Yoga-cph

19/06/2026

More about why higher doses of protein might good for older adults..

The Recommended Dietary Allowance for protein is 0.8 grams per kilogram of body weight per day. For a 70 kg adult, that is 56 grams. The number has been treated for decades as if it represents an optimal target, the amount everyone should aim for. It does not.

The RDA was established through the National Academies' Food and Nutrition Board and traces to classical nitrogen balance studies. It is designed to identify the lowest intake at which nitrogen losses are matched by intake in approximately 97.5% of the population. In other words, the RDA is the floor below which protein deficiency becomes likely. It is a public health threshold, not a recommendation for physiological optimization.

That distinction matters most for older adults. After roughly age 50, skeletal muscle becomes progressively less responsive to the same dose of dietary protein, a phenomenon researchers call anabolic resistance. The amount of leucine and essential amino acids that triggered a full muscle protein synthesis response at 25 produces a blunted response at 70. To get a comparable signal, older adults appear to need more protein per meal and more across the day.

A 2022 systematic review and meta-analysis by Nunes and colleagues, published in the Journal of Cachexia, Sarcopenia and Muscle, pooled 105 randomized controlled trials in 5,402 participants. Looking specifically at adults aged 65 and older, the authors found that gains in lean body mass clustered between 1.2 and 1.59 grams per kilogram per day. Below that range, gains were smaller. Above approximately 1.6 g/kg, additional protein produced little further benefit in non-resistance-trained populations, though resistance-trained individuals may benefit from somewhat higher intakes.

This is not a directive that every older adult should eat 1.6 g/kg. The Nunes meta-analysis describes where benefits cluster in the available trial data. The optimal intake for a given individual depends on resistance training status, kidney function, total caloric intake, protein source quality, and how protein is distributed across meals. The point is that 0.8 is almost certainly too low for muscle-related outcomes in older adults, and the relevant range sits meaningfully above the RDA.

The intake gap matters because most older adults are not even hitting the floor. A 2019 NHANES analysis by Krok-Schoen and colleagues found that up to 46% of US adults over 71 consumed less than 0.8 g/kg of protein per day. The conversation about whether the target should be 1.0, 1.2, or 1.6 is happening at the academic level while a meaningful share of the population is still below the deficiency-prevention threshold.

For scale, a 70 kg older adult eating 1.4 g/kg would consume around 100 grams of protein per day. A cup of plain Greek yogurt delivers approximately 23 grams. Three large eggs add 18. A 4 oz portion of chicken breast contributes about 30. A 4 oz serving of salmon adds another 28. None of those individual portions is unusual. The challenge for many older adults is appetite, dentition, food cost, and meal frequency, not the math.

The honest takeaway. The 0.8 g/kg RDA is a deficiency-prevention threshold from nitrogen balance studies. It was never designed to optimize muscle outcomes in older adults. Modern evidence points toward 1.2 to 1.6 g/kg as the range where muscle-related benefits cluster in pooled trial data, with the precise individual target still debated. The more urgent gap is that a substantial fraction of older adults are not meeting even the floor.

Nunes EA et al., J Cachexia Sarcopenia Muscle 2022
Krok-Schoen JL et al., J Nutr Health Aging 2019

10/06/2026

Yet another reason to do creatin so many promising effects from a cheap safe and easy to use supplement:

Creatine is moving out of the muscle-and-brain box and into cancer immunology

The textbook role of creatine is a phosphate buffer. Creatine kinase keeps a reserve of phosphocreatine on hand, and when a cell burns ATP faster than its mitochondria can replace it, that reserve donates a phosphate to regenerate ATP almost instantly. Muscle relies on this during hard contractions. The same buffering chemistry exists in any cell with sharp, bursty energy demand, and a tumor-infiltrating immune cell is one of the most energy-stressed cells in the body. It has to proliferate, migrate, and execute effector functions inside a microenvironment that is hypoxic and stripped of glucose by the tumor itself.

Di Biase and colleagues at UCLA built the first direct evidence in 2019. Tumor-infiltrating T cells sharply upregulate SLC6A8, the surface transporter that pulls creatine into a cell. Knocking that transporter out in mice severely impaired the antitumor T cell response, and supplementing creatine suppressed tumor growth across several mouse tumor models. They described creatine as a molecular battery that conserves bioenergy to power T cell activity. The result that drew the most attention was a combination effect: creatine plus PD-1/PD-L1 checkpoint blockade suppressed tumors more than either alone. Checkpoint inhibitors are already frontline immunotherapy, so a cheap metabolite that amplifies them is a real translational hook.

The 2026 study from the same lab moved the mechanism one step upstream, and that is what makes it interesting rather than repetitive. T cells do not act on their own. Dendritic cells are the antigen-presenting scouts that capture tumor proteins and activate T cells in the first place, and they were not part of the original story. Kang and colleagues found that intratumoral dendritic cells also upregulate the creatine transporter and depend on creatine uptake to function. Transporter-deficient dendritic cells failed to activate and could not prime an effective CD8 T cell response. Creatine supplementation restored their activation and suppressed tumor growth in a syngeneic melanoma model. Mechanistically, creatine preserved the intracellular ATP these cells need to drive energy-dependent inflammatory signaling, which is the same molecular-battery logic operating in a different cell type. The same activation boost showed up in human monocyte-derived dendritic cells in culture, which is the first signal the biology might carry across species.

Two cautions belong on this directly. The evidence base is preclinical. It is built on mouse tumor models with in vitro human cell confirmation, and no human cancer trial has tested creatine as an immunotherapy adjunct. The senior author also holds UCLA patents on the approach, which is worth knowing when reading the framing of any single paper. Neither caveat is disqualifying, and both are standard for an early translational program, but they set the ceiling on what can honestly be claimed today.

What the two papers together establish is a coherent energetic model: creatine feeds an ATP buffer that both the dendritic cell and the T cell draw on to do metabolically expensive immune work inside a hostile tumor. That reframes a compound most people file under athletic performance as a candidate metabolic adjunct to immunotherapy, and it gives a concrete, testable rationale for the human trials that would have to come before any of this reaches a clinic.

References: Di Biase et al., Journal of Experimental Medicine, 2019 Kazak and Cohen, Nature Reviews Endocrinology, 2020 Kang et al., iScience, 2026

09/06/2026

Funny read on the ever lasting “spritual materialism”..

The European Backpacker Who Calls Everyone Else Basic but Has the Exact Same Banana Pancake Route 🎒🥞🤡

He sits in a trendy vegan cafe in Pai, furiously rolling his own ci******es, and loudly judging the "mainstream tourists" while completely ignoring the fact that his entire gap-year itinerary was essentially copy-pasted from a 2004 Lonely Planet guidebook.

Writing cryptic journal entries on an overnight train to Chiang Mai doesn't make you an intrepid, off-the-grid explorer. It officially makes you just another incredibly generic cog in the heavily commercialized, factory-setting Southeast Asian backpacker machine.

You sit cross-legged on a bamboo mat genuinely convinced that your "spiritual journey" through Thailand is a uniquely untethered awakening. Meanwhile, the brutal truth is that your entire personality is just a carbon copy of every other European with a patchy beard and unwashed elephant pants who has passed through the exact same Khao San Road 7-Eleven since the late nineties. You loudly mock the families staying at resorts in Phuket while literally executing the most perfectly predictable, mass-produced travel loop known to modern mankind: Bangkok, Chiang Mai, Pai, Koh Tao, self-discovery, repeat.

There is absolutely nothing more spectacularly pathetic than watching you stroke your chin and pretend you've discovered "the real Thailand" simply because you rented a wobbly scooter to visit a heavily advertised waterfall alongside forty other foreigners. You aren't an undiscovered bohemian pioneer navigating the wild frontier: you are literally just participating in an incredibly safe, highly sanitized tourist conveyor belt fueled entirely by banana pancakes, cheap Leo beer, and shared shuttle buses.

Put down your dog-eared copy of Siddhartha, stop acting like you personally discovered Koh Tao, and accept that your supposedly profound, "off-the-beaten-path" adventure is literally the most basic vacation package on the continent.

08/06/2026

You need to put way more load on your leg bones than you might think!

07/06/2026

Well boyz and girlz keep enjoying your coffee it is in fact good for you..

Coffee contains roughly 1-2% caffeine by weight. The other 98-99% is chlorogenic acids at 7-10%, melanoidins formed during roasting, trigonelline, and diterpenes. The non-caffeine fraction is what does most of the work on the gut microbiome.

A new study quantified the shifts. 62 adults: 31 daily drinkers at 3-5 cups per day, 31 non-drinkers. 5-week controlled protocol. APC Microbiome Ireland.

Three findings stood out.

Cryptobacterium species increased in drinkers. These bacteria produce indoles from tryptophan. Indoles activate the aryl hydrocarbon receptor on intestinal cells, which supports gut barrier integrity and modulates immune tone.

Eggerthella species also increased. These bacteria metabolize coffee polyphenols, breaking down chlorogenic acids into smaller bioactive metabolites the gut can absorb. The increase is functionally relevant to coffee compound activation, though some Eggerthella species, particularly E. lenta, are linked to inflammation in inflammatory bowel disease and bloodstream infections in immunocompromised patients. The genus has a mixed clinical profile.

Indole-3-propionic acid decreased in drinkers. IPA is a tryptophan-derived metabolite produced by bacteria like Clostridium sporogenes. It's anti-inflammatory and supports tight junction integrity in the gut barrier. Lower IPA correlates with type 2 diabetes risk, gut barrier dysfunction, and inflammation across the literature. A reduction is not a benefit.

The same directional shifts appeared in decaffeinated coffee drinkers. Chlorogenic acids and melanoidins are present in decaf at similar concentrations. Caffeine alone does not explain the microbiome changes.

A few qualifications.

N=62 is small. The findings are exploratory and need replication.

The behavioral component of the study reported a mix of effects. Some measures of cognition shifted in expected directions. Others, including impulsivity and emotional reactivity, also moved. The picture on mood and cognition is more complicated than a single direction.

Whether the IPA reduction reflects a meaningful change in gut barrier function, or is a marker of broader bacterial community changes, isn't resolvable from this data.

Practical framing: coffee changes the gut whether or not it contains caffeine. If caffeine causes problems with sleep, anxiety, or blood pressure, decaf delivers most of the same microbiome effects. The IPA reduction applies to both forms.

Boscaini et al., Nat Commun, 2026 DOI: 10.1038/s41467-026-71264-8

05/06/2026

Yet another clear study demonstrating the crucial importance of strengthening as we age!

“Grip strength is a proxy for whole-body muscle strength. It correlates with quadriceps strength, with overall lean mass, and with neuromuscular function. The European Working Group on Sarcopenia in Older People uses grip as the primary measure of muscle strength in their diagnostic criteria.

The mechanism is straightforward. Skeletal muscle is the largest insulin sensitive tissue in the body. It is the primary engine of glucose disposal, the largest reservoir of amino acids, and an endocrine organ that secretes myokines during contraction. When that tissue degrades, the entire metabolic system loses its main shock absorber. Weaker bodies die earlier across a long list of causes…”

Muscle strength is one of the most reliable predictors of how long you live. The simplest way to measure it is to squeeze a handheld dynamometer for 30 seconds. The kilograms get recorded. That single number tracks with mortality across nearly every cause researchers have measured.

The Prospective Urban Rural Epidemiology study followed 139,691 adults across 17 countries on five continents for a median of 4 years. Every 5 kilogram drop in grip strength tracked with 16% higher all-cause mortality. The same direction and magnitude held up for cardiovascular death, non-cardiovascular death, heart attack, and stroke. 3,379 deaths occurred over the follow-up period and the relationship persisted after adjustment for age, s*x, education, smoking, alcohol, physical activity, and country.

The headline finding came from a separate analysis. When grip strength and systolic blood pressure were both placed in the same model, grip was the stronger predictor of all-cause and cardiovascular mortality. Blood pressure is the most universally measured risk factor on earth. A squeeze test outperformed it.

Grip strength is a proxy for whole-body muscle strength. It correlates with quadriceps strength, with overall lean mass, and with neuromuscular function. The European Working Group on Sarcopenia in Older People uses grip as the primary measure of muscle strength in their diagnostic criteria.

The mechanism is straightforward. Skeletal muscle is the largest insulin sensitive tissue in the body. It is the primary engine of glucose disposal, the largest reservoir of amino acids, and an endocrine organ that secretes myokines during contraction. When that tissue degrades, the entire metabolic system loses its main shock absorber. Weaker bodies die earlier across a long list of causes.

The PURE data is observational. It does not prove that getting stronger causes lower mortality, only that the strength signal is consistent across continents, across country income levels, and across cause of death.

Almost every adult who walks into a clinic gets a blood pressure measurement. Almost none get their grip strength measured. Your blood pressure cuff misses this. A dynamometer doesn't.

Strength is a vital sign.

Leong et al., Lancet, 2015