It may not be general, but everybody knows somebody that ,”wants to live forever.” Thanks to epigenetics the dream of living “forever” is not far out of reach.

The goal of modern medicine has always been to extend human life to its maximum potential, and we have succeeded thus far in doing so. According to statistics compiled by UC Berkeley, The average life expectancy in 1910 was 49 years, while it has now risen to 73 years. 4% of the population of the United States lived to 80 years old in 1910- that statistic has now risen to above 40% for men and has nearly reached 60% for women.

In the 19th and even early 20th centuries it was not uncommon to barely live to meet your own grandchildren. The general population now enjoys the luxury of living to an age where multiple generations can interact comfortably. Unfortunately, the rapid increase in life expectancy that occurred throughout the 20th and into the 21st century has begun to stall; we have simply exhausted the limitations of traditional medicine. One field that has sparked the interest of many medical researchers is epigenetics, the study of the human genome and how it can be modified to our benefit. Potential implications of epigenetic techniques have been found to be enormous. Imagine living to meet your great-great grandchildren, and being spry enough to spend time with them as our grandparents do now.

Aging is a process widely recognized as a product of genetic and environmental factors, with the environmental factors largely playing a role in triggering phenotypic response. It was not until recently that the role of predetermined genetic factors in aging and longevity were realized, with concrete evidence for genetic association amongst long-lived populations coming even later. With the help of modern data analytics we have been able to uncover some of the mysteries behind living beyond our current timetable.

One way that researchers have been developing an understanding of the role that phenotype plays in aging has been through qualitative study of genetic expression triggered by variation in living environment.  Researchers found that variation in stimulus leads to a variation in phenotypic expression. One of the most interesting relationships CJ Kenyon and her team at the University of California at San Francisco was the inverse correlation between the availability of nutrients and lifespan. When access to resources was limited, genes were activated in order to focus on lengthening the life of the organism, a sort of internal self-preservation mechanism. Researchers were then able to isolate the specific genes that were activated and determine their unique correlation with longevity.

These phenotypes take hold not only in gene activation, but also in the form of physical and behavioral changes. As scarcity of resources went up, organisms tended to prioritize individual well being over other processes such as reproduction and territorial expansion. This link between genetics and behavior demonstrates how genetics play into one’s physical and behavioral characteristics due to environmental factors.

Unfortunately, these correlations discovered in microscopic organisms, (that of choice in this particular study led by C.J. Kenyon was C. Elegans), must be taken with a grain of salt. Variations in expression of the same gene has been found to have dramatically different effects in different organisms, and even within different ethnic cohorts. We must therefore take the time to pinpoint these “longevity genes” in organisms and ethnic cohorts individually. Thankfully, modern computational power gives us the ability to sift through genomic data like never before.

Scientists have begun to utilize analysis techniques such as Genome Wide Association Studies (herein referred to as GWAS) to identify macroscopic genetic trends to isolate the secrets to longevity hidden within the massive amounts of data stored in the human genome. According to the Murabito lab at Boston University School of Medicine, GWAS are able to identify trends that were previously invisible to the human observer through massive data analytics. By isolating certain long-lived populations, specifically those that lived into their hundreds (centenarians), researchers were able to pinpoint certain phenotypes that correlated with longevity with limited statistical significance. It was found that you are more likely to live past 85 if your parents did, as well as there being a lower chance of developing age-related disease if one’s parents were a member of the centenarian cohort. Although there was only limited significance in the findings regarding ageing, phenotypes contributing to the development of age related ailments were pinpointed at a much higher significance level.

Other researchers are taking a different approach in their study of longevity by focusing on individual genes that directly contribute to one’s lifespan and quality of life throughout the ageing process. One gene that has sparked the interest of Dr. C.J. Kenyon amongst others is IGF1, an insulin signaling pathway gene that has been found to directly correlate with lifespan with mild statistical significance. Genes like these continue to be discovered and further research is being conducted to determine the strength of their role in longevity.

Future implications of research being conducted currently may include being able to stimulate genetic expression that leads to extended life. By activating mutations that lead to longevity over and over we may be able to effectively double the human life expectancy. Gene therapeutics have had success in stimulating longevity phenotypes in microorganisms and we are now working to apply the same techniques in more complex organisms.

Modern science continually provides us with the ability to push the boundaries of the human interface, with ever increasing lifespan serving as a primary indicator. In 1910 most doctors would have laughed if told the average person would live to 100. The fact that we may soon have the facilities to increase the length of our lives beyond that set by the bounds of nature by a considerable margin is a new concept that can therefore be difficult to comprehend. It is our duty both inside and outside of the scientific community to make sure we use  Researchers continue to push the envelope with epigenetics and similar treatments; who knows, one day we just might live forever.

By: W. Corley

References:

Hoeijmakers, Jan HJ. “DNA Damage, Ageing, and Cancer.” The New England Journal of Medicine, 8 Oct. 2009,https://www-nejm-org.libproxy.lib.unc.edu/doi/full/10.1056/NEJMra0804615

Kenyon, C. J. (2010). The Genetics of Ageing. Nature, 464(7288), 504-12. doi:http://dx.doi.org/10.1038/nature08980

Murabito, J.M., Lunetta, K.L., “The Search for Longevity and Healthy Aging Genes: Insights From Epidemiological Studies and Samples of Long-Lived Individuals,” The Journals of Gerontology: Series A, Volume 67A, Issue 5, May 2012, 470 -479, https://doi.org/10.1093/gerona/gls089

“Life Expectancy in the United States, 1900-98.” Life Expectancy in the USA, 1900-98, UC Berkeley, 2010, u.demog.berkeley.edu/~andrew/1918/figure2.html.

Image Credits:

“3D Rendering of a DNA Double Helix”, Getty Images/iStockphoto, https://thecollege.asu.edu/content/dna-primer

 

According to the National Cancer Institute, in 2019 alone, 1.8 million people would be diagnosed with cancer, and that’s just in the United States. Of these 1.8 million people, 606,880 won’t make it to see themselves win the battle. Of these 1.8 million people, the majority would have to endure some combination of treatment to combat such a disease whether it’s surgery, chemotherapy, or radiation. The majority of these 1.8 million people would have to experience both mental and physical fatigue, weight loss, hair loss, nausea, vomiting, memory and concentration loss, and so much more. For decades, researchers have been looking for a solution that minimizes both effects and incidences, and they might have found just the trick in the form of gene therapy.

Now let’s get familiar with the common forms of cancer treatments.

Surgery removes the cancer and associated tumors and does this by either cutting through skin, muscle, or bone, using cold liquid nitrogen to freeze off abnormal tissue, applying laser beams to tissues or masses to shrink and remove them, or exposing the cells and tissues to extreme heat to kill or weaken what’s present. As for the aftermath of the procedure, along with varying recovery time and surgeon visits, the patient might experience pain, infection, damage to nearby healthy tissues, and bleeding. However, doctors tend to turn to this tactic first in order to have the chance to remove the entire tumor, debulk it, or ease symptoms.

Chemotherapy is typically administered intravenously and treats the cancer by targeting rapidly dividing cells. With such a method, a patient is often confined to a hospital chair anywhere from half an hour to four hours, then left to suffer the hair loss, appetite loss, nausea, diarrhea, and anemia at home for days to weeks at a time before the next round. The ultimate goal of chemotherapy is to get rid of all the cancer cells, eradicating the cancer completely, but others include getting rid of potential cancer cells that might remain after surgery, shrinking the tumor before surgery, and relieving the symptoms and slowing down the growth for those whose development has gone too far.

Radiation therapy involves the use of high doses of radiation in order to damage the DNA of the cancer cells significantly enough to cause them to stop replicating. There are two kinds of radiation therapy: external beam and internal radiation. With an external beam, the patient is to lay down on a table and a machine will move around them to release radiation at certain parts of the body. With internal radiation, the patient is to swallow or be injected with a source of radiation near the tumor site and that radiation will damage the cancer cells from the inside. Each radiation therapy session lasts between 10 to 30 minutes, with several weeks in between sessions, and the patient is left with various types of side effects depending on the location of the tumor; however, some include fatigue, hair loss, skin discoloration, swelling, shortness of breath, diarrhea, and blurry vision. The goal of radiation is the ease the symptoms of the patient, prevent a cancer from returning, and killing/slowing the cancer that is present.

What makes gene therapy so special compared to the current treatments is its mode of attack. Unlike, surgery, chemotherapy, and radiation, gene therapy attacks cancer cells by implanting itself in the core, the genes in the DNA, and altering its expression. In order to do so, scientists employ viral particles or adenoviruses, such as herpes, that are genetically modified to contain a certain genetic expression, so, when injected, the particle is able to go into the cancer cell’s DNA and turn on or off the genetic sequence that is causing it to replicate or form defective proteins, or is able to go into a healthy cell to boost its fighting strength.

Currently, there are three versions of gene therapy: gene transfer, immunotherapy, and oncolytic viral therapy.

Gene transfer consists of the introduction of new genes within the surrounding tissue or cancer cell, typically through intravenous injection. The purpose of gene transfer is to program these viral particles to limit cell growth or just all together cause cell death.

Immunotherapy manipulates a patient’s immune system by stimulating it to aid in fighting and destroying cancer cells. This method is able to perform such tasks by adding the specific genes to the patient’s own blood or bone marrow cells, a viral particle, or a vaccine with manipulated cells. The purpose of immunotherapy is to use the patient’s own immune system to combat the disease rather than using foreign chemicals or rays that can suppress it further.

Oncolytic viral therapy is best suited for the more metastatic cancers because of the replicated nature of both the cells and viral particles. When the viral particles get placed into the body, they invade the rapidly dividing cells, so the viral particles replicate fast within them as well, causing cell destruction.

However, like other treatments, limitations exist, more so with immunotherapy and oncolytic therapy, but there are not as many present in gene therapy like there are in others.

As described by Dr. Deanna Cross and James K Burmester in “Gene Therapy for Cancer Treatment: Past, Present, and Future,” the concern with immunotherapy comes from the vaccination aspect. Since the engineered cells used for the vaccines originate from the individual, it costs a lot of money and takes a substantial amount of time to create and uphold, and very few facilities possess such tools to manufacture the product, thus availability is limited and production might not be able to catch up with the rate of disease.

Moreover, in order for oncolytic therapy to be effective, the viral particles have to be able to out-grow the cancer growth, which is harder for more set masses, therefore, this treatment might have to be paired alongside another. In addition, this method is still relatively new so some key factors, such as the most effective virus to deliver the new genetic message, is still unknown.

Comparatively, gene therapy is associated with fewer side effects since it is more direct at targeting certain cells, maintaining the health of the unaffected, however, that doesn’t eliminate the notion that there aren’t any.

The main side effect that is of concern is toxicity, more specifically, severe adverse effects. There have been cases where after the injection, there has been an increase in certain protein levels, in turn, causing other conditions such as disseminated intravascular coagulation (small clots in the bloodstream) or leukemia. However, it is still unclear on whether it is the gene therapy treatment that is causing these severe adverse effects, or the environment and other genes that the patient may possess. On top of that, it’s hard to predict the severity of the toxicity because the animals used for testing, athymic or SCID mice, lack an immune system which would show the severity effects.

The other main side effect of concern is the replication of the recombinated viruses, a virus with recombined pieces of DNA, used for treatment. If the viruses used to impose treatment were to recombinant and then replicate, then the antibiotics necessary to regulate the problem wouldn’t be available since they do not exist yet, leading to further illness.

Rest assure that such cases have other confounding variables attached to it, so though it happened to a genetic therapy patient, it does not conclude that those effects are a direct result from the treatment itself. As often reiterated and heavily emphasized in science, correlation does not equal causation.

 

Overall, gene therapy is still a relatively new topic, undergoing clinical research trials as we speak, and yet, Dr. Amer showed that it has already been linked to success in chronic lymphocytic leukemia, acute lymphocytic leukemia, and brains tumors.

Once enough research is done to improve on the three types already present, as well as the development of other types, it can be used alongside other treatments or by itself to manage cancers.

Gene therapy possesses the ability to treat a disease like cancer at its base and tailored to the individual, in turn allowing for a more effective and definite fix by stopping the growth and expressing the proper protein to restore normal function. With such qualities, it has the potential to eradicate and prevent the hereditary nature of cancer and be an overall cure to cancer.

Gene therapy will win the battle against cancer for those who couldn’t and protect those from ever having to fight that battle again.

 

 

 

 

 

 

 

 

References

“Acute Lymphocytic Leukemia.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 10 Aug. 2018, https://www.mayoclinic.org/diseases-conditions/acute-lymphocytic-leukemia/symptoms-causes/syc-20369077

“Chronic Lymphocytic Leukemia.” Mayo Clinic, Mayo Foundation for Medical Education and Research, 3 Apr.2019, https://www.mayoclinic.org/diseases-conditions/chronic-lymphocytic-leukemia/symptoms-causes/syc-20352428

“Common Cancer Sites – Cancer Stat Facts.” SEER, seer.cancer.gov/statfacts/html/common.html.

“Gene Expression.” Genome.gov, www.genome.gov/genetics-glossary/Gene-Expression.

“How Does Chemotherapy Work?” InformedHealth.org [Internet]., U.S. National Library of Medicine, 15 Aug. 2019, www.ncbi.nlm.nih.gov/books/NBK279427/.

“Information for Health Care Providers.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 7 Nov. 2019, www.cdc.gov/cancer/preventinfections/providers.htm.

“Radiation Therapy for Cancer.” National Cancer Institute, www.cancer.gov/about-cancer/treatment/types/radiation-therapy#RTCCSE.

“Side Effects of Cancer Treatment.” National Cancer Institute, www.cancer.gov/about-cancer/treatment/side-effects.

“Surgery for Cancer.” National Cancer Institute, www.cancer.gov/about-cancer/treatment/types/surgery#WEBDAS.

Amer, Magid H. “Gene therapy for cancer: present status and future perspective.” Molecular and cellular therapies vol. 2 27. 10 Sep. 2014, doi:10.1186/2052-8426-2-27

Chulpanova, Daria S, et al. “Recombinant Viruses for Cancer Therapy.” Biomedicines, MDPI, 25 Sept, 2018, www.ncbi.nlm.nih.gov/pubmed/30257488

Cross, Deanna, and James K Burmester. “Gene therapy for cancer treatment: past, present and future.” Clinical Medicine & Research vol. 4 iss.3 (2006): 218-27. doi:10.3121/cmr.4.3.218

Hunt, Kelly K., et al. Gene Therapy for Cancer. Humana Press, 2007. IBSN: 978-1-58829-472-2

Wold, William S M, and Karoly Toth. “Adenovirus vectors for gene therapy, vaccination and cancer gene therapy.” Current gene therapy vol. 13,6 (2013): 421-33. doi:10.2174/1566523213666131125095046

By: E. Melbouci

Image Credits

Stepanenko Oksana, Gene therapy DNA 3D chemical molecule structure low poly. Polygonal triangle point line healthy cell part. Innovation., Dreamstime, https://www.dreamstime.com/gene-therapy-dna-d-chemical-molecule-structure-low-poly-polygonal-triangle-point-line-healthy-cell-innovation-blue-medicine-genome-image115746910

Understanding the ketogenic diet’s benefits in athletics, lifestyle, and medical/therapeutic.

What do Lebron James, Katie Couric, and an 18-year-old girl with seizure-like events have in common? 

The ketogenic diet. 

Fats: steak, eggs, cheese, and many more delicious foods are a part of the diet. 

Each of them has used it for a different advantage: Lebron for an athletic application, Katie for maintaining a healthy lifestyle, and the 18-year-old girl with seizure-like events for a medical/therapeutical reasons. All of this has been achieved by comprising a majority of their nutrition with fats.

The fact that the ketogenic diet has these different applications is interesting. 

But, before I get into the different applications of the diet, it is important to understand what the diet actually is made up of and does. The ketogenic or keto diet is a diet in which most of your nutrition is comprised of fat. The other aspect of this diet is a low intake of carbohydrates or sugars (glucose). Because of the low intake of carbs, your body goes into a state of ketosis. Ketosis is a metabolic state characterized by the production of ketone bodies from acetyl-COA. In other words, your body stops using glucose as its main source of metabolic energy and starts using fats.

Let’s start with Lebron.

Lebron James is an NBA athlete. And as a professional paid athlete Lebron’s job is physically taxing especially during games. Now let’s say Lebron ate some carbs before a game. He will feel energized because the carbs that he ate are comprised of glucose. The glucose is used by the mitochondria–the powerhouse of the cell–within his cells to create adenosine triphosphate or if you want to be cool about it, ATP. 

ATP is important because it is basically the energy of life for all living aerobic animals, including us humans.

So Lebron feels energized by the carbs. However, his sugar-induced energy is short-lived because glucose burns very quickly; this means he runs out of carbs. His brain and muscles need the glucose to function properly, so without it, his athletic performance is hindered; not unless he went on a keto diet and ate something fatty before the game. 

But an experiment by Krzysztof Durkalec-Michalski found that Crossfit athletes who went on a ketogenic diet for four weeks and did an incremental cycling test (incremental cycling test measures oxygen consumption and carbon dioxide production by increasing the intensity of the cycling over time), started utilizing fat as an energy source when the maximal oxygen uptake–VO2 max–was up to eighty percent. This shows that fat consumption during exercise is used when a submaximal–heavy work that does not require maximal effort–effort is being exerted. 

Before you say, “Wait the experiment was done on Crossfit athletes how does that apply to King James?”

Both the incremental cycling test and the basketball game are endurance-heavy. 

For this reason, if Lebron had gone on a ketogenic diet before this hypothetical game, he could have done one of two things. The first is as said before, he could have eaten the fat-enriched food and his body would have consumed the fat to burn it for metabolic energy. Lebron will have longer energy on fats compared to carbs. The other way in which Lebron could have used the diet to his advantage is going on the keto diet while eating carbs before the game. The reason for this is because of mitochondrial biogenesis.

Mitochondrial biogenesis is a process by which cells increase mitochondrial mass. This can be induced by ketosis. With mitochondrial biogenesis, there is an increased glucose uptake by muscles. In regards to Lebron, this means better performance during a game compared to just eating carbs without having been on the keto diet. 

This brings me to the next person Katie Couric. 

Katie Couric–and I’m going to go out on a limb here–is not an athlete. Now yes she does workout but she ain’t running back and forth on the basketball court breaking ankles or making three-pointers. Any healthy, average person should do some form of regular exercise, and that’s that. 

Back to Katie though, she has used the keto diet for maintaining a healthy lifestyle. Similarly, an experiment done by Robert DS Pitcheathly & Carlo Viscomi found a ketogenic diet within normal, healthy subjects had no bad effect on muscles. Also in a two and a half year follow up with patients, healthy patients had lost fast and weight. 

The ketogenic diet also has been reported by Vincent Miller and others to help with chronic diseases such as diabetes, obesity, and other diseases resulting from mitochondrial disability. 

This leads me to the last person within the discussion of the versatility of the keto diet, the 18-year-old girl with seizure-like events.

This was a retrospective case study done by M.A.A.P. Willemsen and others. They looked at the 18-year-old girl’s lab results thinking that her blood glucose levels were low resulting in the seizure-like events. However, upon looking for low glucose levels within the spine, they found that the girl had a  GLUT1 deficiency syndrome: weakened glucose movement to the brain. 

The keto diet comes in because the ketones that are produced provided the brain as a replacement for energy, rather than glucose. The ketones are reconverted back into the acetyl-COA which then goes into the Kreb Cycle. The Kreb Cycle is the last step of cellular respiration. The use of the ketogenic diet isn’t new to the medical field: since the 1920s the keto diet has been used to treat patients with epilepsy. 

With all the applications of the keto diet, it is should be known that this diet does mean following a very strict plan of low to no carbs. Lack of vitamins and minerals calls for the need for supplementation. Also, the diet should not be followed for a long period of time because of the aforementioned lack of vitamins and minerals. 

And while the textbook definition of the keto diet is high fat and low carbs, in “Nutritional Ketosis and Mitohormesis: Potential Implications for Mitochondrial Function and Human Health” Vincent J. Miller and others state:

“A [keto diet] less restrictive in carbohydrate[s] and protein[s] … [is] more satisfying, sustainable, and feasible for the general population.” 

At the end of the day be smart about whatever diet you decide to go on. Know that there are pros and cons to each diet; there is no perfect diet. What leads to a healthy life is making the right decision overall that will better your life and your happiness.

By: I Tonuzi

References

Durkalec-Michalski, Krzysztof, et al. “Effect of a Four-Week Ketogenic Diet on Exercise Metabolism in CrossFit-Trained Athletes.” Journal of the International Society of Sports Nutrition, vol. 16, no. 1, 2019, doi:10.1186/s12970-019-0284-9. https://jissn.biomedcentral.com/articles/10.1186/s12970-019-0284-9

Miller, Vincent J., et al. “Nutritional Ketosis and Mitohormesis: Potential Implications for Mitochondrial Function and Human Health.” Journal of Nutrition and Metabolism, vol. 2018, 2018, pp. 1–27., doi:10.1155/2018/5157645. https://www.hindawi.com/journals/jnme/2018/5157645/

Pitceathly, Robert Ds, and Carlo Viscomi. “Effects of ketosis in mitochondrial myopathy: potential benefits of a mitotoxic diet.” EMBO molecular medicine vol. 8,11 1231-1233. 2 Nov. 2016, doi:10.15252/emmm.201606933 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5090656/

Willemsen, M.A.A.P., Soorani‐Lunsing, R.J., Pouwels, E. and Klepper, J. (2003), “Neuroglycopenia in normoglycaemic patients, and the potential benefit of ketosis.” Diabetic Medicine, 20: 481-482. doi:10.1046/j.1464-5491.2003.00952.x https://onlinelibrary.wiley.com/doi/full/10.1046/j.1464-5491.2003.00952.x

Image Credits 

Image 1: Malan, David, Unknown Title, https://www.aarp.org/health/brain-health/info-2015/brain-diet.html

Image 2: Allison, Keith, “Lebron James”, https://en.wikipedia.org/wiki/The_Block_(basketball)

Image 3: Stutz, Douglas H., “NBC Today Show host Katie Couric broadcasts live from Prince Sultan Air Base, Saudi Arabia, as part of the show’s coverage of Operation Southern Watch”, https://commons.wikimedia.org/wiki/File:Katie_Couric.jpg

Image 4: Jaiswal, Jyoti K. , M.S.C., Ph.D., Unkown Title, https://innovationdistrict.childrensnational.org/mitochondria-key-repairing-cell-damage-dmd/

When we think about developing countries and nutrition, a picture of a malnourished child immediately jumps into our heads. 

Ironically, there is a global epidemic of overweight and obesity that coexists with undernutrition. One third of the entire population is either overweight or obese, and, 62 percent of these individuals are living in developing countries. 

This rising trend is particularly seen in children and adolescents which, for the most part, puts them at a greater risk for physical health and psychological effects.

But why is obesity rising in developing countries in the first place? 

The World Health Organization suggests that every aspect of the environment in which children are conceived, born, and raised can contribute to their risk of becoming overweight. In developing countries, some of the determinants of health include: physical activity, dietary changes, socioeconomic status, sociocultural factors, and schooling.  Furthermore, in third world countries, although higher obesity rates are concentrated in high income neighborhoods, children of lower social status are also beginning to show higher rates of obesity, and there are various determinants to account for the rise in child obesity rates in both of these groups.

As low income countries continue to develop, many changes are occurring. Dietary changes in these parts of the world are one of the most concerning factors that contribute to the rise in obesity for both high and low income children. The main reason behind this change in food preferences come from a rise in food prices and continuous advertisements.

According to the Journal of Endocrine Reviews, relatively low cost, energy-dense foods are becoming increasingly popular, and feeding infants high-fat or high-sugar foods such as fries or sodas, are a decisive contributor to childhood obesity. For example, the Oxford Academics Nutrition Reviews Journal says that prices for basic grains have doubled or tripled in various developing countries. If families don’t have access to fair priced healthy foods, there won’t be a variety of food for children to choose from. While unhealthy foods are getting cheaper and more attractively tasting, both parents and children continue to prefer eating them. 

Moreover, there seems to be greater access to unhealthy fast food choices surrounding schools and the school area, which is were children spend the majority of their time. According to the journal of endocrine reviews, school cafeterias and vending machines are usually stocked with cheap fast food choices and high-sugar beverages that are easy for kids to purchase. Furthermore, the school neighborhood is usually surrounded by fast food dining options and street food vendors that give students quick access to highly-processed unhealthy foods. 

Schools and a kid’s family have big influence over what children choose to eat, but they lack the knowledge to tell children what they should be eating. The World Health Organization says that there is a lack of information about what it means to have a healthy diet. In fact, this is also where the sociocultural factors become a determinant. There is a lack of knowledge and various misconceptions surrounding unhealthy nutrition and its possible adverse effects. For example, some people living in African countries think of being overweight as a symbol of wealth and happiness; because of sociocultural constructions about obesity like this one, some people even strive to gain more wight by eating unhealthy foods. To counteract the lack of knowledge and misconceptions, The Nutrition Reviews say that educating children and their families about nutrition is primordial.

Shockingly, socioeconomic status within developing countries also may contribute to where obesity is concentrated. The study published in the international journal of obesity links higher education and urbanization with higher rates of obesity. Although this does not correspond with a lack of knowledge on nutrition, high-SES families give their children more money for food, and as the Endocrine Reviews research suggests, their have more western type of lifestyle. This means, children have more freedom to choose what they eat and where they eat, and they may have a more inactive lifestyle. As urbanization rises, there is fewer opportunities for physical activity. Children living in the city are less likely to be more physically active because according to the world health organization there are not as much open spaces for them to engage in healthy play. 

Lack of physical activity also contributes to the rise in obesity for low-SES children. The neighborhoods where low income children are brought up in can be dangerous and lack a safe space to practice sports and engage in group physical activities. The article on Endocrine Reviews suggests that, usually, are not even safe walk or bicycle routes for kids to get to school. 

Given all of these determinants, obesity has become pretty common in developing countries, and it is affecting the children living in both wealthy and low income households.  

But what are the consequences of this rise in obesity? why is this even important? 

Although, not every overweight child develops the possible consequences that obesity brings, previous research has shown that obesity can affect a child’s physical and mental health as well as their future health as adults.

Cardiovascular disease, diabetes, asthma, and even some types of cancers seem to be linked to obesity. These diseases can negatively impact a person’s life and decrease their life expectancy. According to Best Practice and Research, 58% of obese 5 to 10 year-olds had at least one cardiovascular risk factor. A cardiovascular risk factors can be something like hypertension or insulin resistance, which have been associated with higher obesity rates. Although these words seem daunting, all it means is that children with unhealthy diets increases their risk of being constantly sick as adults. For example, hypertension, in simple terms, is another name for high blood pressure, and eating things such as butter or canned soups can increase a person’s blood pressure, which is bad for their health. 

The International Journal of Obesity also points out that the primary problem with having obesity as a child is that it increases the risk of continuing with obesity in adulthood. In fact, their research shows that the risk of developing obesity in adulthood  is 3.9 to 6.5 times greater for obese than non-obese children. If kids continue to be obese as adults, they will experience even more long term health consequences. In fact, according to the Journal of Hormone Research in Pediatrics, early life obesity is a risk factor for mortality later in life. Imagine that the life of your child is not as long as it could be because of their weight and how they eat. 

Furthermore, there are psychosocial consequences related to childhood obesity that affect a child’s mental health and future. The study conducted by the International Journal of Obesity says that the consequences of obesity among children are usually psychosocial, such as low self esteem, poor peer acceptance, and low participation in social and sports activities. Social isolation and stress seem to be common among overweight children especially during their adolescent years. The Journal of Family Medicine and Primary Care even say that these negative social problems can also affect their academic performance, which affects a child’s future. 

All of the consequences that threaten overweight children in developing countries are a call to action for a change before the effects of obesity get to a point of no return. If the rates of obesity in children continue to rise there is a threat to the health of entire populations. If there is no change in government policy and incentives for individuals to change their dietary habits and levels of physical activity, the growth rate of obesity around the world will continue to increase.

By: D Bayas

References

Facts and figures on childhood obesity. (2019). Retrieved from https://www.who.int/end-childhood-obesity/facts/en/

Maffeis, C. & Tatò, M. (2001). Long-Term Effects of Childhood Obesity on Morbidity and Mortality. Hormone Research in Pediatrics. 55(1), 42-45. https://doi.org/10.1159/000063462

Martorell, R., Khan, L. K., Hughes, M. L., & Grummer-Strawn, L. (2000). Overweight and obesity in preschool children from developing countries. International Journal of Obesity and Related Disorders, 24(8), 959-967. http://dx.doi.org/10.1038/sj.ijo.0801264

Nidhi, G., Kashish, G., Priyali, S. & Anoop, M., (2012). Childhood Obesity in Developing Countries: Epidemiology, Determinants, and Prevention. Endocrine Reviews. 33(1), 48–70. https://doi.org/10.1210/er.2010-0028

Olufunke, A. & Kayode, O. (2013). Trends of Obesity Epidemic and its Socio-cultural Dimensions in Africa: Implications for Health Systems and Environmental Interventions. Emerging Issues in Medical Diagnosis and Treatment. 7(1), 1-8. https://pdfs.semanticscholar.org/5f8d/6ffb1327a837c909bec08d5a209adbde43eb.pdf?_ga=2.50345579.397012989.1581660189-1657725813.1579874040

Popkin, B., Adair, L. & Wen Ng, S. (2012). Global nutrition transition and the pandemic of obesity in developing countries. Nutrition Reviews. 70(1), 3–21. https://doi.org/10.1111/j.1753-4887.2011.00456.x

Reilly, J. (2005). Descriptive epidemiology and health consequences of childhood obesity. Best Practice & Research Clinical Endocrinology & Metabolism, 19(3), 327-341. https://doi.org/10.1016/j.beem.2005.04.002

Sahoo, K., Sahoo, B., Choudhury, A. K., Sofi, N. Y., Kumar, R., & Bhadoria, A. S. (2015). Childhood obesity: causes and consequences. Journal of family medicine and primary care, 4(2), 187–192. doi:10.4103/2249-4863.154628. https://www.ncbi.nlm.nih.gov/pubmed/25949965

Why does childhood overweight and obesity matter? (2014). Retrieved from https://www.who.int/dietphysicalactivity/childhood_consequences/en/

Image Credits

Image 1: Rasfan, Mohod, “A homeless child eats food on a street in Kuala Lumpur”, The Guardian, https://www.theguardian.com/global-development/2016/sep/09/global-food-crisis-cultural-shift-junk-food-researchers-oxfam-ids

Image 2: Unknown author, “Availability of food choices”, Women Fitness, https://www.womenfitness.net/foods-obesity/

Image 3: Asad, KM, “A temporary food stall is seen in a street in Old Dhaka, Bangladesh”, The Guardian, https://www.theguardian.com/global-development/2016/sep/09/global-food-crisis-cultural-shift-junk-food-researchers-oxfam-ids

 

You’ve just been diagnosed with moderate endometriosis. You’ve been in excruciating pain for as long as you can remember, sometimes unable to keep food down because of it, and you’ve been bleeding for months without relief.

Now it’s time to choose a treatment plan. Do you get a hysterectomy? There’s no way you would be able to carry a child and the emotional and mental stress from surgery is intense. Do you get prescribed pain relief medication to deal with it? That doesn’t address the growing endometrial issue that can lead to cytotoxicity and reproductive cancers. Lastly, the main question in front of you: Do you start taking birth control to manage your hormone levels so you’re less likely to grow endometrial tissue? Can you even afford birth control where you are? Will you face judgement from those around you for taking it? Is it even worth it? These are the questions that are asked every day as women around America are diagnosed with abnormal uterine bleeding.

Abnormal uterine bleeding consists of disorders such as endometriosis, PCOS, heavy menstrual bleeding, and others, all entailing of symptoms such as irregular menstruation patterns, anemia, nausea, bowel dysfunction, or pelvic pain, many of which are so drastic that it prevents the patient from taking part in day to day activities. Much of this pain takes place in the uterus, as this is where the dysfunction occurs. While many of these disorders may have their variances of symptoms as whether there is endometrial tissue growing or ovarian cysts forming, the one commonality between them all: they all derive from an irregularity in sex specific hormones and have an effect on a female’s menstrual cycle. This is why birth control is an effective treatment for AUB.

Oral contraceptives work as they consist of both progesterone and estrogen hormones that lead to the thickening of the uterine lining and as you go into taking the fourth week of pills, you take a placebo that triggers “breakthrough bleeding” also known as menstruation, as the body is no longer being supplied the artificial hormones. In AUB, this is effective to maintain a more normal cycle and fluctuation of such hormones, preventing and treating some of the many symptoms of the disorders. If birth control is so effective in treating AUB disorders, why is there so much stigma and hesitation around it?

According to the New England Journal Medicine, the battle over the financial coverage has been a long one, but has significantly increased ever since the Affordable Care Act was passed in 2010. The Obama administration exempted houses of worship from the requirement of offering employee’s coverage of contraceptives. This is because while contraceptives help regulate menstruation, they also work to prevent pregnancies when sexually active, bringing in argument the churches disapproval of premarital sex.

The association between the “shame” of premarital sex and how it goes against religious values has led to many companies not financially covering contraceptives as medical treatment, stating that “If an employee wants birth control, that worker could … just work elsewhere”, thus a disparity in healthcare accessibility across America in these workplaces forms (Alta). These statements and views of the world may bring a perspective about the balance of religion in healthcare, but they also bring about healthcare disparities from their views on birth control.

In a study done in response to the Affordable Care Act, the inaccessibility of oral contraceptives (OCs) is greatly shown. The research done included those who took OCs for more than just to prevent conception, but for also AUB disorders and severe acne. After the coverage OC coverage exemption took place, this resulted in racial/ethnic minorities to be less likely to be OC users and to have a lower OCP usage if using, and minorities and married women were more likely choose more generic brands of OCs (Lin). This illustrates the decline in affordability of such treatments, as well as the increasing lack of accessibility to this treatment after the ACA was put in place, tying a direct relation between the decreasing contraceptive access and social stigma.

Should religiously affiliated institutions be exempt from providing coverage for contraceptives, even if they are used as a form of treatment? If we do not consider contraceptives to be part of the healthcare system, we then revert back to choosing unnecessary and irreversible invasive surgeries that devastate the human body, or to just leave patients that cannot afford those options to go suffer from AUB untreated. These options not only ignore the problem of AUB at hand, but also bring about unnecessary stress, pain, and declines the health of the patient as it progresses.

Without treating AUB directly we leave the patient not only to deal with the physical and mental burden that comes with the disorders, but they are also at risk to develop more destructive conditions such as cytotoxicity, where cell death or damage occurs in the body, take place. In a study by Dr. Donald P. Braun from The American Fertility Society, it was found that in patients with endometriosis, cytotoxicity towards normal cells was more likely to appear in patients that were untreated and later staged than in patients being treated by birth control. This ailment racks the human body; to have the ability to prevent this from occurring by using oral contraceptives is something that should not be overlooked and should never be withheld from a patient, no matter their economic status or religious affiliation.

These discussions of treatment are all contingent on people having an open line of communication with their physicians and being an advocate for their own health. As we delve more and more into the future of medicine, we must recognize the importance of making treatments accessible as well as being aware of the stigmas that surround our society that prevent us from receiving vital healthcare. One day you or a loved one could be sitting in a room fighting to overcome the healthcare obstacles in your way to get the best treatment, but if we keep an understanding and educated mind about ourselves, then we can help prevent so much pain and provide patients with actual choices.

By: K. Peck

References

1. Alta, C. R. (2012). Warning: Contraceptive drugs may cause political headaches. The New England Journal of Medicine, 366(15), 1361-1364. doi.org/10.1056/NEJMp1202701.
2. Bradley, L. D., & Gueye, N.-A. (2016). The medical management of abnormal uterine bleeding in reproductive-aged women. American Journal of Obstetrics and Gynecology, 214(1), 31–44. doi.org/10.1016/j.ajog.2015.07.044.
3. Braun, D. P., Gebel, H., Rotman, C., Rana, N., & Dmowski, W. P. (1992). The development of cytotoxicity in peritoneal macrophages from women with endometriosis. Fertility and Sterility, 57(6), 1203-1210.
4. Lin, H.-C., & Lee, H.-Y. (2015). Utilization of and Adherence to Oral Contraceptive Pills and Associated Disparities in the United States: A Baseline Assessment for the Impact of the Affordable Care Act of 2010. International Journal of Health Services, 45(4), 729–742. doi.org/10.1177/0020731415591244.

Image Credits

1. Blausen, Picture of uterus with endometrium, TeachMeObGyn, https://teachmeobgyn.com/gynaecology/uterine/endometriosis/.