Centro Fisioterapia e Osteopatia Martinelli Gianluca

13/04/2026

Exercising while sleeping less than 7 hours per night might do more harm than good: a study linked that pattern to biological signs of premature aging!

And vice versa: slowed biological aging with more sleep.

😮 I’d never work out again if I stuck to days when I had more than 7 hours sleep!

But here we go with CORRELATIONS again, sigh. Every time you hear “link” or “association,” always ask: rather than causing each other, maybe both caused by something else?

For instance: maybe many people sleep AND age poorly for shared reasons! (Also, self-reported sleep is super sloppy data.)

SOURCE: PMID 38486063

~ Paul Ingraham, PainScience.com publisher

12/04/2026

Vitamin B12 is absorbed through two pathways. The first is intrinsic factor, a protein produced by parietal cells in the stomach. IF binds B12 in the small intestine and carries it across the gut wall via a receptor called cubilin in the distal ileum. This pathway is efficient but has a hard ceiling: it saturates at roughly 1.5 µg per dose. No matter how much B12 you swallow beyond that, IF cannot carry any more.

The second pathway is passive diffusion. About 1 to 2% of any oral dose diffuses across the intestinal lining without IF, and this occurs along the entire length of the gut. At dietary doses, this pathway is negligible. At supplement doses, it becomes the primary route of absorption.
Adams et al. (1971, Scand J Gastroenterol) measured whole body retention of radiolabeled cyanocobalamin at different doses. At 1 µg, roughly 50% was retained. At 5 µg, about 20%. At 25 µg, just over 5%. The NIH Office of Dietary Supplements reports approximately 2% absorption at 500 µg and 1.3% at 1,000 µg.

The fraction drops dramatically. But the total amount absorbed keeps rising. At 1 µg you absorb about 0.5 µg. At 1,000 µg you absorb roughly 13 µg total, of which approximately 10 µg comes from passive diffusion alone. The RDA is 2.4 µg. Even the backup pathway, working at 1% efficiency, delivers more than four times your daily requirement from a single pill.

This is the basis for high-dose oral B12 as an alternative to injections in patients who lack intrinsic factor. The NIH notes that high-dose oral supplementation "may be another treatment option" for pernicious anemia, though injections remain standard first-line therapy and the available randomized controlled trials comparing the two approaches are considered limited in quality.
One important nuance: absorbing B12 into your bloodstream is only the first step. After absorption, B12 must bind to a transport protein called transcobalamin to reach your cells. This complex, holotranscobalamin, is the biologically active fraction. It represents only about 20 to 30% of the total B12 circulating in your blood. The remaining 70 to 80% rides on a separate protein called haptocorrin, which does not deliver B12 to most tissues.

This is why serum B12 can be misleading as a status marker. A person can have a "normal" total serum B12 level while their holotranscobalamin, the fraction that actually delivers B12 to cells, is low. Methylmalonic acid is a more sensitive functional marker because it rises when cellular B12 is genuinely insufficient, regardless of what total serum B12 shows.

Absorption determines how much B12 enters your blood. Transport determines how much reaches your cells. Testing only total serum B12 measures neither of these processes accurately.

Adams et al., Scand J Gastroenterol, 1971
NIH Office of Dietary Supplements, 2024
Allen et al., J Nutr, 2018

12/04/2026

Most people think Vitamin D is “just a vitamin," and, indeed, it is a vitamin… but this chart shows it behaves more like a hormone (a feature of several vitamins) that controls hundreds of processes in your body.

Sunlight hits your skin → your liver rewires the molecule → your kidneys activate it → and then this tiny hormone starts regulating everything from immunity to calcium to gene expression.

This diagram shows what textbooks never make simple:

Vitamin D is controlling your:

☀️ Immune response
☀️ Bone building
☀️ Muscle function
☀️ Hormone signaling
☀️ Cell growth & cell death
☀️ Inflammation
☀️ Cancer-protective pathways
☀️ Calcium & phosphorus absorption
☀️ Even gene transcription inside the nucleus

Every cell with a Vitamin D receptor (VDR) is listening.
That includes your brain, thyroid, pancreas, immune cells, prostate, breast tissue, colon, bones, and more.

Look at what’s happening in the diagram:

🔸 UVB light converts 7-dehydrocholesterol in the skin into previtamin D₃
(this step only activates with the right wavelength of sunlight)

🔸 The liver turns it into 25(OH)D3 (the lab marker everyone measures)
This is the “circulating form” (the one your doctor tests).

🔸 The kidney turns THAT into the active hormone, 1,25(OH₂)D3
This is the molecule that actually controls your genes.

🔸 Immune cells can ALSO activate Vitamin D on their own
Meaning your vitamin D status directly affects how strongly or weakly your immune system reacts.

🔸 Bones, thyroid, parathyroid, and gut are all communicating using this one signaling molecule
A full endocrine network most people never knew existed.

Vitamin D isn't just about “strong bones.”
It’s a biochemical communication system that your entire physiology depends on.

And deficiency doesn’t just cause low energy, it disrupts every node in this network.

Sunlight, diet, supplements, metabolism, inflammation, liver health, kidney function…
They all determine whether this system works or collapses.

source:
Holick, M. F. (2014). Cancer, sunlight and vitamin D. Journal of Clinical & Translational Endocrinology, 1(4), 179–186

06/04/2026

𝐓𝐡𝐞 𝐇𝐢𝐝𝐝𝐞𝐧 𝐂𝐮𝐥𝐩𝐫𝐢𝐭 𝐁𝐞𝐡𝐢𝐧𝐝 𝐋𝐨𝐰𝐞𝐫 𝐁𝐚𝐜𝐤 𝐏𝐚𝐢𝐧: 𝐔𝐧𝐝𝐞𝐫𝐬𝐭𝐚𝐧𝐝𝐢𝐧𝐠 𝐭𝐡𝐞 𝐂𝐚𝐫𝐭𝐢𝐥𝐚𝐠𝐢𝐧𝐨𝐮𝐬 𝐄𝐧𝐝𝐩𝐥𝐚𝐭𝐞 𝐚𝐧𝐝 𝐈𝐧𝐭𝐞𝐫𝐯𝐞𝐫𝐭𝐞𝐛𝐫𝐚𝐥 𝐃𝐢𝐬𝐜 𝐃𝐞𝐠𝐞𝐧𝐞𝐫𝐚𝐭𝐢𝐨𝐧

⬛ Low back pain (LBP) is one of the leading causes of disability worldwide, and a primary driver of this pain is Intervertebral Disc Degeneration (IDD). While many of us imagine IDD as simply a "slipped" or "worn out" disc, a recent comprehensive review article sheds light on a less-discussed but critically important structure in the spine: the cartilaginous endplate (CEP).

𝐓𝐡𝐞 𝐒𝐩𝐢𝐧𝐞’𝐬 𝐍𝐮𝐭𝐫𝐢𝐭𝐢𝐨𝐧𝐚𝐥 𝐁𝐫𝐢𝐝𝐠𝐞: 𝐖𝐡𝐚𝐭 𝐢𝐬 𝐭𝐡𝐞 𝐂𝐄𝐏?

⬛ The intervertebral disc (IVD) holds a unique distinction: it is the largest avascular (blood vessel-free) structure in the human body. Because it lacks a direct blood supply, it relies almost entirely on surrounding structures for nutrients and waste removal.
⬛ The CEP is a thin layer of translucent cartilage located at the top and bottom edges of the vertebral bodies. It serves two vital roles:

🧩 Mechanical Support: It anchors the disc and evenly distributes compressive loads.
🩸 The Nutrient Highway: The CEP houses a dense microvascular network that acts as a "bridge" for nutrient diffusion. Research indicates that axial nutrient diffusion (through the CEP) is three times higher than radial diffusion (through the outer disc).
⬛ When the CEP degrades—becoming stiffer, less permeable, and calcified—it essentially starves the disc of nutrients, initiating the cascade of IDD.

𝐅𝐢𝐯𝐞 𝐊𝐞𝐲 𝐓𝐫𝐢𝐠𝐠𝐞𝐫𝐬 𝐨𝐟 𝐂𝐄𝐏 𝐃𝐞𝐠𝐫𝐚𝐝𝐚𝐭𝐢𝐨𝐧

⬛ The breakdown of the CEP is a slow, complex process driven by several distinct factors.
⏳ Natural Degeneration: The human CEP actually begins degenerating around age 2. As we age, cell apoptosis accelerates, calcified foci form, and the microvascular network shrinks, severely reducing nutrient diffusion.
🧬 Genetics: IDD has a surprisingly strong familial link. Twin studies show that up to 74% of lumbar disc degeneration variation can be attributed to genetic factors. Mutations in genes coding for essential structural collagens, such as COL2A1 and COL9A2, directly accelerate matrix degradation and CEP calcification.
🛡️ Immune Responses: A healthy IVD is considered an "immune-privileged" tissue, completely isolated from the body's immune system by the CEP barrier. When the CEP is damaged, this barrier breaks. Immune cells flood the disc, recognizing the inner tissue as foreign, and launch an aggressive inflammatory response that further destroys the tissue.
🏋️ Mechanical Injury: Chronic high-load axial pressure can crack the weak center of the CEP. This allows the inner disc material to protrude into the bone, forming what are known as Schmorl's nodes.
🚬 Smoking: Ni****ne constricts the microvascular network within the CEP and significantly reduces the concentration of glycosaminoglycan (GAG), a crucial protein for maintaining disc elasticity. Even passive smoking has been shown to alter the circadian rhythms of disc cells.

𝐓𝐡𝐞 𝐕𝐢𝐜𝐢𝐨𝐮𝐬 𝐂𝐲𝐜𝐥𝐞: 𝐌𝐨𝐝𝐢𝐜 𝐂𝐡𝐚𝐧𝐠𝐞𝐬

⬛ The article highlights a critical imaging finding known as Modic changes—which are MRI signal changes in the vertebral bone marrow adjacent to a damaged disc.
⬛ A damaged CEP acts as a leaky filter, allowing inflammatory proteins and matrix-degrading enzymes to escape the disc and irritate the surrounding bone. In turn, the bone marrow's immune response further attacks the CEP.
⬛ This creates a vicious, positive feedback loop of inflammation and degeneration that is notoriously difficult to stop.

𝐄𝐦𝐞𝐫𝐠𝐢𝐧𝐠 𝐓𝐫𝐞𝐚𝐭𝐦𝐞𝐧𝐭𝐬: 𝐅𝐫𝐨𝐦 𝐌𝐨𝐥𝐞𝐜𝐮𝐥𝐞𝐬 𝐭𝐨 𝐒𝐜𝐚𝐟𝐟𝐨𝐥𝐝𝐬

⬛ Current surgical and non-surgical treatments primarily manage symptoms without restoring the disc's biological function. However, modern regenerative medicine is targeting the CEP directly.
🧬 Molecular Therapy: In the early stages of IDD, scientists are experimenting with injecting enzymes (like MMP8) or calcium-binding compounds directly into the CEP to decalcify it and clear out molecular debris, thereby reopening the nutrient pathways.
🧫 Cell Transplantation: Researchers have discovered that the CEP contains its own resident stem cells. Using exosomes derived from these healthy CEP stem cells can suppress cell death pathways in degenerating discs.
🧱 Tissue Engineering: For late-stage IDD, scientists are developing 3D-bioprinted scaffolds and composite biomaterials (like "eDAPS") designed to replace the damaged CEP. These scaffolds encourage native cells to migrate into the implant and generate fresh tissue and blood vessels.

𝐓𝐡𝐞 𝐇𝐨𝐫𝐢𝐳𝐨𝐧 𝐨𝐟 𝐓𝐫𝐚𝐝𝐢𝐭𝐢𝐨𝐧𝐚𝐥 𝐂𝐡𝐢𝐧𝐞𝐬𝐞 𝐌𝐞𝐝𝐢𝐜𝐢𝐧𝐞 (𝐓𝐂𝐌)

⬛ Interestingly, the review details extensive research into natural compounds derived from TCM that protect the CEP at a cellular level.
🌿 Curcumin (from Turmeric): Suppresses cell apoptosis via autophagy pathways and protects the CEP from mechanical stress.
🌱 Icariin (from Epimedium): Protects against CEP calcification by activating mitochondrial autophagy and blocking inflammatory cell death (ferroptosis).
🧪 TCM Compound Formulas: Formulas like Shen Sui Tong Zhi have been shown to target the NF-κB signaling pathway, downregulating inflammatory factors in the CEP.

𝐖𝐡𝐚𝐭’𝐬 𝐍𝐞𝐱𝐭?

⬛ While targeting the cartilaginous endplate represents a massive leap forward in treating the root cause of back pain, challenges remain.
⬛ Many modern bio-scaffolds struggle to mimic the mechanical strength of natural bone and cartilage.
⬛ Furthermore, much of the research—particularly regarding TCM—is currently limited to in vitro studies and requires further in vivo clinical validation.
⬛ Ultimately, the consensus is clear: saving the spine requires saving the endplate.
⬛ By bridging cutting-edge bioengineering with traditional pharmacological therapies, science is inching closer to treatments that don't just mask lower back pain, but actually reverse it.

04/04/2026

Resistance training can reduce body fat percentage while simultaneously improving grip strength, representing an effective management strategy for sarcopenic obesity, reports a systematic review and meta-analysis in BMC Geriatrics.

Link in the comments.

26/03/2026

26/03/2026

Timing of exercise may help with type 2 diabetes

Circadian clock gene rhythms are disrupted in type 2 diabetes, contributing to impaired glucose metabolism and hormonal dysregulation.

Exercise acts as a zeitgeber (time-giver) that modulates internal biological clocks, with timing emerging as an important factor for metabolic outcomes in type 2 diabetes.

Afternoon and evening exercise (moderate to high intensity) consistently improves glycem ic control and insulin sensitivity in type 2 diabetes, whereas morning exercise has little effect or may worsen metabolism by raising blood glucose levels.

Afternoon exercise in type 2 diabetes is associated with lower cortisol and inflammation levels, as well as greater oxidative capacity, compared with morning exercise.

The timing-dependent effects of exercise in type 2 diabetes appear to be intensity dependent, highlighting an important interaction between when and how intensely individuals with type 2 diabetes exercise.

https://www.cell.com/trends/endocrinology-metabolism/fulltext/S1043-2760(26)00030-5
https://sciencemission.com/metabolism-in-T2D

26/03/2026

New science shows Alzheimer’s may be shaped by an organ-brain axis, where the gut, lung, liver, and bladder influence brain inflammation.

1. In Alzheimer’s, immune changes outside the brain may help drive:
- chronic neuroinflammation
- blood-brain barrier breakdown
- harmful microglia and astrocyte activation

2. The gut-brain axis is especially important:
- Healthy gut microbes support anti-inflammatory immune balance
- Gut dysbiosis can shift immunity toward Th17-driven inflammation
- This may worsen brain immune activation and neuronal damage

3. Key protective gut metabolites like SCFAs help:
- strengthen the blood-brain barrier
- support regulatory T cells
- maintain healthy microglia function

4. Other microbial signals, such as AhR-related pathways, may also help suppress excessive inflammation in both the gut and brain.

Reference: Kim Y et al. (2026)

22/03/2026

22/03/2026

𝗦𝗮𝗿𝗰𝗼𝗽𝗲𝗻𝗶𝗮 𝗣𝗿𝗲𝘃𝗲𝗻𝘁𝗶𝗼𝗻 𝗶𝗻 𝗢𝗹𝗱𝗲𝗿 𝗔𝗱𝘂𝗹𝘁𝘀: 𝗔 𝗖𝗼𝗺𝗽𝗿𝗲𝗵𝗲𝗻𝘀𝗶𝘃𝗲 𝗟𝗼𝗼𝗸 𝗮𝘁 𝗡𝗼𝗻-𝗣𝗵𝗮𝗿𝗺𝗮𝗰𝗼𝗹𝗼𝗴𝗶𝗰𝗮𝗹 𝗜𝗻𝘁𝗲𝗿𝘃𝗲𝗻𝘁𝗶𝗼𝗻𝘀

⬛ As the global population ages, maintaining health span and independence in older adults has become a critical societal issue.
⬛ One of the greatest threats to healthy aging is sarcopenia, a condition characterized by the progressive, systemic loss of skeletal muscle mass, strength, and physical performance.
⬛ Affecting an estimated 10% to 16% of the older global population, sarcopenia increases the risk of falls, diminishes the quality of life, and is closely linked to higher mortality rates.
⬛ Because there are currently no established pharmacological treatments for sarcopenia, managing and preventing the condition relies heavily on non-pharmacological interventions.
⬛ A recent 2025 review article by Kim et al., published in Osteoporosis and Sarcopenia, evaluates the most effective strategies to combat this condition.
⬛ Here is a thorough breakdown of the review's findings on how to prevent and treat sarcopenia.

𝗟𝗘𝗫𝗘𝗥𝗖𝗜𝗦𝗘: 𝗧𝗵𝗲 𝗙𝗶𝗿𝘀𝘁-𝗟𝗶𝗻𝗲 𝗗𝗲𝗳𝗲𝗻𝘀𝗲 🏋️

⬛ Immobilization is a primary driver of muscle loss, making exercise the cornerstone of sarcopenia treatment.
⬛ Resistance Training is the Gold Standard: Engaging in machine-based or free-weight resistance training two to three times per week has been proven to significantly improve muscle mass, handgrip strength, lower limb strength, and gait speed in older adults.
⬛ It is highly effective not just as a treatment, but also as a preventive measure in the early stages of muscle decline (pre-sarcopenia).
⬛ Aerobic Exercise Enhances the Benefits: While aerobic training alone does not significantly build muscle strength, it improves metabolic regulation and cardiovascular function.
⬛ When combined with resistance training in "multicomponent" exercise programs, the overall therapeutic benefits are significantly enhanced.
⬛ Home-Based Workouts are Safe but Require Consistency: For those who cannot access a gym, home-based resistance exercises, such as Elastic Band Training (EBT), offer a safe alternative with a lower risk of injury.
⬛ However, because home-based workouts lack supervision, they often yield more modest results, highlighting the need for motivation to maintain adequate training intensity.

𝗡𝗨𝗧𝗥𝗜𝗧𝗜𝗢𝗡: 𝗙𝘂𝗲𝗹𝗶𝗻𝗴 𝗠𝘂𝘀𝗰𝗹𝗲 𝗣𝗿𝗲𝘀𝗲𝗿𝘃𝗮𝘁𝗶𝗼𝗻 🥗

⬛ Older adults frequently face malnutrition and "anabolic resistance" (a blunted muscle-building response to protein), which accelerates sarcopenia.
⬛ Targeted Supplementation: Diets rich in protein, specifically branched-chain amino acids like leucine and its metabolite HMB, can help increase fat-free mass in older individuals.
⬛ However, leucine or HMB alone has limited effects on raw muscle strength unless combined with other nutrients.
⬛ The Power of Vitamin D: Vitamin D suppresses myostatin, a negative regulator of muscle synthesis.
⬛ When older adults combined Vitamin D with whey protein or leucine, they saw massive improvements in lean mass, physical performance, and muscle strength.
⬛ Synergy with Exercise: Nutritional interventions are consistently most effective when paired with exercise.
⬛ Combining a protein-rich diet with resistance training improves muscle mass, lower limb strength, and gait speed far more effectively than either intervention alone.

𝗘𝗟𝗘𝗖𝗧𝗥𝗜𝗖𝗔𝗟 𝗠𝗨𝗦𝗖𝗟𝗘 𝗦𝗧𝗜𝗠𝗨𝗟𝗔𝗧𝗜𝗢𝗡 (𝗘𝗠𝗦): 𝗔𝗻 𝗔𝗹𝘁𝗲𝗿𝗻𝗮𝘁𝗶𝘃𝗲 𝗳𝗼𝗿 𝘁𝗵𝗲 𝗜𝗺𝗺𝗼𝗯𝗶𝗹𝗲 ⚡

⬛ For older adults who suffer from severe mobility limitations or cannot engage in traditional exercise, Whole-Body Electrical Muscle Stimulation (WB-EMS) has emerged as a promising alternative.
⬛ EMS artificially induces muscle contractions, mimicking some microscopic cellular responses of exercise.
⬛ Mid-to-long-term use (2 to 6+ months) has been shown to improve isometric leg strength and appendicular skeletal muscle mass.
⬛ However, WB-EMS comes with strict limitations.
⬛ It is contraindicated for individuals with pacemakers, acute illnesses, untreated hypertension, and neurological disorders, and it carries a risk of rhabdomyolysis, a severe muscle-breakdown condition.

𝗧𝗵𝗲 𝗛𝗶𝗱𝗱𝗲𝗻 𝗖𝘂𝗹𝗽𝗿𝗶𝘁: 𝗖𝗵𝗿𝗼𝗻𝗶𝗰 𝗜𝗻𝗳𝗹𝗮𝗺𝗺𝗮𝘁𝗶𝗼𝗻 𝗮𝗻𝗱 𝗢𝗿𝗮𝗹 𝗙𝗿𝗮𝗶𝗹𝘁𝘆 🦷

⬛ One of the most fascinating aspects of the review is the emerging link between chronic, low-grade inflammation (often called "inflammaging") and muscle degradation.
⬛ Persistent systemic inflammation suppresses muscle protein synthesis and promotes muscle atrophy.
⬛ The Periodontitis Connection: Poor oral health directly impacts muscle health.
⬛ Periodontitis (gum disease) triggers systemic inflammation, elevating pro-inflammatory cytokines like IL-6 and TNF-α, which are known to break down muscle proteins.
⬛ Oral Frailty: Conditions like tooth loss, dry mouth, and difficulty chewing drastically reduce a person's ability to consume adequate protein, accelerating muscle loss.
⬛ Furthermore, oral pathogens can swallow into the digestive tract, altering the gut microbiota and causing metabolic dysfunctions that further drive sarcopenia.

𝗞𝗲𝘆 𝗧𝗮𝗸𝗲𝗮𝘄𝗮𝘆𝘀 𝗳𝗼𝗿 𝗦𝗮𝗿𝗰𝗼𝗽𝗲𝗻𝗶𝗮 𝗣𝗿𝗲𝘃𝗲𝗻𝘁𝗶𝗼𝗻 📌

⬛ The management of sarcopenia cannot rely on a single silver bullet.
⬛ A personalized, comprehensive strategy is strictly required to extend the healthy lifespan of older adults.
⬛ Effective prevention should include:
⬛ Consistent Resistance Training, ideally paired with aerobic activities.
⬛ Adequate Nutritional Support, focusing on protein, Vitamin D, and anti-inflammatory nutrients like Omega-3s.
⬛ Prioritizing Oral Health, treating periodontitis early to stop systemic inflammation at its source.
⬛ By combining physical activity, tailored nutrition, and diligent periodontal care, older adults can effectively preserve their muscle function, independence, and overall quality of life.