Trudy Scott Anxiety Nutrition Solutions & Every Woman Over 29

Hydroxychloroquine and chloroquine (antimalarial drugs): quinism and the risk of sudden and lasting neuropsychiatric effects

July 31, 2020 By Trudy Scott 66 Comments

The Quinism Foundation, a nonprofit charitable organization “promotes and supports education and research on quinism, the family of medical disorders caused by poisoning by mefloquine, tafenoquine, chloroquine, and related quinoline drugs.”

Executive Director of the foundation, Dr. Remington Nevin, MD, MPH, DrPH, is a Johns-Hopkins trained psychiatric epidemiologist and drug safety expert and former U.S. Army public health physician. He has published extensively on the subject.

The foundation share the symptoms of chronic quinoline encephalopathy, also known as neuropsychiatric quinism:

The term “quinism” may seem new, but the symptoms of poisoning by mefloquine (previously marketed as Lariam®), tafenoquine (marketed as Krintafel® and Arakoda™), chloroquine (marketed as Aralen®), and related quinoline drugs are all too familiar: Tinnitus. Dizziness. Vertigo. Paresthesias. Visual disturbances. Gastroesophageal and intestinal problems. Nightmares. Insomnia. Sleep apnea. Anxiety. Agoraphobia. Paranoia. Cognitive dysfunction. Depression. Personality change. Suicidal thoughts.

These symptoms are not “side effects,” they are symptoms of poisoning by a class of drug that is neurotoxic and that injures the brain and brainstem. This poisoning causes a disease, and this disease has a name: Chronic quinoline encephalopathy — also known as quinism.

In March they published this press release: The Quinism Foundation Warns of Dangers from Use of Antimalarial Quinolines Against COVID‑19. Here are some highlights:

A risk of sudden and lasting neuropsychiatric effects from the use of antimalarial quinolines against COVID‑19, the disease caused by the novel coronavirus
In susceptible individuals, these drugs act as idiosyncratic neurotoxicants, potentially causing irreversible brain and brainstem dysfunction, even when used at relatively low doses

What is concerning is lasting neuropsychiatric effects and the fact that even low doses can cause irreversible effects. The Foundation “has urged policy makers, physicians, and members of the public to be alert to such effects.”

Dr. Nevin states that “these are not safe drugs” and “While it may be tempting to attribute anxiety, depression, paranoia, or other mental health symptoms to the psychological effects of the COVID‑19 pandemic, these symptoms may be an early warning sign of idiosyncratic neurotoxicity, and must be taken seriously.”

You can read the entire March 2020 press release here. It contains a link to U.S. Food and Drug Administration’s MedWatch program for reporting adverse effects.

Another press release published late July also cautions the use of tafenoquine against COVID-19 which The Qunism Foundation states “is a neurotoxic quinoline antimalarial drug with a similar adverse effect profile to mefloquine.”

New COVID-19 research on chloroquine and hydroxychloroquine

It’s encouraging to see that new research published on COVID-19 and these medications also highlights the possibility of neuropsychiatric side effects (even through the authors state it’s considered uncommon): Psychiatric Aspects of Chloroquine and Hydroxychloroquine Treatment in the Wake of COVID-19: Psychopharmacological Interactions and Neuropsychiatric Sequelae

…neuropsychiatric side effects are very uncommon but possible, and include a potentially prolonged phenomenon of “psychosis following chloroquine.” Hydroxychloroquine has less information available about its neuropsychiatric side effects than chloroquine, with psychosis literature limited to several case reports

Case reports on psychiatric symptoms induced by hydroxychloroquine

Here is one of these case reports: Psychiatric symptoms induced by hydroxychloroquine. A 36-year-old woman was diagnosed with Systemic Lupus Erythematosus (SLE) and antiphospholipid syndrome, and was treated with prednisone 10 mg and hydroxychloroquine 200 mg every 24 hours. Her arthritis improved but

One month after initiation of treatment, the patient began with generalized anxiety, suicidal ideation and the appearance of auditory and kinaesthetic [tactile] hallucinations.

She had similar adverse effects 5 years later when hydroxychloroquine (without prednisone) was prescribed following an outbreak of cutaneous SLE

A week later, the patient was admitted to the Department of Psychiatry because of suicidal ideation, self-harm and kinaesthetic and auditory hallucinations, which improved after withdrawal of hydroxychloroquine and treatment in a psychiatric setting.

Since then, the patient has not been taking hydroxychloroquine and has had no further episodes of kinaesthetic [tactile] or auditory hallucinations.

Here are two other case reports: Hydroxychloroquine-induced acute psychosis in a systemic lupus erythematosus female and Hydroxychloraquine-induced acute psychotic disorder in a female patient with rheumatoid arthritis: a case report.

Risk factors for susceptibility

This review article from 2018, Neuropsychiatric clinical manifestations in elderly patients treated with hydroxychloroquine: A review article mentions that these adverse events can range from less severe nervousness to “actual psychosis and suicidal tendencies.”

It also lists possible risk factors that may make certain individuals more susceptible:

co-exposure to interacting drugs, alcohol intake, familial history of psychiatric diseases, female gender, and the concomitant use of low-dose glucocorticoids [such as prednisone].

Malaria drug causes brain damage that mimics PTSD

I first learned of this neuropsychiatric connection a number of years ago when I read about the “case of a service member diagnosed with post-traumatic stress disorder but found instead to have brain damage caused by a malaria drug.” You can read about this here – Malaria drug causes brain damage that mimics PTSD: case study.

My concerns about long-term prophylactic use and lack of awareness

My concerns are long-term prophylactic use. There are a number of clinical trials planned or in progress for long-term use in healthcare workers. If they are stressed, anxious, depressed and exhausted because of the COVID-19 work they have been doing, they may incorrectly attribute some of their symptoms to all that rather than the medication side-effects. And if they do get COVID-19, they may confuse the neurological and psychiatric effects of COVID-19 with those of chloroquine or hydroxychloroquine.

What also concerns me is the lack of awareness. None of the advocates of this class of medications mentions quinism, the possible neuropsychiatric side-effects and long-term risks, or who may be susceptible.

I would be very happy if chloroquine or hydroxychloroquine is found to be a solution (or part of a solution) for COVID-19 – alone or in combination with zinc – for certain individuals.

But I believe we do need to be very aware about side-effects as serious as these. I’d also like to see education for healthcare providers and the consumer, as well as informed consent for the consumer.

Similar concerns with other medications

In the past I’ve written about similar concerns with other medications such as benzodiazepines, SSRIs and fluoroquinolone antibiotics:

Your feedback and questions so we can all learn

I encourage you to keep all this in mind as you navigate what you hear in the news, read on social media and/or read in the research on hydroxychloroquine.

Keep all this in mind too if you have future plans to travel to a malaria area for a vacation in the future (wouldn’t we love that – a trip!?).

Have you used chloroquine or hydroxychloroquine for COVID-19 and experienced psychiatric side-effects? Or know someone who has?

Have you used antimalarial medications in the past and experienced psychiatric side-effects? Was this a short-course or long-term prophylactic use?

Have you used these medications for lupus or rheumatoid arthritis with success and without psychiatric side-effects? Or have you experienced adverse effects and had to stop?

If you have had adverse psychiatric effects please share which medication, dosage and frequency? Also do you have any of the predisposing risk factors: alcohol intake at the time, history of psychiatric diseases (you or family members), are female, and were also prescribed low-dose glucocorticoids such as prednisone, and/or other medications (and which ones)?

Feel free to post your questions here too.

I am an emotional eater and eat sugar as a reward and find myself craving it when I am fatigued. Do you have clients on more than one amino acid?!

July 24, 2020 By Trudy Scott 18 Comments

This is a question I received from a stressed out mom in my community. She has identified when she craves sugar and the emotion connected to her cravings. Now she has questions about how to trial and use amino acids to stop her cravings, get her energy back and feel emotionally stable:

I know I am an emotional eater, I know I eat sugar as a reward and I do find myself craving it when I am fatigued. I also seem to crave it after a very savory meal; especially one with garlic. What is THAT about?! Do you have clients on more than one amino acid?!

I have been a caregiver for my son (multiple disabilities) for 30 years; he has uncontrolled seizures and my husband has PTSD. It is a stressful household.

This is what I shared with her about the brain chemical imbalances and amino acids:

Many of my clients need more than one amino acid but it’s best to trial one at a time. When I hear my client say they eat sugar as a reward we immediately consider a trial of DPA (d-phenylalanine) especially if they are also overly emotional/weepy and also have physical pain.
When I hear my client say “I do find myself craving sugar when I am fatigued” we consider low catecholamines and a trial of tyrosine especially if they also have poor focus, low motivation and a flat mood. If the fatigue is caused by low blood sugar this can cause fatigue, irritability/crankiness and anxiety and a trial of glutamine may be a better option. If the DPA helps the emotional-reward-eating after a week or two, then we may do a trial of tyrosine and/or glutamine (one at a time) and use them in addition to the DPA.
When I hear “sugar cravings after a savory meal” we consider low serotonin and a trial of tryptophan if it’s after lunch or dinner. Serotonin dips in the afternoon and evening triggering this type of craving. With low serotonin we also see worry, anxiety, depression, anger, PMS, insomnia and irritability. Let’s assume the DPA helps and the tyrosine helps with the fatigue, then we’d consider a trial of tryptophan and add that.

So yes I do have many clients needing more than one amino acid! But we always trial one at a time and find a good baseline before adding the next one or doing a new trial if the first one didn’t give expected results.

With regards to which amino acid trial to do first, I always ask my client which area is causing the most problem or distress in your life and we start there. Since she mentioned emotional eating and then fatigue and then cravings after a savory meal, this sequence may be best for her. But addressing the fatigue with tyrosine first may be a better approach for someone else.

With regards to cravings after a savory meal we also look into how much protein and healthy fats the client has in that meal. I don’t know why garlic would be a trigger other than it’s possibly stirring up candida. Candida is also a big factor when it comes to sugar cravings, fatigue and feeling sad/emotional so we would also possibly need to address this too.

Adrenal and sleep support is also key and I recommend this resource for additional caregiver support for her – The psychological trauma of coronavirus – nutritional support for doctors, nurses and their loved ones.

For her husband’s PTSD I recommend this resource – PTSD from 3 tours in Afghanistan: Can GABA help with the anxiety?

For her son’s seizures I recommend this paper, Ketogenic Diet and Epilepsy: What We Know So Far, and working with a practitioner who could offer consultation and guidance on a ketogenic diet. Another useful resource is this one – Use of Cannabidiol in the Treatment of Epilepsy: Efficacy and Security in Clinical Trials.

If you suspect low levels of any any of the neurotransmitters and are new to using the amino acids and do not have my book I highly recommend getting it and reading it before jumping in to taking supplements: The Antianxiety Food Solution – How the Foods You Eat Can Help You Calm Your Anxious Mind, Improve Your Mood, and End Cravings.

There is a complete chapter on the amino acids and one for pyroluria, plus information on real whole food, sugar and blood sugar, gluten, digestion and much more. If you’re not a reader there is now also an audible version.

Here is the Amino Acids Mood Questionnaire from The Antianxiety Food Solution and additional information on Anxiety and targeted individual amino acid supplements: a summary

Please also read and follow these Amino Acid Precautions.

This lists The Antianxiety Food Solution Amino Acid and Pyroluria Supplements that I use with my individual clients and those in my group programs. You’ll find DPA, tyrosine and tryptophan listed here.

Please share your emotional eating and sugar craving success story if you have one using DPA.

And let us know if tyrosine helps with your fatigue and low-energy driven sugar cravings?

And does tryptophan help your afternoon and evening sugar cravings?

Feel free to post your questions here too.

Tryptophan ends TMJ pain, headaches and worry, and improves mood and sleep: a success story

July 17, 2020 By Trudy Scott 20 Comments

Today I’m sharing a success story on how the amino acid tryptophan, taken as a supplement, ends TMJ (temporomandibular joint) pain and headaches in a woman in my community. She had the added benefits of an improved mood and less worrying and her sleep improved too.

There is evidence to support the low serotonin connection to TMJ and pain like fibromyalgia and I share that research below.

Before I share the success story, in case you’re new to neurotransmitter imbalances, the other symptoms we see with low serotonin are the worrying-type of anxiety, panic attacks and phobias, lack of confidence, depression, negativity, imposter syndrome, PMS, irritability, anger issues, insomnia and afternoon/evening cravings. Tryptophan can be used to boost serotonin levels and improve these symptoms as you’ll see below.

Right after speaking on the recent Trauma and Mind-Body Super Conference, Renee shared her wonderful success story on Facebook:

Out of all the interviews I felt yours gave the most actionable steps. I was taking amitriptyline for TMJ and didn’t like the side effects, however what other options did I have? Not many according to my GP [general practitioner]. Luckily I found your suggestion of tryptophan. And I can’t explain how much of a change it made! I weaned off the medicine and took tryptophan instead and not only did it help the TMJ but also helped me feel more even emotionally.

I am being referred for trauma therapy and I am optimistic that I will be discomfort free soon.

So huge thanks for sharing your knowledge. It helped me at a time when I was really starting to think there were no ‘natural’ options and conventional meds were all I could take.

I checked in with her, thanking her and acknowledging her wonderful feedback. I also asked how much tryptophan made this difference and how quickly she saw an improvement. And what side-effects she was seeing with the medication. She shared this:

I am a week into taking tryptophan, and I’m taking 500mg. I saw improvements with the TMJ within an hour of taking it. My jaw felt loose and I had no headaches, I also felt more ‘even’ mood wise. Like an underlying worry had gone. [worry is a classic symptom of low serotonin – more on that here]

I also had some stress yesterday that usually would have made me crumble, but instead I was able to stand up for myself and see subjectively the extent of the issue and resolve it. I am amazed!

My original medication (amitriptyline) had given me extreme dry mouth, which I found hard to manage, the headaches were also not relieved as much as I had hoped, plus I was having sessions of palpitations.

I haven’t had any palpitations from the day I started tryptophan whereas the dry mouth took some time to subside.

These really are wonderful results and typical that we’d see results this quickly with tryptophan if the root cause of the TMJ and headaches is low serotonin. It can sometimes take a few weeks to find the ideal dose but Renee found it with the initial trial amount of 500mg.

The tryptophan also improved her sleep (and the palpitations and dry mouth side-effects from the medication stopped):

I was struggling to get to sleep and stay asleep, suffering bouts of insomnia, prior to any medication. I still am sleeping well taking tryptophan which I am pleased about.

She did however share that the timing of the tryptophan was making her too sleepy too early in the evening and she was planning to shift the timing:

I am finding tryptophan is making me feel drowsy in the evening, so I am trying different times during the day to take it. Hopefully I can push back the tiredness to perhaps 8/9 at night to coincide with bedtime.

My advice to her was that I have my clients use tryptophan MA (mid-afternoon) and evening and if MA makes them too sleepy they just do an evening dose. That can be enough for TMJ the next day. Sometimes more than 1 x 500mg in the evening is needed for easing TMJ and headache pain that night and the next day too.

I did check with her about weaning off the medication as cold-turkey quitting of psychiatric medications are dangerous and not advised. She shared this:

I weaned off over 1 week, but I was only in it for 8 weeks in total before I found tryptophan.

A slow taper under the guidance of the prescribing doctor is always recommended (more on this for amitriptyline/Elavil withdrawal here).

Here is some research supporting this serotonin/TMJ connection:

Plasma tryptophan and kynurenine in females with temporomandibular disorders and fibromyalgia – An exploratory pilot study

…both temporomandibular disorders myalgia (TMDM) and fibromyalgia (FM) have been linked to central and peripheral changes in serotonin availability.” (tryptophan is not used in this study which also makes the serotonin/anxiety connection)

The effects of dietary tryptophan on chronic maxillofacial pain and experimental pain tolerance

Over the 4 weeks of the study, there was a greater reduction in reported clinical pain and a greater increase in pain tolerance threshold in the tryptophan group than in the placebo group. The tryptophan group was given “three grams of tryptophan in conjunction with a high carbohydrate, low fat, low protein diet.”

If you suspect low serotonin symptoms and are new to using the amino acids and do not have my book I highly recommend getting it and reading it before jumping in to taking supplements: The Antianxiety Food Solution – How the Foods You Eat Can Help You Calm Your Anxious Mind, Improve Your Mood, and End Cravings.

Here is the Amino Acids Mood Questionnaire from The Antianxiety Food Solution and additional information on Anxiety and targeted individual amino acid supplements: a summary

Please also read and follow these Amino Acid Precautions.

This lists The Antianxiety Food Solution Amino Acid and Pyroluria Supplements that I use with my individual clients and those in my group programs.

We appreciate Renee sharing her success story. Please share your TMJ/headache tryptophan success story if you have one. And feel free to post your questions here too.

Mercury & gadolinium toxicity, iron overload, COVID-19: NBMI research update and potential applications

July 10, 2020 By Trudy Scott 8 Comments

Professor Boyd Haley set out to find a safe and non-toxic heavy metal chelator that would cross the blood-brain barrier, get inside the cells and bind mercury. The compound was initially sold as an antioxidant called OSR and is now called NBMI. In 2018 I wrote a blog about this – Mercury detox: NBMI as a safe and non-toxic heavy metal chelator. At the time NBMI was in phase 2 clinical trials. The blog was a popular one then and still gets many comments and requests for updates. Today I’m sharing some updates on progress, new studies and proposed new applications. I still find NBMI intriguing and look forward to it being readily available once the studies are completed.

The recent newsletter from EmeraMed, reports that their projects are all running according to plan (despite coronavirus setbacks) and “producing the anticipated positive results necessary to bring our drug to market. When we complete the studies requested last year by the FDA, EmeraMed will file a new drug application (NDA), which then starts the FDA approval process.”

Studies on metal binding have shown that NBMI is strongly attracted to mercury, arsenic, lead, cadmium, uranium, gadolinium [used as a contrast agent in MRIs] and free iron and copper.

EmeraMed are expanding the clinical trials to look at other disorders that NBMI can potentially improve. These updates were shared in the newsletter:

The Colombian drug regulatory agency INVIMA approved a trial for mercury intoxication in May 2020:

…mercury intoxication and kidney disease are a serious life-threatening intractable condition and prominent in Colombia

…mercury from fish in the Santa Margareta river is one potential source for kidney injury leading to dialysis treatment. It will be a double-blind placebo controlled pivotal study, the participants health and results will be carefully monitored.

The treatment will be much longer than our earlier trials with gold miners and will look at numerous physiological parameters.

There are two pilot studies on iron overload in Europe:

Excess iron causes many devastating disorders, some lethal. Atypical Parkinson, an always fatal disease, is partially finished.

We expect to receive an interim report by July 2020 on a Thalassemia study that shows a highly significant benefit from NBMI. 8 out of 8 improved without any reported drug induce toxic side effects. “Impressive” in the words of one reviewer.

A potential use for COVID-19 based on NBMI increasing glutathione levels:

The mechanism of action is based on the ability of Emeramide to: 1; enter cells and cross the blood brain barrier, 2; scavenge and remove existing hydroxyl free radicals lowering oxidative stress and 3; chelate into non-reactive and non-toxic complexes several toxic metals and most importantly Fe2+ a redox metal that has been proposed to be displaced from hemoglobin by the COVID-19 infection.

We know NBMI would help because viruses need to release free iron to be able to reproduce. That iron causes oxidative stress possibly leading to a cytokine storm.

Another potential application is environmental clean-up of rivers, lakes and streams:

Arsenic (As) in drinking water is a well-recognized problem but since it is very difficult to remove, EPA maximum drinking water standard allows drinking water to have arsenic levels that cause significant amounts of bladder and lung cancers.

And one more potential application is the improved “treatment of waste-water sewer sludge to remove mercury or other toxic metals before it is spread on farms.”

Here is the mercury feasibility trial mentioned in the newsletter: Efficacy of N,N’bis-(2-mercaptoethyl) Isophthalamide on Mercury Intoxication: A Randomized Controlled Trial, where NBMI was given to 36 gold miners with high levels of mercury in their urine:

Although this study was designed with a small sample size to test for feasibility, the gained results with 300 mg NBMI already showed an effect on physical fatigue with statistical significance and there were indications to positive effects on other symptoms, like sleeping problems.

The newsletter link above has information about which countries are allowing early access. Please contact the company directly rather than ask me about how to obtain the product as I am simply sharing what they have shared with me. I also encourage you to sign up for EmeraMed’s newsletter so you can keep up to date with progress and access information.

I find it intriguing and look forward to it being readily available once the studies are completed.

Please share if you used the original OSR product with any success or if you have managed to obtain NBMI and trial it?

And feel free to post your questions for Professor Boyd Haley. I’m hoping to have him speak on Anxiety Summit 6: Toxins/Meds/Infections.

Anxiety and globus pharyngeus (lump in the throat): GABA to the rescue?

July 3, 2020 By Trudy Scott 31 Comments

Low levels of GABA, a calming neurotransmitter can lead to anxiety, fears and panic attacks. With low GABA, the anxiety is a physical kind of anxiety with muscle tension or muscle spasms. Today you’ll read how low GABA may be one possible root cause of globus pharyngeus, which you may have experienced as a rather scary golf-ball-like lump or constriction in the throat.

Let me describe globus pharyngeus and then I’ll share my story with globus pharyngeus, why low GABA may be a factor (and supplemental sublingual GABA to the rescue) and other possible root causes that should be considered.

This 2015 paper, Globus pharyngeus: an update for general practice, defines it as follows:

Globus pharyngeus or globus sensation is the painless sensation of a lump in the throat and may be described as a foreign body sensation, a tightening or choking feeling.

Globus means globe or sphere and it can actually feel like you have a golf-ball sized object in your throat.

You may have experienced it without even knowing the medical name. Only a few of my clients and those in my community have ever heard the term. I also only learned about the name many years after my episode.

What is very surprising is that, according to the above paper, up to 45% of the population have experienced it.

My story with globus pharyngeus

I’m one of the 45% and for me it was a terrifying experience. As you may know, I experienced anxiety, PMS, fears and panic attacks in my late 30s and early 40s (it’s why I do this work).

Fortunately I only had one episode. It truly felt like I had a golf-ball in my throat and was horrifying. I knew I needed to swallow so I could get rid of this obstruction but at the same time I was terrified to swallow in case it got stuck and choked and killed me.

I remember going to the mirror to try and see this golf-ball sized object in my throat. I was so surprised that I couldn’t see anything.

Looking back, I suspect the addition of GABA Calm to my protocol prevented further episodes. I was also using progesterone cream at the time and this promotes GABA production too.

I’ve had many clients report that looking back they also realized their episodes stopped once they addressed their low GABA levels.

I was also under a great deal of stress at the time: work stress (long hours and my adrenals were a mess) and physical stress (due to amalgam removal, gluten issues, perimenopausal changes and much more).

Globus pharyngeus and GABA

The fact that the throat or pharynx “is a muscular tube that runs from the back of your nose down into your neck” is one reason for considering a muscle spasm and low GABA as a root cause.

The amino acid GABA, when used sublingually, eases muscle spasms within 15 seconds to 2 minutes. Some examples where we see this:

If you’re in the midst of an episode it’s impossible to open a capsule of GABA into your mouth. Until a client knows how much they can tolerate we start with 100-125 mg and increased based on the trial. Taking the powder and dabbing it with a wet finger and putting the finger to the inside cheek a few times is the best way for quick relief.

A product that is GABA-only in a capsule such as Enzymatic Therapy GABA or ProThera 500mg GABA are my choices for in-the moment relief (more on these in my supplement store here).

Source Naturals GABA Calm is my most popular GABA product and is my choice for everyday use.

Of course, I recommend this approach to doing nothing. The authors state: “simple reassurance may be all that is required” or “Advise patients to resist the urge to dry swallow.” We can do better.

Once your GABA levels are sufficient, it’s less likely to happen unless you’re under a great deal of stress and/or there are psychological factors at play:

There is increased reporting of stressful life events prior to development of symptoms and research suggests that as many as 96% of patients with globus sensation report an exacerbation of symptoms during times of emotional intensity.

During times of added stress, folks may experience other “physical symptoms such as palpitations, poor sleep, and feelings of panic.”

Oxalate crystal disease, dietary oxalates and pain: the research & questions

June 26, 2020 By Trudy Scott 79 Comments

This blog post came out of my quest for finding a medical explanation/term for my own pain caused by dietary oxalates and a desire to gain a better understanding for my clients who experience similar pain. It’s been on my writing list for some time and I’ve been gathering articles and research but the current coronavirus pandemic and recommendations for high vitamin C intake had me concerned enough to blog about it and ask for feedback from my community.

This is the blog, Coronavirus and vitamin C for immune support: new pain or more severe pain due to oxalate issues?, where I pose the question about recent increased intake of vitamin C or the addition of large doses for immune support and increased pain: joint pain, eye pain, foot pain, vulvodyndia, bladder issues, insomnia, gut pain, kidney pain, changes in thyroid health/labs, bone pain etc? The feedback on this blog and on Facebook has been huge and confirms the connection. Thank you if you’ve already contributed to the discussion!

Today I’ll share an overview of oxalates, my pain issues with dietary oxalates, a deeper dive into the condition called oxalate crystal disease (with some of my insights and questions), and the autism and atherosclerosis research. It’s by no means a comprehensive blog on all things oxalates but rather a way to try and connect some dots and pose some questions for going deeper.

The next blog will address my vitamin C/oxalate/pain story and the research on vitamin C, oxalates and pain, together with questions.

Oxalates defined and food sources

Before we review oxalate crystal disease, let’s define calcium oxalates. Julie Matthews, my good friend and colleague and an oxalate expert shares this in her blog, Oxalates: Their Influence on Chronic Disease

Oxalates present in our body as sharp crystals or crystalline structures with jagged edges that cause pain, irritation, and distress. They can bind with certain minerals; particularly calcium and magnesium, as well as iron and copper

You’ll find many different lists of low, medium and high oxalate foods. When I started eating low oxalate I found Susan Owen’s site simple and very helpful. I then joined the Trying Low Oxalates Facebook group for support and feedback.

In summary, these are the common medium-oxalate and high-oxalate foods that many folks have problems with: nuts, nut-butters and nut-flour (something to watch when eating Paleo or GAPS), wheat, chocolate, kiwi fruit (very high – see the raphides image below), star fruit (also very high), beets, potatoes, legumes, berries, spinach and soy.

You can see why these needle shaped calcium oxalate crystals found in kiwi fruit could inflict pain. This is just one example – there are many different shapes of calcium oxalate crystals.

raphides purified from kiwifruit — Raphides purified from kiwifruit. Raphides, needle shaped calcium oxalate crystals, were collected from kiwifruit homogenate through heavy media separation using a dense CsCl solution. (A) The SEM image of purified raphides (x400). Shared from: Synergistic Defensive Function of Raphides and Protease through the Needle Effect via Creative Commons.

My oxalate story: severe foot pain and eye pain

I personally had severe dietary oxalate issues in 2012 which manifested as excruciating foot pain. It was a combination of hot-burning-coals-pain and shards-of-glass-pain. It was just after my book, The Antianxiety Solution (my Amazon link), came out. Due to my book tours and events, I would be on my feet all day presenting, often for 3 full consecutive days, so I figured that must be the reason. When I travelled, I took a blender and made smoothies with berries, ate plenty of healthy nuts as my snacks and took kale chips with me to make sure I was getting my greens. Kiwi fruit was a favorite of mine!

I was eating a high oxalate diet and had no idea until I heard Julie present at an Integrative Medicine for Mental Health Conference on dietary oxalates and autism. A light-bulb went off and then I worked with her to learn about oxalates and figure out if it was in fact because of oxalates and sure enough, as soon as I removed high and medium oxalate foods the pain resolved. Note: the advice is NOT to remove all high and medium oxalate foods at once because dumping can occur. I was fortunate that this didn’t happen with me, possibly because of the vitamin B6 I was already taking as part of the pyroluria protocol.

When I eat a low oxalate diet I do really well. However, more recently dietary oxalates have been causing me eye pain when I have a treat like eggplant or carob. It starts out as a kind of scratchy discomfort and mild pain and then gets worse and worse. I also have a goopy kind of discharge from the inner part of my eye and burning/redness crystal-like teariness on the outer parts of my eyes. I recently had one very severe incident where the eye pain in my left eye was agonizing for about 2 hours. I was beside myself and tried GABA, DPA and tryptophan for an attempt at pain relief – with no success. When I took 500mg of vitamin B6 the pain eased immediately.

The theory is that oxalates cause issues where you have a weakness. I injured my left eye walking into a low tree-branch while rock-climbing 15 years ago, so I suspect this is why my left eye is more severely affected.

Oxalate crystal disease

The condition “oxalate crystal disease” is the closest explanation I’ve found that explains the pain I’ve experienced and makes the most sense, other than the fact that all the studies mention kidney disease and yet I don’t have kidney disease and have never had kidney stones. I’ve also never had a problem with my estimated Glomerular Filtration Rate (eGFR). In case eGFR is new to you it measures how well your kidneys filter the wastes from your blood and is the best overall measure of kidney function/damage.

This paper, Update on oxalate crystal disease, summarizes it:

Oxalate arthropathy is a rare cause of arthritis characterized by deposition of calcium oxalate crystals within synovial fluid. This condition typically occurs in patients with underlying primary or secondary hyperoxaluria. Primary hyperoxaluria constitutes a group of genetic disorders resulting in endogenous overproduction of oxalate, whereas secondary hyperoxaluria results from gastrointestinal disorders associated with fat malabsorption and increased absorption of dietary oxalate. In both conditions, oxalate crystals can deposit in the kidney leading to renal failure. Since oxalate is primarily renally eliminated, it accumulates throughout the body in renal failure, a state termed oxalosis. Affected organs can include bones, joints, heart, eyes, and skin. Since patients can present with renal failure and oxalosis before the underlying diagnosis of hyperoxaluria has been made, it is important to consider hyperoxaluria in patients who present with unexplained soft tissue crystal deposition. The best treatment of oxalosis is prevention. If patients present with advanced disease, treatment of oxalate arthritis consists of symptom management and control of the underlying disease process.

Let me break this down because I’ve had to look up terminology and read and re-read papers in order to get a better understanding of things:

#1 Oxalate arthropathy is a rare cause of arthritis characterized by deposition of calcium oxalate crystals within synovial fluid.

Oxalate arthropathy is a disease of the joints caused by oxalates depositing in the synovial fluid of the joints. The paper states it is a rare cause of arthritis, but I suspect it is much more common given what we’re seeing clinically.

Also, because all the research connects oxalate crystal disease with kidney disease, it may be overlooked when there is no kidney disease (more on that below).

Synovial fluid is the fluid between the joints that acts as a lubricant and nutrient source.

#2 This condition typically occurs in patients with underlying primary or secondary hyperoxaluria.

Hyperoxaluria occurs when you have “too much oxalate in your urine.”

#3 Primary hyperoxaluria constitutes a group of genetic disorders resulting in endogenous overproduction of oxalate and… secondary hyperoxaluria results from gastrointestinal disorders associated with fat malabsorption and increased absorption of dietary oxalate.

Primary hyperoxaluria is genetic and results in endogenous or internal overproduction of oxalate, causing too much oxalate in the urine.

The secondary hyperoxaluria description mentions “gastrointestinal disorders associated with fat malabsorption and increased absorption of dietary oxalate.” There are a number of other factors which I’ll address in a future blog.

According to this paper and others, secondary hyperoxaluria also results in too much oxalate in the urine.

#4 In both conditions, oxalate crystals can deposit in the kidney leading to renal failure. Since oxalate is primarily renally eliminated, it accumulates throughout the body in renal failure, a state termed oxalosis.

Affected organs can include bones, joints, heart, eyes, and skin.

Mayo clinic states oxalosis occurs if your kidneys fail. “Because your body can no longer eliminate the extra oxalate, it starts accumulating — first in your blood, then in your eyes, bones, skin, muscles, blood vessels, heart and other organs.”

My comment is that in some instances, oxalates accumulate in various parts of the body without kidney failure. I share more about this aspect and what we see clinically below, plus an autism and atherosclerosis study.

This paper, Oxalate crystal deposition disease, also mentions the following: “osteopathy, acute and chronic arthropathy with chondrocalcinosis, synovial calcification, and miliary skin calcium oxalate deposits and vascular calcifications that affect mainly the hands and feet.” The paper is focused on primary hyperoxaluria (and does also discuss the kidney involvement) but I’m including it because of the conditions listed. You may have received one of these diagnoses and not linked it back to dietary oxalates and/or vitamin C intake possibly playing a role.

The authors do report “systemic life-threatening cardiovascular, neurologic, and hematologic manifestations”, saying they are rare.

Calcium oxalates: anxiety, sleep, headaches, fatigue and other symptoms

Calcium oxalate crystals can also be found in the thyroid, and ear, leading to hearing loss under some circumstances.

Julie Matthews, in her blog, Oxalates: Their Influence on Chronic Disease, also shares that

Clinical studies and anecdotal experience indicate that oxidative stress, mitochondrial disruption and damage, and nutrient depletions, trigger widely varied symptoms including fatigue and inflammatory cascades, joint pain or pain anywhere in the body. Chronic low energy is very common because of a reduction in ATP in the mitochondria. Oxalates could be a hidden source of headaches, urinary pain, genital irritation, joint, muscle, intestinal or eye pain.

Other common oxalate-caused symptoms may include mood conditions, anxiety, sleep problems, weakness, or burning feet. Indicators can be digestive, respiratory, or even bedwetting for children.

What the researchers are saying – always kidney disease

I’ve reached out to a number of researchers, practitioners and labs and they all state that oxalate crystal disease only happens with kidney disease/kidney stones. This is what one researcher shared with me: “Plasma oxalate concentrations only elevate enough to cause systemic disease when there is significant kidney disease (typically GFR <20-30). I have never seen a significantly elevated plasma oxalate without chronic kidney disease.”

Could this be the case because they are kidney specialists and therefore only seeing patients who already have kidney disease?

The good news is that a number of them are intrigued and interested in learning more.

Oxalate crystals in autism and atherosclerosis without kidney issues

However, based on my own experience and according to many in this community and other communities like the Trying Low Oxalates Facebook group, pain issues related to dietary oxalate intake may occur without kidney issues/kidney stones, and often does.

These papers offer some support for what I suspect we are seeing clinically – systemic oxalate deposits can occur deposits without kidney stones or renal failure:

A Potential Pathogenic Role of Oxalate in Autism

Children with ASD [autism spectrum disorder] demonstrated 3-fold greater plasma oxalate levels … and 2.5-fold greater urinary oxalate concentrations. Despite significant hyperoxaluria no evidence of kidney stone disease…was observed

Atherosclerotic Oxalosis in Coronary Arteries

calcium oxalate crystals were observed within atherosclerotic plaques in the coronary arteries. Similar deposits were seen in the thyroid gland and other organs but not in the kidneys. None of the patients had chronic renal failure…. We suggest the phrase “atherosclerotic oxalosis” to describe this finding.

These are the disconnects I’m seeing in the research and questions I have:

Oxalate crystal disease is reported to be rare and it only happens with kidney disease/kidney stones – could it be more common than reported? As Julie states: “New science and clinical experience reveal concerns about oxalates that far exceed traditional kidney stone pathology.”
Should we be calling it hyperoxaluria. “too much oxalate in your urine” if the kidney is not involved? Or do we need to expand the definition of hyperoxaluria to include too much oxalate in other tissues outside the kidney and urine?
Could oxalate crystal disease with no kidney disease be a new syndrome that has yet to be widely and clearly identified in the research?

I mean no disrespect to the study authors and researchers by sharing my insights and questions here and in the section above. I appreciate the work they do and the opportunity to learn from them.

Searching through the literature on this has been extremely challenging because studies always refer to the kidney. It may well be that there is a perfectly logical explanation for much of this and someone has already gone through the research and has answers to all my questions. I am very willing to be enlightened so please do share if you’ve come across a good explanation.

Either way, please share your insights based on what I’ve shared in this blog and in relation to your experiences with pain caused by dietary oxalates and/or pain caused by vitamin C intake. I will be sharing this blog and the comments with the researchers and practitioners who are open to all this.