CHE - Customised Health Essentials - customisedhealth.net

05/06/2026

04/06/2026

31/05/2026

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

24/05/2026

Coffee and tea contain polyphenols that bind non-heme iron in the gut and form insoluble complexes that pass through unabsorbed.
Hurrell and colleagues (1999, Br J Nutr) tested this directly using radio-labeled iron in adult humans eating a standardized bread meal with different beverages. Absorption was quantified by erythrocyte incorporation of the tracer.

Compared to water, beverages containing 20 to 50 mg of polyphenols per serving reduced iron absorption by 50 to 70%. At 100 to 400 mg, the reduction was 60 to 90%. Black tea: 79 to 94%. Peppermint tea: 84%. Cocoa: 71%. Chamomile: 47%. Adding milk did not meaningfully change the effect.

The mechanism is specific to galloyl structure, not total phenolic content. Brune, Rossander, and Hallberg (1989, Eur J Clin Nutr) showed that tannic acid inhibits in a dose-dependent manner that tracks galloyl content: 5 mg cut absorption 20%, 25 mg cut it 67%, and 100 mg cut it 88%. Gallic acid inhibited equivalently per mol of galloyl groups. Catechin, which lacks that structure, showed no inhibition at all. Chlorogenic acid, the dominant polyphenol in coffee, inhibits but less potently than tannins.

Heme iron behaves differently. It's absorbed intact through the HCP1 transporter inside its porphyrin ring, shielded from polyphenol binding entirely. Non-heme iron from plants, eggs, and fortified foods is the vulnerable pool.

Vitamin C counteracts the interaction by reducing Fe³⁺ to Fe²⁺ and forming a soluble ascorbate-iron complex that resists polyphenol binding. Hallberg and Hulthen (2000, Am J Clin Nutr) showed that adding 50 mg of vitamin C to a meal with significant inhibitors increased non-heme iron absorption 3 to 6-fold.

For anyone with borderline iron status, menstruation-related losses, a plant-based diet, or pregnancy, timing matters. A two-hour gap between the beverage and iron-rich foods, or pairing the meal with vitamin C, is the simplest fix.
Hurrell 1999. Brune 1989. The mechanism has been in the literature for three decades. It's rarely in standard dietary counseling, rarely on any bottle, and almost never mentioned by the industry selling iron.

Hurrell et al., Br J Nutr, 1999
Brune et al., Eur J Clin Nutr, 1989
Hallberg & Hulthen, Am J Clin Nutr, 2000

18/05/2026

Short sleep ages you. Long sleep usually means something is already aging you. Same curve. Different stories.

A new paper in Nature, led by Junhao Wen's lab at Columbia, mapped sleep duration against biological aging across 9 organ systems in half a million UK Biobank adults aged 37 to 84. They used 23 different aging clocks built from MRI scans, plasma proteins, and metabolites. The relationship is U-shaped. The slowest measured aging sat between 6.4 and 7.8 hours per night. Outside that window, in either direction, organs looked older than chronological age would predict.

The two arms of the U are not the same biology.

On the short-sleep side, the causal story is well established. Sleeping under 6 hours raises systemic inflammation, impairs glucose tolerance the next morning, suppresses NK cell activity, and associates with markers of poorer overnight brain waste clearance. Mendelian randomization analyses, including in this paper, support a direct causal effect of short sleep on aging biology. Short sleep drives the wear and tear.

On the long-sleep side, the picture flips. Consistently sleeping over 8 or 9 hours is a well-documented marker of underlying disease, not a damaging behavior in itself. It tracks with major depression, undiagnosed sleep apnea, hypothyroidism, chronic inflammation, and neurodegenerative disease. The authors of this paper note that Mendelian randomization could not strongly support reverse causality on the long arm, but they explicitly could not exclude it either. Decades of prior work in sleep medicine and psychiatry argue that for most long sleepers, the long sleep is the body compensating for something already wrong.

This matters because the practical advice for the two groups is opposite.

If you sleep under 6 hours, the levers are direct. Total sleep opportunity. Sleep timing consistency. Morning light exposure. Caffeine cutoff after lunch. Alcohol stopped three hours before bed at minimum. These are the highest-evidence behavioral interventions in sleep medicine. Sleep extension trials adding 45 to 90 minutes a night have shown improvements in metabolic and cardiovascular markers across small studies.

If you consistently sleep 9 or more hours and especially if you still wake unrefreshed, the right move is to investigate what your body is recovering from. The workup is straightforward. A home sleep study to rule out apnea. TSH, free T4, ferritin, CRP, vitamin D, vitamin B12. Depression and anxiety screening. A review of medications that increase sleep need, including antihistamines, gabapentinoids, mirtazapine, and beta blockers.

There is a third scenario worth naming because it gets lumped in with the long sleepers. Athletes in heavy training blocks, adolescents, people recovering from infection, and people in their first trimester of pregnancy genuinely need 9 to 10 hours and the curve does not apply to them in the same way. The paper looked at habitual sleep in adults aged 37 to 84, not acute recovery states.

The cleaner way to state the finding is this. There is a window in the middle where the body looks youngest on every clock the authors built. Both sides of that window correlate with faster organ aging. The reasons differ. Short sleep does the damage. Long sleep usually shows the damage is already underway.

Wen et al., Nature, 2026 Cappuccio et al., Sleep, 2010 Irwin, Nat Rev Immunol, 2019 Spiegel et al., Lancet, 1999 Tasali et al., JAMA Intern Med, 2022 Besedovsky et al., Physiol Rev, 2019

14/05/2026

The most persistent myth about creatine is that it damages your kidneys. The concern comes from a real observation interpreted incorrectly: creatine supplementation raises serum creatinine. On a standard metabolic panel, elevated creatinine triggers a lower estimated glomerular filtration rate, which is the primary marker doctors use to assess kidney function. The number looks worse. The kidney is fine.
Here is why. Creatine is stored in skeletal muscle primarily as phosphocreatine. It degrades spontaneously and irreversibly into creatinine at a rate of approximately 2% per day. Creatinine is a waste product. It is filtered by the kidneys and excreted in urine. Standard kidney function tests measure serum creatinine and use it to calculate eGFR. The assumption built into the equation is that creatinine production is relatively constant. When you supplement creatine and increase total body creatine stores, you produce more creatinine. The equation interprets this as reduced kidney filtration. It is not. It is more substrate producing more waste at the same filtration rate.

A 2025 systematic review and meta-analysis of 21 studies examining the effect of creatine supplementation on kidney function confirmed this directly. Creatine was associated with a small but statistically significant increase in serum creatinine (mean difference: 0.07 micromol/L). However, there were no changes in measured GFR, cystatin C, proteinuria, or albuminuria. These are the markers that actually reflect kidney health independent of creatinine metabolism. The creatinine went up. Every other renal marker was unchanged.

Kreider et al. (2025, JISSN) conducted the largest safety analysis of creatine to date, reviewing 685 human clinical trials involving over 26,000 participants. Side effect prevalence was virtually identical between creatine and placebo groups: 4.60% vs 4.21% (p=0.828). No significant differences were observed in any of the 49 side effects evaluated, including all markers of renal function and health. Some of these trials ran for up to 14 years.

The case reports that occasionally surface involving creatine and kidney injury almost always involve individuals with pre-existing kidney conditions, concurrent use of other substances known to affect renal function, or extreme exercise leading to rhabdomyolysis. These are confounded cases, not evidence of a causal relationship between creatine and kidney damage in healthy individuals.

One practical issue worth noting: if you take creatine and get routine bloodwork, your doctor may flag the creatinine and eGFR numbers. This is not because your kidneys are failing. It is because the standard test was not designed with creatine supplementation in mind. The solution is straightforward. Tell your doctor you take creatine and ask for a cystatin C-based eGFR instead. Cystatin C is produced at a constant rate by all nucleated cells and is not affected by creatine intake. It gives you the real kidney function number without the artifact.

For individuals with pre-existing kidney disease, the data is more limited. Most creatine studies have been conducted in healthy populations. While pilot studies in hemodialysis patients have not shown adverse effects beyond the expected creatinine increase, caution is warranted for anyone with diagnosed renal impairment until more data is available.

Kreider et al., JISSN, 2025
2025 Systematic Review/Meta-Analysis: Effect of creatine supplementation on kidney function