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Influences on skeletal mineralization in children and adolescents: Evidence for varying effects of sexual maturation and physical activity medicine cards buy 15mg remeron otc. Reduced rates of skeletal remodeling are associated with increased bone mineral density dur ing the development of peak skeletal mass 9 medications that cause fatigue order remeron 15 mg with visa. Dietary intake of fat symptoms 7 dpo bfp order 30mg remeron amex, fiber medicine for yeast infection discount remeron 30 mg without a prescription, and other nutrients is related to the use of vitamin and mineral supplements in the United States: the 1992 National Health Interview Survey. Effect of dietary calcium and phospho rus levels on the utilization of iron, copper, and zinc by adult males. Magne sium kinetics in adolescent girls determined using stable isotopes: Effects of high and low calcium intakes. Calcium supplementation and plasma ferritin concentrations in premenopausal women. Effects of vitamin D and calcium on markers of bone metabolism in geriatric patients with low serum 25-hydroxyvitamin D levels. The relationship of bone mass and frac ture history to fluoride and calcium intake: A study of three communities. A prospective study of bone mineral content and fracture in communities with differential fluoride exposure. Dietary Reference Intakes: the Essential Guide to Nutrient Requirements. A prospective study of bone density and pregnancy after an extended period of lactation with bone loss. Biochemical markers of bone turnover in lactating and nonlactat ing postpartum women. Evidence for an interaction between calcium intake and physi cal activity on changes in bone mineral density. Cyclical serum 25-hydroxyvitamin D concentrations paralleling sunshine exposure in exclusively breast-fed infants. Sunshine expo sure and serum 25-hydroxyvitamin D concentrations in exclusively breast-fed infants. Calcium regulating hormones and minerals from birth to 18 months of age: A cross sectional study. Effects of sex, race, age, season, and diet on serum miner als, parathyroid hormone, and calcitonin. Effect of vegetarian diet on serum 1,25-dihydroxyvitamin D concentrations during lactation. Changes in calcium homeostasis over the first year postpartum: Effect of lactation and weaning. Low serum calcium and high parathyroid hormone levels in neonates fed “humanized” cows milk based formula. Randomized trial of varying mineral intake on total body bone mineral accretion during the first year of life. Effect of phosphorus on the absorp tion of calcium and on the calcium balance in man. Dietary Reference Intakes: the Essential Guide to Nutrient Requirements. Comparison of oral 25-hydroxycholecal ciferol, vitamin D, and ultraviolet light as determinants of circulating 25-hy droxyvitamin D. Hematuria associated with hypercalciuria and hyperuricosuria: A practical approach. The reduction of growth-promoting and calcifying properties in a ration by exposure to ultraviolet light. Bone mineralization and growth in term infants fed soy-based or cow milk-based formula. Trabecular bone density in a two year controlled trial of peroral magnesium in osteoporosis. Caries prevalence in northern Scotland before, and 5 years after, water defluoridation. Target cells for 1,25 dihydroxyvitamin D3 in intestinal tract, stomach, kidney, skin, pituitary, and parathyroid. A comparison of symptoms after the consumption of milk or lactose-hydrolyzed milk by people with self-reported severe lactose intolerance. Postnatal development of renal hydrogen ion excretion capacity in relation to age and protein intake. Dietary Reference Intakes: the Essential Guide to Nutrient Requirements. Risk factors in the pathogenesis of arteriosclerotic heart disease and generalized atherosclerosis. Failure of magne sium supplementation to influence marathon running performance or recov ery in magnesium-replete subjects. Axial and peripheral bone density and nutrient intakes of postmenopausal vegetarian and omnivo rous women. Longitudinal monitoring of bone mass accumulation in healthy adoles cents: Evidence for a marked reduction after 16 years of age at the levels of lumbar spine and femoral neck in female subjects. Alterations of red cell glycolytic intermediates and oxygen transport as a consequence of hypophosphatemia in patients receiving intra venous hyperalimentation. The use of epidemiological approaches and meta-analysis to deter mine mineral element requirements. Dietary factors in bone health of elderly lacto ovovegetarian and omnivorous women. Dietary Reference Intakes: the Essential Guide to Nutrient Requirements. Late infantile tetany and secondary hyperparathyroidism in infants fed humanized cow milk formula. Quantification and kinetics of 25-hydroxyvitamin D3 by isotope dilution liquid chromatogra phy/thermospray mass spectrometry. Calcium supplementation during pregnancy may reduce preterm delivery in high-risk populations. Subclinical vitamin D deficiency in postmenopausal women with low vertebral bone mass. Trends in Childhood Use of Dental Care Products Containing Fluoride: United States, 1983–1989. The influence of numerous pregnancies and lactations on bone dimensions in South African Bantu and Caucasian mothers. The effect of lactation on peak adult shaft and ultra distal forearm bone mass in women. Postmenopausal bone loss at multiple skeletal sites: Relationship to estrogen use. Dietary Reference Intakes: the Essential Guide to Nutrient Requirements. Serum inorganic fluoride: Changes re lated to previous fluoride intake, renal function and bone resorption. Influence of season and latitude on the cutaneous synthesis of vitamin D3: Exposure to winter sunlight in Boston and Edmonton will not promote vitamin D3 synthesis in human skin. Sunlight regulates the cutaneous pro duction of vitamin D3 by causing its photodegradation. An evaluation of the relative contributions of exposure to sunlight and of diet to the circulating concentra tions of 25-hydroxyvitamin D in an elderly nursing home population in Bos ton. Death resulting from overzealous total parenteral nutrition: the refeeding syndrome revisited. Serum and mononuclear cell potassium, magnesium, sodium and cal cium in pregnancy and labour and their relation to uterine muscle contrac tion. Comparison of in vitro and in vivo tests for deter mination of availability of calcium from calcium carbonate tablets. Dietary Reference Intakes: the Essential Guide to Nutrient Requirements. Assessment of Fracture Risk and its Applica tion to Screening for Postmenopausal Osteoporosis. Prepared in collaboration with the Food and Agriculture Organization of the United Nations and the International Atomic Energy Agency. Dietary calcium, physical activity, and risk of hip fracture: A prospective study.

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When sulfate is consumed in the form of soluble sulfate salts medications given during dialysis best remeron 15mg, such as potassium sulfate or sodium sulfate medicine definition order remeron 15mg with mastercard, more than 80 percent is absorbed medicine 100 years ago buy discount remeron 15mg. When sulfate is consumed as insoluble salts medications requiring central line remeron 15mg low price, such as barium sulfate, almost no absorption occurs. Unabsorbed sulfate is excreted in the fe ces, reabsorbed in the colon, or reduced by anaerobic bacteria to metabolites. In addition to dietary sulfate intake from food and water, sulfate is derived in the body from methionine and cysteine found in dietary protein and the cysteine component of glutathione. In fact, most body sulfate is produced from the amino acids methionine and cysteine, both of which contain sulfur and are obtained from dietary protein and body protein turnover. Sulfate re quirements are thus met when intakes include recommended levels of sulfur amino acids. Because there is no information from national surveys on sulfate intakes or on supplement usage, the risk of adverse effects within the United States or Canada cannot be characterized. The remaining approximately 64 percent comes from organic com Copyright © National Academy of Sciences. Dietary Reference Intakes: the Essential Guide to Nutrient Requirements. Foods found to be high in inorganic sulfate include dried fruits, certain commercial breads, soya flour, and sausages. Beverages found to be high in sulfate include select juices, beers, wines, and ciders. An analysis of the sulfate content of various diets using foods purchased at supermarkets suggested a large variation in daily inorganic sulfate intake, ranging from 0. The sulfate content of drinking water highly varies depending on where in the country it was obtained. Distilled water contains very little, if any, sul fate, and deionized water contains no sulfate. Dietary Supplements Some people self-prescribe sulfur-containing compounds such as chondroitin sulfate, glucosamine sulfate, and methylsulfonylmethane as possible aids to bones and joints. Evidence has been presented suggesting that the beneficial effects of glucosamine sulfate for osteoarthritis may be due more to the sulfate than to the glucosamine contained in the compound. Thus, a defi ciency of sulfate is not found in people who consume normal protein intakes containing adequate sulfur amino acids. Ingestion of methionine, cysteine, and glutathione in foods, along with consumption of other sulfated compounds in both food and beverages, is sufficient to meet the bodys requirement for sulfate. Research with animals has shown that growth is stunted when dietary sul fate is removed from the food and water supply, and when sulfur amino acids, Copyright © National Academy of Sciences. Dietary Reference Intakes: the Essential Guide to Nutrient Requirements. Osmotic diarrhea resulting from unab sorbed sulfate has been reported and may be of particular concern in infants who consume fluids that are derived from water sources with high levels of sulfate. Sulfate and undigested sulfur compounds have been implicated in the etiology of ulcerative colitis. High levels of hydrogen sulfide, produced in the colon from sulfate by sulfate-reducing bacteria, are thought to overburden mucosal detoxification systems, causing the colonic epithelial inflammation of ulcerative colitis. However, the possible link between dietary sulfate, colonic hydrogen sulfide levels, and ulcerative colitis has not been adequately evaluated. Special Considerations Kidney failure: Increased blood sulfate levels are a common feature of kidney failure. High serum sulfate levels may play a role in parathyroid stimulation and homocysteinemia, both of which commonly occur in people with chronic kid ney disease. Dietary Reference Intakes: the Essential Guide to Nutrient Requirements. Foods found to be high in inorganic sulfate include dried fruits, certain commercial breads, soya flour, and sausages. Beverages found to be high in sulfate include select juices, beers, wines, and ciders. Sulfate is also present in many other sulfur-containing compounds in foods, providing the remaining approximately 64 percent of total sulfate available for bodily needs. Thus, a deficiency of sulfate is not found in people who consume normal protein intakes containing adequate sulfur amino acids. Dietary Reference Intakes: the Essential Guide to Nutrient Requirements. Dietary Reference Intakes: the Essential Guide to Nutrient Requirements. It facilitates several enzy matic processes related to the metabolism of protein, carbohydrates, and Z fats. Zinc also helps form the structure of proteins and enzymes, and is involved in the regulation of gene expression. The adult requirements for zinc are based on metabolic studies of zinc absorption, defined as the minimum amount of dietary zinc necessary to offset total daily losses of the nutrient. Foods rich in zinc include meat, some shellfish, legumes, fortified cereals, and whole grains. Overt human zinc deficiency is rare, and the signs and symp toms of mild deficiency are diverse due to zincs ubiquitous involvement in metabolic processes. There is no evidence of adverse effects from intake of natu rally occurring zinc in food. The adverse effects associated with chronic intake of supplemental zinc include acute gastrointestinal effects and headaches, im paired immune function, changes in lipoprotein and cholesterol levels, reduced copper status, and zinc–iron interactions. Its biological functions can be divided into catalytic, structural, and regulatory. It is necessary for the structure of certain proteins, some of which are involved in gene expression as deoxyribonucleic acid–binding transcription factors. Zinc also provides a structural function for some en zymes, the most notable of which is copper–zinc superoxide dismutase. Addi tionally, zinc plays a role in gene expression and has been shown to influence both apoptosis and protein kinase C activity. Dietary Reference Intakes: the Essential Guide to Nutrient Requirements. The mechanism of absorption appears to be saturable and there is an increase in transport velocity with zinc depletion. The absorbed zinc is bound to albumin and transferred from the intestine via the portal system. More than 85 percent of the bodys total zinc is stored in the skeletal muscle and bone; only about 0. However, the body tightly regulates plasma zinc concentrations to keep them steady at about 10–15 mmol/L. Factors such as stress, acute trauma, and infec tion can cause plasma zinc levels to drop. In humans, plasma zinc concentra tions will remain relatively stable when zinc intake is restricted or increased, unless these changes in intake are severe and prolonged. This tight regulation also means that small amounts of zinc are more efficiently absorbed than large amounts and that people in poor zinc status can absorb the nutrient more effi ciently than those in good status. Normal zinc losses may range from less than 1 mg/day with a zinc-poor diet to greater than 5 mg/day with a zinc-rich diet. Zinc loss through the urine represents only a fraction (less than 10 percent) of normal zinc losses, although urinary losses may increase with conditions such as starvation or trauma. Other modes of zinc loss from the body include skin cell turnover, sweat, semen, hair, and menstruation. Zinc absorption is defined for this purpose as the minimum amount of absorbed zinc necessary to match total daily zinc losses. Special Considerations Children aged 3 years and under: the absorption of zinc from human milk is higher than from cow milk–based infant formula and cow milk. The zinc bioavailability from soy formulas is significantly lower than from milk-based formulas. Zinc nutriture in later infancy is quite different from that in the younger infant. Dietary Reference Intakes: the Essential Guide to Nutrient Requirements.

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The clini should be carried out against nicotine on behalf of their cal picture varies from menstrual abnormalities medications given for migraines purchase 30 mg remeron free shipping, galac fertility and future maternity (17) treatment plan for anxiety cheap 15 mg remeron amex. It is recommended that serum prolactin is measured – Increased levels of testosterone and androstene twice before sellar imaging is requested treatment plan for depression order remeron 30 mg on line, particularly in dione symptoms mono remeron 15 mg, as well as its raised conversion rate to E2. The main changes ex Cushings disease plaining infertility in patients with hypothyroidism are (26): Menstrual dysfunction and decreased fertility are – Altered peripheral estrogen metabolism: de common fndings in this syndrome. Hiperthyroidism Subclinical hypothyroidism the prevalence of primary or secondary infertility as According to the Endocrine Society (27), studies are sociated with hyperthyroidim was described to be 5. Nowadays, the prevalence of irregular cycles is cal hypothyroidism and subclinical hyperthyroidism 21. Concomitant diseases, such as autoimmune tibodies in the rst trimester will develop postpartum thyroid disease and premature ovarian insuffciency thyroiditis. In particular, reduced secre (follicular) phase of the menstrual cycle may result in tion of adiponectin has a crucial role not only in induc inadequate endometrial maturation and impaired em ing insulin resistance, but also in determining the clus bryo implantation (2,29). Increased leptin secretion may be responsible Addisons disease for sympathetic nervous system overactivity and hyper Primary adrenal insuffciency (Addisons disease) is tension, while reduced omentin may have an important characterized by defciency of cortisol, aldosterone and permissive role in the development of atherogenic pro androgen hormonal precursors, usually caused by an cesses. Other adipokines (resistin, visfatin) determine autoimmune reaction towards the adrenal cortex. Even and modulate the infammatory process, which is an es with state-of-the-art replacement therapy with miner sential component of cardiovascular risk. So, hyperprolactinemia should be cal hyperandrogenism and one other criterion for diag treated with dopamine agonists, hypothyroidism re nosis (35). These Pregnancy rates range from 80% to 93% after 6 and 12 patients had a normal body mass index, insulin sensi months respectively, and are mostly single (39). The luteal phase is usu of the follicular pool, or can be attributed to follicular ally supplemented with progesterone. Resistant women, or those who tor produced solely by small, growing follicles in the do not conceive after six months should be offered go 150 Arq Bras Endocrinol Metab. Assessment and a cumulative pregnancy rate of 55% to 70%, with of changes in volume and vascularity of the ovaries during the rates of ovarian hyperstimulation syndrome and mul normal menstrual cycle using three-dimensional power Doppler tiple pregnancy of less than 1% and 6%, respectively. The future for genetic described that co-treatment with metformin and clo studies in reproduction. Risk-taking behaviours and beliefs about fertility in university rates, but not livebirth rate compared with clomiphene students. The relevance of age in resistant to clomiphene, metformin association was de female human reproduction-current situation in Switzerland and pathophysiological background from a comparative perspective. Yilmaz N, Kilic S, Kanat-Pektas M, Gulerman C, Mollamahmutoglu drug is usually not associated with ovarian hyperstimu L. Int J Eat Disclosure: no potential confict of interest relevant to this article Disord. Diagnosis and treatment of hyperprolactinemia: an Endocrine Society clinical practice guideline. Menstrual irregularities and lactation failure may precede thyroid 1991;19(8):597-604. Day 3 serum inhibin-B is predictive of assisted Endocrinologists and the American Thyroid Association. Stagnaro-Green A, Abalovich M, Alexander E, Azizi F, Mestman for the polycystic ovary syndrome: the complete task force J, Negro R, et al. Measuring anti-Mullerian congenital adrenal hyperplasia due to 21-hydroxylase deffciency. Revised 2003 consensus on diagnostic criteria and long women with polycystic ovary syndrome, oligo amenorrhoea and term health risks related to polycystic ovary syndrome. Azziz R, Carmina E, Dewailly D, Diamanti-Kandarakis E, Escobar polycystic ovary syndrome: a systematic review. This affects 15–20% A male factor contributes to infertility in approximately 50% of I of couples. Evaluating the fertility potential of specialist, and gives an overview of the specialist management the male partner represents an important part in the assessment of male infertility. This evaluation should be performed simultaneously with the evaluation of Discussion the female partner, but it is not performed in at least 18% of cases. Male infertility is associated with 12 months of regular, unprotected sexual intercourse, a screening poorer overall health, increased cancer risk and decreased life expectancy. For the male partner this includes history, physical examination, endocrine assessment important role in maximising the fertility potential and improving and semen analysis. Several lifestyle and environmental factors the overall health of the male patient. Causes Male infertility can be caused by a wide range of conditions, encompassing anatomical or genetic abnormalities, systemic or neurological diseases, infections, trauma, iatrogenic injury, gonadotoxins and development of sperm antibodies (Table 1). In 30–40% of male infertility cases, no cause is identified (idiopathic male infertility). Causes of male infertility stratifed by mechanism male partner because of prior history or comorbidities. Men who Pre-testicular are not trying to conceive but have concerns about their fertility can be offered a screening evaluation after appropriate counselling. This includes a detailed reproductive and • Cryptorchidism • Klinefelter syndrome sexual history, followed by a thorough past general medical and • Testicular cancer • Environmental surgical history, exposures and lifestyle, family history, and review • Radiation • Infection of systems. An • Chemotherapy or • Injury or trauma assessment tool that can be used in clinical practice is available pharmacological • Primary ciliary dyskinesia from Andrology Australia ( Post-testicular Physical examination • Coital • Youngs syndrome the main goals of the physical examination are to determine: • Pharmacological • Nerve injury • penile anatomy • Retrograde ejaculation • Spinal cord injury • degree of virilisation • Congenital bilateral absence of • Retroperitoneal lymph node • testicular and epididymal characteristics (ie presence, size, the vas deferens dissection • Ejaculatory duct obstruction or • Systemic disease consistency) seminal vesicle dysfunction • presence of vasa deferentia • Vasectomy or Iatrogenic injury to • presence of varicoceles the vas deferens • abnormalities on digital rectal examination • evidence of previous inguinal, scrotal, pelvic or abdominal Box 1. The prostate, bladder relationship between these hormones allows the source of the • Genital: sexually transmissible infection, epididymo-orchitis, scrotal pain abnormality to be determined in most cases. Typical hormonal • Urinary: lower urinary tract symptoms, prostatitis • Exposures: alcohol, smoking, occupational, environmental, lifestyle (heat profiles of different clinical scenarios are presented in Table 2. Causes include congenital syndromes, brain tumours, infiltrative diseases, trauma, drugs, infection or systemic illness. Management is Spermatogenesis requires a certain level of intratesticular contingent on the primary aetiology. Key aspects of the physical examination infertile and have hormonal abnormalities is complex and requires Physical examination specialist input. Adequate collection of semen • Penis: position of meatus specimen is paramount to obtain a representative result. Different • Scrotum: abstinence periods have been suggested, but two to three – Testicular size, consistency, presence of masses, location days of abstinence may be optimal. The repeat semen analysis is General practice management recommended after one to three months for those with mild or Male fertility can be affected by several lifestyle and environmental moderate derangements, and within two to four weeks for those factors. Patients should be treated as per sensitivities, and in stress and improve semen quality in several small studies case of sexually transmissible infection, the partner also needs without pregnancy and live birth outcomes. Semen analysis – World Health Organization specialist 8 reference values Indications for referral to a specialist in male infertility include: Volume 1. Patient counselling recommendations1 specialist may choose to further investigate and treat a patient Alcohol Consumption of up to three to four units per who has been referred. Smoking Associated with decreased semen quality Obesity Obesity (body mass index >30 kg/m2) is likely Specialist investigation of the male partner to reduce fertility Once a patient is referred to a specialist, a more detailed Scrotal temperature Scrotal exposure to elevated temperatures is investigation of the male partner is done according to findings associated with reduced semen quality from the basic evaluation. Prescription, over Certain drugs can interfere with fertility (eg Post-ejaculatory urine analysis the-counter and testosterone, opioids, psychotropic agents, recreational drugs cannabis) An examination of post-ejaculatory urine allows for exclusion Occupation Certain occupations that involve exposures to of retrograde ejaculation, and is indicated in patients with an heat, ionising radiation, vibrations, pesticides ejaculate volume <1. In patients with azoospermia, detection of any sperm suggests retrograde ejaculation. In patients with low-ejaculate Testicular biopsy and/or fne needle aspiration volume and oligospermia, there is no consensus on the number Diagnostic fine needle aspiration and/or testicular biopsy were of sperm that should be considered significant, as even in historically used to differentiate patients with obstructive and non individuals who are considered normal, there are sperm obstructive azoospermia. However, it has been demonstrated that present in the post-ejaculatory urine analysis. Anti-sperm antibodies can be prognostic information that helps direct further management. Sperm-bound antibodies can decrease motility, block penetration Overview of specialist management of the cervical mucus and prevent fertilisation. This may involve surgery, use of a dopamine infertile, and is associated with worse pregnancy outcomes. Hypogonadotropic hypogonadism tests may provide some prognostic information, its role in of hypothalamic origin can be managed with gonadotropin management of an infertile male is yet to be established. Varicoceles can be corrected by surgical bilateral absence of the vas have other genitourinary anomalies, ligation (eg open, microscopic, laparoscopic) or embolisation.

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In this unseen world minute causes produce mighty effects; the effect medications elderly should not take remeron 30 mg discount, moreover symptoms 6 weeks pregnant quality 15mg remeron, is often seemingly unrelated to the cause symptoms 4-5 weeks pregnant buy discount remeron 15mg on-line, appearing in a part of the body remote from the area where the original injury was sustained treatment definition math remeron 15 mg for sale. When one is concerned with the mysterious and wonderful functioning of the human body, cause and effect are seldom simple and easily demonstrated relationships. To discover the agent of disease and death depends on a patient piecing together of many seemingly distinct and unrelated facts developed through a vast amount of research in widely separated fields. We are accustomed to look for the gross and immediate effect and to ignore all else. Unless this appears promptly and in such obvious form that it cannot be ignored, we deny the existence of hazard. Even research men suffer from the handicap of inadequate methods of detecting the beginnings of injury. The lack of sufficiently delicate methods to detect injury before symptoms appear is one of the great unsolved problems in medicine. Despite the absence of sudden and dramatic symptoms, one who handles such materials is unquestionably storing up toxic materials in his body. Storage of the chlorinated hydrocarbons, as we have seen, is cumulative, beginning with the smallest intake. On examination his fat was found to contain stored dieldrin, which had been metabolised as he lost weight. Several years ago the Journal of the American Medical Association warned strongly of the hazards of insecticide storage in adipose tissue, pointing out that drugs or chemicals that are cumulative require greater caution than those having no tendency to be stored in the tissues. The adipose tissue, we are warned, is not merely a place for the deposition of fat (which makes up about 18 per cent of the body weight), but has many important functions with which the stored poisons may interfere. Furthermore, fats are very widely distributed in the organs and tissues of the whole body, even being constituents of cell membranes. It is important to remember, therefore, that the fat-soluble insecticides become stored in individual cells, where they are in position to interfere with the most vital and necessary functions of oxidation and energy production. One of the most significant facts about the chlorinated hydrocarbon insecticides is their effect on the liver. In its versatility and in the indispensable nature of its functions it has no equal. It presides over so many vital activities that even the slightest damage to it is fraught with serious consequences. Not only does it provide bile for the digestion of fats, but because of its location and the special circulatory pathways that converge upon it, the liver receives blood directly from the digestive tract and is deeply involved in the metabolism of all the principal foodstuffs. It stores sugar in the form of glycogen and releases it as glucose in carefully measured quantities to keep the blood sugar at a normal level. It builds body proteins, including some essential elements of blood plasma concerned with blood-clotting. It maintains cholesterol at its proper level in the blood plasma, and inactivates the male and female hormones when they reach excessive levels. It is a storehouse of many vitamins, some of which in turn contribute to its own proper functioning. Without a normally functioning liver the body would be disarmed—defenceless against the great variety of poisons that continually invade it. Some of these are normal by-products of metabolism, which the liver swiftly and efficiently makes harmless by withdrawing their nitrogen. The harmless insecticides malathion and methoxychlor are less poisonous than their relatives only because a liver enzyme deals with them, altering their molecules in such a way that their capacity for harm is lessened. In similar ways the liver deals with the majority of the toxic materials to which we are exposed. Our line of defense against invading poisons or poisons from within is now weakened and crumbling. A liver damaged by pesticides is not only incapable of protecting us from poisons, the whole wide range of its activities may be interfered with. Not only are the consequences far-reaching, but because of their variety and the fact that they may not immediately appear they may not be attributed to their true cause. In connection with the nearly universal use of insecticides that are liver poisons, it is interesting to note the sharp rise in hepatitis that began during the 1950s and is continuing a fluctuating climb. While it is admittedly difficult, in dealing with human beings rather than laboratory animals, to prove that cause A produces effect B, plain common sense suggests that the relation between a soaring rate of liver disease and the prevalence of liver poisons in the environment is no coincidence. Whether or not the chlorinated hydrocarbons are the primary cause, it seems hardly sensible under the circumstances to expose ourselves to poisons that have a proven ability to damage the liver and so presumably to make it less resistant to disease. Both major types of insecticides, the chlorinated hydrocarbons and the organic phosphates, directly affect the nervous system, although in somewhat different ways. This has been made clear by an infinite number of experiments on animals and by observations on human subjects as well. Abnormal sensations as of prickling, burning, or itching, as well as tremors or even convulsions may follow exposure to appreciable amounts, according to a standard textbook of toxicology. The direct effect on the nervous system is apparent in their eloquent description of their symptoms: The tiredness, heaviness, and aching of limbs were very real things, and the mental state was also most distressing. He then spent three weeks in bed, made miserable by constant aching in limbs, insomnia, nervous tension, and feelings of acute anxiety. The experimenter lost 10 weeks from his work, and at the end of a year, when his case was reported in a British medical journal, recovery was not complete. Typically, such a victim has had a known exposure to one of the insecticides, his symptoms have subsided under treatment which included the exclusion of all insecticides from his environment, and most significantly have returned with each renewed contact with the offending chemicals. This sort of evidence—and no more— forms the basis of a vast amount of medical therapy in many other disorders. There is no reason why it should not serve as a warning that it is no longer sensible to take the calculated risk of saturating our environment with pesticides. There is some evidence that women are more susceptible than men, the very young more than adults, those who lead sedentary, indoor lives more than those leading a rugged life of work or exercise in the open. Beyond these differences are others that are no less real because they are intangible. What makes one person allergic to dust or pollen, sensitive to a poison, or susceptible to an infection whereas another is not is a medical mystery for which there is at present no explanation. The problem nevertheless exists and it affects significant numbers of the population. Some physicians estimate that a third or more of their patients show signs of some form of sensitivity, and that the number is growing. And unfortunately, sensitivity may suddenly develop in a person previously insensitive. In fact, some medical men believe that intermittent exposures to chemicals may produce just such sensitivity. If this is true, it may explain why some studies on men subjected to continuous occupational exposure find little evidence of toxic effects. By their constant contact with the chemicals these men keep themselves desensitized—as an allergist keeps his patients desensitized by repeated small injections of the allergen. The whole problem of pesticide poisoning is enormously complicated by the fact that a human being, unlike a laboratory animal living under rigidly controlled conditions, is never exposed to one chemical alone. Between the major groups of insecticides, and between them and other chemicals, there are interactions that have serious potentials. Whether released into soil or water or a mans blood, these unrelated chemicals do not remain segregated; there are mysterious and unseen changes by which one alters the power of another for harm. There is interaction even between the two major groups of insecticides usually thought to be completely distinct in their action. The power of the organic phosphates, those poisoners of the nerve-protective enzyme cholinesterase, may become greater if the body has first been exposed to a chlorinated hydrocarbon which injures the liver. This is because, when liver function is disturbed, the cholinesterase level drops below normal. The added depressive effect of the organic phosphate may then be enough to precipitate acute symptoms. And as we have seen, pairs of the organic phosphates themselves may interact in such a way as to increase their toxicity a hundredfold. Or the organic phosphates may interact with various drugs, or with synthetic materials, food additives—who can say what else of the infinite number of manmade substances that now pervade our world Yet the liver damage that brings this about might be so slight as to pass unnoticed.


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