Movember

[RassK]

Tänkte kicka igång Movember (http://se.movember.com/) med en serie studier som handlar om kost och risk för prostatacancer. Ska försöka slänga upp en studie om dagen i hela november. Detta för att bidra med min del till att öka medvetenheten om vad man som privatperson kan göra för att minska risken för prostatacancer.


Abstract
The hypothesis that vitamin D deficiency increases the risk of clinical prostate cancer has stimulated an extensive body of research. 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.

Vitamin D, Sunlight, and the Epidemiology of Prostate Cancer. Anticancer Agents Med Chem. 2012 Oct 12.

http://www.ncbi.nlm.nih.gov/pubmed/23094920

Låga nivåer av vitamin d och höga nivåer av kalcium ger ökad risk för prostatacancer. Så tagga ner på kvargen och ät ert vitamin d grabbar!

[Thornblom]

Attans att man dricker 2-3L mjölk om dagen då..

[Eddie Vedder]

Låga nivåer av vitamin d och höga nivåer av kalcium ger ökad risk för prostatacancer. Så tagga ner på kvargen och ät ert vitamin d grabbar!

En hypotes är ju att det senare leder till det förstnämnda vilket då skulle innebära att kalcium inte är den kausala faktorn överhuvudtaget utan snarare en indirekt.

[Glutenkatt]

Attans. Jag överkonsumerar alla slags mjölkprodukter.
Fast å andra sidan tar jag 50 mikrogram D-vitamin var dag.. De jämnar nog ut sig. Snus borde jag sluta med kanske.

[Fishtank]

Första dagen på movember och jag rakar av allt.
Good stuff.

[RassK]

NSAID'er ökar risken för prostatacancer, acetylsalisylsyra minskar den.

Abstract
The cyclooxygenase 2 (COX-2) enzyme overexpression in prostate cancer has led to the hypothesis that COX-2 inhibition may reduce prostate cancer growth. Some previous studies have linked the usage of COX-2 inhibiting non-steroidal anti-inflammatory drugs (NSAIDs) with a decreased prostate cancer risk. We estimated the association between cumulative COX-2 inhibition by NSAID usage and prostate cancer risk at population level. All new prostate cancer cases in Finland during 1995-2002 and matched controls (24,657 case-control pairs) were identified from national registries. Detailed information on medication purchases was obtained from a national prescription database. A total cumulative COX-2 inhibition value was calculated based on total cumulative mg amount of each NSAID drug and the drug-specific COX-1/COX-2 inhibition ratio. Prostate cancer risk was analysed with propensity score-matched conditional logistic regression model. In total, 53.8% of the cases and 46.5% of the controls had any prescription-use of NSAIDs, while 8.1% and 7.9%, respectively, had used aspirin. Compared to the non-users, any NSAID use was associated with an elevated overall prostate cancer risk (46.4% versus 53.6%, respectively; odds ratio [OR] 1.3, 95% confidence interval [CI] 1.3, 1.4) and risk of advanced cancer (11.8% versus 14.1%; OR 1.6, 95% CI 1.5, 1.8). The risk remained elevated despite the amount of cumulative COX-2 inhibition. In a separate analysis, the risk increase was similar for each NSAID with the exception of aspirin, which was associated with a decreased overall prostate cancer risk (OR 0.90, 95% CI 0.84, 0.96) in a dose-dependent fashion. NSAID use is associated with an increased prostate cancer risk at the population level regardless of the COX-2 inhibition. This may be explained by systematic differences between prescription NSAID users and non-users. In contrast, aspirin use is associated with a decreased overall prostate cancer risk. Further studies on aspirin and prostate cancer will be needed.

Use of aspirin, but not other non-steroidal anti-inflammatory drugs is associated with decreased prostate cancer risk at the population level. Eur J Cancer. 2012 Oct 15.

http://www.ncbi.nlm.nih.gov/pubmed/23079475

En aspirin om dagen är inte bra för magen, men för prostatan :thumbup:

[RassK]

Abstract

Pomegranate juice (PJ) is a natural product that inhibits prostate cancer progression. A clinical trial on patients with recurrent prostate cancer resulted in none of the patients progressing to a metastatic stage during the period of the trial. We have previously found that, in addition to causing cell death of hormone-refractory prostate cancer cells, PJ also markedly increases adhesion and decreases migration of the cells that do not die. However, because PJ is a very complex mixture of components and is found in many different formulations, it is important to identify specific components that are effective in inhibiting growth and metastasis. Here, we show that the PJ components luteolin, ellagic acid, and punicic acid together inhibit growth of hormone-dependent and hormone-refractory prostate cancer cells and inhibit their migration and their chemotaxis toward stromal cell-derived factor 1α (SDF1α), a chemokine that is important in prostate cancer metastasis to the bone. These components also increase the expression of cell adhesion genes and decrease expression of genes involved in cell cycle control and cell migration. Furthermore, they increase several well-known tumor-suppression microRNAs (miRNAs), decrease several oncogenic miRNAs, and inhibit the chemokines receptor type 4 (CXCR4)/SDF1α chemotaxis axis. Our results suggest that these components may be more effective in inhibiting prostate cancer growth and metastasis than simply drinking the juice. Chemical modification of these components could further enhance their bioavailability and efficacy of treatment. Moreover, because the mechanisms of metastasis are similar for most cancers, these PJ components may also be effective in the treatment of metastasis of other cancers.

Specific pomegranate juice components as potential inhibitors of prostate cancer metastasis.

http://www.ncbi.nlm.nih.gov/pubmed/23066443

[RassK]

On ni inte orkar läsa så står att granatäpplejuice dödar prostatacancerceller och bromsar sjukdomsförloppet. Något som är känt sen länge men studien är uppdaterad och från 2012.