So to begin. I suffer from palmar and plantar hyperhidrosis and I’m not too keen on a lot of the mainstream treatments suggested for hyperhidrosis and I will explain the reasons for that shortly.
When I google hyperhidrosis treatments, the AI Overview gives the list:
Common Treatments:
- Botox (and estimates that the length of effectiveness would be around 6-12 months)
- Prescription antiperspirants (containing aluminum chloride)
- Topical anticholinergics
- Iontophoresis: “A device that uses a low-voltage electrical current to block sweat glands.”
- miraDry: “Non-invasive, thermal energy (microwaves) that destroys underarm sweat glands.”
- Oral medications (again from the drug class of anticholinergics primarily glycopyrrolate).
- Brella sweat control patch: “A 3-minute, in-office patch treatment.” (appears to be a newer option that I’m only seeing as being available for treatment of underarm sweat)
OTC and Natural Remedies:
- Strong antiperspirants
- Sage tea
- Apple cider vinegar
- Cornstarch
Other options:
- Laser treatments
- “Surgery (Endoscopic Thoracic Sympathectomy – ETS): A last-resort, permanent option to cut nerves responsible for sweating.”
My purpose in writing this post is to gather ideas for consideration in potential ways to try to treat my own hyperhidrosis. I can also explain why I chose not to use many of the “common treatments” as listed above.
First with botox, it’s not widely available. Botox itself is widely available, but not the option to get botox treatments to the palmar or plantar regions, rather it is most commonly available for treatment in the underarm area. I have inquired about this from a dermatologist that I had visited in the past and the dermatologist did not offer this service and was hesitant at the idea of using it as a treatment at all as according to this dermatologist the procedure requires local anesthesia where an anesthetist or anesthesiologist would have to administer a nerve block prior to the procedure.
Second is the topical antiperspirants that contain aluminum chloride, which I hold some reservations on using. This one I am less certain about, but still cautious on. My knowledge on this topic is very limited so I prompted ChatGPT with this: “peer reviewed information about effects of aluminum chloride in antiperspirants on health”, and it gives this rather lengthy response:
“Here’s what the peer-reviewed literature says about aluminum chloride / aluminum chlorohydrate (the aluminum salts used in antiperspirants) and health.
What aluminum salts in antiperspirants actually do
Most antiperspirants use aluminum chlorohydrate (ACH) or related aluminum salts (not always “aluminum chloride,” which is more common in prescription hyperhidrosis products). These salts form temporary plugs in sweat ducts, reducing wetness.
Systemic absorption (how much gets into your body)
Human tracer/pharmacokinetic studies suggest very low dermal absorption:
- A microtracer study using aluminum-26 labeled ACH estimated ~0.012% of applied aluminum was absorbed through skin under study conditions.
- A larger clinical PK study in 12 healthy women using an aluminum-26 microtracer under “real-life” application conditions also found very low systemic exposure, supporting the idea that only tiny amounts enter circulation.
- A follow-up study (also in 12 women) added skin sampling/biopsies to assess local fate, again focusing on minimal systemic exposure and where aluminum remains in skin.
Bottom line: In typical use, absorbed aluminum from antiperspirant appears to be a very small fraction of what’s applied, and generally small compared with dietary aluminum exposure (diet is usually the main source for the general population).
Breast cancer: is there evidence of increased risk?
Epidemiology (human population studies)
- A well-known population-based case-control study (Mirick et al., 2002; ~800 cases and ~800 controls) found no association between underarm antiperspirant/deodorant use (or shaving) and breast cancer risk.
- A systematic review/meta-analysis of observational studies (Allam et al., 2016) concluded the pooled evidence did not show an increased breast cancer risk with deodorant/antiperspirant use.
“Earlier diagnosis” paper (often cited online)
- A retrospective study reported an association between certain underarm habits and earlier age at diagnosis, but this design can’t establish causation and has been widely criticized as insufficient to prove risk.
Bottom line: The best-known epidemiologic evidence and a systematic review do not support antiperspirant use as a breast cancer risk factor.
Alzheimer’s / dementia: what does the evidence say?
Aluminum has long been investigated in neurodegeneration, but the key question is whether antiperspirant aluminum exposure meaningfully increases brain risk.
- A broad review of aluminum toxicology notes that while aluminum exposure is biologically studied, human evidence tying everyday consumer exposures (like antiperspirants) to Alzheimer’s is not conclusive, and absorption from antiperspirants appears low.
- Older papers raised the question mechanistically (and helped fuel public concern), but they are not evidence that antiperspirants cause Alzheimer’s.
Bottom line: There isn’t solid human evidence that aluminum antiperspirant use increases Alzheimer’s risk; the main antiperspirant-specific data point is still very low absorption.
Other health effects with stronger evidence
Skin irritation / dermatitis (most common real issue)
Irritant or allergic reactions can occur, especially with higher-strength products (including aluminum chloride solutions used for hyperhidrosis). Reviews in dermatology discuss cutaneous reactions to aluminum exposure.
Kidney disease (special population concern)
People with advanced kidney disease have reduced ability to excrete aluminum; for them, minimizing avoidable aluminum exposure is sometimes advised clinically (this is more about overall aluminum handling than antiperspirants alone). Toxicology reviews discuss aluminum overload risks particularly in renal impairment.
What’s still uncertain / actively debated
- Some lab and tissue studies explore whether aluminum can have estrogen-like (“metalloestrogen”) or genotoxic effects under certain conditions, but translating that to real-world antiperspirant use in humans remains unresolved, and epidemiology hasn’t confirmed increased risk.
- Shaving/irritated skin could theoretically change absorption, but the best available human microtracer work still points to very low systemic uptake overall.
Practical takeaways
- For most people, the peer-reviewed evidence supports: minimal systemic absorption and no demonstrated increase in breast cancer risk from antiperspirant use.
- If you have very sensitive skin, recurrent rashes, or use prescription-strength aluminum chloride, irritation is the most likely downside; switching formulas or frequency often helps.
- If you have advanced kidney disease, it’s reasonable to discuss aluminum exposure (including antiperspirants) with your clinician in the context of your whole exposure picture.”
In my own conclusion regarding aluminum chloride it seems like it might be safer to err on the side of caution as the research seems to be rather unclear at this time.
As for anticholinergics I am personally strongly against them, but again the deeper research I’ll allow ChatGPT to go over:
“Anticholinergics (drugs that block acetylcholine) have a pretty consistent association in large human studies with higher dementia risk, especially with long-term, higher cumulative exposure. The key nuance: most evidence is observational (association ≠ proven causation), but the pattern is strong enough that many clinicians try to reduce anticholinergic burden in midlife/older adults when alternatives exist.
What the best human evidence shows
Dose–response relationship (stronger signal)
- Prospective cohort (US): higher cumulative use of strong anticholinergics was linked to increased incident dementia, with a clear dose–response pattern.
- Large UK nested case-control (BMJ 2018; Coupland/Richardson group): dementia risk increased with greater cumulative exposure, with the strongest associations for antidepressants with anticholinergic activity, bladder antimuscarinics, and anti-Parkinson drugs.
- Large UK nested case-control (JAMA Intern Med 2019): again found increased dementia risk with anticholinergic exposure; strongest links for anticholinergic antidepressants, bladder antimuscarinics, antipsychotics, antiepileptics.
Meta-analysis / synthesis
- A systematic review/meta-analysis concluded anticholinergic drug use is associated with increased dementia risk (independent risk factor in pooled observational data).
Which anticholinergic categories are most implicated (repeatedly)
Across the big studies above, the most recurrent “signals” are:
- Bladder antimuscarinics (e.g., oxybutynin, tolterodine, solifenacin—specific drugs vary by study)
- Antidepressants with strong anticholinergic effects (often some tricyclics)
- First-generation antihistamines (sleep/allergy meds like diphenhydramine-type drugs are frequently discussed in this class; Gray 2015 noted associations beyond antidepressants)
- Antipsychotics / antiepileptics also show up in some analyses
Is it “dementia” or just short-term brain fog?
Both are concerns, but different time scales:
- Short-term: confusion, sedation, memory problems—well recognized with anticholinergics (especially in older adults).
- Long-term: multiple large datasets suggest a cumulative exposure link with later dementia diagnosis.
Causation and “protopathic bias” (the big caveat)
A real issue is that some anticholinergics treat symptoms that can appear before dementia is diagnosed (sleep problems, depression, urinary symptoms), which can make a drug look guilty when it’s partly a marker of early disease. The Gray 2015 paper explicitly discusses this and still reports elevated risk across drug subclasses.
What to do in real life (practical + evidence-aligned)
Avoid self-medicating with strong OTC anticholinergics for sleep/allergies long-term (these are common hidden sources).
Don’t stop anything abruptly—some of these require tapering or are treating important conditions.
Ask your clinician/pharmacist for an “anticholinergic burden” review (often using scales like ACB).
If you’re on one, the common risk-reduction moves are:
Lower dose, shorter duration, or switch to a lower-anticholinergic alternative (e.g., for overactive bladder there are non-anticholinergic options depending on your situation).”
I responded to this information that: “I heard that one year of daily use of benadryl significantly increases this risk”, this is ChatGPT’s response:
“Short answer: There are peer-reviewed observational studies showing that long-term, frequent use of strong anticholinergics (including first-generation antihistamines like diphenhydramine—the active ingredient in Benadryl) is statistically associated with a higher risk of dementia in older adults. However, this evidence does not prove causation (i.e., it doesn’t prove that taking Benadryl for a year causes dementia).
Here’s the current scientific picture based on published research:
📌 Key Research Findings
1. Cumulative anticholinergic use and dementia risk
A large prospective cohort study published in JAMA Internal Medicine looked at people age 65+ over many years. It found that higher cumulative use of strong anticholinergic medications—including first-generation antihistamines like diphenhydramine—was associated with a significantly increased risk of developing dementia (including Alzheimer’s disease) compared with minimal use.
- Those with the highest cumulative exposure over a 10-year period had a markedly higher risk than those with low exposure.
- The “dose–response” trend (more use → higher risk) was a focus of this study.
However, the typical comparison highlighted in media (e.g., “one year of daily use equals a big risk”) simplifies a more complex research design: risk was calculated over cumulative exposure spanning multiple years and doses, not just a single 12-month period.
2. Systematic evidence suggests the risk increases with duration
A systematic review and meta-analysis of multiple studies found that ≥3 months of anticholinergic use was associated with about a 46 % higher average risk of incident dementia compared to non-use, indicating that longer exposure matters.
3. Observational studies vs. causation
Most of the evidence comes from observational cohort or case-control studies:
- These studies observe correlations between drug use and later dementia diagnoses over time.
- They do not prove that the drugs cause the dementia.
One reason causation is hard to establish is protopathic bias—people may start drugs like Benadryl for early symptoms related to the disease process before a dementia diagnosis.
🧠 Why these drugs are biologically plausible as a risk factor
Anticholinergics block acetylcholine, a neurotransmitter critical for learning and memory. Chronic blocking of this system—especially in older individuals whose baseline acetylcholine levels are already lower—could logically impair cognition over time.
🧪 What about “one year of daily use”?
There’s no specific large, high-quality study that isolates exactly Benadryl daily for one year as the exposure and then shows a quantified dementia risk for that exact scenario.
Most of the strong associations noted in the research refer to:
- Cumulative exposure over many years (often 3+ years measured in “total standard daily doses”).
- Studies that combine many kinds of anticholinergic drugs, not just diphenhydramine.
So while the general concept that longer use increases risk is supported, the specific “1 year of daily Benadryl = X% increased dementia risk” figure floating around on social media is not directly supported by a controlled study of that exact exposure.
🧾 Bottom Line — Evidence Summary
✔️ Older adults using strong anticholinergic drugs chronically (longer periods, higher doses) are more likely to be diagnosed with dementia in observational studies.
✔️ Diphenhydramine (Benadryl) is an anticholinergic and is included in this class.
✔️ Studies show associations, not proven causation.
✔️ The most consistent signals emerge with cumulative exposure (multi-year), especially in older adults.
🧠 Clinical guidance (what experts often say)
- Be cautious with long-term use of strong anticholinergics in older adults when alternatives exist.
- Short-term use (e.g., occasional allergy relief) is less clearly implicated.
- Talk to a clinician before changing use, especially if you’re taking these medications regularly.”
As far as iontophoresis, I own a machine and have found that it can work, but I have my own personal issues with this method. It requires very frequent use (for me at least as I have a severe case), the set up can be irritating, and it’s rather painful because once again my hyperhidrosis is severe and will only respond to high settings. So in my only personal experience from usage: frequent, painful, and rather a chore, especially considering that not maintaining the routine for me immediately resets my progress and can even temporarily worsen my already bad sweat. In my eyes it often just adds unnecessary stress in my life.
MiraDry seems like a decent option in the treatment of hyperhidrosis only mine happens to mostly affect my hands and feet, so it’s not particularly pertinent. I can basically say about the same regarding Brella.
Now as for the less used medical treatment: Surgery (Endoscopic Thoracic Sympathectomy – ETS). That is an entirely separate bag of worms. All I can say is this surgery seems like far more trouble than it’s worth, just look up other people’s experiences. The dermatologist I spoke to also only knew two people, I believe, that had chosen to get it done and according to the dermatologist it did not go well for either of the two patients.
*This information is mostly for my own reference. Please do your own research and consult your doctor for your own health.*
