Addictions and cell phone

Dr. Weeks’ Comment: Most users of cell phones would acknowledge the addictive effects of these devices.



By U of Washington psychologist Henry Lai, who specializes in the biological effects of non ionizing radiation .
 When the nervous system or the brain is disturbed, e.g., by RFR, morphological, electrophysiological, and chemical changes can occur. A significant change in these functions will inevitably lead to a change in behavior. Indeed, neurological effects of RFR reported in the literature include changes in blood-brain-barrier, morphology, electrophysiology, neurotransmitter functions, cellular metabolism, calcium efflux, responses to drugs that affect the nervous system, and behavior [for a review of these effects, see Lai, 1994 and Lai et al., 1987a].
 Our research on the effects of RFR exposure on the nervous system covers topics from DNA damage in brain cells to behavior. My research in this area began in 1980 when I investigated the effects of brief exposure to RFR on the actions of various drugs that act on the nervous system. We found that the actions of several drugs- amphetamine, apomorphine, morphine, barbituates, and ethyl alcohol- were affected in rats after 45 min of exposure to RFR [Lai et al., 1983; 1984 a,b]. One common feature of these responses was that they seemed to be related to the activity of a group of neurotransmitters in the brain known as the endogenous opioids [Lai et al., 1986b]. These are compounds that are generated by the brain and behave like morphine. We proposed that exposure to RFR activates endogenous opioids in the brain of the rat [Lai et al., 1984c]. One interesting finding was that RFR could inhibit morphine withdrawal in rats [1986a, which led me to speculate as to whether low-intensity RFR could be used to treat morphine withdrawal and addiction in humans. When I was in Leningrad, USSR in 1989, a scientist informed me that he had read my paper on ‘RFR decreased morphine withdrawal in rats’, and he had been using RFR to treat morphine withdrawal in humans. Also, unknown to us at that time was that the ‘endogenous opioid hypothesis’ could actually explain the increase of alcohol consumption in RFR-exposed rats that we reported in 1984 [Lai et al., 1984b]. In the summer of 1996, the United States Food and Drug Administration approved the use of the drug naloxone for the treatment of alcoholism. Naloxone is a drug that blocks the action of endogenous opioids. Increase in endogenous opioid activity in the brain can somehow cause alcohol-drinking behavior. In addition, our finding that RFR exposure alters the effect of alcohol on body temperature of the rat [Lai et al., 1984b] was replicated by Hjeresen et al. [1988, 1989] at an SAR half of what we used.
 Interactions between RFR with drugs could have important implications on the health effects of RFR. They suggest that certain individuals in the population could be more susceptible to the effects of RFR. For example, an important discovery in this aspect is that ophthalmic drugs used in the treatment of glaucoma can greatly increase the damaging effects of RFR on the eye [Kues et al., 1992].

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