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How heat methods work

In order to understand how heating the testes is a form of contraception, one needs to understand normal temperature regulation in the testes.

Testes are usually cooler than the rest of the body

Animals whose testes are located outside the abdominal cavity have elaborate temperature regulation systems which keep the testes a few degrees cooler than the rest of the body. Various features of the male reproductive system make this temperature differential possible:

Diagram of the pampiniform plexus and muscles of the male reproductive system
  • Two sets of muscles (cremaster and tunica dartos) help regulate the temperature of the testes. The muscles contract, moving the testes closer to the body when the testes drop below normal temperature. The muscles relax, moving the testes farther away from the body when the testes are warmer than normal;
  • The blood flowing into the testes is cooled below body temperature. Inflowing blood gives some of its heat to the cooler outflowing blood in a dense network of blood vessels in the spermatic cord (pampiniform plexus);
  • The scrotal skin has very little underlying fat tissue, and so does not provide insulating warmth;
  • The scrotal skin also contains abundant sweat glands which allow very effective evaporative cooling (Kandeel 1988).

Small changes in testicular temperature are normal

It is normal for a man’s testes to change temperature by several degrees during the course of a day. Changes in posture can have this effect. Testicular temperature is also affected by the cut and fabric of clothing. Jumping into a hot tub or cold pool will temporarily change testicular temperature. The system for keeping the testes cooler than the body can cope with these small or infrequent fluctuations.

Big changes in testicular temperature result in fertility problems

Prolonged or regular exposure to higher temperatures can override the body’s ability to keep the testes cool. For example, prolonged summer heat spells have a strong correlation to decreased conception rates. Men who work in hot environments every day, such as bakers and furnace operators, may have lower fertility than normal (Dada 2003). Even an increase in testicular temperature of only a few degrees, such as in cryptorchid men, can cause infertility.


Before birth, a boy’s testes are formed inside his abdominal cavity. Around the time he is born, the testes drop down through a channel (inguinal canal) and into the scrotum. In cryptorchid boys, one or both of the testes remain inside the abdomen. Doctors usually recommend surgery to move the undescended testis into the scrotum within a year of birth.

It was common knowledge for many centuries that cryptorchid livestock were infertile, but the cause of the infertility was not understood until the early 1920s. A researcher showed that the production of sperm is extremely sensitive to heat, and that the constant exposure of the testes to slightly higher abdominal temperatures resulted in infertility (Steinberger 1959). Even though the testes are kept only a few degrees warmer than normal in cryptorchid men, the mild heating is so consistent that it has a serious impact on the production of sperm.

What happens when the testes are warmer than usual?

Prolonged or regular exposure of the testes to higher than usual temperatures causes a decreased sperm count and decreased swimming strength of the remaining sperm. Researchers are still trying to understand all the ways in which heat affects sperm production. Some known cellular-level effects are:

  • In the nucleus of developing sperm, exposure to heat results in slowed construction of DNA (Steinberger 1991). Mitosis, one form of cell division, stops in heat stressed cells (Sarge 1997).
  • Male rats exposed to heat showed a 60% decrease in production of inhibin. Inhibin is hormone which forms a negative feedback loop with FSH, another reproductive hormone made in the pituitary gland. Low levels of inhibin create an increase in FSH levels. High FSH levels trigger the cells of the testes to protect themselves by eliminating cell-surface FSH receptors (Steinberger 1991).
  • Some stages of developing sperm (pachytene spermatocytes and early spermatids) are particularly susceptible to heat damage (Setchell 1998). These cells undergo programmed cell death as soon as 6 hours after exposure to heat. These developing sperm use multiple chemical pathways to kill themselves; some are similar to the mechanisms used by other cells in the body, some appear unique. Researchers are still trying to understand how germ cells set their heat stress levels lower than the rest of the body’s cells (Izu 2004, Sinha Hikim 2003).

Will heat provide reliable contraception?

In studies of various forms of heat as male contraceptives, participants’ sperm count has typically been suppressed to subfertility levels of less than 20 million sperm per milliliter. An early trial of heat reported sperm counts of 1-4 million sperm per milliliter, yet still provided effective contraception (Mieusset 1985). By comparison, the researchers working toward a hormonal male contraceptive have agreed that less than 1 million sperm per milliliter is their minimum goal; they would be even happier with no sperm in the ejaculate at all (azoospermia).

This seems like a very large discrepancy. How could heat provide effective contraception with such relatively high sperm counts? Heat effects more than just the number of sperm produced – it effects how sperm are shaped (morphology) and how well they swim (motility). In a fertile man, 60-80% of his sperm have normal motility and morphology. A man treated with heat as a contraceptive will have 20-40% motile sperm and 50-60% normal morphology. The World Health Organization uses 2.1 million motile sperm per milliliter as its standard for contraceptive efficacy, and recent studies of heat methods meet this standard.

There are two different approaches to heat as a potential form of male contraception:

  • Suspensories. This method uses the higher temperature of a man’s body to raise testicular temperature 1 - 2.5 ºC. Because the heating is slight, the duration of the treatment must be long to be effective. A typical regimen requires wearing the suspensory briefs every day during waking hours.
  • External heat. This method uses a source of heat such as a hot sitz bath, a sauna, or a specialized electric warming device to raise testicular temperature up to 10 ºC for about 30 minutes. Depending on the heat source, this treatment would be repeated at varying intervals to provide effective contraception. For example, sitz baths of a certain temperature are effective when used daily for three weeks several times a year.

The effectiveness of suspensories as a male contraceptive has been proven in a modern clinical trial. See the suspensories page for further information. There have been no formal trials of external heat as a contraceptive, but there is ample experiential reporting from a Swiss doctor who taught the method to hundreds of men in India between 1930 and 1950. See the external heat page for further information. Both methods have the potential to provide effective, cheap and safe male contraception.

What are the risks of using heat as a contraceptive?

Some researchers have voiced concerns that prolonged or extreme heating could cause permanent damage to the male reproductive system (Kandeel 1988). However, others assert that the heat required to do such damage is outside the range of physical tolerance (Vogeli 1956). Another concern is the genetic integrity of sperm produced after heat treatment stops. Although the children born after various heat clinical trials have all been normal, the potential for genetic abnormalities merits further study.


  • Dada, R, NP Gupta and K Kucheria (2003) “Spermatogenic arrest in men with testicular hyperthermia.” Teratogenesis, Carcinogenesis, and Mutagenesis S1: 235-43.
  • Goodson, ML, and KD Sarge (1995) “Heat-inducible DNA binding of purified heat shock transcription factor 1.” Journal of Biological Chemistry 270(6): 2447-50.

  • Izu, H, S Inouye, M Fujimoto, K Shiraishi, K Naito and A Nakai (2004) “Heat shock transcription factor 1 is involved in quality-control mechanisms in male germ cells.” Biology of Reproduction 70: 18-24.
  • Kandeel, FR, and RS Swerdloff (1988) “Role of temperature in regulation of spermatogenesis and the use of heating as a method for contraception.” Fertility and Sterility 49(1): 1-23.
  • Mieusset, R, H Grandjean, A Mansat and F Pontonnier (1985) Inhibiting effect of artificial cryptorchidism on spermatogenesis.” Fertility and Sterility 43(4): 589-94.
  • Sarge, KD, and KE Cullen (1997) “Regulation of hsp expression during rodent spermatogenesis.” Cellular and Molecular Life Sciences 53(2): 191-7.
  • Setchell, B (1998) “The Parkes lecture: Heat and the testes.” Fertility and Sterility 114(2): 179-94.
  • Sinha Hikim, AP, Y Lue, CM Yamamoto, Y Vera, S Rodriguez, PH Yen, K Soeng, C Wang and RS Swerdloff (2003) “Key apoptotic pathways for heat-induced programmed germ cell death in the testis.” Endocrinology 144(7): 3167-75.
  • Steinberger, E, and WJ Dixon (1959) “Some observations on the effect of heat on the testicular germinal epithelium.” Fertility and Sterility 10(6): 578-95.
  • Steinberger, A (1991) “Effects of temperature on the biochemistry of the testis.” In Zorgniotti (ed.) Temperature and Environmental Effects on the Testes. Plenum Press, NY.
  • Vogeli, M (1956) “Contraception through temporary male sterilization.” Unpublished. Smith College Archives.


More info on heat methods


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