Basal body temperature and

thyroid function
Why your temperature might be lower than
the average population
Having an underactive thyroid changes the way body heat is
generated and maintained. This is why most people with an
underactive thyroid and Hashimoto’s will have lower body
temperatures than average.
Keeping up basal body temperature (BBT) is
one of the most costly processes in the body.
Many hormones in the body may impact it,
but thyroid hormones are the only ones that
modulate BBT to correspond to the energy
balance in the body. Since an underactive
thyroid means a lack of energy, that is one of
the reasons the BBT of people with an
underactive thyroid will be lower (1).

What is BBT?
Basal body temperature (BBT) is the temperature of your body
at rest. It is usually the lowest body temperature you will
experience throughout the day.

Thyroid hormones are pivotal for BBT generation and

maintenance, and even slight changes in hormone levels will
show the change in BBT (1).
How does the thyroid regulate BBT?
Thyroid hormones regulate body temperature by increasing
available energy in the body, as well as by increasing appetite,
pulse, the amount of oxygen delivered to different body parts,
and fat buildup. Thyroid hormones work together with the
nervous system in order to maintain body temperature.
Thyroid hormones determine how much of the energy molecule
called ATP (adenosine triphosphate) will be produced by the
body (2). ATP is the energy currency in the cell, and the more
you have it, the better you will be at generating heat. If you
generate too much heat, you start sweating; if too little, the
muscles will start to shiver.

The difference in the amount of energy made by the cell might

be quite striking: for any type of muscle work, for example
walking or running, people with an underactive thyroid might
generate up to three times less heat, when comparing to people
with a normally functioning thyroid (3, 4).

This can be corrected with thyroid medication, and it has been

shown that even minimal changes in fT4 levels (within normal
ranges) can have a significant impact on the body temperature
(1, 5, 6).

Where is heat created?

Most basal heat is made in brown fat, or brown adipose tissue. It
is important for adapting to cold weather, as are thyroid
hormones (1). Brown fat contains a lot of enzymes called
deiodinases, which are important for the conversion of T4 into
the active T3. This means that brown fat can generate T3, which
is crucial for producing the energy molecule ATP, and for
creating heat during that process (7).

The thyroid and other body parts

Thyroid hormones might increase the heat-utilizing hormonal
impact on the nervous system (8). They activate adrenaline and
noradrenaline and through this increase T4 to T3 conversion
(6). Most notably, when starving, T4 to T3 conversion drops (9).

Increased temperature also increases the need for more oxygen,

which increases heart function in order to get more oxygen to
different parts of the body (10).

Other causes of changes in BBT

Thyroid hormones are the main regulators of body temperature,
but not the only ones have an impact: insulin, glucagon,
estrogen and progesterone, epinephrine, leptin and ghrelin have
a major impact on BBT (1). While the thyroid can have a more
continuous impact on the BBT, the other hormones are more
temporary.

Genes have a big impact on how a person’s BBT is regulated (11),

and they pre-determine the BBT level.

How does cold exposure impact BBT?

During exposure to cold, thyroid hormones activate brown fat
(12). With an underactive thyroid, the body develops protective
mechanisms to preserve heat, and one might feel this as cold
hands and feet. This mechanism is also governed by thyroid
hormones (1, 13).

Why measure BBT?

Basal body temperature is a good overall indicator of the thyroid
status, and might tell more about how well medications are
compensating for thyroid activity. It can be a first indicator of a
medication overdose.
You can record your BBT in the BOOST
Thyroid app and have a better overview of
how your thyroid function impacts
your body.

BOOST Thyroid app is available for

iPhones and iPadsHow to stop
Hashimoto’s?
An underactive thyroid is one of the consequences of
Hashimoto’s — an autoimmune condition in which our own
immune system mistakenly marks our thyroid as an intruder in
our own body.

What researchers know is that to develop Hashimoto’s there

needs to be a genetic predisposition, meaning the code for
developing the disease is written in our genes, and we have likely
inherited it from our genetic predecessors.
But in the addition to this genetic component,
the environment in which we live is actually
the factor activating the disease.

Why does it happen so often to the

thyroid gland?
Because the three proteins(big molecules) in our body that are
necessary for conveying information from the outside to the
thyroid are quite big.

The bigger the protein, more problems it usually causes with

autoimmunity, and there are a lot of them.

More abundant proteins are more likely to cause an

autoimmune response. These proteins are called thyroid
peroxidase (TPO) and thyroglobulin (Tg), and when they break
our self tolerance (the property of our immune system to
attack only foreign bodies like bacteria and viruses, while letting
our organs alone), we start producing antibodies called anti-TPO
and anti-Tg. The only function of these antibodies is to seek and
destroy anything containing TPO and Tg proteins, which is
mostly the thyroid gland and cells it contains.

Medications, foods, and treatments

increasing autoimmune response
There are certain medications used for other diseases that do
temper with our immune system and may cause autoimmune
flare-up

 Treatment for hepatitis C with interferon (1). Treatments

for multiple sclerosis (2) or some surgical treatments for type
1 diabetes (3)
 Excess iodide (4)
 Microorganisms, possibly including some found in
probiotics
 Low level radiation (5, 6)
 Pregnancy and a certain period after pregnancy can
induce autoimmunity(7, 8)
 Foods such as cassava, cabbage, and raw bok choy can
cause thyroid problems and autoimmune flareups (9, 10).
Breakdown products in these foods include molecules
called thiocyanates, which inhibit thyroid function.
 Viral and bacterial infections, especially the ones causing
digestive problems (11–14)

What can we do?

The “hygiene hypothesis” claims that people regularly exposed
to viruses and bacteria develop less autoimmunity and allergy
than people living in “clean” environments (15, 16). Some
researchers claim that this can lead to a less active or trained
immune system, leading the immune system to start reacting to
the own body.

1. Training one’s immune system is individual, and should be

done under medical doctor supervision only.
2. Take your colds and other infections seriously. The
clean environment might not be a culprit for all of
Hashimoto’s flareups. Prolonged infections caused by viruses
and bacterias can seriously affect the immune system. Make
sure you recover fast — low down if needed and take the time
to heal.
3. Avoid foods that specifically cause you any kind of
digestive problem: bloating, flatulence, diarrhea, or
constipation. Food sensitivities are very individual, but there
are some common patterns.

Track your symptoms with BOOST Thyroid to discover your

health patterns and predict when flareups might come.
BOOST Thyroid app is available for iPhones

References

1. Prummel MF, et al. Interferon-α and autoimmune thyroid

disease, 2003
2. Coles AJ, et al. Pulsed monoclonal antibody treatment and
autoimmune thyroid disease in multiple sclerosis, 1999
3. Gillard P, et al. Graves hyperthyroidism after stopping
immunosuppressive therapy in type 1 diabetic Islet cell
recipients with pretransplant TPO autoantibodies, 2009
4. Carayanniotis G. Molecular parameters linking thyroglobulin
iodination with autoimmune thyroiditis, 2011
5. Eheman CR, et al. Autoimmune thyroid disease associated
with environmental thyroidal irradiation, 2003
6. Pacini F, et al. Prevalence of thyroid autoantibodies in
children and adolescents from Belarus exposed to the
Chernobyl radioactive fallout, 1998
7. Weetman AP. Immunity, thyroid function and pregnancy:
molecular mechanisms, 2010
8. Morshed SA. Delineating the autoimmune mechanisms in
Graves’ disease, 2012
9. Chesney AM, et al. Endemic goiter in rabbits, 1928
10. Chu M. Myxedema coma induced by ingestion of raw bok
choy, 2010
 11.Prummel MF, et al. The environment and autoimmune
thyroid diseases, 2004
12. Burek CL, et al. Environmental triggers of autoimmune
thyroiditis, 2009
13. Tomer Y, et al. Infection, thyroid disease, and
autoimmunity, 1993
14. Hammerstad SS, et al. Inflammation and Increased
Myxovirus Resistance Protein A Expression in Thyroid
Tissue in the Early Stages of Hashimoto’s Thyroiditis, 2013
15. Wills-Karp M, et al. The germless theory of allergic disease:
revisiting the hygiene hypothesis, 2001
16. Yazdanbakhsh M, et al. Allergy, parasites, and the hygiene
hypothesis, 2002
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Dr. Vedrana Högqvist Tabor

CEO @Boost_HealthApp|| TEDx speaker || Cancer hunter || Hashimoto’s patient||

Parentpreneur || Learning from own mistakes since 1977

 Follow

Boosted — by BOOST Thyroid App

Companion health app for people diagnosed with Hashimoto’s and an underactive thyroid ||
Simple Personal Thyroid Insights
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References:

1. Silva JE. Thermogenic Mechanisms and Their Hormonal

Regulation, 2006
2. Silva JE. The thermogenic effect of thyroid hormone and its
clinical implications, 2003
3. Leijendekker WJ et al. Heat production during contraction in
skeletal muscle of hypothyroid mice, 1987
4. Silva JE. Thyroid hormone control of thermogenesis and
energy balance. Thyroid, 1995
5. Boivin M, et al. Uncoupling protein-2 and -3 messenger
ribonucleic acids in adipose tissue and skeletal muscle of
healthy males: variability, factors affecting expression, and
relation to measures of metabolic rate, 2000
6. Arsenijevic D, et al. Disruption of the uncoupling protein-2
gene in mice reveals a role in immunity and reactive oxygen
species production, 2000
7. Timms-Hagen J. Thyroid Hormones and Thermogenesis,
1983
8. Werner & Ingbar’s The Thyroid: A Fundamental and Clinical
Text, 2012
9. Young JB, et al. Effect of diet and cold exposure on
norepinephrine turnover in brown adipose tissue of the rat,
1982.
10. Kahala GJ, et al. Cardiovascular hemodynamics and
exercise tolerance in thyroid disease, 2002
11.R. Rising, et al. Concomitant interindividual variation in
body temperature and metabolic rate, 1992
 12. Andersen S, et al. Thyroid hyperactivity with high
thyroglobulin in serum despite sufficient iodine intake in
chronic cold adaptation in an Arctic Inuit hunter population,
2012
13. Castillo M, et al. Disruption of thyroid hormone activation
in type 2 deiodinase knockout mice causes obesity with
glucose intolerance and liver steatosis only at
thermoneutrality, 2011
 Health
 Hashimotos
 Temperature
 Science
 Thyroid
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Dr. Vedrana Högqvist Tabor

CEO @Boost_HealthApp|| TEDx speaker || Cancer hunter || Hashimoto’s patient||

Parentpreneur || Learning from own mistakes since 1977

 Follow

Boosted — by BOOST Thyroid App

Companion health app for people diagnosed with Hashimoto’s and an underactive thyroid ||
Simple Personal Thyroid Insights

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