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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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