Clay poultice,  a soft composition powder mixed with water and applied
as a mud pack to an inflamed body part for purposes of absorbi ng toxins of
arthritis, cancer , insect stings, diarrhea, and poisons, it has an adsorptive
effect like that of charcoal. The clay poultice aids detoxification. Clay
powder can also be used interna lly to clear gastrointestinal difficulties and
inflammations. The procedure for applying a clay poultice should involve
the following steps:
1. Prepare enough warm water to mix the needed amount of clay powder
into a paste. 2. Apply the paste quickly to a square of clean muslin to prevent cooling. 3. Place the muslin on an area to be treated. 4. Cover the area with plastic and wool cloth. 5. Pin the covering in place and leave it on overnight or until dry . 6. Remove and gently rub the area with a cold wet cloth. 7. Repeat this procedure as required. 8. Discard used clay pack. References for Chapter Nineteen
1Schaefer , A. “Some characterist ics of cancer survivors.” Townsend Letter
for Doctors & Patients. 195:70-71, October 1999. OceanofPDF .comChapter Twenty
GERSON LAB TESTS EXPLAINED
In this chapter we explain the significance of certain laboratory tests that
are necessary for monitoring one’s healing progress. Laboratory testing of
blood and urine are a standard part of follow-up protocols for Gerson
Therapy patients employed by all Gerson-trained health professionals. Among practitio ners invited to administer the Gerson program are medical
doctors, osteopathic physicians, and naturopathic physicians. If you are a patient utilizing the Gerson approach to healing but have no
access to a trained Gerson health practitioner to act as your ombudsman, it’s
still possible to have appropriate  monitoring performed. Accom plish this by
hiring the services of a convent ionally practicing allopathic physician who
is willin g to order laboratory examinations for you or for ill loved ones (of
course, for a fee). Then, using the guidance of this chapter , you probably
will be able to interpret the test results. But, you do need a licensed health
professional’ s prescription to have laboratory tests conducted. Moreover , from observations made over many years of counseling
degenerative disease patients, the coauthors know that combining a doctor ’s
interpretation with information offered below will give you an
understanding of what is happening physiologically in your healing body . We offer this caution, however: Suggestions by allopathic, non-Gerson-
educated practitioners for you to take drugs or make food changes may not
be in your best interest and could very well be contraindicated. Explanations and interpretations are provided here to help our readers
feel less intimidated by unfamiliar medical terms, and to acquaint them with
current knowledge about the required laboratory tests in the even t they must
monitor themselves without assistance by any health professio nal. If you
want education about some specific test other than what is furnished here,
we recommend that you query the laboratory conducting the particularexamination for you. It’s your right to know about tissues and other
specimens taken from your own body . THE SERUM  CALCIUM  LABORA TORY TEST
The laboratory test for serum calcium is a measurement of the levels of
calcium in the blood. Knowing  such levels helps a health professional to
interpret the patient’ s physiologi cal status regarding neuromuscu lar activity ,
enzyme activity , skeletal development, and blood coagulation. Calcium (Ca+) is a predominantly extracellular ion (a cation) derived
from the calcium absorbed in food through the gastrointestinal tract,
provided sufficient vitamin D is present in the food eaten. Excess quantities
of calcium ions in the blood are excreted in the urine and feces, while
insuf ficient calcium concentrations can move out of the storage areas of
bones and teeth to restore low blood levels. Daily ingestion of 1 gram of
calcium is necessary for normal calcium balance. For Gerson patients, this
should not be given in the form  of supplements. Juices and foods contain
more than adequate amounts of calcium. Serum calcium testing aids in diagnosing arrhythmias, blood-clotting
deficiencies, acid-base imbalance, and disorders of the neuromuscular ,
skeletal, and endocrine systems. Normal adult serum calcium levels range
from 8.9 to 10.1 mg/dL (atomic absorption is 2.25 to 2.75 mmo l/L). Serum
calcium levels for children are higher than for adults. When the level of Ca+ is too high, a condition of hyper calcemia  prevails
indicating the possibility of one or more of the following pathologies:
hyperparathyroidism, Paget’ s disease of the bone, multiple myeloma,
metastatic carci noma, multiple  fractures, and prolonged immobilization. From inadequat e excretion of calcium, also shown by elevated serum
calcium, kidney disease and adrenal insuf ficiency may result. In contrast, low calcium levels (known as hypocalcemia)  may come from
hypoparathyroidism, total parathyroidectomy , or malabsorption . Decreased
serum Ca+ levels may arise from calcium loss in Cushing’ s syndrome,
kidney (renal) failure, acute pancreatitis, and periotonitis. Hypercalcemia may bring on deep bone pain, flank pain from renal
calculi, and muscle hypotonicity . Its beginning symptoms are manifested bynausea, vomitin g, and dehydration, leading to stupor and coma, and may
end in cardiac arrest. Hypocalcemia may produce peripheral numbness and tingling, muscle
twitching, facia l muscle spasm (Chvostek’ s sign), carpop edal spasm
(Trousseau’ s sign), seizures, and arrhythmias. THE SERUM  PHOSPHA TES LABORA TORY TEST
The laboratory test for serum phosphates is a measurement of the blood
levels of phosphates to tell the state of body energy, carbohydrate
metabolism, lipid metabolism, and acid-base balance. Phosphate ion (P+) is
the dominant cellular anion, which is essential for bone formation. Testing
for its blood level aids in the diagnosis of acid-base imbalance  plus renal,
endocrine, skeletal, and calcium disorders. In a normal adult, serum phosphate levels range from 2.5 to 4.5 mg/dL
(0.80 to 1.40 mmol/L) or from 1.8 to 2.6 mEq/L. Children show a higher
range that can rise to 7 mg/dL  (2.25 mmol/L) during spurts of increased
bone growth. Phosphates are absorbed through the intestines from dietary sources in
the presence of vitamin D. Excess quantities of them are excreted through
the kidneys, which act as the regulating mechanism. Because calcium and
phospate interact in a reciprocal relationship, urinary excretion of
phosphates incre ases or decreases in inverse proportion to serum calcium
levels. Abnormally high concentrations of phosphates in the blood
(hyperphosphatemia),  which can come from drinking an overabundance of
carbonated beverages, sets up a pathological process of bone loss, tooth
demineralization, poor healing of fractures, hypopara thyroidism,
acromegaly , diabetic acidosis, high intestinal obstruction, and renal failure. Depressed phosp hate levels in the blood (hypophosphatemia)  may result
from malnutrition, malabsorption syndromes, hyperparathyroidism, renal
tubular acidosis , or treatment of diabetic acidosis. In children, such
hypophosphatemia can suppress normal growth. THE SERUM  SODIUM  LABORA TORY TESTThe laboratory test for serum sodium is a measurement of the blood
levels of sodium to determine body water distribution, osmotic  pressure of
extracellular fluid, neuromuscu lar function, and acid-base balance. The
sodium ion (Na+) is the major extracelullar cation, and it influences both
chloride and potassium blood levels. Sodium is absorbed by the intestines and is excreted primarily by the
kidneys; a small amount is lost through the skin by sweating. This mineral
aids the kidneys in regulating body water , for decreased Na+ promotes
water excretion and an increased level promotes water retention (edema). Testing for Na+ aids in evaluat ing fluid electrolytes, acid-base balance,
and certain disorders of the kidneys, adrenals, and neuromuscular system. The sodium blood test also determines the effects of drug therapy such as
diuretics on the body . For an adult, normally serum sodium levels range
from 135 to 145 mEq/L (mmol/L). For Gerson patients, a level of 127 is
still acceptable. Sodium imbalan ce comes from either a change in water volume intake or
variation in how much sodium gets consumed. Elevated serum sodium
levels (hypernatr emia)  may be caused by inadequate water intake, diabetes
insipidus, impa ired renal function, prolonged hyperventilation, severe
vomiting, or severe diarrhea. Sodium retention also comes from consuming
excessive salt. The signs and symptoms of hypernatremia are thirst,
restlessness, dry mouth, sticky mucous membranes, flushed skin, oliguria,
diminished reflexes, hypertension, dyspnea, and edema. Ingesting too little sodium mine ral for serum Na+ (hyponatr emia)  is rare
and doesn’t even happen on the low-sodium dietary program encouraged by
the Gers on Ther apy. There is always some sodium coming from food. Still,
hyponatremia can occur , and its indications appear as apprehension,
lassitude, headache, decreased skin turgor, abdominal cramps, tremors, or
convulsions. It can come on from profuse sweating, gastrointestinal
suctioning, diuretic therapy , diarrhea, vomiting, adrenal insufficiency ,
burns, and chronic renal insuf ficiency with acidosis. If you do have testing
for serum sodium performed, make sure to get a urine sodium
determination simultaneously . THE SERUM  POTASSIUM  LABORA TORY TESTThe laboratory test for serum potassium, a quantitative analysis, is the
measurement of blood potassium for regulation of homeostasis, osmotic
equilibrium, muscle activity , enzyme activity , acid-base balance, and kidney
function. Potassium (K+) is the body’ s major intracellular ion (a cation);
small amounts of it are also found in the extracellular fluid. Since the kidneys excrete nearly all the ingested potassium, a dietary
intake of at least 40 mEq/day (mmol/d) is essential. A normal diet usually
includes 60 to 100 mEq/day of this mineral. In the blood, norm al K+ levels
range from 3.8 to 5.5 mEq/liter (mmol/L). Vital to maintain ing electrical conduction within the cardiac and skeletal
muscles, K+ is affected by variations in the secretion of adrenal steroid
hormones and by fluctuations in pH, serum glucose levels, and serum
sodium levels. A reciprocal relationship exists between K+ and Na+; the
substantial intak e of one causes a corresponding decrease in the other . Although the body readily conserves sodium, potassium deficiency may
develop rapidly and is quite common, because there is no efficient method
for conserving potassium. The laboratory test for serum potassium is used to evaluate clinical signs
of either potassium excess (hyperkalemia)  or potassium depletion
(hypokalemia). It also monitors kidney function, acid-base balance, and
glucose metabo lism, and evaluates arrhythmias, neuromuscular disorders,
and endocrine disorders. Hyperkalemia is common in patients with
excessive cellular K+ entering the blood as in cases of burns, crushing
injuries, diabetic ketoacidosis, and myocardial infarction. It will also be
present where there is reduced sodium excretion from renal failure that
causes an abnor mal Na+-K+ exchange and in Addison’ s disease caused by
the absence of aldosterone, with consequent K+ buildup and Na+ depletion. Note: Although elevated serum potassium is uncommon in Gerson
Therapy patients, if it does occur , supplemental potassium should be
reduced or temporarily discontinued. Then the consulting Gerson-trained
physician should immediately be consulted. The signs and symptoms of hyperkalemia are weakness, malaise, nausea,
diarrhea, colicky pain, muscle irritability progressing to flaccid paralysis,
oliguria, and bradycardia. An electrocardiogram (EKG) reveals a prolonged
PR interval; wide QRS; tall, tented T wave; and ST depression. Indications
of hypokalemia are decreased reflexes; rapid, weak, irregular pulse; mentalconfusion; hypo tension; anorexia; muscle weakness; and paresthesia. The
EKG shows a flattened T wave, ST depression, and U wave elevation. In
severe cases of hypokalemia, ventricular fibrillation, respiratory paralysis,
and cardiac arrest could occur . THE SERUM  CHLORIDE  LABORA TORY TEST
The laboratory test for serum chloride, another quantitative analysis, is a
measurement of blood levels of the chloride ion (Cl-), the major
extracellular fluid anion. Interacting with Na+, Cl- helps maintain the
osmotic pressure, blood volume, arterial pressure, and acid-base balance. Chloride is absorbed from the intestines and is excreted prim arily by the
kidneys. By evaluating the body’ s fluid status, the serum chloride laboratory test
detects two types of fluid imbala nces, acid-base (acidosis and alkalosis) and
extracellular cation-anion. Normally serum chloride levels range from 100
to 108 mEq/liter (mmol/L). Maintaining a normal amount of chloride in the
blood reflects acid-base balance by its inverse relationship to bicarbonate. Excessive loss of gastric juices or other secretions containing chloride may
cause hypochloremic metabolic alkalosis or excessive chloride retention. Ingesting it may lead to hyperchloremic metabolic acidosis. Elevated serum chloride levels (hyper chlor emia ) can come on from
severe dehydration, complete renal shutdown, head injury (which produces
neurogenic hyperventilation), and primary aldosteroism. Manifestations
consist of stupor , rapid and deep breathing, and weakness that leads to
coma. A situation of low chloride levels in the blood (hypochlor emia)  is
associated with reduced blood sodium and potassium levels coming from
prolonged vomiting, gastric suctioning, intestinal fistula, chronic renal
failure, or Addison’ s disease. Congestive heart failure, or edema resulting in
excess extracel lular fluid, can cause dilutional hypochlo remia. The
indications are hypertonicity of muscles, tetany , and depressed respirations. THE LACTIC  DEHYDROGENASE  (LDH) L ABORA TORY TESTThe laboratory test for lactic dehydrogenase (LDH) is a measurement of
five specific isoenzymes which catalyze the reversible conversion of
pyruvic acid present in all muscles of the body into lactic acid. Many
common diseases—myocardial infarction (MI), pulmonary infarction,
anemias, liver disease, kidney disease, erythrocytic damage, and others—
cause elevations  in total lactic dehydrogenase, and the LDH laboratory test
is useful for dif ferentiating between them. The five identified isoenzymes in lactic dehydrogenase are LDH1 and
LDH2 appeari ng in the heart, red blood cells, and kidneys; LDH3 in the
lungs; and LDH4 and LDH5 in the liver and the skeletal muscles. Testing
for these  enzymes is especially appropriate for the delayed measurement of
creatine phosphokinase (CPK) associated with MI and for monitoring
patient respons e to some forms of chemotherapy . Total LDH levels
normally range from 48 to 115 U/L. Normal distribution of the five
isoenzymes is as follows:
 
LDH1: 17.5% to 28.3% of total  
LDH2: 30.4% to 36.4% of total  
LDH3: 19.2% to 24.8% of total  
LDH4: 9.6% to 15.6% of total  
LDH5: 5.5% to 12.7% of total
 
Since a vast number of illnesses involve the enzymes of LDH, this
laboratory test for lactic dehydrogenase is broadly employed for
establishing diagnoses. THE ASPARTATE TRANSAMINASE /SERUM  GLUT AMIC -OXALOACETIC
TRANSAMINASE  (AST/SGOT) L ABORA TORY TEST
The laboratory blood examination for aspartate transaminase and serum
glutamic-oxaloacetic (AST/SGOT) is a measurement of specific amino acid
residues left behind by nitrogenous portions of the metabolized aminoacids. Aspartate aminotransferase (AST) is found in the cytoplasm and
mitochondria of many tissue cells, primarily in the liver, heart, skeletal
muscles, kidneys, pancreas, and red blood cells. AST is released  into blood serum in proportion to cellular damage, and
its detection (together with creatine phosphokinase and lactate
dehydrogenase) indicates myocardial infarction. The test also helps in the
diagnosis of acute liver diseas e. It monitors patient progress in healing. AST adult serum  levels range from 8 to 20 U/L. Normal values for infants
are four times higher . Maximum eleva tions of AST are associated with viral hepatitis, severe
skeletal muscle trauma, extensive surgery, drug-induced liver injury , and
passive liver congestion. Levels ranging from 10 to 20 times normal may
indicate severe MI, severe infectious mononucleosis, and alcoholic
cirrhosis. Moderate-to-high levels ranging from 5 to 10 times normal
indicate Duche nne muscular dystrophy , dermatomyositis, and chronic
hepatitis, along with prodromal and resolving stages of diseas es. Low-to-
moderate levels  of 2 to 5 times normal may show hemolytic anemia,
metastatic liver tumors, acute pancreatitis, pulmonary emboli, alcohol
withdrawal syndrome, fatty liver, and the first stages of biliary duct
obstruction. THE SERUM  BILIRUBIN  LABORA TORY TEST
The laboratory test for serum bilirubin, the main product of hemoglobin
catabolism, is a measurement of bile pigment which indicates the state of
health of the liver and gallbladder . After being formed in the retic-
uloendothelial cells, bilirubin is bound to albumin and then transported to
the liver, where it’s conjugate d with glucuronic acid to form bilirubin
glucuronide and bilirubin diglucuronide. These two compounds are then
excreted in bile. Measurement of indirect or prehepatic (unconjugated)
bilirubin helps to evaluate hepatobiliary and erythropoietic functions. The serum bilirubin laboratory test showing elevated levels often
indicates liver damage in which the parenchymal cells can no longer
conjugate bilirubin with glucuronide. Then indirect bilirubin reenters the
bloodstream. Also, an elevated reading alerts the health professional to the
possibility of severe hemolytic  anemia. This test aids in the differentialdiagnosis of jaundice, biliary obstruction, and dangerous levels of
unconjugated bilirubin. Normally in an adult, indirect serum bilirubin measures 11 mg/d L or less;
direct serum bilirubin of less than 0.5 mg/dL). Neonates have total serum
bilirubin ranging from 1 to 12 mg/dL; if elevated to 20 mg/dL (for them, it
indicates neonatal hepatic immaturity or congenital enzyme deficiencies. An exchange blood transfusion may then be required. If readings of bilirubin are elevated for adults, the test advises about the
possibility of autoimmunity or transfusion reaction, hemolytic or pernicious
anemia or hemorrhage, and hepatocellular dysfunction perhaps from viral
hepatitis. Needl ess to say, elevated levels of direct conjugated bilirubin
usually show biliary obstruction with overflows into the bloodstream. Intrahepatic biliary obstruction may come from viral hepatitis, cirrhosis, or
chlorpromazine reaction. Extrahepatic obstruction may come from
gallstones, gallbladder cancer , pancreatic cancer , or bile duct disease. THE SERUM  GAMMA -GLUT AMYL  TRANSPEPTIDASE  (GGT) L ABORA TORY
TEST
The laboratory test for serum gamma-glutamyl transpeptidase (GGT) is a
measurement of obstructive jaundice in neoplastic liver disease, and it’s
also useful for the detection of excessive alcohol consumption. The GGT
enzyme is sensitive to drug use and detects alcohol ingestion; therefore, it’s
used to determine compliance with alcoholism treatment. It also helps in the
diagnosis of obstructive jaundice and liver cancer . The normal range for GGT varies with age in males but not in females. For men ages 18 to 50 it varies between 10 and 39 U/L. Older than that,
males show a GGT range from 10 to 48 U/L. The normal range in women is
6 to 29 U/L. Elevation signals a cholestatic liver process. Note: The immune-stimulating effect of the Gerson Therapy frequently
causes a rise in GGT blood levels. THE ACID PHOSPHA TASE LABORA TORY TEST
The laboratory test for acid phosphatase is a measurement of the prostatic
and erythrocytic  isoenzymes to detect cancer . Active at a pH of 5, the twophosphatase enzymes appear in the liver, spleen, red blood cells, bone
marrow , platelets, and prostate gland. Successful treatment for prostate cancer decreases acid phosphatase
levels. Its normal values range from 0 to 1.1 Bodansky units/mL; 1 to 4
King Armstrong  units/mL; 0.13 to 0.63 Bessey-Lowery-Broc k units/mL;
and 0 to 6 U/L in S1 units. Normal range of radioimmunoassay results is 0
to 4.0 ng/mL. An elevated prostatic acid phosphatase test indicates Paget’ s disease,
Gaucher ’s disea se, multiple myeloma, and a tumor that has spread beyond
the prostatic capsule. If metast asized to bone, the high acid phosphatase
level accompanied by a high alkaline phosphatase shows increased
osteoblastic activity—metastatic bone cancer . THE ALKALINE  PHOSPHA TASE (AP) L ABORA TORY TEST
An enzyme that is most active  at pH 9.0, alkaline phosphat ase (AP)
influences bone  calcification and the transport of lipids and metabolites. The alkaline phosphatase laboratory test measures combined activities of
those AP isoenzymes found in the liver, bones, kidneys, intestinal lining,
and placenta. Bone and liver AP are always present in adult blood serum,
with liver AP most prominent—except during the third trimester of
pregnancy when the placenta originates half of all AP
The AP laboratory test is particu larly sensitive to mild biliary obstruction
and indicates liver lesions. Its most specific clinical application is in the
diagnosis of metabolic bone disease and detecting skeletal diseases
characterized by osteoblastic activity and local liver lesions causing biliary
obstruction such as tumor or abscess. It furnishes supplemental information
for liver function studies and GI enzyme tests, and it assesses the response
to vitamin D treatment in rickets. The normal range of serum alkaline phosphatase varies in accordance
with the laboratory method employed, but the usual total AP levels range
from 30 to 120 U/L in adults and from 40 to 200 U/L in children. Since AP
concentrations rise during active bone formation and growth, infants,
children, and adolescents normally show levels three times higher than
adults. Additional normal range s for AP are 1.5 to 4 Bodansky  units/dL; 4to 13.5 King-Armstrong units/d L; 0.8 to 2.5 Bessey-Lowry units/dL; 30 to
110 U/L by SMA 1260. High AP blood levels indicate skeletal disease, intrahepatic biliary
obstruction causing cholestasi s, malignant or infectious infiltrations,
fibrosis, Paget’ s disease, bone metastases, hyperparathyroidism , metastatic
bone tumors from pancreatic cancer , and liver diseases before any change in
blood serum bilirubin levels. Moderate rise in AP levels shown by this laboratory test may reflect
acute biliary obstruction from liver inflammation in active cirrhosis,
mononucleosis, osteomalacia, deficiency-induced rickets, and viral
hepatitis. THE ALANINE  TRANSAMINASE , SERUM  GLUT AMIC -PYRUVIC  TRANSAMINASE
(ALT/SGPT) L ABORA TORY TEST
Alanine aminotr ansferase (ALT), one of the two enzymes that catalyze a
reversible amino group trans fer reaction in the Krebs citric acid
(tricarboxylic acid) cycle, is necessary for tissue energy production. (The
second enzyme  is aspartate aminotransferase.) Elevated serum ALT
indicates acute hepatocellular damage before jaundice appears. The
ALT/SGPT laboratory test makes use of spectrophotometric or colorimetric
methods which detect and evaluate treatment progress for hepatitis,
cirrhosis withou t jaundice, liver toxicity , and acute liver disease. It also
distinguishes between myocardial and hepatic tissue damage. ALT values range from 10 to 32 U/L in men; from 9 to 24 U/L in
women; twice those levels in infants. When they are very high—up to 50
times normal—v iral or drug-induced hepatitis must be suspected. Or there
may be other liver disease with extensive necrosis. Moderate-to-high levels of ALT may indicate infectious mononucleosis,
chronic hepatitis, intrahepatic cholestasis, early or improving acute viral
hepatitis, or severe hepatic congestion due to heart failure. Slight-to-moderate ALT elevations may appear with any condition that
produces acute cellular injury in the liver such as active cirrhosis and drug-
induced or alcoholic hepatitis. Marginal elevations possibly show acute myocardial infarction or
secondary hepatic congestion.An interfering factor for the alanine transaminase, serum glutamie-
pyruvic transaminase laboratory test is the taking of opiate analgesics such
as morphine, codeine, and meperidine. THE TOTAL SERUM  CHOLESTEROL  LABORA TORY TEST
This quantitative serum analysi s measures the circulating levels of free
cholesterol and cholesterol esters and reflects the amount of cholesterol
compound appe aring in the body tissues. Both absorbed from the diet and
synthesized in the liver and other body tissues, cholesterol is a structural
component in cell membranes and plasma lipoproteins. It contributes to the
formation of adrenocorticoid steroids, bile salts, androgens, and estrogens. A diet high in saturated fat raises cholesterol levels by stimulating
absorption of lipids, including cholesterol, from the intestine; a diet low in
saturated fat lowers them. Elevated total serum cholesterol is associated
with an increased risk of atherosclerotic cardiovascular disease. Thus, the total serum cholesterol laboratory test assesses the risk of
coronary artery disease (CAD ), evaluates fat metabolism, and aids in
diagnosing kidney disease, pancreatitis, liver disease, hypothyroidism, and
hyperthyroidism. Total cholesterol concentrations vary with age and sex. Its
common range is from 150 to 200 mg/dL. A desirable blood cholesterol is below 200 mg/dL, and levels from 200 to
240 mg/dL are considered borderline or at high risk for CAD. A level in
excess of 250 mg/dL (hyper cholester olemia)  indicates high risk of cardio-
vascuar disease, incipient hepatitis, lipid disorders, bile duct blockage,
nephrotic syndro me, obstructive  jaundice, pancreatitis, and hypothyroidism. They require treatment. Hypercholesterolemia from high dietary intake
requires modific ation of eating habits and possibly medication to retard
absorption. Hypercholesterolemia can occur from taking adrenocorticotropic
hormone, corticosteroids, androgens, bile salts, epinephrine,
chlorpromazine, trifluoperazine, oral contraceptives, salicylates, thiouracils,
and trimetha-dione. Low serum cholesterol (hypocholester olemia)  is associated with
malnutrition, cellular necrosis of the liver, and hyperthyroidism. Cholesteroloften drops below normal in the Gerson program, because patients are
eating an extremely low-fat diet. THE LIPOPROTEIN /CHOLESTEROL  FRACTIONA TION  LABORA TORY TEST
To assess the risk of coronary artery disease, the lipoprotein/cholesterol
fractionation laboratory test is conducted. By centrifugation or
electrophoresis, it isolates and measures the cholesterol in blood, which
appears as low-density lipopro teins (LDL) and high-density lipoproteins
(HDL). It’s known that a lower HDL level in the population gives rise to a
higher incidence  of CAD. Conversely , higher HDL levels produce a lesser
amount of CAD. Note: Since the Gerson Therapy  offers a minimal amount of fat, it often
lowers the risk of coronary artery disease; but it does provide an adequate
supply of certain polyunsaturated essential fatty acids and fat-soluble
vitamins that cannot be synthesized in adequate amounts for optimal body
function. Normal HDL cholesterol ranges from 29 to 77 mg/100 mL of blood, and
normal LDL cholesterol ranges from 62 to 185 mg/100 mL. Too-high LDL
levels increases the risk of CAD, while elevated HDL general ly reflects a
healthy state. Or it might indicate chronic hepatitis, early-stage primary
biliary cirrhosis, or too much alcohol consumption. THE SERUM  TRIGL YCERIDES  LABORA TORY TEST
Triglycerides being the body’ s main storage form of lipids (constituting
95 percent of fatty tissue), the serum triglycerides laboratory test provides a
quantitative analysis of them. It identifies hyerlipemia  in kidney disease and
CAD. The triglyceride values vary according to age:
Age Trigyceride V alues
mg/dL nmol/L
0-29 10-140 0.1-1.5530-39 10-150 0.1-1.65
40-49 10-160 0.1-1.75
50-59 10-190 0.1-2.10
  
Test abnormality suggests that other measurements are needed. High
triglycerides indicate the risk of atherosclerosis or CAD. Mild-to-moderate
levels advise of biliary obstruction, diabetes, kidney disease, endocrin-
opathies, or too much consumpt ion of alcohol. Decreased levels are rare but
may show malnutrition or a betalipoproteinemia. Note: On the Gerson diet, flare-ups and healing reactions are shown by
elevated triglycerides. THE SERUM  PROTEIN  ELECTROPHORESIS  LABORA TORY TEST
The major blood proteins of the body , albumin and four globulins, are
measured in an electric field by separating them into patterns according to
size, shape, and electric charge at pH 8.6. Comprising more than 50 percent
of total serum protein, albumin prevents leakage of capillary plasma by
oncotic pressure (the pressure exerted by plasma proteins on the capillary
wall), and it transports the many water -insoluble substanc es such as
bilirubin, fatty acids, hormones , and drugs. Of the four globulins, alpha1,
alpha2, beta, and gamma, the first three act as carrier proteins for
transporting lipids, hormones, and metals through the blood, and the fourth,
gamma globulin, acts in and upon the immune system. As indicated by its label, the serum protein electrophoresis labor atory test
uses electric current to measure the total serum protein and albumin-
globulin ratio to convert them into absolute values. These values help to
uncover the presence of liver disease, blood dyscrasias, kidney disorders,
gastrointestinal illnesses, neoplastic (benign and malignant) diseases, and/or
protein deficien cy. Here are the normal blood serum ranges for these
proteins:Total serum pr otein 6.6 to 7.9
g/dL
Albumin fraction 3.3 to 4.5
g/dL
Alpha1 globulin fraction0.1 to 0.4
g/dL
Alpha2 globulin0.5 to 1.0
g/dL
Beta globulin 0.7 to 1.2
g/dL
Gamma globulin 0.5 to 1.6
g/dL
  
The balance between total albumin and total globulin (known in
medicine as the A-G ratio) is evaluated in relation to the total protein level. A reversed A-G ratio (decrease d albumin and elevated globulins) and low
total protein shows chronic liver disease; reversed A-G ratio with normal
total protein shows myeloproliferative disease (leukemia and Hodgkin’ s
disease) or certain chronic infectious diseases (tuberculosis and chronic
hepatitis). THE BLOOD  UREA NITROGEN  (BUN) L ABORA TORY TEST
Measurement of the blood’ s nitrogen fraction of urea, the chief product
of protein metabolism, is accom plished by the blood urea nitro gen (BUN)
laboratory test. Formed in the liver from ammonia and excreted by the
kidneys, urea constitutes 40 to 50 percent of the blood’ s nonprotein
nitrogen. The BUN level reflects protein intake and kidney excretory
capacity , but it’s a less reliable indicator of uremia (urine in the blood) than
the serum creatinine level (see the test description which immediately
follows).With normal values ranging from 8 to 20 mg/dL, the BUN test helps to
evaluate kidney  function, aids in the diagnosis of kidney illness, and
assesses the body’ s hydration. An elevated BUN happens in reduced renal
blood flow from  dehydration, renal disease, urinary tract obstruction, and
increased protein catabolism as in burns. Depressed BUN levels occur in
severe liver damage, malnutrition, and overhydration. Note: Due to initial decreased dietary protein intake, a person following
the Gerson Therapy will likely show a slightly r educed level of BUN. THE SERUM  CREA TININE  LABORA TORY TEST
Providing a more sensitive measure of kidney damage than the BUN, the
serum creatinine laboratory test is a quantitative analysis of the non-protein
end product of metabolism, creatinine. Kidney impairment is virtually the
only cause of creatinine elevation in the blood; therefore, creatinine levels
are directly related to the glomerular filtration rate. They assess renal
glomerular function and screen for kidney damage. Creatinine concentration in males normally ranges from 0.8 to 1.2
mg/dL; in females it ranges from 0.6 to 0.9 mg/dL. Elevation of serum
creatinine means that serious renal disease is present with 50 percent
damaged nephrons as in gigantism and acromegaly . Interfering factors are
too much absorption of ascorbic acid, barbiturates, diuretics, and sulfobro-
mophthalein. Also, athletes may have above-average creatinine levels, even
with normal kidney function. THE SERUM  URIC ACID LABORA TORY TEST
Used mainly to detect gout, the serum uric acid laboratory test measures
levels of uric acid, a metabolite of purine in the blood. Glomeru lar filtration
and tubular secretion gets rid of uric acid, but it’s less soluble at a pH of 7.4
or lower  which occurs in certai n diseases such as gout, excessive cellular
generation and destruction as in leukemia, and kidney dysfunction. Uric acid conce ntrations in men range from 4.3 to 8 mg/dL; in women
they range from 2.3 to 6 mg/dL. Although elevated levels of serum uric acid
don’t correlate with severity of disease, they do rise in congestive heart
failure, glycogen storage disease, acute infectious diseases such asinfectious mononucleosis, hemolytic anemia, sickle cell anemia, hemo-
globinopathies, polycythemia, leukemia, lymphoma, metastatic malignancy ,
and psoriasis. Depressed uric acid levels indicate defective acute hepatic
atrophy or tubular absorption as in Wilson’ s disease and Fan-coni’ s
syndrome. Drug factors interfering in the serum uric acid laboratory test include
loop diuretics, ethambutol, vincristine, pyrazinamide, thiazide s, and low
doses of salicylates which elevate blood levels. Also, starvation, a high-
purine diet, stress, and alcohol  abuse raise uric acid. When uric acid is
measured by the colorimetric method, false elevations come from
acetaminophen, ascorbic acid, levodopa, and phenacetin. Decreased uric
acid is caused by high doses of aspirin, Coumadin, clofibrate, cinchophen,
adrenocorticotropic hormone, and phenothiazines. THE GLUCOSE,  FASTING  BLOOD  SUGAR  (FBS) L ABORA TORY TEST
Following a 12- to 14-hour fast, the glucose, fasting blood sugar (FBS)
laboratory test measures glucose metabolism as required in diabetes
mellitus. In the fasting state, blood glucose levels decrease, stimulating
release of the hormone glucagon. Glucagon then raises plasma  glucose by
accelerating glycogenolysis, stimulating glyconeogenesis, and inhibiting
glycogen synthesis. Normally , secretion of insulin checks this rise in
glucose levels. In diabetes, absence or deficiency of insulin allows
persistently high glucose levels. Normal ranges for fasting blood glucose on the FBS laboratory test after
an eight- to twelve-hour fast are:
• fasting serum, 70 to 100 mg/dL;
• fasting whole blood, 60 to 100 mg/dL;
• nonfasting whole blood, 85 to 125 mg/dL in persons over age 50, and
70 to 1 15 mg/dL in persons under age 50. These laboratory readings help to screen for diabetes mellitus and other
disorders of glucose metabolism. They also monitor drug or dietary therapy
for diabetics, insulin requirements for uncontrolled diabetics, and known or
suspected hypoglycemics. Fasting blood glucose levels of 140 to 150 mg/dL or higher obtained on
two or more occasions are diagnostic of diabetes mellitus. Nonfasting levelsthat exceed 200 mg/dL also show diabetes. The elevated blood glucose may
come from pancreatitis, hyperthyroidism, pheochromocytoma, chronic
hepatic disease, brain trauma , chronic illness, chronic malnutrition,
eclampsia, anoxia, and convulsive disorders as well. Depressed blood  glucose occurs from hyperinsulinism, insulin oma, von
Gierke’ s disease, functional or reactive hypoglycemia, hypothyroidism,
adrenal insuf ficiency , congenital adrenal hyperplasia, hypopituitarism, islet
cell carcinoma of the pancreas, hepatic necrosis, and glycogen storage
disease. THE SERUM  IRON AND  TOTAL IRON-BINDING  CAPACITY  LABORA TORY TEST
Two separate blood tests conducted with buffering and coloring reagents
measure (1) the amount of iron bound to the glycoprotein transferrin and (2)
the plasma’ s total iron-binding capacity (TIBC) if all the transferrin were
saturated with iron. The percent age of saturation is obtained by dividing the
serum iron result by the TIBC, which reveals the actual amount of saturated
transferrin. Normal transferrin is 30 percent saturated. Thus, the two tests
(a) estimate total iron storage, (b) diagnose hemochromatosis, (c)
distinguish between iron deficiency anemia and chronic disease anemia,
and (d) evaluate a person’ s nutritional status. Normal serum iron and TIBC values have been determined to be:
In iron deficiency , serum iron falls and TIBC increases to decrease the
saturation. With chronic inflammation as in rheumatoid arthritis, serum iron
is low in the presence of adequate body stores, but TIBC remains
unchanged or drops to preserve normal saturation. Iron overload does not
alter serum levels until relativ ely late in the pathology , but serum iron
increases and TIBC remains the same to increase the saturation. THE ERYTHROCYTE  (RED BLOOD  CELL, RBC) C OUNTTraditionally counted by hand with a hemacytometer , red blood cells
(RBCs) are now commonly counted with electronic devices, which provide
faster , more accurate results. This erythrocyte count does not provide
qualitative information about the RBCs’ hemoglobin content, but it does tell
mean corpuscular volume (MCV) and mean corpuscular hemoglobin
(MCH). Thus, the erythrocyte blood count offers indices for RBC size and
hemoglobin content and supports other hematologic tests in diagnosing
anemia and polycythemia. Depending on age, sex, sample, and geographic location, normal RBC
values in adult males range from 4.5 to 6.2 million/microliter (4.5 to 6.2 x
1,012/L) of venous blood; in adult females from 4.2 to 5.4
million/microliter (4.2 to 5.4 x 1,012/L) of venous blood; in children, 4.6 to
4.8 million /microliter of venous blood; in full-term infants,  4.4 to 5.8
million/ microliter (4.4 to 5.8 x 1,012/L). An elevated RBC count indicates
polycythemia or dehydration; a depressed count shows anemia, fluid
overload, or recent hemorrhag e. With total bed rest, RBC counts drop
considerably from decreased oxygen requirements. THE TOTAL HEMOGLOBIN  (HGB) L ABORA TORY TEST
The total hemoglobin (Hgb) concentration in a deciliter (100ml) of whole
blood is measured by the total hemoglobin laboratory test. The Hgb-RBC
ratio (mean corpuscular hemoglobin or MCH) and free plasma Hgb affect
the RBC count. This test, a usual part of the complete blood count,
measures the severity of anemia or polycythemia, monitors therapy
response, and supplies figures for calculating MCH and mean corpuscular
Hgb concentration. Based on venous blood samples, normal values for dif ferent patients are:
AgeHemoglobin Level
(g/dL)
Less than 7 days 17-22
1 week 15-201 month 11–15
Childr en 11-13
Adult males 14-18
Elderly males 12.4-14.9
Adult females 12-16
Elderly females 11.7–13.8
THE HEMA TOCRIT  (HCT) LABORA TORY TEST
The volume of RBCs packed in a whole blood sample is measur ed by the
hematocrit (Hct) laboratory test. Number and size of the RBCs determine
the Hct concentration, and such a readout aids in the diagnosis of abnormal
states of hydration, polycythemia, anemia, fluid imbalance, blood loss,
blood replacement, and red cell indices. According to a patien t’s sex, age,
laboratory competence, and type of blood sample, the test routinely screens
one’s blood in a complete blood count. Hct reference values range from  40 percent to 54 percent (0.4 to 0.54) for
men and from 37 percent to 47 percent (0.37 to 0.47) for wome n. Low Hct
indicates anemia or hemodilution; high Hct shows polycythemia or
hemoconcentration caused by blood loss. If a hematoma develops at the
venipuncture site, ease discomfo rt by applying ice, followed later by warm
soaks. THE ERYTHROCYTE  INDICES  LABORA TORY TEST
Mean corpuscular volume (MCV), mean corpuscular hemoglobin
(MCH), and mean corpuscular hemoglobin concentration (MCHC) are the
three measurem ents accomplis hed by the erythrocyte indices laboratory
test. The MCV expresses the average size of erythrocytes and indicates
whether they are undersized (microcytic), oversized (mac rocytic), or
normal (normoc ytic). MCH gives the weight of hemoglobin in an averagered cell. MCHC defines the concentration of Hgb in 100 mL of packed red
cells. The normal RBC indices are:
MCV = 84 to 99 cubic microliters/red cell (femtoliters (fl)/red cell)
MCH = 26 to 32 picograms (pg)/red cell
MCHC = 30% to 36% (300 to 360 g/L)
  
These indices aid in diagnosing  and classifying anemia. Low MCV and
MCHC show microcytic hypochromic anemias caused by iron deficiency
anemia, pyridoxine-responsive anemia, or thalassemia. High MCV
indicates macrocytic anemia caused by megaloblastic anemias coming from
folic acid or vitamin B12 deficiency , inherited disorders of DNA synthesis,
or reticulocytosis. THE ERYTHROCYTE  SEDIMENT ATION  RATE (ESR)
Measuring the time required for erythrocytes in a whole blood sample to
settle to the bottom of a vertical tube, the erythrocyte sedimentation rate
(ESR) is a sensitive but nonspecific test that indicates the presence of
disease when other chemical or physical signs are normal. It rises in
widespread inflammatory disorders caused by infection, autoimmune
disease, or malignancy . Thus, the ESR monitors inflammatory or malignant illness and detects
occult disease such as tuberculosis (TB), tissue necrosis, or connective
tissue disorders. The normal ESR ranges from 0 to 20 mm/hour . It rises in
pregnancy , acute or chronic inflammation, TB, paraproteinemias, rheumatic
fever , rheumatoid arthritis, and some cancers. ESR also rises in anemia. ESR drops in polycythemia, sickle cell anemia, hyperviscosi ty, and low
plasma protein.Note: ESR is frequently raised during and after reactions and fevers
induced by the Gerson Therapy . THE PLATELET  COUNT
Platelets, or thrombocytes, are tiny formed elements in the blood which
create the hemostatic plug in vascular injury . They promote coagulation by
supplying phospholipids to the intrinsic thromboplastin pathway . The
platelet count is vital for moni toring chemotherapy , radiation therapy , or
severe thrombocytosis and thrombocytopenia. A platelet count that falls
below 50,000 brings on sponta neous bleeding; below 5,000, fatal central
nervous system bleeding or massive gastrointestinal hemorrhage is possible. The platelet count evaluates platelet production, assesses effects of
cytotoxic therapy , aids the diagnosing of thrombocytopenia and
thrombocytosis, and confirms visual estimate of platelet number and
morphology from  a stained blood film. Normal platelet counts range from
130,000 to 370,000/mm (130 to 370 x 1011/L). A decreased count comes from aplastic or hypoplastic bone marrow; in-
filtrative bone marrow diseases like carcinoma, leukemia, or disseminated
infection; megak aryocytic hypop lasia; ineffective thrombopoiesis caused by
folic acid or vitamin B1 deficiency; pooling of platelets in an enlar ged
spleen; increased platelet destru ction from drug use or immune disorders;
disseminated intravascular coagulation; Bernard-Soulier syndrome; or
mechanical injury to platelets. Medications decreasing the count include acetazolamid, acetohexam-ide,
antimony , antineoplastics, brompheniramine maleate, carbamazepine,
chloramphenicol, ethacrynic acid, furosemide, gold salts,
hydroxychloroquine, indomethacin, isoniazid, mephenytoin, mefenamic
acid, metha-zolamide, methimazole, methyidopa, oral diaoxide,
oxyphenbetazone, penicillamine, penicillin, phenylbutazone, phenytoin,
pyrimethamine, quinidine sulfate, quinine, salicylates, streptomycin,
sulfonamides, thiazide, thiazidelike diuretics, and tricyclic antidepressants. Heparin causes transient reversible thrombocytopenia. An increased platelet count results from such diseases as hemorrhage;
infectious disord ers; malignanc ies; iron deficiency anemia; myelofibrosis;
primary thrombo cytosis; polycy themia vera; myelogenous leuke mia; recentsurgery, pregnancy , or splenectomy; and inflammatory disorders, such as
collagen vascular disease. THE LEUKOCYTE  (W HITE BLOOD  CELL, WBC) C OUNT
Reporting on the number of white blood cells (WBCs) found in a
microliter (cubic  millimeter) of whole blood by use of a hemacytometer or
Coulter counter , the leukocyte count varies with strenuous exercise, stress,
or digestion. It’s used to detec t infection or inflammation, the need for
further tests such as the WBC differential or bone marrow biopsy, and the
response to chemotherapy or radiation therapy . The WBC count  ranges from 4.1 to 10.9 x 10”. An elevated count signals
infection such as an abscess, meningitis, appendicitis, or tonsillitis, and it
may indicate leukemia, tissue necrosis from burns, myocardial infarction, or
gangrene. A low count shows bone marrow depression from viral infections
or from toxic reactions such as those following treatment with
antineoplastics, mercury or other heavy metal toxicity , benzene or arsenic
exposure, and invasion by the organisms of influenza, typhoid fever ,
measles, infectious hepatitis, mononucleosis, and rubella. THE WHITE BLOOD  CELL DIFFERENTIAL
Being a relative number of each type of white blood cell, the white blood
cell differential test is determined by multiplying the percentage value of
each WBC type to give an absol ute number of each kind of the 100 or more
WBCs. There are granulocy tes, agranulocytes, juvenile neutrophils,
segmented neutrophils, basophils, eosinophils, large lymphocytes, small
lymphoctyes, phagocytes, histiocytes, and so on. The WBC differential evalua tes the body’ s capacity to resist and
overcome infection, various types of leukemia, the stage and severity of
infection, allergic reactions, severity of allergic reactions, and parasitic
infections. There is a long list of reference values in the WBC differential
test, divided into adult and child. For example some of them are:For Adults— Relative V alue (%) Absolute V alue (mcL)
Neutr ophils 47.6–76.8 1950–8,400
Lymphocytes 16.2-43 660-4,600
Monocytes 0.6-9.6 24-960
Eosinophils 0.3-7 12-760
Basophils 0.3-2 12-200
  
To make an accurate diagnosis, the test examiner must consider both
relative and absolute values of the differential counts. For the vast number
of variables and illnesses which are diagnosed by them, please see
Appendix I of the Gerson Therapy  Handbook: Companion Workbook to A
Cancer Therapy: Results of Fifty Cases: Practical Guidance, Resour ces
and Recipes for Gerson Ther apy Patients. To acquire a copy of this
handbook /workbook, contact the Gerson Institute, in Bonita, California. THE ROUTINE  URINAL YSIS
Elements of routine urinalysis include the measurement evaluations of
physical characteristics, specific gravity and pH, protein, glucose, and
ketone bodies, plus examination of urine sediment, casts, and blood cell
crystals. The analysis of urine is an exceedingly important test that tells a
lot about the internal workings of a person. Routine urine test results have a
great number of implications for how the physiology is functioning or how
it is responding to the diet, nonpathologic conditions, specimen collection
time, and other factors. For the vast number of variables and illnesses which are evaluated by
urinalysis, please see Appendix I of the Gerson Therapy Handbook:
Companion Workbook to A Cancer Therapy: Results of Fifty Cases:
Practical Guidance, Resour ces and Recipes for Gerson
  Therapy
Patients. To acqu ire a copy of this handbook/workbook, contact the Gers on
Institute in San Diego, California.OceanofPDF .comChapter Twenty-One
SUCCESS ST ORIES BY P ATIENTS
Writing in the Townsend Lette r for Doctors  & Patients,  medical
anthropologist Tim Batchelder advises that people do not arrive at health
care systems for diagnosis and treatments; rather , they come to find
wellness and wholeness.1
People often feel symptoms and even exhibit signs of illness when they
seek the services of a doctor or clinic but return home labeled with a
disease. Other medical anthropologists call such a result the “veterinary
practice of medicine” since the patient’ s experience of illness becomes
irrelevant except as it reveals an underlying presence of disease. A patient’ s
opinions, beliefs and other aspects of sociocultural identity only cloud the
doctor ’s mind-set.2 Preferable for some technically oriented and
conventionally practicing health  professionals is that the patien t be passive
like a sedated animal in a veterinarian’ s clinic. Not so the situa tions for Gerson patients whose case histories of chronic
illness you’re about to read. They have been far from passive  or sedated;
instead these people actively sought out the Gerson Therapy and practiced it
—this despite knowing their selected approach to wellness offers a difficult,
highly restrictive, and isolating  lifestyle. The goal for each of these folks
has been  to live as close as possible to the full complement of mankind’ s
allotted years. The Gerson Therapy has been allowing them to reach that
goal. REVERSING  LATE-STAGE LUNG CANCER
To his shock and dismay , in November 1989, sixty-year -old John Peters
of Pittsbur gh was diagnosed with lung cancer—an adeno carcinoma. Although he had eaten a good diet, swam a thousand yards in his swimmingpool five days each week, never smoked, and had been given an excellent
health report by his doctor just three months before, Mr. Peters still had
come down with non-small-cell  carcinoma of the lung, staged at level IIIA
by his consulting oncologist. Lung Cancer is the second most common cancer and the number -one
cause of death from malignancy  in both men and women. Although there
has always been a higher incidence in men, lung cancer in women has risen
rapidly in recent years. While lung cancer has long been the top cancer
killer of men, it has now surpa ssed breast cancer as the main malignancy
killer of women. In 1997,  178,100 Americans developed lung cancer , and 160,400 died of
it. This high incidence of death is true even though lung cancer is the most
preventable of malignancies; if every bit of tobacco were remov ed from the
earth, the number of all cancer types (not only those affecting the lung)
would fall by 17 percent. Of the two general kinds of lung cancer , small-cell
and non-small-cell, the latter is more common, accounting for
approximately 75 percent of all diagnosed cases. Conventional oncological treatment of lung cancer , which primarily
depends on surgery with chemotherapy , radiation therapy , and sometimes
hyperthermia, has offered a poor prognosis for remaining alive over a
prolonged period of time. • The success rate for five-year survival of stage I lung cancer (no spread
to lymph  nodes) is 30 to 80 percent because the tumor is tiny in size and
surgery removes it. • The success rate for five-year survival of stage II lung cancer (spread to
the hilar nodes) is 10 to 35 percent with both surgery and radiation
therapy administered. (Hilar nodes  are those lung indentations where
arteries enter and veins and lymphatics leave.) • The success rate for five-ye ar survival of stage IIIA lung cancer
(surgery is possible combined with radiation therapy and occasional
chemotherapy) is 10 to 15 percent. • The success rate for five-ye ar survival of stage IIIB lung cancer
(surgery offers no benefit; radiation therapy and experimental
chemotherapy may be attempted) is less than 5 percent because usual
orthodox oncological treatments truly fail the patients. • The success rate for five-year survival of stage IV lung cancer
(metastases to distant sites) is considerably less than 5 percent—perhapsonly 3 percent—for treatment usually is directed merely toward relieving
symptoms. Non-small-cell lung cancer , spreading by the lymphatic system and
through the blood, contains three distinct types: squamous-cell or
epidermoid carcinoma of the lung (most related to smoking), large-cell
carcinoma (associated with brain metastasis), and adenocarcinoma. For no
known reason, adenocarcinoma has steadily increased in frequency (above
30 percent of all lung cancers). Treatment is similar for these three non-
small-cell lung cancer types. Upon an emer gency recommendation of his consulting oncologist, John
Peters underwent immediate open-chest surgery, followed by twenty-four
radiation treatments. Thus, his various symptoms consisting of constant
cough, sometimes containing blood, hoarseness and shortness of breath,
excessive sputum, recurrent episodes of lung infection, weight loss, and
swelling of the face, plus the sense of overwhelming fatigue, lessened to the
point of almost disappearing. A year later, however , the patient’ s original coughing and some of his
other symptoms recurred. Another series of diagnostic tests, including
bronchoscopic examination, revealed that he again required chest surgery
for excising the non-small-cell lung cancer . “When I refused surgery and
chemotherapy , the doctors told me that there was no chance for my survival
at all,” John Peters explained. “I had research ed lung cancer and realized that the only reason I got
cancer was that my body supported it. Thus, if I didn’ t change the internal
environment of my body , the cancer would just come back again. In May
1991, I started on the Gerson Therapy at home,” said Mr. Peters. “I was
very weak, and this Gerson Therapy was demanding, but I was facing the
Grim Reaper , so I was also highly motivated. “In only three weeks, I knew the Gerson treatment was workin g—I was
getting stronger , coughing less, and feeling much better . Most surprising, I
was actually gaining weight on this vegetarian diet. After losing so many
pounds the months before, I was finally becoming more than just skin and
bones,” Mr . Peters wrote in a letter to the Gerson Institute. “I have remained
cancer -free and in good health for the past seven years. I am vegan, avoid
refined flour , sugar , salt, caf feine and alchohol and still press vegetables and
drink their juice s, about twenty-four ounces per day. There is no doubt inmy mind that I would have been in the cemetery six or seven years ago
without the Gerson Therapy . “Incidentally , before going throu gh my 1989 lung removal surgery, I had
obtained a second opinion from the head of the Pittsbur gh Cancer Institute. When I returned  to him for a follow-up cancer test in 1996, he was shocked
to see me survi ving. The lung surgeon told me that I’d never know how
lucky I was to be alive and that with my disease, there was only about a 3
percent chance of five-year survival. Eating the Gerson vegetarian way has
saved my life,” John Peters confirmed. At his latest report to this book ’s two authors, as a former lung cancer
patient who subscribes rather closely to the eating program of the Gerson
Therapy , John Peters has gone  well beyond doubling the usual cancer
patient’ s five-ye ar survival time for adenocarinoma of the lung. (As you’ve
been informed, five-year survival of any cancer is defined by the American
Cancer Society as a “cure. )”
A T WENTY -YEAR CURE OF  INOPERABLE  STAGE IIIB L UNG CANCER
In mid-January 1979, Jesus Lechuga Valdez of Durango, Mexico,
returned from a business trip to Mexico City with a severe cold. A week
later it had deter iorated into a persistent cough and lingering hoarseness that
made it difficult  for him to speak. Senor Lechuga, who, at this writing, is
eighty-six years  old, in 1971 had retired from his position as general
manager and partial owner of a truck and tractor dealership. His travels for
business had been successful but hard on the man’ s body . During the next
six months, his chronic cough and hoarse voice were treated by three
allopathic physi cians and a homeopath, all of whom thought such signs of
illness came from adult-onset asthma. At that time he was sixty-six years
old. The doctors’ diagnosis and treatment were incorrect, for X-ray films
eventually taken  of Senor Lech uga’s thoracic area showed a 5-centimeter
(cm) round spot in the upper region of his right lung. A chest surgeon he
consulted confirmed the existence of a lung tumor 2½ inches across. Since an El Paso, Texas, intern ist, Walter D. Feinber g, M.D., had been
keeping annual records of the patient’ s physical examinations, on June 18,
1979, Senor Lechuga traveled  to Dr. Feinber g’s office for comparingprevious and current radiographs. It turns out that there had been no sign of
the potential for a chest lesion the year before. Within half a dozen months,
therefore, his mass had formed spontaneously and quickly . Pulmonologist E. S. Crossett, M.D., at El Paso’ s Hotel Dieu (French for
“God’ s house”) Hospital performed a bronchioscopy and medi- astinoscopy
during lung surgery to remove the tumor . But because excision would have
left his patient too weak, the surgeon decided not to remove the tumor and
only performed a biopsy . The resulting tissue pathology and
instrumentation reports indicated that Senor Lechuga was victimized by
stage IIIB “large cell undif ferentiated carcinoma with metastasis to the
bronchial and mediastinal areas.”
Staging  in cancer terminology is a relative index of how much cancer
exists in an individual’ s body , including its size, location, and containment
or metastasis.3 Stage III indicates that metastases have spread the cancer to
areas other than the primary site. In lung cancer , stage III is divided into
two types, IIIA and IIIB. Stage IIIB lung cancer  classifies the tumor as not
removable because of technical reasons relating to the surgical technique or
because there would be no benefit to the patient.4 The several malignant
metastases of Jesus Lechuga Valdez were declared inoperable, and his
prognosis became established at only three to six months of life remaining. High-Dosage Radiation Exposur e for Senor Lechuga
Consultation with oncologist Ira A. Horowitz, M.D., medical director of
the El Paso Cancer Treatment Center , followed. Dr. Horowitz emphatically
recommended radiation therapy , but the machine used for this external
radiation failed to be state-of-the-art; its old-fashioned cobalt-60 electron
beams would present the patient with some awful side effects. The
machine’ s radioactive source was housed in a lead container , and as the
cobalt isotope decayed, it produced a beam in the megavoltage range.5
With advice from his family , Senor Lechuga decided instead that he
would take radiation therapy in Chester , Pennsylvania, close to the
Wilmington, Delaware, home of his daughter , Geor gina Lechuga Potter . (Mrs. Potter, who now lives in Vienna, Virginia, acted as transl ator for her
father ’s Spanish -spoken case history . Besides hospital records, she is a mainsource of the information you are reading. The patient’ s wife, Dolores A.
Lechuga, signed the permission form to release this story .) From Wilmington, Mrs. Potter brought her father to consult with
oncologist Robert Enck, M.D., located at the Crozer -Chester Medical
Center in Chester . He confirmed the need for radiation therapy . Upon Dr.
Enck’ s referral, radiologist Warren Sewall, M.D., from July 10 to August
21, 1979 , used a linear accelera tor to administer radiation doses of 4,400
rads (the modern dosage term is centigray  [cGy]) to the right lung and
mediastinum for four weeks. The patient also received 1,600 rads to the
upper lobe of the right lung plus 5,000 rads simultaneously to cancer -filled
“supraclavicular nodules.” He took this high-ener gy therapy five days per
week for four weeks. Then the radiologist added another 5,000 rads to those
supraclavicular nodules for two additional weeks. The linear accelerator , one of the most popular machines now being
used, was truly state-of-the-art  back in 1979. It is available in energies
ranging from 4 to 3 5 megavolts and uses a mixed beam of X rays and
electrons. Electrons are accelerated along a wave guide to their high
velocity . Penetration into tissue is determined by the energy of the beam
selected.6
With the object of relieving his symptoms (not curing the cancer), Jesus
Lechuga Valdez underwent multiple exposures to the hospital’ s linear
accelerator ’s high-ener gy X rays. They were responsible for certain
discomforting side effects and may be responsible for cancer to have
appeared curren tly, twenty years later. The massive amount of X rays given
then to normal tissue supposedly never exceeded safe doses. Through a process of “ionizatio n,” the radiation is designed to kill some
cancer cells by damaging their chromosomes and DNA to stop cell division. Of the centigray dose, one gray equals 100 rads, so that Senor Lechuga each
day actually received 44 cGy plus 16 cGy plus 50 cGy for a four-week total
of 2,200 cGy, and then he accep ted another 1,000 cGy for two weeks more. The 3,200 cGy dosage is enormous and, as you will learn later, such
radiation therapy held significance for the man’ s future health prospects. The beam’s adverse effects caused Senor Lechuga to experience mental
depression, loss of appetite, serious weight loss, darkening of the skin in the
irradiated chest area, and difficulty swallowing from esophageal scarring
that resulted from the radiation burns he sustained. Even today , almosttwenty-one years later, he must swallow carefully because he can be choked
by an overly lar ge food particle getting stuck at the esophageal scar site. By means of follow-up diagnostics back at the El Paso Cancer Treatment
Center , on August 31, 1979, Dr. Horowitz confirmed that his patient’ s lung
tumor had been reduced by about 80 percent. The coughing fits were less
strong and not striking Senor Lechuga as often; his appetite had returned;
and the annoying hoarseness improved. Throughout his examinations and
treatments, the doctors put no dietary restrictions on him whatsoever ,
permitting Danish pastries, fatty hambur gers, french fried potatoes, pizza,
cola drinks, and other assorted junk. He was told merely to avoid sunlight
directly on his irradiated skin areas. When pressed for a prognosis as the result of radiation therapy received,
Dr. Horo witz gave him an estim ated 50 percent chance of either having a
lung cancer recurrence or living somewhat longer . It was then that the man
returned home to Durango and resumed working in his truck  and tractor
dealership. Lung Cancer Returns
Less than a month after conclusion of the radiation, his cancer came
back. Coughing  spells and hoarseness returned worse than ever for Senor
Lechuga. It was then that he and Dolores decided to act upon information
about the Gerson Therapy provided by their daughter , Geor gina Lechuga
Potter . Her friend, practicing pharmacist Irwin Rosenber g, Ph.D. (a
doctorate in nutrition), acquired  information and taught Mrs. Potter about
healing cancer using Dr. Max Gerson’ s dietary/detoxification program. Dr.
Rosenber g is owner of the Apothecary Pharmacy on Geor getown Road in
Bethesda, Maryland (ironically , located across from the National Institutes
of Health). On October 28, 1979, Senor Lechuga accompanied by his wife arrived at
the Gers on Therapy hospital in Tijuana, Mexico. Victor Ortuno, M.D., the
hospital’ s medical director , initially examined the patient and then turned
the Lech uga case over to his cousin, Arturo Ortuno, M.D., who took full
responsibility for supervising treatment. Although very uncomfortable from his numerous healing reactions,
Senor Lechuga’ s physical response was rapidly positive. His cancermarkers and other laboratory tests improved; however , his state of mind hit
bottom—depression set in. Still, from Dr. Arturo Ortuno’ s efforts and with
much encouragement from Dolo res Lechuga, Senor Lechuga stayed on the
dietary/detoxification program at the Gerson hospital and then later at
home. On his own back in Durango, Senor Lechuga struggled with tolerating
the many glasses of Gerson juices, coffee enemas, castor oil treatments,
salads, and eating the well-done  and unsalted foods. The Gerson diet was
contrary to his Mexican cultural background and abhorrent to his psyche. During healing reactions, appet ite left him completely , and such reactions
came on frequently for prolonged periods. Sometimes they lasted for a
week, but the love and support of Dolores, his companion for life, prevailed
over his discouragement. Dolor es prepared the foods, juices, enemas, and
other healing components; she became his self-contained caregiver and the
household’ s Gerson therapist. In effect, his wife saved the life of Senor
Lechuga. By the week between Christmas  and New Years day of 1980, his healing
flare-ups diminished, and he began to feel better . However , the man did
experience extreme weakness and had to force himself to eat anything at all. He preferred to do nothing more than rest in bed and sleep frequently . In
another week he made enough  progress to return to work part-time and
sporadically . Sitting at his desk gave him a renewed will to fight his cancer
with all his might. W ith an of fice a mere five minutes by car from home, the
patient went home for coffee enema cleansings, to eat his meals, and to
drink the green juices. He carrie d carrot juice in a thermos with him to work
for hourly drinking.
_OceanofPDF.com_The_Gerson_Therapy_-_Charlotte_Gerson_Morton_Walker.txt
Summarize the following text section accurately and concisely. Maintain specific details and numerical information, and use anti-repetition mechanisms:

        Clay poultice,  a soft composition powder mixed with water and applied
as a mud pack to an inflamed body part for purposes of absorbi ng toxins of
arthritis, cancer, insect stings, diarrhea, and poisons, it has an adsorptive
effect like that of charcoal. The clay poultice aids detoxification. Clay
powder can also be used interna lly to clear gastrointestinal difficulties and
inflammations. The procedure for applying a clay poultice should involve
the following steps:
1. Prepare enough warm water to mix the needed amount of clay powder
into a paste. 2. Apply the paste quickly to a square of clean muslin to prevent cooling. 3. Place the muslin on an area to be treated. 4. Cover the area with plastic and wool cloth. 5. Pin the covering in place and leave it on overnight or until dry. 6. Remove and gently rub the area with a cold wet cloth. 7. Repeat this procedure as required. 8. Discard used clay pack. References for Chapter Nineteen
1Schaefer, A. “Some characterist ics of cancer survivors. ” Townsend Letter
for Doctors & Patients. 195:70-71, October 1999. OceanofPDF. comChapter Twenty
GERSON LAB TESTS EXPLAINED
In this chapter we explain the significance of certain laboratory tests that
are necessary for monitoring one’s healing progress. Laboratory testing of
blood and urine are a standard part of follow-up protocols for Gerson
Therapy patients employed by all Gerson-trained health professionals. Among practitio ners invited to administer the Gerson program are medical
doctors, osteopathic physicians, and naturopathic physicians. If you are a patient utilizing the Gerson approach to healing but have no
access to a trained Gerson health practitioner to act as your ombudsman, it’s
still possible to have appropriate  monitoring performed. Accom plish this by
hiring the services of a convent ionally practicing allopathic physician who
is willin g to order laboratory examinations for you or for ill loved ones (of
course, for a fee). Then, using the guidance of this chapter, you probably
will be able to interpret the test results. But, you do need a licensed health
professional’ s prescription to have laboratory tests conducted. Moreover, from observations made over many years of counseling
degenerative disease patients, the coauthors know that combining a doctor ’s
interpretation with information offered below will give you an
understanding of what is happening physiologically in your healing body. We offer this caution, however: Suggestions by allopathic, non-Gerson-
educated practitioners for you to take drugs or make food changes may not
be in your best interest and could very well be contraindicated. Explanations and interpretations are provided here to help our readers
feel less intimidated by unfamiliar medical terms, and to acquaint them with
current knowledge about the required laboratory tests in the even t they must
monitor themselves without assistance by any health professio nal. If you
want education about some specific test other than what is furnished here,
we recommend that you query the laboratory conducting the particularexamination for you. It’s your right to know about tissues and other
specimens taken from your own body. THE SERUM  CALCIUM  LABORA TORY TEST
The laboratory test for serum calcium is a measurement of the levels of
calcium in the blood. Knowing  such levels helps a health professional to
interpret the patient’ s physiologi cal status regarding neuromuscu lar activity,
enzyme activity, skeletal development, and blood coagulation. Calcium (Ca+) is a predominantly extracellular ion (a cation) derived
from the calcium absorbed in food through the gastrointestinal tract,
provided sufficient vitamin D is present in the food eaten. Excess quantities
of calcium ions in the blood are excreted in the urine and feces, while
insuf ficient calcium concentrations can move out of the storage areas of
bones and teeth to restore low blood levels. Daily ingestion of 1 gram of
calcium is necessary for normal calcium balance. For Gerson patients, this
should not be given in the form  of supplements. Juices and foods contain
more than adequate amounts of calcium. Serum calcium testing aids in diagnosing arrhythmias, blood-clotting
deficiencies, acid-base imbalance, and disorders of the neuromuscular,
skeletal, and endocrine systems. Normal adult serum calcium levels range
from 8. 9 to 10. 1 mg/dL (atomic absorption is 2. 25 to 2. 75 mmo l/L). Serum
calcium levels for children are higher than for adults. When the level of Ca+ is too high, a condition of hyper calcemia  prevails
indicating the possibility of one or more of the following pathologies:
hyperparathyroidism, Paget’ s disease of the bone, multiple myeloma,
metastatic carci noma, multiple  fractures, and prolonged immobilization. From inadequat e excretion of calcium, also shown by elevated serum
calcium, kidney disease and adrenal insuf ficiency may result. In contrast, low calcium levels (known as hypocalcemia)  may come from
hypoparathyroidism, total parathyroidectomy, or malabsorption. Decreased
serum Ca+ levels may arise from calcium loss in Cushing’ s syndrome,
kidney (renal) failure, acute pancreatitis, and periotonitis. Hypercalcemia may bring on deep bone pain, flank pain from renal
calculi, and muscle hypotonicity. Its beginning symptoms are manifested bynausea, vomitin g, and dehydration, leading to stupor and coma, and may
end in cardiac arrest. Hypocalcemia may produce peripheral numbness and tingling, muscle
twitching, facia l muscle spasm (Chvostek’ s sign), carpop edal spasm
(Trousseau’ s sign), seizures, and arrhythmias. THE SERUM  PHOSPHA TES LABORA TORY TEST
The laboratory test for serum phosphates is a measurement of the blood
levels of phosphates to tell the state of body energy, carbohydrate
metabolism, lipid metabolism, and acid-base balance. Phosphate ion (P+) is
the dominant cellular anion, which is essential for bone formation. Testing
for its blood level aids in the diagnosis of acid-base imbalance  plus renal,
endocrine, skeletal, and calcium disorders. In a normal adult, serum phosphate levels range from 2. 5 to 4. 5 mg/dL
(0. 80 to 1. 40 mmol/L) or from 1. 8 to 2. 6 mEq/L. Children show a higher
range that can rise to 7 mg/dL  (2. 25 mmol/L) during spurts of increased
bone growth. Phosphates are absorbed through the intestines from dietary sources in
the presence of vitamin D. Excess quantities of them are excreted through
the kidneys, which act as the regulating mechanism. Because calcium and
phospate interact in a reciprocal relationship, urinary excretion of
phosphates incre ases or decreases in inverse proportion to serum calcium
levels. Abnormally high concentrations of phosphates in the blood
(hyperphosphatemia),  which can come from drinking an overabundance of
carbonated beverages, sets up a pathological process of bone loss, tooth
demineralization, poor healing of fractures, hypopara thyroidism,
acromegaly, diabetic acidosis, high intestinal obstruction, and renal failure. Depressed phosp hate levels in the blood (hypophosphatemia)  may result
from malnutrition, malabsorption syndromes, hyperparathyroidism, renal
tubular acidosis, or treatment of diabetic acidosis. In children, such
hypophosphatemia can suppress normal growth. THE SERUM  SODIUM  LABORA TORY TESTThe laboratory test for serum sodium is a measurement of the blood
levels of sodium to determine body water distribution, osmotic  pressure of
extracellular fluid, neuromuscu lar function, and acid-base balance. The
sodium ion (Na+) is the major extracelullar cation, and it influences both
chloride and potassium blood levels. Sodium is absorbed by the intestines and is excreted primarily by the
kidneys; a small amount is lost through the skin by sweating. This mineral
aids the kidneys in regulating body water, for decreased Na+ promotes
water excretion and an increased level promotes water retention (edema). Testing for Na+ aids in evaluat ing fluid electrolytes, acid-base balance,
and certain disorders of the kidneys, adrenals, and neuromuscular system. The sodium blood test also determines the effects of drug therapy such as
diuretics on the body. For an adult, normally serum sodium levels range
from 135 to 145 mEq/L (mmol/L). For Gerson patients, a level of 127 is
still acceptable. Sodium imbalan ce comes from either a change in water volume intake or
variation in how much sodium gets consumed. Elevated serum sodium
levels (hypernatr emia)  may be caused by inadequate water intake, diabetes
insipidus, impa ired renal function, prolonged hyperventilation, severe
vomiting, or severe diarrhea. Sodium retention also comes from consuming
excessive salt. The signs and symptoms of hypernatremia are thirst,
restlessness, dry mouth, sticky mucous membranes, flushed skin, oliguria,
diminished reflexes, hypertension, dyspnea, and edema. Ingesting too little sodium mine ral for serum Na+ (hyponatr emia)  is rare
and doesn’t even happen on the low-sodium dietary program encouraged by
the Gers on Ther apy. There is always some sodium coming from food. Still,
hyponatremia can occur, and its indications appear as apprehension,
lassitude, headache, decreased skin turgor, abdominal cramps, tremors, or
convulsions. It can come on from profuse sweating, gastrointestinal
suctioning, diuretic therapy, diarrhea, vomiting, adrenal insufficiency,
burns, and chronic renal insuf ficiency with acidosis. If you do have testing
for serum sodium performed, make sure to get a urine sodium
determination simultaneously. THE SERUM  POTASSIUM  LABORA TORY TESTThe laboratory test for serum potassium, a quantitative analysis, is the
measurement of blood potassium for regulation of homeostasis, osmotic
equilibrium, muscle activity, enzyme activity, acid-base balance, and kidney
function. Potassium (K+) is the body’ s major intracellular ion (a cation);
small amounts of it are also found in the extracellular fluid. Since the kidneys excrete nearly all the ingested potassium, a dietary
intake of at least 40 mEq/day (mmol/d) is essential. A normal diet usually
includes 60 to 100 mEq/day of this mineral. In the blood, norm al K+ levels
range from 3. 8 to 5. 5 mEq/liter (mmol/L). Vital to maintain ing electrical conduction within the cardiac and skeletal
muscles, K+ is affected by variations in the secretion of adrenal steroid
hormones and by fluctuations in pH, serum glucose levels, and serum
sodium levels. A reciprocal relationship exists between K+ and Na+; the
substantial intak e of one causes a corresponding decrease in the other. Although the body readily conserves sodium, potassium deficiency may
develop rapidly and is quite common, because there is no efficient method
for conserving potassium. The laboratory test for serum potassium is used to evaluate clinical signs
of either potassium excess (hyperkalemia)  or potassium depletion
(hypokalemia). It also monitors kidney function, acid-base balance, and
glucose metabo lism, and evaluates arrhythmias, neuromuscular disorders,
and endocrine disorders. Hyperkalemia is common in patients with
excessive cellular K+ entering the blood as in cases of burns, crushing
injuries, diabetic ketoacidosis, and myocardial infarction. It will also be
present where there is reduced sodium excretion from renal failure that
causes an abnor mal Na+-K+ exchange and in Addison’ s disease caused by
the absence of aldosterone, with consequent K+ buildup and Na+ depletion. Note: Although elevated serum potassium is uncommon in Gerson
Therapy patients, if it does occur, supplemental potassium should be
reduced or temporarily discontinued. Then the consulting Gerson-trained
physician should immediately be consulted. The signs and symptoms of hyperkalemia are weakness, malaise, nausea,
diarrhea, colicky pain, muscle irritability progressing to flaccid paralysis,
oliguria, and bradycardia. An electrocardiogram (EKG) reveals a prolonged
PR interval; wide QRS; tall, tented T wave; and ST depression. Indications
of hypokalemia are decreased reflexes; rapid, weak, irregular pulse; mentalconfusion; hypo tension; anorexia; muscle weakness; and paresthesia. The
EKG shows a flattened T wave, ST depression, and U wave elevation. In
severe cases of hypokalemia, ventricular fibrillation, respiratory paralysis,
and cardiac arrest could occur. THE SERUM  CHLORIDE  LABORA TORY TEST
The laboratory test for serum chloride, another quantitative analysis, is a
measurement of blood levels of the chloride ion (Cl-), the major
extracellular fluid anion. Interacting with Na+, Cl- helps maintain the
osmotic pressure, blood volume, arterial pressure, and acid-base balance. Chloride is absorbed from the intestines and is excreted prim arily by the
kidneys. By evaluating the body’ s fluid status, the serum chloride laboratory test
detects two types of fluid imbala nces, acid-base (acidosis and alkalosis) and
extracellular cation-anion. Normally serum chloride levels range from 100
to 108 mEq/liter (mmol/L). Maintaining a normal amount of chloride in the
blood reflects acid-base balance by its inverse relationship to bicarbonate. Excessive loss of gastric juices or other secretions containing chloride may
cause hypochloremic metabolic alkalosis or excessive chloride retention. Ingesting it may lead to hyperchloremic metabolic acidosis. Elevated serum chloride levels (hyper chlor emia ) can come on from
severe dehydration, complete renal shutdown, head injury (which produces
neurogenic hyperventilation), and primary aldosteroism. Manifestations
consist of stupor, rapid and deep breathing, and weakness that leads to
coma. A situation of low chloride levels in the blood (hypochlor emia)  is
associated with reduced blood sodium and potassium levels coming from
prolonged vomiting, gastric suctioning, intestinal fistula, chronic renal
failure, or Addison’ s disease. Congestive heart failure, or edema resulting in
excess extracel lular fluid, can cause dilutional hypochlo remia. The
indications are hypertonicity of muscles, tetany, and depressed respirations. THE LACTIC  DEHYDROGENASE  (LDH) L ABORA TORY TESTThe laboratory test for lactic dehydrogenase (LDH) is a measurement of
five specific isoenzymes which catalyze the reversible conversion of
pyruvic acid present in all muscles of the body into lactic acid. Many
common diseases—myocardial infarction (MI), pulmonary infarction,
anemias, liver disease, kidney disease, erythrocytic damage, and others—
cause elevations  in total lactic dehydrogenase, and the LDH laboratory test
is useful for dif ferentiating between them. The five identified isoenzymes in lactic dehydrogenase are LDH1 and
LDH2 appeari ng in the heart, red blood cells, and kidneys; LDH3 in the
lungs; and LDH4 and LDH5 in the liver and the skeletal muscles. Testing
for these  enzymes is especially appropriate for the delayed measurement of
creatine phosphokinase (CPK) associated with MI and for monitoring
patient respons e to some forms of chemotherapy. Total LDH levels
normally range from 48 to 115 U/L. Normal distribution of the five
isoenzymes is as follows:
 
LDH1: 17. 5% to 28. 3% of total  
LDH2: 30. 4% to 36. 4% of total  
LDH3: 19. 2% to 24. 8% of total  
LDH4: 9. 6% to 15. 6% of total  
LDH5: 5. 5% to 12. 7% of total
 
Since a vast number of illnesses involve the enzymes of LDH, this
laboratory test for lactic dehydrogenase is broadly employed for
establishing diagnoses. THE ASPARTATE TRANSAMINASE /SERUM  GLUT AMIC -OXALOACETIC
TRANSAMINASE  (AST/SGOT) L ABORA TORY TEST
The laboratory blood examination for aspartate transaminase and serum
glutamic-oxaloacetic (AST/SGOT) is a measurement of specific amino acid
residues left behind by nitrogenous portions of the metabolized aminoacids. Aspartate aminotransferase (AST) is found in the cytoplasm and
mitochondria of many tissue cells, primarily in the liver, heart, skeletal
muscles, kidneys, pancreas, and red blood cells. AST is released  into blood serum in proportion to cellular damage, and
its detection (together with creatine phosphokinase and lactate
dehydrogenase) indicates myocardial infarction. The test also helps in the
diagnosis of acute liver diseas e. It monitors patient progress in healing. AST adult serum  levels range from 8 to 20 U/L. Normal values for infants
are four times higher. Maximum eleva tions of AST are associated with viral hepatitis, severe
skeletal muscle trauma, extensive surgery, drug-induced liver injury, and
passive liver congestion. Levels ranging from 10 to 20 times normal may
indicate severe MI, severe infectious mononucleosis, and alcoholic
cirrhosis. Moderate-to-high levels ranging from 5 to 10 times normal
indicate Duche nne muscular dystrophy, dermatomyositis, and chronic
hepatitis, along with prodromal and resolving stages of diseas es. Low-to-
moderate levels  of 2 to 5 times normal may show hemolytic anemia,
metastatic liver tumors, acute pancreatitis, pulmonary emboli, alcohol
withdrawal syndrome, fatty liver, and the first stages of biliary duct
obstruction. THE SERUM  BILIRUBIN  LABORA TORY TEST
The laboratory test for serum bilirubin, the main product of hemoglobin
catabolism, is a measurement of bile pigment which indicates the state of
health of the liver and gallbladder. After being formed in the retic-
uloendothelial cells, bilirubin is bound to albumin and then transported to
the liver, where it’s conjugate d with glucuronic acid to form bilirubin
glucuronide and bilirubin diglucuronide. These two compounds are then
excreted in bile. Measurement of indirect or prehepatic (unconjugated)
bilirubin helps to evaluate hepatobiliary and erythropoietic functions. The serum bilirubin laboratory test showing elevated levels often
indicates liver damage in which the parenchymal cells can no longer
conjugate bilirubin with glucuronide. Then indirect bilirubin reenters the
bloodstream. Also, an elevated reading alerts the health professional to the
possibility of severe hemolytic  anemia. This test aids in the differentialdiagnosis of jaundice, biliary obstruction, and dangerous levels of
unconjugated bilirubin. Normally in an adult, indirect serum bilirubin measures 11 mg/d L or less;
direct serum bilirubin of less than 0. 5 mg/dL). Neonates have total serum
bilirubin ranging from 1 to 12 mg/dL; if elevated to 20 mg/dL (for them, it
indicates neonatal hepatic immaturity or congenital enzyme deficiencies. An exchange blood transfusion may then be required. If readings of bilirubin are elevated for adults, the test advises about the
possibility of autoimmunity or transfusion reaction, hemolytic or pernicious
anemia or hemorrhage, and hepatocellular dysfunction perhaps from viral
hepatitis. Needl ess to say, elevated levels of direct conjugated bilirubin
usually show biliary obstruction with overflows into the bloodstream. Intrahepatic biliary obstruction may come from viral hepatitis, cirrhosis, or
chlorpromazine reaction. Extrahepatic obstruction may come from
gallstones, gallbladder cancer, pancreatic cancer, or bile duct disease. THE SERUM  GAMMA -GLUT AMYL  TRANSPEPTIDASE  (GGT) L ABORA TORY
TEST
The laboratory test for serum gamma-glutamyl transpeptidase (GGT) is a
measurement of obstructive jaundice in neoplastic liver disease, and it’s
also useful for the detection of excessive alcohol consumption. The GGT
enzyme is sensitive to drug use and detects alcohol ingestion; therefore, it’s
used to determine compliance with alcoholism treatment. It also helps in the
diagnosis of obstructive jaundice and liver cancer. The normal range for GGT varies with age in males but not in females. For men ages 18 to 50 it varies between 10 and 39 U/L. Older than that,
males show a GGT range from 10 to 48 U/L. The normal range in women is
6 to 29 U/L. Elevation signals a cholestatic liver process. Note: The immune-stimulating effect of the Gerson Therapy frequently
causes a rise in GGT blood levels. THE ACID PHOSPHA TASE LABORA TORY TEST
The laboratory test for acid phosphatase is a measurement of the prostatic
and erythrocytic  isoenzymes to detect cancer. Active at a pH of 5, the twophosphatase enzymes appear in the liver, spleen, red blood cells, bone
marrow, platelets, and prostate gland. Successful treatment for prostate cancer decreases acid phosphatase
levels. Its normal values range from 0 to 1. 1 Bodansky units/mL; 1 to 4
King Armstrong  units/mL; 0. 13 to 0. 63 Bessey-Lowery-Broc k units/mL;
and 0 to 6 U/L in S1 units. Normal range of radioimmunoassay results is 0
to 4. 0 ng/mL. An elevated prostatic acid phosphatase test indicates Paget’ s disease,
Gaucher ’s disea se, multiple myeloma, and a tumor that has spread beyond
the prostatic capsule. If metast asized to bone, the high acid phosphatase
level accompanied by a high alkaline phosphatase shows increased
osteoblastic activity—metastatic bone cancer. THE ALKALINE  PHOSPHA TASE (AP) L ABORA TORY TEST
An enzyme that is most active  at pH 9. 0, alkaline phosphat ase (AP)
influences bone  calcification and the transport of lipids and metabolites. The alkaline phosphatase laboratory test measures combined activities of
those AP isoenzymes found in the liver, bones, kidneys, intestinal lining,
and placenta. Bone and liver AP are always present in adult blood serum,
with liver AP most prominent—except during the third trimester of
pregnancy when the placenta originates half of all AP
The AP laboratory test is particu larly sensitive to mild biliary obstruction
and indicates liver lesions. Its most specific clinical application is in the
diagnosis of metabolic bone disease and detecting skeletal diseases
characterized by osteoblastic activity and local liver lesions causing biliary
obstruction such as tumor or abscess. It furnishes supplemental information
for liver function studies and GI enzyme tests, and it assesses the response
to vitamin D treatment in rickets. The normal range of serum alkaline phosphatase varies in accordance
with the laboratory method employed, but the usual total AP levels range
from 30 to 120 U/L in adults and from 40 to 200 U/L in children. Since AP
concentrations rise during active bone formation and growth, infants,
children, and adolescents normally show levels three times higher than
adults. Additional normal range s for AP are 1. 5 to 4 Bodansky  units/dL; 4to 13. 5 King-Armstrong units/d L; 0.
A soft composition powder mixed with water, applied as a mud pack to an inflamed body part to absorb toxins and aid in detoxification.
What is the purpose of a clay poultice?
The text does not provide specific information on normal calcium levels for children, but it does mention that the Gerson Therapy typically lowers calcium levels.
What is the normal range for serum calcium levels in children?
The text does not provide a specific normal range for total serum cholesterol.
What is the normal range for total serum cholesterol?
The test is used to regulate homeostasis, osmotic pressure, and neuromuscular function, and to diagnose various diseases.
What is the purpose of the serum potassium test?
The test provides information about the internal workings of a person's body and is used to diagnose various diseases.
What is the purpose of the routine urinalysis test?