Answer From Brent A. Bauer, M.D.
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An infrared sauna is a type of sauna that uses light to make heat. This type of sauna is sometimes called a far-infrared sauna. "Far" describes where the infrared waves fall on the light spectrum. A regular sauna uses heat to warm the air, which in turn warms your body. An infrared sauna heats your body directly without warming the air around you.
Generally, people like saunas because they cause reactions like those caused by moderate exercise, such as vigorous sweating and an increased heart rate. An infrared sauna gives these results at lower temperatures than does a regular sauna. This makes an infrared sauna a choice for people who can't stand the heat of a sauna. But does that mean there are clear health benefits? Perhaps.
Many studies have looked at using infrared saunas in the treatment of long-lasting health problems and found some proof that saunas may help. Conditions studied include high blood pressure, heart failure, dementia and Alzheimer's disease, headache, type 2 diabetes, and arthritis. But larger and more-exact studies are needed to prove these results. Some of these studies were also performed with people using a regular sauna.
On the other hand, no harmful effects have been reported with infrared saunas. So if you're thinking of trying a sauna to relax, an infrared sauna might be an option.
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Ishibashi et al. [ 8 ] did an in vitro study with five human cancer cell lines (A431, vulva; HSC3, tongue; Sa3, gingival; A549, lung; and MCF7, breast) to assess the effects of FIR irradiation. For that purpose, they used a tissue culture incubator with an imbedded FIR lamp that could continuously irradiate cells with FIR (lamp operating wavelength range being 4&#;20 μm with an emission peak height at 7 &#;12 μm). The overall observation was that the FIR effect varied in these five cancer cell line types, as can be expected. The study results showed that basal expression level of heat shock protein (HSP) 70A mRNA was higher in A431 and MCF7 cell lines in comparison with the FIR-sensitive HSC3, Sa3, and A549 cell lines. The study showed that the over expression of HSP70 inhibited FIR-induced growth arrest in HSC3 cells, and that HSP70 siRNA inhibited the proliferation of A431 cells after FIR treatment. A summary of the results of this study indicated that the proliferation-suppressing effect of FIR, in some cancer cell lines, is controlled by the basal expression level of the HSP70A. These findings suggest that FIR irradiation may be used as an effective medical treatment avenue for some cancer cells which have low levels of HSP70.
Along the same lines, Akasaki et al. [ 7 ] studied in vivo the effects of repeated FIR irradiation on angiogenesis in a mouse model of hindlimb ischemia. Following reports that FIR therapy upregulated the expression of arterial eNOS in hamsters (and it is known that NO constitutively produced by eNOS plays an important role in angiogenesis) they took a step further to investigate whether the FIR therapy increases angiogenesis in mice with the hindlimb ischemia. In their study, unilateral hindlimb ischemia was induced in apolipoprotein E-deficient mice and the group to receive the FIR irradiation was placed in a FIR dry sauna at 41°C for 15 min and then at 34°C for 20 min once daily, with total duration of the experiment of 5 weeks. Laser-Doppler perfusion imaging demonstrated that at the ischemic limb, blood perfusion ratio in the irradiated group increased significantly in comparison with the control group (0.79±0.04 vs. 0.54±0.08, p<0.001). Also, in the treated group, significantly greater capillary density was observed (757±123 per mm 2 vs. 416±20 per mm 2 , p<0.01). Western blotting showed that thermal therapy has increased markedly the hindlimb eNOS expression. Furthermore, to study possible involvement of eNOS in thermally induced angiogenesis, the same FIR therapy was given to mice with hindlimb ischemia with or without N(G)-nitro-L-arginine methyl ester (L-NAME) administration for the duration of 5 weeks. It was observed that L-NAME treatment eliminated angiogenesis induced using the FIR thermal therapy and that the therapy did not increase angiogenesis in eNOS-deficient mice. The study led to the conclusion that angiogenesis can be induced via eNOS using FIR thermal therapy in mice with hindlimb ischemia.
There have been a few laboratory studies that have reported the biological effects of FIR. A recent important paper describes the in vitro use of an FIR generator (WS TY-301R ® ; M/s WS Far Infrared Medical Technology Co., Ltd., Taipei, Taiwan; see ) as a radiation source to irradiate human umbilical vein endothelial cells (HUVECs) [ 4 ]. In the study, FIR exposure (a low non-thermal irradiance) of 0.13 mW/cm 2 for 30 min inhibited proliferation and the vascular endothelial growth factor (VEGF)-induced phosphorylation of extracellular signal-regulated kinases in HUVECs. Furthermore, FIR exposure induced the phosphorylation of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) generation in VEGF-treated HUVECs. Both VEGF-induced NO and reactive oxygen species (ROS) generation was involved in the inhibitory effect of FIR. Nitrotyrosine formation increased significantly in HUVECs treated with VEGF and FIR together. Inhibition of phosphoinositide 3-kinase (PI3K) by wortmannin abolished both the FIR-induced phosphorylation of eNOS and serine/threonine-specific protein kinase in HUVECs. In addition to that, FIR exposure upregulated the expression of PI3K p85 at the transcriptional level. It was observed that FIR exposure induced the nuclear translocation of promyelocytic leukemia zinc finger protein in the cells. These data provide information on how FIR exposure could affect microcirculation, independent from thermal effects. The same group had previously shown that non-thermal FIR therapy increased skin blood flow in rats [ 5 ]. Toyokawa et al. [ 6 ] used home-made ceramic FIR emitters to stimulate full thickness excisional skin wound healing in rats. After constant exposure to FIR, wound healing was significantly quickened and transforming growth factor (TGF)-beta1 expressing myofibroblasts and collagen content were increased.
There have been many attempts to use FIR as a therapeutic intervention where devices known as &#;infrared heat lamps&#; that emit more or less FIR are been used. Unfortunately, &#; pure &#; FIR emitting lamps are expensive, and thus, in some instances lamps that have &#;mixed&#; emission, i.e., emit in shorter (mid infrared, MIR; near infrared, NIR and even visible light) wavelength ranges are been used. A common type of specialized infrared heat lamp emits 2&#;25 μm radiation. IR saunas are often used and the most effective types have ceramic FIR emitting panels that remain cool to the touch. However, most IR saunas on the market do not use the expensive FIR panels, which can be touched since they remain always cold.
FIR emitting ceramics have been known for some time [9, 10]. All ceramics have the property of emitting IR radiation depending on their temperature. In the age of gas lighting, ceramic mantles were heated by gas flames to emit both IR and visible radiation depending on the temperature attained. The exact chemical composition of the ceramic material governs the relationship between the temperature and the amount of IR radiation. The radiated energy follows the Stefan-Boltzmann law which says that the total energy radiated per unit of surface area per unit of time is directly proportional to the fourth power of the black body&#;s absolute temperature. The wavelength range also depends strictly on the temperature according to Wien&#;s displacement law [11].
The boron-silicate mineral, tourmaline (known as a gemstone in its crystalline form) when milled into fine powders also emits FIR [12] and the characteristics of the FIR emission depend on the particle size. Preparations containing tourmaline powder have been applied to the skin with the aim of affecting the blood flow [13]. In a similar manner discs of FIR emitting ceramics have been attached to the skin with the intent of producing a beneficial effect (see later).
Small particles (nanoparticles and microparticles) of FIR-emitting ceramic material have been incorporated into fibers that are then woven into fabrics. These fabrics can be manufactured into various garments that can be worn on different parts of the body.
When FIR emitting ceramics or fabrics are employed as therapeutic devices, it is pertinent to analyze the thermodynamics of the process. The first law of thermodynamics states that energy can neither be created nor destroyed. Heat (molecular vibrational energy) is transferred from one body to another in three forms: radiation, convection and conduction. Thus, it is clear that the principle source of energy needed to power the FIR emission from the garments comes from the human body, since it is at a significantly higher temperature than the surrounding air. So energy from the human body is transferred to these ceramic particles, which are acting as &#;perfect absorbers&#;, maintain their temperature at sufficiently high levels and then emit FIR back to the body. It is plausible that FIR emitted from the skin is absorbed by the ceramic particles, which then re-emit the same FIR back to the skin. Although this may appear to be an energy neutral process and to cancel itself out, this is not in fact the case because the FIR emitting material will prevent the loss of FIR that would otherwise have escaped through normal clothing. However the same effect could have been achieved with a FIR reflective foil suit or suchlike. Other sources of heat that can transfer energy from the body to the ceramic particles with a net gain of FIR are either convection, conduction, or both. The balance between conduction and convection will depend on how close the contact is between the garment and the skin. If the garment is skin tight, then conduction may be important, while if it is loose fitting then convection (heating up a layer of air between the skin and the garment) may be important.
Ting-Kai Leung and colleagues have studied the effect of FIR-emitting ceramic powders in a range of biological studies [14 &#;19]. In one set of studies, they cultured murine myoblast cells (C2C12) with bags of ceramic powder under the culture plates and found that FIR irradiation improved cell viability and prevented lactate dehydrogenase release under hydrogen peroxide (H2O2)-mediated oxidative stress, and also elevated the intracellular levels of NO and calmodulin [14]. In the study, they used electro-stimulation of amphibian skeletal muscle and found that FIR emitting ceramics delayed the onset of fatigue, induced by muscle contractions [14]. In another set of studies, they showed that ceramic-emitted FIR (cFIR) could increase the generation of intracellular NO in breast cancer cells [15] and inhibit growth of murine melanoma cells [16]. Similarly, they found that cFIR increased calmodulin and NO production in RAW 264.7 macrophages [17]. cFIR also has been shown to increase the viability of murine macrophages with different concentrations of H2O2 [15]. In this study [15] it was shown that cFIR significantly inhibited intracellular peroxide levels and lipopolysaccharide (LPS)-induced peroxide production by macrophages. In the same study, it was also demonstrated that cFIR blocked ROS-mediated cytotoxicity (shown by measurements of cytochrome c and the ratio of NADP+/NADPH) [15].
The same research group went on to study a rabbit model of rheumatoid arthritis in which rabbits received intra-articular injections of LPS to induce inflammation that mimics the rheumatoid arthritis [18]. Fluorodeoxyglucose(18F) coupled with positron emission tomography (FDG-PET) scans were used to monitor the inflammation in 16 h and 7 days after the LPS injection. Rabbits to be treated with cFIR were placed in a cage surrounded by paper sheets impregnated with a thin layer of the ceramic powder, while the control group was surrounded by the same sheet without the material. Comparison of the final and initial uptakes of FDG isotopes in the LPS-injected left knee-joints of the rabbits indicated larger decreases in the cFIR exposed group than in the control group indicating that FIR reduced inflammation.
In their most recent study the Leung group studied the repair effect of cFIR in human breast epithelial cells (MCF-10A) after H2O2 and after ionizing radiation from an X-ray source [19]. Their results show that in both, H2O2 toxicity and radiation exposure models, the cFIR treated cells demonstrated significantly higher cell survival rates than the control groups. In view of the experimental results and taking into account the relationship between indirect ionizing radiation and the oxidative stress-induced cell damage, and accumulation of free radicals, they proposed that the ionizing radiation protective ability of cFIR occurs predominantly through an antioxidant mechanism. They are suggesting that cFIR provides cells with a defensive mechanism during the irradiation process and promotes cell repair during post exposure period through hydrogen peroxide scavenging and COX-2 inhibiting activities.
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