Well, maybe an easy way (consider many of us are overweight and love to eat), but still a way to get better erections without pills, creams, or pumps: simply restrict calories.
How much? That is a good question, but probably enough to lose weight.
Here is a study (below) that examined this question in mice. Mice are not people; for one thing, their bodies handle calorie restriction differently than humans. But there is no evidence that it is different in people.
Here is the study. Food for thought. (FROM: http://www.ncbi.nlm.nih.gov/pubmed/20512454)
Ketonen J1, Pilvi T, Mervaala E. Caloric restriction reverses high-fat diet-induced endothelial dysfunction and vascular superoxide production in C57Bl/6 mice. Heart Vessels. 2010 May;25(3):254-62.
Obesity is frequently associated with endothelial dysfunction. We hypothesized that high-fat feeding dysregulates the balance between endothelial derived nitric oxide and superoxide formation. Furthermore, we examined whether caloric restriction could reverse the detrimental vascular effects related to obesity. Male C57Bl/6 mice were fed with normal-fat diet (fat 17%) or high-fat diet (fat 60%) for 150 days. After establishment of obesity at day 100, a subgroup of obese mice were put on caloric restriction (CR) (70% of ad libitum energy intake) for an additional 50 days. At day 100, aortic rings from obese mice receiving high-fat diet showed impaired endothelium-dependent vasodilation in response to acetylcholine (ACh). Caloric restriction reversed high-fat diet-induced endothelial dysfunction. At day 150, impaired vasodilatory responses to ACh in obese mice without caloric restriction were markedly improved by preincubation with the tetrahydrobiopterin (BH(4)) precursor sepiapterin and L-arginine, a substrate for endothelial nitric oxide synthase (eNOS). Additionally, inhibition of vascular arginase by L-norvaline partially, and superoxide scavenging by Tiron completely, restored endothelial cell function. Obese mice showed increased vascular superoxide production, which was diminished by endothelial denudation, pretreated of the vascular rings with apocynin (an inhibitor of reduced nicotinamide adenine dinucleotide phosphate [NADPH] oxidase), oxypurinol (an inhibitor of xanthine oxidase), N(G)-nitro-L-arginine methyl ester (LNAME; an inhibitor of eNOS), or by adding the BH(4) precursor sepiapterin. Caloric restriction markedly attenuated vascular superoxide production. In obese mice on CR, endothelial denudation increased superoxide formation whereas vascular superoxide production was unaffected by L-NAME. Western blot analysis revealed decreased phosphorylated eNOS (Ser1177)-to-total eNOS expression ratio in obese mice as compared to lean controls, whereas the phospho-eNOS/NOS ratio in obese mice on CR did not differ from the lean controls. In conclusion, the present study suggests that caloric restriction reverses obesity induced endothelial dysfunction and vascular oxidative stress, and underscores the importance of uncoupled eNOS in the pathogenesis.
Here’s another study, in Rats:
Arch Ital Urol Androl. 2013 Sep 26;85(3):113-7. doi: 10.4081/aiua.2013.3.113.
Caloric restriction increases internal iliac artery and penil nitric oxide synthase expression in rat: comparison of aged and adult rats.
Ozbek E1, Simsek A, Ozbek M, Somay A.
Because of the positive corelation between healthy cardiovascular system and sexual life we aimed to evaluate the effect of caloric restriction (CR) on endothelial and neuronal nitric oxide synthase (eNOS, nNOS) expression in cavernousal tissues and eNOS expression in the internal iliac artery in young and aged rats. Young (3 mo, n = 7) and aged (24 mo, n = 7) male Sprague-Dawley rats were subjected to 40% CR and were allowed free access to water for 3 months. Control rats (n = 14) fed ad libitum had free access to food and water at all times. On day 90, rats were sacrificed and internal iliac arteries and penis were removed and parafinized, eNOS and nNOS expression evaluated with immunohistochemistry. Results were evaluated semiquantitatively. eNOS and nNOS expression in cavernousal tis- sue in CR rats were more strong than in control group in both young and old rats. eNOS expression was also higher in the internal iliac arteries of CR rats than in control in young and old rats. As a result of our study we can say that there is a positive link between CR and neurotransmitter of erection in cavernousal tissues and internal iliac arteries. CR has beneficial effect to prevent sexual dysfunction in young and old animals and possible humans.
Even better…combine CR (calorie restriction) with exercise.
Hannan JL1, Heaton JP, Adams MA. Recovery of erectile function in aging hypertensive and normotensive rats using exercise and caloric restriction. J Sex Med. 2007 Jul;4(4 Pt 1):886-97.
INTRODUCTION: Using aging spontaneously hypertensive rats (SHR), we established that antihypertensive drugs can improve erections and penile vascular structure, and lower arterial pressure. Using kidney cross-transplantations, our findings revealed that the benefit of this treatment resulted from drug-induced changes specific to the penile circulation, and not to the kidney-mediated lowering of pressure.
AIM: The objective of the present study was to determine whether increased exercise and/or caloric restriction (CR) can reverse the decline in sexual responses in aging hypertensive and normotensive rats.
METHODS: From 30 to 40 weeks, food intake was restricted (10-40%), and SHR, Wistar, and Sprague-Dawley rats ran on treadmills (30 minutes/day, 5 days/week). Exercise was withdrawn at 40 weeks, and CR was stopped at 50 weeks. Using a separate group of older Wistars (56 weeks) and Sprague-Dawley rats (67 weeks), the effects of 10% CR or exercise plus 10-40% CR on erectile function were determined.
MAIN OUTCOME MEASURE: Apomorphine-induced erectile responses and body weight were monitored weekly.
RESULTS: An age-related decline in erections was seen from 15 to 29 weeks of age in all strains. This decline paralleled increases in body weight, particularly in the normotensive strains. Exercise and CR induced a 10% weight loss in normotensive rats and improved erections in all animals. In SHR, increased erections occurred without decreasing body weight. Body weight and erectile responses were maintained by CR alone after exercise was withdrawn, but erectile function rapidly declined soon after CR was stopped and paralleled increases in body weight. In aged Wistar and Sprague-Dawley rats treated with exercise and CR, erectile function was also significantly improved.
CONCLUSIONS: Similar to previous studies, erectile function progressively decreased with age in both hypertensive and normotensive rats. Erectile responses were found to be substantially improved by an intervention involving exercise and CR, but not necessarily involving weight loss.