Hello David- I was diagnosed with stage 3C HER2+ oestrogen and progesterone + receptors (breast cancer). I am 54 years old. I have had one course of “red devil” – (Adrianycin and cytoxian). I have been able to begin swimming and in my 3rd week after my 1st round am able to swim 40 lengths of a 12 meter pool. It takes me about 20 minutes. Please advice on how to avoid breast cancer side effects of this chemotherapy and protect my heart from the toxins I will be getting.
I am not one for exercise usually, but do walk a lot during my working day. I am 5.5 feet tall and weigh 67 kg.
Any assistance will be appreciated. Thanks Carol
I am sorry to read of your BC diagnosis. You are off to a great start however, in reducing your risk of heart damage from breast cancer side effects. The cardio toxicity of both adriamycin and cytoxan are well documented. Regular exercise (swimming, walking, etc.) stimulates your heart muscle and has been shown to reduce your risk of heart failure from BC chemotherapy. Excellent start.
I will link other studies about therapies to reduce your risk of heart disease and enhance your heart health below.
Regarding the info below, two issues to keep in mind. First, my experience and belief is that anecdotal info is useless without studies to support them. Secondly, I have broadened my definition of “evidence-based practice” to include research such as in-vivo and in-vitro studies. In other words, I look beyond FDA approved research…
Doxorubicin is the same as adriamycin- feel free to ask any and all questions.
” ω-3 PUFA have also been shown to prevent harmful side-effects (including cardiotoxicity and heart failure) induced by conventional and innovative anti-cancer drugs in both animals and patients…
The ability of these fatty acids to reduce the toxic side-effects of these drugs has been largely proven [63,64,65], and several results have also concurred to demonstrate their chemosensitizing effects, as well as their ability to prevent drug-resistance [66,67,68]…
ω-3 PUFA appear as ideal candidates in preventing the development of cardiac events induced by ATC chemotherapy, since these fatty acids are known to induce benefits at a cardiovascular level by positively modulating some of the cellular processes and molecular pathways that, conversely, are harmfully altered by ATC and other chemotherapeutic agents…”
“Doxorubicin (Dox) induces cardiotoxicity, thereby limiting its clinical application for chemotherapy of cancer. The mechanism of cardiotoxicity includes the production of excess intracellular ROS. 14-3-3s have been found to protect the myocardium against various types of injury…
Curcumin (Cur) is a polyphenolic compound that is derived from turmeric and has multiple bioactivities, including anti-oxidative and radical-scavenging activities that exert cytoprotection…
Our results showed that Dox-induced injury to the myocardium was decreased by Cur treatment via upregulating the protein expression of 14-3-3γ in total protein and Bcl-2 expression on mitochondria, activating Bad (S112) phosphorylation, reducing the heart rate and ST segment, and reducing LDH and CK activities in the serum, thereby causing a reduction in caspase-3 activity, the apoptosis rate, and histopathological changes of the myocardium (in vivo)…
In conclusion, this is the first study to demonstrate that Cur protected the myocardium against Dox-induced injury via upregulating 14-3-3γ expression, thereby promoting the translocation of Bcl-2 to mitochondria, suppressing oxidative stress, and improving mitochondrial function…”
“Doxorubicin (DOX) is a widely prescribed antineoplastic and although the precise mechanism(s) have yet to be identified, DOX-induced oxidative stress to mitochondrial membranes is implicated in the pathogenic process…
Treatment with a cumulative dose of 14 mg/kg DOX caused mitochondrial cardiomyopathy as evidenced by histology, accumulation of oxidized cardiac proteins, and a significant decrease in mitochondrial calcium loading capacity.
Maintaining rats on the alpha-tocopherol supplemented diet resulted in a significant (two- to four-fold) enrichment of cardiac mitochondrial membranes with alpha-tocopherol and diminished the content of oxidized cardiac proteins associated with DOX treatment.
However, dietary alpha-tocopherol succinate failed to protect against mitochondrial dysfunction and cardiac histopathology.
From this we conclude that although dietary vitamin E supplementation enriches cardiac mitochondrial membranes with alpha-tocopherol, either (1) this tocopherol enrichment is not sufficient to protect cardiac mitochondrial membranes from DOX toxicity or (2) oxidative stress alone is not responsible for the persistent mitochondrial cardiomyopathy caused by long-term DOX therapy.”
“Increase in oxidative/nitrosative stress is one of the mechanisms associated with the development of cardiotoxicity due to doxorubicin (Dox), a potent chemotherapy drug.
In the present in vivo study in rats, we investigated the effect of prophylactic treatment with Vit C on Dox-induced apoptosis, inflammation, oxidative/nitrosative stress, cardiac dysfunction, and Vit C transporter proteins.
Dox (cumulative dose: 15 mg/kg) in rats reduced systolic and diastolic cardiac function and caused structural damage. These changes were associated with a myocardial increase in reactive oxygen species, reduction in antioxidant enzyme activities, increased expression of apoptotic proteins, and inflammation.
These results suggest a cardioprotective role of Vit C in Dox-induced cardiomyopathy by reducing oxidative/nitrosative stress, inflammation, and apoptosis, as well as improving Vit C transporter proteins.
NEW & NOTEWORTHY This in vivo study provides novel data that vitamin C improves cardiac structure and function in doxorubicin-induced cardiomyopathy by reducing oxidative/nitrosative stress, apoptosis, and inflammation along with upregulation of cardiac vitamin C transporter proteins. The latter may have a crucial role in improving antioxidant status in this cardiomyopathy.”