At this point I think most of us have either complained about our “sore back” or have heard someone in our life complain about the same. Lower back pain, in particular, is the world’s leading cause of disability and missed work. That alarming fact is making low back pain a hot topic and one that deserves a lot of attention. The vast majority of low back pain is due to mechanical or non-organic causes. Which basically means that most of the time we have no idea why our back is in pain or what caused it. Often there is no
Erectile dysfunction (ED) is mostly addressed as a psychogenic disorder, but an organic form of ED occurs in about 10-15% of all cases1 and in 72% of cases in men under the age of 40 years.2
The organic cause of ED is strongly linked to low testosterone levels as well as atherosclerosis and cardiovascular disease (CVD). ED is typically age-related with many similar risk factors to CVD including hypertension, diabetes, smoking, obesity, dyslipidemia.3
In the Massachusetts Male Aging Study (MMAS), 1057 men aged 40-70 years who did not have CVD or diabetes at baseline were followed for roughly 10-13 years.4 Over that time about 25% developed CVD, and 27% of those (71 men) died of a cardiac event during the study. Researchers found a significant association between the incidence of ED and CVD risk (Framingham risk score) and concluded that ED could predict the development or occurrence of CVD, independent of age.
Although ED and CVD are strongly associated, ED has not been found to cause CVD, but may instead be a marker of CVD or increased CVD risk. In a study by Inman et al.5 the greatest incidence of CVD per age group occurred in the youngest participants that had ED: Those aged 40-50 years. Men in this age group had a CVD incidence of 48.5 per 1000-person years if they had ED, compared with 0.94 per 1000-person years in those without ED. Those aged 50-70 years also had a higher incidence of CVD when ED was also present, but beyond 70 years old, the difference was much smaller.5
When common cardiovascular risk factors were accounted for, men with ED had about an 80% increased risk of having coronary artery disease. Other studies have quoted values closer to 45-65%3,5 which is still quite substantial. The risk of stroke and mortality has also been found significantly higher for those with ED.3
Organic Erectile Dysfunction
Endothelial dysfunction and inflammation, which can occur from decreased availability of nitric oxide (NO), can trigger the development of atherosclerosis and reduce vasodilation. As atherosclerosis develops, obstruction occurs much earlier in very small arteries such as penile arteries, compared to coronary arteries.6
Peripheral cavernosal arteries of the penis are end arteries and therefore do not have any alternate source of blood flow to compensate for the loss. The arteries then degenerate resulting in penile ischemia.5 Organic ED manifests from limited or absent blood flow. Compared to this occurring in the coronary arteries, reduced penile blood flow is more likely to lead to a recognizable symptom and problem.6
This organic form of ED develops gradually. In these cases we’re more likely to see a normal healthy libido but with the inability to achieve or maintain an erection due to decreased blood flow.2 Conversely, when ED occurs suddenly or around a significant life event, and where masturbation may still produce a strong erection, the etiology is likely psychogenic. Psychogenic ED can also present as the ability to initiate but not maintain an erection.
Based on this distinction, ED as a whole can’t be considered a risk factor for CVD, but identifying organic ED serves as a marker of early CVD, or a significantly increased risk of developing CVD. This could be key for addressing CV risk earlier and making appropriate lifestyle changes before it’s too late. In a 2013 prospective cohort study including data from 95,038 men over the age of 45 years, there were 7,855 cardiovascular events and 2,304 deaths which occurred on average 2.2 years for CVD admission and 2.8 years for mortality from the study’s baseline.7 The severity of ED also increased the risk of a CV event and death.
Researchers from this study found a significantly increased risk of ischemic heart disease, heart failure, peripheral artery disease, acute myocardial infarction (MI), and atrioventricular and left bundle branch block, but there was no difference in risk for primary hypertension. So in addition to ED and CVD having overlapping risk factors, they also have the same pathophysiology. ED doesn’t cause CVD; it is the early presentation of small arteries carrying decreased flow due to endothelial dysfunction and represents high CVD risk. The timeline on this isn’t long: ED has been shown to occur about two to five years before symptoms of CVD show up.6
Their similar pathophysiology would indicate that treating one would benefit the other and that treating both concurrently would have an even greater beneficial effect. In a seven-year cohort study in Sweden of men who had been diagnosed with an MI, researchers compared the effect that treatment with ED medications (specifically phosphodiesterase-5 inhibitors or alprostadil) had on recurrent MI, heart failure and death.8 Of the 43,145 patients in this study, 3,068 were treated with an ED medication. These men were less likely to have diabetes, heart failure, COPD and stroke at baseline.
During this study’s follow-up period, cardiovascular death occurred in 5.4% of the non-ED treated group, compared to 1.5% in the group treated for ED. Overall, treatment with ED medication was found to reduce the risk of heart failure by 40% and reduce the risk of death by 33%.
Early recognition of ED is key. Cardiac stress tests only detect moderate to severe stenosis (50-70%), which is also independent of the risk of plaque rupture. Other early risk factors that can be investigated include hs-CRP, HbA1C, and lipoprotein-associated phospholipase A2.6 Waist circumference and physical activity should also be used to evaluate risk. Central adiposity and low levels of physical activity are associated with numerous negative CV effects in addition to a 50% greater likelihood of having ED compared to those with normal BMI and/or waist circumference.9 Regardless of BMI, maintaining a waist circumference under 102 cm and participating in regular moderate-intensity physical activity can promote proper erectile function.9
- Miner M, Kim ED. (2015). Cardiovascular disease and male sexual dysfunction. Asian J Androl. 17(1): 3-4
- Papagiannnopoulos D, Khare N, Nehra A. (2015). Evaluation of young men with organic erectile dysfunction. Asian J Androl. 17(1): 11–16.
- Mostafaei H, Mori K, Hajebrahimi S, et al. (2021). Association of erectile dysfunction and cardiovascular disease: an umbrella review of systematic reviews and meta-analyses. BJU Int. 128(1): 3-11
- Araujo AB, Hall SA, Ganz P, et al. (2010). Does erectile dysfunction contribute to cardiovascular disease risk prediction beyond the Framingham risk score? J Am College Cardiol. 55, 350-356
- Inman BA, St Sauver JL, Jacobson DJ, et al. (2009). A population-based, longitudinal study of erectile dysfunction and future coronary artery disease. Mayo Clin Proc. 84(2): 108-13
- Randrup E, Baum N, Feibus A. (2015) Erectile dysfunction and cardiovascular disease. Postgrad Med. 127(2): 166-72
- Banks E, Joshy G, Abhayaratna WP, et al. (2013). Erectile dysfunction severity as a risk marker for cardiovascular disease hospitalization and all-cause mortality: A prospective cohort study. PLoS Med. 10(1): e1001372
- Andersson DP, Lagerros YT, Grotta A, et al. (2017). Association between treatment for erectile dysfunction and death or cardiovascular outcomes after myocardial infarction. Heart. 103(16): 1264-70
- Janiszewski PM, Janssen I, Ross R. (2009). Abdominal obesity and physical inactivity are associated with erectile dysfunction independent of body mass index. J Sex Med. 6(7): 1990-8