In the 5+ weeks I’ve been off smokeing last weekend was the worst. I try not to post negativities here but I’m going to try to get some stuff out of my system so please forgive me. I have been feeling anger that borders on rage and for no good reason. I’ve been lashing out at those closest to me and I feel like a total heel over this. I realize that this is due to the breaking of my mental addiction but it doesn’t make it any easier. This morning I started to get the “I don’t care if I quit or not” feeling. “It really doesn’t matter”. Obviously the fact that I am posting instead of  smoking shows that I haven’t surrendered and I’m not going to. Thinking about my list of reasons I ask myself are these really valid.

The urges and cravings I can handle. They come and go. What is dificult is the mental state that won’t leave me alone hour after hour. My only solace is that I do know deep down that this too shall pass.

Like bread, everybody knows it’s good while it’s hot!!!!

Inhibition of chronic ulcerative colitis associated adenocarcinoma
development in mice by inositol compounds
Authors: Liao, Jie; Seril, Darren N.; Yang, Allison L.; Lu, Gary G.;
Yang, Guang-Yu

Source: Carcinogenesis, Volume 28, Number 2, February 2007, pp.446-454(9)

Publisher: Oxford University Press

Abstract:

Chronic inflammation is a well recognized risk factor for cancer and patients with long-standing ulcerative colitis (UC) are at an increased risk for colorectal carcinoma development. In order to prevent UC associated carcinogenesis, we tested the effects of
inositol compounds (including inositol and hexaphosphate inositol) on UC-associated carcinogenesis in our novel mouse model. Female C57BL/6 mice were subjected to long-term, cyclic dextran sulfate sodium (DSS) treatment and fed a 2-fold iron-enriched diet. The inositol compounds  were administered via the drinking fluid. In the DSS-plus-2-fold iron
positive control group, colorectal adenocarcinoma incidence was 70.6% (24/34 mice) after 15 cycles of DSS treatment (1 DSS cycle = 7 day DSS treatment period followed by a 10 day recovery period). Tumor multiplicity was 1.26 ± 1.05 and tumor volume was 21.4 ± 5.2 mm3.
Adding 1% inositol, tumor incidence was statistically significantly reduced (42%, 9 of 21 mice with tumors), as was tumor multiplicity (0.5 ± 0.7) and tumor volume (4.2 ± 1.9 mm3). Administration of hexaphosphate inositol noticeably reduced tumor incidence (50%, 12 mice with tumors out of 24 total), tumor multiplicity (0.8 ± 0.9) and tumor volume (12.3 ± 4.1 mm3); however, the results were not statistically significant (P > 0.05). Further mechanistic studies showed that the inhibition of UC-associated carcinogenesis by inositol
compounds might relate to their function on the modulation of macrophage mediated inflammation, nitro-oxidative stress and cell proliferation in UC-associated carcinogenesis. This study indicates that inositol compounds may have the potential to serve as preventive agents for chronic inflammation-carcinogenesis.

Document Type: Research article