Anyone with Ehlers Danlos and chronic pain flare ups find a solution?

@notmcas It's my understanding that thiamine resolves inflammation by lowering lactic acidosis.

I've also read that thiamine "modulates" nitric oxide (NO), meaning that thiamine deficiency can cause cardiovascular disease and thiamine deficiency also can cause increased brain endothelial nitric oxide synthase (brain inflammation). Nitric oxide is inflammatory; the right amount at the right place at the right time is helpful; too much for too long is dangerous. It is important to understand that thiamine deficiency derails the control of nitric oxide release. It makes sense that thiamine deficiency would do so because thiamine is required for the autonomic nervous system to function properly.
additional links:
Ray Peat audios about nitric oxide
Ray Peat's written work about nitric oxide
Thiamine and magnesium deficiencies: Keys to disease

@notmcas said in Anyone with Ehlers Danlos and chronic pain flare ups find a solution?:

I think a full estrogen test is definitely warranted in these cases. Unfortunately it's not an uncommon a story anymore, and even more unfortunate is that doctors seem pretty unwilling to order a test for even estradiol at least in the US. I think I want to order one for total e, estradiol, and progesterone. Another big thing is that progesterone can remove estrogen from the cell/tissues but like you noted it's possible to get a detox reaction from the freed estrogen especially with an impaired liver.

According to Ray Peat, all estrogen is carcinogenic; they vary a little in how strongly each is carcinogenic, but the fact that each can morph into another makes me think that simply focusing on things that lower estrogen in general is the important thing. PUFA (polyunsaturated fats) are all estrogenic so banishing it from the diet is very important. There's lots of toxic estrogenic pollution floating all around us. Lots of plastics (all?) are estrogenic. So purging the pantry and the bathroom of iffy items would be a really good idea.

The role of environmental estrogens and autoimmunity

Ray Peat on estrogen in his written work
Ray Peat on estrogen in his interviews

Liver function is very important
Ray Peat on liver function, audio shows
Ray Peat on liver function, written work

also this one may be of interest:
https://www.functionalps.com/blog/2012/07/05/menstrual-cycle/

frankincense

@notmcas based on what you’re describing and you mentioning that prednisone brings relief, have you considered that mold exposure could be contributing? Have you been tested for mycotoxins?

BartL

@mostlylurking have you ever tried to get off the supplements ? If metabolism starts working in theory you should be able to back of the supplements and getting the nutrients from food would you agree?

Btw, really appreciate you sharing your (healing) story. It gives hope. I'm in a similar bad spot. I'm working on my healing, I take high dose benfo, thiaminHCL seem to crash my bg hard. But it's a long road, my digestion is so poor, continuous bloating and get really dizzy and week from food

@BartL said in Anyone with Ehlers Danlos and chronic pain flare ups find a solution?:

have you ever tried to get off the supplements ? If metabolism starts working in theory you should be able to back of the supplements and getting the nutrients from food would you agree?

If you do not have a lifetime to toxins stored in your body that include things like mercury (like I do), and if your genetics are such that your body is oriented to work perfectly with minimal nutrients, I suppose that might be possible.

I have mercury toxicity from mercury amalgam fillings that were put in my teeth when I was a child. When I was in my early twenties they started crumbling out of my teeth. Each time one fell out, the dentist replaced it with a gold inlay. No safety protocol was ever used, not even a dental dam. So I have long term health problems. The mercury causes my body to have high oxidative stress/reactive oxygen species. I am able to live better with my supplements than I am without them. The mercury inside me is not going to just go away; it's there for the duration. Here's a list of sources for mercury exposure.

@BartL said in Anyone with Ehlers Danlos and chronic pain flare ups find a solution?:

Btw, really appreciate you sharing your (healing) story. It gives hope. I'm in a similar bad spot. I'm working on my healing, I take high dose benfo, thiaminHCL seem to crash my bg hard. But it's a long road, my digestion is so poor, continuous bloating and get really dizzy and week from food

Thanks.

About your blood glucose crashing hard from the thiamine hcl: I've sort of amalgamated Ray Peat's teaching with Dr. Derrick Lonsdale's teaching; it works for me but others may have trouble reconciling the two schools of thought in their minds.

Ray Peat taught that sugar is good because it counteracts the stress hormones. Dr. Lonsdale teaches that sugar is bad because lots of people get thiamine deficiency from consuming it. Ray Peat taught that if you don't consume carbohydrates/sugars that your body will make the glucose it requires by dissolving your muscles so your brain and organs will have the energy to function so you don't die. Dissolving your own muscles with cortisol is a really stressful way to provide glucose to survive. So I have chosen to take high dose thiamine hcl (it's literally changed my life) so that I can consume a healthy diet that includes soft, ripe, juicy fruit, OJ, milk, cheese, eggs, gelatin, some beef, etc. and also have enough thiamine (B1) to utilize the nutrients I get from my diet.

Thiamine does more than just being a co-factor for multiple steps in the Krebs cycle which converts glucose into energy. Thiamine is also used to counteract/resolve high stress. Thiamine resolves body/brain stress.

Interactions of oxidative stress with thiamine homeostasis promote neurodegeneration
"Abstract: Thiamine-dependent processes are diminished in brains of patients with several neurodegenerative diseases. The decline in thiamine-dependent enzymes can be readily linked to the symptoms and pathology of the disorders. Why the reductions in thiamine linked processes occur is an important experimental and clinical question. Oxidative stress (i.e. abnormal metabolism of free radicals) accompanies neurodegeneration and causes abnormalities in thiamine-dependent processes. The vulnerability of thiamine homeostasis to oxidative stress may explain deficits in thiamine homeostasis in numerous neurological disorders. The interactions of thiamine with oxidative processes may be part of a spiral of events that lead to neurodegeneration, because reductions in thiamine and thiamine-dependent processes promote neurodegeneration and cause oxidative stress. The reversal of the effects of thiamine deficiency by antioxidants, and amelioration of other forms of oxidative stress by thiamine, suggest that thiamine may act as a site-directed antioxidant. The data indicate that the interactions of thiamine-dependent processes with oxidative stress are critical in neurodegenerative processes."

also:

"Conclusions:
Regarding thiamine as a select antioxidant may be useful in terms of revealing the role of thiamine dependent processes in disease and other conditions that lead to altered neuronal function** (Fig. 5). Overwhelming evidence indicates that oxidative stress accompanies neurodegeneration. Several lines of evidence suggest that thiamine homeostasis may reflect the oxidative state of cells. The reduction in thiamine-dependent enzymes in multiple neurodegenerative disorders may indicate that the cells...."

also this article:
The impact of oxidative stress in thiamine deficiency: A multifactorial targeting issue

"Vitamin B1 (thiamine) deficiency is a disorder involving impairment of oxidative metabolism in which selective cerebral vulnerability is a major consequence. This is manifested in the form of Wernicke–Korsakoff syndrome (WKS), a serious and potentially life-threatening neuropsychiatric disorder (Carmichael and Stern, 1931) consisting of Wernicke’s encephalopathy (WE), the neurological component of the disorder characterized by acute thiamine deficiency (TD) in association with confusion, ophthalmoplegia, and ataxia but no permanent structural damage, and Korsakoff’s psychosis, a debilitating amnesic state due to chronic TD and accompanied by irreversible diencephalic lesions. Neuropathologically, the disorder is characterized by focal areas of the brain developing symmetrical hemorrhagic and ischemic-like lesions, occuring most frequently in diencephalic structures, in particular the thalamus and mammillary bodies (Fig. 1), extending caudally through the midbrain (inferior colliculus) and brainstem areas that include the vestibular nuclei and inferior olivary complex (Victor et al., 1989)."

"Pathophysiology of thiamine deficiency: The pathophysiological mechanisms involved in TD are complex. Four major enzyme systems utilize thiamine in the form of thiamine diphosphate (TDP) as a major cofactor, i.e. pyruvate dehydrogenase (EC 1.2.4.1) complex (PDHC), an organized enzyme assembly that connects glycolysis with the tricarboxylic acid (TCA) cycle, α-ketoglutarate dehydrogenase (EC 1.2.4.2) complex (KGDHC), a multicomponent enzyme complex associated with the TCA cycle, transketolase (EC 2.2.1.1) (TK), a key participant in...

Oxidative stress and excitotoxicity in TD: Considerable evidence for development of oxidative stress has been demonstrated in TD, including the presence of increased production of reactive oxygen species (ROS) (Langlais and Zhang, 1997), and increased expression of heme oxygenase (HO-1) and intercellular adhesion molecule-1 (ICAM-1) (Gibson and Zhang, 2002) as well as microglial activation (Todd and Butterworth, 1999), along with induction of the endothelial isoform of nitric oxide synthase (eNOS) (Hazell and Butterworth, 2009).

Oxidative stress and inflammatory processes: Neuroinflammation is now recognized as a key component of a variety of neurological diseases that include stroke, multiple sclerosis and Alzheimer’s disease (AD), along with other problems of the brain such as brain trauma. During the 1960s, alterations in glial cell morphology in TD including evidence of swelling and the appearance of phagocytic vacuoles (Collins, 1967, Robertson et al., 1968) were first reported. These findings are consistent with pathological changes that can be attributable...

Oxidative stress and mitochondrial dysfunction: Mitochondria have three main functions: generation of ATP, production of reactive oxygen species (ROS) and inhibition of apoptosis. FADH2 and NADH formed in glycolysis, fatty acid oxidation, and the citric acid cycle are used to reduce oxygen to water by a series of electron carriers located in the inner mitochondrial membrane. Mitochondria are a major source of ROS, and also a target, in which case structural damage and activation of signaling pathways can result. Loss of mitochondrial...

Apoptosis and oxidative stress in TD: Every day millions of cells die due to physiological and pathological causes. Oxidative stress is a major contributor to the demise of these cells, with a diverse protective system having evolved to enable adaptation to such oxidative environments and preventing the progression of the oxidative stress and further damage to cells (Limón-Pacheco and Gonsebatt, 2009). However when these protective mechanisms become compromised, e.g. under conditions of impaired mitochondrial function, such...

BBB dysfunction and oxidative stress in TD: The BBB consists of a complex of capillary endothelial cells, pericytes and astroglial perivascular macrophages that serve as a barrier to the entry of lipophobic substances into the brain, and thus performs an important function in regulating transport, both into and out of the brain (Provenzale et al., 2005; Bart et al., 2000). Numerous studies in the past indicate that breakdown of the BBB occurs in TD (Warnock and Burkhalter, 1968, Manz and Robertson, 1972, Watanabe, 1978, Harata and...

Role of oxidative stress on nucleic acid function: As indicated above, several studies have demonstrated evidence for oxidative stress in TD. ROS production under these conditions can target both proteins and nucleic acids, and in the case of the latter, has the capacity to cause changes in these nucleic acids, altering their structure and leading to fragmentation (Jena, 2012). Mitochondrial (mt)DNA is most affected, probably due to their greater proximity to these ROS (Wei et al., 1998). The lesions in nucleic acids can occur due to direct
Influence of oxidative stress on neural stem cells

Future treatment strategies for WKS may involve the use of stem/progenitor cells. Since oxidative stress is a major contributor to brain pathology in TD, understanding how these cells respond following exposure to ROS is an important consideration. Oxidative stress is suspected to be a major cause of cell death in neural stem cells (NSCs) implanted in the CNS. The injection of cells into the cerebral parenchyma can produce oxidative stress at the site of administration following penetration
Therapeutic strategies targeting oxidative stress in neurodegenerative disease

While TD provides a useful template for studying the pathophysiology of neurodegenerative diseases (Jhala and Hazell, 2011), the incidence of conditions like PD and AD continues to increase with life expectancy, especially in industrialized countries. Such neurodegenerative disease states carry a heavy burden for the patients affected and also the health care system. The neurodegeneration observed in these diseases can be caused by oxidative stress. During neurodegeneration, the main ROS...

Conclusions: Due to its influence on cerebral energy metabolism, TD has major consequences on a variety of cellular processes, particularly those that require a plentiful supply of glucose. Oxidative stress targets many of these processes and, once initiated, can therefore reduce the threshold for developing injury, resulting in earlier onset of functional impairment than would otherwise be expected in its absence. This multifactorial attack on many vital functions of the cell suggests that once initiated...."
-end paste-

All living matter require thiamine to live. Evidently, something is happening on the planet that is reducing the availability of thiamine. Researchers have noticed and are trying to sound the alarm.

@BartL said in Anyone with Ehlers Danlos and chronic pain flare ups find a solution?:

I take high dose benfo, thiaminHCL seem to crash my bg hard. But it's a long road, my digestion is so poor, continuous bloating and get really dizzy and week from food

I want to suggest that you spend some time over at Dr. Costantini's website. He was a neurologist in Italy who successfully treated thousands of Parkinson's Disease patients with thiamine hcl. He treated his patients mainly with injections of thiamine hcl, but he also used oral thiamine hcl. His Therapy page provides the information needed to convert the dose of 100mg thiamine by injection into what is needed if taking thiamine hcl by mouth. You see, thiamine hcl has a very poor absorption rate via the intestine so a massive amount needs to be taken orally compared to if taking it by injection.
links:
Who was Dr. Costantini
Therapy
Frequently Asked Questions
Patients' before and after videos
Dr. Costantini's research papers

Dr. Costantini said that people should not have any negative reactions to high dose thiamine hcl if the dose is calibrated correctly for them. The information provided on the Therapy page gave me the courage and understanding to increase my oral dose to 1 gram of thiamine hcl, taken 2Xday, with water only, 30 minutes away from consuming food.

The only time I had a negative reaction to taking high dose thiamine hcl was when I tried taking 2.5 grams of it in one day. That night, I experienced shooting electrical zapping pains in my thighs when I went to bed. That experience told me that I had overdone it so I resumed taking 1 gram of thiamine hcl, 2Xday, with the understanding that this indeed is my optimum dose.

notmcas

@frankincense I’m suspicious of mycotoxins for sure. But the tests aren’t very accessible, I have to argue with the doctors to insist they do them. They seem to not want to test anything.

notmcas

@mostlylurking Have you had any experiences with sublingual thiamine to avoid risk of digestive upset? I know it’s not fat soluble but maybe it could work in a ethanol solution or something?

@notmcas said in Anyone with Ehlers Danlos and chronic pain flare ups find a solution?:

Have you had any experiences with sublingual thiamine to avoid risk of digestive upset? I know it’s not fat soluble but maybe it could work in a ethanol solution or something?

I did try it. I was aware that it did get into my brain. It gets rave reviews from people who have tried it. Daphne Bryan's book is a good read and worth the money.

My problem with it is that I was having tremendous positive results via oral high dose thiamine hcl and I was having a hard time reconciling the dosage I should take of the sublingual versus my optimal dosage I had already worked out for thiamine hcl. By that time, I had gotten used to the taste so it didn't bother me anymore.

From memory:
2 grams of thiamine hcl, taken daily for 7 days equals to one 100mg of thiamine hcl taken by injection per week.
and
One 100mg tablet of sublingual thiamine mononitrate equals to one 100mg of thiamine hcl taken by injection.

I simply couldn't get it square in my mind that a single sublingual 100mg tablet per WEEK was going to do for me what 2 grams of thiamine hcl taken daily was doing for me. Thiamine doesn't stick around in the body very long because it is water soluble. Even the so called "fat soluble" thiamines are water soluble. So I don't understand it well enough and so I went back to taking the 2 grams of thiamine hcl daily. Thiamine hcl is considered a "safe" supplement and has been around for decades. Even Ray Peat considered it a "safe" supplement.

@Granbien said in Anyone with Ehlers Danlos and chronic pain flare ups find a solution?:

I have some sort of connective tissue disorder and am currently going very hard trying to fix my thyroid, promising results but to be seen what happens. But in my experience stock, mainly thick home made beef stock, has been the single best thing for me by far. Another and I was surprised by this recently is Vitamin E, I have been ingesting tons of it from food sources and been noticing huge effects instantly.

I think people in this thread may be having the same kinds of responses to changes in health. If you try to 'build yourself up' like with thyroid or something, you'll start doing better but then fall apart soon after. I'm currently going in extremely hard trying to max out basically every nutrient I can think of while eating thyroid and it seems like it may be working.

But does anyone here deal with extremely low amounts of energy and have any kind of solution? I can never really figure out what causes low energy and what helps me raise it occasionally.

I consume a LOT of gelatin too; I do think it is very helpful.

I managed to get my hypothyroidism corrected with the help of a good endo in 2015. But I still had many problems with my health. I got my thiamine function blocked summer of 2020 via Bactrim antibiotic and had started adding some thiamine that fall, but I developed hypothyroidism symptoms (low body temp, brain fog, zero energy). I got my thyroid panel run 2 months early because I thought I'd gotten a bad batch of NP Thyroid by Acella. The test results showed that my free 3 was was through the roof.

Evidently, my thyroid gland had awakened via the thiamine supplement and I no longer needed so much thyroid hormone supplement. My doctor lowered my dose of NP Thyroid from 180mgs down to 135mgs and explained to me that taking too much thyroid hormone causes hyperthyroidism, and hyperthyroidism causes a thiamine deficiency. So I began taking 135 mg of NP Thyroid and continued to increase my thiamine hcl dosage to 1 gram, 2Xday. I've been doing very well on this combination for 3 years. My connective tissue is good; my joints are good. My energy level is good. I'm 74.

Reconciling how much thyroid supplement you need to take with how much thiamine you need can be tricky because a deficit in either one of them can cause very similar symptoms. This is because lack of either T3 or thiamine will block oxidative metabolism. This reduction in my thyroid med dose happened December of 2020; I have continued to take (and need) 135mg of NP Thyroid and I have been taking 1 gram of thiamine hcl, 2Xday since February of 2021. This combination seems to be what I need. My doctor though, has been making noises that make me think he wants to lower my thyroid med again, because of my age. I may actually be able to lower it now with no problem because my body seems to be working so well with the addition of the high dose thiamine hcl. Maybe my thyroid is able to crank out more hormone on its own now because it's getting the thiamine it needs? Maybe.

@Granbien said in Anyone with Ehlers Danlos and chronic pain flare ups find a solution?:

Another and I was surprised by this recently is Vitamin E, I have been ingesting tons of it from food sources and been noticing huge effects instantly.

Have you banished polyunsaturated fats (PUFA) from your diet? According to Ray Peat, PUFA is very bad for the connective tissue. It is my understanding that the body can use vitamin E to saturate PUFA so it's not so toxic. So it may be that you have PUFA stored in your fat cells and when it gets into circulation as free fatty acids you get symptoms. Niacinamide can be very helpful by keeping free fatty acids low. I take 100mg 4Xday. It is water soluble so it only sticks around maybe 2 hours so it works better if you take smaller doses more frequently.

Ray Peat on polyunsaturated fats
Ray Peat on niacinamide
Ray Peat on vitamin E

edit: Please note that an article shows up on one of the linked lists about caffeine. I found that coffee and black tea are things that I cannot tolerate at all because both of these block thiamine function.

notmcas

I remember Ray saying something along the lines of vitamin e products not being as good anymore. I’m not sure where the one in progeste e is sourced from because that could be useful

@notmcas said in Anyone with Ehlers Danlos and chronic pain flare ups find a solution?:

I remember Ray saying something along the lines of vitamin e products not being as good anymore. I’m not sure where the one in progeste e is sourced from because that could be useful

This company's vitamin E products are good. I've used them to dissolve progesterone in and the E is high enough quality to dissolve the progesterone completely and it stays in suspension fine. I'm pretty sure that Ray Peat also singled out this company's vitamin E as being good. Of course now I can't find that quote. I'm not affiliated with the company.

If memory serves, I think that the problem about the vitamine E that Ray was talking about was that people were cutting corners when making his progesterone product to the point that what they were using was "almost" vitamin E and "almost" progesterone in order to make more money on the product they were supposed to be manufacturing. So Peat severed that relationship with whoever that business partner was. This was a long time ago. There's no problem with the current Progest-E.

skywxlker

I've long suspected EDS in myself after seeing some links between EDS and ME/CFS.

Some casual tests on myself show I am mild on the EDS scale. However I also have mild tissue deformities like a crooked rib, slight underbite, semi-flat feet, difficult to gain muscle, Osgood-Schlatter's in both knees growing up...

I suspect a glycine, vitamin A and K deficiencies along with any number of B vitamin deficiencies. Zinc, copper, manganese, possibly iron and cholesterol.

High estrogen, low androgens.

Idk if Weston A. Price ever talks about this specifically, but he emphasizes the importance of these nutrients coming from animal foods and organs.

And in my casual observations, it seems quite clear that deficiencies in these nutrients, create for a weak, feeble, dysgenic body as opposed to the strong archetypical high androgenized bodies.

Growing up I played sports and I was the runt of the pack while on the other hand I had some friends were absolute beasts. My body was flimsy, theirs were sturdy and built. Thick skinned as well. Never lifted weights but strong and powerful. And I noticed those friends ate beef and butter, home cooked meals. While the runts like myself ate processed foods and grains.

Personally I've getting success eating 5-6 eggs yolks, beef liver, cheese and supplementing with vitamin K, A, E, zinc picolinate, selenium, manganese, coq10, shilahit, raw honey and ghee.

cleaning up your environment, avoiding zeno-estrogens, soy, plastics, pesticides. living a more wild lifestyle, ie nature/hiking.

EDS people simply appear low T, low androgens. while the opposite are usually the strong among us... faster wound repairs, can take on more damage, not flexible, more gravitas in their physique.

LinDaiyu

This post lowkey been popping off

Ecstatic_Hamster

@mostlylurking said in Anyone with Ehlers Danlos and chronic pain flare ups find a solution?:

@Ecstatic_Hamster I was taking a higher dose of pregnenolone (around 200-225mg/day). However, my cholesterol spiked up and my normally sane endocrinologist threatened me with statins. So I cut my dose of pregnenolone in half and my cholesterol normalized within 6 months.

You may have to up it to a gram a day for this condition.
I can’t see why high cholesterol is a problem, frankly.

@Ecstatic_Hamster said in Anyone with Ehlers Danlos and chronic pain flare ups find a solution?:

You may have to up it to a gram a day for this condition.
I can’t see why high cholesterol is a problem, frankly.

Well, I didn't understand why my 250mg of pregnenolone would spike my cholesterol level either. But it made sense to me that it might be the cause of my higher cholesterol (total 236). I've never had that issue before and I take 135mg of prescription desiccated thyroid daily (NP Thyroid by Accella, great stuff). Increasing my thyroid prescription dose was clearly off the table as a solution.

My higher cholesterol really didn't bother me but it really got both of my doctors' attention and threats of statin drugs to lower it got my attention as statins are really dangerous. I had doubled my pregnenolone dose when I got so sick in 2020 from taking Bactrim antibiotic which blocked my thiamine function. My cholesterol was around 203-208 for a long time and the jump to 236 that got the doctors' attention happened in 2022. By then I had recovered my health (re. the thiamine functional blockage/deficiency). I didn't notice any negative symptoms when I lowered my pregnenolone dose back down. Maybe I simply didn't need the higher dose of it anymore.

The body converts cholesterol into pregnenolone as the first step on the way to other beneficial things like progesterone, etc. I reasoned that if my body felt that I had plenty of pregnenolone (from supplementation) that it wouldn't bother converting more cholesterol into pregnenolone. So I cut the dose of pregnenolone and my body resumed converting cholesterol into pregnenolone which normalized my cholesterol level.

Ray Peat on pregnenolone, written work
Ray Peat on pregnenolone, interviews

notmcas

@mostlylurking I'm surprised that they'd give you such trouble at a total of 236. Mine was 300 and my doctor wouldn't even consider thyroid despite my tsh being ~3 and I'm still young. I was able to game tests by upping selenium, vitamin A, and taurine pretty high but they still just call it a fluke and won't consider any kind of thyroid which I bet would lower it. My dad has the same issue of high cholesterol and temps around 95-96 and doc is constantly threatening statins and yelling at him, his tsh is about 3.8. Did you have to have an over range tsh to get thyroid? My temps are okay if I eat often but drop otherwise so I suspect low sustaining t4.

Ecstatic_Hamster

@mostlylurking i suppose it depends on your relationship with the health “professionals.” I wouldn’t have budged and that isn’t high at all. I know a physician who has dealt with Ehlers Danlos in his patients and he and I have talked for hours about it, and high dose pregnenolone is very helpful.

Also low dose naltrexone is something I would be all over:
https://www.ldnscience.org/research/low-dose-naltrexone-in-the-management-of-ehlers-danlos-syndrome-associated-pain

This is a case of a 35 year old female with history of Ehlers Danlos syndrome, small fiber neuropathy in her left lower extremity, and lumbar radiculopathy who presented to our pain clinic suffering from chronic widespread muscular and joint pain along with persistent neuropathic pain in the lower extremity. Her pain regimen included anticonvulsants, narcotics, and NSAIDS. Over time, her pain regimen as described was inadequately controlling her pain. She was weaned off her narcotics and started on the low dose naltrexone therapy (4.5mg per day). The patient had excellent response with reduction in her pain severity and increase in her daily functionality. At 12 months follow up, she continues to report excellent symptom control without any escalation in adjuvant medications and has resumed her occupation. The patient has tolerated the therapy without any adverse side effects.