DCA Dosage – Please help confirm!

Home Forums General DCA Discussion DCA Dosage – Please help confirm!

This topic contains 9 replies, has 6 voices, and was last updated by  Dan52 7 years, 1 month ago.

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    My mum was diagnosed with colon cancer back in 2007, since then every year she has battled more and more hurdles. Following that operation 7 months later it travelled to her spleen (which she got removed) then to one of her ovaries (also removed) they then they noticed there were segments in the liver which were cancerous (they did offer her the liver resection but she refused), also noticing pertineal disease which is cancer in the lower abdomen and the latest is a spot on the lung which looks suspicious. She has had chemo via either IV and tablet form after most operations but did not respond well to it and was in bed for most days so docs recommened it was not a great option later on in the track.

    Its now 2012, she has been placed in Palliative care (at home) – on numerous medications to control pain and nausea. I am her main carer and am looking after her. She is 48, still too young and i cant afford to lose her without trying my hardest.

    After researching online i came across DCA and have managed to import it into Australia from a reputable DCA site. Mum has been on it for 4 days so far.

    Her body weight is 66kg. Ive got her taking 10mg/kg, which becomes 660mg, which in grams is 0.66grams. I give her that only once a day (approx. 11am) after food.

    I also have her on B1 Thiamine tablets which she is averaging between 500-750mg. I also make her organic caffinated green tea, which i double bag, but she really only manages to drink 1-2 cups max.

    Can someone please confirm that i am doing it right and that this is the correct dosage as i have heard different things from all over the web.

    Look forward to your replies. Sam



    Dosage is ok. I suggest twice a day. 50 % each one.

    May be you can increase to 12.5 mg/ kg after the first week. Take into acount to left 2 days off.



    Hi Elias,

    Thanks for your fast reply. Ok im glad, and yes i will consider that.

    Do you think its worthwhile me buying her caffiene tablets as she struggles to drink several cups of green tea, if so at what dose if you do know?




    Unfortunately, I dont know because my dad is used to drink green tea.



    Sammy, I think that if your mum is struggling with consuming the tea, that you might cut back a little and supplement it with caffeine tablets.  The quality of her life is important and she is dealing with pain and nauesa, so why have her stuggle with trying to drink more tea.  Just a suggestion to see if it helps.

    All my best to you and your mum.




    Hi Susan, yes I was thinking along the same lines. Just got to find some pure caffeine tablets in Melbourne, chemist don’t seem to sell pure tablets…



    Just a question… On the off days of DCA should she still be having caffeine and vitamin B1?

    Would appreciate if someone could let me know how they do it.




    No caffeine Sammy , B1 is fine



    I am a medical oncologist and have spent hundreds of hours reading the literature on DCA, writing a protocol for DCA (for the Bahamas) and looking at the adjuvant agents that are said to be important for DCA.  The latter is really a hodge-podge of advice that appears to be in the category of urban legends.   DCA inhibits  PDK (pyruvate dehydrogenase kinase) which allows PDH to work pushing pyruvate into the Kreb's cycle and lessening the cancer's cell use of glycolysis.  This approach supposedly relates to the need of the cancer cell for glucose as a major source of energy.  We know the cancer cell also uses glutamate, as well as  LDL and also omega 6 fatty acids.  Caffeine causes insulin resistance and in studies leads to elevated blood sugars. In contrast, coffee does the opposite.  It appears that there is something in coffee, perhaps caffeic acid or chlorogenic acid, that accounts for the apparent value of coffee to lower blood sugars. 

    Basically, the literature is confusing on this topic and there is a need to clarify what combinations should be used with DCA.  Adjuvants like benfotiamine, thiamine, R-lipoic acid are purported to reduce the neurologic toxicity that can occur with DCA. Most of this advice is based on the use of these agents in reducing neuropathy from chemotherapy agents  e.g., oxaliplatin or on the improvement seen using them in diabetic patients  with polyneuropathy. Other agents tried in patients with various discorders to lessen neuropathy also include  CoQ10 and L-carnitine.  The literature on these reports is conflicting, especially since DCA is often used in treating a disorder  called MELAS which in and of itself has neurologic problems.  Rat studies did show improvement by thiamine when high doses of DCA ( 50  mg/kg/d) were given. In a study by Spruijt from 2001, humans were given thiamine (B1) at a dose of 100mg per day in patients receiving DCA. These were children who have a much lower incidence of  peripheral neuropathy (PN). Note the DCA dose was the same as that used in the rat studies. " Overall, more than 50% of the patients given DCA displayed a significant decrease of nerve conduction velocity and response amplitude." "All the patients in our study were comedicated with a daily oral dose of 100 mg thiamine. This management was adopted because of reported experience with rats treated with DCA in which the parenteral administration of thiamine reduced the incidence of polyneuropathy as indicated by hindlimb weakness.17"  

    The authors also noted: "The concept that peripheral neuropathy is caused by thiamine depletion appears less likely from our experience, because all our patients received thiamine continuously, yet the development of peripheral neuropathy was not prevented. Because enteral thiamine absorption is limited to about 5 mg/day,7,19 we treated patients who became symptomatic with intramuscular injections of thiamine at 50 mg daily for 1 week and then weekly as long as symptoms persisted. At the same time, the dose of DCA was reduced. Three patients who received this treatment reported some improvement of symptoms, but no significant electrophysiologic amelioration was detected at 6 and 12 months."

    And "In conclusion, it appears that peripheral neuropathy is a common side effect of chronic treatment with DCA. Only by studies of nerve conduction can such treatment be adequately monitored. Serial nerve conduction studies of untreated patients and patients treated with DCA would be valuable to determine the incidence and natural history of peripheral neuropathy in mitochondrial disease."

    The reference and abstract of this paper is below: 


    1.  Spruijt L, Naviaux RK, McGowan KA, et al: Nerve conduction changes in patients with mitochondrial diseases treated with dichloroacetate. Muscle Nerve 24:916-924, 2001, PMID: 11410919.                                                             


    Serial measurements of nerve conduction velocities and amplitudes were performed in 27 patients with congenital lactic acidemia over 1 year of sodium dichloroacetate (DCA) administration. Patients were treated with oral thiamine (100 mg) and DCA (initial dose of 50 mg/kg) daily. Nerve conduction velocity and response amplitude were measured in the median, radial, tibial, and sural nerves at 0, 3, 6, and 12 months, and plasma DCA pharmacokinetics were measured at 3 and 12 months. Baseline electrophysiologic parameters in this population were generally below normal but as a group were within 2 standard deviations of normal means. Although symptoms of neuropathy were reported by only three patients or their families, nerve conduction declined in 12 patients with normal baseline studies, and worsening of nerve conduction occurred in the two who had abnormalities at baseline. Peripheral neuropathy appears to be a common side effect during chronic DCA treatment, even with coadministration of oral thiamine. Nerve conduction should be monitored during DCA treatment.


    The vast majority of those using DCA in human therapy conclude that only by stopping the DCA can the neurologic abnormalities be improved. 


    The bottom line is that there is no clear evidence of what is important to use with DCA  to either enhance activity or lessen toxicity.  


    If anyone has medical literature or some form of proof of efficacy please share it with me.  Our protocol which will be carried out in the Bahamas will use coffee containing chlorogenic acid and caffeine, and also use benfotiamine, R-lipoic acid. The benfotiamine also contains a small amount of thiamine.  BUT…. the only reason that these agents are being used is that in the few cases where we have obtained medical records of DCA efficacy, the patients used these "adjuncts".  This is anecdotal information and nothing more at this time. 


    If anyone can add clarity to this discussion, I would be highly grateful. 


    Stephen B. Strum, MD

    Board Certified Medical Oncologist



    I get 600mg vitamine B1 with 10 mg/kg/day DCA for 5 days/week by two months and have good results for neuropathy.

    I think urgent research is needed about the four PDK isoenzymes: you may take a look at my post   http://www.thedcasite.com/dca-forum/topic/high-reading  

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