Dr. Josh Axe

For each of these substances there is research suggesting a link with mitochondrial health, but the strength of the evidence varies considerably between substances and is far from convincing in humans in many cases. Urolithin A has a plausible mechanism of action through the clearance of damaged mitochondria, but the human studies are small, partly failed to reach their primary endpoints and largely come from the manufacturer. NAD+ supplements measurably raise NAD+ levels, but whether this actually leads to better mitochondrial health in humans has not yet been demonstrated. CoQ10 has the strongest human evidence, but specifically in people with heart failure, not as a general mitochondrial supplement. For PQQ, the available data are insufficient to reach a verdict. The claim that all these substances 'support' mitochondrial health therefore goes beyond what the current evidence justifies.

Research confirms that the brain cleans itself during sleep via the glymphatic system, and sleep is mentioned as one of the ways to keep autophagy active. The claim that autophagy processes are specifically activated during sleep to clear cellular waste is therefore broadly correct. However, the direct link between sleep and the activation of autophagy in cells is not well supported by the available evidence, and existing knowledge about sleep and the brain relates primarily to the glymphatic system, not to autophagy as such.

Research shows that chronically sleeping too little disrupts blood sugar regulation and increases the risk of type 2 diabetes in the long term. This effect occurs after just a few nights of insufficient sleep and works through several biological mechanisms. However, the claim that fewer than six hours of sleep causes an acute and significant rise in insulin levels goes beyond what the evidence firmly establishes: the studies demonstrate disrupted blood sugar regulation and an increased diabetes risk, but an acute, substantial insulin spike as a direct consequence is not confirmed that specifically.

Research does confirm that insulin and cortisol influence each other and other systems, but there is no evidence that normalizing these two hormones alone is sufficient to restore virtually all other hormones automatically. Chronically elevated cortisol affects multiple systems, including immune function, sleep and body composition, and recovery depends on more factors than cortisol and insulin levels alone. The claim suggests a direct and near-complete chain reaction that the available research does not support. The reality is more complex: hormonal balance is an interplay of many systems, each with its own regulatory mechanisms.

Research points to multiple biological processes that together contribute to the development of cancer: the accumulation of DNA damage, a weakened immune system, and chronic inflammation are all well established. The immune system certainly plays a role, but research does not identify it as one of two key players. The "detoxification system" as a distinct key organ system in cancer development is not named or substantiated as such in the available evidence. The claim suggests a neat two-part division that research does not support.

The claim asserts a causal link between unprocessed emotions and damage to the colon and the immune system. Research does show that the gut and the immune system are closely connected, and that disruptions to the gut barrier or gut microbiome can dysregulate the immune system. However, there is no evidence that holding on to past emotions triggers that process. The leap from psychological emotions to concrete intestinal damage has not been demonstrated and goes far beyond what available research shows.

Emotional trauma and psychological stress can contribute to hormonal dysregulation through the cortisol system, but the evidence for this is limited to specific subgroups and far from strong enough to speak of one of the biggest causes. For digestive problems, available research does not address this link. When it comes to cancer, research points to physical factors such as obesity and physical inactivity as well-established risk factors, not emotional baggage. The claim presents trauma as a primary cause of three serious conditions simultaneously, and that has not been demonstrated.

That the body adapts to higher carbon dioxide levels through practising breath-holding is plausible and has been observed in divers. Systemic vasodilation, however, is an oversimplification: during breath-holding, activity in the sympathetic nervous system also rises, causing blood vessels in the arms and legs to contract while those in the brain dilate. The body does both at the same time, in different places.

That carbon dioxide dilates blood vessels is correct and well documented, particularly in the brain: at higher CO2 levels, blood flow there increases measurably. However, the reversal of the claim goes too far. Nitric oxide is the substance through which the vessel wall itself regulates blood flow, a role established by Nobel Prize-winning research. These are two distinct mechanisms, not competitors for first place.

That the body responds to oxygen deprivation with adaptations in the mitochondria is well established from altitude and exercise research. The leap to a lower biological age is an entirely different matter: it would require measuring an ageing clock before and after, in a controlled study design, and that research does not exist. The first part is physiology; the second is a promise.

Research shows that berberine measurably lowers blood sugar and can offer broader metabolic benefits for people with type 2 diabetes, so the general direction of the claim is correct. However, the wording goes further than the evidence justifies: the evidence is moderate and the claim lacks the necessary caveats. The European food safety authority was unable to establish a safe intake level due to indications of DNA and liver damage, and berberine has strong interactions with many medications, including diabetes medication itself. Presenting berberine as a support for insulin resistance and diabetes without these qualifications is incomplete.

There are indications that microplastics can affect male fertility and hormonal balance, but these indications come largely from laboratory and animal studies. It has not yet been demonstrated in humans that everyday exposure to microplastics leads to a significant drop in testosterone levels. The claim therefore goes further than current research can substantiate.

That synthetic clothing releases microplastics and that these particles enter the body through breathing and possibly through the skin is consistent with what research shows: microplastics have demonstrably been found in the human body. There is also research showing that some hormone-disrupting substances are present in everyday plastic products and are measurable in blood and fatty tissue. However, the claim states too categorically that polyester clothing acts as a hormone disruptor through these routes: the evidence for that specific mechanism in humans is still predominantly associative and comes largely from laboratory and animal studies. How significant the risk of clothing as a source is during everyday exposure, and whether it genuinely leads to hormonal disruption, has not yet been scientifically established.

Smoking demonstrably accelerates skin ageing through oxidative stress and inflammation, and multiple systematic reviews confirm that smoking is an independent risk factor for wrinkles and loss of elasticity. However, the claim goes beyond what the research shows: there is no evidence that nicotine specifically causes dehydration as a mechanism behind skin ageing, and the claim focuses on nicotine in particular while the evidence concerns smoking as a whole. Moreover, evidence for the role of dehydration in this context cannot be found in the available research.

The Mediterranean diet does indeed reduce the risk of heart attacks and strokes by around 25 to 30 percent, and this has been demonstrated consistently in large randomised trials and population studies. However, the claim attributes that benefit specifically to the extra virgin olive oil, whereas the research shows that it is the overall dietary pattern that matters. Which component of the diet contributes most has not yet been established. The olive oil is one part of that pattern, not the decisive factor in itself.

Eating fibre is indeed robustly linked to a lower risk of premature death, but the claim that 10 extra grams of fibre per day extends life expectancy by more than 5 years goes well beyond the available evidence. The research speaks of a lower risk of premature death and chronic disease, not of a concrete number of years gained. That precise figure of five years cannot be substantiated on the basis of current research.

Large analyses show that the Mediterranean diet is associated with lower mortality and fewer cardiovascular diseases, but a concrete gain of 7.5 years in life expectancy is not supported by the available research. Those studies point to a lower risk of death and a reduced disease burden, not to an established number of extra years lived. Moreover, the evidence comes largely from observational research, in which cause and effect cannot be fully separated, which makes such a precise claim untenable from the outset.

Chronically elevated cortisol does indeed have measurable effects on the brain and memory: prolonged stress impairs cognitive resilience, and the evidence for this comes from large review studies. However, the answers mention no direct link between chronically elevated cortisol and physical shrinkage of memory regions such as the hippocampus. Brain shrinkage in ageing is well documented, but in the available research it is attributed more to ageing and high blood pressure than specifically to cortisol levels. The direction of the claim is plausible, but the relationship between cortisol and measurable shrinkage of memory regions cannot be firmly established on the basis of this research.

Research shows that insulin resistance is already measurable through elevated fasting insulin while blood sugar is still completely normal. Standard blood sugar tests respond too late to pick up this early signal. This supports the claim that fasting insulin rises before changes in fasting blood sugar become visible. However, the exact size of that time difference is not expressed in concrete years in the research.

Research into GLP-1 medications shows that a quarter of the weight lost consists of muscle and other non-fat tissue. This pattern is consistent with what is known from aggressive dieting as well: alongside fat, you also lose muscle mass. Strength training is the most well-supported way to limit this, and without it you face a greater risk of muscle loss. The claim therefore accurately reflects the current state of the evidence.

The recommendation of 1 gram per pound of body weight per day amounts to approximately 2.2 grams per kilogram per day. Research indicates that for maintaining and building muscle after the age of forty, an intake of 1.2 to 1.6 grams per kilogram per day is well supported, and up to 1.6 to 2.4 grams per kilogram when losing weight. The amount in the claim is therefore considerably higher than what the evidence recommends. Furthermore, research shows that strength training is at least as important as protein intake itself, something the claim does not mention at all.

Large-scale research consistently shows that low grip strength is associated with a higher risk of premature death, and that association is robustly supported. The direction of the claim is therefore correct. However, the specific figure of a 16 percent increase in risk per 10 to 11 pounds decrease in grip strength cannot be firmly established based on the available research. Moreover, this concerns an association, not a proven cause: grip strength reflects your overall muscular health and is not a direct cause of earlier death.

Remarkably precise, because this comes from a randomised study by Stanford. People who ate fermented foods for ten weeks developed a more diverse microbiome and showed a decrease in nineteen inflammatory proteins. The group that increased their fibre intake did not see that effect. It is one of the few solid findings in microbiome research.

This figure is repeated everywhere, but it is a rough estimate. What is true is that a large proportion of your immune cells are found in and around your gut, in the lymphatic tissue along the intestinal wall. Seventy or eighty percent is a rule of thumb for that, not a measurement. More important than the percentage is that your gut and your immune system are in constant dialogue with each other.

Correct, and this is the finding from a large review study. Half an hour to an hour of strength training per week goes hand in hand with a ten to twenty percent lower risk of death, cardiovascular disease and cancer. Notably, more than an hour per week did not yield any additional benefit in that same study.

Correct, and this has been measured precisely. In a study of older adults with elevated blood sugar, three short walks of a quarter of an hour after meals performed at least as well as a single three-quarter-hour walk, and even better after the evening meal. The timing matters more than the total duration.

The study exists and is large: in tens of thousands of people wearing a wrist tracker, a regular sleep schedule turned out to be more strongly associated with mortality risk than sleep duration itself. That is a striking and useful finding. However, the range of 20 to 48 percent comes from a single study, and irregular sleep is linked to shift work, illness, and poverty.

Correct, and this is one of the best-known findings from the long-running American Nurses' Health Study. Five habits combined: not smoking, maintaining a healthy weight, exercising, drinking in moderation, and eating well, were associated with more than twelve extra years of life expectancy at age fifty. It remains observational research, but its scale and duration make it compelling.