NEWS REPORT RESEARCH MEIDCINE AWARENESS

MEDIUNITE THE JOURNAL’S VITAL MAGAZINE

ISSUE N.6. THE MEDIUNITE JOURNAL VITAL MAGASINE. MARCH 2024

MEDICAL
AWARENESS, HOW
WE’RE CHANGING
GLOBAL WELLBEING
Pg 2. Alzheimer's Brain Changes,
Read the article on Pathophysiology
for Alzheimer's disease
Pg 4. Nerve Cell Vulnerability?
Read the article on RSV’s Impact
Pg 5. What’s the Rationale? Read
the article on PPIs in H. pylori
treatment
Pg 7. Feed Your Gut, Feed Your
Mind, Read the article on gut health
Pg 8. What is the battle against
antibiotics? Read the article on
antiobiotic immunity
Pg 9. Radiant Skin or Dire
Consequences? Read the article on
Retinol’s Dermatological Useage
Pg 11. Should We Be Worried?
Read the article on pharmaceuticals

GET TO KNOW THE LATEST, RELEVANT, AND

VITAL MEDICAL-RELATED INSIGHTS IN THE
GLOBAL WORLD
Have content to submit? contact us at
mediunitejournal@gmail.com
MEDIUNITEJOURNAL.CA
ISSUE N.6
A Kamran Shukoor and Ibrahim Tariq Initiative
 MEDIUNITE JOURNAL
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 Beta-
Amyloid 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.
MEDIUNITE.CA
MONTHLY MAGASINE
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).
ISSUE N.6
 MEDIUNITE JOURNAL MONTHLY MAGASINE

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 References

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.
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. https://molecularneurodegeneration.biomedcentral.com/article
s/10.1186/s13024-024-00702-2
5. Wang, Y. (2016). Tau in physiology and pathology. PubMed.
https://pubmed.ncbi.nlm.nih.gov/26631930/

MEDIUNITE.CA ISSUE N.6

 MEDIUNITE JOURNAL
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
References
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.
MEDIUNITE.CA
MONTHLY MAGASINE
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 over-
the-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.
1. Infectious Disease Special Edition. (n.d.). RSV may cause nerve
inflammation and damage. https://www.idse.net/Viral-
Infections/Article/01-24/RSV-May-Cause-Nerve-Inflammation-
and-
Damage/72592#:~:text=Since%20RSV%20was%20first%20discovere
d,fluid%20of%20children%20with%20seizures
2. Perk, Y. (2018). Respiratory syncytial virus infections in neonates
and infants. PubMed Central (PMC).
3. 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-child-
deaths-under-age-5-study-estimates-1.6149304
4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6089794/#:~:text=
Respiratory%20syncytial%20virus%20is%20the,the%20neonatal%20
period%20(1)
5. 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-release-
detail/us-fda-approves-abrysvotm-pfizers-vaccine-prevention-
0#:~: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-cause-
inflammation-and-damage
ISSUE N.6
 MEDIUNITE JOURNAL MONTHLY MAGASINE

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.

MEDIUNITE.CA ISSUE N.6

 MEDIUNITE JOURNAL MONTHLY MAGASINE

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.
6. 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.
7. 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.

MEDIUNITE.CA ISSUE N.6

 MEDIUNITE JOURNAL MONTHLY MAGASINE

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 well-
being. 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/
2. The gut microbiota in anxiety and depression – A systematic
review. (2021). ScienceDirect.
https://www.sciencedirect.com/science/article/abs/pii/S0272735820
301318?casa_token=Fo-
PLItjhxEAAAAA:XEFGyyGC0HVUvcjosZmnHobtIS-
RGWiGL6sRcDvjMLtV9TY1DAzVvvNa8cdTooW7ImmqSFsh#bb0080
3. The gut-brain axis: Interactions between enteric microbiota,
central and enteric nervous systems. (2015, April). PubMed Central
(PMC).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4367209/#:~:text=
The%20gut%2Dbrain%20axis%20
4. 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/PMC4991899/#:~:text=
Thoroughly%20revised%20est

MEDIUNITE.CA ISSUE N.6

 MEDIUNITE JOURNAL
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.
MEDIUNITE.CA
MONTHLY MAGASINE
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
1. Antibiotics: When you need them and what to expect. (n.d.). Cleveland
Clinic. https://my.clevelandclinic.org/health/treatments/16386-antibiotics
2. Antimicrobial resistance. (2021, November 17). World Health Organization
(WHO). https://www.who.int/news-room/fact-
sheets/detail/antimicrobial-resistance
3. Combating antibiotic resistance. (2019, October 29). U.S. Food and Drug
Administration. https://www.fda.gov/consumers/consumer-
updates/combating-antibiotic-resistance
4. 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/
5. Measuring outpatient antibiotic prescribing. (2023, November 14). Centers
for Disease Control and Prevention. https://www.cdc.gov/antibiotic-
use/data/outpatient-
prescribing/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
6. Outpatient antibiotic use and the need for increased antibiotic
stewardship efforts. (2018, June 1). American Academy of Pediatrics.
https://publications.aap.org/pediatrics/article-
abstract/141/6/e20174124/37685/Outpatient-Antibiotic-Use-and-the-Need-
for?redirectedFrom=fulltext
7. Patient stories. (2023, May 31). EUROPEAN ANTIBIOTIC AWARENESS DAY.
https://antibiotic.ecdc.europa.eu/en/patient-stories
ISSUE N.6
 MEDIUNITE JOURNAL MONTHLY MAGASINE

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 fat-
soluble 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.
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.

The terms retinol and retinoids, although used

interchangeably, carry nuanced distinctions.
Typically, retinoids lean towards prescription-
grade 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).

MEDIUNITE.CA ISSUE N.6

 MEDIUNITE JOURNAL MONTHLY MAGASINE

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.

References
1. Curology Team. (2023, March 22). The potential side effects of
Clinical trials demand significant funds, often from retinol, explained. Curology.
taxes, and cosmetics, defined as enhancers of https://curology.com/blog/retinols-potential-side-effects-
experts-weigh-
appearance, don't top the priority list for rigorous in/#:~:text=Most%20often%20%2C%20retinol%20side%20effe
testing. Consequently, skincare brands often conduct cts,more%20vulnerable%20to%20UV%20rays
2. Lab Muffin Beauty Science. (2023). Does retinol in skincare
their experiments, creating a potential conflict of even work? [Video]. YouTube.
interest as they promote their products (2). https://www.youtube.com/watch?v=e6Z5Vr7uSiA
3. RETINOL VS RETINOID: WHAT'S THE DIFFERENCE? (n.d.).
LaRoche Posay. https://www.laroche-
Yet, it's crucial not to dismiss the efficacy of retinol posay.com.au/blog/retinol-vs-
retinoid.html#:~:text=Both%20of%20these%2%200anti%2Da
entirely. Tretinoin, a well-researched geing,and%20formulated%20for%20%20everyday%20use%20
retinoid drug, stands as a clinically proven testament to https://pubmed.ncbi.nlm.nih.gov/33871811/#:~:text=Since%20
the%20US%20Food%20and,the%20%20mainstay%20of%20ac
the family's effectiveness. Interestingly, some biological ne%20treatment
4. Retinol: Cream, serum, what it is, benefits, how to use. (n.d.).
pathways in our body naturally convert retinol into Cleveland Clinic.
tretinoin, hinting at the potential benefits of the https://my.clevelandclinic.org/health/treatments/23293-
retinol
former. With additional medical research, the beauty of 5. Zasada, M. (2019). Retinoids: Active molecules influencing
tomorrow is within reach; And retinol, in all its glory, is skin structure formation in cosmetic and dermatological
treatments. PubMed Central (PMC).
just a glimpse into the exciting possibilities yet to https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6791161/#:~:t
unfold in the skincare world. ext=Retinol%20stimulates%20fibro

MEDIUNITE.CA ISSUE N.6

 MEDIUNITE JOURNAL
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).
MEDIUNITE.CA
MONTHLY MAGASINE
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-pharmaceutical-
industry/#topicOverview
ISSUE N.6