Dave Asprey

It is true that creatine plays a role in the energy metabolism of brain cells through the ATP system, and there are positive indications that it can relieve cognitive complaints during sleep deprivation. However, the effect has not been broadly proven: it is strongest in people with elevated fatigue, sleep deprivation, or a plant-based diet, and for healthy, well-rested people creatine appears to do little. The claim gives the impression that creatine improves cognition in everyone experiencing sleep deprivation or stress, while the research for this is still too limited and too inconsistent.

Research does indeed show that ashwagandha can measurably lower cortisol levels, but the best available meta-analysis shows no consistent or convincing effect on how stressed people actually feel. The specific figure of 28 percent does not appear in the available research, and results vary across studies, doses, and populations. So while the direction is correct, that precise percentage cannot be substantiated based on the available evidence.

Our answer on fibre intake confirms that a daily intake of 25 to 29 grams of fibre is associated with a 15 to 30% lower risk of premature death, which supports the direction of the claim. However, the claim differs on one point: the upper limit stated is 30 grams, whereas our answer cites 29 grams as the amount studied. In addition, the research concerns an association, not a proven causal effect, so the phrasing 'reduces total mortality' is more definitive than the evidence allows.

There is plausible evidence that too little sunlight is associated with a higher risk of cardiovascular disease, but a proven causal relationship has yet to be established. The claim that exposure to bright daylight reduces the risk of dying from cardiovascular disease and metabolic disorders goes beyond what research can currently support. Moreover, the available evidence focuses on the harmful effects of too little sunlight, not specifically on 'bright' daylight or on mortality from metabolic disorders. The direction is plausible, but the claim is more definitive than the evidence warrants.

The only controlled human study shows that GlyNAC does indeed have positive effects on glutathione levels and oxidative stress. However, the claim goes beyond the evidence by stating that those levels are restored 'to the levels of young people', given that the study included only 24 participants over 16 weeks. That is too small and too short to justify such a far-reaching conclusion. The direction is correct, but the claim is more definitive than the available research supports.

Research shows that four or more sauna sessions per week are associated with greater health benefits, including a lower risk of cardiovascular disease and premature death, and that this association is dose-dependent. However, the specific percentages in the claim (63 percent reduction in sudden cardiac death and 40 percent reduction in overall mortality) do not emerge from the research and therefore cannot be confirmed. Moreover, the research emphasises that it is purely observational and that a causal relationship has not been established. The claim presents the figures as established fact, whereas the reality is more nuanced.

Research shows that there are indications that omega-3 slows biological ageing, but these indications are explicitly preliminary and contradictory. The claim is too categorical: it specifies a dose of 1 gram, targets people over 70, and refers to epigenetic ageing, while the available evidence does not support that level of detail. The direction cannot be ruled out, but the certainty and specificity of the claim go beyond what the available evidence allows.

Research shows that berberine measurably lowers blood sugar, which is consistent with the claim. However, the claim suggests that berberine does so effectively and without reservation, whereas the EFSA has been unable to establish a safe intake level due to indications of DNA and liver damage. In addition, berberine has strong interactions with medications, making its use in practice risky. The blood sugar-lowering effect is therefore real, but the word "effectively" creates an overly positive and incomplete picture.

Multiple studies show that creatine can improve muscle strength and muscle mass in older adults, which supports the direction of the claim. However, the evidence is strongest when creatine is combined with resistance training; without that combination, the effects are less clear. The claim presents an increase in lean muscle mass as an established fact, but that goes somewhat beyond what the research, which is of moderate quality, justifies.

This comes from a real 2013 study that caused a great stir: during sleep, the space between brain cells increased by about 60 percent and waste was flushed out more quickly. However, the research was conducted in mice. In humans, the brain's waste-clearing system has been visualised, but that precise percentage has not been measured.

This is exactly what the research concludes. In the UK Biobank, with more than three thousand deaths over seven years, the regularity of sleep was a stronger predictor of mortality than the number of hours slept. Going to bed and waking up at the same time every day therefore matters more than the exact duration. It remains observational research.

The direction is correct and there is genuine research on this: in a Japanese cohort of seven hundred older adults, people who slept with light in the bedroom developed diabetes nearly four times as often as people who slept in the dark. That is a far larger difference than the 53 to 67 percent mentioned here, so those figures come from somewhere else. Moreover, this is observational research in older adults with nineteen new cases, making it a small study.

The idea that cooling the sleep environment improves sleep is plausible and is being investigated. However, the specific difference between men and women mentioned here, deep sleep in one group and REM sleep in the other, is not something I have been able to find in the literature. Sex differences of this kind require large studies, and those do not exist on this point.

It has been demonstrated that apigenin acts on the site in the GABA system where sleep medications also work, but this has been shown in test-tube and animal studies. 'Calming without sedation' is a marketing phrase: the dose at which it calms without causing drowsiness has not been established in humans, and the amounts used in those studies are far higher than what you can get from chamomile.

Deep sleep does decrease with age, that is true, and more so in men than in women. But 'almost completely lost' by the age of 45 is not what measurements show: in sleep research, middle-aged men still have perfectly normal deep sleep, just less than they had in their twenties. The decline is gradual and there is no age at which it suddenly tips over.

There are small studies in which participants felt less fatigued, particularly during prolonged stress. However, the research is poorly designed, the effects on cortisol have not been found consistently, and most of the work comes from manufacturers. As an herb with a possible effect it is interesting, but presenting it as established fact goes too far.

The description of how it works is broadly correct: modafinil inhibits the reuptake of dopamine and lasts roughly as long as a working day. But this is a prescription drug for narcolepsy, not a focus aid. It causes headaches, insomnia, and palpitations, interacts with hormonal contraceptives, and in the Netherlands it cannot legally be obtained without a prescription.

There is no optimal ratio, because none has ever been studied. The studies used a range of different doses and not one of them compared ratios against each other. Two to one is a number that stuck in the supplement world, not a research finding.

This is one of the few combinations from the nootropics world that actually holds up in randomised research. Theanine combined with caffeine improves task-switching and accuracy more than caffeine alone, largely because it takes the edge off the restlessness caffeine causes. The effects are small, though, and were measured in brief tests rather than across a working week.

The alpha waves are accurate: this has been observed in multiple EEG measurements and is the clearest effect of theanine. The rest is weaker. The evidence for reduced anxiety is modest and comes from short-term studies, and the claim that it lowers your cortisol has not been confirmed in the best-quality studies.

Tyrosine is indeed the building block your body uses to make dopamine and noradrenaline, and taking it demonstrably raises the levels of these substances in your blood. However, this only leads to increased production in the brain when your reserves are actually depleted, for example after sleep deprivation, exposure to cold, or prolonged stress. In someone who is well-rested, nothing happens.

Brief, vigorous exercise just before mental work measurably improves your attention; that has been observed in multiple studies. What exactly happens in your brain is less clear: the assumption that more neurotransmitters are produced is derived from animal studies and has not been measured in humans.

That sleep deprivation seriously impairs concentration is well established and is one of the most consistently measured effects in sleep science. The accompanying explanation, however, is an oversimplification: it involves far more than two neurotransmitters, and the threshold of 60 to 90 minutes is a round number without any research to back it up. Moreover, every person responds differently to the same degree of sleep loss.

For people with existing cardiovascular disease or kidney problems, GLP-1 medications are well supported by evidence, but the claim that they promote a longer lifespan and protect against Alzheimer's is not yet backed up conclusively. The signals regarding brain protection and the prevention of dementia are promising, but have not been confirmed in randomised trials. The claim presents something as an established fact, while research in healthy individuals on this point is not yet complete. Moreover, the available research says little specifically about low doses as a distinct category.

Testosterone therapy has been studied for specific outcomes in people with an established deficiency, and the results are mixed: there is evidence of benefits in terms of body composition, libido and mood, but also real risks of atrial fibrillation, pulmonary embolism and kidney failure. A broader protective effect on all-cause mortality, in both men and women, has not been demonstrated in the available studies. The claim therefore goes considerably further than what the research has shown so far.

The claim makes two specific assertions at once: that bio-identical hormone therapy is clearly superior to conventional therapy, and that starting early reduces all-cause mortality. What the research actually shows is more nuanced: hormone therapy has well-established benefits for symptoms and bone health, and those who start early have the most favourable balance of benefits and risks, but a demonstrable reduction in all-cause mortality has not been proven. For bio-identical hormone therapy specifically, no completed trials with relevant outcomes are available, so there is no evidence that this variant outperforms other forms in this regard.

Mitochondria play a role in ageing, and there is evidence that mitochondrial mutations contribute to accelerated ageing, but the step to 'improved mitochondrial function reduces overall mortality and slows ageing' has not been demonstrated in humans. Exercise can improve mitochondrial health, but whether that translates into a longer lifespan in humans remains an open question. The claim presents as established fact what research regards, at most, as a plausible mechanism.

Senescent cells accumulate inflammatory substances and thus form a source of chronic low-grade inflammation; that mechanism is well documented. It is plausible that such local inflammation can also have systemic effects in the body, but the specific route via an ageing skin barrier has not yet been causally demonstrated in humans. The direction of the claim is therefore correct, but the emphasis on the skin as the starting point goes beyond what current research firmly establishes.

That exercise raises BDNF has been measured in humans and is one of the best-supported links between physical activity and the brain. The step towards neurogenesis is less firmly established, because whether adult humans generate new brain cells remains a matter of debate.

Large observational studies consistently show that abdominal fat strongly increases the risk of premature death, even in people with a normal weight and no other measurable metabolic problems. The direction of the claim is therefore correct. However, the specific figure of 'an almost twice as high risk of dying' cannot be firmly established based on the available research, and moreover these are observational associations in which cause and effect have not been fully proven.