psychiatric

Psychiatric Complications of Primary Hyperparathyroidism and Mild Hypercalcemia: anxiety, depression, anger, irritability, delusions and impaired cognition

July 7, 2023 By Trudy Scott 38 Comments

In samples of patients undergoing parathyroidectomy for primary hyperparathyroidism (PHPT), these disturbances have been identified at a rate of 43.1%–53.0% for anxiety, 33.0%–62.1% for depression, 22.0% for thoughts of death or suicide, 51.9% for anger and irritability, 5.0%–20.0% for hallucinations and delusions, and 37.3%–46.5% for impaired cognition.

In fact, it has been noted that there are more neuropsychiatric phenomena in PHPT than is often recognized and that these symptoms are easily missed, particularly in the elderly population.

This excerpt is from, Psychiatric Complications of Primary Hyperparathyroidism and Mild Hypercalcemia, published in Psychiatry Online.

I’ve recently been reading as much as I can about this condition, for personal and professional reasons. As soon as I learn about something new I go digging to see if there is an anxiety connection. And I must say I was very surprised to read these stats. It’s not something I’ve heard discussed or taught at mental health conferences.

The authors also state this about the condition:

The incidence of primary hyperparathyroidism (PHPT) is about 21 cases per 100,000 person-years, and the disorder is usually caused by a solitary parathyroid adenoma. PHPT has traditionally been recognized by its characteristic symptoms, including urolithiasis (“stones”); osteopenia and osteoporosis (“bones”); abdominal cramping, nausea, and peptic ulceration (“moans”); and depression, anxiety, cognitive dysfunction, insomnia, confusion, and personality changes (“psychiatric overtones”).

How do changes in serum calcium levels contribute to mental health and cognitive symptoms?

It’s always helpful to understand the mechanism and it was the first thought that went through my mind – how does hyperparathyroidism and changes in serum calcium levels cause these mental health and cognitive symptoms? The authors share this:

Although the pathogenesis [or cause] of psychiatric symptoms in primary hyperparathyroidism remains unclear, calcium is thought to figure prominently in determining changes in monoamine metabolism in the central nervous system(CNS), thereby modifying neurotransmission and resulting in alterations in mood and cognition.

I went digging and found this paper – Acute psychosis secondary to suspected hyperparathyroidism: A case report and literature review.

The authors also state that the mechanism isn’t known for certain. And although they are referring specifically to psychosis, the explanation could be applied to other symptoms too: “It is thought that the changes in serum calcium level slow down nerve function and neurotransmission rate, inducing psychosis (and other symptoms like anxiety, depression, anger, irritability and suicidal thoughts).

Understanding this possible mechanism helps us find a temporary solution for these symptoms until the hyperparathyroidism is addressed with surgery i.e. using amino acids as supplements.

Using amino acids to ease symptoms while you are seeking the root cause/s

If you’ve been following my work and have read my book The Antianxiety Food Solution, you’ll be familiar with using targeted amino acids as supplements to support low levels of neurotransmitters. These provide quick relief of symptoms (in a day or less) while you are seeking the root cause.

If we look at the above symptoms:

Anxiety can be a sign of low serotonin (worry type of anxiety) and/or low GABA (physical type of anxiety) – and tryptophan/5-HTP and/or GABA help ease symptoms.
Depression can be a sign of low serotonin (negativity), low dopamine (curl-up-in-bed depression) an/or low endorphins (weepy depression) – and tryptophan/5-HTP, tyrosine and/or DPA help ease symptoms.
Irritability and anger are common with low serotonin – and tryptophan/5-HTP helps to ease symptoms.
Low GABA can also be involved with anger and rage
Cognitive issues can be caused by low dopamine and low GABA – and tyrosine and/or GABA help ease symptoms

(You can find the symptoms questionnaire here. As always, amino acids are used based on symptom clusters and dosed according to your unique needs.)

If you find you have been using the amino acids long term and have explored all the possible root causes described in my book and summarized here, it may be worth investigating primary hyperthyroidism especially if you’re menopausal.

Case: “I had to have a parathyroid gland removed a few years ago… I literally felt better from the moment I came round from the surgery”

We always want to find the root cause when we have various symptoms. With this condition, it’s common to observe very quick resolution of symptoms after parathyroid surgery to remove the adenoma/s. Someone in our community shared this:

I had to have a parathyroid gland removed a few years ago … I literally felt better from the moment I came round from the surgery. It’s a miserable disease. I thought I was going to die! Lots of people get so low that they don’t feel like they can go on.

Bone pain was awful. Fatigue, depression etc.

I had had some dental issues around that time. One of my teeth crumbled. My Vitamin D went down to 9 so I am sure that was a large part of the puzzle.

I was actually diagnosed fairly quickly but was retested many times. I self-referred to a surgeon that was in-network in the end as my insurance wouldn’t cover various surgeons that my doctor wanted me to go too.

I had had breast cancer a few years ago and so had had weekly blood tests and, when I went back and looked, my calcium had been high for years. So important to read our own results.

The surgery was so easy.

What an amazing outcome for this woman and I appreciate her for sharing so we all get to learn and benefit from her journey. And yes, I agree, we need to advocate for ourselves and ask for and keep copies of all our labs. And get educated and ask questions. It’s really unfortunate that high calcium and hyperparathyroidism is so often missed.

Not everyone has all the listed symptoms of primary hyperparathyroidism. This woman did experience fatigue, depression and bone pain. She did not experience anxiety and didn’t have kidney stones. I do suspect dietary oxalate issues (without kidney stones) can be an issue for some folks because of the calcium disruption.

Some reasons why hyperparathyroidism is underdiagnosed

In the last few months I have learned that primary hyperparathyroidism is underdiagnosed. PTH (parathyroid hormone) is not routinely tested and I believe that it should be. Also, as you read above, elevated calcium levels are often ignored or brushed off as being a non-issue. And to complicate things further calcium is not always elevated. Hyperparathyroidism is also underdiagnosed and undertreated in the elderly.

For many women (and men) the discovery happens after they are diagnosed with osteoporosis and then calcium and PTH are tested, and/or past elevated calcium levels are “discovered.” If the hyperparathyroidism diagnosis happens first then osteoporosis screening is not always done and I believe it should be. And don’t get me started on when I believe osteoporosis screening should start (at 45 and not 65 or 70 years old) and issues with DEXA screening (more to come on this).

The good news is that primary hyperparathyroidism is a well-established cause of secondary osteoporosis which starts to resolve after the surgery too.

I’m still very much in learning mode

Primary hyperparathyroidism only recently appeared on my radar as a result of the 2023 osteoporosis summit, hosted by my friend and colleague, Margie Bissinger, Physical Therapist and osteoporosis coach. Dr. Deva Boone was a speaker on this condition on the summit and her site is a wealth of information. I appreciate them both.

As I mentioned above, I am also amazed it’s not something I’ve heard about at mental health or integrative health conferences and when doing continuing education.

I will admit I’m no expert and I’m still very much in learning mode – for myself and for you and this community. But, as you know, I like to share what I learn. As I continue to learn, I plan to share additional perspectives and the osteoporosis/menopause and oxalate links.

I am also in the process of creating a hyperparathyroidism questionnaire to use with my clients. Not everyone has all the above symptoms and not all the papers and resources list all the symptoms covered here today. For example, fatigue is listed on many sites but not in the above two papers and very few sites emphasize the mental health symptoms.

I’m also learning there are clues to look for – like forearm results on the DEXA scan and a good TBS/trabecular bone score has some significance. Stay tuned.

Resources if you are new to using amino acids as supplements

If you are new to using amino acids as supplements, here is the Amino Acids Mood Questionnaire from The Antianxiety Food Solution (you can see all the symptoms of neurotransmitter imbalances, including low GABA, low serotonin, low dopamine and low endorphins).

If you suspect low levels of any of the neurotransmitters and do not yet have my book, The Antianxiety Food Solution – How the Foods You Eat Can Help You Calm Your Anxious Mind, Improve Your Mood, and End Cravings, I highly recommend getting it and reading it before jumping in and using amino acids on your own so you are knowledgeable. And be sure to share it with the practitioner/health team you or your loved one is working with.

There is an entire chapter on the amino acids and they are discussed throughout the book in the sections on gut health, gluten, blood sugar control, sugar cravings, anxiety and mood issues.

The book doesn’t include product names (per the publisher’s request) so this blog, The Antianxiety Food Solution Amino Acid and Pyroluria Supplements, lists the amino acids that I use with my individual clients and those in my group programs. You can find them all in my online store.

If, after reading this blog and my book, you don’t feel comfortable figuring things out on your own (i.e. doing the symptoms questionnaire and respective amino acids trials), a good place to get help is the GABA QuickStart Program (if you have low GABA symptoms too). This is a paid online/virtual group program where you get my guidance and community support.

If you are a practitioner, join us in The Balancing Neurotransmitters: the Fundamentals program. This is also a paid online/virtual program with an opportunity to interact with me and other practitioners who are also using the amino acids.

If you’ve been diagnosed with hyperparathyroidism (or a family member has been) you can likely relate to much of this. Please share your/their journey. I’d love to hear how long it took for a diagnosis and treatment and what symptoms resolved after surgery, and how quickly.

Did you find the amino acids helped anxiety, mood and cognition symptoms in the short term, and then were no longer needed after surgery?

If you’re new to hyperparathyroidism, feel free to ask your questions and share what you’d like to hear more about in the follow-up blog.

If you are a practitioner, is primary hyperparathyroidism on your radar and do you recommend PTH testing in addition to calcium testing? Have you found the amino acids to be a good short-term solution for your clients/patients?

And if hyperparathyroidism is your area of expertise, feel free to add to the discussion.

Feel free to post your feedback here in the comments.

Fatigue, sleep disorders, depression, anxiety, fibromyalgia and cardiac troubles as the expression of a classic mild thiamine deficiency

October 8, 2021 By Trudy Scott 15 Comments

Fatigue, sleep disorders, depression, anxiety, fibromyalgia and cardiac troubles are some of the symptoms we see as the expression of a classic mild thiamine deficiency. Thiamine deficiency is very under-rated and under-recognized, and can have far reaching ramifications. And a magnesium deficiency and high dose magnesium can actually cause a thiamine deficiency. There are also many other causes of thiamine deficiency that may not be on your radar: a high carb/processed food/sugar diet, coffee, tea, alcohol, genetics, environmental toxins, medications, celiac disease, leaky gut, bariatric surgery and malabsorption.

It’s for this reason that I invited Chandler Marrs, PhD to speak on the Anxiety Summit 5: Gut-Brain Axis. We had so much to cover and it ended up being so long, that we split it into part 1 and part 2.

This is what we cover in Thiamine Deficiency in Anxiety and Gut Health (Part 1)

Excessive carbs, alcohol, medications and genetics as causes of low B1/thiamine
Dysbiosis, dysmotility, constipation, anxiety, depression, panic attacks, low energy
Psychiatric and digestive effects: research, history and other symptoms

This is what we cover in Thiamine Deficiency in Anxiety and Gut Health (Part 2)

The mitochondria, dysautonomia and POTS
Other symptoms: hyperemesis, exercise intolerance, muscle pain, neuropathy
Thiamine supplementation – forms, dosing and paradoxical reactions

Thiamine deficiency is under-rated and under-recognized

We start with why it’s an under-rated and under-recognized deficiency and Dr. Marrs shares that the assumption is that deficiency is not common and even when you test it looks like you are not deficient:

“The assumption is that there is no such thing [as a thiamine deficiency] and that it’s rare unless you are a chronic alcoholic. And even then, it’s missed 80% of the time. Or you have a severe injury or illness that depletes thiamine rapidly.
The presumption is that we’ve solved it, and it’s rare, and it only happens in countries where food availability is problematic.
The reality is that the chemistry of our foods, the chemistry of our environment, the medications that we take all combine and accrue to not only deplete the available thiamine on the basis of intake but to increase the need and to damage a lot of the enzymes involved in the processing of thiamine.
So a lot of folks are functionally deficient in that even though by definition they meet the daily requirement and they may, based upon lab testing, show up as being sufficient and not frankly deficient.
And so, I think that we just have taken our eye off of the ball with regard to this particular nutrient.”

Magnesium deficiency (and high dose magnesium) can actually cause a thiamine deficiency

Dr. Marrs also shares how a magnesium deficiency (which is very common) can actually cause a thiamine deficiency:

“One of the things that’s interesting is it requires magnesium to activate thiamine into its active form.
If someone is thiamine sufficient and magnesium deficient, then they are actually functionally deficient in thiamine because you cannot take the free thiamine and activate it into thiamine pyrophosphate.
So magnesium deficiency itself can cause thiamine deficiency. And there’s a good percentage of the population that doesn’t get enough magnesium.”

And she also shares how when taking high dose magnesium it’s so crucial to also be addressing low thiamine in order to prevent them becoming more thiamine deficient:

“Now, the flip side of that is really interesting. And I think this is important for your audience, in particular, is that magnesium supplementation, when someone has a problem with thiamine, will actually shut down thiamine processing and mitochondrial processing at one of the enzymes. Because if you don’t have thiamine with magnesium, then the enzyme α-ketoglutarate dehydrogenase kind of shuts the whole sequence down.
So if you are giving someone high dose magnesium, which is common to supplement, and not tackling the thiamine as well, you risk them becoming more thiamine deficient and reducing ATP output, energy output even further. So everything has to be in balance to some extent or another.”

I can think of one situation where this could be common. You use high dose magnesium due to constipation. Low thiamine may be one of the underlying causes of your constipation and now high dose magnesium is going to make the low thiamine situation worse.

Up to 30% of psychiatric patients have a thiamine deficiency

We talk about how up to 30% of psychiatric patients have a thiamine deficiency but that there hasn’t been enough work on psychiatric disorders which Dr. Marrs says “is strange given the fact that some of the strongest symptoms involve brain function and the most dangerous or some of the more dangerous damage is relative to areas of the brain.”

I share some quotes from a 2019 paper that does actually look at the psychiatric aspects – Neurological, Psychiatric, and Biochemical Aspects of Thiamine Deficiency in Children and Adults:

“The brain is highly vulnerable to thiamine deficiency due to its heavy reliance on mitochondrial ATP production. This is more evident during rapid growth, i.e., perinatal and children.
Thiamine deficiency contributes to a number of conditions spanning from mild neurological and psychiatric symptoms, confusion, reduced memory, sleep disturbances, and severe encephalopathy, ataxia, congestive heart failure, muscle atrophy, and even death.”

This paper also looks at the beneficial effect of thiamine supplementation in autism spectrum disorder (ASD) and other neurological conditions.

Below, I share some additional studies that we didn’t talk about in the interview but add value to the topic.

Fatigue, sleep disorders, depression, anxiety, fibromyalgia and cardiac troubles as the expression of a classic mild thiamine deficiency

This paper, High-dose thiamine improves the symptoms of fibromyalgia, states that “It is our opinion that fatigue, sleep disorders, depression, anxiety and cardiac troubles are the expressions of a classic mild thiamine deficiency.”

The authors share 3 cases where thiamine/vitamin B1 improved symptoms in all areas for all these women:

Patient 1: Female, 58 years old, weight 59 kg. From 1998, the patient began to have widespread pain accompanied by severe fatigue, depression, anxiety, irritability, sleep disorders, trouble concentrating, dry skin, general sickness, continuous headache, intolerance to low temperatures and, more recently, episodes of tachycardia and extrasystolia [alteration in heart rhythm].
Patient 2: Female, 37 years old, weight 74 kg. From 1999, the patient has had widespread pain and all the symptoms described for patient 1, with the only exception being that of cardiac symptoms.
Patient 3: Female, 60 years old, weight 65 kg. From 2006, the patient began to have widespread pain, fatigue, depression, anxiety, sleep disorders. Trouble concentrating.

As you can see the symptoms can be very varied and this is what makes it challenging to identify low thiamine as being the issue.

Thiamine deficiency after bariatric surgery

Here one case study where thiamine deficiency occurred after bariatric surgery: Wernicke’s encephalopathy mimicking multiple sclerosis in a young female patient post-bariatric gastric sleeve surgery:

We describe a case of Wernicke’s encephalopathy secondary to thiamine (B1) deficiency in a patient status post-bariatric sleeve gastrectomy.

The presenting symptoms of new-onset weakness, diplopia [double-vision], and confusion in a young female patient raised suspicion for multiple sclerosis (MS), but given a history of bariatric surgery, thiamine levels were checked, revealing significant Vitamin B1 (thiamine) deficiency.

This case highlights the importance of thorough history taking, as a misdiagnosis of MS in this case could have resulted in irreversible neurological deterioration and hematological and infectious consequences associated with the inappropriate administration of disease-modifying therapies.

Bariatric surgery is one of many causes of thiamine deficiency.

Some of the other many causes of thiamine deficiency

Other causes of thiamine deficiency include factors that may not be on your radar: a high carb/processed food/sugar diet (and even consistent smaller amounts of “healthy” sweeteners), coffee and tea consumption, alcohol consumption (excessive consumption and even moderate consumption i.e. social drinking), genetics (we talk about specific genes in the interview), environmental toxins, certain medications, celiac disease, leaky gut and malabsorption etc.

We do a deep dive into all this in the two interviews (and much more).

chandler marrs interview — (As you can see, when I do interviews I take notes throughout for a few reasons: writing consolidates the information into my brain and it allows me to make notes for follow-up questions. It also helps the video editing process later.)

Interviews that dove-tail well with this topic are these ones:

Michael Collins – Sugar/Fructose Addiction: Anxiety, ADHD and Aggression (because sugar and carbs lead to low thiamine)
My interviews, Glutamine, DPA and Tyrosine for Anxiety and Sugar Cravings and GABA & Tryptophan: Gut-Anxiety Connections (because the amino acids help you quit sugar/carbs, coffee and alcohol easily)
Tara Hunkin, NTP, CGP, RWP – Mitochondrial Dysfunction in Anxiety (because low thiamine adversely affects the mitochondria)

I encourage you to tune in if you have:

Anxiety & feel overwhelmed & stressed by little things
Panic attacks &/or obsessive thoughts or behaviors
Social anxiety/pyroluria
Phobias or fears (flying, spiders or even driving on a highway)

And also if you suffer from…

Food sensitivities, IBS/SIBO, parasites or gallbladder issues
Constipation, diarrhea, bloating, gas, pain & other digestive issues
Leaky gut, a leaky blood-brain barrier or vagus nerve issues

Join us if you are also an emotional eater with intense sugar cravings (and know you suffer from low blood sugar), experience insomnia, low mood, PMS, poor focus and/or low motivation.

This is THE online event to learn about the powerful individual amino acids – GABA, theanine, tryptophan, 5-HTP, glutamine, DPA and tyrosine – to quickly ease anxiety and help with gut symptoms while you are dealing with other root causes which take longer to address. (They also help with cravings as with this example, and sleep and immunity).

With research-based anxiety nutritional solutions and practical steps, you can determine your root causes, ease your anxiety and prevent it from coming back so you can feel on top of the world again!

If you are a practitioner, please join us too and find advanced solutions for your clients or patients too!

You’ve heard me say the Anxiety Summit has been called “a bouquet of hope!” My wish for you is that this summit is your bouquet of hope!

I hope you’ll join me and these incredible speakers, be enlightened and find YOUR solutions! More about this summit and other Anxiety Summits here.

Here’s to no more anxiety and you feeling on top of the world again!

Please share if these thiamine deficiency symptoms are new to you.

Also let us know if you’ve benefited from thiamine in the past or are currently using some form of thiamine – and how helped/is helping.

Have you seen this correlation between low magnesium and low thiamine OR taking high doses of magnesium and low thiamine symptoms?

Feel free to post your questions here too.

Learn more/purchase now

Case Study: Bartonella and Sudden-Onset Adolescent Schizophrenia

March 22, 2019 By Trudy Scott 26 Comments

According to a press release from North Carolina State University, researchers share a case study describing an adolescent human patient diagnosed with rapid onset schizophrenia who was found instead to have a Bartonella henselae infection. This study adds to the growing body of evidence that Bartonella infection can mimic a host of chronic illnesses, including mental illness, and could open up new avenues of research into bacterial or microbial causes of mental disorders.

Bartonella is a bacteria most commonly associated with cat scratch disease, which until recently was thought to be a short-lived (or self-limiting) infection. There are at least 30 different known species of Bartonella, and 13 of those have been found to infect human beings. The ability to find and diagnose Bartonella infection in animals and humans – it is notorious for “hiding” in the linings of blood vessels – has led to its identification in patients with a host of chronic illnesses ranging from migraines to seizures to rheumatoid illnesses that the medical community previously hadn’t been able to attribute to a specific cause.

In the case study published in the Journal of Central Nervous Disease, an adolescent with sudden onset psychotic behavior – diagnosed as schizophrenia – was seen and treated by numerous specialists and therapists over an 18-month period. All conventional treatments for both psychosis and autoimmune disorders failed. Finally, a physician recognized lesions on the patient’s skin that are often associated with Bartonella, and the patient tested positive for the infection. Combination antimicrobial chemotherapy led to full recovery.

According to the case report above, Bartonella henselae Bloodstream Infection in a Boy With Pediatric Acute-Onset Neuropsychiatric Syndrome, these are some of the many symptoms he experienced over the 18-month period:

He reported feeling overwhelmed, confused, depressed, and agitated.
He said that he was an “evil, damned son of the devil” and wanted to kill himself because he was afraid of his new-onset homicidal thoughts toward those he cared about
Weeks after initial hospitalization in October, he became more dysfunctional; school was not possible; he developed progressively severe psychiatric symptoms including obsessional intrusive thoughts, phobias, irrational fears, emotional lability, unpredictable rage outbursts, and increased psychotic thinking. He believed that he had special powers and that a family cat wanted to kill him.
By December 2015, his illness had progressed in severity, causing his mother to quit her job to provide full-time supervision. In addition to persecutory delusions related to his pets, he developed auditory, visual, and tactile hallucinations and began refusing to leave the house.
In January 2016, following discharge after a week-long hospitalization, he developed non-specific somatic symptoms, including excessive fatigue, daily headaches, chest pains, shortness of breath (possible panic anxiety), and urinary frequency

I suspect some of his later symptoms were related to side-effects from many of the medications he was prescribed over the course of his treatment. Some symptoms may also be attributed to withdrawal from some of these medications. One example mentioned in the case study was “abrupt withdrawal of clozapine and tramadol” where “he experienced severe anorexia, nausea, and vomiting, which resulted in hospitalization and a 20.5-kg weight loss over 40 days.” It’s well- documented that withdrawal signs and symptoms of antipsychotic medications such as clozapine “may include insomnia, nausea, vomiting, anxiety, and agitation.”

This figure lists the medications he was prescribed during his treatment. The pink area was during his psychotic 18-month period and the yellow area was during his antimicrobial treatment of the Bartonella.

Figure 2. Drug administration timeline for the boy, reprinted from the study

The skin lesions or “stretch mark-like” lesions on his thigh (A) and armpit (B) are tell-tale signs of a Bartonella bacterial infection or neurobartonellosis. Here are photographs taken by his parents.

A successful outcome for this young boy came about as a result of antimicrobial treatment in the way of antibiotics and antifungals. His skin lesions healed, his psychosis and other symptoms resolved, he was able to quit his psychiatric medications and go back to being a typical young boy. How wonderful for this young boy! And this gives me so much hope for others who may be in a similar situation and looking for solutions.

Other than the hope I felt, these are my other thoughts that came to my mind as I read this case study:

How many people are being prescribed psychiatric medications when they actually have an infection or physiological condition? The authors state: “Beyond suggesting that Bartonella infection itself could contribute to progressive neuropsychiatric disorders like schizophrenia, it raises the question of how often infection may be involved with psychiatric disorders generally.”
How can a young boy of this age be prescribed this many psychiatric medications over an 18-month period? I’m sure his doctors were doing their best but what is it going to take for doctors to look for infectious (and/or physiological or biological or nutritional or environmental) causes for psychiatric symptoms as the first approach or certainly at the same time in a situation like this where psychosis was a factor?
What will it take for mainstream practitioners to get up to speed with this epidemic of Lyme disease? And when will testing for Lyme disease and co-infections be used by all doctors and not just Lyme-literate doctors and functional medicine doctors like Dr. Darin Ingels. the author of “The Lyme Solution.” (Here is my review of his excellent book.) It is worth noting that Dr. Ingels uses very successful treatments that are purely herbal, dietary and immune-supportive, and don’t require antibiotics.

We already know there is a huge psychiatric connection with Lyme disease and co-infections: anxiety, depression, panic attacks, and OCD too. This case adds to the evidence. Even though neuropsychiatric Lyme disease is well-recognized in the world of functional medicine, keep in mind that Lyme disease bacteria such as Borrelia and co-infections such as Bartonella are only one of many possible trigger/root cause of symptoms like this young boy experienced.

Other infectious causes of psychiatric conditions include chronic strep (in the case of PANDAS/PANS) and toxoplasma gondii.

Other physiological root causes of psychiatric conditions like schizophrenia, anxiety, bipolar disorder and depression could include a thyroid condition, heavy metal toxicity from say lead or mercury, mycotoxins, and even gluten.

We need to be shouting case studies like this from the rooftops so more doctors, more psychologists, more functional medicine practitioners, and more parents are aware and start to look for infectious/physiological/biological/nutritional/environmental root causes.

We appreciate those involved in publishing this case and the family for giving permission. Hopefully, case studies like these will drive future research and treatment approaches.

What do you think and what came to your mind when you read this case study?

Feel free to post your questions here too.