Daniel sent us this one — he's someone who's always run a bit hot, grew up in Ireland, now lives in Israel, and noticed it got significantly worse after starting SSRIs. He's not asking about the sweating side of things specifically. He's asking about the deeper physiology. What actually governs how we deal with heat? Why can some people work outside in August and barely notice while others are wrecked by a warm afternoon? And there's this interesting tension in his prompt between using air conditioning therapeutically and worrying about becoming dependent on it. So the real question is, what determines our thermal tolerance, and how much of it is fixed versus trainable?
This is one of those questions that seems simple and then you start pulling on it and realize there are about six different systems all talking to each other. The autonomic nervous system is the conductor, sure, but the orchestra includes your hypothalamus, your thyroid, your blood volume, your sweat gland distribution, your brown adipose tissue, and something called heat shock proteins that most people have never heard of.
Heat shock proteins. Sounds like what happens when you open a furnace door without gloves.
They're actually fascinating. They're molecular chaperones — their job is to prevent other proteins from denaturing when your core temperature rises. Some people naturally express more of them. That's one of the first things that separates someone who tolerates heat well from someone who doesn't. Before we even get to sweat or blood flow, there's a molecular level of protection that varies person to person.
Some people's proteins are literally better at not falling apart in the heat.
And it's not fixed. Repeated heat exposure upregulates those heat shock proteins. That's part of heat acclimatization. But the baseline — where you start — that's partly genetic. There's a study from the Journal of Applied Physiology that looked at HSP72 specifically, which is the major heat shock protein in humans, and found that some individuals have a blunted HSP72 response to heat stress. They don't ramp up production the way others do. Those people struggle more in the heat, and they take longer to acclimatize.
Some people are starting from a molecular disadvantage and they don't even know it. They just think they're bad at summer.
Here's where it gets medically relevant to the prompt. SSRIs increase serotonin availability in the synaptic cleft. But serotonin isn't just a brain chemical. About ninety percent of your body's serotonin is in your gut, and it's also a major player in the hypothalamus for thermoregulation. The hypothalamus has serotonin receptors — specifically the five-HT one A and five-HT two A receptors — that are directly involved in setting your body's temperature set point.
So serotonin is partly a thermostat chemical?
The hypothalamus uses serotonin signaling to decide whether to trigger heat dissipation or heat conservation. When you take an SSRI, you're essentially changing the gain on that thermostat. Some people get a slightly elevated set point. They're running at, say, thirty-seven point three instead of thirty-seven point zero. That doesn't sound like much, but for thermal comfort it's huge. You're already closer to the threshold where your body starts panicking about overheating.
It's not just that the SSRIs make you sweat more. They've actually nudged your internal target temperature upward, and now any external heat pushes you into the danger zone faster.
And there's a secondary effect too. Serotonin influences vasodilation — how much your blood vessels near the skin open up to dump heat. Some SSRIs seem to blunt that vasodilation response. So you're generating heat at a slightly higher baseline, and you're less efficient at radiating it away. It's a double hit.
That explains the shirt-off-under-the-air-conditioning ritual. There's something genuinely therapeutic about forcing that heat exchange when your body's own mechanisms are a bit sluggish.
The glass of water he mentions is doing real work too. Plasma volume is one of the biggest determinants of heat tolerance. Your blood is your coolant. If you're even mildly hypohydrated — notice I said hypohydrated, not dehydrated, there's a distinction in the literature — your blood volume drops, your cardiac output has to work harder to push blood to the skin for cooling, and your sweat rate drops. Someone with naturally higher plasma volume, or someone who's really on top of hydration, has a bigger thermal buffer.
That's the state of being not quite optimally hydrated, as opposed to clinically dehydrated.
Dehydration is the medical endpoint. Hypohydration is the zone most people live in, especially in hot climates. And it matters. A two percent drop in body mass from fluid loss measurably impairs thermoregulation. In Israel in August, you can lose that in an hour of outdoor work.
We've got heat shock proteins, serotonin-affected hypothalamic set points, vasodilation efficiency, and plasma volume. What about the thing Daniel mentioned — becoming dependent on air conditioning? Is that physiologically real?
It is, and the literature calls it the adaptive comfort model or sometimes thermal monotony. Your thermoregulatory system is use-it-or-lose-it. When you spend all your time in a narrow temperature band — say, twenty-one to twenty-three degrees Celsius — your body stops investing in the machinery for handling temperature extremes. Heat shock protein expression drops. Sweat gland sensitivity decreases. Your blood vessels become less responsive to thermal signals. It's not addiction in the pharmacological sense, but it's a genuine physiological downregulation.
You're deconditioning your thermal resilience.
And there's a measurable timeline. Full heat acclimatization takes about ten to fourteen days of repeated exposure. But de-acclimatization happens faster — you start losing adaptations within a week of constant air conditioning. After two weeks, you're back to baseline. So someone who works in an air-conditioned office all day and only experiences heat walking to the car is essentially never acclimatized.
Which means the advice to be judicious with air conditioning isn't just about energy consumption. It's about maintaining your body's ability to cope.
There's a fascinating study from Japan that looked at something called toasty, which is the term some researchers use for mild cold or heat exposure that's not quite stressful enough to trigger full acclimatization but enough to maintain some metabolic flexibility. They found that people who allowed their indoor temperature to fluctuate seasonally — warmer in summer, cooler in winter — had better metabolic health markers, including better insulin sensitivity and more active brown adipose tissue.
Brown adipose tissue. That's the metabolically active fat that generates heat, right?
Yes, and it's relevant here in a counterintuitive way. Brown fat is mostly discussed in the context of cold tolerance — it burns calories to generate heat. But brown fat activity is also linked to overall metabolic flexibility, which affects how efficiently your body can shift between heat generation and heat dissipation. People with more active brown fat tend to have more responsive thermoregulation overall. And here's the wild part — brown fat activity is partly genetically determined, but it's also highly trainable through temperature exposure.
Some people are walking around with more biological HVAC capacity than others.
A better furnace and a better air conditioner, yes. And SSRIs complicate this too. There's some evidence that serotonergic signaling influences brown fat activation. The mechanisms aren't fully mapped yet, but it's an active area of research. The five-HT three receptor, which some SSRIs affect indirectly, is expressed in brown adipose tissue.
Let me pull on another thread from the prompt. He mentions that some people seem to tolerate heat much better than others, and he asks what governs that besides disease states like diabetes. What about sex differences?
Significant and under-discussed. Women, on average, have a lower sweat rate than men — fewer activated sweat glands per unit of skin area, and each gland produces less sweat. Women also tend to have a higher core temperature during the luteal phase of the menstrual cycle, which is driven by progesterone. Progesterone is thermogenic — it raises the hypothalamic set point. So a woman in the week before her period is running hotter at baseline, just like someone on an SSRI. And if she's on both, the effects can compound.
Someone could be taking an SSRI and be in their luteal phase and wondering why they feel like they're melting while their male colleague seems fine. And the answer is, their thermostat has been nudged upward by two different mechanisms simultaneously.
Neither of those is a disease state. These are normal physiological variations. Add in body composition — muscle generates more heat at rest than fat, so a more muscular person has a higher basal metabolic rate and produces more heat — and you've got multiple factors that have nothing to do with being unhealthy.
What about aging? I assume that changes things too.
It does, and not in a good direction. As people age, their sweat glands become less responsive. Skin blood flow during heat exposure decreases. The thirst sensation becomes less acute, so older adults tend to be more hypohydrated without realizing it. And the cardiovascular system has less reserve capacity to pump blood to the skin for cooling. All of this is why heat waves are disproportionately dangerous for the elderly. It's not just that they're frail — their thermoregulatory system is literally less capable.
Which makes the Israeli summer a genuine public health concern for an aging population.
Israel is interesting here because the population has such diverse genetic backgrounds. There are populations that have lived in hot climates for thousands of years — Yemenite Jews, for example, or Bedouin communities — and there's some evidence of genetic adaptations related to heat tolerance. Nothing as dramatic as the cold adaptations you see in Arctic populations, but subtle differences in sweat sodium retention and vasodilation efficiency.
That raises a question I hadn't thought about. Is heat tolerance heritable in a straightforward way, or is it mostly environmental?
Twin studies suggest it's about fifty percent heritable. The other fifty percent is acclimatization, conditioning, hydration status, body composition, and all the factors we've been discussing. So you're not stuck with whatever you inherited. But you're also not starting from a blank slate. And that fifty percent heritability covers things like sweat gland density, which is set in early childhood. The number of sweat glands you have is determined by about age two or three. After that, you don't grow new ones. The ones you have can become more or less active, but the total count is fixed.
So if you spent your first three years in a cold climate, you have fewer sweat glands for life?
The evidence suggests yes. There's a famous study from the nineteen sixties — a Japanese researcher named Kuno — that found people raised in tropical climates had more active sweat glands than those raised in temperate zones. The total number isn't wildly different, but the proportion that become functional is influenced by early heat exposure. It's one of those developmental windows that closes early.
Daniel growing up in Ireland — cool, temperate, famously not tropical — may have literally developed a different sweat gland activation profile than someone who grew up in Tel Aviv.
He then moved to one of the hotter countries on earth and added an SSRI. The deck is stacked.
Let's talk about the practical side of this. He mentioned that if he uses air conditioning too aggressively, he becomes dependent. He's clearly noticed the de-acclimatization effect. What's the sweet spot? How do you stay functional without losing your thermal resilience?
The research on this points to a few evidence-based approaches. One is temperature cycling — allowing indoor temperatures to rise during the day and using air conditioning more strategically. Instead of keeping a space at twenty-two degrees all day, let it drift up to twenty-six or twenty-seven during the afternoon and cool it down for sleep. Sleep is actually the one time where aggressive cooling is physiologically justified, because your core temperature needs to drop by about one degree Celsius to initiate and maintain deep sleep.
The air conditioning at night is doing real biological work. It's not just comfort.
And for someone on an SSRI whose baseline temperature is already slightly elevated, that nighttime cooling becomes even more important. The body's natural temperature drop for sleep might be blunted, and a cool room compensates. There's good evidence that a bedroom temperature of eighteen to twenty degrees Celsius improves sleep quality, especially for people with thermoregulatory challenges.
During the day, you're saying, let it be warmer.
The goal is to stay below the threshold of heat stress — where you're uncomfortable but not impaired — for enough hours per day to maintain acclimatization. For most people, that's somewhere in the twenty-six to twenty-nine degree range. You don't need to be suffering. You just need enough thermal variation that your body remembers how to respond.
Like adopting a feral cat. You don't want it fully domesticated.
That's a good analogy. You want your thermoregulatory system to retain some wildness. And there are other ways to maintain acclimatization. Exercise is a major one. When you exercise, your core temperature rises, and that triggers the same heat shock protein response as environmental heat exposure. So someone who exercises regularly, even in air conditioning, is getting some cross-training for their heat tolerance. Not as effective as actual heat exposure, but it helps.
What about the shirt-off, lie-under-the-air-conditioning thing he described? Is that actually therapeutic, or does it feel good for reasons that might be counterproductive?
It's therapeutic in the moment and probably fine as a recovery strategy. What he's doing is maximizing conductive and convective heat loss. Skin-to-cool-surface contact is conductive cooling, and the air blowing over skin is convective cooling. Both are highly efficient. And there's a parasympathetic response to rapid cooling — it can trigger what's called the mammalian dive reflex, a vagal response that slows heart rate and promotes a sense of calm. So the "it relaxes me" part is real physiology. It's not just the relief of being cooler. The rapid skin temperature change is activating the parasympathetic nervous system.
It's essentially a vagal maneuver you do with air conditioning instead of cold water.
That's exactly what it is. And after physical labor in the heat, rapid cooling is actually recommended to bring core temperature down. The old advice was to cool gradually, but the evidence now supports faster cooling for heat-related exhaustion. So his instinct is spot on.
I want to go back to something you mentioned earlier — the difference between people who handle heat well and people who don't. You said heat shock proteins, sweat gland density, plasma volume. Is there a single biggest predictor? If you had to bet on whether someone will struggle in the heat, what's the number one thing you'd look at?
VO2 max — maximal oxygen uptake — is the single best predictor of heat tolerance. A high VO2 max means a strong heart, high blood volume, efficient vasodilation, and better sweat response. All of the thermoregulatory machinery runs on the cardiovascular system. If your heart and blood vessels are in good shape, everything else works better.
The guy who runs marathons and the guy who sits on the couch are experiencing the same August day completely differently, and it's not just about fitness in the abstract. It's about their actual physical capacity to move heat from their core to their skin.
It's trainable. VO2 max improves with aerobic exercise, and heat tolerance improves alongside it. There's a study of middle-aged men who did a twelve-week aerobic training program. Their heat tolerance improved by about twenty percent, measured by how long they could work in a hot environment before their core temperature reached a threshold. And their sweat rate increased and their sweat became more dilute — they were retaining more sodium, which is what a heat-acclimatized body does.
More sweat, but saltier sweat. So you're losing less sodium per liter.
The sweat glands become more efficient at reabsorbing sodium. That's a hallmark of heat acclimatization, and it matters because sodium loss affects nerve function and muscle contraction. Someone who's not acclimatized loses more sodium in their sweat and is more prone to cramping and fatigue.
I'm realizing we should probably address the elephant in the room, which is that climate change is making all of this more relevant for more people. There was a piece in Nature Climate Change a few years back that projected that by twenty thirty, about two billion people will be living in areas where the average summer temperature exceeds what's considered survivable without artificial cooling.
That's the tension at the heart of this prompt, isn't it? Air conditioning is both a lifesaving technology and something that, used excessively, makes people less resilient to the very conditions it's protecting them from. It's not a clean trade-off.
The conference story he told — three days in a suit in a warm country that had dialed back the air conditioning for sustainability reasons — that's a preview of what more people are going to experience. And it's not just about comfort. Cognitive performance drops measurably in heat stress. Decision-making gets worse. Reaction time slows.
There's a well-known study from Harvard's T.Chan School of Public Health that looked at students in dormitories during a heat wave. Students in air-conditioned dorms performed significantly better on cognitive tests than students in non-air-conditioned dorms. The effect was largest for working memory and processing speed. So it's not trivial. If you're at a conference trying to absorb information and network effectively, being thermally stressed is a genuine cognitive impairment.
Which means the sustainability argument for reducing air conditioning has to contend with the productivity argument. You can't just say "tough it out" when people's ability to think clearly is at stake.
That's where the adaptive approach becomes so important. The goal shouldn't be no air conditioning or constant air conditioning. It should be strategic cooling combined with deliberate heat exposure to maintain acclimatization. Use cooling when it matters most — for sleep, for cognitively demanding work, for recovery after heat exposure. But don't live in a thermal bubble twenty-four seven.
There's also a social dimension here that doesn't get discussed much. Heat tolerance affects who can participate in what. If you're someone who struggles in the heat, outdoor social events, physical activities, even walking to lunch become burdens that other people don't experience. It's an invisible barrier.
It intersects with medication use in a way that doctors rarely discuss with patients. How many people are prescribed an SSRI and told that it might affect their heat tolerance? The conversation is usually about sexual side effects, weight changes, maybe sleep. Not about the fact that you might feel five degrees hotter all summer.
I've seen the prescribing information for several SSRIs. Excessive sweating is listed as a side effect, usually in the fine print. But the broader thermoregulatory shift — the set point change, the vasodilation issue — that's not really communicated.
It should be, especially for people living in hot climates or people with outdoor occupations. If you're a construction worker in Phoenix and you're prescribed an SSRI, the heat implications are relevant to your safety. Heat-related illness is not rare. In the United States alone, there are about seven hundred heat-related deaths per year, and that's almost certainly an undercount because heat exacerbates cardiovascular events that get coded as heart attacks or strokes.
What would you tell someone who's on an SSRI, living in a hot climate, and trying to figure out their relationship with air conditioning and heat tolerance? What's the Herman Poppleberry protocol?
First, separate sleep from waking hours. Cool your bedroom aggressively at night — eighteen to twenty degrees is ideal. That's non-negotiable. Sleep quality affects everything, and the temperature drop needed for sleep initiation is harder to achieve when your serotonergic thermostat is nudged upward.
Second, get your cardiovascular fitness up. Even moderate aerobic exercise — brisk walking, cycling, swimming — will improve your heat tolerance more than anything else. Swimming is especially good because you're getting the exercise while the water conducts heat away, so you can work harder without overheating.
You're in Israel, so the Mediterranean is right there.
Third, stay ahead of hydration. Not just water — electrolytes. Someone on an SSRI who's sweating more than they used to is losing sodium. If you're drinking plain water to replace sweat losses without replacing sodium, you can actually dilute your blood sodium to dangerous levels. It's called exercise-associated hyponatremia, and it's more common than people realize.
Not just water. Water plus something with electrolytes.
Even just salting your food adequately makes a difference. Fourth, use air conditioning strategically rather than constantly. Cool down when you need to recover or concentrate. Let the temperature drift upward at other times. And fifth, consider timing. The SSRI half-life matters here. If you take your dose in the morning and peak plasma concentration hits in the afternoon — which is also the hottest part of the day — you might talk to your doctor about shifting to evening dosing. The thermoregulatory effects track with plasma levels to some degree.
That's a concrete, actionable thing that most people would never think to ask about.
It's not a guaranteed fix — the relationship between plasma levels and thermoregulatory effects isn't perfectly linear — but it's a low-risk intervention worth discussing with a prescribing physician.
I want to circle back to something you said earlier about the developmental window for sweat glands. If your sweat gland activation is set in early childhood, and Daniel grew up in Ireland, he's got an Irish sweat system living in an Israeli climate. Can that system still adapt, or is there a ceiling on what acclimatization can achieve?
It can adapt significantly. The sweat glands you have can become more active, more efficient at sodium reabsorption, and more responsive to lower core temperature thresholds. What doesn't change much is the total count of active glands. But the capacity of each gland can increase. So someone from a cool climate can absolutely acclimatize to a hot one — it just might take longer and the ceiling might be slightly lower than someone who developed in a hot climate.
The SSRI is essentially raising the difficulty level on that adaptation process.
It's like trying to acclimatize while someone keeps nudging your thermostat up by half a degree. You can still do it, but it's harder and you're going to feel the heat more acutely throughout the process.
One thing we haven't touched on — he mentioned diabetes as a disease state that affects thermoregulation. What's the mechanism there?
Diabetic neuropathy damages the autonomic nerves that control sweating and skin blood flow. So someone with diabetes might not sweat enough, or might sweat in the wrong places, or might have impaired vasodilation. They're also at higher risk for heat-related illness because their cardiovascular system is often compromised and their thirst sensation can be blunted. It's a triple or quadruple hit.
That's before we even get to obesity, which is often comorbid with diabetes and adds its own thermal burden. More mass means more heat generation, and adipose tissue is insulating — it traps heat.
The physics are unforgiving. A larger body has a lower surface-area-to-volume ratio, which means less skin area per unit of mass for heat dissipation. And subcutaneous fat acts as insulation. So someone with obesity is generating more heat and is less able to get rid of it.
We've built up quite a picture here. Heat tolerance is a product of genetics, early development, cardiovascular fitness, hydration, body composition, acclimatization history, and — for a significant number of people — medication side effects that nobody warned them about.
It's dynamic. It changes day to day based on sleep, hydration, recent heat exposure, and even mood. There's a bidirectional relationship between thermal comfort and emotional state. Being hot makes people irritable. Being stressed raises core temperature slightly. The systems are deeply intertwined.
Which brings us back to the air conditioning as therapy thing. He said after lying under the air conditioning with a glass of water, he feels more like himself. That's not just physical recovery. That's the restoration of a psychological baseline that heat had disrupted.
That's a legitimate use of environmental cooling. The key is not letting it become the only way you can feel like yourself. If you can only function in a narrow temperature band, you've lost something valuable. But using cooling as a recovery tool after heat exposure — that's just good practice.
The conference story really sticks with me. Three days in a suit, uncomfortable, in a place that had turned down the air conditioning. That's a preview of a future where cooling is more contested — either because of energy costs, grid constraints, or sustainability policies. And the people who will suffer most are the ones with the least physiological margin. The elderly, the medically compromised, people on medications that affect thermoregulation.
There's an equity dimension that doesn't get enough attention. Access to cooling is already unequal. As grids get strained and energy prices rise, that inequality will widen. And the people who need cooling the most — for medical reasons, not just comfort — are often the least able to advocate for themselves.
The question of "what governs how we deal with heat" turns out to be partly a question about biology and partly a question about infrastructure and policy.
As most good questions do. The biology is fascinating — heat shock proteins, serotonergic set points, brown fat, sweat gland development — but it all plays out in a social and environmental context that determines who gets to deploy which cooling strategies.
For someone on an SSRI in a hot climate, the practical takeaways are real. Cool nights, cardiovascular fitness, electrolyte-aware hydration, strategic air conditioning, and maybe a conversation with the doctor about dose timing. None of those are magic bullets, but together they're a meaningful shift.
Don't underestimate the value of just understanding what's happening. Knowing that your thermostat has been nudged upward by serotonin — that the heat you're feeling isn't just in your head, it's a real pharmacological effect — that knowledge helps. It takes the experience from "why can't I handle this" to "my body is responding predictably to a known mechanism.
Naming the thing. That's half the battle.
Now: Hilbert's daily fun fact.
Hilbert: The Newfoundland cave amphipod, Stygobromus canadensis, discovered in the nineteen thirties, is named after Canada — not because the species is particularly patriotic, but because the cave system where it was found was thought at the time to be the only subterranean ecosystem in the entire country.
A cave shrimp with a national identity crisis.
Now I want to know if there are others.
This has been My Weird Prompts. Thanks to our producer, Hilbert Flumingtop. If you enjoyed this episode, leave us a review wherever you get your podcasts — it helps other people find the show. I'm Herman Poppleberry.
I'm Corn. Stay cool out there.
