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Invisible Illness Research

The research of Genetic Disease Investigators LLC,  Diana Driscoll, OD, President, is resulting in dramatic treatment paradigm shifts for numerous illnesses currently considered “invisible”. Dr. Driscoll’s research began with autonomic dysfunction, POTS, and Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and has expanded to include interstitial cystitis, Multiple Sclerosis, Ehlers-Danlos syndrome (EDS), vascular disorders and brain health.

“Traditional treatment for many invisible illnesses focuses on managing symptoms, but has nothing to do with treating the underlying medical problems causing the illnesses. We can stay in the science for answers, but we must dig deeper. The future of these patients depends on it.”       — Dr. Diana Driscoll, Optometrist

COVID and the Vagus Nerve – An amazing discovery

COVID and the Vagus Nerve – An amazing discovery

Document

COVID and the Vagus Nerve - An amazing discovery

By Dr. Diana Driscoll, Optometrist, FAAO

The vagus nerve is affected in post-COVID Longhaulers! This contributes to dysautonomia (dysfunction of parts of the autonomic nervous system). This ground-breaking information was recently released in peer-reviewed literature (see Reference below).

So what can you do? Do you need to stimulate the vagus nerve? No. This nerve is autonomic - it works with no effort on your part. Instead, you can take Parasym PlusTM , an oral supplement that uniquely stimulates the receptors of the vagus nerve, allowing normal function.

Parasym PlusTM works despite the reason for the vagus nerve problem. The nerve can be damaged, infected, inflamed, or destroyed, but the receptors are still viable. Parasym PlusTM is patented and works directly on the receptors of the vagus nerve (and other parasympathetic nerves).

The publication in Acta Neuropathologica validates the research completed by Genetic Disease Investigators approximately 15 years ago. Inventor, Dr. Diana Driscoll, Optometrist, FAAO proved the receptors of the vagus nerve were viable, leap-frogging the research in attempts to stimulate the nerve.

From Dr. Driscoll:
“As an eye doctor, I knew from researching Sjogren’s syndrome that stimulating a parasympathetic nerve when the patient was inflamed was of minimal help. Instead, we should trigger the receptors themselves and the organs respond immediately. We do not need to wait for a new drug to do this. Parasym PlusTM is patented and works directly on these receptors and is available today.”

For more information on Parasym PlusTM : https://vagusnervesupport.com/vagus-nerve-support- parasym-plus/

For more information on Inflammatory POTS: https://potscare.com/inflammatory-pots/

Reference:

Woo MS, Shafiq M, Fitzek A, et al. Vagus nerve inflammation contributes to dysautonomia in COVID-19. Acta Neuropathol. 2023;146(3):387- 394. doi:10.1007/s00401-023-02612-x

More Information Concerning the Vagus Nerve:

The vagus nerve is the major nerve controlling the parasympathetic nervous system -- the system of the body that allows us to rest and digest.

The vagus nerve controls virtually every aspect of digestion -- from stomach acid production to motility. When this nerve fails, digestion suffers and malabsorption can occur.

After you experience “fight or flight” (the sympathetic nervous system is activated), the vagus nerve also allows you to calm down and normalize your heart rate and breathing. It is the “rest and digest” system of the body.

The vagus nerve is also the anti-inflammatory nerve of the body! Once the need for inflammation passes, the vagus nerve sends out signals to the inflammatory cells to stop releasing damaging inflammatory cytokines and other chemicals. When the vagus nerve is not working well, inflammation can become chronic (and cause further damage).

Do you need to stimulate your vagus nerve?

With the new science released on the importance of the vagus nerve, I’ve seen many people go to great lengths to stimulate their vagus nerve. They may splash water on their face, sing or hum, or meditate, for example. Many patients are buying vagus nerve stimulators to get their vagus nerve working. But is this necessary, effective, or even desirable?

If you have been stimulating your vagus nerve, but not getting the results you hoped for, something may be missing!

It is critical to understand that the vagus nerve is part of the autonomic nervous system -- the system of the body that works without our effort (it is automatic). As the “automatic” nervous system, no one should need to make it work. You shouldn’t need to “make” your stomach produce stomach acid, nor do you need to “tell” your gallbladder to release bile for digestion, for example. This happens all by itself as a part of the autonomic nervous system. And thank goodness! Can you imagine going through life needing to tell your body when to produce tears, change your blood pressure, eject pancreatic enzymes, or have a bowel movement? The body is magnificently made so that the autonomic nervous system doesn’t need our input! We shouldn’t need to make the vagus nerve work!

We shouldn’t need to stimulate our vagus nerve.

So if the nerve doesn’t appear to be working well, or if stimulation is not getting the desired response, what can we do? Let’s look closely at the science.

What else could cause a vagus nerve problem and how can we return to normal autonomic functioning without actively stimulating the nerve?

First, we need to understand that nerves work by receiving a signal, then the signal travels down to the end of the nerve where a chemical is released (the neurotransmitter) which then jumps over a small gap (a “synapse”) to land on a receptor, causing an action.

synapse illustration

Secondly, we need to consider that the vagus nerve problem could be a secondary issue. If the problem is actually a neurotransmitter problem, correcting this problem can return normal nerve function. What can affect the neurotransmitter used by the vagus nerve?

This neurotransmitter is acetylcholine. There are some genetic conditions that influence its production. A genetic problem with the manufacturing of acetylcholine means that you cannot produce enough for maximal vagus nerve function. Again, stimulating the nerve will not correct the problem -- it is a neurotransmitter problem, not a nerve problem.

Also critical for acetylcholine production are specific nutrients. If you suffer with nutrient malabsorption for any reason, the production of acetylcholine can be restricted.

Some inflammatory cytokines and chemokines block the release of acetylcholine. If this is occurring, stimulating the nerve will not be effective.

How can you recognize a problem with acetylcholine as the issue resulting in vagus nerve problems?

When problems with acetylcholine occur, the symptoms extend beyond the vagus nerve. If these symptoms are present, the true problem may be an acetylcholine problem -- not a vagus nerve problem. What symptoms or signs should you consider?

When acetylcholine is not being produced or released properly, symptoms of anticholinergic syndrome occur. Anticholinergic syndrome occurs when a patient has ingested a drug that breaks down acetylcholine (such as atropine -- eye drops that dilate the pupil). These symptoms include brain fog, easy irritation, moodiness, visual snow, fatigue, constipation, poor cognition and a decrease in short-term memory, dry eyes and dry mouth. These symptoms reach far beyond vagus nerve problems.

Dr. Diana Driscoll discusses the results of her research in anticholinergic syndrome in Chronic Fatigue Syndrome at AAEM 2019:

If the true problem involves the neurotransmitter, the problem with the neurotransmitter must be corrected (as opposed to the vagus nerve). Correcting the acetylcholine problem can then resolve the symptoms of vagus nerve problems AND the additional symptoms of low acetylcholine.

Remember -

  • If the vagus nerve is damaged, stimulating the nerve will not work.
  • If there is a genetic issue with the production of acetylcholine, stimulating the nerve will not work.
  • Some nutrients are essential in the production of acetylcholine. Deficiencies of these nutrients result in insufficient acetylcholine and stimulating the vagus nerve will not work.
  • If the problem is one of acetylcholine, stimulating the vagus nerve will do nothing to help with other systems of the body that depend upon acetylcholine (tear production by the lacrimal nerve and cognition by the central nervous system, for example).

It took years for me to work through this problem! I collected symptom spreadsheets over 4 ½ years for patients with numerous “invisible illnesses” such as ME/CFS (Chronic Fatigue Syndrome), Fibromyalgia, POTS (Postural Orthostatic Tachycardia Syndrome), PTSD (Post Traumatic Stress Disorder), and TBI (Traumatic Brain Injury). The majority of patients displayed the majority of symptoms of anticholinergic syndrome -- a new finding never before reported.

It took even longer to test my hypothesis (beginning with my own body), then begin to approach treatment in a unique fashion. I asked myself if it was possible to come up with an oral supplement that could come into the body quickly to stimulate the (postganglionic) vagus nerve or the receptor itself and yet work around any of the problems with the nerve or with the neurotransmitter affecting the patient. My goals were numerous and included the following:

  • The supplement had to work around any genetic issues with acetylcholine production.
  • It had to cross the blood-brain barrier to supply acetylcholine for cognition.
  • It had to supply necessary nutrients to cover for any deficiency that can lead to low acetylcholine.
  • It had to work even if the (preganglionic) vagus nerve was damaged. Instead, it had to work on the postganglionic vagus nerve (or the receptor itself).
  • To judge effectiveness, I needed to see a bowel movement.
  • It had to support acetylcholine for the lacrimal nerve, normalizing tear production (dry eyes).

No one had ever tried to do this orally before. As such, the result of my work has received four patents to date.

Staying firmly in science gives us the answers. Although my intuition told me that I shouldn’t need to stimulate the vagus nerve with a stimulator (it should work all by itself), the true problems can be easy to miss.

Supporting your vagus nerve with Parasym PlusTM will cover you for any reason you have a problem with the neurotransmitter. You don’t need to know if you have genetic problems with acetylcholine or if your (preganglionic or postganglionic) vagus nerve is damaged. Stimulating your vagus nerve is not necessary.

Supporting your vagus nerve with Parasym PlusTM will cover you for any reason you have a problem with the neurotransmitter. It was critical for my return to health and for that of my children.

Dr. Diana Driscoll, Optometrist, FAAO

https://vagusnervesupport.com/vagus-nerve-support-parasym-plus/
Do you need to stimulate your vagus nerve?

Do you need to stimulate your vagus nerve?

Do You Need to Stimulate Your Vagus Nerve? What You May Be Missing!

By Dr. Diana Driscoll, Optometrist

The vagus nerve is the major nerve controlling the parasympathetic nervous system - the system of the body that allows us to rest and digest.

The vagus nerve controls virtually every aspect of digestion - from stomach acid production to motility. When this nerve fails, digestion suffers, and malabsorption can occur.

After you experience "fight or flight" (the sympathetic nervous system is activated), the vagus nerve also allows you to calm down and normalize your heart rate and breathing. It is the "rest and digest" system of the body.

The vagus nerve is also the anti-inflammatory nerve of the body! Once the need for inflammation passes, the vagus nerve sends out signals to the inflammatory cells to stop releasing damaging inflammatory cytokines and other chemicals. When the vagus nerve is not working well, inflammation can become chronic (and cause further damage).

So, Do You Need to Stimulate Your Vagus Nerve?

With the new science released on the importance of the vagus nerve, I’ve seen many people go to great lengths to stimulate their vagus nerve. They may splash water on their face, sing or hum, or meditate, for example. Many patients are buying vagus nerve stimulators to get their vagus nerve working. But is this necessary, effective, or even desirable?

If you have been stimulating your vagus nerve, but not getting the results you hoped for, something may be missing!

It is critical to understand that the vagus nerve is part of the autonomic nervous system - the system of the body that works without our effort (it is automatic). As the "automatic" nervous system, no one should need to make it work. You shouldn’t need to “make” your stomach produce stomach acid, nor do you need to “tell” your gallbladder to release bile for digestion, for example. This happens all by itself as a part of the autonomic nervous system. And thank goodness! Can you imagine going through life needing to tell your body when to produce tears, change your blood pressure, eject pancreatic enzymes, or have a bowel movement? The body is magnificently made so that the autonomic nervous system doesn’t need our input! We shouldn’t need to make the vagus nerve work!

We shouldn’t need to stimulate our vagus nerve.

So if the nerve doesn’t appear to be working well, or if stimulation is not getting the desired response, what can we do? Let’s look closely at the science.

What else could cause a vagus nerve problem and how can we return to normal autonomic functioning without actively stimulating the nerve?

First, we need to understand that nerves work by receiving a signal, then the signal travels down to the end of the nerve where a chemical is released (the neurotransmitter) which then jumps over a small gap (a “synapse”) to land on a receptor, causing an action.

When this process is broken, we need to consider the possibility that the nerve is damaged. The vagus nerve (“the wandering nerve”) is the longest cranial nerve in the body and is prone to damage. Abdominal surgery, heart ablation, gastric sleeve, and whiplash, for example, can all damage this delicate nerve. If your nerve is damaged, stimulating it will do nothing. The signal will not pass through the damaged portion in order to release the neurotransmitter.

Secondly, we need to consider that the vagus nerve problem could be a secondary issue. If the problem is actually a neurotransmitter problem, correcting this problem can return normal nerve function. What can affect the neurotransmitter used by the vagus nerve?

This neurotransmitter is acetylcholine. There are some genetic conditions that influence its production. A genetic problem with the manufacturing of acetylcholine means that you cannot produce enough for maximal vagus nerve function. Again, stimulating the nerve will not correct the problem -- it is a neurotransmitter problem, not a nerve problem.

Also critical for acetylcholine production are specific nutrients. If you suffer with nutrient malabsorption for any reason, the production of acetylcholine can be restricted.

Some inflammatory cytokines and chemokines block the release of acetylcholine. If this is occurring, stimulating the nerve will not be effective.

How can you recognize a problem with acetylcholine as the issue resulting in vagus nerve problems?

When problems with acetylcholine occur, the symptoms extend beyond the vagus nerve. If these symptoms are present, the true problem may be an acetylcholine problem -- not a vagus nerve problem. What symptoms or signs should you consider?

When acetylcholine is not being produced or released properly, symptoms of anticholinergic syndrome occur. Anticholinergic syndrome occurs when a patient has ingested a drug that breaks down acetylcholine (such as atropine -- eye drops that dilate the pupil). These symptoms include brain fog, easy irritation, moodiness, visual snow, fatigue, constipation, poor cognition and a decrease in short-term memory, dry eyes and dry mouth. These symptoms reach far beyond vagus nerve problems.

Watch Dr. Diana Driscoll discuss the results of her research in anticholinergic syndrome in Chronic Fatigue Syndrome at AAEM 2019

If the true problem involves the neurotransmitter, the problem with the neurotransmitter must be corrected (as opposed to the vagus nerve). Correcting the acetylcholine problem can then resolve the symptoms of vagus nerve problems AND the additional symptoms of low acetylcholine.

Remember

  • If the vagus nerve is damaged, stimulating the nerve will not work.
  • If there is a genetic issue with the production of acetylcholine, stimulating the nerve will not work.
  • Some nutrients are essential in the production of acetylcholine. Deficiencies of these nutrients result in insufficient acetylcholine and stimulating the vagus nerve will not work.
  • If the problem is one of acetylcholine, stimulating the vagus nerve will do nothing to help with other systems of the body that depend upon acetylcholine (tear production by the lacrimal nerve and cognition by the central nervous system, for example).

It took years for me to work through this problem! I collected symptom spreadsheets over 4 ½ years for patients with numerous “invisible illnesses” such as ME/CFS (Chronic Fatigue Syndrome), Fibromyalgia, POTS (Postural Orthostatic Tachycardia Syndrome), PTSD (Post Traumatic Stress Disorder), and TBI (Traumatic Brain Injury). The majority of patients displayed the majority of symptoms of anticholinergic syndrome -- a new finding never before reported.

It took even longer to test my hypothesis (beginning with my own body), then begin to approach treatment in a unique fashion. I asked myself if it was possible to come up with an oral supplement that could come into the body quickly to stimulate the (postganglionic) vagus nerve or the receptor itself and yet work around any of the problems with the nerve or with the neurotransmitter affecting the patient. My goals were numerous and included the following:

  • The supplement had to work around any genetic issues with acetylcholine production.
  • It had to cross the blood-brain barrier to supply acetylcholine for cognition.
  • It had to supply necessary nutrients to cover for any deficiency that can lead to low acetylcholine.
  • It had to work even if the (preganglionic) vagus nerve was damaged. Instead, it had to work on the postganglionic vagus nerve (or the receptor itself).
  • To judge effectiveness, I needed to see a bowel movement.
  • It had to support acetylcholine for the lacrimal nerve, normalizing tear production (dry eyes).

No one had ever tried to do this orally before. As such, the result of my work has received four patents to date.

Staying firmly in science gives us the answers. Although my intuition told me that I shouldn’t need to stimulate the vagus nerve with a stimulator (it should work all by itself), the true problems can be easy to miss.

Supporting your vagus nerve with Parasym PlusTM will cover you for any reason you have a problem with the neurotransmitter. You don’t need to know if you have genetic problems with acetylcholine or if your (preganglionic) vagus nerve is damaged. Stimulating your vagus nerve is not necessary.

Supporting your vagus nerve with Parasym PlusTM will cover you for any reason you have a problem with the neurotransmitter. It was critical for my return to health and for that of my children.

Dr. Diana Driscoll, Optometrist

Learn more about Vagus Nerve Support with Parasym PlusTM

Vascular fundus changes in patients with high probability of chronic cerebrospinal venous insufficiency

Vascular fundus changes in patients with high probability of chronic cerebrospinal venous insufficiency

Presented February 2012- International Society of Neurovascular Disease.

This study included co-authors Dr. Clair Francomano and Diana Driscoll, OD and involved the evaluation of 60 fundus images of patients with EDS/POTS or multiple sclerosis, as compared to age-matched normals. The vascular abnormalities found allowed a “blinded” doctor to correctly identify patients with EDS/POTS with 90% accuracy. The search for answers then shifted to the cause of these anomalies.

Acetazolomide as a medical treatment option for patients with neurodegenerative disease

Acetazolomide as a medical treatment option for patients with neurodegenerative disease

Presented February 2012 — International Society of Neurovascular Disease

This study, co-authored by Dr. William Code and Diana Driscoll, OD revealed the improvement of symptoms of headache, poor sleep, fatigue and cognition in patients with multiple sclerosis with the use of acetazolamide. Although likely multifactorial, undiagnosed idiopathic intraocular hypertension (“IIH”) as a likely cause of symptoms turned research efforts toward the cause of this abnormally high intracranial pressure.

Cardiac effects in the multiple sclerosis patient

Cardiac effects in the multiple sclerosis patient

Presented February 2012: International Society Neurovascular Disease

This study, co-authored by Dr. Clair Francomano and Diana Driscoll, OD began the study of the potential role of inflammatory cytokines in the development of left ventricular diastolic dysfunction typically found in both multiple sclerosis and Ehlers-Danlos syndrome patients. By evaluating similarities and differences in these conditions, proposed etiologies were revealed.

Vascular fundus changes in patients with high probability of chronic cerebrospinal venous insufficiency

Vascular fundus changes in patients with high probability of chronic cerebrospinal venous insufficiency

June 2012- Optometry’s Meeting

Clinicaltrials.org NCT#01356134 This study included co-authors Dr. Clair Francomano and Diana Driscoll, OD and involved the evaluation of 60 fundus images of patients with EDS/POTS or multiple sclerosis, as compared to age-matched normals. The vascular abnormalities found allowed a “blinded” doctor to correctly identify patients with EDS/POTS with 90% accuracy. The search for answers then shifted to the cause of these anomalies.

Head circumference growth in children with Ehlers-Danlos syndrome who developed dysautonomia later in life

Clinicaltrials.org NCT#01367977 Preliminary results of this study revealed abnormally fast growth of head circumferences (as opposed to the lengths and weights) in babies who were later diagnosed with EDS (“Ehlers-Danlos syndrome”) / POTS (“Postural Orthostatic Tachycardia Syndrome”). Enlarged head circumferences as found by this study hinted at, yet could not prove, the presence of high intraocular pressure (“IIH”) in these children. Many of these children were not well and many suffered from an array of neurological symptoms such as seizures, epilepsy, cataplexy, and narcolepsy. Attention then turned to the role of idiopathic intraocular hypertension in both children and adults with EDS/POTS.

Options for Care

CONSULT

$275

30-minute phone consultation with Dr. Diana Driscoll, Optometrist and Clinical Director

Are you lost in your case? Do you need direction, advice, or encouragement? Although not a medical examination, Dr. Driscoll is a recovered patient, a researcher, and a practitioner and can offer high-level support. She can share her thoughts concerning Inflammatory POTS, IIH, family dynamics, school issues, validation, and recovery. Dr. Driscoll will also send you selected resources following your consultation that may help you.

THE POTS CARE PACKAGE™

$775

Three month program to begin recovery including:

  • An app on your cell phone to guide you through Inflammatory POTS (what does the latest research tell us and how can this guide your recovery)
  • 30-minute consultation with Dr. Diana Driscoll
  • Biweekly audios by Dr. Diana Driscoll to educate, inform, and support
  • Over $500 in supplements that may offer you some immediate relief, even if your doctors have not yet identified your inflammation.
  • Heart rate variability monitor to help guide your recovery
  • A recovery journal/workbook
  • Guidance on exercise, sleep, and dietary planning
  • This package covers the commonalities in POTS patients including a tendency to develop abnormal intracranial pressure, parasympathetic nervous system problems, digestive issues, nutrient malabsorption, cognitive decline, immune disorders, and inflammatory states.
  • If you would like to approach POTS with as few medications as possible, or if you are not familiar with Inflammatory POTS, this POTS Care Package™ may be a great place to start.

CASE EVALUATION (COMING SOON)

$2,900

This is an evaluation of your case to date, with specific guidance for you and your
medical team. Not everyone can be a POTS expert nor up on the latest research. We will do this for you!

We will carefully evaluate your medical records to date (including blood work, your brain MRI if you’ve had one, and your ocular records) as well as over 200 potential symptoms and what these may mean.

We will offer specific thoughts and guidance based on your individual case with recommendations for further testing that your medical team can likely complete, differential diagnoses to consider, and ways can get answers or relief with the least invasive procedures. Are you extraordinarily sensitive? We will discuss that, as well as psychiatric symptoms that can be misinterpreted by those uninformed.

FULL POTS CARE TREATMENT

$9,300

Full case evaluation with a treatment plan and two months of follow-up.
This includes:

  • A careful review of your previous medical records
  • Customized blood work
  • Ocular testing (non-invasive and can be completed by your eye doctor)
  • Three days of appointments with our team
  • You receive a Preliminary Plan after the three day visit, and a Final Treatment Plan at one month.
  • We continue to work with you for an additional month.
  • Audio and workbook guidance continues for three months.
  • You will graduate from us with the knowledge, medicine, and power to not only
    recover from POTS, but to be healthier throughout your life.

Currently on a waiting list.