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Elsevier Australia
Clinical Naturopathic Medicine
Leah Hechtman
MSci Med [RHHG] (USYD), BHSc (UNE), ND (NCC) MACNEM,
MASRM, MATMS, MESHRE, MFSA, MNHAA
President, The National Herbalists Association of Australia (NHAA)
Lecturer UG and PG, School of Biomedical and Health Science,
University of Western Sydney, NSW
Faculty Member and Lecturer, Green Medicine Institute (GMI)
Director, The Natural Health and Fertility Centre, Natural Health and Fertility Pty Ltd
Private Practitioner, Sydney, NSW
Sydney Edinburgh London New York Philadelphia St Louis Toronto
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Elsevier Australia
Churchill Livingstone
is an imprint of Elsevier
Elsevier Australia. ACN 001 002 357
(a division of Reed International Books Australia Pty Ltd)
Tower 1, 475 Victoria Avenue, Chatswood, NSW 2067
FIGURE 17.2 Flow diagram of negative feedback between glucagon and
insulin.
[4]
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PA R T 3 : T H E B O DY S Y S T E MS 1030
leads to more contractions, and so the cycle continues
until the delivery of the child. This feedback system has
been used traditionally to ensure the prompt delivery of
the placenta after the birth of a child, as the stimulation
caused by breastfeeding immediately after birth further
enhances the release of oxytocin, thus aiding the contrac-
tion of the uterus.
ROLE OF THE NATUROPATH
TRADITIONAL INTERPRETATION
The traditional understanding of the endocrine glands
was largely reliant upon symptomatic evidence, as there
was no deeper knowledge of the functions of the endo-
crine system until the mid 19th century. More com-
prehensive theories were developed in the mid to late
twentieth century, but many questions still remain to be
answered today.
The developmental changes caused by the castration of
calves and humans (as evident in eunuchs) caught the
attention of many enquiring minds in ancient Egypt and
China, and led philosophers of those times to wonder at
the mechanism of action of the testes. Similarly goitres
were rst recognised in China in 2700 BC,
[391]
and repeat-
edly noted in numerous cultures since. Avicenna (Abou
Ali Sina, 980 1037), in his medicinal and philosophical
masterpiece al-Qanun (The Cannon of Medicine), out-
lined the physical symptoms of both insulin-dependent
and non-insulin-dependent diabetes.
[392]
However, it was
many centuries later, in 1869, before the pancreatic insula
were discovered by Langerhans.
The anatomical discoveries of each of the endocrine
glands greatly pre-dated the understanding of their func-
tions. The thymus gland was known to the Alexandrians
in the 3rd century BC , and the thyroid, pineal and pitu-
itary glands were anatomically described by Galen.
[393]
The adrenal glands were not discovered until the 16th
century and the pancreatic and parathyroid glands in the
latter 19th century. Pre-dating each of these discoveries
was the anatomical observation by the earliest physicians
of both the gonads and the liver.
[393]
Although the functions of individual endocrine hor-
mones (a term rst used by Starling in 1905)
[394]
were
unknown, symptomatic treatment of endocrine diseases
was widespread. For example, goats rue ( Galega ofci-
nalis ) was used in medieval Europe for the treatment
of diabetes and became the basis of the modern drug
metformin. Goats rue continues to be used by modern
herbalists for its blood sugar regulating actions. Similarly
fenugreek ( Trigonella foenum-graecum ) was used by Avi-
cenna in the treatment of diabetes, and also continues to
be used for this condition in modern naturopathic treat-
ment.
[395]
The treatment of the endocrine system initially
centred on the humoral beliefs of Galen. The pituitary
was thought to be a sump for phlegm (waste products)
from the brain which were then expelled via the nasal
passage.
[396]
Similarly, goitres were thought to be caused
from excess phlegm; however, they were treated with
empirical treatments of marine sponge and seaweed.
[391]
These humoral theories were largely believed until 1855,
when a number of scientists and physicians disproved
them, although they had been anatomically disproved
some 200 years previously by anatomists such as Conrad
Victor Schneider and Richard Lower.
[394]
MODERN INTERPRETATION
The modern interpretation of the endocrine system is
based on both the traditional use of herbs (for both
symptomatic relief and treating the cause) and the sci-
entic understanding of the connection between the
nervous and endocrine systems. The scientic experi-
mentation of the mid 19th century saw a radical shift
and deeper understanding of the endocrine system, as
experiments such as those carried out by A.A. Berthold
(in 1849) were able to show that the action of the endo-
crine glands was not local, but systemic.
[397]
Berthold cas-
trated four out of six young male chickens. Two of these
four had their testes transplanted to the abdominal cav-
ity, while the remaining two had their testes removed
completely. The growth of the two uncastrated chickens
was normal, and they developed into roosters with fully
developed cones, wattles and plumage. The two fully cas-
trated chickens failed to develop any male rooster char-
acteristics, displaying only atrophied combs and wattles.
Surprisingly for the scientists of the time, the two chick-
ens with the transplanted testes grew to become fully
developed roosters, displaying the same male character-
istics as the control roosters. This was among the rst evi-
dence that hormones existed, that they were transported
throughout the body in the bloodstream, and that they
had a decisive role in sexual growth and maturation. Fur-
ther experiments and observations conducted around
this time helped to prove this theory, such as the observa-
tions of Thomas Addison (also in 1849) on patients with
what he termed melasma suprarenale (adrenal disease),
a disorder which is now called Addisons disease in his
honour.
[393]
The understanding of the endocrine system progressed
rapidly from this point, as these internal secretions
DNA damage
p53
Cyclin A-cdk2
Cyclin E-cdk2
Cyclin D-cdk4/6
E2F
RB-E2F
?
Growth
factors
p21
cip1
p14
ARF
DHFR
DNA
Polymerase
Cyclin A
Cyclin E
Cyclin A-cdk-2
Cyclin E-cdk-2
E2F-DP
P
DP- P
E2F- P
P
RB- P
p27
kip1
p57
kip2
p16
INK4a
p15
INK4b
p18
INK4c
Replication
FIGURE 17.3 Flow diagram of negative and positive feedback systems.
[5]
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Chapter 17 The Endocr i ne System 1031
were eventually shown to be chemical structures called
hormones.
[393]
The discovery of each individual hor-
mone quickly ensued at the turn of the 20th century.
Following this the role of the hormones on the overall
process of metabolism (a term rst used by Michael
Foster in 1876) and regulation was discovered via the
work of Harvey Cushing and Langdon-Brown.
[393]
Until
the mid 20th century the symptomatic approach to
treatment remained, with varying results. This is evi-
dent in the quote below from Ellingwood (1910)
[398]
discussing the treatment and prognosis of diabetes
mellitus:
Treatment: As yet no specics have been discovered, either for
this disease as a whole, or for any of its attendant conditions.
Various measures have been devised but these have usually been
ultimately abandoned. While dietary measures are by far the
most important.
Prognosis: The prognosis as to cure is always unfavourable.
The most recent development in the understanding and
subsequent treatment approach to the endocrine system
has developed since the 1920s due to the knowledge
of the interconnected nature of both the endocrine and
nervous systems.
[8]
Specically, it is the vast amount of
research conducted in the latter part of the 20th century
regarding the hypothalamic pituitary adrenal (HPA)
axis and psychoneuroimmunology (PNI) that has most
signicantly altered the understanding of the endo-
crine system.
[399]
This innate link between the brain,
the body and health has given a greater scientic basis
to the holistic nature of the naturopathic treatment
approach. For example, studies conducted in Russia
on Siberian ginseng ( Eleutherococcus senticosus ) during
the great space race have helped to establish that the
use of single herbs can alter immune function, physical
stamina and aid stress adaptation, all via the endocrine
system.
[283]
This holistic treatment of the endocrine sys-
tem is often a key factor in treatment due to the role
stress plays in many patients lives. However, the power
of what Bellamy and Pster (1992)
[368]
term the largest
endocrine gland (the brain) is yet to be fully realised.
They quote Albert Schweizers musings to better explain
their point:
The witch doctor succeeds for the same reason all the rest of us
succeed. Each patient carries his own doctor inside him. They
come to us not knowing that cure. We are at our best when we
give the doctor who resides within each patient a chance to go
to work. (p. 259)
This concept of the patients innate healing ability is cen-
tral to the naturopathic approach to treatment, and is
rapidly being given a scientic basis of evidence via the
function of the endocrine system.
INVESTIGATIONS
Investigations used in endocrine disorders are sum-
marised in Table 17.4 .
TESTOSTERONE AND SEX HORMONE BINDING
GLOBULIN (SHBG)
Normal values of testosterone and sex hormone binding
globulin are shown in Table 17.5 .
HUMAN CHORIONIC GONADOTROPHIN (HCG)
TEST (URINE PREGNANCY TEST)
This test is used to diagnose pregnancy, monitor high
risk pregnancy, and as a tumour marker for certain
tumours ( Table 17.6 ). Human chorionic gonadotro-
phin hormone is normally secreted by the placental
tissue after the ovum is fertilised (i.e. from the earli-
est stages of development). HCG will appear in the
blood of pregnant women as early as 10 days after
conception.
URINARY HORMONE ASSESSMENT
Oestrogen metabolites an assessment of the urinary
levels of oestrogen metabolites 2-hydroxyoestrone
(2-OHE1) and 16 -hydroxyoestrone (16 -OHE1) pro-
vides information about the way in which oestrogen is
being metabolised by the patient. A result showing a
low ratio (a reduced 2-hydroxyoestrone) indicates that
there is a state of oestrogen excess within the patient.
Alternatively a high ratio (increased 2-hydroxyoestrone)
indicates an oestrogen decient state. This test is suit-
able for males and females and is conducted using the
rst morning urine sample (the patient must fast from
10 p.m. the evening before). Females taking the test are
advised to take it between days 18 and 25 of their men-
strual cycle.
URINARY IODINE
Excess iodine is excreted via the kidneys, thus providing
an accurate measurement of recent iodine usage/require-
ment ( Table 17.7 ). First morning urine samples provide
the most accurate results; 24-hour urine samples are not
required for this test. A study conducted in Indonesian
children found urinary iodine excretion to be the best
method for detecting iodine deciency when compared
with TSH, goitre palpation, ultasonography, intellectual
performance and anthropometric indices (Pardede, Hard-
jowasito et al. 1998).
Nutritional medicine treatment of endocrine disorders
is described in Table 17.2 . Some useful herbal medicines
are listed in Table 17.3 . And Table 17.8 lists some poten-
tial herb drug interactions.
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PA R T 3 : T H E B O DY S Y S T E MS 1032
TABLE 17.2 Nutritional Medicine
Requirement Justifcation RDI
[350]
Therapeutic Dose Food Sources
A high strength,
sustained release
multivitamin/
mineral
preparation
The excess production of thyroid hormones
that occurs in hyperthyroidism leads to a higher
metabolic rate and subsequently nutrients are
depleted at a higher rate. Additionally, in hyper-
thyroidism there is malabsorption. Due to these
factors a greater number of nutrients are required
by the body. Similarly where there is adrenal
exhaustion higher requirements will be required
by the body to meet increased demands
N/A
Vitamin B complex The B vitamins provide energy and support
during physically demanding periods. They
are involved in maintaining the health of the
hormone- producing glands
[351]
Comprehensive
complex containing
individual B vitamins as
per below:
Legumes, whole
grains, nuts, beans,
brewers yeast, leafy
green vegetables
Thiamin
(vitamin B
1
)
Vitamin B
1
is involved with other B vitamins in
energy metabolism and the normal functioning of
nerves. Vitamin B
1
may be needed during periods
of increased physical and mental stress and has
been clinically proven to protect the adrenal
gland from functional exhaustion
Men:
19 30 years 1.2 mg/d
31 50 years 1.2 mg/d
51 70 years 1.2 mg/d
> 70 years 1.0 1.2 mg/d
Women:
19 30 years 1.1 mg/d
31 50 years 1.1 mg/d
51 70 years 1.1 mg/d
> 70 years 1.1 mg/d
5 150 mg/d Legumes,
liver, nuts,
whole grains,
wheatgerm
Vitamin B
2
Vitamin B
2
is crucial in the production of energy
and may be needed in periods of heightened
stress. Along with vitamins B
5
, B
12
, folic acid,
potassium and sodium it stabilises the activity of
the adrenal glands
Men:
19 30 years 1.3 mg/d
31 50 years 1.3 mg/d
51 70 years 1.3 mg/d
>70 years 1.6 mg/d
Women:
19 30 years 1.1 mg/d
31 50 years 1.1 mg/d
51 70 years 1.1 mg/d
>70 years 1.3 mg/d
10 200 mg/d Avocados, beans,
currants, eggs,
milk and dairy
products, sprouts,
whole grains
Vitamin B
3
Nicotinamide is converted into the active forms
of niacin in the body. Niacin is required for the
function of more than 200 enzymes throughout
the body and is a component of the glucose toler-
ance factor, which helps to control blood glucose
delaying or preventing the need for insulin by
interfering with immune-mediated beta cell
destruction. Vitamin B
3
has also been found to
help slow down the development of nephropathy
in diabetes
[351]
(As niacin equivalents)
Men:
19 30 years 16 mg/d
31 50 years 16 mg/d
51 70 years 16 mg/d
>70 years 16 mg/d
Women:
19 30 years 14 mg/d
31 50 years 14 mg/d
51 70 years 14 mg/d
>70 years 14 mg/d
10 3000 mg/d Almonds, eggs,
chicken, mackerel,
meat, peanuts,
salmon, sardines,
sunfower seeds
Vitamin B
5
Vitamin B
5
enhances adrenal cortex function.
Defciency leads to a compromised adrenal cortex
function. Vitamin B
5
down-regulates hypersecre-
tion of cortisol secondary to high stress situations
Men:
19 30 years 6 mg/d
31 50 years 6 mg/d
51 70 years 6 mg/d
>70 years 6 mg/d
Women:
19 30 years 4 mg/d
31 50 years 4 mg/d
51 70 years 4 mg/d
>70 years 4 mg/d
20 500 mg/d Avocado, beans,
egg yolks, green
vegetables, milk,
mushrooms,
oranges,
royal jelly,
sweet potato,
wholegrain
cereals
Vitamin B
6
Along with the other B vitamins, vitamin B
6
is
important during periods of stress, providing sup-
port to the nervous system and adrenal glands.
Vitamin B
6
defciency has been shown to cause
symptoms of hypoglycaemia, increased insulin
sensitivity and degeneration of beta cells
Men:
19 50 years 1.3 mg/d
51 70 years 1.7 mg/d
Women:
19 50 years 1.3 mg/d
51 70 years 1.5 mg/d
10 150 mg/d Brewers yeast,
chicken, yolk,
legumes, mack-
erel, oatmeal,
salmon, tuna,
walnuts
Vitamin B
9
Along with vitamins B
2
, B
5
, B
12
, potassium and
sodium vitamin B
9
stabilises the activity of the
adrenal glands
Men:
19 70 years 400 g/d
Women:
19 70 years 400 g/d
1000 5000 g/d Beans, eggs,
green leafy
vegetables, lentils,
yeast
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Elsevier Australia
Chapter 17 The Endocr i ne System 1033
TABLE 17.2 Nutritional Medicinecontd
Requirement Justifcation RDI
[350]
Therapeutic Dose Food Sources
Vitamin B
12
Along with vitamins B
2
, B
5
, folic acid, potassium
and sodium, vitamin B
12
stabilises the activity of
the adrenal glands
Men:
19 70 years 2.4 g/d
Women:
19 70 years 2.4 g/d
300 800 g Bacterial synthesis
in the gut
Clams, egg yolk,
herring, milk,
meat, oysters,
salmon, sardines
Biotin Supplementation with biotin has been found to
help maintain healthy blood sugar levels in indi-
viduals with diabetes as the generation of glucose
is dependent on a biotin-containing enzyme
Men:
19 70 years: 30 g/d
Women:
19 70 years: 25 g/d
0.5 15 mg/d Bean sprouts,
egg yolk, milk,
peanuts, soy
beans, wholegrain
cereals
Vitamin C Vitamin C is a water soluble antioxidant that
protects against oxidative stress associated with
thyroid diseases. The adrenal gland is among the
organs with the highest concentration of vitamin C
in the body. Interestingly, both the adrenal cortex
and the medulla accumulate such high levels of
ascorbate. Vitamin C is a co-factor required both
in catecholamine biosynthesis and in adrenal
steroidogenesis. Production of adrenaline and
noradrenaline are dependent on vitamin C.
[352]
Vitamin C can also help to regulate blood glucose
Men:
19 70 years 45 mg/d
Women:
19 70 years 45 mg/d
250 10,000 mg/d Blackcurrant,
broccoli, citrus
fruits, kiwis,
strawberries,
rosehips, guava,
mangoes,
pineapple
Vitamin D Glucose intolerance and insulin secretion has
been observed during vitamin D defciency,
resulting in type 2 diabetes. It is theorised that
this is due to vitamin D receptors in several tissues
and cells, including the pancreatic beta-cells
Men:
19 50 years 5.0 g/d
51 70 years 10.0 g/d
>70 years 15.0 g/d
Women:
19 50 years 5.0 g/d
51 70 years 10.0 g/d
>70 years 15.0 g/d
400 1600 IU/d Synthesised by
the action of
sunlight on skin,
fsh liver oils cod,
halibut, herring,
tuna, egg yolk,
milk, sprouted
seeds
Vitamin E Hypothyroidism is accompanied with increased
oxidative stress and fat soluble antioxidant vita-
min E supplementation exerts benefcial efects
on this situation. Vitamin E can enhance insulin
sensitivity thus reducing the need for insulin and
other hypoglycaemics
[351]
Men:
19 70 years 300 mg/d
Women:
19 70 years 300 mg/d
100 800 mg/d Almonds, beef,
corn, egg yolks,
nuts, saf ower,
sunfower,
wheatgerm
L-tyrosine L-tyrosine is an essential precursor for the synthe-
sis of the catecholamines adrenaline, noradrena-
line and dopamine and the thyroid hormone
thyroxine. Supplementation with tyrosine aids
adrenal function helping during periods of pro-
longed stress, to support the body and improve
stress adaptation.
1120 mg/d 1120 mg/d Almonds, beef,
cheese, chicken,
eggs, fsh, soy
beans, wild game
Zinc Zinc is required for healthy thyroid function
and the synthesis and metabolism of thyroid
hormones. Defciency of zinc dependent enzymes
may result in decreased thyroid hormone levels
and resting metabolic rate (RMR). Changes in zinc
metabolism are commonly observed in diabetic
patients
Men:
19 70 years 14 mg/d
Women:
19 50 years 6 mg/d
10 100 mg/d Beef, baked beans,
cashews, egg
yolks, ginger, her-
rings, liver, milk,
lamb, oysters,
sunfower and
pumpkin seeds,
whole grains
Selenium Selenium is essential for the biosynthesis and
function of the iodothyronine deiodinase
enzymes that are essential for the conversion
of T
4
to T
3
. Selenium-dependent glutathione
peroxidases protect against oxidative damage to
the thyroid gland. Defciency leads to decreased
conversion of T
4
to T
3
, and oxidative stress on the
thyroid gland as a result of reduced glutathione
peroxidise activity. The thyroid gland contains
more selenium per gram than any other tissue in
the body. Selenium is also important for healthy
blood sugar regulation. Defciency may reduce
insulin secretion
Men:
19 70 years 70 g/d
Women:
19 70 years 60 g/d
200 600 g/d Alfalfa, brazil
nuts, cashews,
crab, eggs, fsh,
garlic, kidney,
liver, mackerel,
oysters, peanuts,
tuna, whole grain
cereals, broccoli,
onions
Continued
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PA R T 3 : T H E B O DY S Y S T E MS 1034
TABLE 17.2 Nutritional Medicinecontd
Requirement Justifcation RDI
[350]
Therapeutic Dose Food Sources
Magnesium Magnesium assists in the maintenance of normal
healthy blood glucose metabolism. Hypo-
magnesaemia is frequently present in diabetic
patients hence magnesium is often suggested
in patients with diabetes mellitus who have
proven hypomagnesaemia and the presence of its
complications
Men:
19 30 years 410 mg/d
31 70 years 420 mg/d
Women:
19 30 years 310 mg/d
31 70 years 320 mg/d
300 1000 mg/d Eggs, cocoa,
almonds, brewers
yeast, cashews,
kelp, wheatbran,
wheatgerm,
buckwheat
Manganese Manganese plays a crucial role as part of its role
in the glucose tolerance factor and is required
for metabolism of carbohydrates as the synthesis
of new glucose from puyruvate is necessary on
manganese-containing enzymes as well as for
normal insulin secretion. Defciency may contrib-
ute to blood sugar abnormalities and reduced
pancreatic cell function
Manganese is required for thyroid hormone
function
Men:
19 70 years 5.5 mg/d
Women:
19 70 years 5 mg/d
2 50 mg/d Almonds, beans,
coconuts, corn,
kelp, sunfower
seeds, legumes,
walnuts, whole
grains
Alpha lipoic acid Alpha lipoic acid, also known as thioctic acid,
is an antioxidant and decreases the risk of cell
damage attributed to free radicals. Alpha lipoic
acid is unique in that it is soluble in water as
well as fat and is therefore able to scavenge
both fat- and water-soluble free radicals. It also
has the ability to recycle or regenerate endog-
enous antioxidants including vitamins C and E,
CoQ10 and glutathione. Alpha lipoic acid plays
a role in glucose metabolism and is involved in
the transport of blood glucose into cells. It may
therefore help maintain healthy blood sugar
levels and has been used in diabetics to assist
with the conversion of sugar to energy and is
thought to be beneficial in reducing the effects
of oxidative stress
[353]
which are associated with
this condition, as well as decreasing symptoms
associated with diabetes such as diabetic
polyneuropathy
[354]
50 600 mg/d
[355]
600 mg/d
[353,355]
Typical dietary
sources of lipoic
acid are muscle
meats, heart,
kidney, and liver,
and to a lesser
degree, fruits
and vegetables;
potatoes
Chromium Chromium is an essential micronutrient for
humans. It plays a role as a co-factor in all
insulin-regulated activities including carbo-
hydrate, lipid and protein metabolism and is
an essential component of glucose tolerance
factor, a compound that helps to regulate blood
sugar. Chromium is particularly important for
normal carbohydrate metabolism and assists
in maintaining healthy blood glucose levels, by
aiding the transport of glucose from the blood
into the cells
Chromium may be used where diets are high
in simple sugars and refned carbohydrates,
which may have increased chromium
requirements
Men:
19 70 years 45 g/d
Women:
19 70 years 35 g/d
100 400 g
[356,357]
Asparagus, beer,
cheese, egg yolk,
molasses, nuts,
oysters, peanuts,
prunes, raisins
Iodine Iodine is an essential component of the thyroid
hormones thyroxine (T
4
) and triiodothyronine
(T
3
), and defciency impairs synthesis of these
hormones. Approximately 60 g of iodine
is absorbed each day by the thyroid gland;
however, it is estimated that 150 g is required
each day for optimum functioning of the thyroid
gland
[358]
Men:
19 70 years 150 g/d
Women:
19 70 years 150 g/d
100 1100
[356,359]
Seaweed
(e.g.wakame),
cod, iodised
salt, lima beans,
mushrooms,
oysters
Sources: see end of chapter
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Elsevier Australia
Chapter 17 The Endocr i ne System 1035
TABLE 17.3 Herbal Medicine
Class Example Justifcation
Adaptogen Eleuthrococcus senticosus
(Siberian ginseng)
Adaptogens improve non-specifc responses to stress by increasing the resistance of the
recipient to a variety of physical, chemical, or biological stressors while also promoting
recovery and acting as a general regulator in the body. Siberian ginseng has traditionally
been used as a prophylactic to build resistance, reduce susceptibility to illness, and pro-
mote health and longevity. Its activity appears to be based on whole body efects rather
than particular organs or systems, which lends support to the traditional view that ginseng
is a tonic that can revitalise the functioning of the organism as a whole. Siberian ginseng
increases levels of noradrenaline, serotonin, adrenaline and cortisol (improving positive
and negative responses to stress)
Adrenal restorative Rehmannia glutinosa
(rehmannia)
Rehmannia is an adrenal tonic that has been used in Traditional Chinese Medicine to
nourish qi (vital energy). Rehmannia works by supporting the adrenal cortex and pituitary
gland during prolonged stress and regulates cortisol levels. In trials done on rabbits, rehm-
annia reversed morphological changes to the pituitary and adrenal cortex, antagonising
the suppressive efect of glucocorticoids on the hypothalamus pituitary adrenal axis
[360]
Tonic Withania somnifera
(ashwagandha)
Withania somnifera is a gentle tonic that is considered to be the pre-eminent adaptogen
from the Ayurvedic medical system. Withania improves responses to stress, possibly via an
action on the adrenal glands, and also has anti-infammatory and sedative efects. Withania
is used to treat nervous exhaustion, convalescence and debility associated with chronic
infammatory conditions
Aldose reductase
inhibitor
Glycyrrhiza glabra
(liquorice)
Aldose reductase is an enzyme in carbohydrate metabolism that converts glucose to
sorbitol. Its activity increases as the glucose concentration rises in diabetes particularly
in the lens of the eyes, the peripheral nerves and glomerulus, leading to retinopathy and
neuropathy. Liquorice in its role as an aldose reductase inhibitor helps to prevent eye and
nerve damage in people with diabetes
Antiobesity Coleus forskohlii (coleus) The exact mechanism of C oleus forskohlii in weight loss is unknown; however, based on in
vitro data it is hypothesised that Coleus forskohlii may cause an increase in cyclic adenosine
phosphate (cAMP) which in turn leads to an activation of protein kinase which activates
lipase (an enzyme involved in the breakdown of triglycerides, fatty substances in the blood
and components of LDL cholesterol). This results in thermogenesis, loss of body fat and the
maintenance of lean body mass.
[361]
Coleus forskohlii may have a thyroid stimulating action,
thus possibly increasing metabolic rate and thermogenesis and may regulate insulin
secretion thus positively afecting fat and protein metabolism
Appetite inhibiting Gymnema sylvestre
(gymnema)
Gymnema is an Ayurvedic herb with the ability to inhibit the taste of sweetness, hence its
nickname sugar destroyer. Gymnema reduces desire for food, particularly those that are
sweet in taste, leading to its action as an appetite inhibitor. This action also means it is a
useful addition to any weight-loss programme
Hypoglycaemic Galega of cinalis
(goats rue)
Galegine in goats rue has been associated with marked reductions in blood sugar levels.
Studies in the 1970s demonstrated that the alkaloid galegine within goats rue is respon-
sible for reducing blood sugar levels.
[362]
The British Herbal Pharmacopeia confrms the
action of galega as a hypoglycaemic agent with anti-diabetic activity and indicates its use
for diabetes
[363]
Hepatic,
hepatoprotective,
hepatotrophorestor-
ative
Bupleurum falcatum
(bupleurum)
The liver plays an important role in the efective metabolism of the thyroid hormones as
well as the regulation of their systemic endocrine efects. Suboptimal liver function can
afect thyroid hormone metabolism hence the application of hepatics in the management
of thyroid conditions. Bupleurum falcatum is a Traditional Chinese Medicine which displays
hepatoprotective activity. It is highly indicated where there is poor liver function
Pancreatic
trophorestorative
(endocrine functions)
Gymnema sylvestre
(gymnema)
The exact mode of action by which gymnema exerts its pancreatic trophorestorative action
is unknown. It appears that gymnema helps to support healthy pancreatic function via a
wide array of actions rather than just one; these include the inhibition of intestinal absorp-
tion of glucose and promotion of glucose homeostasis, and also increasing the number of
cells in the pancreas responsible for insulin production
Thyroid stimulant Fucus vesiculosus
(bladderwrack)
Fucus vesiculosus is a valuable source of iodine, a trace element necessary for regulating the
bodys metabolism and normal production of thyroid hormones. Organic iodine, such as
that found in bladderwrack, is likely to be better utilised by the body in terms of bioavail-
ability and less likely to be excreted than potassium iodide
[364]
Thyroid suppressant/
regulator
Lycopus spp. (bugleweed) Lycopus is a perennial herb containing phenolic acids. In the 19th century Lycopus was
given to calm the nerves. Today Lycopus is primarily used to help manage hyperthyroid
conditions as well as the associated cardiac symptoms. High doses of Lycopus cause a
reduction of thyroid stimulating hormone in animal experiments; conversely in hyperthy-
roid patients treated with low doses of Lycopus improvement of cardiac symptoms was
reported
[365]
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Elsevier Australia
PA R T 3 : T H E B O DY S Y S T E MS 1040
TABLE 17.8 Potential Interactions
Drug Classes Commonly Used Herb/Supplement Potential Outcome Recommendation
Diabetes mellitus
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (glipizide,
glibenclamide, glimepiride)
Insulin analogue (lispro, aspart, isophane,
lente, ultralente, detemir, glargine)
Alpha lipoic acid (ALA) Possible additive or synergistic efect;
hypoglycaemia may result; however,
clinical signifcance uncertain
ALA may protect insulin action under
oxidative stress
Consider co-administra-
tion: the use of ALA as
an adjunctive to other
diabetic treatment may act
as in a preventative mode,
particularly in dysglycae-
mic patients
Monitor patient closely
in conjunction with other
health professionals
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (glibenclamide,
glimepiride)
Coenzyme Q10 Possible benefcial efect; some hypo-
glycaemic drugs inhibit the CoQ10
enzyme NADH-oxidase, which may
exert further adverse efects on insulin
biosynthesis in individuals with diabe-
tes mellitus
Consider co-administra-
tion: monitor glucose
levels closely
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (glipizide,
glibenclamide, glimepiride)
Oral hypoglycaemic agents/Insulin sensi-
tisers/ -glucosidase inhibitors (acarbose)
Oral hypoglycaemic agents/insulin
secretagogues/glitinides (repaglinide)
Oral hypoglycaemic agents/insulin
sensitisers/ glitazones/thiazolidinediones
(rosiglitazone, troglitazone, pioglitazone)
Insulin analogue (lispro, aspart, isophane,
lente, ultralente, detemir, glargine)
Conjugated linoleic
acid (CLA)
Interaction inconclusive; CLA has been
shown to improve glucose tolerance,
but also to increase fasting plasma
glucose concentrations
Low risk: monitor patient
closely in conjunction with
other health professionals
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (glipizide,
glibenclamide, glimepiride)
Insulin analogue (lispro, aspart, isophane,
lente, ultralente, detemir, glargine)
Omega-3 fatty acids Interaction uncertain; adverse efects
of fsh oil on glucose control medica-
tions are unlikely, possibly short-lived,
and may vary according to the patient
Low risk: clinical implica-
tions of interaction will
depend on a variety of
factors: monitor patient
Lifestyle interventions also
recommended to moderate
possible adverse efects of
omega-3 fatty acid therapy
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (glipizide,
glibenclamide, glimepiride)
Oral hypoglycaemic agents/insulin sensi-
tisers/ -glucosidase inhibitors (acarbose)
Oral hypoglycaemic agents/insulin
secretagogues/glitinides (repaglinide)
Oral hypoglycaemic agents/insulin
sensitisers/ glitazones/thiazolidinediones
(rosiglitazone, troglitazone, pioglitazone)
Acetyl- L -carnitine Possible additive efect; L -carnitine
signifcantly lowers fasting plasma
glucose in type 2 diabetic patients.
However, fasting triglyceride levels are
increased
Low risk: consider
co-administration in
patients with healthy lipid
profle. Monitor lipid levels
in conjunction with other
health professionals
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (glipizide,
glibenclamide, glimepiride)
Oral hypoglycaemic agents/insulin
sensitisers/ -glucosidase inhibitors
(acarbose)
Oral hypoglycaemic agents/insulin
secretagogues/glitinides (repaglinide)
Oral hypoglycaemic agents/insulin
sensitisers/ glitazones/thiazolidinediones
(rosiglitazone, troglitazone, pioglitazone)
Insulin analogue (lispro, aspart, isophane,
lente, ultralente, detemir, glargine)
Chromium Possible additive efect; chromium
potentiates insulin activity through
multiple mechanisms and has hypogly-
caemic activity in some individuals
Possible benefcial efect; compromised
chromium status may contribute to
insulin resistance, dysglycaemia and
onset of diabetes
Caution: monitor drug and
nutrient requirements,
and patient glucose levels
closely
Consider co-administration
if defciency is indicated.
Monitor patient in
conjunction with other
health professionals
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Chapter 17 The Endocr i ne System 1041
TABLE 17.8 Potential Interactionscontd
Drug Classes Commonly Used Herb/Supplement Potential Outcome Recommendation
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (glipizide,
glibenclamide, glimepiride)
Magnesium Possible benefcial interaction; mag-
nesium intake may improve insulin
sensitivity and secretion, thus increas-
ing drug activity on glucose. Enhanced
drug response may cause hypoglycae-
mia or facilitate therapeutic strategy
Consider co-adminis-
tration: Monitor patient
closely and titrate drug
dose
Insulin analogue (lispro, aspart, isophane,
lente, ultralente, detemir, glargine)
Magnesium Possible benefcial efect; magnesium
can improve insulin sensitivity and
secretion
Consider co-adminis-
tration: monitor patient
closely
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Vitamin B
1
Possible adverse efect; taken together,
thiamine and metformin may increase
the risk of lactic acidosis, and reduce
thiamine activity
Low risk: co-administer if
indicated. Separate doses
by 2 4 hours
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
sensitisers/ glitazones/thiazolidinediones
(rosiglitazone, troglitazone, pioglitazone)
Oral hypoglycaemic agents/insulin
sensitisers/ -glucosidase inhibitors
(acarbose)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (gliclazide,
glipizide, glibenclamide, glimepiride)
Oral hypoglycaemic agents/insulin
secretagogues/glitinides (repaglinide)
Insulin analogue (lispro, aspart, isophane,
lente, ultralente, detemir, glargine)
Vitamin B
3
Possible adverse efect: high-dose
niacin administration could interfere
with the therapeutic activity of glucose
control medications, resulting in
hyperglycaemia
Possible benefcial efect: niacinamide
may enhance secretion and increase
insulin sensitivity, and may be ben-
efcial in preventing and/or delaying
type 1 diabetes. Niacinamide does
not appear to interfere with insulin or
hypoglycaemic medications
Moderate risk: consider co-
administration of low-dose
niacin or niacinamide in
defcient patients. Monitor
patient closely and regu-
larly in conjunction with
other health professionals
(plasma glucose and liver
enzymes)
Lifestyle interventions also
recommended
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Vitamin B
9
(folate) Possible adverse efect: metformin
may reduce folate levels in diabetics by
reducing folic acid absorption
Low risk: consider co-
administration. Diabetic
patients may need folic
acid supplements to
reduce hyperhomocyste-
inaemia and their risk of
cardiovascular disease
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Vitamin B
12
Benefcial nutritional efect: metformin
therapy causes reduced vitamin B
12
absorption and low serum total vitamin
B
12
by depressing intrinsic factor (IF)
secretion and uptake of B
12
-IF complex.
May also reduce folate
Low risk: consider
co-administration.
Supplement also with folic
acid and calcium
Monitor folate and
cobalamin status
Insulin analogue (lispro, aspart, isophane,
lente, ultralente, detemir, glargine)
Vitamin E Interaction uncertain; vitamin E may
improve glucose tolerance in diabetics
Low risk: caution is
warranted against high
doses of vitamin E in obese
patients. Monitor patient
in conjunction with other
health professionals
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
sensitisers/ glitazones/thiazolidinediones
(rosiglitazone, troglitazone, pioglitazone)
Oral hypoglycaemic agents/Insulin
sensitisers/ -glucosidase inhibitors
(acarbose)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (gliclazide,
glipizide, glibenclamide, glimepiride)
Oral hypoglycaemic agents/insulin
secretagogues/glitinides (repaglinide)
Insulin analogue (lispro, aspart, isophane,
lente, ultralente, detemir, glargine)
Zinc Possible additive efect; zinc may
improve both insulin secretion and
insulin sensitivity and may exert
insulin-like efects
Low risk: use cautiously
with diabetes medications.
Monitor patient closely
Continued
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PA R T 3 : T H E B O DY S Y S T E MS 1042
TABLE 17.8 Potential Interactionscontd
Drug Classes Commonly Used Herb/Supplement Potential Outcome Recommendation
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (gliclazide,
glipizide, glibenclamide, glimepiride)
Insulin analogue (lispro, aspart, isophane,
lente, ultralente, detemir, glargine)
Allium cepa
Allium sativum
Possible additive efect; signifcant
hypoglycaemic efects of garlic and
onion are preliminary
Garlic extracts may provide other, ben-
efcial and cardioprotective efects
Low risk: consider co-
administration in some
patients, but not as a strat-
egy for reducing blood
glucose levels
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (gliclazide,
glipizide, glibenclamide, glimepiride)
Cinnamomum
zeylanicum
Possible additive efects; cinnamon has
been shown to potentiate insulin activ-
ity and increase glucose metabolism
May produce synergistic, benefcial
efect under professional supervision
Low risk: consider co-
administration. Monitor
patient and drug levels
closely
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
sensitisers/ glitazones/thiazolidinediones
(rosiglitazone, troglitazone, pioglitazone)
Oral hypoglycaemic agents/insulin
sensitisers/ -glucosidase inhibitors (acarbose)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (gliclazide,
glipizide, glibenclamide, glimepiride)
Oral hypoglycaemic agents/insulin
secretagogues/glitinides (repaglinide)
Insulin analogue (lispro, aspart, isophane,
lente, ultralente, detemir, glargine)
Coleus forskohlii Possible additive efect; coleus stimu-
lates insulin release and may enhance
the efect of hypoglycaemic agents or
exogenous insulin
Moderate risk: use with
caution. Monitor serum
glucose levels in conjunc-
tion with other health
professionals. Drug dose
may require adjustment
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
sensitisers/ glitazones/thiazolidinediones
(rosiglitazone, troglitazone, pioglitazone)
Oral hypoglycaemic agents/insulin
sensitisers/ -glucosidase inhibitors (acarbose)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (gliclazide,
glipizide, glibenclamide, glimepiride)
Oral hypoglycaemic agents/insulin
secretagogues/glitinides (repaglinide)
Insulin analogue (lispro, aspart, isophane,
lente, ultralente, detemir, glargine)
Gymnema sylvestre Possible additive efect; the hypo-
glycaemic efects of gymnema may
potentiate the efects of hypoglycae-
mic drugs in diabetic patients
May produce synergistic, benefcial
efect under professional supervision
Moderate risk: monitor
serum glucose levels in
conjunction with other
health professionals.
Drug dose may require
adjustment
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (gliclazide,
glipizide, glibenclamide, glimepiride)
Momordica charantia Possible additive efects; Bitter melon
has been shown to produce hypogly-
caemic activity
May produce benefcial efect under
professional supervision
Moderate risk: monitor
patient and drug require-
ments closely in conjunc-
tion with other health
professionals
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (gliclazide,
glipizide, glibenclamide, glimepiride)
Insulin analogue (lispro, aspart, isophane,
lente, ultralente, detemir, glargine)
Panax quinquefolius Possible adverse efect; American gin-
seng can induce lowering of postpran-
dial glucose levels in humans
Moderate risk: prescription
for glycaemic control is
not indicated for this herb,
particularly in conjunction
with antidiabetic drugs
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (gliclazide,
glipizide, glibenclamide, glimepiride)
Insulin analogue (lispro, aspart, isophane,
lente, ultralente, detemir, glargine)
Panax ginseng Interaction uncertain; theoretical
adverse interaction is based on estab-
lished property of American ginseng
to induce lowering of postprandial
glucose levels
Low risk: prescription for
glycaemic control is not
indicated for this herb
Oral hypoglycaemic agents/insulin
sensitisers/biguanides (metformin)
Oral hypoglycaemic agents/insulin
secretagogues/sulfonylureas (gliclazide,
glipizide, glibenclamide, glimepiride)
Trigonella
foenum-graecum
Possible additive efects; fenugreek
exerts hypoglycaemic activity by delay-
ing glucose absorption and enhancing
its utilisation
May produce benefcial efect under
professional supervision
Moderate risk: monitor
blood sugar levels closely
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Elsevier Australia
Chapter 17 The Endocr i ne System 1043
TABLE 17.8 Potential Interactionscontd
Drug Classes Commonly Used Herb/Supplement Potential Outcome Recommendation
Analgesic/acetylsalicylic acid (aspirin) Omega-3 fatty acids Inconclusive; the combination of
omega-3 fatty acids and aspirin may be
benefcial under certain circumstances
(e.g. heart disease due to improved
blood fow characteristics, relaxation
of endothelial cells, etc.) but problem-
atic in other conditions (e.g. warfarin
therapy due to increased risk of bleed-
ing complications)
Risk variable: closely
monitor patients at risk for
excessive bleeding
Analgesic/acetylsalicylic acid (aspirin) Chromium Possible adverse efects; interaction
inconclusive. Aspirin may theoretically
increase chromium levels, which could
increase the risk and magnitude of
side-efects
Low risk: monitor patient
closely. Check chromium
levels in patients on long-
term chromium therapy
Analgesic/acetylsalicylic acid (aspirin) Vitamin B
2
Interaction uncertain; concurrent
intake of aspirin and ribofavin has
been reported to cause gastric intoler-
ance in some patients
Low risk: monitor patient
closely
Analgesic/acetylsalicylic acid (aspirin) Vitamin B
3
Possible benefcial efect; aspirin can
moderate niacin-induced cutaneous
fushing and other niacin-induced
efects
Low risk: consider
co-administration
Caution: closely monitor
patients at risk for bleed-
ing. Monitor liver enzymes
Analgesic/acetylsalicylic acid (aspirin) Vitamin C Possible benefcial efect; aspirin
increases urinary excretion of ascorbic
acid and decreases its metabolic avail-
ability. Vitamin C can reduce aspirin-
induced gastric mucosal damage
and toxicity, and enhance its activity.
However, vitamin C may increase blood
levels and adverse efects of aspirin
Consider co-adminis-
tration, especially with
potential ascorbic acid
depletion. Promote nutri-
tional diet in patients on
long-term aspirin therapy
Analgesic/acetylsalicylic acid (aspirin) Vitamin E Possible additive efect; vitamin E may
reduce platelet aggregation and hence
cardiovascular risk
Low risk: consider
co-administration with
multiple antioxidants,
including mixed tocopher-
ols and coenzyme Q10
Analgesic/acetylsalicylic acid (aspirin) Zinc Interaction uncertain Regular monitoring is
essential if aspirin and zinc
are used concomitantly.
Separate doses by at least
2 hours
Analgesic/acetylsalicylic acid (aspirin) Allium sativum Possible additive efect; may pro-
vide additional antiplatelet activity,
increasing the risk of bleeding. Co-
administration in antithrombotic pro-
tocols may enable lower doses of the
drugs, and reduce adverse drug efects
Moderate risk
Avoid or adopt and moni-
tor bleed times
Anticoagulants/antiplatelet drugs
(aspirin, warfarin)
Codonopsis pilosula Possible additive efect; Codonopsis
may inhibit platelet aggregation,
enhancing drug efect
Low risk: monitor patient
bleeding times in conjunc-
tion with other health
professionals
Analgesics/acetylsalicylic acid (aspirin) Coleus forskohlii Possible adverse efect; coleus may
increase the risk of bleeding associated
with some pain relievers
Moderate risk: use with
caution
Analgesic/acetylsalicylic acid (aspirin) Glycyrrhiza glabra Possible benefcial efect; liquorice
helps reduce gastroirritant adverse
efects of aspirin
Consider co-administration
using deglycyrrhizinated
liquorice ( DGL)
Lipid-lowering therapies (statins) Chromium Interaction uncertain; chromium may
increase HDL levels
Low risk: monitor patient
closely. Check HDL levels
in patients on long-term
chromium therapy
Continued
sample proofs only
Elsevier Australia