Link: https://youtu.be/yUdg7drjrZY

Duration: 38 min

Transcript: Download plain text

Short Summary

Andrew Huberman interviews Dr. Susanna Søberg, a brown fat and thermogenesis researcher who studies how deliberate cold and heat exposure change metabolism, insulin sensitivity and inflammation. She argues cold exposure should feel hard and end in the cold, that it works through trainable hormesis rather than extreme suffering, and that small daily doses (a 19 °C bedroom, cold wind, a cooling vest) can grow brown fat without a cold plunge. She also lays out the data from a winter-swimming study and Hansen et al. 2017 on sleeping cold.

Key Quotes

1. "So I think it's just you should get uncomfortable cold." (00:00:54)
2. "So the cold shock is activation of your sympathetic nervous system and these activation of the the catecholamines." (00:01:02)
3. "You think about cold water and cold water immersion as something that is comfortable. It should be hard because that's the point of it, right?" (00:01:58)
4. "You can go in the water for one to two minutes um per session, but go up to 11 minutes per week in total." (00:27:52)
5. "And if you overdo it, you exhaust the cells and that will increase your risk of cardiovascular disease also." (00:28:31)

Detailed Summary

Dr. Susanna Søberg on Brown Fat, Cold Exposure, and Thermogenesis

Andrew Huberman interviews Dr. Susanna Søberg about how cold and heat exposure affect brown fat, metabolism, insulin sensitivity, inflammation, and cardiovascular health. The discussion moves from cold-shock physiology and thermogenesis to detailed winter-swimming and sleeping-cold studies, then ends with practical ways to design a deliberate cold exposure routine.

Research Background and the Søberg Principle

Søberg began her research in 2016 while looking for a group activity capable of activating brown fat. Winter swimming provided the initial model because people who repeatedly enter cold water should, in principle, stimulate brown adipose tissue.

• Søberg is frequently associated with the “Søberg principle,” rendered as “Soburg” or “Søburg” in the transcript: begin and end a cold exposure session in cold water so that the body must actively rewarm itself afterward.
• Her research methods include PET-CT imaging, infrared thermography, and oral glucose tolerance tests conducted with winter-swimming cohorts.
• The broader research question is how deliberate temperature stress changes metabolic health, particularly insulin sensitivity, glucose handling, inflammation, and the function of brown fat and skeletal muscle.
• The episode treats cold and heat as potentially trainable physiological stressors rather than merely sources of discomfort.

Cold Shock and the Autonomic Nervous System

Cold exposure initially produces a pronounced autonomic response. Søberg describes this cold shock as an activation of the sympathetic nervous system and catecholamines, visible as rapid or hyperventilated breathing.

• Cold shock can produce hyperventilation and a faster breathing rate as the sympathetic nervous system responds to the abrupt temperature change.
• The gasping response is trainable: with repeated exposure, Søberg says people generally become more comfortable and the magnitude of the initial cold-shock response diminishes.
• Immersion activates a mammalian diving response that slows oxygen consumption, allowing the body to preserve oxygen and avoid becoming hypothermic too quickly.
• Within roughly one to two minutes of immersion, she says both the sympathetic and parasympathetic branches of the autonomic nervous system can become fully activated.
• The more skin covered by cold water, the more cold receptors are stimulated, producing a faster and stronger autonomic response than standing outdoors in a T-shirt and cold wind.
• Standing in cold air still raises norepinephrine and activates brown fat, so immersion is not required for the initial sympathetic response.

Brown Fat and the Thermogenic Pathway

Brown fat and skeletal muscle form two complementary thermogenic systems. Brown fat continuously helps regulate body temperature, while muscles generate additional heat through shivering.

• Cold receptors in the skin send signals to the hypothalamus, which produces a rapid increase in norepinephrine, adrenaline, and cortisol.
• Brown fat is highly sensitive to norepinephrine and can therefore respond quickly after the nervous system detects cold.
• Adapted brown fat cells develop more mitochondria and draw glucose and fatty acids from the bloodstream to fuel sustained heat production.
• Brown fat is activated by both cold and warmth through different pathways; a third pathway runs directly from shivering muscles.
• Muscle and brown fat therefore cooperate to prevent the body from becoming either too cold or too hot.
• Activated brown fat is described as reducing excess unhealthy white fat, the energy-storage tissue around the thighs and internal organs.

Small-Scale Experiments and the Face-Cold Hypothesis

Søberg describes an experiment in which a hand was immersed in water at 4 °C for four minutes while blood pressure, heart rate, and brown-fat activity were monitored. Infrared thermography revealed brown-fat activation and a temperature increase within only a few minutes.

• The largest brown-fat depot lies just beneath the clavicles and close to the skin surface, which makes changes in that region easier to detect with infrared thermography.
• Other brown-fat depots are located more centrally, including around the central nervous system.
• Because the face contains many cold receptors, she proposes that cold exposure to the face during sleep may stimulate brown-fat growth.
• The face-to-sleeping-cold hypothesis connects directly to the later evidence that sleeping in a cool room can increase brown fat.
• Søberg notes that no studies quantify how much brown fat is activated by cold showers, so the metabolic benefit of that practice remains theoretical rather than directly measured.

Shivering, Vasoconstriction, and Afterdrop

Shivering is presented as a useful response rather than something to fear, provided the exposure does not cause hypothermia. Søberg links shivering to the brown-fat and muscle activity needed to restore body temperature.

• On entering cold water, blood vessels constrict to preserve heat around the core and protect vital organs.
• On leaving the water, those vessels dilate, allowing warm blood to flow toward the still-cold skin and limbs.
• The post-immersion fall in core temperature is called “afterdrop,” and Søberg describes it as an unavoidable consequence of exiting cold water.
• Afterdrop also triggers shivering and thermogenesis as the body responds to the renewed cooling.
• The main risk she identifies from remaining in cold water too long is excessive afterdrop, which is why she rejects extreme durations such as half an hour as a routine strategy.

Hormesis and Repeated Adaptation

The episode’s central biological framework is hormesis: a short, manageable stress makes cells more resistant to the next exposure. Søberg compares this adaptation to the way repeated exercise makes muscle stronger and more efficient.

• Exercise, cold, and heat can raise heat-shock proteins and cold-shock proteins, improving cells’ capacity for repair and subsequent stress.
• Repeated cold exposure makes brown fat more responsive and increases the number and efficiency of its mitochondria.
• Skin capillaries also become better at constricting during cold exposure, while the catecholamine and initial stress response becomes less pronounced.
• Over repeated sessions, metabolism and insulin sensitivity can improve alongside greater brown-fat activation.
• Søberg says many people notice a qualitative change after approximately three, four, or five exposures, finding it easier to feel and maintain warmth.
• Excessive exposure can exhaust cells and potentially increase cardiovascular risk, so she advocates a low-dose threshold rather than escalating to severe or prolonged cold exposure.

The Winter-Swimming Protocol

The winter-swimming research began with people who had already swum for two to three seasons rather than complete beginners. Sessions were short, and the outdoor environment was intentionally treated as a real-world rather than tightly controlled setting.

• Participants generally remained in cold water for only one to two minutes per session.
• Water temperatures ranged from approximately 15 °C downward, often reaching roughly 2–4 °C, while outdoor swimming remained highly uncontrolled.
• Each session involved three rounds of cold-water immersion combined with two sauna sessions per day.
• The protocol was performed two to three times per week and followed the Søberg principle by beginning and ending the sequence in cold water.
• Sauna sessions lasted approximately 10 to 15 minutes at a temperature near 80 °C.
• Across the study, participants accumulated about 11 minutes of cold-water exposure per week over two or three visits, compared with approximately 57 minutes of sauna exposure per week.
• The control group was matched on multiple parameters, allowing Søberg and her colleagues to compare the swimming group with a more conventional comparison group.

Insulin Sensitivity, Glucose Clearance, and Heat Production

Winter swimmers displayed several metabolic differences from controls after following the combined cold-water and sauna protocol. These changes were measured after the participants’ final meal under fasting and resting conditions.

• The swimmers had greater insulin sensitivity and produced less insulin on all experimental days.
• For the metabolic measurements, participants fasted and lay still in bed for eight hours after their last meal.
• In an oral glucose tolerance test used for screening, the swimmers cleared glucose faster; at the two-hour point, their blood-glucose curve had fallen farther and sat lower than the control group’s.
• On laboratory sleep days, the swimmers were warmer at the skin surface than controls while resting outside the cold, evidence of greater thermogenic activity.
• Søberg attributes their higher heat loss to more vascular skin produced by repeated transitions between cold water and sauna heat.
• A separate 2016 study followed middle-aged men and women through a four-to-five-month winter-swimming season and found lower blood pressure, lower heart rate, and improved insulin sensitivity by the end of the season.
• That 2016 study did not measure brown fat, which Søberg identifies as a possible missing link in explaining the reduction in inflammation.

Inflammatory Markers

The research also examined inflammatory signaling rather than concentrating only on glucose and insulin. Søberg describes the observed sequence as consistent with patterns already known in the literature.

• Interleukin-6, or IL-6, rose during the intervention.
• IL-10 subsequently increased, producing the sequential inflammatory-marker pattern reported in the study.
• Søberg proposes that the greater brown-fat activation found in other experiments could help explain why the winter swimmers exhibited this pattern.
• The episode connects lower inflammation with potential protection against metabolic and neurological disease, although the research presented does not establish that brown fat alone caused the full set of health outcomes.

Hansen et al. 2017 and Sleeping Cold

Hansen et al. 2017 used PET-CT and metabolic measurements to examine what happens when people sleep in different ambient temperatures. The study provides the clearest evidence in the episode for a low-effort brown-fat intervention.

• Participants first slept at 24 °C and completed a baseline brown-fat measurement.
• After one month of sleeping at 19 °C, they showed increased brown fat and increased insulin sensitivity.
• The participants remained clothed and under a duvet during the cool sleeping condition.
• After a second month at 24 °C, both brown-fat activation and insulin sensitivity decreased slightly.
• By a fourth month at 27 °C, brown-fat activation and insulin sensitivity were lower still.
• The practical implication is that sleeping in a 19 °C bedroom may grow brown fat without the sleeper consciously noticing the effect or ever entering cold water.

Designing a Deliberate Cold Exposure Routine

Søberg’s prescription emphasizes that cold exposure should be challenging and that the body should be left with work to do afterward. Her starting recommendation is to enter the cold, allow the cold response to subside, and finish while still cold so that active rewarming follows.

• She argues that ending a session in the cold keeps brown fat, muscle, and neurotransmitter activity elevated after the immersion ends.
• The resulting thermogenesis can operate for hours, making the adaptation more consequential than the brief time physically spent in the plunge.
• Because the body remains cold after exposure, she says neurotransmitter activity supports the efficiency of brown-fat and muscle cells and encourages mitochondria to generate heat rapidly.
• Her stance is that cold water should feel hard rather than pleasant; if the water is very cold and the participant feels very cold, she advises staying in slightly longer.
• The goal is not to maximize suffering but to finish with enough active rewarming to train the cells, muscles, and metabolism.
• For someone limited to two days per week, she endorsed splitting a session into one or two minutes in the cold, stepping out, and then returning for another couple of minutes, helping accumulate roughly four to five minutes per exposure toward the 11-minute weekly target.

Cold Exposure Without a Full Immersion

A cold plunge is presented as one option rather than a requirement. Søberg emphasizes several less demanding ways to stimulate the same general adaptation pathways.

• Wearing a cooling vest for 10 days has been shown to grow brown fat in the evidence discussed during the episode.
• Cold wind alone can activate brown fat, so outdoor exposure may be sufficient without entering water.
• People who work outdoors or regularly move between contrasting temperatures tend to have more brown fat.
• A 19 °C sleeping environment can provide a repeated low-dose stimulus without a shower or plunge.
• Søberg’s two-day-per-week example shows that a limited schedule can still work if the available sessions are divided into multiple short entries and exits.
• The temperature changes themselves strengthen the cells by repeatedly challenging them to adapt.

The Role of Warm–Cold Transitions

Søberg gives particular emphasis to starting and ending in the cold, while Huberman reframes the broader principle around transitions. Their formulations emphasize different but related aspects of the same routine.

• Søberg’s approach focuses on finishing cold so that the body must generate heat to return to normal temperature.
• Huberman emphasizes the repeated transitions from warm to cold and cold to warm as the source of the adaptation.
• The transition-oriented view allows more flexibility than a rigid requirement for one temperature, duration, or number of weekly sessions.
• This framing makes the routine easier to vary through cold wind, cool sleeping, cooling vests, and immersion.
• The underlying goal remains a short, repeatable hormetic challenge rather than a contest involving extreme discomfort.

Heat Exposure and Sauna

Heat is treated as another trainable stressor rather than simply a reward after cold. The winter-swimming protocol deliberately combines both forms of exposure.

• Cold and heat activate different thermogenic pathways while both contributing to the broader hormetic response.
• Sauna exposure in the study occurred at approximately 80 °C for 10 to 15 minutes per session.
• The cold-water and sauna combination was designed to create repeated contrast and adaptation rather than isolate a single temperature.
• Winter swimmers accumulated about 57 minutes of sauna time per week alongside approximately 11 minutes of cold-water immersion.
• The contrasting exposures were associated with increased insulin sensitivity, faster glucose clearance, greater thermogenesis, and the described inflammatory-marker pattern.

Broader Metabolic and Public-Health Implications

The episode places deliberate temperature exposure within the broader history of modern lifestyle and chronic disease. Søberg argues that people have become unusually insulated from both cold and heat.

• Insulated homes, sedentary indoor living, and temperature-controlled environments have made many people largely temperature-neutral for decades.
• She associates more comfortable lifestyles beginning in the 1960s and 1970s with rising obesity, which she says increased further during the 1980s according to the statistics she cites.
• Cold and heat are framed as natural stressors that return physiology toward homeostasis and support cellular repair.
• Lower inflammation could, in principle, reduce the risk of conditions linked to it, including type 2 diabetes, depression, anxiety, and Alzheimer’s disease.
• The episode’s overall message is that short, repeated, manageable hormetic stress may provide metabolic and cardiovascular benefits at a relatively low exposure threshold.
• At the same time, the discussion rejects extreme suffering as the goal and repeatedly emphasizes adaptation, dose control, and the need to avoid hypothermia or excessive cardiovascular strain.