein have remained rigid as the virus mutates; one such area is the stem helix.  Because of its lack of mutation, scientists believe that this area is essential to SARS-CoV-2 and if disrupted can limit its ability to mutate and cause harm to our bodies.  

Although the new drug from Sherbrooke uses 2 antibodies that attack the spike protein in a more conventional way, the new third antibody attacking the more rigid areas of the protein has proven effective in all trials that have been undertaken.

Another recent paper has also attempted to amend antibody treatment to target more stable sections of the spike protein: the fusion peptide.  According to the chief of the Antibody Biology unit of the National Institute of Allergy and Infectious Diseases, this structure “acts like a grappling hook and inserts into the human cell membrane, pulling the membrane closer to the virus membrane.”  Researchers hope to use these rigid structures to help develop more reliable treatments and preventions for COVID-19.

This system of antibodies protecting our bodies from illness is similar to what we are currently learning in Biology class.  In class, we learned that in the body’s humoral response to pathogens, B-plasma cells secrete antibodies that bind to pathogens, thereby neutralizing them, allowing them to be quickly engulfed by macrophages and destroyed.  Monoclonal antibody treatment leverages this function of antibodies, creating artificial antibodies to facilitate this interaction more strongly.

While these new developments in COVID-19 treatment are exciting, Finzi warned that “we shouldn’t underestimate the capacity of a coronavirus to mutate.”  Other scientists, including Harvard professor of pediatrics Bing Chen, believe that antibody treatment research should not take the place of other disease-fighting tactics; according to Chen “we need much more effective vaccines, for sure.”  But one thing remains true, and that is that SARS-CoV-2 continues to mutate, and will continue to be a serious problem if we fail or adequately treat and prevent it, and while the number of cases is decreasing, it still remains strikingly high for us to write off the disease as harmless.

The Science Of Addiction

Overview of the brain

There are three main parts of the brain: the cerebrum, the cerebellum, and the brain stem. The cerebrum controls most of our functions such as movements, thoughts, and even our senses. The cerebrum is roughly two-thirds of the brain as a whole and is divided into four lobes: the frontal, parietal, temporal, and occipital. These lobes control emotions, pain receptors, hearing, vision, and more. Second, the cerebellum is located right behind and a little below the cerebrum, and controls most of our motor functions. Finally, the brain stem is the smallest portion of the brain, sitting beneath the cerebrum and in front of the cerebellum. The brain stem controls both breathing and heart rate, making it just as important as the other parts of the brain regardless of its small size.

Diagram of the brain. Wellcome L0008294

Addiction 

Abusive drugs increase the amount of dopamine in the brain which is produced by the brain stem. Often brain activity that would often be seen from a simple social interaction or through eating food will be seen after addictive drugs are consumed, but the activity will be much more powerful and persistent, leading to the addiction. The brain recognizes the pleasure the drug may grant the user and this numbs the user, over time, to natural releases of dopamine. Further, a study conducted on mice proved that the prefrontal cortex controls social behavior and as social behavior is affected by addiction, one of the major parts of the brain is damaged by drug use.

Connection to biology

The original article articulates how drugs of abuse target circuits in the brain and affect how the reward centers are damaged by drug use. Further, the article focuses on how cortisol levels can affect how quickly a person can recover from an addiction. This is important for addiction research as recovery windows will be more accurate if doctors can test how much cortisol a person has. However, this is not nearly as important as the study of the effects drugs have on our brains. This connects to our biology class so far this year as the plants we’ve been experimenting on in the lab have been watered daily. However, if we suddenly just decided to stop watering them the plants would have the same reaction as someone who was addicted to drugs being cut off: yearning for what was taken from them. In the same way that plants depend on water, a drug addiction makes the addict depend on the drug for functionality as the person’s brain is so damaged that it can no longer produce dopamine without synthetic production through drugs.

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Shhhhhhh! Some Viruses Can Sneak into Cells and Cause Cancer

Viruses! We all hate the colds we get in the fall that come with a cough, a runny nose, and a sore throat.  These bugs have gone around since nursery school, so we were taught that viruses were transmitted through touching door knobs, getting coughed on, and touching someone who is sick.  While these are how viruses are spread from person to person, the infection that occurs on a cellular level is much more complex.  

For starters, only a handful of viruses are known to actually cause illness in humans, but the ones that do have adapted to do it very efficiently, and some are even known to cause cancer.  Viruses that cause cancer include human papillomavirus, Kaposi Sarcoma-associated Herpesvirus, and Epstein-Barr virus.  The way that these viruses get into the cells is very unique compared to the common cold virus, and a team at the University of Michigan Medical School decided to take a closer look at just how they invade to try and get a better grasp on how to prevent cancers caused by viruses in humans.

The virus they researched is called SV40 and it causes tumors in monkeys.  The way that SV40 infects monkey cells is by burrowing itself through the cell membrane and then into its nucleus in order to duplicate itself.  SV40 is used as a tool to understand how the cancer causing viruses work because of the biological similarities that monkeys and humans have.  An earlier team studied how SV40 travels through the cell.  It goes from the surface, through the endosome, the ER, and then enters the cytosol.  

The most recent study illuminates the rest of the virus’ passage through the cell. The way SV40 gets into the nucleus is through the nuclear pore complex.  This is how many viruses enter the nucleus, but the SV40 is too large to enter through this pore.   The virus must disassemble in order to gain access to the nucleus. This process partially disassembles the virus into a smaller package made of two proteins and genetic material (DNA).  As we have learned in class, the DNA is the macromolecule that codes for how to build the proteins that build the virus.  When the DNA for the virus is connected with the two proteins, it uses both the nuclear pore complex and another complex called LINC.  LINC connects the two membranes of the nucleus together.  Many other viruses grab onto the little fingers sticking out of the nuclear pore complex (seen below), while SV40 seeks out LINC in order to get into the nucleus.  

202012 Nuclear pore complex

The difference in entrances between more common viruses and SV40 could be what makes SV40 cancer-causing.  The next step is to research how SV40 exploits LINC in order to expand upon how other diseases could enter the nucleus, and hopefully find a way to trigger the immune system in order to expel or digest the viruses before it is too late.  

Is a Vaccine for Cancer Getting Closer?

Vaccines for cancer have long been seen as a possible, but incredibly far-fetched idea. However, the possibility of being vaccinated for cancer, like a polio or flu shot, is getting closer. Scientists and medical doctors are becoming increasingly optimistic about the possibility for a successful vaccine to certain forms of cancer.

Testing vaccine in laboratory. Holding syringe with protective medical gloves closeup. (51714051263)

One type of these vaccines is a dsRNA vaccine, which is designed to replicate the protein that is able to take over a cell by tricking the receptor proteins on the plasma membrane into accepting it. The immune system then learns how to respond to this event and can do so in the future with actual malignant proteins. This works similarly to the COVID-19 mRNA vaccine.

Pancreatic cancer is a promising target – for those in remission, the chance of fatal recurrence is 70-80%, yet relatively easy to detect early with careful testing. The safety study, conducted by the Johns Hopkins Hospital Cancer Center, had no recurrence out of 12 patients. Although very early in the trial process, these are promising initial results that bode well for the future of the trial.

Although not every study is quite as promising. In a more comprehensive, though also not peer-reviewed, study of vaccination against colon cancer, there was no significant difference between the cancer rates of the control group and the experimental group. However, there is promise in the concept, and the field must be explored further before judgment can be cast. At the same time as these other therapies are being developed, inoculation such as the HPV vaccine is preventing cancer by protecting against cancer-causing illnesses. Cancer prevention is a recent, but flourishing field, and one that must be developed further.

Know Someone addicted to Opioids or Painkiller? This Biomedical Advancement May Be Able to Help.

First and foremost, the opioid crisis effects Americans nationwide. The United States is facing a major health crisis that rarely is even mentioned on the news. In the last 20 years(1999-2020) National overdose deaths involving any opioid have risen by more than a factor of six. Nearly 70,000 Americans died in 2020 rising by over 44% since just 2017. Whether given after a major surgery or sports injury, the addictive nature of opioids combined with the difficult side effects have left researchers looking for a better solution.

The general goal for this research was to target different receptors in the cell to do away with the harmful side effects of opioids. An international team of researchers led by the Chair of Pharmaceutical Chemistry at Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) are “focusing particularly on the molecular structures of the receptors that dock onto the pharmaceutical substances”. In short, they are looking to activate adrenaline receptors instead of opioid receptors.

Researchers looked at the central nervous system to discover receptors in cells that lacked the sedative effect. While many of these adrenaline receptors are involved in pain processing, few have been cleared for use in therapies. This is where a team of researchers from Erlangen, China turned their attention to the adrenaline producing alpha 2A adrenergic receptor. One problem is that the analgesics that target the alpha 2A receptor produce a strong sedative effect. Gmeiner, one of the researchers, quotes “Dexmedetomidine(an analgesic) relieves pain, but has a strong sedative effect, which means its use is restricted to intensive care in hospital settings and is not suitable for broader patient groups”.

The goal for the researchers was to separate the sedative effect from the adrenaline receptors to ensure that this therapy could be used on a wider scale. Through the use of extremely high-resolution cryo-electron microscopic imaging, researchers were able to develop agonists that like Dexmedetomidine send large amounts of adrenaline to the brain thus, revealing  the sensation of pain very well. But, the real development was the “fact that none of the new compounds caused sedation, even at considerably higher doses than those that would be required for pain relief.”

In AP Biology, we have looked at the active transport of molecules through the phospholipid bilayer of the cell. Using ATP energy, cells in your body are able to move particles from a high concentration outside the cell to a lower concentration inside the cell. One process cells use to move these particles is Receptor Mediated Endocytosis. Specific ligands (ions, small molecules, or proteins) bind to a coated pit in the receptor while the receptor matches the ligands shape. Next, the ligands pass through the phospholipid bilayer and are put into a coated vesicle to be transported around the cell. A similar process takes place when receptors receive pain relieving drugs.

The prospect of removing the addictive and violent side effects of opioid use through the use of adrenaline receptors sounds promising, but it is important to keep in mind that this is still just research in the lab. With enough funding and time, the possibility of saving thousands of lives by developing non-opioid pain medication is a very exciting advancement and worth the investment.

Can Reactive Oxygen Species Maintain Stem Cell Function and Prevent Inflammation?

Have you ever wondered what “gut health” really means? What keeps your gut microbiome functioning properly, maintaining homeostasis, and preventing inflammation? Originating from oxygen, reactive oxygen species (ROS) that are highly reactive function as central indicators of cellular flaws and issues in the body, such as inflammation. Nai-Yun Hsu of Mount Sinai has stated that “Reactive oxygen species released by stem cells are critical in maintaining a heathy gut via maintaining proper balance of intestine barrier cell types.”

File:Inflammatory Bowel Disease MTK.jpg 

A team of researchers from the Ichan School of Medicine at Mount Sinai have gone in depth about the importance of these oxygen species for stem cell function, avoiding inflammation, and repairing wounds in a recent study. Using mice as models, the researchers were also able to conclude that microfold cells, called “m cells” regulate an organism’s gut immune response, and emerged from a loss of ROS in mice and humans. 

 

The experiment was conducted in vino and in vitro conditions with the mice cells, and ex vivo conditions with human intestinal biopsies post-colonoscopy. Both the human intestinal biopsies and mouse cells were utilized to determine the amount of ROS in the body to support a finding. In addition to determining the amount of the oxygen species, the biopsies and mice were used to analyze the “gene expression profile” of barrier cells in intestines of mice and humans that are diagnosed with a “subtype of IBD known as ulcerative colitis.”  

 

A decrease in these oxygen species can lead to TNF’s emergence in the body, which is a substance that attempts to maintain homeostasis in the body and avoid inflammatory diseases, like IBD and ulcerative colitis. They have concluded that losing species like NOX1, a protein that creates these species, is directly linked with inflammatory diseases like Inflammatory Bowel Disease (IBD). Judy H. Cho, MD, has stated that the study is a breakthrough “in defining the key role of oxygen species in maintaining a healthy epithelial barrier for IBD.” These reactive oxygen species are relevant to AP Bio considering the information we have learned about general biological systems and cells, which function to maintain homeostasis in the body. The mitochondria, which is an organelle of the cell covered in AP Bio, receives signals from gut bacteria that reveals inflammation. While the mitochondria is typically known as the site of cell respiration and performing reactions, new evidence has shown a relationship between the gut microbiota and mitochondria to trigger immune responses and activate barrier cell function. These processes relate to changes to the mitochondria that occur from gut-related issues in IBD patients, meaning that there is a connection to ROS. 

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Gut Microbiota

As a conclusion to proving the direct link between the highly reactive oxygen species and treating inflammation, these researchers encourage and plan to conduct further study on this topic, but for using “oxygen species-stem cell modulation therapy” to potentially treat IBD patients. 

 

 

Neuralink: Science Fiction or Reality?

Throughout centuries of scientific discoveries, most of the human body has been discovered and fully understood. Now this would be completely true if it wasn’t for one organ in our body: the brain. The brain is a humans most complex organ, but it is something that we only understand about 10% of how it works. There is a common misconception that we only use 10% of our brain, but “it’s not that we use 10 percent of our brains, merely that we only understand about 10 percent of how it functions.” This is both scary and interesting as the organ that runs our body is hardly understood. While we only understand 10% of its function, there have still been many advancements in technology: one more notable one in the future being Elon Musks’ Neura Link          

The name Neura Link might not ring a bell, and that’s okay because it is something that if fairly new and still in somewhat of a developmental stage. For those who do not know, Neura Link is a device that “place electrodes near neurons in order to detect action potentials. Recording from many neurons allows us to decode the information represented by those cells. In the movement-related areas of the brain, for example, neurons represent intended movements. There are neurons in the brain that carry information about everything we see, feel, touch, or think.” In summary, this is a device that interprets your neurons signals, records it, decodes it, and can then represent the intended message.

All this might sound like some fancy new technology with its only purpose being to interpret what the brain is saying, and that is basically what Neura Link does. However, the implications of this can be very helpful in the world of modern treatments. One thing that is very promising about Neura Link is that the procedure is preformed by robot, so the risk of human error is out of the equation, and it can be done for cheaper than it might have been if a human doctor was preforming the surgery. They are actively trying to make it affordable for the average person that needs it. It is hypothesized that Nuera Link can help bring back motor function to paralyzed people by being an intermediary between damaged neurons. In Neura Links own words, their device could “help people who are paralyzed with spinal or brain injuries, by giving them the ability to control computerized devices with their minds. This would provide paraplegics, quadriplegics and stroke victims the liberating experience of doing things by themselves again.

One thing we have learned in this bio class this year is how there are many processes for many parts of the body. These processes (such as cellular respiration) require many resources as well as a lot of moving parts, and have to be executed very well. There are processes like these for the healing process of certain parts of the body as well. One thing, however, is that neurons and certain nerves, when damaged, can not be recovered or reproduced. There is no system in the body to heal these damaged neurons or nerves. With the absence of a system in place to recovery these damaged parts of the body, they are left there damaged. One thing that is very interesting is that many scientists have tried to find ways to repair this tissue, but Neura Link, instead of trying to repair it, is almost trying to replace it.

While the idea of placing technology inside your brain may seem a little creepy, it might just be the solution to many seemingly unsolvable issues in the body. I think that if these ambitions of the Neura Link team are met with reality (through thorough rigorous testing and safety protocols) that there should be no limit to what it can help with. Since the brain plays a pivotal roll all over the body, there is no telling what Neura Link could do decades from now.

Are You Happy With Your Current Cell Provider?

Stem cells are defined as a specific type of cell that is capable of evolving into many different types of cells throughout the human body. Although they may be one of the most promising medical and biological discoveries, not many people know enough about them. The term “stem cell” has actually been dated back to the 19th century, but it wasn’t until 1981 that the first embryonic cells were isolated. In the year 1981, scientists Martin Evans and Gail Martin conducted separate studies and they were able to derive pluripotent stem cells from the embryos of mice.

Why Are They Useful?

In 1959 Physician E. Donnall Thomas conducted the first human hematopoietic stem cell transplant. The transplant was actually conducted on twin sisters. One sister with end stage leukemia received total body irradiation in order to kill the cancer. Soon after, her twin sister donated bone marrow, resulting in the regression of her twin sister’s leukemia. Because of stem cells’ ability to repair, regenerate and develop into specific specialized cell types, they prove to be therapy for many diseases and disorders. People that benefit from stem cell therapy are people who suffer from:

  • Spinal cord injuries
  • Type 1 diabetes
  • Parkinson’s disease
  • Amyotrophic lateral sclerosis
  • Alzheimer’s disease
  • Heart disease
  • Stroke
  • Burns
  • Cancer
  • Osteoarthritis

422 Feature Stem Cell new.png

Types of Stem Cells and Their Therapies

There are three types of stem cells, each with their own respective therapies and uses. The first types are Adult Stem Cells (ASCs). ASCs are found in small numbers in tissues such as bone marrow or fat. Researchers used to think that ASCs could create only similar types of cells. New evidence shows that ASCs may be able to create various types of cells. This means that bone marrow stem cells, for example, could be able to create bone and heart muscle cells. The other kind of stem cells are Embryonic Stem Cells (ESCs). ESCs come from embryos that are three to five days old. These stem cells are pluripotent, which means they can divide into more stem cells or become any cell in the body. This means that ESCs can be used to regenerate and repair diseased tissue and organs. The third kind of stem cells are induced pluripotent stem cells (iPSCs). These kinds of stem cells are ones created in a laboratory and they are a mixture of adult stem cells and embryonic stem cells. Scientists altering genes in adult cells allows them to reprogram the cells into behaving like embryonic stem cells.

 

 

 

 

 

 

 

Understanding Merck’s Molnupiravir

Since the beginning of the pandemic, research of antiviral medicines and drugs have only become more specific with combating the Coronavirus. Merck’s new drug, Molnupiravir, was a result of pharmaceuticals amplifying research on Covid. The foreshadowing of this drug shows a bright future and an end to Covid-19 once and for all.

Merck applied for authorization first in October and many praised the new drug as a potential game-changer. Pfizer submitted their version of medication called Paxlovid in November. The Food and Drug Administration has provided emergency use authorizations for pills from both Merck and Pfizer while scientists continue to study the real-world effectiveness of both. Molnupiravir is administered as four 200 milligram capsules taken orally every 12 hours for five days, for a total of 40 capsules. It is not authorized for use for longer than five consecutive days where its use seems to be feasible to all users.

Molnupiravir works by introducing errors into the SARS-CoV-2 virus’ genetic code where it prevents the virus from further replicating. Dr. Shaw, a Yale Medicine infectious diseases specialist, explains when the drug enters your bloodstream, it blocks the ability of the SARS-CoV-2 virus to replicate, a Yale Medicine infectious diseases specialist, Dr. Shaw explains. The coronavirus uses RNA as its genetic material. The structure of Molnupiravir resembles the nucleosides (or chemical building blocks) used to make the virus’s RNA. The drug works by incorporating itself into the RNA as it’s being synthesized where it “results in many mutations, or changes in the RNA genetic code, introduced into the viral RNA,” says Dr. Shaw. “And when this RNA is translated into viral proteins, these proteins contain too many mutations for the virus to function.” If this disables replication and RNA’s ability to infect our cells, we will not be as sick from Covid no longer.

An early report showed the Merck drug cut the risk of hospitalization and death to 50% in patients who had mild-to-moderate cases. Results from the Molnupiravir clinical trial, conducted in the U.S. and other countries, suggested the drug would be effective against CDC “variants of concern,” including the Delta, Gamma, and Mu mutations. Scientists are still studying how well the drug works to treat Omicron and are optimistic since its application is the same with Omicron’s RNA.

While this is exciting news, the vaccine many researchers, scientist, and doctors say is still our first line of defense. Some are even concerned that the attention on Molnupiravir will “draw attention away from vaccination,” says Dr. Meyer. “Some people might say, ‘I’m not getting vaccinated because I’ll have access to these medications’—to this pill or to remdesivir or other treatments. But you can’t trade one for the other. If you haven’t done so already, the most important thing is still to get the vaccine.”

Vitamin D Points to Potential Life-saving Therapeutics for Severe Cases of SARS-CoV-2

A promising new joint study by Purdue University and the National Institutes of Health (NIH) suggests that active metabolites of vitamin D are linked to reducing lung inflammation after SARS-COV2 infection. And no, before you break out your vitamin D pills, the vitamins inside your capsules are quite different from the active metabolites studied. Because of this, these researchers are warning those infected with COVID-19 against taking excessive supplements of vitamin D in hopes of reducing lung inflammation.

The researchers identified an autocrine loop involving vitamin D which allows T-helper (Type 1) cells to activate and respond to the active metabolites of Vitamin D which represses the signaling protein, Interferon Gamma. Distinguishing features of Interferon Gamma is the central role it plays in promoting inflammation

Interferon Gamma

Structure of interferon gamma. The two chains are colored in red (chain A) and green (chain B).

Although interferon gamma sounds wildly unrecognizable at first, we have actually learned about these proteins more broadly in our AP Biology class. Interferon Gamma is actually a type of cytokine! Regarding this cytokine’s structure, the proteins that compose interferon gamma are dimerized (sounds familiar? This is because we have also previously learned about dimerization through the tyrosine kinase receptor pathway in class!). 

Along with the suppression of Interferon Gamma, Interleukin 10, a cytokine with potent anti-inflammatory properties, is amplified. This is significant because this cytokine prevents damage to the host and maintains normal tissue homeostasis by reducing inflammation.

IL10 Crystal Structure.rsh

Structure of interleukin 10 as published in the Protein Data Bank.

In the near future, these pathways could be exploited therapeutically to accelerate the shutdown program of hyper-inflammatory lung cells in patients with severe SARS-CoV-2 infections. But for now, before vitamin D is adopted to treat COVID-19, clinical trials are still needed. However, research findings like these are critical to creating effective treatment not just for those infected with SARS-CoV-2, but also other respiratory diseases as well.

What do you think about this new discovery? Do you think this could lead to scientific progress regarding the treatment of inflammation?

The Common Misconception Around Antibiotics & New Findings

Gfp-medicine-container-and-medicine-tabletAntibiotics as a treatment are never fun – not only are you most likely dealing with a bacterial infection, but you need to take them on a strict cycle and can be quite aggressive on your stomach. I once had to go on antibiotics for treating a sinus infection, and it didn’t quite make me feel better after taking it. So after, I went on the same antibiotic, Cefuroxime, and took a higher dose, but I was not consistent in taking it and started feeling ill. This reaction was due to the antibiotics impact on the protective bacteria in my stomach’s microbiome. I soon learned more about the effects the antibiotics had on my stomach’s microbiome, and realized the common misconception around antibiotics – that they only benefit one’s health – and how some of the symbiotic relationships with bacteria in there are essential to digestion and immune protection. 

Biological overview

Antibiotics have been around since 1928 and help save millions of lives each year. Once antibiotics were introduced to treat infections that were to previously kill patients, the average human life expectancy jumped by eight years. Antibiotics are used to treat against a wide variety of bacterial infections, and are considered a wonder of modern medicine. However, they can harm the helpful bacteria that live in our gut.

The word antibiotic means “against life”, and they work just like that – antibiotics keep bacterial cells from copying themselves and reproducing. They are designed to target bacterial infections within (or on) the body. They do this through inhibiting the various essential processes we learned in Unit 1 about a bacterial cell: RNA/DNA synthesis, cell wall synthesis, and protein synthesis. Some antibiotics are highly specialized to be effective against certain bacteria, while others, known as broad-spectrum antibiotics, can attack a wide range of bacteria, including ones that are beneficial to us. Conversely, narrow spectrum antibiotics only impact specific microbes.

Antibiotic resistance mechanisms

The Human stomach is home to a diverse and intricate community of different microbial species- these include many viruses, bacteria, and even fungi. They are collectively referred to as the gut microbiome, and they affect our body from birth and throughout life by controlling the digestion of food, immune system, central nervous system, and other bodily processes. There are trillions of bacterial cells made of up about 1,000 different species of bacteria, each playing a different role in our bodies. It would be very difficult to live without this microbiome – they break down fiber to help produce short-chain fatty acids, which are good for gut health – they also help in controlling how our bodies respond to infection. Many antibiotics are known to inhibit the growth of a wide range of pathogenic bacteria. So, when the gut microbiome is interfered with using similar antibiotics, there is a high chance that the healthy and supportive microbes in our stomachs are targeted as well. Common side effects of collateral damage caused by antibiotics can be gastrointestinal problems or long-term health problems (such as metabolic, allergic, or immunological diseases). There is a lot of new research on the gut microbiome, some even suggesting that it impacts brain health by influencing the central nervous system. It is essential that we know more about how we can optimize its overall well-being.

New Research

Tackling the Collateral Damage to Our Health From Antibiotics

Researchers from the Maier lab EMBL Heidelberg at the University of Tübingen have substantially improved our understanding of antibiotics’ effects on gut microbiomes. They have analyzed the effects of 144 antibiotics on our most common gut microbes. The researchers determined how a given antibiotic would affect 27 different bacterial strains; they performed studies on more than 800 antibiotics.

The studies revealed that tetracyclines and macrolides – two commonly used antibiotic families – led to bacterial cell death, rather than just inhibiting reproduction. These antibiotic classes were considered to have bactericidal effects – meaning that it kills bacteria rather than just inhibiting their reproduction. The assumption that most antibiotics had only bacteriostatic effects was proven not to be true; about half of the gut microbes were killed upon being treated with several antibiotics, whereas the rest were just inhibited in their reproduction. 

These results expanded existing datasets on antibiotic spectra in gut bacterial species by 75%. When certain bacteria in the gut are dead, and others are not, there can exist an reduction of microflora diversity in the microbiota composition; this concept is referred to as dysbiosis. This can result in diarrhea, or even long term consequences such as food allergies or asthma. Luckily, the Researchers at EMBL Heidelberg have suggested a new approach to mitigating the adverse effects of antibiotics on the gut microbiome. They found that it would be possible to add a particular non-antibiotic drug to mask the negative effects the antibiotics had. The Researchers used a combination of antibiotic and non-antibiotic drug on a mouse and found that it mitigated the loss of particular gut microflora in the mouse gut. When in combination with several non-antibiotic drugs, the gut microbes could be saved. Additionally, they found that the combination used to rescue the microbes did not compromise the efficacy of the antibiotic.

It has been known for a while that antibiotics were impactful on gut microbiome, but its true extent had not been studied much until recently.  More time is needed to identify the optimal dosing and combinations, but the research coming from the Maier lab is very substantial as it fills in “major gaps in our understanding of which type of antibiotic affects which types of bacteria, and in what way,” said Nassos Typas, Senior Scientist at EMBL Heidelberg.

Healthcare Inequality Within the United States

The healthcare field, that is painted to be a blessing for many Americans, happens to also be a huge source of fear for many Americans as well. Throughout history, our healthcare system has shown to ignore and strike fear into specific groups of people. For this reason, through years of trauma and story telling, the fear of these same healthcare systems tend to be passed down as generations pass by. Many Americans then grow up with the constant fear of the healthcare system and seeking assistance when something alarming may appear.

According to CenterJD:

  • The Harvard Medical Practice Study found, “there were significant differences between hospitals that serve a predominantly minority population and other hospitals. That is, Blacks were more likely to be hospitalized at institutions with more AEs [adverse events] and higher rates of negligence.”
  • The Agency for Healthcare Research and Quality, a division of the U.S. Department of Health and Human Services, found, “Blacks received poorer quality of care than Whites in 43 percent of the core measures” and “disparities in quality and access to care are growing wider in the Hispanic population.”
  • Racial and ethnic minorities are uninsured more often than non-Hispanic Whites, a status that frequently results in less than adequate care.
    • A study by the Robert Wood Johnson Foundation found that compared with the insured, those without health coverage who are hospitalized are more likely to receive fewer services, experience second-rate care, and die in the hospital.

Although this CenterJD post is from 2008, it puts into perspective how medical malpractice is not only a problem of the past during chaotic events such as WWI and WWII and how medical malpractice still very much affects our society today.

As Covid-19 is the modern issue at hand for most people in the United States, we often take into question who and how quickly is Covid-19 affecting people. Pasted below are statistics around Covid-19 in relation to race and ethnicity in America.

Evidently from the statistics given by the CDC, American Indian/Alaska Natives, Black/African Americans and Hispanic/Latino persons are way more likely to die and be hospitalized by Covid-19 than their White counterparts. This may be due to a multitude of reasons stated by the CDC. They claim that “Race and ethnicity are risk markers for other underlying conditions that affect health including socioeconomic status, access to health care, and exposure to the virus related to occupation, e.g., frontline, essential, and critical infrastructure workers.”

One very prominent example of this inequality in the healthcare field is Black women in America’s healthcare system. According to Black Women’s Health Imperative, “Black women are 3-4 times more likely to die from pregnancy-related complications and 3-4 times more likely to suffer from severe disability resulting from childbirth compared to White women.”  Black women are also much more likely to experience birth injuries and deaths due to other factors that are engraved in our societal structure. According to AJMC, When analyzing preterm birth numbers, it is evident that women living in areas of high violent crime and high air pollution that have the highest risk of preterm birth. “Black women are 4 times more likely to live in a neighborhood with high violent crime and high air pollution than White women,” which may partially explain why there is such a difference in the birth characteristics of these two groups.  Heather Burris, a current medical doctor, stated that “both physical and psychological stressors can lead to low birth weight and other health disparities” as well. This is why we must view these issues with historical context in mind. Discrimination and Racism, such as redlining, food deserts and many other forms of control by the American systems were used and ultimately affect the way that many Black Americans and other American groups function to this day.

According to Endofound, Health conditions that disproportionately affect Black women receive less government research funding than other similar diseases. They state that “estimates reveal that nearly a quarter of Black women between the ages of 18 and 30 have [uterine] fibroids — compared with 7 percent of White women. By age 35, that number increases to 60 percent. However, NIH annual funding for the condition is $17 million — compared to $86 million for cystic fibrosis, which impacts far fewer people each year (though the great majority of those impacted are Caucasian).” Cystic Fibrosis is a much rarer disease according to Cystic Fibrosis Foundation as there are around 70,000 currently living people worldwide with this condition. There are more than 200,000 cases of Uterine Fibrosis in the United States alone. Cystic Fibrosis appears to be much deadlier, however, the lack of funding in a department for an illness that is extremely common should be of concern. With more demand, more funding would seem like a plausible reaction, however, the current funding clearly shows otherwise.

 

As shown by the article’s data presented by Nature’s Alice B. Popejoy and Stephanie M. Fullerton, many racial and ethnic minority groups are still not present in genome wide association studies funded by the National Institute of Health. Popejoy and Fullerton state that “together, individuals of African and Latin American ancestry, Hispanic people (individuals descended from Spanish-speaking cultures in central or South America living in the United States) and native or indigenous peoples represent less than 4% of all samples analysed.” These numbers are ridiculous and makes it very hard for many people of color to feel as safe as their White counterparts, since there is significantly less statistical data that provides the same support and comfort in their own safety.

According to an article by Lauren Frayer, the NHS, which is the state funded company that funds health care for all in Britain, polls better than the queen, showing that British citizens are extremely fond of the system that is set in place to help all of its citizens. Richard Murray, a policy director for a health care think tank named the Kings Fund, says that it would be “electoral poison” for any political figure in the UK to advocate for privatizing the NHS. This feeling is mutual among many citizens of other countries with some form of universal health care as well. Many other countries such as Canada, Sweden, Spain and many more have very similar policies set in place to help aid citizens in getting better health care coverage. In a similar fashion the Affordable Care Act (ACA) in the United States made health insurance much more attainable for some citizens but also made more complications for others citizens as well. According to healthline, “more than 16 million Americans obtained health insurance coverage within the first 5 years of the ACA. A more affordable health insurance would help many groups such as the large amounts of people who live in high crime areas and high levels of poverty such as big cities like Chicago, Los Angeles and many other similar areas. Although our country is yet to promote policies that provide realistic health care policies for all, there is always room for change and progress as we try to become more united as a country.

Universal health care coverage can be achieved in a multitude of ways and this graphic by commonwealth fund displays methods of achieving the end goal of universal health care.

 

This is evidently a multi-faceted issue as the health care problems for many groups in America are not only caused by one specific source. Our country must start by fixing the issue of widespread poverty in our country because it directly correlates to so many problems within our country including health care inequality. We must use our resources to help build up and fortify the communities that are not properly funded nor given the opportunities as many of the wealthier communities in the United States due to this lack of funding and lack of emphasis to support these areas. Without proper steps towards building these communities and making health care a more realistic option, a large amount of the United States’ population will continue to suffer and struggle for years to follow.

Bias in Science: History, Representation, and Medicine

Science is not objective. Scientists may value fact, but they are still people too, influenced by identity and implicit and explicit biases in their research. Racism has pervaded every aspect of society since the country’s founding, and scientific institutions are no exception. From historical racist research practices to a modern reluctance to support Black Lives Matter or actively diversify the field, scientists have participated in and promoted racism for centuries. Scientists cannot claim objectivity now as an excuse to not be antiracist.

Throughout American history, unethical, racist research has contributed to scientific “progress”, but that is not regularly acknowledged. Although the past cannot be undone, fields should at least recognize the horrific means by which some research was done. For example, gynecology was borne of unethical experiments done on enslaved women and children. The “Tuskegee Experiment” withheld treatment of syphilis from hundreds of Black men just to see how the disease progressed. Henrietta Lacks, a Black woman with cervical cancer in 1951, had some cells taken from her tumor without being informed of this. The cells from her tumor, now known as HeLa cells, have been used since the 1950s for biomedical research. Since cancer is characterized by an improperly regulated cell cycle, with either too much cell growth or too little cell death, cancer cells can grow and divide excessively. This particular line of cells has been able to grow and divide endlessly, due to the presence of an active version of telomerase during cell division. This enzyme prevents the typical shortening of telomeres in cell division that leads to cell aging and death, making the cells “immortal” and the cell line usable to this day. Though they have been used in various research advances, her name was only connected to them in the 1970s. Her family, still with limited access to healthcare themselves, received no financial benefits and had no say in how the cells were used. Henrietta Lacks’ case is a more recent example of unethical research practices affecting Black people.

The questions scientists choose to study, whom they choose to include, and how they apply their results all bias research. Scientists of marginalized identities are much more likely to explore topics relevant to minority groups. So then, the lack of diversity among scientists also contributes to biased research priorities. In 2016, only 9% and 13.5% of science bachelors degrees were given to African Americans and Latinos respectively, and only 5% and 3.8% of doctoral degrees in science and engineering went to women and men from underrepresented minorities. Almost 70% of scientists and engineers employed full time are white. When issues like COVID-19 and climate change disproportionately affect marginalized groups, the lack of diverse representation can prevent representative research or solutions. Scientific institutions need to work on hiring and retention of Black, Latinx, and Indigenous scientists, in part by creating less hostile work environments and increasing DEI efforts.

The lack of diversity in clinical trials also decreases the inclusivity of science and medicine. Even though about 40% of Americans are nonwhite or Hispanic, the clinical trials for new drugs tend to have much whiter samples, with some having 80 to 90% white participants. Since these drugs will be used to treat all people, diverse samples are needed to determine the efficacy and side effects that can vary across ethnicity and sex. The 1993 National Institutes of Health Revitalization Act that required greater inclusion of women and minorities in NIH research samples did improve the proportion of female subjects, but not so much for minority groups. Even for diseases that disproportionately affect marginalized groups, those groups are grievously underrepresented in the clinical trials. 

One such disease is COVID-19. Even though the rates of infection, severity, and death are greater for Black, Latinx, and Indigenous Americans, these groups are underrepresented in clinical trials. Trials for drugs to treat COVID-19 did not accurately reflect the most affected populations at the research sites. Some studies also did not report the race and ethnicity of participants as required by the FDA. Remdesivir has shown to somewhat decrease recovery time, but since disease severity and outcomes are worse for minority groups, the benefits of improvement may not necessarily extend to them. This is why proportional representation of affected populations is so important in clinical trials for drugs.

One cause for lack of diversity in clinical trials is that minority groups can be unwilling or unable to take part, for reasons including fear of discrimination, lack of time or resources, inaccessibility of recruitment centers, language barriers, and fear of exploitation based in historical precedent. However, these barriers should be on the researchers to address, not on the marginalized groups. A possible solution could be to have the FDA enforce that drugs should be tested on samples that demographically reflect the populations that will be using them.

In the end, research institutions and scientists need to examine their biases in order to determine who they are serving, and then who they mean to serve. Efforts to increase diversity cannot be passive, but instead should involve active recruitment and work to eliminate the barriers in place. In an academic institution, that might mean a more inclusive work environment and better outreach and mentorship programs. For clinical trials, this could be reducing the financial burden of participation and building better relationships with minority communities that may have been hurt in the past. Science is meant to help people, so we need to be better moving forward, as well as acknowledge the damage scientists have done in the past.

I Have a Gut Feeling that Microbiomes Are the Next Step in Medicine

We as humans are a very genetically diverse species. But what if we could find microorganisms that have over 150 times more genes right within our own guts. Scientists believe that human microbiomes is the key to treating diseases in the future and some analysts believe that the field of human microbiome market will reach $3.2 billion by 2024.

Lack of microbiome diversity has shown to cause diseases like MS, diabetes, and asthma. So microbiomes have demonstrated themselves to be a key component of our health. To better understand these links, many projects launched in the past few years have focused on mapping microbial genesthat are associated with disease. For example, there are certain microbiomes that make cancer drugs ineffective whereas others are actually necessary to make these drugs work. Thus, a patient’s microbiome makeup directly correlates to their survival chances. So the next step in the Microbiome market is modifying the microbiome to work for the patient.

One older technique of doing this is traced back to China thousands of years ago where they would transplant whole microbial communities to treat diarrhea also known as Fecal microbiota transplant (FMT). A more defined approach is where beneficial bacterial strains are delivered, alive, to the patient’s gut.

In the UK, a company called Microbiotica transfers non-pathogenic strains of C. difficile to fight C. difficileinfections, IBD, and cancer. Even though these approaches have drawn a lot of attention to the field, some scientists argue that the bacteria we ingest are not as well adapted to living in our gut as those that have been living there for years thus are not effective.

In France, an opposite approach is used by Enterome where drugs target specific bacteria leaving the rest to the gut microbiome intact. This approach is aimed at treating Chron’s diseaseand cancer.

Another approach is using bacteriophages to kill specific bacteria strains. Eligo Bioscience takes it a step further by using the bacteriophages to deliver CRISPR/Cas9 into the bacteria to kill it by cutting the DNA of the strain carrying the disease only.

Finally, certain companies like Blue Turtle Bio engineer bacteria to make them produce drugs directly within the human gut.

Since this is a rather new field, there are newly emerging companies along with groups who do not believe in the practice. Personally, I do believe in this practice because there is already a strong correlation between our immune system and specific microbiome strands. With microbiome treatments comes microbiome diagnostics to determine which patients can benefit from these therapies. Thus a high number of approaches will initially fail to treat disease. So far, gut infections and inflammatory diseases seem to be strongly correlated to the gut microbiota, so that will be an area where more research should be applied.  A crucial challenge for the field will be to move from correlation to causation, and a lot of research is still needed for that.

 

What are Biofilms?

 

Biofilm being formed. (Pixnio)

Medicine has made great advancements in patient care and treatment over the last decade. However, everyday viruses and bacteria alike have become stronger and more resilient – even to the latest antibiotics. One such threat that has led to “…thousands of deaths…” in “…American Hospitals alone…” are biofilms. These bacterial cells “…gather [together] and develop structures that bond them in a gooey substance…” insulating them from the outside world. Biofilms ability to become impervious to antibiotics at a moment’s notice has led biologists to wonder both how they develop, and how to stop them.

To find out how and why these bacteria form biofilms, researchers at the Levchenko Lab, at Yale University, as well as from the University of California – San Diego, “…designed and built microfluidic devices and novel gels that housed uropathogenic E. coli cells, which are often the cause of urinary tract infections. These devices mimicked the environment inside human cells that host the invading bacteria during infections.” From this experiment, the scientist discovered that the bacteria would multiply until physical constraints inhibited them from further reproduction. At this point, the bacteria would become “stressed” and thus this “stress would induce the formation of a biofilm.

With the numerous mimicking devices that the researchers utilized in the experiment, they can now create many biofilms in predictable ways, and further analyze their behavior in similar environments. “This would allow for screening drugs that could potentially breach the protective layer of the biofilms and break it down.”  It is an amazing solution to a stubborn and persistent biological threat, that has already robbed enough, otherwise healthy, people of their lives.

It is imperative that we continue to make great strides in the advancement of medical technologies and treatments, as this will enable us to live healthier, more disease-free lives for the future to come. As viruses and bacteria get stronger, we need to make sure to keep up.

Sleep In for Heart Surgery!

Now if you’re on the operating table, likely passed out and opened up, its a fair bet that what time of day it is will have absolutely no importance to you. But maybe it should.

Recently, a study spanning over 6 years and conducted on over 600 patients, was based on recovering from heart surgery had noticed a strong correlation with time of day and rate/outcome of recovery.

These patients who underwent a heart valve replacement had shown an interesting relationship with a humans circadian rhythm. Those who underwent surgery in the afternoon had much better results and recovery than those in the morning. Additionally, in the following 500 days after the surgery, patients who were operated on during the afternoon were half as likely to have a major cardiac event such as myocardial infarction (commonly known as a heart attack) or acute heart failure.

The team conducted a second study in which a total of 88 random patients were put into two groups, morning and afternoon. The results showed that those in the afternoon had lower levels of myocardial ischemia.

In a further examination of these findings in an attempt to find a cause, an article from Scientific American states, “The researchers isolated heart tissue samples from a subgroup of 30 patients from the randomized controlled trial. In laboratory tests, tissue from afternoon surgeries more quickly regained its ability to contract when researchers imitated the process of the heart refilling with blood as surgery concludes.”

While operating in the afternoon may have its benefits, doctors say that altogether abandoning surgery in the morning is simply out of the question. However, other practical applications of this are being studied, such as how it may affect cancer treatment in patients and whether or not circadian rhythm affects a variety of medical procedures. But until then, let the anesthesia kick in and enjoy the operation.

What do you think will be the next application of circadian rhythm or other anatomical and biological features?

Want to find out more? Sources below.

http://www.telegraph.co.uk/science/2017/10/26/surgery-safer-afternoon-bodys-circadian-rhythm-study-suggests/

https://www.scientificamerican.com/article/why-heart-surgery-may-be-better-in-the-afternoon/

http://www.independent.co.uk/news/science/heart-surgery-afternoon-morning-safety-post-illness-recovery-circadian-rhythm-body-clock-a8023736.html

Australian and PNG doctors and nurses performing surgery in Operation Open Heart. Port Moresby General Hospital, Papua New Guinea. Picture by Rocky Roe/AusAID

The First Ever Human Head Transplant

Exactly 200 years after Marry Shelley’s Frankenstein, neurosurgeon Sergio Canavero has announced that he will be performing the first ever human head transplant in 2017, until recent reports say that it will not take place until early 2018. However, this is not the first head transplant, as nearly 50 years ago a rhesus monkey was the first recipient of such an operation. Additionally, Canavero has found a partner for the operation, Xiaoping Ren, who states that he has practiced this on over 1,000 mice.

Until April 28th of 2017, our human guinea pig was 31 year old Russian man, Valery Spiridonov. He suffers from Werdnig-Hoffman disease, a form of muscular atrophy. However, the Italian neurosurgeon announced that Spiridonov will not be the head donor, but in his place a volunteer from China. Canavero stated the reason for this is due to the surgery taking place in China, and getting a Chinese donor is much more convenient/practical.

As for the procedure, the operation is said to take 36 hours. During these hours, the donor head and body will have to be cooled down to a temperature of -15˚C so the cells last more than a few minutes without oxygen. They will cut the tissue around the neck, having the major blood vessels linked by tiny tubes. Then, the spiral cord on both the head and body will be severed cleanly with an extremely sharp blade to minimize damage to the spinal cord. Finally, the head is ready to be connected. The two ends of the spinal cord will be fused with a chemical known as polyethylene glycol, a chemical used in certain medicines such as laxatives, but has been shown to act as a catalyst to the growth of spinal cord nerves. Following the connection of the muscles and blood vessels, the patient will be put into a coma for a month to decrease and limit any movement so that the electrodes can stimulate the spinal cord to grow and strengthen connections.

Sergio Canavero, Photo taken by 诗凯 陆 (@flickr)

As for the reaction to this so called “taboo-medicine”, the scientific community is not only skeptical but horrified as well. Many argue that the procedure is simply unethical and a twisted, gruesome form of medicine. However, Canavero states that it is simply giving a chance for paralyzed people to hopefully be able to walk and function on their own. What do you think of this? Is it unethical and taboo? Or is it an opportunity for progress?

For more information visit these sources:

http://www.alphr.com/science/1001145/human-head-transplant
http://www.iflscience.com/health-and-medicine/human-head-transplant
http://www.newsweek.com/head-transplant-sergio-canavero-valery-spiridonov-china-2017-591772

Parents Take Warning: Antibiotics Can Be Harmful to Infants

Antibiotics are the marvel of modern medicine. They have brought about incredible medical advances, treating bacterial diseases and helping to prolong lifespans in modern times. But a new study conducted by researchers at the Massachusetts General Hospital and the Broad Institute has shined a light on the potential negative effects antibiotics can have on an infant’s health.

https://www.flickr.com/photos/herebedragons/2573487530

The study, conducted in partnership with a team of Finnish researchers, took monthly fecal samples from 39 children from birth until they were 36 months old and analyzed the sample using standard, RNA sequencing procedure to identify different microbes. During the study, 20 of the children had taken antibiotics for respiratory or ear infections ranging from 9 to 15 treatments over the course of the study. From this data, the researchers could analyze the diversity of the gut microbiome of these participants with respect to their antibiotic usage.

The researchers had chosen to analyze the effect antibiotics have on the gut microbiome in young children because of the pivotal role antibiotics appear to play in human health during early development. Low diversity in the early years of life of this collection of bacteria residing in the intestines has been linked to allergies and autoimmune diseases.

The results of this study show a decrease in the diversity of the microbial gut populations in infants who took antibiotics. This was even more pronounced when the infants were marked with a specific signature low in a bacteria known as Bacteriodes (this decrease in Bacteriodes has been speculated to be linked to Caesarean section births in the past but the researchers found this rationale to be inconclusive as well as another rationale that prolonged breastfeeding led to a stronger gut microbiome with higher levels of Bifidobacteria).

When the infants had taken antibiotics, a single strain of bacteria tended to rule their gut with only a few species surviving. On the whole, the gut microbiomes of these participants were less stable and had higher levels of antibiotic resistant genes.

Don’t get me wrong: antibiotics are an incredible innovation that has saved millions of lives. But, be careful in thinking they are a cure all. They’re side-effects might be more harmful than you think, especially in children.

How does this research change your perception of antibiotics?

 

Is There a Limit to How Old Humans Will Get?

In the 1900s, the life expectancy for humans in the United States was approximately 50 years. Since then, the age to which humans can live has only grown. In 1997, a woman by the name of Jeanne Calment died at the age of 122- an astounding increase from the life expectancy less than a hundred years ago. A new study written about in the New York Times explains that Dr. Vijg, an expert on aging at the Albert Einstein College of Medicine, feels that we have now reached our “ceiling. From now on, this is it: Humans will never get older than 115.” Dr. Vijg and his graduate students published their pessimistic study in the journal Nature, presenting the evidence for their claim.

For their study, Dr. Vijg and his colleagues looked at how many people of varying ages were alive in a given year. Then they compared the figures from year to year, in order to calculate how fast the population grew at each age. For a while, it looked as though the fastest-growing group was constantly becoming older; “By the 1990s, the fastest growing group of Frenchwomen was the 102-year-olds. If that trend had continued, the fastest-growing group today might well be the 110-year-olds.” (NY Times Article). Instead, the increases slowed and eventually stopped, leading Dr. Vijg and his colleagues to conclude that humans have finally hit an upper limit to their longevity. Further research into the International Database of Longevity seemed to validate their findings; No one, except in rare cases like Ms. Calment, had lived beyond the age of 115. It appears as though human beings have hit the ceiling of longevity.

There was a varied mix of responses to the study. Some, like Leonard P. Guarente, a biology professor at MIT, praised it, saying “it confirms an intuition he has developed over decades of research on aging.” Others, like James W. Vaupel, the director of the Max-Planck Odense Center on the Biodemography of Aging, called the new study a travesty and said, “It is disheartening how many times the same mistake can be made in science and published in respectable journals.”

This study is by no means conclusive. It is simply one more piece of research in the ongoing debate over whether human beings will continue to live longer, and will continue to be debated by many experts in the field.

However, one must wonder whether living longer should be the goal. After all, as Dr. Vijg pointed out, “aging is the accumulation of damage to DNA and other molecules. Our bodies can slow the process by repairing some of this damage. But in the end, it’s too much to fix. At some point, everything goes wrong, and you collapse.” While morbid, he makes a valid observation: Humans can only go so long until necessary bodily functions begin to break down. Rather than worrying about whether we will live to an extraordinary age such as Ms. Calment, I concur with Dr. Vijg; the focus should be on living the most amount of healthy years and taking care of our bodies. While it may seem like a great idea to live to the age of 125, what good would that do if you aren’t able to continue with the activities you enjoy because your body is breaking down?

 

Other Relevant Articles:

In Depth Explanation of Longevity: https://en.wikipedia.org/wiki/Longevity

A brief summary of Dr. Vijg’s findings (a bit shorter than the NY Times article): http://www.newser.com/story/232121/human-lifespan-has-likely-maxed-out.html

An interesting article about an entrepreneur’s quest to make people live even longer: https://www.theguardian.com/science/2015/jan/11/-sp-live-forever-extend-life-calico-google-longevity

 

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