functional medicine and nutritional genomics - American Association ...

AAPI’S NUTRITION GUIDE TO OPTIMAL HEALTH: USING PRINCIPLES OF FUNCTIONAL MEDICINE AND NUTRITIONAL GENOMICS
In this particular case, one could rationalize that this
patient has had evidence of a physiologic environment
consistent with longstanding chronic inflammation. Atopy
and asthma are obvious. Less obvious was that each
pregnancy was complicated by symptoms of preterm
labor, which is thought to be mediated in part by
abnormal prostaglandin synthesis and degradation, i.e.
inflammation. She also experienced unexplained
‚allergic‛ type reactions during two of the four
pregnancies, one of which required hospitalization.
Pregnancy places a tremendous stress on the immune
system and hormonal physiology, requiring the host to
adapt to a non-self fetus as well as adjusting to the
hemodynamic and metabolic needs of the pregnancy.
Pregnancy depletes nutrients as well as causes
hormone imbalance and these may have been part of
the pathway to the inflammatory responses that
ultimately manifest themselves as chronic bladder pain.
This chronic pain played a role in poor sleep
andcertainly ‚stressed‛ the adrenal systems production
of cortisol.
So, we see a potentially common thread: atopy and
asthma since childhood; pregnancy(stress and hormone
imbalance) temporarily unmasks the patients underlying
immune system imbalance, which creates the symptoms
of preterm labor and ‚allergic‛ reaction; chronic bladder
pain (inflammation) develops which further stresses
the physiology; lack of restorative sleep due to pain,
which may contribute to intestinal hyper-permeability
and development of multiple food and chemical
sensitivity; development of subclinical hypothyroidism
and autoantibodies; development of autoimmune
thyroiditis and Graves’ disease.
We know that the balance of the cellular and humoral
arms of the immune system is regulated in part by the
hormonal environment with testosterone, DHT, DHEA
and DHEA-S favoring a shift toward cellular (Th1
immunity and glucocorticoids, estrogens, and
catecholamines favoring a shift toward the humoral
(Th2) arm of the immune system. In this patient’s
case, we could argue for a generally estrogen
dominant hormone environment to her low cortisol, low
17-OHP, and weight gain; this may have been part of
what tipped the scales further towards autoimmune
thyroiditis.
80
2012
Once established, Graves’ disease is difficult to treat.
There is little in the literature giving clinical guidance
to the prevention and treatment of eye disease.
Antibodies directed toward the TSH receptor are
involved in eye disease, as expression of the TSH
receptor has been shown present in the adipocytes
and connective tissue of the diseased Grave’s orbital
tissues. Very recent research has found a human
monoclonal antibody which stimulates the TSH receptor
and adipogenesis in the human Grave’s orbit via a
known signaling cascade. Inhibition of this cascade
may be a potential treatment strategy for Grave’s
opthalmopathy.
I find it fascinating that this patient has such a
constellation of disease processes (atopy,
asthma, preterm labor, interstitial cystitis, arthritis, and
Graves’ disease) and the most logical link among
these conditions is the immune system and
inflammation. Although the etiology of interstitial cystitis
is unknown, as is the cause of Graves’ and most
autoimmune disease, recent interest in the use of
hyperbaric oxygen therapy for urological conditions like
interstitial cystitis has been reported in the Italian
literature.(3)
HBOT has been used in a variety of other
inflammatory and autoimmune conditions.
HBOT stimulates stem cell mobilization from the bone
marrow and decreases oxidative stress in tissues
thereby reducing inflammation and may have potential
to help IC. IC may indeed be another manifestation of
autoimmunity. This patient had undergone 10 hours of
HBOT therapy in a mild chamber and had reported
improvement in bladder symptoms.
The cornerstone of treatment for this patient will be
long term hormone management, nutritional support and
anti-oxidant therapy. Periodic re-evaluation of food
intolerances and monitoring of gut flora will aid in
restoration or prevention of intestinal hyperpermeability.
Summary
Food Sensitivity is not a ‚food‛ problem. Rather, it is
an immune phenomena driven by a myriad of variable
metabolic imbalances occurring within the
gastrointestinal tract, over time, within the unique
genetic environment of the host, which culminates in
some degree of immune activation. This immune