Erectile Dysfunction Now!
Controlling Erectile Problems Before They Start - Reducing The Risk Due To Physical Factors
It's an observable fact that millions of men are affected by erectile dysfunction. The extraordinary thing is that little is understood about the frequency with which men spontaneously recover from this condition. You might think, and you would probably be right, that spontaneous recovery is a rare event: certainly there are clinical data which support this view.
Treatments for erectile dysfunction have been very invasive up to this point in time, and often linked with low levels of compliance from patients. Even though Viagra is now available, and shows a high success rate, it may well be that prevention of erectile dysfunction (ED) is the most effective way of reducing the consequences of ED on the male population.
Carol Derby and her colleagues reported a study in Adult Urology, 2000, pages 302-306, on how modifiable risk factors for erectile dysfunction respond to lifestyle changes.
There have been many previous studies which have revealed the association between erectile dysfunction and many other conditions such as heart disease, stroke, peripheral vascular disease, cigarette smoking, high lipid levels in the bloodstream, obesity, chronic alcoholism, cigarette smoking, and sedentary behavior.
Obviously many of these studies suggest that ED can be an indicator for atherosclerosis. Nonetheless, data is lacking on how the risk of ED may be modified by changes to these causative factors. Derby and her colleagues reviewed how changes in smoking, drinking, sedentary lifestyle, and obesity are related to the risk of ED.
They used data from the well-known Massachusetts male aging study. This is a longitudinal study in a randomly selected group of men aged between 40 and 70 years. The correlation of health status and aging originated between 1987 and 1989 when over 1700 respondents completed their baseline evaluation. A follow-up questionnaire was completed by 70% of the men who were alive and eligible to do so between 1995 and 1997. Of those men, 593 who had no signs of ED, who were not being treated for heart disease or diabetes, and who did not have any indication of prostate cancer were used as the cohort for the study referred to in the current article.
The average age, prevalence of smoking, lifestyle -- whether sedentary or not -- and body mass index were generally comparable to the US male population, although levels of education and income were rather higher.
For the purpose of this research obesity was defined as a person having a body mass index of 30 kg per cubic meter or more. Levels of cigarette consumption and alcohol usage were derived from self reporting -- heavy drinking being defined as more than 36 g of ethanol consumed per day.
The level of physical activity was assessed by the patient's own report on his level of activity, the frequency of his physical activity, and the duration of his activity, a calculation which allowed an estimation of the individual's total weekly energy expenditure: once attained, this was allocated to four categories of sedentary, moderate exercise, vigorous exercise, and heavy exercise.
Treatment for any condition of hypertension and diabetes or heart disease was ascertained by reference to medication being taken for these conditions.
The Center For Epidemiological Studies depression scale was used to assess whether men taking part in this showed depressive symptoms.
Testosterone levels were measured by radio immunoassay and a low level of testosterone for the purpose of this research was scored as less than 250 ng per deciliter.
One of the interesting aspects of this research was that a man's level of sexual activity was investigated by means of a self administered questionnaire completed in private. This immediately raises fundamental questions about the level of accuracy of such data; this methodology may be regarded as suspect.
The questionnaire included one question for a man to assess his level of erectile dysfunction: the categories were none, minimal, moderate, or complete.
Derby and colleagues used follow-up data to perform discriminant analysis of the relationship between global self-assessment and specific item responses.
This produced the probability that an individual with a particular set of answers to the questionnaire at follow-up would fall into a specific ED category.
These functions were applied to every subject at the original baseline of the study and at follow-up. This allowed respondents to be assigned to a category of erectile dysfunction by level of probability.
The analysis simply split men into two categories: the absence or presence of moderate or complete ED. Further analysis was undertaken on the descriptive characteristics, which were compared using chi-square and Student's t-test.
Multiple logistic regression models with the dependent variable of ED at follow-up were used to evaluate the relationship of risk factor change to ED risk. The variables used in the research were baseline and follow-up status of the following characteristics: heavy drinking, obesity, smoking, and sedentary behavior.
Each of these characteristics was represented by a four level categorical variable: present at baseline and follow-up [maintained risk factor]; present at follow-up only [acquired risk factor]; present at baseline only [stopped risk factor]; and not present at either time.
Adjusting for age and the use of anti-hypertension medication, depression, or low testosterone levels, separate models were fit for each risk factor. To check for any interaction among the risk factors various other models with fit adjusting individually for the individual risk factors were used. Trends in ED risk across sequential levels were tested by devising appropriate linear contrasts in those models which were used and adjusted for baseline risk status.
The majority of men in the study showed healthy behaviors at both baseline and follow-up. Half of the baseline smokers were no longer engaged in cigarette smoking at the time of the follow-up which was nine years later.
Equally almost 50% of the heavy drinkers at baseline claimed that they had reduce their alcohol consumption by the time of the follow-up evaluation. There were 87 men classified as obese at the time of the baseline study and by the time of the follow-up 18% had lost weight. In the light of this it is perhaps not surprising to learn that 55% of 173 men at the baseline had begun to undertake moderate to intense physical activity by the time of the follow-up.
The overall incidence of erection problems as defined by the authors of the study at the time of the follow-up was approximately 1 in5, or 17%. Unadjusted proportions of men developing erectile difficulties were broadly speaking similar between the categories of smoking and alcohol consumption.
Those men who had been classified as obese at the time of the baseline study did in fact have a higher incidence of erectile difficulties regardless of the follow-up status. Furthermore, the incidence of erectile dysfunction was also rather higher in the group of men who were sedentary at follow-up, and again regardless of their baseline activity level.
The adjusted logistic regression models revealed that changes in whether men smoked a lot and changes in drinking levels were not in fact associated with ED risk, but changes in obesity and sedentary behavior status were actually related to ED risk. In the case of obesity, the lowest probabilities of erectile issues arising were in men who were not obese at the time of the initial study, regardless of their status at the time of the follow-up.
For sedentary behavior, the highest risk of erectile difficulties was among men who remained sedentary, while the lowest risk of erectile difficulties was, perhaps not surprisingly, among those who either began to take physical activity or who continued to exercise between the time of the baseline study and the follow-up evaluation.
The researchers tested for a dose response relationship by assessing the risk of erectile difficulties by quartiles of follow-up physical activity level, after making adjustments in respect of the level of baseline activity.
They discovered a graded inverse association across the lowest three quartiles, while the test for linear trend was actually borderline statistically significant. In relation to those men who were to be found in the lowest quartile, the odds ratio for erectile difficulties was 0.8 [the 95% confidence interval 0.4 to 1.4] in the second quartile, while for those men who occurred in the third quartile it was 0.5 [95% confidence interval 0.3 to 0.9], and for men in the fourth quartile it was 0.6 [95% confidence interval 0.3 to 1.2].
The researchers observed that there was a dearth of information about the relationship between these factors and the incidence of erectile dysfunction, perhaps one reason why little attention has actually been paid to the possibility of discouraging ED from developing by using some kind of prophylactic regime.
This appears to be especially important in view of the fact that clinically spontaneous recovery is rather a rare event, and medical treatments have been highly invasive and unpopular. Even Viagra has a large group of users for whom it is ineffective. Any other method of identifying potential means of prevention would clearly be of great assistance to large numbers of men.
In the Massachusetts Male Aging Study smoking was associated with an increased risk of erectile dysfunction. This result suggests that smoking cessation in middle-aged does not in fact play a large part in reducing ED risk: the was no significant difference in risk between men who stop smoking and those who continue to do so.
Smoking has many effects on the body including hypercoagulability and enhanced platelet aggregation, a marked imbalance between thromboxane and prostacyclin, as well as toxic and damaging effects on the endothelium of the vascular system.
Indeed, the long-term effects of smoking on the vascular system may persist after smoking has stopped. Fried and colleagues have demonstrated that there is an inverse association between having ever smoked and the diameter of the coronary arteries, in other words both current and ex-smokers show the same alteration in arterial diameter.
The authors were not able to establish the consequence of long-term cessation or stopping smoking on the risk of erectile difficulties in later life. What was clear was that men who stopped smoking in the MMAS had almost all been smoking from around 16 years of age and had a very high exposure to cigarette smoke in their lifetime.
This provided circumstantial evidence that stopping smoking in the early years of adulthood, or never smoking at tall, may be preconditions for the risk of developing erectile to be lowered.
This raises the question of whether the prospect of suffering erectile difficulties might turn out to be more of an effective way of deterring young men from smoking than focusing on other consequences of smoking: although one rather suspects that that is unlikely!
A change in heavy drinking levels was not apparently associated with the risk of developing erectile dysfunction. However, it is true that chronic heavy alcohol consumption has an irreversible effect on a man's capacity to sustain an erection because of damage to the nerves in his pelvis and penis.
This means that changing one's drinking habits in middle age may not do much to improve erectile function, although the lack of an association as reported in this study could have been due to underreporting and misclassification of exposure status.
Those men who were classified as overweight at the time of the baseline study were indeed at an increased risk of developing erectile difficulties regardless of any change in weight by the time of the follow up assessment..
Adverse lipid levels in the bloodstream, diabetes, and hypertension are all associated with obesity, and indeed these factors may have an independent association with a atherosclerotic heart disease. It is therefore possible that by the time of middle age the long-term damage to the vascular system caused by obesity and the other risk factors associated with it on penile blood flow are rather difficult to reverse.
Most studies have been conducted on the subject of revealed a reduced risk of cardiovascular disease in men who take physical activity. There of various possible mechanisms by which this may happen: the various hypotheses put forward to explain this include the inhibition of atherosclerosis, improvement in the profile of lipids in the blood stream, and favorable effects on thrombosis.
Clearly it is possible that exercise produces similar positive effects on blood flow through the blood vessels of the penis, although few studies have been conducted to assess the impact of physical activity on the frequency of erectile difficulties.
In the population on which the MMAS was undertaken, the adjusted odds ratio for erectile difficulty was 0.3 [95% confidence and 0.1 to 0.6] for men who began to undertake physical activity compared to those who remained sedentary.
It was similar for men who were active both at the time of the baseline study and at the time of follow-up evaluation [odds ratio 0.5, 95% confidence interval 0.2 to 0.8]. All of this suggests that sedentary men may well be able to decrease the risk of developing erectile dysfunction by adopting regular physical activity at a comparatively modest level of 200 kg calories per day -- this corresponds to only a two-mile brisk walk.
This data is actually consistent with the study by White and colleagues which demonstrated increased sexual function as well as enhanced sexual responsiveness among middle-aged men who participated in a random trial of aerobic exercise.
Where research is being conducted on the relationship in physical activity and cardiovascular disease, the results have demonstrated an inverse dose response gradient. The results of the study currently under discussion seem to indicate the possibility of a similar relationship, although it was not demonstrated a level of statistical significance.
One limitation of the analysis which Derby and colleagues undertook is that only two time points were examined: the base line time study of the original MMAS date, and the time point of the follow-up evaluation. As may well be clear by now, the risk factor of these men was not evaluated before the baseline study, a fact which may be important in terms of lifetime exposure.
Changes in risk between the two points could not be assessed, and change in risk was actually measured over a comparatively short period between these two points -- that's especially true in relation to the naturally longer developmental period associated with vascular disease.
Another objection to the study methodology is that the small sample size for the various risk factors limited the power to detect associations and indeed to test for any kind of dose response relationship.
And the final objection to the methodology of this study is that one restriction on the men initially recruited was that they were free of erectile dysfunction -- a fact which may have been responsible for selecting out the men most susceptible to the development of ED, and that may possibly be the same group for whom a change in vascular risk may be most significant.
Additionally, any changes in behavior in midlife may actually be the result of some kind of underlying ill health or chronic disease, and this could obscure any kind of association between behavioral change and erectile dysfunction prevention.
That is especially true around the association between behavioral change and prevention of erectile difficulties. This may explain the rather unexpected finding in the study of a higher ED risk among men who have lost weight, although data on comorbidity does not support this hypothesis.
Men treated for heart disease and diabetes were excluded, and the occurrence of treated blood pressure was similar among men who had made favorable changes and those who did not.
Comparisons of smoking, alcohol use, body mass index, sedentary behavior and depression also revealed no significant differences between men who have made favorable changes in the other factors, although once again this may be a limitation of the study sample size.
It is in fact possible that the effect of exercise on a man's mood is an additional factor in the relationship between physical exercise and ED.
However, this study was adjusted for depression and it has been previously demonstrated with other members of the group of men who were investigated that depression was not in fact related to the incidence of erectile dysfunction, a finding supported by the fact the frequency depression was similar among men who took up activity and those who did not.
The authors conclude that the prevention of erectile dysfunction through addressing modifiable risk factors is something that may require a man to take up these alterations in lifestyle earlier rather than later.
One clear finding seems to be that moderate to vigorous exercise can reduce the risk of erectile dysfunction, even if it is started in midlife. Further investigation is needed, however, to explain how behaviors directly modifying these risk factors would affect men's risk of developing ED in earlier adulthood.
All in all, the data surveyed definitely adds weight to the suggestion that not smoking, taking regular exercise, and other health-oriented lifestyle change may amount to protective and/or prophylactic measures against ED in a population where increasing numbers of aging men are otherwise likely to experience erectile difficulties.
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