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THE NUTRI-SPEC LETTER

Volume 9 Number 12








From:
Guy R. Schenker, D.C.
December, 1998


Dear Doctor,

     Without the slightest bit of exaggeration or 
sensationalism we can unhesitatingly claim that you can save 
lives with your NUTRI-SPEC protocol for Electrolyte Stress 
Imbalance.  As you know -- cardiovascular disease (CVD) kills 
50% of all Americans.  And as you also know, nearly every 
person who suffers from CVD has a NUTRI-SPEC Electrolyte 
Stress Imbalance.  Since half the people you know -- half your 
patients, half your friends, and half your family -- are going 
to die of CVD ...

    DO YOU NOT FULLY APPRECIATE HOW SIGNIFICANT IT IS THAT
 MANY HUNDREDS OF NUTRI-SPEC PATIENTS ACROSS THE COUNTRY HAVE
  HAD THIS ELECTROLYTE STRESS/CVD COMPLEX SLOWED AT THE VERY
  LEAST, ALMOST ALWAYS STOPPED, AND IN MANY CASES REVERSED?

How many people do you know who have had heart attacks, who 
are plagued with high blood pressure, who have high 
cholesterol, or who suffer from angina -- who desperately need 
your help?  Remember, despite the "best" of medical science 
the mortality from cardiovascular disease just keeps lingering 
at about the 50% mark.

     Since virtually every person who suffers from CVD has a 
NUTRI-SPEC Electrolyte Stress Imbalance, let us ask    
ourselves ...

        JUST WHAT IS AN ELECTROLYTE STRESS IMBALANCE?

Reduced to its most basic NUTRI-SPEC essentials -- this 
imbalance is the destruction of the electronegative colloidal 
properties of the body fluids.  Once the polarity of these 
body fluids begins to drop (in association with excess 
electrolyte load and with the loss of tissue membrane 
integrity resulting from oxidative damage) you get a vicious 
cycle.  The loss of electronegativity accelerates the rate of 
oxidative tissue destruction -- and the tissue destruction 
further decreases the electronegativity.
                            - 2 -


     When analyzing your patient's NUTRI-SPEC test results,  
your Quick Reference Guide (QRG) protocol will tell you in 
seconds to what extent that patient is suffering the 
cardiovascular ramifications of fluid and electrolyte dynamics 
that are out of control.

     It is by addressing the causes of CVD that your Formula 
ES works its wonders on the heart and vascular system.  
Formula ES:

- retards arteriosclerotic and aging processes within the      
  arterial wall                                                 
- possesses lipid clearing activity for both cholesterol and    
  triglycerides                                                
- significantly reduces angina                                  
- maintains arterial elasticity                                 
- protects against thrombus formation                          
- facilitates normal myocardial metabolism                     
- increases RNA and DNA synthesis in the heart                  
- supplies magnesium aspartate to facilitate myocardial         
  strength and dilate coronary arteries                         
- inhibits platelet aggregation and decreases platelet          
  deposition                                                    
- improves exercise tolerance                                   
- prevents cardiac arrhythmias                                  
- lowers blood pressure

     Never lose sight of the fact that when you are working 
with a CVD patient with an electrolyte stress you are 
effecting these changes not by drugging and blocking 
physiological activity as is done by the pharmacological 
approach to CVD.  Rather ...

        YOU ARE RESTORING NORMAL OXIDATION AND NORMAL
         FLUID DYNAMICS TO THE HEART AND VASCULATURE.

     As discussed in last month's Letter, we have taken 
another quantum leap in the specificity with which we can 
analyze our patients.  We have given you with the latest 
revision of your QRG ...

         THE MEANS TO IDENTIFY AND SPECIFICALLY TREAT
          SEVERAL SUB-CATEGORIES OF ES/CVD PATIENTS.

     Combining Formula ES with the proper dispersing agents, 
we NUTRI-SPEC practitioners have had dramatic successes at 
restoring health to those with severely deteriorated 
cardiovascular function.  However, we have also had the 
occasional unresponsive patient.


                            - 3 -


     Several years of literature searches and related clinical 
experimentation have taught us how you can differentiate 
between several causative factors, selecting those factors 
that are having the biggest impact on any individual ES/CVD 
patient.  With your new QRG, a favorable response is even more 
assured.

     Review our introduction to water and electrolyte dynamics 
from the November Letter.  The concept was introduced of 
normal vs. abnormal extracellular and intracellular fluid 
composition and movement.  Much of what goes wrong in ES/CVD 
patients involves either abnormal solutes and abnormal pH of 
one of the body fluid compartments, or, involves the inability 
to move biologically active water and/or electrolytes into the 
proper body fluid compartment.

     Another ES/CVD problem is the flocculation of the body 
fluids.  Red blood cells begin to clump and platelets begin to
aggregate.  These changes are largely associated with the loss 
of normal electronegative charge on the platelets and the 
RBC's.  In restoring this electronegative colloid we are 
lowering the tendency to develop thrombosis.

     Our ability to lower cholesterol and triglycerides is 
also tied in with our ability to maintain water and 
electrolyte dynamics.  It is only when damage to the arterial 
intima creates a loss of tissue membrane polarity that 
cholesterol and the other components of atherosclerotic 
plaquing are pulled into the lesion.

     Now with your new QRG protocol you can not only identify 
the existence of ES/CVD in a matter of seconds, but you can 
identify the specific causative factors in each individual 
patient.

     Look at the accompanying chart.  The chart breaks down 
your ES patients into two broad sub-categories.  Then, you see  
some variations of the main theme within each of the two 
columns.

       THE PRINCIPAL SUB-CATEGORIZATION OF ES PATIENTS
           BREAKS THEM DOWN INTO THOSE WITH EITHER
         EXCESS RENIN ACTIVITY OR LOW RENIN ACTIVITY.

Recall that renin is the hormone associated with the kidneys 
that relates to sodium excretion and retention as well as 
arterial constriction and dilation.  The column in the chart 
for the high renin activity patients is labeled "ES/R+"; the 
column for the low renin patients is headed "ES/R-".


                            - 4 -


     The first distinctions made between these two 
sub-categories of ES patients involve the primary stress 
hormones that are found to be excessive in these patients as 
well as the NUTRI-SPEC metabolic imbalances that are typical
of these patients.

     Next, you see the serum pH typical of each category.  
That is followed by a description of the fluid distribution 
aberrations plus the sodium and chloride status of each 
category.

     Then, the major mechanism by which this category of 
electrolyte stress is effected is described.  Essentially what 
we have here is one category of ES patients that is extremely 
chloride sensitive and one category which is extremely sodium 
sensitive.

     The chart is completed with a list of typical clinical 
test findings.  These, as you might expect, are built into 
your QRG protocol so they do not require specific thought on 
your part.

     You have certainly noticed that the ES supplement page of 
your QRG gives you three choices -- a, b, or c -- of how to 
enter the ES supplementation selection protocol.  The choice 
"a" is designed to address the needs of your patients who are 
very obviously ES/R+.  Choice "b" is to specifically meet the 
needs of those that are ES/R-.  Choice "c" is to handle the 
patients that have a significant stress problem with both sets 
of stress hormones, or, who have a mix of NUTRI-SPEC metabolic 
imbalances.

     It is interesting to look at where sodium chloride (salt) 
fits into these sub-categories.  NUTRI-SPEC has long promoted 
the Riddick paradigm of dispersing agents.  Essentially, the 
good electrolytes are those that combine a monovalent cation 
(sodium or potassium) with a polyvalent anion such as a 
citrate or even a phosphate.  The most devastating 
electrolytes to the electronegative colloidal properties of 
the body fluids are those that combine a polyvalent cation 
such as aluminum with a monovalent anion such as chloride.

     Since we ran into problems with quantitative excesses of 
sodium chloride in electrolyte stress patients very early in 
the game, we have long recommended avoidance of salt for all 
ES patients.  We made the mistaken assumption that it was the 
sodium component of salt that was the big trouble maker.  We 
did not give enough emphasis to the potential harm of the 
monovalent chloride anion.  After several years of intensive 
literature review backed up by clinical experience, we find 
that the chloride ion is the major problem for a substantial
                            - 5 -


percentage of your ES patients.  I have six scientific studies 
which show the complete inability to elevate hypertensive test 
animals' blood pressure with sodium unless it is accompanied 
by chloride.

     Other studies on water/electrolyte dynamics show that 
inadequate sodium intake for ES/R+ hypertensives will actually 
further increase renin activity and exacerbate the blood 
pressure problem.

     Many of you were astounded (and called to see if it was a 
misprint) when you saw sodium salts appearing on the ES 
supplement page.  Now you know why -- you have only a minority 
of your electrolyte stress patients that are harmed by sodium 
and a substantial percentage that actually need sodium as long 
as it is not accompanied by chloride (and is accompanied by 
adequate water).

     As you might expect, not too many of your patients are 
going to be considerate enough to fall neatly into one of 
these two ES sub-categories.  To be honest, most of your ES/
CVD patients will have elements from both columns in their 
clinical picture.  In other words, they will have excess
catecholamines and excess cortisol.  Or, they will be both 
dysaerobic and parasympathetic, for instance, or perhaps both 
glucogenic and anaerobic.

     Your QRG protocol does a very nice job of focusing on the 
most pressing needs of your patient at the moment.  It also 
does a nice job of adapting to the changes in your patient's 
body chemistry as your NUTRI-SPEC regimen begins to show its 
effects.

     This is why we cannot emphasize strongly enough the 
absolute essentiality of the first follow-up test being within 
a week of your initial testing.  Significant changes are 
likely to be required in the supplement regimen within a week.  
You want changes to happen that quickly.  The supplements you 
recommend after the patient's initial testing are to be 
thought of in two ways -- both as therapeutic and as a 
clinical challenge.  Seeing how the patient responds to the 
initial supplementation tells you as much or more as the 
initial testing did.

     Now that your protocol for analyzing and treating ES/CVD 
patients is even more comprehensive, more specific, and more 
effective, you and your patients will be amazed to see how 
quickly symptoms respond and how quickly in many cases 
medications can be reduced or eliminated as the patient's:


                            - 6 -


- body fluids are restored to proper electronegativity

- kidney function is normalized

- electrolyte levels are balanced quantitatively and            
  qualitatively in each fluid compartment

- pH is restored to normal in each fluid compartment

- vascular tone is normalized

- myocardium is strengthened

- serum and tissues are cleared of excess lipids

- oxidative stress is reduced in both the heart and the         
  vasculature

              NO ONE UNDERSTANDS THE MECHANISMS
                    OF CVD THE WAY YOU DO.

     If you see the logic to an objective testing and 
treatment plan -- one that addresses the causes of CVD -- then 
do not let this ES/CVD protocol go under-utilized in your 
practice.  You can and will save lives, and save your patients 
from untold suffering.  If you and your patients will make a 
reasonably small investment of time and money you will be 
rewarded with astonishing results.


                               Sincerely,

                               Guy R. Schenker, D.C.


____________________________ES (R+)                  ES (R-)_________________

Renin Activity                    +                      -
_____________________________________________________________________________

Primary Stress Hormones     Catecholamines           Adrenal Corticoids
                                                         (& Insulin)
_____________________________________________________________________________

Metabolic Imbalances        DYSAEROBIC               ANAEROBIC
                            GLUCOGENIC               KETOGENIC
                            SYMPATHETIC              PARASYMPATHETIC
                            RESP ACID                K DEPLETION ALK
_____________________________________________________________________________

Fluid Distribution          Plasma Volume Hi         Plasma Volume Hi
                            Interstitial Hi (?)      Interstitial Hi (?)
                            Intracellular Lo         Intracellular Lo (or Hi)
_____________________________________________________________________________

Fluid pH                    Serum Acid               Serum Alkaline
                            Interstitium Alkaline    Interstitium Acid
_____________________________________________________________________________
                                                                               
Na+ Status                  Must not restrict in-    Excess retention; must
                            take (but needs H20)       restrict intake
_____________________________________________________________________________

Cl- Status                  Cl- Sensitive hyper-     Lo  Retention of Cl-
                                 tension                   (& K+ & H+)
_____________________________________________________________________________

Mechanism                   Cl- excess causes vaso-  Natriuretic peptide
                            constriction of the      deficiency = decreased
                            efferent renal tubule    vasodilation & Hi Na+,
                            arteriole, = Hi renin,   (& renin decreased to
                            = Hi vasoconstriction    <1/3 normal)
                            systemically = Hi BP
_____________________________________________________________________________

Common Test Findings        - SBP & DBP Hi by same % - SBP Hi, but DBP near
                                                         normal
                            - P1 normal to Hi        - P1 normal to  Lo

                            - Clinostatic pulse      - Clinostatic pulse
                              response extreme         response not extreme
                              (unless DYS)             (unless ANA)
                              P4-P1=12+              - Highest P-P1=12+

                            - Spgr = Hi              - Spgr = Lo
                              Ox Indx=Hi               Ox Indx = Lo

                            - SpH = Lo (unless DYS)  - SpH = Hi (due to Lo
                              (SpH-50)Spgr

                            - BH  = Lo               - BH  = Hi

                            - Insomnia               - Lo  RR (unless
                                                               Parasym)
                            - SBP2-SBP1=5+           - SBP2-SBP1=0-

                            - P2=84+; P4=80+
                            - P4-P1=12+; P2-P1=13+
_______________________EI (A-)____________________EI (R-)_______________

Hormonal Input         Aldosterone Lo             Renin Lo

                       Catecholamines Hi          Catecholamines Lo
                       (nor-epinephrine)          (alpha adrenergic)

                       (Renin Lo?)
_____________________________________________________________________________

Metabolic Imbalances   DYSAEROBIC                 ANAEROBIC
                       GLUCOGENIC                 KETOGENIC
                       SYMPATHETIC                PARASYMPATHETIC
                       RENAL/K EXC                RESP ALKALOSIS
                         ACIDOSIS
_____________________________________________________________________________

Fluid Distribution     Plasma Volume Lo           Plasma Volume Lo
                       Interstitial Hi            Interstitial Lo (or Hi)
                       Intracellular Hi or Lo     Intracellular Lo (or Hi)

_____________________________________________________________________________

Fluid pH               Serum Acid                 Serum Alkaline
                       Interstitium Alkaline      Interstitium Acid
_____________________________________________________________________________

Na + Status            Must increase intake       Moderate increased
                       significantly (but must    intake needed.
                       increase H20 even more)
_____________________________________________________________________________

Mechanisms             Aldosterone Lo =loss of    Renin Lo = Loss of Na+
                       Na+ & excess K+ = Inter-   & extreme hypovolemia
                       stitial alkalosis & sys-   = Lo BP & tachycardia
                       temic acidosis, & Lo BP.

                       Serum Albumin Lo = Lo      ISFV drops even more than
                       oncotic pressure = Inter-  plasma V since oncotic
                       stitial edema & alkalosis  pressure OK, &, since ISF
                                                  translocates to plasma to
                       ISF edema may pass         compensate.
                       into cells if DYS
                       membrane dysfunction.

                       Na+ needed to absorb       Fatigued or over-stim
                       glucose & decrease ex-     cell absorbs excess
                       cess catecholamines.       Na+ & H2O.  Na+ is
                                                  anti-adrenergic.
                       Na+ removes excess
                       Ca++ from cell = anti-
                       DYS & anti-SYMP.
_____________________________________________________________________________

Common Test Findings   Spgr = Hi                  Sp gr = Lo
                       Ox Index = normal or Hi    Ox Index = Lo
                       Orthostatic BP failure     Orthostatic BP failure ++
                       P1 = Lo (unless SYMP)      P1 = Lo or normal
                       Clinostatic Pulse failure  Clinostatic Pulse failure

                       RR = Hi                    RR = Hi (unless KETO)
                       BH = Lo                    BH = normal or Hi
                       RR-(BH/5))=8+
                       ASpH = Hi (unless GLUCO)   ASpH = Hi (unless ANA)

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