Health & Wellness – Dev Aditya Tomar

Defecation-Induced Memory Loss: Understanding Transient Global Amnesia

Dev Aditya Tomar — Sun, 19 Apr 2026 09:43:26 +0000

A recent viral case from Hong Kong described a woman who reportedly “lost 10 years of memory” after excessive straining due to constipation. Even though it sounds absurd, and borderline impossible, the condition is a benign but rare neurological problem known as Transient Global Amnesia (TGA). This article explains the case, underlying mechanisms, and key clinical insights.

Table of Contents

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WHAT HAPPENED IN THE HONG KONG CASE?

WHAT IS TRANSIENT GLOBAL AMNESIA?

Diagnostic Criteria

Risk Factors

THE HIDDEN MECHANISMS

Impairment of Brain Venous Drainage

Disturbance of Venous Flow Patterns

THE CAUSE OF MEMORY LOSS

DIFFERENTIAL DIAGNOSIS

PROGNOSIS

REFERENCES

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WHAT HAPPENED IN THE HONG KONG CASE?

A middle-aged female from Hong Kong presented with the chief complaints of :

Sudden memory loss (reported as ~10 years)
Confusion with preserved consciousness
Repetitive questioning

She was suffering from constipation for the past 2 weeks, and the symptoms started while she was straining during defecation for a long time.

The episode lasted several hours and resolved spontaneously, with the patient having no memory of the event itself. This presentation is classical for TGA.

WHAT IS TRANSIENT GLOBAL AMNESIA?

Transient Global Amnesia (TGA) is a benign and temporary loss of anterograde memory with the preservation of remote memories and immediate recall. It is characterised by:

Inability to form new memories (anterograde amnesia)
Partial loss of past memories (retrograde amnesia)
Repetitive questioning
Preservation of identity and alertness

Diagnostic Criteria

Hodge and Warlow (1990) described the criteria to be used for diagnosing a patient as TGA.

The attack was witnessed and reported.
There was obvious anterograde amnesia during the attack.
There was an absence of clouding of consciousness.
There were no focal neurological signs or deficits during or after the attack.
There were no features of epilepsy.
The attack resolved within 24 h.
The patient did not have any recent head injury or active epilepsy

Risk Factors

Physical exertion, swimming, sexual intercourse and use of marijuana and Viagra are some of the factors but the greatest risk factor for TGA is a history of migraines.

THE HIDDEN MECHANISMS

Although the exact pathogenesis is not confirmed yet, there are a few existing theories.

Impairment of Brain Venous Drainage

A 2019 research article published in Frontiers in Neurology investigated if TGA could be caused by cerebral venous outflow abnormalities using imaging techniques like Doppler ultrasound and MRI. They compared internal jugular and vertebral venous flow during rest and Valsalva manoeuvre against healthy controls.

Results indicated that many TGA patients displayed abnormal venous hemodynamics, such as insufficient internal jugular vein drainage or reflux, especially during increased intrathoracic pressure. They support a link between venous congestion and transient hippocampal ischemia or metabolic disturbance as a plausible TGA mechanism.

Disturbance of Venous Flow Patterns

Hans H. Bartsch et al also try to find a link between TGA and abnormal internal jugular venous drainage. They too proposed the mechanism to be venous congestion during Valsalva-like manoeuvres. Using duplex ultrasonography, they found that a substantial proportion of TGA patients displayed retrograde flow or incompetent valves in the internal jugular veins, abnormalities rarely observed in controls. These flow disturbances were thought to cause transient venous hypertension within the brain’s memory-critical regions [hippocampus]

In a 2006 research paper published in the Nederlands Tijdschrift voor Geneeskunde, The authors observed that many TGA episodes occurred following conditions elevating central venous pressure, such as Valsalva-like maneuvers, emotional stress, or immersion in cold water.

THE CAUSE OF MEMORY LOSS

The hippocampus, especially the CA1 region, is highly sensitive to:

Reduced blood flow
Venous congestion

During a Valsalva maneuver:

Transient dysfunction of hippocampal neurons occurs
This leads to temporary inability to form and retrieve memories

Importantly, this is functional impairment, not permanent brain damage.

DIFFERENTIAL DIAGNOSIS

Before diagnosing TGA, it is essential to rule out:

Transient Ischemic Attack (TIA)
Seizure (post-ictal confusion)
Syncope-related hypoperfusion
Psychogenic amnesia

The absence of focal deficits and complete recovery helps confirm TGA.

PROGNOSIS

The prognosis is great, with full recovery expected

REFERENCES

Spiegel, David R et al. “Transient global amnesia: current perspectives.” Neuropsychiatric disease and treatment vol. 13 2691-2703. 24 Oct. 2017, doi:10.2147/NDT.S130710

Sander D, Winbeck K, Etgen T, Knapp R, Klingelhöfer J, Conrad B. Disturbance of venous flow patterns in patients with transient global amnesia. Lancet. 2000 Dec 9;356(9246):1982-4. doi: 10.1016/S0140-6736(00)03313-4. PMID: 11130530.

Han, Ke et al. “Transient Global Amnesia Linked to Impairment of Brain Venous Drainage: An Ultrasound Investigation.” Frontiers in neurology vol. 10 67. 5 Feb. 2019, doi:10.3389/fneur.2019.00067

Harrison, Magnus, and Mark Williams. “The diagnosis and management of transient global amnesia in the emergency department.” Emergency medicine journal : EMJ vol. 24,6 (2007): 444-5. doi:10.1136/emj.2007.046565

Telemedicine: The Guide to Digital Healthcare in 2026

Dev Aditya Tomar — Sun, 01 Mar 2026 13:08:27 +0000

Telemedicine is no longer a futuristic concept, but rather a reality of how people receive healthcare nowadays. In simple terms, telemedicine is the practice of delivering medical services remotely, using technology such as video calls, apps, messaging, and remote‑monitoring devices. That is, one can get expert opinion with only a click now!

The COVID-19 pandemic has significantly accelerated its evolution from a niche “backup option” into a mainstream model of care. It is now being used for routine check-ups, chronic‑disease management, mental‑health counselling, emergency triage, and even remote‑surgical support.

In India, eSanjeevani portal and private‑sector apps are already being promoted and put into use.

Table of Contents

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WHAT IS TELEMEDICINE?

PATIENT'S BENEFITS

DOCTORS AND TELEMEDICINE

REGULATIONS, PRIVACY AND ETHICS

TELEMEDICINE IMPLEMENTATION GUIDE BY WHO

CASE STUDY: eSANJEEVANI

Lessons & Future Plans

CHALLENGES AND LIMITATIONS

THE FUTURE OF TELEMEDICINE

REFERENCES

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WHAT IS TELEMEDICINE?

Many people use “telemedicine” and “telehealth” interchangeably, but :

Telemedicine refers to clinical services delivered at a distance [like consultations, prescriptions, and follow-ups]
Telehealth is a broader umbrella comprising of telemedicine, remote monitoring, health‑education courses, and public‑health campaigns delivered through digital channels.

Within telemedicine, there are three main modes:

Live‑interactive video visits
Store‑and‑forward: Patients or local clinics send photos, scans, and lab reports to a specialist who reviews them later and issues a report or recommendation
Remote patient monitoring (RPM): Patients use devices (blood‑pressure cuffs, glucose meters, smartwatches, ECG patches) that transmit data to clinicians, who then track trends and intervene when needed.

In India, telemedicine has been formally guided by the Telemedicine Practice Guidelines (2020), updated in 2026. It requires the doctors to be registered, patient identity to be verified, proper documentation, informed consent, and treatment with the same professional standards as in-person visits.

PATIENT'S BENEFITS

For patients, telemedicine is primarily about access, convenience, and continuity.

Telemedicine removes geography as a barrier to expertise.
No long queues, no crowded waiting rooms. Also, greater compliance would be observed in cases of multiple regular follow-ups.
For Chronic‑disease management, like diabetes, hypertension, heart failure, chronic kidney disease, and autoimmune conditions. It can schedule regular check-ins, track lab results, and watch trends from home devices, helping the patient prevent avoidable hospitalizations.
Tele‑counselling and tele‑psychiatry let people seek help from the privacy of their homes, reducing stigma and shame
Post‑treatment and rehabilitation. After surgery, or hospital discharge, patients can receive physiotherapy guidance and nutrition coaching easily.

DOCTORS AND TELEMEDICINE

With a skewed doctor-to-population ratio here in India, telemedicine can provide a structure, thus decreasing OPD crowd, waiting time, and delivery of urgent care.

The following are some possible scenarios:

Pre‑visit triage: A patient can fill out an online, listing his symptoms, medications, and allergies. This information is then forwarded to the physician before the call starts.
During the visit: The platform can access the patient’s medical history, lab results.
Post‑visit automation: After the call, the system can auto‑generate notes, send prescription orders as suggested, schedule follow-up reminders, and flag patients with notifiable diseases.

REGULATIONS, PRIVACY AND ETHICS

Because telemedicine deals with highly sensitive health data, it sits at the intersection of law, ethics, and technology.

In India, the 2026‑updated Telemedicine Practice Guidelines stress that the same professional standards apply whether care is given in‑person or remotely.
Patients must be clearly informed about how their data are stored, who can access it, and how long records are kept. Teleconsultation records must be as complete and secure as physical‑chart notes.
End-to-end encryption is a must, for maintaining patient’s privacy. Another possibility could be integrating the private telemedicine data into national digital‑health platforms such as India’s Ayushman Bharat Digital Mission (ABDM).

Telemedicine Practice Guidelines, India

Strict scrutiny over AI-generated results should be kept. Confirming the result with a physician could be one step towards it.

TELEMEDICINE IMPLEMENTATION GUIDE BY WHO

CASE STUDY: eSANJEEVANI

Launched in 2018 by the Ministry of Health & Family Welfare, Government of India, eSanjeevani is a cloud-based national telemedicine platform developed by C-DAC, Mohali. It was integrated with Ayushman Bharat Health & Wellness Centres (HWCs).

Objectives

Its main objectives were to:

Address shortage of doctors and specialists at primary level
Reduce burden on district and tertiary hospitals
Create electronic health records and ensure continuity of care

During COVID-19 lockdown (when OPDs were closed), it was expanded into eSanjeevaniOPD, a free patient-to-doctor teleconsultation service for all citizens.

Parts of eSanjeevani

Patient to Doctor Telemedicine

Assisted Telemedicine

It has two components :

eSanjeevaniHWC (Hub-and-Spoke Model)
- Health worker to doctor teleconsultation
- Used at rural HWCs
- EMR created → patient connected to doctor → ePrescription issued → medicines dispensed locally
eSanjeevaniOPD
- Direct patient-to-doctor consultation via web/mobile app
- Patient registers → receives token → waits in virtual queue → doctor consults → prescription issued

Issues Faced

Scaling issues
No SOPs initially [Standard Operating Procedures]
Digital illiteracy among health workers
Low public trust in telemedicine
Demand spikes

Their Solutions

Shifted to hyperscale cloud system
Developed and revised SOPs with MoHFW
Extensive training & trial sessions
Awareness campaigns & user guides
Continuous monitoring & forecasting

Lessons & Future Plans

Higher internet penetration increased usage, but demand was strong even in low-connectivity and remote areas.
Strong local technical support ensured 99.5% uptime.
Integrated with Ayushman Bharat Digital Mission for health records linkage.
Expanding to eSanjeevani 2.0 with AI features, multilingual interface, and capacity for 1 million consultations/day.

CHALLENGES AND LIMITATIONS

Despite having positive effects on the current healthcare infrastructure, it comes along with some challenges.

Digital divide: People may lack stable internet, smartphones, or the digital literacy to use apps.
Physical‑exam limitations: Conditions like acute abdominal pain, complex injuries, and certain surgical cases would still require in-person exams, palpation, or imaging that cannot be fully replicated remotely.
Privacy and commercialization risks: Breaches, misuse of data, or aggressive marketing practices can erode patient trust too.

THE FUTURE OF TELEMEDICINE

Instead of “in‑person vs. telemedicine,” the future is hybrid care—mixing face‑to‑face visits, video consults, phone calls, and remote monitoring based on each patient’s needs and condition.
As smartwatches, continuous glucose monitors, ECG patches, and implantable devices become more accurate and affordable, telemedicine dashboards will receive richer, real-time data streams, thus enabling earlier intervention.
Telemedicine will be a key tool for delivering specialist care in low‑resource and remote regions, including tribal belts and underserved districts of India, where building enough hospitals and training enough specialists in‑person is physically and financially challenging.

REFERENCES

Consolidated telemedicine implementation guide. 9 November 2022 Publication. ISBN: 978 92 4 005918 4

eSanjeevani, National Telemedicine Service. Link.

Is HbA1c not useful in Indian Population?

Dev Aditya Tomar — Sun, 22 Feb 2026 07:33:50 +0000

HbA1c or Glycated Haemoglobin is a term known to almost all Indians, thanks to the high prevalence of diabetes not only in their direct family but also in their community. Be it a healthcare worker or a member of the general public, I can surely say that you must know a diabetes patient personally, may it be your friend, family or a loved one.

HbA1c is widely used as a diagnostic and monitoring method for diabetes in general. Even with the availability of other tests like OGTT, FBS, PPBS, it still remains the preferred mode of classifying people into diabetics and non-diabetics. This is perhaps due to the following advantages:

No fasting required
Depicts the trend of the previous 2-3 months
Adopted in guidelines [WHO, ADA]

However, depending on HbA1c as the sole criteria for diagnosis and monitoring of diabetes can lead to the misinterpretation, specially in Indian populations. This effect is seen due to the enormous burden of haematological abnormalities [IDA], genetic factors [G6PD deficiency], social and metabolic influences.

The Article “The limitations and fallacies of relying on glycosylated haemoglobin for diagnosing and monitoring diabetes in Indian population” highlights the discordance between HbA1c and blood glucose levels, with a special focus on people with altered erythrocytic dynamics.

My article tries to describe all of it in a much simpler way, so that you can digest the information easily and also get to know about medical topics, without obsessing over the minute details.

Special thanks to Shambik Sir [my Physics teacher] for telling me about this article published in The Lancet Regional Health – Southeast Asia, 2026.

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STRUCTURE OF THE STUDY

Search Terms

HbA1c
glycated haemoglobin
diabetes
diagnosis
oral glucose tolerance test (OGTT)
iron deficiency anaemia
hemoglobinopathies
G6PD deficiency
Polycythaemia
erythrocyte lifespan
South Asians
India

Filters

To select

observational studies
randomized controlled trials
meta-analyses
national survey reports
clinical guidelines

Grouping

HbA1c as a :

Diagnostic tool [Compared to OGTT, FBS]
Monitoring marker [Compared to SMBG, CGM, Fructosamine, Glycated albumin]

Selection Criteria

If they provided data on

Discordance between HbA1c and glucose-based indices
Diagnostic or monitoring performance in the presence of hematologic disorders
Alternative biomarkers such as fructosamine, glycated albumin, or 1,5-anhydroglucitol.

Special Emphasis

On studies focused on the effect of haematological conditions on HbA1c.

HbA1c AND BLOOD GLUCOSE

Blood Test for HbA1c

HbA1c is hailed as the gold standard test for assessment of glycaemic control. It is used for the diagnosis of prediabetes and diabetes. This choice can be attributed to:

Convenience [no fasting]
Stability before analysis
Relatively low variation among individuals

The American Diabetes Association guidelines give the following cut-offs for classification of diabetes :

< 5.7% : Normal
5.7 to < 6.5% : Prediabetes
> 6.5% : Diabetes

On the other hand, here’s what WHO says about it :

HbA1c can be used as a diagnostic test for diabetes if stringent quality assurance tests are in place and assays are standardized to criteria aligned to the international reference values, and there are no conditions present which preclude its accurate measurement.
An HbA1c of 6.5% is recommended as the cut point for diagnosing diabetes.
A value of less than 6.5% does not exclude diabetes diagnosed using glucose tests.
Quality of evidence assessed by GRADE: moderate
Strength of recommendation based on GRADE criteria: conditional

In short, it has pointed out the specific requirements, only under which the credibility of the test is assured.

American Diabetes Association Guidelines

In the Indian scenario, these are quite often overlooked, thus simplifying and increasing the “efficiency” of the diagnostic and monitoring process. It leads to either misdiagnosing or overdiagnosis of diabetes, hindering the treatment plan, prolonging the latent period, and increasing the risk of complications like diabetic neuropathy, retinopathy, etc.

When the HbA1c and mean glucose concentrations were compared using various methods like Continuous Glucose Monitoring Systems [CGMS], Fasting Plasma Glucose, Self-Monitoring of Blood Glucose, a discordance was observed between them. The causes of the variations are individually discussed in the upcoming topic.

So, to remove such variations, the researchers proposed 2 related indices.

Glycation Gap [GGap] : Predicted HbA1c from plasma fructosamine – Measured HbA1c
Haemoglobin Glycation Index [HGI] : Measured HbA1c – Predicted HbA1c from fasting plasma glucose level

CAUSES OF DIVERGENCE IN INDIA

Four major causes are underlined in the paper. They are :

Haematological Abnormalities
Standardisation of Assays
National Glyco-haemoglobin Standardisation Programme
Seasonal variation

Haematological Abnormalities

Here, a table was provided with different causes and their underlying mechanisms. In short, it talks about three cases in general:

FALSE LOW HbA1c

Due to the following causes, RBC lifespan decreases, thus decreasing the time it gets for glycation of Haemoglobin.

Haemolytic anaemia
G6PD deficiency (subclinical haemolysis)
Acute blood loss (increased young RBCs)
Pregnancy (increased RBC turnover, haemodilution)
Chronic liver disease (hypersplenism, bleeding)
Chronic renal failure (Decreased RBC survival)
Recent blood transfusion (dilution effect)
High-dose vitamin C (assay interference / Decreased glycation)

FALSE HIGH HbA1c

It is opposite to false low HbA1c. Here, the lifespan increases, thus increasing glycation time.

Iron deficiency anaemia (IDA) (Increased glycation, prolonged RBC life)
Polycythaemia (prolonged RBC lifespan)

UNRELIABLE OR VARIABLE HbA1c

It is due to a mix of the mechanisms or because it interferes with the assay.

Hemoglobinopathies (variant & method dependent)
Chronic renal failure (carbamylated Hb interference)
Alcohol abuse
Liver disease
High BMI (obesity)
Race/ethnicity differences (e.g., South Asians, African origin)
Elderly (RBC morphology changes)
Recent transfusion
Hypertriglyceridemia, hyperbilirubinemia
Lead poisoning
Drugs: opioids, salicylates, ribavirin, vitamin E
Asplenia
Assay variation
Seasonal variation (noted in Indian population)

In India, we see high rates of IDA (affecting an estimated 25%–68% depending on age, sex, and study region), hemoglobinopathies ((0.37%-5.9%), with regional and ethnic variation), and G6PD deficiency (7.7–8.5% with high prevalence in tribal group).

G6PD deficiency alone resulted in a median delay of 4.1 years in diabetes diagnosis and a 37% increase in microvascular complications.

Standardisation of Assays

Many laboratories use methods other than High-performance liquid chromatography (HPLC) for the assessment of HbA1c. Even ion-exchange HPLC, which is widely employed in Indian labs, may yield uninterpretable results in individuals with silent haemoglobin variants.

National Glyco-haemoglobin Standardisation Programme

A survey of 310 Indian laboratories found that 75% used HbA1c for diabetes mellitus diagnosis, but only 70% of these assays were National Glyco-haemoglobin Standardization Programme (NGSP)- certified. It shows the possibility of gaps in quality assurance between different labs throughout India.

Thus, the labs need to adopt standardised NGSP-certified HbA1c methods for better diagnosis.

Seasonal Variations

HbA1c levels are highest during the monsoon (June–September) and lowest during autumn (October–November). In patients with well-controlled diabetes, HbA1c tends to rise during winter and the monsoon. However, in patients with HbA1c ≥ 6.5%, levels tend to decrease during the monsoon and autumn.

OTHER APPROACHES

To assess glycemia, we can adopt alternative and complementary approaches as listed below.

Self-Monitoring of Blood Glucose [SMBG]
Fructosamine
Continuous Glucose Monitoring
Flash Glucose Monitoring
Glycated Albumin
1,5-Anhydroglucitol
Haemoglobin Glycation Index

Self Monitoring of Blood Glucose

CLINICAL & POLICY IMPLICATIONS

For Diagnosis

Standardised OGTT as Gold Standard

For Monitoring

HbA1c (measured using a standardized and NGSP-certified assay) should be interpreted
With serial fasting and postprandial blood glucose values.
CGMS if affordable and available.

REFERENCE

The limitations and fallacies of relying on glycosylated hemoglobin for diagnosing and monitoring diabetes in Indian populations. Samajdar, Shambo Samrat et al. The Lancet Regional Health - Southeast Asia, Volume 45, 100724

Use of Glycated Haemoglobin (HbA1c) in the Diagnosis of Diabetes Mellitus. Abbreviated Report of a WHO Consultation. WHO/NMH/CHP/CPM/11.1

Nipah Virus : Is it an Emergency?

Dev Aditya Tomar — Sun, 01 Feb 2026 07:27:22 +0000

Nipah virus (NiV) is a highly virulent zoonotic pathogen that represents a major public health concern because of its high fatality rate and ability to spread between humans. The virus was first recognized during an outbreak in Malaysia in 1998–1999 and is classified under the Henipavirus genus of the Paramyxoviridae family. Fruit bats of the Pteropus genus serve as the natural reservoir, and human infection can occur through direct contact with bats, via intermediate animal hosts such as pigs, or through close contact with infected persons.

Clinically, Nipah virus infection demonstrates a broad spectrum of manifestations, ranging from asymptomatic cases to severe respiratory disease and lethal encephalitis. Reported case fatality rates vary from 40% to 75%, depending on the outbreak and the level of healthcare support available. Repeated outbreaks in South and Southeast Asia, particularly in India and Bangladesh, underscore the virus’s significant epidemic potential.

We'll discus the topic under the epidemiological triad [Agent, Host, Environment], Transmission, its Symptoms, Treatment and Prevention.

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AGENT FACTOR

Structure

Genome Organization

Mechanism of Viral Entry

Role of Epherin Receptor

HOST FACTORS

Natural Reservoir

Intermediate Animal Hosts

Human Host

Human to Human Transmission

ENVIRONMENTAL FACTORS

Habitat Loss and Deforestation

Urbanisation and Agricultural Expansion

Climate and Seasons

Food Contamination Practices

Livestock and Animal Housing

PATHOGENESIS

Viral Entry into Host

Primary Replication

Viremia and Dissemination

Endothelial Infection and Vasculitis

Neuroinvasion

Respiratory System Involvement

Immunopathology

Unique Feature

MODES OF TRANSMISSION

Neurological Involvement

Differential Diagnosis

MANAGEMENT

Symptomatic Treatment

Drugs under Study

PREVENTATIVE MEASURES

Prevention of Bat-to-Human Transmission

Prevention of Animal-to-Human Transmission

Prevention of Human-to-Human Transmission

Infection Control in Healthcare Settings

Public Health Measures

Vaccination

SITUATION IN INDIA

REFERENCES

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AGENT FACTOR

Nipah virus (NiV) belongs to the Paramyxoviridae family and is classified under the Henipavirus genus. Owing to its high virulence, significant mortality rate, and the lack of an effective antiviral therapy or licensed vaccine, NiV is designated as a Biosafety Level-4 (BSL-4) pathogen.

Structure

Although NiV shares similarities with other paramyxoviruses, it exhibits certain distinct structural features.

Presence of reticular cytoplasmic inclusions located near the endoplasmic reticulum
Comparatively larger virion size.

Such ultrastructural differences help distinguish NiV from classical paramyxoviruses, despite overall structural resemblance.

Nipah Virus under Microscope

Genome Organization

Nipah virus is a negative-sense, single-stranded, non-segmented, enveloped RNA virus exhibiting helical symmetry. The viral genome is approximately 18.2 kilobases in length and consists of six genes arranged in a 3′–5′ orientation.

These genes encode essential viral proteins : Nucleocapsid protein, Phosphoprotein, Matrix protein, Fusion glycoprotein, Attachment glycoprotein, and the Large polymerase protein.

The nucleocapsid protein, phosphoprotein, and large polymerase protein together form the viral ribonucleoprotein complex, which is essential for viral replication and transcription.
The matrix protein plays a crucial role in viral assembly and budding, linking the ribonucleoprotein core to the viral envelope.

Mechanism of Viral Entry

Viral entry into host cells is mediated by two surface glycoproteins: the attachment glycoprotein and the fusion glycoprotein.
The attachment glycoprotein binds to specific host cell receptors, initiating viral entry.
This interaction triggers activation of the fusion glycoprotein, which undergoes cleavage into two subunits, F1 and F2.
The F1 subunit is primarily responsible for mediating the fusion of the viral envelope with the host cell membrane, allowing entry of the viral genome into the cell.

Role of Epherin Receptor

Research has shown that binding of the host cell receptor ephrin-B2 to the Nipah virus attachment glycoprotein induces allosteric conformational changes. These changes activate the fusion glycoprotein and facilitate receptor-dependent viral entry into host cells, particularly in endothelial and neuronal tissues.

HOST FACTORS

Host factors play a crucial role in determining susceptibility, disease severity, and transmission dynamics of Nipah virus (NiV) infection.

Fruit Bats

Natural Reservoir

Fruit bats of the Pteropus genus serve as the natural reservoir of Nipah virus. Infected bats remain largely asymptomatic while shedding the virus in saliva, urine, feces, and partially eaten fruits. Their ability to fly long distances and their close proximity to human habitats facilitate viral spillover events.

Intermediate Animal Hosts

Certain domestic animals can act as intermediate hosts, amplifying viral transmission. Pigs played a major role during the initial outbreak in Malaysia, where close contact between infected pigs and humans led to widespread transmission. Other animals, such as horses and goats, have also been found to be susceptible, although their role in large-scale outbreaks remains limited.

Human Host

Humans are accidental hosts of Nipah virus infection. Factors such as close contact with infected animals, consumption of contaminated food products, and exposure to infected individuals increase the risk of infection. Healthcare workers and family caregivers are particularly vulnerable due to prolonged and close exposure to infected patients.

Nipah virus exhibits a strong affinity for ephrin-B2 and ephrin-B3 receptors present on host cells. These receptors are highly expressed on endothelial cells, neurons, and respiratory epithelium, explaining the virus’s predilection for the nervous system and lungs. Binding of the viral attachment glycoprotein to these receptors facilitates viral entry and cell-to-cell spread.

The innate immune response is the first line of defense against Nipah virus infection. However, NiV has developed mechanisms to evade host immunity, particularly by inhibiting interferon signaling pathways. Impaired early immune responses contribute to high viral replication and severe disease.

Disease severity is influenced by host-related factors such as age, nutritional status, comorbidities, and immune competence. Delayed healthcare access and inadequate supportive care further exacerbate disease outcomes. Host genetic factors may also play a role, although these are not yet fully understood.

Human to Human Transmission

Host behaviours significantly affect transmission. Practices such as inadequate infection control, lack of personal protective equipment, and close physical contact with infected individuals increase the risk of secondary transmission. Cultural practices involving caregiving and burial rituals may also contribute to virus spread during outbreaks.

ENVIRONMENTAL FACTORS

Environmental factors play a critical role in the emergence, transmission, and recurrence of Nipah virus outbreaks. These factors influence bat ecology, human–animal interactions, and opportunities for viral spillover.

Habitat Loss and Deforestation

Deforestation and large-scale land-use changes disrupt the natural habitats of fruit bats (Pteropus species), forcing them to migrate closer to human settlements. Loss of forest cover reduces natural food sources for bats, increasing their reliance on cultivated fruits and agricultural areas, thereby enhancing the risk of viral transmission to humans and domestic animals.

Urbanisation and Agricultural Expansion

Rapid urbanization and expansion of agricultural activities bring humans, livestock, and wildlife into closer contact.

Deforestation and Habitat Loss

Orchards and farms established near bat roosting sites facilitate contamination of fruits, animal feed, and water sources with bat saliva, urine, or feces, creating conditions favorable for Nipah virus spillover.

Climate and Seasons

Seasonal variations significantly influence Nipah virus transmission. In South Asia, outbreaks commonly occur during winter months, coinciding with increased consumption of raw date palm sap. Climatic factors such as temperature changes, rainfall patterns, and drought affect bat feeding behavior, viral shedding, and human exposure risks.

Date Pal Sap Collection

Food Contamination Practices

Traditional food-harvesting and storage practices contribute to environmental exposure. Collection of raw date palm sap in open containers allows contamination by bats, serving as a major route of Nipah virus transmission in Bangladesh and parts of India.

Similarly, consumption of partially eaten fruits discarded by bats increases infection risk.

Livestock and Animal Housing

Poor livestock housing conditions, particularly pig farming near fruit trees or bat habitats, increase the risk of animal infection and viral amplification. Environmental contamination of animal feed and water sources can facilitate rapid spread among livestock, which may then transmit the virus to humans.

PATHOGENESIS

Viral Entry into Host

Infection begins when Nipah virus enters the human body through the respiratory tract, oral mucosa, or gastrointestinal tract. The viral attachment glycoprotein binds to host cell receptors, primarily ephrin-B2 and ephrin-B3, which are abundantly expressed on endothelial cells, neurons, and respiratory epithelial cells.

This receptor binding triggers activation of the viral fusion glycoprotein, allowing fusion of the viral envelope with the host cell membrane and entry of the viral genome into the cell.

Primary Replication

Following entry, the virus undergoes primary replication at the site of entry, particularly in respiratory epithelial cells. The viral ribonucleoprotein complex initiates transcription and replication of viral RNA in the host cell cytoplasm, leading to production of new virions.

Viremia and Dissemination

Pathogenesis of Nipah Virus Infection

After initial replication, Nipah virus spreads through the bloodstream, resulting in viremia. The virus disseminates to multiple organs, including the lungs, central nervous system, spleen, kidneys, and heart. Endothelial cells serve as major targets, facilitating widespread vascular involvement.

Endothelial Infection and Vasculitis

A hallmark of Nipah virus pathogenesis is infection of vascular endothelial cells, leading to endothelial dysfunction and systemic vasculitis. Viral replication in endothelial cells causes inflammation, thrombosis, increased vascular permeability, and microinfarctions. These vascular changes contribute significantly to tissue ischemia and organ damage.

Neuroinvasion

Nipah virus demonstrates marked neurotropism. The virus gains access to the central nervous system either through hematogenous spread across the blood–brain barrier or via infected endothelial cells. Once in the brain, viral replication leads to neuronal damage, inflammation, and necrosis, resulting in acute encephalitis, seizures, altered consciousness, and coma.

Respiratory System Involvement

Infection of respiratory epithelium and pulmonary endothelium leads to acute respiratory distress characterized by cough, dyspnea, and hypoxia. Extensive alveolar damage and pulmonary edema may occur, contributing to high mortality and increased risk of human-to-human transmission via respiratory secretions.

Immunopathology

Nipah virus has evolved mechanisms to suppress the host innate immune response, particularly by inhibiting interferon signaling pathways. This immune evasion allows uncontrolled viral replication and delays effective antiviral responses, contributing to disease severity.

Excessive immune activation in later stages may lead to cytokine release and inflammatory tissue damage. The combined effects of direct viral cytotoxicity and immune-mediated injury exacerbate organ dysfunction.

Unique Feature

A unique feature of Nipah virus infection is the occurrence of relapsing or late-onset encephalitis weeks to months after apparent recovery. This is believed to result from persistent viral infection or reactivation within the central nervous system.

MODES OF TRANSMISSION

Bat-To-Human, Animal-To-Human, Human-To-Human Transmission

Bat-To-Human

Fruit bats (Pteropus species), the natural reservoir of Nipah virus, transmit the virus to humans through contamination of food or water with their saliva, urine, or feces. Consumption of raw or partially processed date palm sap contaminated by bats is a well-documented route of transmission. Eating fruits partially eaten or contaminated by bats also increases the risk of infection.

Animal-To-Human

Domestic animals, particularly pigs, can act as intermediate hosts and amplify the virus. Humans may become infected through close contact with infected animals, their respiratory secretions, blood, or tissues. This mode of transmission was prominent during the initial outbreaks in Malaysia among pig farmers and slaughterhouse workers.

Human-To-Human

Person-to-person transmission has been documented in several outbreaks, especially in healthcare and household settings. Transmission occurs through close contact with infected individuals, exposure to respiratory droplets, body fluids, or contaminated surfaces.

Transmission

Caregivers and healthcare workers are at increased risk in the absence of adequate infection control measures.

Nosocomial

Hospital-based transmission occurs when appropriate infection prevention and control practices are not followed. Aerosol-generating procedures, improper use of personal protective equipment, and inadequate isolation facilities contribute to nosocomial spread.

CLINICAL FEATURES

The incubation period typically ranges from 5 to 14 days, but in some cases may extend up to 45 days.

Some individuals may remain asymptomatic or develop only mild illness. However, even mild cases may progress rapidly to severe disease.

Prodromal Symptoms

Initial symptoms are non-specific and may resemble common viral illnesses, including : Fever, Headache, Myalgia, Fatigue, Sore throat, Nausea and vomiting.

Respiratory Symptoms

Respiratory involvement is common and may be mild or severe. Features include:

Cough, Shortness of breath,
Chest discomfort
Acute respiratory distress syndrome (ARDS) in severe cases

Respiratory symptoms increase the risk of human-to-human transmission.

Neurological Involvement

Neurological involvement is a hallmark of Nipah virus infection and often indicates severe disease. Features include:

Altered sensorium
Drowsiness or confusion
Seizures
Focal neurological deficits
Acute encephalitis leading to coma

Other Symptoms

Systemic involvement may result from widespread vasculitis and endothelial damage, leading to:

Hypotension
Tachycardia
Multiorgan dysfunction

A distinctive feature of Nipah virus infection is relapsing or late-onset encephalitis, occurring weeks to months after apparent recovery. Symptoms include behavioral changes, seizures, and neurological deterioration.

Complications

Severe encephalitis
Respiratory failure
Multiorgan failure
Death [Case Fatality Rate is 40-75%]

DIAGNOSIS

Early and accurate diagnosis of Nipah virus infection is essential for patient management and outbreak control. Due to the high infectivity of the virus, diagnostic testing is performed in specialized high-containment laboratories.

Specimen

Blood (serum, plasma)
Cerebrospinal fluid (CSF)
Throat and nasal swabs
Urine
Respiratory secretions

RNA Detection

Reverse Transcriptase–Polymerase Chain Reaction (RT-PCR) is the gold standard for early diagnosis. It detects Nipah virus RNA in clinical specimens and is highly sensitive and specific. RT-PCR is most useful during the acute phase of infection.

Serology

Serological assays are used to detect antibodies against Nipah virus:

IgM antibodies - recent or acute infection
IgG antibodies - past exposure or recovery

Enzyme-linked immunosorbent assay (ELISA) is commonly used for antibody detection.

Nipah Virus (VERO NR596 Cells) Malaysia Strain

Virus Isolation

Virus isolation can be performed in cell culture but is restricted to Biosafety Level-4 (BSL-4) laboratories due to the high risk involved. This method is primarily used for research and confirmatory purposes rather than routine diagnosis.

Imaging

Although not confirmatory, imaging studies support diagnosis:

MRI brain may show multiple small hyperintense lesions suggestive of encephalitis
Chest X-ray / CT scan may reveal pulmonary infiltrates or ARDS

Immunohistochemistry

Immunohistochemical staining of tissue samples can detect viral antigens in affected organs, particularly in fatal cases. This method helps in post-mortem diagnosis and pathological studies.

Differential Diagnosis

Japanese encephalitis,
Herpes simplex encephalitis,
Dengue,
Leptospirosis, and
COVID-19.

MANAGEMENT

Currently, there is no specific antiviral therapy or licensed vaccine available for Nipah virus infection. Management is largely supportive, with emphasis on early diagnosis, intensive care, and strict infection control measures.

Symptomatic Treatment

Management of fever and pain
Adequate hydration and electrolyte balance
Nutritional support
Patients with severe disease require admission to intensive care units.
Respiratory Support :
- Respiratory complications are common and may progress rapidly. Management includes:
- Oxygen therapy
- Non-invasive or invasive mechanical ventilation in cases of respiratory failure
- Management of acute respiratory distress syndrome (ARDS)
Neurological Management :
- Patients with encephalitis require careful neurological monitoring. Management includes:
- Control of seizures using antiepileptic drugs
- Measures to reduce raised intracranial pressure
- Maintenance of airway protection in unconscious patients

Drugs under Study

Drug Name	Effect in Humans	Effect in Animals	In-Vitro Test
Ribavirin	In Malaysia outbreak during 1998/1999, a 36% reduction in mortality. In 2018 outbreak in Kerala, out of 23 cases showed 2 survivors. (drug given orally)	No effect in animals	-
Remdesivir (GS-5734; Veklury®)	Not tested in humans	Shows 100% survival rate in AGM model against NiV-B	-
Favipiravir (T-705; Avigan®)	Not tested in humans	Full protection against NiV- M	-
Griffithsin (GRFT)	Not tested in humans	In syrian hamster model against NiV-B shows 15% and 35% survival rate.	-
4’ azidocytidine (R1479)	Not tested in humans	Not tested in animals	Shows activity against NiV, but its prodrug is inactive; therefore withdrawn from clinical trials
4′-chloromethyl-2′-deoxy-2′-fluorocytidine (ALS-8112)	Phase I and II of clinical trials against respiratory syncytial virus infection	Not tested in animals	Strong effect against NiV in vitro at low micromolar range.
Lipopeptide fusion inhibitors	50% survival rate in Syrian golden hamster’s model. In AGMs model shows 33% survival rate.	-	-

PREVENTATIVE MEASURES

Prevention of Bat-to-Human Transmission

Avoid consumption of raw or unprocessed date palm sap.
Use physical barriers (such as bamboo skirts or covers) to prevent bats from accessing sap collection pots.
Wash and peel fruits thoroughly before consumption.
Avoid eating fruits that appear partially eaten or contaminated by bats.

Prevention of Animal-to-Human Transmission

Maintain proper animal housing away from fruit trees and bat habitats.
Implement biosecurity measures in livestock farms, especially pig farms.
Use protective gloves and clothing when handling sick animals.
Promptly isolate and report illness in domestic animals.

Prevention of Human-to-Human Transmission

Early identification and isolation of suspected and confirmed cases.
Use of personal protective equipment (PPE) by healthcare workers and caregivers.
Avoid direct contact with body fluids of infected individuals.
Safe burial practices with minimal handling of the deceased.

Infection Control in Healthcare Settings

Adherence to standard, contact, and droplet precautions.
Use of N95 masks during aerosol-generating procedures.
Proper disinfection of hospital equipment and patient environments.
Training healthcare workers in infection prevention and control practices.

Public Health Measures

Strengthening surveillance systems for early outbreak detection.
Rapid contact tracing and monitoring of exposed individuals.
Quarantine of high-risk contacts when necessary.
Timely risk communication and public awareness campaigns.

Vaccination

Vaccine Name	Country	Phase of Trial
ChAdOx1	United States (Oxford)	Phase 2
PHV02	United States	Phase 1
mRNA-1215	United States	Phase 1
HeV-sG-V	USA	Phase 1
CD40.NiV	Vaccine Research Institute of the ANRS MIE/Inserm	-

SITUATION IN INDIA

Scroll.in

In West Bengal (North 24 Parganas district), two laboratory-confirmed cases of Nipah virus infection were reported in late December 2025 and confirmed in January 2026. Both patients are young healthcare workers (nurses) from the same private hospital.

One patient has shown clinical improvement while the other remained critically ill as of the latest reports.

Over ~190 contacts (including health workers and community contacts) were identified and tested; none have tested positive or shown symptoms.

The World Health Organization said that the risk posed by the Nipah virus was “moderate at the sub-national level, and low at the national, the regional and global levels”. The World Health Organization said it assessed the risk from Nipah to be “moderate” at the sub-national level as no specific drugs or vaccines against it are available, and because early diagnosis is difficult.

REFERENCES

Pandey H, Pandey P, Jakhmola V, et al. A Comprehensive Review of Nipah Virus: From Epidemics to Approaches of Management. J Pure Appl Microbiol. 2024;18(3):1502-1514. doi: 10.22207/JPAM.18.3.33

Rana S, Negi P, Devi M, Butola M, Ansori ANM, Jakhmola V. Systematic Review On New Face of Monkeypox Virus. J Pure Appl Microbiol. 2022;16(suppl 1):3119-3129.

Thomas B, Chandran P, Lilabi MP, et al. Nipah virus infection in Kozhikode, Kerala, South India, in 2018: epidemiology of an outbreak of an emerging disease. Indian J Community Med. 2019;44(4):383-387.

Looi LM, Chua KB. Lessons from the Nipah virus outbreak in Malaysia. Malays J Pathol. 2007;29(2):63-67.

Clayton BA. Nipah virus: transmission of a zoonotic paramyxovirus. Curr Opin Virol. 2017;22:97-104.

Johnson K, Vu M, Freiberg AN. Recent advances in combating Nipah virus. Fac Rev. 2021;10.

Oxford scientists launch first human vaccine trials for deadly Nipah virus. 2024. Retrieved from Link.

Monath TP, Nichols R, Feldmann F, et al. Immunological correlates of protection afforded by PHV02 live, attenuated recombinant vesicular stomatitis virus vector vaccine against Nipah virus disease. Front Immunol. 2023;14:1216225

National Institutes of Health. NIH launches clinical trial of mRNA Nipah virus vaccine.2022. Retrieved from Link.

Rodrigue V, Gravagna K, Yao J, Nafade V, Basta NE. Current progress towards prevention of Nipah and Hendra disease in humans: A scoping review of vaccine and monoclonal antibody candidates being evaluated in clinical trials. Trop Med Int Health. 202429(5):354-364.

A promising vaccine against Nipah virus infection. 2024. Retrieved from Link.

Nipah virus fact sheet. WHO. Retrieved from WHO.

Nipah virus: WHO says low risk of disease spreading beyond India, no travel curbs needed. Scroll.in. Retrieved from Scroll.in.

Artificial Sweeteners and Cognitive Decline: How Low-Calorie Sweeteners Impact Brain Health

Dev Aditya Tomar — Wed, 22 Oct 2025 06:45:32 +0000

Artificial sweeteners have become a popular alternative to sugar, promising the same sweetness without the added calories. From diet sodas to sugar-free desserts, these low- and no-calorie sweeteners are widely used by individuals aiming to manage weight, control blood sugar, or reduce sugar intake. While their short-term metabolic benefits are well-documented, emerging research is raising concerns about their long-term effects on brain health. Recent studies suggest that regular consumption of artificial sweeteners may be linked to cognitive decline, memory impairment, and neuroinflammation. In this article, we explore the mechanisms behind these effects, review the latest scientific evidence, and discuss what this means for individuals concerned about mental and metabolic health.

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ARTIFICIAL SWEETENERS

EXTRA-ORAL MECHANISMS:

EFFECTS OF ARTIFICIAL SWEETENERS

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ARTIFICIAL SWEETENERS

Artificial sweeteners are synthetic sugar substitutes that provide a sweet taste without the added calories of regular sugar. They are widely used in foods and beverages such as diet sodas, sugar-free desserts, and chewing gums to help reduce calorie intake and manage blood sugar levels. Common examples include aspartame, saccharin, sucralose, and stevia (a plant-derived natural sweetener often grouped with artificial ones).

These sweeteners are much sweeter than sugar, meaning only small amounts are needed to achieve the desired

sweetness. They are particularly beneficial for people with diabetes or those aiming to control weight. However, their long-term safety and health effects have been subjects of scientific debate, prompting ongoing research and regulatory monitoring.

But Why?

Artificial sweeteners were created as substitutes for sugar to address the increasing demand for low-calorie and diabetes-friendly alternatives. During the early 20th century, growing concern about health issues such as obesity, diabetes, and tooth decay encouraged the search for safer sweetening options that could provide sweetness without harmful effects. These substitutes were intended to help lower calorie consumption, support weight control, and maintain stable blood sugar levels. They also proved especially useful during periods of sugar scarcity—like World War I and II—when alternative sweeteners were needed for food manufacturing.

Are they sweet?

Mechanism of Action

Non-nutritive sweeteners (NNSs) are not physiologically inert and can influence feeding and metabolism through various peripheral and central mechanisms. These mechanisms include actions on oral and extra-oral sweet taste receptors, effects on metabolic hormone secretion, cognitive processes like reward learning, memory, and taste perception, and gut microbiota.

ORAL MECHANISMS:

Sweet taste perception begins in the oral cavity when sweet tastants bind to T1R2/T1R3 G-protein coupled receptors. NNSs bind with high affinity to these receptors, even at low concentrations, to elicit sweet taste.
Prolonged NNS stimulation might increase sensory adaptation and reduce sweet taste sensitivity, potentially affecting the acceptability of both caloric and non-caloric sweeteners.
In vitro studies suggest NNSs cause greater down-regulation of taste receptor subunits compared to caloric sweeteners, indicating that adaptation magnitude may depend on binding affinity or receptor interactions.
Unlike caloric sweeteners, NNSs do not consistently produce cross-adaptation and can sometimes enhance the intensity of sweet stimuli, especially caloric ones.
Early exposure to NNSs, such as acesulfame potassium (AceK) in maternal milk, has been shown to increase preference thresholds for saccharin and sucrose in adult mice, accompanied by changes in taste signal transduction proteins.
Neuroimaging studies in heavy NNS users have revealed altered taste processing, including an inverse association between NNS use and brain responses (BOLD) in the amygdala and insula to sucrose.

EXTRA-ORAL MECHANISMS:

Functional sweet taste receptors are present in various extra-oral tissues, including the brain, pancreas, and gut, where they are involved in metabolic processes like glucose sensing, satiety hormone secretion, and glycemic control.
In vitro, both caloric and non-caloric sweeteners can stimulate the secretion of incretin hormones (GLP-1 and GIP) from enteroendocrine cells via a T1R3-dependent mechanism.
Both natural and non-nutritive sweeteners increase the expression and membrane trafficking of glucose transporters SGLT-1 and GLUT2 through their actions on intestinal sweet taste receptors.
Studies in mice have demonstrated that NNS administration increases SGLT-1- and GLUT2-dependent glucose absorption. However, some studies have not observed acute effects of NNS consumption on hormone secretion or glycemic excursion in naive rats.

EFFECTS OF ARTIFICIAL SWEETENERS

Alternative sweeteners and potential action mechanisms.

The potential mechanisms by which artificial sweeteners (AS) influence the development of type 2 diabetes (T2D) and cardiovascular complications are complex and multifactorial. By interacting with the sweet taste receptor family (T1R), artificial sweeteners can enhance insulin sensitivity, promote glucose uptake, and increase the expression of LDL receptors. Additionally, they may help reduce the formation of advanced glycation end products (AGEs), reactive oxygen species (ROS), and inflammatory mediators such as TNF-α, IL-6, and intracellular NF-κB.

However, overstimulation of the associated G protein pathways due to excessive intake of artificial sweeteners may have adverse effects.

This includes promoting weight gain, insulin resistance, increased intestinal permeability, and chronic inflammation, all of which contribute to the development of metabolic disorders and related comorbidities.

COGNITIVE DECLINE

An 8-Year Prospective Study was done to find out the "Association Between Consumption of Low- and No-Calorie Artificial Sweeteners and Cognitive Decline". It was published on 3rd September, 2025 and here's what it says :

Stats

12,772 participants
Mean age 51.9 ± 9.0 years
54.8% women
43.2% Black/mixed race
Mean consumption of LNCSs was 92.1 ± 90.1 mg/d.

Summary

Recent research has suggested a possible link between the consumption of certain low- and no-calorie sweeteners (LNCSs) — including aspartame, saccharin, acesulfame-K, erythritol, sorbitol, and xylitol — and accelerated cognitive decline. Higher intake of these sweeteners has been associated with a faster reduction in global cognitive performance, particularly affecting memory and verbal fluency. Participants consuming the highest amounts of combined LNCSs demonstrated a more rapid decline in verbal fluency and overall cognition in non-diabetic individuals, and a greater decline in memory and cognitive function among those with diabetes.

The most recent evidence, published in Neurology — the medical journal of the American Academy of Neurology, was supported by the Brazilian Ministry of Health, the Ministry of Science, Technology, and Innovation, and the National Council for Scientific and Technological Development.

It found that regular consumption of these sweeteners, including tagatose, was linked to declines in memory and overall cognitive ability equivalent to approximately 1.6 years of additional brain aging. These findings suggest that frequent intake of artificial and low-calorie sweeteners may have potential long-term implications for brain health.

Researchers found a link in people under 60 but not older than 60. Do note that, while the study found links, it does not prove that sweeteners cause cognitive decline.

"Correlation does not equal to Causation"

Similar Studies

While numerous animal studies have demonstrated a link between excessive sugar intake and impaired cognitive function, the precise effects of sugars on human cognition remained uncertain.

On 25th Dec, 2023, a systematic review and meta-analysis aimed to assess existing evidence, and the overall quality of research exploring the impact of free and added sugars on cognitive performance in healthy individuals.

Most cohort studies and eight of nine cross-sectional studies reported a significant positive association between higher added sugar consumption and an increased risk of cognitive decline. Conversely, four studies noted a lower risk of cognitive impairment among individuals consuming natural fructose-rich foods, such as fruits.

The majority of randomized controlled trials focused on the short-term effects of glucose on cognitive facilitation, emphasizing that optimal brain function depends on well-regulated blood glucose levels tailored to individual physiology. Overall, the findings underscore the potential harmful effects of excessive, long-term, or prenatal exposure to added sugars on cognitive health.

However, further research is still necessary to clarify the distinct roles of free and added sugars in influencing human cognition.

Mechanism

Effects of Artificial Sweeteners on Brain Health.

Dr. Arbind Kumar Choudhary, Associate Professor, Department of Physiology, All India Institute of Medical Science, Raebareli, Uttar Pradesh, India in his research suggests that artificial sweeteners such as aspartame, sucralose, and saccharin may contribute to oxidative stress and neuroinflammation, disrupt the integrity of the blood-brain barrier, and alter cerebral blood flow, potentially accelerating cognitive decline.

These sweeteners may also affect the gut microbiome, impairing the gut-brain axis and exacerbating neurocognitive issues. Individuals with metabolic conditions such as type 2 diabetes and obesity may be particularly vulnerable, facing an increased risk of cognitive impairment and neurodegenerative diseases.

While artificial sweeteners can provide short-term metabolic benefits, their potential long-term effects on brain health remain a concern. Given their widespread use in India amid rising rates of metabolic and neurodegenerative disorders, there is an urgent need for targeted research to evaluate their safety and long-term neurological impact.

REFERENCES

Aspartame and Other Sweeteners in Food. US FDA.

Burke MV, Small DM. Physiological mechanisms by which non-nutritive sweeteners may impact body weight and metabolism. Physiol Behav. 2015 Dec 1;152(Pt B):381-8. doi: 10.1016/j.physbeh.2015.05.036. Epub 2015 Jun 3. PMID: 26048305; PMCID: PMC4661139.

Concetta Schiano, Vincenzo Grimaldi, Michele Scognamiglio, Dario Costa, Andrea Soricelli, Giovanni Francesco Nicoletti, Claudio Napoli, Soft drinks and sweeteners intake: Possible contribution to the development of metabolic syndrome and cardiovascular diseases. Beneficial or detrimental action of alternative sweeteners?, Food Research International, Volume 142,
2021, 110220, ISSN 0963-9969, https://doi.org/10.1016/j.foodres.2021.110220.

Gillespie KM, White MJ, Kemps E, Moore H, Dymond A, Bartlett SE. The Impact of Free and Added Sugars on Cognitive Function: A Systematic Review and Meta-Analysis. Nutrients. 2023 Dec 25;16(1):75. doi: 10.3390/nu16010075. PMID: 38201905; PMCID: PMC10780393.

CHOUDHARY, Arbind Kumar. Artificial Sweeteners on Brain Health: Neurovascular Changes and Cognitive Decline in Indian Population. Medical Research Archives, [S.l.], v. 13, n. 4, apr. 2025. ISSN 2375-1924. Available at: <https://esmed.org/MRA/mra/article/view/6388>. Date accessed: 22 oct. 2025. doi: https://doi.org/10.18103/mra.v13i4.6388.

Natalia Gomes Gonçalves, Euridice Martinez-Steele, Paulo A. Lotufo , Isabela Bensenor , Alessandra C. Goulart, Sandhi Maria Barreto , Luana Giatti , Carolina Perim de Faria, Maria del Carmen Bisi Molina, Paulo Caramelli , Dirce Maria Marchioni, and Claudia Kimie Suemoto.

Association Between Consumption of Low- and No-Calorie Artificial Sweeteners and Cognitive Decline. Neurology Journals. Volume 105 | Number 7. October 07, 2025

ORS : Oral Rehydration Salt Solution

Dev Aditya Tomar — Sat, 18 Oct 2025 09:04:06 +0000

On 15th October, 2025, the Food Safety and Standards Authority of India (FSSAI), has issued a directive requiring all food and beverage companies to cease using the term “ORS” (Oral Rehydration Solution) on their products. The order extends to all instances where the term appears on its own, with any prefix or suffix, or as part of a trademark or brand name.

On this note, I would like to expand more on the topic of Oral Rehydration Solution, its constituents and uses as directed by WHO while touching on the clarification issued by FSSAI.

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BASIC TERMINOLOGIES

Dehydration

Rehydration

Oral Rehydration Therapy (ORT)

ORAL REHYDRATION SALT SOLUTION

Constituents

Difference between the Old and the New

Role of the Constituents

Previous Stance on ORS

Clarification dated 15th Oct, 2025

Dr. Sivaranjani Santosh

References

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BASIC TERMINOLOGIES

Dehydration

Loss of water and dissolved salts from the body, occurring, for instance, as a result of diarrhoea.

Rehydration

The correction of dehydration.

Oral Rehydration Therapy (ORT)

The administration of fluid by mouth to prevent or correct the dehydration that is a consequence of diarrhoea.

ORAL REHYDRATION SALT SOLUTION

Oral Rehydration Salts (ORS) is the internationally recognized non-proprietary name for a scientifically formulated glucose-electrolyte solution developed in 1969. It was approved, recommended, and distributed by the World Health Organization (WHO) and UNICEF as a life-saving medical formulation for the prevention and treatment of dehydration caused by diarrhea and other conditions leading to fluid loss. It remains a cornerstone of primary healthcare and is classified as an essential medicine by the WHO for its proven safety, affordability, and effectiveness.

Constituents

Given below is the list of ingredients present in the New ORS solution as advised by WHO.

Dissolution of an ORS sachet in drinking water yields the following concentrations :

Difference between the Old and the New

The 'Old' ORS formulation is known as the Standard WHO ORS whereas the 'New' one is called the Reduced Osmolarity ORS. Previously, the ORS had a total osmolarity of 311 mOsm/l, but a consultative technical meeting held in New York (USA) in July 2001 reviewed various studies evaluating this approach. During the meeting, experts provided technical recommendations to WHO and UNICEF regarding the efficacy and safety of reduced osmolarity ORS for treating children with acute non-cholera diarrhea, as well as adults and children suffering from cholera.

These studies showed that the efficacy of ORS solution for treatment of children with acute non-cholera diarrhoea is improved by reducing its osmolarity. In a combined analysis of this study and studies with other reduced osmolarity ORS solutions stool output was also reduced by about 20% and the incidence of vomiting by about 30%.

However, it remains uncertain whether this finding can be confidently applied to patients with severe cholera-induced diarrhea, in whom electrolyte losses are extensive. In such cases, the risk of developing hyponatremia may be heightened, potentially leading to adverse clinical outcomes and diminishing the benefits of using reduced osmolarity ORS.

Role of the Constituents

Glucose : Facilitates the absorption of sodium (and hence water) on a 1:1 molar basis in the
small intestine
Sodium and Potassium : To replace the body losses of these essential ions during
diarrhoea (and vomiting)
Citrate : Corrects the acidosis that occurs as a result of diarrhoea and dehydration.

Uses

DEHYDRATION :

While the mortality rate among children under five suffering from acute diarrhea has declined remarkably—from about 4.5 million deaths annually in 1979 to 1.6 million in 2002—acute diarrhea still remains a significant cause of illness and death among children in developing countries.

The introduction of Oral Rehydration Salts (ORS) and Oral Rehydration Therapy (ORT) by UNICEF and WHO in the late 1970s represented a major milestone in global child health. During the 1990s, these therapies were estimated to have saved more than one million young lives each year by effectively preventing deaths from dehydration caused by diarrhea.

Nevertheless, recent trends indicate a concerning decline in both awareness and the correct use of home-based treatments for diarrhea, including ORT, in several countries—threatening to undermine decades of progress in reducing child mortality.

Hence, the healthcare workers are advised to : [Detailed]

Treat dehydration with ORS solution (or with an IV electrolyte solution in cases of severe dehydration) &

Provide children with 20 mg per day of zinc supplementation for 10–14 days (10 mg per day for infants under six months old)

For cause-specific mortality: The World Health Report2003, WHO, Geneva. For malnutrition: Pelletier, D. L., E. A. Frongillo, and J. P. Habicht, ‘Epidemiologic evidence for a potentiating effect of malnutrition on child mortality’,American Journal of Public Health, vol. 83, no. 8, August 1993, pp. 1130-1133.

OTHERS :

In a study about ORS as alternative to IV fluids in adult burn patients with >15% TBSA burn injuries, it was observed that :

there were no major significant differences between the study group and control group.
Even where there was a significant difference, apart from blood pressure in the first hour of the first day, the study group never crossed safe limits for other parameters.
WHO-ORS with 5gm salt tablets, given according to Sørenson’s formula, is a safe and efficient alternative for IV resuscitation.
It could even be a substitute, particularly in low resource settings and fire disasters.

FSSAI

FSSAI, or the Food Safety and Standards Authority of India, is an independent statutory body responsible for establishing and enforcing food standards in India, ensuring that all food products are safe, hygienic, and fit for human consumption.

Previous Stance on ORS

Earlier directives from the Centre, issued on July 14, 2022, and February 2, 2024, permitted the use of the term “ORS” on product labels as part of a trademark with a prefix or suffix. This was allowed only provided the label included the disclaimer: “The product is NOT an ORS formula as recommended by WHO.”

Clarification dated 15th Oct, 2025

FSSAI has reiterated that, following a fresh review, the use of the term “ORS” in any form—whether as part of a trademark or otherwise—on products like fruit-based, non-carbonated, or ready-to-drink beverages violates the Food Safety and Standards Act.

The authority emphasized that such labeling can mislead consumers by being false, deceptive, ambiguous, or inaccurate.

Additionally, FSSAI warned that products in breach of this rule may incur penalties under Sections 52 and 53 of the Food Safety and Standards Act, 2006.

Dr. Sivaranjani Santosh

Dr Sivaranjani Santosh, paediatrician, says the following...

“It's a huge relief. That means now I know that no child will die, no adult will die because of worsening of diarrhoea, because of these drinks. ORS is supposed to save lives. It's a wonder drug of the 20th century. It's supposed to save lives. It's supposed to rehydrate us. It is like Amrut for us. And here, people have labelled their high sugar drinks as ORS with a suffix or prefix. And for the past 14 years, they have been cheating the public, deceptive labelling, unethical marketing, pharmacies, hospitals, schools, everywhere,”

In 2022, Dr. Santosh filed a PIL in the Telangana High Court against companies labeling sweetened fruit juices as ORS without meeting WHO standards, citing high sugar content and inconsistent electrolytes.

The case drew the attention of then Health Secretary Rajesh Bhushan, prompting judicial and regulatory review. FSSAI initially restricted the use of ‘ORS’ on labels and ads on April 8, 2022, but temporarily relaxed the rule on July 14, 2022, allowing companies with registered trademarks to continue using the term until a final ruling by the Controller General of Patents, Designs and Trademarks.

Dr. Santosh’s eight-year campaign shed light on companies marketing sugar-heavy drinks as ORS, falsely suggesting health benefits. Her advocacy emphasized the risks these products pose, especially to children and people with diabetes. And finally, FSSAI has now given is new directive in favour of her campaign.

References

Kim Y, Hahn S, Garner P. Reduced osmolarity oral rehydration solution for treating dehydration caused by acute diarrhoea in children. Cochrane Database Syst Rev. 2001;2002(2):CD002847. doi: 10.1002/14651858.CD002847. Update in: Cochrane Database Syst Rev. 2002;(1):CD002847. doi: 10.1002/14651858.CD002847. PMID: 11406049; PMCID: PMC6532752.

Moghazy AM, Adly OA, Elbadawy MA, Hashem RE. Evaluation of who oral rehydration solution (ORS) and salt tablets in resuscitating adult patients with burns covering more than 15% of total body surface area (TBSA). Ann Burns Fire Disasters. 2016 Mar 31;29(1):43-47. PMID: 27857652; PMCID: PMC5108229.

Clarification regarding Order dated 14.10.2025 on withdrawal of permissions for use of the term “ORS” along with brand names. Dated 15th October 2025. FSSAI. Retrieved from https://fssai.gov.in/advisories.php.

Oral rehydration salts. Production of the new ORS. 1 January 2006 | Guideline. WHO. Link.

Clinical Management of Acute Diarrhea. WHO/UNICEF Joint Statement.

Antimicrobial Resistance : A Report by WHO

Dev Aditya Tomar — Fri, 17 Oct 2025 08:17:20 +0000

The WHO’s Global Antimicrobial Resistance Surveillance System (GLASS) report highlights a sharp increase in antibiotic resistance, particularly in low- and middle-income nations such as India, where healthcare systems are often fragile.

Drawing on data from more than 23 million bacterial infections reported in over 100 countries, the report reveals that between 2018 and 2023, over 40% of antibiotics have become ineffective against common infections of the bloodstream, urinary tract, digestive system, and reproductive organs.

In 2021 alone, bacterial infections caused an estimated 7.7 million deaths globally, with drug resistance contributing to 4.71 million of those and directly causing 1.14 million fatalities.

This article delves deeper into the topic of antimicrobial resistance and its current effects worldwide and in India.

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INTRODUCTION

Antimicrobial resistance (AMR) is emerging as one of the most serious challenges to global health, weakening the power of critical medicines and increasing the danger posed by infections that were once easily treatable, as well as by routine medical procedures.

Through its Global Antimicrobial Resistance and Use Surveillance System (GLASS), the World Health Organization (WHO) helps nations establish robust surveillance systems and produce comparable data that can drive informed public health policies.

On 13 October 2025, WHO published Global antibiotic resistance surveillance report 2025, which offers a comprehensive global picture of antibiotic resistance patterns, drawing on evidence from more than 23 million confirmed cases of bloodstream, urinary, gastrointestinal, and urogenital infections (including gonorrhoea). The findings are based on data submitted by 104 countries in 2023 and 110 countries over the 2016–2023 period.

If you'd like to understand what AMR [Antimicrobial Resistance] is, then please look at this article. The following is a synopsis of the detailed analysis provided by WHO.

AT A GLANCE

Since the launch of GLASS in 2016, antimicrobial resistance (AMR) data have been submitted by 110 countries, including three territories and regions. Participation has expanded significantly—from just 25 countries in 2016 to 104 in 2023, reflecting a growth of more than 300%.

The steady increase in reporting underscores the growing global recognition of the importance of sharing surveillance data as a collective public health responsibility. Despite these improvements, considerable gaps in data availability and reporting continue to hinder a complete global picture.

In 2023, antibiotic resistance was detected in roughly one out of every six laboratory-confirmed bacterial infections worldwide. The highest resistance levels were found in urinary tract infections (1:3 cases) and bloodstream infections (1:6).

Lower resistance rates were observed in gastrointestinal infections (1:15) and urogenital gonorrhoeal infections (1:125).

Trends of AMR: median annual change in percentage, 2018–2023.

Geographically, the South-East Asia and Eastern Mediterranean regions reported the greatest burden, with nearly one in three infections showing resistance, followed by the African Region, where one in five infections were resistant—both surpassing the global median.

Conversely, resistance was less prevalent in the European Region (one in ten) and lowest in the Western Pacific Region (one in eleven), highlighting marked regional differences.

Median national percentage of AMR in bloodstream infections by AMR surveillance coverage, 2023.

Between 2018 and 2023, antimicrobial resistance (AMR) has risen in 40% of the pathogen–antibiotic combinations tracked for global trends, with annual relative increases ranging from 5% to 15%, depending on the specific combination.

Resistance is notably growing against “Watch” antibiotics in the AWaRe (Access, Watch, Reserve) classification—particularly carbapenems and fluoroquinolones—among major Gram-negative pathogens such as Acinetobacter spp., E. coli, K. pneumoniae, and Salmonella spp.

This trend is concerning because these drugs are critical for treating severe infections. The rise in AMR is narrowing empirical treatment options and prompting a shift from oral to intravenous therapies, with increased dependence on second-line and last-resort antibiotics.

Here are some representations of the Percentage antibiotic resistance to ceftriaxone in N. gonorrhoeae urogenital infections, 2023

Percentage AMR

Global trends in percentage AMR by infection type: median annual change (2018–2023) and 2023 percentage resistance estimates :

INDIAN STATS

The numbers below were a part of Global antibiotic resistance surveillance report 2025 :

Blood Stream Infections

DRUGS

NO. OF INFECTIONS WITH AST, 2023

NO. OF INFECTIONS WITH AST, 2018-2023

% RESISTANCE

Acinetobacter - Imipenem

9946

30,983

71.2

E. coli - Cefotaxime

6564

25,744

78.5

E. coli - Imipenem

8962

30,295

32.3

E. coli - IIIrd Gen Cephalosporins

6564

17,527

79.4

K. pneumoniae - Cefotaxime

6132

24,864

79.6

K. pneumoniae - Imipenem

9065

32,301

61.2

Salmonella - Ciprofloxacin

S. aureus - Methicillin

8373

37,592

50.9

S. pneumoniae - Penicillin G

Gastrointestinal Infections

DRUGS

NO. OF INFECTIONS WITH AST, 2023

NO. OF INFECTIONS WITH AST, 2018-2023

% RESISTANCE

Salmonella - Ciprofloxacin

340

1084

28.9

Shigella - Ciprofloxacin

186

82.1

Urinary Tract Infections

DRUGS

NO. OF INFECTIONS WITH AST, 2023

NO. OF INFECTIONS WITH AST, 2018-2023

% RESISTANCE

E. coli - Cefotaxime

51,874

174,593

73.5

E. coli - Imipenem

64,488

206,402

19.2

K. pneumoniae - Cefotaxime

13,440

44,535

69.9

K. pneumoniae - Imipenem

18,739

59,460

40.3

Urogenital Infections

DRUGS

NO. OF INFECTIONS WITH AST, 2023

NO. OF INFECTIONS WITH AST, 2018-2023

% RESISTANCE

N. gonorrhoea - Ceftriaxone

AMRSN, 2013

Antimicrobial resistance (AMR) represents a significant public health challenge in India, a country with a high prevalence of infectious diseases and extensive, often unregulated, antibiotic use. Accurate assessment of the AMR burden is essential to understand its consequences, while knowledge of local resistance trends is critical for developing both empirical and pathogen-specific treatment strategies suited to varied epidemiological contexts.

In view of this, to generate relevant evidence on the extent of drug resistance and a nationally representative reliable data on AMR which was not existent from India, ICMR initiated Antimicrobial Resistance Surveillance and Research Network (AMRSN) in 2013.

Goals :

Establish network of hospitals to monitor trends in the antimicrobial susceptibility profile of clinically important bacteria and fungi limited to human health.
Include comprehensive molecular studies for identifying the clonality of drug-resistant pathogens and their transmission dynamics to enable better understanding of AMR in the Indian context and develop suitable interventions.
Disseminate information on AMR in pathogenic organisms to stakeholders to promote interventions that reduce AMR.
Create data management system for data collection and analysis.

Focus :

Enterobacteriaceae causing sepsis,
Gram negative non-fermenters,
Enteric fever pathogens,
Diarrheagenic bacterial organisms,
Gram positives: staphylococci and enterococci and
Fungal pathogens (excluded in WHO priority pathogens)-yeasts (Candida and Cryptococcus spp.) and mycelial fungi (Aspergillus spp. and Zygomycetes spp.)

Collaboration with Institutes :

Diarrheagenic bacterial organisms, CMC, Vellore
Enteric fever pathogens: AIIMS, New Delhi
Enterobacteriaceae causing sepsis: PGIMER, Chandigarh
Gram negative non fermenters: CMC, Vellore
Gram positives including MRSA: JIPMER, Pondicherry
Fungal infections: PGIMER, Chandigarh

REFERENCES

India's Antimicrobial Resistance Surveillance & Research Initiative, ICMR. Link.

Global antibiotic resistance surveillance report 2025. 13 October 2025 | Global report. WHO. ISBN: 978924011633. Link.

Global antibiotic resistance surveillance report 2025: summary13 October 2025 | Executive summary. WHO Reference Number: B09585. Link.

Vitamin B12 : Sources & Deficiency

Dev Aditya Tomar — Wed, 30 Aug 2023 12:58:43 +0000

Unlocking the secrets of optimal health often leads us to explore the intricate world of vitamins, and among them, vitamin B12 takes center stage. With its pivotal role in functions ranging from nerve health to red blood cell formation, vitamin B12 is an essential nutrient that our bodies depend on. However, unlike some vitamins, our bodies can't manufacture B12 on their own.

This article serves as a comprehensive guide, delving into the diverse sources that provide us with this vital nutrient and examining the potential risks and consequences associated with vitamin B12 deficiency. If you want a quick briefing about B12, you can read 'Introduction to Vitamin B12'.in B12 Vitamin B12Vitamin B12 Vitamin B12 Vitamin B12 Vitamin B12 Vitamin B12 Vitamin B12 Vitamin B12 Vitamin B12 Vitamin B12 Vitamin B1 Vitamin B12 Vitamin B12 Vitamin B12 Vitamin B12 Vitamin B12

Table of Contents

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SOURCES OF VITAMIN B12

DEFICIENCY OF VITAMIN B12

CAUSES OF DEFICIENCY:

Autoimmune Cause

Dietary Insufficiency

Malabsorption

HIGH RISK POPULATIONS:

SYMPTOMS:

PREVENTION OF B12 DEFICIENCY

REFERENCES

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SOURCES OF VITAMIN B12

Food	Micrograms per Serving	Percentage DV
Cooked Clams (without shells), 85gm	17	708
Fortified nutritional yeast, 1/4 cup	8.3 - 24	346 - 1000
Cooked Atlantic Salmon, 85gm	2.6	108
Light Tuna (canned in water), 85gm	2.5	104
Milk with 2% Milkfat, 1 cup	1.3	54
Plain Fat-free Yoghurt, 170gm	1	43
Fortified Breakfast Cereal, 1 serving	0.6	25*
Cheddar Cheese, 42.5gm	0.5	19
Whole Cooked Egg, 1 large	0.5	19
Roasted Turkey Breast, 85gm	0.3	14
Tempeh, 1/2 cup	0.1	3
Banana, 1 medium	0	0
Kidney Beans, 1/2 cup	0	0

The U.S. Food and Drug Administration (FDA) devised Daily Values (DVs) to facilitate informed comparisons of nutrient compositions among foods and dietary supplements in the broader context of dietary intake.

In the case of vitamin B12, the recommended Daily Value stands at 2.4 mcg for both adult individuals and children aged 4 years and older. Foods that furnish 20% or more of this DV are categorized as high sources of the nutrient. However, it is important to note that even foods delivering lower percentages of the DV play a meaningful role in cultivating a health-conscious diet.

The U.S. Department of Agriculture's FoodData Central is catalogues the nutrient profiles of diverse foods. This resource presents a comprehensive list of vitamin B12-rich foods, organized based on their nutrient content and food name. The accompanying table showcases some of the major sources of vitamin B12 within this compilation.

*depends on the amount of fortification

Analyzing the table, it is apparent that most of the sources are of animal-origin; meat, egg, milk, yoghurt, cheese, fish. This acts as an evidence to the fact that vegetarians and vegans are more prone to deficiency of vitamin B12.

Some other sources that one can take are dietary supplements and prescription medications. The most common form of supplement is cyanocobalamin. It is also taken in the form of adenosylcobalamin, methylcobalamin, and hydroxycobalamin.

DEFICIENCY OF VITAMIN B12

Vitamin B12 deficiency, medically referred to as cobalamin deficiency, occurs when the levels of vitamin B12 in the
blood and tissues are below the normal range.

But relying solely on blood tests to gauge deficiency isn't the most accurate method, as certain individuals with a deficiency might exhibit regular vitamin B12 blood levels. More reliable indicators of actual vitamin B12 activity are the blood concentrations of methylmalonic acid, a byproduct of protein breakdown, and homocysteine. These values rise in the presence of a vitamin B12 deficiency.

CAUSES OF DEFICIENCY:

Vitamin B12 deficiency primarily has 3 etiologies : Dietary Insufficiency, Malabsorption, and Autoimmune.

Autoimmune Cause

Pernicious anemia is a relatively rare autoimmune condition that hampers the absorption of dietary vitamin B12, leading to a deficiency of B12 and then megaloblastic anemia. In this disorder, antibodies against intrinsic factor, a protein necessary for B12 absorption, are generated.

These anti-intrinsic factor antibodies attach themselves to intrinsic factor, impeding its functionality, which in turn renders the terminal ileum incapable of absorbing B12.

Dietary Insufficiency

Vitamin B12 accumulates in surplus within the liver; nevertheless, individuals who have strictly adhered to a vegan diet for roughly three years might encounter a B12 deficiency due to insufficient dietary intake.

Individuals who exclude meat, fish, poultry, and dairy from their diets face the possibility of lacking in vitamin B12, as it is exclusively present in animal-derived products. Research has indicated that individuals following a vegetarian lifestyle tend to exhibit diminished levels of vitamin B12 in their bloodstreams.

Therefore, individuals practicing a vegetarian or vegan dietary regimen should incorporate B12-fortified foods or take B12 supplements. This is of particular significance for pregnant women, as proper vitamin B12 is crucial for fetal neurological development, and deficiency can result in permanent neurological impairment.

Malabsorption

There are various reasons for malabsorption, ranging from medication to physical inability to absorb.

SURGERY :

Parietal cells are a specialized form of gastric cells (in stomach) that secrete Intrinsic Factor and ileum (small intestine) is the site of absorption of B12. So, any surgery related to these locations may lead to the deficiency of B12. For example, a patient with a history of gastric bypass

surgery (weight loss surgery) may develop the deficiency. Also, a surgical resection of terminal ileum (due to Crohn's disease) may increase the risk of deficiency. To know more about Crohn's disease and its holistic treatment, you may visit Ayurvedic Herbalist.

GASTROINTESTINAL DISORDERS :

Certain diseases including Crohn’s and celiac disease that negatively impact the digestive tract also increase the risk of deficiency. Other than that, gastritis (inflammation of stomach lining) is a common cause of B12 deficiency. This occurs due to a lack of hydrochloric acid, which is a key component for absorption. You can understand more about the way B12 is absorbed in 'Introduction to Vitamin B12'.

MEDICATIONS:

The extended usage of metformin, a commonly prescribed drug for type 2 diabetes, is strongly linked to deficiencies in vitamin B12 and lower levels of folic acid. This is primarily because metformin can hinder the absorption of these essential nutrients, potentially resulting in elevated levels of homocysteine and an increased risk of cardiovascular disease. Similarly, individuals taking proton pump inhibitors and histamine blockers, medications aimed at reducing stomach acid, are also at risk of experiencing reduced vitamin B12 levels.

Individuals who frequently rely on medications that suppress stomach acid due to conditions like gastroesophageal reflux disease (GERD) or peptic ulcer disease—such as proton-pump inhibitors, H2 blockers, or other antacids—may encounter difficulties in absorbing sufficient vitamin B12 from their diets.

These medications can slow down the release of stomach acid or reduce its production, which could potentially impede the conversion of vitamin B12 into a usable form in the stomach. Nevertheless, current research has not provided evidence for a significantly higher incidence of vitamin B12 deficiency in people using these medications.

HIGH RISK POPULATIONS:

AGE OVER 75 : Individuals above the age of 75 are more susceptible to developing vitamin B12 deficiency due to potential difficulties in fully absorbing the vitamin by their bodies.
GI DISORDER : Conditions like celiac disease and Crohn’s disease can complicate the absorption of vitamin B12 in the body.
STRICT VEGAN OR VEGETARIAN DIET : Those who follow this diet are at an increased risk of vitamin B12 deficiency if their diet lacks sufficient fortified foods containing the vitamin.
TAKING SPECIFIC MEDICATIONS : Certain medications can lead to decreased levels of vitamin B12 in the body. These include metformin (a medication used to manage diabetes), proton pump inhibitors (PPIs used to treat GERD and peptic ulcers), histamine H2 blockers (used to reduce stomach acid production), and oral birth control pills (oral contraceptives).

SYMPTOMS:

The outlook (prognosis) for individuals with vitamin B12 deficiency relies on the promptness of diagnosis and treatment. When the deficiency is identified early, most individuals can alleviate their symptoms through treatment. The duration of medication needed varies depending on the underlying cause of the deficiency; it could be a short-term regimen or require lifelong medication.

GENERAL :

Feeling very tired or weak.
Experiencing nausea, vomiting or diarrhea.
Not feeling as hungry as usual.
Weight loss.
Having a sore mouth or tongue.
Having yellowish skin.

NEUROLOGICAL :

Numbness or tingling in your hands and feet.
Vision loss.
Having a hard time remembering things or getting confused easily.
Having a difficult time walking or speaking like you usually do.

PHYSIOLOGICAL :

Feeling depressed, irritable and
Experiencing a change in the way you feel and behave.

Neglecting to address vitamin B12 deficiency can lead to enduring and significant consequences that impact the nervous system and brain. Some of the more severe and lasting effects of untreated vitamin B12 deficiency are :

Megaloblastic Anemia: It is characterized by red blood cells that are larger than normal. As the red blood cells are too large, they may not be able to exit the bone marrow to enter the bloodstream and deliver oxygen.
Nerve damage with numbness, tingling in the hands and legs
Depression
Paranoia and delusions
Memory loss

PREVENTION OF B12 DEFICIENCY

Preventing vitamin B12 deficiency involves ensuring an adequate intake of this essential nutrient through various dietary and supplemental means. It is achievable for most individuals through the consumption of foods and beverages containing vitamin B12. Here are some foods you can add to your diet :

ANIMAL-DERIVED FOODS : Vitamin B12 is present in red meat, fish, poultry, eggs, as well as milk and other dairy products.

FORTIFIED FOOD : Fortified foods are enriched with vitamins and nutrients they naturally lack. Examples include select breakfast cereals, nutritional yeast, plant-based milk, and specific types of bread. Ensure you review the food label (nutritional information) to determine if the item has been fortified with vitamin B12.

VITAMIN B12 SUPPLEMENTS : Numerous multivitamins contain vitamin B12, and standalone supplements focused solely on vitamin B12 are also available. This is one of the few options available to vegans and vegetarians, apart from fortified foods.

REFERENCES

Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B(6), Folate, Vitamin B(12), Pantothenic Acid, Biotin, and Choline. Washington, DC: National Academies Press; 1998. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK114310/

Vitamin B12-Fact Sheet for Medical Professionals. National Institutes of Health (NHI). Retrieved from https://ods.od.nih.gov/factsheets/VitaminB12-HealthProfessional/#en1

Vitamin B12 Deficiency. Diseases and Conditions, Health Library, Cleveland Clinic. Retrieved from https://my.clevelandclinic.org/health/diseases/22831-vitamin-b12-deficiency

Vitamin B12. The Nutrition Source, Harvard T.H. Chan. Retrieved from https://www.hsph.harvard.edu/nutritionsource/vitamin-b12/

Vitamin B-12. By Mayo Clinic Staff. Retrieved from https://www.mayoclinic.org/drugs-supplements-vitamin-b12/art-20363663

Ankar A, Kumar A. Vitamin B12 Deficiency. [Updated 2022 Oct 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK441923/

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Introduction to Vitamin B12

Dev Aditya Tomar — Wed, 05 Jul 2023 08:49:32 +0000

Vitamin B12 stands out as an extraordinary nutrient with distinctive characteristics. It is the sole vitamin containing a metal ion and relies solely on external sources for our daily intake. Its versatility extends to a wide range of functions, making it a true powerhouse for our health. Without sufficient B12, disorders affecting the cardiovascular, neural, and psychological systems can emerge.

In this series of articles, we aim to present the topics in a simple and accessible manner. Here, we strive to provide a comprehensive understanding of this extraordinary vitamin and its significance for overall health and well-being.

Table of Contents

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INTRODUCTION

METHODS OF ABSORPTION

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INTRODUCTION

Vitamin B12 is a part of a group of compounds called cobalamins. They share similarities in their structure and can serve as substitutes of B12 in its absence. Hence, they are also termed as vitamers of B12.

Some examples are adenosylcobalamin, hydroxocobalamin, and cyanocobalamin. Methylcobalamin & 5-deoxyadenosylcobalamin are metabolically active forms in humans, but hydroxycobalamin & cyanocobalamin can also be used after being converted into the former forms.

Notably, Vitamin B12 is the only vitamin to contain a metal ion. It is present as cobalt-corrin complex which gives the compound its characteristic deep red color. The red crystalline vitamin forms a red solution when dissolved in water.

It is the most chemically complex vitamin, and it can’t be synthesized by our body. This means the only source of the vitamin is from either food or supplements.

METHODS OF ABSORPTION

There are two ways for absorption of Vitamin B12. The first one is by passive absorption due to a difference in its concentration between the lumen and the cells of the intestine.

The other way is via active transport with the help of protein carriers. Vitamin B12 is usually bound to a protein in the foods we eat. So, the first step is dissociating the food-bound B12 with the help of HCl (stomach acid) and pepsin (protease) in the stomach.

The freed B12 now binds to a cobalamin-binding protein secreted by the salivary glands & the gastric mucosa (moist inner lining of stomach). When the partially digested chyme enters the small intestine, the protein-bound B12 is attacked by pancreatic proteases. This results in the separation of B12 from the protein.

Now, B12 forms a complex with intrinsic factor which was secreted by the parietal cells of stomach. The intrinsic factor has two functions; to assist the vitamin’s absorption & to protect it from catabolism by intestinal bacteria. This B12-IF complex can be absorbed by enterocytes (cells lining the intestine) of distal ileum via receptor-mediated endocytosis.

STORAGE & EXCRETION

Around 2-5 mg of vitamin B12 is found in adults. Most of it is stored in the liver. As this vitamin is stored in substantial amounts in comparison to its utilization rate, the reservoir usually takes 3-5 years to get exhausted.

A part of it is secreted in the bile, which is then recycled via enterohepatic circulation. That is, the vitamin is secreted from liver into bile, which enters the small intestine, gets absorbed by enterocytes, and transported back to the liver. This process is not completely efficient and results in a minor loss the vitamin.

Another mode of excretion is by urine. When there is an excess B12 in the blood, it gets filtered by kidneys and excreted through urine.

FUNCTIONS

Given below are the diverse functions of Vitamin B12:

Being a part of Vitamin Bs, it is involved in the metabolism of proteins, fats, and carbohydrates.
It also has a role in erythropoiesis or red blood cell formation.
It is required for DNA & RNA synthesis and is important for the development and maturation of red blood cells.
Also, for proper cell division, growth and repair, an adequate amount of vitamin B12 is essential.
It is involved in synthesis of myelin. Myelin is found in the long axonal region of a neuron. It facilitates fast impulse transmission and acts as a protective layer.
Adequate B12 levels are also associated with good cardiovascular and mental health.

RECOMMENDED INTAKE

Vitamin B12 recommended intake values vary with age and gender. They are provided in the Dietary Reference Intakes (DRIs) developed by the Food and Nutrition Board (FNB) at the National Academies of Sciences, Engineering, and Medicine.

Adequate Intake (AI) : set for recommended intake for infants
0-6 months	0.4 μg/day	≈0.05 μg/kg
7-12 months	0.5 μg/day	≈0.05 μg/kg

Recommended Dietary Allowance (RDA) : measures an average daily intake that is sufficient to meet the nutrient requirements of nearly all healthy individuals.
1-3 yrs	For children	0.9 μg/day
4-8 yrs	For children	1.2 μg/day
9-13 yrs	For boys	1.8 μg/day
9-13 yrs	For girls	1.8 μg/day
14-18 yrs	For boys	2.4 μg/day
	For girls	2.4 μg/day
	For pregnancy	2.6 μg/day
	For lactation	2.8 μg/day
19-30 yrs	For men	2.4 μg/day
	For women	2.4 μg/day
	For pregnancy	2.6 μg/day
	For lactation	2.8 μg/day
31-50 yrs	For men	2.4 μg/day
	For women	2.4 μg/day
	For pregnancy	2.6 μg/day
	For lactation	2.8 μg/day
51-70 yrs	For men	2.4 μg/day
51-70 yrs	For women	2.4 μg/day
>70 yrs	For men	2.4 μg/day
>70 yrs	For women	2.4 μg/day

Estimated Average Requirement (EAR) measures an average daily intake that meets the requirements of 50% of healthy individuals.
1-3 yrs	For children	0.7 μg/day
4-8 yrs	For children	1 μg/day
9-13 yrs	For boys	1.5 μg/day
9-13 yrs	For girls	1.5 μg/day
14-18 yrs	For boys	2 μg/day
	For girls	2 μg/day
	For pregnancy	2.2 μg/day
	For lactation	2.4 μg/day
19-30 yrs	For men	2 μg/day
	For women	2 μg/day
	For pregnancy	2.2 μg/day
	For lactation	2.4 μg/day
31-50 yrs	For men	2 μg/day
	For women	2 μg/day
	For pregnancy	2.2 μg/day
	For lactation	2.4 μg/day
51-70 yrs	For men	2 μg/day
51-70 yrs	For women	2 μg/day
>70 yrs	For men	2 μg/day
>70 yrs	For women	2 μg/day

REFERENCES

Institute of Medicine (US) Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. Washington (DC): National Academies Press (US); 1998. 9, Vitamin B12. Available from: https://www.ncbi.nlm.nih.gov/books/NBK114302/

Institute of Medicine (1998). "Vitamin B₁₂". Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B₆, Folate, Vitamin B₁₂, Pantothenic Acid, Biotin, and Choline. Washington, DC: The National Academies Press. pp. 306–356. ISBN 978-0-309-06554-2.

Vitamin B12-Fact Sheet for Medical Professionals. National Institutes of Health (NHI). Retrieved from https://ods.od.nih.gov/factsheets/VitaminB12-HealthProfessional/#en1

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Aloe Vera : A Sustainable Disinfectant

Dev Aditya Tomar — Sat, 15 Oct 2022 11:30:12 +0000

The name Aloe vera derives from the Arabic word “Alloeh” meaning “shining bitter substance,” while “vera” in Latin means “true.” 2000 years ago, the Greek scientists regarded Aloe vera as the universal panacea. The Egyptians called Aloe “the plant of immortality.”

The botanical name of Aloe vera is Aloe barbadensis miller. It belongs to the Asphodelaceae (Liliaceae) family, and is a shrubby or arborescent, perennial, xerophytic, succulent, pea- green color plant. It grows mainly in the dry regions of Africa, Asia, Europe, and America. In India, it is found in Rajasthan, Andhra Pradesh, Gujarat, Maharashtra, and Tamil Nadu. [1]

This post is a continuation of 'Hazards of Disinfectants' and is the second part of my Class 12th Chemistry Investigatory Project 'Isolation, Evaluation and Analysis of Anti-Microbial Agents from Aloe vera'. It describes with the historical significance of Aloe vera and its uses in Ayurveda. The post also expands on the properties and side effects of Aloe and the reason why the plant exhibits these properties (i.e. Active Components). This condensed information is provided so as to encourage and prove that there are more holistic and sustainable methods of acquiring disinfectants from nature.

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HISTORY

Fig 1-1: Papyrus Eber

The first known written report of the aloe vera plant reach as far back as 6,000 years ago in ancient Egypt. Aloe was regarded as a pious plant the “blood” of which held the secrets to beauty, health, and immortality. Even the dead were embalmed with aloe vera because of its anti-microbial qualities. Its anti-inflammatory effects were written down in the “papyrus Eber” of 1,550 BC (Fig 1-1).

The earliest documentation of Aloe vera was identified on the clay boards from Nippur(Mesopotamia) which dates back as long ago as 2,200 BC. The people of this era were aware of the cleansing and soothing effect of aloe on the intestines. In this period of history, illnesses were always regarded as demonic possession of the body and only a divine plant such as aloe had the natural power to exorcise the demons.

The Japanese culture also greatly values the aloe plant, in Japan it was known as the “royal plant”, the juice was consumed as an elixir and the samurai used it for embrocation.

Fig 1-2: Ayurvedic Tridoshas

In Sanskrit, aloe vera is known as Ghrita-Kumari. Kumari means girl and it was believed that this plant supplied the energy of youth to women and had a rejuvenating effect on the female nature. In the Indian ayurvedic medicine, aloe is applied in numerous applications such as rejuvenating remedies, for menorrhoea problems and to stabilise the cardiovascular system. Aloe is regarded as the plant of balance between pitta, kapha and vata (Fig 1-2) – the aloe is one of very few plants that hold these qualities!

During the 16th century, the Indian tribes also became familiar with the aloe healing plant. Aloe was one of the 16 holy plants which were worshiped with a god like status. The diluted aloe juice that they applied to their skin worked as an insect repellent protecting them on their exhausting marches through the infested swamp areas. The Indians also used the aloe insect repellent on wood and other vulnerable materials that were likely to be damaged by insects; this treatment preserved the materials with great effect.[2]

ALOE VERA AND AYURVEDA

Medicine is an ancient art and drugs have been used as long far back as history can take us. Human life has remained dependent on plants for daily life purposes as well as medicinal uses.

Vedas are the foremost text of Hindus. Rigveda has quoted that drugs are three yuga older than gods. Vedas have given importance of drugs and classified them. Later, in Samhitas and Nighantus knowledge of drugs developed vigorously, causing detailed knowledge as well as controversies.

Kumari (or Aloe vera) is one of the non-controversial plant and extremely popular these days. It is the known drug for wound healing, burns, hepatoprotective and immunomodulator. Kumari was first described in Bhela Samhita as an ingredient of Rasna tail in Vatavyadhichikitsa.

Acharya Madhava, in his Madhava Dravya Guna, has mentioned it in Vividha Aushadhi Varga and indicated it in Yakrit roga (Liver-related disease), Pliha roga (Spleen-related disease), Kapha roga and Jwara (Fever).

In Rasa Ratna Samuchchaya, the application of the paste of Kumari juice with Jiraka (Cumin) has been indicated to pacify the burning sensation and suppuration in Lingapaka.

Ravna in Arkaprakasha has written in Netrya gana that Girikanya’s Arka(distilllation) is useful in leprosy, pain, wounds, and poisoning. He has again mentioned that Kumari is indicated in burning etc.

The properties of kumari (mentioned in Ayurveda Vigyanam) are :

Agnijanana (digestive), Pittanirharana, Balakara (strength promoter), Rechana (laxative), Garbhpatana (abortificent).

It has been indicated in constipation, Krimiroga (Worm-related intestinal infection), anxiety, epilepsy, amenorrhea, urticaria, headache, fever, spleen diseases and Mandaagni (Excessive Kapha).

ANATOMY OF ALOE VERA

Fig 3-3: Anatomy of Aloe vera

(Fig 3-3) The plant has triangular, fleshy leaves with serrated edges, yellow tubular flowers and fruits that contain numerous seeds. Each leaf is composed of three layers:

An inner clear gel that contains 99% water and rest is made of glucomannans, amino acids, lipids, sterols, and vitamins.
The middle layer of latex which is the bitter yellow sap and contains anthraquinones and glycosides.
The outer thick layer of 15–20 cells called as rind which has protective function and synthesizes carbohydrates and proteins. Inside the rind are vascular bundles responsible for transportation of substances such as water (xylem) and starch (phloem). [3]

PROPERTIES AND ACTIONS

HEALING PROPERTY:

Active compounds in aloe vera gel interact with growth factor receptors on the fibroblast, thereby stimulating its activity and proliferation, which in turn significantly increases collagen synthesis.
Aloe gel not only increased collagen content of the wound but also changed collagen composition and increased the degree of collagen cross linking.
Due to this, it accelerated wound contraction and increased the breaking strength of resulting scar tissue. [4]

EFFECT ON SKIN EXPOSURE TO UV & GAMMA RADIATION:

Aloe vera gel has been reported to have a protective effect against radiation damage to the skin. [5] [6]
It reduces the production and release of skin keratinocyte-derived immunosuppressive cytokines and hence prevents UV-induced suppression of delayed type hypersensitivity. [7]

LAXATIVE EFFECT:

Active ingredients like anthraquinones present in latex are a potent laxative.
It increases intestinal water content, stimulates mucus secretion, and increases intestinal peristalsis. [8]

ANTISEPTIC EFFECT:

Aloe vera contains 6 antiseptic agents: Lupeol, salicylic acid, urea, nitrogen, cinnamomic acid, phenols, and sulphur; and have inhibitory action on fungi, bacteria, and viruses.

ANTI-VIRAL & ANTI-TUMOR ACTIVITY:

These actions may be due to indirect or direct effects. Indirect effect is due to stimulation of the immune system and direct effect is due to anthraquinones.
The anthraquinone aloin inactivates various enveloped viruses such as herpes simplex, varicella zoster and influenza. [9]

MOISTURIZING & ANTI-AGING EFFECT:

Mucopolysaccharides help in binding moisture into the skin. Aloe stimulates fibroblast which produces the collagen and elastin fibres making the skin more elastic and less wrinkled.
It also has cohesive effects on the superficial flaking epidermal cells by sticking them together, which softens the skin.

SIDE EFFECTS

TOPICAL:

It may cause redness, burning, stinging sensation and rarely generalized dermatitis in sensitive individuals.
Allergic reactions are mostly due to anthraquinones, such as aloin and barbaloin.

ORAL:

Abdominal cramps, diarrhoea, red urine, hepatitis, dependency or worsening of constipation.
Prolonged use has been reported to increase the risk of colorectal cancer.oLaxative effect may cause electrolyte imbalances (low potassium levels)

PREGNANCY & BREASTFEEDING:

Oral aloe is not recommended during pregnancy due to theoretical stimulation of uterine contractions.
In breastfeeding mothers, it may sometime cause gastrointestinal distress in the nursing infant.

Thus, though Aloe vera has wide spectrum of the properties and uses, some of them could be myths and some of them could be the truth. In future, controlled studies are required to prove the effectiveness of Aloe vera under various conditions.

ACTIVE COMPOUNDS IN ALOE

Any component that provides pharmacological activity or other direct effect in the diagnosis, cure, mitigation, treatment, or prevention of disease, or affects the structure or any function of the body of man or animals.[10]

Aloe vera contains 75 potentially active compounds like: [11]

VITAMINS:

Fig 6.1-4: Vitamin structures

It contains vitamins A (beta-carotene), C and E, which are antioxidants. It also contains vitamin B12, folic acid, and choline.
Function - Neutralizes free radicals.

ENZYMES:

It contains 8 enzymes: aliiase, alkaline phosphatase, amylase, bradykinase, carboxypeptidase, catalase, cellulase, lipase, and peroxidase.
Functions -
Bradykinase helps to reduce excessive inflammation when applied to the skin topically
Others help in the breakdown of sugars and fats.

MINERALS:

It provides calcium, chromium, copper, selenium, magnesium, manganese, potassium, sodium, and zinc.
Functions - They are essential for the proper functioning of various enzyme systems in different metabolic pathways and few are antioxidants.

SUGARS:

Fig 6.4-5: Mannose-6-phosphate

It provides monosaccharides (glucose and fructose) and polysaccharides: (glucomannans/polymannose).
These are derived from the mucilage layer of the plant and are known as mucopolysaccharides.
The most prominent monosaccharide is mannose-6-phosphate (Fig 6.4-5), and the most common polysaccharides are called glucomannans.

ANTHRAQUINONES:

It provides 12 anthraquinones, which are phenolic compounds traditionally known as laxatives.
Function – Aloin and emodin act as analgesics, antibacterials and antivirals.

FATTY ACIDS:

It provides 4 plant steroids: cholesterol, campesterol, β-sisosterol and lupeol.
Function - All these have anti-inflammatory action and lupeol also possesses antiseptic and analgesic properties.

HORMONES:

Auxins and gibberellins that help in wound healing and have anti-inflammatory action.

OTHERS:

Fig 6.8-6: Lignin

It provides 20 of the 22-human required amino acids and 7 of the 8 essential amino acids.
It also contains salicylic acid that possesses anti-inflammatory and antibacterial properties.
Lignin (Fig 6.8-6), an inert substance, enhances penetrative effect of the other ingredients into the skin.
Saponins that are the soapy substances form about 3% of the gel and have cleansing and antiseptic properties.

ANTIMICROBIAL ACTIVITY OF ACTIVE COMPOUNDS

There are mentions of many compounds with anti-bacterial anti-viral and anti-septic properties in the topic above. Some examples are Aloin, Emodin, Lupeol, Salicylic acid and Saponins. Following is a brief about their properties.

ALOIN & ALOE EMODIN [ANTHRAQUINONE]:

Fig 7.1-8 : Structure of Aloin and Aloe Emodin

Aloin is a bitter yellow brown coloured compound noted in the exudate of many Aloe species. Aloin, extracted from natural sources, is a mix of two diastereomers; namely, Aloin A (Barbaloin) [12] and Aloin B (Isobarbaloin), with both having similar chemical properties. (Fig 7.1-8) It increases peristaltic movements in the colon, inducing bowel movements. It also prevents the colon from reabsorbing water, resulting is softer stools.

Aloe Emodin, one of many types of Emodin, is also found in the exudate of many Aloe species.

Fig 7.1-7 : Activity of Aloin and Aloe Emodin

In a joint research by Institute of Environmental and Agricultural Chemistry, Università Cattolica del Sacro Cuore, Italy; Department of Crop Science, Breeding and Plant Medicine, Mendel University in Czech Republic; & Department of Agrochemistry, Soil Science, Microbiology and Plant Nutrition, Mendel University in Czech Republic; an observation was made that Aloin and aloe emodin mostly act on gram positive bacteria. (Tab 7.1-7) [13]

The pure aloin standard solution was the most effective against B. licheniformis, while S. boulardii was the least affected microorganism. Pure aloe emodin standard solution reduced the growth of B. licheniformis. [13]

The standard solution of aloin showed a middle or lower effect against all microorganisms and, except S. boulardii, with the antibacterial activity increasing with time. The standard solution of aloe emodin had a stronger effect than the previous and showed fluctuating activity against B. licheniformis, S. boulardii, and S. epidermidis, first increasing, plummeting, and then increasing again. [13]

LUPEOL [FATTY ACID]:

Fig 7.2-9 : Structure of Lupeol

(Fig 7.2-9) Lupeol, naturally found in mango, pepper, cucumber, strawberry, red grapes, and Aloe species, has complex pharmacological activities. It is displaying antiprotozoal, antimicrobial, anti-inflammatory, anti-tumor, and chemo preventive properties. [14]

SALICYLIC ACIDS:

Fig 7.3-10 : Structure of Salicylic acid

(Fig 7.3-10) Salicylic acid is lipophilic mono-hydroxy benzoic acid and is also a ß-hydroxy acid. It is a colourless crystalline organic acid and is called as the safest and most effective medicines needed in a health care system - bye WHO’s List of Essential Medicines. [15]

Salicylic acid as a medication is used most to help remove the outer layer of the skin. Bismuth subsalicylate is used as stomach relief aid and is a salt of bismuth and salicylic acid. It is. Also used as food preservative, a bactericidal and an antiseptic. [16]

SAPONINS:

Fig 7.4-11 : Structure of Saponins

(Fig 7.4-11) Saponins are phytochemicals which can be found in most vegetables, beans, and herbs. The best-known sources of saponins are peas, soybeans, and some herbs. They are soapy substances and have cleansing and antiseptic properties.

REFERENCES

[1] Surjushe, A., Vasani, R., & Saale, D.G. (2008). Aloe vera: A Short Review. Indian Journal of Dermatology. 53:163-6
[2] Medicinal plants of ancient (n.d.). Aloe Medical Group International. Retrieved June 13 2020 from https://www.aloe-medical-group.com/en/aloe-vera/history.html
[3] Tyler V. The honest herbal: A sensible guide to the use of herbs and related remedies. 3rd ed. Binghamton, New York: Pharmaceutical Products Press; 1993.
[4] Heggers JP, Kucukcelebi A, Listengarten D, Stabenau J, Ko F, Broemeling LD, Robson MC, Winters WD J Altern Complement Med. 1996 Summer; 2(2):271-7.
[5] Roberts DB, Travis EL Int J Radiat Oncol Biol Phys. 1995 Jul 15; 32(4):1047-52.
[6] Sato Y, Ohta S, Shinoda M Yakugaku Zasshi. 1990 Nov; 110(11):876-84.
[7] Byeon SW, Pelley RP, Ullrich SE, Waller TA, Bucana CD, Strickland FM J Invest Dermatol. 1998 May; 110(5):811-7.
[8] Ishii Y, Tanizawa H, Takino Y Biol Pharm Bull. 1994 May; 17(5):651-3.
[9] Sydiskis RJ, Owen DG, Lohr JL, Rosler KH, Blomster RN Antimicrob Agents Chemother. 1991 Dec; 35(12):2463-6.
[10] active ingredient. (n.d.) Medical Dictionary for the Health Professions and Nursing. (2012). Retrieved June 13 2020 from https://medical-dictionary.thefreedictionary.com
[11] Amar Surjushe, Resham Vasani, D G Saple. Aloe vera: A Short Review. Indian J Dermatol. 2008; 53(4): 163–166. doi:10.4103/0019-5154.44785
[12] Reynolds T, ed. (January 2004). Aloes: the genus Aloe. CRC press.

[13] Pellizzoni, M., Ruzickova, G., Kalhotka, L. and Lucini, L. Antimicrobial activity of different Aloe barbadensis Mill. and Aloe arborescens Mill. leaf fractions. Journal of Medicinal Plants Research Vol. 6(10), pp. 1975-1981, 16 March 2012
[14] Margareth B. C. Gallo; Miranda J. Sarachine (2009). "Biological activities of Lupeol" (PDF). International Journal of Biomedical and Pharmaceutical Sciences. 3 (Special Issue 1): 46–66.
[15] World Health Organization (2019). World Health Organization model list of essential medicines: 21st list 2019. Geneva: World Health Organization.
[16] "Definition of Salicylic acid". Retrieved from MedicineNet.com.

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