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Welcome to the Cushing's Help and Support Newsletters!
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that the entire newsletter is not here, or you prefer to
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4-4-2007.htm.
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Dr. Theodore Friedman from Charles R. Drew University, Division of Endocrinology is currently seeking patients to participate in a research study of pituitary dysfunction. More info.
March 30, 2007
Alena Renea Weeks Greenhill
(Died March 30, 2007)
Sign Guest Book | Send Private Condolences
AIKEN – Ms. Alena Renea Weeks Greenhill, 31, of Aiken, died Friday, March 30, 2007 at her residence. Funeral services will be held at 3:00 PM Wednesday in the Shellhouse-Rivers Funeral Home Chapel. Reverend Robert Rish will officiate. Interment will follow in the Clearwater Branch Baptist Church Cemetery.
Pallbearers will be Joshua Weeks, Jim Rutland, Morgan Weeks, Greg Smith, Jimmy Jones, and Charles Jones.
Renea was born in Aiken, a daughter of Gail Weeks, Aiken; and James "Randy" and Debbie Weeks, Aiken. She was a lifelong resident, and worked as a medical assistant at the Women's Health Association.
In addition to her children, Olivia Ann "Libby" and David Randall "DJ" Greenhill, survivors are a sister, Dawn Rutland (Jim) Aiken; a brother Joshua Weeks (Melissa) Aiken; Nikki Weeks, Aiken, Danielle Smith, Aiken; Greg Smith (Maria), Aiken; Kasey Smith, Aiken; JerriLynn Smith, Lincolnton; a maternal grandmother, Joyce Weeks, Aiken; a paternal grandmother, Harriette Weeks, Aiken; twelve nieces and nephews; and her special friend, Jimmy Jones, Aiken.
A niece, Taylor Weeks, and a grandfather, Gene Weeks, preceded her in death.
Please visit Renea's online memorial at shellhouseriversfuneralhome.com
The family will receive friends at the residence of Joshua Weeks, 2334 Wire Road, Aiken on Tuesday from 12-5 PM and from 6-8 PM Tuesday evening at Shellhouse-Rivers Funeral Home, Inc., 715 East Pine Log Rd., Aiken, SC.
From my email:
Mary, I got a call tonight from Renea Greenhill's mom who told me that Renea died Friday night. Renea was from Aiken, SC and was on the board until she did not have a computer anymore. She had tried to get groups together in SC. She had left a note that if she died that her mother was to call me and I was to let everyone on the Cushing's board know of her death. Her mother had seen her on Friday night and talked with her later. Her boyfriend came over and found her on the floor. He called her mother who told him to call 911. He did and her mother got right over there. 911 got there, but did not attempt to revive her and she was to be an organ donor and the organs could not be used. She was dead. An autopsy found nothing wrong with her physically. I told her mother that I bet she died of an adrenal crisis and told her mother to call the coroner to have them do tests for that. She was very appreciative of my thinking of this and was going to call. Renea had been to see Dr. Laws for surgery several years ago. She ended up with meningitis from surgery there. She ended up in critical care at the Medical University of SC. Later had her adrenal glands removed. She had "beat" cushings her mother said. She had lost over 300 lbs. She has two young children who are now without a mother. Her husband had divorced her several years ago, so she was rearing the children as a single mom. Please pass this on to everyone for me for Renea at her request if this happened to her. She loved her Cushing's friends. Below is her obit. Memorials are to be made to the Cushing's group.
• I knew Renea - I met her the Tennessee CUSH Conference. What a shame
• I am sorry to hear of Renea's passing...thank you for sharing with us. Condolences to her family, friends and loved ones.
• So very young -- so very sad.
• My Goodness, she was so very young. This is a startling reminder how serious an adrenal crisis can be. Thank you for carrying out her wishes to let us know.
• Oh my...
I talked with Renea a few months ago. It may not have been adrenal crisis, but it may have, as Renea, after her BLA, didn't need replacement. She hadn't taken hydro for some year(s), and yet her cortisol was always "0". The doctors would just scratch their heads.
Thanks for posting Mary. My prayers are with her and her family.• I am so sorry to hear about this. My prayers go out to her children and her family. What is scary to me is the fact that, considering her history no one there thought to check to see if an adrenal crisis was responsible.
• How terribly sad. And the two young kiddies too. She sounds a remarkable woman. Very sad indeed.
• I am absolutely heartbroken over Renea's death. She was far too young and she already suffered so much. I hope her kids know how much she loved them. I have been struggling with my own health issues lately and her death brings home just how dangerous our lives can be.
I hope she is at peace and that her family is able to cope with her death. I am so very sorry that we lost such a great person. Renea was a great source of strength for me and I will miss her dearly.• Very sad news! My thoughts are with her family and her children.
• Thoughts with her family and children. Her mother must be devastated. I hope she can read the posts and know she's thought of.
Very sad for these children to lose their mother at such a young age.• My deepest condolences to her family and friends.
• How very sad. So young, and had already been through so much.
My thoughts are with her family & friends• So very sad. So young , & so much still ahead of her.
In my prayers• I wonder if they checked her for Nelson's also? She looks very tan. My deepest condolences to her family and friends.
• Such a sad ending to a beautiful life. Sending peaceful thoughts to her family..
• It is very sad to fight that hard... and then the family does not know why... my thoughts and prayers are with them... It breaks my heart to think that she had to suffer so much, but she must have been such a strong, brave person to go through it. My prayers are with the family..
• How sad - she was so young. My sympathies to her children and all of her family.
• I'm so sorry to hear that another Dear Cushie was lost, I remember Renea from the old board mostly and remember how, very sick she was after her surgery, as others said she was way too young, and I'm sure her family and friends will miss her so very much. Someone we have to get all doctors on board to realize how very serious this illness is, not just a few who are out West, we all know they are good doctors, but we need some good ones in the Midwest, in the South, in the East, I know there are some, but we need more pit centers and more pit spealist on understands the devastating and life or death realality some of these pituitary tumors or adrenal tumors can cause.
I'm so sorry to learn on this happening to a dear cushie I remember from the boards.• My prayers to her family. May God bless and keep her children. I can't imagine how hard this is for them.
• Testimonials http://www.cushings-help.com/testimonials.htm I thank God everyday that I found this site and have met (on the boards,
and some in person) so many wonderful people! Without your hard work, none of
this would be possible! Give me a "M", give me an "A", give me a "R", give me a
"Y"- "MARY!!!!!" I am now post op, confirmed cyclical pituitary Cushing’s Disease. I had
pituitary surgery in April 2004, then a BLA in March 2006. I credit this board
with saving my life! From
JenS' bio Mary, I love it. Now we big kids can hunt Easter
eggs for a week! And while I have your attention, thank you so much for this
board. I have no idea where we would be without it. My family was close to
desinigrating from the stress of the last two years with my son sick. Now we are
healing even though we have no diagnosis yet. but have a more positive outlook.
THANKS From:
http://bjp.rcpsych.org/cgi/content/full/190/4/363
Understanding Animal Behavior So We Can Understand Our Own By Dan Paskowitz Behavioral scientists have long sought to understand the detailed mechanisms
by which the brain, and the endocrine systems under its control, govern animal
behavior. In a paper from the March 1 issue of Nature, Japanese researchers have
described a pathway that appears to play a major role in social and reproductive
behavior in mice. The hormone oxytocin is made by neurons in the hypothalamus, a remarkable
part of the brain that regulates appetite, water balance, temperature control,
circadian rhythms and most of the body’s endocrine glands. The oxytocin-producing
neurons send processes to the pituitary gland, from which they release the
hormone. Oxytocin is known to promote uterine contraction and lactation, but has
also been implicated in a variety of sexual and social behaviors. The researchers focused on a protein expressed in the oxytocin-producing
hypothalamic neurons called CD38. The structure of this protein suggested that
it might play a role in the release of oxytocin. In mutant mice lacking the gene
for CD38, oxytocin levels were lower than normal in cerebrospinal fluid and
blood, but elevated in the hypothalamus and posterior pituitary, arguing for an
inability to secrete the hormone into circulation. Circulating levels of a
similar hypothalamic hormone were not affected, implying a specific abnormality
in the oxytocin system. The CD38 mutant mice grew normally and appeared to be generally healthy.
Various behavioral tests suggested that the mice had normal sensory and learning
abilities. However, the mutant mice exhibited several changes in social
behavior. Males displayed a defect in social memory. Unlike normal mice, they
always reacted to female mice as if meeting them for the first time, even after
multiple encounters with the same individual. Mothers appeared to be less
interested in nurturing their pups. When normal mothers were placed at the
opposite side of a cage from their pups, they retrieved the pups quickly and
crouched over them to keep them warm. CD38 mutant mothers retrieved the pups
after a long delay and crouched over them only briefly. Injection of oxytocin restored normal behavior, implicating the deficit in
secreted oxytocin as the cause of the abnormalities in social behavior. Delivery
of a CD38 gene to the hypothalamus using viral vectors restored both oxytocin
secretion and normal social behavior. Further experiments elaborated the
mechanism of oxytocin release by CD38. These experiments may offer insight into some aspects of human behavior. One
of the cardinal features of autism and related developmental disorders is a lack
of normal social interaction. Some recent research has suggested that oxytocin
levels are decreased in autistic children, and that administration of oxytocin
can ameliorate some of their behavioral abnormalities, although it does not
restore normal social behavior. It is possible that abnormalities of CD38 or
other components of the oxytocin release machinery during development could play
a role in some patients with developmental disorders. Hollis-Eden Pharmaceuticals Announces Filing of IND for Phase I Clinical
Trial with Next-Generation Drug Candidate HE3286 in Metabolic Disorders -- Successful Safety Study Would Also Support
Potential Phase II Study with HE3286 in Autoimmune Disorders under Separate
IND Filing --
SAN DIEGO--(BUSINESS WIRE)--Hollis-Eden Pharmaceuticals,
Inc. (NASDAQ:HEPH) announced that it is filing today an
Investigational New Drug (IND) application with the U.S.
Food and Drug Administration (FDA) to begin a Phase I
clinical trial with its next-generation drug candidate
HE3286 for the treatment of metabolic disorders, which
include diabetes, obesity and dyslipidemia. The Phase I
trial program, designed to assess the safety of HE3286 in
healthy volunteers, could support both a Phase II study in
type 2 diabetes patients, as well as a Phase II study in
rheumatoid arthritis patients under a separate IND the
Company plans to file for autoimmune disorders later this
year. In preclinical studies, HE3286 has been shown to
regulate signaling pathways of inflammation common to both
metabolic and autoimmune disorders. As previously reported at a scientific conference on diabetes, HE3286
produced glucose lowering activity and increased insulin sensitivity when
administered orally in preclinical models of type 2 diabetes. The Company'>s
findings suggest that HE3286 may be the first in a new class of insulin
sensitizers with a novel mechanism of action, since it appears to regulate
the pro-inflammatory NF-kappa B pathway without acting on the PPARgamma
receptor, which is the target of insulin sensitizing drugs currently
prescribed today. By working through this new pathway, HE3286 appears in
preclinical studies to avoid the undesirable side effect of weight gain
commonly seen with these existing therapies. HE3286 is a derivative of an endogenous hormone the Company believes is
central to regulating glucose metabolism. Studies in rats fed with a diet
containing the parent hormone of HE3286 showed a reduction in the expression
levels of certain genes encoding key enzymes involved in glucose and
cortisol metabolism (e.g., PEPCK or 11beta-HSD1), an effect which should
lessen the severity or impact of type 2 diabetes on insulin resistance.
Through the application of medicinal chemistry, Hollis-Eden has developed a
chemical analog of that hormone, HE3286, a compound with a more
pharmaceutically suitable profile. In preclinical studies conducted to date, HE3286 administered orally to
genetically obese mice prone to diabetes (db/db model), significantly
(p <0.02) suppressed after 10 days the
progression of hyperglycemia typically observed in these animals. In an
animal model of diet-induced insulin resistance, HE3286 significantly (p < 0.01)
improved glucose handling in an oral glucose tolerance test (OGTT) when
compared to the control group, and at the end of the study was superior (p < 0.003)
to the active control (rosiglitazone). In addition, HE3286 demonstrated a
statistically significant (p<0.006)
reduction in fasting glucose values when compared to controls at days 14 and
29 of the study, and the activity was similar to the active control
(rosiglitazone) ( p<0.05). Additional evidence of improvement in glucose disposal by HE3286 comes
from a hyperinsulinemic/euglycemic clamp study, widely acknowledged as the
"gold standard" model to
measure insulin sensitivity in vivo. In this study, administration of
HE3286 to diabetic db/db mice markedly increased the glucose infusion
rate (GIR) required to maintain normal levels of blood glucose following an
intravenous infusion of a high dose of insulin. The GIR is a key parameter
used to determine the degree of insulin sensitivity in vivo, and its
increase following treatment with HE3286 indicates that this compound acts
physiologically as an insulin sensitizer in the diabetic state. In parallel experiments designed to elucidate the possible mechanism of
action of HE3286 to produce these metabolic effects, it was found that
HE3286 regulates the pro-inflammatory NF-kappa B pathway in cultured mouse
macrophages or human monocytes. This may be an important finding because
over the last several years reports in the scientific literature suggest
that chronic activation of inflammatory pathways such as NF-kappa B can also
lead to insulin resistance and may play a role in the progression towards
type 2 diabetes. HE3286 has also demonstrated a dramatic benefit in rodent models of both
initial-onset and established rheumatoid arthritis. Potential mechanisms of
action for HE3286 in this indication include regulation of NF-kappa B
and increasing the production of regulatory T cells, or Treg cells. Treg
cells play a key role in keeping the immune system from attacking the body
itself, and are being cited increasingly in the medical literature as
therapeutic targets in a range of diseases and disorders including
autoimmune conditions. "Filing an IND for HE3286 is a significant
milestone for Hollis-Eden and for our development program targeting
metabolism," stated Richard B. Hollis, Chairman
and Chief Executive Officer of Hollis-Eden."HE3286
represents a potential first-in-class treatment with a new class of hormones
to control glucose metabolism in type 2 diabetes. The role that hormones
play in metabolism is well documented in the scientific literature, and
HE3286 is an analog of a naturally occurring parent hormone believed to play
a fundamental role in regulating glucose metabolism. Given this biological
lineage, along with the preclinical data we have generated to date with
HE3286, we are optimistic about the compound's
potential as a novel therapy for the treatment of type 2 diabetes and
possibly other metabolic disorders. In addition, based on the role of
inflammation common to both metabolic and autoimmune disorders, we believe
that HE3286 offers potential therapeutic benefit in autoimmune conditions
such as rheumatoid arthritis given its demonstrated ability to
simultaneously regulate signaling pathways central to inflammation and
immune function. "Advancing HE3286 to this stage of development
further demonstrates the progress we are making with our next-generation
drug development program" added Hollis.
"In addition to our expectation of initiating
clinical development of HE3286 in metabolic disorders, we plan to file an
IND for HE3286 for autoimmune disorders later this year, as well as an IND
for our cancer drug candidate HE3235 in late 2007 or early 2008. At the same
time, we are profiling additional follow-on oral next-generation compounds
for a variety of diseases and disorders. Through these efforts, we are
translating our proprietary class of adrenal steroid hormones into potential
pharmaceutical products with competitive advantages in indications that have
well-defined clinical paths and large, well-established markets.
About Diabetes Diabetes, a disease characterized by high levels of glucose in the blood,
is reaching epidemic proportions in the U.S. and other developed countries.
Approximately 20 million Americans and over 160 million people worldwide
have type 2 diabetes. As a result of an aging population and a rise in
obesity rates, a common risk factor in this disease, the prevalence of type
2 diabetes is increasing rapidly. In diabetes, the body does not produce sufficient quantities of, or
properly use, insulin. Insulin is a hormone needed to carry glucose from the
blood into cells, where it is converted to energy necessary for proper
cellular function. When insulin is not available in sufficient quantities or
does not function properly, glucose levels in the blood become elevated,
leading to a variety of severe medical conditions. Included among the therapeutic approaches to type 2 diabetes are drugs
designed to increase insulin production by the pancreas, drugs to reduce
glucose production by the liver, and drugs to increase the body's
sensitivity to insulin, thereby improving glucose disposal by the
bloodstream. Of these, insulin sensitizers represent the largest class of
oral anti-diabetic agents, representing 48% of the annual sales in the $12
billion per year global oral anti-diabetic market. Currently approved
insulin sensitizers, known as glitazones, appear to act primarily through
the activation of the nuclear hormone receptor known as PPARgamma. While
these agents can lower blood glucose, they have been associated with
undesirable side effects such as weight gain and edema. Hollis-Eden Pharmaceuticals Hollis-Eden Pharmaceuticals, Inc. is a world leader in the development of
a proprietary class of adrenal steroid hormones as novel pharmaceuticals for
human health. Through its Hormonal Signaling Technology Platform,
Hollis-Eden is developing a new series of small molecule compounds that are
metabolites or synthetic analogs of endogenous hormones derived by the
adrenal glands from the body' most abundant
circulating steroid. These steroid hormones, designed to restore the
biological activity of cellular signaling pathways disrupted by disease and
aging, have been demonstrated in humans to possess several properties with
potential therapeutic benefit -- they regulate innate and adaptive immunity,
reduce nonproductive inflammation and stimulate cell proliferation. The
Company's clinical drug development candidates
include HE3286, a next-generation compound being prepared for clinical
trials in treating type 2 diabetes and potentially rheumatoid arthritis. A
second next-generation candidate, HE3235, has been selected for clinical
development in cancer. In addition to these clinical development candidates,
Hollis-Eden has an active research program that is generating additional new
clinical leads that are being further evaluated in preclinical models of a
number of different diseases. For more information on Hollis-Eden, visit the
Company's website at
www.holliseden.com. This press release contains forward-looking statements within the
meaning of the federal securities laws concerning, among other things, the
potential and prospects of the Company's drug discovery program and its drug
candidates. Any statement included in this press release that are not a
description of historical facts are forward-looking statements that involve
risks, uncertainties, assumptions and other factors which, if they do not
materialize or prove correct, could cause the Company's actual results to
differ materially from historical results or those expressed or implied by
such forward-looking statements. Such statements are subject to certain
risks and uncertainties inherent in the Company's
business, including, but not limited to: the ability to complete preclinical
and clinical trials successfully and within specified timelines, if at all;
the ability to obtain regulatory approval for HE3286, HE3235 or any other
investigational drug candidate; the Company's future capital needs; the
Company's ability to obtain additional funding; the ability of the Company
to protect its intellectual property rights and to not infringe the
intellectual property rights of others; the development of competitive
products by other companies; and other risks detailed from time to time in
the Company's filings with the Securities and Exchange Commission.
Existing and prospective investors are cautioned not to place undue reliance
on these forward-looking statements, which speak only as of the date of this
press release. Except as required by law, the Company undertakes no
obligation to update or revise the information contained in this press
release as a result of new information, future events or circumstances
arising after the date of this press release.
• From
http://aapnews.aappublications.org/cgi/content/full/28/4/20-a • From
http://www.immunesupport.com/library/showarticle.cfm/ID/4532 Question: Dr. Holtorf,
in a past article on the effective treatment of Chronic Fatigue Syndrome and
Fibromyalgia** you stated that “individuals with these syndromes have measurable
hypothalamic, pituitary, immune and coagulation dysfunction. These abnormalities
then result in a cascade of further abnormalities, in which stress plays a
role.” Could you discuss in detail how you approach testing for and treating
these problems in CFS and FM patients? Dr. Holtorf: There is a
mixture of underlying causes of Chronic Fatigue Syndrome (CFS) and Fibromyalgia
(FM), and each underlying abnormality can trigger further problems. This results
in a cascade of multiple physiologic abnormalities and a perpetuating vicious
cycle. Successful treatment requires that this vicious cycle be addressed on
multiple levels. This cascade of abnormalities [beginning with the "Genetic
Predisposition" and then "Triggering Event of Physiologic Stress"] is
graphically depicted below - and a few of the abnormalities are also discussed.
Thank you Mary for everything!!
News Items:
Media:
• Sam who has been on The Mystery Diagnosis TV Show (Discovery Health) has been invited to appear on Dr. Phil taping soon. More info as it becomes available.
Cushing's:
• From
http://aapnews.aappublications.org/cgi/content/full/28/4/20-a
Polycystic ovary syndrome in adolescence associated with obesity
AAP News (subscription) - USA
... anovulation and include disorders such as nonclassic congenital adrenal
hyperplasia, hyperprolactinemia, Cushing's disease, and, rarely, neoplasm. ...
Adrenal:
• From
http://bjp.rcpsych.org/cgi/content/abstract/190/4/357
Hypothalamic–pituitary–adrenal axis response in borderline ...
British Journal of Psychiatry (subscription) - UK
Hypothalamic–pituitary–adrenal (HPA) axis sensitivity was investigated in 32
non-medicated patients with borderline personality disorder without comorbid ...
Suicide risk and perinatal circumstances
British Journal of Psychiatry (subscription) - UK
As suggested by Riordan et al, foetal nutrition, intra-uterine stressors,
hypothalamic–pituitary–adrenal axis dysfunction and attachment theory may all be
...
Pituitary:
• From
http://www.ucsf.edu/synapse/content/32207/behavior.html
Science Editor
Diabetes:
• From
http://home.businesswire.com
March 29, 2007 07:00 AM Eastern Daylight Time
General Health:
Polycystic ovary syndrome in adolescence associated with obesity
AAP News (subscription) - USA
... anovulation and include disorders such as nonclassic congenital adrenal
hyperplasia, hyperprolactinemia, Cushing's disease, and, rarely, neoplasm. ...
Kent Holtorf, MD, on
Treating Chronic Fatigue Syndrome & Fibromyalgia - An Update
Dr. Kent Holtorf, MD, is Medical Director of the Holtorf Medical Group Center
for Hormone Imbalance, Hypothyroidism and Fatigue in Torrance, California.* He
specializes in treatment of CFS and FM patients.
ImmuneSupport.com
03-27-2007
[ click to enlarge ]
Immune Dysfunction
If a complete immune panel is done on CFS and FM patients, almost all have immune dysfunction, which often includes poor natural killer cell function and/or high RNAse-L activity.
Natural killer cell function. These cells are very important in killing viruses and bacteria. It is very difficult to eradicate chronic infections when these cells are not functioning well.
Antibiotics and antivirals do not work well and are often infective if the immune system is not stimulated as well. You are never able to kill all the infectious agents unless the body is able to clean up the residual left by the antibiotic or antiviral.
There are a number of methods to do this. What we use depends on the infection present, but includes both natural and pharmaceutical antivirals, antibiotics, immune boosters and immune modulators. Growth hormone, thyroid and cortisol (adrenal hormone) are also very good immune enhancers.
Yes, I said cortisol - low doses of cortisol for people who have adrenal insufficiency act as an immune enhancer. Large doses are immune suppressors. Your body normally increases cortisol in times of infection. Oxidative therapies, discussed below, can be very powerful. We customize the specific treatment for the patient.
RNase-L activity: In response to infection, the body can produce an enzyme called RNase-L that breaks down the viral RNA to rid the body of the infection. When the infection is gone this enzyme is then turned off. In CFS, however, the presence of chronic infections can result in the stimulation of an abnormal “super” RNase-L enzyme that also breaks down the cell’s own RNA that is used to code for proteins and required for normal functioning.
The result is poorly functioning cells and an increase in cellular apoptosis (programmed cell death). Treatment consists of eradication of the chronic infection and immune modulators. The RNase-L activity test can be done by Redlabs USA (http://www.RedlabsUSA.com ). (No affiliation).
Coagulation Problems
This is diagnosed with a specialized laboratory test that includes soluble fibrin monomer, prothrombin fragment 1 +2, fibrinogen and thrombin/antithrombin complex.
Defects are typically treated with heparin and vascular enzymes such as lumbrokinase and serapeptidase to stop the excessive production of soluble fibrin monomers and to help clean up the fibrin already laid down.
Eradication of chronic infections is also important, as there is often a chronic infection as the underlying stimulus of the abnormal activation of coagulation.
Low Thyroid
CFS and FM patients almost always have low tissue levels of thryoid hormones due to hypothalamic and pituitary dysfunction and thyroid resistance, which has been documented in a number of studies.
Unfortunately, this hypothryiodism is missed 80% to 90% of the time because standard thyroid tests and TSH [thyroid-stimuating hormone] levels are usually normal, and this is what 90% of doctors are accustomed to using to diagnose low thyroid. Currently, the best method to diagnose low thyroid in these conditions is to look at the T3/reverseT3 ratio. [TSH causes the thyroid gland to produce two hormones: triiodothyronine (T3) and thyroxine (T4).]
When CFS and FM patients are treated with thyroid, they are almost always under-dosed because their pituitary dysfunction results in their TSH becoming quickly suppressed, which normally indicates too much thyroid.
Because these patients have pituitary dysfunction, one must not rely on the TSH, and not treat based on this parameter. In addition, due to the thyroid resistance, T4 preparations such as Synthroid and Levoxyl cannot provide adequate tissue levels of the active hormone. T4/T3 combinations such as Armour thyroid can be of benefit, but many patients also find that these preparations also do not provide adequate relief. Straight timed released T3 is often the best preparation to obtain adequate tissue levels.
Adrenal Insufficiency
Standard blood testing will almost always miss this deficiency. Studies show that with sophisticated testing, close to 100% of CFS and FM have adrenal dysfunction and treatment can be very beneficial.
To diagnose, we typically use symptoms and a combination of blood sugar, free cortisol, and HgA1C%. Again, one must have a high clinical suspicion and not just think in terms of 'normal' and 'abnormal'. These normal levels are determined for healthy individuals, not the chronically ill, so the cortisol levels should be higher with this illness. 24-hour urine and saliva tests can be done, but these can also result in false positive and false negative results.
Growth Hormone Deficiency
Many CFS and FM patients are low in growth hormone. This hormone is produced in the pituitary, and with the documented pituitary dysfunction in CFS and FM, it is not unexpected that there is such a deficiency in these illnesses.
Treatment can sometimes make a tremendous impact and because the cost has come down significantly in recent years, it is a viable treatment for more patients. IGF-1 is the best indication for growth hormone levels, but again, one cannot use the standard laboratory normal ranges to diagnose.
Question: Once you’ve determined which problems a CFS or FM patient has, do you prescribe both traditional and alternative treatments, or do you focus on a single method at a time?
Dr. Holtorf: In order to treat these diseases adequately, one must simultaneously use both traditional and so-called alternative treatments. If one treatment were used at a time it would take many years before the patient feels better. Many treatments can be withdrawn as the patient improves.
Question: Please tell us a little bit about the Holtorf Medical Group, Inc: The Center for Hormone Imbalance, Hypothyroidism and Fatigue (http://www.HoltorfMed.com) where you practice.
Dr. Holtorf: I started the Holtorf Medical Group to concentrate on the treatment of complex endocrine dysfunction, hypothyroidism, fatigue, CFS and fibromyalgia. Eighty percent of our practice is for patients complaining of fatigue, with CFS and FM probably being the biggest part of the practice.
Question: What are the biggest challenges you face with treating CFS and FM patients?
Dr. Holtorf: Although we have good success with CFS and FM, these are challenging cases that require doctors to spend significant time with the patient. It cannot be accomplished with seven-minute office visits.
Question: What are the biggest successes you’ve experienced in treating CFS and FM?
Dr. Holtorf: Many of these patients are very sick and have given up. It is so gratifying to get these patients back to having a life. They are just so grateful. Many have been unable to work and/or have been on disability and now, following treatment, are happy, functional and productive.
Question: Are you working on any promising new treatments at this time – either through research or through a trial and error process with your patients?
Dr. Holtorf: We are continually working on and implementing new treatments every day in practice. We have been using and refining many of the so-called “new” treatments for many years. For instance, Valcyte is considered a new, novel treatment for CFS, but we have been using it for 4 years, since it was first approved.
Question: What are the most exciting developments you’ve seen recently in treatment options for CFS and FM?
Dr. Holtorf: Recent developments are taking place in a stepwise manner, but I do not believe it will be through the so-called ‘mainstream’ medicine one-drug cures. I think these are very treatable conditions, and advances will only continue to improve treatment.
I do believe, however, that the incidences of CFS and FM will significantly increase and at some point will be considered an epidemic because they are very poorly treated through the standard healthcare delivery system.
____
* For more information about the Holtorf Medical Group’s Center for Hormone
Imbalance, Hypothyroidism and Fatigue, visit their website at
http://www.HoltorfMed.com
or phone 310-375-2705
** To review Dr. Holtorf's earlier summary article on the effective treatment
of CFS and FM, archived in the ImmuneSupport.com library,
click
here.
Note: This information has not been evaluated by the FDA. It is not intended to prevent, diagnose, treat, or cure any illness, condition, or disease. It is very important that you make no change in your healthcare plan or regimen without researching and discussing it in collaboration with your professional healthcare team.
Add your Helpful Hints for Dealing with Cushing's to the website and the email Newsletters.
| Newest Bios: | ||
| To add or edit your bio, http://www.cushings-help.com/forms/bio.htm | ||
| Not Yet Diagnosed Patients | ||
| Carol (Deirdre) | Carol is an nursing student with tentative Cushing's diagnosis. She asks if anyone with the experience or knowledge of Cushing's, surgery and or nursing school or other physically and mentally demanding situations, please offer info. | Houston, Texas |
| Kim (kat) | Kim has not yet been diagnosed with Cushing's but has many symptoms and has been diagnosed with an adrenal adenoma and PCOS | Covington, Kentucky. |
| Krista (KristaKorz) | Krista has not yet been diagnosed with Cushing's but was diagnosed with PCOS at 16. She also has a blood disorder (thrombophilia ) and carries the Epstein Barr virus. | Mount
Carmel, Pennsylvania Currently at Bridgewater State College, Massachusetts. |
| Kristina (Kristina82) | Kristina is not yet diagnosed with Cushing's but has a great many symptoms. | Burlington, Massachusetts |
| Natasha (Natasha) | Natasha has been diagnosed with diabetes and PCOS so far. She's had an elevated dexamethasone test and will be seeing a new endo in April. | St. Albans, West Virginia |
| Pituitary Patients | ||
| Jennifer (JenS) |  Jennifer was confirmed with cyclical pituitary Cushing’s Disease. She had pituitary surgery in April 2004, then a BLA in March 2006. Jennifer has also had her thyroid and several enlarged lymph nodes removed. Subsequent diagnosis/illnesses include PCOS, endometriosis, mono, lymphadenopathy, thrombocytopathy, menieres syndrome, and fibromyalgia. She now has Addison's and is growth hormone deficient with suspected unconfirmed Nelson's. |
New Jersey |
| Steroid-Induced Patients | ||
| Mary (mari) | After Mary hurt her back in March 2004, her doctor started injecting her with medrol which she thought was a pain reliever. After taking these steroids, she's noticed symptoms of Cushing's. | Jacksonville, Florida. |
| Pat (Patches) | Pat uses steroids and she has Adult Growth Hormone deficiency as well as adrenal insufficiency. | Portageville, Missouri |
| To add or edit your bio, http://www.cushings-help.com/forms/bio.htm | ||
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| Newest Helpful Doctors: | ||
|
Dr William Ludlam Swedish Hospital Seattle, WA Phone: 206-320-2800 Fax: 206-320-2827 Email: Bill.Ludlam@swedish.org |
My doctor is Dr. Bill Ludlum. I just spoke with him today and made an appointment after finally tracking him down. He just moved up to Seattle from Portland, OR. He has set up a center here. He also works with the expert in Neuro-science, surgeon Marc Mayberg. |
Seattle, WA |
| To add your helpful doctor, http://www.cushings-help.com/forms/doctor.htm | ||
Fundraising:
The Cushing's Store for all kinds of Cushing's Labeled clothing, US Postage Stamps, Teddy Bears, coffee mugs, totebags and much more. Great for your endo or Secret Someone. |
| Remember iGive.com... |
| ... all year round. iGive.com allows online stores to donate a percentage of their profit to running these Cushing's Support sites: the message boards at http://cushings.invisionzone.com/index.php, http://www.cushings-help.com, http://www.cushings-info.com,http://www.cushings-support.com and http://www.cushingsonline.com. See the list of participating merchants 
===> FREE $5 DONATIONS!
<=== Thank you so much for your support. |
Upcoming Conventions, Meetings and Seminars:
• DC Metro Area, TBA More
info as it becomes available.
• June 2-5, 2007, ENDO 2007, Toronto, Canada, Metro
Toronto Center. More info as it becomes
available.
• October 6, 2007,
Rockford, IL. More info as it becomes
available.
• More upcoming local meetings are listed here
Online Chats:
Please join us in the Chat
Room TONIGHT at 9 PM Eastern. Click
to access through the message boards
If you are not yet a member of the message boards,
please use this page: http://cushings.invisionzone.com/chatroom.htm
This room is always open, and has convenient links so that you can get needed information while you're chatting.
I hope to see you tonight!
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