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The following outlines explain the MECHANISMS of 
   growth PROMOTION by REDUCTANTS and 
   growth INHIBITION by OXIDANTS. 

         ~~~  GRAND  SCHEME  OF  MANAGING 
      THE DISTRIBUTION OF REDUCING EQUIVALENTS  ~~~
FOOD  SOURCES: 
 Carbohydrates, Fats, Proteins, Supplements 
ACTIVATION  MECHANISMS: 
 Glycolysis, Hexose Monophosphate Shunt, 
 Tricarboxylic Acid Cycle, Oxidative Detoxification 
CARRIER  POOLS: 
 NADH, NADPH, GSH, Certain Phenols 
UTILIZATION  CHANNELS: 
 myriad BETS 
FUNCTIONS: 
 Synthesis, Energy Production, Reduction of Oxidants, 
 Various Reductases, Physiologic Controls, 
 Mixed Function Oxidases 

                        
Proliferation of cells requires a high level 
  of synthetic activity. 
Many synthetic processes require ample supplies 
  of reducing equivalents. 
Alteration of the relative demand of each 
  reductant consuming pathway will alter 
  the final distribution of reducing equivalents. 
Diversion of reducing equivalents to energy production 
  or to oxidant removal depletes the carrier pool. 
Depleted carrier pools result in decreased supplies 
  for synthesis. 
Inhibition of synthesis inhibits proliferation. 

~~~ KEY PROCESSES NECESSARY TO PROLIFERATION 
        WHICH DEPEND ON REDUCTANTS ~~~
activation of FOLATE to tetrahydrofolate: 
	needed to produce thymine from uracil etc. 
activation of THIOREDOXIN: 
	needed to produce deoxyribonucleosides 
activation of ORNITHINE DECARBOXYLASE: 
	needed to produce putrescine and polyamines 
activation of GLYOXALASE by reduced glutathione: 
	needed to remove alpha-keto-aldehydes 
activation of beta-ketoacyl-ACP-REDUCTASE, 
  crotonyl-ACP-REDUCTASE, other reductases:  
	needed to synthesize fatty acids 
activation of beta-hydroxy-beta-methylglutaryl-
  CoA-REDUCTASE: 
	needed to synthesize turpenoids and cholesterol 

	~~~  DISEASES  ASSOCIATED  WITH  ~~~
 PROLIFERATION & SYNTHESIS & REDUCTANT DEPENDENCY 
     = ALLERGIES:  humoral
                   cellular
               = INFECTIONS:  viral
                              inclusion
                              bacterial
                              fungal
                              parasitic
                         = NEOPLASMS:  benign
                                       malignant

~~~  "OXIDATION-REDUCTION  POTENTIALS 
      IN  BACTERIOLOGY  AND  BIOCHEMISTRY"  ~~~
by LF HEWITT, 6th Ed, E. & S. LIVINGSTONE LTD., 1950
TOPICS:   oxidation-reduction processes
          electrode potentials and polarography
          redox indicator methods
          effects of pH
          biologic electron/hydrogen carriers
          metabolic reductant production systems
          lag phase versus log growth phase
          peroxide resistance
          bactericidal dyes, mold products, quinones
          redox potentials of different bacteria
          redox potentials and virulence

~~~ REFERENCES BY ALBERT SZENT-GYORGYI, MD, PhD, NI ~~~
 BIOELECTRONICS - A STUDY IN CELLULAR REGULATION,
   DEFENSE, AND CANCER         1968, Academic Press
 THE LIVING STATE - WITH OBSERVATIONS ON CANCER
                               1972, Academic Press
 THE LIVING STATE AND CANCER   1978, Marcel Dekker
	TOPICS  DISCUSSED:
- semiconductor characteristics of hydrated proteins 
- pools of exchangeable hydrogen carriers 
- how primitive and dividing cells require 
    an abundance of reductants 
- phenol oxidases and peroxidases as defense systems 
    against infection in higher plants 
- physiologic effects of ratios of alphaketoaldehydes 
    to thiols and to amines 
- methylglyoxal as growth regulator 
- mechanism of glyoxalase activation by reduced glutathione 

	BIOCHEMICAL PECULIARITIES OF TUMORS 
	WHICH CAUSE INTERNAL REDOSIS:
1)  glucose / insulin receptors overabundant 
2)  hexose monophosphate shunt upregulated 
3)  glycerol-3-phosphate dehydrogenase deficient 
4)  cysteine sequestration upregulated 
5)  glutathione peroxidase deficient 

	BIOCHEMICAL ADVANTAGES OF REDOSIS 
	WHICH FAVOR TUMOR GROWTH AND SURVIVAL:
1)  ensure sufficient hydrogen donors for synthesis 
2)  toggle transcription factors and growth factors 
      towards  mode 
3)  enhance antioxidant protection against environment 
4)  enhance resistance to oxyradical attack by killer cells 
5)  maintain apoptosis triggers in  mode 

	~~~  HOW  TO  DIVERT  REDUCING  EQUIVALENTS 
		TOWARDS  ENERGY  PRODUCTION  ~~~

EXERCISE  - - - - - ADP activates mitochondrial ETC function
                    increases perfusion
RIBOFLAVIN  - - - - precursor to FAD oxidoreductases
THYROID & DHEA  - - both induce G3PDH
QUINONES  - - - - - shuttle reductants to cytochromes
HYDROGEN PEROXIDE - activates cytochromes
OXYGEN  - - - - - - activates cytochrome A
COPPER  - - - - - - ensures adequate cytochrome A
LIGAND DETOX *  - - ensures active cytochrome A
AMMONIA DETOX - - - ensures active carbonyl carriers
MANGANESE - - - - - ensures adequate mitochondrial SOD
                      *  HS-  CN-  NN-  CO
               
	~~~  HOW  TO  DIVERT  REDUCING  EQUIVALENTS 
	TOWARDS  OXIDANT  QUENCHING  PATHWAYS  ~~~

OXYRADICALS (bad choice): 
	radiation, selenium deficiency, toxic metals, 
	iron overload or quinone overdose 
HYDROGEN PEROXIDE: 
	IV-H2O2, PO-H2O2, PO-MgO2 
	ozone, quinones, autoregeneration 
LIPID PEROXIDES: 
	auto-oxidation of PUFA's, 
	ene reaction of singlet oxygen 
OXIDES OF CHLORINE:  ClO2  HClO  HClO2  HClO3  HClO4 
ULTRAVIOLET BLOOD IRRADIATION: 
	photoreduction consumes reductants 
	singlet oxygen produces peroxides and quinones 
	produces vitamin D a redifferentiator 
COPPER:      activates many endogenous oxidases 
SELENIUM:    activates glutathione peroxidase pathway 
GLUTATHIONE: activates glutathione peroxidase pathway 
             activates reductive antioxidant family 
             activates oxidant sensitive immunoreceptors 

~~~  HOW  EXCESS  ACCUMULATION  OF  REDUCTANTS  OCCURS  ~~~

	CAUSES:                    MECHANISMS:
overeating - - - - - - - - substrates for NADPH production 
inactivity - - - - - - - - depressed reductant consumption 
hypothyroidism - - - - - - depressed reductant consumption 
                           depressed GPDH shuttling 
DHEA deficiency  - - - - - elevates G6PDH activity 
cortisol excess  - - - - - elevated gluconeogenesis 
insulin insensitivity  - - elevated glucose 
Se deficiency  - - - - - - failure of glutathione peroxidase 
                           failure of T4 to T3 conversion 
Cu deficiency  - - - - - - failure of numerous oxidases 
carbon monoxide  - - - - - blocks Hb and CytA 
hydrogen sulfide - - - - - blocks CytA and other Cu enzymes 
xenobiotic exposure  - - - depletes glutathione 
                           induces quinone reductases 

    ~~~  HOW  TO  STARVE  THE  SUPPLY  SIDE  ~~~

		LOW  CALORIE  DIET 
		FASTING 
		EXERCISE 
		CORRECT  HYPERGLYCEMIA 
		HYDRAZINE  SULFATE 
		GLUCOCORTICOID  AVOIDANCE 
		G6PDH  DEFICIENCY 
		DHEA 
		SILVER 
		XENOBIOTIC  AVOIDANCE 
		MAGADOSE  REDUCTANT  AVOIDANCE
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