477 Health claim verifications avg. score 5.0/10 172 rated true or mostly true 305 rated false or misleading
“During acute stress, pulmonary blood flow increases mainly because cardiac output increases.”
The central mechanism is correct for typical acute stress in healthy people: sympathetic activation raises cardiac output, and pulmonary blood flow usually rises with it. The statement becomes too broad if applied to all stressors or all patients, because acute hypoxia and diseases such as severe pulmonary hypertension can make pulmonary vascular resistance or right-heart afterload more important.
“After proteases finish digesting food in the duodenum, they move with chyme into the middle and distal small intestine and then digest themselves and other enzymes into amino acids.”
Reliable physiology sources show that pancreatic proteases do travel through the small intestine and are progressively inactivated and degraded there. But the claim misstates the sequence and emphasis: protein digestion does not simply end in the duodenum, and distal enzyme breakdown is not shown to be the main or intended next step. It blends a real phenomenon with an overstated physiological narrative.
“Most intestinal juice in the small intestine comes from the contents released when small-intestinal epithelial cells rupture and slough off, rather than from fluid actively secreted by intestinal glands.”
The evidence does not support the claim. Authoritative physiology sources describe intestinal juice as mainly water and electrolytes actively secreted by crypt epithelium and glands, not fluid released from ruptured, sloughed cells. The main cited support concerns protein content in cellular debris from an older animal study, which does not establish that most intestinal juice volume comes from cell shedding.
“Under normal conditions, only a very small fraction of dietary amino acids in the small-intestinal lumen are diverted by other substances or are consumed by colonic bacteria before being absorbed, so amino-acid loss is very low.”
Most dietary amino acids are absorbed in the small intestine under normal, healthy conditions, so losses before absorption are generally low. Human studies and reviews commonly report ileal amino-acid digestibility above 90%, often above 95%. The wording is somewhat broad because digestibility differs by protein source and some proteinaceous material still reaches the colon, but that does not overturn the main conclusion for typical diets.
“In humans, taste buds that detect sweet taste are concentrated at the tip of the tongue.”
The evidence does not support a sweet-specific cluster of taste buds at the tongue tip. Modern taste research has rejected the old textbook “tongue map”: sweet-responsive cells are found across multiple tongue regions, with only minor regional sensitivity differences at most. Those sensitivity differences do not mean sweet-detecting taste buds are concentrated at the tip.
“Drinking coffee stains teeth yellow.”
Coffee is a well-established cause of extrinsic tooth staining, and the discoloration often appears yellow-brown over time. The evidence from dental studies is strong, but the effect is not uniform or inevitable for every coffee drinker. Staining depends on exposure, enamel condition, and oral hygiene, and some studies use lab conditions that can overstate real-world effects.
“Eating chocolate cures depression.”
The evidence does not support chocolate as a cure for depression. Some studies suggest small, short-term mood improvements from cocoa-rich products, but they do not show that eating chocolate resolves diagnosed depressive disorder or provides lasting clinical recovery. Major health authorities and systematic reviews do not endorse chocolate as a treatment for depression.
“Among patients 12 months after ST-elevation myocardial infarction, those with high-sensitivity C-reactive protein levels greater than 26.4 mg/L had a 12% rate of major adverse cardiovascular events, compared with a 4% rate among those with high-sensitivity C-reactive protein levels at or below 26.4 mg/L.”
The quoted 12% versus 4% event rates are supported by a 2024 peer-reviewed STEMI study. However, those numbers came from a selected cohort followed for about 12 months, and the 26.4 mg/L threshold was the study’s median hs-CRP level, not a broadly accepted universal cutoff. The data are accurate, but the wording is slightly broader than the underlying evidence.
“A prospective Fudan University study of 724 patients with recent myocardial infarction found that soluble interleukin-2 receptor (sIL-2R) was an independent predictor of long-term major adverse cardiac events, reporting an unadjusted hazard ratio of 9.123 (95% CI 5.883–14.147) and an adjusted hazard ratio of 3.761 (95% CI 2.269–6.233) with p < 0.001.”
The cited study details are supported by the published record. Multiple authoritative versions of the same Fudan/Zhongshan cohort paper report 724 patients, a prospective design, and the exact unadjusted and adjusted hazard ratios with p<0.001. The main caveat is a likely misindexed older database entry, plus the study’s single-center design and cutoff-based analysis.
“A follow-up study of 382 adults younger than 60 years old, assessed 3 months after a first myocardial infarction and followed for 20 years, reported that participants in the highest tertile of interleukin-6 had a 2.70-fold higher risk of hospitalization for heart failure than those in the lowest tertile (hazard ratio 2.70; 95% CI 1.32–5.50).”
The reported hazard ratio appears in the literature, but the claim’s age-specific framing is not reliably established. One abstract describes 382 adults younger than 60, yet other peer-reviewed sources assign the same 2.70 estimate and sample to patients aged 60–74, and a related report cites 391 participants. Because age materially affects interpretation, the statement overstates certainty about which cohort produced this result.
“Creatine supplementation reduces S-adenosylmethionine (SAMe) demand by decreasing endogenous creatine synthesis.”
Available evidence supports this mechanism. Creatine supplementation suppresses endogenous creatine synthesis, and that synthesis normally uses SAMe to methylate guanidinoacetate into creatine, so the pathway’s SAMe demand falls. Unchanged blood SAM, SAH, or homocysteine in some trials does not negate this, because those markers do not directly measure pathway flux.
“Creatine supplementation improves brain fog in humans.”
Creatine may help some cognitive functions linked to what people call brain fog, but the evidence does not directly show that it generally improves “brain fog” in humans. Most studies measured objective cognitive tasks, not the symptom itself, and positive effects are most apparent in specific settings such as sleep deprivation, older adults, or other higher-demand conditions. The broad, unqualified wording goes beyond the evidence.
“Bipolar disorder is characterized by episodes of mania or hypomania and episodes of depression.”
This is a generally accurate description of bipolar disorder, but it is not a universal diagnostic rule. Major medical sources describe bipolar disorder as involving periods of mania or hypomania and depression, yet Bipolar I can be diagnosed without any prior depressive episode. The claim is best read as a broad characterization rather than a strict criterion.
“A 2025 Robert Koch Institute report found that, in Germany, the proportion of adults diagnosed with a mental disorder in outpatient care increased from 35.0% in 2012 to 40.9% in 2022.”
The increase itself is supported, but the claim overstates what the evidence shows. Available sources back a rise from 35.0% in 2012 to more than 40% in recent years, yet they do not substantiate the exact figure of 40.9% for 2022 or clearly tie it to a distinct 2025 Robert Koch Institute report. The wording also blurs that this is outpatient administrative diagnosis data, not overall population prevalence.
“The increase in outpatient diagnoses of mental disorders in Germany from 2012 to 2022 was largely caused by previously untreated or unrecorded mental health problems becoming visible due to increased help-seeking.”
Increased help-seeking likely made many previously untreated or unrecorded mental health problems visible in Germany’s outpatient system, but the evidence does not show this was the main cause of the 2012–2022 rise in diagnoses. Authoritative sources describe several concurrent drivers, including coding and documentation changes, billing incentives, and service expansion. Because those contributions cannot be reliably separated, “largely caused” overstates what the evidence supports.
“A 2025 report by the Robert Koch Institute stated that a key explanation for the increase in outpatient diagnoses of mental disorders is that people may be increasingly seeking help due to destigmatisation.”
The cited evidence does not verify that a 2025 Robert Koch Institute report made this specific statement. The only clearly identified 2025 RKI publication in the record addresses survey-based prevalence and methodological differences, not rising outpatient diagnoses attributed to destigmatisation. Reduced stigma may indeed increase help-seeking, but that broader idea does not prove the claimed RKI wording or attribution.
“Using prescription acne medication at any point during pregnancy is problematic for pregnant women.”
The evidence does not support a blanket claim that prescription acne medication is problematic at any point in pregnancy. Major medical guidance says risk is drug-specific: retinoids are contraindicated, while several prescription options, such as topical clindamycin and azelaic acid, are commonly considered acceptable in pregnancy. The statement wrongly treats the entire category as unsafe.
“Alternative medicine works as well as or better than conventional medicine.”
The evidence does not support the idea that alternative medicine broadly works as well as or better than conventional medicine. A few approaches, such as acupuncture for some pain conditions, may offer modest benefit, but they generally do not outperform standard care. Many others, especially homeopathy, fail rigorous testing, and replacing proven treatment with alternatives can increase harm and mortality.
“Sugar-free soft drinks sweetened with non-sugar sweeteners (for example, Coca-Cola Zero Sugar) are as harmful to teeth as sugar-sweetened soft drinks.”
The claim overstates what the evidence shows. Sugar-free soft drinks can damage teeth about as much as sugary soft drinks in terms of enamel erosion, because both are acidic. But sugary soft drinks also promote cavities by feeding oral bacteria, so they are not generally equal in overall dental harm.
“Salivary amylase cannot break down starch into glucose because the enzyme molecule is too large.”
The evidence shows the claim is not supported. Salivary amylase does begin starch digestion by cutting starch into smaller sugars such as maltose and dextrins, and its molecular size is not a barrier to that action. If the intended point was that salivary amylase does not usually produce free glucose by itself, that is a different and much narrower statement.