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Your All Energy Blockages Will Be Cleared, If You Eat This For 3 Days - William LiLongevity and heart health -
Doctors may recommend that people with CHF eliminate excess salt or sodium from their diet. Too much sodium causes the body to retain fluids.
Doctors may also suggest reducing or limiting alcohol and overall fluid intake. Regular aerobic exercise may improve heart health and lead to a better quality of life in people with CHF.
It can reduce hospitalization rates in people with heart failure. Aerobic exercise is any activity that elevates the heart and breathing rates. Such activities include swimming , cycling , or jogging. However, increasing physical activity may not be practical for everyone with CHF.
A person can talk with their doctor before starting any exercise regimen. People with CHF tend to retain fluid in their bodies. Consuming too much liquid may cancel out the effects of diuretic medications. While it is essential to stay hydrated, a doctor can recommend just how much fluid a person can safely consume in a day.
Obesity is a known risk factor for heart failure. Research shows that weight loss and subsequent management can be effective in the prevention of heart failure. However, a doctor may not always advise weight loss for people with CHF.
In some circumstances, rapid weight loss may be an early sign of other conditions, such as cachexia. Doctors often ask people to monitor their weight daily to check for any sudden or fast weight gains , which may be a sign of fluid retention. Research estimates that more than half of all people with congestive heart failure will survive for 5 years after diagnosis.
There is no cure for CHF. It may be time for hospice care for a person with CHF when they begin to experience persistent, severe symptoms that interfere with their everyday life. Hospice care might also be considered if a person has recurrent or complicated hospitalizations, such as an ICU stay.
Each person with CHF will have a different experience. Life expectancy for the disease varies significantly between individuals. People who have received an early diagnosis may have a better outlook than those who did not.
Many people find that positive lifestyle changes can significantly improve their CHF symptoms and well-being. In addition, medications help many people with CHF. Doctors sometimes recommend surgery. A person with CHF can work directly with their doctor and medical team to make an individualized treatment plan to have the best possible outlook.
Systolic congestive heart failure makes it difficult for the heart to pump blood through the body. Learn more here. How does a heart attack differ to heart failure? Read on to learn more about these two types of heart disease, such as how they differ, their causes…. Congestive heart failure can cause a persistent, wet cough that produces white or blood-tinged mucus.
End stage heart failure happens when the body can no longer compensate for the reduced amount of blood the heart can pump.
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Franco OH , de Laet C , Peeters A , Jonker J , Mackenbach J , Nusselder W. Effects of Physical Activity on Life Expectancy With Cardiovascular Disease.
Arch Intern Med. Author Affiliations: Department of Public Health, Erasmus MC University Medical Center Rotterdam, Rotterdam, the Netherlands Drs Franco, de Laet, Peeters, Mackenbach, and Nusselder and Ms Jonker ; and Department of Epidemiology and Preventive Medicine, Monash University Central and Eastern Clinical School, Melbourne, Australia Dr Peeters.
Background Physical inactivity is a modifiable risk factor for cardiovascular disease. However, little is known about the effects of physical activity on life expectancy with and without cardiovascular disease.
Our objective was to calculate the consequences of different physical activity levels after age 50 years on total life expectancy and life expectancy with and without cardiovascular disease. Methods We constructed multistate life tables using data from the Framingham Heart Study to calculate the effects of 3 levels of physical activity low, moderate, and high among populations older than 50 years.
For the life table calculations, we used hazard ratios for 3 transitions healthy to death, healthy to disease, and disease to death by levels of physical activity and adjusted for age, sex, smoking, any comorbidity cancer, left ventricular hypertrophy, arthritis, diabetes, ankle edema, or pulmonary disease , and examination at start of follow-up period.
Results Moderate and high physical activity levels led to 1. For women the differences were 1. Conclusions Avoiding a sedentary lifestyle during adulthood not only prevents cardiovascular disease independently of other risk factors but also substantially expands the total life expectancy and the cardiovascular disease—free life expectancy for men and women.
This effect is already seen at moderate levels of physical activity, and the gains in cardiovascular disease—free life expectancy are twice as large at higher activity levels. The beneficial effect of physical activity in the prevention of cardiovascular disease is widely known and is supported by a large amount of evidence.
This is crucial to assess the contribution of physical activity in cardiovascular risk management. In this study we calculated the effects of different levels of physical activity on life expectancy and years lived with and without cardiovascular disease at age 50 years or older.
Using data from the original Framingham Heart Study, 18 we built life tables to calculate the relation between different levels of physical activity and total life expectancy and life expectancy with and without cardiovascular disease at age 50 years in the general population.
The Framingham cohort consisted of respondents residing in Framingham, Mass, between and The cohort has been examined biannually for 46 years. Further description can be found elsewhere.
To calculate transition rates by levels of physical activity, we pooled 3 nonoverlapping follow-up periods of 12 years. Each period started with a measurement of physical activity.
In the present investigation, the follow-up periods started at examinations 4, 11 if present, otherwise 12 , and 19 if present, otherwise Using the pooling of repeated observations method, 19 we pooled follow-up information over 3 follow-up periods, compiling a total of observation intervals.
The same participant could thus be observed during 3 periods until the event first onset of cardiovascular disease or death occurred or the subject was censored. However, follow-up time and physical activity status were reevaluated in each interval. We used observation intervals of no more than 12 years to avoid overlapping periods of follow-up.
Participants were asked to estimate how long they spent in a typical day at various levels of activity: sleeping, resting, or engaging in light, moderate, or heavy physical activity.
The reported levels of activity were weighted based on the estimated oxygen consumption for each activity to reflect metabolic expenditure corresponding to metabolic equivalents. Weights used were as follows: for sleeping, 1; for being sedentary, 1. Finally, a daily physical activity score was calculated by adding the sum of the weighted hours for each level of activity.
The minimum possible score was 24 for a participant sleeping 24 hours a day. Further detail on the assessment of physical activity and calculation of the daily physical activity score can be found elsewhere.
The primary outcome measure of our study is incident or fatal cardiovascular disease. Cardiovascular disease included coronary heart disease angina, coronary insufficiency, myocardial infarction, and sudden or not-sudden death as a consequence of coronary disease , congestive heart failure, stroke, transient ischemic attack, and intermittent claudication.
A panel of 3 physicians evaluated all events; agreement of all 3 was required. More detail on the evaluation of outcomes in the Framingham Heart Study is available elsewhere. Potential confounders were measured at each baseline except for education, which was only measured once.
All analyses were adjusted or stratified by age and sex. The examination at the start of the follow-up period was included to correct for a potential cohort and period effect, since the participants could belong to 3 different periods of follow-up and different birth cohorts.
Intermediate variables considered were hypertension and body mass index BMI calculated as weight in kilograms divided by the square of height in meters. Hypertension was defined as systolic blood pressure of mm Hg or higher or diastolic blood pressure of 90 mm Hg or higher. No backflows were allowed, and only the first entry into a state was considered.
To evaluate the differences in risk among persons 50 years or older for the 3 levels of activity, we first calculated the overall sex- and age-specific transition rates for each transition. Then we calculated hazard ratios by levels of activity using Poisson regression Gompertz distribution and adjusting for sex, age, potential confounders, and intermediate variables.
Three final models were selected. One basic model adjusted for age and sex. The second model adjusted for confounders that substantially changed the effect of physical activity on cardiovascular disease or mortality in addition to age and sex. The third model also included intermediate variables BMI and hypertension.
Finally, the 3 sets of transition rates were calculated for each physical activity level using the overall transition rates, the adjusted hazard ratios of cardiovascular disease by activity level, and the prevalence of physical activity level by sex and presence of cardiovascular disease.
Similar calculations have been described previously, 24 , 25 and the data spreadsheets are available on request. Separate life tables were created for each sex and each level of physical activity incorporating each of the 3 transitions.
The multistate life table was started at age 50 years and was closed at age years. The measures available from the life table include total life expectancy and life expectancy with and without cardiovascular disease by levels of physical activity and sex.
All statistical analyses were performed using STATA version 8. We calculated confidence intervals for all life expectancies and their differences using Monte Carlo simulation parametric bootstrapping. All the analyses were repeated for different periods of follow-up: 12, 10, 8, and 6 years.
In general, participants in the low physical activity group tended to be older mean age, 62 years than the participants in the moderate and high activity groups mean ages, 58 and 59 years, respectively.
The levels of each of the comorbidities, mean systolic blood pressure, diastolic blood pressure, and total cholesterol were higher among the participants with low physical activity Table 1.
All transition hazard ratios corrected for age and sex were inversely related to the level of physical activity Table 2. Overall there was a dose-response protective relation between physical activity level and incident cardiovascular disease or death among participants free of cardiovascular disease and for mortality among participants with cardiovascular disease.
Selected confounders were smoking status, presence of comorbidity cancer, left ventricular hypertrophy, diabetes, arthritis, ankle edema, or any pulmonary disease , and the starting date of the follow-up period. Other variables like education, marital status, and total cholesterol level were also tested but not included in the final model since they did not alter the relative risks for cardiovascular disease and mortality substantially.
For the group with a moderate level of activity, the protective effect of physical activity was significant for the transition from no cardiovascular disease to death but not for the other 2 transitions.
The directions and significance but not the magnitude—which was reduced—of these relations remained the same after adjusting for both confounders and intermediate variables Table 2. Total life expectancy increased proportionally with higher levels of physical activity Figure.
After adjustment for the selected confounders, participants in the moderate and high activity groups, respectively, lived more than 1.
This longer total life expectancy for both sexes comprised more years lived without cardiovascular disease and also—although to a lesser degree and not statistically significant—more years lived with cardiovascular disease Table 3.
The effect of physical activity on cardiovascular disease and mortality was consistent for all lengths of follow-up, although its magnitude increased as the period of follow-up was reduced; the shorter the period of follow-up, the higher the differences in life expectancies between physical activity groups Table 4.
Life expectancy for sedentary people at age 50 years was found to be 1. These differences were similar for both sexes. The longer total life expectancy measured for participants with higher levels of physical activity was the result of the larger number of years lived without cardiovascular disease and a slightly longer life expectancy with cardiovascular disease.
The increased life expectancy with cardiovascular disease among participants at moderate and high physical activity levels compared with the group at low physical activity level was not statistically significant. In all cases it was less than 0. The longer cardiovascular disease—free life expectancy was due to a protective effect of physical activity on the incidence of cardiovascular disease combined with a protective effect of physical activity on mortality among participants free of cardiovascular disease.
On the other hand, the slightly longer life expectancy with cardiovascular disease was caused by the effect of physical activity on mortality among participants with cardiovascular disease: people with cardiovascular disease at higher levels of physical activity lived longer and therefore experienced an increased burden of cardiovascular disease.
Another reason for the increase in years with cardiovascular disease is that higher physical activity is associated with increased survival to advanced ages when the risks of cardiovascular disease are higher. The diluting effect of increasing time of follow-up in the preventive role of physical activity on cardiovascular disease and mortality that we found in this study has been reported before.
However, the dilution may also be owing to less selection and reverse causation although we corrected for known comorbidity in all analyses , which are the potential biases associated with shorter terms of follow-up. We chose 12 years of follow-up to maximize power and minimize the risks for selection and reverse causation.
Importantly, in our study length of follow-up affected mainly the magnitude of effect. These observed differences in effects secondary to length of follow-up should not affect the interpretation of the results, though, because the direction of the relation we found between physical activity and cardiovascular disease and mortality was consistent over the different terms of follow-up.
The hazard ratios we found fall well within the range of the published measures of effect of physical activity on cardiovascular disease and total mortality. In the case of primary prevention of cardiovascular disease, the protective effect of physical activity that we found is moderately higher than that found by past investigations of the Framingham population.
However, the earlier studies used longer periods of follow-up years , which could explain their lower effects. A strength of our study was the use of a well-organized historic cohort that has been observed biannually for decades we used 36 years with readily available upgraded information on covariates and outcomes.
Some limitations of this study must be considered. This is a prospective observational study in which no intervention was performed; therefore, it has the inherent weaknesses of all cohort studies and lacks the strength of causality that a randomized trial could offer.
Reverse causation, which means that lower physical activity levels are caused by disease and not the other way around, is an important issue to consider because it could introduce bias in the evaluation of the effect of physical activity.
Different approaches exist to reduce the effect of reverse causation, but there is no method to eliminate it completely. To correct for reverse causation, we adjusted our analyses for comorbidities at baseline instead of excluding the subjects with disease at the start of follow-up, since our original objective was to evaluate the effect of physical activity in the general population and not on selected healthy populations.
Also we ran additional analyses excluding the participants with the lowest levels of physical activity who also represented the highest risk of reverse causation and found no substantial changes in our hazard ratios data not shown.
Another limitation of our study is the way exposure was assessed in the Framingham study. During the Framingham Heart Study, physical activity levels were evaluated by self-report, which may introduce misclassification of exposure. However, this misclassification is likely to be nondifferential, which can only attenuate our results, making them less than the true association.
A relevant limitation of our study is that we could not evaluate the effect of physical activity levels completely independently of other risk factors of cardiovascular disease such as diet and alcohol and aspirin intake.
Although we accounted in our analyses for some risk factors at baseline by correcting for BMI, blood pressure, education, cholesterol, smoking, sex, and comorbidities cancer, left ventricular hypertrophy, diabetes, arthritis, ankle edema, or any pulmonary disease , the data for diet and alcohol and aspirin intake were incomplete, unreliable, or unavailable for a large proportion or all of our population.
It is possible that part of the observed differences in life expectancy within the 3 physical activity groups might be explained by the differences in diet and alcohol and aspirin intake levels or that our results do not correspond fully to isolated differences in physical activity but to a more general effect of following a healthy lifestyle.
However, the extent of this diet-intake effect cannot be calculated with the available data. Other important risk factors for cardiovascular disease were accounted for in our analysis: sex, age, BMI, smoking, blood pressure, left ventricular hypertrophy, diabetes, cholesterol, and education.
An added value of this study is the combination of assessing the relation between physical activity and onset of cardiovascular disease and mortality in a large prospective study and the translation of these relations into life expectancy with and without cardiovascular disease.
This study shows that higher levels of physical activity not only prolong total life expectancy but also life expectancy free of cardiovascular disease at age 50 years.
This effect is already seen at moderate levels of physical activity, and the gains in cardiovascular disease—free life expectancy at higher levels are more than twice as large.
Our results underline current recommendations for physical activity, which call for even moderate levels of activity to enjoy the benefits of a healthier and longer life.
The protective effect of physical activity on cardiovascular disease is also significant in terms of life expectancy free of cardiovascular disease. The role that physical activity plays in cardiovascular risk management should be emphasized to achieve a worldwide implementation of an active pattern of life.
Our study suggests that following an active lifestyle is an effective way to achieve healthy aging. Correspondence: Oscar H. Franco, MD, PhD, Erasmus MC University Medical Center Rotterdam, Department of Public Health, Office Ee , PO Box , DR Rotterdam, the Netherlands o.
francoduran erasmusmc. Dr Peeters was partly funded as a VicHealth Public Health Research Fellow. Previous Presentation: This study was presented at the International Conference on Preventive Cardiology; May 21, ; Foz do Iguasu, Brazil.
Additional Information: The Framingham Study is conducted and supported by the National Heart, Lung and Blood Institute NHLBI in collaboration with the Framingham Heart Study Investigators.
Longwvity to live longer? Ueart research shows a Calcium and cancer prevention between strong Longevity and heart health Gut healing foods and Longeviyy biological aging — and there are certain steps that can help you get healtj. The Longevity and heart health, using data from heat, adults who participated in the to National Health and Nutrition Examination Survey, found that having high yeart health may slow the pace of biological aging. Adults with high cardiovascular health were about 6 years younger biologically than their chronological age, according to the research. We also found a dose-dependent association — as heart health goes up, biological aging goes down," study senior author Nour Makarem, an assistant professor of epidemiology at the Mailman School of Public Health at Columbia University Irving Medical Center in New York, said in a news release from the American Heart Association. The inverse was also true: For those with a lower level of heart health, phenotypic age went up, meaning they were biologically "older" than expected.
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