Dr. Hanjabam Barun, Medical-Clinical & Interventional Physiologist

25/10/2025

📌Physiology of balance.

👉 (A) The visual system provides information on the surrounding environment; the vestibular system, consisting of the two inner-ear balance organs and several nervous structures (nerves and central nuclei), encodes angular and linear accelerations of the head to support the clear vision and balance control via rapid eye movements (vestibulo-ocular reflexes) and postural reflexes (vestibulo-spinal reflexes); the somatosensory system senses self-movement and body position through specialised sensory receptors located in the muscles (muscle spindles), joints (Ruffini endings, Pacinian corpuscles, and Golgi-like receptors), tendons (Golgi tendon organs), and skin (Merkel cells, Ruffini endings, Meissner corpuscles, and Pacinian corpuscles) .

👉 (B) Multisensory signals from visual, vestibular and somatosensory receptors are integrated in the central nervous system to provide an internal postural model and in turn, descending motor commands to muscles.

👉(C) Reactive postural strategies and anticipatory postural adjustments allow balance control under environmental circumstances (e.g., external postural perturbations) and motor initiative (e.g., voluntary movement), respectively.

Article 👇

25/10/2025

Breathing during core exercises can be broken down in three main core categories including long and short breathing, braced breathing, and pulsed breathing. Learn more in Developing the Core and click on the comments below to get a link to the book.

25/10/2025

Factors affecting microbiota-associated chronic inflammation in healthy and disease state👇

✅Healthy State (Left Side)

🔴Balanced microbiota: Diverse, stable microbial populations produce beneficial metabolites such as short-chain fatty acids (SCFAs).

🔴Protective mucus layer: SCFAs stimulate the production of antimicrobial peptides and mucin, which strengthen the mucus barrier.

🔴Intestinal barrier: The epithelial layer remains intact and impermeable, preventing bacterial entry into underlying tissues.

🔴Immune balance:

📎Increased Treg (regulatory T cells) maintain immune tolerance.

📎Decreased Teff (effector T cells) reduce inflammatory responses.

📎Production of anti-inflammatory cytokines dominates.

🔴Outcome: Proper barrier function and immune homeostasis prevent inflammation.

✅Disease State (Right Side)

🔴Microbial imbalance (dysbiosis): Loss of beneficial bacteria and expansion of pathobionts (potentially harmful bacteria).

🔴LPS (lipopolysaccharides): Released from pathogenic bacteria, triggering inflammation.

🔴Reduced mucus protection: Decreased secretion of mucin and antimicrobial peptides, allowing bacterial pe*******on into epithelial tissues.

🔴Dysfunctional barrier: The epithelial layer becomes leaky, enabling microbes and toxins to cross.

🔴Immune dysregulation:

📎Decreased Treg cells and increased Teff cells.

📎Overproduction of proinflammatory cytokines.

📎Activation of macrophages and dendritic cells (DCs) leads to chronic inflammation.

🔴Outcome: Persistent immune activation and tissue damage perpetuate inflammation.
💡 Hou, K., Wu, ZX., Chen, XY. et al. Microbiota in health and diseases. Sig Transduct Target Ther 7, 135 (2022).

25/10/2025

Comparing biomarker profiles measured at similar ages, but earlier in life, among exceptionally long-lived individuals and their shorter-lived peers can improve our understanding of aging processes. This study aimed to (i) describe and compare biomarker profiles at similar ages between 64 and 99 among individuals eventually becoming centenarians and their shorter-lived peers, (ii) investigate the association between specific biomarker values and the chance of reaching age 100, and (iii) examine to what extent centenarians have homogenous biomarker profiles earlier in life. Participants in the population-based AMORIS cohort with information on blood-based biomarkers measured during 1985–1996 were followed in Swedish register data for up to 35 years. We examined biomarkers of metabolism, inflammation, liver, renal, anemia, and nutritional status using descriptive statistics, logistic regression, and cluster analysis. In total, 1224 participants (84.6% females) lived to their 100th birthday. Higher levels of total cholesterol and iron and lower levels of glucose, creatinine, uric acid, aspartate aminotransferase, gamma-glutamyl transferase, alkaline phosphatase, lactate dehydrogenase, and total iron-binding capacity were associated with reaching 100 years. Centenarians overall displayed rather homogenous biomarker profiles. Already from age 65 and onwards, centenarians displayed more favorable biomarker values in commonly available biomarkers than individuals dying before age 100. The differences in biomarker values between centenarians and non-centenarians more than one decade prior death suggest that genetic and/or possibly modifiable lifestyle factors reflected in these biomarker levels may play an important role for exceptional longevity.

Comparing biomarker profiles measured at similar ages, but earlier in life, among exceptionally long-lived individuals and their shorter-lived peers can improve our understanding of aging processes. This study aimed to (i) describe and compare biomarker profiles at similar ages between 64 and 99 amo...

24/10/2025

24/10/2025

The gut-brain axis integrates 4 primary streams of signals:

🧠 1. Neural Pathway
The vagus nerve and enteric nervous system (ENS) transmit afferent signals from the gut to the brain. Microbial metabolites and host-derived neurotransmitters (e.g., serotonin, dopamine, GABA) influence mood, cognition, and stress responses. Enteroendocrine and enterochromaffin cells release neuroactive compounds in response to microbial cues.

🧬 2. Endocrine Pathway
The gut microbiota modulates HPA axis activity through changes in gut barrier integrity, circulating metabolites, and stress hormones. Cortisol, released from the adrenal cortex, affects both systemic inflammation and brain function. Microbiota-regulated hormones such as GLP-1, CCK, and ghrelin further influence appetite, mood, and behavior.

🦠 3. Immune Pathway
Microbial antigens (PAMPs) and metabolites interact with intestinal immune cells (e.g., Th1, Th17, dendritic cells), influencing systemic and neuroinflammatory tone. Elevated cytokines like TNF-α, IL-1, and IL-6 have been linked to blood-brain barrier disruption, depression, and cognitive impairment.

🔁 4. Metabolic Pathway
The gut microbiota ferments dietary components (e.g., fiber, protein, bile acids) into signaling molecules including:

-SCFAs (butyrate, propionate)
-Secondary bile acids
-Branched-chain amino acids (BCAAs)

These metabolites affect energy regulation, neurotransmission, and epigenetic signaling within the CNS and peripheral tissues.

23/10/2025

🧠 The Neuroscience Of Why Sleep Teaches Better Than Studying

Most people think learning happens when they’re reading, revising, or solving problems. But neuroscience reveals something more powerful, real learning happens while you sleep.

When you study, your brain’s hippocampus acts like a temporary storage drive. It holds new information and short-term memories. But these connections are fragile and can fade within hours unless they’re consolidated.

That’s where deep sleep comes in.

During the slow-wave phase of non-REM sleep, the hippocampus replays neural activity patterns that occurred during learning. This replay activates the neocortex, which gradually integrates those memories into long-term storage. Think of it as the hippocampus “teaching” the neocortex what you learned that day.

This process is known as memory consolidation, and it’s essential for turning short-term knowledge into stable, retrievable memories.

Brain imaging studies at the University of Lübeck and Harvard Medical School show that students who sleep after studying perform significantly better on recall and problem-solving tests compared to those who stay awake. Sleep not only strengthens existing connections but also prunes irrelevant ones, sharpening understanding and retention.

Pulling all-nighters, on the other hand, floods the brain with stress hormones, disrupts hippocampal replay, and blocks the very mechanisms needed to store what you studied. It’s like writing an essay and never pressing save.

Sleep Smart: Why You Learn More in Bed Than at Your Desk: https://www.patreon.com/posts/141878781

23/10/2025

💔 NSTEMI vs STEMI: When the Heart Cries for Help 💔

Every heartbeat fuels life — but when the heart’s own blood supply is cut off, time becomes muscle. This visual shows the dramatic difference between NSTEMI (Non-ST Elevation Myocardial Infarction) and STEMI (ST Elevation Myocardial Infarction) — two emergencies with one common enemy: coronary artery blockage.

🔸 NSTEMI occurs when a coronary artery is severely narrowed but not completely blocked. Blood flow still trickles through, but not enough to meet the heart’s oxygen demand. The result? Partial-thickness damage or subendocardial necrosis — the inner layer of the heart muscle begins to die.
On the ECG, there’s ST-segment depression or T-wave inversion, subtle hints that the heart is struggling. The patient may feel pressure, heaviness, or chest discomfort — but without the dramatic ECG spikes seen in STEMI. It’s a silent but serious warning that a complete blockage may soon follow if untreated.

🔴 STEMI, on the other hand, is an all-out attack. Here, the artery is completely occluded, and blood flow stops entirely. The heart muscle supplied by that vessel begins to die across its full thickness — a transmural necrosis. On ECG, this appears as the classic ST-segment elevation, a red flag screaming for immediate reperfusion. The faster the artery is reopened — via PCI (angioplasty) or thrombolytic therapy — the more muscle can be saved.

In short:
⚡ NSTEMI = Partial blockage → partial muscle death → ST depression
🔥 STEMI = Complete blockage → full-thickness muscle death → ST elevation

Both are heart attacks — but STEMI is the five-alarm fire, demanding rapid, aggressive action. The ECG tells the story, but the heart tells the truth. Every minute counts because in myocardial infarction, time truly is muscle. ❤️‍🔥

Disclaimer: Image Credit to the rightful Owner.

23/10/2025

23/10/2025

Temporal control of eating and body weight by GHSR-expressing suprachiasmatic nucleus neurons

http://dlvr.it/TNrD6v

23/10/2025

Do we need to move from 'MTSS' to 'LIMP' 🤔

Our latest digs into why the labelling of what we currently know as Medial Tibial Stress Syndrome should change...

Read why 👉 https://ow.ly/CqpB50X6tpr