Effects of Radiation on the Human Body

Effects of Radiation on the Human Body

Click on a number to learn about the effects of radiation on the body

(1) Hair

The losing of hair quickly and in clumps occurs with radiation exposure at 200 rems or higher.

(2) Brain

Since brain cells do not reproduce, they won't be damaged directly unless the exposure is 5,000 rems or greater. Like the heart, radiation kills nerve cells and small blood vessels, and can cause seizures and immediate death.

(3) Thyroid

The certain body parts are more specifically affected by exposure to different types of radiation sources. The thyroid gland is susceptible to radioactive iodine. In sufficient amounts, radioactive iodine can destroy all or part of the thyroid. By taking potassium iodide, one can reduce the effects of exposure.

(4) Blood System

When a person is exposed to around 100 rems, the blood's lymphocyte cell count will be reduced, leaving the victim more susceptible to infection. This is often refered to as mild radiation sickness. Early symptoms of radiation sickness mimic those of flu and may go unnoticed unless a blood count is done.According to data from Hiroshima and Nagaski, show that symptoms may persist for up to 10 years and may also have an increased long-term risk for leukemia and lymphoma.

(5) Heart

Intense exposure to radioactive material at 1,000 to 5,000 rems would do immediate damage to small blood vessels and probably cause heart failure and death directly.

(6) Gastrointestinal Tract

Radiation damage to the intestinal tract lining will cause nausea, bloody vomiting and diarrhea. This is occurs when the victim's exposure is 200 rems or more. The radiation will begin to destroy the cells in the body that divide rapidly. These including blood, GI tract, reproductive and hair cells, and harms their DNA and RNA of surviving cells.

(7) Reproductive Tract

Because reproductive tract cells divide rapidly, these areas of the body can be damaged at rem levels as low as 200. Long-term, some radiation sickness victims will become sterile.

Weight loss

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/ This article may require cleanup to meet Wikipedia's quality standards. Please improve this article if you can. (May 2008)

For the episode of the United States version of The Office, see Weight Loss (The Office).

A weightloss pyramid made on the model by BCM

Weight loss, in the context of medicine or health or physical fitness, is a reduction of the total body weight, due to a mean loss of fluid, body fat or adipose tissue and/or lean mass, namely bone mineral deposits, muscle, tendon and other connective tissue.

It can occur unintentionally due to an underlying disease or can come about through conscious effort to improve an overweight or obese state.

Contents

[hide]

• 1Unintentional weight loss
• 2Intentional weight loss
• 2.1Therapeutic weight loss techniques
• 2.2Crash dieting
• 2.3Weight loss industry
• 3See also
• 4References
• 5External links

[edit]Unintentional weight loss

Poor management of type 1 diabetes mellitus, also known as insulin-dependent diabetes mellitus (IDDM), leads to an excessive amount of glucose and an insufficient amount of insulin in the bloodstream. This triggers the release of triglycerides from adipose (fat) tissue and catabolism (breakdown) of amino acids in muscle tissue. This results in a loss of both fat and lean mass, leading to a significant reduction in total body weight. Note that untreated type 1 diabetes mellitus will usually not produce weight loss, as these patients get acutely ill before they would have had time to lose weight.

Myriad additional scientific considerations are applicable to weight loss: physiological and exercise sciences, nutrition science, behavioral sciences, and other sciences.

One area involves the science of bioenergetics including biochemical and physiological energy production and utilization systems, that is frequently evidence of diabetes, and ketone bodies, acetone particles occurring in body fluids and tissues involved in acidosis, also known as ketosis, somewhat common in severe diabetes.

In addition to weight loss due to a reduction in fat and lean mass, illnesses such as diabetes, certain medications, lack of fluid intake and other factors can trigger fluid loss. And fluid loss in addition to a reduction in fat and lean mass exacerbates the risk for cachexia.

Infections such as HIV may alter metabolism, leading to weight loss.[1]

Hormonal disruptions, such as an overactive thyroid (hyperthyroidism), may also exhibit as weight loss.[2]

Recent research has shown fidgeting to result in significant weight loss. [3]

[edit]Intentional weight loss

Weight loss refers to the loss of total body mass in an effort to improve fitness, health, and/or appearance.

Therapeutic weight loss, in individuals who are overweight or obese, can decrease the likelihood of developing diseases such as diabetes,[4]heart disease, high blood pressure, stroke, osteoarthritis,[5] and certain types of cancer.

Weight loss occurs when an individual is in a state of negative energy balance. When the human body is spending more energy in work and heat than it is gaining from food or other nutritional supplements, it will use stored reserves of fat or muscle.

It is not uncommon for some people who are currently at their ideal body weight to seek additional weight loss [6] in order to improve athletic performance, and/or meet required weight classification for participation in a sport. However, others may be driven by achieving a more attractive body image [7]. Consequently, being underweight is associated with health risks such as difficulty fighting off infection, osteoporosis, decreased muscle strength, trouble regulating body temperature and even increased risk of death.[8]

[edit]Therapeutic weight loss techniques

See also: Obesity#Managementand Bariatrics

The least intrusive weight loss methods, and those most often recommended by physicians, are adjustments to eating patterns and increased physical exercise. Physicians will usually recommend that their overweight patients combine a reduction of processed[9] and caloric content of the diet with an increase in physical activity.[10]

Other methods of losing weight include use of drugs and supplements that decrease appetite, block fat absorption, or reduce stomach volume. Medicines with herbs such as Fucus vesiculosus are popular.[11] Finally, surgery may be used in more severe cases. Bariatric surgery artificially reduces the size of the stomach, limiting the intake of food energy.

[edit]Crash dieting

A crash diet is where a person willfully restricts themselves of all nourishment (except water) for more than 12 hours. The desired result is to have the body burn fat for energy with the goal of losing a significant amount of weight in a short time. Crash dieting is not the same as intermittent fasting, in which the individual periodically abstains from food (e.g., every other day).

[edit]Weight loss industry

There is a substantial market for products which promise to make weight loss easier, quicker, cheaper, more reliable, or less painful. These include books, CDs, cremes, lotions, pills, rings and earrings, body wraps, body belts and other materials, not to mention fitness centers, personal coaches, weight loss groups, and food products and supplements. US residents in 1992 spent an estimated $30 billion a year on all types of diet programs and products, including diet foods and drinks.[12]

Between $33 billion and $55 billion is spent annually on weight loss products and services, including medical procedures and pharmaceuticals, with weight loss centers garnering between 6 percent and 12 percent of total annual expenditure. About 70 percent of Americans' dieting attempts are of a self-help nature. Although often short-lived, these diet fads are a positive trend for this sector as Americans ultimately turn to professionals to help them meet their weight loss goals.[13]

The Journal of Clinical Endocrinology & Metabolism Vol. 92, No. 2 583-588
Copyright © 2007 by The Endocrine Society

Effect of Human Body Weight Changes on Circulating Levels of Peptide YY and Peptide YY3–36

P. T. Pfluger1, J. Kampe1, T. R. Castaneda, T. Vahl, D. A. D’Alessio, T. Kruthaupt, S. C. Benoit, U. Cuntz, H. J. Rochlitz, M. Moehlig, A. F. H. Pfeiffer, C. Koebnick, M. O. Weickert, B. Otto, J. Spranger and M. H. Tschöp

Departments of Psychiatry and Medicine (P.T.P., J.K., T.R.C., T.V., D.A.D., T.K., S.C.B., M.H.T.), Obesity Research Center, University of Cincinnati–Genome Research Institute, Cincinnati, Ohio 45237; Department of Physiology (J.K.), Monash University, Melbourne 3800, Australia; Center for Psychosomatic Medicine (U.C.), D-83209 Prien, Germany; German Institute of Human Nutrition (H.J.R., M.M., A.F.H.P., C.K., M.O.W., J.S.), 10551 Nuthetal, Germany; Department of Preventive Medicine (C.K.), University of Southern California, Los Angeles, California 90089; and Department of Gastroenterology (B.O.), University Hospital, D-81377 Munich, Germany

Address all correspondence and requests for reprints to: Matthias H. Tschöp, M.D., Associate Professor, Departments of Psychiatry and Medicine, University of Cincinnati, Office E-217, Genome Research Institute, 2170 East Galbraith Road, Cincinnati, Ohio 45237. E-mail: .

/ Abstract

Background: Recent findings suggest that low plasma peptideYY (PYY) levels may contribute to diet-induced human obesityand justify PYY replacement therapy. Although the pharmacologicalvalue of PYY is controversial, further study of the secretionof the precursor PYY1–36 and the pharmacologically activePYY3–36 is indicated to determine the potential role inenergy balance regulation.

Aim: Our objective was to determine the effects of acute andchronic changes in human body weight on circulating levels ofthe putative satiety hormone peptide YY.

Design: Total plasma PYY levels (PYY1–36 + PYY3–36)were measured in 66 lean, 18 anorectic, 63 obese, and 16 morbidlyobese humans. In addition, total PYY was measured in 17 of theobese patients after weight loss and in the 18 anorectic patientsafter weight gain. Fasting PYY3–36 levels were measuredin 17 lean and 15 obese individuals.

Results: Fasting total plasma PYY levels were highest in patientswith anorexia nervosa (80.9 ± 12.9 pg/ml, P < 0.05)compared with lean (52.4 ± 4.6 pg/ml), obese (43.9 ±3.8 pg/ml), or morbidly obese (45.6 ± 11.2 pg/ml) subjects.In obese patients, weight loss of 5.4% was associated with a30% decrease in fasting total PYY plasma levels. In anorecticpatients, weight gain had no effect on fasting PYY. PYY3–36levels did not differ between lean (96.2 ± 8.6 pg/ml)and obese (91.5 ± 6.9 pg/ml) subjects.

Conclusion: Our findings do not support a role for abnormalcirculating PYY in human obesity. We conclude that circulatingPYY levels in humans are significantly elevated in anorexianervosa and, given the controversially discussed anorectic effectof PYY, could theoretically contribute to that syndrome.

Introduction

PEPTIDE YY (PYY) is an intestinal peptide that has been advancedas a satiety factor (1, 2, 3). PYY belongs to the pancreaticpolypeptide family, which includes pancreatic polypeptide (PP)and neuropeptide Y (NPY). These related peptides display a highsequence homology and share a common tertiary structure (PP-fold).PYY mRNA has been identified in the intestine and the pancreas,and, like many other gastrointestinal hormones, it can be detectedin distinct brainstem neurons (4). The peptide is predominantlysecreted into circulation by endocrine L cells, which line thedistal small bowel and colon.

PYY is metabolized by the enzyme dipeptidyl peptidase-IV, whichhydrolyzes PYY at the Pro2-Ile3 bond, converting a precursorform PYY1–36 to PYY3–36 (5, 6). Because of the extentand rapidity of this process, the main circulating form of PYYin postprandial human plasma is PYY3–36 (5). Both formsof PYY bind to the Y2 isoform of the NPY receptor (7, 8). PYY1–36also binds theY1 and Y5R isoforms (8). Both PYY1–36 andPYY3–36 inhibit gastric acid and pancreatic enzyme secretionand suppress gastrointestinal motility (9, 10, 11, 12, 13, 14).Similar to NPY, PYY1–36 and PYY3–36 are potent stimulifor feeding in the brain, producing massive and immediate hyperphagiawhen injected into cerebral ventricles, the paraventricularnucleus, or the hippocampus (15).

In contrast to the effects in the central nervous system, Batterhamand Bloom (1) reported that circulating PYY3–36 is anendogenous satiety factor, mediating this effect through theY2R subtype. In these experiments, iv PYY3–36 suppressedfood intake in rodents and humans and decreased body weightgain in rodents (3). These observations were hailed as a potentialadvance toward an effective antiobesity treatment (2). Thisfinding has not been universally confirmed, and 12 independentstudy groups recently reported that they were unable to reproduceany anorexigenic or weight-reducing effects of PYY3–36in rodents (16).

There is little published information on plasma levels of PYYin response to changes in energy balance. PYY levels reach anadir after fasting and increase after meals. Over the courseof a day, PYY levels are lowest in the morning and increasesteadily after breakfast, lunch, and the evening meal (17).After ingestion of a test meal, plasma levels increase proportionallyto the amount of ingested calories within 15 min, reaching apeak at approximately 90 min, and then remain elevated for upto 6 h (14). To determine the effects of chronic energy balanceon plasma PYY, we compared circulating PYY1–36 and PYY3–36levels in plasma of anorectic, lean, obese, and morbidly obesesubjects.

Patients and Methods

Anorexia patients

Plasma samples from 18 female patients [body mass index (BMI),15.4 ± 0.3 kg/m2; age, 25.6 ± 1.0 yr] with anorexianervosa according to the criteria of the Diagnostic and StatisticalManual of Mental Disorders, 4th edition (DSM-IV, American PsychiatricAssociation, 1994) were measured in this study. The patientshad been admitted to a psychosomatic treatment center (KlinikRoseneck, Prien, Germany) for an inpatient intervention program.All patients had been examined and were in good health apartfrom their eating disorder. Fasting blood samples were takenat three different times: 1) within the first 3 d after admission(no weight gain since admission or in the last 2 wk before),2) after a weight gain of at least 2 kg twice consecutivelywhen weighing the patients twice a week (1–7 wk afteradmission), 3) in the last week before discharge [6–19(mean, 10.6 ± 0.8) wk in hospital]. None of the patientsreceived parenteral nutritional support at any time of the treatment.The procedure was reviewed and approved by the ethics committeeof the Medical Faculty of the Ludwig-Maximilians-University,Munich, Germany.

Lean, obese, and morbidly obese individuals

Fasting blood samples from 66 lean individuals (24 males, 42females; BMI, 22.1 ± 0.2 kg/m2; age, 41.5 ± 2.2yr), 63 obese individuals (20 males, 43 females; BMI, 32.7 ±0.3 kg/m2; age, 48.4 ± 2.4 yr), and 16 morbidly obeseindividuals (one male, 15 females; BMI, 44.5 ± 0.9 kg/m2;age, 44.7 ± 2.8 yr) were drawn at the Department of ClinicalNutrition at the German Institute of Human Nutrition Potsdam-Rehbruecke,Nuthetal, Germany. In addition, PYY3–36 was measured in17 lean (all female; BMI, 22.0 ± 0.5 kg/m2; age, 51.6± 1.9 yr) and 15 obese (all female; BMI, 31.1 ±0.5 kg/m2; age, 52.0 ± 2.0 yr) individuals. For anothersubset of obese subjects (three males, 14 females; BMI, 35.1± 1.4 kg/m2) blood samples were drawn approximately 12wk after undergoing a therapeutic weight loss program (averageBMI, –1.9 kg/m2; 5.4%; P < 0.001). BMI was classifiedaccording to World Health Organization and Centers for DiseaseControl criteria: normal BMI, 18.5–25 kg/m2; overweightBMI, 25–30 kg/m2; obese BMI, 30–40 kg/m2; morbidlyobese BMI, more than 40 kg/m2 (18, 19). All patients gave writteninformed consent for their participation in the study, whichwas approved by the Ethical Committee of the University Potsdam.

Meal study

PYY1–36 and PYY3–36 were measured after ingestionof water or a high-caloric-density meal in six lean, healthyvolunteers (three male, three female; age, 29.0 ± 1.2yr; BMI, 20.7 ± 1.1 kg/m2). On two consecutive days,blood samples were taken before and after a test ingestion (–5,0, 15, 30, 60, 90, and 120 min), starting at 0900 h. On 1 d,250 ml water was consumed. On the second day, a high-caloriemeal [Burger King Croissan’wich with ham, cheese, andeggs, hash brown rounds, orange juice, and one can of EnsurePlus (Abbott, Chicago, IL); total, 1030 kcal] was consumed within15 min and blood sampled as described above. This study wasreviewed and approved by the Human Subjects Committee at theUniversity of Cincinnati.

Measurement of total PYY

Blood samples were drawn into EDTA tubes in the morning afteran overnight fast of 12 h, the plasma separated within 1 h bycentrifugation at 3000 xg and 4 C and stored at –80 C.Human total PYY plasma levels were measured using an ELISA kit(ACTIVE Total Peptide YY) from Diagnostic Systems Laboratories(Webster, TX). The ELISA quantifies both PYY1–36 and PYY3–36.The cross-reactivity against mouse PYY1–36 and human PYY1–36is 100%. Intra- and interassay coefficients of variation (CV)are less than 3.3 and 7.6%, respectively. The sensitivity (minimumdetection limit), as calculated by interpolation, is 9.5 pg/ml.All measurements were performed in duplicate according to themanufacturer’s instructions.

Measurement of PYY3–36

For specific measurement of PYY3–36, blood samples weredrawn after an overnight fast into chilled tubes containingEDTA and a protease inhibitor (Trasylol, 500 kIU/ml; Bayer,Leverkusen, Germany) and centrifuged at 3000 xg and 4 C. Forquantification of PYY3–36, a RIA from Linco [human PYY(3–36Specific RIA Kit; Linco Research, St. Charles, MO] was used.The assay specifically detects human PYY3–36 and has nodetectable cross-reactivity with human PYY1–36. Intraand interassay CV are less than 11.0 and 15.0%, respectively,and the lowest level of PYY3–36 that can be detected is20 pg/ml. All measurements were performed in duplicate accordingto the manufacturer’s instructions.

Measurement of leptin and leptin-binding protein

Blood samples were drawn into EDTA tubes in the morning afteran overnight fast of 12 h, the plasma separated within 1 h bycentrifugation at 3000 xg and 4 C and stored at –80 C.Human leptin and human leptin-binding protein were measuredby using ELISA kits (Active Human Leptin and Active Leptin SolubleReceptor, respectively) from Diagnostic Systems Laboratories.For the detection of leptin, no cross-reactivity was observedwith bovine or porcine sera as well as with human leptin fragmentsLP 1 (5–21), LP 2 (22–42), LP 3 (61–85), andLP 4 (114–146). Recombinant leptin was shown to have nocross-reactivity in the leptin-binding protein ELISA. Intra-and interassay CV were less than 6.2 and 5.3% for the determinationof leptin and less than 13.3 and 9.6% for the determinationof leptin-binding protein, respectively. The theoretical sensitivity(minimum detection limit) of the assays, as calculated by interpolation,was 0.05 ng/ml for leptin and 0.14 ng/ml for leptin-bindingprotein. All samples were measured in duplicate according tothe manufacturer’s instructions.

Statistical analysis

BMI and PYY levels of anorectic, control, obese, and morbidlyobese subjects were compared using one-way ANOVA followed byDunnett’s post hoc test. Significant changes of BMI andPYY levels in obese subjects subjected to weight loss and anorecticpatients on weight-gain therapy were analyzed by paired t testsand repeated-measures ANOVA with post hoc Bonferroni’smultiple comparison tests, respectively. BMI and PYY3–36levels in the additional sets of control and obese patientswere compared by unpaired (two-tailed) t tests. Differencesin the fasting or postprandial release of total PYY and PYY3–36were examined by two-way ANOVA followed by Bonferroni’smultiple comparison tests. Correlations of PYY levels with age,BMI, leptin, and leptin-binding protein levels were analyzedby two-tailed Pearson correlation. All statistical analyseswere performed using GraphPad Prism version 4.0 (GraphPad Software,San Diego, CA). Results are presented as means ± SEMor as individual levels with median values.