Can apple cider vinegar treat erectile dysfunction? Apple cider vinegar is thought to have many health benefits, but can it help treat erectile dysfunction (ED)? ED can result from cardiovascular problems, diabetes, and other factors. Apple cider vinegar may help improve symptoms of conditions related to ED. Find out how it may help, and how to use it safely. Read now
ED can also occur among younger men. A 2013 study found that one in four men seeking their first treatment for ED were under the age of 40. The researchers found a stronger correlation between smoking and illicit drug use and ED in men under 40 than among older men. That suggests that lifestyle choices may be a main contributing factor for ED in younger men.
Factors that mediate contraction in the penis include noradrenaline, endothelin-1, neuropeptide Y, prostanoids, angiotensin II, and others not yet identified. Factors that mediate relaxation include acetylcholine, nitric oxide (NO), vasoactive intestinal polypeptide, pituitary adenylyl cyclase–activating peptide, calcitonin gene–related peptide, adrenomedullin, adenosine triphosphate, and adenosine prostanoids.
As blood levels of testosterone increase, this feeds back to suppress the production of gonadotrophin-releasing hormone from the hypothalamus which, in turn, suppresses production of luteinising hormone by the pituitary gland. Levels of testosterone begin to fall as a result, so negative feedback decreases and the hypothalamus resumes secretion of gonadotrophin-releasing hormone.
The other interesting thing about the study: men’s testosterone levels were lowest in March (at the end of winter) and highest in August (at the end of summer). Sunlight affects your vitamin D production, so you have seasonal dips and peaks. Get a blood test to check your levels, and if you’re low, take a high-quality vitamin D3 supplement. If you’re going to take D3, take vitamin K2 and vitamin A with it. The three work in sync, so you want them all to be balanced. Here are my dosage recommendations.
^ Jump up to: a b Travison TG, Vesper HW, Orwoll E, Wu F, Kaufman JM, Wang Y, Lapauw B, Fiers T, Matsumoto AM, Bhasin S (April 2017). "Harmonized Reference Ranges for Circulating Testosterone Levels in Men of Four Cohort Studies in the United States and Europe". The Journal of Clinical Endocrinology and Metabolism. 102 (4): 1161–1173. doi:10.1210/jc.2016-2935. PMC 5460736. PMID 28324103.
Diabetes is a well-recognized risk factor for ED. A systematic review and meta-analysis found that the prevalence of ED was 37.5% in type 1 diabetes, 66.3% in type 2 diabetes, and 52.5% in diabetes overall—a rate approximately 3.5 times higher than that in controls.  The etiology of ED in diabetic men probably involves both vascular and neurogenic mechanisms. Evidence indicates that establishing good glycemic control can minimize this risk.
Studies also show a consistent negative correlation of testosterone with blood pressure (Barrett-Connor and Khaw 1988; Khaw and Barrett-Connor 1988; Svartberg, von Muhlen, Schirmer et al 2004). Data specific to the ageing male population suggests that this relationship is particularly powerful for systolic hypertension (Fogari et al 2005). Interventional trials have not found a significant effect of testosterone replacement on blood pressure (Kapoor et al 2006).
Several pathways have been described to explain how information travels from the hypothalamus to the sacral autonomic centers. One pathway travels from the dorsomedial hypothalamus through the dorsal and central gray matter, descends to the locus ceruleus, and projects ventrally in the mesencephalic reticular formation. Input from the brain is conveyed through the dorsal spinal columns to the thoracolumbar and sacral autonomic nuclei.
Patients at high cardiovascular risk should not be treated for ED until their cardiac condition is stabilize. These conditions include unstable or refractory angina, myocardial infarction or cerebrovascular accident within the past 2 weeks, uncontrolled hypertension, New York Heart Association (NYHA) Functional Classification III-IV congestive heart failure, high-risk arrhythmias, hypertrophic obstructive cardiomyopathies, and moderate-to-severe valvular disease.25 This class of drugs is also contraindicated in patients who use nitroglycerin or nitrate-containing compounds.26, 27
Of the drugs used for depression, tricyclic antidepressants may be associated with erectile problems and other drugs may be substituted to prevent this complication. Currently available substitutes include bupropion, nefazodone, and trazodone. The selective serotonin reuptake inhibitors (eg, fluoxetine, sertraline, paroxetine, citalopram) can also cause difficulties with ED, but they might also have other significant sexual side effects, including decreased libido and anorgasmia.
Both testosterone and 5α-DHT are metabolized mainly in the liver. Approximately 50% of testosterone is metabolized via conjugation into testosterone glucuronide and to a lesser extent testosterone sulfate by glucuronosyltransferases and sulfotransferases, respectively. An additional 40% of testosterone is metabolized in equal proportions into the 17-ketosteroids androsterone and etiocholanolone via the combined actions of 5α- and 5β-reductases, 3α-hydroxysteroid dehydrogenase, and 17β-HSD, in that order. Androsterone and etiocholanolone are then glucuronidated and to a lesser extent sulfated similarly to testosterone. The conjugates of testosterone and its hepatic metabolites are released from the liver into circulation and excreted in the urine and bile. Only a small fraction (2%) of testosterone is excreted unchanged in the urine.
Trauma to the pelvic blood vessels or nerves can also lead result in ED. Bicycle riding for long periods has been implicated as an etiologic factor; direct compression of the perineum by the bicycle seat may cause vascular and nerve injury.  On the other hand, bicycling for less than 3 hours per week may be somewhat protective against ED.  Some of the newer bicycle seats have been designed to diminish pressure on the perineum. [37, 38]
The Food and Drug Administration (FDA) does not recommend alternative therapies to treat sexual dysfunction. Many products are advertised as "herbal viagra" or "natural" sexual enhancement products, but no clinical trials or scientific studies support the effectiveness of these products for the treatment of ED, and synthetic chemical compounds similar to sildenafil have been found as adulterants in many of these products. The FDA has warned consumers that any sexual enhancement product that claims to work as well as prescription products is likely to contain such a contaminant.
Longitudinal studies in male aging studies have shown that serum testosterone levels decline with age (Harman et al 2001; Feldman et al 2002). Total testosterone levels fall at an average of 1.6% per year whilst free and bioavailable levels fall by 2%–3% per year. The reduction in free and bioavailable testosterone levels is larger because aging is also associated with increases in SHBG levels (Feldman et al 2002). Cross-sectional data supports these trends but has usually shown smaller reductions in testosterone levels with aging (Feldman et al 2002). This is likely to reflect strict entry criteria to cross-sectional studies so that young healthy men are compared to older healthy men. During the course of longitudinal studies some men may develop pathologies which accentuate decreases in testosterone levels.
Exercise and lifestyle modifications may improve erectile function. Weight loss may help by decreasing inflammation, increasing testosterone, and improving self-esteem. Patients should be educated to increase activity, reduce weight, and stop smoking, as these efforts can improve or restore erectile function in men without comorbidities. Precise glycemic control in diabetic patients and pharmacologic treatment of hypertension may be important in preventing or reducing sexual dysfunction. 
medicines called alpha-blockers such as Hytrin (terazosin HCl), Flomax (tamsulosin HCl), Cardura (doxazosin mesylate), Minipress (prazosin HCl), Uroxatral (alfuzosin HCl), Jalyn (dutasteride and tamsulosin HCl), or Rapaflo (silodosin). Alpha-blockers are sometimes prescribed for prostate problems or high blood pressure. In some patients, the use of Sildenafil with alpha-blockers can lead to a drop in blood pressure or to fainting
The Massachusetts Male Aging Study (MMAS) documented an inverse correlation between ED risk and high-density lipoprotein (HDL) cholesterol levels but did not identify any effect from elevated total cholesterol levels.  Another study involving male subjects aged 45-54 years found a correlation with abnormal HDL cholesterol levels but also found a correlation with elevated total cholesterol levels. The MMAS included a preponderance of older men.
In males, testosterone is synthesized primarily in Leydig cells. The number of Leydig cells in turn is regulated by luteinizing hormone (LH) and follicle-stimulating hormone (FSH). In addition, the amount of testosterone produced by existing Leydig cells is under the control of LH, which regulates the expression of 17β-hydroxysteroid dehydrogenase.
Other side effects include increased risk of heart problems in older men with poor mobility, according to a 2009 study at Boston Medical Center. A 2017 study published in JAMA found that treatments increase coronary artery plaque volume. Additionally, the Food and Drug Administration (FDA) requires manufactures to include a notice on the labeling that states taking testosterone treatments can lead to possible increased risk of heart attacks and strokes. The FDA recommends that patients using testosterone should seek medical attention right away if they have these symptoms:
All devices that are currently approved by the FDA are considered safe for use in magnetic resonance imaging environments. However, 2 previously approved devices–the OmniPhase and the DuraPhase penile prostheses–are not considered safe in this environment. Other surgical procedures–including venous ligation to limit penile venous outflow and penile revascularization procedures–are rarely successful and are not recommended.19 These surgeries are only indicated when a patient demonstrates recent-onset ED and an occlusive lesion seen on angiogram or magnetic resonance angiography and should be performed only in centers of excellence for ED.
The mechanism of age related decreases in serum testosterone levels has also been the subject of investigation. Metabolic clearance declines with age but this effect is less pronounced than a reduction in testosterone production, so the overall effect is to reduce serum testosterone levels. Gonadotrophin levels rise during aging (Feldman et al 2002) and testicular secretory responses to recombinant human chorionic gonadotrophin (hCG) are reduced (Mulligan et al 1999, 2001). This implies that the reduced production may be caused by primary testicular failure but in fact these changes are not adequate to fully explain the fall in testosterone levels. There are changes in the lutenising hormone (LH) production which consist of decreased LH pulse frequency and amplitude, (Veldhuis et al 1992; Pincus et al 1997) although pituitary production of LH in response to pharmacological stimulation with exogenous GnRH analogues is preserved (Mulligan et al 1999). It therefore seems likely that there are changes in endogenous production of GnRH which underlie the changes in LH secretion and have a role in the age related decline in testosterone. Thus the decreases in testosterone levels with aging seem to reflect changes at all levels of the hypothalamic-pituitary-testicular axis. With advancing age there is also a reduction in androgen receptor concentration in some target tissues and this may contribute to the clinical syndrome of LOH (Ono et al 1988; Gallon et al 1989).
Testosterone replacement therapy may improve energy, mood, and bone density, increase muscle mass and weight, and heighten sexual interest in older men who may have deficient levels of testosterone. Testosterone supplementation is not recommended for men who have normal testosterone levels for their age group due to the risk of prostate enlargement and other side effects. Testosterone replacement therapy is available as a cream or gel, topical solution, skin patch, injectable form and pellet form placed under the skin.
Transdermal preparations of testosterone utilize the fact that the skin readily absorbs steroid hormones. Initial transdermal preparations took the form of scrotal patches with testosterone loaded on to a membranous patch. Absorption from the scrotal skin was particularly good and physiological levels of testosterone with diurnal variation were reliably attained. The scrotal patches are now rarely used because they require regular shaving or clipping of scrotal hair and because they produce rather high levels of dihydrotestosterone compared to testosterone (Behre et al 1999). Subsequently, non-scrotal patches were developed but the absorptive capacity of non-scrotal skin is much lower, so these patches contain additional chemicals which enhance absorption. The non-scrotal skin patches produce physiological testosterone levels without supraphysiological dihydrotestosterone levels. Unfortunately, the patches produce a high rate of local skin reactions often leading to discontinuation (Parker and Armitage 1999). In the last few years, transdermal testosterone gel preparations have become available. These require daily application by patients and produce steady state physiological testosterone levels within a few days in most patients (Swerdloff et al 2000; Steidle et al 2003). The advantages compared with testosterone patches include invisibility, reduced skin irritation and the ability to adjust dosage, but concerns about transfer to women and children on close skin contact necessitate showering after application or coverage with clothes.
Lifestyle choices that impair blood circulation can contribute to ED. Smoking, excessive drinking, and drug abuse may damage the blood vessels and reduce blood flow to the penis. Smoking makes men with atherosclerosis particularly vulnerable to ED. Being overweight and getting too little exercise also contribute to ED. Studies indicate that men who exercise regularly have a lower risk of ED.
Even before the study yields its findings, Dr. Swerdloff said a few important points should be emphasized. "I want to make it clear that this is not a made-up disease," he said. "It is well known in younger men that if you have a failure to produce normal testosterone, there are certain signs and symptoms that create a kind of syndrome. Treatment for low testosterone has been documented to be beneficial."
A large number of side-effects have been attributed to testosterone. In our clinical experience, the incidence of significant adverse effects with treatment producing physiological testosterone levels is low, and many side effects attributed to testosterone are mainly relevant to supraphysiological replacement. Some adverse effects are specific to a given mode of delivery and have already been described. Potential adverse effects concerning the prostate have also been discussed and require appropriate monitoring of symptoms, PSA and digital rectal examination. Other tumors which may be androgen responsive include cancer of the breast and primary liver tumors, and these are both contraindications to testosterone treatment
^ David KG, Dingemanse E, Freud JL (May 1935). "Über krystallinisches mannliches Hormon aus Hoden (Testosteron) wirksamer als aus harn oder aus Cholesterin bereitetes Androsteron" [On crystalline male hormone from testicles (testosterone) effective as from urine or from cholesterol]. Hoppe-Seyler's Z Physiol Chem (in German). 233 (5–6): 281–83. doi:10.1515/bchm2.1935.233.5-6.281.
The rise in testosterone levels during competition predicted aggression in males but not in females. Subjects who interacted with hand guns and an experimental game showed rise in testosterone and aggression. Natural selection might have evolved males to be more sensitive to competitive and status challenge situations and that the interacting roles of testosterone are the essential ingredient for aggressive behaviour in these situations. Testosterone produces aggression by activating subcortical areas in the brain, which may also be inhibited or suppressed by social norms or familial situations while still manifesting in diverse intensities and ways through thoughts, anger, verbal aggression, competition, dominance and physical violence. Testosterone mediates attraction to cruel and violent cues in men by promoting extended viewing of violent stimuli. Testosterone specific structural brain characteristic can predict aggressive behaviour in individuals.
In one study, 9.6% reported ‘occasional’ erectile dysfunction, 8.9% reported erectile dysfunction occurring ‘often’, and 18.6% reported erectile dysfunction occurring ‘all the time’. Of these, only 11.6% had received treatment.In another study, only 14.1% of men reported that they had received treatment, despite experiencing erectile dysfunction for longer than 12 months.
Studies have demonstrated reduced testosterone levels in men with heart failure as well as other endocrine changes (Tappler and Katz 1979; Kontoleon et al 2003). Treatment of cardiac failure with chronic mechanical circulatory support normalizes many of these changes, including testosterone levels (Noirhomme et al 1999). More recently, two double-blind randomized controlled trials of testosterone treatment for men with low or low-normal serum testosterone levels and heart failure have shown improvements in exercise capacity and symptoms (Pugh et al 2004; Malkin et al 2006). The mechanism of these benefits is currently unclear, although a study of the acute effects of buccal testosterone given to men with chronic cardiac failure under invasive monitoring showed that testosterone increased cardiac index and reduced systemic vascular resistance (Pugh et al 2003). Testosterone may prove useful in the management of cardiac failure but further research is needed.
It appears that testosterone has NOS-independent pathways as well. In one study, castrated rats were implanted with testosterone pellets and then divided into a group that received an NOS inhibitor (L-nitro-L-arginine methyl ester [L-NAME]) and a control group that received no enzyme.  The castrated rats that were given testosterone pellets and L-NAME still had partial erections, a result suggesting the presence of a pathway independent of NOS activity.