The effect of weak magnetic fields on biosystems is the subject matter of the science of magnetobiology. There are objective factors, due to theory lagging far behind experiment, that are hindering the development of this science. Academic interest in the subject is restrained by the fact that experimental data lack a clear physical explanation. Besides, there is a strong imbalance in how physics and biology are involved in magnetobiology, the former being still in infancy in this respect. It is this imbalance which is currently the driving force for the development of the theory of magnetobiology. This brief analytical review focuses on the physical aspects of magnetobiological research. The task of magnetobiology is to explore the biological effects of weak magnetic fields and to understand mechanisms behind these effects. Magnetobiology is part of a more general issue of the biological impact of weak and hyperweak physico-chemical factors. It is believed that such factors operate even below the trigger threshold for protective biological mechanisms and are therefore capable of accumulating at the subcellular level. The so-called 'kT-problem' is discussed in detail, and the interference mechanisms of the molecular gyroscope and of molecular states in an idealized protein cavity are suggested as candidate solutions.

Effects of weak magnetic fields on biological systems: physical aspects

Based on earlier work by several groups, in 1989 Selkoe and colleagues [1,2] suggested that amyloid beta (A beta) found in cerebral blood vessels, skin tissue, and elsewhere might come from a peripheral source and might contribute to the Alzheimer's disease (AD) pathogenesis. Independently, using four clinical series and four different types of controls, Sobel et al. [3,4] found that having a primary occupation likely to have resulted in medium-to-high extremely low frequency (ELF) electromagnetic field (EMF) exposure significantly increases the risk of AD. The means by which EMF (or any other) exposure might precipitate the Alzheimer pathogenesis are currently unknown. One possibility is that EMF exposure might affect the peripheral or neuronal processing of the amyloid precursor protein. We outlined a cascade of events as a hypothesis of how EMF exposure may be associated with AD onset.

In two published papers, Sobel et al. [3,4] found elevated risk of AD associated with having a primary occupation likely to have resulted in medium-to-high EMF exposure. The four clinical series examined were widely separated by time or distance and the data were collected without any consideration of EMF exposure.

(Table 1) provides information about patients and control subjects and the ascertainment period for each series. The total number of AD patients in the four series was 713 and the total number of control subjects was 627. Surrogate-derived data were used for all patients and for control subjects from Finnish Series 1 and the Rancho Los Amigos Medical Center (RLAMC), Los Angeles, series because these subjects were demented. Following standard practice, we defined high EMF exposure as averaging above 10 milligauss (mG) or often above 100 mG and medium EMF exposure as averaging between 2 and 10 mG or often above 10 mG. We classified all other EMF exposures as low. The …

Electromagnetic field exposure may cause increased production of amyloid beta and eventually lead to Alzheimer's disease

Effects of an ELF (50 Hz, 1 mT) electromagnetic field (EMF) on concentration in visual attention, perception and memory including effects of EMF sensitivity.

EFFECTS OF EXPOSURE TO ELECTROMAGNETIC RADIATION AT 835 MHz ON GROWTH, MORPHOLOGY AND SECRETORY CHARACTERISTICS OF A MAST CELL ANALOGUE, RBL‐2H3

Acute effects of whole body exposure to static magnetic field (SMF) on pharmacologically induced hypertension in a conscious rabbit were evaluated. Hypertensive and vasoconstrictive actions were induced by norepinephrine (NE) or a nonselective nitric oxide synthase (NOS) inhibitor, N(omega)-nitro-l-arginine methyl ester (l-NAME). The hemodynamics in a central artery of the ear lobe was measured continuously and analyzed by penetrating microphotoelectric plethysmography (MPPG). Concurrently, blood pressure (BP) changes in a central artery, contralateral to that of the MPPG measured ear lobe, were monitored. Magnetic flux densities were 5.5 mT (Bmax), the magnetic gradient peaked in the throat at the level of approximately 0.09 mT/mm, and the duration of exposure was 30 min. The results demonstrated that under normal physiological conditions without treatment of pharmacological agents, there were no statistically significant differences in the hemodynamics and BP changes between the sham and the SMF exposure alone. Under pharmacologically induced hypertensive conditions, the whole body exposure to nonuniform SMF with peak magnetic gradient in the carotid sinus baroreceptor significantly attenuated the vasoconstriction and suppressed the elevation of BPs. These findings suggest that antipressor effects of the SMF on the hemodynamics under NE or l-NAME induced high vascular tone might be, in part, dependent on modulation of NE mediated response in conjunction with alteration in NOS activity, thereby modulating BPs.

Anti-pressor effects of whole body exposure to static magnetic field on pharmacologically induced hypertension in conscious rabbits.

Experiments on the effects of extremely-low-frequency (ELF) electric and magnetic fields on cells of the immune system, T-lymphocytes in particular, suggest that the external field interacts with the cell at the level of intracellular signal transduction pathways. These are directly connected with changes in the calcium-signaling processes of the cell. Based on these findings, a theoretical model for receptor-controlled cytosolic calcium oscillations and for external influences on the signal transduction pathway is presented. The authors discuss the possibility that the external field acts on the kinetics of the signal transduction between the activated receptors at the cell membrane and the G-proteins. It is shown that, depending on the specific combination of cell internal biochemical and external physical parameters, entirely different responses of the cell can occur. The authors compare the effects of a coherent (periodic) modulation and of incoherent perturbations (noise). The model and the calculations are based on the theory of self-sustained, nonlinear oscillators. It is argued that these systems form an ideal basis for information-encoding processes in biological systems.

F. Kaiser

Papers

Model for external influences on cellular signal transduction pathways including cytosolic calcium oscillations.