Fulda conference #8: New approaches in biological tumour therapy (Dr Florian Schilling)


The Christmas Market at Fulda

Updated March 2016 – For more information on GcMAF, please join the GcMAF and GcMAF Cancer forums on Facebook – they are closed groups, so you have to wait for your membership to be confirmed.  They contain up-to-date information on sources of GcMAF, and also feedback and contributions  by people who are using GcMAF.

Florian Schilling presented another talk at the conference:  Leaky-Gut:  Dietary regimen with MAP and GcMAF

Florian Schilling studied pre-clinical medicine at the Ludwig-Maximillian-Universitat Munchen (LMU), and then trained as an alternative practitioner, with his own clinic since 2006, specialising in integrated and complementary tumour therapy, CFS/ME, general regulatory medicine and detoxification.  He has been a lecturer at the Paracelsus College in Munich since 2007, and lectures both in Germany and internationally.

info.schilling@googlemail.com, http://www.nhz-buchloe.de/


Like Dr Ionnescu, Dr Schilling also emphasised the importance of not using glutathione if there is a tumour.

What was also interesting is his protocol in treating tumours. It is no use just using anti-oxidative or oxidative therapies by themselves:  if negative – no sustainable effect (tumour will grow back) – you put niche pressure on the tumour.  If positive – shrink the tumour mass.  You need both oxidative and anti-oxidative therapies for them to work.  So using IV C by itself doesn’t work, which accounts for why it didn’t work with me.  Such a pity the pracitioner I went to in the UK wasn’t aware of this.



copyright Dr Schilling

The genetic cause of cancer theory is flawed

SCID (severe combined immunodeficiency) mice (with no tumour growing in it) – a transplanted tumour does not grow in it.

In tumours you find stem cells, which prompts the growth of tumours

Chemotherapy only affects the active, differentiated cells.

Stressed stem cells (1) develop resistance and (2) when really annoyed increase cell division

Residual tumour post-chemotherapy increases resistant stem cells with subsequent courses of chemo-resistance

Genetic disposition – detox system, anti-oxidaive system.

Stem cells can regenerate the organ if needed

Chronic inflammation – if protective mechanisms are decompensating, then we have cancer

If you have a tumour, you can’t work with anti-oxidation therapies.  Detox is no longer going to save the patient.

Tumour growth is triggered by tumour stem cells – there are different degrees of malignancy in stem cells:

1.  Multi-potent stem cells – most tumours – can switch to pluripotent in conditions of hypoxia

2.  Pluripotent stem cells – tissue and organs

3.  Totipotent stem cells – can build a whole human being.  How differentiated? Not differentiated at all

Stem cells in a permanently hypoxic milieu will switch to fermentation which stimulates cell division and vice versa – it is a vicious cycle.

Iron deficiency – 10% of Europeans are iron-deficient.  We need iron.  Iron is used in cytochrome building and blood-building (priority).  Lack of iron means that cells go into fermentation mode.

Check for ferritin status to determine whether or not there is iron deficiency.

Embryonic stem cells shouldn’t exist (adults shouldn’t have them).  These are the most malignant.  The poorest prognosis is from this.

Trophoblast in stem cells form the placenta – destroy uterus tissue.  Nidation – if this is not stopped, pregnancy would be lethal.

Treatment of tumours

Tumour metabolism relies on the Warburg effect – doesn’t want to burn oxygen, relies on energy via glycolysis.

Tumour cells – high concentration of glutathione.  Upregulated genetically.  Redosis – intra-cellular alkalinity.  NK cells don’t like the acid trench.

Lactate is an anti-oxidant in high concentrations – so redosis increases.

So don’t administer glutathione.

Detox with glutathione in Phase 2 detox

If redosis can be reduced, the tumour cell is vulnerable.

Antioxidative therapies and oxidative therapies = negative – no sustainable effect (tumour will grow back) – you put niche pressure on the tumour.  positive – shrink the tumour mass.  You need both oxidative and anti-oxidative therapies.


Tests check for:  positive LDH-Isoenzyme

Positive M2PK

Positive Lactate/Pyruvate

Hypoketogenic Diet – use MAP

High Dose IV C – high acid.  MAP allows safe use


DCA – increases the activity of mitochondria.  Starts the combustion in fermentating cells. – increases ATP level – apoptosis.  Increases free radicals


copyright Dr Schilling

Tumour anaemia (ferritin levels elevated).  Metal overload (Ni, Cu, Cr)

Vitamin C


Vitamin C and artesunate

Fenton reaction

Take a metal and expose to Vitamin C – oxygen radical, oxidated metal – in the tumour cell but not in healthy cells.

Doses of Vitamin C:  Start at 50g and move to 150g IV C – problems – very acidic, and this degrades into oxalid acid and can cause kidney issues.  So add a buffer – do a test to see what buffer is in the blood.

Iron – anaemia – blood transfusion is safest.

Alpha Lipoic Acid protects hepatocytes (not glutathione)



– down-regulate the suppressor cells.  Incubate in labs and see what can bring up the NK cell activity and decrease suppressor cells.

– test every 4 weeks

GcMAF and macrophages

– more than 100ng/week.  Each dose 400ng and higher, administered IV with high vitamin D level.

Dendritic cells – very expensive


Vitamin B17/Laetrile


copyright Dr Schilling

Enzyme treatment – bromelain, papain.

– Pancreatic enzymes – high dose.  Clear stop of growth.  Trophoblasts ends with pancreatic enzymes.  Trypsin, Chymotrypsin.  Only works with beta HCG.

Histamin – pro-inflammatory.  Eliminate Type 1 allergens.  Cimetidine (inhibits histamine, stiumlates CTL).

Curcumin – 8-9,000 g/day

Selenium – anti-inflammatory


copyright Dr Schilling

One response

  1. You clearly have a lot of good information, but I cannot understand much of it. Has anybody written an explanation for those of us without medical degrees? I can get some of it, but definitely not enough.

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