551 Health claim verifications avg. score 5.1/10 219 rated (mostly) true 266 rated (mostly) false
“Physiologic stress can increase intestinal permeability by disrupting tight junctions between enterocytes, which increases translocation of luminal antigens and bacteria.”
The literature strongly supports that stress can impair the intestinal barrier by altering tight-junction function and increasing permeability. Reviews, animal studies, and cell studies also link this barrier disruption to greater passage of luminal antigens and, in some models, bacteria. The main caveat is that the full causal chain is demonstrated most directly in animal and in vitro research; human evidence is stronger for permeability changes than for direct bacterial translocation.
“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 mid and distal small intestine and begin digesting themselves and other enzymes into amino acids.”
The evidence supports that pancreatic proteases continue moving with chyme beyond the duodenum and may be degraded during transit. But the claim misstates both timing and mechanism: protein digestion is not simply finished in the duodenum, and free amino acids are produced mainly through brush-border and intracellular peptidases, not primarily by proteases digesting themselves and other enzymes.
“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 sweetness are concentrated at the tip of the tongue.”
The evidence does not support the idea that sweetness-detecting taste buds are concentrated at the tip of the human tongue. Modern research shows sweet receptors and taste buds are distributed across the tongue, and the classic “tongue map” is widely regarded as a myth. At most, some studies suggest slight sensitivity differences at the tip, but that is not the same as a concentration of sweet-detecting taste buds.
“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 cohort study of 382 adults younger than 60 years old, assessed 3 months after a first myocardial infarction and followed for 20 years, found that participants in the highest tertile of interleukin-6 had a 2.70-fold higher risk of heart-failure hospitalization than those in the lowest tertile (hazard ratio 2.70; 95% CI 1.32–5.50).”
The described study appears real, and the available evidence supports that higher IL-6 levels measured three months after a first myocardial infarction were linked to higher later risk of heart-failure hospitalization in 382 adults under 60. However, the exact figure cited—hazard ratio 2.70 with 95% CI 1.32–5.50—and the stated 20-year follow-up are not directly verified in the provided evidence. The core association is supported; the precise numerical claim is not fully substantiated here.
“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.
“The cervical region of a tooth (near the cementoenamel junction) contains both enamel and cementum at the same location.”
The core anatomical idea is correct: the cervical/CEJ region is where enamel and cementum meet, and cementum commonly overlaps enamel. But the wording is too absolute. Teeth show several CEJ patterns, including edge-to-edge contact and small gaps exposing dentin, so both tissues are not literally present at the exact same spot in every case.
“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 share of adults with statutory health insurance outpatient claims who had at least one documented mental disorder diagnosis (ICD-10 F00–F99) increased from 35.0% in 2012 to 40.9% in 2022.”
The RKI did report an upward trend, but not the one stated here. For 2012–2022, official RKI sources report 33.4% rising to 37.9%, while the 40.9% figure belongs to 2024 in a different RKI indicator series. The claim therefore combines real RKI numbers from different years and datasets, which materially changes the factual takeaway.
“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.”
Available evidence does not support increased help-seeking as the main driver of Germany’s 2012–2022 rise in outpatient mental-disorder diagnoses. Authoritative RKI and peer-reviewed analyses describe several plausible contributors, including diagnostic and documentation changes, coding and system effects, longer treatment duration, demographic factors, and COVID-related influences. The increase in diagnoses is well documented, but the claimed dominant cause is not.
“A 2025 Robert Koch Institute (RKI) report stated that a key explanation for the increase in outpatient diagnoses of mental disorders is that people may be increasingly seeking help due to destigmatization.”
The report did say that increasing outpatient mental-disorder diagnoses may partly reflect more people seeking help, including because mental disorders are becoming less stigmatized. However, it presented this as one possible explanation among several and also pointed to longer diagnosis or treatment duration as an important driver. The claim is substantively accurate but slightly overstates the report’s emphasis.
“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.