6 Needs context
In chronic caffeine users, caffeine consumption does not significantly increase cortisol levels.
"Turns out caffeine, if you're a chronic caffeine user, such as me, such as you, doesn't actually increase cortisol that much." (said at 0:03:02)
Randomized crossover evidence indicates that chronic daily caffeine consumption induces partial tolerance to caffeine's cortisol-stimulating effects. In a controlled trial of healthy adults, 5 days of habitual caffeine intake (300 to 600 mg/day) abolished the salivary cortisol response to a morning caffeine challenge, whereas abstinent individuals showed robust cortisol increases. However, tolerance is incomplete: repeated doses taken later in the day or caffeine consumed during acute psychosocial stress can still elicit significant cortisol elevations in habitual consumers.
Cold water immersion in a cold plunge reduces cortisol levels while increasing adrenaline, dopamine, and norepinephrine.
"Cold plunge reduces your cortisol levels. You can look at the data. The data show that it goes down. Adrenaline goes up. Dopamine goes up. Norepinephrine goes up." (said at 0:03:18)
The claim is partially accurate but needs qualification regarding cortisol and adrenaline. The widely cited study on cold water immersion (Šrámek et al., 2000; PMID: 10751106) evaluated 1-hour immersion in water at 14 °C and found large increases in plasma noradrenaline (by 530%) and dopamine (by 250%). In that trial, cortisol concentrations did not rise and tended to decrease (as is typical with head-out water immersion due to hydrostatic pressure), while plasma adrenaline remained unchanged. However, other cold-exposure and winter-swimming protocols show variable responses: acute cold stress can elevate or leave adrenaline unchanged, and cortisol levels can either decline due to immersion hydrostatic effects/circadian rhythm or increase transiently during more severe or painful cold stress. Thus, while dopamine and norepinephrine robustly increase, cold water immersion does not uniformly reduce cortisol or increase adrenaline across all contexts.
- supports: Human physiological responses to immersion into water of different temperatures. (European journal of applied physiology 2000) · cited 346x in the literature
"Cold water immersion (14 degrees C) lowered rectal temperature and increased metabolic rate (by 350%), heart rate and systolic and diastolic blood pressure (by 5%, 7%, and 8%, respectively). Plasma noradrenaline and dopamine concentrations were increased by 530% and by 250% respectively, while diuresis increased by 163% (more than at 32 degrees C)... Cortisol concentrations tended to decrease. Plasma adrenaline concentrations remained unchanged. Immersion in water of different temperatures did not increase blood concentrations of cortisol." (abstract, results, passage verified)
pubmedfull study (doi) - context: Some endocrine responses to sauna, shower and ice water immersion. (Arctic medical research 1989) · cited 34x in the literature
"The initial, post-exposure and post-recovery concentrations of plasma ACTH, serum cortisol, serum melatonin, plasma norepinephrine and plasma epinephrine were determined. ACTH and cortisol indicated a slightly increased post-exposure level... Post-exposure norepinephrine levels increased (P less than 0.05) from the initial. Post-exposure epinephrine indicated a tendency to elevated levels" (abstract, results, passage verified)
pubmed
Switching from a standard macronutrient diet containing starches to a low-carbohydrate diet significantly increases cortisol levels.
"But if you shift from a sort of standard macronutrient distribution of, you know, 40/30 or whatever it is where you're eating starches to a low-carbohydrate diet, your cortisol levels go up significantly. This has been explored." (said at 0:25:58)
Meta-analytic evidence indicates that transitioning from a high-carbohydrate to a low-carbohydrate diet (≤35% carbohydrates) moderately elevates resting cortisol during the acute adaptation phase (<3 weeks) and amplifies cortisol release following prolonged exercise. However, in longer-term interventions (≥3 weeks), resting cortisol levels do not remain significantly elevated and return toward baseline.
After three weeks or more on a low-carbohydrate diet, baseline cortisol levels remain consistently higher across the 24-hour cycle than on a carbohydrate-containing diet.
"If you're on a low-carbohydrate diet for a period of time, I think in this case it was 3 weeks or more, your cortisol curve, that high in the morning, low in the afternoon and evening, kind of normalizes a bit. It's still a little bit higher at every point than it normally would be." (said at 0:25:30)
Evidence from controlled feeding trials indicates that adhering to a very low-carbohydrate diet for several weeks (such as 4 weeks) significantly increases 24-hour cortisol excretion compared with isocaloric higher-carbohydrate diets. In a randomized 3-way crossover trial in overweight and obese adults (Ebbeling et al., 2012; PMID: 22735432), a very low-carbohydrate diet (10% carbohydrates) maintained over 4-week periods resulted in significantly higher 24-hour urinary cortisol levels (P = .005) compared to low-glycemic and low-fat diets. While this reflects an overall elevation in 24-hour cortisol output, the measurement in such pivotal trials was total 24-hour urinary excretion rather than repeated continuous salivary/serum sampling proving elevations at every individual diurnal timepoint.
- partial: Effects of dietary composition on energy expenditure during weight-loss maintenance. (JAMA 2012) · cited 433x in the literature
"Hormone levels and metabolic syndrome components also varied during weight maintenance by diet (leptin, P < .001; 24-hour urinary cortisol, P = .005; indexes of peripheral [P = .02] and hepatic [P = .03] insulin sensitivity; high-density lipoprotein [HDL] cholesterol, P < .001; non-HDL cholesterol, P < .001; triglycerides, P < .001; plasminogen activator inhibitor 1, P for trend = .04; and C-reactive protein, P for trend = .05), but no consistent favorable pattern emerged." (abstract, results, passage verified)
pubmedfull study (doi)
Lichen planus is an autoimmune condition that causes bruise-like lesions on the wrists, genitals, and tops of the feet triggered by excessive stress and sleep deprivation.
"it's an autoimmune condition where the immune system because of stress and excessively long days, etc., excessive caffeine, push, push, push, people will get um it's almost like looks like bruising um on the wrists. They can get them on their genitals, on the tops of their feet." (said at 2:46:52)
Lichen planus is a chronic immune-mediated/autoimmune inflammatory disorder characterized by pruritic, flat-topped, polygonal, violaceous (purple) papules and plaques that commonly affect the flexor surfaces of the wrists, extremities (including dorsal aspects of feet/legs), and genital or oral mucosa. While psychological stress is frequently reported as an exacerbating factor or trigger for disease flares, asserting that it is directly caused by excessive caffeine, long work days, or sleep deprivation is an oversimplification and not established as a primary etiology.
- context: Diagnosis and treatment of lichen planus. (American family physician 2011) · cited 56x in the literature
"Lichen planus is a chronic, inflammatory, autoimmune disease that affects the skin, oral mucosa, genital mucosa, scalp, and nails. Lichen planus lesions are described using the six P's (planar [flat-topped], purple, polygonal, pruritic, papules, plaques). Onset is usually acute, affecting the flexor surfaces of the wrists, forearms, and legs." (abstract, results, passage verified)
pubmed
Finasteride taken for hair loss can lead to post-finasteride syndrome, causing persistent sexual and psychological health issues after cessation.
"young men who took drugs for to avoid hair loss: post-finasteride syndrome. You know, the medical community, the standard medical community thinks it's it's nonsense. But you talk to these guys that are having serious and at least till now permanent—hopefully some of this stuff can be reversed—sexual sexual health issues, psychological issues." (said at 2:46:10)
Post-finasteride syndrome (PFS) is described in the medical literature as a constellation of persistent sexual dysfunction (such as decreased libido and erectile dysfunction), somatic, and neuropsychiatric/psychological symptoms that endure after discontinuing finasteride taken for androgenetic alopecia. The speaker accurately notes both the existence of patients reporting these persistent symptoms and the widespread skepticism within mainstream medicine. However, the evidence supporting PFS as a distinct, causally established biological entity remains very low in certainty, relying primarily on patient surveys, pharmacovigilance reports, and uncontrolled case series with high potential for selection bias and nocebo effects, without confirmation from prospective randomized trials.
- supports: Persistent sexual, emotional, and cognitive impairment post-finasteride: a survey of men r… (American journal of men's health 2015) · cited 115x in the literature
"Responses from 131 generally healthy men (mean age, 24 years) who had taken finasteride for male pattern hair loss was included in the analysis. The most notable finding was that adverse effects persisted in each of the domains, indicating the possible presence of a "post-finasteride syndrome."" (abstract, results, passage verified)
pubmedfull study (doi) - context: Post-Finasteride Syndrome: An Induced Delusional Disorder with the Potential of a Mass Psy… (Skin appendage disorders 2019) · cited 29x in the literature
"By definition, the condition is characterized by sexual dysfunction, somatic symptoms, and psychological disorders that persist after cessation of finasteride treatment. As yet, the condition is not recognized by the medical community, although individuals who suffer from PFS present with relatively homogenous symptoms. The concept of PFS has emerged from reports of non-dermatologists, neuroendocrinological research and reflections, and uncontrolled studies of low quality and with a strong bias selection, while a significant nocebo effect among patients informed about possible side effects of finasteride is recognized." (abstract, passage verified)
pubmedfull study (doi) - context: Post-finasteride syndrome - a true clinical entity? (International journal of impotence research 2025) · cited 9x in the literature
"This review critically examines Post-Finasteride Syndrome (PFS), a condition eventually reported by men who have used finasteride for androgenetic alopecia or benign prostatic enlargement and experienced persistent adverse effects after discontinuation. We explore the clinical manifestations, including sexual dysfunction, neuropsychiatric symptoms, and physical changes, that collectively challenge both diagnosis and management. This review evaluates the evidence for PFS, discusses potential mechanisms including neurobiological alterations, genetic predispositions, and addresses the controversies surrounding its existence and recognition by the medical community." (abstract, passage verified)
pubmedfull study (doi)
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