MediUnite Journal Monthly Magasine "Vital" - March 2024

MEDIUNITE

THE JOURNAL’S VITAL MAGAZINE

MEDICAL AWARENESS, HOW WE’RE CHANGING

GLOBAL WELLBEING

Pg2. Alzheimer'sBrainChanges, ReadthearticleonPathophysiology forAlzheimer'sdisease

Pg4. NerveCellVulnerability? ReadthearticleonRSV’sImpact

Pg5. What’stheRationale?Read thearticleonPPIsinHpylori treatment

Pg7 FeedYourGut,FeedYour Mind,Readthearticleonguthealth

Pg8 Whatisthebattleagainst antibiotics?Readthearticleon antiobioticimmunity

Pg9 RadiantSkinorDire Consequences?Readthearticleon Retinol’sDermatologicalUseage

Pg11. ShouldWeBeWorried? Readthearticleonpharmaceuticals

UNRAVELING THE PATHOPHYSIOLOGY OF ALZHEIMER'S DISEASE

By Olivia Kim

Alzheimer’s disease (AD) is a neurodegenerative disease that largely affects older adults. AD is the most common form of dementia, a form of memory and cognitive loss, in the world (1). Symptoms patients typically experience include: impairments in cognitive ability such as language, long-term and short-term memory loss, personality changes including increased aggression and irritability.

Understanding the pathophysiology of AD is integral in developing effective treatments and prevention methods for those who are at a high risk for developing AD later on in life or those who suffer from the disease. Based on previous and ongoing research, the two main pathological signs in AD patients are BetaAmyloid plaques (AB) and neurofibrillary tangles (NFT) which lead to brain atrophy, producing the various symptoms associated with AD.

Tau proteins are microtubule associated proteins in neuronal cells (4). In other words, Tau proteins participate in the structure of neurons. Specifically, in the structure of microtubules in axons. Axons are the part of the neuron responsible for transmitting any action potentials that are initiated at the axon hillock towards the axon terminal where neurotransmitters are released. In several neurodegenerative diseases, including AD, these Tau proteins are hyperphosphorylated which causes them to aggregate and form structures known as NFT.

Naturally, aggregation of Tau proteins leads to axonal dysfunction and cell death over a long period of time. Diseases that are caused, or partially caused by Tau protein misfolding, are categorized as taupathic. Early research suggested that NFT themselves cause neurotoxicity and result in atrophy of the cortex, however, current research suggests that NFT may be the result of the brain trying to protect itself from a different soluble neurotoxic form of Tau.

One reason for the change in hypothesis is that NFT occur in the brain in individuals who never develop AD later on in life. More research is needed on the exact mechanisms behind Tau pathology that leads to AD. Despite the uncertainty on the details of NFT’s involvement, the field still agrees that NFT is an integral part of AD pathophysiology because of their constant, heightened presence in AD patients (1). AB are extracellular protein aggregates produced by improper cleavage of amyloid precursor proteins (1).

When improperly cleaved protein fragments clump together, they precipitate together into a clump outside of the cell. AB are associated with a cell state called oxidative stress (OS) (3). OS is a state in which a cell experiences accumulation of reactive oxygen species due to an inability to produce antioxidants or a deficiency in antioxidants (2). OS is extremely harmful to the cell and will often result in cell death and mitochondrial dysfunction. AB have been proven to cause OS in the mitochondria in vitro and in vivo which causes cell death and brain atrophy. Although the exact mechanism behind the link between AB and OS is not fully known, AB does increase OS in neurons which trigger further OS and produce more AB in a cycle (1). Both OS and AB also enhance the hyperphosphorylation of Tau proteins producing increased levels of NFTs which contribute to cell death.

Further research into developing potential therapeutics targeting AB appears to be a fruitful approach based on the evidence for AB’s role in producing cell death through mitochondrial OS in neurons. AD is a highly prevalent form of dementia amongst older individuals. Evidence from decades of research points to NFTs and AB as the two key pathological players in the development of AD by impairing neuron function and synapses which cause extensive cell death. With enough neuronal death, the cortex starts to atrophy which leads to impairments in functions the atrophic area is involved in.

Current research is focused on discovering the mechanisms that link NFTs and AB with OS and necrosis in the brain.

References

1

Perspective chapter: Alzheimer - A complex genetic background (2021, December 28) IntechOpen - Open Science Open Minds | IntechOpen.

https://www intechopen com/chapters/79831

2.

Real-time imaging of mitochondrial redox reveals increased mitochondrial oxidative stress associated with amyloid β aggregates in vivo in a mouse model of Alzheimer’s disease. (2024, January 18) BioMed Central

3.

PubMed. (n.d.). Imaging beta amyloid aggregation and iron accumulation in Alzheimer's disease using quantitative susceptibility mapping MRI

https://pubmed ncbi nlm nih gov/30739060/

4

5

https://molecularneurodegeneration biomedcentral com/article s/10 1186/s13024-024-00702-2

Wang, Y (2016) Tau in physiology and pathology PubMed https://pubmed ncbi nlm nih gov/26631930/

NERVE CELL VULNERABILITY AND RSV'S IMPACT

By Farhnaz Fazli

Background:

RSV is known as the second leading cause of infancy death globally, after malaria (1) It is an infection that commonly causes severe complications in premature infants and infants 6 months and younger. Some symptoms in infants include: irritability, decreased activity, and breathing difficulties (2). Since its discovery, RSV has been thought to only infect the respiratory tract and system.

A recent study by Tulane University in the United States however, reveals that it can penetrate nerve cells too (6). Neurological issues in RSV infected patients is thought to be caused by the body’s inflammatory response to the virus indirectly affecting nerve cells. This latest finding could potentially lead to an alternate explanation behind the neurological issues that arise in some RSV infected patients (6) If RSV is capable of penetrating nerve cells as the study findings conclude, it raises the alarming possibility that infections could affect neurological development in infants.

Preventative Treatment:

As of 2023, the FDA in the United States has approved the world’s first preventative treatment of RSV (5). RSV antibodies can be administered into mothers that are 32-36 weeks pregnant during RSV season and for babies younger than 8 months old (entering or born during the RSV season) RSV season varies upon region. It is important to note that this antibody treatment does not stop infection from occurring but rather prevents severe cases of RSV.

There are currently no other treatments available to tackle RSV. For severe cases, infants are often hospitalized and provided with oxygen, IV fluids, mechanical ventilation, tube feeding, and mucus suctioning (3). For milder cases of RSV, patients are told to wait out the infection by resting, staying hydrated and taking overthe-counter medication for pain or fever.

Thus, it is evident that public and global health authorities shall prioritize a preventative approach to RSV via antibody treatment and reduce its severity as one of the leading causes of death in infants, globally.

References

2

3

4

1. Perk, Y (2018) Respiratory syncytial virus infections in neonates and infants PubMed Central (PMC)

5.

Infectious Disease Special Edition. (n.d.). RSV may cause nerve inflammation and damage https://www idse net/ViralInfections/Article/01-24/RSV-May-Cause-Nerve-Inflammationand-

Damage/72592#: :text=Since%20RSV%20was%20first%20discovere d,fluid%20of%20children%20with%20seizures

RSV responsible for 1 in 50 child deaths under age 5, study estimates (2022, November 11) CTVNews

https://www ctvnews ca/health/rsv-responsible-for-1-in-50-childdeaths-under-age-5-study-estimates-1.6149304

https://www ncbi nlm nih gov/pmc/articles/PMC6089794/#:~:text Respiratory%20syncytial%20virus%20is%20the,the%20neonatal%20 period%20(1)

U.S. FDA approves ABRYSVO™, Pfizer’s vaccine for the prevention of respiratory syncytial virus (RSV) in infants through active immunization of pregnant individuals 32-36 weeks of gestational age | Pfizer (2023) Pfizer: One of the world's premier biopharmaceutical companies.

https://www pfizer com/news/press-release/press-releasedetail/us-fda-approves-abrysvotm-pfizers-vaccine-prevention0#: :text=In%20May%202023%2C%20the%20U S ,years%20of%20ag e%20or%20older

6

Yawn, A (2024) RSV shown to infect nerve cells, cause inflammation and damage Tulane University News

https://news tulane edu/pr/rsv-shown-infect-nerve-cells-causeinflammation-and-damage

PPIS ARE KEY INGREDIENTS IN H. PYLORI TREATMENT. WHAT’S THE RATIONALE?

By Feras Qays

1.

The difference between a PPI-free and PPI-included eradication therapy. In the study, MACH (1), four groups of patients were enrolled to demonstrate the H. pylori eradication rates with and without a PPI.

Group AC: Amoxicillin/Clarithromycin

Group OAC:

Omeprazole/Amoxicillin/Clarithromycin

Group MC: Metronidazole/Clarithromycin

Group OMC:

Omeprazole/Metronidazole/Clarithromycin

As shown in (figure 1), the addition of omeprazole significantly increased the eradication therapy of both regimens

2. How does PPI contribute to a higher eradication rate?

PPIs tend to have a direct and in‐direct effect on H pylori eradication (2‐4)

Direct effects:

1. PPIs have a weak antibacterial effect. Acid converted metabolites of PPIs have been shown to have a more potent antibacterial effect than parent PPIs.

2. They also bind and deactivate the urease and ATPase enzymes of H. pylori, which are important for its survival It has been doubtful that these direct effects alone are responsible for the significant increase in eradication rates, as it has been shown in the GU‐ MACH2 study that omeprazole alone had an eradication rate of 4% only. Therefore, it has been suggested that PPIs contribution to a higher eradication rate comes from its synergistic or in‐direct effects to Amoxicillin + Clarithromycin OR Metronidazole + Clarithromycin.

Indirect effects:

1. PPIs inhibit acid secretion and increases intragastric pH levels. Several papers have showed that the minimum inhibitor concentration (MIC) of these antibiotics is pH dependent. Amoxicillin and Clarithromycin antibacterial activity against H. pylori is increased by 8 and 20 times, respectively after PPI administration. However, metronidazole’s activity is no pH dependent.

2. As a result of acid inhibition, antibiotics concentration within the stomach is increased providing a stronger action

3. H. Pylori replicates/grows at neutral pH of 6‐7, and it turns into the coccoid form that is resistant to antibiotics. The coccoid form is non‐replicative and non‐growing (6). Therefore, it is important to maintain a neutral pH to allow the bacteria to turn back into its replicative form, a form that is resistant to antibiotics, unlike the resistant coccoid form.

3. What is the most optimal PPI?

As stated earlier, it is very important to have a neutral or high pH levels as soon as possible to synergize the antibiotics effect. The time that a PPI require to inhibit acid secretion is critical to a successful therapy. The usual duration for an eradication therapy is 7 days. If acid suppression is achieved within 3 days of taking PPI, then the actual effective duration of the antibiotics is only 4 days. Saitoh and colleagues conducted research that examined the time (in days) needed to inhibit acid secretion by omeprazole, lansoprazole and rabeprazole. As shown in (figure 2), Rabeprazole acid suppression is achieved after 1 day and are faster than lansoprazole and omeprazole that took 3 days to provide acid suppression. Therefore, Rabeprazole is recommended over the latter.

But what about esomeprazole?

Hunfield examined the difference between esomeprazole and rabeprazole. He found that within the first 24hour the intragastric pH were significantly higher with esomeprazole than with rabeprazole. Therefore, Esomeprazole is superior to rabeprazole in terms of time needed to maintain a high pH levels for optimum eradication therapy.

References

1

Lind T, Megraud F, Unge P, et al: The MACH2 study: role of omeprazole in eradication of Helicobacter pylori with 1-week triple therapies Gastroenterology 1999;116:248–253

2.

Nagata K, Satoh H, Iwahi T, et al: Proton inhibitory action of the gastric proton pump inhibitor lansoprazole against urease activity of Helicobacter pylori: unique action selective for H. pylori cells. Antimicrob Agents Chemother 1993;37:769–774 19

3.

Mauch F, Bode G, Malfertheiner P: Identification and characterization of an ATPase system of Helicobacter pylori and effect of proton pump inhibitors. Am J Gastroenterol 1993;88:1801–1802 20

4

Grayson ML, Elipoulos GM, Ferraro MJ, et al: Effect of varying pH on the susceptibility of Campylobacter pylori to antimicrobial agents Eur J Clin Microbiol Infect Dis 1989;8:888–889

5

McNulty CA, Dent JC, Ford GA, et al: Inhibitory antimicrobial concentrations against Campylobacter pylori in gastric mucosa J Antimicrob Chemother 1988;22:729–738

7.

6 Hunfeld, N.G. et al. (2012) “A comparison of the acid-inhibitory effects of ESOMEPRAZOLE and rabeprazole in relation to pharmacokinetics and CYP2C19 polymorphism,” Alimentary Pharmacology & Therapeutics, 35(7), pp 810–818 Available at: https://doi org/10 1111/j 1365- 2036 2012 05014 x

Ierardi E, Losurdo G, Fortezza RF, Principi M, Barone M, Leo AD Optimizing proton pump inhibitors in Helicobacter pylori treatment: Old and new tricks to improve effectiveness World J Gastroenterol. 2019 Sep 14;25(34):5097-5104. doi:

10 3748/wjg v25 i34 5097 PMID: 31558859; PMCID: PMC6747288

FOOD & MOOD: THE SURPRISING CONNECTION BETWEEN GUT-HEALTH AND MENTAL WELL-BEING

By Maya Madhvani

We are an ecosystem that houses at least about 38 trillion bacteria in our bodies. The gut is often called the 'second brain'; It is home to trillions of bacteria that play a crucial role in digestion, immune function, and mood regulation. The gut-brain axis (GBA) is a two-way connection between the brain and the gut, linking emotions and thoughts with intestinal activities. This means that not only does your brain influence your gut, but it is also influenced by the gut. Can you relate to having noticed changes in your mental state after eating poorly or having digestive problems when you felt distressed? Scientists have uncovered a profound link between gut health and mental well-being in recent years.

"The gut provides approximately 95% of total body serotonin" (1). Serotonin is a neurotransmitter for longer-lasting happiness, satisfaction, and overall wellbeing. Low levels of serotonin are found in people who are diagnosed with depression.

Moreover, researchers found that people with anxiety and depression tend to differ from others in the kind and amount of gut microbiota (2). The results reported that individuals with anxiety and depression tend to harbor gut bacteria associated with inflammation, alongside a decrease in microbes producing short-chain fatty acids, known to regulate the central nervous system

References

1

Appleton, J (2018) The gut-brain Axis: Influence of microbiota on mood and mental health PubMed Central (PMC)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6469458/

The gut microbiota in anxiety and depression – A systematic review. (2021). ScienceDirect.

2 The gut-brain axis: Interactions between enteric microbiota, central and enteric nervous systems. (2015, April). PubMed Central (PMC)

4

https://www sciencedirect com/science/article/abs/pii/S0272735820 301318?casa token=FoPLItjhxEAAAAA:XEFGyyGC0HVUvcjosZmnHobtISRGWiGL6sRcDvjMLtV9TY1DAzVvvNa8cdTooW7ImmqSFsh#bb0080

3 Revised estimates for the number of human and bacteria cells in the body (n d ) PubMed Central (PMC)

https://www ncbi nlm nih gov/pmc/articles/PMC4367209/#: :text= The%20gut%2Dbrain%20axis%20

https://www ncbi nlm nih gov/pmc/articles/PMC4991899/#:~:text Thoroughly%20revised%20est

COMBATING ANTIBIOTIC RESISTANCE

By Yatharshana Prabhu

Antibiotics, vital in treating bacterial infections like strep throat and pneumonia, are often misused for viral illnesses, fostering antibiotic resistance. (1) This phenomenon, rampant globally, poses severe threats to public health and healthcare systems. Up to 50% of antibiotics prescribed in outpatient settings are unnecessary or inappropriate, accelerating resistance development (5). Antibiotic resistance leads to longer illnesses, increased transmission of infections, and heightened healthcare utilization (2).

Strict adherence to antibiotic stewardship principles is crucial. In one study, only 48% of patients adhered fully to prescribed antibiotic regimens, contributing to resistance (American Academy of Pediatrics). Case studies highlight the human toll of resistance: Iñaki Morán's battle with recurrent infections after COPD-related transplant and David Ricci's multiple antibiotic-resistant infections following a train accident Such cases underscore the urgency for global action (5).

In elucidating the gravity of antibiotic resistance, a compendium of case studies underscores the human toll exacted by this phenomenon Iñaki Morán, a recipient of pulmonary transplant necessitated by chronic obstructive pulmonary disease (COPD), grappled with the perils of antimicrobial resistance, enduring recurrent hospitalizations and psychological distress. His plight epitomizes the exigency for concerted global efforts to combat the lethal ramifications of antibiotic resistance.

Similarly, David Ricci, a 19-year-old from the environs of Seattle, confronted a series of NDM-1 positive antibiotic-resistant infections subsequent to a life-altering train accident in Calcutta, India, culminating in the amputation of his right leg (7) Meanwhile, George Semakula, aged 57, confronted a life-threatening infection impervious to conventional antibiotics following a mugging incident in Tanzania. (7) His salvation materialized through treatment with an experimental Japanese drug, spotlighting the urgent imperative for the development of novel antibiotics.

Consultation with healthcare providers is pivotal. However, research indicates that only 35% of patients sought medical advice before self-medicating with antibiotics (4) Healthcare professionals play a pivotal role in guiding appropriate antibiotic usage, thereby mitigating resistance development and safeguarding public health.

References

2

1 Antimicrobial resistance (2021, November 17) World Health Organization (WHO) https://www who int/news-room/factsheets/detail/antimicrobial-resistance

3.

Antibiotics: When you need them and what to expect (n d ) Cleveland Clinic https://my clevelandclinic org/health/treatments/16386-antibiotics

Combating antibiotic resistance. (2019, October 29). U.S. Food and Drug Administration https://www fda gov/consumers/consumerupdates/combating-antibiotic-resistance

A cross-sectional study of antimicrobial use among self-medicating COVID-19 cases in Nyeri County, Kenya. (n.d.). PubMed Central (PMC). https://www ncbi nlm nih gov/pmc/articles/PMC9427085/

4 Measuring outpatient antibiotic prescribing. (2023, November 14). Centers for Disease Control and Prevention https://www cdc gov/antibioticuse/data/outpatientprescribing/index html#: :text=CDC%20estimates%20that%20at%20least ,antibiotic%20was%20needed%20at%20all &text=2-,Total%20inappropria te%20antibiotic%20use%2C%20inclusive%20of%20unnecessary%20use%2 0and%20inappropriate,of%20all%20outpatient%20antibiotic%20use

5. Outpatient antibiotic use and the need for increased antibiotic stewardship efforts (2018, June 1) American Academy of Pediatrics https://publications aap org/pediatrics/articleabstract/141/6/e20174124/37685/Outpatient-Antibiotic-Use-and-the-Needfor?redirectedFrom=fulltext

6 Patient stories (2023, May 31) EUROPEAN ANTIBIOTIC AWARENESS DAY https://antibiotic.ecdc.europa.eu/en/patient-stories

EXPLORING THE ANTI-AGING WONDERS OF RETINOL IN SKINCARE BLISS

By Terence Liu

Retinol, the skincare buzzword that promises miraculous transformations for aging skin, has become a staple in beauty conversations. Its reputation for turning wrinkled lines into a smooth, youthful complexion raises questions about its nature: is this seemingly magical elixir the result of complex chemical mixtures? How does it work?

Retinol, a form of vitamin A, is a fat-soluble compound classified under retinoids. While it can be ingested through foods rich in fatsoluble vitamins, like liver and certain fish. It's crucial to note that the impact of topical application on the skin differs significantly from diet. Excessive consumption of these vitamin-packed foods doesn't equate to the targeted benefits achieved through topical use; in fact, it risks a potentially harmful vitamin overdose.

The terms retinol and retinoids, although used interchangeably, carry nuanced distinctions. Typically, retinoids lean towards prescriptiongrade potency, reserved for higher-stakes skin care interventions. Conversely, retinol, available over-the-counter, denotes a milder strength, making it more accessible for routine use. The ascent of retinoids in skin care traces back to 1971 when it earned approval from the Food and Drug Administration (FDA). Since then, this potent compound has become a stalwart in skincare regimens, treating not only acne and breakouts but emerging as a key remedy against wrinkles (4).

How does retinol supposedly possess transformative effects? Firstly, it amplifies skin cell proliferation, creating the supposed “look” of diminished fine lines and wrinkles by promoting the growth of keratinocytes, the predominant cells in the outermost layer of the skin (epidermis).

Further, retinol inhibits metalloproteinase, an enzyme responsible for breaking down collagen (5). By preserving collagen, the skin gains elasticity and suppleness, contributing to a more youthful look. However, the increased turnover of the epidermis, triggered by retinol, reduces the likelihood of breakouts and acne. Taken together, retinol facilitates a combination of cellular processes, compounding cell proliferation, collagen preservation, and enhanced skin turnover to deliver the remarkable effect of a younger and more vibrant complexion.

While acknowledging it’s mainstream use, some individuals may experience redness, irritation, and peeling, due to the accelerated shedding of skin cells during the initial phases of retinol use (1). As the old makes way for the new, the process can lead to heightened skin sensitivity and flaking. Moreover, using retinol in the morning might amplify the skin's susceptibility to UV rays, potentially causing irritation and itching. These reactions are the body's response to the potency of the retinol; as such, these side effects are not insurmountable obstacles. They can be mitigated through measures such as opting for lower doses and gradually acclimating your skin to larger doses.

Here's the reality check: products are divided into two main classifications, drugs and cosmetics (3). Drugs undergo rigorous research and testing to ensure suitability for the masses. However, when it comes to cosmetics like retinol, the landscape is less populated with high-quality, peer-reviewed papers.

The reason? Money.

Clinical trials demand significant funds, often from taxes, and cosmetics, defined as enhancers of appearance, don't top the priority list for rigorous testing. Consequently, skincare brands often conduct their experiments, creating a potential conflict of interest as they promote their products (2).

Yet, it's crucial not to dismiss the efficacy of retinol entirely. Tretinoin, a well-researched retinoid drug, stands as a clinically proven testament to the family's effectiveness. Interestingly, some biological pathways in our body naturally convert retinol into tretinoin, hinting at the potential benefits of the former. With additional medical research, the beauty of tomorrow is within reach; And retinol, in all its glory, is just a glimpse into the exciting possibilities yet to unfold in the skincare world.

References

2.

1 Lab Muffin Beauty Science. (2023). Does retinol in skincare even work? [Video] YouTube

3

Curology Team (2023, March 22) The potential side effects of retinol, explained Curology

https://curology.com/blog/retinols-potential-side-effectsexperts-weighin/#: :text=Most%20often%20%2C%20retinol%20side%20effe cts,more%20vulnerable%20to%20UV%20rays

https://www.youtube.com/watch?v=e6Z5Vr7uSiA

RETINOL VS RETINOID: WHAT'S THE DIFFERENCE? (n d ) LaRoche Posay. https://www.larocheposay com au/blog/retinol-vsretinoid html#: :text=Both%20of%20these%2%200anti%2Da geing,and%20formulated%20for%20%20everyday%20use%20

https://pubmed ncbi nlm nih gov/33871811/#: :text=Since%20 the%20US%20Food%20and,the%20%20mainstay%20of%20ac ne%20treatment

4.

Retinol: Cream, serum, what it is, benefits, how to use. (n.d.). Cleveland Clinic

https://my.clevelandclinic.org/health/treatments/23293retinol

5.

Zasada, M. (2019). Retinoids: Active molecules influencing skin structure formation in cosmetic and dermatological treatments. PubMed Central (PMC).

https://www ncbi nlm nih gov/pmc/articles/PMC6791161/#:~:t ext=Retinol%20stimulates%20fibro

SHOULD WE RESEARCH OUR MEDICATIONS?

By Naima Rauf

In the realm of the pharmaceutical world, where there is always groundbreaking research emerging, it is normal for us to place our trust in information we receive through word of mouth or the media. But is this enough? Do we possess the prerogative to scrutinise and comprehend the medications we take?

Embracing my role as a dedicated student pursuing a Bachelor of Arts in Health Sciences and double minoring in Human Studies and Rehabilitation Services, I wholeheartedly affirm that we should! Although the Pharmaceutical world is closely integrated into the world of healthcare, some things can go unsaid. Most healthcare providers aim to prescribe their patients the medications they need to embrace their quality of life and provide cures, but this may not be the same in the world of pharmaceuticals.

In 2022, the pharmaceutical revenues worldwide totaled to 1.48 trillion USD (2). Over the last two decades, the pharmaceutical market has experienced a notable surge in profits, unveiling a multitude of innovative formulas and medications each year. Prioritising our well-being is necessary, and we should urge ourselves to research medications and formulas before introducing them to our bodies, to see what is right for us; Because medication errors harm at least 1.5 million people annually in the United States (1).

Chances are, that the new medication you just bought contains the same formula as the past three you had on your counter. But, with the rise of marketing and social media, the promotion of reused formulas is very common. Some medications may pose harm that we overlook, as some information and research are suppressed to encourage consumers to continue taking drugs.

By researching the prescriptions, we are putting in our bodies, we can discover what is suitable for us and sometimes make decisions about what is necessary for us by discussing with their providers. On the negative scope of things, there can also be side effects. There are millions of cases every year where rare or undiscovered side effects of medications like aspirin or discovered and because of the small margin of risk involved, patients are blinded to this information. Even when considering seemingly forward choices of over-the-counter medication like Tylenol or Aleve painkillers, delving into research on these products could reshape our perspective on how often we choose to rely on them. Although medications are approved by the FDA, risks of profit and benefit for the promises of the global world are high.

So the next time you open your medicine cabinet, meet with your provider, or visit your local drugstore to buy medication, do some research before that, or consult with a medical professional about what is best for you.

References

1.

A just culture approach to managing medication errors. (n.d.). PubMed Central (PMC)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5424837/#: :text=In%20the %20United%20States%2C%20medication,result%20of%20a%20medication%2 0error

2

Topic: Global pharmaceutical industry (2022, October 12) Statista

https://www.statista.com/topics/1764/global-pharmaceuticalindustry/#topicOverview