Prostate Cancer: Everything You Need To Know

Prostate cancer

This blog is only partly written, I will be editing it and expanding upon it over the coming weeks but I wanted to publish a ‘first draft’ as soon as I could my dad was recently diagnosed with prostate cancer. So this one’s for you dad.

According to Prostate Cancer UK, 144 men every day are diagnosed with prostate cancer in the UK. Not only was my dad diagnosed, but his dad was too.

So this blog is for all you men out there – know the risk factors. Know the signs and symptoms. Get informed.

Risk Factors For Prostate Cancer

The traditional risk factors for prostate cancer include tall stature, male sex, known family history, obesity, high blood pressure, lack of fitness, higher levels of testosterone for a long time, increasing age, and ethnicity are well known (source).

Looking at the research we may also include infections, poor gut health, inflammation and nutrient status too.

Ultimately the body is a highly complex system made up of numerous interconnected systems.

Inflammation And Prostate Cancer

Chronic inflammation is now known to contribute to several forms of cancer, with an estimated 20% of adult cancers attributable to chronic inflammatory conditions caused by infectious agents, chronic non-infectious inflammatory diseases and/or other environmental factors.

Chronic inflammation is now regarded as an ‘enabling characteristic’ of human cancer. (source)

Prostate Cancer Basics

Commonly, the diagnosis of prostate cancer is made based on elevated blood levels of PSA (>4 ng/mL). The androgenic hormones regulate normal prostate gland growth and function by interacting with the androgen receptor, whose gene expression in prostate cancer appears to be deregulated; this plays a central role in development and metastatic progression.

Prostate cancer is considered an androgen-dependent cancer. This is because its growth depends on androgens (for example testosterone and dihydrotestosterone often just referred to as asDHT).

This is why androgen deprivation therapy (ADT) leads to prostate tumour regression in up to 80% of cases.

Despite this, tumours eventually begin to grow, despite continued anti-androgen treatment.

This isn’t surprising, unfortunately, as the underlying issue(s) aren’t being addressed.

Conventional Treatment For Prostate Cancer

Treatment depends on a number of factors including how big the cancer is, whether it has spread anywhere else in your body and your general health.

There are a number of different treatments for prostate cancer. You may have a choice of treatments such as surgery or radiotherapy. Or your doctor might suggest that you have monitoring of your cancer instead of treatment straight away.

Tt might include one of the following:

  • Surgery to remove your prostate
  • External radiotherapy
  • Internal radiotherapy (brachytherapy)
  • Hormone therapy (androgen deprivation therapy)

Side Effects Of Treatment

Osteoporosis

Osteoporosis is a common side effect of treatment with androgen deprivation therapy (ADT) in men with prostate cancer. ADT may prolong survival; however, deterioration of bone mass density occurs soon after initiation. A systematic review of current literature revealed the importance of adequate nutrition during treatment with ADT to reduce the risk of osteoporosis. More specifically, this literature stressed achieving adequate intake of calcium and vitamin D through a combination of supplements and food. The necessity of providing nutrition education to patients with prostate cancer at initiation of ADT was identified. (source)

Infections And Prostate Cancer

Multiple different bacterial species are known to infect the human prostate and induce inflammation, and many of these organisms have been identified from studying patients with bacterial prostatitis. (source)

There are also several lines of evidence that support a potential role for asymptomatic (i.e. subclinical) prostatic inflammation caused by infectious microorganisms and prostate cancer development. An organism of particular interest in this respect is E. coli. Apart from being one of the most frequently isolated microorganisms from patients with bacterial prostatitis, E. coli has also been identified in both BPH and prostate cancer tissues using both culture-dependent and culture-independent molecular techniques. (source)

Additional organisms such as Pseudomonas spp., Proteus mirabilis, Klebsiella spp. and Serratia spp. have also been identified. Several sexually transmitted organisms have also been implicated in bacterial prostatitis or prostatic inflammation, and these include Chlamydia trachomatis, Gonococcal organisms, Trichomonas vaginalis and Treponema pallidum. Mycoplasma spp. have also been implicated in chronic prostatitis. (source)

Additional microorganisms (both bacterial and viral) have been implicated in stimulating prostatic inflammation that may contribute to the development of prostate carcinogenesis. For example, C. trachomatis has been detected in prostatitis, BPH and prostate cancer, although multiple epidemiological studies have reported no association between C. trachomatis seropositivity and prostate cancer risk. Studies have shown that C. trachomatis can infect rat prostate epithelial cells in vitro, leading to the production of proinflammatory cytokines and chemokines. (source)

Another bacterial species that has gained recent attention in the prostate cancer field is Propionibacterium acnes, a proinflammatory bacterium that is considered to be the aetiological agent in the skin condition acne, as well as several other inflammatory conditions including endocarditis and post-surgical infections. (source)

Obesity And Prostate Cancer

The physiological mechanisms associating obesity with poor prostate cancer outcomes remain largely unknown; however, an increased inflammatory environment and metabolic irregularities associated with excess fat mass are commonly postulated. Although research is limited, fat loss strategies using exercise and nutrition programmes may slow down prostate cancer progression and improve a patient’s prognosis. (source).

Insulin And Prostate Cancer

Hyperinsulinemia is associated with prostate cancer development, progression and aggressiveness. Prostate cancer patients who undergo androgen deprivation therapy are at risk of diabetes in survivorship. It is unclear whether this is a direct result of treatment or related to pre-existing metabolic features (e.g. hyperinsulinemia and obesity). Obesity and metabolic syndrome are also associated with prostate cancer development and poorer outcomes for cancer survivors, which may be driven by hyperinsulinemia, pro-inflammation, hyperleptinemia and/or hypoadiponectinemia. (source)

Independently evaluating changes in glucose metabolism near the time of prostate cancer diagnosis and during long-term ADT treatment is important to distinguish their unique contributions to the development of metabolic disturbances. Integrative approaches, including metabolic, clinical and body composition measures, are needed to understand the role of adiposity and insulin resistance in prostate cancer and to develop effective nutrition and exercise interventions to improve secondary diseases in survivorship. (source)

Resistance Training And Prostate Cancer

Prostate cancer patients on androgen deprivation therapy (ADT) experience adverse effects such as lean mass loss, known as sarcopenia, fat gain, and changes in cardiometabolic factors that increase risk of metabolic syndrome (MetS). Resistance training can increase lean mass, reduce body fat, and improve physical function and quality of life, but no exercise interventions in prostate cancer patients on ADT have concomitantly improved body composition and MetS. This pilot trial investigated 12 weeks of resistance training on body composition and MetS changes in prostate cancer patients on ADT. An exploratory aim examined if a combined approach of training and protein supplementation would elicit greater changes in body composition.

A 12-week resistance training intervention effectively improved sarcopenia, body fat %, strength and quality of life in hypogonadal prostate cancer patients, but did not change MetS or physical function. (source)

Sarcopenia And Prostate Cancer

The possibility of sarcopenia being a prognostic factor in advanced prostate cancer patients has recently become a subject of interest.

Patients with advanced prostate cancer and sarcopenia were found to have a shorter progression-free survival (the length of time during and after treatment of a cancer that the patient lives with the disease but it does not get worse), but sarcopenia did not have much influence on the overall survival and cancer-specific survival (the length of time from either the date of diagnosis or the start of treatment to the date of death due to the cancer).

Diet And Prostate Cancer

The incidence of prostate cancer (PCa) displays widespread regional differences, probably owing to differences in dietary habits. Nutrients, including fat, protein, carbohydrates, vitamins (vitamin A, D, and E), and polyphenols, potentially affect PCa pathogenesis and progression, as previously reported using animal models; however, clinical studies have reported controversial results for almost all nutrients. The effects of these nutrients may be manifested through various mechanisms including inflammation, antioxidant effects, and the action of sex hormones. (source)

human studies comparing the consumption of individual nutrient factors or the presence or absence of vitamin or polyphenol supplementation often result in unclear outcomes. This might be due to significant differences in the original diet and lifestyle, among other factors, such as region, age, and race. Interactions and synergies between nutrient factors might also need to be considered to determine the effects of diets on PCa. Therefore, some studies report using cohorts that were classified and compared according to dietary pattern rather than individual nutrient factors.

Gut Microbiome And Prostate Cancer

Human studies reported an increase in the abundance of specific gut bacteria in prostate cancer patients. (source)

Interestingly, studies suggest that gut microbiome is involved not only in intestinal diseases but also in diseases in other organs, with several laboratory and human studies suggesting its involvement in Alzheimer’s disease, rheumatoid arthritis, and diabetes. Additionally, the influence of gut microbiota on cancer is a research area that has received substantial attention based on findings that gut microbiota, which is altered by various external factors, including dietary composition, is involved in all stages of cancer, including initiation, progression, treatment outcomes, and adverse reactions. (source)

A previous study of the gut microbiota of 133 patients undergoing prostate biopsies in the United States showed an association between the presence or absence of PCa and microbial composition, and that Bacteroides and Streptococcus spp. were significantly enriched in the gut microbiota of patients with PCa. This suggests that gut microbiota might be involved in not only gastrointestinal cancers but also PCa. Because the composition of gut microbiota differs greatly according to region, it remains unclear how gut microbiota (or a particular bacterial species) is involved in PCa for a given population. Furthermore, the mechanisms by which gut microbiota control PCa have not been elucidated.

Although the prostate is not an organ directly affected by gut microbiota, the prostate could be affected indirectly by cytokines and immune cells modified by microbiota in the gut or bacterial metabolites and components absorbed from the intestine that enter systemic circulation (i.e., a “microbiota-gut-prostate axis”). (source)

These findings suggest the potential influence of diet and nutrition on PCa and its partial mediation by gut microbiota. We anticipate that future studies will reveal more about the “microbiota-gut-prostate axis”. (source)

Protein And Prostate Cancer

Several clinical studies exploring the relationship between dietary protein intake and risk of PCa reported inconsistent findings. Recently, a meta-analysis of 12 articles comprising 13,483 PCa cases and 286,245 participants revealed that protein intake has no effect on PCa. In this report, the RR of the highest protein intake versus the lowest protein intake on PCa incidence was 0.993. Further, there was no significant association between PCa risk and intake of animal or plant protein. (source)

Regarding intake of animal meat and carcinogenesis, heterocyclic amines (HCAs) are formed when cooking all of the components in meat (e.g., creatine, amino acids, and sugar) at high temperatures and have been described as mutagenic compounds. Previous studies analysing the relationship between HCAs and men with PCa report well-cooked meat as being associated with increased PCa risk. (source)

Carbohydrates And Prostate Cancer

There have been few human studies focused on the relationship between carbohydrate intake and PCa risk. In a prospective study of 3,184 adults from the Framingham Offspring cohort, the quantity and quality of carbohydrates and sugars were investigated in relation to obesity-related cancers (breast, prostate, and colorectal). They reported that higher intake of fruit juice was significantly associated with PCa risk, whereas there was no significant association between PCa risk and total consumption of carbohydrate-heavy or sugary beverages. However, a study comprising 22,720 men reported that sugar intake from fruit juice was unrelated to PCa risk, whereas intake of sugar-sweetened beverages was related to this risk.

These findings suggest that the quality of carbohydrates might be more important than their quantity regarding the relationship between carbohydrate consumption and PCa risk, although more research in future clinical trials is required. (source)

Vitamin A And Prostate Cancer

Vitamin A (also known as retinol or carotene) is found in liver, eggs, and vegetables. Essentially, vitamin A and its derivatives are required for sustaining vision and early development. The relationship between prostate cancer and vitamin A, particularly lycopene, a type of carotene, has been heavily studied due to its ability to prevent prostate cancer. Three meta-analyses suggest that dietary intake of tomatoes or lycopene lowered prostate cancer risk, and a recent a meta-analysis of 42 studies reported that not only dietary intake but also circulating concentrations of lycopene were significantly associated with reduced prostate cancer risk according to dose-response relationships.

Lycopene in tomatoes is suggested to be the factor most likely associated with reduction of prostate cancer risk reduction by vitamin A. (source)

Vitamin D, Sunlight, and Prostate Cancer

Vitamin D is synthesized from a derivative of cholesterol by organisms exposed to sunlight; however, humans can easily experience vitamin D deficiency, and must obtain it from supplements or vitamin D-rich food, such as fish, dairy products, and mushrooms. The primary active form of vitamin D is a hormone that regulates the metabolism of calcium and phosphorus, with calcitriol shown to induce differentiation of immune cells and reduce cancer proliferation. Additionally, calcitriol administration reduced PSA levels by >25% in 20% of patients with localised prostate cancer after 3 months of treatment.

Despite the expected benefit of vitamin D for preventing PCa, the results of epidemiological studies are debatable, as some studies indicate that higher vitamin D levels negatively affect PCa status, whereas others suggest the exact opposite. Furthermore, a meta-analysis of 25 studies provided little evidence to support a major role for vitamin D in preventing PCa development and progression. (source)

Ecologic studies have shown that mortality rates from prostate cancer are inversely correlated with levels of ultraviolet radiation, the principal source of vitamin D. Human prostate cells express receptors for 1,25-Dihydroxyvitamin D which exerts pleitropic anticancer effects on these cells in vitro and in animal models. Moreover, normal prostate cells synthesize 1,25-Dihydroxyvitamin D from circulating levels of 25-OHD, whose levels are dependent on exposure to ultraviolet light. Analytic epidemiologic studies of vitamin D and prostate cancer have focused on polymorphisms in the vitamin D receptor (VDR), on serum vitamin D levels, and on solar exposure.

A role for VDR polymorphisms in prostate cancer risk and progression is established.

Prospective studies of serum 25(OH)D do not support a protective role for higher levels of 25(OH)D on prostate cancer risk overall, but a role for vitamin D deficiency is supported by several studies. Conversely, a growing body of evidence implicates low levels of 25-OHD with an increased risk of fatal prostate cancer.

The results of most epidemiologic studies of sunlight exposure are consistent with a protective effect of exposure to ultraviolet radiation. The discrepancy between the results of studies of solar exposure and studies of serum 25-OHD may be related to methodological differences and to uncertainties regarding the critical period for vitamin D exposure. Additionally, both high dietary intake of calcium and high levels of calcium in serum are positively associated with prostate cancer risk. The relationship between serum 25(OH)D levels and risk of prostate cancer may differ by calcium intake. (source)

Vitamin E And Prostate Cancer

Vitamin E includes tocopherols and tocotrienols, and depending on their presence or absence and the position of the methyl group, they are further classified into four different isoforms: α, β, γ, and δ. Vegetable oils contain high amounts of vitamin E. In particular, soybean, sunflower, corn, walnut, cottonseed, palm, and wheat-germ oils are rich in vitamin E, with the proportions of its isoforms varying depending on the type of oil. (source)

Vitamin E exhibits strong antioxidant, anti-inflammatory, and anti-thrombolytic effects, and preclinical investigations suggest that it inhibits tumor growth. A large prospective study of 29,000 men on the efficacy of vitamin E in reducing lung cancer risk concluded that vitamin E intake did not affect the risk of lung cancer but reduced PCa incidence However, since the release of those results, epidemiological studies have reported no association between vitamin E supplementation and PCa risk. (source)

Recent studies focused on differences between the effects of different isoforms of vitamin E on PCa, revealing that δ-tocopherol inhibits PCa progression by attenuating AKT activation via phosphorylation at T308 in PCa cell lines and prostate-specific Pten−/− mice. Additionally, δ-tocotrienol reportedly inhibits PCa cell proliferation in vitro. δ-Tocotrienol exhibits antitumor activity via endoplasmic reticulum stress, which induces vacuolation, and autophagy pathways. In many previous clinical studies, including SELECT, α-tocopherol was supplied as vitamin E, which might explain why vitamin E showed no effect on reducing PCa risk in those studies. (source)

Polyphenols And Prostate Cancer

Polyphenols are the most abundant and vital plant metabolites and are present in different proportions in most plants. Unlike vitamins, polyphenols are not essential for human survival but exhibit various biological activities, mainly antioxidant and anti-inflammatory. Polyphenols have been studied for their beneficial effects on human health, such as treatment of hypertension and prevention of cancer or cardiovascular disease. The association of prostate cancer with the polyphenols catechin (found in green tea) and isoflavone is well documented. (source)

Green Tea And Prostate Cancer

Catechin is found mainly in green tea, with EGCG the most commonly identified catechin in green tea (>50% of the total polyphenol content) and exhibiting a strong physiological activity. Previous studies report inhibitory effects of EGCG on prostate cancer progression and its molecular targets in vivo and in vitro. (source)

Many epidemiologic studies have explored the association between tea intake and prostate cancer, with inconsistent results regarding the benefits of tea. Notably, almost none of the studies categorized the tea (black vs. green) and included populations that consume black tea, which might not accurately reflect the association between green tea intake and prostate cancer. A large-scale prospective study of 49,920 Japanese men including a high prevalence of green tea drinkers examined the relationship between consumption of green tea and PCa risk, revealing that men who drank five or more cups of green tea daily had a lower risk of advanced prostate cancer relative to those drinking less than one cup daily.

Additionally, a meta-analysis of 10 epidemiological studies on green tea and prostate cancer incidence reported that prostate cancer risk decreased in a dose-dependent manner along with increased green tea consumption, with a significant risk reduction for those who consumed more than seven cups daily.

These results indicate that green tea has an inhibitory effect on prostate cancer carcinogenesis but must be consumed in large amounts to be effective. (source)

Isoflavones And Prostate Cancer

Isoflavones are abundant in most leguminous plants such as beans, soybeans, chickpeas, peanuts, lentils. Additionally, soy isoflavones and their derivatives, genistein and daidzein, reportedly show efficacy in preventing prostate cancer, with a study showing a reduced risk of prostate cancer associated with soy isoflavone intake. Soy isoflavones are similar in structure to 17β-estradiol; therefore, they can bind to the estrogen receptor (ER) and act as phytoestrogens.

Additionally, soy isoflavones are more likely to induce the transcriptional activity of ER-β than of ER-α. The intensity of expression of ER-α or -β varies among different tissue types, with prostate and bone expressing higher levels of ER-β. Therefore, isoflavones are more likely to exhibit estrogenic effects in prostate tissue.

A randomised control study of 158 men in eight Japanese centres using a purified isoflavone supplement reported no significant change in the PSA value before and after treatment, and the incidence of prostate cancer showed no significant difference between isoflavone and placebo groups, although for patients aged >65 years, prostate cancer incidence in the isoflavone group was significantly lower (28.0% vs. 57.1%). Reports of isoflavone supplementation in patients with prostate cancer include multiple randomised controlled trials that suggest that isoflavones show a suppressive effect on prostate cancer progression based on biomarkers, such as serum PSA and testosterone levels, although the results have been inconsistent.

Such inconsistencies might be related to differences in dosage, duration, and dietary intake by the cohorts in each study.

Omega 3 And Prostate Cancer

Recent epidemiological investigations have proven that continuous oily fish intake was associated with decreased prostate cancer risk. PUFAs, both ω-3 and omega-6 fatty acid (ω-6), are changed to eicosanoids in the body. These compounds are commonly engaged in cell growth and differentiation, anti-inflammatory process, and immune modulation.

The mechanism by which omeega-3 prevents carcinogenesis involves the suppressive effect on arachidonic acid synthesised eicosanoids. Eicosanoids extracted from arachidonic acid exert pro-inflammatory activity while omrga-3 derived eicosanoids exert anti-inflammatory activity, thus preventing prostate cancer. In eicosanoid synthesis, cyclooxygenase-2 (COX-2) acts as a core enzyme. Investigations have revealed that there is an overproduction of COX-2 in prostate cancer.

Eicosanoids derived from ω-3s have a suppressive effect on COX-2 overproduction, thus preventing prostate cancer.

However one paper concluded that there is a general paucity of research that includes essential measurements like consumed fish type and tissue ω-3 concentrations, there is scarce evidence to confirm that an association exists between human cancer and marine fatty acid consumption. (source)

Endocrine Disruptors And Prostate Cancer

Endocrine disruptors, defined as exogenous substances or a mixture that “alters function(s) of the endocrine system, causing adverse health effects in an intact organism, or its progeny, or in a (sub)populations”. Endocrine disruptors can act at a low dose and are found in many daily products, such as beverage and plastic bottles, food cans and overall food packaging, epoxy plastic-based electronics, recycled paper, and so on. The main exposure to these contaminants occurs through the intake of contaminated water and food, but can also be taken through other sources, such as direct dermal contact or inhalation of polluted air.

Most endocrine disruptors act similarly to hormone-like chemicals, mostly as estrogen-like or antiandrogens, because they possess a chemical structure similar to natural endogenous hormones. Thus, endocrine disruptors can mimic or block different hormonal pathways. In fact, endocrine disruptors interact with sexual receptors, both ER and AR, and with other non-nuclear receptors.

There are several in vitro studies in human prostate epithelial cells and in vivo studies in animal models as well as epidemiologic studies that indicate a possible association between endocrine disruptors and prostate cancer risk.

The role of endocrine disruptors in the human prostate gland is an overlooked issue even though the prostate is essential for male fertility. From experimental models, it is known that endocrine disruptors can influence several molecular mechanisms involved in prostate homeostasis and diseases, including prostate cancer, one of the most common cancers in the male, whose onset and progression is characterised by the deregulation of several cellular pathways including androgen receptor (AR) signalling.

Autophagy And Prostate Cancer

The role of autophagy in cancer is controversial and still not completely clarified: it has been described as a double-edged sword because of its involvement in both cell survival and tumor suppression, depending on cell type, genetic context, stage of tumor development and nature of the stressor

Autophagy is a homeostatic mechanism through which intracellular organelles and proteins are degraded and recycled in response to increased metabolic demand or stress. Essentially components of the cell can broken down and recycled – and this is a really important thing to happen to maintain a healthy cell.

Autophagy dysfunction is often associated with many diseases, including cancer. Because of its role in tumorigenesis, autophagy can represent a new therapeutic target for cancer treatment. Prostate cancer is one of the most common cancers in aged men. The evidence on alterations of autophagy related genes and/or protein levels in prostate cancer cells suggests a potential implication of autophagy in prostate cancer onset and progression.

The use of natural compounds, characterized by low toxicity to normal tissue associated with specific anticancer effects at physiological levels in vivo, is receiving increasing attention for prevention and/or treatment of prostate cancer. (source)

The loss of autophagic functions can result in accumulation of protein aggregates and damaged organelles, above all damaged mitochondria, and consequently in reactive oxygen species (ROS) production, which then promotes genome instability furthering oncogenic transformation and cancer progression. This evidence is indicative of the anticancer role of autophagy. (source)

Again, what we’re saying here is that if we lose healthy autohpagic function – components of cells get damaged and this may contribute to cancer and cancer progression.

Natural Compounds For Autophagy

Natural products are receiving increasing attention for the prevention and/or treatment of cancer because of their promising efficacy and low toxicity to normal tissue. Therefore there is a great interest in identifying new natural products active against prostate cancer and in understanding the mechanisms of action of these compounds to exploit their properties in the development of new therapeutic or preventive treatments. Since autophagy may become a new therapeutic target for prostate cancer treatment, in this section we will report the evidence on natural compounds able to modulate autophagy influencing prostate cancer cell fate. (source)

Isothiocyanates

Isothiocyanates are a family of compounds derived from the myrosinase-mediated hydrolysis of glucosinolates contained in cruciferous vegetables. High intake of cruciferous vegetables may be associated with reduced risk of aggressive prostate cancer , and isothiocyanates are believed to be responsible for the anticancer effects of these vegetables. (source)

Polyphenols

Polyphenols constitute one of the largest and ubiquitous group of phytochemicals: flavonoids and phenolic acids represent the most common ones in food. Epidemiological evidence suggests lower prostate cancer risk in populations with higher consumption of major polyphenols. Several naturally occurring polyphenols, including resveratrol, green tea catechins and curcumin, are currently being studied for their potential role in prostate cancer prevention and treatment. These compounds can induce both apoptotic and autophagic cell death in various type of cancers. (source)

Vitamin C and K

In recent years, various reports have shown that vitamins, such as vitamin C and vitamin K, exhibit antioncogenic effects. In various cancer cell lines, autophagy has been evidenced to be evoked as a response to vitamin K or ascorbic acid treatment. Autophagy triggered by vitamins has mainly been described as an alternative caspase-independent cell death pathway that supports apoptosis. (source)

Black Pepper

Piperine and piperlongumine, two alkaloids present in black (Piper nigrum Linn) and long (Piper longum Linn) peppers, have been recently reported to mediate antitumoral effects on human prostate cancer cells in vitro and in vivo, and autophagy was one of the mechanism triggered by this active compounds (source)

Melatonin And Prostate Cancer

Melatonin exerts its oncostatic effect by inhibiting angiogenesis, preventing cancer spread and growth, and improving the sensitivity of cancer cells to radiation and chemotherapy in both prostate and breast cancer. (source)

A dose of melatonin within the nanomolar (nM) range (≤10-9 M) usually leads to cytostatic effects, while apoptosis occurs at higher concentrations. At a dose of 10 nM, it demonstrates antiproliferative effects, while at 50 nM, it influences cell growth, and at 1 millimolar (mM), it influences cell viability. Unlike the traditional chemotherapeutic agents, melatonin induces death only in cancerous cells sparing the normal cells. In addition, melatonin administration at various doses from 1 mg to 10 mg/kg, either as short, intermediate, or long-term administration, is shown to offer very minimal side effects compared to medications serving a similar purpose as melatonin. Mild adverse effects reported include headache, nausea, sleepiness, and dizziness.

A recent retrospective study in Russia that spanned 20 years assessed the effect of melatonin on the survival rate of prostate cancer patients with varied prognoses. Out of 955 participants, 113 had a favorable prognosis, 187 had an intermediate, and 655 had a poor prognosis. All participants received combined hormonal and radiation therapy with or without 3 mg of melatonin daily. The study revealed a statistically significant improvement in the five-year survival rate of those with poor prognosis treated with melatonin compared to those not treated with melatonin. However, there was no statistically significant improvement among the patients with favorable and intermediate prognoses.

This reflects the beneficial effects of melatonin in advanced prostate cancer patients with poor prognosis, and more research is encouraged to investigate when it is feasible to start melatonin treatment in those with intermediate prognosis who might progress to poor prognosis.

Melatonin has also been shown to reduce proliferation and angiogenesis and inhibit migration of cancer cells.

Illness Uncertainty And Prostate Cancer

Illness uncertainty is a significant source of psychological distress that affects cancer patients’ quality of life (QOL). Mishel’s uncertainty in illness theory (UIT) proposes that illness uncertainty influences an individual’s use of coping strategies, and directly and indirectly influences their QOL.

Patients’ illness uncertainty directly, negatively influenced their physical well-being and mental well-being. Patients’ illness uncertainty was positively related to their avoidant coping strategies. Patients’ active and avoidant coping strategies influenced their mental well-being. Uncertainty also negatively influenced mental well-being through avoidant coping strategies. The model had excellent fit to the data.

Our findings have indicated the potential of improving QOL by decreasing illness uncertainty and reducing avoidant coping strategies.

avoidant coping enhanced the negative effects of uncertainty on mental well-being. These results are consistent with Kurita’s study of patients with lung cancer. When a situation is or appears to be highly uncertain, patients’ coping strategies are very limited because there is no clear goal for their active coping strategies. In this situation, patients may choose avoidant coping strategies including denial and disengagement to help them ignore the fact, distract from the stressor, and/or its related emotions. Although using avoidant coping strategies might temporarily make an individual feel less stressed, over the long term, these strategies are ineffective to manage the uncertainty because they do not provide an individual with the techniques to solve the problem.

Use of avoidance coping strategies may also cause new problems, accumulate more stress or intensify stress, and ultimately exacerbate the individual’s mental well-being

A number of studies have shown that uncertainty management interventions can improve QOL among prostate cancer patients. For example, an intervention has shown to be effective in uncertainty management when it is designed to help patients to identify their specific concerns, reframe cognitive perception of the cancer situation, and provide relevant cancer information. Care providers can help patients reduce their use of avoidant coping strategies in order to improve patients’ QOL. Although previous studies have suggested that interventions focused on active coping might improve QOL, our findings suggest that interventions targeted at reducing avoidant coping strategies may particularly benefit the mental QOL of patients with prostate cancer.

Summary

An intervention of dietary patterns could contribute to the prevention of prostate cancer. (source)

There are important things to ebb ware of when it comes to side effects of conventional treatment.

It’s important to take a preventative approach – my dad and dad’s dad had prostate cancer and therefore I need to be more mindful of the way I live. Prevention is much easier than treatment!

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