Dedication:
To my beloved children: Jean-Yves, Colette, Melanie, David-Benoît, Yahmeah, and Ezechiel, and stepchildren: Samuel and Adam.
Acknowledgements
Most scientists develop methods that improve over time through trial and error. The methods used in this book were conceived when I was a fellow in Allergy and Clinical Immunology at the Johns Hopkins Asthma and Allergy Center in Baltimore, Maryland. Over the years, through practice, my methods have much improved and many patients who have used them have enjoyed good health outcomes. I would therefore like to thank my patients from the University of Texas Health Sciences Center at Tyler (UTHSCT); those at the Center for Asthma, Allergy, Immunology & Hormone Health in Tyler, TX, and Woodbridge, VA; those at Fort Belvoir, VA; and finally, my current patients at Altru Health System, who have taught me so much and continue to reveal to me the etiology of allergic diseases and how to treat them. Those of you who have gone through my clinics and have seen the impact on your lives and have written to me about your satisfaction, I thank you for your useful comments, belief, and trust in me. I would like to thank my colleagues and the staff at Altru Health System, Fort Belvoir, and UTHSCT, who support my ideas and who are too many to list here, for their encouragements.
I would like to also thank the scientists at AhrQ for the HCUP data that provided solid evidence about allergic rhinitis, sinusitis, and conjunctivitis, and Bienvenue Tien, my nephew, who greatly helped in the making of the diagrams in this book.
I would like to thank my copy editor and proofreader Amberly Finarelli for her systematic line-by-line editing and her suggestions that have made this book a better finished product, and Stephanie Chandler and her team at Authority Publishing for their advice, encouragements, and efficient, timely production of this book.
Finally, I would like to thank Fatima, my wife and companion, who has continued to be my captive audience, for her patience, support, and love.
In the end, I must, as always, agree with Descartes that knowing that we know nothing is the beginning of real knowledge, and if knowledge comes from a higher power, then all thanks and praise should go to that higher power.
Benoît Tano, M.D., Ph.D
Grand Forks, 2011
The Allergy Detective
Allergic Rhinitis Treatment Secrets Your Doctor May Not Tell You
by
Benoît Tano
Published by Integrative Medical Press at Smashwords
Copyright © 2011 by Benoît Tano. All rights reserved.
Smashwords Edition, License Notes
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Limit of Liability/Disclaimer of Warranty: While the publisher and author have used their best efforts in preparing this book, they make no representations or warranties with respect to the accuracy or completeness of the contents of this book and specifically disclaim any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives or written sales materials. The advice and strategies contained herein may not be suitable for your situation. You should consult with a professional when appropriate. Neither the publisher nor the author shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, personal, or other damages.
1. Health & Fitness : Diseases - Immune System 2. Health & Fitness : Alternative Therapies 3. Health & Fitness : Allergies
ISBN: 978-0-9834192-3-5
Original Copyright © 2011 by Benoît Tano
Revised Edition
This book is available in print at www.DrBTano.com
Table of Contents
ALLERGIC RHINITIS, SINUSITIS, AND CONJUNCTIVITIS ED DISCHARGES
ESTROGEN EPIDEMIC AND ADULT-ONSET RHINITIS
SKIN TESTING AND ALLERGY VACCINE
MEDICATION THERAPY AND TREATMENT TECHNIQUES
Warning and disclaimer
Integrative Medical Press has designed this book to provide information about allergic rhinitis, perennial non-allergic rhinitis, sinusitis, and conjunctivitis. This information is derived from the author’s practice of allergy and is not intended to replace your primary care physician or allergist. The publisher and the author are not liable for the misconception or misuse of the information provided in this book.
Every effort has been made to ensure that the information contained in this book is complete and accurate. The author and publisher assume neither liability nor responsibility to any person or entity with respect to any direct or indirect loss or damage caused, or alleged to be caused by the information contained herein, or for errors, omissions, inaccuracies, or any other inconsistency within these pages. The author has no conflict of interest to declare and does not have any financial interests and does not do any consulting or other business with the companies whose products are included in this book. The author is not promoting any particular products mentioned in this book.
Nose, eye, and sinus symptoms, commonly called allergies, fall under four major categories: allergic rhinitis (inflammation of the nasal membranes due to pollens, dust, dust mites, molds, pet dander, etc.), non-allergic rhinitis (inflammation of the nasal membranes due to chemicals — household cleaning agents, cigarette smoke, perfumes, flower scents, scented candles, air fresheners, petrochemicals, fumes, etc.), allergic conjunctivitis (inflammation of the eyes causing itchy, watery, puffy, swollen, red eyes), and sinusitis (acute and chronic sinus infections).
The bulk of allergy cases are treated by primary care health care providers. Many patients also self-treat, and the multiple over-the-counter (OTC) antihistamines available to the public attest to that. However, many health care providers do not have a deep understanding of the pathophysiology of rhinitis symptoms. Also, many patients who self-medicate use the weakest antihistamines, and often the more dangerous medications that lead to rhinitis medicamentosa (rebound nasal congestion), such as oxymetazoline (Afrin®). Others use nasal decongestants such as phenylephrine (Neo-Synephrine®) compounds and a combination of antihistamines and decongestants that can lead to high blood pressure. Understanding the mechanisms behind nasal symptoms and using an optimal combination of medications is necessary for effective treatment of nasal symptoms that are not benign. Untreated or poorly treated allergic and non-allergic rhinitis can lead to chronic and recurrent sinus infections, sinus pressure, headaches, and even asthma symptoms of chest tightness, shortness of breath, coughing, and wheezing. Postnasal drip, which is present in most allergy patients, is one of the most annoying, difficult-to-treat, and lingering rhinitis symptoms.
This guide, drawn from my own practice experience as an allergist, is intended to help all allergy sufferers take better control of their allergies. Health care professionals may also learn a brief pathophysiology of allergic and non-allergic rhinitis, as well as treatment protocols and techniques that will help their patients. In most cases of rhinitis, finding out the allergens by skin testing and desensitization by allergy vaccine leads to long-term relief, and qualified allergists (fellowship-trained allergists) will offer this service. If allergy sufferers are only interested in palliation (lessening) of their symptoms, they can often get good results by knowing what OTC medications work best and which ones to avoid. In this guide, you will learn about the medications that can give you relief, and how to save yourself money and grief.
Adult-onset nasal symptoms are on the rise, and are often frustrating for lack of understanding how to properly treat them. This guide explores the origins of this adult-onset allergy epidemic and the most effective ways to correct these symptoms. I will focus on both allergic and non-allergic rhinitis and their attendant derivatives of acute and chronic sinusitis, as well as allergic conjunctivitis. Chapter 1 presents rhinitis, sinusitis, and conjunctivitis statistics. In this chapter, the evidence of increasing allergic conditions is demonstrated by the emergency department (ED) discharges of these conditions for the year 2008, reported by the Healthcare Cost and Utilization Project (HCUP) data. This chapter opens a window to hormone imbalance that contributes to multiple pathological conditions prevalent in women, including rhinitis symptoms. Once the evidence is understood, the why, what, and how will be covered by understanding the pathophysiology of atopic diseases. The pathophysiology discussion is divided into two chapters: Chapter 2 presents allergy in childhood, and Chapter 3 presents the case of the estrogen epidemic and adult-onset rhinitis symptoms. The treatment of rhinitis begins with skin testing and an allergy vaccine, as discussed in Chapter 4, followed by medication therapy and treatment techniques, covered in Chapter 5. Finally, Chapter 6 offers some concluding remarks in an overall summary.
Allergic diseases are multiple and include:
* Allergic rhinitis
* Asthma
* Atopic dermatitis (eczema)
* Food allergy and anaphylaxis
* Drug allergy and anaphylaxis
* Urticaria and angioedema
* Sinusitis (which is a consequence of allergic and non-allergic rhinitis)
* Allergic conjunctivitis
This chapter covers rhinitis, sinusitis, and conjunctivitis from HCUP ED discharges data.
Tables 1-19, in Appendix A, present ED discharges for these allergic conditions for the year 2008 (U.S. only). The reported statistics seek to tease out the prevalence of allergic rhinitis, sinusitis, and conjunctivitis in women compared to men, and adults compared to children.
Summary
Tables 1-19 in Appendix A show that all cases of rhinitis, sinusitis, and conjunctivitis are more prevalent in women than in men. These allergic conditions are more prevalent in the 18-44 age groups. The South has the highest disease burden, followed by the Midwest, the Northeast, and the West. The increased disease burden in prime-age women may be due to hormone imbalance, until proven otherwise, and estrogen may be the culprit. The South and Midwest have the highest rates, possibly due to the high propensity of pesticides/herbicides used in farmlands in these two regions that lead to increased environmental estrogens.
Many of these conditions have high prevalence in women due to the increased endogenous estrogen production that couples with xenoestrogens (pesticides and herbicides, and the myriad of estrogenic products in cosmetics) and phytoestrogens (plant-based estrogens) to wreak havoc in women. This super-estrogen dominance in women manifests as the “multiple allergy” and other disease symptoms reported later on in this chapter. The next section will shed some light on the endogenous estrogen production process in men and women.
Sources of Endogenous Estrogens
Most endogenous estrogens in women are produced during the menstrual cycle but can also be produced by the adrenal glands and by conversion of testosterone to estrogen. Aromatase is the enzyme that facilitates the conversion of testosterone to estrogen. Obesity increases the activity of aromatase and hence, obese men and women tend to have more estrogens than lean individuals. Men produce estrogen by their bodies converting testosterone to estrogens via aromatase. Estrogen is responsible for the gynecomastia (man boobs) that men develop with increasing age, obesity, and alcohol abuse.
Estrogens in women and men are not benign, and the consequences will be covered in the following sections. The next section will cover the production of endogenous hormones.
Progesterone Deficiency, Estrogen Dominance, Leptin Resistance, Insulin Resistance, and Obesity
Our good hormones come from what is known as “bad” LDL cholesterol, which generates pregnenolone. Pregnenolone divides into two other hormones, progesterone and DHEA (DeHydroEpiAndrosterone); these two in turn produce estradiol, estrone, and testosterone. When we get older, we lose some of these hormones and others increase. The changes in hormones cause a hormonal disequilibrium, which is the source of many diseases and symptoms treated by health care providers. The diagram below is a rough illustration of endogenous hormone production cascade and consequences.
In this diagram, start with progesterone on the left: progesterone deficiency leads to increased estradiol and estrone, which lead to increased insulin. When insulin increases, initially glucose decreases, causing hypoglycemic episodes, and the individual often feels shaky and lightheaded. Adrenalin and glucagon therefore increase to augment the glucose level in the blood; insulin increase causes craving for sweets that also increase the glucose level.
Insulin then puts the excess glucose into adipocytes (fat cells) that cause obesity; filled adipocytes produce leptin to signal to the hypothalamus (center for satiety and craving) for decompression. The hypothalamus sends a message down to the insulin to stop the craving and reduce the appetite for weight loss; however, weight loss does not occur overnight — the adipocytes, not seeing the effect of their message to the hypothalamus, therefore continue to “complain” by producing more leptin. When the leptin message is too high, the hypothalamus ignores it and leptin resistance is created.
Leptin resistance causes a decrease in serotonin that leads to depression, anxiety, and panic attacks. Leptin resistance also leads to insulin resistance. Insulin resistance means that adipocytes shield themselves and do not want to absorb any more glucose. The glucose therefore remains in the blood and a high level creates what is called diabetes. The adipocytes also produce inflammatory cytokines such as TNF-α and IL-6 that cause aches and pains, arthritis, and allergic diseases such as asthma and rhinitis symptoms. The adipocytes also help the skin cells and adrenal glands to produce more estrogens (estradiol and estrone).
This endogenous increase in estrogens, coupled with environmental estrogens and plant-based estrogens, lead to benign tumors such as fibroid tumors, ovarian cysts, cervical dysplasia, fibrocystic breast disease in women, and benign prostatic hypertrophy (BPH) in men, and many other conditions. If you are not lucky and do not get a benign tumor, you may get a malignant tumor such as breast, uterine, ovarian, vaginal, cervical, or colon cancers in women and prostate or colon cancers in men. Estrogens have a receptor (binding site) on mast cells and basophils and when the estrogens attach to their receptor-alpha on these cells, the cells pour out histamine and leukotrienes just like pollens do.
Hence, increased estrogens not only directly increase allergies but also increase allergies through obesity. When progesterone decreases, thyroid function decreases, which leads to obesity. DHEA is the mother of all hormones. DHEA decreases with age and stress, which leads to insulin increase. Increase in insulin causes salt retention in kidney tubules that leads to hypertension. The decrease in DHEA therefore leads to obesity that eventually leads to allergic diseases, via increase in TNF-α and IL-6. The following will summarize the consequences of progesterone deficiency/estrogen dominance.
Progesterone Deficiency/Estrogen Dominance Creates a Chain Reaction
* Cortisol decrease (initially)
* Thyroid function decreases
* T4 does not always convert to T3
* TSH and free T4 may be in the “normal range” and free T3 may be low
* Measuring of TSH, free T4, and free T3 in a thyroid function test is therefore necessary
* Insulin increases
* Initially, hypoglycemia occurs
* Adrenaline is produced to increase glucose
* Glucagon is also produced to increase glucose
* Insulin causes an increase in carbohydrate consumption that leads to an increase in glucose
* Excess glucose is pushed into adipocytes by insulin
* Filled adipocytes produce leptin, adiponectin, visfatin, apelin
* Leptin signals to the hypothalamus that adipocytes are filled up
* The hypothalamus responds briefly, then stops when the demand is excessive
* Lack of response from the hypothalamus leads to leptin resistance
* Leptin resistance leads to a decrease in serotonin
* Decrease in serotonin leads to depression, anxiety, and panic attacks
* Leptin resistance also leads to insulin resistance
* Leptin and insulin resistance lead to type 2 diabetes
* Leptin resistance leads to increased ghrelin/NPY activities that lead to hunger and obesity
* Besides leptin and many other adipokines (chemicals used for communication by fat cells), adipocytes also make inflammatory cytokines such TNF-α and IL-6 that cause inflammation in the body such as arthritis, asthma, and allergic rhinitis
* Adipocytes help skin cells and adrenal glands to produce estradiol and estrone
* Estrogens increase both insulin and thyroid-binding globulin
* Increased thyroid-binding globulin further decreases thyroid function, which leads to more obesity
* Endogenous estrogens, environmental estrogens, and plant-based estrogens cause mast cells and basophils to release allergy-causing mediators that lead to allergy symptoms
* DHEA decreases with age and stress
* Decrease in DHEA causes insulin to increase
* Insulin increase causes salt retention that leads to hypertension
* Decrease in DHEA and progesterone lead to decreased testosterone
* Testosterone also converts to estrogens that lead to benign tumors, cancer, and allergic reactions
* When there is a hormone imbalance, the body tries to replenish the hormone by increasing the ingredient used to make the hormone
* Cholesterol — especially LDL cholesterol — increases so as to increase the production of the hormones
* Cholesterol is made in the liver and mixes with bile for better digestion of fat
* Sometimes bile salts are missing when the cholesterol gets to the gallbladder
* When bile salts are missing, the cholesterol precipitates and forms gallstones
* Gallstones block the common bile duct and therefore lead to inflammation of the gallbladder, called cholecystitis
* Cholecystitis leads to surgical removal of the gallbladder, called cholecystectomy
* In medical training, cholecystitis is known to be the disease of females, fat, fertile, and forty (the four F’s)
* This condition is clearly related to hormone imbalance that occurs in women when they are in their 40s
* Decrease in progesterone and DHEA and increase in estradiol and estrone tend to increase insulin
* Progesterone modulates thyroid hormone activity by keeping potassium, zinc, and selenium in the cells. Potassium, zinc, and selenium are known to help convert T4 into T3 for increased metabolism
* Decrease in progesterone leads to estrogen dominance, and estrogen dominance leads to an increase in insulin and a further decrease in thyroid hormone activity. (Never rely on TSH alone as a thyroid function test. It is not uncommon to find elevated or decreased TSH level in the face of normal T4 and T3, and it is also common to find low free T3 in the face of normal free T4 and TSH.) It is also possible to see women on Synthroid with more weight problems, which suggests a suboptimal treatment of hypothyroidism.
Effects of Progesterone/Estrogen Imbalance on Women
This hormone imbalance creates:
* Premenstrual asthma (PMA)
* Premenstrual migraines
* Premenstrual dermatitis
* Non-allergic rhinitis and enhanced seasonal/perennial allergic rhinitis
* Fibromyalgia
* Menstrual disturbances
* Interstitial cystitis (IC), also known as overactive bladder. (IC is a mast-cell disease and is more prevalent in women than men; I suspect that estrogen dominance in women causes IC. When estrogen binds to its receptor-α on the mast cell, it causes mast cell degranulation in the detrusor muscle of the bladder that leads to the IC symptoms. Hence, balancing estrogen by giving adequate amounts of progesterone and DIM or I-3-C may help IC patients.)
* Arthritis
* Non-allergic rhinitis and seasonal/perennial allergic rhinitis
* Obesity and asthma
What do obesity and asthma have in common? They are both influenced by estrogen.
Progesterone Deficiency and Consequences
Both men and women produce progesterone. While progesterone is produced by the adrenal glands and testes in men, progesterone in women is produced during the menstrual cycle by the ovaries and adrenal glands. The low progesterone gene can be inherited from the mother, and low progesterone in the mother can lead to low progesterone in the daughter or son.
When girls inherit the low progesterone gene, they developed progesterone deficiency symptoms early in life. Right after menarche (onset of menstrual periods), the young girl starts experiencing menorrhagia (heavy menstrual periods) and/or dysmenorrhea (painful menstrual cramps), often accompanied by nausea, vomiting, and diarrhea. This is quite debilitating for many young girls. These women also often have difficulty conceiving and if they conceive, they have difficulty carrying the pregnancy to term. They tend to have multiple miscarriages, and if an astute OB/GYN physician realizes the low progesterone problem and injects even synthetic progesterone, the pregnancy can go to term.
If the low-progesterone woman becomes pregnant, the first trimester could represent a real challenge. She will have nausea and vomiting throughout the pregnancy, but these symptoms are worse in the first trimester when the progesterone production is still average. During the second trimester, the placenta produces about 400 mg of progesterone a day, and that helps resolve the nausea and vomiting problem. After delivery, when the placenta is gone, the progesterone production decreases to average and the woman becomes depressed. This may explain much of the postpartum depression experienced by many women. The low progesterone also causes many symptoms, and many of these symptoms are the same as estrogen dominance because estrogen dominance is simply normal or high estrogen in the face of low progesterone.
Adult-Onset Progesterone Deficiency
If a woman does not have low progesterone to begin with, as she gets older she tends to lose her progesterone because of anovulatory menstrual cycles (menstrual cycles without ovulation). Women also lose their progesterone because of progesterone-containing birth control pills (progestins) that suppress the natural production of progesterone. Women produce progesterone during their menstrual cycle as follows:
Progesterone is produced after ovulation. In women who have a normal cycle of 28 days, the 14th day is known as ovulation or when the egg (ovum) is released from the ovary. When the egg is released, the pocket where the egg came from does not disappear. It becomes yellow and is known as the “yellow body,” or corpus luteum in Latin. The female menstrual cycle is therefore divided into three phases: pre-ovulatory phase or follicular phase, ovulatory phase, and post-ovulatory phase, also known as the luteal phase because of the activity of the corpus luteum. Before ovulation, the estrogens estradiol and estrone increase, reach their peak around ovulation time, and decline thereafter. Progesterone is flat prior to ovulation, but right after ovulation it starts to increase and peaks about seven days before a woman’s period. Three to five days (but sometimes a week) before the period, many women develop premenstrual syndrome (PMS) or premenstrual dysphoric disorder (PMDD).
PMS and PMDD can consist of an uneasy feeling, emotional lability, bloating, acne, premenstrual asthma exacerbations for post-pubertal women with asthma, premenstrual migraines, premenstrual dermatitis (hives), and most women around the world crave sweets — chocolate is only one of them. The sugar craving is due to the activity of insulin, which is the sugar-craving hormone. Insulin increases when progesterone decreases below estrogen in the last week of the menstrual cycle. This transient insulin increase is responsible for the sugar craving.
Women tend to have anovulatory menstrual cycles in their late 20s, early 30s, mid-30s, and beyond. This leads to progressive dwindling of the protective hormone progesterone, and the ensuing unopposed estrogen leads to a persistent, instead of transient, insulin increase. This permanent insulin increase in turn leads to constant craving for sweets. Eating sweets or high-sugar-content foods leads to increase in blood glucose. The insulin has to quickly dispose of the glucose so as to prevent it from spilling in the blood. The quickest way of getting rid of the glucose in the blood is to put it into the fat cells. Fat cells convert the glucose into fatty acids for storage and the end result is obesity. Hence, it is not surprising to see women gain weight after age 35, or even sooner if their progesterone deficiency starts earlier.
When progesterone decreases, thyroid function also decreases, which compounds the weight gain problem.
How does thyroid function connect to progesterone? Progesterone aids in the retention of zinc, potassium, and selenium in our cells. Zinc, potassium, and selenium allow the thyroid hormone T4 to enter the cell and then to be converted to the active form T3 that is used for metabolism. Low progesterone decreases this mineral retention in cells. As a result, T4 does not convert to T3. Patients with hypothyroidism are given a T4 equivalent: levothyroxine (Synthroid). If the patient has low progesterone, as occurs in menopausal women, then this treatment remains ineffective. These patients do not readily lose the weight and if T3 is measured, it is found to be low. T3 may be within the standardized specified range that no one should deviate from, but on the low end of the range. The TSH in this case is often greater than 2. If 0.49-4.47 is the normal range, and 0.49 is considered perfectly optimal thyroid function, then anything above 0.49 is not perfect. Anything above this perfect number is signaling that the body needs a little more thyroid to optimally achieve metabolism. Unfortunately, the rigid standard of care does not even consider a patient’s possible symptoms of continued fatigue and difficulty in losing weight despite the thyroid supplementation. Patients continue to be treated with the same medications, even though the results are not there. This leads to frustration, and patients seek alternative therapies on their own.
Increased estrogen leads to increased thyroid binding globulin that binds both T4 and T3 tightly and does not relinquish them for metabolism. Some scientists have therefore suggested that women be supplemented with thyroid medication when they are on birth control pills. Birth control pills prevent ovulation and therefore decrease the progesterone level in the users. Hence, many women on these pills tend to gain weight.
Estrogen is also associated with copper. Copper is required for the synthesis and release of estrogen and also forms enzymes in the liver, which help to break down leftover estrogen into harmless substances. Estrogen can cause copper retention if zinc or progesterone levels are too low or calcium level is high. Since copper contributes to the increase in estrogen, an increase in copper level in the body may therefore decrease thyroid function.
If calcium and copper increase together, they can have a detrimental effect on thyroid function. By antagonizing estrogen and allowing potassium, selenium, and zinc to remain in cells, progesterone reverses all these negative mineral effects on thyroid function. Unfortunately, TSH, measured by most physicians to test for thyroid function, often does not capture this imbalance.
Estrogens also cause benign tumors in women as mentioned above. In men, prostate enlargement, called benign prostatic hypertrophy, may be due to too much estrogen. This condition is usually linked to dihydrotestosterone, a more potent form of testosterone, blamed for causing male pattern baldness and prostate enlargement.
Estrogens, Benign Tumors, and Many Other Conditions in Women
* Fibroid tumors
* Fibrocystic breast disease
* Ovarian cysts
* Cervical dysplasia (non-HPV related)
* Endometriosis
Estrogens and Cancer
* Studies of estrogen metabolism have led to the hypothesis that reaction of certain estrogen metabolites, predominantly catechol estrogen-3,4-quinones with DNA, can generate the critical mutations initiating breast, prostate, and other cancers.
* The endogenous estrogens estrone (E1) and estradiol (E2) are oxidized to catechol estrogens (CE), 2- and 4-hydroxylated estrogens, which can be further oxidized to CE quinones that are involved in breast and prostate cancers.
Estrogen is associated with the following cancers and perhaps many more:
* Breast cancer
* Uterine cancer
* Ovarian cancer
* Cervical cancer
* Vaginal cancer
* Colon cancer
* Prostate cancer
Estrogen and Progesterone Receptors in Breast Cancer
* ER (estrogen-receptor) positive/PR (progesterone-receptor) positive (this type of breast cancer is more prevalent than other types of breast cancer)
* ER positive/PR negative
* ER negative/PR positive
* ER negative/PR negative
Estrogenic Chemicals and Allergic Diseases: The Case of BPA
A 2010 study on mice has concluded that perinatal exposure to 10 micrograms/mL of BPA in drinking water enhances allergic sensitization and bronchial inflammation and responsiveness in an animal model of asthma (adult-onset allergies due to estrogen dominance will be covered in Chapter 3).
Endocrine Disrupting Chemicals, Hormone Imbalance, and Diseases in Humans
Women tend to produce more estrogens from their late 20s on. Most women become estrogen dominant because their endogenous production of estrogens increases when they lose their progesterone due to anovulatory menstrual cycles. Women who go on birth control pills tend to develop hormone disruption sooner. Increased endogenous estrogens, coupled with environmental estrogens (xenoestrogens and phytoestrogens), lead to multiple symptoms that women present with to their doctors. Unfortunately, since there is no true training in hormone disruption and correction of its ill effects in medical schools or residency programs, and since most endocrinologists are busy dealing with diabetes, thyroid diseases, and more familiar endocrine conditions, there are few physicians who will touch these symptoms. The few physicians who try to investigate these conditions do well by helping these patients. However, since most medical professionals are not well versed in the literature regarding the effects of endocrine disruptors, they pose as judges of the few who try to find solutions.
What Causes Estrogen Dominance?
* Endogenous estrogens
* Exogenous estrogens
Xenoestrogens: herbicides, pesticides, and other household chemicals, including cosmetics and cosmeceuticals.
Phytoestrogens: Plant estrogens such as found in bay leaf, celery, nutmeg, cloves, cinnamon, alfalfa sprouts, cottonseed oil, cumin, tea, tea tree oil, oregano, Melaleuca products, dates, thyme, peppermint, turmeric, fenugreek, feverfew, pomegranate, flax oil, wheat (weak phytoestrogen), garlic, hemp oil, red clover, hops (beer), rosemary, caffeine, coffee (including decaffeinated coffee), safflower, safflower oil, canola oil, chamomile, chamomile tea, licorice, soy, chocolate and its main product cocoa, clover, mint, sunflower oil, sunflower seeds, only to name a few. (See additional xenoestrogens and phytoestrogens listed by Peter Eckhart, M.D., at www.woomhoo.com.)
Progesterone deficiency and estrogen dominance therefore lead to multiple pathological conditions treated by health care professionals.
Some of these progesterone/estrogen imbalance symptoms are:
* Abdominal bloating
* Absence of maternal instinct and behavior
* Acne
* Agitation
* Agoraphobia
* Alcohol abuse
* Allergies or sensitivities to foods or chemicals
* Allergy shiners in adults (dark circles under the eyes)
* Anovulatory menstrual cycles
* Anxiety
* Asthma
* Binges
* Blood clots
* Breast and/or ovarian cysts