Suspended animation shows up early in science fiction after a long history in prior literature. In Shakespeare, it’s the result of taking a “distilling liquor” (thus Juliet’s ‘sleep,’ which drives Romeo to suicide). In the SF realm, an early classic is John Campbell’s 1938 story “Who Goes There?”, which became the basis for the wonderful “The Thing from Another World” (1951). Here an alien whose spacecraft has crashed remains in frozen suspension for millennia, only to re-emerge as the barely recognizable James Arness. In the essay below, Don Wilkins points us toward a new study that could have implications for achieving the kind of suspended animation that one day might get a crew through a voyage lasting centuries. A frequent contributor to Centauri Dreams, Don is an adjunct instructor of electronics at Washington University, where the work took place. Echoes of van Vogt’s “Far Centaurus”? Read on. I’ll have another take on this topic in the next post.

by Don Wilkins

Humans have often observed with envy the ability of certain animals to extend sleeping periods from mere hours to months. If bears can do it, why cannot a suitably prepared person do it? Artificial hibernation is often used in science fiction to transport an individual into a distant future without the bother of aging or achieving relativistic speeds or conserving scarce resources. A practical hibernation system, in a more terrestrial function, provides medical support, improving survival by decreasing metabolic activity of a critically ill patient. Some writers hypothesize that a certain number of sleepers, particularly hibernations of decades or more, will suffer disabilities or death.

Research has focused on inducing torpor, a condition of significantly decreased metabolic rates and body activity, producing hibernation without adverse side-effects or horrifying experiments with cryogenics. A practical system remains within the realm of science fiction.

Torpor, like hibernation, is a physiological state in which various animals, including certain fish, reptiles, insects and mammals, actively suppress metabolism, lower body temperature and slow other life processes to conserve energy and survive fatal conditions and cold environmental temperatures.

A research team led by Yaoheng Yang (Washington University, St. Louis) has demonstrated a novel method for inducing torpor in rodents: Deep ultrasonic stimulation of a mammal’s brain [1]. Animals in torpor states experience reduced metabolism and body temperatures. Ultrasound was selected as the stimuli as it noninvasively and safely penetrates bone, and can be tightly focused with millimeter precision. The team hypothesizes that the central nervous system organizes the multitude of reactions needed to induce torpor.

In the experiments, as shown in Figure 1, a mouse wore a tiny “hat”, a lead zirconate titanate ceramic piezoelectric ultrasonic device with a center frequency of 3.2 MHz. The output was focused on the animal’s brain in the hypothalamus preoptic area (POA). Activating the POA neurons induced a torpor state for periods greater than 24 hours.

Fig. 1: Ultrasound device for inducing a torpor-like hypothermic and hypometabolic state. a, Illustration of ultrasound (US)-induced torpor-like state. b, Illustration of the wearable US probe (top). The probe was plugged into a baseplate that was glued on the mouse’s head. MRI of the mouse head with the wearable US probe shows that ultrasound was noninvasively targeted at the POA (insert). Photograph of a freely moving mouse with the wearable US probe attached is shown at the bottom. c, Illustration of the US stimulation waveform used in this study. ISI, inter-stimulus interval; PD, pulse duration; PRF, pulse repetition frequency. d, Calibration of the temperature (T) rise on the surface (top) and inside (bottom) the US probe. The temperature inside the probe was measured between the piezoelectric material and the mouse head when US probes were targeted at the POA or the cortex.

When the POA was stimulated, the body temperatures of the test animals dropped approximately three degrees C, although the environment was held to room temperature. Metabolism switched from carbohydrates and fat to solely fat. Heart rates declined about 47%.

The system used an automatic closed-loop feedback controller with the animal’s body temperature as the feedback variable. Tests which kept the subject’s body 32.95 ℃ for 24 hours were successfully concluded when the ultrasonic influence was removed and the animal returned to normal body temperature. According to previous studies, the body temperature must be below 34 ℃ to induce torpor.

Increasing the acoustic pressure and duration of the ultrasound stimulus further lowered body temperature and slowed metabolism. Each ultrasonic pulse produced consistent neuronal activity increases together with body temperature reductions in the test subjects.

The team, through genetic sequencing, discovered ultrasound could restrain the TRPM2 ultrasound-sensitive ion channel in the POA neurons. The precise mechanism providing the torpid state is unknown.

In a rat, which does not naturally enter torpor or hibernation, ultrasound simulation of POA neurons reduced skin temperature and core body temperature.

Ultrasonics can, with great spatial accuracy, reach deeply within the brain to stimulate the POA neurons. This approach could serve as the foundation of a system providing long term, noninvasive, and safe induction of torpor.


1. Yang, Y., Yuan, J., Field, R.L. et al., “Induction of a torpor-like hypothermic and hypometabolic state in rodents by ultrasound,” Nature Metabolism 5, 789–803 (2023). Full text.