Kelsey Matichuk, RMT

06/07/2026

Here's a snapshot of the biological insult from international travel. It takes your body over two weeks to fully recover.

It's a big price tag.

One international trip per quarter is a reasonable balance.

Time to recover:
> sleep duration: 2 days
> grip strength: 5 days
> mood: 1 wk
> cortisol: 9 days
> sleep quality: 2 wks
> blood glucose: 2 wks

06/07/2026

Scientists have created what they call a "ghost heart" — and it may be the most important medical breakthrough of our lifetime.

Here is how it works. They take a pig heart, wash it gently with a mild detergent until every single cell dissolves away. The blood drains out. The color fades. What is left behind is a ghostly white protein scaffold — the architectural skeleton of a heart, perfectly intact, right down to the tiniest blood vessel channels.

Then they inject it with the patient's own stem cells.

The cells find their way into the scaffold, settle in, and begin to grow. Scientists have already watched these hybrid hearts start beating in the lab.

The reason this changes everything is rejection. Every year, thousands of transplant patients die not because they did not get an organ — but because their body attacked it. With a ghost heart rebuilt from your own stem cells, there is nothing foreign for your immune system to fight. No rejection. No lifelong anti-rejection drugs.

Right now, over 103,000 Americans are on the transplant waiting list. 13 people die every day waiting for an organ that never comes. One in three heart patients dies before a donor heart even becomes available.

And here is the part that should be on the front page of every newspaper. In June 2025, this technology was used on a real human patient for the first time — not the heart yet, but a bioengineered liver built using the exact same method. It worked. The organ performed all the functions of a healthy liver in a patient who had no other options.

The heart is next. Researchers say a fully transplantable ghost heart could be ready within the next 6 to 7 years.

We may be the last generation that dies waiting for a donor organ.

06/06/2026

06/06/2026

The glass of wine with dinner is the amount almost everyone treats as safe. For seven cancers, it is already enough to raise your risk.

A 2026 analysis in Nature Health pooled 843 studies using a conservative method designed to report the smallest effect the data can support. Across all ten cancers examined, risk rose with intake, and for seven of them it was already elevated below one standard drink a day: pharynx, colorectum, esophagus, breast, liver, pancreas, and prostate. There was no threshold below which the risk disappeared.

The magnitude is not the same for every cancer, and the graphic shows that honestly. The strongest signal is in the upper aerodigestive tract. Pharyngeal cancer carried by far the highest minimum excess risk in the analysis, with laryngeal cancer next, and the other aerodigestive sites following. Colorectal and breast cancer showed clear, consistent dose-response relationships of smaller size. Liver, pancreatic, and prostate cancer showed the smallest excess risk with wider uncertainty, but still no safe floor. The direction never reversed. Only the size changed.

This is where alcohol differs from most things people argue about. The same paper found genuinely mixed and weak evidence for several cardiometabolic and neurological outcomes, where low-to-moderate intake was associated with slightly lower risk that weakened or reversed at higher amounts. For cancer there was no such ambiguity. The senior author described the cancer evidence as consistent and unambiguous: risk rises at any level.

The practical point is not about heavy drinking. The cancer signal is already present at the amount most people consider harmless. A single daily drink is not a safe lane for cancer risk. It is the low end of a line that only goes up.

Dai et al., Nature Health, 2026

06/03/2026

06/03/2026

https://www.facebook.com/share/p/18eegueKnT/

Spinal manipulation

06/01/2026

🧬 Your weekly science updates. Read more 👇🏻

Cancer: https://bit.ly/4viowhR
Exercise: https://bit.ly/43578kQ
Pigeon: https://bit.ly/4u4jVyU
Memory: https://bit.ly/4dW1J4z
Neurons: https://bit.ly/4uJ76eD
Peppermint: https://bit.ly/4u4qjG8

This Week in Science (25 May - 31 May 2026)

05/30/2026

Just published 🔥

𝗖𝗿𝗼𝘀𝘀-𝗲𝗱𝘂𝗰𝗮𝘁𝗶𝗼𝗻 𝗼𝗳 𝘂𝗻𝗶𝗹𝗮𝘁𝗲𝗿𝗮𝗹 𝗿𝗲𝘀𝗶𝘀𝘁𝗮𝗻𝗰𝗲 𝘁𝗿𝗮𝗶𝗻𝗶𝗻𝗴 𝗮𝘀 𝗮 𝘀𝘁𝗿𝗮𝘁𝗲𝗴𝘆 𝘁𝗼 𝗺𝗶𝘁𝗶𝗴𝗮𝘁𝗲 𝗶𝗺𝗺𝗼𝗯𝗶𝗹𝗶𝘀𝗮𝘁𝗶𝗼𝗻-𝗶𝗻𝗱𝘂𝗰𝗲𝗱 𝗻𝗲𝘂𝗿𝗼𝗺𝘂𝘀𝗰𝘂𝗹𝗮𝗿 𝗱𝗲𝗰𝗹𝗶𝗻𝗲: 𝗔 𝘀𝘆𝘀𝘁𝗲𝗺𝗮𝘁𝗶𝗰 𝗿𝗲𝘃𝗶𝗲𝘄 𝗮𝗻𝗱 𝗺𝗲𝘁𝗮-𝗮𝗻𝗮𝗹𝘆𝘀𝗶𝘀

▶️ Immobilisation has been used in the treatment of upper and lower extremity injuries since ancient times in order to reduce pain, allow tissue healing, and prevent further damage (). However, modern forms of immobilisation such as casting, bracing, or surgical fixation substantially reduce mechanical loading and therefore induce rapid declines in muscle strength and muscle mass (https://pubmed.ncbi.nlm.nih.gov/19727027/, https://pubmed.ncbi.nlm.nih.gov/38895777/).

⬇️ These neuromuscular losses occur particularly quickly during the first days of immobilisation before beginning to plateau after approximately two weeks (https://pubmed.ncbi.nlm.nih.gov/36883219/). Daily strength losses of approximately 2.0% in the knee extensors and 1.2% in the elbow flexors have been reported (https://pubmed.ncbi.nlm.nih.gov/30900205/).

💡 Importantly, these early declines in strength are thought to be driven predominantly by neural mechanisms — including reductions in neural drive, motor unit excitability, and firing frequency — rather than by muscle atrophy itself (https://pubmed.ncbi.nlm.nih.gov/41106072/, https://pubmed.ncbi.nlm.nih.gov/33981206/, https://pubmed.ncbi.nlm.nih.gov/36088611/).

⬆️ Since persistent strength deficits and asymmetries are associated with an increased risk of reinjury and delayed return to sport or work (https://pubmed.ncbi.nlm.nih.gov/36965459/, https://pubmed.ncbi.nlm.nih.gov/35141554/), cross-education of the contralateral non-immobilised limb has emerged as a promising strategy to attenuate neuromuscular decline during periods of immobilisation itself.

📘 Carroll et al. (https://pubmed.ncbi.nlm.nih.gov/17043329/) showed that these contralateral strength gains reach approximately 52% of those observed in the trained limb, highlighting the importance of maximising trained limb strength to optimise the cross-education effect in the untrained contralateral limb.

💪 Effective cross-education interventions require near-maximal training intensities to maximise strength gains in the untrained limb (https://pubmed.ncbi.nlm.nih.gov/28936703/, https://pubmed.ncbi.nlm.nih.gov/37156010/, https://pubmed.ncbi.nlm.nih.gov/33984253/).

🧠 The magnitude of strength transfer is greatest when training emphasises eccentric muscle actions, which induce greater reductions in intracortical inhibition and greater increases in corticospinal excitability compared to other contraction types (https://pubmed.ncbi.nlm.nih.gov/26037804/, https://pubmed.ncbi.nlm.nih.gov/34488881/).

📘 In a brand-new study, Rodríguez-Coloma and colleagues (https://pubmed.ncbi.nlm.nih.gov/42141765/) quantified the effects of cross-education on muscle strength and size during unilateral limb immobilisation in healthy individuals. Subgroup analyses examined the moderating influence of training modality (i.e., eccentric, concentric, isometric, or combined), immobilisation model (i.e., proximal vs distal limb musculature), and muscle group specificity for preserving neuromuscular function.

👫 The review included eight experimental studies with a total of 189 healthy participants. In all studies, one upper limb was immobilised for 3 to 4 weeks while the opposite limb performed resistance training.

𝗠𝗮𝗶𝗻 𝗙𝗶𝗻𝗱𝗶𝗻𝗴𝘀

📊 Cross- education attenuated strength loss compared with immobilisation alone (g = 0.53, p < 0.001), with effect magnitude moderated by immobilisation location and training modality.

💪Proximal immobilisation (i.e. shoulder joint) yielded greater attenuation (overall: g = 0.62; eccentric: g = 0.82; concentric- eccentric: g = 0.68) than distal immobilisation (i.e. wrist joint, overall: g = 0.42; eccentric: g = 0.34; isometric: 43 g = 0.63).

📊 Regarding muscle size, cross education produced a small preservation effect in the immobilised limb (g = 0.19, p = 0.01). This effect was only evident in proximal immobilisation (g = 0.40) compared to distal (g = 0.06). Quantitatively, proximal effects were about 1.5 times greater than distal effects for strength, but markedly greater—about 6.7 times—for muscle size.

🧠 Possible neuroanatomical Explanation: Proximal muscles receive enhanced descending drive from the reticulospinal tract (mediating diffuse bilateral adaptations), whereas distal fine motor movements of the hand/forearm rely heavily on the corticospinal tract. This localized control restricts the cross-activation effect, rendering cross-education far less effective at protecting distal wrist musculature from structural atrophy.

📊 Strong positive associations were observed between adaptations in the trained and immobilised limbs for strength (r = 0.79) and muscle size (r = 0.81). These findings indicate that cross-education attenuates losses in muscle strength and size during immobilisation. However, these results should be interpreted with caution due to the varying risk of bias among the included studies.

💡 Several distinct neurophysiological and morphological mechanisms might explain theses results:

👉 Strength Sparing is Primarily Neural: Early strength losses during disuse are predominantly driven by neural decrements, such as reduced neural drive and altered motor unit firing rates, rather than immediate muscle atrophy. Cross-education acts as a direct countermeasure by maintaining cortical excitability and neural drive to the immobilised limb.

👉 Size Sparing is Limited by Lack of Load: Muscle hypertrophy and mass preservation are fundamentally dependent on direct external mechanical loading. Because the immobilised limb experiences no actual load, the cross-education effect on muscle size is predictably small.

👉 Potential Protein Synthesis Modulation: The small amount of muscle size preservation that does occur might be driven by sustained neural activation, which may weakly modulate local signaling pathways to abated decreases in muscle protein synthesis, effectively slowing down tissue atrophy.

𝗪𝗵𝗮𝘁 𝗮𝗿𝗲 𝘁𝗵𝗲 𝗽𝗼𝘀𝘀𝗶𝗯𝗹𝗲 𝗺𝗲𝗰𝗵𝗮𝗻𝗶𝘀𝗺𝘀?

The broader neural cross-transfer of strength is justified by two primary candidate cortical mechanisms:

🧠 The Cross-Activation Hypothesis (https://pubmed.ncbi.nlm.nih.gov/23908616/): Unilateral motor training produces spillover activation facilitating neural adaptations in both hemispheres, driving concurrent neural adaptations in both the trained and untrained descending pathways.

🧠 The Bilateral Access Hypothesis: The neuroplastic adaptations remain localized within the hemisphere controlling the trained limb, but the untrained hemisphere can directly "access" these motor schemes via transcallosal pathways (the corpus callosum) when trying to recruit the immobilised limb (https://pubmed.ncbi.nlm.nih.gov/23908616/).

📋 Exercise Prescription Guidelines

1️⃣ Implement cross-education immediately during the acute immobilisation phase to blunt the steep initial drops in voluntary neural drive.

2️⃣ Prioritize Eccentric Load: Incorporate high-intensity eccentric actions (e.g., eccentric preacher curls) where feasible to optimize neuroplasticity and maximize transfer magnitude.

3️⃣ Demand Near-Maximal Intensity: Exercise prescription should utilize near-maximal intensities, as cross-education effects are highly dose-dependent.

4️⃣ Target Homologous Pairs: Ensure targeting of the exact homologous contralateral muscle groups to exploit muscle-specificity advantages.

05/29/2026

Five seconds was never the part that mattered most.

Two food-science labs actually tested the five-second rule, dropping food on surfaces and counting how many bacteria moved across. Here is the part people get wrong: the rule isn't completely false. Longer contact really does move more bacteria. Time is real. It just isn't the thing doing most of the work.

What you dropped matters more than how fast you grabbed it. The wettest food they tested, watermelon, picked up the most, in some conditions up to 97% of the bacteria sitting on the surface. The driest, a gummy candy, picked up as little as 0.1%. Same drop, same floor, completely different outcome, and the difference came from the food, not the clock. Bacteria move in water, and a wet surface hands them over fast.

Where you dropped it matters too. Smooth hard surfaces like tile transfer readily. Carpet transferred the least, probably because food only touches a fraction of its surface.

And there is no perfectly safe window. Some bacteria transfer in under a second. Grabbing it fast helps a little, but it does not reset the clock to zero.

So the real version is simple. Drop dry food on a clean dry surface and you are mostly fine, fast or not. Drop wet food on a dirty hard floor and the five-second timer will not save you.

Two honest notes. These studies used a harmless tracer bacterium, not a live pathogen, so they measured transfer, not how sick you would actually get. And the real risk comes down to what is on the floor in the first place. A clean kitchen tile and a public bathroom floor are not the same bet.

Miranda & Schaffner, Appl Environ Microbiol, 2016
Dawson et al., J Appl Microbiol, 2007

05/28/2026

A banana cancels most of your berry smoothie's antioxidants.

Firstly, bananas are a good food. This is about an enzyme and what it does to a specific group of compounds.

Flavanols are antioxidants found in berries, cocoa, grapes, and apples that have been linked to heart and brain health. Bananas are high in polyphenol oxidase (PPO), the enzyme that turns a cut banana brown within minutes. PPO breaks flavanols down into forms the body absorbs poorly.

The study that measured this was careful about one thing worth understanding. Ottaviani et al. (2023) did not simply compare a berry smoothie to a banana smoothie and assume berries had more to begin with. They added the same standardized dose of cocoa flavanols to every drink, so the starting amount was identical. Then they gave healthy volunteers three things on separate days: that flavanol dose in a capsule, the same dose in a low-PPO berry smoothie, and the same dose in a high-PPO banana smoothie.

The capsule produced peak blood flavanols of about 680 nmol/L. The berry smoothie landed in the same range. The banana smoothie reached only about 96 nmol/L, roughly 84 percent lower than the capsule, from an identical starting dose. The only thing that changed was the enzyme it was blended with.

A second detail sharpens the mechanism. When the banana drink and the flavanols were swallowed together but not blended beforehand, levels still dropped. That points to PPO continuing to act after you swallow it, likely in the stomach, not only during blending.

Two honest limits. This was a small mechanistic study. The comparison behind the 84 percent figure was a crossover in eight healthy men, and it measured absorption, not a long-term health outcome. It was also funded by Mars, Inc., which has a commercial interest in cocoa flavanols. That does not change the underlying chemistry, which is well established, but it is worth knowing.

The practical takeaway is narrow and specific. This does not mean bananas reduce the nutritional value of your food, and it is not a reason to stop eating them. It means that if flavanol intake is something you care about, the fruit you blend with your flavanol source is worth considering. Berries and pineapple are low in PPO. If you want those compounds to reach your blood, keeping the banana out of that particular smoothie, or eating it on the side, is a reasonable choice.

Ottaviani et al., Food & Function, 2023 (DOI: 10.1039/d3fo01599h)