Rachael F. Heller

Membrane Perturbations and Mediation of Gap Junction Formation in Response to Taurine Treatment in Normal and Injured Alveolar Epithelia

Nitrogen dioxide is an air pollutant that causes pulmonary alterations. Employing light and transmission electron microscopy, we examined plastic sections and freeze-fracture replicas of alveolar epithelium of groups of hamsters exposed to nitrogen for 24 h to determine taurine-induced changes in intercellular junctions. Prior to exposure, one group of hamsters was given 0.5% taurine in their drinking water for 2 weeks. A second group of hamsters was given taurine-free water. The taurine-treated group was divided into three subgroups. The first subgroup was exposed to nitrogen dioxide at a concentration of 7 ppm for 24 h, the second subgroup was exposed to nitrogen dioxide at a concentration of 30 ppm for 24 h, and the third subgroup was exposed to normal room air for 24 h. The nontaurine-treated animals were similarly divided into three subgroups and treated as described above. The lungs of the hamsters exposed to nitrogen dioxide without the taurine pretreatment exhibited extensive inflammatory cell infiltration in the walls of the terminal bronchioles, alveolar ducts, and peribronchiolar alveoli. The degree of infiltration was proportional to the degree of nitrogen dioxide concentration. The taurine-treated animals exposed to nitrogen dioxide and the nontaurine-treated animals exposed to room aid did not show any inflammatory infiltrate. Freeze-fracture replicas of the tight junctional regions of the type I and type II pneumocytes revealed significant fragmentation in the nitrogen dioxide-exposed lungs. It was also observed that the tight junctions between the type I pneumocytes of the taurine-treated groups, whether exposed or not, revealed gap junction-like aggregates among the tight junction fibrils. The 30-ppm nitrogen dioxide exposed group exhibited larger and more frequent gap junctions between the pneumocytes than those observed in the 7-ppm nitrogen dioxide exposed group. The evidence suggests that taurine may have an effect on plasma membranes and intercellular communications. Changes in intercellular communication may contribute to decreased susceptibility to injury and increased pneumocyte survival.

Hyperinsulinemic obesity and carbohydrate addiction: the missing link is the carbohydrate frequency factor

It is proposed that chronic hyperinsulinemia is largely responsible for hunger, cravings and weight gain observed in many obese. This form of obesity can be treated by decreasing frequency of daily intake of carbohydrates to one well-balance meal each day and allowing for additional meals that are low in fat, low carbohydrates and high fiber. Animal experimentation and epidemiological evidence support the role of chronic hyperinsulinemia as a major factor in obesity and accounts for the frequent failures of diet and behavioral modification programs. Chronic hyperinsulinemia upsets metabolic balances and favors anabolic metabolism; fosters carbohydrate cravings; promotes insulin resistance which further promotes anabolic metabolism; and insulin resistance in turn exacerbates chronic hyperinsulinemia. This vicious cycle maintains excess weight and defeats diet and behavioral modification attempts to treat obesity. An eating program focused on reduction of chronic hyperinsulinemia coupled with appropriate exercise and behavior modification can successfully and permanently bring down cravings, hunger and body weight.

Profactor-H (elevated circulating insulin): The link to health risk factors and diseases of civilization

We propose the term Profactor-H for chronic elevated circulating insulin. Profactor-H is common in atherosclerosis, essential hypertension, non-insulin dependent diabetes mellitus, some forms of obesity, some forms of cancer, cardiovascular disease, peripheral vascular disease and some forms of stroke. Profactor-H appears to be the central pathophysiologic consideration in the etiology of many diseases and health risk factors. Profactor-Hs impact depends on genetic predisposition, frequency consumption of refined simple and complex carbohydrates, deficiency in dietary chromium, sedentary life style and stresses of modern day living. In many obese individuals, Profactor-H disturbs metabolic balance, favoring anabolic metabolism, and is exacerbated through chronic insulin production and impairment of insulin action. This vicious cycle also appears to be common in many apparently healthy, non-obese individuals destined to develop health risks and diseases in response to long-term adverse consequences of Profactor-H. We believe that a four-pronged program which 1) reduces the daily frequency of carbohydrate consumption, particularly refined foods and simple sugars, 2) supplements the daily dietary intake of chromium, 3) encourages activity, and 4) reduces stress, will minimize the impact of Profactor-H and thereby reduce health risks and result in improved health.