From: Centers For Disease Control and Prevention at http://www.cdc.gov/tobacco/data_statistics/fact_sheets/health_effects/effects_cig_smoking/
Smoking harms nearly every organ of the body. Smoking causes many diseases and reduces the health of smokers in general.1
Smoking causes death.
Compared with nonsmokers, smoking is estimated to increase the risk of—
Centers for Disease Control and Prevention
National Center for Chronic Disease Prevention and Health Promotion
Office on Smoking and Health
“Studies have shown that workers facing job strain (or its components—high job demands and low job control) smoke more (if they are smokers) or have greater difficulty quitting smoking [110-113]. In some studies, workers with job strain are heavier and exercise less [110, 114, 115]. Workers with low job control have higher levels of plasma fibrinogen, a chemical in the blood that contributes to atherosclerosis, that is, hardening of the arteries [116, 117]. And workers with low job control or job strain, in some studies, show greater atherosclerosis in the arteries in the heart or the arteries going to the brain [118-121]. High blood pressure also contributes to atherosclerosis .”
Taken from: Schnall PL, Dobson M, Rosskam E, Editors Unhealthy Work: Causes, Consequences, Cures. Baywood Publishing, 2009.
110. Hellerstedt, W. L. and R. W. Jeffery, The Association of Job Strain and Health Behaviours in Men and Women, International Journal of Epidemiology, 26:3, pp. 575-583, 1997.
111. Kawakami, N., T. Haratani, and S. Araki, Job Strain and Arterial Blood Pressure, Serum Cholesterol, and Smoking as Risk Factors for Coronary Heart Disease in Japan, International Archives of Occupational and Environmental Health, 71:6, pp. 429-432, 1998.
112. Green, K. L. and J. V. Johnson, The Effects of Psychosocial Work Organization on Patterns of Cigarette Smoking among Male Chemical Plant Employees, American Journal of Public Health, 80, pp. 1368-1371, 1990.
113. Landsbergis, P. A., P. L. Schnall, D. K. Deitz, K. Warren, T. G. Pickering, and J. E. Schwartz, Job Strain and Health Behaviors: Results of a Prospective Study, American Journal of Health Promotion, 12:4, pp. 237-245, 1998.
114. Siegrist, J. and A. Rodel, Work Stress and Health Risk Behavior, Scandinavian Journal of Work Environment and Health, 32:6, pp. 473-481, 2006.
115. Johansson, G., J. V. Johnson, and E. M. Hall, Smoking and Sedentary Behavior as Related to Work Organization, Social Science and Medicine, 32, pp. 837-846, 1991.
116. Markowe, H. L., M. G. Marmot, M. J. Shipley, et al., Fibrinogen: A Possible Link between Social Class and Coronary Heart Disease, British Medical Journal, 291, pp. 1312-1314, 1985.
117. Brunner, E. J., G. D. Smith, M. G. Marmot, R. Canner, M. Beksinska, and J. O’Brien, Chi l dhood Soci al Ci r cumst ances and Psychosoci al and Behavi or al Fact or s as Determinants of Plasma Fibrinogen, Lancet, 347, pp. 1008-1013, 1996.
118. Langosch, W., B. Brodner, and M. Borcherding, Psychosocial and Vocational Long- Term Outcomes of Cardiac Rehabilitation with Postinfarction Patients under the Age of Forty, Psychosomatic Medicine, 40, pp. 115-128, 1983.
119. Muntaner, C., F. J. Nieto, L. Cooper, J. Meyer, M. Szklo, and H. A. Tyroler, Work Organization and Atherosclerosis: Findings from the Aric Study. Atherosclerosis Risk in Communities, American Journal of Preventive Medicine, 14, pp. 9-18,
120. Hintsanen, M., M. Kivimaki, M. Elovainio, et al., Job Strain and Early Atherosclerosis: The Cardiovascular Risk in Young Finns Study, Psychosomatic Medicine, 67:5, pp. 740-747, 2005.
121. Rosvall, M., P. O. Ostergren, B. Hedblad, S. O. Isacsson, L. Janzon, and G. Berglund, Work-Related Psychosocial Factors and Carotid Atherosclerosis, International Journal of Epidemiology, 31:6, pp. 1169-1178, 2002.
122. Steptoe, A. and M. Marmot, Atherogenesis, Coagulation and Stress Mechanisms, Occupational Medicine: State of the Art Reviews, 15:1, pp. 136-138, 2000.
DIABETES & OBESITY:
“Studies show that diabetes impacts employment, absenteeism, and work productivity [55, 76] and that obesity is strongly associated with absenteeism and other health risks . Moreover, obesity also may act as a co-risk factor for the development of a number of work-related diseases, such as occupational asthma and cardiovascular disease. It is theorized that obesity may modify the worker’s response to occupational stress, immune response to chemical exposures, and risk of disease from occupational neurotoxins .
Work-induced risk factors, such as long work hours and sedentary work, are contributing to the epidemic of obesity, one which will be far greater than the epidemic of the present, while the changing ethnic fabric of the population in the coming decades will no doubt exacerbate significantly the epidemic of diabetes. The anticipated and alarming growth in the epidemics of obesity and diabetes, influenced by both changing patterns of work and ethnicity, will act like a tsunami, contributing to both hypertension and cardiovascular diseases which will, in turn, have tremendous impacts at both the societal and individual levels. Given the poor efforts toward preventing and treating the present epidemics of obesity and diabetes, there is little reason to think that status quo measures will be more successful in addressing epidemics of a far greater scale. Prevention is, and will continue to be, critical.”
Taken from: Schnall PL, Dobson M, Rosskam E, Editors Unhealthy Work: Causes, Consequences, Cures. Baywood Publishing, 2009.
47. Schulte, P. A., G. R. Wagner, A. Ostry, et al., Work, Obesity, and Occupational Safety and Health, 97:3, pp. 428-436, 2007.
55. Stewart, W. F., J. A. Ricci, E. Chee, A. G. Hirsch, and N. A. Brandenburg, Lost Productive Time and Costs Due to Diabetes and Diabetic Neuropathic Pain in the US Workforce, Journal of Occupational and Environmental Medicine, 49:6, pp. 672-679,
76. Tunceli, K., C. J. Bradley, D. Nerenz, L. K. Williams, M. Pladevall, and J. Elston Lafata, The Impact of Diabetes on Employment and Work Productivity, Diabetes Care, 28:11, pp. 2662-2667, 2005.
There are several methods used to calculate distribution of body fat:
1. Waist-hip ratios are valuable in clinical use as they are easily measured and analyzed. It is the method used to primarily measure abdominal and visceral fat, as more fat is located in the waist area and less in the hip area. Waist refers to the circumference of the body at the level of the umbilicus (belly button) and hip refers to circumference of the body around the trochanter (at the level of the hip). The normal waist-hip ratio for men is 1.0, and for women is 0.8. Individuals with ratios above the normal are considered upper-body obese.
2. Body Mass Index (BMI) is commonly used to compare subjects in a research study. It can be calculated using the formula, weight (kg)/height(m)2. The average male BMI is 25 (considered normal). A body mass index of 28 for males is considered overweight, while 31 depicts obesity. For females, the numbers are slightly smaller: 21 is normal, 25 is overweight, and 29 is obese.
Both waist-hip ratios and BMI are good predictors of hypertension.
3. Skin fold thickness is another measure of percentage of body fat and distribution of body fat. Skinfolds of the subscapular and triceps among others are measured to calculate subcutaneous fat. An analysis reported in the Health and Nutrition Examination Survey (HANES) suggests that centrally located fat measured by the subscapular skinfolds are better predictors of hypertension than the triceps skinfold. In addition, CT and MR scans measure subcutaneous and visceral fat. Other determinations of fat have been accomplished by underwater weighing and fat biopsy.
Genetics (data from studies of twins), overeating, smoking cessation, alcohol consumption, lack of exercise, change in life-style, energy intake vs. energy expenditure (consider resting metabolic expenditure), environmental factors, salt/potassium retention, major depression/anxiety/other psychological, medical illness, medications, during and after pregnancy, cultural (perceptions on obesity), socioeconomic factors.
Fatigue (especially with exercise), shortness of breath, decreased energy, palpitations, irregular heart beat, edema (especially swelling of the feet and legs), sleep apnea (Pickwickian syndrome), respiratory obstruction (for obesity to cause sleep apnea and repitory obstruction it must be severe).
Hypertension (increased blood pressure), coronary heart disease, predisposition to diabetes, hyperlipidemia (increased cholesterol level), metabolic abnormalities, increased risk for gallbladder disease, gout, some types of cancer, development of osteoarthritis of the weight-bearing joints.
Being overweight is a significant risk factor for the development of hypertension. The prevalence of hypertension in the U.S. is greatly increased by the fact that one quarter to one half of all adults (prevalence varies by study) are overweight. Although the association between higher body fat and blood pressure has been recognized for years, recent studies have discovered a 50% to 300% higher incidence of hypertension among adults who consider themselves overweight compared to those classified as normal weight. Similar findings are revealed from studies involving children and young adults, in which the correlation coefficient between weight and blood pressure has been observed to be as high as 0.4. Two proposed mechanisms underlying this correlation are the stimulation of sodium retention and increased catecholamine release, which are results of increased sodium sensitivity and hyperinsulinemia. Age, gender, and race are modifiers/confounders of obesity, and should be considered when studying preventive interventions. Hypertension and obesity treatment are necessary to avoid potential morbidity and mortality from coronary heart disease or stroke.
1. Nonpharmacologic treatment of mild hypertension could include dietary salt restriction (NaCl), dietary potassium supplementation, and/or weight reduction, physical exercise, meditation and other therapies (e.g., biofeedback).
Salt restriction is recommended for those individuals with hypertension who are “salt-sensitive,” or are prone to retaining sodium, gaining weight, and developing a rise in blood pressure as a result of a high-salt diet. Those who are “salt-resistant,” on the other hand, do not experience change in weight or blood pressure on either high or low-salt diets. For the salt-sensitive population, extreme amounts of salt restriction are not needed for improvement of blood pressure. Several studies have shown that diets containing 1600 to 2300 mg of sodium per day are associated with average reductions in systolic pressure of -9 to -15 mm Hg and in diastolic pressure of -7 to -16 mm Hg in salt sensitive individuals. Thus, salt restriction in this range is recommended in the dietary management of most individuals with hypertension.
The blood pressure lowering effect of supplemental potassium may be greater in patients receiving a high-salt diet. The amount of dietary potassium required to obtain this effect, however, is not easily obtained.
Six controlled studies of patients with hypertension concluded that short-term weight loss is usually associated with a reduction of blood pressure. In patients who experienced a weight loss of 11.7 kg (~25.7 lb.), an average blood pressure reduction of -20.7/-12.7 mm Hg was recorded. A similar study found that a decrease in blood pressure of -2.5/-1.5 mm Hg per kilogram of reduction of weight, further demonstrated a significant correlation between weight change and blood pressure change.
Physical exercise is a critical component of any program to reduce and control weight on a long term basis. See the following website for additional information on exercise (link under construction).
2. Pharmacologic treatment of hypertension is essential when the disease has advanced to a more chronic phase. The most common forms of treatment are diuretics, beta blockers, and calcium channel blockers. Controversial and expensive alternatives to dieting in treating obesity are surgery and/or liposuction, which should be used only as a last alternative. Future research for treating obesity includes inhibiting gastric emptying, stimulating lipid oxidation, increasing thermogenesis, and blocking carbohydrate or lipid digestion.
Dietary change, exercise, behavior modification, drug treatment, and/or a combination of these interventions. Limitations on dietary intake, the most common method used for weight loss, can last several weeks to months, depending on individual need and motivation. Altering dietary proportions of fat, protein, carbohydrate, using macronutrient substitutes, and taking vitamins, diet supplements or meal replacements are all techniques to modify food intake. In addition, low calorie diets (1000-1500 calories/day) and very low calorie diets (800 or less calories/day) help patients lose weight. Physician supervision is recommended, however, to prevent adverse side effects, such as excessive loss of lean body mass, particularly in individuals with chronic health problems such as hypertension. Eating and chewing food slowly will send nervous system signals to the stomach that it is “full,” and will assist in weight loss and deter weight gain after dieting, especially if a healthy diet is selected. Exercising is another way to lose weight, although the average weight loss from exercise alone is 4-7 lb. (8.8-15.4 kg.), greater weight loss is possible. Regular workouts are advantageous to increasing high-density lipoprotein cholesterol and lean body mass, and diminishing rapid weight gain. Along with changing eating patterns and increasing physical activity, behavior modification produces gradual change.
Four steps to behavior modification include: 1) identifying eating or related life-style behaviors to be modified, 2) setting specific behavioral goals, 3) modifying determinants of the behavior to be changed, and 4) reinforcing the desired behavior. Drug treatment is another method used for weight loss. With prolonged use, however, loss of weight is minimized as it reaches a plateau. Some side effects are common. An example of an over the counter drug is phenylpropanolamine which, however, has a negative effect on blood pressure, and little is known about it’s long-term side-effects.
On average, 1-1.5 lb./week (~.45-.68 kg./week) are lost by combining excercise, reducing dietary intake, and behavior modification. Successful weight loss involves a combination of these methods that are suitable to the individual in a slow and steady process. Remember who won the race.
1. Fraser G. Preventive Cardiology. Oxford University Press, New York, 1986, pp. 134-5.
2. Gerber L, Schnall P, and Pickering T. Body fat and its distribution in relation to casual and ambulatory blood pressure. Endocrinology and Metabolism Clinics of North America, Sept. 1995, 24(3).
3. Hurst JW, Logue RB, Rackley CE, et. al. The Heart, Sixth Edition. McGraw-Hill Book Company, New York, 1986, pp. 1078-9.
4. Methods for voluntary weight loss and control. NIH Technology Assessment Statement, 1992 March 30-April 1,(10).
5. Moore T and McKnight J. Dietary factors and blood pressure regulation. Endocrinology and Metabolism Clinics of North America, Sept. 1995, 24(3).