Claim checker

Several studies in humans, including a carefully designed four-week randomised study and a twelve-week study, find no clear changes in the composition of gut bacteria from daily stevia use. A review article even concludes that stevia may be beneficial for the diversity of gut bacteria. One study in rats did find changes in the gut flora, but results in animals are no proof of what happens in humans. The claim that two weeks of daily stevia use changes gut bacteria in a negative way is not supported by the available research in humans and is even at odds with the findings of those human studies.

Several large observational studies, in which participants are followed without researchers intervening, show that higher levels of erythritol in the blood are associated with an increased risk of serious cardiovascular problems, including heart attack and stroke. A study in which healthy volunteers were given erythritol also shows that consuming erythritol makes platelets more active, which can promote clotting. There is, however, an important caveat: those first-mentioned studies measure erythritol in the blood, but a large proportion of it is produced by the body itself as a sign of a disrupted sugar metabolism. It has therefore not yet been proven that erythritol as a sweetener in food is the cause of the risks identified. Long-term studies into the effects of erythritol as a dietary ingredient on cardiovascular disease are still lacking.

Research in healthy adults shows that allulose can indeed cause gastrointestinal complaints at higher doses, including diarrhoea and bloating (abdominal distension). The claim is therefore broadly correct. However, it goes slightly beyond what the evidence supports: these complaints only occur at quite high single doses, and with regular intake in large amounts other complaints also occurred, such as nausea and abdominal pain. "Loose stools" as a separate complaint is not mentioned as such; diarrhoea is. The claim also suggests that this happens to everyone who consumes large amounts, whereas the research shows that the threshold depends on body weight and the manner of intake.

Your body can use more protein per meal than the well-known threshold of 20 to 25 grams, but that does not mean that 100 grams in one go is fully utilised. Research shows that the exact threshold depends on the composition of the meal and the rate at which protein is digested, and that absorption is higher with a mixed meal than with fast protein on an empty stomach. For the best results, you should still spread your daily intake across four or more meals of around 0.4 grams per kilogram of body weight; with a single very large portion, you are likely to lose some of the potential benefit.

Research confirms that obesity among American adults has risen sharply: from around 30% around the turn of the century to well over 40% in recent years. That is a significant increase, but not a quadrupling. The claim that genes play no role is also not entirely accurate: research actually shows that certain genes make people more susceptible to an environment that promotes obesity, and that epigenetic factors play a major role. The core point is correct, however: the rise has been so rapid that a changed gene pool cannot explain it, and environmental and lifestyle factors are seen as the main cause.

Exercise does indeed help limit weight gain and is an important part of maintaining a healthy weight, but the research nuances the second part of the claim. Losing weight through exercise alone is not so much "difficult" as it is fundamentally less effective: only above 250 minutes of exercise per week does the effect on the scales become truly noticeable, and combining exercise with caloric restriction is demonstrably more effective than exercise alone. The claim is therefore broadly correct, but it suggests that exercise in itself is a reasonable path to weight loss that simply requires a bit more effort, whereas the evidence shows that diet is the decisive factor.

The claim that exercise and fasting influence cellular repair and maintenance mechanisms via mTOR and AMPK is broadly correct, but the details are more nuanced than the statement suggests. As for mTOR, fasting and protein restriction lower its activity in a way that appears beneficial for cellular maintenance; for AMPK, however, human studies show that fasting alone produces barely measurable activation in muscles. Combining exercise with low carbohydrate availability, such as training in a fasted state, is the best-supported way to activate AMPK. The statement gives the impression that both triggers act equally strongly on both mechanisms, and that is not consistent with the available research.

Zinc does indeed play a role in bone health: people with a low zinc intake are at greater risk of bone loss, and supplementation improves bone density, particularly at the hip. However, the claim that zinc contributes to the "formation" of bone tissue goes slightly further than the research supports. The evidence points mainly to the preservation of bone density and the prevention of loss, and the benefit is greatest in people with a low zinc intake.

For sleep, there are cautious indications that magnesium glycinate may offer a modest benefit, particularly if you get little magnesium through your diet. The claim that it "helps improve" sleep goes slightly further than the evidence justifies: the studies are small, of low quality and partly contradictory. For ordinary nocturnal leg cramps, magnesium offers no demonstrable benefit, so that part of the claim does not hold up.

Several review studies show that boron plays a role in bone health, partly through the metabolism of calcium, vitamin D and sex hormones. A narrative review from 2020 (11 studies, 594 participants) concludes that a daily supplement of 3 mg of boron can positively influence bone mineral density in humans. At the same time, other reviews emphasise that the body of evidence is still limited and the findings are mixed, and that boron is generally studied as one of many trace elements. The claim that boron protects against bone loss is broadly correct in its direction, but is more definitive than the current research fully supports: the evidence base is still relatively small and the effects depend on dose, duration and individual circumstances.

The part about insulin is broadly correct: several studies show that intermittent fasting lowers fasting insulin levels and improves insulin sensitivity, although the evidence is partly of limited quality. The claim about free oestrogen and testosterone is a different matter: our answers only note that hormonal fluctuations are a point of concern with fasting and intense exercise, not that fasting significantly raises these hormones. The word "significantly" in relation to insulin also goes further than the studies support, and the hormonal claim about oestrogen and testosterone cannot be substantiated on the basis of the available research.

A published case report (a scientific article on a small number of individual patients, registered under number 39981248 in an international database) discusses two MS patients who received ibogaine and subsequently showed improvement, including changes in pain and brain scan outcomes. The claim about rapid pain reduction, fatigue and improved motor endurance is consistent with the direction of that report, but a description of only two patients is not strong evidence. Moreover, the authors have a financial interest in the company offering the treatment. The remaining available studies concern ibogaine in rats or traditional rituals, not MS patients. No well-designed studies in people with secondary progressive MS have yet been completed that confirm these effects.

The cardiac risks of ibogaine are serious and documented, including in people without pre-existing heart conditions, and deaths have been reported. However, the mechanism described in the claim, namely reduced potassium uptake in heart cells as the cause of QT prolongation, is not supported by the available research. That ibogaine prolongs the QT interval and can cause serious arrhythmias is consistent with what is known, but the precise effect on potassium channels cannot be established on the basis of this evidence.

A study of 30 male veterans with traumatic brain injury shows that ibogaine is indeed associated with changes in blood flow in brain areas, measured by fMRI directly after treatment and after one month. Blood flow increased gradually in several brain areas, and changes in blood flow were associated with improvement in symptoms. The claim is therefore correct regarding the blood flow and the fMRI measurement, but it also mentions "electrical activity", which the study did not measure: the researchers looked at blood flow and functional connectivity, not at electrical brain activity. Furthermore, it is a small, uncontrolled study involving exclusively male military veterans, and the researchers themselves emphasise that larger, controlled studies are needed to confirm the findings.

There is one published case report, identifiable by a unique registration number in a scientific database, on ibogaine for severe nerve pain. It concerns a man who had suffered persistent pain for twenty years following nerve damage. The report indicates that the treatment was promising and that the pain decreased significantly. However, the figure of forty percent does not appear in the available abstract of that report, so this specific figure cannot be confirmed on the basis of this study. Moreover, it is a single case, which means no general conclusions about patients with nerve pain can be drawn from it. Other research focuses on ibogaine for addiction problems, or on related substances in animals, not on pain reduction in humans.

There is biological evidence that green tea catechins such as EGCG can influence thermogenesis, and the most modest but most consistent benefit found in research is a slight additional weight loss when catechins are combined with exercise. However, the effects observed in the laboratory translate only to a limited extent into demonstrable benefits in humans. The claim that EGCG "can activate" thermogenesis is therefore not wrong in its direction, but suggests more certainty than the available evidence in humans justifies.

The claim is partly correct: research shows that finely milling grains damages cell walls, causing carbohydrates to be broken down earlier by digestive enzymes in the small intestine and therefore reaching the large intestine in smaller amounts. This applies in particular to starch and protected macronutrients in intact cells. The picture is more nuanced, however: dietary fibre (a type of carbohydrate) does reach the large intestine, and laboratory research shows that soluble and insoluble fibres from processed grain flour are fermented just as well in the large intestine. Mouse studies also show that the type of processing (cooking versus extrusion) affects what reaches the gut flora and how the flora responds, but this has not yet been studied in humans. The claim is therefore too broad: it applies more strongly to starch than to fibre, and to some forms of processing more than others.

The claim states that omega-6 fatty acids improve insulin sensitivity, lower long-term blood sugar levels, lower bad cholesterol and raise good cholesterol. Research in humans paints a more nuanced and partly contradictory picture. A large review combining many studies found no link between eating more omega-6 and a lower risk of a combination of conditions such as obesity, high blood pressure and disturbed blood sugar, whereas omega-3 did show such a link. Studies on linoleic acid (an omega-6 fatty acid) and blood sugar control yield mixed results: one review sees a possible protective role, but an observational study in diabetic patients shows that higher omega-6 levels are actually associated with poorer blood sugar regulation. For a specific type of omega-6 fatty acid naturally found in dairy and ruminant meat, research even shows a rise in fasting blood sugar with no effect on long-term blood sugar levels or insulin sensitivity. The specific effects on bad and good cholesterol are not confirmed for omega-6 by this research.

For nuts, the picture is more nuanced than the claim suggests: studies show that nuts have no clear effect on weight, which supports the claim, but "no evidence of weight gain" is a different assertion from "nuts do not help with weight loss". For olive oil, calories ultimately do count towards weight, and the available research does not specifically address whether olive oil causes weight gain or not. The general scientific consensus that calorie intake determines weight regardless of its source makes the claim too categorical in absolute terms: the direction is correct for normal use, but "no evidence" is a stronger statement than what the research demonstrably supports.

Several animal studies show that curcumin can activate thermogenesis: the substance stimulates the conversion of white adipose tissue into heat-producing brown adipose tissue in mice and increases the production of proteins required for this process. This effect has been consistently found in mice under a variety of conditions, including obesity induced by a high-fat diet, exposure to chemical substances, and even through the gut bacteria of the mother. In humans, this effect on thermogenesis has not yet been tested in clinical research involving actual patients or participants, which means the claim is currently supported only by animal research.

Research shows that there is a link between ultra-processed foods and a higher blood sugar response after eating. One analysis of 98 ready-made products found a strong association between the degree of processing and the blood sugar response. Review studies and mechanistic research in humans cite a higher blood sugar response as one of the possible explanations for the health risks of ultra-processed foods. The claim is therefore broadly correct, but in most studies the relationship is indirect or measured as an average risk across groups of people, rather than as a directly demonstrated difference in blood sugar rise in individuals. Moreover, a small-scale study with chickpeas shows that the blood sugar response does not always increase with greater processing, indicating that the effect does not apply universally to all products.

The claim that exercise without dietary changes does little to reduce weight is roughly correct: the evidence shows that exercise mainly helps to limit muscle loss, not primarily as a means of making the scales go down. The evidence for building muscle mass through exercise also fits the claim. However, the part about fat around the organs, so-called visceral fat, is not addressed in the available research data, so that specific claim cannot be substantiated here. The claim thus combines a well-supported direction with an assertion that is not covered by the available sources.

Research into the heating of oils actually shows the opposite: when frying, rapeseed oil produced more volatile harmful substances (aldehydes) than extra virgin olive oil, not fewer. A study in which potatoes were fried in both extra virgin olive oil and rapeseed oil also found that rapeseed oil yielded higher amounts of harmful breakdown products because it contains more polyunsaturated fatty acids, which are more susceptible to oxidation. A study on the thermal stability of rapeseed oil does show that selective breeding can reduce the polyunsaturated fatty acid content and thereby greatly improve stability, but this concerns specially developed varieties, not ordinary rapeseed oil as found in shops. The research therefore provides no support for the claim that standard rapeseed oil is more stable than extra virgin olive oil when heated.

Research in humans shows that replacing saturated fat with unsaturated fats (such as polyunsaturated fats) lowers LDL cholesterol and reduces the risk of cardiovascular disease. However, the claim reverses the reasoning: it is not starches and sugars that replace saturated fat, but rather saturated fat that is replaced by healthy fats. Studies actually show that replacing saturated fat with refined carbohydrates and sugars is not beneficial for LDL and does not even reduce the risk of cardiovascular disease. Moreover, replacing saturated fat with unsaturated fats also lowers HDL cholesterol, so the effects are not simply "cancelled out". The direction of the message is partly correct, but the wording suggests that you can freely eat saturated fat as long as you avoid enough sugars and starches, and that goes beyond what the research demonstrates.

A study in which 57 people were randomly assigned to groups shows that butter raised LDL cholesterol, while whipping cream (rich in milk fat globule membrane) did not, which supports the core of the claim. However, the claim is too categorical: the researchers attribute the difference to the presence of the milk fat globule membrane in whipping cream, and not simply to the fact that it is whipping cream. Moreover, another study in healthy individuals looked specifically at blood triglycerides after a meal and found no difference in LDL between butter and whipping cream in that regard. The claim therefore lacks the caveat that the difference appears to depend on a specific property of whipping cream, and that not all studies show the same result.

A study of 30 male veterans with (predominantly mild) brain injury does indeed show major improvements in PTSD, depression and anxiety following treatment with ibogaine and magnesium, and those effects were still present at a follow-up measurement up to 12 months later. The improvement in sleep, however, was measured in a study in which ibogaine was combined with another substance (5-MeO-DMT), not exclusively with magnesium. The claim about sleep therefore cannot, on the basis of this research, be firmly linked to the combination of ibogaine and magnesium alone. Moreover, all studies involved are small and lack a comparison group, meaning the researchers cannot compare outcomes with those of people who received a different treatment or no treatment at all. The researchers themselves state that larger and more rigorously designed studies, in which participants are randomly assigned to groups, are needed to confirm the findings.

Research in yeast cells and mouse neurons does indeed show that ibogaine first lowers ATP levels and temporarily suppresses energy production, after which a recovery or even an enhancement of energy production occurs. This pattern is described in multiple studies and is also referred to as "metabolic preconditioning". The claim is therefore correct in its direction, but so far it is based solely on animal and cell research, not on studies in humans. Whether the same effect occurs in the human body has not yet been tested.

Early research in animals and in the laboratory showed that omega-3 fatty acids can stabilise the electrical activity of heart cells and may thereby prevent cardiac arrhythmias, including in humans. However, large, carefully designed studies and meta-analyses involving tens of thousands of people show that taking omega-3 supplements has no clear effect on cardiac arrhythmias or sudden cardiac death. At high doses, these supplements even increase the risk of atrial fibrillation. The idea that omega-3 prevents arrhythmias during a heart attack by stabilising heart cells is therefore not confirmed by research in humans themselves, and recent studies point rather to the opposite. → Do omega-3s help against heart rhythm disorders?

Several review studies and a large population study in humans show that excess iron increases the risk of diabetes and that beta cells play an important role in this. Iron can damage these cells by triggering harmful reactions inside them, which can lead to cell death and reduced insulin production. The claim is therefore essentially correct, but somewhat too simple: in humans, the evidence for the risk of diabetes runs more strongly through reduced insulin sensitivity and liver burden than through direct damage to beta cells alone, and the direct causal evidence for beta cell damage comes largely from animal studies. Moreover, the role of iron from meat specifically, such as in red meat, is not separately substantiated in the studies provided; these concern iron overload and iron intake in general.

Large follow-up studies show that people who eat yoghurt regularly develop type 2 diabetes less often, and cheese shows similar, slightly weaker associations. In addition, fermented dairy products noticeably lower blood sugar and insulin resistance in people with diabetes or prediabetes. The word "may" in the claim fits well with the state of the research: the associations are consistent, but that is not proof that fermented dairy is the only or decisive factor.

Research in humans shows that artificial sweeteners can, through changes in the gut microbiome, lead to a reduced ability of the body to process blood sugar properly, and review studies also link them to a reduced sensitivity of the body to insulin. At the same time, a randomised controlled study found no effect on insulin sensitivity after two weeks of sucralose or aspartame use in healthy adults. For natural sweeteners, some, such as stevia, may actually have a protective effect and are not directly linked to reduced insulin sensitivity. The claim is therefore partly correct for some artificial sweeteners, but goes too far by also including natural sweeteners and by presenting the effect as established, whereas the evidence in humans is not yet conclusive and long-term research is lacking. → Are diet soft drinks and sweeteners bad for you, and if so, why?

The associations between red meat and colorectal cancer on the one hand and type 2 diabetes on the other are indeed well documented, but the research also describes a clear association with cardiovascular disease. No ranking has been demonstrated in which colorectal cancer and diabetes come out more strongly than cardiovascular disease; on the contrary, the evidence indicates that the associations are clear for all three conditions. The claim therefore draws a comparison that the available evidence does not support.

Several review studies show that omega-3 fatty acids can activate fat burning, particularly through certain types of adipose tissue. This effect has been demonstrated consistently in animal studies and laboratory studies. In humans, however, the evidence is still limited: one review study notes that human fat cells can take on a different composition in response to EPA, and another review study discusses studies in humans on energy expenditure, but concludes that the potential use as a treatment for humans needs to be investigated further. The claim is therefore correct in its direction, but is broader than what the evidence in humans firmly supports so far.

Two copies of the ApoE4 gene do indeed confer a significantly increased risk of Alzheimer's disease. ApoE4 is the strongest known genetic risk factor for the common form of the disease, and having two copies raises that risk more than having one. Nevertheless, two copies are no guarantee of developing the disease: many carriers never become ill, and lifestyle factors such as exercise and healthy eating have been shown to have a measurable protective effect even for them.

A study involving people who ran a 5 km race at maximum speed showed exactly the opposite: immediately after the effort, both insulin levels and blood sugar levels were higher than on a rest day, and insulin sensitivity was reduced. Multiple review studies confirm that exercise increases the insulin sensitivity of muscles in the longer term, but that immediately after intense exercise, insulin levels in response to food do not necessarily need to be lower. The claim that the body produces less insulin in response to a meal after a 3-mile run is not supported by the available research in humans and, for short-term maximal exercise, even appears to be contradicted by it.

For red and processed meat and colorectal cancer, there is indeed strong evidence from dozens of long-running studies, and the association is consistent: higher meat consumption is linked to a higher risk. That pattern resembles a dose-response relationship, but the claim goes further than what the research establishes: the relationship applies mainly to colorectal cancer, and most strongly to processed meat. For other types of cancer, the indications are considerably weaker. The broad category of 'long-term cancer risk' is therefore not well supported by the available evidence.

Large review studies in humans show that eating less saturated fat moderately reduces the risk of cardiovascular disease, and that replacing it with polyunsaturated fats appears to be a useful strategy in this regard, particularly for people at high cardiovascular risk. Nevertheless, the picture is not straightforwardly 'better for everyone': for people with a low baseline risk, the benefit appears minimal, and one analysis that includes only well-controlled trials finds no clearly demonstrable effect on heart disease or mortality. Furthermore, the benefit applies mainly to cardiovascular events; little or no effect was found on all-cause mortality. The claim is therefore too broadly formulated: the evidence is stronger for people at elevated risk and specifically for cardiovascular outcomes, not for health in general.

Research shows that red meat contains a sugar molecule (Neu5Gc) that humans absorb through their diet and that ends up on cell membranes. Because humans do not produce this molecule themselves, they respond to it with antibodies, and that response is accompanied by mild chronic inflammatory symptoms (xenosialitis). However, Neu5Gc is a sugar acid (a specific sialic acid), not a glycoprotein in the broad sense of the word; the claim identifies glycoproteins as the activating substances, whereas the evidence specifically concerns this sugar molecule on glycans. Moreover, the mechanism in humans has largely been described on the basis of animal and laboratory studies; direct evidence that the inflammatory response in humans is clinically relevant has not yet been fully established.

A high-quality plant-based diet is associated with lower rates of premature death and favourable changes in gut bacteria, but that benefit lies primarily in the quality of the food, not simply in eliminating animal products. Strictly vegetarian or vegan eating has not been proven to be better than a varied diet that occasionally includes meat or fish, and for older adults and pregnant women a strictly plant-based diet carries real risks of nutritional deficiencies. The claim that plant-based food makes people "generally" healthier is therefore too broad: the quality and composition of the overall dietary pattern matter more than the category alone.

Research shows that grains and legumes together can indeed provide a nearly complete amino acid profile, as they complement each other's shortcomings. However, studies add the nuance that "complete" does not automatically mean that all amino acids are equally well absorbed: plant-based proteins generally contain fewer essential amino acids than animal proteins, and their absorption by the body is lower. Moreover, the composition varies considerably depending on the specific combination of grain and legume, meaning that not every combination automatically delivers a full spectrum. The claim is broadly correct, but it creates the impression that the combination is fully equivalent to animal protein sources, which the research does not confirm.

Several reviews of scientific research in people with type 2 diabetes show that a low-carbohydrate diet can contribute to weight loss, improved blood sugar levels, and even remission of the disease in some participants. One large meta-analysis found that after six months, well over half of the people on a low-carbohydrate diet no longer had diabetes, compared to nearly a third in the group that did not follow the diet. The claim that it "can be life-changing for some people" is consistent with these findings. However, the studies also add nuance: the effects diminished after twelve months, the evidence is not very strong, and the specific condition that food must be "minimally processed" is not examined in the studies. The qualification "some people" aligns with the findings, but the emphasis on minimal processing goes beyond what the research has actually tested.

A large meta-analysis pooling many human studies shows that when total protein intake is taken into account, the timing of intake has no measurable additional effect on muscle growth. That part of the claim is correct. At the same time, however, multiple human studies show that how protein is distributed throughout the day does matter: spreading intake evenly stimulates muscle tissue synthesis noticeably more than concentrating everything in one meal. The prevailing scientific consensus therefore recommends distributing protein at intervals of roughly three hours. The claim that timing has "no clear effect" thus goes further than the research supports: it applies specifically to timing around training, whereas daily distribution turns out to be a separate factor. → When is the best time to eat protein for your muscles?

Ultra-processed food is associated with a broad and consistent range of health risks, including depression, but the studies provided do not mention cognitive decline and Alzheimer's disease as specifically examined outcomes. The associations that have been found are all observational, meaning that causality has not been established even for the conditions that were examined. The direction of the claim is plausible, but the specific link with cognition and Alzheimer's disease cannot be substantiated on the basis of the available evidence.

That chronically elevated insulin levels are associated with more age-related diseases, including cardiovascular disease and cognitive decline, is consistent with the available research. However, the claim goes much further: it asserts that insulin causally contributes to virtually all chronic diseases. The research shows mainly associations, not proven causal relationships, and the links often run via excess weight and other factors. Furthermore, the association with cancer is indirect and has certainly not been demonstrated for sugar or insulin as an independent cause. The leap to "virtually all chronic diseases" and "causally" is not supported by the available evidence.

Sugary drinks are indeed associated with a higher risk of type 2 diabetes and fatty liver disease, and fatty liver disease in turn is associated with an increased risk of inflammation-related conditions. However, the claim makes it sound like a simple, established chain reaction: liquid sugars are absorbed, the liver turns them into fat, and that directly leads to fatty liver disease and inflammatory molecules. Evidence exists for the individual steps, but the direct causal link from start to finish has not yet been fully demonstrated in humans. Moreover, fatty liver disease is a condition determined by more factors than liquid sugars alone, such as excess weight and physical inactivity.

Research has consistently shown that sugary drinks such as soft drinks increase the risk of type 2 diabetes. The direction of the claim is therefore correct. However, the specific figure of a 23 percent increase in risk for one can per day does not appear in the available research, and such precise figures from meta-analyses vary considerably between studies and populations. The relationship is clear, but that exact percentage cannot be substantiated.

Research shows that sweeteners, when used normally, do not cause weight gain and even appear to be slightly beneficial for weight compared to regular sugar. The observational studies that seem to show a link with health problems are probably explained by the fact that people who are overweight or ill more often opt for light products, not the other way around. The idea that sweeteners trigger compensatory behaviour that leads to a higher calorie intake is therefore not supported by the available research.

Several large review studies in humans do indeed show that eating more ultra-processed food is associated with a higher risk of type 2 diabetes. The direction of the claim is therefore correct. However, the figure of 10 percent higher risk per 10 percent more ultra-processed food deviates from what research shows: the figures found range between 12 and 14 percent higher risk per 10 percent more ultra-processed food, not exactly 10 percent. Moreover, these are observed associations from population studies, in which cause and effect have not been fully established, and the risk varies depending on the type of ultra-processed product.

A study of 138 first-time marathon runners found exactly the drops mentioned after six months of training: 4 mmHg systolic and 3 mmHg diastolic in central (aortic) blood pressure. An eight-month study with 45 participants showed comparable results, and two large meta-analyses on endurance sports confirm that blood pressure reductions of this magnitude are realistic. The claim states the figures correctly and rightly specifies that it concerns central blood pressure.

The MARC-2 study, a study of 289 middle-aged to older men followed for over six years, does show that exercising at very high intensity is associated with a greater increase in calcium deposits in the coronary arteries, while exercising at high but slightly lower intensity is associated with less increase. The direction of the claim is therefore correct. However, the claim is worded more broadly than the available evidence justifies: this study looked only at middle-aged men, and other studies, such as a large-scale meta-analysis and cross-sectional studies, focus primarily on total exercise volume rather than specifically on the comparison between the two intensity levels mentioned in the claim. Furthermore, some studies suggest that a higher average intensity is actually associated with less calcification, and that the participant's sex plays a role. The claim omits these nuances and presents the association as though it applies universally, while the evidence comes primarily from a single long-term study in men.

Research in humans does show that endurance athletes have calcified plaques more often than non-athletes, but the claim that non-endurance athletes in turn have soft (non-calcified) plaques more often does not hold up against the findings. The large Master@Heart study shows that lifelong endurance athletes also have significantly more non-calcified and mixed plaques than healthy non-athletes, meaning that the more dangerous plaque types are actually more common in the athletes themselves. The notion that non-athletes account for the high-risk soft plaques is therefore not supported by the available research and contradicts what the studies show.

The finding that marathon training is associated with a lower biological age is consistent with what research shows: regular intensive exercise is consistently linked to a biological age that is roughly one to three years lower on epigenetic measures. However, the claim specifically mentions the aorta and a reduction of four years, and that level of precision goes beyond what the available evidence supports. Moreover, it has not yet been proven that a lower score on a biological age clock actually guarantees better health or a longer life.

Cortisol and insulin resistance are demonstrably linked, but the evidence in the research concerns chronically elevated cortisol, not a brief rise. With prolonged excessive cortisol levels, several mechanisms have been described that lead to the accumulation of deep abdominal fat and insulin resistance. The word 'directly' in the claim suggests an immediate effect with every rise in cortisol, whereas research shows that this is a process that develops over a longer period of time. The direction is correct, then, but the claim makes it sharper and faster than the evidence justifies.

That oestrogen plays a role in how the brain functions, including in substances that influence mood and cognition, is supported by research: studies on memory and concentration show that a declining oestrogen level has measurable effects on brain function. However, the claim names a specific series of substances, including dopamine, serotonin, acetylcholine, oxytocin and BDNF, and that precise list cannot be substantiated on the basis of available research. Moreover, "stimulates" suggests a straightforwardly upward effect, whereas in reality the picture depends on factors such as timing, type of oestrogen and individual circumstances.

Research in humans shows that mindfulness and meditation can generally lower cortisol and may influence the immune system, but the claim goes further than the evidence supports on one important point. A large randomised study with 313 participants actually shows that focused attention training does not lower the cortisol stress response, whereas social forms of training such as compassion training do. At the same time, meta-analyses show that mindfulness and meditation as a broad category positively influence cortisol and some heart-related measures, and that effects on the immune system are still small and mixed. The combination of focused attention, open awareness and kind intention has not been tested as a package in the available studies, and the claimed effects do not apply equally to all three components. → How healthy is meditation, and what does it actually do for you?

Extra protein during weight loss helps preserve muscle mass, and intakes higher than the official minimum guideline are well supported. However, the studies that inform our answers point to a range of 1.2 to 1.6 grams per kilogram per day as a well-supported target for maintaining muscle mass, not to 2.2 grams as the ideal figure for lean people losing weight. The claim also mentions 'lean people' as a separate group, but that distinction is not made in the available evidence. The direction of the claim is correct, but the specific threshold of 2.2 grams cannot be substantiated on the basis of the research.

Research in humans shows no protective effect of high Lp(a) levels during a COVID-19 infection. One study of 211 hospitalised patients found no association between Lp(a) and in-hospital mortality or discharge. Another study of 50 patients links high Lp(a) to more severe illness, such as more serious kidney damage. Yet another study of 219 patients shows that a rise in Lp(a) during admission is strongly associated with more thrombotic complications, and a further study links higher Lp(a) to increased mortality and worse outcomes. The research therefore provides no indication that high Lp(a) protects people; if anything, the findings point in the opposite direction.

Research shows that AGEs adversely affect the mechanical properties of tendons: in a laboratory study using human shoulder tendon tissue (ex vivo), tensile strength was markedly lower after exposure to AGEs, and studies using rat and bovine tendon tissue show similar effects on fibre sliding and deformability. The claim is therefore correct in its direction, but the direct evidence for reduced tensile strength in shoulder tendons comes from tissue outside the body, not from living humans. Whether these findings also lead to measurable loss of strength in the living human body has not yet been demonstrated.

A large review study pooling data from more than one million patients found a protective effect of rosuvastatin on rotator cuff conditions (HR 0.41), which roughly corresponds to the "half the risk" mentioned. However, the results for other statins and other tendon inflammations are contradictory: some studies actually find an increased risk of tendon problems, and one study found a considerably higher chance of re-rupture of the tendon after surgery in people taking statins. The claim suggests that the effect applies to statins in general and to all people with high cholesterol, whereas research shows that the effect depends strongly on the type of statin, the type of tendon and individual characteristics. The direction of the claim is therefore correct for a specific case, but it is formulated too broadly for the available evidence.

There is one small study in humans (12 participants) showing that adults with slightly elevated LDL cholesterol do indeed have stiffer Achilles tendons than people with normal cholesterol levels. That direction is therefore correct. However, the study is very small, and other research in people with a hereditary cholesterol disorder shows mixed results: sometimes less stiffness or no difference in stiffness, depending on how and when it is measured. The claim that this causes "considerably" stiffer tendons goes further than the body of evidence robustly supports, especially since the groups were small and the findings still need to be confirmed in larger studies.

Research on older women with sleep problems shows that a hot bath (around 40 degrees) an hour and a half before bedtime improves sleep quality and leads to more deep sleep, and that participants experience their sleep as deeper. These findings come from small studies with nine and fourteen participants respectively, and a review study summarising three such studies confirms the same picture. The claim therefore holds for hot baths, but for lukewarm baths the results are weaker: in one study, lukewarm water showed only a slight indication of more deep sleep, with no clearly demonstrable effect. The claim suggests that lukewarm and warm work equally well, whereas the evidence does not support that distinction.

There is research showing a link between the glycaemic index of an evening meal and how quickly you fall asleep, and the direction of the claim is consistent with what is known about carbohydrates, blood sugar and sleep. However, the specific combination of rice, a high glycaemic index and the timing of four hours before bedtime as a condition for a shorter sleep-onset latency cannot be firmly established on the basis of the available research. What does emerge consistently is that the timing of meals and their composition together influence sleep quality, but concrete thresholds for timing or food type have not yet been sufficiently studied.

There is one study that examines exactly this: a randomised controlled trial in which obese adults with pre-diabetes or diabetes ate between 8:00 and 18:00 for twelve weeks, compared to eating until midnight. That study measured sleep objectively using a wrist-worn accelerometer and did indeed find approximately 55 minutes more sleep in the time-restricted group. The claim therefore comes directly from this research. At the same time, the group was small (38 participants, almost all African-American women with obesity) and the finding came from an analysis conducted after the fact, meaning the result cannot straightforwardly be generalised to broader populations. Other review studies and trials using different eating windows or different groups find no effect on sleep duration, which shows that the result depends heavily on the specific eating window, the population and the measurement method. → Does the timing of your meals affect how well you sleep?

A literature review describes that symptoms of food sensitivities can indeed appear with a delay: hours to days after exposure, and not necessarily every time. Several studies, including well-designed randomised controlled trials in people with migraines, support the idea that delayed food sensitivities (measured via IgG antibodies) play a role in triggering migraine attacks. That said, the evidence for the precise time delay is largely descriptive in nature, and the researchers themselves characterise the overall quality of the evidence as limited. The claim that symptoms can appear only "days" later is supported by the literature, although the mechanism and exact timing have not yet been fully established.

Psyllium fibres do indeed form a gel, and this slows the absorption of nutrients, which dampens the rise in blood sugar after a meal. This effect has been most firmly demonstrated in people with type 2 diabetes. The claim that psyllium therefore also suppresses appetite goes beyond what the research shows: that specific effect on appetite is not well established.

A pilot study involving people who received NAD infusions in a commercial wellness setting does indeed describe moderate to severe side effects: gastrointestinal complaints, an elevated heart rate and chest pressure during administration. All symptoms resolved as soon as the infusion was finished. This is a small study in which participants were not randomly assigned to groups, and the findings have not yet been confirmed in larger trials; however, the side effects mentioned correspond precisely to what is stated in the claim. → Does a NAD infusion (IV drip) make sense?

Sprint interval training does indeed produce VO2 max gains comparable to regular endurance training, but the claim is more specific about the number of sprints per session. What the research shows is that you need at least 15 minutes of active work per session for VO2 max to increase substantially, and that blocks of 2 minutes or longer are the most effective. Whether exactly 8 to 10 sprints offer no advantage over 2 to 3 sprints is a specification that cannot be substantiated based on the available evidence.

Short sprints can indeed increase VO2 max, and research shows that sprint interval training produces comparable results to regular endurance training. However, the direction and the precise figures in the claim cannot be substantiated: there is no evidence that such a minimal volume (two to three 20-second sprints, three times a week) specifically produces an improvement of 10 to 19 percent. Moreover, the strongest evidence points to longer intervals of at least 2 minutes as the most effective protocol for VO2 max gains.

Research in rats, mice and human cells shows that the body can indeed convert vitamin K1 (phylloquinone) into a form of vitamin K2, namely menaquinone-4 (MK-4). This process takes place in the body's own tissues via a specific enzyme (UBIAD1), which has also been found in humans. However, the conversion is not straightforwardly complete: it proceeds via an intermediate step, is tissue-specific and has been demonstrated in animal and cell research. Whether the conversion in humans is sufficient to meaningfully convert K1 consumed through vegetables into K2 has not yet been directly tested in humans. The claim gives the impression that this is a simple and complete process, whereas the evidence in humans is still limited.

One study in women shows that higher oestrogen levels are associated with faces rated as more feminine, more attractive and healthier, which directly supports the claim. However, other studies paint a more nuanced picture: one study found that it was actually progesterone (and its interaction with oestrogen) that predicted the attractiveness of faces and voices, while a large-scale cross-cultural study found only very small and unreliable effects of cyclical changes in fertility on the rated attractiveness of faces. A smaller study also found that women with lower oestrogen levels were rated higher by men who also had low oestrogen levels. The claim is therefore too categorical: the direction is correct for part of the research, but the evidence is mixed and the effects are not always robust.

Two to three training days per week is indeed the well-supported basic recommendation for muscle building, and the threshold of half an hour to one hour per week also appears in the research. However, that time threshold applies to health benefits in a broad sense, not specifically to muscle building, and the evidence for the most pronounced effects is strongest in beginners. For more advanced athletes, volume matters more, which means one hour per week may then be insufficient. The claim is therefore correct in its general direction, but the phrasing "are already enough to achieve good results in muscle building" goes slightly further than what the research broadly supports.

Several review studies confirm that the fermentation of protein by gut bacteria does indeed produce substances such as ammonia, hydrogen sulphide, amines and phenols. The claim is therefore correct with regard to the mechanism and the substances mentioned. One review study does note, however, that at the concentrations normally found in the large intestine these substances may not cause harmful effects, and that their harmfulness has been demonstrated mainly in the laboratory and has not yet been sufficiently established in humans. The qualification "potentially harmful" in the claim does justice to this uncertainty, but the suggestion that this inevitably occurs whenever fibre is absent goes slightly further than what research has so far been able to establish in humans.

Research shows that, over the longer term, the difference in muscle mass and strength between soy protein and animal protein during strength training is not demonstrable, and that 1.2 to 1.6 grams of protein per kilogram per day is a well-supported amount for maintaining and building muscle. However, the claim goes further than the evidence allows: it specifically concerns a fully plant-based diet, whereas the studies compare almost exclusively soy protein versus animal protein. People who eat a fully plant-based diet also have to contend with lower digestibility and less leucine per gram, and research shows that plant-based eaters are wise to combine protein sources and consume slightly larger portions. The conclusion that 1.6 grams of plant-based protein per kilogram produces just as much muscle growth as animal protein is therefore plausible and points in the right direction, but has not yet been firmly established for a fully plant-based dietary pattern.

Laboratory studies with rat liver cells and mice convincingly show that caffeine and paraxanthine suppress the production of connective tissue growth factor (CTGF), and that paraxanthine is even more potent in this regard than caffeine. In rats, paraxanthine also demonstrably reduces the accumulation of scar tissue in the liver. The direction of the claim is therefore well supported, but the evidence rests almost entirely on animal and cell studies. This effect has not yet been tested in large-scale scientific trials involving human patients, and researchers themselves call for further research before this can be considered established.

Research confirms that unfiltered coffee raises cholesterol levels, and kahweol and cafestol are the substances considered responsible for this. The available findings show that unfiltered coffee raises cholesterol while filtered coffee does not, which indirectly supports the claim. However, a direct comparison of kahweol and cafestol levels between French press, espresso and Turkish coffee on the one hand and paper-filtered coffee on the other is not present in the research available for assessment here. The direction of the claim is plausible, but the precise claim about those specific brewing methods cannot be substantiated on the basis of what is available.

Research in rats and partly in human cells shows that kahweol and cafestol do indeed stimulate certain detoxification enzymes in the liver, such as glutathione S-transferase and glucuronosyltransferase. However, the claim about the enzyme CYP2E1 is incorrect: in the only study that specifically measured this enzyme, its activity did not change following treatment with kahweol and cafestol. Other comparable liver enzymes were inhibited, but CYP2E1 was not. Moreover, most of the evidence comes from animal studies, and it remains unclear to what extent these findings also apply to humans.

Per meal, soy protein stimulates muscle growth less effectively than animal protein, because it contains fewer essential amino acids and less leucine. Over a longer period of strength training, however, the difference in muscle mass and strength between soy and animal protein is not demonstrable. The claim that soy is 'just as effective' is therefore correct in the long term, but misses the caveat that you need to combine soy sources cleverly and take slightly larger portions to achieve the same result.

Diet can influence GLP-1, but lentils are not specifically identified in the research as a stimulating food source. The strongest evidence points to tryptophan-rich protein sources such as dairy and chicken, and partially hydrolysed milk proteins. Dietary fibre, of which lentils are a rich source, has also been studied, but so far only in people who have undergone gastric surgery, which makes it uncertain whether the findings translate to the general population. The claim about lentils in particular therefore cannot be substantiated on the basis of the available research.

Research in mice and rats shows that compounds from cloves, such as the essential oil and allylguaiacol, can increase BDNF levels in the brain. Studies found, for example, that the essential oil of cloves increased BDNF production in the hippocampus of mice under chronic stress, and that allylguaiacol stimulated BDNF production both in brain cell research and in mice. However, no research has yet been conducted in humans, which means it cannot be said that this effect also occurs in humans.

Research shows that chlorogenic acid activates AMPK, thereby inhibiting fat production in the liver and stimulating fat burning. This has been demonstrated in cell studies using liver cells and in animal studies in mice, chickens and rats. The claim is therefore correct in its direction, but all of this research has been conducted in the lab or in animals and has not yet been tested in humans, while the claim is presented as a universally applicable statement. Whether the same effect also occurs in humans at comparable doses has not yet been investigated.

Research in humans shows that insulin stimulates the kidneys to retain sodium (salt), and that this effect is also preserved in people with insulin resistance. The reasoning in the claim is therefore broadly correct: higher insulin means more salt retention, and lower insulin would then lead to greater salt loss and thus fluid loss. However, the studies focus primarily on the effects of high insulin levels, and one study in dogs shows that chronically high insulin has only a temporary effect on sodium retention, without causing lasting blood pressure elevation. The claim that a falling insulin level "directly" leads to fluid loss therefore goes somewhat further than what the research unambiguously demonstrates: the mechanisms are more complex, and the direct relationship in the context of falling insulin has not yet been properly tested in humans.

Research in humans shows that immediately after a meal, hunger is determined primarily by the amount actually eaten, but two to three hours later this reverses: at that point, the memory of what you thought you had eaten is the strongest predictor of how hungry you feel. This has been demonstrated, among other things, in an experiment in which participants received more or less soup than they saw via a hidden pump, so that the volume seen and the volume consumed could be varied independently of each other. Several studies in humans confirm that meal memories play an independent role in regulating appetite and subsequent intake. The claim closely matches what this research shows.

Research in humans shows that participants who were asked to think about what they had eaten earlier that day subsequently ate less during a snack test than people who were not reminded of this. This effect was found in women without dietary restrictions and proved to be specific to the lunch of that same day: being reminded of the previous day's lunch had no effect on snack intake. Several review articles confirm that this so-called meal-memory effect is a robust phenomenon in healthy adults. One study adds that the effect also occurs when people imagine their lunch as larger than it actually was, but that thinking back to the meal in detail does not strengthen the effect.

Animal research shows that the sensory fibres of the vagus nerve from the gastrointestinal tract play an important role in transmitting the satiety signal of the body's own GLP-1. Studies in rodents show that disabling or damaging these vagal nerve pathways strongly reduces or abolishes the appetite-suppressing effect of GLP-1. However, several studies nuance this picture: the reduction in food intake is sometimes only weakened rather than completely absent, and there are indications that other signalling pathways can partially take over. Furthermore, one study shows that the effect of the body's own GLP-1 partly depends on the simultaneous presence of other gut hormones, which means the claim is formulated somewhat too absolutely.

GLP-1 demonstrably suppresses hunger via both the gut and the brain: it slows gastric emptying and influences brain regions that regulate satiety. The claim that both systems operate independently of each other goes beyond what the available research shows. That independence has not been demonstrated in the sources currently available.

Research in rats and mice does indeed show that a junk food or Western diet causes memory problems. One study in female rats found that memory problems persisted after switching to a healthy diet, but a study in mice found that memory problems and brain metabolism problems fully resolved after eight weeks of normal eating. The findings are therefore partly contradictory: whether the damage persists or resolves appears to depend on factors such as species, sex, age, and the precise composition and duration of the diet. The claim that memory problems always persist after returning to a healthy diet is therefore too categorical given the available animal research.

Multiple studies and clinical reviews confirm that night blindness is an early and characteristic symptom of vitamin A deficiency in humans. A comprehensive clinical review describes how eye complaints develop when vitamin A levels are severely reduced, with night blindness as one of the first manifestations. Case reports in adults show that night blindness, sometimes caused by poor absorption following gastric surgery or liver disease, resolves after vitamin A supplementation. This is further supported by early laboratory research describing the relationship between vitamin A and loss of vision in low light.

Research in humans actually shows the opposite: in many situations, men respond more strongly to cortisol than women. A large-scale analysis of 34 studies shows that men have higher cortisol peaks after a stress test than women. A study in people with opioid addiction confirms that men show a stronger cortisol response, while women report more subjective stress. A review study in people with depression finds that depressed women even have a lower cortisol response to stress than depressed men. One study does show that in women a particular hereditary trait influences the cortisol response, but this applies only to a specific subgroup and not to women in general.

A large study that combined the results of 44 separate studies shows that yoga, of all the forms of exercise examined, is most strongly associated with a reduction in cortisol, particularly in people experiencing psychological stress. Broader review studies on relaxation and exercise methods in humans also confirm that cortisol levels drop. The claim is therefore broadly correct. However, the supporting evidence applies to yoga in general, not specifically to sun salutations: studies focusing on that one exercise form in isolation were not included here. Moreover, one carefully designed study in depressed patients who practised Hatha yoga alongside their medication found no additional effect of yoga on cortisol beyond that of the medication, which indicates that the effect does not occur in every situation.

Research shows that eating too little can disrupt hormonal balance, but the studies cited in this context primarily mention reproductive hormones and sleep hormones, not cortisol specifically. The idea that eating too little raises cortisol levels is plausible, since the body experiences a significant calorie deficit as a stressor, but that specific claim cannot be firmly established on the basis of the available research. The statement therefore goes beyond what the evidence concretely supports.

Research shows that prolonged stress disrupts hormonal balance, with leptin (the satiety hormone) falling and ghrelin (the hunger hormone) rising, leading to increased hunger. This is described in a review article on stress in children and adolescents. At the same time, another carefully conducted analysis of medical studies found that cortisol, leptin, and ghrelin levels did not change noticeably as a result of sleep deprivation, suggesting that the relationship is not always straightforward. Moreover, the available research focuses mainly on stress in general or in specific groups, and the direct causal link between chronically elevated cortisol and the described hormonal changes in humans has not yet been convincingly demonstrated in controlled studies.

Studies in animals (rats, hamsters, guinea pigs, and dogs) consistently show that soluble fibre increases the excretion of bile acids through the stool, and a study pooling and comparing the results of multiple animal studies confirms this pattern across several species. A review article on cholesterol reduction also identifies increased faecal bile acid excretion as one of the mechanisms underlying soluble fibre. The claim is therefore correct in terms of direction, but the evidence comes almost entirely from animal studies. Whether this effect is equally pronounced in humans, and whether it is truly "significant", has not yet been established on the basis of this research. Moreover, the effect appears to vary depending on the type of fibre and the composition of the diet.

The evidence for muscle building and strength recovery with creatine is reasonably strong, especially in combination with resistance training. The part about fat loss is not accurate: creatine is not a slimming agent, and its effect on fat mass is small and indirect, working through strength training rather than through direct fat burning. As for anti-inflammatory effects, the available studies provide no support for this claim, leaving it entirely unsubstantiated.

An MRI study of 45 men (15 natural bodybuilders, 15 steroid users and 15 recreationally active men) showed that the organ volumes of natural bodybuilders did not differ from those of regular athletes, while steroid users had clearly larger organs, including a larger heart and a larger liver. Several other studies and reviews confirm that anabolic steroids lead to cardiac enlargement and damage to organs such as the liver and kidneys. The claim corresponds precisely to what this human study demonstrates.

Several review studies and human trials show that testosterone is associated with less abdominal fat in men with low testosterone levels and excess weight, and that testosterone treatment can reduce waist circumference. However, the findings are contradictory: one randomised controlled trial in obese men with low-normal testosterone levels actually showed that testosterone injections did not reduce abdominal fat and sometimes even increased it. Review studies emphasise that a reduction in abdominal fat is mainly to be expected in men with genuinely low testosterone and a high body weight, and that the evidence largely comes from studies that only measure associations or are insufficiently well designed. The claim is broadly correct in terms of direction, but too categorical because the effect is not found in all studies and depends strongly on the form of treatment used and the characteristics of the patient. → Does testosterone help after 50, and is it dangerous?

Research consistently shows that moist-heat preparation (boiling, steaming) produces significantly fewer AGEs than dry heat such as roasting, grilling or frying. One study reports that dry heat increases AGE formation by a factor of 10 to 100 compared to raw food, and another study confirms that boiling yields the lowest AGE levels compared to grilling, roasting and frying. The claim that moist-heat preparation results in 'less than a quarter' is a specific figure that can be inferred from some cases, but the studies show that the difference depends strongly on the type of meat, the temperature and the cooking time. Moreover, one study on lamb found that the cooking method had hardly any effect on certain AGE markers, indicating that the relationship is not always so straightforward.

Several animal studies, conducted in rats, piglets and minipigs, consistently show that threonine plays a key role in the production of intestinal mucus (mucin) and that a threonine deficiency specifically reduces that production. The claim is therefore correct in its direction. Nevertheless, it goes slightly beyond what the available evidence justifies: all experimental studies were conducted in animals, not in humans. One review article does note that the findings are relevant to both animals and humans, but direct human trials are absent from this body of research. Furthermore, threonine does not come exclusively from dietary proteins; the gut can also partially extract it from the blood, which makes the claim somewhat too simple.

Research points to a daily amount of 25 to 29 grams of fibre as the threshold at which the risk of cardiovascular disease, diabetes and bowel cancer is clearly lower. A recommendation of 40 grams specifically for men is not supported by that evidence, nor does the evidence make a distinction between men and women. The claim therefore goes beyond what research has demonstrated so far.

Meditation increases telomerase activity across multiple randomised studies, most likely through stress reduction, and this is consistent with the idea that it can influence ageing at the cellular level. However, whether telomeres themselves actually grow longer as a result of meditation has not yet been demonstrated, and the studies are too small to draw firm conclusions. The claim that a specific exercise with "three pillars" optimises telomerase and thereby slows the biological ageing process goes beyond what research has shown so far: the mechanistic chain from meditation to telomere length to a slowing of ageing has not been conclusively proven.

The cortisol peak after waking is a well-established phenomenon in humans: research shows that cortisol rises sharply in the first thirty to sixty minutes after waking. Human research also shows that this peak is associated with the activity and connectivity of the prefrontal cortex later in the day, which supports the idea of brain priming. However, the claim about glucose release from the liver does not hold up without qualification: one study that specifically examined this in humans found no evidence for a gluconeogenic role of the morning cortisol peak, and the 60 to 90-minute timeframe mentioned in the claim also differs from the 30 to 60 minutes reported in the studies. The claim thus combines a well-supported brain effect with a metabolic effect that has not been confirmed by human research.

That insulin inhibits fat breakdown is a well-described mechanism: chronically high insulin levels are associated with insulin resistance, and intermittent fasting demonstrably improves insulin sensitivity and lowers fasting insulin levels. The general direction of the claim is therefore correct. However, the step that the body therefore uses fat as fuel less efficiently during fasting goes beyond what the research directly shows: the available studies measure insulin values and insulin sensitivity, not the efficiency of fat burning during fasting as a separate outcome measure. Moreover, the evidence for the underlying insulin studies comes predominantly from small, short-term trials, which calls for caution with such categorical statements.

Fermentation does indeed improve the digestibility of food, and this is supported by research into fermented products. However, the specific claim that carbohydrates yield less digestible glucose during fermentation and that phytates and tannins are broken down considerably goes beyond what the available evidence concretely shows: it focuses on broader effects such as antioxidant activity and overall digestibility, not on these individual mechanisms. The general direction of the claim is plausible, but the precise details regarding antinutrients and glucose content cannot be substantiated on the basis of the available research.

The ratio of fat to carbohydrates in a meal makes little difference to weight gain in the long term, as long as total calorie intake remains the same. This is shown by multiple randomised studies and meta-analyses. The claim that an insulin spike combined with a high fat intake strongly promotes fat storage goes beyond what the research supports: total caloric surplus is the determining factor, not the specific combination of macronutrients. The idea that fat is stored extra rapidly in the presence of insulin has not been demonstrated as a mechanism that operates independently of energy balance.

Research in humans shows that both endurance training (such as running or cycling) and strength training increase NAMPT in muscles, including in older adults. One study with young and older participants found, after twelve weeks of endurance training, an increase of 28 % in older adults and, after strength training, an increase of 30 %, which strongly supports the core of the claim. A meta-analysis pooling the results of five separate studies confirms this general picture, but also notes that the likelihood of an increase in older adults (68.7 %) is somewhat lower than in younger adults (75.6 %), and that the likelihood is somewhat higher for endurance training (75.1 %) than for strength training (66.4 %). The claim suggests a certain outcome for both types of training in older adults, whereas the evidence shows that an increase is probable but not guaranteed, and that the magnitude differs by group and training type.

Screen light in the evening demonstrably suppresses melatonin production and keeps you awake longer, and this effect is strongest with bright or prolonged exposure. The biological mechanism is well described and applies specifically to light-emitting screens, which supports the comparison with a printed book that emits no light of its own. The precise magnitude of the effect during everyday smartphone use is somewhat less clear-cut, but the direction of the claim rests on solid evidence.

The first part of the claim is correct: an omega-3 deficiency during early development has measurable effects on brain development, and that is reasonably well supported. The second part goes beyond what the evidence allows. Population studies suggest a link between omega-3 and Alzheimer's disease, but omega-3 supplements have shown little protective effect against the disease in research, and there is also no hard evidence for the broader idea that a deficiency in childhood increases the risk of Alzheimer's later in life. The claim draws a straight line from childhood to old age that current studies cannot support.

That low omega-3 levels harm the brain and are associated with depression is reasonably well supported, but the claim puts three conditions on the same footing while the evidence differs considerably from one condition to the next. For depression: omega-3 as a supplement to antidepressants works, but as a standalone treatment it does not. For dementia, supplements deliver less than population studies suggest, and for ADHD the available research provides no solid support. The link with cardiovascular disease also deserves a nuance: high doses of omega-3 actually increase the risk of atrial fibrillation, which contradicts the picture of omega-3 as straightforward protection.

GLP-1 agonists do indeed reduce fatty liver disease, and this effect is partly driven by weight loss and reduced appetite. Loss of muscle mass is a genuine concern, although the research supports this as a concern particularly in older adults rather than as a proven standard side effect in the same category as nausea. Malnutrition is not substantiated as a specific side effect in the available research; the most well-documented side effects are gastrointestinal complaints. The claim overlaps with the evidence on several points, but it presents muscle loss and malnutrition too categorically as established side effects.

Lifestyle changes, especially weight loss of 10% or more, can genuinely reverse fatty liver disease in most patients, and even early fibrosis is reversible in many cases. However, the specific figure of more than 90 percent cannot be substantiated on the basis of available research. Moreover, the evidence rests largely on observational studies and clinical reviews rather than large randomised trials, so the general direction is correct, but such a precise claim goes beyond what current research supports.

That a low-carbohydrate diet, which typically contains a lot of fat, raises LDL cholesterol in most people is well supported by several large reviews of randomised studies. The link with apoB is plausible, because apoB measures the number of harmful lipid particles and is associated with LDL, but our sources do not directly establish that link with a high-fat diet. The claim is therefore correct for LDL, but for apoB specifically, the evidence cannot be derived directly from what is available.

hs-CRP is precisely used to detect low-grade, chronic inflammation, and a value of 3 mg/l falls into the elevated risk category, not necessarily "significant inflammation". The research describes hs-CRP as a predictor of long-term cardiovascular problems, where even mildly elevated values are clinically relevant. The claim gives the impression that a pronounced inflammatory process is present, but that is not what this measurement reflects: it concerns a smouldering, low-grade inflammation that does not feel acute or intense at all. An acute infection or severe inflammation produces values many times higher.

Several large review studies and a fifty-year prospective study involving tens of thousands of male physicians confirm that long-term smoking is the most important risk factor for the development and progression of COPD, and that COPD is associated with considerable mortality. In these studies, smoking is directly linked to death from respiratory diseases. One review describes COPD as claiming the lives of more than three million people worldwide each year, with smoking as the primary cause. The claim that a long history of smoking can lead to death from COPD is thus broadly supported by research in humans.

The mechanism is correct: warm feet dilate the blood vessels in the skin, allowing heat to escape from the body more quickly and lowering the core temperature, which promotes falling asleep. This fits with the broader picture that a slight drop in body temperature is needed to fall asleep well. However, the evidence for socks specifically is exploratory and comes from small studies involving young healthy men, so the claim does not apply to everyone without qualification. Whether sleeping naked is the decisive factor in this is not firmly established by the research.

A lower body temperature does indeed play a role in falling asleep: research shows that heat disrupts sleep and that a cooler environment helps. Stress and anxiety are also demonstrably linked to sleep, and people who are less anxious fall asleep more easily. However, the research does not identify heart rate as a separate condition that one must consciously lower, and the claim gives the impression that all three factors are equally well supported and equally necessary, which goes further than the evidence shows.

Research in humans shows that the thermic effect of protein is between 20 and 30%, meaning that proportion of calories is lost as heat during digestion and processing. The figure of "about 20%" therefore falls at the lower end of that range and is not incorrect, but the full range extends to 30%. Furthermore, it is not only digestion that plays a role, but also the initial metabolic steps and the storage of nutrients. The claim is therefore broadly correct, but formulated somewhat too narrowly.

Animal studies show that the liver does indeed produce less cholesterol when more is consumed through the diet; this is called negative feedback. Studies in rats and hamsters demonstrate that hepatic cholesterol synthesis decreases as dietary cholesterol intake rises. In baboons (primates), however, this inhibition only becomes fully active at fairly high levels of absorption, and it only works when the enterohepatic circulation is intact. The claim is therefore broadly correct, but the compensation is not always complete: at higher cholesterol intakes, cholesterol accumulates in the liver and blood cholesterol levels still rise, showing that the compensation has its limits. Studies that have directly tested this mechanism in humans are not available in this research.

The protein leverage hypothesis is described and supported by multiple studies: research in humans shows that a lower proportion of protein in the diet is associated with a higher total energy intake, suggesting compensatory overeating to meet protein needs. Both controlled experiments and studies tracking people in their daily lives support this direction. The claim is therefore broadly correct, but the mechanistic assertion that the body "keeps sending hunger signals until protein needs are met" goes somewhat beyond what the studies actually demonstrate: they describe the behavioural pattern (eating more when protein intake is lower), but do not directly substantiate the underlying signalling process. Moreover, some studies indicate that the relationship is not equally strong across all groups, and that in studies tracking people in their daily lives it is difficult to distinguish cause from effect.

Research in humans shows that growth hormone rises sharply during fasting and plays an important role in protecting muscle mass, partly by inhibiting protein breakdown. Studies also show that intermittent fasting largely preserves muscle mass in humans. However, the claim goes too far: growth hormone reduces and strongly slows muscle breakdown, but does not prevent it entirely. Moreover, studies in humans show that other factors also play a role, such as the amount of protein in the diet, and that muscle mass can still decrease with longer or more severe fasting.

Research in healthy people shows that blood sugar is indeed kept relatively stable by the liver during fasting, but the claim that it stays between 70 and 80 mg/dL does not hold for everyone. In people with type 2 diabetes, blood sugar dropped from 158 to 104 mg/dL after 24 hours of fasting, which is well above that range. The study on liver regulation shows how the liver tries to keep blood sugar stable, but does not specify a concrete range for healthy people during fasting. The claim therefore goes too far by citing a specific and narrow range that does not apply to certain groups of people.

Research in humans shows that liver glycogen drops substantially after a night of fasting and that stores are completely depleted after 36 to 48 hours of fasting, not already after 24 hours. The claim that 90 percent has been used up after 24 hours therefore goes beyond what human studies indicate. The figure of 8 hours for a 50 percent reduction is not confirmed as a specific number by the available research in humans. Studies in rats do describe glycogen breakdown as the primary energy source during the first 24 hours, but those findings apply to rats and cannot be transferred directly to humans.

Curcuminoids are indeed the active compounds in turmeric to which an anti-inflammatory effect is attributed, and the evidence for curcumin is strongest for lowering CRP. However, whether curcuminoids make up exactly 3 to 5 percent of the plant is not established in the available research, and the claim that they are the "most effective component" goes beyond what has been proven: comparative research with other components of turmeric is lacking. Moreover, the anti-inflammatory effect is preliminary and has not yet been convincingly demonstrated for outcomes other than CRP.

The results of curcumin for joint complaints are encouraging but preliminary: the evidence is not strong enough to make firm claims, let alone to declare curcumin equivalent to NSAIDs. The claim that curcumin causes no side effects also goes beyond what the research shows, and absorption is so poor that without piperine or a special formulation, barely any curcumin ends up in the bloodstream. The comparison with NSAIDs has not been established at this time.

Piperine from black pepper does indeed significantly improve the absorption of curcumin, and research shows that combining the two measurably raises blood levels. However, the figure of 2,000 percent cannot be substantiated on the basis of the available evidence: research confirms the direction of the effect, but not that specific percentage. Moreover, it remains unclear whether this improved absorption actually leads to better health outcomes.

Several human studies support this claim. Research in obese people on a very low-fat diet shows that the gallbladder empties considerably less well after low-fat meals than after meals with more fat, and that this is associated with a higher rate of gallstone formation. A threshold of around 10 grams of fat per day is mentioned as the minimum needed for the gallbladder to contract sufficiently. A small-scale experiment in healthy volunteers also found that a fat-free meal caused barely any gallbladder contraction. Review articles explicitly identify a fat-free or extremely low-fat diet as a risk factor for gallstone formation during weight loss.

The thermogenic effect of carbohydrates versus fats is a frequently cited mechanism, but the evidence does not address this directly. What the research does show is that the ratio of fat to carbohydrates makes little difference to your weight in the long term, as long as total calorie intake remains the same. That undermines the second part of the claim: the idea that dietary fat is more easily stored as body fat than carbohydrates is not supported by the research. The available studies suggest that dietary adherence and total intake matter far more than which macronutrient you eat.

Research in humans does indeed show that women burn proportionally more fat during endurance exercise than men, and that this difference disappears after the menopause when oestrogen levels fall, which suggests that oestrogen plays a role. However, the evidence that oestrogen directly causes this higher rate of fat burning is less solid: one review study reports that oestrogen supplements produce less convincing results in humans than in rodents, and a human study with 36 participants was unable to explain the sex difference in fat burning during exercise on the basis of proteins measured in muscle and fat tissue. The claim that oestrogen drives the female body to burn more fat is therefore broadly correct, but the underlying mechanism in humans has not yet been fully elucidated and the role of oestrogen is less straightforward than the claim suggests.

Several studies in healthy women without diabetes find no clear difference in blood sugar regulation or insulin sensitivity between the luteal and follicular phases. A study of 110 women found no difference in blood sugar levels or the amount of insulin the body produces after consuming a sugary drink, and a study of 13 healthy women likewise found no clear difference in how well the body responds to insulin between the two phases. Research in young women also confirms that the way the body processes carbohydrates does not change noticeably across the cycle. Only in women with type 1 diabetes is there any indication that some of them may be slightly less sensitive to insulin during the luteal phase, but even there the evidence is not unequivocal and the quality of the studies is limited.

Research in women and female rats shows that progesterone can stimulate appetite, and a review article on women also explicitly mentions this. Nevertheless, the picture is not clear-cut: a study in female rats without ovaries actually shows that progesterone reduces food intake and body weight. The effect appears to be strongly dependent on the hormonal context, such as the presence of oestrogen. Furthermore, progesterone does not act directly as a 'hunger hormone' in the brain the way ghrelin does; rather, it indirectly influences other signalling substances in the brain that regulate hunger.

Research shows that 1.2 to 1.6 grams of protein per kilogram of body weight per day is more effective for muscle maintenance than the official minimum guideline, and that a high-protein diet is one of the best-supported ways to increase energy expenditure. However, the claim that 'various metabolic markers' improve within that protein range goes further than what the available research concretely demonstrates: the studies focus primarily on muscle mass and energy expenditure, not on a broad range of metabolic outcomes. Moreover, the lower limit stated in the claim (1.1 grams) differs from the threshold most studies use (1.2 grams), which means the direction is right but the precise range is not fully substantiated.

Several studies show that methionine is converted to cysteine via the so-called transsulfuration pathway, and that cysteine is subsequently the primary building block for glutathione production. A review article on sulfur-containing amino acids describes how methionine is broken down in the body into cysteine, which can then be converted into glutathione. Another study shows that methionine acts as an effective precursor to cysteine and thereby contributes to glutathione synthesis in tissues, including in humans. Laboratory research on mouse and human brain tissue confirms this by tracing radioactively labelled methionine directly in glutathione. The claim that methionine contributes to the production of glutathione is therefore well supported.

In a study of 29 healthy control subjects who underwent a 72-hour fasting test, blood glucose levels at the end of the fast ranged from 47 to 89 mg/dL, with a median of 63 mg/dL. This means that some healthy participants did fall below the threshold of 70 mg/dL, which is classified as hypoglycaemia. In addition, research using continuous glucose monitoring in healthy, non-diabetic individuals shows that they spend an average of around 1.1% of their time (approximately 15 minutes per day) below 70 mg/dL, even without prolonged fasting. The claim that healthy people never experience hypoglycaemia during a 72-hour fast is therefore not fully supported by this research.

Research shows that the ketone beta-hydroxybutyrate (BHB) can inhibit a specific inflammatory mechanism in the body. This effect has been demonstrated in human immune cells and in experiments with mice. Multiple review studies also describe broader anti-inflammatory signalling functions of ketones. However, the claim that "ketones have a natural anti-inflammatory effect" goes further than the evidence supports: not all ketones have this effect (research points specifically to BHB, not to acetoacetate), the effect does not apply to all inflammatory pathways, and large-scale evidence from patient studies in humans is largely still lacking. Researchers emphasise that confirmation through large human studies is still needed.

Autophagy is not exclusively linked to fasting. Research shows that exercise also activates autophagy in muscle cells, through multiple independent biological mechanisms. In addition, protein intake and caloric reduction play a role, independently of full fasting. The claim therefore misses an important part of the picture: fasting is one way to stimulate autophagy, but certainly not the only one.

What research actually shows is the opposite: low blood sugar activates stress hormones and the sympathetic nervous system, not high blood sugar. In hypoglycaemia, stress hormones rise and symptoms such as trembling and sweating occur, which are typical of sympathetic activation. Whether a high blood sugar level triggers the same mechanism cannot be substantiated on the basis of the available research. So the direction of the claim is wrong, even though blood sugar and the autonomic nervous system do genuinely interact.

Multiple studies confirm that damage to the blood-forming system is a common and serious consequence of chemotherapy in humans. A clinical source states that bone marrow suppression is the most common side effect that determines the maximum dose of anticancer drugs, and a separate source on nitrosoureas explicitly names bone marrow suppression as one of the serious side effects of these agents. A study in people with colorectal cancer shows that 40% of patients developed serious blood abnormalities during chemotherapy. Two meta-analyses summarising the results of multiple carefully designed randomised controlled trials treat bone marrow suppression after chemotherapy in lung cancer patients as an established and common clinical problem for which additional treatments are being investigated.

Animal research shows that nicotinoyl-GABA (picamilon) crosses the blood-brain barrier, and one study in mice reports that the permeability of nicotinoyl-GABA is even ten times higher than that of regular GABA. Another study in guinea pigs confirms that radiolabelled nicotinoyl-GABA reaches brain tissue after subcutaneous injection. The claim is therefore correct in its direction, but all of this evidence comes exclusively from animal and laboratory studies. Whether this also applies to humans has not yet been demonstrated on the basis of this research.

Multiple studies in rodents (mice and rats) show that exercise, particularly voluntary running, clearly stimulates the production of new brain cells in the hippocampus. This effect has also been found in animal research into depression, where running increased cell proliferation in the hippocampus. The claim explicitly limits itself to animal research, and rightly so: the studies described were conducted almost exclusively in animals. Some studies do show, however, that the effect is less straightforward in wild rodents than in laboratory animals, and that motivation and environmental factors may play a role.

Of all forms of creatine, monohydrate has the strongest evidence for its efficacy as well as the best safety data. No alternative variant has proven in research to perform better than monohydrate, and creatine ethyl ester even scores worse because it gives a false impression on a kidney blood test. The claim therefore closely reflects what the available research shows.

Research in humans shows that creatine users can experience gastrointestinal complaints, including bloating, but this association is reported mainly at higher doses during the so-called loading phase (typically 20 to 30 grams per day spread across multiple moments). The claim mentions a daily dose of 5 grams, whereas the complaints in studies appear more often at considerably higher doses and have not been specifically investigated at 5 grams. The reports of gastrointestinal complaints also come largely from athletes' self-reports and review studies, not from carefully designed studies in which researchers tracked and measured bloating as the primary outcome. The direction of the claim (creatine can cause gastrointestinal complaints) is correct, but the specific link to 5 grams per day goes beyond what the available research demonstrates.

That creatine draws fluid into the muscles is a well-known mechanism consistent with how creatine works: it increases water retention in muscle tissue. This part of the claim is indirectly supported by the available research on creatine and muscle mass. However, the figure of 70 percent water in muscles does not appear in the study we assessed, so that specific percentage cannot be substantiated on the basis of what is available.

Animal studies and large analyses of patient data show that GLP-1 agonists can curb the craving for alcohol, nicotine and high-calorie foods, which is consistent with a suppressive effect on the reward system. The nucleus accumbens and dopamine are cited as the likely mechanism, but clinical trials in humans that confirm this specific mechanism are still scarce and yield mixed results. The claim therefore describes a plausible mode of action, but it has not yet been demonstrated that this also occurs in humans via dopamine in the nucleus accumbens.

Animal studies consistently point to reduced alcohol consumption with GLP-1 agonists, and large analyses of patient data show an association in humans with fewer hospital admissions due to alcohol-related problems. The direction of the claim is therefore correct, but clinical trials in humans are scarce and yield mixed results. Furthermore, the evidence is still too limited to say anything specific about people with severe addiction; in humans, this is currently being tested in early-stage trials.

Research does indeed show that a weight loss of 10% or more leads to resolution of liver inflammation and regression of fibrosis in most patients. The direction of the claim is therefore correct. However, the precise figures of 90% (resolution of liver inflammation) and 45% (reduction in fibrosis) cannot be firmly established on the basis of the available evidence, and the research rests primarily on observational data and clinical reviews rather than large randomised trials with hard endpoints.

There are indications that vitamin E may have some effect in fatty liver disease, but the only proven approach to reducing liver inflammation and fibrosis is weight loss of 10% or more. The phrase "highly effective" goes beyond what the available evidence supports: it is well established that vitamin E does nothing for the heart, and for other applications the evidence is too thin. Moreover, weight loss and lifestyle change are the foundation of treatment, with medication only coming into the picture as a supplementary option if that is not enough.

The figures in the claim come directly from a carefully designed study in which 99 patients with confirmed fatty liver disease (NASH) were randomly assigned to groups. Neither the patients nor the researchers knew who was receiving the real treatment and who was receiving a placebo, in order to prevent bias. Of the patients who took 700 mg of silymarin three times a day, 22.4 percent had less liver scarring after 48 weeks, compared with 6 percent of the patients who received the placebo. That difference is large enough not to be attributable to chance. The researchers themselves note that this result warrants confirmation in a larger study. A second, similarly designed study using the same dosage found a more favourable outcome in the placebo group with regard to the degree of scarring, but that study had serious problems with the way patients were selected.

It is plausible that cinnamon can lower blood sugar to some extent in type 2 diabetes, but "reversing diabetes" goes far beyond what the research shows. Fasting blood sugar probably drops a little, but whether this also leads to better long-term values has not been convincingly demonstrated. At best, cinnamon is a modest addition to proven treatment, not a means of reversing diabetes.

Several large studies in humans show that a larger waist circumference is associated with a higher risk of fatty liver disease. The direction of the claim is therefore correct. However, not all studies use the specific cut-off values of 80 cm for women and 94 cm for men: one study uses 85 cm for men and 80 cm for women, and the remaining studies look at waist circumference as a continuous measure or at the ratio of waist circumference to height, without mentioning those precise thresholds. The claim is therefore somewhat more assertive about the cut-off values than the research directly supports.

One study that followed people who actually went on to develop dementia found that doing crossword puzzles in later life delayed the accelerated memory decline by 2.54 years. That figure is therefore correct. However, the claim implies that this applies to everyone who does crossword puzzles regularly, whereas the study only looked at people who had already developed dementia, and it concerns an association, not a proven causal relationship. Broader review studies show that staying mentally active is generally associated with less memory decline, but specific evidence from controlled trials in which participants are randomly assigned to groups is still lacking for crossword puzzles. The researchers themselves call for future randomised controlled trials to confirm this.

There is one human study (328 patients with mild Alzheimer's disease or mild memory problems) in which neither the participants nor the researchers knew who received which treatment. That study shows that plasmalogens from scallops clearly improved certain memory scores in women and younger participants, but the primary outcome for the group as a whole showed no clear improvement. The term "reverse" goes further than what that study demonstrates: there was partial improvement in some of the participants, but no overall recovery. Additional research has been conducted in mice and in review articles, but this does not strengthen the conclusions for humans. The claim is therefore broadly pointing in the right direction, but overstates the strength and breadth of the evidence.

Research shows that as little as 15 minutes of exercise per day is associated with a lower risk of death, and that the biggest leap occurs precisely when going from completely inactive to minimally active. However, exercising for 15 minutes a few times a week is less than daily exercise, and studies also indicate that a combination of cardiovascular and strength training is most beneficial for older adults. Moreover, the evidence concerns mortality risk in a general sense, not "decline" specifically as a separate outcome. The direction of the claim is therefore correct, but the wording creates the impression that a very small dose is sufficient, whereas the research points to a minimum threshold, not an optimum.

Exercising in middle age is associated with a lower risk of dementia, and this is one of the better-supported lifestyle recommendations. However, a reduction of at least 80 per cent is not supported by the available research. That research shows that the certainty about the size of the effect is moderate, and that the protection is probably strongest when several factors are addressed simultaneously, such as exercise, a healthy diet, cognitive stimulation and blood pressure management. Such a high and specific figure for exercise alone cannot be substantiated.

Research in humans does indeed show that caffeine reduces deep sleep, but the figure of 30 minutes does not match what studies find. A large meta-analysis combining and comparing the results of multiple studies shows an average reduction in deep sleep of just over 11 minutes, and another comparable review reports a decrease in the proportion of deep sleep of around 1 per cent. The study that specifically tested 400 mg of caffeine four hours before bedtime does confirm that this high dose causes a clearly measurable disruption to sleep, but does not report a figure of 30 minutes for deep sleep. The figure of 30 minutes corresponds most closely to the reduction in total sleep time found in some studies, not to the reduction in deep sleep specifically.

That quercetin inhibits the enzyme xanthine oxidase is well established: laboratory studies show that quercetin binds directly to the active site of the enzyme and blocks the production of uric acid, and an X-ray image of this complex is even available. Uric acid production also decreases after quercetin administration in liver cells and in animal studies. One small randomised controlled trial shows that quercetin supplementation lowers uric acid levels in the blood, but urinary excretion was not affected in that study, which suggests that mechanisms other than xanthine oxidase inhibition also play a role. The claim is therefore largely correct, but the current data in humans are limited and the evidence that xanthine oxidase inhibition is the sole or decisive cause in humans has not yet been convincingly established.

A large Korean study that followed more than 12 million adults for many years does indeed show a U-shaped relationship between total cholesterol levels and the risk of death. The lowest risk of death was found at a cholesterol level between 210 and 249 mg/dL, which aligns with the core of the claim. However, in younger women the most favourable range was lower, namely below 200, meaning the ideal level is not the same for everyone. Moreover, this concerns an association that researchers observed without changing anything: people with a low cholesterol level may die sooner because they are already ill, not because that low cholesterol is inherently dangerous. A large study in which researchers randomly assigned people to groups and actively lowered LDL cholesterol in some of them actually shows that this reduces the risk of death, which tells a different story from the idea that a lower level would itself be more harmful. → What is a healthy cholesterol level and when should I be concerned?

The claim states that dietary fibre stimulates GLP-1 production more effectively in women and that intensive exercise does so more strongly in men. However, the research shows the opposite for exercise: GLP-1 rose after both moderate and intensive exertion only in women, not in men. Habitual physical activity was indeed linked to a greater GLP-1 response to glucose in men, but this concerns everyday movement habits, not intensive training sessions. The relationship between dietary fibre and sex differences in GLP-1 is not examined in these studies at all, and the direction of the exercise effect is precisely the opposite of what the claim asserts.

Research shows that cooking does indeed introduce harmful substances into indoor air, but the studies point not so much to proteins at high temperatures as to fuel combustion, such as coal, wood or biomass, as the main source. One study measures these harmful substances in fumes produced when frying chicken legs in oil, which does involve proteins at high temperatures, but the study does not explicitly link this to indoor air pollution as such. The claim is therefore correct in its general direction (harmful substances from cooking in indoor air), but identifies proteins as the key factor, whereas the research points to fuel type and combustion method as the primary source.

Research in humans shows that at least 3 grams of water are stored in muscle per gram of glycogen, which confirms the lower end of the claim. A study in humans examining small pieces of muscle tissue found a ratio of 1 to 3 under restricted fluid intake, but upon full restoration of fluid levels that ratio rose to 1 to 17, because water not bound to glycogen is also stored in muscle. A recent review article furthermore concludes that the relationship between glycogen and body water has not yet been established with certainty. The figure of '3 to 4 grams' is therefore correct for the lower bound, but implies a fixed range, whereas the actual range is far wider and less certain.

A walk immediately after a meal demonstrably lowers the blood sugar spike, and this effect has been confirmed repeatedly. However, the claim goes beyond the evidence on two points: that muscles absorb glucose without insulin in the process is a mechanistic explanation that is not supported by the available research, and for squats specifically this effect has not been demonstrated in humans. The evidence therefore applies to walking after a meal, not automatically to every form of light exercise you might substitute for it.

The order in which you eat demonstrably affects the blood sugar spike after a meal: eating vegetables and protein first and carbohydrates last measurably dampens that spike. The effect on insulin points in the same direction, but the evidence for this is more preliminary and has been shown most convincingly in people with type 2 diabetes. The claim presents this as a general fact that applies to everyone, whereas the research is most persuasive in that specific group.

Eating early in the day does indeed improve insulin sensitivity, and this effect has been demonstrated in humans. However, the claim that oxidative stress decreases is not well supported by the available research. Moreover, the studies are predominantly small and short-term, which means the claim goes beyond what the evidence can currently support. The addition of "even without weight loss" is directionally correct: meal timing has an independent effect on metabolism, but that conclusion too rests on research of limited quality.

Research in healthy volunteers and people with diabetes shows that fluctuating blood sugar levels can indeed lead to changes in the eye's lens, such as thickening and changes in shape due to fluid shifts, which can be accompanied by intermittently blurred vision. A study in seven healthy subjects found that elevated blood sugar made the lens thicker and caused the vision to become more short-sighted, while normalisation reversed this. However, another study in five healthy subjects found no measurable lens change in most participants, and a study in 25 people with diabetes found no clearly demonstrable changes in lens shape, concluding that blurred vision is not always explained by lens changes. The claim is therefore broadly correct, but the evidence is not clear-cut: this effect occurs in some people but not in others, and the mechanism is more complex than the claim suggests.

Research in humans shows that excessively high blood sugar leads to glucose in the urine, which draws water along with it through osmotic diuresis, resulting in excessive urine production (polyuria). A study in patients with hyperglycaemia confirms this mechanism and shows that glucose makes up a large part of the urine composition. A review study bringing together all available research on nighttime urination in hormonal disorders explicitly names diabetes mellitus as a cause of nocturia through this mechanism. A study in children with type 1 diabetes also shows that higher blood sugar is associated with more nighttime bedwetting. The claim accurately and clearly describes the mechanism.

Several studies in humans show that people with skin tags have higher HOMA-IR values than people without skin tags. For instance, HOMA-IR was clearly higher in patients with skin tags compared to healthy controls, and markedly elevated HOMA-IR values (above 3.8) were almost seven times as common in people with multiple skin tags. One study also found that the mean HOMA-IR in people with skin tags was nearly twice as high as in controls. The claim is thus broadly supported by research in humans. → What are the earliest signs of insulin resistance?

Several review studies and clinical trials in humans show that chronically elevated insulin levels (hyperinsulinaemia) are associated with excessive growth of skin cells, which manifests as rough, thickened skin (acanthosis nigricans) and skin tags (acrochordons). One study describes how high insulin levels activate certain proteins in skin cells that are sensitive to growth signals, causing those cells to divide and proliferate more rapidly. The presence of skin tags and acanthosis nigricans is therefore regarded in research as a visible indicator of insulin resistance and elevated insulin levels in humans. The claim aligns well with what the research shows.

Several review studies in humans confirm that problems with the cell's energy factories (the mitochondria) are strongly associated with insulin resistance, both in muscles and in the liver. However, these studies also emphasize that it remains unclear whether problems with the energy factories are the cause of insulin resistance or rather its consequence. The claim suggests a close association, which is indeed described, but the direction of the relationship has not yet been established. Moreover, the studies also mention other tissues and mechanisms, such as adipose tissue and fat accumulation, that play an equally important role.

The claim contains two specific assertions: that highly processed food increases hunger for up to three to four days after consumption, and that this occurs because the production of GLP-1, a hormone that regulates satiety, is shut down. Research in humans tests both assertions and finds no evidence for them. A carefully designed study in which 32 people were randomly assigned to two groups shows that after fourteen days on a diet rich in highly processed products, the GLP-1 response to a meal was no different from what it had been at the start of the study. The daily hunger score measured early in the morning also remained stable throughout each diet. The assertion that the effect persists for three to four days is not supported anywhere. A review study does note that GLP-1 could theoretically be affected, but concludes that the findings to date are inconsistent. The claim as formulated therefore goes beyond what research in humans shows, and is flatly contradicted by a targeted study as regards both the lasting duration and the suppression of GLP-1. → How bad is ultra-processed food, and what does it do to you?

Research in humans shows that legumes such as beans and lentils can increase the feeling of satiety after a meal, particularly in short-term studies lasting a day or less. The delayed gastric emptying effect is attributed in the studies to the soluble fibre in legumes, which forms a gel in the gastrointestinal tract that slows transit, but this mechanism is not tested specifically for beans and lentils individually. Moreover, the studies describe this effect mainly in the context of energy-controlled meals or combination products containing multiple ingredients, and the long-term effects on satiety have not yet been sufficiently studied. The claim is therefore broadly correct, but is worded more broadly than what the available research can support with certainty.

That fibre slows the rise in blood sugar after a meal has been demonstrated in humans on multiple occasions, and the overall composition of a meal plays a role in this. However, the claim goes further: it states that combining fibre with both protein and fat slows digestion and prolongs the feeling of satiety. The available research provides no direct support for this. What is clear is that the order and composition of a meal affect the blood sugar response, but that is not the same as a demonstrated prolonged feeling of satiety resulting from that specific combination.

Research shows that oleocanthal, a compound in extra virgin olive oil, blocks the same proteins in the body as ibuprofen, namely those that drive inflammation and pain. Other plant compounds from olive oil appear to share this ability. This has been demonstrated in laboratory experiments and computer models, and an analgesic effect on uterine cramps has been observed in mice. One human study measured a reduction in inflammatory markers in the blood after a meal containing extra virgin olive oil. However, the claim that these compounds actually reduce pain and inflammation in humans goes beyond what the available research has shown so far: the evidence in humans is limited and the direct pain-relieving effect in humans has not yet been adequately studied.

A small randomised trial conducted in people with poor blood circulation in the legs showed that daily cocoa consumption (15 g of cocoa powder) over six months significantly improved mitochondrial function in the calf muscles compared to a placebo. The claim is therefore essentially correct, but two observations are warranted. First, this was an exploratory study with only 44 participants; the researchers themselves state that follow-up research is needed to confirm the findings. Second, the study used a cocoa drink containing a specific combination of cocoa powder and a high dose of a particular cocoa compound, not cocoa powder alone. A second study examined cocoa components in mouse muscle cells in a laboratory setting and is therefore not directly applicable to humans.

The study on which this claim is based does exist: a small-scale trial in which 44 people with peripheral artery disease were randomly assigned to groups did indeed show an improvement in walking distance of approximately 42.6 metres after six months of daily cocoa consumption (15 grams of cocoa powder with 75 mg of epicatechin), measured 2.5 hours after drinking. That figure is therefore almost exactly right. However, the claim refers to "three tablespoons of cocoa powder", whereas the study used a ready-made cocoa drink with a specific dose of an active compound, not an ordinary kitchen measure. Moreover, this was a small-scale pilot study that the researchers themselves describe as preliminary and that requires further investigation; the claim suggests more certainty than the evidence provides.

A cold bath immediately after strength training demonstrably inhibits muscle growth, and several consistent studies confirm this effect. The claim goes one step further, however, by identifying the mechanism: the suppression of inflammatory signals. That mechanism is put forward as an explanation in the available research, but has not been conclusively demonstrated in humans. The practical conclusion, avoid cold water immediately after strength training if you want to build muscle mass, is therefore correct, but the precise reason behind it has not yet been proven.

Research in humans shows that muscle protein synthesis remains elevated far longer than 2 to 3 hours after intense strength training. For example, synthesis was more than doubled at 24 hours after training and only returned to baseline around 36 hours. Another study in humans also shows that post-training nutrition can sustain the elevated muscle protein synthesis for even longer, for more than 12 hours. A different timeline was found only in rats, where synthesis did not rise until after 12 hours. The claim that the process returns to baseline after just 2 to 3 hours therefore directly contradicts what studies in humans show.

Multiple studies in children and adolescents show that mouth breathing is associated with measurable changes in facial structure: the jaw tilts backward and downward, the palate is narrower and higher, and the dental arches are narrower. A meta-analysis combining the results of ten individual studies confirms this pattern, as do individual medical studies and a descriptive review article. The airways are also narrower on average in people who breathe through their mouth. Regarding broader health effects, the evidence is less well developed, but the review articles mention associated conditions such as sleep problems and changes in muscle function as additional risks. The claim that mouth breathing is detrimental to the development of facial structure is thus well supported; the part about "possibly to health" is consistent with what the studies describe as accompanying complaints.

Regarding hormonal disruption through drinking water, studies conducted in a heavily contaminated area of Sweden find an increased risk of a hormonal condition in which the ovaries do not function properly (a condition known as polycystic ovary syndrome) in women, but that same study finds no association with a condition in which uterine lining grows outside the uterus. One analysis concludes, on the contrary, that the influence of PFAS in drinking water on hormonal balance is negligibly small compared to other sources. As for gut health, PFAS-induced disruptions of gut bacteria have been demonstrated primarily in mouse studies and in infants exposed to these substances through breast milk, and not directly through drinking water in adults. Furthermore, the Ronneby drinking water study found no convincing evidence that PFAS in drinking water causes inflammatory bowel disease. The claim is partially correct in its direction, but goes further than what research has so far demonstrated for all three of the mentioned effects through drinking water in humans.

One double-blind study conducted in obese Japanese adults shows that taking 15 or 30 millilitres of vinegar daily for 12 weeks did indeed lead to significantly lower values for visceral fat, waist circumference and blood fats (triglycerides) compared to a group that received a placebo. Those findings are therefore consistent with the claim. However, more recent review studies paint a more nuanced picture: a broad analysis of multiple randomised controlled trials found no clear effect of vinegar consumption on blood fats or waist circumference when all studies are considered together, and another review concludes that the evidence is still insufficient for firm conclusions. The claim is thus based on a single study whose results are not consistently confirmed in summaries of the broader research, and a retracted study that no longer carries any weight either.

One study in humans (152 overweight adults) does indeed show that a breakfast of two eggs, compared to a bagel, led to 65 percent more weight loss after 8 weeks. However, this only applied to the group that was simultaneously following a low-calorie diet: without such a diet, the type of breakfast made no difference. The claim leaves out that crucial condition. Furthermore, the study shows a 34 percent greater reduction in waist circumference, not 83 percent more fat loss around the waist: that figure does not match the research. A later study in more than a hundred people found no difference in weight loss between an egg breakfast and a grain-based breakfast.

A study in which 210 healthy Japanese adults with a high level of visceral fat were randomly assigned to groups, and in which neither the participants nor the researchers knew who received which product, shows that daily consumption of fermented milk containing the bacterium Lactobacillus gasseri SBT2055 for 12 weeks reduced visceral fat by an average of 8.5 percent in the group with the intermediate amount. That outcome matches exactly the stated 8.5 percent and 12 weeks. An earlier study in overweight adults using the same probiotic bacterium also found a clear, measurable reduction in abdominal fat, but of 4.6 percent. The claim is therefore well supported for this specific bacterium and quantity, although the results apply to a Japanese study population with high levels of abdominal fat.

Several laboratory studies directly compare inulin and wheat dextrin in terms of gas production during intestinal fermentation. Two studies consistently show that inulin produces clearly more hydrogen and total gas than wheat dextrin. A third study confirms this picture and shows that wheat dextrin actually produces the least gas of all the fibres tested. The claim concerns laboratory research, and that is exactly right: all of the findings mentioned come from laboratory models that simulate intestinal fermentation.

One human study shows that creatine combined with strength training increases the number of muscle stem cells and cell nuclei in muscle fibres, which goes hand in hand with greater muscle growth. Review articles and laboratory studies, in cultured cells and in rats, support the idea that creatine can promote the activity of muscle stem cells and the recovery process. The claim therefore points in the right direction, but the evidence in humans is limited to one study in which creatine was always combined with strength training. Whether creatine also increases the number of muscle stem cells without training and thereby contributes to recovery in ordinary people has not yet been properly studied. → Does creatine speed up muscle recovery?

Several human studies show that creatine can increase glycogen storage in muscles, especially at high doses or when combined with carbohydrate intake after exercise. However, not all studies find this effect: one human study found no difference in muscle glycogen compared to a placebo during carbohydrate loading. The liver was not examined in any of these studies, so that part of the claim has not yet been demonstrated in humans. The claim is therefore partly correct for muscle tissue, but goes too far by also mentioning the liver.

The idea that creatine draws fluid into the muscles and can thereby lead to weight gain without fat accumulation is a widely recognised mechanism behind the early weight gain seen with creatine use. The evidence confirms that creatine improves muscle mass and strength, but the specific figure of one to two pounds (approximately 0.5 to 1 kilogram) of weight gain due to fluid retention is not firmly supported by the available research. The direction of the claim is correct, but the precise figure cannot be substantiated based on what is currently known.

Several review studies show that ketamine stimulates the formation of new connections between brain cells, thereby making the brain more adaptable. This effect is well documented in animal research, where ketamine demonstrably promotes the growth of connections in the cerebral cortex. In humans, the evidence is encouraging but less complete: studies with patients show that ketamine has rapid antidepressant effects that go hand in hand with changes in brain connectivity, but directly measuring structural changes in those connections in humans is still limited. The claim is therefore essentially correct, but it implies more certainty than the research in humans currently provides.

Several human studies show that ketamine weakens the connections within the default mode network (DMN), but the network is not simply "shut down". Researchers found, for example, that in healthy volunteers ketamine reduced the connection between the medial prefrontal cortex and the rest of the network, while connections in other parts of the brain actually increased. A review study that carefully pooled all available research on patients with depression also describes primarily reductions in DMN connectivity, not a complete shutdown. The claim implies an all-or-nothing effect, whereas the research shows that ketamine partially and selectively disrupts the network, with some connections decreasing while others change or remain intact.

Research actually shows that fibre does affect the gut microbiome, though the effect is not the same for everyone. Additional fibre increased bacterial diversity in people who already had a diverse microbiome, and in people with excess weight, eating more fibre-rich food through avocado led to measurable shifts in beneficial bacterial species. The claim that fibre also fails to reduce pro-inflammatory proteins goes beyond what our sources directly confirm or refute, but the broader picture, in which a high-fat, lower-fibre diet actually fuels low-grade inflammation through a damaged gut wall, points in the opposite direction.

It is true that by far the largest part of the body's serotonin is produced in the gut, and research shows that gut bacteria play an important role in this. What the claim confuses, however, is that the serotonin in the gut is not produced by the microbes themselves, but by specialised gut cells that are stimulated by bacteria and their compounds. One study does identify gut bacteria that can produce serotonin directly, but this concerns a specific bacterial consortium doing so under laboratory conditions. The precise figure of 90% does not appear in the available studies, and the claim that microbes "produce" the serotonin goes beyond what the studies show.

Research shows that mannoheptulose inhibits glucokinase, including human liver glucokinase used in laboratory studies. However, these studies have not directly demonstrated that mannoheptulose also slows down hepatic glucose processing in the human body after a meal: they involve laboratory experiments with isolated enzymes and liver cells, not trials with people eating avocado. Moreover, most research focuses on inhibition in pancreatic tissue and tumour cells, rather than specifically on the situation after a meal. The claim therefore draws a conclusion about the whole human body that goes beyond what the available laboratory research shows. → Does avocado help lower your blood sugar spike after a meal?

It is plausible that small peptides from collagen are biologically active, and this is supported by research: there is evidence that collagen peptides can contribute to muscle growth in older adults, particularly in combination with strength training, and it is biologically plausible that they stimulate skin cells. However, for both muscle growth and skin effects there are conditions that the claim leaves out: the effect on muscles is strongest in combination with exercise, and the evidence for skin effects comes almost exclusively from manufacturer-funded research. The specific claim that peptides stimulate the production of hyaluronic acid goes beyond what the available research unambiguously shows.

Research shows that both half and a whole avocado can blunt the blood sugar and insulin response after a meal, but only when they replace carbohydrates. The claim that both amounts are equally effective cannot be substantiated: no data are available that directly compare the two doses and find them equivalent. Moreover, the evidence is limited overall and partly funded by the avocado industry, which calls for caution with specific claims of this kind.

Diet does indeed affect the composition of your gut flora quickly: research shows that effects can be measured within days. However, the claim that this change is "significant" deserves some nuance. The overall pattern of your gut flora is strongly tied to how you have been eating for years and does not shift easily. Heavily processed foods can measurably damage the flora within two weeks, but anyone who wants to structurally change their gut flora as an adult needs a lasting adjustment to their diet, not a one-week intervention.

Research in humans does indeed show that a high fibre intake can lead to bloating and flatulence, and that this occurs especially with highly fermentable fibres. A large review of medical studies confirms that excessive fibre intake causes gastrointestinal complaints, and that tolerance varies greatly depending on the type of fibre. The claim that this occurs "quickly" when jumping from 10 to 50 grams is broadly correct in direction, but the research also shows that the threshold differs greatly per type of fibre and that factors such as eating habits and individual sensitivity play a major role. The claim is therefore too categorical: how quickly and how severely the symptoms occur depends on which type of fibre you consume and how your body responds to it.

Several studies in people with irritable bowel syndrome (IBS) show that inulin and galacto-oligosaccharides can trigger symptoms such as gas, bloating and cramps. A systematic review and meta-analysis shows that inulin-type fibres worsen the sensation of flatulence in people with IBS. A separate well-designed MRI study confirms that inulin produces more intestinal gas and that symptoms occur more frequently in IBS patients after ingestion than in healthy individuals, probably because the intestine of IBS patients reacts more sensitively to distension. Research into the so-called low-FODMAP diet, an eating pattern that avoids certain fermentable carbohydrates, including the group to which inulin and galacto-oligosaccharides belong, also shows that restricting these substances reduces gastrointestinal symptoms. The claim is therefore correct for inulin. For galacto-oligosaccharides, the evidence is slightly less direct, but it fits within the broader picture of what research into this dietary pattern has shown in humans. → Do probiotics help with irritable bowel syndrome itself, or only when taken alongside antibiotics?

Psyllium forms a gel in the intestine, thereby slowing the absorption of sugars, which fits well with the picture of a fibre that retains water. The available studies on psyllium cite gel formation as the biological mechanism, which does indeed point to water retention. The claim that psyllium is relatively resistant to fermentation and therefore works differently from rapidly fermentable fibres is a distinction that is made in the research, but is not specifically substantiated in the available evidence. The direction of the claim is plausible, but the precise comparison with fermentation cannot be firmly established here.

Research in mice does indeed show that Akkermansia can influence goblet cells and mucin production, and laboratory research shows that substances derived from Akkermansia can stimulate mucin production in goblet cells. The claim is therefore correct in its direction. However, the picture is more nuanced: one mouse study actually shows that Akkermansia makes the mucus layer thinner in certain situations and inhibits the differentiation of goblet cells, while yet another mouse study shows that the number of goblet cells does not change but the composition of the mucus does. The claim that the breakdown of mucus stimulates goblet cells to produce more is therefore not unambiguously confirmed, and in humans this mechanism has not yet been tested.

The claim suggests that today's children have almost an 80% chance of developing overweight or obesity at some point in their lives. None of the available research supports this figure for children in general. The 80% threshold does appear in a large American study, but there it refers to the proportion of adults who are already overweight or obese in certain US states, not to a lifetime risk for children. Another study shows that 80% of young people with obesity still have it in adulthood, but that concerns only young people who are already obese, not all children. There is also research showing that 56% of children with obesity and 29% of children with overweight go on to become severely obese, but here too the focus is on specific high-risk groups, not on all children. The claim as formulated is therefore not supported by the evidence examined, and there are indications that the figure has been misapplied or taken out of context.

Research shows that the ketone body beta-hydroxybutyrate (BHB) does indeed act as a signalling molecule in the body and can stimulate mitophagy, which supports the core of the claim. Mitophagy is the process by which cells clear out and recycle damaged mitochondria, the cell's energy-producing units. Studies in rats and cell cultures show that BHB promotes this process via specific pathways within the cell, and research in rabbits shows that BHB enhances this process in both young and ageing heart cells. However, the claim is broader than the evidence justifies: most research has been conducted in animals and cell cultures, and the assertion that ketones prompt mitochondria to both protect themselves and recycle goes beyond the fact that BHB works less effectively in heart failure, because the normal process of merging and splitting mitochondria is disrupted in that condition. Moreover, part of the evidence focuses on other forms of mitochondrial protection, such as the production of small vesicles that remove damaged components, rather than exclusively on the process of clearing out and recycling.

A randomised study conducted in older adults shows that taking 4 grams of omega-3 fatty acids daily for eight weeks does enhance muscle protein synthesis, but only in combination with increased intake of amino acids and insulin, not at rest. The signalling pathway in the muscles that drives muscle growth was indeed more active in that context. A separate large study in older adults found no positive effect on muscle protein synthesis when fish oil was combined with protein over 24 weeks. Animal studies and laboratory studies likewise show activation of that signalling pathway, but those results do not automatically apply to humans. The claim suggests a general and independent effect of omega-3, whereas the evidence in humans is limited and contradictory, and the positive effect in the favourable study only occurred with an additional supply of amino acids.

A study with 24 trained men shows that 20 grams of whey protein every 3 hours did indeed produce more muscle protein synthesis than smaller or larger portions, with a difference of 31 to 48 percent. That aligns well with the claim. However, the claim goes slightly further than the evidence supports: the percentage in the claim (30 to 50 percent) is roughly correct, but the study only measured muscle protein synthesis over 12 hours after a single training session, not actual long-term muscle growth. Whether this difference also translates into greater muscle mass over weeks or months was not demonstrated in this study.

Research in humans actually shows the opposite pattern: low-carbohydrate and ketogenic diets raise both SHBG and total testosterone in obese men, while free testosterone barely changes or rises as well. One study in obese men found that SHBG increased after a very low-calorie ketogenic diet, but that calculated free testosterone did not change appreciably. Another study in obese men found an increase in both SHBG and free testosterone after weight loss, regardless of whether the diet was low-carbohydrate or high-carbohydrate. A study in healthy-weight men found no change whatsoever in SHBG or testosterone after six weeks of carbohydrate restriction. The claim that free testosterone falls as a result of rising SHBG is therefore not supported by this research.

A carefully designed randomised study conducted in men with obesity shows that ghrelin actually rises during a calorie-restricted diet, and that taking probiotics made no difference: both groups (probiotics and placebo) showed the same increase in ghrelin. A second study in adults with obesity who combined probiotic yogurt with a calorie-restricted diet did measure ghrelin, but found no clear effect on ghrelin. In addition, a laboratory study using stomach cells shows that a specific probiotic yogurt strain can actually increase ghrelin production. The claim that probiotic yogurt prevents ghrelin from rising during a calorie-restricted diet is therefore not supported by the research and is directly contradicted by one study.

Black seed oil shows measurable effects on blood fats, blood pressure and inflammatory markers in meta-analyses, and this direction is consistent. The claim that the supplement specifically leads to significantly greater weight loss and a greater reduction in waist circumference in people with obesity who are also following a low-calorie diet goes beyond what the available research can substantiate. Only a handful of small trials in humans have been conducted, none of which have published results in a trial registry, and there is no clear dosage recommendation of 3 grams per day. The combination with a low-calorie diet is promising, but "significantly more" has not been demonstrated at this point.

One small study of 20 patients with poor circulation in the legs showed that dark chocolate (more than 85% cocoa) measurably improved maximum walking distance and walking time two hours after consumption, compared to milk chocolate. A second, slightly larger pilot study (44 patients) also found an improvement in walking distance after six months of daily cocoa consumption, but only when measured shortly after intake; the effect 24 hours later was so small that it could have been due to chance. A third study examined blood vessels after eating dark chocolate in 21 patients and found no improvement in circulation. The evidence thus points cautiously in the right direction, but the studies are small, the results are contradictory, and solid evidence for long-term effects is lacking. → Does dark chocolate or cocoa help your heart?

Research shows that cocoa flavanols can improve blood vessel elasticity, and some studies focus specifically on smokers, whose arteries stiffen more rapidly. The direction of the claim is therefore biologically plausible and is supported by research into chocolate and blood vessels. Nevertheless, the claim goes further than the evidence can firmly establish: the precise two-hour time window and the qualification "significantly" for smokers as a separate group cannot be substantiated on the basis of the available research. The effects of cocoa on blood pressure and vascular walls are described in the literature as modest, not significant.

Meditation does have measurable effects that point to a beneficial influence on the body, but the claim is broader than the available evidence justifies. The strongest evidence concerns depression, anxiety and pain, with a moderate but demonstrated effect that lasts for at least six months. Effects at the cellular level, such as increased telomerase activity, are promising but come from small studies. That meditation has a beneficial effect on the nervous system as a whole is a plausible direction, but as a general claim it goes beyond what research has been able to firmly establish so far.

For depression and anxiety the claim holds up: the effect of meditation is moderate but well established and lasts for at least six months. For burnout and focus, the evidence is currently insufficient to support those claims. The assertion about changes in brain structure goes beyond what the available research can firmly support: there are indications at the cellular level, such as increased telomerase activity, but that is not the same as demonstrated structural changes in the brain. The claim rightly bundles proven effects with claims that do not yet stand on solid enough ground.

In guided settings, psilocybin shows positive signals in terms of mood and brain function, but the studies are still small and often lack a proper control group, which means "long-lasting psychological benefits" goes beyond what the current evidence firmly supports. The inflammation claim stands on even shakier ground: whether psilocybin reduces inflammation in humans has not yet been demonstrated, and the early clinical trials investigating this have not yet published their results. The claim thus combines a cautiously supported effect with one for which human evidence is currently lacking.

Research consistently shows that strength training is a necessary condition for muscle growth, even when protein intake is adequate. Protein alone helps to preserve muscle mass, but a clear anabolic effect has only been demonstrated in combination with training. This applies with particular force to people over fifty, who already have more difficulty responding to protein stimuli due to a reduced sensitivity to protein. The claim is therefore consistent with what the research shows.

A study in healthy people shows that delaying carbohydrates after a workout does not improve insulin function compared to immediate refuelling: the group that ate immediately after training actually scored best on insulin function (a 44% improvement versus 19% in the delayed group). The direction of the claim is therefore not straightforwardly correct. Rat and mouse studies do show that the timing of carbohydrates after exercise influences how muscles take up glucose and store glycogen, but those findings cannot simply be extrapolated to humans. It has not yet been demonstrated in humans that waiting to eat carbohydrates leads to better insulin function than refuelling immediately.

Two studies in humans show that endurance exercise improves the sensitivity of subcutaneous fat tissue to insulin: one older study that compared trained and untrained men, and one randomised study conducted over ten weeks in young men. A review article confirms that the physical adaptations caused by exercise also occur outside muscle tissue, including in fat tissue. On the other hand, a study in women found no improvement after twelve weeks of intensive exercise in the way fat tissue takes up glucose in response to insulin, and a study shows that fat tissue's response to exercise with respect to insulin and glucose is actually the opposite of that of muscle tissue. The claim that endurance exercise "directly" improves the insulin sensitivity of subcutaneous fat tissue is therefore not accurate without qualification: results vary and appear to differ depending on sex, type of training, and method of measurement.

Research shows that fat cells forced to store extra glycogen do indeed display a pro-inflammatory response that is associated with insulin resistance. This has been demonstrated in both human fat cells and in experiments with mice. The claim is therefore broadly correct, but there is an important nuance: the research shows an association and an effect in laboratory and animal experiments, and the translation to what this means in the living human body at a population level has not yet been fully established. Moreover, the context of obesity and oxygen deficiency also plays a role in glycogen accumulation, which makes the claim somewhat too simple.

Research in transgenic mice with extremely high glycogen levels in fat cells shows that those cells do indeed release fewer free fatty acids, both at rest and after stimulation. That pattern is consistent with the claim. However, the evidence comes exclusively from animal and cell studies, not from research in humans, and it concerns artificially elevated glycogen levels that are not normally seen in humans. Furthermore, a study using rat fat cells shows that high glucose concentrations can simultaneously increase both glycogen and lipolysis, which demonstrates that the relationship is more complex than the claim suggests.

Research in humans shows that adipose tissue does indeed store more glycogen in obesity and insulin resistance, and that this accumulation is linked to inflammatory processes. So the direction of the claim is correct. However, the relationship is more complex than the claim suggests: the accumulation appears to be a consequence of oxygen deficiency in adipose tissue in overweight individuals rather than a direct consequence of increasing insulin resistance in itself. Moreover, research in mice shows that less glycogen formation in fat cells actually worsens insulin resistance, which further nuances the picture. The claim presents the relationship as simple and straightforward, while the evidence calls for more caution.

Research shows that polyphenols such as resveratrol and quercetin do indeed influence energy metabolism, fat storage and energy expenditure. One human study shows that resveratrol produces metabolic changes in obese men that resemble the effects of caloric restriction. For most polyphenols, however, the evidence comes largely from cell studies and animal research, and human studies are still largely absent or limited. Fisetin is not specifically addressed in these studies, and the claim that polyphenols 'boost' metabolism is too simplistic: some substances actually lower resting metabolism, while others appear to increase energy expenditure, depending on the substance and the context.

The claim that people with Laron syndrome have very low IGF-1 levels due to a defective growth hormone receptor and develop remarkably little cancer and diabetes points in the right direction: research into growth hormone activity does indeed suggest that lower activity in later life may be beneficial for cancer risk. However, the claim presents this as an established fact about this specific group, whereas the available research in humans has not yet been demonstrated unequivocally. The link to diabetes is likewise not firmly established in the underlying research. The claim therefore goes beyond what the evidence currently supports.

Two studies show that mice without a functioning NLRP3 inflammasome, or mice given a compound that blocks the NLRP3 inflammasome, lived longer than mice without that intervention. This applies to normally ageing mice (see scientific article 31625260), to mice with obesity induced by a high-fat diet (see scientific article 31975052) and to mice with an accelerated ageing syndrome (see scientific article 34448355). The claim concerns mice and the evidence was collected exclusively in mice, which means the claim is correct as stated.

The research shows that FOXO4-DRI improves fitness, coat density and kidney function in mice that have been genetically modified to age at an accelerated rate. This is because the compound triggers senescent cells to destroy themselves. This is precisely what the claim states: rejuvenating effects in mice with accelerated ageing. The claim explicitly states that it concerns mice, and the evidence was indeed gathered in mice, so the claim does not go beyond the available evidence.

Bremelanotide is well documented as a drug that can increase sexual desire in women, and several completed phase 3 trials in women with hypoactive sexual desire disorder support this picture. The claim is therefore broadly correct. What is missing is an important nuance: bremelanotide is not routinely available in the Netherlands, which means the threshold for its use in practice is considerably higher than the claim suggests.

Several laboratory studies show that eugenol, the main active compound in cloves, enhances the effect of certain antibiotics against resistant bacteria. In some combinations the required dose does indeed drop substantially, and one study reports an 8- to 64-fold reduction in dose for eugenol combined with carvacrol. However, this synergy does not always occur: some combinations with other antibiotics show no effect at all, and the factor achieved varies considerably depending on the bacterial species and the antibiotic involved. Moreover, all these results come exclusively from laboratory research rather than from studies in humans, which means the claim goes further than the current evidence supports.

Research in rats shows that eugenol promotes GLP-1 release and thereby influences fat metabolism in the liver, but in that rat study eugenol had no measurable effect on food intake or weight gain. A review article on cinnamon-related compounds mentions eugenol as a possible influencer of GLP-1 signalling and appetite, but that article provides an overview of mechanisms rather than trials in humans. There is therefore no evidence in humans that eugenol reduces hunger or supports insulin release via GLP-1, and the rat research actually suggests that its effect on appetite is limited.

Research shows that creatine can support memory and cognitive performance, particularly when the brain is under pressure, such as during sleep deprivation. That direction is therefore correct. However, the specific dose of 0.35 grams per kilogram of body weight as a single dose that fully reverses cognitive decline after 21 hours of sleep deprivation cannot be substantiated based on the available evidence. The doses studied for cognition are generally based on daily use over several weeks, not on a single acute dose.

A large study summarising the results of 23 earlier studies does indeed confirm that adults under 50 who use creatine alongside strength training develop an average of 4.43 kg more strength in their upper body and 11.35 kg more in their lower body compared to strength training alone. The figures cited are therefore largely correct. There is, however, an important caveat: the same study shows that the effect in women was so small as to be barely measurable or reliable, while the claim makes no distinction between men and women. A second, larger study summarising 69 studies finds smaller and more variable effects in younger adults, depending on which exercise is measured. The claim is correct with regard to the figures, but gives the impression that the result applies to all adults under 50, whereas the evidence for women is considerably weaker.

Several review studies in humans show that long-term use of testosterone or anabolic steroids can strongly suppress sperm production and lead to a severely reduced or absent sperm count, shrinkage of the seminiferous tubules and reduced sperm motility. However, the word 'die off' in the claim goes further than what research in humans shows: in animals there are indications of direct cellular damage in the testes, but in humans the research focuses mainly on suppression of sperm production. Furthermore, in most cases infertility is reversible after stopping, although recovery can take years and is incomplete in some men. Permanent infertility is therefore a real risk, but not the rule.

Poor sleep does indeed disrupt hormones and impairs blood sugar regulation, and this is well documented for cortisol. The same applies to ghrelin: sleep deprivation affects appetite through hormonal pathways, and the evidence for poorer blood sugar processing the following day is plausible. However, PYY is not specifically identified in the research as part of this mechanism, so mentioning that hormone goes beyond what the evidence supports. The direction of the claim is correct, but the specific mention of PYY cannot be substantiated.

Research in humans shows that cortisol rises and the insulin/glucagon ratio falls both during fasting and during starvation. AMPK does indeed play a role as an energy sensor during fasting, and glucagon activates AMPK, but these two factors are not exclusive to fasting: they also play a role during starvation. Moreover, cortisol is already measurably elevated during short-term fasting, not only during starvation. The claim suggests too sharp a division, in which AMPK and glucagon belong to fasting and cortisol exclusively to starvation, but research shows that these hormones are active in both situations, albeit in varying proportions.

Research in humans shows that during fasting, glycerol accounts for only a small share of glucose production via gluconeogenesis. After an overnight fast, that share is approximately 4 to 22 percent of total glucose production, depending on how long the person has fasted. Most glucose produced via gluconeogenesis actually comes from other substrates, such as lactate and amino acids. The claim that glycerol is the source of the majority of glucose produced via gluconeogenesis is therefore contradicted by research in humans.

Seaweed does indeed contain iodine, and iodine is essential for a properly functioning thyroid gland. That connection is well established. However, the claim is missing an important side: both too little and too much iodine can disrupt the thyroid gland, and seaweed can contain highly variable amounts of iodine per serving. For people with an existing thyroid condition, eating seaweed regularly can actually throw the gland out of balance. The phrase "thereby supports the thyroid gland" is therefore formulated too unconditionally.

Research in humans shows that T3 declines during fasting, but that resuming eating does not double this level. In one study of healthy men, T3 did not change measurably after eating was resumed, compared to its level during fasting. Another study of people on caloric restriction actually shows a decline in T3, with no mention of a doubling upon resumption of eating. Research in rats and chickens does show T3 recovering to pre-fasting levels, but no doubling is reported there either.

Studies in people with an underactive thyroid show no rise in thyroid-stimulating hormone (TSH) as a result of fasting. A study in people with a mildly underperforming thyroid compared alternate-day fasting with daily caloric restriction and found no change in TSH or thyroid hormone after six months. A study on 16/8 fasting in healthy, trained men likewise found no clear change in TSH. A well-designed study in thyroid patients who fasted during Ramadan showed that TSH remained stable. A study in people with a disrupted metabolism also found no noticeable change in TSH in the group that ate only within a limited time window. The claim that 16 hours of fasting raises TSH in people with an underactive thyroid is not supported by any available human research; the opposite appears to be more likely the case.

It is well established for iodine that both a deficiency and an excess can disrupt the thyroid and cause disorders. For the other minerals mentioned, such as selenium, iron, copper, zinc, calcium and magnesium, the available research does not directly support the role the claim attributes to them in thyroid disorders. The direction of the claim is plausible for iodine, but the broad enumeration of all these minerals as equally proven causes of thyroid disorders goes beyond what the research shows.

Several human studies show that slow breathing with a prolonged exhalation makes the calming part of the nervous system more active, as measured by heart rate variability. One study in Covid patients and one in healthy adults found clear effects, and a review article describes that relaxed exhalation activates the nerves responsible for rest and recovery. The claim is therefore broadly correct. However, the studies almost always look at a combination of factors: a particular breathing rate, a slow exhalation, and often a deep inhalation as well. That exhaling longer than inhaling on its own activates the calming part of the nervous system, independently of the overall breathing pattern, has not yet been demonstrated separately in humans.

Research shows the opposite of what the claim states: melatonin is produced by the pineal gland based on the light-dark cycle, controlled by the suprachiasmatic nucleus in the brain, and melatonin itself then causes a drop in body temperature. It is not the temperature drop that signals the brain to release melatonin; rather, melatonin contributes to the temperature drop. Human studies also confirm that heat dissipation from the body to the skin is associated with sleep, but this is driven by the circadian rhythm and not by temperature as a trigger signal for melatonin production.

Several human studies support the claim. A trial in which over 200 stomach ulcer patients were randomly assigned to groups shows that zinc carnosine (polaprezinc) is as effective as a standard gastroprotective agent in healing stomach ulcers. A meta-analysis of three such trials shows that zinc carnosine, as an addition to standard antibiotic treatment, improves the eradication of the stomach bacterium H. pylori. Two review articles describe broader applications for stomach complaints, including damage to the gastric mucosa and nausea, and note that the compound has been officially approved for stomach ulcers in Japan. The evidence is promising but still limited in scale, and larger studies are needed to confirm the findings.

In the lab, GHK-Cu does indeed show effects on collagen production and tissue repair, and its biological activity is plausible. In living humans, however, this has not been demonstrated: the peptide penetrates the skin barrier poorly, and clinical evidence is lacking. The claim implies that applying it to the skin actually produces these effects, but that goes a step further than what research has shown so far.

Two large studies that pooled the results of many individual studies examined healthy adults and show that men and women achieve comparable relative increases in muscle size through strength training. There is a small difference in absolute gains in favour of men, but this disappears when you account for how muscular a person already was before starting to train. The claim that boys after puberty achieve greater muscle growth than girls is therefore not supported when looking at percentage gains. For absolute gains in kilograms of muscle tissue, the difference is small and limited mainly to the upper body. Research into how hormones respond to strength training does describe possible explanations for this difference, but when looking directly at muscle size itself, the evidence does not support the claim.

A study of 250 patients with a ruptured aneurysm did indeed find that straining hard during a bowel movement makes the risk seven times greater. Several other studies in humans confirm that straining is a common trigger for an aneurysm rupture. The factor of seven comes from one specific study with a particular design, and another study that also examined humans found a smaller increase in risk associated with straining, namely approximately a tripling of the risk. The claim is correct in terms of direction, but the precise factor of seven comes from a single study and is not found in all research.

A review of multiple published studies shows that eating an average of 14 grams of extra fibre per day is associated with a reduction in calorie intake of around 10 percent. That figure is therefore consistent with the claim. However, it is an average across several studies, and the effect was greater in people with excess weight than in people with a healthy weight. The other studies confirm that fibre can help reduce calorie intake, but they do not all point to the same figure of 10 percent. The claim is thus largely supported, but slightly too categorical, as it concerns an average and the effect can vary considerably from person to person.

Sermorelin is a synthetic peptide that works identically to the body's natural growth hormone-releasing hormone from the hypothalamus. Several human studies, including clinical studies in children with growth hormone deficiency, show that sermorelin specifically signals the pituitary gland to release growth hormone. This effect has been demonstrated both with intravenous administration and with subcutaneous injection. The mechanism of action via the pituitary gland is therefore well supported, and the claim describes it correctly.

Eating late disrupts metabolism, and research shows that the timing of meals affects blood sugar levels, hormone balance and body weight. However, the specific effect of an evening snack on fat burning during the night, compared with that same snack in the morning, has not been established so concretely in the available research. The broader direction is correct: eating earlier appears to be more beneficial for metabolism than eating late. That a snack of exactly 190 calories in the evening 'significantly' reduces fat burning compared with the same snack in the morning goes beyond what research has firmly established so far.

Research in healthy people does indeed show that tasting and chewing food without swallowing it substantially raises the production of pancreatic polypeptide, and one study in healthy subjects reports an increase of around 100 percent. However, other studies show that this depends strongly on what is being tasted: with mixed foods the effect is reliable, whereas sweet or salty liquids and chewing gum barely or not noticeably raise pancreatic polypeptide levels. The response also varies from person to person and according to the composition of the food. The claim that simply chewing and tasting raises pancreatic polypeptide levels by 100 percent is therefore not straightforwardly correct: that increase does not apply to all types of food and is not always the same.

Multiple human studies, including a randomised controlled trial and a large study summarising the results of many earlier studies, show that eating soy and taking isoflavones generally does not negatively affect sperm quality in healthy men. The picture is not clear-cut, however: one observational study conducted among men at a fertility clinic found an association between higher soy intake and lower sperm concentration, while another large study identified high daidzein consumption as actually protective. Moreover, the experiments that were conducted did not involve 'almost twenty servings per day' but considerably lower amounts, which means the claim goes beyond what the available research directly demonstrates. The conclusion that there is no adverse effect is therefore too categorical for such an extremely high intake. → Is soy healthy, or not because of the phyto-oestrogens?

Research into dietary stimulation of GLP-1 points to specific ingredients, such as tryptophan-rich protein sources and partially hydrolysed milk proteins, as the best-supported stimulants. The claim that a wide variety of ingredients in a meal specifically increases GLP-1 production finds no support in the available evidence. The link between a diverse microbiome and GLP-1 has not been demonstrated; the broader relationship between the gut microbiome and satiety hormones comes largely from association studies and animal research, and is too general to substantiate this specific claim.

One randomised controlled trial compared exactly this: walking for ten to fifteen minutes after each meal versus medication (domperidone plus simethicone). Walking did indeed prove more effective than the medication for postprandial fullness and bloating. For the remaining gastrointestinal complaints, there was no difference between the two groups. The claim is therefore correct for that specific symptom, but implies that walking is superior to medication in all respects, whereas the study only demonstrates this for postprandial bloating. Moreover, it is a single relatively small trial, which makes the claim somewhat too categorical.

Several systematic reviews and randomised controlled trials in people with irritable bowel syndrome show that a low-FODMAP diet significantly reduces symptoms compared to a normal diet or standard dietary advice. The direction of the claim is therefore correct. However, it goes slightly too far: the most recent and comprehensive meta-analysis (2025, 28 randomised controlled trials) shows that a low-carbohydrate diet low in starch and sucrose performs as well as or better than the low-FODMAP diet for some symptoms, and that the low-FODMAP diet ranks fourth for overall symptom relief. A large randomised controlled trial also found that a low-carbohydrate diet produced comparable results. The claim that a low-FODMAP diet works better than all other dietary approaches is therefore not fully supported by the evidence.

Leucine does indeed play a role in mTOR activation, and eating less protein lowers mTOR activity, which is consistent with the claim. However, research points to multiple factors that influence mTOR, such as fasting, calorie intake and the energy status of the cell. Identifying leucine as the "most important factor" goes beyond what the available evidence supports.

Several studies in people taking sirolimus (rapamycin) after an organ transplant show that impaired wound healing is a well-known side effect, and medical review articles confirm this pattern. Animal studies support this as well: rapamycin slowed wound healing in animals with poorly vascularised wounds, while another animal study found that a related drug targeting the same pathway in the body could actually promote wound healing in diabetic mice. The claim therefore holds for people taking rapamycin to prevent transplant rejection, but the picture is not clear-cut for all situations: the effect depends on the context, such as a healthy wound versus a wound in someone with diabetes or a wound with insufficient oxygen supply.

Fructose does indeed put more strain on the liver than glucose and raises triglycerides and abdominal fat more, which promotes fatty liver disease. However, the claim goes beyond the evidence on two points: at moderate intakes, direct harm in humans has not yet been conclusively demonstrated, and fructose is not the only driver of fatty liver disease. Excess weight, diabetes and a calorie surplus in general play an equally important role. The claim that fructose is specifically stored "around the liver" is moreover a simplification that the available research does not confirm so precisely.

Research in rats shows that high doses of eugenol, the active substance in clove oil, can cause structural and functional liver damage. In addition, there is a case report of a toddler who developed liver failure after ingesting 10 ml of undiluted clove oil. Laboratory research with liver cells supports the picture that eugenol can be harmful to the liver at high concentrations. The claim is therefore correct in its general direction, but the word "irritate" only partially covers what is actually happening: at high doses, the concern is serious liver damage up to and including acute liver failure, not merely mild irritation. Moreover, the human evidence is limited to individual cases, not controlled studies.

There is one small pilot study in humans (13 healthy volunteers and people with prediabetes) showing that 250 mg of clove extract daily can produce a clearly measurable reduction in blood sugar after meals. That direction is therefore correct. However, this is a very small study in which everyone knew which substance they were receiving and there was no comparison group receiving a placebo, carried out by researchers with ties to the company selling the product, which limits its reliability. The remaining studies were conducted in rats and mice, not in humans, and use different forms of clove extract or different dosages. The claim that 250 mg of clove 'significantly' lowers blood sugar therefore goes further than what the current evidence in humans can firmly support.

One controlled study with 24 office workers does indeed show scores 61% higher in a clean ('green') building and 101% higher in a green building with extra ventilation, compared to a conventional building. Those exact percentages are therefore correct. However, the claim omits an important nuance: the 101% gain applied only to the variant with increased fresh air supply, not to the clean building in itself. Moreover, this is a single small study, and broader research shows that the effects of better ventilation on cognitive performance are far more modest and variable, with improvements of a few percent that are by no means always clearly demonstrable. The claim presents the most favourable outcome as a general conclusion, while the evidence for it rests on a single study.

Research in humans shows that inhaling scent molecules does indeed produce measurable changes in blood pressure, heart rate and brain activity (EEG), as demonstrated in two studies with human participants who inhaled volatile substances. The idea that scent molecules can travel to the brain via the olfactory nerve is supported by research into what is known as the olfacto-cerebral route. One study also shows that a specific scent molecule (diacetyl) can actually cross the blood-brain barrier, but this concerns animal and laboratory research and does not yet constitute evidence in humans. The claim combines two mechanisms: crossing the blood-brain barrier and direct effects on blood pressure, brain activity and heart rate, yet these two have not been demonstrated simultaneously in humans in the research. Moreover, the physiological effects are also likely explained via the nervous system, not solely by direct passage across the blood-brain barrier.

Human research does indeed show that butter can raise good cholesterol, but the picture is more nuanced than the claim suggests. One study found a rise in good cholesterol compared to a regular diet, but not compared to olive oil. Another study found that coconut oil raised good cholesterol considerably more than butter did, and a third study found no changes in cholesterol levels due to butter in people who were overweight and had a disturbed metabolism. This is therefore not a straightforward protective effect: butter simultaneously raises bad cholesterol as well, which is considered a risk factor, and whether the rise in good cholesterol actually proves protective depends on what you compare butter with and in which group.

Several review studies summarising the results of well-designed trials in adults show that taking CLA as a supplement is associated with a small reduction in fat mass and body weight. The direction of the claim is therefore correct. However, the researchers themselves are cautious: the effects are small and in practice they by no means always make a meaningful difference in people. Moreover, an analysis that includes only the best studies shows no clear reduction in fat mass. Animal studies show stronger effects than human studies, and there are indications that the effect depends on how long someone takes the supplement, what dose is used, and which group is involved (for example, people who are overweight).

Vitamin K2 activates proteins that direct calcium to bone tissue and slow down calcification of the arteries, and that mechanism is broadly correct. Research shows that K2 improves bone density and slows the build-up of calcium deposits in the coronary arteries. However, the claim suggests a precise and fully proven transport mechanism, whereas the observed effects are modest and apply primarily to people with bone problems or existing arterial calcification, not necessarily to everyone.

Several large review studies in humans show that the claim is incorrect. Two Cochrane reviews involving tens of thousands of participants find that reducing saturated fat lowers the risk of cardiovascular disease by 17 to 21% compared to a normal diet. A third review confirms this pattern and adds that the effect is strongest in people who already have an elevated risk, and that replacing saturated fat with polyunsaturated fat provides additional benefit. Only one review study from 2015, based on observational data without researcher intervention, found no clearly demonstrable association for saturated fat on its own. However, that study did not examine what happens when saturated fat is replaced by unsaturated fat. The picture from studies in which researchers directly adjusted participants' diets is therefore clear enough to contradict the claim.

Research on the malaria mosquito Anopheles stephensi shows that a low dose of IGF-1 ingested through a blood meal extended the average lifespan of mosquitoes by 23% compared to a control group. The claim is therefore correct for that specific mosquito species and that specific dose. However, a second study on the same species adds nuance: only the low dose of IGF-1 extended lifespan, while the high dose did not have that effect. Moreover, research on a different mosquito species, Anopheles arabiensis, shows that IGF-1 actually shortened lifespan in a susceptible strain, indicating that the effect does not apply to all mosquitoes. The claim presents the 23% figure as if it applies to mosquitoes in general, whereas in reality it is tied to one species and one dose.

Diet plays a role in body fat, but does not determine it on its own. Research shows that the ratio of fat to carbohydrates makes little difference to weight in the long term as long as total calorie intake remains the same, and that exercise is at least as important a lever as diet. Moreover, hormones and body fat reinforce each other with age in an interplay that is independent of diet. The claim therefore overlooks the role of other factors such as exercise, hormones and genetics.

Research in humans shows that air purification with filters that capture very small particles from the air can lead to improvements in allergic asthma and allergic rhinitis: quality of life and asthma control improve, and airway inflammation also decreases. However, the complaints do not disappear entirely: other outcomes, such as symptom severity, medication use and lung function, do not improve to a degree large enough to be certain it is not due to chance. The claim that complaints can "disappear" therefore goes beyond what the research shows, as the effects are modest and cannot be demonstrated for all measures of complaints.

Research in humans shows that exposure to mould and damp in homes is associated with a range of health complaints. There is sufficient evidence for a link with asthma, allergic respiratory conditions, rhinitis and pneumonia. In addition, there is limited evidence for a link with eczema, COPD and mood disorders. A comprehensive medical guideline confirms these associations and distinguishes between the strength of the evidence for each condition. The claim that mould in a home can lead to serious health complaints is therefore well supported by research in humans.

Research shows that sensory stimuli from food, such as smell, taste and appearance, do indeed trigger reflexes that activate the gastrointestinal tract: more gastric juice and digestive enzymes are released even before you start eating. This mechanism, known as the cephalic phase response, has been described in multiple studies in humans and animals. The idea that producing saliva itself is the driving force is partly correct: saliva production is part of the same reflex, but the release of digestive enzymes is controlled via the nervous system, not by the saliva itself. As for nutrient absorption, a thorough review study from 2020, based on fifty studies in humans, concludes that there is little evidence that these reflexes make a measurable difference in practice for absorption or blood sugar regulation.

Several studies in humans do indeed show that blood vitamin D levels can rise after weight loss, and one study in people with obesity found a link between a decrease in fat mass and an increase in vitamin D. The idea that stored vitamin D is released from fat cells during weight loss is a frequently cited explanation, but researchers also mention other causes. For instance, when body fat is greater, vitamin D may be distributed across a larger volume, causing blood levels to drop; weight loss would then reverse this effect. Moreover, one large meta-analysis, which summarised and compared the results of many individual studies, shows that the effect of weight loss on vitamin D is small and that the findings are contradictory. The claim presents the released-from-fat-cells explanation as an established fact, whereas the research shows that this mechanism has not yet been proven and that several explanations exist alongside one another.

Two major studies in humans, conducted by Karolinska University and based on measuring radioactive carbon from nuclear tests in the DNA and fats of fat cells, directly support this claim. The first study shows that approximately ten percent of fat cells are renewed each year, which corresponds to an average lifespan of around ten years. The second study explicitly mentions 'the average lifespan of ten years of human fat cells' as an established fact. Both studies were conducted in adults, both of healthy weight and with obesity, and the finding applies to all adult ages and weight categories.

Several studies examined precisely this question: whether the breakdown products of plasticisers activate certain hormone receptors. Those studies consistently found the same result, namely the opposite of what one might expect. The main breakdown products showed no effect on these hormone receptors in laboratory research, whereas some of the original substances themselves had a weak hormone-like effect. A study examining the plasticiser BBP and its breakdown products also concluded that those breakdown products had no hormonal activity, and that only the original substance itself was active. One exception is a study on an alternative plasticiser that is not a phthalate, namely DEHT. One particular breakdown product of that substance did have a weak hormone-like effect, but DEHT does not belong to the same group of substances as the phthalates.

A study of 20 participants found BPA in the sweat of 16 of them, including people whose blood and urine tests showed no BPA. That supports the claim. However, a second, larger study of 50 participants used sweat patches and found no BPA above background levels in most participants, not even in someone with a demonstrably high BPA concentration in their urine. That study suggested as possible explanations that the amount of sweat collected per patch was too small, or that BPA concentrations in sweat are simply very low. The two studies taken together show that there is still uncertainty about how reliable sweat is as a measurement method, and the claim presents the finding more definitively than the research justifies.

Research shows that so-called 'obesogens', including substances that mimic hormones such as oestrogen, can indeed influence fat storage and body weight. Several review studies describe how these kinds of endocrine-disrupting substances stimulate fat cells to grow and divide, disrupt metabolism, and interfere with appetite and satiety signals. The claim is broadly correct, but oversimplifies things in two respects. First, the relevant group of substances is broader than just oestrogen mimics: substances that affect other hormonal pathways also fall into this category. Second, the evidence in humans is not yet conclusive: the strongest indications come from laboratory and animal research, and in humans the findings are primarily epidemiological associations rather than proven cause-and-effect relationships.

Research in humans shows that xylitol and erythritol in the blood are associated with poorer kidney function. A large study identifies xylitol and erythritol as substances that are elevated in both regular kidney patients and kidney transplant patients, but describes this as an association across different stages of kidney disease, not explicitly as a rising trend as kidney function declines step by step. A smaller older study found elevated erythritol levels in all six patients with kidney problems, but does not mention xylitol as elevated in that context. The claim is therefore largely correct for erythritol, but the evidence that xylitol rises systematically as kidney function further declines is less clear-cut.

Cell studies show that higher sugar levels in the cell and damage caused by free radicals (a form of cellular damage arising from an imbalance between harmful and protective substances in the body) increase erythritol production, but this does not apply to all human cell types. In lung cancer cells (A549) and muscle cells (C2C12), erythritol production rises with more sugar and with this form of cellular damage. Kidney cells (HK-2), however, respond only to higher sugar levels, not to that cellular damage. The claim states that this applies to human cells in general, but the research shows precisely that the effect differs by cell type. Furthermore, this involves laboratory research with cultured cells, so whether this also occurs in the living body has not yet been demonstrated.

Research in humans does indeed show that the body produces erythritol on its own, via a metabolic pathway linked to glucose processing, and that higher blood levels are associated with obesity, diabetes and cardiovascular disease. A review article also confirms that the body produces xylitol itself, but the details of when and in whom levels rise are far less studied for xylitol than for erythritol. Moreover, the link between metabolic problems and elevated erythritol levels is not as straightforward as the claim suggests: one study found that age, not blood sugar or insulin, was the strongest predictor of erythritol levels in fasting blood. The claim is therefore broadly correct for erythritol, but goes beyond what the evidence shows for xylitol, and lacks the nuance that the relationship with metabolic dysfunction is more complex and has not yet been fully elucidated.

Sleep deprivation and stress can seriously disrupt the intestines, but "shutting down" goes further than what the research shows. Stress causes abdominal pain, irregular bowel movements, and gastrointestinal complaints in many people, and sleep deprivation affects the diversity of gut bacteria. These are real effects, but a complete shutdown of intestinal function has not been demonstrated. The claim paints a more complete and more serious picture than science currently supports.

Research shows that a high-fat diet, certain fatty acids (such as palmitate), and food additives such as carrageenan can disrupt the functioning of L-cells and reduce GLP-1 production. Some of this evidence comes from mouse studies and laboratory studies using cultured cells; only a limited portion has been investigated in humans. The claim is partly correct in its direction: ultra-processed foods do indeed contain substances that can harm L-cells. However, "toxic oils" as a separate category is not identified as such in the research, and the claim that GLP-1 production is completely "shut down" goes beyond what studies show: there is reduced secretion and impaired function, not a complete cessation.

Dietary fibres and their fermentation products, including short-chain fatty acids, are associated with higher GLP-1 secretion, but the direct mechanism via L-cells has not been well established in humans. Research into fibres and GLP-1 in humans is also limited: studies using dietary fibres such as oat bran have so far only been conducted in people who had undergone gastric surgery. The direction of the claim is therefore plausible, but the word "directly" goes beyond what the available evidence in humans can firmly support.

A large meta-analysis combining and comparing the results of many earlier studies shows that a high intake of vitamin E through food is associated with a lower risk of Alzheimer's disease, and a comparable association is also found for supplements. The large Rotterdam Study confirms the protective effect of dietary vitamin E, but one other follow-up study found no association at all, either for food or for supplements. Research into vitamin E supplements as a treatment shows little to no effect on the risk of or decline from Alzheimer's disease. The picture for supplements and risk reduction is therefore not as clearly negative as the claim suggests: the studies contradict each other, and one meta-analysis also finds an association for supplements, which makes the claim too categorical in its distinction. → Does taking vitamin E have any proven benefit?

There is one well-designed study involving people with fatigue complaints (burnout), in which participants were randomly assigned to a group receiving Rhodiola rosea extract or a group receiving a placebo, without participants or researchers knowing who received what. That study shows that the extract reduced fatigue and lowered cortisol levels after waking compared to the placebo. This supports the direction of the claim. However, a broader review that combines multiple human studies concludes that the effects of herbal supplements on cortisol in humans remain largely unclear and that more research is needed. Studies in rabbits and rats do show cortisol-lowering effects, but these say nothing directly about people with burnout. The claim gives the impression that the effect is more solidly and broadly proven than the available human research justifies: the only human study is small (60 participants) and the broader review is more cautious about the effect on cortisol.

Caffeine does indeed raise cortisol, and the body only partially adapts to this, including to the morning peak. However, the claim that coffee immediately after waking drives cortisol levels "higher than desirable" goes beyond the evidence: for most people, a temporary rise in cortisol caused by caffeine is not an acute health problem. People who are already under a lot of stress or who are sensitive to stress hormones would do well to pay attention to timing and quantity, but that does not automatically apply to everyone.

Research shows that magnesium plays a role as a cofactor in the production of serotonin and melatonin, and that magnesium supplementation in older people with insomnia is associated with higher melatonin levels. A review study also identifies magnesium as a cofactor in the synthesis and metabolism of serotonin. However, the claim that magnesium is "necessary" for that production goes beyond what the studies demonstrate: they show that magnesium plays a supporting or modulating role, not that it is an indispensable prerequisite in the way that tryptophan is as a building block. Moreover, in the studies tryptophan is the primary building block for serotonin and melatonin, while magnesium contributes as a cofactor but is not identified as the sole determining factor.

Magnesium threonate does reach the brain more effectively than common magnesium supplements, and there are preliminary indications that it raises magnesium levels in the brain. However, the evidence for this comes largely from animal studies and small human studies, at least one of which had a conflict of interest. The claim sounds more definitive than what current human research can firmly establish.

Orally ingested collagen peptides do show positive effects on both skin hydration and collagen density in research, and a duration of at least eight weeks is cited as a guideline. However, the claim goes slightly beyond what the evidence supports: the study that demonstrated these effects involves a conflict of interest, which limits confidence in the results. Moreover, the effect depends on the quality of the product, specifically its active peptide content, and not merely on taking it over a given period.

Multiple randomised studies show that taking extra leucine does not counteract the loss of muscle mass and muscle strength during immobilisation or bed rest. Three controlled trials in young and older adults found no difference between leucine and a placebo in muscle mass or strength after limb immobilisation. One study in middle-aged adults did find a partial protective effect of leucine on muscle strength and muscle quality during 14 days of bed rest, but this effect was limited and partly disappeared after 14 days. A review study on essential amino acids combined with glutamine does see potential in taking those amino acids in patients in a clinical setting, but this concerns a different composition than leucine alone, and different groups of people. On balance, most direct research in humans indicates that taking extra leucine alone does not prevent muscle and strength loss during bed rest or immobilisation.

Research in large groups of people shows that discontinuation rates are high, but tend to occur within one year rather than two: among people without diabetes, more than half had already stopped within twelve months, and among people with diabetes, nearly half had done so. The claim's reference to 'within two years' therefore underestimates how quickly people stop. The second part of the claim, that people subsequently regain weight, is strongly supported by multiple large systematic reviews in which researchers summarise and compare all available studies on this topic: weight regain after stopping has been demonstrated time and again, regardless of the type of medication or the duration of treatment. The claim is therefore broadly correct, but the timeline for stopping is shorter than two years in the research.

Research shows that gut bacteria stimulate GLP-1 production through substances such as short-chain fatty acids, and that GLP-1 plays a role in satiety via the vagus nerve and brain areas such as the hypothalamus. Several review studies describe this relationship, but they focus primarily on how gut bacteria influence GLP-1 secretion, not specifically on "prolonging" the effect of GLP-1 in the brain. The claim that bacterial metabolites prolong the satiating effect of GLP-1 in the brain therefore goes further than what the available research actually demonstrates, and most studies are reviews without direct evidence from clinical experiments for this specific mechanism.

Several studies show that polyphenols, including compounds from cocoa and berries, can stimulate thermogenesis in brown fat. However, this effect has only been demonstrated in animal and laboratory research: the studies were conducted in mice and rats, and one study tested a synthetic polyphenol compound. A review article mentions that there are also indications from human research, but provides no concrete results regarding this specific effect. The claim makes it sound as though this is a proven effect in humans, whereas the evidence so far remains limited to animal studies.

Several randomised studies and meta-analyses show that the ratio of fat to carbohydrates makes little long-term difference to weight loss, as long as total calorie intake remains the same. The specific claim that a low-fat diet reduces resting energy expenditure by 300 to 400 calories per day while a high-fat, low-glycaemic-load diet keeps that expenditure at the same level is not supported by the available research. What actually matters is how well you can sustain an eating pattern, not the precise macronutrient composition.

A small case series of three patients has been published in which stem cells from umbilical cord blood were used for forms of hair loss, including one case of complete hair loss over the entire body. In those patients, hair growth began after a few months, which broadly confirms the stated period of 6 to 12 months. At the same time, review studies describe stem cell therapy as promising but still at an early stage, with further research needed into its long-term safety and efficacy. The claim that the therapy works specifically in cases of total scalp hair loss by simultaneously influencing both the immune system and stem cells goes beyond what these limited case descriptions demonstrate: this mechanism of action has not been confirmed in controlled research in humans, and moreover the three reported cases do not all involve the same form of hair loss.

Several studies confirm that egg yolks are exceptionally rich in phosphatidylcholine. A review study, for instance, describes egg yolk as the richest natural source of phospholipids, with phosphatidylcholine as the most prevalent type. Another source states that egg yolk phospholipids consist of approximately 80% phosphatidylcholine. Egg yolk is also consistently cited in the broader scientific literature as one of the most important sources of phosphatidylcholine in the Western diet. The claim is thus well supported.

Collagen does indeed play a structural role in the intestinal wall: research in humans shows that collagen in the submucosa and muscular wall of the intestine provides strength, and animal research in rats shows that protein deficiency leads to less collagen in the intestinal wall and lower breaking strength. Glycine is also a crucial building block of collagen, as demonstrated by studies showing that replacing glycine in collagen severely disrupts the structure of collagen fibres. The claim is therefore correct regarding the role of collagen in the intestinal wall and the importance of glycine for it; however, the assertion that glycine is specifically essential for the connective tissue of the intestinal wall has not been directly tested in humans in the available research, and one study adds the nuance that free glycine is less effective than complete collagen peptides in protecting intestinal cells.

In research on non-ruminants such as dogs and rats, glutamine is indeed described as an important fuel for intestinal epithelial cells, and one review explicitly names it as the primary energy source for rapidly dividing cells. However, the picture is more nuanced: in sheep, intestinal epithelial cells appear to be less dependent on glutamine and more flexible in their fuel use; in chickens, glutamate rather than glutamine is the main energy source; and in dogs and rats, other substances such as butyrate and glucose also compete for oxidation. The claim that glutamine is the most important energy source therefore goes beyond what research broadly demonstrates: it depends strongly on the animal species and the available nutrients.

Research shows that elevated IL-6 is regularly associated with mood complaints: a large-scale summary of longitudinal studies finds a clear link between higher IL-6 and CRP levels and subsequent depressive complaints in people, and a similar summary confirms that older adults with depression have higher IL-6 levels than people without depression. For cognitive function, studies in people with Alzheimer's disease do find elevated IL-6 levels in the blood, but in mild memory complaints and in the context of CRP and Alzheimer's disease, the picture is less clear-cut. The association with CRP is also not consistent: one large-scale summary finds no clear difference in CRP between older adults with depression and healthy individuals. The claim is therefore correct for IL-6 and mood, but the assertion that CRP is equally consistently associated, and that this also applies to cognitive problems, goes beyond what research clearly demonstrates.

The combination of hydrolysed collagen with vitamin C is indeed supported by evidence for skin and joints, and vitamin C is mentioned in the research as a worthwhile addition. However, the specific advice to take collagen about an hour before a morning workout to support connective tissue goes beyond what the available evidence shows: studies look at daily intake over weeks to months, not at the precise timing relative to a workout. The general direction is correct, but the timing advice cannot be substantiated based on current research.

Insulin plays a role in fat storage and fat metabolism, and excess weight is indeed associated with insulin resistance, which decreases when weight is lost. However, the claim that weight loss is purely a hormonal process in which lowering insulin is the key goes beyond what the evidence justifies. Research shows that losing weight works through exercise, diet, and a combination of both, and that the approach matters less than sticking with it. Insulin is one factor in this, not the overriding mechanism.

Research in humans shows that slow breathing exercises before bedtime can shorten the time it takes to fall asleep and improve sleep quality. For example, a study in people with insomnia found that 20 minutes of slow breathing before sleep reduced the time to fall asleep and increased sleep efficiency, through increased activity of the calming part of the nervous system. The claim that slow breathing lowers heart rate is partly correct: studies show more of an increase in heart rate variability and greater influence of the calming part of the nervous system than a direct drop in heart rate. Moreover, the studies do not specifically show that a lower heart rate is the reason people reach deep sleep stages more quickly, and direct evidence for that specific mechanism is lacking in the available research.

It is well documented that stress disrupts sleep: multiple studies show that stress and poor sleep reinforce each other. However, the claim goes a step further by asserting that it is specifically the perception of a situation as a threat versus a challenge that matters. That distinction, known as cognitive appraisal, is not firmly established in the underlying research. The direction of the claim is correct, but the wording suggests a level of precision that the evidence does not support.

Research actually shows that heating breaks down the polyphenols in extra virgin olive oil itself: at temperatures between 98 and 180°C, the amount of polyphenols measurably decreases, and the higher the temperature, the faster this happens. A review concludes that extra virgin olive oil is best used at low temperatures and for short periods, precisely because the polyphenols are lost during heating. The polyphenols do offer some protection against oxidation, but are themselves consumed and broken down in the process; they do not fully compensate for the damage, and with prolonged or intense heating, both the polyphenol content and the total antioxidant capacity of the oil decrease sharply.

Green tea does modestly support brain function, but the claim is not entirely accurate as formulated. The evidence indicates that the effect of green tea on concentration and working memory stems primarily from the interaction between caffeine and L-theanine, not from EGCG as an antioxidant alone. The role of EGCG specifically as the active antioxidant for the brain therefore cannot be substantiated on the basis of research in humans.

That caffeine stimulates the breakdown of fat cells and thereby releases fatty acids from adipose tissue is broadly supported by research. A study in rat cells shows how this process works, studies in humans demonstrate that caffeine promotes the release of fatty acids, and review studies confirm that caffeine can increase fat burning. However, the claim that the caffeine in question comes specifically from green tea is not tested in any of the research: green tea also contains other active compounds, such as a substance naturally occurring in green tea, which may play a role, and it has not yet been demonstrated in humans that caffeine from green tea has the same fat-burning effect as caffeine on its own.

A review article on cerebral oxygen consumption explicitly confirms that the human brain accounts for about 2% of body weight but is responsible for approximately 20% of total oxygen consumption. A second study, which summarises and compares findings from multiple human studies, also cites an increase of around 20% in brain metabolism during exercise as a baseline, indicating an already high resting consumption. The claim therefore holds for humans and is directly supported by the available research.

Research shows that MCT oil can improve brain energy, but the common mechanism is that MCTs are converted in the liver into ketones, which the brain then uses as fuel. This works even without a low-carbohydrate diet or ketosis: several studies in people with mild cognitive complaints and Alzheimer's show elevated blood ketone levels and indications of improved brain metabolism after MCT use, even without a ketogenic diet. In addition, laboratory and animal research suggests that the fatty acids in MCT oil can also serve the brain directly as fuel, independently of ketone production, but this direct effect in healthy people who eat carbohydrates normally has not yet been well established. The claim that MCT oil "directly" improves brain energy even outside of ketosis is partly correct, but the direction and extent of the effect depend on how well someone's own glucose metabolism is still functioning, and in people with a healthy glucose metabolism the evidence is still limited.

Several review studies in humans confirm that GLP-1 medications (a group of drugs that affect the pancreas and the brain) slow down gastric emptying, suppress hunger and cause nausea as a common side effect. That direction is therefore correct. However, the claim states that the slower gastric emptying is "strong" and directly causes hunger to "disappear", whereas the studies show that the disappearance of hunger also works through processes in the brain that have nothing to do with how quickly the stomach empties. Moreover, animal research shows that the brain regions that regulate satiety and those that cause nausea are separate from each other. This means that nausea does not simply have to be a consequence of larger meals alone, but operates in its own way. The claim oversimplifies the whole picture and places too much emphasis on slower gastric emptying as the explanation for both effects.

High zinc doses demonstrably block copper absorption in the intestines, with clinically proven consequences such as anaemia and, in severe cases, spinal cord damage. The evidence is solid for very high doses and plausible for prolonged use above the safe upper limit. The claim describes this mechanism correctly: the combination of prolonged use and excessive amounts is precisely where the risk lies.

Research shows that fermentable fibres can stimulate GLP-1, but no clear threshold of 10 grams per day has been established anywhere. One study in humans did use 10 grams per day of a specific fibre-propionate compound and observed a rise in GLP-1, but this applied to that particular substance, not to fermentable fibres in general. A large review of 52 studies in humans concludes that the effects vary considerably by fibre type and that the results are not consistent. The claim suggests a universal and precise daily dose that the evidence does not support. → How can you naturally stimulate GLP-1 through diet?

Several systematic reviews show that taking zinc supplements in children has no clearly measurable effect on general cognitive function. A large international study in middle-aged and older adults also finds no meaningful effect on cognitive functioning. Nevertheless, the picture is not entirely clear-cut: one small study in schoolchildren reports improvements on specific subtests of an IQ test, and an observational study shows an association between higher blood zinc levels and a lower risk of cognitive decline in later life. Moreover, most studies focus on children in developing countries, whereas the claim makes no distinction by age group or nutritional status. The claim is largely consistent with the available research, but lacks the nuance that the situation may differ for people with a zinc deficiency or in certain population groups.

Several randomised controlled trials conducted in people with (early-stage) Alzheimer's disease show that Souvenaid probably does not reduce the risk of dementia and has no convincing effect on most measures of cognitive function. That part of the claim is correct. However, the picture is not black and white: a long-term study of 36 months found a clear slowing of cognitive decline and decline in daily functioning in people with early-stage Alzheimer's disease, and a meta-analysis combining multiple studies shows that a composite measure of disease progression favours omega-3 supplements, including Souvenaid. The claim that Souvenaid 'does not improve' cognitive function therefore goes beyond what the evidence supports, because for certain outcomes and early disease stages there are indications of some effect.

Several large studies actually show a modest benefit of a daily multivitamin on memory and cognitive performance in older adults, comparable to two to three years less age-related decline. This effect occurs mainly in people at risk of nutritional deficiencies or with a history of heart disease, and is most pronounced after at least one to three years of use. One long-running study of well-nourished older physicians found no benefit after twelve years, but that is a specific group that is not representative of all older men.

Several large human studies show that a combination of vitamin C, vitamin E and beta-carotene generally does not improve cognitive function or protect against cognitive decline. A large randomised study of women with cardiovascular disease found no effect of the combination on cognitive decline, and an overview study of trials involving tens of thousands of participants concludes that no meaningful effect has been found. That said, some findings point to possible benefits with long-term use or in certain groups of people, and one smaller study in older adults actually showed improvement on cognitive tests. The claim that the supplement "offers no benefit" is therefore too categorical: the evidence largely points in that direction, but is not clear-cut enough to support such an absolute conclusion.

A large randomised study conducted among older male physicians (the Physicians' Health Study II) does indeed show that men who had used beta-carotene for an average of eighteen years scored slightly better on cognitive tests than men who received a placebo. The direction of the claim is therefore correct, but the stated eleven years is inaccurate: the study found an effect specifically at an average duration of use of eighteen years, and no benefit was found with shorter treatment. Moreover, a Cochrane review and an overview study pooling all available research conclude that the evidence is of low certainty, and in another large study of women with cardiovascular disease, no effect of beta-carotene on cognitive function was found. Furthermore, the only positive study used a dose of 50 mg every other day, not daily.

The claim suggests that there is an almost perfect geographical overlap in the United States between glyphosate use and cancer incidence, but this is not supported by the research. Several large long-running studies that followed pesticide users in Iowa and North Carolina for many years find no link between glyphosate exposure and cancer in general, or with most specific types of cancer. Pooled analyses of multiple studies do show an elevated risk of certain blood cancers, such as non-Hodgkin lymphoma, in those most heavily exposed, but that is very different from a broad geographical association with cancer as a whole. Moreover, whether glyphosate actually causes that blood cancer has not yet been proven, and researchers point to limitations in the research, such as imprecise measurement of the level of exposure. → Does glyphosate increase your risk of lymph node cancer?

The picture among regulators is divided, not clear-cut. The IARC classified glyphosate as "probably carcinogenic to humans", but other major bodies, such as the European Food Safety Authority and the US Environmental Protection Agency, reached a different conclusion. There is therefore no broad recognition of a causal link by "several major regulatory bodies". The research itself is also contradictory: some meta-analyses find a moderately elevated risk of lymphoma with intensive exposure, while others do not find that link once they correct for other pesticides.

Research into glyphosate and cancer risk does not, in fact, produce a clear picture: several large analyses contradict one another, and a link with lymphoma sometimes disappears when you correct for other pesticides. There is no question of anything being "irrefutably proven by medical science". The evidence is contradictory enough that researchers neither rule out the risk nor confirm it. The claim therefore goes considerably further than the available research supports.

Research does indeed show that puberty in girls begins earlier than in the past, but the two to three years mentioned do not match the figures found. A large meta-analysis based on data from 1977 to 2013 finds a shift of nearly three months per decade, which amounts to approximately one and a half years over fifty years. European research cites a decline of six to twelve months per century for the onset of menstruation, and a Chilean study finds around 3.7 months per decade. A shift of two to three years over fifty years is not supported anywhere and is considerably larger than what research shows. → Can an unhealthy diet cause puberty to start earlier?

Biological age is measurable and is associated with health risks, but evidence that the pace of biological ageing can be deliberately influenced is currently lacking; let alone that this pace can be reduced to a specific ratio such as six months per twelve calendar months. No study with solid clinical support has shown that such a precise deceleration is achievable; the available studies are small and methodologically immature. The claim therefore goes considerably beyond what research has demonstrated so far.

An intervention study with ten healthy volunteers shows that taking 30 grams of erythritol increases platelet reactivity, while 30 grams of glucose does not. The claim is therefore correct regarding dose, population and direction of the effect. Nevertheless, it goes slightly beyond the evidence: the study is small (ten participants per group), and no exact measurement at thirty minutes is reported in the abstract; only that an acute effect occurred after ingestion. A separate review article also notes that no increased platelet activation has been found in people with chronically elevated erythritol levels, and that long-term data in humans are still lacking, which nuances the overall conclusion.

Research does support the idea that berberine influences blood sugar and insulin sensitivity: it lowers blood sugar and HbA1c in people with type 2 diabetes, with an effect comparable to a mild oral diabetes medication. The AMPK mechanism is a frequently cited explanation for this, but whether it also concretely reduces the liver's burden from fructose has not been demonstrated in the available research. The claim combines a mechanism with a clinical outcome (less fructose burden on the liver) for which the evidence is lacking.

Studies in humans show that the uric acid-excreting effect of vitamin C only occurred at very high doses (4 grams or more), not at the amounts obtained through diet. Moreover, one human study at those same high doses found no effect on uric acid excretion at all. The underlying mechanism suggested, competition in the kidneys, has been studied in the context of megadose supplementation, not of vitamin C from whole foods. The claim that vitamin C from ordinary food excretes more uric acid through this mechanism is therefore not supported by the research.

Tart cherry juice does contain melatonin, but whether the amount is large enough to noticeably improve sleep quality has not been examined in the available studies. The response about the sleepy girl mocktail makes clear that cherry juice as a sleep aid has barely been studied and that evidence for an effect is lacking. The claim that it "can support" sleep quality therefore goes beyond what the research has shown so far.

Several reviews confirm that the liver produces uric acid when breaking down fructose, and that elevated uric acid levels are associated with insulin resistance and metabolic syndrome. Research in children shows, for example, that high fructose intake is linked to insulin resistance, even in children of normal weight. Nevertheless, the causal relationship in humans has not yet been fully elucidated: most mechanistic evidence comes from animal and laboratory studies, and reviewers emphasise that the precise role of fructose-derived uric acid in the development of insulin resistance, independently of calorie intake, has not yet been fully clarified. The claim is therefore broadly correct, but goes slightly beyond what the evidence in humans can establish with certainty so far.

Research shows that high uric acid levels cause harmful processes in fat cells through free radical damage, and that this is associated with an impaired response to insulin. Studies in cultured mouse fat cells and rat models demonstrate this mechanism, and a review study also summarises evidence from human research. However, the evidence for the part of the claim relating to the cell's energy centres comes primarily from animal experiments and cell studies; in humans, the precise sequence of cause and effect has not yet been fully established. The review study also notes that the exact interaction at the cellular level between uric acid and insulin action is still incompletely understood and requires further research.

Several review studies in humans show that high uric acid levels reduce the availability of nitric oxide, which is consistent with the first part of the claim. However, the link with reduced blood flow to the muscles and lower glucose uptake by the muscles is not described in the research: the studies focus on vascular function, cardiovascular disease and insulin resistance in general, not specifically on the muscles as the target organ. Moreover, the studies indicate that it is not yet certain whether uric acid itself is the direct cause of these effects, or whether it acts through harmful processes in the cells that arise during the production of uric acid.

Several studies show that grass-fed beef does contain measurable amounts of omega-3 fatty acids, and clearly more than grain-fed beef. One Australian study shows that only grass-fed beef meets the recommended threshold of 30 mg of long-chain omega-3 per 100 grams required to officially label a product as an omega-3 source. At the same time, review studies confirm that the absolute amount of omega-3 in grass-fed beef is much lower than in fatty fish, and that the amount per serving is too small for most people to meet their daily needs. The claim that grass-fed beef contains "no meaningful amount" of omega-3 therefore goes too far: it genuinely contains more omega-3 than grain-fed beef and can make a contribution, even though fatty fish is a far richer source.

Research shows that eating low-carb noticeably reduces belly fat and liver fat, and that this effect occurs relatively quickly, especially in people who are overweight or have metabolic complaints. However, the claim that this happens "selectively" and "much faster" than the loss of total body fat goes beyond what the available research firmly establishes: studies show a beneficial effect on belly fat, but a direct comparison with the rate of total body fat percentage loss is not demonstrated in those studies. Moreover, the weight-loss advantage of low-carbohydrate diets over other diets largely disappears over time, which puts the emphasis on "much faster" into perspective.

A carefully designed scientific study, the so-called MASTERS trial, in which adults aged 65 and over were randomly assigned to two groups that each received a different treatment without knowing which one they were taking, produced the following findings. Participants who took metformin gained significantly less muscle mass and muscle density during strength training than participants who received a placebo. The claim is therefore correct for older adults, but the evidence explicitly applies only to that age group and has not yet been studied in younger, healthy adults. Moreover, a closer analysis of the same study shows that concurrent use of cholesterol-lowering drugs may cancel out the inhibitory effect of metformin on muscle growth, meaning that the outcome depends on other medication a person is taking. The claim is therefore too broadly formulated, as it makes no distinction by age group and includes no caveat for this type of drug interaction.

Research shows that strength training can improve VO2 max, but the evidence for this is stronger for circuit training or combined training than for classical strength training alone. A study of men aged 70 to 80 found an increase in VO2 max of around 8% after 16 weeks of strength training, but those gains disappeared again after four weeks of detraining. A large-scale review of multiple studies in healthy adults showed clear improvements in VO2 max following resistance circuit training. In previously sedentary, middle-aged individuals, circuit training once a week was sufficient to maintain VO2 max but did not clearly increase it. A study of older, low-active adults at elevated cardiovascular risk did find an improvement in VO2 max after combined training, but not after strength training alone. The claim that strength training by itself modestly improves VO2 max in older adults or untrained individuals is partly correct: the direction is plausible for specific forms such as circuit training or in people starting from a low baseline, but the evidence for regular strength training alone is limited.

Research does indeed show that nitric oxide production decreases with age, but the studies that support this with specific figures were conducted in rats, not in humans. For example, one study in old rats (33 months) found a 50% decline in a specific activating step in the production process, while another study in rats found a similar halving in the functioning of a particular protein that drives production. Studies conducted in humans do describe the decline, but do not mention a specific percentage and do not link it to the age of forty. The claim that the body produces only 50 percent around the age of forty compared to the age of twenty has not been demonstrated in this way in humans.

Research shows that exposure to pesticides increases the risk of Parkinson's disease, and avoiding them is therefore considered a meaningful measure. For glyphosate specifically, however, the evidence is mixed: some analyses find an increased risk of certain types of cancer, but the associations are not consistent and partly disappear when corrected for other pesticides. The link with autism is not described in the research we have reviewed, which means that part of the claim cannot be substantiated. The claim thus conveys more certainty about these associations than the available evidence justifies.

Several large review studies show that people with sleep apnoea more often have a vitamin D deficiency than people without this condition, and that the deficiency is greater as sleep apnoea is more severe. The first part of the claim is therefore well supported. The second part, that supplementation improves throat muscle function and inflammation, goes beyond what research has demonstrated so far. One review study mentions that vitamin D supplementation may improve sleep quality and reduce the severity of sleep apnoea, but emphasises that further research is needed to confirm this. No evidence has yet been found for the specific effect on throat muscle function and inflammation in humans: a small human study found no association between vitamin D and inflammation levels, and barely any clinical trials involving supplementation in sleep apnoea patients have been conducted.

One study in humans (56 Japanese middle-aged women) shows that both strength training and endurance training improve skin elasticity and the upper skin layer after 16 weeks, and that strength training additionally improves dermal thickness. This supports the core of the claim. However, the claim states that strength training "slows" skin ageing, while the study concerns a specific group (sedentary middle-aged women) and is only a single study. The remaining abstracts concern collagen supplements and the cell biology of skin ageing, and do not test the claim. The conclusion that strength training slows skin ageing in humans in general therefore goes beyond what this one study can demonstrate.

Ultra-processed food is associated in observational research with increased risks of diabetes, cardiovascular disease, depression and premature death, and there are indications that high sugar intake damages the gut lining and chronically stimulates immune cells. However, fatigue, poorer sleep and acid reflux as separate consequences are not firmly established by the available research. The immune effect is plausible with structurally excessive sugar intake, but even then, "more frequent infections" goes a step further than what the evidence shows. The claim combines a range of complaints as though they are all equally well supported, whereas the evidence for most of those specific effects has not been demonstrated.

A large study pooling and comparing the results of 23 long-running studies in humans shows that retirement has no negative effect on cognitive ability in general, and at most a small adverse effect on memory. A review of 10 studies finds mixed results: some studies find an association between earlier retirement and cognitive decline, but five studies actually show that retiring later reduces the risk of dementia. More recent research in large populations suggests that the timing of retirement itself has little influence on the risk of dementia, and that the way in which someone stops working, as well as health reasons related to work, matter more. The claim that retiring earlier both causes earlier and faster cognitive decline is not supported by the available research in humans.

Research in older adults shows that regular rest and activity patterns throughout the day are associated with a lower risk of dementia and better executive functioning. Irregular napping patterns have also been linked to greater Alzheimer's pathology. However, the claim is specifically about consistent bedtimes as a marker of neurological health, whereas the studies take a broader look at day-night rhythms and activity patterns in general, not exclusively at the time a person goes to bed. Moreover, the findings concern associations, not evidence that consistent bedtimes themselves cause better brain health.

The association between glyphosate and lymph node cancer has been studied, but the evidence is contradictory: some meta-analyses find a moderately elevated risk with intensive occupational exposure, others find nothing, and the association partly disappears when correcting for other pesticides. As for direct toxicity to the liver and kidneys at the exposure levels people normally encounter, the available research contains nothing that is concretely substantiated. The claim therefore draws two conclusions at once, of which the cancer link is at least disputed and liver and kidney toxicity in humans cannot be firmly established on the basis of current research.

Research shows that hydralazine inhibits AGE formation, but the mechanism is more complex than simply scavenging free glucose molecules. Studies in diabetic rats and mice show that hydralazine lowers AGEs through 'transglycation' (detaching glucose from proteins) and by scavenging reactive carbonyl compounds such as glyoxal and methylglyoxal, not primarily free glucose. Cell studies even show that hydralazine does not effectively scavenge glyoxal itself, but instead acts as an antioxidant. The claim that hydralazine specifically scavenges free glucose molecules is therefore not fully correct: the active mechanisms are different and have moreover been demonstrated mainly in animal and cell studies, not in humans.

Several human studies show that pioglitazone favourably alters the ratio of visceral to subcutaneous fat: visceral fat decreases or increases relatively less, while subcutaneous fat increases. One study in people with diabetes shows that visceral fat decreased and subcutaneous fat increased after treatment. However, another study in non-diabetic people with overweight shows that the improvement in fat distribution is driven mainly by an increase in fat in the lower body regions, not by genuine mobilization of visceral fat. The claim that pioglitazone actively 'mobilizes' visceral fat and moves it to another compartment goes beyond what the studies demonstrate: it is more a matter of redistribution in which newly stored fat is preferentially deposited subcutaneously, rather than a direct transfer of existing visceral fat.

Research shows that ageing processes are indeed already active during embryonic development: in mammals, including humans, programmed cellular senescence occurs in the embryos themselves, and factors such as the mother's weight gain, blood pressure and obesity influence the epigenetic ageing of the placenta. Research also shows that adverse conditions in the womb, such as poor nutrition or exposure to harmful substances, increase the risk of ageing-related diseases later in life. The claim is therefore broadly correct, but "the mother's lifestyle" is somewhat broader than what the studies specifically demonstrate: they focus in particular on weight gain during pregnancy, blood pressure and obesity, not on lifestyle in the wider sense, such as exercise, sleep or stress.

A medical study does indeed show that three rounds of the Fasting Mimicking Diet in adults are associated with a reduction in biological age of 2.5 years according to a reliably validated blood test, independent of weight loss, and a second smaller study confirmed similar findings. The claim is therefore correct in terms of the figure and direction. Some nuance is warranted, however: this involves a secondary and exploratory analysis of an existing study, not a study designed from the outset to measure biological age, and the researchers have financial ties to the manufacturer of the diet. In addition, another study measures a different marker in people with multiple sclerosis, and the remaining studies concern other outcomes such as blood sugar or cancer, meaning that the evidence for the claim of 2.5 years currently rests on a single main study.

Research in humans actually shows the opposite of what the claim states. In a study of adults who fasted on water alone for an average of 14 days, as much as 74 % of the weight lost during fasting consisted of fat-free mass (muscle mass and fluid), not two thirds of muscle mass. A review study that pooled and compared the results of 49 separate studies confirms that prolonged fasting is accompanied by substantial decreases in both fat-free mass and body water, but found no consistent pattern in which fat accounts for two thirds of the loss. A study of hunger strikers fasting for 43 days showed that body fat decreased by far the most. The two-thirds muscle / one-third fat ratio is therefore not supported by the available research.

Research in humans does indeed show that fasting substantially increases growth hormone release, but the figures and durations vary considerably. One study in older adults found a fourfold increase after two days of fasting, whereas the claim refers to a factor of two for a window of 18 to 24 hours. Studies in younger healthy individuals show comparable effects, but no separate figure for the 18-to-24-hour window is available from these studies. Moreover, one mouse study reached the opposite conclusion: in that study, 16 hours of overnight fasting actually suppressed growth hormone release. The direction is correct for humans, but the specific duration and the factor of two have not been directly confirmed.

Research into diabetes and bone fractures shows that GLP-1 agonists have a neutral to mildly beneficial effect on bone health, not a harmful one. Osteoporosis and bone fractures are listed as risks for other diabetes medications, but are not linked to GLP-1 agonists as a class. Only one human trial has been registered, and it was terminated early, which does not point to a strong suspicion of harm. The claim therefore goes against the direction of the available evidence.

Several studies show that acetic acid activates AMPK in liver cells and that this leads to greater fat oxidation. This has been demonstrated in mice, rats, cows and in cultured liver cells in the laboratory. A review study confirms that acetate can increase fat oxidation in humans, but also notes that human data are scarce. For the specific combination of AMPK activation in the liver and the direct link to fat oxidation in humans, no solid human evidence is yet available. The claim suggests an established mechanism in humans, whereas to date it has been shown primarily in animal and laboratory research.

Research in humans shows that vinegar (including apple cider vinegar) can indeed reduce the rise in blood sugar after a carbohydrate-rich meal. One study found a reduction of approximately 20% compared to a placebo, and another study with healthy participants reported a reduction of approximately 55% in the blood sugar response after 60 minutes, but that result was only clearly measurable with a meal that causes a sharp rise in blood sugar. The figure of "more than 31%" is a specific number that does not follow directly from these studies: the percentages found vary considerably between studies, meal types and measurement methods. The direction of the effect is correct, but the precise size of the reduction depends on factors such as the type of carbohydrates, the dose and the timing of intake.

The claim is based on a single scientific study involving healthy participants, who were exposed to red light with a wavelength of 670 nanometres for 15 minutes. That study does indeed show that blood sugar levels over the two hours following sugar intake were on average 27.7% lower, but the peak blood sugar value fell by only 7.5%. The claim speaks of "approximately a 28% reduction in the blood sugar peak", but in the study that figure refers to the total amount of sugar in the blood over the entire two-hour period, not to the highest value the blood reached. The peak therefore dropped far less than 28%. Furthermore, it is a single small study in healthy people, and whether the light source was directed at the back is not mentioned in the study's abstract.

Research in mice shows that suppressing inflammation in the hypothalamus is associated with a longer lifespan: mice given life-extending drugs had less hypothalamic inflammation, and that reduction ran parallel to the increase in lifespan. Review studies confirm that hypothalamic inflammation plays a role in ageing and that counteracting it is promising. The claim therefore holds for laboratory animals (mice), but the evidence is largely indirect: studies demonstrate an association and a parallel effect, not a direct manipulation in which only the inflammation was reduced and lifespan was then measured as a result. In humans, this relationship has not yet been tested.

Several review studies and a pilot study confirm that stem cells can indeed transfer mitochondria to damaged cells, restoring energy production and cell survival. This has been demonstrated in both laboratory and animal research, and studies investigating this in humans are under way. The claim is therefore correct in its general direction, but goes beyond what the evidence firmly supports on two points: the effect has not yet been well demonstrated in humans, and the transfer to specifically 'ageing' cells has not been examined as a separate category in the summaries. Moreover, one review study points out that mitochondrial transfer also has a downside, for example in cancer. → Does stem cell therapy work against ageing in people?

Exercise demonstrably stimulates the production and function of mitochondria, but the evidence that substances such as curcumin, berberine and resveratrol act as exercise mimetics in humans is not yet solid. Supplements targeting mitochondrial energy metabolism are being actively studied, but show mixed results and lack strong clinical evidence behind them. The claim therefore runs considerably ahead of what the research has shown so far.

Mitochondrial mutations accumulate with ageing and disrupt energy production, while chronic low-grade inflammation and cellular ageing demonstrably reinforce each other. However, the claim that mitochondrial DNA leaks into the bloodstream and is recognised there as foreign by the immune system is a more specific mechanism than the available research supports: the studies cited do not describe the link between mitochondrial damage and inflammation at that level of detail. The broader idea that mitochondrial problems contribute to chronic inflammation during ageing is plausible, but this precise mechanism cannot yet be established on the basis of current research.

A small study in older adults who respond poorly to a vaccine shows that spermidine supplementation measurably improves the immune response, and that is consistent with the claim about the antibody response after vaccination. However, the claim that it also demonstrably reduces cellular ageing markers cannot be substantiated on the basis of the available research in humans. The claim is therefore too categorical: the direction is promising, but the evidence base is narrow and the ongoing trials have yet to deliver results.

Research into a low-dose spermidine supplement does indeed show that twelve months of supplementation provided no cognitive benefit, which supports the claim. Moreover, after high-dose supplementation, spermidine levels in the blood did not even rise, which further increases doubts about the effectiveness of supplements. The claim is therefore well in line with the available evidence, although the research is limited and this is far from the final word on spermidine and memory.

Large-scale global analyses show that while a high sodium intake is one of the most significant diet-related risk factors, it is not the leading one. A major international study from 2017 found that high sodium intake, low consumption of whole grains and low consumption of fruit each account for approximately 3 million deaths per year, placing them on an equal footing. A comparable study from 2019 ranks unhealthy dietary patterns as a whole below non-dietary risk factors such as high blood pressure and smoking. The claim that sodium is the leading diet-related risk factor for mortality is therefore incorrect based on these studies: sodium and whole grains score comparably, and the international research data show no clear top position for sodium. → Do you live longer if you eat more salt?

Muscle mass does indeed begin to decline around the age of thirty, and research confirms that this is a gradual process. However, the claim cites a specific figure of 3 to 8 percent per decade, whereas the available data concern muscle strength loss (around 3 to 4 percent per year after the age of fifty) rather than muscle mass loss within that precise range. Those specific figures for muscle mass per decade cannot be substantiated based on what the research shows, and strength declines considerably faster than mass.