there IS Electrophysiological evidence of chemo brain

[Lani]

again, I feel non-anecdotal information deserves reading by the larger audience (the articles section does not seem to attract such a large readership and I felt this info would make many feel better about that their symptoms were not "just in their head" OR REALLY THAT THEY REALLY ARE! ABSTRACT: Effects of High-Dose and Conventional-Dose Adjuvant Chemotherapy on Long-Term Cognitive Sequelae in Patients with Breast Cancer: An Electrophysiologic Study [Clinical Breast Cancer]
Background: The mechanisms underlying cognitive deficits found in a number of patients with breast cancer treated with adjuvant chemotherapy are still unclear. In the current study, we used a combination of measures of brain electric activity and cognitive performance during information processing to elucidate the origin of these cognitive deficits.

Patients and Methods: Twenty-nine patients at high risk with breast cancer treated with adjuvant conventional-dose cyclophosphamide/epirubicin/5-fluorouracil or adjuvant high-dose cyclophosphamide/thiotepa/carboplatin were compared with 23 patients with stage I breast cancer not treated with chemotherapy approximately 4 years after completion of treatment. We studied reaction times and the amplitudes and latencies of the P3, an electrophysiologic index of information processing, in a task with different conditions related to input, central, and output processing of information.

Results: The amplitude of the P3 component was significantly reduced in patients with breast cancer treated with high-dose cyclophosphamide/thiotepa/carboplatin compared with patients with breast cancer not treated with chemotherapy. We observed no significant differences in reaction times and P3 latency between the treatment groups.

Conclusion: Our data show electrophysiologic alterations in patients with breast cancer treated with high-dose chemotherapy 4 years after completion of treatment. The observed P3 reduction might be a result of suboptimal phasic cortical arousal and problems with the allocation of processing resources in these patients.

[Susan2]

You are right. Confirmation of what so many of us have seen first-hand.

[saleboat]

Hi Lani,

Case in point-- I'm confused by this. Was it the patients who had high-dose chemo, as opposed to 'regular' dose chemo who showed the greatest cognitive impairment? Did those who received regular dose chemo have the same cognitive ability as those who did not receive any chemo?

Thanks for your help with this.

Jen

[R.B.]

I have not looked at the way chemo agents work.

But Herceptin is reported in papers to block FAS.

Fas blockers are reported as having significant in vivo antitumour activity in BC.

IF Fas blocking by Herceptin is body wide (and there is evidence of expression if not over expression of HER2 in other areas of the body e.g. arthritis) and if applicable to all longer chain fatty acid production in whole or in part it would reduce DHA production. (the body can make dha from linolenic acid omega three, as it does arachidonic acid AA a percusor of COX 2 from linoleic omega six - shutting down AA might well be good news in a body that is awash with omega six, but shutting down omega three in the absence of supplementation may have negative impact (and may increase with time ???) as DHA etc is essential to human health, particularly brain and eyes.

In pregnant women it is suggested that the developing foetus is capable of drawing down DHA from the bodies likley largest source of DHA - so in people with low DHA synthesys and low intake could the body be robbing the brain to keep other things going and how long is that an option before the impact on the brain of low DHA manifests.

Smart Fats by A Scmidt cites trials which suggest brain tumours have high omega and low DHA.

Statistics show DHA consumption has dropped dramatically and inflamatory omega sixes increased.

Lack of DHA in the brain has been linked at various levels to a number of brain disorders and general lack of cognitive process.

IF a consequence of treatment is blocking disrupting fatty acid sythesys pathways the body would have to rely on ingested sources.

Conclusion - there are a lot of potential upsides to Fish oil, algae, DHA supplementation and few evident downsides.

AND trials suggest that adequate omega three intake reduces the risk of BC.

I do not have the answers I am just raising questions based on papers I have been reading - images in the fog.

As ever please discuss dietary changes with your advisors.

RB

[R.B.]

Herceptin does impact in arthritic joints.

See above.

RB


ABSTRACT

http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum


1: Arthritis Rheum. 2001 Feb;44(2):260-5. Related Articles, Links

Involvement of ErbB-2 in rheumatoid synovial cell growth.

Satoh K, Kikuchi S, Sekimata M, Kabuyama Y, Homma MK, Homma Y.

Department of Orthopaedic Surgery, Fukushima Medical University School of Medicine, Japan.

OBJECTIVE: The synovial tissue affected by rheumatoid arthritis (RA) is characterized by hyperproliferation of synovial cells. High amounts of epidermal growth factor (EGF) in the synovial fluid of RA patients contribute to the growth of rheumatoid synovial cells. To characterize the receptor for EGF in rheumatoid synovial cells, the expression and function of ErbB family members were examined. METHODS: Synovial tissues were obtained from surgical excisions. The expression of ErbB products was examined by immunohistochemistry and immunoblotting by using specific antibodies. Primary cultures were established from the surgical materials. Cell growth was measured using MTT. The levels and phosphorylation state of the ErbB-2 protein were analyzed by immunoprecipitation and immunoblotting. RESULTS: The expression of ErbB-2, but not other ErbB-related products, was detected in synovium with RA as compared with that with osteoarthritis (OA) and ligament injury. Growth of primary synovial cells with RA was inhibited by genistein, a tyrosine kinase inhibitor, and herceptin, a specific monoclonal antibody against ErbB-2. Herceptin showed a small effect on growth of primary synovial cells with OA. EGF stimulated the phosphorylation of ErbB-2 in primary synovial cells with RA. This EGF-stimulated phosphorylation was completely abrogated by genistein and herceptin. CONCLUSION: ErbB-2 is expressed in rheumatoid synovial cells and may function as the receptor for EGF. Our data suggest that mitotic signals from EGF family members are transduced by ErbB-2 in these cells. Inhibition of ErbB-2 may provide a new approach to the effective treatment for RA.

PMID: 11229455 [PubMed - indexed for MEDLINE]

[Sherryg683]

Thanks Lani, I knew my brain isn't working like it use to, every one looks at me like I'm crazy when I say this, even though I stumble through my words as I say it...sherryg683