Suspected Hypothyroidism: Treat, Ignore, or Feed?
Robert Thiel, Naturopath

Thiel R. Suspected hypothyroidism: Treat, ignore, or feed. Int J Naturopathy, 2003;1(1):12-22

Abstract: People who have symptoms associated with hypothyroidism do not always test
positive for thyroid conditions when standard thyroid panels are run. Health professionals
are thus faced with the choice to treat suspected cases with synthetic hormone replacement or
ignoring the symptomatology. This paper suggests that another alternative, feeding through
various forms of nutrition, offers potential benefits without the risks associated with possibly
unnecessary thyroid medications. Specific nutrients suggested included iodine, l-tyrosine,
selenium, zinc, and vitamin B2, whereas foods suggested included kelp, alfalfa, burdock,
scullcap, and various bovine glandular extracts. Certain possible roles, including nutritional
and possible anti-autoimmune properties, of some of these nutrients/foods are mentioned.
For those suspected of having hypothyroidism, it notes that there are reports that problems
with arrythmias, fatigue, depression/mood, headaches, body fat, weight, circulatory
complaints, and other symptoms frequently respond to thyroid nutrition. The paper
concludes that nutrition is a logical approach to consider when mild cases of hypothyroidism
are suspected — even when not confirmed by any blood test.

Key words: hypothyroidism, nutrition, food, glandulars, herbs

INTRODUCTION
The thyroid produces hormones that have been found to speed metabolism (such as
thyroxine) and affect concentrations of calcium (calcitonin) [1,2]. Symptoms associated with
a low thyroid function include fatigue, cold extremities, depression, mood swings, behavioral
disorders, weight issues (both weight gain and inability to gain weight), circulatory
complaints, hypercholesterolemia, hypertension, headaches, arrythmias, lower tolerance for
temperature fluctuations, menstrual problems, dry skin, and constipation [1,3,4]. Poor
nutrition has sometimes been positively correlated to low serum thyroid hormone levels [5].
Thyroid problems are exceptionally common [i.e. 6-13]. One study involving 46,000
Americans found that 11% had one or more undiagnosed thyroid conditions [7]; a non-
American study found that 9.7% of elderly males and 18.2% of elderly females had
hypothyroidism [12]. Subclinical hypothyroidism, which is rarely diagnosed, is considered
by some researchers to be the most prevalent [13]. Hypothyroidism is the most common
endocrine disorder for those afflicted with Down syndrome (trisomy 21) [14]. People with
overt or subclinical hypothyroidism are more likely to develop atherosclerosis and
cardiovascular diseases [15].

This paper will focus on suspected hypothyroidism. For the purposes of this paper, suspected
hypothyroidism will be considered to include 1) clinical hypothyroidism, where T-4
(thyroxine) levels are below the low end of the acceptable range, 2) subclinical
hypothyroidism, where TSH (thyroid stimulating hormone) levels are elevated and T-4 is not
below the acceptable range, 3) borderline hypothyroidism, where T-4 is near the low end of
the acceptable range, and 4) symptomatic hypothyroidism, where T-4 and TSH levels are
acceptable, yet symptomatology suggests possible hypothyroidism. For purposes of this
paper, suspected hypothyroidism does not include thyroid problems where the thyroid has
been surgically removed, has been ablated through radiation, or is incapable of producing
thyroxine.

Certain foods, perhaps most notably soy (it contains several goitrogenic substances [16]),
have been linked to the development of hypothyroid problems, but this controversy has not
yet been fully resolved [17,18]. Caffeine also may contribute to, or at least mask [19,20],
some symptoms associated with hypothyroidism (it has been reported that caffeine “slows
the thyroid by suppressing the adrenal gland’s production of cortisol, a hormone essential to
thyroid function” [21]). Another environmental factor, cigarette smoking, tends to increase
concentrations of the goitrogen thiocyanate [22].

Although being female [23], smoking [22], experiencing depression [24-27], being poorly
nourished [5], being under stress [28] and advancing age [6,12] are all factors for developing
hypothyroidism (though men, children, and non-smokers get them as well [7,12,22]), these
causes are rarely emphasized in standard medical education. Medical textbooks generally
suggest that hypothyroidism is caused by genetic factors, autoimmune disorders,
developmental anomalies, ablation of thyroid due to radiation or surgery, thyroid cancer,
antithyroid drug administration, and hypopituitarism [e.g. 29-31]. Nutrition tends to get a
cursory mention, but mostly is mentioned for societies who live in iodine deficient areas who
consume little iodized salt [29-32]. This type of training essentially leaves the practitioner
with the impression that hypothyroid conditions seen in Western nations are due to factors
beyond the patient’s control, thus medicating with a synthetic hormone replacement is the
logical (and even preferred) choice for many practitioners [33]. Other practitioners, wary of
contributing to possible thyroid atrophy, medication dependence, or other problems tend not
to prescribe anything--in essence ignoring many cases of suspected hypothyroidism
[11,24,34].

Are these the only two choices? (Most papers on this subject seem to suggest only those two
though, in clinical practice, some medical doctors will prescribe some type of antidepressant,
even when depression is not a symptom [35], which at least give the patients the appearance
that something has been done).
There is another option.

NUTRITION
Natural health practitioners have long worked with nutrition and the thyroid [36]. Nutritional
support has been used in the U.S. since at least 1916 [37] and in China for thousands of years
[38].

Nutrition is a logical supporter of thyroid health. The primary thyroid hormone is made up of
iodine and tyrosine and undergoes several metabolic processes to become T-4 (commonly
called thyroxine) and T-3 (triiodothyronine) [2,32]. “One of the factors affecting the output
of thyroid hormone by the thyroid gland is iodine” [38]. Many foods contain iodine (such as
sea vegetables) and protein-containing foods contain between 1.4-5.8% tyrosine by mass
[39]. The thyroid must trap about 60mcg of iodine each day to maintain an adequate amount
of thyroxine and at least one billion people living in developing countries are currently
believed to be deficient in it [32]. Although salt has been iodized since the 1920s, with all
the warnings about salt consumption and hypertension, this source of iodine has been
reduced unnecessarily in the diet’s of many [40].

Tyrosine is an amino acid which is essential for the “synthesis of proteins, catecholamines,
melanin pigment, and thyroid hormones. The body naturally produces tyrosine...Tyrosine
provides energy when catabolized through p-hydroxyphenylpyruvate to fumarate and
acetoacetate” [39]. Hypothyroidism can be associated with low levels of tyrosine [41].
Tyrosine has an effect on nerve impulse transmission and may “improve vigilance and lessen
anxiety” [42]. Some naturopathic physicians have reported success using l-tyrosine to help
nutritionally support the thyroid gland [43].

Some natural health practitioners recommend supplements containing selenium, zinc, and
other minerals to provide nutritional support for the conversion of T4 to T3 [40-41] and
chromium for general support [43]. “The iodothyronine deiodinases, types I-III are all
selenoproteins. These enzymes catalyze the deiodination of thyroxine, triiodothyronine, and
reverse triiodothyronine and thereby regulate the concentration of the active hormone
triiodothyronine” [44]. “Circulating triiodothyronine and thyroxine are decreased in zinc
deficiency, as is the hypothalamic thyroid-releasing hormone” [45]. The deiodinase type II
enzyme needed to convert T4 to T3 is a selenium-zinc protein [44,46]. Selenium deficiency
seems to deplete thyroidal iodine and thyroid hormones [47], thus both should possibly be
taken together [48]. People with Down syndrome tend to have below normal plasma levels
of selenium and zinc [49]--many such individuals are suspected on being hypothyroid [14].
One study found that selenium deficient rats had lower levels of T3 and T4 than controls and
that zinc deficient animals had 30% decreased concentrations of zinc than controls [51].
Several studies show that zinc supplementation can generally improve thyroid serum results.
One found that zinc reduced TSH by 34% for hypothyroid Down syndrome patients [51],
while another found it reduced TSH in other disabled persons by 50% while increasing T-3
by 13% [46]. Sometimes results are different, as another study found that zinc increased
TSH by 28%, increased T-4 by 52%, and increased T-3 by 30% for some with end stage
chronic renal failure [52].

Vitamins B2 deficiencies seem to be higher in people with overt hypothyroidism [53]. A
vitamin B2 derived coenzyme, flavin adenine dinucleotide, appears to be sensitive to thyroid
status [53]. Research has also indicated that vitamin B2 is helpful in some headaches [54],
which others have found can be related to thyroid function [4,8].

Herbs
Some of the herbs used by herbalists to support the thyroid include kelp (nereocytis luetkana
or laminaria hyperborea), alfalfa (medicago sativa), burdock (arctium lappa, previously
known as lappa officinalis), and scullcap (scutellaria lateriflora) [55-57]. As a rule, these
herbs contain minerals and phytonutrients which can nutritionally support the thyroid
[58,59].

Kelp is the classic herb that is used for thyroid support [38,57]. It is high in minerals [60,61]
and may have immune-enhancing properties [61]. Kelp has long been used to provide
nutritional support for the thyroid gland [3,38,43,62]. Gary Null, Ph.D., has written, “Kelp
can rebalance thyroid metabolism, resulting in successful weight management and the
reversal of many conditions which are caused by a thyroid imbalance, including stomach and
respiratory disorders” [43]. One study concluded that ‘living food’ eating vegetarians need to
consume kelp (or take kelp supplements) in order to maintain normal iodine levels for proper
thyroid functioning [62]. Kelp and other sea vegetables are rich food sources of iodine,
which may be their most active nutritional ingredient [38]. It has been recently been reported
that kelp may be able to effect TSH levels [59]. Kelp is a food [58,62]. Although it is
categorized by the American Herbal Products Association as “Class 2d - Therapeutic use is
not recommended in hyperthyroidism; long-term use is not recommended” [58], this
contradicts other findings which suggests it is beneficial, for at least certain vegetarians,
long-term [62]. Also, it appears that it is the quantity of kelp that may have negative effects
[57,59], as opposed to kelp itself (the danger of inducing hyperthyroidism exists when it
supplies over 150 grams of iodine per day [57], a massively high amount). Some evidence
suggests negative effects of kelp or iodine-containing supplements on thyroid serum results is
often [62,], but not always [64], temporary.

Some herbalists believe alfalfa has a “beneficial effect on the pituitary gland”, “helps in
chemical imbalance”, and “is useful as a food to prevent cholesterol accumulation in the
veins” [56]. In supplement form, alfalfa is “rich in proteins, calcium and trace minerals,
vitamins E and K, (and) unidentified factors” [38]. Some believe burdock “aids the pituitary
gland to help adjust hormone balance” [56]. Perhaps for that reason, burdock has sometimes
been recommended for thyroid health [56,65]. Scullcap (also spelled “skullcap”) is a
member of the mint family which contains various flavonoid glycoside pigments such as
scutellarein, wogonin, isoscutellarian, and baicalin [66]. It is often used as a tonic for
‘female weakness’ [37,66,67]. The United States Pharmacopoeia has long recognized
scullcap as a nervine (nutritional nervous system support) and tonic [37]. It also is
recommended by some herbalists for thyroid concerns [56]. Alfalfa, burdock, and scullcap
are all categorized by the American Herbal Products Association as “Class 1: Herbs which
can be safely consumed when used appropriately” [58].

Glandulars
Bovine glands, such as adrenal, liver, thyroid, and pituitary have been consumed as
nutritional support for decades; they have been part of the human diet for much longer [68].
Glandular extracts are natural food complexes which contain minerals, peptides, enzymes
(when freeze or vacuumed-dried), fatty acids, and substances believed to be hormone
precursors [32,44,69-75]. Proponents normally believe that the specific glandular consumed
will tend to have benefits for the corresponding gland within the human body [70-75].
Glands contain about the highest concentration of selenium of any food [44], good amounts
of zinc [69], and in the case of thyroid, high concentrations of iodine [32].
A small amount of glandular peptides are absorbed and some appear to provide nutritional
support in performing various anabolic and catabolic processes [70-75]. Howell and others
have reported that the amount of enzymes which pass through the stomach may be as high as
50% [76] (raw glandulars contain enzymes [70,76]). Enzymes encourage a variety of
metabolic processes, including anabolic (rebuilding) reactions [76]--they may be the key to
the body utilizing thyroid nutrients such as iodine and tyrosine.

In the 1930s, Dr. Royal Lee hypothesized that problems with endocrine glands, such as the
thyroid, were caused by the body attacking the organ (autoimmunity) and that consumption
of glandulars was effective, not so much because of the nutrients they provided, but because
they “neutralize such attacks, allowing the organs to heal themselves” [77] or put another
way, Lee speculated that glandulars may have anti-autoimmune properties. This should be
considered as speculation, however, as this researcher is not aware of any recent published
study which clearly confirms this belief.

Natural health professionals frequently prefer thyroid glandulars over the synthetic
counterparts for nutritional applications [8,70,78,79]. “Thus a patient given thyroid
concentrate will manifest improvement in thyroid panels and other tests that demonstrate
thyroid activity. Apparently the body is able to ‘recognize’ the specific ‘blueprints’
(nucleoproteins including DNA and RNA coding), protein configuration and other aspects of
the specific gland or organ, and receptors of the target gland (i.e. thyroid) pick up the
substances from the circulation” [70]. According to the 1916 guide to the United States
Pharmacopoeia, bovine thyroid glandulars are foods which are capable of “exerting a strong
influence on nutritive and metabolic processes” [37]. Unlike porcine thyroid glandulars [80],
commercially processed bovine thyroid glandular extracts do not contain detectable amounts
of thyroxine. Thyroid glandular supplements specifically have been recommended for a
variety of thyroid-related conditions including low T4 production, chronic fatigue,
headaches, obesity, and depression [37,78]. “Glandular products have been produced and
used in the U.S. for over 60 years with absolutely no reports of microbial contamination or
resultant illness...Since hormones are not part of the substance, overdosing is not a concern.
Even when excess amounts have been ingested, the body can easily deaminize them” [70].

CLINICAL PRACTICE
The most common serum tests ran in clinical practice for hypothyroidism are total T4, the
free thyroxine index, and TSH [81]. Tests of T3 are sometimes also run [81]. Unfortunately,
these tests essentially just measure how the body is dealing with T4, but do not measure
calcitonin, thyroglobulin, T1, or T2 which are also produced by the thyroid (which may or
may not affect symptoms associated with mild hypothyroidism) [2,81].
Natural health practitioners tend to use a variety of techniques to determine whether or not
nutritional support for the thyroid can be helpful, as well as to determine which combination
of substances will be most beneficial. The most common is probably based upon
symptomatology [7,10], whereas others are based on less stringent interpretation of thyroid
panel results [6,7,77], iodine absorption tests [77], low basal temperature [77,79,82], muscle
testing [78,82], and factors such as gender and weight [10,37]. Some use combinations of
these methods [10,65,77,82].

Preliminary studies, clinical research, and other reports, have concluded that nutritional
support of the thyroid at least results in symptomatic improvement for most who receive that
support with the best results for symptoms such as arrythmias, circulatory complaints,
fatigue, headaches, mood/depression issues, and being underweight [8,18,37,53,54,78,82-
86]. Nutritional support for the thyroid has long been believed to be helpful as part of a
program to lose weight [37], but the results are not universal (this researcher found that it
helped only about 60% of those overweight suspected to have hypothyroidism lose body fat,
while about 31% actually gained body fat during the same study [84]).

A Dutch study found that synthetic thyroid therapy helped 25-30% of those with subclinical
hypothyroidism [13]. Several researchers and practitioners have reported that nutritional
support for the thyroid is more effective when hypothyroidism is suspected than standard
thyroid medications [8,18,70,79,82].

DISCUSSION
Two studies concluded that 6-10% of the population suffers from subclinical hypothyroidism
[9,13] while another concluded that up to 48% of U.S. and U.K. seniors (over age 60) had
subclinical hypothyroidism [6]. While some consider subclinical hypothyroidism to be a
condition diagnosable from serum TSH tests [87], in this investigator’s opinion, true
subclinical hypothyroidism includes assessment from symptoms only. Since thyroid blood
tests do not always reveal that thyroid may be involved, actual symptoms can be much more
significant factors in determining whether a nutritional intervention may be effective; other
doctors have reached similar conclusions [8,10,24,82,88].

There is medical debate about what to do about suspected hypothyroidism [10,11,89]--the
major points are that in many cases hypothyroidism exists, but that there are negative
consequences associated with synthetic thyroxine replacement therapy as it leads to thyroid
atrophy and dependency [10,23,89]. Doesn’t nutritional support appear to be the logical
choice in such situations? It should also be added that the two do not have to be mutually
exclusive--this investigator’s clinical experience has taught him that individuals who take
synthetic thyroid medications often have symptomatic improvement when nutrition for the
thyroid is used as an adjuvant (others have come to similar conclusions [i.e. 82]).

Thyroxine is sometimes prescribed in a specific effort to induce thyroid atrophy [80]; even
when that is not the goal, synthetic thyroxine does not nutritionally support the thyroid gland.
Thyroxine therapies are suspected to possibly increase the incidence of the nutritional
problem of osteoporosis [90-94]. It may be because they interfere with estrogens or it may
be that the atrophy of the thyroid gland leads to a reduced production of calcitonin or other
substances [9,95]. Synthetic thyroid hormone therapy often leads to dependency [80], which
should not be necessary in cases where the thyroid is capable of producing hormones. That is
not to say there is no place for hormone therapies (there clearly are [80]), but nutrition-based
approaches may be the key to improving the health of those who suffer from nutritionallydeficient
thyroid glands [8,18,39,82-85,96].

Since thyroid problems are common, most health professionals believe that they require
management with external agents to reduce their occurrence [24,80]. While this investigator
concurs with this belief in many cases, is it necessary that these agents always be synthetic?
Nutritional interventions administered by properly trained professionals tend to have fewer
negative consequences (pregnancy and other cautions, though do apply) than the synthetic
counterparts offered by some practitioners [9,80,82,95]. Since food and nutritional problems
do contribute to causing thyroid problems [5,32], this researcher encourages doctors and
health researchers to be willing to challenge current paradigms about the thyroid and to work
toward cooperative interventions to help those with thyroid concerns improve and lead better
lives.

REFERENCES
[1] Robinson J, Rall JE, Gordon P. The Thyroid and Iodine Metabolism. In: Duncan’s Diseases of Metabolism,
7th ed. B Saunders, Phil.:1009-1104, 1974.
[2] Guyton AC, Hall JE. Textbook of Medical Physiology, 9th ed. WB Saunders, Phil., 1996.
[3] The Merck Manual of Diagnosis and Therapy, 17th ed. Merck & Co: West Point (PA), 1999.
[4] Mishkin, B. Standards of Care for Headache Diagnosis and Treatment. National Headache Foundation:
Chicago, 1996.
[5] Ricart-Engel W, et al. The relation between thyroid function and nutritional status in HIV-infected patients.
Clin Endocrinol 44(1):53-58, 1996.
[6] Sawin CT. Subclinical hypothyroidism in older persons. Clin Ger Med 11(2):231-238, 1995.
[7] Many thyroid conditions are underdiagnosed. Med Tribune: 2, Jan 25, 1996.
[8] Ingram C. Who Needs Headaches? Literary Visions, Hiawatha (IA), 1991.
[9] Woeber KA. Subclinical hypothyroid dysfunction. Arch Int Med 157:1065-1068, 1997.
[10] Bakke J. Rethinking thyroid guidelines. Cortlandt Forum 46-20:79, 1991.
[11] Lerch M, Meier C, Staub JJ. Is there a need for treatment in subclinical hypo- and hyperthyroidism? Ther
Umch 56(7):369-373, 1999.
[12] Luboshitzky R, et al. Prevalence of cognitive dysfunction and hypothyroidism in an elderly community
population. Isr J Med Sci 32(1):60-65, 1996.
[13] Wiersinga WM. Subclinical hypothyroidism and hyperthyroidism: prevalence in clinical practice. Neth J
Med 46:197-204, 1995.
[14] Karlsson B, et al. Thyroid dysfunction in Down’s syndrome: relation to age and thyroid antibody. Arch
Dis Childhood 79:242-245, 1998.
[15] Bruckert E, Chadarevian R, Turpin G. Low free-thyroxine levels are a risk factor for subclinical
atherosclerosis in euthyroid hyperlipidemic patients. J Cardiovasc Risk 6(5):327-331, 1999.
19
[16] Divi RL, et al. Anti-thyroid isoflavones from soybean. Biochem Pharmacol 54:1087-1096, 1997.
[17] Duncan AM, et al. Modest hormonal effects of soy isoflavones in postmenopausal women. J Clin
Endocrinol Metab 84(10):3479-3484, 1999.
[18] DeCava JA. Underactive and overactive thyroid. Nutr News & Views 3(4):108, 1999.
[19] Iancu I, Dolberg OT. Is caffeine involved in the pathogenesis of combat-stress reaction? Military Med
161(4):230-232, 1996.
[20] Caffeine-withdrawal headache in post-operative patients. Fam Pract Recert 14(8):47, 1992.
[21] Thyroid health. Whitman News Brief 74:2, 2000.
[22] Colzani R, Fang SL, Alex S, Braverman LE. The effect of nicotine on thyroid function in rats. Metabol
47(2):154-157, 1998.
[23] Mulder JE. Thyroid disease in women. Med Clin North Am 82(1):103-125, 1998.
[24] Franklyn J. Subclinical hypothyroidism: To treat or not to treat, that is the question. Clin Endocrinol
43:443-444, 1995.
[25] Haggerty JJ, et al. Subclinical hypothyroidism: A modifiable risk factor for depression? Am J Psychiatry
150(3):508-510, 1993.
[26] Hickie I, et al. Clinical and subclinical hypothyroidism in patients with chronic and treatment-resistant
depression. Aust NZ J Psychiatry 30(2):246-252, 1996.
[27] Pies RW. The diagnosis and treatment of subclinical hypothyroid states in depressed patients. Gen Hosp
Psychiatry 19(5):344-354, 1997.
[28] Mason J, et al. Elevation of serum free triiodothyronine, total triiodothyronine, thyroxine-binding globulin,
and total thyroxine levels in combat-related posttraumatic stress disorder. Arch Gen Psychiatry 51:629-641,
1994.
[29] Franssila KO. Thyroid gland. In Anderson’s Pathology, 9th ed. CV Mosby, St, Louis:1544-1569, 1990.
[30] Cotran RS, Kumar V, Collins T. Robbins’ Pathological Basis of Disease, 6th ed. WB Saunders Co., Phil.,
1999.
[31] Lloyd RV. Endocrine Pathology. Springer-Verlag, New York, 1990.
[32] Hetzel BS, Clugston GA. Iodine. In Modern Nutrition in Health and Disease, 9th ed. Williams & Wilkins,
Balt.:253-264, 1999.
[33] Massol J. Treatment of hypothyroidism. Rev Prat 48(18):2027-2033, 1998.
[34] Pines A, et al. L-thyroxine prevents the bone-conserving effect of HRT in postmenopausal women with
subclinical hypothyroidism. Gynecol Endocrinol 13(3):196-201, 1999.
[35] Whitaker J. Four things to do for fibromyalgia. Health & Healing 6(9):3-4, 1996.
20
[36] Profiles in Nutritional Progress. Rubicon Productions, Bakersfield, 1993.
[37] Wright JS. A Guide to Organic Drugs of the United States Pharmacopoeia 1916. Eli Lilly, Indianapolis,
1917.
[38] Ensminger AH, Ensminger ME, Konlande JE, Robson JRK. Food & Nutrition Encyclopedia, 2nd ed.
CRC Press, New York, 1993.
[39] Elsas LJ, Acosta PB. Nutritional support of inherited metabolic disease. In Modern Nutrition in Health
and Disease, 9th ed. Williams & Wilkins, Balt.: 1003-1056, 1999.
[40] Arroll B. Salt restriction and physical activity in treated hypertensives. NZ Med J:266-268, Jul 14, 1995.
[41] Rivlin RS, Melman KL, Sjoerdsma A. An oral tyrosine tolerance test in thyrotoxicosis and myxedema.
New Engl J Med 272:1143-1148, 1965.
[42] Specific nutrients aid in high-performance activity. Nutr Week:7, June 4, 1994.
[43] Null G. The Complete Encyclopedia of Natural Healing. Kensington Books, New York, 1998.
[44] Burk R, Levander O. Selenium. In Modern Nutrition in Health and Disease, 9th ed. Williams and
Wilkins, Baltimore:265-282, 1999.
[45] Cunnane S. Zinc: Clinical and Biological Significance. CRC Press, Boca Raton, 1988.
[46] Nishiyama S, et al. Zinc supplementation alters thyroid hormone metabolism in disabled patients with zinc
deficiency. J Am Coll Nutr 13(1):62-67, 1994.
[47] Berry MJ, Larsen PR. The role of selenium in thyroid hormone activation. Endocrine Rev 13(2):207-220,
1992.
[48] Contempre B, et al. Effects of selenium supplementation on thyroid hormone metabolism in an iodine and
selenium deficient population. Clin Endocrinol 36:579-583, 1992.
[49] Kadrabova J, et al. Changed serum trace element profile in Down’s syndrome. Biol Trace Elem Res
64(3):201-206, 1996.
[50] Kralik A, et al. Influence of zinc and selenium deficiency on parameters related to thyroid metabolism.
Hormone Metabol Res 28:223-226, 1996.
[51] Bucci I, et al. Zinc sulfate supplementation improves thyroid function in hypozincemic Down children.
Biol Trace Elem Res 67(3):257-268, 1999.
[52] Arreola F, et al. Effect of zinc treatment on serum thyroid hormones in uremic patients under peritoneal
dialysis. Horm Metabol Res 25:539-542, 1993.
[53] Bell IR, et al. Low thyroxine levels in female psychiatric patients with riboflavin deficiency: implications
for folate methylation. ACTA Pyschiatrica Scand 85:360-363, 1992.
[54] Schoenen J, et al. High-dose riboflavin as a prophylactic treatment of migraine: results of an open pilot
study. Cephalgia 14:328-329, 1994.
21
[55] Scalzo R. Naturopathic Handbook of Herbal Formulas. Kivaki Press, Durango (CO), 1994.
[56] Tenney L. Herb Handbook. Woodland Books, Provo, 1987.
[57] PDR for Herbal Medicines, 2nd ed. Medical Economics, Montvale (NJ), 2000.
[58] McGuffin, et al. American Herbal Products Association’s Botanical Safety Handbook, CRC Press, New
York, 1997.
[59] Key, et al. Raised thyroid stimulating hormone associated with kelp intakes in British vegan men. J
Human Nutr 5:323-326, 1992.
[60] Seaweed, kelp, raw. USDA Nutrient Database for Standard Reference, Release 11-1, August 1997.
[61] Lau B. Edible plant extracts modulate macrophage activity and bacterial mutagenesis. Intl J Clin Nutr
12(3):147-155, 1992.
[62] Rauma AI, et al. Iodine status in vegans consuming a living food diet. Nutr Res 14(12):1789-1795, 1994.
[63] Lesher JL. Subclinical hypothyroidism during potassium iodide therapy for lymphacutaneous
sporotrichosis. Cutis 53:128-130, 1994.
[64] Galofre JC, et al. Increased incidence of thyrotoxicosis after iodine supplementation in an iodine sufficient
area. J Endocrinol Invest 17:23027, 1994.
[65] Thiel RJ. Serious Nutrition for Health Care Professionals, 3rd ed. Center for Natural Health Research,
Arroyo Grande (CA), 1997.
[66] Scullcap. The Lawrence Review of Natural Products. Facts and Comparisons, St. Louis, Feb 1990.
[67] Hoffman D. The Herb Handbook. Healing Arts Press, Rochester (VT), 1988.
[68] Dunbar R. Foraging for nature’s balanced diet. New Scientist: 25-28, August 31, 1991.
[69] King JC, Keen CL. Zinc. In Modern Nutrition in Health and Disease, 9th ed. Williams & Wilkins,
Balt.:223-239, 1999.
[70] DeCava JA. Glandular supplements. Nutr News & Views 1(3):1-10, 1997.
[71] Burns D. Growing scientific evidence support glandular therapy. Digest Chiropractic Econ: 74-79,
Nov/Dec 1987.
[72] Schwartz EF. Glandular therapy. Am Chiropractor: 14-18, Jan/Feb 1983.
[73] Harrower H. Practical Organotherapy, 3rd ed. W.B. Conkey, Hammond (IN), 1921.
[74] Gardner M. Intestinal absorption of intact peptides and protein from the diet - a neglected field? Biologic
Rev 59:289-331, 1984.
[75] Popov IM, et al. Cell therapy. J Intl Acad Prev Med 3:74-82, 1977.
22
[76] Howell E. Enzyme Nutrition. Avery Publishing, Wayne (NJ),1985.
[77] Balch JF, Balch PA. Prescription for a Nutritional Healing. Avery Publishing, Garden City (NY), 1997.
[78] Versendaal DA. Contact Reflex Analysis and Applied Trophology. D.A. Versendaal, Holland (MI), 1990.
[79] Williams DG. They’re finally catching on. Alternatives 8(10):77-78, 2000.
[80] Physician’s Desk Reference, 54th ed. Medical Economics, Montvale (NJ), 2000.
[81] Fischbach F. A Manual of Laboratory Diagnostic Tests, 2nd ed. JB Lipponcott, Phil.,1984.
[82] Cutler EW. Winning the war against immune disorders and allergies. Delmar, NY, 1998.
[83] Thiel R. Natural interventions for migraine headache sufferers. ANMA Monitor 2(3):5-9, 1998.
[84] Thiel R. Nutritional interventions for the thyroid. ANMA Monitor 4(1):6-14, 2000.
[85] Thiel R. Chronic fatigue assessment and intervention: The result of 101 cases. ANMA & AANC J 1(3)17-
19, 1996.
[86] Lathan R. Chronic fatigue? Consider hypothyroidism. Phys & Sports Med 19(10):67-70,66, 1991.
[87] Nunez S, Leclere J. Diagnosis of hypothyroidism in the adult. Rev Prat 48(18):1993-1998, 1998.
[88] Zulewski H, et al. Estimation of tissue hypothyroidism by a new clinical score: evaluation of patients with
various grades of hypothyroidism and controls. J Clin Endocrinol Metab 82(3):771-776, 1997.
[89] Adlin V. Subclinical hypothyroidism: deciding when to treat. Am Fam Physician 57(4):776-780, 1998.
[90] Wartofsky L. Use of sensitive TSH assay to determine optimal thyroid hormone therapy to avoid
osteoporosis. Annu Rev Med 42:341-345, 1991.
[91] Foldes J, et al. Bone mineral density in patients with endogenous subclinical hyperthyroidism: is this
thyroid status a risk factor for osteoporosis. Clin Endocrinol 39(5):521-527, 1993.
[92] Langdahl BL. Is skeletal responsiveness to thyroid hormone altered in primary osteoporosis or following
estrogen replacement therapy? J Bone Min Res 12(1):78-88, 1997.
[93] Fowler PB, McIvor J, Sykes L, Macrae KD. The effect of long-term thyroxine on bone mineral density
and serum cholesterol. J R Coll Physicians Lond 30(6):527-532, 1996.
[94] Erlacher L, et al. Salmon calcitonin and calcium in the treatment of male osteoporosis: the effect on bone
mineral density. Wein Klin Wochenschr 109(8):270-274, 1997.
[95] Dellovade TL, Zhu YS, Krey L, Pfaff DW. Thyroid hormone and estrogen interact to regulate behavior.
Proc Natl Acad Sci 93:12581-12586, 1996.
[96] Wagner W, Nootbaar-Wagner U. Prophylactic treatment of migraine with gamma-linolenic and alphalinolenic
acids. Cephalgia 17(2):127-130, 1997.