Sweat enzymes may weaken healing skin by cutting the protein links between surface cells
In restored skin models from donors aged 20–30 and 40–60 years, sweat enzymes may transfer vulnerability regardless of recipient age. Unchanged strength after verified enzyme removal, with protection from changing mechanical constraints on swelling, would reject the proposed mechanism.
Stage of verification
- Hypothesis published2026-09-25
- Indirect evidenceAssessed at 4 of 10
- Direct testAwaited
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Where in the body
Biological function
Kind of knowledge gap
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Target map
Every target of every published hypothesis, each with the actions a hypothesis can propose on it. The targets and the actions of this hypothesis are drawn solid.

Enzyme
Proteases
Enzymes that break down proteins
Where this hypothesis actsSweat contacting recently healed skin under moist clothing
Hypotheses on this target 7
Inhibition6
Activation
Lower level1
Higher level
Replacement
Protection from degradation
Cofactor removal
Synthesis suppression
Function preservation

What is proposed
Lower level
Suppress protease activity to prevent cleavage of corneodesmosomal proteins
With whatRemoval from a body fluid
HowSelectively remove the active protease fraction from sweat while preserving sweating and evaporative heat loss
Possible result
Possible preservation of the mechanical damage threshold and stabilization of SPV_3
From the recordпот после удаления активной протеазной фракции
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Every target read from the published hypotheses, each kind around its pictogram. A larger mark means more hypotheses act on that target. Point at a mark and the actions proposed on it branch out of it.
Solid and named: the targets of this hypothesis
Explore in depth
The logic
The train of thought that ends in this hypothesis. Each stage is the reason the next exists. The master question narrows to a goal, the goal to an unknown nobody has closed, the unknown to the hypothesis proposed here. Every step below says what it rests on and what carries it.
Recently healed skin may remain easy to damage even after the surrounding sweat has dried. The unexpected proposal is that sweat cuts the protein connections holding surface cells together, leaving lasting weakness that can be transferred between skin samples with the enzyme-containing portion of sweat. This is a hypothesis generated by the pipeline, not a measured result.
- Sweat from surrounding skin carries protein-cutting enzymes to the healing area.
- Wet clothing prolongs contact between those enzymes and the newly restored outer skin layer.
- The enzymes cut protein connections between surface cells before rubbing begins.
- The surface changes from connected cells that resist rubbing to cells with missing connections and a lower damage threshold.
- Drying restores water content but, under the proposal, leaves the missing connections and resulting weakness behind.
- Selectively preventing the cutting is predicted to preserve strength while sweating and heat loss through evaporation remain unchanged.
A fabric can stay weak after drying if some of the stitches holding it together have been cut. Moving the scissors to another piece can move the source of damage with them.
Where the picture breaks: Skin connections are biological structures rather than stitches, and the presence of an enzyme does not establish that it can reach and cut those connections under actual clothing conditions. The picture also leaves out the competing possibility that uneven swelling creates weakness without cutting connections.
- Master questionstep 01 of 04
The goal is a treatment that restores the functional condition of middle-aged people’s skin to that of young people.
Rests on: The supplied goal names younger skin as the target for functional improvement.
Stated in the chain - Goal pillarstep 02 of 04
Protection, healing and the return to physical demands need coordinated timing.
Rests on: The goal concerns skin function, but does not explain why coordinating these three periods is a route to restoring younger function.
AssumptionThe chain assumes that coordinating protection, healing and renewed physical demands is a necessary part of the intended treatment.
- Gap questionstep 03 of 04
More sweating around a healing area might reduce its resistance to rubbing when clothing holds additional moisture against it without increasing heat loss through evaporation.
Rests on: The preceding stage identifies protection during healing and return to physical demands as concerns. This stage selects sweating, retained moisture and friction as a particular situation in which those concerns could conflict.
AssumptionThe selected situation assumes that moisture under clothing can increase while heat loss through evaporation stays unchanged; the preceding stage does not establish that exposure pattern or its effect on strength.
- Hypothesisstep 04 of 04
Proteases, enzymes that cut proteins, carried by sweat are proposed to become the main limit on the strength of the recently restored stratum corneum, the outer layer of flattened skin cells. They would cut corneodesmosomes, the protein connections between those cells, leaving weakness after drying. Transferring the active enzyme-containing portion of sweat is predicted to transfer vulnerability between samples with comparable starting strength, regardless of the receiving tissue’s age.S4S6
Rests on: The preceding question supplies the wet-clothing and friction setting. S4, in Journal of proteomics (2017), reports identifying protein-cutting enzymes and proteins that restrain them in human sweat, but does not establish their activity against healing skin or their effect on strength. S6, in Microorganisms (2026), describes loss of cell attachment through destruction of a connecting protein in work on a purified bacterial enzyme, but does not establish that sweat produces this effect in recently healed skin.
Supported by literature
What is carried, and what is not. Two links have relevant screened-source support: sweat contains protein-cutting enzymes, and cutting a connecting protein can undermine attachment between skin cells. The supplied literature does not establish the complete sequence from ordinary sweat exposure under clothing to persistent weakness after drying, transfer between samples or protection through selective enzyme blocking.
Where the reasoning is carried by something unstated · 2
- Goal pillar. The chain assumes that coordinating protection, healing and renewed physical demands is a necessary part of the intended treatment.
- Gap question. The selected situation assumes that moisture under clothing can increase while heat loss through evaporation stays unchanged; the preceding stage does not establish that exposure pattern or its effect on strength.
How a result here could mislead · 3
- Removing the enzyme-containing portion of sweat could also remove other proteins or alter the preparation, so a strength improvement could be incorrectly credited to loss of enzyme activity. What closes it: The specification requires a mock removal procedure and checks for other proteins removed alongside the enzymes. Enzyme activity and preparation composition must be measured before removal, after removal and after restoration; the prescribed matching of temperature, water content through the skin’s depth, acidity, dissolved-particle concentration and applied sideways force per area must also be verified.
- Equal water content could be mistaken for equal mechanical conditions. The rival explanation attributes weakness to unequal swelling between layers, constrained expansion and resulting folds; matching water content alone does not establish that these effects are equal. What closes it: The test must measure or control constraints on swelling and the resulting folds or retained internal forces. The specification names changing the constraint on swelling as a discriminating intervention, but does not give its implementation. Protein-connection cutting must be measured before rubbing, alongside strength after water content returns to its starting level.
- Damage caused by a concentrated preparation or unusually long exposure could be read as evidence that ordinary sweating is the main limit on healing-skin strength. What closes it: The supplied specification requires effects at concentrations and contact durations actually measured under clothing before participant studies. Those exposure measurements and the amounts used in the test must be reported; none are supplied here.
What would make this wrong. The central claim would fail if verified removal of the sweat preparation’s protein-cutting activity left strength unchanged under matched conditions, while changing the mechanical constraint on swelling removed the vulnerability. Failure of the active portion to transfer weakness between samples with comparable starting strength would separately contradict the proposal’s strong transfer claim.
What it would change. If the prediction held, restoring skin function would require attention to the integrity of surface-cell connections as well as whether a healing area had dried. The work would identify selective prevention of protein cutting as a candidate way to coordinate protection and return to physical demands while retaining sweating and evaporative cooling. Results in the proposed laboratory skin models made from cells of donors aged 20–30 and 40–60 would still not establish a treatment that restores middle-aged people’s skin to young function. The supplied material also does not define SPV_3, its intended outcome measure, so improvement in that measure cannot yet be translated into a concrete functional benefit.
Sources read · 10
Sweat allergy: Extrinsic or intrinsic? · Journal of dermatological science · 2017
“Sweat contains small amount of proteins including proteases, protease inhibitors, and anti-microbial peptides.”
Does not settle: Источник не устанавливает протеолитическую активность пота на заживающей коже, расщепление белков корнеодесмосом, влияние влажной одежды, длительность уязвимости после высыхания, перенос уязвимости между образцами или влияние селективного подавления протеолиза на SPV_3 и теплоотдачу.
Kallikrein-related Peptidase 5 (KLK5) Expression and Distribution in Canine Cutaneous Squamous Cell Carcinoma. · Journal of comparative pathology · 2020
“KLK5 was highly expressed in the upper stratum granulosum, stratum corneum, hair follicles and sweat glands, skin sites where human KLK5 has been shown to be involved in physiological processes including keratinocyte desquamation, antimicrobial defence, lipid permeability and pigmentation.”
Does not settle: This canine skin and cutaneous squamous cell carcinoma study does not establish proteolytic activity in sweat, exposure of healing human skin under wet clothing, cleavage of corneodesmosomes, persistence of weakness after drying, transferability between samples, tissue-strength outcomes, or selective prevention while preserving sweating and evaporative heat loss.
The protease corin regulates electrolyte homeostasis in eccrine sweat glands. · PLoS biology · 2021
“Unexpectedly, we detected corin expression in the luminal epithelial cells of human and mouse eccrine sweat glands.”
Does not settle: Источник не устанавливает наличие протеолитической активности в выделившемся поте, её действие на корнеодесмосомы или прочность зажившего рогового слоя, перенос уязвимости между образцами либо эффект селективного ингибирования при сохранении потоотделения.
Proteomic and peptidomic analysis of human sweat with emphasis on proteolysis. · Journal of proteomics · 2017
“Several skin proteases and protease inhibitors were identified in human sweat, highlighting the intense proteolytic activity of human skin.”
Does not settle: Источник не устанавливает физиологические концентрации или активность ферментов на заживающей коже, их воздействие на белки корнеодесмосом, прочность рогового слоя, перенос уязвимости между образцами либо эффект селективного предотвращения расщепления.
Staphylococcal epidermolysins. · Current opinion in infectious diseases · 2003
“While different observations suggested a proteolytic action to these toxins, the histological parallel made with pemphigus foliaceus greatly helped in the characterization of the targets for epidermolysins ETA, ETB, ETD: desmoglein-1, a desmosome-constitutive protein, and incidentally melanocyte-stimulating hormones, which accounts for the blisters observed clinically.”
Does not settle: Источник описывает бактериальные эпидермолизины и их мишени при инфекционных заболеваниях. Он не устанавливает протеолитическую активность пота, физиологические концентрации, воздействие влажной одежды, недавно восстановленный роговой слой, корнеодесмосомы, перенос уязвимости между образцами или эффект селективного предотвращения расщепления на SPV_3 и теплоотдачу.
An Ex Vivo 'Leaky Skin' Model to Study Early Events Induced by Staphylococcus aureus Protease. · Microorganisms · 2026
“Desmoglein-1, a desmosomal cadherin essential for corneocyte adhesion in the upper epidermis, represents another critical target of S. aureus proteases, whose degradation compromises mechanical cohesion and facilitates microbial access to deeper tissue layers [ , ].”
Does not settle: Источник изучает очищенную протеазу SspA Staphylococcus aureus, а не ферментную фракцию пота. Он не устанавливает физиологические концентрации пота, воздействие влажной одежды, недавно восстановленный роговой слой, перенос уязвимости между образцами, сохранение последствий после высыхания, SPV_3 или сохранение потоотделения и испарительной теплоотдачи.
Physiological and pathological roles of kallikrein-related peptidases in the epidermis. · Journal of dermatological science · 2019
“In Netherton syndrome, unrestricted activity of KLK5 due to loss of the major endogenous inhibitor, lymphoepithelial Kazal-type-related inhibitor (LEKTI), destroys the component molecules of corneodesmosome, leading to Th2 and Th17 inflammation.”
Does not settle: Источник не устанавливает, что протеолитическая активность переносится с потом окружающей кожи, действует при физиологических концентрациях под влажной одеждой или является главным ограничителем прочности недавно восстановленного рогового слоя. Он также не проверяет перенос уязвимости ферментной фракцией пота между образцами, сохранение эффекта после высыхания, показатель SPV_3, селективное предотвращение расщепления либо сохранение потоотделения и испарительной теплоотдачи.
Deletion of the Epidermal Protease KLK5 Aggravates the Symptoms of Congenital Ichthyosis CDSN-nEDD. · International journal of molecular sciences · 2025
“Contrary to our original hypothesis, KLK5 exacerbated the CDSN -nEDD phenotype.”
Does not settle: This source does not test sweat, wet clothing, physiological sweat-enzyme concentrations, recently healed human skin, transfer of vulnerability between samples, SPV_3, or evaporative heat loss.
Chitosan and Cellulose-Based Hydrogels for Wound Management. · International journal of molecular sciences · 2020
“Although there are several interesting properties of hydrogels in the field of wound management, they also suffer from some limitations such as dehydration if they are not covered, result in skin maceration, they need a secondary dressing, it is not easy to secure them, and they possess poor mechanical stability at swollen state [ ].”
Does not settle: This source does not establish that sweat carries proteolytic activity, that it cleaves corneodesmosome proteins in healing skin, any physiologic concentration or exposure duration, persistent loss after drying, transfer of vulnerability between samples, or selective stabilization of SPV_3 without altering sweating or evaporative heat loss.
Skin Ulcers: Wound Management. · FP essentials · 2020
“The ideal dressing provides moisture to the wound and dryness to the periwound area.”
Does not settle: Источник не рассматривает пот, протеолитическую активность, корнеодесмосомы, прочность недавно восстановленного рогового слоя, перенос уязвимости между образцами или селективное предотвращение расщепления.
The gap this hypothesis explains
What is measured here stands in for what matters, and may not track it.
Does increased sweating around healing skin reduce its resistance to rubbing?
Original wording · exactly as the pipeline generated it
Снижает ли усиление потоотделения окружающей кожи устойчивость заживающего участка к трению, если под одеждой растёт увлажнение, а испарительная теплоотдача остаётся прежней?
What this question is asking
The question asks whether extra sweat from skin surrounding a healing area makes that area easier to damage by rubbing. It concerns everyday warming under clothing, comparing greater surrounding sweating with less surrounding sweating and measuring how well the healing area withstands subsequent rubbing. It assumes that moisture under clothing increases while the heat removed by sweat evaporating stays unchanged. The broader uncertainty is whether responses in nearby skin protect the healing area or leave it wetter and more vulnerable.
- Healing skin
- Skin undergoing repair after injury. The question concerns this ongoing process, whose stage is unspecified; it is not interchangeable with the already healed scar tissue described in S2.
- Sweat glands
- Structures in skin that release sweat, a liquid consisting mainly of water containing dissolved salts. S3 describes their role in temperature regulation, while the question concerns sweat produced around a healing area.
- Evaporation and evaporative heat loss
- Evaporation is the conversion of liquid water into vapor; evaporative heat loss is the heat removed through that process. Sweat production and heat removed by evaporation are different quantities, and the question assumes that only the former increases.
- Skin moisture content
- The amount of water held in skin, also called skin hydration. Moisture beneath clothing and water held within the skin are related measurements in the proposed question, but the supplied sources do not establish how one changes the other in this setting.
- Resistance to rubbing
- How well skin withstands repeated contact and movement against another surface without damage. It is the specific outcome asked about, but no measurement method or damage criterion is supplied.
- Mechanical properties
- A group of characteristics describing how tissue responds to physical forces, including deformation and damage. General findings about these properties do not by themselves establish resistance to rubbing.
- Skin barrier function
- The skin's ability to limit water loss and passage of substances between the body and its surroundings. The gap description includes preservation of this function among the desired outcomes, but supplies no defined acceptable limits.
- Scar
- Repair tissue that remains after an injury heals. S2 reports that it generally differs from intact skin in mechanical properties and in the presence of structures such as sweat glands.
- Glycerol
- A compound that S4 associates with improved moisture content, barrier function, and mechanical properties of skin. Those findings concern glycerol and do not establish the effects of accumulated sweat.
- Skin's outermost layer
- The surface layer of skin, called the stratum corneum in S4. Its moisture content is one of the outcomes discussed in that source.
- Skin blood flow
- The movement of blood through vessels in the skin. S8 discusses the timing of its increase as part of the body's heat-loss responses, without measuring the rubbing resistance of healing skin.
- Surrounding skin responses
- Changes in nearby skin, such as sweating and blood flow, that the pipeline proposes might help protect a healing area. Calling these responses compensation expresses a proposed protective role; the supplied sources do not establish that role in the conditions asked about.
Increased sweating in the surrounding skin raises moisture under clothing while evaporative heat loss remains unchanged.
Sweat is liquid released onto the skin, and evaporation removes heat when that liquid becomes vapor. The question assumes that additional sweat increases moisture beneath clothing without increasing this heat removal. That condition would allow the question to focus on whether added moisture compromises resistance to rubbing despite providing no additional evaporative cooling.
None of the supplied excerpts establishes this combination of surrounding sweating, increased moisture under clothing, and unchanged evaporative heat loss. S3 describes the temperature-regulating role of sweat glands, while S8 and S10 report other influences on sweating. The supplied material contains no direct assessment of the assumed condition and insufficient search information to judge whether it is established elsewhere.S3S8S10
The same question asked without the part nothing read establishes:
- When surrounding skin sweats more during everyday warming, does healing skin become less resistant to rubbing, and how do moisture under clothing and evaporative cooling change?
- How does increased sweating around healing skin affect its resistance to rubbing under clothing?
- Resistance to rubbing decreases Under the question's assumed conditions, increased surrounding sweating would accompany additional moisture without additional evaporative cooling, and the healing area would withstand rubbing less well. Treating the sweating response as evidence of protection would therefore misrepresent the measured mechanical outcome; attributing that outcome specifically to moisture would still require evidence connecting the steps.
- Resistance to rubbing does not decrease Under the same assumed conditions, additional moisture would not translate into greater damage from rubbing. Increased sweating would still not demonstrate additional evaporative cooling, but the proposed loss of resistance would not occur under the conditions assessed.
The proposed chain runs from increased surrounding sweating to greater moisture under clothing and then to a change in the healing area's resistance to rubbing. If evaporation removes no additional heat, increased sweat production alone cannot demonstrate increased cooling. If resistance also falls, interpreting more sweating as protection would overlook increased vulnerability to rubbing. Conversely, assuming that increased moisture necessarily weakens skin would also go beyond the supplied evidence: S4 reports improved moisture content and mechanical properties with glycerol, although it does not establish what sweat does to healing skin.
Физиологические узлы, RL-2, описывают секрецию и перфузию; их прирост отдельно не подтверждает эффективное охлаждение и сохранение механической устойчивости.
Во время бытового нагревания региональная компенсация включается своевременно; температура, гидратация и барьер остаются в установленных пределах при последующем трении.
Не установлено, при каких условиях региональная компенсация защищает заживающий участок, а при каких повышает его уязвимость через накопление влаги.
The mechanism it proposes
The engine's own statement of the hypothesis, in full.
Проверяемая гипотеза: пот окружающей кожи переносит протеолитическую активность, которая при физиологических концентрациях становится главным ограничителем прочности недавно восстановленного рогового слоя. Под влажной одеждой ферменты получают длительный контакт с участком заживления и расщепляют белки корнеодесмосом, соединяющих роговые клетки. Состояние уязвимости сохраняется в виде утраченных молекулярных соединений после высыхания. Сильное утверждение состоит в том, что замена ферментной фракции пота способна переносить повышенную уязвимость между образцами независимо от возраста ткани-получателя, если исходная прочность сопоставима. Селективное предотвращение такого расщепления должно стабилизировать SPV_3 при сохранении потоотделения и прежней испарительной теплоотдачи.
What a later run added
A later run reached the same claim about the same subject. Its version was withdrawn in favour of this earlier one, and what it added is kept here, quoted exactly.
Предполагается, что раннее потоотделение увеличивает продолжительность контакта эпидермиса с каталитически активными протеазами пота.
Connects earlier sweating specifically to longer protease exposure; EARLIER attributes prolonged contact to wet clothing.
При задержке жидкости под одеждой ферменты, включая калликреиноподобную пептидазу KLK8, усиливают протеолитические реакции на поверхности кожи и нарушают сцепление корнеоцитов.
Names KLK8 as a candidate enzyme within the shared proteolytic mechanism.
Каталитически неактивный белок эффекта не восстановит.
Adds an inactive-protein control to distinguish catalytic damage from effects of the protein's presence.
Testing and possible results
The prediction that would tell it apart
A hypothesis that predicts what its rivals predict is not worth running an experiment over. This is the observation on which this one differs.
В перекрёстном опыте на восстановленных кожных моделях из клеток доноров 20–30 и 40–60 лет сравнивают исходный пот, пот после удаления активной протеазной фракции и тот же препарат после возвращения этой фракции до исходной активности. Выравнивают температуру, гидратацию по глубине, pH, осмоляльность и приложенное касательное напряжение. Гипотеза предсказывает перенос низкого порога механического повреждения вместе с активной фракцией, восстановление порога после её удаления и повторное снижение после возвращения. Расщепление белков корнеодесмосом должно предшествовать трению; слабость должна сохраняться после восстановления исходной гидратации. Если удаление ферментов при подтверждённой потере их активности не меняет прочность, а изменение механического ограничения набухания устраняет уязвимость, результат поддерживает IH_Q_L3_M_G3_4_02.
Would tell it apart from at least one rival. The prediction specifies observable changes in mechanical damage threshold after fraction removal and restoration, temporal ordering, persistence after hydration restoration, and an explicit alternative-supporting condition. No rival prediction is supplied. Only a bench experiment would settle it.
What testing it would take
The engine's own read on whether this is testable with methods that already exist.
Активность ферментов, состав фракций и продукты расщепления доступны для измерения биохимическими методами. Удаление фракции требует имитационной процедуры и контроля сопутствующего удаления других белков. Разрушающие испытания проводят только на отдельных образцах и кожных моделях. До исследований на участниках необходимо показать эффект при концентрациях и длительности контакта, действительно измеренных под одеждой.
Other explanations
Every other hypothesis the engine wrote for the same gap, and the observation that would separate the two.
В перекрёстном опыте на восстановленных кожных моделях из клеток доноров 20–30 и 40–60 лет сравнивают исходный пот, пот после удаления активной протеазной фракции и тот же препарат после возвращения этой фракции до исходной активности. Выравнивают температуру, гидратацию по глубине, pH, осмоляльность и приложенное касательное напряжение. Гипотеза предсказывает перенос низкого порога механического повреждения вместе с активной фракцией, восстановление порога после её удаления и повторное снижение после возвращения. Расщепление белков корнеодесмосом должно предшествовать трению; слабость должна сохраняться после восстановления исходной гидратации. Если удаление ферментов при подтверждённой потере их активности не меняет прочность, а изменение механического ограничения набухания устраняет уязвимость, результат поддерживает Uneven swelling may buckle healing skin and make it vulnerable to friction.
- What would separate them
Uneven swelling may buckle healing skin and make it vulnerable to friction predicts: На образцах с одинаковыми составом жидкости, гидратацией по глубине и температурой изменяют боковое механическое закрепление при увлажнении. Гипотеза предсказывает пороговое появление складок до трения, зависимость их пространственного шага от толщины и механических свойств поверхностного слоя, а также совпадение будущих повреждений с рассчитанными максимумами деформации. Разрешение свободного бокового расширения во время увлажнения должно предотвращать складки и сохранять прочность при последующем одинаковом испытании. Эффект должен воспроизводиться с жидкостью без протеаз. Если освобождение от ограничения не защищает ткань, а удаление протеаз сохраняет прочность при неизменной геометрии, результат поддерживает this hypothesis.
Why this is not the mainstream account
The engine is asked to say what its hypothesis would overturn and what would surprise a specialist. This is its answer.
В первичной работе показана активная калликреин-подобная пептидаза KLK8 в человеческом поте и её участие в протеолитическом каскаде кожи. Это делает биологически правдоподобным перенос каталитической активности с потом, но не доказывает предложенный перенос механической уязвимости. [Исследование активности KLK8 в эпидермисе и поте](https://pmc.ncbi.nlm.nih.gov/articles/PMC3013028/).
Физиология эккринных желёз и биомеханика заживления; пересмотра потребовал бы учебный раздел «Потоотделение, десквамация и восстановление механической защиты». При подтверждении соседние железы придётся включить в модель как внешний источник ферментов, способный определять прочность восстановленного участка и переносить её возрастной дефицит между тканями.
При одинаковых температуре, гидратации и нагрузке молодой восстановленный эпидермис приобретает механическую уязвимость после получения активной фракции пота определённых доноров 40–60 лет, а возрастной эпидермис сохраняет прочность после её удаления. Возвращение очищенной активной фракции воспроизводит эффект без воспалительных клеток и без изменения геометрии ткани.
Участие калликреинов в десквамации уже известно и само по себе не является еретическим утверждением. В выполненном целевом поиске не найдено обоснования более сильного тезиса: физиологическая ферментная фракция пота переносит возрастную механическую уязвимость между сопоставимыми заживающими тканями и определяет её независимо от возраста получателя. Полное отсутствие такого тезиса в литературе не доказано; соответствие этому критерию остаётся предварительным.
What stands behind it
Which of the figures above have a study behind them, which are the engine's own, and what it would take to refute the hypothesis. This audit never judges the idea.
This hypothesis states no figure and cites no study, so there is nothing here to trace.
What it would take to refute it. Nothing already retrieved carries the prediction’s terms and it names no measurement this layer can route to a public dataset, so the bench is the residual — not a finding against it.
0 citation handles extracted; 1 Europe PMC search run; 0 records examined; 0 sources stored for enrichment, 0 with full text. A citation that did not resolve is a bibliographic failure, not proof that no such paper exists, and no hypothesis is blocked by this audit.