Volume 26, No. 1
January 2003
NUTRITIONAL PERSPECTIVES
_______________________________________________________________________________________
_______________________________________________________________________________________
EDITOR-IN-CHIEF
NUTRITIONAL PERSPECTIVES
Gary J. Post, D.C.
is published quarterly by the
ACA Council on Nutrition
ASSOCIATE EDITORS
Arthur A. Fierro, D.C.
G. R. Moon, D.C.
Jerrold Simon, D.C.
Juanee Surprise, D.C.
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COUNCIL OFFICERS
PRESIDENT
VICE PRESIDENT
EXECUTIVE SECRETARY
EXECUTIVE DIRECTOR
Dr. Juanee Surprise
1100 Dallas Drive, Suite 122
Denton, Texas 76205
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PAST PRESIDENT
Dr. Jerrold Simon
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Dr. J. Michael Flynn
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PRODUCTION
MANAGER
Bonnie Sealock
COUNCIL DIRECTORS
Dr. Mitchell Pearce
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The Council on Nutrition is dedicated to encouraging and promoting a more advanced knowledge and use of nutrition in the
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Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
Contents
Guest Editorial
Juanne Surprise, R.N., D.C., D.A.C.B.N., D.A.A.P.M., C.C.N., F.A.C.C.N.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 3
Rational For Nutritional Management of Osteporosis
George G. Junkin, D.C.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 5
Insulin/Cortisol Imbalances – The Place To Begin Nutritionally
When Dealing With The Chronically Ill Patient – Part II
Jeffrey Moss, D.D.S., C.N.S. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 13
Cellular Detoxification: The Chiropractic Perspective
James Adair, D.C., Steven Corcoran, D.C.,
Allen M. Kratz, PharmD and Jack Taylor, M.S., D.C., D.A.C.B.N.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 24
Nutritional Considerations in the Diagnosis and Treatment of
Attention Deficit Disorder
Michael J. Swiller, D.C., M.S., C.C.N., D.A.C.B.N.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 34
Seminar . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Pages 39-40
Guest Editorial
Juanee Surprise, R.N., D.C., D.A.C.B.N., D.A.A.P.M., C.C.N., F.A.C.C.N.
Here it is, the beginning of a New Year. The 29th for
your Council on Nutrition. It is time to remind everyone
that our annual meeting and seminar is scheduled from
April 24-27, 2003 in Washington DC. The main topic is
Longevity with emphasis on cardiovascular and cancer
detection and treatment. Also, the 4 mandatory ACBN
hours are part of the 20 available hours.
It is also time to remind everyone once again that membership in our parent organization, the American
Chiropractic Association, is necessary to be a voting member of the Council on Nutrition. So, with election ballots to
be mailed and returned before the seminar and other critical, upcoming business to conduct at our meeting on
Friday, April 25, it is time to make sure you have current
membership in both organizations. If you are not sure about
your membership status in the Council, call Bonnie at 540-
635-8844 and, for the ACA, call 800-986-4636. If you are
not currently an ACA member and dollar amount is an
issue, please call me at 972-292-1434. I will help you
obtain a lower 1st year new member rate!
The entire Executive Board and Appointed Directors
want to extend a personal invitation and request for each of
you to attend the meeting and seminar. In addition to the
obvious education, the camaraderie and sharing of information on the informal level is food for the soul of each of
us who practice nutrition. Remember, the success of our
seminar is critical to the financial well being of our Council
and your participation helps ensure success. Attendance is
a win for you and a win for the Council!
We wish you a happy, healthy and successful New Year
and look forward to seeing you in April.
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
January 2003
3
Rationale for Nutritional Management
of Osteoporosis
George G. Junkin, D.C.
TREATMENT OF THE OSTEOPOROTIC PATIENT WITH NUTRITION can be a challenge since there are so many nutrients
and metabolic processes involved in the health of bone tissue. This article is first a summary of the various causative metabolic processes involved with osteoporosis. Next, the medical options with prescription drugs are examined. The final section
will cover the basis for nutritional management of this condition.
Osteoporosis is not a disease per se, but the end result of
severe prolonged bone loss. It is a disorder of bone metabolism that causes a loss of bone mass from the skeleton, with
subsequent weakening of bone. Approximately 25 million
Americans have this condition and the annual cost of medical care is about 10 billion dollars.2, 3, 21 The U.S. Bureau
of Census has estimated that by the year 2050 21.7% of the
American population will be older than 65. Since our population is aging, there will be a proportionate increase in the
number of cases and the cost to treat this condition. Numerous research studies yielded very positive findings that
dietary and lifestyle changes can prevent and treat osteoporosis.
Bone tissue is a dynamic structure which is in a constant
state of change, always breaking down and reforming. This
process is carried out by specialized bone cells, the osteoclasts and the osteoblasts. The osteoclasts, or bone
breakers, dismantle the minerals and protein layers that
make up the bone. The osteoblasts secrete the protein
matrix, collagen, proteoglycans, and glycoproteins onto the
surface of the bone. The osteoclasts and osteoblasts are the
gatekeepers of the body’s calcium.8 The body’s calcium
needs are immense, including nerve pathways, blood clotting, hormone regulation, and initiation of numerous nerve
pathways. Hormones communicate to the gatekeepers, the
osteoclasts and osteoblasts, when the body’s calcium and
mineral balance needs to change according to the body’s
need for calcium.
HORMONAL CONTROL OF BONE DENSITY
Estrogen is the most important hormone associated with
primary osteoporosis. Women normally reach menopause
between the ages 48 to 52. With the drop in estrogen, the
rate of bone loss peaks at 3 to 5 percent per year for the
next 5 to 10 years. Estrogen is manufactured from cholesterol and this is one reason a low cholesterol level is not
advisable. Estrogen has an indirect effect on bone resorption by interfering with the parathyroid hormone. Estrogen
causes a decrease in the rate of bone breakdown by binding
to receptors on the osteoclast cells and this interferes with
their activity.
Parathyroid hormone (PTH) is secreted into the circulation if the calcium blood levels drop even the slightest
amount. Under normal conditions the calcium concentration
in the extracellular fluid rarely varies more than 5 percent.
This hormone increases the bone resorption activity of the
osteoclast, resulting in an increased level of blood calcium.
Also PTH increases the production of the active form of vitamin D, calciferol, which will elevate blood calcium.6, 13, 26
Vitamin D is obtained from food and thru exposure to
sunlight. The ultraviolet light changes dihydrocholesterol
into vitamin D. If the blood calcium levels drop, parathyroid
hormone is secreted which causes the kidneys to increase the
conversion of vitamin D to calciferol, its active form. Calciferol acts on the intestines to increase calcium absorption and
on bone to increase break down and resorption.7, 10, 13
Calcitonin is a hormone secreted by the parafollicular
cells of the thyroid in response to hypercalcemia. This hormone decreases the activity of the osteoclasts and increases
the activity of the osteoblasts resulting in a decreased bone
resorption. Also the kidneys respond with increased calcium excretion.
IMMUNE SYSTEM AND BONE DENSITY
Research indicates that osteoporosis can be the result of
an autoimmune disorder via cytokines, protein messengers
that affect the skeletal and immune system regulating the
development of osteoporosis. Estrogen deficient postmenopausal women are found to have high levels of a
cytokine, interleukin-1, which seems to promote bone loss
by stimulating the activity of the osteoclast. Increasing the
estrogen levels protects the bone by decreasing the interleukin-1, which decreases the osteoclastic activity.6
Simultaneously, the cytokine gamma interferon is stimulated by estrogen and osteoblastic activity is increased
helping to build bone.27
Other proinflammatory cytokines that have been found
to be involved with osteoporosis and the autoimmune
response are interleukin-8, interleukin-1, and interleukin-6.
IL-8 assists in the communication between parathyroid hormone and the osteoclast, directing them to break down
bone. It has been found that Vitamin D has a calming effect
on the proinflammatory IL-1. Interleukin-6, which
increases the activity of osteoclasts is shown to reduce with
consumption of soy products.22, 27
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
January 2003
5
Rationale for Nutritional Management of Osteoporosis
Nitric oxide, which macrophages normally release during periods of inflammation and infection, act as a
neurotransmitter in the nervous system. Nitric oxide in low
concentrations inhibit the osteoclast, but in high concentrations nitric oxide stimulates osteoclast to break down bone.
Pycnogenol from pine bark can significantly decrease nitric
oxide production and help with osteoporosis. Also ipriflavone from soy products decreases nitric oxide activity.27
Research has uncovered several plant compounds that
help to reduce the activity of the inflammatory cytokines. If
the level of Vitamin E drops too low, this allows interleukin-6 to increase, which promotes osteoporosis by
increasing the activity of the osteoclast. Quercetin is an
antioxidant of the bioflavinoid family shown to inhibit the
induction of interleukin-8.18 Curcumin, also known as
tumeric, has powerful anti-tumor, anti-oxidant, and antiinflammatory effects that have been shown to decrease the
activity of the inflammatory cytokines, especially IL-1 and
IL-8. Bosellia has powerful anti-inflammatory and antiarthritic effects which inhibit pro-inflammatory
prostaglandins. (The omega-3 fatty acids, derived from fish
oils or algae, reduce the activity of IL-1 and IL-6, as well as
the pro-inflammatory prostaglandins.27)
LIFESTYLE FACTORS
Secondary osteoporosis can be avoided through several
lifestyle and dietary modifications that can be accomplished with good old fashioned willpower. An increase of
calcium from 400 mg to 800 mg per day can decrease bone
loss. The RDA is 1200 mg per day for men and women,
and 1500 mg for a postmenopausal woman treating for
osteoporosis. Smoking is known to inactivate estrogen and
create a relative estrogen deficiency. Caffeine levels that are
high, more than two cups of coffee per day, cause the body
to excrete enough calcium and other minerals to stimulate
bone break down. Excessive alcohol intake can lead to
decreased vitamin D metabolism via liver damage. Alcoholics also tend to be malnourished and do not get adequate
intake of bone essential minerals.13
MEDICAL MANAGEMENT
The traditional treatments for osteoporosis that have
been developed by the medical profession usually have
supplementation with calcium and vitamin D. Weight bearing exercise is generally recommended to increase bone
density according to Wolf’s Law. Prescription drugs are the
standard choice of therapy by the allopathic profession, but
most all have health risks and side effects.
Estrogen is a widely prescribed hormone to postmenopausal women which is proven to reduce bone loss.
Studies have shown a reduction of hip fractures by fifty per-
cent. The downside is considerable in that it causes a much
higher risk for cancer of the endometrium and twice the
incidence of breast cancer. Also, women on estrogen are
two to three times more likely to have blood clots in the
deep veins which can result in a pulmonary embolism.13
Studies in the 1970’s showed an increased risk for uterine
cancer if taken alone, but if taken with progesterone the risk
was decreased. The problem with adding progesterone is
that it causes an increase of LDL with a decrease of the
good HDL cholesterol level.4
Calcitonin, which requires a prescription, which helps
with bone density by increasing the absorption of calcium
and phosphorus from the blood and increases bone mineralization. Another action is that it binds to the osteoclasts
and renders them ineffective. Synthetic calcitonin is derived
from salmon, and is actually more effective than the body’s
own calcitonin. Calcitonin is administered in two forms:
the first is a nasal spray which can cause nose bleeds and
itching; and the second is injectable which can cause nausea and flushing. Also, calcitonin can cause secondary
hyperparathyroidism which will increase PTH and result in
the opposite effect, increased bone loss.4, 8
Fosamax, a trade name for alendronate (a group of compounds called biphosphonates), is the only non-hormonal
preparation in tablet form. Fosamax has been shown to
increase bone density in the hip by seven percent and prevent fractures of the long bones and vertebrae. As with
most medications there are unwanted side effects that
include gastrointestinal disturbances with nausea and constipation as well as irritation of the lining of the esophagus
and the stomach. This compound can collect in the bones.8
Raloxifene is a prescription drug that stops bone loss and
increases bone density without increasing breast cancer
rates. It also lowers cholesterol and enhances the mood of
postmenopausal women. Once again there are side effects
in that it increases hot flashes and can cause blood clots.8
Several experimental drugs being tested have shown
similar results in the ability to increase bone density, but
they also have unwanted side effects. Sodium fluoride has
the ability to elevate the number of osteoblasts, but creates
a poor quality of bone tissue which is brittle and actually
increases the risk of fracture.17 Also, this substance causes
gastrointestinal disturbances and may cause bone cancer.8
Calcitrol, 1,25 dihydroxy-vitamin D, has the ability to
increase calcium absorption and therefore blood calcium
levels, but can result in kidney stones. Tamoxifen has beneficial effects on bone similar to estrogen, but increases the
risk of uterine cancer.27
DIET AND BONE
To get the most out of a treatment regimen for osteo-
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
January 2003
7
Rationale for Nutritional Management of Osteoporosis
porosis, the dietary influences on calcium availability must
be fully understood with consumption of carbohydrates and
sugars. Too much simple sugar in the diet will cause excretion of calcium in the urine. The average American
consumes 150 grams per day. Fiber, an indigestible form of
carbohydrate, can have positive or negative effects on calcium depending on if it is soluble or insoluble. Soluble
fibers such as oats, legumes, apples, and citrus fruits
enhance absorption of calcium and magnesium by slowing
the digestive tract. On the other hand, insoluble fiber, such
as wheat, wheat bran, flax seed, psyllium husks and other
grains speed the movement of food through the intestines
which makes calcium less available.5, 7, 17 Green vegetables
that contain oxalic acid which binds to calcium and prevents absorption. So calcium should not be taken with
spinach, Swiss chard, beet tops, and rhubarb. Also legumes
are high in phytic acid that bind with calcium and prevent
absorption.1
For optimum bone health, the intake of dietary oils and
fats should be monitored, since large quantities increase
calcium excretion and inhibit the absorption of calcium
from the gastrointestinal tract. Findings are that saturated
fats bind calcium and other minerals, and form insoluble
compounds which can not be absorbed. Saturated fats will
also bind with vitamin D, which will further inhibit absorption of calcium.12 Another problem is that too much fat
raises LDL cholesterol, which inhibits production of certain enzymes associated with bone formation.
It is generally accepted that the protein content of the
American diet is too high, with an average intake of over
100 grams per day. The RDA for a male weighing 174lbs
is 63 grams per day and for a woman at 138lbs is 50 grams
per day. This is calculated at .08 grams per kilogram of
body weight. The breakdown of this excessive level of protein leaves highly acidic by-products in the body. Since the
body wants to maintain a balance between the acid and
alkaline levels, it mobilizes the alkaline compound bicarbonate, which is taken from the bone, and calcium is then
lost via the urine.7, 8, 12, 20
Research has found that isoflavone, a phytoestrogen that
is abundant in soy products, can reduce the risk of osteoporosis. The chemical structure of isoflavone is very similar
to estrogen and this allows it to compete for receptor sites
that estrogens fill.11 Isoflavones appear to enhance bone
growth by boosting the activity of the osteoblasts and
increasing the production of bone matrix proteins. One
study showed that genistein, a type of isoflavone, inhibits
the activity of nitric oxide which causes a decrease in the
activity of the osteoclast and therefore resorption of bone.
Also, it is known to decrease the loss of minerals from
bones that occurs when the diet is deficient in calcium and
vitamin D. The rates of osteoporosis are much lower in
8
Japan where the intake of soy products are 30 to 50 grams
per day as compared to the U.S. intake of 3 grams per day.
Isoflavone can be synthesized into a supplement, which is
then termed ipraflavone. Studies found that ipraflavone
inhibited parathyroid hormone-, vitamin D-, PGE2-, and
interleukin-1 stimulated bone resorption.19
One of the most important dietary influences on bone,
calcium, can be obtained from several sources. Milk products are high in calcium, but with pasteurization denaturing
its usefulness and the fact that many people are lactose
intolerant, other sources should be considered. One cup of
dark green leafy vegetables has almost as much calcium as
a cup of milk, and sea vegetables are higher. Other good
alternatives are rice and soy milk which have as much calcium as milk.
Coffee can have a detrimental effect on calcium levels
and is found to decrease blood calcium levels by increasing
calcium excretion.11 Coffee is found to increase the secretion of parathyroid hormone which stimulates bone
breakdown. Also, coffee works to decrease the available
male testosterone which can lead to an increased risk for
osteoporosis in the male. It is recommended not to drink
more than one or two cups per day.
Carbonated soft drinks should be avoided if concerned
with osteoporosis, since they contain phosphorous in the
form of phosphoric acid, a preservative. If the blood levels
of phosphorous exceed the ideal serum levels of the calcium to phosphorous ratio, which is 2.5 to 1, the body
reacts by breaking down bone to release calcium into the
blood. Also, high phosphorous levels suppresses vitamin D
which is needed for absorption of calcium. Other food
sources that are high in phosphorous are restructured meat
products, dairy products, and fish.3, 6, 7, 17
The ingestion of alcohol should be held to one or two
drinks per day if treating osteoporosis. High intake of alcohol has been associated with numerous health issues, but
relative to bone density there are several ways it can impact
your health. The most direct route is that it increases the
rate of bone resorption by stimulating the activity of the
osteoclast.4 There are several mechanisms that are interrupted that magnesium is involved with, since too much
alcohol will increase the excretion of magnesium.7 Most
alcoholics tend to be malnourished and are deficient in
essential nutrients needed for bone. Also chronic alcoholism can damage the liver which can effect the Vitamin
D pathway and ultimately calcium absorption.13
NUTRITIONAL SUPPLEMENTATION
Supplementation with calcium is the foundational building block in a nutritional protocol for osteoporosis, but we
must remember it is only one substance in a whole range of
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
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Rationale for Nutritional Management of Osteoporosis
factors affecting bone health. This is brought to light since
it has been found that in several cases of osteoporosis there
is no evidence of calcium depletion.16 One study indicated
that if the body’s loss of calcium during the first five years
of menopause is more than 15 percent, then calcium intake
will be ineffective at stopping bone loss. Building peak
bone mass with adequate calcium intake prior to
menopause is crucial to this period of accelerated bone
loss.34 Various studies have revealed that supplementation
at levels of 1,000 to 1,500 mg per day can help reduce bone
loss by 30 to 50 percent. A 1998 study in the Calcified Tissue International Journal showed that calcium
supplementation of 1,000 mg per day suppressed bone
breakdown by decreasing blood levels of the parathyroid
hormone. For best absorption use chelated calcium which
is bound to an amino acid or carbohydrate. Research indicates that dosing in the evening produced the best result.
Magnesium is a critical ingredient in bone health. It is
found to increase soft bone mineralization. Magnesium
prevents bone fragility by destabilizing the hydroxyapatite
crystals, and works synergistically with ATP to stabilize
amorphous calcium phosphate and prevent hydroxyapatite
formation. Magnesium helps to activate the bone building
osteoblasts. It facilitates the normal functioning of the
parathyroid glands and enhances the sensitivity of bone tissue to PTH and active vitamin D. Another important
function is that it facilitates the transportation of calcium in
and out of bone.22 The normal blood level ratio of calcium
to magnesium should be 5 to 1. Magnesium can be
obtained from the following food sources: brown rice,
buckwheat, corn, dandelion greens, dark green vegetables,
legumes, nuts, rye, sunflower seeds, sesame seeds, pumpkin seeds, wheat germ, and whole grains cereals.11
Vitamin D is an important nutrient for bone metabolism
which enhances calcium absorption in the intestines and
decreases its excretion via the kidneys. The human body
will manufacture an adequate supply with fifteen minutes
of sunlight per day, but the elderly, a high risk group for
osteoporosis, may not get enough exposure to supply their
need. Therefore, dietary supplementation may be necessary, but since Vitamin D can be toxic, a person should not
take more than 800 IU per day. The RDA for vitamin D is
200 IU, with a therapeutic dose of 400 to 800 IU per day.16
Food sources for vitamin D include: butter, cheese, egg
yolks, fish liver oils, herring, mackerel, oysters, salmon,
fortified cereals and milk.11
Vitamin K is a group of compounds, K1 (phylloquinone) derived from food, K2 (menaquinone) made from
bacteria in the intestines, and K3 (menadione) a synthetic
compound, which are cofactors in the synthesis of y-carboxyglutamic acid (Gla) residues in proteins.9, 24
Osteocalcin is a noncollagen Gla protein produced by the
10
osteoblasts, and is believed to be the first step in bone mineralization. Decreased levels of osteocalcin in blood have
been reported in postmenopausal women with hip fractures
and can indicate a deficiency of Vitamin K. It has also been
shown that vitamin K supplementation increases the serum
markers for bone formation (including osteocalcin and
bone alkaline phosphatase) and may decrease urinary calcium and hydroxyproline. The RDA for vitamin K is 150
mcg per day. Food sources for vitamin K include: broccoli,
brussel sprouts, cauliflower, garbanzo beans, dairy products, eggs, kale, seeds, olive and canola oil.27
Boron is an essential trace element necessary for the
conversion of Vitamin D to its active form. It also helps to
activate estrogen, and is shown to markedly increase blood
concentration of 17-beta-estradiol. The RDA for boron is 3
to 5 mg per day. Food sources include: apples, beet greens,
broccoli, cabbage, cherries, grapes, legumes, nuts, peaches,
pears.27
Silicon is an essential trace element that is needed for
bone development when the protein matrix is under construction. Studies indicate that silicon increases bone
mineralization thru its role in the formation of apatite crystals, the primary constituent of bone. There is no RDA for
this trace element, but 25 to 50 mg per day is suggested.
Silicon can be found in a variety of whole unprocessed
foods, but is deficient in today’s modern diet. Food sources
include the following: asparagus, cabbage, cucumbers, dandelion greens, lettuce, mustard greens, olives, parsnips,
radishes, white onions and whole grains.27
Zinc is an important mineral that is found in its highest
concentrations in the prostate, eyes, liver and bone. In
regard to bone it has a direct effect on osteoblastic activity,
the production of collagen and chondroitin sulfate, and is a
component of alkaline phosphatase. Insulin-like growth
factor 1 (IGF1) is a critical regulator of bone formation,
remodeling, and calcium homeostasis. Recently it has been
shown that zinc is the main regulating factor in blood levels
of insulin-like growth factor.14 It regulates secretion of calcitonin from the thyroid gland. Studies have found that
postmenopausal women secrete more zinc than other
women and that they should take 30 to 60 mg of chelated
zinc a day. Recent studies indicate that zinc is a highly
potent and selective inhibitor of osteoclast bone resorption
even at very low concentrations. Good food sources of zinc
are brazil nuts, oats, oysters, peanuts, pecans, pumpkin
seeds, rye, and split peas.
Approximately 19 percent of the body’s total copper is
found in the skeletal system. It contributes to the immune
function, artery function, protects against oxidation, inflammatory diseases and bone health. Copper is a cofactor for
lysyl oxidase and is required for incorporation of collagen
and elastin into the organic component of bone.16 Copper
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
Vol. 26, No. 1
Rationale for Nutritional Management of Osteoporosis
affects bone metabolism by inducing low bone turnover by
suppressing activity of the osteoclasts and by contributing
to the bone matrix.8 Food sources for copper include the
following: buckwheat, crab, liver, mushrooms, peanut butter, seeds, nuts, split peas, and olive oils.
A 1997 study in the Journal of Epidemiology and Community Health revealed over a ten-year period that women
taking Vitamin C had a higher bone density. An interesting
finding was that vitamin C from food sources did not have
any affect. Recommendations for treatment for osteoporosis is 500 to 1,000 mg per day.
NUTRITIONAL SUMMARY
A specific summary of all the necessary steps to meet
the nutritional and lifestyle treatment and prevention of
osteoporosis is as follows:
1. Avoid excess protein, average of 50 to 63 grams per
day.
2. Reduce caffeine, especially coffee.
3. Reduce sugar.
4. Moderate alcohol consumption.
5. Stay active, especially weight bearing exercise.
6. Quit smoking.
7. Consume more soy products.
8. Increase calcium and other minerals.
9. Estrogen replacement formula—Ipriflavone 600
mg per day and isoflavones 100 mg from soy.
10. Bone building formula—calcium citrate 1,000 to
1,500 mg per day;
Vitamin D 400 mg per day;
Vitamin K 150 mg per day;
Boron 3 mg per day;
Zinc 30 mg per day;
Copper 3 mg per day;
Silicon 25 mg per day;
Vitamin C 500 to 1,000 mg per day.
As a chiropractor, many patients will seek out your help
with what they perceive as a backache, and upon further
evaluation, osteoporosis may be uncovered as a contributing factor to their condition. It will be your job to inform
your patient of their options for treatment, and the ramifications of such. In light of the information that has been
presented concerning a medical versus a nutritional man-
agement of this condition, it is apparent that nutritional
management should be utilized for a more favorable outcome.
REFERENCES
1. Aloia, John F. Osteoporosis: “A Guide to Prevention
and Treatment.” Champaign, Illinois, 1989.
2. Brewer, Earl J. The Arthritis Sourcebook. Chicago, Illinois, 1993.
3. Calvo, Mona S. Dietary Considerations To Prevent
Loss Of Bone And Renal Function. July 8, 2000, pp.
564-566.
4. Cooper, Kenneth H. Preventing Osteoporosis. New
York, 1989.
5. Coudray, C. Effect Of Soluble Dietary Fibres Supplementation On Absorption And Balance Of Calcium,
Magnesium, Iron, And Zinc, In Healthy Young Men.
European Journal of Clinical Nutrition, February 17,
1997, pp. 375-380.
6. Gallagher, Christopher J. The Role Of Vitamin D In
The Pathogenesis And Treatment Of Osteoporosis.
Journal of Rheumatology, Vol. 23, 1996, pp. 15-18.
7. Heaney, Robert P. Calcium Nutrition And Bone Health
In The Elderly. The American Journal of Clinical
Nutrition, November 1982, pp. 986-1013.
8. Kessler, George J. The Bone Density Diet: “6 Weeks
To A Strong Body And Mind.” New York, 2000.
9. Knapen, Marjo H.J. The Effect Of Vitamin K Supplementation On Circulating Osteocalcin (Bone Gla
Protein) And Urinary Calcium Excretion. Annals of
Internal Medicine, December 15, 1989, pp. 1001-1005.
10. Leboff, Meryl S. Occult Vitamin D Deficiency In Postmenopausal US Women With Acute Hip Fracture.
JAMA, April 28, 1999, pp. 1505-1511.
11. Nelson, Miriam E. Strong Women, Strong Bones:
“Everything You Need To Know To Prevent, Treat,
And Beat Osteoporosis.” Canada, 2000.
12. New et al. Nutritional Influences On Bone Mineral
Density: “A Cross sectional Study In Premenopausal
Women.” American Journal Of Clinical Nutrition, January 31, 1997, pp. 1831-1838.
13. Notelovitz, Morris. Stand Tall! “The Informed
Woman’s Guide To Preventing Osteoporosis.” Canada,
2000.
14. Ovesen, Janne. The Positive Effects Of Zinc On Skeletal Strength In Growing Rats. Bone, Vol. 29, No. 6,
December 2001, pp. 565-570.
15. Papanicolaou, Dimitris A. The Pathophysiologic Roles
Of Interleukin–6 In Human Disease. Annals of International Medicine, Vol. 128, No. 2, January 15, 1998,
pp. 127-134.
Contined on page 22
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
January 2003
11
COMMENTARY
Insulin/Cortisol Imbalances – The Place to Begin Nutritionally
When Dealing with the Chronically Ill Patient – Part II
Jeffrey Moss, DDS, CNS
IN PART I OF THIS SERIES I concluded with one of the more highly publicized relationships between dysinsulinism and disease, the connection between cardiovascular disease (CVD) and insulin resistance, which has been classically referred to as
“Syndrome X.” However, I should note that, while volumes have been written during the last ten years or so on this relationship, if dysinsulinism were only significant in relation to CVD, I probably would not be writing this series. For, in reality, I feel
that there is little more I can add to all that has already been stated. The main reason I am writing about insulin metabolism
is that I am finding that chronically ill patients with obvious problems with insulin management are presenting with a whole
lot more than just signs and symptoms that relate to CVD. As you are probably well aware, they are presenting with a sometimes bewildering array of clinical findings ranging from fatigue to gout to constipation to reproductive disorders and
everything in between. What I am trying to demonstrate to you in this series is that there are virtually no chronic ailments
that you will typically encounter in your practices that will not be related to insulin/cortisol dysregulation in some way. Furthermore, in many instances, simple methodologies using diet and supplementation can not only have far reaching effects in
correcting dysinsulinism/cortisol dysregulation but will, more often than not, have a significant positive impact on the primary symptomatic picture, no matter what it may be. Therefore, based on this premise, issues relating to insulin/cortisol
metabolism (I will be explaining in future segments the role of cortisol and stress in dysinsulinism) or metabolic syndrome X
(MSX), the term I mentioned last issue, are foundational for almost all chronic illnesses. Finally, and maybe even more importantly, addressing these issues as your first course of action may very well transform a very complicated case into one that is
much easier to resolve.
HOMOCYSTEINE AND MSX
Since I concluded with CVD in part , I felt that an appropriate beginning to this discussion would be homocysteine,
which has been linked to CVD and a whole variety of other
chronic diseases. Of course, elevated homocysteine has
often been suggested as a primary cause of illness. However, in reality, could elevated homocysteine be secondary
to an even more primary issue, MSX? This question was
recently examined by Emoto et al1 in the paper “Impact of
insulin resistance and nephropathy on homocysteine in type
2 diabetes.” In this paper the authors state:
“The present study clearly demonstrated
that…insulin resistance was an independent
determinant of plasma tHcy level in type 2 diabetes. Furthermore, this independent contribution
of insulin resistance to plasma tHcy level was also
found when the group of patients with type 2 diabetes was limited to those with normal renal
function.”
How does insulin resistance cause homocysteine elevations? Emoto et al1 comment:
“A few studies have demonstrated that insulin
may affect activities of enzymes involved in homocysteine metabolism, cystathione ß-synthase and
5,10 methylenetetrahydrofolate reductase, which
are the key enzymes of homocysteine transsulfation and remethylation pathways respectively.”
Before leaving this subject, though, it is important to put
the above mentioned findings into their proper perspective.
Please recall from the quote above that the individuals evaluated already were demonstrating significant metabolic
imbalances (They were type 2 diabetics). Would the same
relationship be noted in a healthy population? According to
Godsland et al,2 no. They state:
“These findings strengthen the possibility that in
healthy humans, homocysteine metabolism is not
substantially affected by insulin action.”
As you may recall, I have often stated that the results
from research performed on healthy people cannot necessarily be extrapolated to sick people. This certainly seems
to be the case in terms of the relationship between insulin
resistance and homocysteine. Therefore, if the person you
are treating is ailing, it is quite likely that any accompanying insulin resistance that is present can cause elevations in
homocysteine. However, if the individual is healthy, it
appears that the presence of insulin resistance alone will not
appreciably affect homocysteine levels.
GOUT AND MSX
The key factor in the pathogenesis of gout is elevations
in serum uric acid. Could the insulin resistance that is a key
factor in MSX play a role in causing these elevations? In
their study of this relationship, Vuorienen-Markkola and
Yki-Jarvinen3 state:
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Insulin/Cortisol Imbalances – The Place To Begin Nutritionally When Dealing With The Chronically Ill Patient – Part II
“…insulin resistance and hyperinsulinemia represent almost universal features of PCOS.”
is the best way to determine levels of free circulating
steroid hormones? While controversy still exists, more and
more research is suggesting that salivary measurement of
sex steroids is an excellent way of determining circulating
levels of free hormone. Of course, the typical serum test
measures both free and protein bound fractions. Therefore,
as you might deduce, if SHBG decreased but total levels
remained the same, it would be impossible to determine
from the typical serum steroid analysis whether the free
levels of androgen, which are crucial to the development of
PCOS, are elevated.
Before continuing, please note again from the above
quote by Yen,11 the word “obesity.” As you will see in the
discussion on underlying causes of MSX, disturbances in
fat metabolism play a major causational role. Of course, as
was noted above, PCOS can exist without obesity. However, Yen11 notes the following about obesity and PCOS:
Is saliva a valid way to measure levels of free steroid
hormones in women? As many of you know, the validity of
salivary cortisol measurement has been documented in several studies. However, as suggested above, salivary
measurement of free reproductive hormones in females is
much more controversial. Read and Walker14 state:
“PCOS is associated with peripheral insulin resistance and hyperinsulinemia, and the degree of
both abnormalities is amplified by the presence of
obesity.”
“The estimation of testosterone in the female
remains much more controversial. In the absence
of acceptable validation of immunoassays in
plasma samples which fall into the ‘female range’
i.e. <3mmol/L, consideration of the corresponding
saliva samples must be otiose at this time. Similarly, there is little consensus on the levels of
salivary oestradiol reached during the menstrual
cycle; nor is there compelling evidence that the
estimated concentrations accurately reflect the
circulating levels of either the plasma-free or
plasma-total levels.”
androstenedione. Chronic anovulation is associated with oligomenorrhea or amenorrhea and the
presence of bilateral polycystic ovaries on ultrasound examination. Obesity is common but not a
prerequisite for the development of PCOS because
50 percent of PCOS women are not obese.”
How common is the presence of insulin resistance and
hyperinsulinemia with PCOS? Nestler12 states:
How does dysinsulinism produce hyperandrogenism,
one of the more important abnormalities in PCOS? Nestler
states:13
“Hyperinsulinemia produces hyperandrogenism
in women with PCOS via two distinct and independent mechanisms: 1) by stimulating ovarian
androgen production, and 2) by directly and independently reducing serum sex hormone binding
globulin (SHBG) levels. The net result of these
actions is to increase circulating free testosterone
concentrations. It appears likely that an inherent
(genetically determined) ovarian defect needs be
present in women with PCOS, which makes the
ovary, either susceptible to, or more sensitive to,
insulin’s stimulation of androgen production.
Limited evidence suggests that hyperinsulinemia
might also promote ovarian androgen production
by
influencing
pituitary
release
of
gonadotrophins.”
Please note again that one way dysinsulinism promotes
hyperandrogenism is through the decrease of SHBG, the
primary binding protein for sex steroid hormones. This
statement carries tremendous clinical significance. For it
emphasizes the fact that the key issue is not the fact that
women with PCOS have elevated levels of circulating
androgens, but they have higher levels of circulating free
androgens. Why is this fact important? As you may recall
from your basic endocrinology courses, it is only the free,
as opposed to the protein-bound, fraction of steroid hormone levels that have any physiologic activity at all. What
16
However, other studies, most performed more recently,
have looked upon salivary analysis of estradiol and progesterone in females very favorably.15-18 The quote below by
Lu et al18 summarizes the attitudes of the above mentioned
researchers:
“Salivary measurements of estradiol and progesterone can be used as noninvasive methods for
assessment of ovarian function. Salivary specimens can be collected at home and brought to the
laboratory for analysis, obviating the need for frequent phlebotomy. The sensitivity and precision of
the salivary estradiol assay make it comparable
with assays of serum estradiol for assessing
changes in hormone levels.”
Is there a reason for these conflicting findings? One possible explanation has to do with the fact that some labs
collect the saliva by having the patient suck on a cotton roll.
In a recent study by Shirtcliff et al19 the following was
noted:
“Salivary assay results for testosterone, DHEA,
progesterone, and estradiol are artificially high,
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Insulin/Cortisol Imbalances – The Place To Begin Nutritionally When Dealing With The Chronically Ill Patient – Part II
and for sIgA artificially low, when samples are collected using cotton absorbent materials. In
contrast, results for salivary cortisol, DHEA-S,
and cotinine are not affected by the use of cotton
collection methods.”
Similar findings were reported by Kruger et al20 concerning 17-hydroxyprogesterone measurements. Why
might the cotton collection method be inaccurate? Kruger
et al20 suggest:
“We speculate that the cotton wool swabs contain
a material, possibly derived from the biological
source of the cotton wool, which cross-reacts with
the antibody in the assay or affects binding affinity.”
Therefore, those of you who have concluded that salivary hormone measurement has no value beyond cortisol
may want to re-examine the issue using a lab that does not
use a cotton-based collection system.
Before leaving this subject, a side note. Many have
reported substantial increases in salivary progesterone after
patients have used topical progesterone creams. This was
not a spurious finding or your imagination. O’Leary et al21
found in six premenopausal women after a single 64 mg
topical application of micronized progesterone a significant
rise in salivary progesterone but not serum or urinary progesterone.
Of course, whatever your view on the controversy concerning salivary hormone analysis, it cannot be denied that,
since SHBG levels decrease with PCOS, knowledge of free
hormone levels is extremely important for proper case
management. Furthermore, it should be noted decreases of
SHBG are not just a manifestation of PCOS. In fact,
decreased SHBG is almost universally found whenever
dysinsulinism exists. Hautanen 22 states:
“A positive association between SHBG and various measures of insulin sensitivity has been
demonstrated in both sexes, suggesting that
decreased SHBG levels may be one of the components of the metabolic syndrome.”
In addition, Nestler23 notes:
“More recently, as commented elsewhere, results
of in vivo studies suggest that insulin regulates
SHBG not only in obese women with PCOS but in
normal men and women as well. The results of
these studies suggest that regulation of SHBG
metabolism by insulin may be a generalized physiologic phenomenon, and that SHBG may serve as
a biological marker for hyperinsulinemic insulin
resistance in humans.”
In what other clinical situations might decreased SHBG
be evident? Hautenen22 points out:
“Clinical studies have shown that SHBG levels
decrease in puberty, obesity, hypothyroidism and
during androgen treatment…”
Given how frequent decreased SHBG and increased levels of free reproductive hormones are going to be present in
your patients, you may want to consider measuring serum
SHBG (Contact your local lab for availability) or salivary
reproductive hormones on a more regular basis. However,
if this is not possible or practical, it appears from the literature quoted above that if you just assume that these findings
exist in almost all your patients (Assuming my hypothesis
that universal presence of MSX is correct), you will probably be correct in the vast majority of instances.
Before leaving this section, I would like to briefly
address a thought that I assume is going through your
minds right now, that diet and lifestyle modifications
should be extremely helpful in alleviating many of the findings associated with PCOS. According to Yen,11 you would
be correct with this line of thinking. Just with caloric
restriction alone the following was noted:
“Improvement of endocrine-metabolic parameters occurs after 4 to 12 weeks of dietary
restriction; a twofold increase in SHBG is accompanied by a fall in free testosterone levels with
parallel changes in serum insulin and IGF-1 concentrations.”
Furthermore:
“In accord with these findings, weight loss in
obese PCOS patients is attended by a substantial
reduction of hyperandrogenism and a return of
the ovulatory cycle in 30 percent of patients.”
Can exercise be helpful? Yen11 points out:
“…when combined with dietary restriction, exercise serves as an important adjunct to therapeutic
success in PCOS patients.”
I will be discussing the use of diet, supplementation, and
other lifestyle interventions in much more detail concerning PCOS and other manifestations of MSX in the
concluding issue of this series.
OTHER FEMALE REPRODUCTIVE ABNORMALITIES
AND MSX
Gestational diabetes – Given the above, you would
expect that patients in this category would also demonstrate
lowered SHBG levels. As noted by Bartha et al,24 this,
indeed, is the case.
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Insulin/Cortisol Imbalances – The Place To Begin Nutritionally When Dealing With The Chronically Ill Patient – Part II
Hypertension and preeclampsia during pregnancy –
Several studies have found that insulin resistance is prevalent in this situation. In a review of the literature, Solomon
and Seely25 state:
“…insulin resistance may be involved in the
pathogenesis of pregnancy-induced hypertension
and that approaches that improve insulin sensitivity might have benefit in the prevention or
treatment of this syndrome…”
Endometriosis – In a reply to a letter to the editor Mathias and Franklin26 note:
“I also suggest that many of us have disease
because of eating too much of the wrong foods
resulting in cellular imbalance from the hypersecretion of insulin and an unbalanced eicosanoid
system. Endometriosis, in our experience, is one
such disease.”
NUTRIENT DEFICIENCIES AND MSX
intimate relationship with insulin metabolism. However, as
noted by Tosiello,29 this relationship is fairly complex.
Therefore, I would like to now present some highlights
from Tosiello’s excellent paper so that the relationship
between insulin and magnesium can be fully explained.
To introduce the relationship between magnesium and
insulin, consider these statements by Tosiello:29
“Low levels of magnesium can reduce secretion of
insulin by the pancreas.”
In addition:
“…magnesium deficiency has been shown to promote insulin resistance in multiple studies.”
Furthermore, the negative impact of magnesium deficiency on insulin resistance is not seen just in diabetic
patients:
“There is also evidence that magnesium deficiency
itself produces insulin resistance in normal subjects.”
Magnesium – Many Americans consume a diet that is
deficient in magnesium. As noted by Rude :27
How does magnesium deficiency cause insulin resistance? Tosiello29 suggests one intriguing theory:
“…with the consumption of more refined foods,
dietary intake of magnesium has been estimated
to fall below recommended levels in up to 75% of
subjects surveyed in the United States.”
“…a low erythrocyte magnesium content can
alter membrane viscosity, and this may impair the
interaction of insulin with its receptor on the
membrane.”
However, is the answer to the magnesium problem more
magnesium? Those of you who have experienced the frustration of gaining little or no improvement when
supplementing magnesium with patients who are suffering
from obvious magnesium deficiency related symptoms
might think the answer to this question is obvious. Could
the answer to some of the frustrations we have clinically in
managing magnesium homeostasis lie with MSX? To
answer this question, first consider this statement by
Humphries et al :28
However, the story of magnesium and insulin does not
end here. What makes this relationship even more interesting and more complicated is the fact that not only does
magnesium deficiency cause insulin resistance but insulin
resistance causes reduced magnesium uptake. Tosiello29
states:
“Disturbance in magnesium metabolism is widely
recognized in diabetes, a disorder commonly associated with magnesium deficiency. The incidence
of hypomagnesemia in diabetes mellitus has been
reported to be from 25% to 39%.”
Of course, it would be easy to say that the cause of the
above statistic is low dietary intake. However, while this is
probably the case in a certain amount of instances, anecdotal reports of a lack of clinical results with magnesium
supplements alone would suggest that there is more to this
issue than one of simple deficiency.
al28
and Tosiello,29
As suggested by both Humphries et
one of the key factors that is often overlooked in relationship to magnesium physiology is the fact that it has an
18
“…low levels of magnesium induce insulin resistance, which in turn attenuates magnesium
uptake by insulin-responsive tissues.”
Humphries et al28 elaborate on this issue:
“Both the intracellular magnesium concentration
and intracellular magnesium transport correlate
with insulin-mediated glucose uptake. Hence, the
intracellular accumulation of magnesium is
dependent upon insulin action. Intracellular magnesium deficiency may be the consequence of
insulin resistance, but the data of Paolisso et al
and Garland suggest that magnesium deficiency
may also worsen insulin resistance.”
Thus, as I hope you can see, a true vicious circle exists
where magnesium deficiency causes insulin resistance
which, in turn, causes magnesium deficiency.
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Insulin/Cortisol Imbalances – The Place To Begin Nutritionally When Dealing With The Chronically Ill Patient – Part II
Antioxidants – In individuals who were insulin resistant but not diabetic, Facchini et al30 found that insulin
resistance was related to depressed levels of plasma acarotene, b-carotene, lutein, a-tocopherol, and
d-tocopherol. Also, as you might expect, lower levels of
these antioxidants were correlated with elevated levels of
lipid hydroperoxides.
THE METABOLIC SYNDROME X: MUCH MORE
THAN JUST INSULIN RESISTANCE
Of course, you may now be thinking that the list of illnesses I have discussed so far falls way short of being
inclusive of virtually every clinical entity you might
encounter, which is the central premise of this series. This
brings me to a key point that has been mentioned but not
emphasized. Up to this point I have been primarily discussing illnesses that have been directly related to insulin
resistance. However, as I have suggested, MSX is much
more than just insulin resistance. As I have alluded, one of
the factors that makes MSX so damaging to human physiology is that insulin resistance never exists in isolation in
the chronically ill patient. Instead, insulin resistance will
always lead to hyperinsulinemia and visa versa. Lowe31
states:
“In individuals with glucose intolerance due to cellular resistance to insulin, insulin levels may be
elevated during the fasting state and after meals.
If as a result, the ability of the beta cells of the
pancreas to synthesize and secrete insulin becomes
impaired, diabetes mellitus results.”
Conversely, Wolever32 points out:
“Excess insulin secretion may eventually reduce bcell function due to amyloid deposition, leading to
raised blood glucose and further deterioration of
ß-cell function and insulin sensitivity via glucose
toxicity.”
Thus, Wolever32 makes the following, very appropriate,
observation:
“The metabolic syndrome represents a vicious circle whereby insulin resistance leads to
compensatory hyperinsulinemia, which maintains
normal plasma glucose but may exacerbate
insulin resistance.”
With the above in mind, I would now like to present
some thoughts on how hyperinsulinemia, independently of
insulin resistance, can create ill health. First, I would like to
discuss a fascinating hypothesis paper by Facchini et al,33
the title of which makes a bold and all-encompassing suggestion: “Hyperinsulinemia: The missing link among
oxidative stress and age-related diseases?” One way that
20
Facchini et al33 suggest that hyperinsulinemia leads to agerelated diseases has to do with an enzyme called
proteasome. What does this enzyme do? According to the
authors:
“Oxidized protein degradation is catalyzed by an
enzyme called proteasome.”
What is the relationship between insulin and proteasome? Facchini et al33 continue:
“…it is established that insulin’s major effect on
cellular protein turnover is inhibition of protein
degradation. Recent studies have clearly demonstrated that the major effect of insulin on cellular
protein degradation is in fact due to inhibition of
proteasome. Therefore, the higher the insulin levels, the lower the proteasome activity and,
presumably, the faster the accumulation of oxidized proteins.”
In addition, the authors suggest:
“…insulin may facilitate protein oxidation by
increasing steady-state levels of oxidative stress,
independently from hyperglycemia.”
How else might hyperinsulinemia create ill health? Facchini et al33 suggest the following:
1. “Since hyperinsulinemia appears to be interacting with size of body iron stores, there are
multiple mechanisms by which, either directly
or indirectly, it might accelerate the HaberWeiss reaction and generation of hydroxyl
radical.” (For those of you who are not familiar
with hydroxyl radical, you should know that it is
one of the most destructive, instantly reacting with
almost every substance it encounters.)
2. “Insulin also causes nitric oxide-mediated
vasodilation in skeletal muscle by stimulating
nitric oxide synthase…Nitric oxide in micromolar amounts, inhibits respiration and by rapid
reaction with superoxide anion, generates peroxynitrite. (Peroxynitrite is another very destructive
free radical.)
3. Finally, consider an in important point that has been
emphasized by many, including Sears:
“…it should be mentioned that insulin upregulates liver ▲6, ▲5-desaturase activity.”
Of course, as most of you know, activity of these
enzymes is important for prostaglandin formation. Could
over activity induced by hyperinsulinemia create problems?
This is exactly what Facchini et al33 suggest:
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Insulin/Cortisol Imbalances – The Place To Begin Nutritionally When Dealing With The Chronically Ill Patient – Part II
“The utility of such function might, however, be
offset by the greater susceptibility of n-6 longchain polyunsaturated fatty acids to peroxidation.
In fact, mitochondrial susceptibility to peroxidation was found to be increased by greater
desaturation of membrane fatty acids and postulated to play a role in explaining differences in
longevity of long- versus short-lived mammals
with similar basal metabolic rates.”
Finally, it should be noted that even with polycystic
ovary syndrome where, as was discussed above, insulin
resistance is clearly correlated, insulin resistance may not
be the actual factor that causes the deleterious imbalances
in sex hormones. Nestler 12 states:
“An important conclusion that can be drawn from
the above studies is that hyperinsulinemia is the
culprit that stimulates ovarian androgen production and suppresses serum SHBG in PCOS. That
is, it is not insulin resistance at the ovarian or
hepatic level that is pathogenic—rather, it is the
elevation in circulating insulin.”
Of course, even with hyperinsulinemia taken into
account, it still could be asserted that, based on what I have
presented so far, my hypothesis that MSX is a fundamental
cause of virtually all the chronic illnesses you see in your
practices has not been adequately supported. In reply, I
would say that this assertion is absolutely correct. Statements about insulin metabolism alone are not enough to
explain the all-encompassing effect of MSX. For MSX, as
you will see, is more, much more, than just insulin resistance and hyperinsulinism. What is the additional factor
that truly lends credence to the idea that MSX is epidemic?
For me, as the title of this series suggests, it is the combination of disturbances in cortisol metabolism and related
adrenocortical imbalances along with dysinsulinism that
makes MSX the potent negative force it is in today’s patient
population.
In part III of this series, I will show how adrenal dysfunction intertwines with disturbances in insulin
metabolism to make conditions such as PCOS, magnesium
deficiency, and a whole host of others not yet mentioned
increasingly common in your patients.
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1. Emoto M et al, Impact of insulin resistance and
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2. Godsland IF et al, Plasma total homocysteine concentrations are unrelated to insulin sensitivity and
components of the metabolic syndrome in healthy
men. J Clin Endocrinol Metab, 2001. 86(3): p. 719-23.
3. Vuorinen-Markkola H and Yki-Jarvinen H, Hyperuricemia and insulin resistance. J Clin Endocrinol
Metab, 1994. 78(1): p. 25-9.
4. Modan M et al, Elevated serum uric acid—a facet of
hyperinsulinemia. Diabetologia, 1987. 30(9): p. 713-8.
5. Chou P et al, Gender differences in the relationships of
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16. Bolaji II, Sero-salivary progesterone correlation. Int J
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17. Chearskul S & Visutakul P, Non-invasive hormonal
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1994. 77(4): p. 176-86.
18. Lu Y et al, Salivary estradiol and progesterone levels in
conception and nonconception cycles in women: evaluation of a new assay for salivary estradiol. Fertility
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20. Kruger C et al, Problems with salivary 17-hyroxyprogesterone determinations using the Salivette device. Eur
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21. O’Leary P et al, Salivary, but not serum or urinary levels of progesterone are elevated after topical
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2000. 53(5): p. 615-20.
22. Hautanen A, Synthesis and regulation of sex hormonebinding globulin in obesity. Int J Obesity, 2000. 24(7):
p. S64-S70.
23. Nestler, J.E., Insulin and ovarian androgen excess, in
Androgen Excess Disorders in Women, R. Azziz and
et al, Editors. 1997, Lippincott-Raven: Philadelphia. p.
473-483.
24. Bartha JL et al, Sex hormone-binding globulin in gestational diabetes. Acta Obstet Gynecol Scand, 2000.
79(10): p. 839-45.
25. Solomon CG & Seely EW, Brief review: hypertension
in pregnancy: a manifestation of the insulin resistance
syndrome? Hypertension, 2001. 37(2): p. 232-9.
26. Mathias JR & Franklin RR, Enteric nervous system
and Endometriosis-Connection? (Reply to letter to the
editor). Fertility and Sterility, 1999. 71(1): p. 182.
27. Rude RK, Magnesium, in Biochemical and Physiological Aspects of Human Nutrition, Stipanuk MH, Editor.
2000, W.B. Saunders Co.: Philadelphia. p. 671-685.
28. Humphries S et al, Low dietary magnesium is associated with insulin resistance in a sample of young,
nondiabetic black Americans. Am J Hypertension,
1999. 12(8): p. 747-756.
29. Tosiello L, Hypomagnesemia and diabetes mellitus.
Arch Intern Med, 1996. 156(11): p. 1143-1148.
30. Facchini FS et al, Relation between insulin resistance
and plasma concentrations of lipid hydroperoxides,
carotenoids, and tocopherols. Am J Clin Nutr, 2000.
72(3): p. 776-9.
31. Lowe JC, The Metabolic Treatment of Fibromyalgia.
2000, Boulder, CO: McDowell Publ.Co. p. 542.
32. Wolever TMS, Dietary carbohydrates and insulin
action in humans. Br J Nutr, 2000. 83(Suppl 1): p. S97S102.
33. Facchini FS et al, Hyperinsulinemia: The missing link
among oxidative stress and age-related diseases? Free
Rad Biol Med, 2000. 29(12): p. 1302-6.
Rationale For Nutritional Management of Osteoporosis Continued from page 11
16. Patrick, Lyn. Comparative Absorption Of Calcium
Sources And Calcium Citrate Malate Of Osteoporosis.
Alternate Medicine Review, Vol. 4, No. 4, 1999, pp.
74-85.
17. Sasaki, Satoshi. Association Between Current Nutrient
Intakes and BMD. At Calcaneous in Pre and Postmenopausal Women, Journal of Nutritional Science
and Vitaminology, January 9, 2001, pp. 289-294.
18. Sato, Motoyoshi. Quercitin, A Bioflavonoid, Inhibits
The Induction Of Interleukin 8 and Monocyte
Chemoattractant Protein-1 Expression By Tumor
Necrosis Factor-A In Cultured Human Synovial Cells.
The Journal of Rheumatology, February 21, 1997, pp.
1680-1683.
19. Sato, Yoshihiro. Effect Of Ipriflavone On Bone In
Elderly Hemiplegic Stroke Patients With Hypovitaminosis D1. American Journal of Medical
Rehabilitation, October-September 1999, pp. 457-463.
20. Seidner, Douglas L. Nutrition In Clinical Practice,
August 2000, pp. 163-170.
22
21. Siegel, Irwin M. All About Bone: An Owner’s Manual.
New York, 1998.
22. Sojka, J.E. Brief Critical Reviews “Magnesium Supplementation And Osteoporosis.” Nutrition Reviews,
Vol. 53, No. 3, March 1995, pp. 71-73.
23. Weaver, Connie M. Calcium And Magnesium Requirements Of Children And Adolescents And Peak Bone
Mass. Nutrition, Vol. 16, Nov. 7/8, July 8, 2000, pp.
514-516.
24. Cees, Vemeer. Bridgit L.M.G. Glisbers, Alexandra M.
Craciun, Monique M.C.L. Groenen-VanDooren and
Majo H.J. Knapen. Effects of Vitamin K on Bone Mass
and Bone Metabolism. American Institute of Nutrition,
1996.
25. Ipriflavone. Alternate Medical Review, Vol. 5, No. 3,
2000.
26. Guyton, Arthur C. Textbook of Medical Physiology,
1971.
27. Germano, Carl, RD, CNS, LDN. The Osteoporosis
Solution. Kensington Publishing Corp., 1999.
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
Vol. 26, No. 1
Cellular Detoxification: The Chiropractic Perspective
James Adair, D.C., Steven Corcoran, D.C.
Allen M. Kratz, PharmD and Jack Taylor, M.S., D.C., D.A.C.B.N.
A TOXIN IS ANY AGENT THAT IS CAPABLE OF A DELETERIOUS RESPONSE in a biologic system which can contribute to
premature aging.
Toxins that adversely effect humans come from a variety of sources: processed food, tap water, prescribed and
recreational drugs, working environments, our homes, the
air we breathe, amalgams in our teeth, even from our clothing and laundry detergents. Almost every known chemical
substance has the potential to produce cellular injury, which
might ultimately lead to death of the organism. As we enter
the new millennium, we have become more aware of the
constant challenge by compounds that are without nutritive
value. These foreign materials are both the by-products of
our modern industrial age, called xenobiotics (toxins capable of modifying biological systems) as well as toxins that
are generated by our own cellular catabolism.1
HEPATIC DETOXIFICATION
Xenobiotics biotransformed by the liver are released into
the intestine through the bile. The liver has at least seven
transport systems for active excretion of toxins into the
bile.2 These include glycination, glucaronidation, mercapturation, sulphation, sulphoxidation, methylation and
acetylation. Once the bile and its by-products enter the
intestine, they can either be reabsorbed or excreted. Reabsorption can lead to very long half-lives for xenobiotics.
Intestinal excretion of toxins often causes “loose” bowel
movements due to an increase in intestinal motility and a
reduced intestinal transit time. This observable clinical
effect suggests a higher rate of intestinal excretion of toxins
In this article we will explore various sources of xenobiwhich probably irritate the intestinal lining after bile secreotics and propose some ways to deal with them on a
tion to promote faster elimination. All body secretions are
cellular level.
able to excrete toxic byDIAGRAM 1
products which can be
retrieved in sweat, tears,
XENOBIOTICS AS
XENOBIOTIC DETOXIFICATION PATHWAYS
and breast milk.3
CELLULAR TOXINS
Xenobiotics are among
CELLULAR
the most damaging foreign
XENOBIOTIC
toxic substances, capable
Enzyme inactivation:
of modifying biological
Effects mitochondrial functions,
DNA repair, intracellular systems.
systems.2
They
are
ingested, inhaled and
absorbed through the skin.
Under ideal circumstances
(perfect health), the body
can eliminate most toxins,
performing the ongoing
task of detoxification. The
primary organ for detoxifiEND PRODUCTS
cation is the liver, and
OF XENOBIOTIC
many toxins must first be
Water soluble
Polar
biotransformed from fatAble to be
soluble to water-soluble
excreted/eliminated
compounds before they
via kidneys and/or bowels
can be excreted through
the bile and by the kidneys. This first phase of biotransformation produces abundant amounts of free radicals that
need to be buffered by intrahepatic and extrahepatic antioxidants systems. The new toxic by-products need to be dealt
with by Phase II liver detox processes, mostly conjugation
processes. First among them is the selenium dependent
gluthathione peroxidase enzymatic system. See Diagram 1.
24
energetic release
EXTRACELLULAR
XENOBIOTIC
Lipid soluble
Non-polar
Not readily excreted
PHASE I
Cytochrome P450 activity/Liver
PHASE I I
Conjugation/Liver
INTERMEDIATE
METABOLITES
Many disease states
are the result of the adaptive response of the body
to a toxic load. The
body’s attempt to adapt
and return to a state of
equilibrium or homeostasis depends upon its
ability to properly eliminate endogenous and
exogenous toxins. Failure to clear the body of
accumulating
toxins
leads, at some point, to
the balance shifting in
favor of the environment
and against the living
organism.4-
DIS-EASE VERSUS ILLNESS STATES
In the process to regain balance, “symptoms” of “disease” (maladaptive responses) might appear and should not
be dealt with by drugs aimed at eliminating symptoms. In
this phase, corrective measures dealing with the underlying
problem are more appropriate. The body’s natural correc-
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
Vol. 26, No. 1
Cellular Detoxification: The Chiropractic Perspective
tive cleansing measure can cause temporary discomfort.
Conventional drug treatments frequently interfere with the
important process of hepatic detoxification, often leading
to further intrahepatic and systemic recirculation of toxic
compounds. This might lead to illness states. Many autoimmune conditions may be the result of xenobiotic
retoxification. Toxins that should have been eliminated,
when reincorporated lead to accelerated free radical damage (oxidative stress). Oxidative stress on newly formed
tissues might lead to imperfect peptide formation. These
abnormal peptides are then recognized as foreign tissues by
our immune surveillance, creating the chain of events of
autoimmune disorders.5,6 Oxidative stress is also a major
factor in premature aging.
alarming report from the Environmental Protection Agency
demonstrating that 100% of samples of human body fat
contained toxic doses of chemicals including styrene (Styrofoam), 1,4-dichlorobenzene (moth balls, house
deodorizers), and xylene (paints, gasoline). See Table 1 for
this EPA study. Dr. Rea informs us that “over 300 foreign
chemicals have been identified in the ubiquitous adipose
tissue, which is especially high in the brain, as well as in
the liver. Every cell membrane contains buffering lipids.12
Where do these xenobiotics come from? Consider the
following discouraging statistics from another EPA publication, the 1989 Toxics Release Inventory National Report
from its Office of Toxic Substances:13
• 2,427,061,906 pounds of chemicals emitted into the
Factors such as lifestyle, dietary habits, and stress play a
air in 1989.
role in affecting the body’s ability to detoxify. Constant
• 1,180,831,181 pounds of chemicals released into
exposure to occupational and/or environmental toxins can
the ground threatening our supply of drinking water
lead to exhaustion of the buffering intrahepatic and sysin one year (1989).
temic mechanisms. Changes in lifestyle, including stress
reduction, proper physical activity, dietary changes and
• 551,034,696 pounds of industrial chemicals
adequate nutrients, are required to support detoxification.
dumped into public sewage systems that same year.
Vitamin deficiencies of C, E, and B complex and mineral
• 188,953,884 pounds of chemicals discharged into
deficiencies of calcium, magnesium, molybdenum, selesurface waters annually.
nium and zinc can reduce the rates of xenobiotic
biotransformation. Many of these nutrients are in short supIs it any wonder that these substances wind up in our
ply in today’s highly refined and nutrient depleted diets.7
cells?
Intake of foods made of incomplete essential amino acids
As for toxic metals,
have also been found to
according
to
some
increase markedly the toxicTABLE 1: EPA National Adipose Tissue Survey
researchers, the five most
ity of a number of
frequently encountered are
xenobiotics.8 Conversely,
Compound
Sources
% Observation
cadmium, mercury, lead,
foods from the brassica
Styrene
disposable cups
100
beryllium, and antimony.
family (especially kale and
carpet backing
Henry Schroeder, M.D., Probrussel sprouts) as well as
fessor
Emeritus
at
lemonine rich foods (rose1,4-dichlorobenzene mothballs
100
Dartmouth Medical School
mary, lemons, limes) can
house deodorizers
in his classic book The Poiassist liver detoxification
OCDD (dioxin)
herbicides
100
sons Around Us, stated that
auto exhaust
“these five toxic trace metals
SOURCES OF TOXICare involved in at least half
Xylene
gasoline
100
ITY
the deaths in the US and
paints
Another important step
much of the disabling disHxCDD(dioxin)
wood treatment
98
toward detoxification is
ease.14 Aluminum toxicity
herbicides
avoidance of toxic expohas also emerged as a recogsure, whenever possible.
nized threat to overall
Benzene
gasoline
96
Toxic chemicals and toxic
cellular integrity, especially
Source: National Human Adipose Tissue Survey, FY82, US Environmental Protection
metals are among our most
of the brain.
Agency. Volumes I-V, EPA-560/5-86-039, Dec. 1986.
pervasive cellular toxins.
Currently
more
than
DETERMINING CELLULAR TOXICITY
100,000 chemicals are in commercial use: over 25% are
known to be hazardous.9,10,11 William J. Rea, M.D., one of
Form our experiences, all chronic “dis-eases” have a celthe true pioneers in the emerging field of environmental
lular toxicity component as a contributing causation.
medicine, in his book Chemical Sensitivity discusses an
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
January 2003
25
Cellular Detoxification: The Chiropractic Perspective
Everyone is exposed to environmental toxins. Specifically, a practitioner should always consider this component
when faced with unexplainable symptom clusters, such as
fatigue, malaise, lack of energy, frequent colds and nonspecific lowered immune responses. Even in immune disease
processes, such as AIDS, the toxic load plays a major role.
The search for the toxic load should start with a careful
amanuensis. Investigation should begin with occupational
exposure, second hand smoke, sick building syndrome,
automobile exhaust and exposure to industrial by-products.
Indoor air pollution may be an even more pervasive issue
than outdoor sources of pollution.
HOMEOVITICS
aimed at promoting the removal of substances that
they have an affinity for; as an example, homeovitic
preparations for chemicals or for toxic metal challenge. Homeovitic formulations are also available
for specific biotoxins. The choice of appropriate formulations will be discussed later.
3. Cellular Support: Homeovitic support of cellular
regeneration is recommended during both clearing
and cellular detox. This cellular support is aimed at
minimizing oxidative stress that might occur as a
result of toxin release during clearing or cellular
detox.
THE REBUILDING PHASE
Cellular toxicity is a primary contributing factor in
chronic diseases such as arthritis, diabetes and hypertension.15 It should be addressed as part of an integrated
wellness program. We will focus primarily on one system
of detoxification, called homeovitics16-19 without required
weekly visits to a physician’s office. Homeovitics are
homeopathically vitalized nutraceuticals.20 They are prepared according to the Homeopathic Pharmacopoeia of the
United States (HPUS) standards and are regulated by the
FDA. Homeovitics are used to support cellular detoxification, a normal function of the body to maintain
homeostasis. As stated, we are convinced that cellular toxicity is a primary contributing factor in chronic conditions
such as arthritis, diabetes, hypertension… and aging!
The rebuilding phase begins after the 3-step cleansing
phase. Supplementation with specific nutrients and herbal
preparations are an essential part of cellular regeneration
and organ/system rebuilding. The previous 3 steps of detoxification facilitate optimal uptake of the rebuilding phase
nutrients. Vitamins A, C, E and B Complex and minerals
such as calcium, magnesium, molybdenum, zinc and selenium are the most important nutrients of the rebuilding
phase of detoxification. Homeovitic support can facilitate
incorporation of these nutrients into specific enzymes or tissues. We also recommend the use of foods rich in nutrients
and low in toxicity (organic, pesticide-free produce and free
range meats).
THE CLEANSING PHASE OF DETOXIFICATION
DETOXIFICATION TESTS AND LABORATORY
EVALUATIONS
Although the burden of detoxification lies primarily with
the liver, it takes place in every cell of the body. Positive
modifications in diet and lifestyle and adequate nutritional
supplementation support Phase 1 and 2 liver detoxification.
Coupled with avoidance of toxic exposure, they constitute
the first steps of detoxification. These measures should be
accompanied by more aggressive interventions. These
interventions consist of three cleansing phase steps: clearing, cellular detox and cellular support.
1. Clearing: An enhancement of eliminative functions
that prepares the body for further detoxification. We
are “priming the pump” to facilitate the removal of
toxins. The homeovitic approach to clearing works
on the energy level of our physiology. Other modalities that work on a more physical level are bowel
cleansing, juice fasting, herbal laxatives, skin brushing, etc. These are valuable complements to
homeovitic clearing. More on this later under integrative approaches to detox.
2. Cellular Detox: After 12 days of clearing we use
specific homeopathically prepared substances
26
A number of clinical laboratories are recognizing the
importance of detoxification and have developed tests to
evaluate detox pathways, particularly in the liver. Specific
heavy metal testing (eg. mercury) can also be utilized. It is
important to realize that during cellular detox, the level of
toxins in the blood, urine, sweat and sebaceous secretions
will increase. As toxic by-products are forced to be released
from cell storage sites, their content in the excretory systems will then probably reach high levels. The excretory
systems, therefore, need to be cleared and also protected
with homeovitic cellular support.
Recently, new laboratory tests have been developed to
determine exposure to xenobiotics on a cellular level. One
test measures both urinary and cellular DNA protein
adducts which reflect the function of DNA repair enzymes
that are involved in excising these nucleic acid adducts
from imperfect DNA.21 Excisional repair of DNA is essential for cellular regeneration and it can be compromised by
exposure to chemicals and metals. Another innovative laboratory test measures serum thiols as a predictor of DNA
repair.22 These tests can be used to validate the effective-
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
Vol. 26, No. 1
Cellular Detoxification: The Chiropractic Perspective
ness of cellular detox. In addition, current research is suggesting that detecting improvement of cellular immune
functions such as natural killer cell activity and the decrease
in programmed cell death (apoptosis) also measures the
effectiveness of cellular detoxification.23
RECENT RESEARCH
A clinical study completed in the summer of 2000 by
Darryl See, M.D., and his colleagues incorporated the
serum thiol analysis as a measure of DNA repair in a 48
day protocol of homeovitic cellular detoxification for
chemicals, heavy metals and latent viruses. These
researchers also evaluated the immune enhancing activity
of cellular detox by measuring glutathione (GSH) levels,
natural killer cell (NK) activity and antioxidant capacity.
All three of these outcome parameters were significantly
increased (p = <.05) indicating beneficial effects on
immune function and also on DNA repair.24
RELEASE RESPONSES TO CLEARING AND
CELLULAR DETOX
The term “release response” is used to describe the
symptomatic (and positive) effects on cellular detox. A
change in bowel functions, headache or flu-like symptoms
(often without fever), or low energy may all be “release
responses” of cellular detoxification during active detoxification interventions. The main reason that a clearing (Step
1) is completed prior to specific cellular detox is to minimize any unpleasant responses by activating and supporting
organs and systems of elimination to deal with released cellular toxins. Under these circumstances, if a release
response does occur, it is usually mild, transient, and selflimiting. The practitioner or pharmacist may instruct the
patient to recognize such a response as a positive sign of
cellular detoxification. The entire cleansing phase requires
the direct supervision of a health care professional
acquainted with the effects of cellular detox.
FREQUENCY OF CELLULAR DETOX
In a world increasingly more toxic, it is advisable to
embark on periodic detoxification procedures. This frequency depends upon the source of exposure and its
intensity. The following are some criteria for evaluation:
•
Has the source of the toxicity been eliminated?
•
Have lifestyle changes been made?
•
Has occupational exposure been minimized?
A cleansing protocol is advisable for everyone. And, if
toxic exposure is still present, homeovitic formulations may
then be employed on a weekly basis with cellular support.
28
This maintenance regimen will minimize toxic build-up
and preserve cellular detoxification pathways.
Some individuals may need to ease into a detox program
by first supporting cellular regeneration homeovitically
along with adequate nutrients and diet. It is also advisable
to primarily “destress” these individuals as much as possible.
Conditions such as allergies, chronic bacterial, viral or
yeast infections and parasitic infestation will benefit from
specific interventions. In our experience, therapeutic measures to eliminate infections and reduce the allergic
diathesis will not be totally effective if one does not reduce
the “toxic load” of chemicals and toxic metals. Therefore,
any detox protocol should address these primary cellular
toxicities.
INTEGRATIVE APPROACHES TO DETOX
The homeovitic approach to detox is based on the bioenergetic principle of homeopathy. It supports and intensifies
the body’s own cellular detoxification mechanisms. As
already mentioned, there are other physical detox modalities that are complementary to this energetic approach. A
number of factors should influence the practitioner’s choice
of detoxification procedure(s):
a. Age of the individual.
b. Overall health status and degree of toxicity suspected.
c. Associated health challenges such as chronic illness,
allergies, etc.
d. The use of prescribed or self-administered pharmaceutical and nutraceutical products.
e. Expected cooperativeness and compliance.
f.
Awareness of detoxification responses.
g. Financial constraints.
Many practitioners will elect to use homeovitic detox as
the primary protocol, while others will use a combination
of modalities.
PARTNERS IN WELLNESS
We invite all chiropractic physicians and their patients to
become more aware of the importance of cellular detoxification. Vigilant professional supervision is a prerequisite
for a successful detoxification and rebuilding program. In
this article we placed special emphasis on the homeovitic
approach to cellular detoxification as a first step on the path
to improved health. It is prudent to remove toxic residue
before one can begin to create a stimulus to new cell
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
Vol. 26, No. 1
Cellular Detoxification: The Chiropractic Perspective
growth. Homeovitic protocols support cellular detoxification and initiate positive, anti-aging effects. In a
contemporary chiropractic practice it is necessary to educate patients, to make them willing partners in the healing
process… as true “partners in wellness.”
NOTE: a portion of this article has been excerpted from the
chapter on Cellular Detoxification in “Advanced Guide to
Longevity Medicine,” IMPAKT Communications.
REFERENCES
1. Jakoby, W.B., Ziegler, D.M. The enzymes of detoxification. Journal of Biological Chemistry, 265(34):pp.
20715-20718, 1990.
2. Klaassen, C.D., Eaton, D.L. Principles of toxicology.
In: Casarett and Doull’s Toxicology, MO Amdur, J
Doull and CD Klaassen (Eds). New York: McGrawHill, Inc., Fourth Edition, pp. 26-30, 1993.
3. Stowe, C.M., Plaa, G.L. Extrarenal excretion of drugs
and chemicals. Annual Review of Pharmacology. 8:pp.
337-356, 1968.
4. Selye, H. The Stress of Life (revised edition). New
York, McGraw-Hill, Inc., 1978.
5. Rooney, P.J., et al. A short review of the relationship
between intestinal permeability and inflammatory joint
disease. Clinical & Experimental Rheumatology. 8:pp.
75-83. 1990
6. Smith, M.D., et al. Abnormal bowel permeability in
ankylosing spondylitis and rheumatoid arthritis. Journal of Rheumatology. 12:pp. 299-305, 1985.
7. United States Department of Agriculture, Report #2.
USRDA, Dietary Intake Studies, 1986.
8. Sipes, I.G., Gandolphi, A.J.. Biotransformation of toxicants. In: Casarett and Doull’s Toxicology, MO Amdur,
J Doull and CD Klaassen (Eds). New York: McGrawHill, Inc., Fourth Edition, p. 118, 1993.
9. Lappe, M. Chemical Deception. Sierra Club Books,
San Francisco, 1991.
10. Bellini, J. High Tech Holocaust. Sierra Club Books,
San Francisco, 1989.
11. DNA repair works its way to the top. Science.
226(Dec. 23):1926, 1994.
12. Rea, W.J. Chemical Sensitivity. Volume 4. CRC Lewis
Publishers. Boca Raton, FL, p. 2435, 1997.
13. U.S. Environmental Protection Agency, 1991. Toxins
in the Community: National and Local Perspectives,
The 1989 Toxics Release Inventory National Report,
Office of Toxic Substances, Washington, D.C.
14. Schroeder, H.A. The Poisons Around Us. Indiana University Press (1974) Keats Publishing, New Canaan,
CT, 1994.
15. Ghen, M.J. Xenobiotics and cellular detoxification.
Journal of the American Nutraceutical Association. pp.
33-35, 1999.
16. Gennaro, A.R. REMINGTON: The Science and Practice of Pharmacy. 19th Edition. Chapter 50: Alternative
Healthcare.. Mack Publishing, p. 834, 1995.
17. Pizzorno, J.E., Murray, M.T. A Textbook of Natural
Medicine. 2nd Edition, Section 3, Contemporary
Homeopathy. Churchill Livingstone, p. 281, 1999.
18. Clark, C.C. Encyclopedia of Contemporary Health
Practice. Part IV, Practices and Treatments. Springer
Publishing, p. 391, 1999.
19. Kratz, A.M. Homeovitics… contemporary, innovative
homeopathy. The Journal of Applied Nutrition. 48:pp.
7-9, 1996.
20. Ghen, M.J., Kratz, A.M. Homeopathic nutraceuticals… a new frontier. Journal of the American
Nutraceutical Association. 2:1, pp. 12-13, 1999.
21. Vojdani, A. Immunosciences Lab, Inc. Beverly Hills,
CA. Personal communication, August 30, 1999.
22. Pero, R.W. Oxigene, Inc., Boston, MA. Personal communication, March 2, 1999.
23. See, D. Jeunesse, Inc., Huntington Beach, CA. Personal communication, September 14, 1999.
24. Clinical Data on file, HVS Laboratories, Naples,
Florida.
25. Diamond, W.J., Cowden, W.L., Goldberg, B. An Alternative Medicine Definitive Guide to Cancer. Future
Medicine Publishing, Tiburon, CA, ppp. 472-3, 1997.
__________
For more information or comment contact Dr. Jack Taylor
at [email protected] or visit www.metabolic
map.com
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
January 2003
29
Nutritional Considerations in the Diagnosis and Treatment of
Attention Deficit Disorder
Michael J. Swiller, D.C., M.S., C.C.N., D.A.C.B.N.
DEFINITION1—A clinical syndrome, usually noted in a child younger than 7, with many of the following: 1. Hyperactivity–Aggressiveness, temper tantrums, constant movement; 2. Impulsiveness–Destructiveness, rapid mood changes; 3. Short
attention span–Inability to concentrate, neglected schoolwork; 4. Low tolerance to frustration–Nervousness, fears, nightmares, headaches; 5. Irritability–Abusiveness, stubbornness.
ASSOCIATED FINDINGS
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
Craving for sweets.
Food allergies.
Food sensitivities.
Chemical sensitivities.
Excessive thirst.
Mineral deficiencies.
Vitamin deficiencies.
Protein deficiencies.
Essential fatty acid deficiencies.
Toxic metal overload/Multiple chemical sensitivities.
Hypoglycemia.
Candida (yeast) infection.
Subclinical hypothyroidism.
Neurotransmitter deficiency.
REVIEWING THE ASSOCIATED FINDINGS
1. Craving for sweets.
Reactive hypoglycemia. Glucose and insulin high
and glycohemoglobin below 5.5. May require:
ketogenic diet, chromium.
2. Food allergies.
Immediate allergies. IgE mediated.
One food only breakfast followed by pulse testing. Pulse increase by more than 12 beats/min.
is positive. Eliminate this food from diet.
Delayed allergies. IgG mediated.
RAST testing for groups of foods. Eliminate
those foods. May require pantothenic acid,
quercetin.
Milk allergy is associated with chronic ear
infections, circles under the eyes and chronic
throat clearing. May require lactose-free diet.
Wheat allergy is associated with abdominal
pain, gas and diarrhea. May require gluten-free
diet.
3. Food sensitivities.
Rice, olive oil, turkey, lettuce, peeled pears,
salt, water and tea.2 As soon as symptoms
begin to subside, introduce one new food every
three days. Do not start with foods normally
eaten on a daily basis.
May have a sensitivity to gluten (Anti-gliadin
antibody, anti-reticulin and antibody high).
Must stop wheat, rye, oats, barley. May have a
sensitivity to milk (anti-casein antibody high).
Must stop all dairy products.
May require the anti-inflammatory omega-3 fatty
acids.
4. Chemical sensitivities.
Read labels. Eliminate any food that contains
food additives, artificial coloring (tartrazine,
Ponceau 4R) or preservatives (BHA, BHT).
Eliminate caffeine (chocolate, tea, coffee).
Keep environment smoke-free.
Stop aspirin use and avoid aspirin-factor foods3
(apples, apple juice, apple cider vinegar, apricots, grapes, grape jelly, raisins, oranges,
orange juice, fruit punch, nectarines, currants,
almonds, blackberries, boysenberries, gooseberries, raspberries, strawberries, cherries,
peaches, plums, prunes, cucumbers, pickles,
tomatoes and catsup). Food flavoring/chemical
agents that contain the aspirin-like salicylates
are found in: some bakery goods, some ice
creams, chewing gums, some soft drinks (rootbeer), some gelatin products, and anything with
mint flavor, wintergreen, lime, lemon, strawberry, raspberry or grape flavors.
May require tryptophan, vitamin B6.
5. Excessive thirst.
A common sign of an essential fatty acid deficiency.4
May require borage oil, safflower oil, flax seed oil.
May require a diet that allows only:
30
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
Vol. 26, No. 1
Attention Deficit Disorder
6. Mineral deficiencies.
More than 50% of hyperactive children were
found to have a zinc deficiency (Bad body
order, smelly feet, loss of taste sensation, loss
of smell sensation, eyes sensitive to bright
lights).
May require zinc, vitamin B6.
Calcium deficiency:
Muscle tightness (stiff achey neck/lower back).
Magnesium deficiency:
Craves chocolate, constipation, back pain.
May require calcium, magnesium.
7. Vitamin deficiencies.
Poor dream recall and poor concentration ability is characteristic of a vitamin B6 deficiency.
May require vitamin B6 at 50-100 mg/day.
Greasy skin may be the result of a riboflavin
deficiency.
Allergies may be the result of a pantothenic
acid deficiency.
A vitamin A deficiency may cause itchy skin
and eyes that are sensitive to bright lights.
8. Protein deficiencies.
Insomnia, nervousness, and obsessive-compulsive behavior are characteristics of poor
tryptophan, serotonin synthesis.
Hyperactivity is often a sign of a deficiency of
the brain calming neurotransmitter GABA.
Glutamine can neutralize the hyperactivating
ammonia overload.
9. Essential fatty acid deficiency.
Every nerve is covered by a waxy material, the
myelin sheath. The white matter of the brain is
made up of a waxy material. All of this matter
is derived from essential fatty acids. This protects and prevents nerve short circuiting. Is
diminished in Alzheimer’s disease, Parkinson’s
disease and multiple sclerosis.
All fatty acids are derived from linoleic acid or
linolenic acid.
10. Toxic metal exposure/Multiple chemical sensitivity.
Lead poisoning is a brain activity suppressant
and may only be detected in a hair analysis.5
32
May come from use of foreign made pottery
used as a food container, from exposure to batteries, to some hair coloring agents, to lead
containing paints.
Fluoride intoxication should be suspected when
the child has hyperactivity and chronic ear
infections.
May require cod liver oil, vitamin A, magnesium.
Cadmium from cigarette smoke, from tire dust
if live near a busy road. Coffee and tea
double/triple cadmium uptake from food.
11. Hypoglycemia may be a cause of hyperactivity,
inability to concentrate and short term memory loss.
May require a diet low in simple sugars, that
includes: chromium, zinc, vitamin B-complex,
5-6 small meals/day.
Chronic hypoglycemia causes the body to
destroy its own protein, thereby raising the
ammonia levels, i.e. irritating the brain.
A magnesium deficiency prevents the body
from changing its glycogen supply into glucose, i.e. brain starvation.
12. Chronic Candida infection.
May cause itchy skin, severe sensitivity to
smells/odors, i.e. perfumes, cigarette smoke,
detergents, etc. Nail fungus, athlete’s foot,
smelly feet.
Causes the production of acetaldehyde, a
severe neuro-toxin. May require a ketogenic
diet, caprylic acid, vitamin A, yogurt, acidophilus plantarum and thiamin.
Chronic inflammation of the colon leads to
lymphoid nodular hyperplasia. This is characterized by high urinary methylmalonic acid
(vitamin B12 deficiency), low hemoglobin, Ig
A, CD3 (natural killer cells), CD4+ and
CD8+6.
13. Sluggish thyroid that may only be detected by finding a low basal temperature.
May be the cause of poor concentration ability,
lack of stamina, complaints of always being
cold, itchy skin and loss of hair at the lateral
eyebrows.
May require thyroid, manganese, phenylalanine, ocean fish, kelp.
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
Vol. 26, No. 1
Attention Deficit Disorder
14. Neurotransmitter deficiency/destruction.
Norepinephrine deficiency causes poor
inhibitory control resulting in hyperactivity.
Norepinephrine deficiencies are associated
with reversed drug reactions, i.e. stimulants
have a calming effect, tranquilizers have a stimulating effect.
9. Nausea.
10. Dizziness.
11. Heart racing, irregular heart rate.
12. Headaches.
13. Drowsiness.
Associated with lightheadedness, dizziness
when changing position.
THE DIFFERENTIAL EVALUATION OF ADD
MUST EXCLUDE:
May require vitamin B-complex, vitamin C,
pantothenic acid, adrenal substance, ginkgo
biloba, siberian ginseng.
Symptom
Other cause
Irritability:
Hyperthyroidism.8
Gamma-linolenic acid deficiency.9
Protein starvation.
Diet high in tuna fish. May cause mercury
poisoning.
Hyperactivity:
Hyperthyroidism.
Food allergies.
Osteopenia. Lack of sufficient calcium.
Mania. Manic depression. Lack of
lithium, chromium, calcium.
Concentration
Poor:
Destruction of white matter of the brain.
Gamma-linolenic acid deficiency.
Reye’s syndrome. Aspirin poisoning.
Celiac disease (anti-gliadin antibody, antireticulin antibody high).
Hypoglycemia
Cerebral anoxia. Anemia.
Pulse Rapid:
Mitral valve prolapse.
Magnesium deficiency.
Hyperthyroidism.
Depressed gamma-amino butyric acid
synthesis.
Insomnia:
Defective brain synthesis of tryptophan/
serotonin.
Hyperthyroidism.
Reactive hypoglycemia. Wakes up and
then can’t get back to sleep.
Growth spurt uses all available calcium.
Calcium is a synaptic buffer; prevents
nerve messages from jumping from one
neuron to the next while on a trip to the
brain.
Starvation. Causes loss of all brain calming proteins.
Nervousness:
Hyperthyroidism.
Osteopenia. Lack of calcium.
Adrenal exhaustion due to stress/excess
sugar intake.
Dopamine deficiency due to adrenal failure.
COURSE IF UNTREATED
As older children:
Antisocial behavior.
School dropouts.
Delinquency.
As adults:
Become hyperactive adults.7
Apathy/disinterest in life.
Depression.
Drug dependency.
Alcoholism.
Criminal behavior.
COMMON MEDICAL TREATMENT
Ritalin (Is actually a neurological stimulant).
Side effects of ritalin.
1. Stunted growth.
2. Seizures/muscle spasms, in those with a preritalin history of seizures.
3. Depression, suicidal thoughts if ritalin is
abruptly discontinued (forgotten, left home
while on vacation, lost at school, etc.)
4. Nervousness.
5. Insomnia.
6. Skin rashes.
7. Joint pains.
8. Loss of appetite.
34
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
Vol. 26, No. 1
Hyperactivity Questionnaire
_________________________________________________
0
1
2
3
Not
Just A
Almost
Several
At All
Little
Every Day Times Daily
_________________________________________________________________________________
1. Picks at things (nails, fingers, nose,
hair, clothing).
_________________________________________________________________________________
2.
Sassy/talks back to adults.
_________________________________________________________________________________
3. Problem making and keeping
friends.
_________________________________________________________________________________
4.
Is excitable, impulsive.
_________________________________________________________________________________
5. Wants to run things.
_________________________________________________________________________________
6. Sucks/chews things (thumbs, clothing, blanket).
_________________________________________________________________________________
7. Cries often or easily.
_________________________________________________________________________________
8. Has an attitude/chip on shoulder.
_________________________________________________________________________________
9. Daydreams often.
_________________________________________________________________________________
10. Difficulty learning.
_________________________________________________________________________________
11. Restless/can’t sit still/“squirmy”.
_________________________________________________________________________________
12. Fearful of new situations, new people, school.
_________________________________________________________________________________
13. Is restless, up and on go, resists
going to sleep.
_________________________________________________________________________________
14.
Is destructive.
_________________________________________________________________________________
15. Tells lies (no homework,
grandma/mom/dad said).
_________________________________________________________________________________
16.
Is shy.
_________________________________________________________________________________
17. Into more trouble than others of
same age.
_________________________________________________________________________________
18. Affected speech (baby talk, hard to
understand).
_________________________________________________________________________________
19. Denies mistakes/blames others.
_________________________________________________________________________________
20. Is quarrelsome.
_________________________________________________________________________________
21. Pouts/sulks.
_________________________________________________________________________________
22. Steals.
_________________________________________________________________________________
23. Obeys resentfully. Is disobedient.
_________________________________________________________________________________
24. Worrier (being along, illness, death).
_________________________________________________________________________________
25. Fails to finish things.
_________________________________________________________________________________
26. Feelings easily hurt.
_________________________________________________________________________________
27. Bullies others.
_________________________________________________________________________________
28. Childish/immature.
_________________________________________________________________________________
29. Easily distracted from project. Attention short.
_________________________________________________________________________________
30.
Headaches.
_________________________________________________________________________________
31.
Mood changes are rapid and drastic.
_________________________________________________________________________________
32. Doesn’t follow rules or restrictions.
_________________________________________________________________________________
33. Excessive intestinal gas.
_________________________________________________________________________________
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
January 2003
35
Attention Deficit Disorder
Mood Changes, Gamma-linolenic acid deficiency.
Rapid:
Reactive hypoglycemia.
Megaloblastic anemia. Due to vitamin
B12 deficiency.
Attention Span Acetylcholine deficiency is reflected in
Short:
lack of energy/strength.
Solanine intoxication. “Nightshade” poisoning. From peppers (red or green),
potatoes (white only), eggplant and tomatoes (and all foods derived from tomatoes,
i.e. catsup, pasta sauce).
Gamma-linolenic acid deficiency.
Vitamin B6 deficiency. Allows build-up of
excitatory neurotoxins.
Anxiety:
Gamma-linolenic acid deficiency.
Hyperthyroidism.
Serotonin/tryptophan deficiency.
Folic acid deficiency. Associated with
fatigue, skin problems, psoriasis.
Headaches:
Allergies:
Thirst
Excessive:
36
Excessive protein destruction. Raises
ammonia levels.
Wilson’s disease. Copper overload.
Zinc deficiency.
Gamma-linolenic acid deficiency.
Iron deficiency.
Blood vessel constriction.
Arterial constriction/compression in neck.
Toxic metal overload.
Glycogen storage disease.
Histamine overload due to platelet
destruction.
Chronic intestinal bacterial overload.
Gamma-linolenic acid deficiency.
Adrenal exhaustion.
Bioflavinoid deficiency.
Toxic metal overload.
Zinc deficiency.
Vitamin B12 deficiency.
Diabetes (Glycohemoglobin high).
Chromium, calcium, and arginine deficiencies.
Essential fatty acid deficiency (linoleic
acid, alpha-linolenic acid, gammalinolenic acid low
Protein malabsorption syndrome.
Anorexia.
Toxemia.
Lactic acidemia.
Defective anti-diuretic hormone synthesis. Arginine deficiency.
SUMMARY
Attention deficit syndrome, with or without the hyperactive label, is a complex health care problem. Rather than
mask the symptoms with a drug of questionable and risky
value, the role of the clinical nutritionist is to discover the
specific biochemical dysfunction for each specific patient.
Once the biochemical defect has been found, the clinical
nutritionist will design a nutritional program to reverse any
discovered chemical defect.
From this article it should be clear that step one, in the
road to recovery, requires a thorough history analysis and
then having the appropriate laboratory tests performed.
There is no fixed price for these tests as the history analysis
will suggest tests that will vary from patient to patient.
This is what I tell my patients:
When the test results are returned to the office they are
immediately reviewed. When a very significant test is
reported to be markedly abnormal you will be required to
come into the office for a consultation. If there is some
immediate nutritional protocol that should help, that advice
will be given to you at this time. If the abnormal test indicates that another test is required to explain this abnormal
finding, you will be given another lab request form.
When all of the requested lab tests are returned to the
office by the various laboratories, these results will be
entered into the office computers for analysis and report
production. The computer compares the results of each test
with the levels of every other test. When a pattern is discovered that relates to a specific defect and a special nutritional
treatment, these facts are printed to a report.
You will be given a copy of this report and asked to
answer numerous specific questions to explain the abnormal chemistries.
When you return the answered report to our office, we
being an in-depth study to develop the best treatment program for the fastest recovery.
It is generally understood that the best nutritional program requires about 4-6 months to reach its fullest
potential. During this time you will return for periodic history and physical re-evaluation. Based upon your changing
history and physical findings, the treatment protocol may
be modified.
While we do expect slow and steady improvement, it is
imperative that the development of any new symptoms or
worsening old symptoms to be reported to the office at
once.
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
Vol. 26, No. 1
Attention Deficit Disorder
TESTS TO CONSIDER IN ATTENTION DEFICIT
DISORDER
Acetaldehyde
Alpha-1-acid glycoprotein
Alpha-linolenic acid
Ammonia
Anti-casein antibody
Anti-diuretic hormone
Anti-reticulin antibody
Arachidonic acid
Arginine
Asparagine
Beta-alanine
Candida antibody 1g A
Candida antibody 1g G
Candida antibody 1g M
Carnitine
Carotene
Catecholamines
Ceruloplasmin
Docosahexaenioc acid
Dopamine
Eicosapentaenoic acid
Epinephrine
Ferritin
Folic acid
Galactose-1-phosphate
Gamma-amino butyric acid
Gamma-linolenic acid
Gastrin
Glucose-6-phosphate
Glutathione peroxidase
Glutamine
Glycohemoglobin
Hair cadmium
Hair calcium
Hair chromium
Hair cobalt
Hair iodine
Hair lead
Hair lithium
Hair magnesium
Hair mercury
Hair zinc
Helicobacter pylori
Histamine
Histidine
Hydroxylysine
Ig E
Ig G
Insulin
Iron-binding capacity
Lactic acid
38
Linoleic acid
Lipid peroxide
Magnesium
Norepinephrine
Phenylalanine
Pulse rate
R.B.C. cholinesterase
R.B.C. folate
Retinol-binding protein
Riboflavin
Salicylic acid
Serotonin
T-3
Thiamin
Thyroid
Thyroid-stimulating hormone
Transferrin
Transferrin saturation
Tryptophan
Underarm basal temperature
Urine copper
Urine homovanillic acid
Urine kynurenic acid
Urine vanilylmandelic acid
Urine xanthurenic acid
Vitamin A
Vitamin B12
Vitamin B6
Vitamin C
Zinc
REFERENCES
1. Mahan, L., RD, Arlin, M., RD. Krause’s Food, Nutrition & Diet Therapy. Philadelphia, PA: W.B. Saunders
Co., 1992, Pg. 229.
2. Werbach, M., MD. Nutritional Influences on Illness.
Tarzana, CA: Third Line Press, 1996, Pg. 45.
3. Feingold, Ben F., MD. Why Your Child is Hyperactive.
New York, NY: Random House, 1975, Pg. 169-170.
4. Graham, J. Evening Primrose Oil. Rochester, VT:
Healing Arts Press, 1989, Pg. 58.
5. Hull, Gay, PhD. Nutrition and the Mind. New York,
NY: Four Walls Eight Windows, 1995, Pg. 154.
6. Wakefield, Andrew MB, BS. The Gut-Brain Axis in
Childhood Developmental Disorders. Program Syllabus. ACAM 5/1999:280.
7. Braly, J., MD, Torbet, L. Dr. Braly’s Food Allergy and
Nutritional Revolution. New Canaan, CT: Keats Publishing, Inc., 1992, Pg. 14.
8. Murray, M., ND, Pizzorno, J., ND. Encyclopedia of
Natural Medicine. Rocklin, CA: Prima Publishing,
1991, Pg. 387.
9. Ibid, Graham, J. Pg. 37.
Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
Vol. 26, No. 1
Improving Longevity
Diagnosis and Nutritional Support for
Cancer and Cardiovascular Disease
ACA Council on Nutrition and
American Clinical Board of Nutrition
April 24-27, 2003 • Washington, DC
COUNCIL ON NUTRITION SEMINAR ATTENDEES ONLY:
WOW!!! Free!! Early Bird Special Trip!
PHILIP A. DUTERME, PhD.
A lecture by internationally
recognized herbal authority
“Value and Limitations of Phytonutrients in Health Care”
❶ Scientific review of the effectiveness of phytonutrients in liver dysfunctions
❷ Interactions between phytonutrients and OTC drugs
ALSO, receive a complimentary round trip bus trip from the seminar hotel to the National Museum of Health and Medicine where attendees will
be treated to a guided tour of several of the permanent exhibits including Living in a World with AIDS and Research Matters: Environmental and Toxicological
Effects of Arsenic (health problems from toxic minerals).
When: Thursday, April 24, 2003 Time: 12:15 p.m. to 7:00 p.m. Sponsored by: Himalaya USA
Instructors
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
FACC
Four hour mandatory
ACBN credit:
John G. Rupolo, DC, MA, FICC,
Philip A. Duterme, PhD
Early Detection of Cardiovascular Disease
Using Tomography and Conventional
Treatment
Value and Limitations of Phytonutrients
in Health Care
Gary D. Stoner, PhD
Interpreting Role Delineation Survey
Results
Jay Robbins, DC, CCN, DACBN
NCI Identifies Dietary Factors That Inhibit
Cancer: The Protective Effect Of Berries
Jerrold Simon, DC, DACBN, CCN,
Michael Dobbins, DC
Fundamental Principles for
Cardiovascular Nutrition
Objective Diagnostic Interruptions Using
the Acustocardiograph
John A. Rumberger, PhD, MD,
DACBN, FACCN
DACRB, FACCN, DABDA, FACCRS, FICC
Developing the Role Delineation Survey
Jeffrey E. Weber, DC, MS,
DACBN, FACCN
Using the Algorithm
Travel & Accommodations . . . . . . . . . .
HYATT REGENCY ON CAPITOL HILL
TRUMP TRAVEL
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Room Rate: $159 Single/Double Parking $26
660 Merrick Road, Baldwin, NY 11510
800-937-3878
Reservation cut-off date March 21, 2003
(Tel) 202-737-1234
PLEASE CALL Claudia Rabin-Manning to
reserve your room at the discount rate and to be sure your Council on Nutrition receives the credit
for your room. Ask for extra day at the same great rate on either end and make this a mini-vacation.
Tuition (includes seminar, luncheon meetings/buffets . . . . . . . . . . . . . . . .
DOCTORS
Members
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Spouse (non-DC), CA
Chiropractic Student
Prior to
March 15, 2003
$389.00
$499.00
$189.00
After
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$289.00
Cancellation Fee:
Prior to April 1 $25.00 NO Refunds after April 1
The CN reserves the right to cancel or adjust program dates, times, speakers
or locations if the need arises. CN is not responsible for registrants’ expenses
should any program changes occur.
Register Now.
Additional Luncheon Ticket
. . . . . . . . . . $45.00 for each day.
Must be purchased prior to seminar. Not available on-site.
Co-sponsored and Continuing
Education Credit by Texas
Chiropractic College:
20 hours of CE credit applied for in most
states through Texas Chiropractic College.
Call 800-533-9822 to determine whether
credit is available in your state.
. . . . . . . . . . . . . . . . .
Call Bonnie at Council Headquarters! Phone (540) 635-8844 Fax: (540) 635-3669
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Nutritional Perspectives: Journal of the Council on Nutrition of the America Chiropractic Association
Vol. 26, No. 1