The Ultimate Human

Research does indeed show that the pace of ageing varies considerably between individuals and that lifestyle, income and biological factors account for a large part of that variation. Excess weight, smoking and an unhealthy metabolic profile demonstrably accelerate the biological clock, and metabolism only declines noticeably after the age of sixty, not automatically before then. This lends support to the idea that much of the decline is not inevitable. However, the claim goes further than the evidence supports: research shows that many health problems can be influenced, but not that they are not a natural consequence of ageing. The distinction between what is modifiable and what is inherent to ageing has not yet been settled by science.

It is true that oak leaves contain gallic acid, ellagic acid, and tannins. How much of these actually ends up in the water when you brew them is unknown, and there is no research showing any health benefit. Moreover, high tannin levels can inhibit iron absorption.

These properties come from test-tube experiments using concentrated extracts, which tells us nothing about a cup of tea. The HIV claim is the most harmful: there is not a single human study to support it, while effective HIV-suppressing medications do exist.

Correct. Raw egg white contains avidin, which binds biotin so tightly that it can no longer be absorbed. Heating destroys the avidin. Added to this, the proteins in cooked egg white are far better digested than those in raw egg white, at around 90 percent versus 50 percent.

Two things go wrong here. Singlet oxygen is not a free radical, and it is not the substance that hydrogen gas acts on according to the research; that concerns hydroxyl radicals. Furthermore, virtually all the evidence comes from animal studies and small short-term trials. Whether hydrogen has any effect in humans is an open question, and inhaling it for four hours a day goes far beyond what can be concluded from that research.

Carotenoids are fat-soluble, so without fat in the same meal the intestine absorbs only a fraction of them. This has been measured repeatedly, including with salads with and without dressing. Milk fat works well for this purpose, but any source of fat does the same; olive oil or avocado works just as well.

The first part is correct: goat's, sheep's and buffalo milk contain no A1 beta-casein, so in that sense they are A2. They are not naturally homogenised, however. Goat's milk has smaller fat globules and lacks the substance that causes fat to cluster together, which means the cream rises more slowly. That is not the same as homogenisation, and in the case of buffalo milk it does not apply at all: buffalo milk is particularly high in fat and the cream separates quickly.

The claim that muscle strength declines faster than muscle mass is correct: research shows that strength decreases by around 3 to 4% per year after the age of fifty, which is indeed far more than muscle mass loss alone would explain. The precise rate of muscle mass loss (0.5% per year, or 4 to 5% per decade) cannot be firmly established based on the available evidence, and the exact ratio of "two to five times faster" for strength is more specific than the research supports. The direction of the claim is therefore correct, but the precise figures are stated with more certainty than the evidence allows.

European guidelines on sarcopenia do indeed use a grip strength threshold in women as part of the screening process, and our answers confirm that grip strength plays a central role in the diagnostic pathway. However, the cut-off values differ between international guidelines, which has already caused confusion in research. The specific value of 16 can therefore not be substantiated on the basis of the available evidence.

The direction is correct: a large waist circumference is an independent risk marker for premature death, diabetes and cardiovascular disease, regardless of overall body weight. However, the claim goes further by stating precise cut-off values for the waist-to-height ratio (below 0.5 safe, 0.6 or higher high risk), and those figures cannot be substantiated on the basis of the available research. The evidence on waist circumference focuses on waist size as a measure in its own right, not on a specific ratio with accompanying threshold values.

The decline of NAD+ with age and the role of chronic inflammation in this have been consistently established in both humans and animals. An important mechanism is indeed the increase of pro-inflammatory cells that actively break down NAD+. The claim attributes this specifically to the enzyme CD38, but that specific mechanism is not elaborated on by name in the available research. The general direction is correct, but that precise detail cannot be substantiated on the basis of current evidence in humans.

Research shows that both processes play a role in the age-related decline of NAD+. Increased breakdown by pro-inflammatory cells is indeed an important mechanism, but production also decreases, partly because proteins that counteract cellular aging become less active. The claim that reduced production plays no role goes beyond what the research supports.

Research shows that a confirmed testosterone deficiency is associated with health risks, and that treatment can be beneficial for men with a confirmed deficiency. However, the second part of the claim goes too far: large studies such as TRAVERSE show that heart attacks do not occur more frequently with supplementation, but there are real risks of atrial fibrillation and pulmonary embolism. The claim that this treatment reduces the risk of cardiovascular disease is therefore not supported, and the benefits moreover explicitly do not apply to men whose testosterone decline is caused solely by ageing or excess weight.

Large randomised trials, including the 2023 TRAVERSE study, found no increased risk of prostate cancer in men with low testosterone levels during testosterone therapy. That part holds up. The claim that the therapy does not worsen existing prostate cancer goes further than the research supports: those studies followed screened men without active cancer, and in men with prostate cancer the evidence is limited to small case series.

That figure comes from nowhere. The commonly reported observation that sweetness tastes more intense after a period of reduced sugar intake is plausible, but that is a matter of taste adaptation and not the same as the recovery of dopamine receptors. In humans, receptor sensitivity has never been measured after ten days without sugar, so the timeframe is simply made up.

The claim that sugar engages the opioid system comes mainly from animal studies, where the effect is clear. In humans it has been demonstrated more indirectly, partly through the finding that a drug blocking opioid receptors reduces the preference for sweetness. The direction is correct, but the certainty goes beyond what has actually been measured in humans.

Correct. Fibre slows gastric emptying and forms a layer through which glucose passes more slowly, and fat also slows gastric emptying. As a result, the same amount of carbohydrates produces a lower peak. This is one of the best-supported pieces of advice on blood sugar management.

Protein at breakfast does dampen the blood sugar spike and keeps you feeling full for longer; that is well established. The specifics are not. Where the figure of thirty grams comes from, why it has to be within an hour, and the claim that it prevents cravings later in the day are not supported by any evidence. A reasonable habit dressed up with an invented number.

That a craving subsides on its own is correct. An urge peaks and fades, usually within a few minutes, and waiting before acting is a well-established way of not giving in to it. The glass of water is not an active ingredient in that process; the waiting is. And claiming that ten minutes is always enough is stated more precisely than the evidence warrants.

The gut does indeed communicate with the brain via the vagus nerve; that is well established. That bacteria thriving on sugar influence your dopamine and serotonin levels through that pathway has not been demonstrated in humans. Ghrelin does not belong in this list in the first place, as it is produced by the stomach. Most of the evidence comes from germ-free mice, and that does not translate straightforwardly to humans.

In rats that binge on sugar, the number of dopamine receptors demonstrably decreases. In humans, that pattern has been observed in obesity, but it is impossible to separate what is caused by sugar from what is caused by excess weight itself. That the prefrontal cortex suffers as a result is a plausible but not yet proven next step.