1、母乳喂养的儿童不易患肥胖症

　　德国研究人员最近发现，母乳喂养长大的儿童患肥胖症的可能性相对较小。

　　慕尼黑的科学家在《英国医学杂志》上介绍说，他们在研究中共调查了德国巴伐利亚地区的9357名儿童。结果发现，在出生后头三至五个月中完全接受母乳喂养的婴儿长到学龄阶段时，患肥胖症的可能性比未接受母乳哺育的同龄儿童要低35％左右。研究还显示，接受母乳喂养的时间越长，婴儿长到学龄阶段后患肥胖症的可能性越小。

　　研究发现，母乳中所含的特殊成分是减少儿童患肥胖症的主要因素。返回

2、北京地区468名少儿肥胖及血压改变的八年随访观察

　吴光驰　郭素怡　王乃坤　朱宇平

　　目的　

调查北京地区少年儿童肥胖发生、发展状况，以及对血压的影响，为预防少儿肥胖和高血压病的措施提供依据。方法　连续8年现场观察468名6～13岁少儿的身高、体重、皮脂厚度及血压等项目，并逐年分析不同性别、年龄的肥胖及超重儿的检出率和肥胖度及与血压的关系。结果　肥胖少儿检出率由6岁的4.9%上升到13岁的16.2%，肥胖发病高峰年龄段是9～11岁，男生发病多于女生，13岁男、女生肥胖检出率分别为21.5%和11.9%。13岁肥胖少儿高血压发生率为14.3%；为同龄非肥少儿的3倍半。结论　北京地区少儿肥胖随年龄增长而逐渐增多，肥胖少儿中高血压者明显增多。抓住肥胖发生的高峰年龄段和肥胖前的超重期是预防肥胖的两个关键。

　　关键词　体重和量体重　　肥胖　　高血压

Follow-up study on children with obesity and hypertension　Wu Guangchi, Guo Suyi, Wang Naikun, et al. Capital Institute of Pediatrics, Beijing 100020 　　Objective　 To study obesity development and its relationship between obesity and hyperetension of children in China.Method　A 8-year follow-up study was conducted in 468 children aged 6 years by the criteria of hight, weight, thickness of skin fat and blood pressure. Results　Obesity morbidity rose from 6 years (4.9%) to 13 years (16.2%), with the peak at 9 to 11 years. Both sexes developed obesity, which dominated in males. Children with obesity developed hypertension at age of 13, the morbidity increased 3.5 times than that of those without obesity. Conclusion　Prevention of malnutrition is important in China but interventions to children with obesity in China are in urgent need. 　　Key words　Obesity　　Hypertension　　Overweight. (Natl Med J China, 1997, 77:14-17)

　　少儿时期的肥胖，特别是青春期肥胖很容易发展为成人肥胖。肥胖是高血压病发病的危险因素，因此，肥胖的防治已成为少儿保健的一个重大课题，我们在未给与干预措施的情况下，于1987～1994年，连续8年观察肥胖儿检出率的变迁及对血压的影响，现就少儿肥胖及血压的改变情况分析总结如下。

对象和方法

　　一、对象

　　1987年9～10月，选择北京市朝阳区(东南片)，西城区(西南片)及海淀区(北片)，中等生活条件的6所小学一年级6岁学生共468人作为研究对象。以后每年9～10月对这些学生都进行一次检查至其13岁(1994年)，连续观察8年。逐年筛出肥胖儿，并将其与肥胖儿同性别、同年龄(相差不超过3个月)，同身高(相差不超过3cm)的非肥胖对照组配对比较。

　　二、方法

　　1.体格检查：对学生进行健康检查的项目、包括身高、体重，左肩胛下皮脂厚度，心、肺、腹、肝、脾等，发现异常者到医院进一步检查，删除体检异常者。

　　2.血压测查：参考美国心肺血管研究中心推荐的“儿童血压测量方法”，及1978年世界卫生组织高血压专家座谈会规定标准进行血压测量，采取坐式连续测量血压3次，每次间隔1分钟，并抬高上臂5～6秒，取后2次血压平均值作为受检者当时的血压。两次测得血压数相差应小于0.533kPa(4mmHg,1kPa=7.5 mmHg)，取Korotkott第一音为收缩压，第4音为舒张压。

　　3.测查人员培训：参加调查的人员要接受培训、统一要求、统一标准。以后每年测查前先进行复训。

　　4.仪器准备：仪器设备统一购置。RGT-140型体重计，TG-2型身高坐高计及仿日本荣研式改良型国产皮下脂肪测量计均为国家体委科学研究所监制。每次测量前先对血压表进行仪器校对，无误后方可使用。

　　5.评价标准：

(1) 肥胖：以WHO推荐的身高相应标准体重法进行评价。超过身高相应标准体重的20%为肥胖，超过10%而不到20%者为超重。

　　超重：体重达标准体重的10%～＜20%；轻度肥胖：体重达标准体重的20%～＜30%；中度肥胖：体重达标准体重的30%～＜50%；重度肥胖：体重达标准体重的50%以上。

(2) 高血压：按年龄、性别、收缩压和(或)舒张压在95百分位以上者为高血压。在第90与第95百分位之间者为临界高血压(正常高限血压)。

结果

　　一、追踪观察率

　　以1987年调查的468名儿童为基数，为保证观察对象不漏失，采取在校调查和多次补查方式，使逐年追踪观察少儿的比率均在90.0%以上，1994年(13岁)时的追踪观察率仍保持在98.9%的高水平。男女生的追踪观察率分别为98.7%和99.2%(表1)。

　　二、肥胖及超重少儿检出率

　　肥胖少儿检出率从6～13岁逐年增多，依次为4.9%、5.4%、5.3%、7.7%、12.7%、14.2%、14.7%及16.4%。从9岁起肥胖少儿数急剧增加，13岁时肥胖少儿检出率为6岁时的3倍。相比之下超重少儿的检出率比较稳定，6～13岁依次为5.1%，6.8%、7.9%、7.2%、7.0%、8.8%、11.2%及6.7%。

　　三、不同性别肥胖及超重少儿检出率

　　男生肥胖检出率自6岁起依次为5.0%、6.0%、6.9%、9.9%、15.8%、21.3%、20.5%及21.5%，增长4倍，增长的加速期从9岁开始。女生肥胖检出率自6岁起依次为4.9%、4.6%、3.9%、5.7%、9.9%、7.9%、9.4%及11.9%，增长2倍，较男生低，其增长加速期从10岁开始，比男生晚1年(图2)。

　　超重儿检出率随年龄的增长略有增加，男生由6岁的5.4%增至13岁的7.8%，女生由6岁的4.9%增至13岁的5.7%。超重男生检出率亦比女生高，与肥胖相似。

　　四、肥胖发病年龄及肥胖度

　　在追踪观察的8年中，新患病的肥胖儿有74例，男生49例，女生25例，发病的高峰年龄段是9～12岁，男生比女生提前1年。13岁肥胖少儿中，轻度29例，占38.2%；中度35例，占46.0%；重度12例，占15.8%。

　　五、肥胖少儿体重指数及肩胛下皮脂厚度

　　1994年检出肥胖少儿76例，体重指数随肥胖加重而增高，轻、中、重度肥胖的体重指数与对照组比差异均有非常显著意义(P＜0.01)。肥胖儿童肩胛下皮脂厚度二倍于对照组，两者相比差异均有非常显著意义(P＜0.01，表2)。

　　六、肥胖度变迁

　　少儿在不断地生长发育，肥胖少儿的身高、体重也处在较大的动态变化之中。与6岁相比，13岁时监测到的463名少儿中，354名(76.5%)身高相应体重保持在原有体型状态。出现新的超重、肥胖或原有肥胖度加重者93例(20.0%)，肥胖及超重少儿体重减轻或转为正常者16例(3.5%)。少儿体重向肥胖发展趋势明显高于体重减轻的趋势(P＜0.001，表3)。在23例6岁肥胖儿中，有7例肥胖度不变，10例肥胖度加重，6例肥胖度减少，其中1例转为正常。正常少儿发展为肥胖都要经过超重阶段。追踪观察期新出现的74例肥胖儿中，有60例(81.1%)在超重阶段已被检查出来，维持超重的时间在1～7年，维持1年者18例(24.3%)，2年者25例(33.8%)，3～7年者17例(28.3%)。另有14例肥胖儿(18.9%)未观察到超重阶段。

　　七、肥胖与血压

　　肥胖对血压的影响极为明显。从表4可见，13岁时正常少儿收缩压平均值为13.6kPa，超重少儿收缩压已开始升高，轻度、中度及重度肥胖少儿的收缩压平均值与正常儿收缩压的差异均有显著和非常显著意义。肥胖舒张压的变化与收缩压相似，肥胖少儿舒张压升高，中、重度肥胖少儿舒张压值明显高于正常少儿，差异均有非常显著意义(表4)。

讨论

　　少年儿童肥胖呈全球性分布，主要分布在发达国家及经济发展迅速的发展中国家。我国自80年代起肥胖少儿有增多的趋势。1986年全国抽样调查0～7岁儿童肥胖检出率为0.91%［1］，同年北京市7～18岁青少年肥胖者为3.28%［2］。90年代为11.25%［3］。1995年全国30个省、市、自治区30万7～22岁青少年学生调查，男生超重与肥胖由10年前的2.75%上升到8.65%，女生由3.38%上升到7.18%，城市男生超重及肥胖发生率高达12.03%。提示我国少儿肥胖明显增多的趋势不容忽视。

　　本组肥胖少儿检出率相当高。刚入学的6岁儿童肥胖检出率就已达4.9%，小学毕业(11岁)时，上升到14.2%，增加近2倍，初中二年级(13岁)达到16.2%，3倍于6岁儿童。男生肥胖率明显高于女生，这可能反映家长或少儿的饮食观念，对于男孩饮食不限制，甚至鼓励多食，而女孩则考虑到体型，以致要控制饮食摄入量。总之，少儿肥胖迅速增多，将严重危害他们的身心健康，特别是青春期肥胖将有80%发展为成人肥胖，以致容易合并高脂血症、高血压病、冠心病、糖尿病、脑卒中等疾病。我国少儿保健工作面临着贫穷和富贵两方面的挑战。

　　高血压病所引起的脑卒中，是我国成人死亡的主要原因，高血压病与肥胖密切相关，甚至年青时期超重也是以后发生高血压病强有力的危险因素，而减肥可以降低血压。Dustan［4］在1979年观察到，减肥后83.6%的收缩压和78.3%的舒张压恢复正常，大多数的血压先于肥胖恢复正常。Verma［5］报道肥胖儿合并高血压者有13.7%，为非肥胖儿的34倍，Mossberg［6］对超重儿童追踪40年，发现肥胖合并高血压者13.6%，对照组为8.1%，而10～29岁时肥胖合并高血压者为5.1%，对照组为0.1%。我们的观察表明，有14.7%的肥胖少儿合并高血压，为正常少儿的3倍；肥胖少儿合并临界高血压者为20.0%，为正常少儿的2倍。因此，在防治高血压病工作中，不能忽视肥胖因素。肥胖合并高血压的机制至今尚未定论，早期认为与盐的摄入有关，近期血液动力学的研究提示与心搏出量和血容量增加有关，其末稍循环阻力高于未合并高血压的肥胖患者。内分泌和神经因素的研究尚不能解释某些肥胖患者出现高血压而另一些患者不出现［5］。

　　肥胖一旦形成，治疗相当困难，因此重点在于预防。预防的措施很多，如健康教育、合理的营养膳食，适当的运动锻炼，去除不良的生活方式等，对具有肥胖遗传因素的儿童更应采取积极的预防措施。根据我们的观察，预防应抓住两个关键环节：一个是在肥胖发生的高峰年龄段，抓紧预防；另一个是超重，少儿发生肥胖必然经过体重超重阶段。我们每年进行一次体格检查，能够发现80%的肥胖少儿在出现肥胖前有一个超重阶段，其持续时期为1～7年。而若从肥胖发生的高峰年龄段之前开始，每学期检查一次，肥胖前超重少儿的检出比例可能会更多，我们认为在少儿肥胖发病的高峰年龄段，及处于超重时期加强预防，能收到积极的效果。

　　作者单位：100020　北京，首都儿科研究所(吴光驰、郭素怡)；首都医科大学附属北京儿童医院(王乃坤)；首都医科大学附属北京安贞医院(朱宇平) 返回

3、怎樣才算肥胖？

想知道自己體型是否屬於肥胖，先要明白“身體質量指數”的計算方法： 身體質量指數 (BMI)= 體重 (公斤) / 身高(米) 的平方 根據世界衛生組織所訂的標準，成人的身體質量指數介乎25至29.9者為過重；介乎30至39.9者為肥胖；若達到40或以上者便屬於非常肥胖。亦可參考成年人標準體重表，若體重超過標準的20%以內為過重，超過20%以上者為肥胖。 肥胖對健康的影響？ 綜合多項研究結果發現，過重或肥胖會增加多種疾病的發病率；有關疾病包括： 高血壓、高脂血症、冠心病、中風等血和血管的病 退化性關節炎 睡眠窒息症及膽囊疾病 過重或肥胖更被發現與乳癌、前列腺癌和結腸癌有關 故此，現在肥胖已被視為一種要認真處理的慢性疾病。 肥胖的成因是什麼？ 肥胖的原因是多方面的，包括先天的遺傳因素和後天的環境因素 後天的環境因素的因素 包括： 飲食習慣 運動和生活習慣：(如看電視的時間和遙控的習慣...) 文化背景等 由於過剩的能量在人體內以脂肪形式儲存，故此簡單而言，肥胖是身體內能量攝取及消耗失去平衡的結果。 肥胖應如何處理？ 肥胖的處理可分三個步驟： 防止體重進一步增加。 減輕現時的體重。 長期維持體重在減磅後的水平。 具體來說，控制體重的方法包括飲食調節、運動、行為治療和減肥藥物。 治療過程中，不應期望體重迅速下降，這樣對健康是弊多於利，恰當的速度為在六個月內減輕10%的體重。 另外，由於肥胖者較多同時患有其他疾病，減肥方法應配合其他疾病的治療。 哪種減肥方法最好？ 飲食調節的原理為減少能量攝取，方法是限制日常飲食中的脂肪和熱量，最好在營養師指導下進行，注意每人每天所需的能量有不同，沒有所有人都合適的減肥餐單，更重要的是，過度節食會造成營養不良而百病叢生，甚至引起危及生命的厭食症。 很多人都知道運動的益處及重要性，對減肥者而言，最好每天有30分鐘或以上的中等程度的運動，日常生活裏應多步行，或以行樓梯代替生升降機。行為治療的內容主要是分析肥胖者的生活習慣(例如飲食、工作、工餘活動等)，從而提出有助減肥的建議，在減肥的過程中，定期的會面可增加減肥者的決心，和及時解決他們面臨的問題，避免半途而廢的出現。 使用減肥藥物應視作減肥治療中的一部分，不應單憑減肥藥物而忽略上述的方法，否則，即使減磅成功亦難以長期維持。事實上，由於肥胖是一種慢性病，治療必需是綜合性的，沒有一種單獨的方法是最好，最有效的反而是上面幾種方法的配合。 減肥藥為什麼能減輕體重？ 目前，經詳細臨床研究並證實有效的減肥藥物主要作用為影響對能量的攝取、吸收或消耗，其中以前兩者較常用，例如部分藥物作用於大腦的攝食中樞，使服用者食慾下降，減少進食，或是作用於胃腸，使飽腹的感覺延長，這些藥物具有相同的特點，就是停藥後食慾會恢復，體重可能隨之上升。 近期一種較熱門的減肥藥，則主要影響人體對脂肪的吸收，另有部分藥物通過對新陳代謝的影響，加快能量的消耗。 減肥藥有什麼副作用？ 常用減肥藥的副作用可以由輕微的例如口乾、失眠、煩燥、腹瀉，到較嚴重的影響血壓、心跳，甚至因影響心肺功能而危及生命。 太急進地節食可引引至胃病、暈眩 故此，服用減肥藥前應先徵詢醫生的意見，及作有關的體格檢查，不應單憑身邊朋友同事的介紹，同時要明白，減肥藥只是肥胖治療中的一部分。返回

4、The World's Oldest Metabolic Disorder

by Michael Blumenkrantz, M.D., F.A.C.P, F.A.C.N.

Contents

The World's Oldest Metabolic Disorder

Indices of Overweight

Assessment of Body Fat

Morbidity and Mortality Associated with Obesity

Obesity and Hypertension

Obesity and Diabetes

Cardiovascular Disease and Fat Distribution

Obesity and Cancer

Obesity and Endocrine Abnormalities

Obesity and Gall Bladder

Obesity and Pulmonary Abnormalities

Obesity and Arthritis

Obesity and Functional and Psychological Disorders

About the Author Dr.

Michael Blumenkrantz, a recognized authority in the treatment of obesity-related disorders, holds Diplomates in the American Boards of Internal Medicine, Nephrology and Clinical Nutrition. His medical practice, in Beverly Hills, California, specializes in Internal Medicine, Nutrition, Kidney Disease and Dialysis, and Hypertension.

The World's Oldest Metabolic Disorder

Obesity is probably the oldest metabolic disturbance; an obese Stone Age statue has been unearthed. Similar evidence of obesity is found in Egyptian mummies and in Greek sculpture. People in a society become obese as soon as enough food and leisure are available to cause an imbalance between energy intake and energy expenditure. Sustained caloric imbalance with consequent obesity is becoming the behavioral norm of the American population. Forty million adult Americans weigh more than 20% above their desirable weight. Its prevalence is increasing in all major race/sex groups including younger adults age 25 to 44. This increase in the prevalence of obesity is against the trend in the last few decades toward lower dietary fat and cholesterol intake, increased exercise, decreased cigarette smoking and increased treatment for hypertension. Obesity is, therefore, becoming a more important risk factor for the development of diabetes, hypertension and cardiovascular disease. Obesity has multiple causes; the development of obesity is a complex interaction between genetic, psychological, socioeconomic and cultural factors. Americans with less education and income are, on the average, more obese. Individuals have unique genetic and environmental factors which affect how food is processed; there are, therefore, individual differences in susceptibility to obesity. Indices of Overweight In the past, obesity has often been measured by "desirable" or "relative" weight. Life insurance tables of desirable weight are based on weights associated with the lowest mortality, among the insured population, who are predominantly upper middle class Caucasian individuals. Relative weight is calculated by dividing the patient's weight by a standard weight that is based on the patient's height, age and sex. There are several problems with the appropriateness of these two measures. They are not applicable to the entire population. They do not reflect current weight or mortality relationships in the American population. Frame size is subjectively determined. They do not provide data predicting the longevity of young persons weighed in their early 20s and followed until their death. A newer, more clinically useful measure of overweight, is the so-called Body Mass Index (BMI). The BMI is obtained by dividing the weight in kilograms by height measured in meters, squared (W/H2). Identical standard values can be used for all adult patients, both men and women. The lowest morbidity and mortality, for both sexes occur in persons with a BMI of 22-25 kg/m2. Life insurance and other epidemiological studies have suggested that mortality rates begin to increase substantially at weights 20% greater than desirable, this corresponds to a BMI of 27 kg/m2. Individuals with a BMI of 30 kg/m2 or greater clearly increased mortality. All of these indices are only measures of overweight. They only estimate body fat. A heavily muscled athlete may be overweight with any of these indices and have a very low fat content. Overweight lean men have lower blood pressures, lipid levels and better glucose tolerance than obese overweight men. To determine whether an individual is obese or simply overweight because of increased muscle mass, one needs techniques for quantitating body fat. Assessment of Body Fat Skinfold measurements can be used to measure body fat. They are easy to do, inexpensive, and portable; if one measures appropriate skinfolds, an equation may be used to estimate body fat. Approximately half the fat in the body is deposited in the skin. The percentage of internal fat increases with increasing weight. Skinfold measurements are often not accurate or reproducible, especially if the observer is inexperienced. Skinfolds are not equally compressible and skin thickness is not necessarily constant. More precise and technically sophisticated methods for determining body fat include underwater weighing, which requires total submersion of an individual and an accurate estimation of lung and abdominal gas, the assessment of total body water by dilution of tritiated water, and measurement of body fat by dilution of an inert fat-soluble gas such as Xenon. CT, ultrasound, and MRI have also been used to determine body fat. These measures are all expensive, difficult to do, time consuming and not applicable to office practice. Bioelectrical impedance analysis appears to be the first easy-to-use, reproducible method for determining body composition in office practice. Body impedance is measured when a small amount of current, applied through electrodes, flows through the body. Resistance is inversely proportional to total body water through which the current travels. Lean body mass and body fat are derived from total body water. Impedance measurements correlate quite well with total body water measured by other means. Morbidity and Mortality Associated with Obesity The major health risks of obesity increase in a curvilinear relationship, with prevalences increasing progressively and disproportionately with increasing weight. Weight increases beginning during adulthood and continuing for many years have the greatest adverse affects. Men 20% above desirable weight show an overall increase of 20% in the likelihood of death from all causes, a 25% increase in death from coronary artery disease, a 10% increase from stroke, twice the risk of diabetes, and a 40% increase in gall bladder disease. In men age 15 to 39 whose relative body weight when initially measured is 125% to 135% of normal, there is an aggregate mortality of 170% of usual at 15-22 year follow-up. In men 40% above desirable, there is a 55% increase in mortality from all causes, 70% increase from coronary artery disease, 75% increase from stroke, and a 400% increased mortality from diabetes. "Malignant obesity" is a term now used to define persons 60% above desirable weight; this corresponds to an absolute excess of a minimum of 100 lbs. With this degree of obesity, there is a minimum doubling of the prevalences of all causes of morbidity and mortality. Weight reduction should be recommended for patients with BMIs equal to or above 27. Weight reduction is also desirable at all levels of obesity if the patient has concomitant diabetes, hypertension, heart disease or other cardiovascular risk factors. The trend toward increasing levels of obesity in the industrial world has to be reversed. Public health measures including education, counseling and possible legislation similar to that done with smoking are necessary to counteract this serious disease. Obesity and Hypertension Hypertension is a common concomitant of obesity. In overweight young adults, age 20-45, the prevalence of hypertension is 6 times that of their normal-weight peers. Weight gain in young adult life is a potent risk factor for the later development of hypertension. Hypertension is infrequent in "primitive" populations who tend to weigh less with advancing years. The distribution of fat in the body may have an important affect on blood pressure risk, with central or upper body fat being more likely to raise blood pressure than lower body fat in the gluteal or thigh region. In obese patients, an accumulation of abdominal fat results in the release of free fatty acids into the portal vein which causes an excess hepatic synthesis of triglycerides, insulin resistance and hyperinsulinemia. Obesity and Diabetes Even moderate obesity, particularly abdominal obesity, can increase the risk of non-insulin dependent diabetes mellitus (NIDDM) ten-fold. Fat tissue apparently has two roles in promoting diabetes: it increases the demand for insulin and, in obese individuals, it creates insulin resistance, and, therefore, hyperinsulinemia. Adipose tissue sensitivity to insulin remains high. It is therefore possible that nutrients are preferably sent into fat for storage. Some of the insulin resistance in obesity can be attributed to a decrease in insulin receptors; there are also intracellular post-receptor defects. Weight reduction in the obese NIDDM will lead to improvement of glycemic control as well as improvement of concomitant medical problems such as hypertension or hyperlipidemia. Cardiovascular Disease and Fat Distribution In long duration studies, such as the Framingham Study, an increased risk of cardiovascular disease is noted with increasing levels or obesity independent of other risk factors. It is calculated that, in men, for each 10% increase in body weight there is approximately a 20% increase in the incidence of coronary artery disease. For every 10% increase in relative body weight, systolic blood pressure increases 6.5 mm/Hg, plasma cholesterol 12 mg/dL and fasting blood glucose 2 mg/dL. Acquired obesity in men tends to be localized to the trunk. Both the degree of obesity and the distribution of body fat, independently and additively, contribute to the risk factors for cardiovascular disease. The simplest way to measure the degree of abdominal obesity is to record the waist circumference and divide it by the hip circumference. In men, the risk of cardiovascular disease increases sharply when waist/hip ratio (WHR) is above 1.0, and in women above 0.8. Numerous reports have indicated that a high proportion of either truncal or abdominal fat is associated with insulin resistance, hyperinsulinemia, impaired glucose tolerance, diabetes, an athrogenic plasma lipid profile and an elevated blood pressure. It has been postulated that high levels of total body fat must be present to observe the deleterious effects of visceral fat on plasma lipoprotein metabolism. Human adipose cells specifically bind HDL. This binding is related to fat cell size. In patients with abdominal obesity, there may be a disproportionate uptake of HDL cholesterol contributing to the reduction in plasma levels. The abdominal visceral fat depot primarily functions for storage of easily and rapidly mobilizable energy reserves. In women the femoral-gluteal depot functions primarily as a storage organ dedicated to female stresses such as pregnancy and lactation. This anatomical and functional specialization is governed by sex hormone balance. In premenopausal obese women, as the waist/hip ratio increases, there is a progressive decrease in sex hormone binding globulin and an increase in free testosterone levels. Increased androgenic activity also increases plasma free fatty acid levels and contributes to abnormalities in insulin dynamics. It has been suggested that the abdominal fat pattern may represent an increase in the size and the number of metabolically active intra-abdominal fat cells. Hypertrophy of the abdominal adipocytes in the upper-body obese might also be a manifestation of hyperandrogenicity. These fat cells release fatty acids directly into the portal circulation and might interfere with insulin clearance in the liver and thus affect various metabolic processes. The association of abdominal fat with metabolic abnormalities is additive to the effects of generalized body obesity. Even mild to moderate obesity should be treated if excess adipose tissue is found mainly in the abdominal region. To assess cardiovascular risk, it is recommended that the WHR be used simultaneously with the determination of total body fat. Obesity and Cancer Overweight men have a significantly higher mortality rate for colorectal and prostate cancer; men whose weight is 130% or more above average are 2.5 times more likely to die of prostate cancer during a 20 year follow-up compared to men of average weight. Menopausal women with upper body fat localization have an increased risk of developing breast cancer. Overweight women also have higher rates of cancer of tile uterus and ovaries. Obesity is also correlated with increased estrogenicity of cervical smears. These problems may reflect an increase in the conversion of estrone to androstenedion by the stromal elements of adipose tissue. Obesity and Endocrine Abnormalities Obese women, especially those with upper body obesity, show more irregularity in menstrual cycles as well as greater frequency of other menstrual abnormalities than normal weight women. They also have more problems during pregnancy with an increased frequency of toxemia and hypertension. In obese girls, the onset of menarche occurs at a younger age than in normal weight girls. Menstruation is probably initiated when body weight reaches a critical mass. Obesity and Gall Bladder Obese women in the 20-30 year age range have a six-fold increase in the risk of developing gall bladder disease compared to normal-weight women. By age 60, nearly one-third of obese women can be expected to have developed gall bladder disease. For each kilogram of fat, approximately 20 mg/dL of cholesterol is synthesized. In obese persons, the bile is therefore more saturated with cholesterol. There is also hypomotility of the gall bladder. Fatty infiltration of the liver, steatosis, is associated with obesity. However, this abnormality is generally not associated with abnormal liver function tests. Obesity and Pulmonary Abnormalities There are several abnormalities in pulmonary function in obese individuals. At one extreme are patients with so-called Pickwickian syndrome, or the obesity-hypoventilation syndrome, which is characterized by somnolence and hypoventilation; it eventually leads to cor pulmonale. In patients who are less obese, there is a fairly uniform decrease in expiratory reserve volume and a tendency to reduction in all lung volumes. A low maximum rate of voluntary ventilation and venous admixture is also present. As an individual becomes more obese, the muscular work required for ventilation increases. In addition, respiratory muscles may not function normally in obese individuals. Obesity and Arthritis Although the cause is unclear, there is a significant correlation between uric acid levels and weight. In the 45-64 year old age group, the prevalence of gout goes up dramatically when relative weight is greater than 130% above desirable. An increase in body weight adds trauma to weight bearing joints and in middle age women excess body weight is a major predictor of osteoarthritis of the knee. This is a mechanical problem and not a metabolic one. Weight loss will markedly decrease the chance of developing osteoarthritis. Obesity and Functional and Psychological Disorders The obese individual has functional impairment in the activities of daily living. This dysfunction is related to sleep, recreation, work and social interactions. Obese patients also have physical incapacity due to back and joint problems and shortness of breath. This contributes to their proneness to fatal accidents. In the severely obese there is an increased incidence of absenteeism and unemployment. Discrimination against obese persons is common in both academic and work settings. Impairment in body image is the major form of psychological disturbance specific to obese persons. However, psychological disturbances do not appear more commonly in overweight persons than in those with normal weight. Emotional disturbances are often likely to be a consequence of obesity rather than the cause. In some studies, obese persons were found to be significantly less anxious and depressed than normal weight persons. 返回

5、专家网上发出警告

肥胖儿易患性发育障碍

　　本报讯 小儿肥胖综合症已成为危害儿童健康，特别是性健康的大敌。据健康报报道，男性病专家李继琦近日通过卫生部金卫医疗网络在省级远程会诊时发出警告：肥胖将成为21世纪青少年健康的第一杀手。

　　富裕的生活，全方位的“呵护”，哺育出越来越多的肥胖儿童。专家介绍，肥胖儿不仅皮下脂肪严重堆积，内脏器官的细胞也在悄悄地脂肪化。更为可怕的是，指挥孩子生长发育的“司令部”——大脑垂体细胞也正在逐渐被脂肪细胞所代替，由此造成性激素的分泌紊乱，可导致男孩女性化、女孩男性化，成年后导致性无能和生殖无能。

　　专家忠告肥胖儿父母：应经常注意孩子生殖系统的发育，孩子7周岁就应配合医生开始监测，8周岁每年要检查两次，9周岁每年要检查3次，12岁半之前是肥胖儿性发育的“红灯期”，一定要勤于检查，以保证孩子能进入正常的青春发育期。 返回