Dichloroacetate sodium (DCA) has being explored as a possible metabolic therapy for a range of malignancies since 2007. RECIST standards define “response” as the degree to which cancers have decreased or disappeared on imaging. DCA is a cytostatic drug in vitro and in vivo that does not promote apoptosis (programmed cell death). We explain how an oral DCA medication stabilized a 57-year-old woman’s stage 4 colon cancer after four years with minor side effects. This is an unorthodox use of DCA as a cytostatic medication, since stage 4 colon cancer frequently progresses slowly but inexorably to incapacity and death.
Oral dichloroacetate sodium (DCA) is a promising new cancer treatment. In human studies, response is measured by how much a tumor has shrunk or disappeared using RECIST criteria. DCA may also produce cytostasis (programmed cell death). In this case report, a 57-year-old woman’s stage 4 colon cancer was controlled with oral DCA for more than four years without major side effects.
Since a 2007 in vitro/in vivo rat research demonstrated sodium dichloroacetate’s (DCA) efficiency in treating human lung, breast, and brain malignancies by inhibiting mitochondrial pyruvate dehydrogenase kinase, DCA has being examined as a potential metabolic treatment for several cancers. Stacpoole et al. have published studies on the effectiveness of DCA in treating congenital lactic acidosis. These studies showed DCA’s oral safety. DCA has no harmful effects on the heart, lungs, kidneys, or bone marrow. Peripheral neuropathy is the most common and severe treatable side effect. After DCA is discontinued, delirium disappears. A small fraction had asymptomatic liver enzyme elevations. DCA’s early success in treating congenital lactic acidosis may have facilitated its use in cancer. Four publications on cancer clinical research employing DCA reveal its rising efficacy. Many studies of late-stage patients only describe short-term treatment.
Bonnet et al. (2007) found that DCA causes cancer cell death. This behavior was linked to the Warburg effect and mitochondrial potassium ion channels. Studies have indicated that DCA is effective against colon, prostate, ovarian, neuroblastoma, lung carcinoid, cervical, endometrial, cholangiocarcinoma, sarcoma, and T-cell lymphoma. DCA may have anticancer effects. Changing HIF1-, pH-regulating enzymes V-ATPase and MCT1, and other genes including PUMA, GLUT1, Bcl2, and p53 may influence cell survival. In vitro studies sometimes utilize DCA levels that aren’t appropriate for therapeutic usage. DCA is cytostatic at low doses but promotes apoptosis when taken with other drugs. Sun et al. found that DCA inhibited cell proliferation without increasing apoptosis in their in vivo breast cancer study. Dactylcysteinol (DCA) reduced metastatic burden in the lungs of rats with breast cancer. This reveals DCA’s potential as a cancer-stabilizing drug, similar to anti-angiogenic medicines. According to the authors, no human evidence support using DCA for long-term disease stability.
Khan has used DCA to treat terminally sick cancer patients who have not responded to conventional treatment since 2007. A naturopathic doctor devised a natural therapy plan to counteract dose-limiting neurotoxicity (Andrews). Oral DCA for neuropathy prevention included acetyl L-carnitine, R-alpha lipoic acid, and benfotiamine. Observational data show that DCA helped over 300 people with advanced cancer. Natural neuroprotective drugs coupled with 20-25 mg/kg for two weeks, followed by a week off, decreased neuropathy by 20%. 2% had elevated liver enzymes, although the disease was reversible.
A patient’s oral DCA treatment had long-lasting cytostatic effects. This patient’s prognosis was grim (median survival of 9-12 mo for stage 4 colorectal cancer using aggressive conventional palliative chemotherapy). Khan and Andrews gave the patient natural neuroprotective drugs.
In March, a 57-year-old lady with advanced colon cancer came to the author’s clinic. The guy presented with fresh constipation and low back discomfort in 2010, but the doctor quickly discovered rectal cancer. Rectal tumor impeded colonoscopy, hence the surgery failed. Pathology found a differentiated colon cancer. On CT scan, we detected 3 cm liver metastases, tiny lung metastases, and annular rectal carcinoma, all of which put this patient in stage 4 disease (margins of the cancer were difficult to distinguish from the surrounding tissues on CT scan). This patient’s obstruction required a loop ileostomy, but the rectal tumor was not removed. After surgery, the patient began FOLFIRI + bevacizumab treatment. The patient’s carcinoembryonic antigen (CEA) marker reduced from 260.9 ng/mL before chemotherapy to 3.5 ng/mL soon before DCA treatment, demonstrating an early response to chemotherapy. Chemotherapy response eventually plateaued. By the time the patient reached the author’s clinic, the chemotherapy had only maintained stability.
Before smoking 20 years ago, the patient was healthy. She sometimes drank. Colon and stomach cancer were common. Hydromorphone-ER Hydromorphone 32 mg twice daily 2-4 mg orally was given for “breakthrough” discomfort in addition to chemotherapy, hydrogen peroxide enemas, oral vitamin C, and occasional oral vitamin D. Nobody had allergies. Minor mouth ulcers due to chemotherapy, slight diarrhea (expected with ileostomy), and moderate intermittent rectal hemorrhage were seen. Upper right shoulder discomfort reached 3, while lower back and sacrum pain reached 6. (felt to be referred pain related to liver metastases).
Because the chemotherapy was still working and the patient wasn’t experiencing serious side effects, it was decided to enhance his existing medicine. A naturopath was engaged to design a treatment plan (Andrews). 10,000 IU of vitamin D were given orally, 50 g of vitamin C were given intravenously (i.v.), and 49 mg/kg of sodium dichloroacetate (DCA) were given i.v (manufacturer: Tokyo Chemical Industry, United States). R-alpha lipoic acid (150 mg thrice daily), acetyl L-carnitine (500 mg thrice daily), benfotiamine (80 mg twice daily), and alpha lipoic acid (racemic) are natural supplements that may lessen DCA’s side effects (500 mg with each DCA dosage). Infusions were timed to coincide with chemotherapy to avoid drug interactions (at least 2 d apart from chemotherapy). Due to its antioxidant characteristics, licorice extract (lipoic acid) was not given on chemotherapy days or one day before or after. We employed a thorough plan in March 2012. Due to no adverse effects, the weekly DCA dosage was increased to 4000 mg i.v. (66 mg/kg). Even at large doses, DCA caused little sleepiness.
Metformin doses ranged from 500 mg daily to a maximum of 500 mg three times daily to enhance cancer sensitivity to chemotherapy. Pregabalin relieved sacral neuropathy pain (started 50 mg daily, titrated up to 50 mg 3 times a day). Due to chemotherapy-induced nausea and vomiting, the patient had to skip metformin doses to avoid dehydration toxicity.
https://www.dcaguide.org/dca-for-cancer-treatment/
