Lifestyle factors

Convincing evidence indicates that ROS generated both endogenously and also in response to diet and lifestyle factors may play a significant role in the etiology of atherosclerosis and CHD. Indeed, free radicals are responsible for LDL oxidation, which is involved in the initiation and promotion of atherosclerosis. Thus, protection from LDL oxidation by antioxidants such as carotenoids may lead to protection against human CHD. 

It is important for the clinician to identify the cause(s) of AHF in order to maximize treatment efficacy and reduce future disease exacerbations. Cardiovascular, metabolic, and lifestyle factors can all precipitate AHF. The most common precipitating factors for acute decompensation and how they contribute pathophysiologically are listed in Table 3-3. 

Non-modifiable risk factors include age, gender, race/ ethnicity, and heredity. Ischemic stroke risk is increased in those greater than 55 years of age, in men, and in African-Americans, Hispanics, and Asian-Pacific Islanders. It is also increased in those with a family history of stroke. Modifiable risk factors include a number of treatable disease states and lifestyle factors that can greatly influence overall stroke risk. Hypertension is... 

Hypercholesterolemia Lifestyle factors Cigarette smoking Excessive alcohol use Physical inactivity Obesity Diet... 

Review the patient history for contributing lifestyle factors and other disease states that may help guide therapy. 

In summary, the true association between most dietary factors and the risk of colon cancer is unclear. The protective effects of fiber, calcium, and a diet low in fat are not completely known. Lifestyle factors such as NSAID use and hormone use appear to decrease the risk of colorectal cancer, whereas physical inactivity, alcohol use, and smoking appear to increase the risk of colon cancer. Clinical risk factors and genetic mutations are well-known risks for colon cancer. 

Heaney, R., Bone mass, nutrition and other lifestyle factors, American Journal of Medicine, 95, 29S, 1993. 

Selection of an adjuvant regimen (Table 62-1) is based on patient specific factors including performance status, comorbid conditions, and patient preference based on lifestyle factors. 

ROCK C L, THORNQUIST M D, KRISTAL A R, PATTERSON R E, COOPER D A, NEUHOUSER M L, neumark-sztainer D and cheskin l j (1999), Demographic, dietary and lifestyle factors differentially explain variability in serum carotenoids and fat-soluble vitamins baseline results from the sentinel site of the Olestra Post-Marketing Surveillance Study , J Nutr, 129(4), 855-64. rodale (1996), The Prevention Index - a report card on the nation s health, 1996 summary report. Rodale Press, Inc, Emmaus, Pennsylvania. SANDLER R S, ZORICH N L, FILLOON T G, WISEMAN H B, LIETZ D J, BROCK M H, ROYER M G and MIDAY R K (1999), Gastrointestinal symptoms in 3181 volunteers ingesting snack foods containing olestra or triglycerides , Annals Internal Med, 130, 253-61. 

Reduced penetrance probably results from a combination of genetic, environmental, and lifestyle factors, many of which are unknown. This phenomenon can make it challenging for genetics professionals to interpret a person s family medical history and predict the risk of passing a genetic condition to future generations. 

As with reduced penetrance, variable expressivity is probably caused by a combination of genetic, environmental, and lifestyle factors, most of which have not been identified. If a genetic condition has highly variable signs and symptoms, it may be challenging to diagnose. 

It has become customary among cancer epidemiologists to talk about certain lifestyle factors as important contributors to cancer risk. Lifestyle factors (smoking, dietary patterns, alcohol consumption) are assumed to be largely under the control of individuals. These are distinguishable from factors that are less directly in the control of individuals (occupation, medicines, consumer products), and those over which individuals have little or no control (food additives, pesticides, environmental pollutants). Just how much control individuals have over the various lifestyle factors is of course much debated. 

In 1981, two eminent British cancer experts. Sir Richard Doll and Richard Peto published a paper in the Journal of the National Cancer Institute entitled The causes of cancer Quantitative estimates of avoidable risks of cancer in the United States today. The authors drew upon a vast body of literature of the type mentioned above, and attempted to allocate the deaths caused by cancers among various responsible factors. The authors concluded that a certain percentage of human cancer deaths could be avoided if exposure to the responsible factors could be eliminated or controlled in some way, although the appropriate degree and nature of control for some of the lifestyle factors, especially diet, is still highly uncertain. The Doll and Peto estimates are presented in Table 5.2. The factors are listed in a somewhat different order from how they were listed by the original authors, because of our interest in clearly separating lifestyle factors (the first... 

The Doll-Peto estimates, and others as well, nevertheless suggest a primary role for lifestyle factors, not chemical pollution and industrial products, in cancer causation. 

The substances we have described in this book turn out to be, for the most part, minor threats to our health. There are, however, perhaps thousands of these threats, and so a regulatory system has evolved to reduce the risks of individual substances to very low levels. There is considerable work yet to be done, to learn the toxic properties of many poorly tested chemicals, and to assess their health risks, but once this is done, regulatory officials have available strong weapons (which they do not always choose to deploy) to reduce exposures when necessary. The burden for exposure reduction falls not on exposed individuals (as in the case of lifestyle factors), but rather upon those who have caused the exposures to occur. 

Several lifestyle factors predispose to cancer development, including smoking tobacco and exposure to sunlight (especially for children and the fair-skinned). It should be noted that low levels of continuous sun exposure may protect against breast and colon cancer, perhaps as a result of raising vitamin D levels which has already been discussed described. 

Some limited information (i.e., anecdotal, single acute-duration exposure, and workplace exposure) is available on the health effects of human exposure to 1,4-dichlorobenzene via inhalation and the oral route. For persons exposed via inhalation, there is information on death, systemic effects, neurologic effects, or the role of lifestyle factors resulting from intermediate- and chronic-duration exposure. There is also information on systemic effects in humans resulting from acute-, intermediate-, and chronic-duration oral exposure. It is important to note that most of this information was obtained from case studies in which levels and durations of exposure to 1,4-dichlorobenzene were unknown or uncertain. 

Scientific procedures for risk assessment include assessment of risk for human health as well as risk for the environment. A substantial part of the EU risk assessment work was in 1997 delegated to the DG SANCO, in relation to the scandal surrounding BSE (bovine spongiform encephalopathy or mad cow disease ). Risk assessment work not under DG SANCO includes pharmaceuticals, working environment, and health effects caused by lifestyle factors such as diet, smoking, and alcohol consumption (EU 2006f). 

In general, a poor nutritional state and a diseased state can be expected to influence the sensitivity to chemicals. This is of special concern when the target organ of the toxic effect is affected by the disease, or when the metabolism and elimination are disturbed. Also lifestyle factors such as alcohol, tobacco smoke, and drugs may modify the toxic responses of chemicals. 

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