Taurine’s effects are more subtle while you will feel creatine’s effects almost immediately.
My go to creatine variant of choice is creatine HCL since I do not seem to get any negative side effects like bloating, sickness, insomnia etc. from it like I do with monohydrate.
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Yeah, that’s interesting. I imagine feeling the effects of creatine is individual. In my situation, I’m struggling to see why I should take it. The usual reasons don’t seem to apply for me. I have no issues with muscle training, my muscles have always been super responsive to exercise, very easy hypertrophy etc., no issues with recovery (and FWIW, rapamycin seems to assist in this department too!) and I don’t feel like I need more water in my muscles or elsewhere (taurine is just fine in that respect). Neurological effects - well, I don’t notice any deficits at this point (I’m 67), perhaps that’s something that will be of help when I’m older, I don’t know. I look over the list of supposed creatine benefits, and see nothing that I appear to need or would be helped with. So for me, creatine is a wait and see thing - maybe one day. For now, I see no reason to add to my already too extensive a stack. YMMV.
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I have been using creatine monohydrate for 15-20 years. Whatever’s the cheapest.
Usual dosages of 5-10 grams, sometimes more, never once have I gotten the runs.
Provides a useful increment of strength/endurance.
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I use the KreAlkalyn form. I find it to be more gentle on my stomach than the monohydrate. .
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Thanks, I’ve never noticed anything whatsoever from creatine so if my break impacts my puffy eyes in a positive way I might test out the brand you take.
Creatine linked to helping prevent erectile dysfunction.
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I think it’s a little overrated myself but I’ve been taking it for 20 years
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I had a close call , 20g a day , a few days of pushing the work outs and not hydrating enough
Man down for 3 days , eGfr33 , and extreme kidney pain
Please make sure you hydrate enough
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Some good and some bad regarding creatine:
Tumor metabolic reprogramming is critical for providing energy to support proliferation and resistance to stress-induced cell death. However, the regulatory mechanisms linking these processes remain incompletely understood. Here, using untargeted metabolomics, we demonstrate that creatine potently induces ferroptosis in colorectal cancer (CRC). Mechanistically, creatine binds extracellular signal-regulated kinase 2 (ERK2), impairing its activation by mitogen-activated protein kinase kinase 1 (MEK1). Inhibiting the creatine transporter SLC6A8 reduces creatine uptake and activates ERK2. Activated ERK2 then binds, phosphorylates ferroptosis suppressor protein 1 (FSP1) at Thr109, and stabilizes it to inhibit ferroptosis. Creatine supplementation suppresses tumor growth, enhances CD8+ T cell infiltration, and sensitizes tumors to anti-programmed cell death protein 1 (PD-1) immunotherapy. Our study identifies ERK2 as a creatine sensor regulating FSP1 stability and ferroptosis resistance, highlighting the therapeutic potential of creatine supplementation in combination cancer immunotherapy.
As one of the most popular nutrient supplements, creatine has been highly used to increase muscle mass and improve exercise performance. Here, we report an adverse effect of creatine using orthotopic mouse models, showing that creatine promotes colorectal and breast cancer metastasis and shortens mouse survival. We show that glycine amidinotransferase (GATM), the rate-limiting enzyme for creatine synthesis, is upregulated in liver metastases. Dietary uptake, or GATM-mediated de novo synthesis of creatine, enhances cancer metastasis and shortens mouse survival by upregulation of Snail and Slug expression via monopolar spindle 1 (MPS1)-activated Smad2 and Smad3 phosphorylation. GATM knockdown or MPS1 inhibition suppresses cancer metastasis and benefits mouse survival by downregulating Snail and Slug. Our findings call for using caution when considering dietary creatine to improve muscle mass or treat diseases and suggest that targeting GATM or MPS1 prevents cancer metastasis, especially metastasis of transforming growth factor beta receptor mutant colorectal cancers.
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On the other hand:
“Our study identified a significant linear negative correlation between dietary creatine intake and cancer risk among U.S. adults, particularly in males and overweight individuals. Age remains a key factor influencing cancer risk.”
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Full paper (PDF) here: Combined creatine and HMB co-supplementation improves functional strength independent of muscle mass in physically active older adults: a randomized crossover trial
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Still not convinced.
I have been taking creatine on and off for several decades, doing the loading phase and maintenance phase for months at a time. I started taking it because of the hype from bodybuilders, who almost universally endorse it.
Because it was cheap, I ignored the fact that I felt no subjective or measurable benefits.
Because I am a natural-born skeptic, I am relatively immune to any placebo effects. The fact is, as many as 40% taking a placebo pill described to them as having amazing benefits will feel the described benefits at least for a short time. Then they will be happy to add to the hype. Hype begets hype.
I have never felt the slightest effect from creatine at home or at the gym. Some people may be hyper-responders to creatine, but I am not.
I have not been taking creatine for several months now, and I don’t miss it.
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I am, but I also barely eat any red meat which might be a factor.
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Sharing the latest Optispan podcast where Matt addresses high dose creatine recommendations from people like Rhonda Patrick…
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CGPT5.1 Summary:
A. Executive Summary (≈200 words)
The episode is a critique of current creatine hype rather than a “pro–creatine” pitch. Matt Kaeberlein’s core position: creatine monohydrate at ~5 g/day, taken consistently and combined with resistance training, probably deserves a place in a “top 5 supplements” list, but the mega-dosing and miracle claims pushed by influencers are not supported by evidence.
On muscle and bone, meta-analyses show that creatine plus resistance training yields modest, incremental gains in lean mass and strength, especially in older adults, but it is not transformative, and higher chronic doses (>5 g/day) have not clearly outperformed standard dosing. ([PubMed][1]) Evidence for bone is mixed: some earlier small trials suggested benefit with RT, but a recent 2-year RCT in postmenopausal women found no added effect on bone mineral density, even with long-term creatine. ([PMC][2])
For cognition, short-term creatine (5–20 g) can improve certain memory and attention tasks, particularly in older adults and under stress or sleep deprivation, but effects are small and not stimulant-like; dose–response is weak, and 20 g/day is not clearly superior to 5 g/day. ([PubMed][3])
Claims that creatine reverses aging or meaningfully alters Parkinson’s disease, multiple sclerosis, or brain aging lack convincing human data; major Parkinson’s trials were stopped for futility. ([HealthPartners][4]) Safety is good at 3–5 g/day in healthy people, with GI upset and water retention the main issues at higher doses, and no clear signal of kidney damage or hair loss in modern trials. ([PMC][5])
The broader lesson: don’t treat creatine as a hack or a drug; treat it as a modest adjunct layered on top of sleep, diet, and resistance training.
B. Bullet Summary (12–20 standalone points)
- Creatine is heavily hyped in 2025, with influencers promoting mega-dosing and dramatic brain/aging effects that exceed the data.
- Kaeberlein places creatine in his “top 5” supplements but emphasizes modest effect sizes and the need for resistance training.
- Standard dosing of ~5 g/day creatine monohydrate with resistance training modestly improves lean mass and strength on average, especially in older adults. ([PubMed][1])
- Data on bone health are equivocal: some shorter trials with RT suggested benefit, but a 2-year RCT in postmenopausal women found no improvement in bone mineral density vs placebo. ([PMC][2])
- Influencers commonly imply “higher is better” (8–10 g/day for bone; 20 g/day for brain), but comparative data do not show clear superiority over 5 g/day. ([PubMed][3])
- Meta-analyses show creatine can improve memory and some cognitive tasks, with older adults and stressed/sleep-deprived individuals deriving the most benefit; young, healthy people often see little effect. ([PubMed][3])
- Dose, duration, sex, and geography do not strongly modify cognitive outcomes in pooled analyses, contradicting “20 g or nothing” narratives. ([PubMed][3])
- Small RCTs suggest creatine augments antidepressant therapy in major depressive disorder, but samples are tiny and sex-specific; this remains preliminary. ([PubMed][6])
- A large, multi-year Parkinson’s trial (>900 participants) showed no disease-modifying effect of creatine and was terminated for futility. ([HealthPartners][4])
- Multiple-sclerosis studies using 20 g/day short term did not meaningfully improve muscle performance or fatigue, and sometimes showed poor creatine uptake. ([University of Toledo][7])
- Claims that creatine feels “like speed” or is “on par with caffeine or nicotine” for focus are not supported by clinical data and conflict with most users’ experience.
- Mechanistically, creatine serves as substrate for phosphocreatine, a short-term ATP buffer; it is not itself a stimulant. ([MDPI][8])
- Kaeberlein stresses evaluating influencers by expertise, track record, and conflicts of interest—especially when they own the creatine brand they are promoting.
- Statements like “no downside” are flagged as inherently non-credible; everything that perturbs metabolism has some risk, however small. ([PMC][5])
- At 3–5 g/day, creatine has a strong safety record in healthy people; kidney function and hair loss concerns are not supported by modern trials. ([PMC][5])
- High doses (≥20 g/day) increase rates of GI symptoms and water retention; long-term safety of chronic mega-dosing is under-characterized. ([Healthline][9])
- The recommended practical strategy: 5 g/day creatine monohydrate, taken consistently, plus progressive resistance training, on top of foundational lifestyle factors (sleep, diet, social connection).
Full response here:
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That’s my take 5 grams past 2 years… in coffee every morning… extra scoop in a small coffee, just before gym on my workout days 
.
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Physionic video:
chatGPT:
Below is a tidy transcript, followed by a summary and critique. I have treated the uploaded transcript text as the source.
Tidy transcript
Introduction
There was an older view of depression that centred on a simple imbalance of neurotransmitters exchanged between neurons. As more research has emerged, that view has had to become more complex.
A new high-impact study now implicates creatine — the same molecule many people supplement with — in depression. Interestingly, the mechanism seems to involve the gut. This is especially notable because previous research on creatine and depression has produced mixed results.
The presenter says he analysed 17 studies to understand how the new study fits with the existing literature.
Chapter 2: “Dude, where’s my creatine?”
The new study compared people with major depressive disorder against people without depression. Researchers measured creatine levels in blood, faeces, and cerebrospinal fluid.
The key finding was that people with depression had lower creatine levels in blood and cerebrospinal fluid, but higher creatine levels in faeces. This suggests that creatine was less available in important body compartments, including around the brain, despite being more abundant in stool.
Creatine is important for cellular energy, especially for short bursts of activity that cannot be supported as efficiently by glucose or fat alone.
The gut is important here because it is the transition point between faecal contents and the bloodstream, and it contains the gut microbiome. The study also transplanted gut microbes from depressed and non-depressed people into mice. Mice receiving microbes from depressed patients developed lower blood creatine.
The presenter interprets this as evidence that the microbiome can directly affect blood creatine levels, and that people with depression may have gut microbes that reduce body creatine stores. Specific bacterial differences were linked to reduced intestinal creatine absorption.
The proposed pathway is:
altered microbiome → reduced intestinal creatine uptake → reduced blood creatine → reduced brain creatine delivery → possible contribution to depression.
Chapter 3: Seven studies disagree
Human studies on creatine supplementation and depression are mixed. The presenter says he reviewed 17 studies:
- nine suggested a benefit from creatine;
- seven showed no effect;
- one meta-analysis of 11 randomised controlled trials found a statistically significant benefit.
However, the meta-analysis effect was described as statistically detectable but probably too small to be clinically meaningful.
The presenter argues that the pattern becomes clearer when looking at the study populations. Most studies that failed to find benefit were either very small, used specialised populations such as stroke or Parkinson’s disease, or did not primarily study people with clinically diagnosed depression.
By contrast, the studies showing benefit generally involved people with clinically diagnosed depression, often treatment-resistant depression, and often in combination with antidepressant medication.
The presenter’s main conclusion from this section is that creatine appears most promising as an adjunct treatment in people with clinical, often treatment-resistant depression, rather than as a general mood enhancer in people without diagnosed depression.
Chapter 4: Something critical is missing
The older clinical studies did not account for microbiome differences, because the new microbiome-creatine study had not yet been published.
The new study included a small clinical trial. People with clinically diagnosed depression were randomly assigned to placebo or creatine plus a bacterium implicated in creatine metabolism. Depression severity was measured using the Hamilton Depression Rating Scale, or HAM-D.
The group receiving creatine plus the bacterium improved more than placebo. The presenter describes the improvement as substantial, around a nine-point change on the 17-item HAM-D scale, although placebo also produced a meaningful improvement.
The presenter then adds several cautions:
- the trial was small;
- it lasted only one month;
- there was no third arm separating creatine alone from the bacterium alone;
- therefore, it is unclear whether the benefit came from creatine, the bacterium, or the combination.
The presenter concludes that current evidence leans toward creatine being useful for people with clinical depression, especially as an adjunct to antidepressant treatment, but likely not very useful for people without clinical depression.
He also suggests that the microbiome may influence whether creatine works. Finally, he notes that many studies used 5 g/day creatine, but higher doses, perhaps closer to 20 g/day, may be relevant when trying to raise brain creatine levels.
Summary
The video argues that creatine may be relevant to depression through a gut–creatine–brain pathway. A new study reportedly found that people with major depressive disorder had lower creatine in blood and cerebrospinal fluid, but higher creatine in faeces, suggesting impaired absorption or altered handling of creatine. Microbiome transfer experiments in mice suggested that gut bacteria from depressed patients could reduce blood creatine.
The presenter then reviews prior human creatine studies. He argues that the mixed evidence becomes more coherent if one separates studies in clinically depressed patients from studies in other populations. Creatine looks more promising in people with diagnosed, often treatment-resistant depression, especially when used alongside antidepressants. It looks less convincing as a general intervention for non-clinical low mood.
The strongest new claim is that the gut microbiome may partly determine whether creatine reaches the blood and brain. A small trial using creatine plus a bacterium reportedly improved depression scores more than placebo, but the study design cannot tell whether creatine, the bacterium, or the combination caused the effect.
Critique
The video’s strongest point is that it does not treat “creatine and depression” as a single simple question. It correctly separates different populations: people with major depressive disorder, people with treatment-resistant depression, people with Parkinson’s or stroke, and people without clinical depression. That distinction matters, because an intervention may work in a deficient or metabolically altered subgroup but not in a general population.
The gut-creatine hypothesis is also plausible. Creatine is biologically relevant to energy buffering, and depression has repeatedly been linked to metabolic, mitochondrial, inflammatory, and microbiome changes. A mechanism involving altered intestinal uptake and reduced brain creatine availability is therefore worth investigating.
However, the clinical claim remains preliminary. The video itself notes an important weakness: the creatine-plus-bacterium trial did not include separate creatine-only and bacterium-only arms. Without those, the trial cannot establish that creatine was the active ingredient, nor that the combination is necessary.
The dosing discussion also needs caution. Suggesting that higher doses such as 20 g/day may be needed to raise brain creatine is mechanistically interesting, but it should not be treated as a clinical recommendation. Higher doses may have more gastrointestinal side effects, and depression trials would need to test dose, duration, safety, and subgroup response directly.
The video is also somewhat vulnerable to “pattern-finding” across heterogeneous studies. Dividing studies into responders and non-responders by population type may be reasonable, but it can become post hoc unless pre-specified. Small trials, different depression scales, different background medications, and different populations make the evidence hard to combine cleanly.
Overall, the video’s cautious conclusion is fair: creatine is not a proven stand-alone treatment for depression, but it is a biologically plausible adjunct worth further study, especially in clinically depressed or treatment-resistant patients. The microbiome angle is novel and interesting, but not yet clinically settled.
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