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RESPIRATORY DISEASES (COPD)

Abstract: Respiratory disease or COPD is now a very major life terminating disease in the US. Its principal cause has been and is cigarette smoking, and most deaths in US vital statistics are for those that smoke. Other air pollution - and especially that from the smoking of others - contributes further. Exercise is a key program that is recommended to those suffering COPD, and a good program of exercise that improves cardiofitness probably can reduce risk of suffering the disease substantially. Adequate consumption of Vitamin C, Beta Carotene, and other antioxidants can reduce risk. Of particular probable benefit is the regular daily eating of grapefruit, oranges, and melons. Omega-3 fats included in fish also appear to reduce the risk of COPD diseases significantly.

Backgound: Respiratory diseases now called chronic obstructive pulmonary disease or COPD is the fourth largest cause of death in the US and rivals stroke as a cause of major disabling disease, hospitalization and premature death. COPD includes chronic bronchitis, emphysema, asthma, and some other diseases of the respiratory system. Most of these diseases when present to the extent that some hospitalization is needed may be irreversible. At this level, a diminished lung function and perhaps requirement for continued use of oxygen to assist breathing can seriously reduce the quality and subsequent length of life. Risks of COPD disease occur at widely differing levels depending the extent they limit a person's expiratory air flow. A clear diagnosis of the disease often suggests that it may be irreversible and progressive. Life Ahead identifies risk of these diseases at the rather severe if approximate level that usually requires hospitalization and may not be reversible.

Respiratory disease is measured by the amount of air that can be processed by the lung, and how fast this air can be processed The term FEV1 identifies the amount of air that can be exhaled in one second. The term FVC identifies the amount of air in the lungs at maximum inhale. The ratio of FEV1 to FVC shows the proportion of inhaled air that can be exhaled in measured time, and thus identifies the rate at which the lungs can process air. As obstructions accumulate in the airways this percentage declines from a healthy value of above 80% to 30% or less for those with serious COPD. Another measure is the FEV1 as a percentage of a predicted population value for a person of the same size in height, sex and age. This is called FEV1 vs. predicted. As either or both of these two key measures drop much below about 80% the severity of COPD increases. Values much below 70% can indicate possible irreversible disease that is serious. Values much below 50% often will lead to hospitalization. Values for healthy individuals can vary considerably, as for example from 80 to 110%. But a decline of values over time even at the higher levels can indicate the building up of lung obstructions. Thus doctors usually monitor the health of the lung function if any indication of a problem exists.

Smoking Risks: Cigarette smoking is by far the major cause of this most important COPD or respiratory disease. In fact most of this disease presently classified in US health statistics was experienced by present or former smokers. Some typical percents of risk and risk ratios of male smokers vs. nonsmokers of age 50 in a next 10 year period are:

Non Smokers Smoking typical 30 Ratio of Risk

cigarettes per day

For Respiratory Disease 0.56 6.1 10.9

For Lung Cancer 0.22 7.2 32.7

Risks for either respiratory disease or lung cancer usually are quite small for average non-smokers. But risks of COPD disease are 10 times larger for smokers and reach a substantial 6% and are near equal to the risks of lung cancer during just during this 10 year period. These added risks grow far higher during years following. Note that the risks of suffering one of these two major problems is 13%, or about one in 7 of all average smokers of age 50 will be afflicted in a subsequent 10 years. And many more will suffer increased risks of heart disease and other forms of cancer during this same future time. Risks will be even higher for those that smoke more than average, that are exposed to above average air pollution or passive smoking, or that have other above average following risk factors for COPD. The Life Ahead program will compute and display actual user risks of these diseases or of death from these diseases for any desired time ahead from any starting age to future ages up to life expectancy. Risks of women for these diseases are similar to those for men. Much more about risks of smoking is included in the article on smoking risks.

Other Air Pollution: Other forms of air pollution create another risk of COPD . Although smoking is an actionable health habit that can be modified, most risks of air pollution may not be controllable. But people should become aware of such risks because they add to the risks of habits that are actionable. High non-actionable or inherent risks can increase the need for better than usual actionable habits. Two forms of this Other Air Pollution are the general air we breath in our environment, and the air breathed that includes the smoke of others and that is called passive smoking. Life Ahead approximates these health effects as pollution equivalents of regular smoker's cigarettes per day. An exception here is that some effects of air pollution including its risk of lung cancer differ somewhat from that of actual cigarette smoking. These equivalents are as follows:

Environment Passive Smoking

Usual Living Area Equivalent Cigarettes/Day Usual Exposure Equivalent Cigarettes/Day

Rural 0.2 Little 0.1 (very small exposure)

Rural/Suburban 0.6 Average 0.5 (usual today)

Suburban/Industrial 0.9 Fair Amount 1.0 (work or home)

Industrial 1.1 Quite a Bit 2.5 (work and home)

These numbers of cigarettes are small vs. those consumed by habitual smokers. But keep in mind that the health effect of cigarettes operates to a 0.5 power of the number smoked. Or 2.5 per day produces half of the health equivalent of 10 per day. And that combinations of best vs. poorest environment can make a difference of 3.6 vs 0.3 or 3.3 cigarettes per day of life time smoking. Also in the past many men were exposed to much higher equivalents of Other Air Pollution in asbestos and chemical plants and other industrial facilities. But the more stringent environmental regulations of today and the many fewer persons engaged in such occupations have made such environments less frequent.

An average level of this Other Air Pollution is now estimated at the equivalent of 1.4 cigarettes per day. This is a much smaller risk than that existing in past years both from the then higher levels of general air pollution and from the then usual environments that then included up to more than half of men smoking cigarettes in nearly every workplace and restaurant. A test with Life Ahead suggests that a lowest above level of 'Other Air Pollution' vs. average would add about 450 Well-Days or about 1.2 years to healthful life. A highest general level would subtract 630 Well-Days or 1.7 years of healthful life from average. Thus over the range now measured a difference between highest and lowest Other Air Pollution would develop a difference of about 3 years of healthful life. But the probable differences in overall Other Air Pollution that most people today experience more probably would produce differences in the order of perhaps one year or less of healthful life. Thus in spite of vast publicity about these environmental effects on our public health, Other Air Pollution probably is of far lesser importance to today's average person than is the effect of actionable habits of exercise, diet, and cigarette smoking that can accumulate to produce 10, 20 and even 30 years of healthy life. But those than can reduce risk of this health factor should try to take useful action. More on air pollution is included elsewhere on this web site.

Exercise and Cardiofitness: After COPD is diagnosed, doctors recommend a variety of approaches than can include smoking cessation, exercise, airway dilators, hydration, vaccinations, oxygen, antibiotics, decongestants, and breathing exercises. Important on this list is the use of medically monitored exercise programs. Much research has shown that carefully programmed exercise will usefully improve cardiofitness as measured by a distance walked in 6 or 12 minutes or by other fitness tests. Results from a such a program carried out for a few weeks can improve physical capability and perceived health for up to two following years. And continued exercise although rarely a complete cure for COPD can provide somewhat better enjoyment of and length of life.

More than hundred studies have been published on the results of these monitored exercise programs for COPD patients. Incredibly, an extensive search through a thousand studies of COPD fails to find even one single useful direct research of the value of exercise or cardiofitness in preventing the disease! If exercise is such a help to those that contracted it, a fairly obvious question is "Why not try to prevent COPD by more exercise before it happens? This is a illustration of the large attention our medical establishment pays to the curing diseases versus the tiny fraction of this effort spent in preventing them from occurring in the first place Yet there should be little question that the exercise that helps patients having the disease also would prevent or slow it from occurring in those that are healthy. This was demonstrated by results from the Cooper Institute's important study of effects of cardiofitness on the respiratory function. (Cheng, YJ, 2003, Br J Sports Med 37:521-8). Results of this study that are easily translated from the published times of individuals on a treadmill to the the more useful fitness measure of CFR are:

Cardiofitness in CFR FEV1/FVC

For Men For Women

90 poor cardiofitness 70.3 73.0

100 Avg sedentary 76.3 77.0

120 Good cardiofitness 79.4 78.9

140 Excellent cardiofitness 85.4 82.8

At the poor cardiofitness of 90 CFR values of FEV1/FVC already are borderline levels for mild COPD. Values for those of excellent cardiofitness are a healthier 15 units higher for men and 10 units higher for women. FEV1/FVC typically declines at about 1.4% for each decade of average healthy life, and perhaps 4-5% per 10 years of age for those contracting COPD. Thus the improved margin of 4-6% for good vs. poor fitness should delay onset of the disease by at least 10 years for those destined eventually to suffer it. And it can be far more efficient to exercise before getting COPD because a deprived lung function can make it much more difficult to exercise effectively after the disease is suffered.

There are a variety of ways for translating this information into estimated risks of disease at age. A very conservative approach suggests that each improvement of one in CFR should reduce risk of COPD by about 3% or a factor of 0.97. This would reduce risk about 26% for a 10 improvement in CFR, and 46% for a 20 improvement in CFR. This is a much smaller reduction in risk for COPD than those for cardiofitness in reducing risks of heart disease and cancer. But this basis is now used in Life Ahead to give at least some recognition to the highly probable value of cardiofitness in reducing risks of respiratory diseases. Life Ahead focuses on what individuals can do for themselves to protect health, and thus does not attempt to value the benefits of medical treatments or interventions such at the above mentioned exercise programs for those having COPD.

Diet Antioxidants: Diet can have a significant effect of an individuals' risk of respiratory disease. Results from nearly 50 different research papers were studied in developing the diet factors on COPD that now are included in Life Ahead version #3. Key diet factors that can improve the lung function are the antioxidant vitamins mostly included in consumption of fruits and vegetables. Low vitamin values result in significantly diminished lung capacity and function, and in higher risks of these very disabling COPD diseases.

The benefits of Vitamin C on lung function have been reported in nearly two dozen papers. Nearly all show that lung function is related to amounts of Vitamin C either in diet or plasma (blood). Most studies reported only a rough value of improved FEV1 or this plus improved FVC for some higher level of Vitamin C. The only useful dose related relationship found was in (McKeever, TM, Am J Respir Crit Care Med 2002, 165:1299.) This relationship suggested effects of dietary Vitamin C values of 50, 100, 200, and 300 mg/day to develop values of -30, 0, +45, and +60 ml of FEV1. Results from other studies varied considerably, but in aggregate were roughly consistent with this relationship. It appeared that the largest negative effect on lung function resulted when Vitamin C levels dropped below about 100 mg/day, with decreased benefit if any for values above 200 mg/day. Usual study populations values were in the range of 100 to 150 mg/day, and a typical population value in the US now is about 150 mg/day of Vitamin C from diet per se.

It seems likely that a variety of other antioxidant nutrients probably will improve lung function. A study of (Holger,S, Am J Respir Crit Care Med 163:1246) showed that plasma or blood values of Vitamins C, E, Beta Carotene, Retinol and Lycopene were related similarly to respiratory function. Vitamin E was studied in several studies and usually showed a benefit. But problems were encountered in quantifying effects of most other antioxidants. Nearly all studies appeared based on dietary nutrients only in foods, and seriously lacking was adequate study of the effect of dietary supplements. The effects noted for differences of only 1-3 mg/day of Vitamin E were far too large to be credible as resulting from this factor per se - and thus other factors probably were involved. Favorable effects of Vitamin A or Beta Carotene were confirmed best, and it seemed likely that effects of multiple agents probably were additive at least to some extent. But there was a lack of any data on nutrients in amounts much larger than 200 mg of Vitamin C equivalent per day, and this is a quite low amount vs. the antioxidant needs for best reducing risks of more extensively studied heart disease and cancer.

A final dietary antioxidant model selected for risk of COPD recognizes the benefit of Vitamin C on FEV1 via a formula that produces the above listed dose related benefits, and recognizes Beta Carotene as a secondary contributor to equivalent amounts of Vitamin C at 0.0126 mg/day per IU of Beta Carotene. But a maximum value accepted for Vitamin C equivalents is now set at 300 mg/day because of the lack of actual confirming research data for values above this amount. It seems possible that larger amounts of antioxidants in either diet or supplements might produce further benefit. But a study in Finland on smokers only (Rautalahahti, M, Am J Respir Crit Care Med 1997; 156:1447) found useful benefits for beta-carotene and Vitamin E in diet, but no benefit for supplements during a 6 year test period.

A final problem in identifying the value of diet is that of relating values of lung function as FEV1 to actual risk ratios of COPD. A value adopted from the few results found available suggested that risk of COPD approximated 0.9926 ^ FEV1 difference. This produces risk ratios of COPD for +30 ml FEV1 and +50 ml FEV1 of 0.80 and 0.69 respectively. A minimum risk of 0.50 is accepted for any diet antioxidant improvement as no research found confirms larger benefits than this. Life Ahead relates this and all other risks to those for an average US population that is assumed to consume 150 mg/day of Vitamin C and 6,300 IU/Day of Beta Carotene.

Life Ahead identifies amounts of 23 nutrients that include Vitamin C and Beta Carotene in any entered diet. Because these nutrients are best present in fruits and vegetables, these foods will contribute most to benefiting antioxidant risk of COPD from diet. Studies have confirmed that dietary fruit consumption relates to FEV1 and probable risk of COPD. But the types of fruits studied were not identified, and individual fruits and vegetables can have vastly differing amounts of contributing nutrients. Life Ahead technology provides for valuing benefits of individual foods- a valuation that usually is not feasible using population type research studies because of their large error margins. Some Life Ahead valuations of the benefit to risk of COPD for eating single daily diet portions of individual foods based on their included amounts of Vitamin C and Beta Carotene are:

Fruit Risk Change Fruit Risk Change

of COPD of COPD

1 Banana -3.4% 1/2 Grapefruit -10.9%

4 oz Blueberries -2.4% 1 Orange -9.3%

4 oz of Grapes -0.6% 1/2 Cantaloupe Melon -19.3%

4 oz Canned Peaches -1.4% 4 oz of Raspberries -3.6%

Note the vastly differing potential benefits of different fruits. This difference is computed due to the correspondingly different amounts of key vitamins in these specific fruits. Grapes are lowest in and melon is highest in amounts of both Vitamin C and Beta Carotene. Life Ahead can compute the benefit of any of the 340 included foods for each of the 15 included major causes of death and for likely life expectancy, and do this for any man or woman of any age having any other combination of lifestyle risks. These differences in computed risk will be much lower for a person that uses substantial dietary supplements of these key vitamins.

Another observation on the benefits of fruits on COPD emerged from a study by Cary, IM (Am J Respir Crit Care Med 1998; 158:728). Fruits improved FEV1 measured at age, but did not appear to contribute to the longer term and usually irreversible decline in lung function that is produced by smoking. Many lifestyles that reduce risk of disease produce gradually increasing benefits only when present for long periods of time. An inference here is that eating fruits and vegetables will improve lung function in present time, and do not have to be taken over long time for benefit. This reinforces the suggestion that any person with risk of or actually suffering COPD should be eating oranges, melons, and grapefruit every day.

Omega-3 Fats: Four studies found confirm that omega-3 fats DHA+EPA mostly in fish reduce risk of COPD. A key study of this (Shahar, E; N Engl J Med 1994; 331:228) found a substantial dose related relationship between population quartiles of omega-3 fats from dietary fish and risk of both individual and total COPD diseases. Risk ratios for n-3 fatty acids in amounts of 50, 130, 230, and 480 mg per day produced risk ratios of 1.0(base), 0.88, 0.77, and 0.54 in COPD, with similar results found for results unadjusted or adjusted for various other factors. The results of the other studies were less definitive, but confirmed this level of benefit found by Shahar. Life Ahead develops the amounts of DHA+EPA in any diet entered.

The potential benefit of the other key omega-3 fat of linolenic acid was not found studied. It seems likely that higher than usual amounts of this fat also will reduce risk of COPD, but until data on this are obtained no effect of linolenic acid can be included in Life Ahead. The present program does adjust the computed risk of COPD for amounts of DHA+EPA included in any entered diet, and this risk is considered together with the above risks for antioxidants as overall diet contributions to risk of this disease.

Weight and BMI: Surprisingly, body weight or BMI usually is not substantially related to the effectiveness of the lung function. The formulas for normalizing or predicting values for FEV1 and FVC recognize height as an important factor of body size, and height and sex relate importantly to lung capacity. But except for extremely obese people, body weight usually is not significantly involved. It has been observed that when individuals stop smoking that they usually gain weight, and this gain has been accompanied by a small loss in lung function. One study found each pound gain in weight subtracted 7 ml from FVC and another study found a 10 ml lower FVC for men. These studies found about 40% lower values subtracted for women. But these differences are small vs. the usual 4,500 and 3,200 ml lung capacity of men and women and would produce a small effect on risk vs. the important effects of weight and BMI on risks of other major diseases and premature death.

People suffering COPD often lose much weight, and those losing too much can incur a much higher risk of death from the disease. Two studies have found that those with BMI values below 20 suffer a 2 to 3 times higher risk of death from the disease than do those with BMI in the usually healthy 20 to 25 range. This effect probably results from the COPD per se causing this unusual weight loss. Thus treatment for the disease usually includes programs to increase weight for those having COPD that have lost too much weight. No effect of body weight is now included the Life Ahead on the usual or general risk of COPD, and anyone suffering this disease should avoid excessive weight loss and be taking proper medical care to avoid having such risks.

Serum Cholesterol: The theory that respiratory disease might be related to serum cholesterol was tested by a large study (Iribarren C, International Journal of Epidemiology, 1997 26:1191) . This study of 559 cases of bronchitis and emphysema from 37,000 men and 476 events from 43,000 women produced a variety of statistics for different age groups and levels of cholesterol that mostly were confusing and not significant. A probable best overall result was that of the continuous risks for men and women of 0.9841 and 0.9921 per 10 mg/dl increase in serum cholesterol over a range of below 160 to well above 240 mg/dl. These difference of only -1.6% and -0.8% for men and women respectively in favor of higher cholesterol were too small to be considered as useful. Although no other useful results on this relationship were found published, this small if any effect from such a very large population sample is adequate to dismiss cholesterol as a factor of significance affecting COPD. Similar small and usually non-significant effects were found for for cholesterol on asthma and other miscellaneous respiratory diseases in this study.