Benign prostate hyperplasia (BPH) is the most common urological condition among elderly men, beginning around the age of 30 and reaching a prevalence of up to 90% in men in their 80s. It is a non-cancerous enlargement of the prostate which may develop gradually over a number of years. The gradual increase in size may be symptom free until it has enlarged sufficiently to press on the urethra and impede the flow of urine. Symptoms of increased urinary frequency, urgency, night-time urination, difficult and slow urination may be experienced as a result; they may be mild through to severe, impacting quality of life.
The prostate gland
The prostate is a small gland found only in men. Initially the size of a walnut, it gets larger with age. The prostate surrounds the urethra just below the urinary bladder and is responsible for making the thick white fluid that mixes with sperm to create semen. It is surrounded by a layer of muscle and a fibrous capsule. In BPH the connective tissue (stromal) cells and epithelial cells proliferate excessively and this is coupled with reduced cell death.
Causes of benign prostate hyperplasia
A number of factors have been implicated in the aetiology of BPH including hormonal changes, oxidative stress, inflammation as well as ageing and metabolic syndrome.
Hormonal changes – In the prostate and other tissues, the male androgen testosterone is converted to dihydrotestosterone (DHT) by the intracellular enzyme 5-alpha reductase. DHT has growth promoting effects which in early life are responsible for the development of the prostate, penis and scrotum. In later years these effects can lead to prostatic hyperplasia. DHT is 10x more potent than testosterone and has been a target for drug therapy. To reduce the conversion of testosterone to DHT, men with BPH may be prescribed an inhibitor of the 5-alpha reductase enzyme. These drugs have been found to be effective in reducing prostate size and associated symptoms but have a number of adverse effects ranging from impotence to gynaecomastia (breast tissue enlargement).
It was thought that high levels of testosterone increased BPH and that testosterone replacement therapy therefore increased the risk, but this has not been supported by research and in fact low levels of testosterone (eg which occur in ageing) may increase the risk, possibly because testosterone has anti-inflammatory effects. In addition, there have now been a number of studies which show a link between low DHT levels and increased inflammation. Current thinking is that androgens have a role but other factors are necessary for the development of BPH.
Oestrogen may also play a role – the prostate is an oestrogen target tissue and ageing and obesity increase the plasma oestrogen to androgen ratio. Environmental oestrogens which are endocrine disruptors may also play a role – oestrogens in the water, plastics (eg BPA) etc. They are certainly having an effect on sperm counts and earlier this week it was reported that men’s sperm counts have halved in the last 40 years. On the other hand, dietary phyto-oestrogens may have a protective effect on the prostate, they are weakly oestrogenic and compete for oestrogen receptors thus blocking and reducing the more potent endogenous (internal) and exogenous (external) oestrogens from binding.
Oxidative Stress – has been considered to be one of the mechanisms that triggers the development and progression of BPH. Levels of antioxidants, including zinc, are decreased in prostatic hyperplasia. In addition, animal models with BPH have shown increased prostatic lipid peroxidation and reduced endogenous antioxidants (eg glutathione, superoxide dismutase and catalase).
Inflammation – Chronic inflammation is a common finding in BPH. A significant correlation has been found between prostate size and both acute and chronic inflammation and data suggest that this could be a causative effect, rather than occurring simply as a consequence. Potential causes include infectious agents, environmental factors (toxins), diet, lifestyle, hormonal or metabolic imbalances or a combination of these. Low testosterone is also associated with increased inflammatory mediators; and there have been a number of studies that show a link between decreased DHT levels and increased inflammation.
Research has shown the prostate gland is one of the tissues where dietary polyphenols exert their actions and studies are reviewed in a paper by Elazu et al (2017). Polyphenols are plant based molecules with antioxidant properties. They may also have phyto-oestrogenic activity. They are classified into 5 groups including flavonoids (eg quercetin, rutin), curcuminoids (eg curcumin), phenolic acids (eg gallic acid), stilbenes (eg resveratrol), and lignans (eg beta-sitosterol).
The different polyphenols have been shown to exert one or more of a number of actions on prostate tissues including:
- decreasing growth factor expression
- inhibiting inflammatory mediators
- inhibiting 5-alpha reductase enzyme
- acting as selective androgen modulators ie decreasing DHT action;
- inducing cell death
- repairing antioxidant defence mechanisms (eg superoxide dismutase and glutathione peroxidase); and
- having phyto-oestrogenic activity
Foods rich in polyphenols include tomatoes, seeds (eg pumpkin, flax, sesame), nuts, green tea, cocoa, olives, parsley, celery, kale, broccoli, spinach, legumes and berries/grapes.
Tomatoes – are an excellent source of lycopene, a carotenoid responsible for its red colour. Lycopene is also found in a number of other foods including watermelon, pink grapefruit and guava. A beneficial role suggested for lycopene in patients diagnosed with BPH resulted in a pilot study of elderly men diagnosed with BPH. The effects of the intervention on carotenoid status, clinical diagnostic markers of prostate proliferation and symptoms of disease were assessed. Those taking lycopene had increased plasma concentrations of the carotenoid and showed no further enlargement of the prostate; in contrast progression of BPH continued in the placebo group. The researchers concluded that lycopene inhibited the progression of benign prostate enlargement.
Pumpkin seeds – contain a wide range of vitamins, minerals and amino acids and are a source of mono- and polyunsaturated fats. They are well known for their zinc content and men with prostate problems have been noted to have dramatically decreased zinc levels. Pumpkin seed has historically featured in the natural approach to treatment for BPH in a number of countries. Potential anti-androgen and anti-inflammatory properties were suggested as the benefit of the pumpkin seed to the prostate – research showing significant results achieved on the International Prostate Symptom Score (IPPS). Results showed IPPS score was reduced after 3 months of pumpkin seed supplementation, with the urinary flow rate showing improvement of statistical significance after six months.
Nuts – contain the plant sterol beta-sitosterol. The various plant sterols have shown a number of potential health benefits with beta-sitosterol demonstrating specific benefits in benign prostatic hyperplasia. A 1998 systematic review of 4 randomised controlled trials involving 519 men found that beta-sitosterol significantly reduced the International Prostate Symptom Score at 4 to 26 weeks.
If you have any questions regarding the topics that have been raised, or any other health matters please do contact me (Clare) by phone or email at any time.
firstname.lastname@example.org, 01684 310099
Clare Daley and the Cytoplan Editorial Team
Prostate Support – Urtica Dioica, Beta-sitosterol, Pumpkin seed, Lycopene and Zinc in a wholefood base
Phytoshield – Mixed flavonoids and carotenoids in a brassica base
CytoRenew – Acetyl-L-Carnitine, Alpha Lipoic Acid, Ginkgo Biloba, CoQ10, N-Acetyl-L-Cysteine and Rosemary extract 5:1
Phyte Inflam – Curcumin from turmeric and gingerols from ginger root
Liposomal Glutathione – N-Acetyl L Carnitine, Alpha Lipoic Acid, Gingko Biloba, Rosemary Leaf Extract, Liposomal Glutathione and Resveratrol
CoQ10 Multi – CoQ10, Beta 1-3, 1-6 Glucan, vitamins B and D12, Acerola Cherry and carotenoids
Elazu C, Elazu K and Kalu W (2017) – Management of benign prostatic hyperplasia: could dietary polyphenols be an alternative to existing therapies? Frontiers in Pharmacology, 8, 234
Hong H et al (2009) – Effects of pumpkin seed oil and saw palmetto oil in Korean men with symptomatic benign prostatic hyperplasia. Nutrition Research and Practice, 3, (4), 323-327
McNicholas T & Kirby R (2011) – Benign prostatic hyperplasia and male lower urinary tract symptoms (LUTS). BMJ Clin Evid, 1801
Nicholson T M & Ricke W A (2012) – Androgens and estrogens in benign prostatic hyperplasia: past, present and future. Differentiation, 82, 4-5, 184-199
Schwarz S et al (2008) – Lycopene inhibits disease progression in patients with benign prostate hyperplasia. J of Nutr, 138, 49-53
Unnikrishnan R et al (2017) – Benign prostatic hyperplasia: Evaluation and medical management in primary care. Cleveland Clinic Journal of Medicine, 84, 1, 53-63
Vignozzi L et al (2012) – Anti-inflammatory effect of androgen receptor activation in human benign prostatic hyperplasia cells. J Endocrinol, 214, 31-43
Yana M et ak (2010) – Differential response to zinc induced apoptosis in benign prostate hyperplasia and prostate cancer cells. J of Nutritional Biochemistry, Vol 21, 8, 687-694.
Last updated on 2nd August 2017 by cytoffice