🦓 Day 23, Cushing’s Awareness Challenge 2022

bestday

I wrote parts of this in 2008, so all the “yesterdays” and “last weeks” are a little off. 

Wow.  That’s about all I can say.  Yesterday was possibly the best day of my life since I started getting Cushing’s symptoms, and that was over 30 years ago.  More than a quarter of a century of feeling exhausted, fatigued.  A quarter of my life spent taking naps and sleeping.

Last week  in this post I wrote in part:

I went to the endo yesterday.  Nothing has changed for me.  Nothing will.  He wants me to take more cortef.  I don’t want to gain weight again.  He looked up Provigil and it’s not indicated for panhypopituitarism.  So he won’t prescribe it.  My kidney surgeon probably won’t let me take, anyway, but it was worth a try.

He did mention that in “only” 2.5 years maybe I can go back on growth hormone.  I don’t want to live like this another year let alone 2.5.  But then, when I was on GH before it didn’t help me like it helps most everyone else.

I’m tired of catering to a kidney that may or may not fail sometime anyway, tired of being so exhausted all the time.  I feel like I’ve lost nearly half my life to this Cushing’s stuff already.

So, yesterday I was supposed to go to a conference on web design for churches.  My church sent me because they want me to spiff up their site and make them a new one for Christmas.  I wanted to go because, well, I like learning new stuff about the web.  I figured that I would learn stuff that would also be useful to me in others of my sites.

And I did!

But the amazing thing is this.  My son had told me  about a medication that was very similar to Provigil, that he had tried it while he was writing his doctoral thesis and it had helped him.

So, having tried the official doctor route and being rebuffed – again – I had decided to try this stuff on my own.

Just the night before I had written a response on Robin’s wonderful blog that reads in part:

I hate this disease, too.

I was just talking to a friend today about how I’d try nearly anything – even if it ruined my one remaining kidney – to have a few days where I felt good, normal, where I could wake up in the morning rested and be able to have energy for the day.

I want to go out and have fun, to be able to drive for more than 45 minutes without needing to rest, to be have people over for dinner, whatever. I hate being restricted by my lack of energy.

My endo says to cheer up. In two and a half years I can try the growth hormone again. Whoopee. Didn’t work the first time and maybe gave me, or contributed to, cancer growth. Why would I want to look forward to trying that again?

I want to feel good now. Today.

I hate that this disease kills but I also hate that it’s robbed me of half my life already.

I wish doctors would understand that even though we’ve “survived”, there’s no quality of life there.

I hate Cushing’s. It robs so much from so many of us. 🙁

As I said earlier, I have a history of daily naps of at least 3 hours a day.  It cuts into everything and prevents me from doing many things.  I have to schedule my life around these naps and it’s awful.

rockford-2006-sue 12-18-2006 2-09-18 pmA few years ago I went on a Cushie trip to Rockford.  I’ve been there a few times and it’s always so much fun.  But this first year, we were going to another Cushie’s home for barbecue.  I didn’t drive, I rested in the back of the car during the drive.  We got there and I managed to stay awake for a little while.  Them I put my head down on the dining room table and fell asleep. Our hostess kindly suggested that I move over to the sofa.

So, I have a long history of daily naps, not getting through the day, yadda, yadda.

So, I was a little nervous about yesterday.  I really wanted to go to this conference, and was afraid I’d have to go nap in my car.

I got up at 5:30 am yesterday.  Before I left at 7:15, I took my Cortef and then I took my non-FDA approved simulated Provigil.  (Although it’s not FDA approved, it is not illegal to possess without a prescription and can be imported privately by citizens)

I stayed awake for the whole conference, went to a bell rehearsal, did Stacey’s interview, had dinner and went to bed about 10:30PM.  NO NAP!  I did close my eyes a little during the 4:00PM session but it was also b-o-r-i-n-g.

I stayed awake, I enjoyed myself, I learned stuff, I participated in conversations (completely unlike shy me!).

I felt like I think normal people feel.  I was amazed.  Half my life wasted and I finally (thank you Michael!) had a good day.

My kidney doctor and my endo would probably be appalled but it’s about time that I had some life again!  Maybe in another 25 years, I’ll take another pill.  LOL


Well, the energy from the Adrafinil was a one day thing.  I felt great on Thursday.   Friday and Saturday I slept more than usual.  Saturday, today, was one of those days where I sleep nearly all day.  Maybe if I took the drug more it would build up in my system, maybe not.  But it was still worth having that one day where I felt what I imagine normal to be.

While I was being a slug today, my husband painted the entire house.

I’m not sure if I would have been this tired today or if I was somehow making up for the nap I didn’t get on Thursday.  Whatever the case, I’m glad that I had the opportunity to try this and to experience the wonderful effects, if only for one day.

Information from a site that sells this:

Alertness Without Stimulation

Adrafinil is the prototype of a new class of smart drug – the eugeroics (ie, “good arousal”) designed to promote vigilance and alertness. Developed by the French pharmaceutical company Lafon Laboratories, adrafinil (brand name, Olmifon) has been approved in many European countries for treating narcolepsy, a condition characterized by excessive daytime sleepiness and other unusual symptoms.

Non-narcoleptic users generally find that adrafinil gives them increased energy and reduces fatigue, while improving cognitive function, mental focus, concentration, and memory. It has been reported that quiet people who take adrafinil become more talkative, reserved people become more open, and passive people become more active.

Of course, many stimulant drugs, ranging from caffeine to methamphetamine, are known to produce similar alerting/energizing effects. Adrafinil has been described by some users as a “kinder, gentler” stimulant, because it provides these benefits but usually with much less of the anxiety, agitation, insomnia, associated with conventional stimulants.

Adrafinil’s effects are more subtle than those of the stimulants you may be used to, building over a period of days to months. They appear to be based on its ability to selectively stimulate 1-adrenergic receptors in the brain.2 These receptors normally respond to norepinephrine (noradrenaline), a neurotransmitter linked to alertness, learning, and memory. This is in contrast to conventional stimulants, which stimulate a broader spectrum of brain receptors, including those involving dopamine. Its more focused activity profile may account for adrafinil’s relative lack of adverse side effects.

There’s more info about Adrafinil on Wikipedia

It’s interesting that that snipped report that people become more talkative.  I reported that in the original post, too, even though I didn’t realize that this was a possibility.

A good quote that I wish I could relate to better:

“Time is limited, so I better wake up every morning fresh and know that I have just one chance to live this particular day right, and to string my days together into a life of action and purpose.”

Lance Armstrong (1971 – )
Cyclist, seven-time Tour de France champion and cancer survivor


2011 stuff starts here:

Awhile ago I went to a handbell festival. I took a bit of adrafinil on the main day to try to stay awake for the whole day. It didn’t seem to keep me as on as it did before. I can’t be used to it already. Maybe I’m just that much more tired than I was before.

Our son lives in New York and every few years he gives us tickets to see a Broadway show.  A couple years ago we took the train to NY to see Wicked.  Usually my DH wants to go out and see sights while we’re there.  I usually want to nap.

This time we got up on Saturday morning, went out for breakfast.  I wanted to take in the whole day and enjoy Wicked so I took some Adrafinil.  We got back to the hotel and got ready to go to a museum or other point of interest.

But, DH wanted to rest a bit first.  Then our son closed his eyes for a bit…

So, I found myself the only one awake for the afternoon.  They both work up in time for the show…

Sigh  It was a great show, though.

A recent Christmas I was going to get my son some Adrafinil as a gift.  The original place we bought it didn’t have any more stock so I tracked it down as a surprise.  He was going to give me some, as well, but couldn’t get it from the original source, either.  So he found something very similar called Modafinil.  GMTA!


And 2016..

Saturday, 4/23/16 really was one of the best days I’ve had in a long time.

I’ll be writing a longer post about that later on my travel blog but here’s the original plan: https://maryoblog.com/2016/04/23/busy-saturday/

Suffice it to say, we arrived at the Tattoo and I got no nap at all, all day!

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🎤 Archived Interview: JenS discussed Bilateral Adrenalectomy (BLA)

Jen had Pituitary surgery by Dr. Shahinian 4/28/04, removed ACTH secreting corticotroph hyperplasia and prolactinoma.

She was diagnosed by Dr. Theodore Friedman as cyclical pituitary Cushings.

Her second Surgery 7/21/04 for infection resulted in neuralgia. She had a BLA in March 2006 as Corticol Hyperplasia returned and she now has possible Nelson’s syndrome. Jen also has Thyroid Issues (Hashimoto’s, multiple nodules and entire thyroid removed 2003) and she is Growth Hormone Deficient (3/2006)

Listen at http://www.blogtalkradio.com/cushingshelp/2008/02/29/jens-discusses-bilateral-adrenalectomy-bla

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Basics: Testing: IGF-1 (Insulin-like growth factor 1)

Aim—To contribute to the debate about whether growth hormone (GH) and insulin-like growth factor 1 (IGF-1) act independently on the growth process.

Methods—To describe growth in human and animal models of isolated IGF-1 deficiency (IGHD), such as in Laron syndrome (LS; primary IGF-1 deficiency and GH resistance) and IGF-1 gene or GH receptor gene knockout (KO) mice.

Results—Since the description of LS in 1966, 51 patients were followed, many since infancy. Newborns with LS are shorter (42–47 cm) than healthy babies (49–52 cm), suggesting that IGF-1 has some influence on intrauterine growth. Newborn mice with IGF-1 gene KO are 30% smaller. The postnatal growth rate of patients with LS is very slow, the distance from the lowest normal centile increasing progressively. If untreated, the final height is 100–136 cm for female and 109–138 cm for male patients. They have acromicia, organomicria including the brain, heart, gonads, genitalia, and retardation of skeletal maturation. The availability of biosynthetic IGF-1 since 1988 has enabled it to be administered to children with LS. It accelerated linear growth rates to 8–9 cm in the first year of treatment, compared with 10–12 cm/year during GH treatment of IGHD. The growth rate in following years was 5–6.5 cm/year.

Conclusion—IGF-1 is an important growth hormone, mediating the protein anabolic and linear growth promoting effect of pituitary GH. It has a GH independent growth stimulating effect, which with respect to cartilage cells is possibly optimised by the synergistic action with GH.

Keywords: insulin-like growth factor I, growth hormones, Laron syndrome, growth

In recent years, new technologies have enabled many advances in the so called growth hormone (GH) axis (fig 1). Thus, it has been found that GH secretion from the anterior pituitary is regulated not only by GH releasing hormone (GHRH) and somatostatin (GH secretion inhibiting hormone), but also by other hypothalamic peptides called GH secretagogues, which seem to act in synergism with GHRH by inhibiting somatostatin. One of these has been cloned and named Ghrelin. The interplay between GHRH and somatostatin induces a pulsatile GH secretion, which is highest during puberty. GH induces the generation of insulin-like growth factor 1 (IGF-1, also called somatomedin 1) in the liver and regulates the paracrine production of IGF-1 in many other tissues.

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The cascade of the growth hormone axis. CNS, central nervous system; GH, growth hormone; GHBP, GH binding protein; GH-S, GH secretagogues; IGF-1, insulin-like growth factor 1; IGFBPs, IGF binding proteins; +, stimulation; –, inhibition.

IGF-1

IGF-1 and IGF-2 were identified in 1957 by Salmon and Daughaday and designated “sulphation factor” by their ability to stimulate 35-sulphate incorporation into rat cartilage. Froesch et al described the non-suppressible insulin-like activity (NSILA) of two soluble serum components (NSILA I and II). In 1972, the labels sulphation factor and NSILA were replaced by the term “somatomedin”, denoting a substance under control and mediating the effects of GH. In 1976, Rinderknecht and Humbel isolated two active substances from human serum, which owing to their structural resemblance to proinsulin were renamed “insulin-like growth factor 1 and 2” (IGF-1 and 2). IGF-1 is the mediator of the anabolic and mitogenic activity of GH.

CHEMICAL STRUCTURE

The IGFs are members of a family of insulin related peptides that include relaxin and several peptides isolated from lower invertebrates. IGF-1 is a small peptide consisting of 70 amino acids with a molecular weight of 7649 Da. Similar to insulin, IGF-1 has an A and B chain connected by disulphide bonds. The C peptide region has 12 amino acids. The structural similarity to insulin explains the ability of IGF-1 to bind (with low affinity) to the insulin receptor.

THE IGF-1 GENE

The IGF-1 gene is on the long arm of chromosome 12q23–23. The human IGF-1 gene consists of six exons, including two leader exons, and has two promoters.

IGF binding proteins (IGFBPs)

In the plasma, 99% of IGFs are complexed to a family of binding proteins, which modulate the availability of free IGF-1 to the tissues. There are six binding proteins. In humans, almost 80% of circulating IGF-1 is carried by IGFBP-3, a ternary complex consisting of one molecule of IGF-1, one molecule of IGFBP-3, and one molecule of an 88 kDa protein named acid labile subunit. IGFBP-1 is regulated by insulin and IGF-1; IGFBP-3 is regulated mainly by GH but also to some degree by IGF-1.

The IGF-1 receptor

The human IGF-1 receptor (type 1 receptor) is the product of a single copy gene spanning over 100 kb of genomic DNA at the end of the long arm of chromosome 15q25–26. The gene contains 21 exons (fig 2) and its organisation resembles that of the structurally related insulin receptor (fig 3). The type 1 IGF receptor gene is expressed by almost all tissues and cell types during embryogenesis. In the liver, the organ with the highest IGF-1 ligand expression, IGF-1 receptor mRNA is almost undetectable, possibly because of the “downregulation” of the receptor by the local production of IGF-1. The type 1 IGF receptor is a heterotetramer composed of two extracellular spanning α subunits and transmembrane β subunits. The α subunits have binding sites for IGF-1 and are linked by disulphide bonds (fig 3). The β subunit has a short extracellular domain, a transmembrane domain, and an intracellular domain. The intracellular part contains a tyrosine kinase domain, which constitutes the signal transduction mechanism. Similar to the insulin receptor, the IGF-1 receptor undergoes ligand induced autophosphorylation. The activated IGF-1 receptor is capable of phosphorylating other tyrosine containing substrates, such as insulin receptor substrate 1 (IRS-1), and continues a cascade of enzyme activations via phosphatidylinositol-3 kinase (PI3-kinase), Grb2 (growth factor receptor bound protein 2), Syp (a phophotyrosine phosphatase), Nck (an oncogenic protein), and Shc (src homology domain protein), which associated to Grb2, activates Raf, leading to a cascade of protein kinases including Raf, mitogen activated protein (MAP) kinase, 5 G kinase, and others.

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Type 1 insulin-like growth factor receptor gene and mRNA. Reproduced with permission from Werner.

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Resemblance between the insulin and insulin-like growth factor 1 (IGF-1) receptors.

Physiology

IGF-1 is secreted by many tissues and the secretory site seems to determine its actions. Most IGF-1 is secreted by the liver and is transported to other tissues, acting as an endocrine hormone. IGF-1 is also secreted by other tissues, including cartilagenous cells, and acts locally as a paracrine hormone (fig 4). It is also assumed that IGF-1 can act in an autocrine manner as an oncogene. The role of IGF-1 in the metabolism of many tissues including growth has been reviewed recently.

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Paracrine insulin-like growth factor 1 (IGF-1) secretion and endocrine IGF-1 targets in the various zones of the epiphyseal cartilage growth zone.

The following is an analysis of whether IGF-1, the anabolic effector hormone of pituitary GH, is the “real growth hormone”.

Is IGF-1 “a” or “the” growth hormone?

The discussion on the role of IGF-1 in body growth will be based on growth in states of IGF-1 deficiency and the effects of exogenous IGF-1 administration. Experiments in nature (gene deletion or gene mutations) or experimental models in animals, such as gene knockouts, help us in this endeavour. In 1966 and 1968, we described a new type of dwarfism indistinguishable from genetic isolated GH deficiency (IGHD), but characterised by high serum GH values. Subsequent studies revealed that these patients cannot generate IGF-1.

This syndrome of GH resistance (insensitivity) was named by Elders et al as Laron dwarfism, a name subsequently changed to Laron syndrome (LS). Molecular studies revealed that the causes of GH resistance are deletions or mutations in the GH receptor gene, resulting in the failure to generate IGF-1 and a reduction in the synthesis of several other substances, including IGFBP-3. This unique model in humans has enabled the study of the differential effects of GH and IGF-1.

Growth and development in congenital (primary) IGF-1 deficiency (LS)

Our group has studied and followed 52 patients (many since birth) throughout childhood, puberty, and into adulthood. We found that newborns with LS are slightly shorter at birth (42–47 cm) than healthy babies (49–52 cm), suggesting that IGF-1 has some influence on intrauterine linear growth. This fact is enforced by the findings that already at birth, and throughout childhood, skeletal maturation is retarded, as is organ growth. These growth abnormalities include a small brain (as expressed by head circumference), a small heart (cardiomicria), and acromicria (small chin, resulting from underdevelopment of the facial bones, small hands, and small feet). IGF-1 deficiency also causes underdevelopment and weakness of the muscular system, and impairs and weakens hair and nail growth. These findings are identical to those described in IGHD. IGF-1 deficiency throughout childhood causes dwarfism (final height if untreated, 100–135 cm in female and 110–142 cm in male patients), with an abnormally high upper to lower body ratio. One patient reported from the UK was found to have a deletion of exons 4 and 5 of the IGF-1 gene and he too was found to have severe growth retardation.

Impaired growth and skeletal development in the absence of IGF-1 were confirmed in mice using knockout (KO) of the IGF-1 gene or GH receptor gene.

Knockout of the IGF-1 gene or the IGF-1 receptor gene reduces the size of mice by 40–45%. Lack of the IGF-1 receptor is lethal at birth in mice owing to respiratory failure caused by impaired development of the diaphragm and intercostal muscles. In another model, the mice remained alive and their postnatal growth was reduced.

In conclusion, findings in humans and in animals show that IGF-1 deficiencies causes pronounced growth retardation in the presence of increased GH values.

The following is a summary of the results of the growth stimulating effects of the administration of exogenous IGF-1 to children and experimental data.

Growth promoting effects of IGF-1

The first demonstration that exogenous IGF-1 stimulates growth was the administration of purified hormone to hypophysectomised rats. After the biosynthesis of IGF-1 identical to the native hormone, trials of its use in humans were begun; first in adults and then in children. Our group was the first to introduce long term administration of biosynthetic IGF-1 to children with primary IGF-1 deficiency—primary GH insensitivity or LS. The finding that daily IGF-1 administration raises serum alkaline phosphatose, which is an indicator of osteoblastic activity, and serum procollagen, in addition to IGFBP-3, led to long term treatment. Treatment of patients with LS was also initiated in other parts of the world. The difference between us and the other groups was that we used a once daily dose, whereas the others administered IGF-1 twice daily. Table 1 compares the linear growth response of children with LS treated by four different groups. It can be seen that before treatment the mean growth velocity was 3–4.7 cm/year and that this increased after IGF-1 treatment to 8.2–9.1 cm/year, followed by a lower velocity of 5.5–6.4 cm/year in the next two years. (In GH treatment the highest growth velocity registered is also in the first year of treatment.) Figure 5 illustrates the growth response to IGF-1 in eight children during the first years of treatment. Ranke and colleagues reported that two of their patients had reached the third centile (Tanner), as did the patient of Krzisnik and Battelino; however, most patients did not reach a normal final height. The reasons may be late initiation of treatment, irregular IGF-1 administration, underdosage, etc. Ranke et al conclude that long term treatment of patients with LS promoted growth and, if treatment is started at an early age, there is a considerable potential for achieving height normalisation. Because no patient in our group was treated since early infancy to final height we cannot confirm this opinion.

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Growth velocity before and during insulin-like growth factor 1 (IGF-1) treatment. Note that in infancy, when the non-growth hormone/IGF-1 dependent growth velocity is relatively high (but low for age), the change induced by IGF-1 administration is less than in older children.

Table 1

Linear growth response of children with Laron syndrome treated by means of insulin-like growth factor 1 (IGF-1)

At start Growth velocity (cm/year) Year of treatment
Authors Year Ref. N Age range (years) BA (years) Ht SDS (m) IGF-1 dose (μg/kg/day) 0 1st 2nd 3rd
(n = 26) (n = 18)
Ranke et al 1995 31 3.7–19 1.8–13.3 −6.5 40–120 b.i.d. 3.9 (1.8) 8.5 (2.1) 6.4 (2.2)
(n = 5) (n = 5) (n = 1)
Backeljauw et al 1996 5 2–11 0.3–6.8 −5.6 80–120 b.i.d. 4.0 9.3 6.2 6.2
(n = 9) (n = 6) (n = 5)
Klinger and Laron 1995 9 0.5–14 0.2–11 −5.6 150–200 i.d 4.7 (1.3) 8.2 (0.8) 6 (1.3) 4.8 (1.3)*
(n = 15) (n = 15) (n = 6)
Guevarra-Aguirre et al 1997 15 3.1–17 4.5–9.3 120 b.i.d. 3.4 (1.4) 8.8 (11) 6.4 (1.1) 5.7 (1.4)
(n = 8) (n = 8)
Guevarra-Aguire et al 8 80 b.i.d. 3.0 (1.8) 9.1 (2.2) 5.6 (2.1)

Growth velocity values are mean (SD).

*The younger children had a growth velocity of 5.5 and 6.5 cm/year.

BA, bone age; b.i.d., twice daily; CA, chronological age; i.d., once daily; Ht SDS, height standard deviation score.

When the growth response to GH treatment in infants with IGHD was compared with that of IGF-1 in infants with LS we found that the infants with IGHD responded faster and better than those with LS. However, the small number of patients and the differences in growth retardation between the two groups makes it difficult to reach a conclusion.

Both hormones stimulated linear growth, but GH seemed more effective than IGF-1. One cause may be the greater growth deficit of the infants with LS than those with IGHD, an insufficient dose of IGF-1, or that there is a need for some GH to provide an adequate stem cell population of prechondrocytes to enable full expression of the growth promoting action of IGF-1, as postulated by Green and colleagues and Ohlson et al. All the above findings based on a few clinical studies with small groups of patients and a few experimental studies remain at present controversial. The crucial question is whether there are any, and if so, whether there are sufficient IGF-1 receptors in the “progenitor cartilage zone” of the epiphyseal cartilage (fig 4) to respond to endocrine and exogenous IGF-1. Using the mandibular condyle of 2 day old ICR mice, Maor et al showed that these condyles, which resemble the epiphyseal plates of the long bones, contain IGF-1 and high affinity IGF-1 receptors also in the chondroprogenitor cell layers, which enables them to respond to IGF-1 in vitro.

Sims et al, using mice with GH receptor KO showed that IGF-1 administration stimulates the growth (width) of the tibial growth plate and that IGF-1 has a GH independent effect on the growth plate. These findings are similar to those found when treating hypophysectomised rats with IGF-1.

In conclusion, IGF-1 is an important growth hormone, mediating the anabolic and linear growth promoting effect of pituitary GH protein. It has a GH independent growth stimulating effect, which with respect to cartilage cells is possibly optimised by the synergistic action with GH.

References

1. Tannenbaum GS, Ling N. The interrelationship of growth hormone (GH)-releasing factor and somatostatin in generation of the ultradian rhythm of GH secretion. Endocrinology 1984;115:1952–7. [PubMed[]
2. Laron Z. Growth hormone secretagogues: clinical experience and therapeutic potential. Drugs 1995;50:595–601. [PubMed[]
3. Ghigo E, Boghen M, Casanueva FF, et al., eds. Growth hormone secretagogues. Basic findings and clinical implications. Amsterdam: Elsevier, 1994.
4. Jaffe CA, Ho PJ, Demott-Friberg R, et al. Effects of a prolonged growth hormone (GH)-releasing peptide infusion on pulsatile GH secretion in normal men. J Clin Endocrinol Metab 1993;77:1641–7. [PubMed[]
5. Kojima M, Hosada H, Date Y, et al. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature 1999;402:656–60. [PubMed[]
6. Devesa J, Lima L, Tresquerres AF. Neuroendocrine control of growth hormone secretion in humans. Trends Endocrinol Metab 1992;3:175–83. [PubMed[]
7. Laron Z. The somatostatin-GHRH-GH-IGF-I axis. In: Merimee T, Laron Z, eds. Growth hormone, IGF-I and growth: new views of old concepts. Modern endocrinology and diabetes, Vol. 4. London-Tel Aviv: Freund Publishing House Ltd, 1996:5–10.
8. Salmon WD, Jr, Daughaday W. A hormonally controlled serum factor which stimulates sulfate incorporation by cartilage in vitro. J Lab Clin Med 1957;49:825–36. [PubMed[]
9. Froesch ER, Burgi H, Ramseier EB, et al. Antibody-suppressible and nonsuppressible insulin-like activities in human serum and their physiologic significance. An insulin assay with adipose tissue of increased precision and specificity. J Clin Invest 1963;42:1816–34. [PMC free article] [PubMed[]
10. Daughaday WH, Hall K, Raben MS, et al. Somatomedin: a proposed designation for the sulfation factor. Nature 1972;235:107. [PubMed[]
11. Rinderknecht E, Humbel RE. Polypeptides with non-suppressible insulin-like and cell-growth promoting activities in human serum: isolation, chemical characterization, and some biological properties of forms I and II. Proc Natl Acad Sci U S A 1976;73:2365–9. [PMC free article] [PubMed[]
12. Laron Z. Somatomedin-1 (recombinant insulin-like growth factor-I). Clinical pharmacology and potential treatment of endocrine and metabolic disorders. Biodrugs 1999;11:55–70. [PubMed[]
13. Blundell TL, Humbel RE. Hormone families: pancreatic hormones and homologous growth factors. Nature 1980;287:781–7. [PubMed[]
14. Rinderknecht E, Humbel RE. The amino acid sequence of human insulin like growth factor I and its structural homology, with proinsulin. J Biol Chem 1978;253:2769–76. [PubMed[]
15. Brissenden JE, Ullrich A, Francke U. Human chromosomal mapping of genes for insulin-like growth factors I and II and epidermal growth factor. Nature 1984;310:781–4. [PubMed[]
16. Mullis PE, Patel MS, Brickell PM, et al. Growth characteristics and response to growth hormone therapy in patients with hypochondroplasia: genetic linkage of the insulin-like growth factor I gene at chromosome 12q23 to the disease in a subgroup of these patients. Clin Endocrinol 1991;34:265–74. [PubMed[]
17. Rotwein P. Structure, evolution, expression and regulation of insulin-like growth factors I and II. Growth Factors 1991;5:3–18. [PubMed[]
18. Hwa V, Oh Y, Rosenfeld RG. The insulin-like growth factor binding protein (IGFBP) superfamily. Endocr Rev 1999;20:761–87 [PubMed[]
19. Lewitt MS, Saunders H, Phuyal JL, et al. Complex formation by human insulin-like growth factor-binding protein-3 and human acid-labile subunit in growth hormone-deficient rats. Endocrinology 1994;134:2402–9. [PubMed[]
20. Laron Z, Suikkairi AM, Klinger B, et al. Growth hormone and insulin-like growth factor regulate insulin-like growth factor-binding protein-1 in Laron type dwarfism, growth hormone deficiency and constitutional short stature. Acta Endocrinol 1992;127:351–8. [PubMed[]
21. Kanety H, Karasik A, Klinger B, et al. Long-term treatment of Laron type dwarfs with insulin-like growth factor I increases serum insulin-like growth factor-binding protein 3 in the absence of growth hormone activity. Acta Endocrinol 1993;128:144–9. [PubMed[]
22. Werner H. Molecular biology of the type I IGF receptor. In: Rosenfeld RG, Roberts CT, Jr, eds. The IGF system—molecular biology, physiology and clinical applications. Totowa, NJ: Humana Press, 1999:63–88.
23. Seino S, Seino M, Nishi S, et al. Structure of the human insulin receptor gene and characterization of its promoter. Proc Natl Acad Sci U S A 1989;86:114–18. [PMC free article] [PubMed[]
24. Bondy CA, Werner H, Roberts CT, Jr, et al. Cellular pattern of insulin-like growth factor I (IGF-I) and type I IGF receptor gene expression in early organogenesis: comparison with IGF-II gene expression. Mol Endocrinol 1990;4:1386–98. [PubMed[]
25. Kato H, Faria TN, Stannard B, et al. Essential role of tyrosine residues 1131, 1135, and 1136 of the insulin-like growth factor-I (IGF-I) receptor in IGF-I action. Mol Endocrinol 1994;8:40–50. [PubMed[]
26. LeRoith D, Werner H, Beitner-Johnson D, et al. Molecular and cellular aspects of the insulin-like growth factor I receptor. Endocr Rev 1995;16:143–63. [PubMed[]
27. Merimee T, Laron Z, eds. Growth hormone, IGF-I and growth: new views of old concepts. Modern endocrinology and diabetes, Vol. 4. London-Tel Aviv: Freund Publishing House Ltd, 1996.
28. D’Ercole AJ, Applewhite GT, Underwood LE. Evidence that somatomedin is synthesized by multiple tissues in the fetus. Dev Biol 1980;75:315–28 [PubMed[]
29. Nilsson A, Isgaard J, Lindhahl A, et al. Regulation by growth hormone of number of chondrocytes containing IGF-I in rat growth plate. Science 1986;233:571–4. [PubMed[]
30. Baserga R. The IGF-I receptor in cancer research. Exp Cell Res 1999;253:1–6. [PubMed[]
31. Rosenfeld RG, Roberts CT, Jr, eds. The IGF system—molecular biology, physiology and clinical applications. Totowa, NY: Humana Press, 1999.
32. Zapf J, Froesch ER. Insulin-like growth factor I actions on somatic growth. In: Kostyo J, ed. Handbook of physiology, Vol. V, Section 7. Philadelphia: American Physiological Society, 1999:663–99.
33. Laron Z, Pertzelan A, Mannheimer S. Genetic pituitary dwarfism with high serum concentration of growth hormone. A new inborn error of metabolism? Isr J Med Sci 1966;2:153–5. [PubMed[]
34. Laron Z, Pertzelan A, Karp M. Pituitary dwarfism with high serum levels of growth hormone. Isr J Med Sci 1968;4:883–94. [PubMed[]
35. Laron Z, Pertzelan A, Karp M, et al. Administration of growth hormone to patients with familial dwarfism with high plasma immunoreactive growth hormone. Measurement of sulfation factor, metabolic and linear growth responses. J Clin Endocrinol Metab 1971;33:332–42. [PubMed[]
36. Elders MJ, Garland JT, Daughaday WH, et al. Laron’s dwarfism: studies on the nature of the defect. J Pediatr 1973;83:253–63. [PubMed[]
37. Laron Z, Parks JS, eds. Lessons from Laron syndrome (LS) 1966–1992. A model of GH and IGF-I action and interaction. Pediatric and Adolescent Endocrinology 1993;24:1–367. []
38. Godowski PJ, Leung DW, Meacham LR, et al. Characterization of the human growth hormone receptor gene and demonstration of a partial gene deletion in 2 patients with Laron type dwarfism. Proc Natl Acad Sci U S A 1989;86:8083–7. [PMC free article] [PubMed[]
39. Amselem S, Duquesnoy P, Attree O, et al. Laron dwarfism and mutations of the growth hormone-receptor gene. N Engl J Med 1989;321:989–95. [PubMed[]
40. Laron Z. Laron syndrome—primary growth hormone resistance. In: Jameson JL, ed. Hormone resistance syndromes. Contemporary endocrinology, Vol. 2. Totowa, NJ: Humana Press, 1999:17–37.
41. Laron Z. Laron type dwarfism (hereditary somatomedin deficiency): a review. In: Frick P, Von Harnack GA, Kochsiek GA, et al, eds. Advances in internal medicine and pediatrics. Berlin-Heidelberg: Springer-Verlag, 1984:117–50. [PubMed]
42. Feinberg MS, Scheinowitz M, Laron Z. Echocardiographic dimensions and function in adults with primary growth hormone resistance (Laron syndrome). Am J Cardiol 2000;85:209–13. [PubMed[]
43. Brat O, Ziv I, Klinger B, et al. Muscle force and endurance in untreated and human growth hormone or insulin-like growth factor-I-treated patients with growth hormone deficiency or Laron syndrome. Horm Res 1997;47:45–8. [PubMed[]
44. Lurie R, Ben-Amitai D, Laron Z. Impaired hair growth and structural defects in patients with Laron syndrome (primary IGF-I deficiency) [abstract]. Horm Res 2001 [In press.]
45. Gluckman PD, Gunn AJ, Wray A, et al. Congenital idiopathic growth hormone deficiency associated with prenatal and early postnatal growth failure. J Pediatr 1992;121:920–3. [PubMed[]
46. Woods KA, Camacho-Hubner C, Savage MO, et al. Intrauterine growth retardation and postnatal growth failure associated with deletion of the insulin-like growth factor I gene. N Engl J Med 1996;335:1363–7. [PubMed[]
47. Zhou Y, Xu BC, Maheshwari HG, et al. A mammalian model for Laron syndrome produced by targeted disruption of the mouse growth hormone receptor/binding protein gene (the Laron mouse). Proc Natl Acad Sci U S A 1997;94:13215–20. [PMC free article] [PubMed[]
48. Sjogren K, Bohlooly YM, Olsson B, et al. Disproportional skeletal growth and markedly decreased bone mineral content in growth hormone receptor –/– mice. Biochem Biophys Res Commun 2000;267:603–8. [PubMed[]
49. Accili D, Nakae J, Kim JJ, et al. Targeted gene mutations define the roles of insulin and IGF-I receptors in mouse embryonic development. J Pediatr Endocrinol Metab 1999;12:475–85. [PubMed[]
50. Holzenberger M, Leneuve P, Hamard G, et al. A targeted partial invalidation of the insulin-like growth factor-I receptor gene in mice causes a postnatal growth deficit. Endocrinology 2000;141:2557–66. [PubMed[]
51. Schoenle E, Zapf J, Humbel RE, et al. Insulin-like growth factor I stimulates growth in hypophysectomized rats. Nature 1982;296:252–3. [PubMed[]
52. Guler H-P, Zapf J, Scheiwiller E, et al. Recombinant human insulin-like growth factor I stimulates growth and has distinct effects on organ size in hypophysectomized rats. Proc Natl Acad Sci U S A 1988;85:4889–93. [PMC free article] [PubMed[]
53. Niwa M, Sato Y, Saito Y, et al. Chemical synthesis, cloning and expression of genes for human somatomedin C (insulin like growth factor I) and 59Val somatomedin C. Ann N Y Acad Sci 1986;469:31–52. [PubMed[]
54. Guler HP, Zapf J, Froesch ER. Short term metabolic effects of recombinant human insulin like growth factor in healthy adults. N Engl J Med 1987;317:137–40. [PubMed[]
55. Laron Z, Klinger B, Silbergeld A, et al. Intravenous administration of recombinant IGF-I lowers serum GHRH and TSH. Acta Endocrinol 1990;123:378–82. [PubMed[]
56. Klinger B, Garty M, Silbergeld A, et al. Elimination characteristics of intravenously administered rIGF-I in Laron type dwarfs (LTD). Dev Pharmacol Ther 1990;15:196–9. [PubMed[]
57. Laron Z, Klinger B, Jensen LT, et al. Biochemical and hormonal changes induced by one week of administration of rIGF-I to patients with Laron type dwarfism. Clin Endocrinol 1991;35:145–50. [PubMed[]
58. Klinger B, Jensen LT, Silbergeld A, et al. Insulin-like growth factor-I raises serum procollagen levels in children and adults with Laron syndrome. Clin Endocrinol 1996;45:423–9. [PubMed[]
59. Underwood LE, Backeljauw P. IGFs: function and clinical importance of therapy with recombinant human insulin-like growth factor I in children with insensitivity to growth hormone and in catabolic conditions. J Intern Med 1993;234:571–7. [PubMed[]
60. Ranke MB, Savage MO, Chatelain PG, et al. Long-term treatment of growth hormone insensitivity syndrome with IGF-I. Horm Res 1999;51:128–34. [PubMed[]
61. Ranke MB, Savage MO, Chatelain PG, et al. Insulin-like growth factor (IGF-I) improves height in growth hormone insensitivity: two years results. Horm Res 1995;44:253–64. [PubMed[]
62. Backeljauw PF, Underwood LE, The GHIS Collaborative Group. Prolonged treatment with recombinant insulin-like growth factor I in children with growth hormone insensitivity syndrome—a clinical research center study. J Clin Endocrinol Metab 1996;81:3312–17. [PubMed[]
63. Klinger B, Laron Z. Three year IGF-I treatment of children with Laron syndrome. J Pediatr Endocrinol Metab 1995;8:149–58. [PubMed[]
64. Guevara-Aguirre J, Rosenbloom AL, Vasconez O, et al. Two year treatment of growth hormone (GH) receptor deficiency with recombinant insulin-like growth factor-I in 22 children: comparison of two dosage levels and to GH treated GH deficiency. J Clin Endocrinol Metab 1997;82:629–33. [PubMed[]
65. Laron Z, Lilos P, Klinger B. Growth curves for Laron syndrome. Arch Dis Child 1993;68:768–70. [PMC free article] [PubMed[]
66. Krzisnik C, Battelino T. Five year treatment with IGF-I of a patient with Laron syndrome in Slovenia (a follow-up report). J Pediatr Endocrinol Metab 1997;10:443–7. [PubMed[]
67. Laron Z, Klinger B. Comparison of the growth-promoting effects of insulin-like growth factor I and growth hormone in the early years of life. Acta Paediatr 2000;89:38–41. [PubMed[]
68. Green H, Morikawa M, Nixon T. A dual effector theory of growth hormone action. Differentiation 1985;29:195–8. [PubMed[]
69. Ohlson C, Bengtsson BA, Isaksson OG, et al. Growth hormone and bone. Endocr Rev 1998;19:55–79. [PubMed[]
70. Maor G, Laron Z, Eshet R, et al. The early postnatal development of the murine mandibular condyle is regulated by endogenous insulin-like growth factor-I. J Endocrinol 1993;137:21–6. [PubMed[]
71. Sims NA, Clement-Lacroix P, Da Ponte F, et al. Bone homeostatis in growth hormone receptor-null mice is restored by IGF-I but independent of Stat5. J Clin Invest 2001;106:1095–103. [PMC free article] [PubMed[]

$Growth Hormone Study Opportunity

 

Here’s your chance to make your voice heard on Growth Hormone Issues.

Anyone interested would sign up with Rare Patient Voice using the CushingsHelp referral Link. You would then get an email invite to the actual study.
Study Opportunity for Idiopathic Short Stature (ISS) Caregivers
This is a 30 min online survey and Compensation is $50
Please sign up at the link below for more information or to see if you qualify

💙 Post-Op Pituitary COVID Injection 1

 

Quick takeaway: I have adrenal insufficiency (one adrenal was removed with my kidney due to cancer, steroid-dependent (post-Cushing’s Disease), growth hormone insufficiency, panhypopituitary.  I had some issues after my first COVID-19 injection (Moderna) but not too bad.  My second injection will be March 15.


January 12, 2021 my Mom’s doctor called and offered her the vaccine but she didn’t want it. She said she didn’t go anywhere.  True but my DH and I do – and she has a friend visit once a month.  I joked to a friend that I could put on a wig and go as her since we have the same first name.

I have been doing the COVID-19 Patient Monitoring System through my doctor’s office since it was first offered.  Just a few boxes of how I’m feeling, if I wore a mask and so on.  I am a strong believer in helping to participate in medical trials, as I mention below.  This one is very easy and takes about a minute out of my day.  Easy-peasy.

I’ve been on the Fairfax Waiting List since January 19, 2021.  As of right now, they are still scheduling people from January 18 – I read somewhere that 41,000-some people registered on the 18th, so it may be a while to get to my date.  They have set up an interesting dashboard to track how things are going  https://www.fairfaxcounty.gov/health/novel-coronavirus/vaccine/data

I got a link from a friend when CVS opened up clinics in my state – https://www.cvs.com/vaccine/intake/store/covid-screener/covid-qns

I kept the CVS link open and checked it every morning.  Everything was full until Saturday, February 13.  I was able to register at about 5 am.  When I went back about 20 minutes later, everything was gone.

 

CVS sent out an informative email with directions, dates, ics file to easily add to calendar,

On the day of your appointment:

•Please arrive early enough to check in before your scheduled appointment. Arriving late for your appointment may result in an extended wait time.

•Bring your ID and insurance card, voucher or other coverage

•Don’t forget a face covering—wearing it throughout your visit is required

•When you arrive, please check in at the pharmacy area inside the store or follow the signs for the COVID-19 vaccine

CVS tips for vaccine shots:

•Wearing short sleeves makes getting a shot easier and faster

•If you must wear long sleeves, dress in layers with the short sleeves underneath

Review the patient fact sheet about the specific vaccine you are receiving

What to do if you feel sick or have COVID-19 symptoms:

•Contact your health care provider immediately

•If your provider recommends it, get tested for COVID-19

Cancel your appointment

•Don’t come to the pharmacy

•Schedule a new appointment when you’re well

After your vaccine:

•Be prepared to stay for 15 to 30 minutes after the COVID-19 vaccination so you can be observed for side effects.

•If you experience side effects from your COVID-19 vaccine dose, you may find some guidance at Coronavirus: Vaccine, Prevention Tips & FAQs

•The CDC has created a way for you to report how you feel after the COVID-19 vaccination through a smartphone-based tool that uses text messaging and web surveys to check in with you. Learn about v-safe and sign up today.

And a short survey, which I took – just add up to 5 stars and write a short paragraph.

Monday, February 15, 2021: When I got to CVS, I found that everything was very well run.

I got a text from CVS asking me to click a link when I arrived at 3:30 and it gave me directions on where to go.

I was met by someone at door who checked my name – I showed him my phone screen – he showed me where to walk following arrows on floor.  Then I was met by so someone who checked my name and he asked if I had done the texting thing (yes!).

There were 4 people ahead of me that I could see.  It went very fast.  I was in the little room within less than 10 minutes.

The nurse asked if left arm was ok to use.

She told me to treat the little quarantine form like gold.  Take a picture on my phone, just in case.  Maybe laminate after second shot.  Keep it with passport.

She said that old folks (like me!) didn’t have as many issues after second shot.

The shot was very fast – I never felt it.

The nurse said if I get a headache, take Tylenol only.  I said that was all I could take anyway because I have only one kidney.

I sat in the waiting area for 15 minutes to be sure there were no problems  There were about 10 or so people sitting around the store that I could see at various stages of their 15 minutes.

I was glad to see that it was Moderna (MRNA) although I would have taken either.  I have a long-standing issue with the other drug company, unrelated to COVID vaccines.

I posted on FB that I had done my first injection and a friend told me about registering at vsafe.cdc.gov for them to keep track of me after the vaccination.  I signed up for that right away – and I noticed that CVS had also given me that link.

About 12 hours later (3:30 am) I got up to go to the bathroom and noticed that my arm was a little sore. No biggie.

Tuesday, February 16, 2021:  I just got my first dose of Moderna yesterday – sore arm, so far.

The nurse told me yesterday that older people like myself (I’m 72) had fewer side effects since we had been exposed to more things over the years.  I’m not sure how accurate that is but I’ll hold on to that hope until I get my second dose on March 15!

Wednesday, February 17, 2021:  I had weird dreams overnight but I got up about 4:00 am.  I did some work and fell back asleep until 10:15.

We didn’t go to water exercise. I decided at the very last minute, walking out the door. Reaction to Monday shot?  I had a little headache, dizzy, congested, very tired.  I should have taken more cortisone at this time but didn’t remember until 8:30 pm.

I slept more until about 2 pm and had very weird dreams – I don’t know if the dreams are part of it or not but I reported them to the safe.cdc.gov questionnaire.

I cancelled piano lessons for the day.  I wrote to my students:

I am so sorry but I need to cancel today’s lesson.  I had the first COVID vaccination on Monday afternoon.  I was feeling fine yesterday so I assumed that I wasn’t going to have any side effects but they caught up with me today.  It’s just a headache , a bit of congestion and fatigue (I’ve been sleeping all day so far) but I don’t think I would be at my best during XXX’s lesson.

See you next week…

After cancelling lessons, I went back to sleep until time for Pender’s 7 pm Ash Wednesday service.  I was felling cold but I don’t know if it was chills or really a cold.  I started coughing a little.

At night, I remembered I should have up-dosed. I told my DH that night if he ever noticed me like this again, it was the perfect time to tell me to stress dose.  It never occurred to me during the day.

At that point, I realized I hadn’t eaten all day.  I had dinner (I was surprised that I could eat it) at 9:25 and did my growth hormone injection.

I went to bed at 11 p.

Thursday, February 18, 2021: I’m a little more tired than usual but ok.  I spent time napping and working alternated through the day.

Friday, February 19, 2021: Just the normal tiredness.  Hooray!


Info below from https://medshadow.org/covid19-vaccine-side-effects/  I’ve had the bold ones so far after the first injection.

Moderna

Moderna started Phase III clinical trials for its vaccine candidate in July. In earlier trials, nearly half of patients experienced common adverse effects like injection site pain, rash, headaches, muscle soreness, nausea and fevers after the second injection. These effects generally subsided within two days. CNBC spoke to a few individuals, some participating in Moderna’s trial and some in Pfizer’s trial who said much the same thing: the side effects were intense and included a high fever, body aches, bad headaches and exhaustion, but were worth it for protection from Covid-19.

In the FDA report published in December, the most common side effects were pain at injection site (91.6% of patients), fatigue (68.5%), headache (63.0%), muscle pain (59.6%), joint pain (44.8%), and chills (43.4%). Three patients experienced Bell’s Palsy, a sudden, and usually temporary, weakening or paralysis of the facial muscles.

A few patients with facial fillers experienced swelling after receiving the vaccine. They were treated with antihistamines and steroids. In California, officials halted the use of one particular batch of Moderna vaccines (lot 41L20A) after a small cluster (fewer than 10) of patients at one particular site experienced allergic reactions that required medical attention.

Out of the first 7.5 million doses administered from Dec 14- Jan 18, 19 cases of anaphylaxis were reported to VAERS after the Moderna vaccine. No patients have died from anaphylaxis. Patients are now being monitored for 15-30 minutes after receiving the vaccine to watch for signs of anaphylaxis.

Many patients are reporting injection site reactions that show up shortly after the injection or up to a week later. These reactions — which are characterized by swelling, redness, itching, rashes, heat and pain — are expected to last a day to a week. Physicians emphasize that while these effects can be scary, they are not dangerous and should not prevent someone from getting the second shot. So far, doctors do not report seeing these reactions after the second shot, however so few have been given so far that scientists are not sure how common it will be on round two.

The CDC reports that 11% of patients experienced swollen lymph nodes after the first shot. That raised to 16% after the second shot.

A study posted on Feb 1 showed that patients who received the vaccine after having been previously infected with COVID-19 showed greater immune response to the first shot and more intense side effects that are associated with strong immune responses like fever and muscle aches. The study included patients who received either the Moderna or Pfizer vaccine. Some scientists believe these patients may only need a single shot to provide sufficient immunity, but more research is needed.

Moderna has announced that it will begin testing its vaccine in children and adolescents, who they believe may have stronger immune responses, leading to more intense side effects.

This page has information about the other brands of vaccine: https://fairfaxcountyemergency.wpcomstaging.com/2021/02/16/what-you-need-to-know-when-you-get-vaccinated-and-after-you-get-vaccinated/

📞 Webinar: Growth Hormone Deficiency, PCOS or Cushing’s: How do You Tell Them Apart?

Dr. Theodore Friedman (The Wiz) will host a webinar on Growth Hormone Deficiency, PCOS or Cushing’s: How do You Tell Them Apart?

Dr. Friedman will discuss topics including:

  • Signs and Symptoms of Cushing’s Syndrome
  • Testing for Cushing’s
  • Signs and Symptoms of Growth Hormone Deficiency
  • Testing for Growth Hormone Deficiency
  • Signs and Symptoms of PCOS
  • Testing for PCOS
  • How do you tell them apart?

Sunday • August 2 • 6 PM PDT
Click here on start your meeting or
https://axisconciergemeetings.webex.com/axisconciergemeetings/j.php?MTID=m4eda0c468071bd2daf33e6189aca3489
OR
Join by phone: (855) 797-9485

Meeting Number (Access Code): 133 727 0164 Your phone/computer will be muted on entry.
Slides will be available on the day of the talk here
There will be plenty of time for questions using the chat button. Meeting Password: pcos
For more information, email us at mail@goodhormonehealth.com

🦓 Day 25, Cushing’s Awareness Challenge 2020

bestday

I wrote parts of this in 2008, so all the “yesterdays” and “last weeks” are a little off. 

Wow.  That’s about all I can say.  Yesterday was possibly the best day of my life since I started getting Cushing’s symptoms, and that was over 25 years ago.  A quarter of a century of feeling exhausted, fatigued.  A quarter of my life spent taking naps and sleeping.

Last week  in this post I wrote in part:

I went to the endo yesterday.  Nothing has changed for me.  Nothing will.  He wants me to take more cortef.  I don’t want to gain weight again.  He looked up Provigil and it’s not indicated for panhypopituitarism.  So he won’t prescribe it.  My kidney surgeon probably won’t let me take, anyway, but it was worth a try.

He did mention that in “only” 2.5 years maybe I can go back on growth hormone.  I don’t want to live like this another year let alone 2.5.  But then, when I was on GH before it didn’t help me like it helps most everyone else.

I’m tired of catering to a kidney that may or may not fail sometime anyway, tired of being so exhausted all the time.  I feel like I’ve lost nearly half my life to this Cushing’s stuff already.

So, yesterday I was supposed to go to a conference on web design for churches.  My church sent me because they want me to spiff up their site and make them a new one for Christmas.  I wanted to go because, well, I like learning new stuff about the web.  I figured that I would learn stuff that would also be useful to me in others of my sites.

And I did!

But the amazing thing is this.  My son had told me  about a medication that was very similar to Provigil, that he had tried it while he was writing his doctoral thesis and it had helped him.

So, having tried the official doctor route and being rebuffed – again – I had decided to try this stuff on my own.

Just the night before I had written a response on Robin’s wonderful blog that reads in part:

I hate this disease, too.

I was just talking to a friend today about how I’d try nearly anything – even if it ruined my one remaining kidney – to have a few days where I felt good, normal, where I could wake up in the morning rested and be able to have energy for the day.

I want to go out and have fun, to be able to drive for more than 45 minutes without needing to rest, to be have people over for dinner, whatever. I hate being restricted by my lack of energy.

My endo says to cheer up. In two and a half years I can try the growth hormone again. Whoopee. Didn’t work the first time and maybe gave me, or contributed to, cancer growth. Why would I want to look forward to trying that again?

I want to feel good now. Today.

I hate that this disease kills but I also hate that it’s robbed me of half my life already.

I wish doctors would understand that even though we’ve “survived”, there’s no quality of life there.

I hate Cushing’s. It robs so much from so many of us. 🙁

As I said earlier, I have a history of daily naps of at least 3 hours a day.  It cuts into everything and prevents me from doing many things.  I have to schedule my life around these naps and it’s awful.

rockford-2006-sue 12-18-2006 2-09-18 pmA few years ago I went on a Cushie trip to Rockford.  I’ve been there a few times and it’s always so much fun.  But this first year, we were going to another Cushie’s home for barbecue.  I didn’t drive, I rested in the back of the car during the drive.  We got there and I managed to stay awake for a little while.  Them I put my head down on the dining room table and fell asleep. Our hostess kindly suggested that I move over to the sofa.

So, I have a long history of daily naps, not getting through the day, yadda, yadda.

So, I was a little nervous about yesterday.  I really wanted to go to this conference, and was afraid I’d have to go nap in my car.

I got up at 5:30 am yesterday.  Before I left at 7:15, I took my Cortef and then I took my non-FDA approved simulated Provigil.  (Although it’s not FDA approved, it is not illegal to possess without a prescription and can be imported privately by citizens)

I stayed awake for the whole conference, went to a bell rehearsal, did Stacey’s interview, had dinner and went to bed about 10:30PM.  NO NAP!  I did close my eyes a little during the 4:00PM session but it was also b-o-r-i-n-g.

I stayed awake, I enjoyed myself, I learned stuff, I participated in conversations (completely unlike shy me!).

I felt like I think normal people feel.  I was amazed.  Half my life wasted and I finally (thank you Michael!) had a good day.

My kidney doctor and my endo would probably be appalled but it’s about time that I had some life again!  Maybe in another 25 years, I’ll take another pill.  LOL


Well, the energy from the Adrafinil was a one day thing.  I felt great on Thursday.   Friday and Saturday I slept more than usual.  Saturday, today, was one of those days where I sleep nearly all day.  Maybe if I took the drug more it would build up in my system, maybe not.  But it was still worth having that one day where I felt what I imagine normal to be.

While I was being a slug today, my husband painted the entire house.

I’m not sure if I would have been this tired today or if I was somehow making up for the nap I didn’t get on Thursday.  Whatever the case, I’m glad that I had the opportunity to try this and to experience the wonderful effects, if only for one day.

Information from a site that sells this:

Alertness Without Stimulation

Adrafinil is the prototype of a new class of smart drug – the eugeroics (ie, “good arousal”) designed to promote vigilance and alertness. Developed by the French pharmaceutical company Lafon Laboratories, adrafinil (brand name, Olmifon) has been approved in many European countries for treating narcolepsy, a condition characterized by excessive daytime sleepiness and other unusual symptoms.

Non-narcoleptic users generally find that adrafinil gives them increased energy and reduces fatigue, while improving cognitive function, mental focus, concentration, and memory. It has been reported that quiet people who take adrafinil become more talkative, reserved people become more open, and passive people become more active.

Of course, many stimulant drugs, ranging from caffeine to methamphetamine, are known to produce similar alerting/energizing effects. Adrafinil has been described by some users as a “kinder, gentler” stimulant, because it provides these benefits but usually with much less of the anxiety, agitation, insomnia, associated with conventional stimulants.

Adrafinil’s effects are more subtle than those of the stimulants you may be used to, building over a period of days to months. They appear to be based on its ability to selectively stimulate 1-adrenergic receptors in the brain.2 These receptors normally respond to norepinephrine (noradrenaline), a neurotransmitter linked to alertness, learning, and memory. This is in contrast to conventional stimulants, which stimulate a broader spectrum of brain receptors, including those involving dopamine. Its more focused activity profile may account for adrafinil’s relative lack of adverse side effects.

There’s more info about Adrafinil on Wikipedia

It’s interesting that that snipped report that people become more talkative.  I reported that in the original post, too, even though I didn’t realize that this was a possibility.

A good quote that I wish I could relate to better:

“Time is limited, so I better wake up every morning fresh and know that I have just one chance to live this particular day right, and to string my days together into a life of action and purpose.”

Lance Armstrong (1971 – )
Cyclist, seven-time Tour de France champion and cancer survivor


2011 stuff starts here:

Awhile ago I went to a handbell festival. I took a bit of adrafinil on the main day to try to stay awake for the whole day. It didn’t seem to keep me as on as it did before. I can’t be used to it already. Maybe I’m just that much more tired than I was before.

Our son lives in New York and every few years he gives us tickets to see a Broadway show.  A couple years ago we took the train to NY to see Wicked.  Usually my DH wants to go out and see sights while we’re there.  I usually want to nap.

This time we got up on Saturday morning, went out for breakfast.  I wanted to take in the whole day and enjoy Wicked so I took some Adrafinil.  We got back to the hotel and got ready to go to a museum or other point of interest.

But, DH wanted to rest a bit first.  Then our son closed his eyes for a bit…

So, I found myself the only one awake for the afternoon.  They both work up in time for the show…

Sigh  It was a great show, though.

A recent Christmas I was going to get my son some Adrafinil as a gift.  The original place we bought it didn’t have any more stock so I tracked it down as a surprise.  He was going to give me some, as well, but couldn’t get it from the original source, either.  So he found something very similar called Modafinil.  GMTA!


20-years-vaf

And this year…

Saturday, 4/23/16 really was one of the best days I’ve had in a long time.

I’ll be writing a longer post about that later on my travel blog but here’s the original plan: https://maryoblog.com/2016/04/23/busy-saturday/

Suffice it to say, we arrived at the Tattoo and I got no nap at all, all day!

IMG_0936

IMG_0940

🎤 Archived Interview: JenS discussed Bilateral Adrenalectomy (BLA)

 

Jen had Pituitary surgery by Dr. Shahinian 4/28/04, removed ACTH secreting corticotroph hyperplasia and prolactinoma.

She was diagnosed by Dr. Theodore Friedman as cyclical pituitary Cushings.

Her second Surgery 7/21/04 for infection resulted in neuralgia. She had a BLA in March 2006 as Corticol Hyperplasia returned and she now has possible Nelson’s syndrome. Jen also has Thyroid Issues (Hashimoto’s, multiple nodules and entire thyroid removed 2003) and she is Growth Hormone Deficient (3/2006)

Listen at http://www.blogtalkradio.com/cushingshelp/2008/02/29/jens-discusses-bilateral-adrenalectomy-bla

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🦓 Day 27: Cushing’s Awareness Challenge 2019

bestday

 

I wrote parts of this in 2008 and other years, so all the “yesterdays” and “last weeks” are a quite a bit off. This year’s update is at the very bottom.

Wow.  That’s about all I can say.  Yesterday was possibly the best day of my life since I started getting Cushing’s symptoms, and that was over 25 years ago.  A quarter of a century of feeling exhausted, fatigued.  A quarter of my life spent taking naps and sleeping.

Last week  in this post I wrote in part:

I went to the endo yesterday.  Nothing has changed for me.  Nothing will.  He wants me to take more cortef.  I don’t want to gain weight again.  He looked up Provigil and it’s not indicated for panhypopituitarism.  So he won’t prescribe it.  My kidney surgeon probably won’t let me take, anyway, but it was worth a try.

He did mention that in “only” 2.5 years maybe I can go back on growth hormone.  I don’t want to live like this another year let alone 2.5.  But then, when I was on GH before it didn’t help me like it helps most everyone else.

I’m tired of catering to a kidney that may or may not fail sometime anyway, tired of being so exhausted all the time.  I feel like I’ve lost nearly half my life to this Cushing’s stuff already.

So, yesterday I was supposed to go to a conference on web design for churches.  My church sent me because they want me to spiff up their site and make them a new one for Christmas.  I wanted to go because, well, I like learning new stuff about the web.  I figured that I would learn stuff that would also be useful to me in others of my sites.

And I did!

But the amazing thing is this.  My son had told me about a medication that was very similar to Provigil, that he had tried it while he was writing his doctoral thesis and it had helped him.

So, having tried the official doctor route and being rebuffed – again – I had decided to try this stuff on my own.

Just the night before I had written a response on Robin’s wonderful blog that reads in part:

I hate this disease, too.

I was just talking to a friend today about how I’d try nearly anything – even if it ruined my one remaining kidney – to have a few days where I felt good, normal, where I could wake up in the morning rested and be able to have energy for the day.

I want to go out and have fun, to be able to drive for more than 45 minutes without needing to rest, to be have people over for dinner, whatever. I hate being restricted by my lack of energy.

My endo says to cheer up. In two and a half years I can try the growth hormone again. Whoopee. Didn’t work the first time and maybe gave me, or contributed to, cancer growth. Why would I want to look forward to trying that again?

I want to feel good now. Today.

I hate that this disease kills but I also hate that it’s robbed me of half my life already.

I wish doctors would understand that even though we’ve “survived”, there’s no quality of life there.

I hate Cushing’s. It robs so much from so many of us. 🙁

As I said earlier, I have a history of daily naps of at least 3 hours a day.  It cuts into everything and prevents me from doing many things.  I have to schedule my life around these naps and it’s awful.

rockford-2006-sue 12-18-2006 2-09-18 pmA few years ago I went on a Cushie trip to Rockford.  I’ve been there a few times and it’s always so much fun.  But this first year, we were going to another Cushie’s home for a barbecue.  I didn’t drive, I rested in the back of the car during the drive.  We got there and I managed to stay awake for a little while.  Them I put my head down on the dining room table and fell asleep. Our hostess kindly suggested that I move over to the sofa.

So, I have a long history of daily naps, not getting through the day, yadda, yadda.

So, I was a little nervous about yesterday.  I really wanted to go to this conference and was afraid I’d have to go nap in my car.

I got up at 5:30 am yesterday.  Before I left at 7:15, I took my Cortef and then I took my non-FDA approved simulated Provigil.  (Although it’s not FDA approved, it is not illegal to possess without a prescription and can be imported privately by citizens)

I stayed awake for the whole conference, went to a bell rehearsal, did Stacey’s interview, had dinner and went to bed about 10:30PM.  NO NAP!  I did close my eyes a little during the 4:00PM session but it was also b-o-r-i-n-g.

I stayed awake, I enjoyed myself, I learned stuff, I participated in conversations (completely unlike shy me!).

I felt like I think normal people feel.  I was amazed.  Half my life wasted and I finally (thank you Michael!) had a good day.

My kidney doctor and my endo would probably be appalled but it’s about time that I had some life again!  Maybe in another 25 years, I’ll take another pill.  LOL


Well, the energy from the Adrafinil was a one-day thing.  I felt great on Thursday.   Friday and Saturday I slept more than usual.  Saturday, today, was one of those days where I sleep nearly all day.  Maybe if I took the drug more it would build up in my system, maybe not.  But it was still worth having that one day where I felt what I imagine normal to be.

While I was being a slug today, my husband painted the entire house.

I’m not sure if I would have been this tired today or if I was somehow making up for the nap I didn’t get on Thursday.  Whatever the case, I’m glad that I had the opportunity to try this and to experience the wonderful effects, if only for one day.

Information from a site that sells this:

Alertness Without Stimulation

Adrafinil is the prototype of a new class of smart drug – the eugeroics (ie, “good arousal”) designed to promote vigilance and alertness. Developed by the French pharmaceutical company Lafon Laboratories, adrafinil (brand name, Olmifon) has been approved in many European countries for treating narcolepsy, a condition characterized by excessive daytime sleepiness and other unusual symptoms.

Non-narcoleptic users generally find that adrafinil gives them increased energy and reduces fatigue, while improving cognitive function, mental focus, concentration, and memory. It has been reported that quiet people who take adrafinil become more talkative, reserved people become more open, and passive people become more active.

Of course, many stimulant drugs, ranging from caffeine to methamphetamine, are known to produce similar alerting/energizing effects. Adrafinil has been described by some users as a “kinder, gentler” stimulant, because it provides these benefits but usually with much less of the anxiety, agitation, insomnia, associated with conventional stimulants.

Adrafinil’s effects are more subtle than those of the stimulants you may be used to, building over a period of days to months. They appear to be based on its ability to selectively stimulate 1-adrenergic receptors in the brain.2 These receptors normally respond to norepinephrine (noradrenaline), a neurotransmitter linked to alertness, learning, and memory. This is in contrast to conventional stimulants, which stimulate a broader spectrum of brain receptors, including those involving dopamine. Its more focused activity profile may account for adrafinil’s relative lack of adverse side effects.

There’s more info about Adrafinil on Wikipedia

It’s interesting that that snipped report that people become more talkative.  I reported that in the original post, too, even though I didn’t realize that this was a possibility.

A good quote that I wish I could relate to better:

“Time is limited, so I better wake up every morning fresh and know that I have just one chance to live this particular day right, and to string my days together into a life of action and purpose.”

Lance Armstrong (1971 – )
Cyclist, seven-time Tour de France champion and cancer survivor


2011 stuff starts here:

A while ago I went to a handbell festival. I took a bit of adrafinil on the main day to try to stay awake for the whole day. It didn’t seem to keep me as on as it did before. I can’t be used to it already. Maybe I’m just that much more tired than I was before.

Our son lives in New York and every few years he gives us tickets to see a Broadway show.  A couple years ago we took the train to NY to see Wicked.  Usually, my DH wants to go out and see sights while we’re there.  I usually want to nap.

This time we got up on Saturday morning, went out for breakfast.  I wanted to take in the whole day and enjoy Wicked so I took some Adrafinil.  We got back to the hotel and got ready to go to a museum or other point of interest.

But, DH wanted to rest a bit first.  Then our son closed his eyes for a bit…

So, I found myself the only one awake for the afternoon.  They both work up in time for the show…

Sigh  It was a great show, though.

A recent Christmas I was going to get my son some Adrafinil as a gift.  The original place we bought it didn’t have any more stock so I tracked it down as a surprise.  He was going to give me some, as well, but couldn’t get it from the original source, either.  So he found something very similar called Modafinil.  GMTA!


20-years-vaf

And 2016…

Saturday, 4/23/16 really was one of the best days I’ve had in a long time.

I’ll be writing a longer post about that later on my travel blog but here’s the original plan: https://maryoblog.com/2016/04/23/busy-saturday/

Suffice it to say, we arrived at the Tattoo and I got no nap at all, all day!

IMG_0936

IMG_0940

 

And 2017.

We just came home from a great weekend in New York City with our son.  I haven’t written about it yet in my Travel Blog but will soon.  I did put a bit about it in my Little Free Library blog (do I have too many blogs??)  I was amazed to make it through the entire weekend with no Adrafinil – sadly, there’s nowhere to get it anymore.  I carried extra cortisol, just in case.  And slept all the way home on the train.

2018.

We went back to the Virginia International Tattoo again and it was everything I remembered from 2016.  A wonderful, but very exhausting time!

This time around we went to some of the band competition, then went back to the hotel for a nap before the show.  Fortunately, most of the afternoon events were live-streamed on Facebook so I didn’t miss much.

All of the 2018 Tattoo is on YouTube already.

A couple of my favorite acts:

and

 

And the Finale:

 

When they showed the videos of the Medal of Honor recipients, I thought it was amazing.  There is no way I could do any part of what they had done.

Just before leaving, I bought a teeshirt which said More Bagpipes.

When we got home this afternoon, it was a 4-hour nap.

 

 

 

Last but not least, 2019 – my best day was Tuesday, April 23.  I just got a cortisol shot in my knee and I’m starting to feel hopeful for the future…

 

🎤 Archived Interview: Karen Nolan, Cyclic Cushing’s, part 2

 

Karen (Rooon55), part 2, March 20, 2008. Karen’s disease started when she was a little girl (7) and she finally got a diagnosis in 2005. She had cycling Cushing’s, Thyroid disease, GH deficiency, and Autoimmune Alopecia. She believes she is cured after two Pituitary surgeries. A doctor didn’t advise Vermont’s Karen Nolan (Rooon on the boards) that she might be one of the scant 3.5 per million people diagnosed annually with Cushing’s disease – another Cushing’s patient did.

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