Jorge Costa, Osteopath, Aerospace Physiologist

Dear colleagues,

in today’s speech, I would like to give a new and complementary perspective on how to approach those extremely difficult cases regarding CHRONIC LOWER BACK PAIN (CLBP)

Epidemiology

Lower back pain is known worldwide as a public health problem, and is one of the main reasons patients resort to primary health care. Either for the therapeutic and diagnostic resources spent, or the high rate of disability it causes to patients, lower back pain is a real challenge for family physicians, making the thorough characterization of the multidisciplinary team associated with this condition a matter of the upmost importance.

The spectrum of disease and morbidity associated with LBP is broad. For many patients, LBP episodes are self‐limited and resolved without specific treatment. For others, however, back pain is recurrent or chronic, causing significant pain that interferes with employment and quality of life. Muscle‐ligamentary and degenerative causes are the most frequent (> 85%), and often cause exhaustion to patients, services and complementary means of diagnosis. LBP is rarely a sign of serious pathology, including infection, neoplasia or other systemic disease.

According to the Global Burden of Disease (GBD) 2013 study, backache is among the top five causes of DALYs (disability‐adjusted life years), along with ischaemic heart disease, lower respiratory tract infections, cerebrovascular disease and road accidents.

It affects a large part of the working‐age population, leading to absenteeism from work and a significant drop in productivity. It is estimated that up to 80% of all adults will have LBP on at least one occasion during their life, and this is one of the most frequent complaints at the General Practice/Family Medicine consultation.

Risk Factors

The risk factors associated with back pain remain poorly understood, however the most frequently reported ones include smoking, obesity, age over 45, female gender, physical and/or psychologically vigorous occupations, sedentariness, low level education, professional dissatisfaction, and psychological factors such as anxiety, depression, and somatization.

Definition and classification

LBP can be defined as pain or discomfort located in the lumbar region between the lower costal ridge and the folds of the lower back, with or without irradiation to one or both lower limbs.

LBP can be classified according to the type of pain into acute, sub‐acute and chronic.

Acute lower back pain can be defined as pain or discomfort located in the region between the lower costal ridge and the folds of the lower back, which starts abruptly, usually after an effort and worsens with mobilization, lasting no more than four weeks, with or without irradiation to one or both lower limbs. Patients who continue to have lower back pain beyond the acute period have subacute lower back pain (lasting between 4 and 12 weeks). After this period, it is called chronic back pain.

Recurrent LBP is defined as a new episode of lumbar pain after an asymptomatic period of six months, with the exception of exacerbation of chronic lower back pain.

Depending on the etiopathogenic mechanism, lumbar pain can be classified as mechanical or non‐mechanical (Table 1). Mechanical pain contributes to 97% of cases and is therefore usually called common. Mechanics implies that the pain is the consequence of a structural anomaly, trauma or degeneration of a normal anatomical structure without a considerable inflammatory component and may be due to excessive overload/force, secondary to trauma/deformation or secondary to a degenerative change of disc or posterior interapophyseal joints.

(Table 1)

The difficulty in establishing a definitive diagnosis in most LBP cases has given rise to the term “non‐specific lombalgy”, a condition which is considered benign. More than 85% have non‐specific back pain, which is defined as back pain that is not attributed to a specific known or recognizable pathology (e.g. infection, tumor, osteoporosis, ankylosing spondylitis, fracture, inflammatory process, root syndrome or equine tail syndrome).

Prognosis

According to the World Health Organization (WHO, 1998), CLBP results from the progression of unresolved acute LBP which can be caused by inflammatory, degenerative diseases, congenital changes, muscle weakness, osteo‐articular predisposition, as well as signs of intervertebral disc degeneration, among others.

In order to avoid the evolution towards chronicity, acute LBP should be properly valued and treated. The following risk factors must be taken into account in regards to the development of chronic LBP and delayed recovery: age; duration of the initial episode; duration of stopping work; relapses; hospitalization; low educational level; low level of resources; family dysfunction; previous history/previous history of depression and anxiety; poor working conditions; low qualifications and professional dissatisfaction; precarious employment; existence of conflict following an accident at work; inappropriate use of diagnostic and therapeutic resources; tobacco, alcohol or drug abuse; history of trauma; poor cardiovascular condition.

Clinical experience

In my practice I’ve found that chronic LBP develops more frequently in individuals who present with maladjusted coping strategies, functional limitations, poor general health, presence of psychiatric comorbidities, presence of non‐organic symptoms or who are in labor litigation.

For the detection of psychological risk factors that influence the prognosis, a set of signs known in the international literature as “yellow flags” are constituted.

1. Beliefs and inappropriate attitudes towards back pain;
2. Behavior of pain with exaggerated rest;
3. Labor problems or compensation process;
4. Emotional problems (depression, anxiety, tendency to isolation).

The identification of “yellow flags” should lead to appropriate cognitive‐behavioral follow‐ups. Psychosocial evaluation is generally advised in patients presenting with one or more of these yellow flags.

CLINICAL EVALUATION IN CONSULTATION

A simple and practical classification, proposed by the Agency for Health Care Policy and Research – USA, and which has gained international recognition, divides LBP into one of three categories – the so‐called “diagnostic screening”:

• Complicated backache (tumor, fracture, infection, equine tail syndrome)
• Lombalgy with sciatica (herniated disc)
• Non‐specific backache

This first observation (sufficient in most cases because most of our patients already tried everything in the conventional medicine and appear in the consultation in despair) should be aimed at excluding complicated back pain.

Finally, it should be noted that the clinical evaluation should also include an evaluation of psychosocial risk factors, which is predictive for the evolution to chronic complaints.

Did you know?

“According to the report “The state of health care quality 2015” by the “National Committee for Quality Assurance” (USA), approximately one quarter of patients with BP and aged between 18 and 50 have had imaging examinations for which they had no indication. It should be noted that inappropriate use of lumbar imaging can lead to irrelevant findings, unnecessary treatments and unjustifiable surgical interventions.

Joint guidelines of the American College of Physicians and the American Pain Society (2007) explicitly recommend that “Doctors should not routinely obtain images or other diagnostic tests in patients with non‐specific lower back pain…”

Osteopathy and BICOM®

Facing this reality, Osteopathy gets more and more fans because of its approach and results.

Osteopathy is a system and philosophy of health care that separated from traditional (allopathic) medical practice about a century ago. It places emphasis on the musculoskeletal system, hence the name  ́Osteo ́ refers to bone and ́path ́ refers to disease. Osteopaths also believe strongly in the healing power of the body and do their best to facilitate that strength.

Pain is the chief reason patients seek musculoskeletal treatment. Pain is a symptom, not a disease by itself. Of critical importance is first to determine the cause of the pain. Cancers, brain or spinal cord disease, and many other causes may be lying beneath this symptom. Once it is clear that the pain is originating in the musculoskeletal system, treatment, that includes manipulation, is appropriate.

My experience

As an osteopath and regardless of the great importance of osteopathy in CLBP, I had a few patients who didn’t have good results or the results were not lasting and this was the main reason why I started working with this combination: Osteopathy/ BICOM® bioresonance.

What I noticed was the huge increase in the success of treatments and lasting results.

Case 1

Chronic lower back pain for the past 3 years especially when waking up and at the end of the day.

Woman, 53 y/o

Mother of 2, 2 cesarean sections, divorced 10 years ago, entrepreneur

Medical history

Several consultations carried out by a family doctor, orthopedics (Lumbar MRI, CAT without relevant data)

Medication for the past 2 years: non‐steroidal anti‐inflammatories, painkillers, muscle relaxant)

Several treatments in physiotherapy.

In my consultation

Severe lumbar hypomobility with no reference to lower limbs.

Patient refers to constipation, insomnia (difficult to maintain sleep), extreme fatigue, lack of energy.

1st treatment

Observation

I could verify that the patient is in extreme difficultly when getting up from the chair

Treatment

Maintains medication

Osteopathy

Lumbar myofascial release

Scar myofascial release

BICOM® bioresonance

Basic therapy

Support elimination organs (liver and kidneys)

3017.0 Clear deep blockages

910.3 Eliminate scar interference (BRT oil OC)

3022.0 Blood circulation, regulate (BRT oil OC)

For vertebral blockage: 197.0 (CTT kit orthopedics, ampule O056), chip

Observation

Although the patient hasn’t said anything, I could see that she moves with less difficulty.

Supplementation

Start increase of water intake, Magnesium malate (1+1+1), melatonin (8 sub‐lingual drops when already in bed).

2nd treatment (1 week after)
Patient report
Patient mentions that she felt “lighter” but still has pain, however not so strong. Can sleep better but still wakes up several times during the night.
Treatment
Osteopathy
Visceral osteopathy abdominal cavity (very painful for the patient)
Harmonic techniques lumbar spine
Traction lumbar/sacrum
BICOM® bioresonance
Basic therapy
3066.0 Lymph activation
910.3 Eliminate scar interference (BRT oil OC)
To stabilize lumbar spine: 198.0 (CTT Kit orthopedics, ampule O032)
198.0 (CTT kit hormones, ampules Dopamine HON 009 + Serotonin HON 026)

3022.0 Regulate the blood circulation (BRT oil OC)
Observation
Patient refers that she feels “great”, still has pain but happier
Supplementation
Maintain the medication and the supplementation.

3rd treatment (1 week after)
Patient report
Diarrhea
Sleeps much better, during the week only took medication for 3 days

Refers to a decrease of 60% of pain.

Treatment
Osteopathy
Visceral osteopathy abdominal cavity.

Manipulation HVLA (High Velocity Low Amplitude) L4‐L5‐S1

BICOM® bioresonance

Basic therapy

3022.0 Regulate the blood circulation (BRT oil OC)

For vertebral blockage: 197.0 (CTT kit orthopedics, ampule O056)

To stabilize ligaments: 198.0 (CTT kit orthopedics, ampule O040)

Chip on the L4/L5 region

Observation

Patient reveals she has a totally different posture regarding life. “Now I have time to think about other things than my pain”

Patient started to do yoga, pilates.

Supplementation

Reduction of Magnesium because of the diarrhea (1+0+1) if diarrhea remains reduction to 0+0+1

4th treatment (2 weeks after)
Patient report
Doesn’t take any medication
Refers to a decrease of 80% of pain, restful sleep, feels very happy with life

Treatment

Maintain Magnesium (1+0+1) and melatonin

Osteopathy

Myofascial diaphragm

Manipulation HVLA T12

BICOM® bioresonance

Basic therapy

3017.0 Clear deep blockages

To stabilize ligaments: 198.0 Test program (CTT kit orthopedics, ampule O024) (BRT oil OC)

To stabilize muscles: 198.0 (CTT kit orthopedics, ampule O039) (BRT oil OC)

Observation

No reference of pain, great lumbar mobility.

5th treatment (1 month later)

Patient report

Feels like a new person, no medication, no LBP, restful sleep, decrease of melatonin (4 drops) and has a new boyfriend.

Treatment
BICOM® bioresonance
Basic therapy
To stabilize ligaments: 198.0 (CTT kit orthopedics, ampule O024) (BRT oil OC)

951.1 Blockage in tissue
3036.0 Regulate detoxication
Observation
Every 3 months she makes a follow up treatment.
Supplementation
Maintain magnesium 1+0+1, melatonin (4 drops)

Case 2

Chronic lower back pain for the past 2 years after hernia surgery (L4/L5)

Male, 62 y/o, bank accountant, retired, married, 1 daughter

Medical history

High blood pressure (medicated)

Stopped taking medication after several attempts.

Hernia surgery 2 years ago

Pain on palpation L3‐L4‐L5 region with associated hypomoblity

Has a good quality of sleep

When he wakes up, needs to stay sat in bed before getting up because of the pain.

Pain is worse when he needs to start moving after a few minutes of being in a standing position

Small swelling in L4/L5/S1 area

1st treatment
Osteopathy
Myofascial release LB
Harmonic techniques lumbar spine

Gentle traction L4‐L5‐S1

BICOM® bioresonance

Basic therapy
Support elimination organs
For lumbar anesthesia: 197.0 (CTT kit orthopedics, ampule O055) (BRT oil OC)

3037.0 Inflammations (Input: pain area) (chip)
197.0 (CTT kit orthopedics, ampule O051) (BRT oil OC)
Chip on pain area
Observation
At this point nothing has changed except that the patient feels tired.

2nd treatment (1 week after)

Patient report

2 days of diarrhea after treatment and felt extremely tired, the pain was worse in those two days but started to improve after that and now he has no pain.

Osteopathy

Myofascial release psoas

Harmonic technics LB

BICOM® bioresonance

Basic therapy

For vertebral blockage: 197.0 (CTT kit orthopedics ampoule O056) (BRT oil OC)

3086.0 Oxygen regulation (chip)

3125.0 Cell regeneration, chronic (chip)

Solar Plexus Chakra: 970.2 Chakra therapy for 1st to 3rd chakra (3 min) + CH2 Mineral: citrine

Observation

Patient returned for follow up 6 months later with no complaints.

Case 3 (special case)

This patient has had CLBP (since forever he said). However he came to my clinic with an acute LBP for the past 2 days.

Male. 58 y/o, lawyer, divorced, 1 son

Medical history

Patient doesn’t remember when started to have LBP, acute LBP for the past 2 days during sleep.

In severe pain with every move he makes, highly depressive, dyspepsia. Takes painkillers every day, gastric protector, multivitamin for the brain.

After talking with the patient we could find a timeline to discover when the LBP started and he says that after the divorce everything got much worse. (10 years ago)

1st treatment

Osteopathy

Myofascial release diaphragm

Sacrocraneal therapy pelvic diaphragm

BICOM® bioresonance

Basic therapy

Support the elimination organs (liver, kidneys)

Solar plexus Chakra: 3,3 Hz; H 1,2; Di 7,0; 4 min (according Dr. Hennecke and Mrs. Ma‐ quinay‐Hennecke ) (BRT oil OC)

Root Chakra: 970.2 Chakra therapy for 1st to 3rd chakra (3 min) (BRT oil OC) 198.0 (CTT kit orthopedics, ampoule O045) + CH2 Tryptophan ampule (CTT kit orthomolecular substances, ampule OS048) (chip)
For shock: 197.0 (CTT kit orthopedics, ampule O053) (chip)

3017.0 Clear deep blockages + CH2 MSM ampule (CTT kit orthomolecular substances, ampule OS056)

Observation

Patient is still in severe pain however he mentioned that he feels strange, nausea, slight vertigo but able to walk by himself.

Advice

Water intake, avoid milk

2nd treatment (1 week after):

Patient report

Patient refers to hot flashes 1 day after, he kept taking painkillers and feels better. The pain he feels is the one that he has for the past 10 years, mentions that it is slightly better regarding dyspepsia

Treatment

Osteopathy

Although he says is better he still has a lot of difficulty with all movements.

Harmonic technics lumbar spine

Myofascial release sacrum area

HVLA ilium (bilateral)

HVLA L4/5

BICOM® bioresonance

Basic therapy

951.1 Blockage in tissue (BRT oil OC)

3036.0 Regulate detoxication + CH2 MSM ampule (CTT kit orthomolecular substances, ampule OS056) (BRT oil OC)

Throat Chakra: 940.1 Chakra therapy for the 5th to 7th chakra (3 min) + CH2 mineral: azurite‐chrysocolla

Solar Plexus Chakra: 970.2 Chakra therapy for 1st to 3rd chakra (3 min) + CH2 mineral: citrine

Observation

Patient refers that he feels sad but with more movement and less pain

Advice

Maintain water intake, avoid milk

3rd treatment (2 weeks after)

Appointment should take place one week after but patient cancelled and reschedule one week after.

Patient report

Refers that he cancelled because started to feel much better and wanted to try if things would keep improving without treatment. After the treatment he cried without reason (he said…). In two weeks only took painkillers 3 times.

When sitting in the chair, did it with almost no pain and very easily.

Treatment

BICOM® bioresonance

Basic therapy

3086.0 Oxygen regulation + CH2 Adrenal gland ampule (CTT kit hormones, ampule HON036) (chip)

Splenic Chakra: Mineral: fire opal, 970.2 Chakra therapy for 1st to 3rd chakra (3 min) + CH2 Dopamine ampule (CTT kit hormones, ampule HON009), Tryptophan ampule (CTT kit orthomolecular substances, OS048) (BRT oil OC)

To stabilize lumbar spine: 198.0 (CTT kit orthopedics ampoule O032)

Observation

Patient refers that he feels younger, lighter and even in court he has more energy to fight for the client.

We made an appointment for one month later for follow up but he canceled few days before. What I know is that some days later I saw him jogging just like a normal healthy person.

In conclusion

We can’t just use “one size fits all” for the same condition. Every patient is a challenge and looking beyond what they say, looking the way they move, behavior, speech, their life history, their energy, is needed for the success of the treatment.

We cannot be responsible for what they do in their lives but we are responsible to help them as best we can from “our side” and make them trust that we do our very best in our job. They need to understand every single touch, and move we make. Explaining this for them and telling them what we are doing makes the cells “understand” better.

For that we have a huge tool – the BICOM® optima.

I have to say that I presented only 3 cases. I could also present many more regarding other pathologies but these were cases that were extremely difficult because the patients were desperate and hopeless, just wishing that something could take that pain away. And here BICOM® is a success by itself and is also very powerful in conjunction with other medical specialties.

Thank you for your time.

Torsten Hartmeier, Naturopath, Lübbecke, Germany

All of us are afraid sometimes. Fear can actually help protect us by alerting us to potentially dangerous situations. There are times, however, when fear runs amok and permanently disrupts our daily lives long term.

Take a moment and imagine what life would be like for anxiety sufferers if they were no longer anxious. It is not difficult for us as therapists to imagine that overcoming anxiety would significantly change the lives of anxiety patients for the better.

All of us have to face our fears at some point. How we deal with our fears determines whether we experience our lives as an exciting adventure or whether we are trapped in our fears.

The question is: Where do fears come from in the first place?

Neuroscientists claim that we humans are the most anxious creatures on the planet. This is because we can learn with our mind, think with it, and also create fear with it (in the amygdala).

Furthermore, these experts say that the anxious feeling we have when we are afraid is a standard biological response. They are more or less the same body signals (activation patterns) whether we’re afraid of being bitten by a dog, being rejected on a date or being audited by the tax office. Fear, like all other emotions, is basically information, nothing more – but also nothing less.

Although the biological reactions that take place in the body are always the same, a distinction can be made between the following manifestations of anxiety disorders: panic disorder, generalised anxiety disorder and phobias. Phobias can be divided into agoraphobia, social phobias and specific phobias.

The physicist and successful author Dr Karl Albrecht postulates 5 basic fears upon which all other fears are built.

1. Extinction – the fear of annihilation, the fear of death. The fear of ceasing to exist. The thought of being no more arouses an existential fear in all people.
2. Mutilation – the fear of losing a part of our body (amputation, accident); the thought that the boundaries of our body will be violated; or the health of an organ. Fear of animals like beetles, spiders, snakes and other creepy things comes from fear of mutilation. A similar fear is observed in elephants when they sleep at night. They are afraid of small animals or insects creeping into their trunk. Hence the joke about elephants and mice.

3. Loss of autonomy – the fear of being immobilised, paralysed, restricted, over‐whelmed, locked up, confined, or otherwise controlled by circumstances beyond our control. In physical form, it is commonly known as claustrophobia, but it also extends to our social interactions and relationships.
4. Separation – the fear of being abandoned; rejection and loss of commonalities; being seen as persona non grata – not wanted, respected or valued by anyone else. “Silent rejection”, when imposed by a group, can have devastating effects on human behaviour.
5. Ego death – the fear of humiliation, profound disapproval, loss of integrity of the self.

Topics we will cover in this presentation

In this presentation we will look at the aspect that anxiety in particular can have a somatic trigger and look at possible alternatives for support. We will not delve into conventional medical methods, procedures and therapies. You can find enough information on those on the Internet.

We will address the following points in particular:

• How we can distinguish anxiety from ordinary worry.
• What symptoms can occur with anxiety.
• What changes you should clarify at the structural/organic level.
• Possible causes/triggers.
• Anxiety and possible comorbidities.
• Neurotransmitters/hormones and fears.
• Possible effective supplements.

How to distinguish fears and worries well – the 7 cues

Cue 1: Worry is specific. Anxiety is vague.

Worries are based on realistic concerns that are specific and can be named.

Fear, on the other hand, is fear of the general “unknown”. Fear usually cannot be named or explained by someone who experiences it.

Cue 2: Worry makes us want to fix the problem. Anxiety causes paralysis.

Because worries are based on specific and often realistic concerns, we respond accordingly. We would like to fix the problems and eliminate the cause of our concern. This is also successful in most cases.

Fear does just the opposite. People with anxiety are unable to pinpoint the reasons for their fears. This creates an inability to take appropriate countermeasures. Many patients also report feeling paralysed and unable to take action. Since people like to be in control, sufferers often adopt compulsive behaviours in order to have at least some degree of control over themselves.

Cue 3: Worry causes mild emotional reactions. Anxiety causes severe emotional reactions.

Worry is a natural human reaction. There is no way humans would have survived this long if we had no “concerns”. This only leads to a minimal emotional reaction, as we are still able to fight against our worries.

Those who struggle with chronic and unconscious anxiety exhibit over‐reactive emotional responses to their environment and circumstances. This hinders their ability to take action against whatever is causing the anxiety.

Cue 4: Worry is controllable. Anxiety controls you.

Precisely because worry is a natural human reaction, we can use our consciousness to control that worry, meaning that we can control the emotions that arise from that.

Anxiety, however, is very different. Because chronic anxiety or fear occurs outside of our cognitive awareness, we cannot take full responsibility for our responses to it. Anxiety manifests itself unconsciously and controls our body’s physical reactions to it without it being aware of what is causing it.

Cue 5: Worry is relatively temporary. There’s no time limit to fear.

Because worry is based on realistic concerns, it is primarily temporary. It motivates us to act so that we can eliminate the cause in a timely manner. The more disciplined we are about it, the sooner we are free from worry.

Anxiety that is chronic and disordered is a common fear of the unknown and is difficult to explain. Since anxiety is hard to name and almost impossible to fix, it can last for days, weeks or months. Fear that lasts overnight is most likely a sign of chronic or disordered anxiety.

Cue 6: Worry takes place in the mind. Anxiety manifests itself in the body.

As we have already mentioned a few times, worry is a cognitive response in the mind. When explaining what is causing concern, there is usually a linear and logical explanation that can be communicated verbally and lead to the timely resolution of the concern.

A chronic, generalised anxiety disorder triggers permanent physical reactions. This can lead to a significant restriction of our normal daily routine.

Cue 7: Worry does not negatively impact our personal or professional functions. Anxiety interferes with our ability to function normally.

Worry is usually a reaction to a problem. Outside of this concern, we function normally and without limitations. This means that although worry may preoccupy us, they allow us to lead a normal life to a large extent without losing our head.

Anxiety – even if sufferers have no idea what is causing it – affects our ability to function normally. Those who struggle with chronic anxiety cannot concentrate, are often tired to the point of CFS (chronic fatigue syndrome). Fear always means worst case scenarios. It is the brain’s coping mechanism, which has to fight against it permanently and causes the exhaustion.

Certain centres in our brain are involved: the limbic system and the amygdala are responsible for processing emotions and storing them. According to scientists, these two centres are overactive in people with anxiety, worry and distress. In addition, the balance of certain messenger substances (neurotransmitters) in the brain seems to be disturbed. The so‐called abdominal brain (gut‐brain axis) can no longer process information properly, either.

What are the symptoms of anxiety?

What are the common physical symptoms?

➡Panic attacks ➡Tachycardia ➡Chest pain ➡Heart palpitations ➡Headache ➡Breathing difficulties ➡Extreme sweating ➡Stomach problems ➡Nausea ➡General fatigue ➡Dizziness ➡Sleeplessness ➡Butterflies in the stomach ➡Difficulty swallowing

In many cases, emotional and psychological symptoms are added, which are even more difficult to bear:

➡Constant fear and anxiety of impending doom ➡Depression ➡Agoraphobia ➡Sudden panic attacks ➡Irritability ➡Feeling of going crazy and/or losing control ➡Feeling of being left alone and restless ➡Feeling helpless and not normal ➡Social phobias ➡Nightmares and anxious thoughts ➡Fear of being abandoned by partner ➡Existential fears ➡Jealousy

Anxiety and possible comorbidities.

➡Bipolar disorder ➡Bulimia ➡Depersonalisation ➡Depression ➡Claustrophobia ➡Hunger craving ➡Globus hystericus ➡Sleeplessness ➡Misophonia (“hatred of sound”) ➡Night terrors ➡Cryptopyrroluria (KPU) ➡Psychosis ➡PTSD ➡Anger attacks ➡Suicidal thoughts ➡Trichotillomania

Anxiety and possible comorbidities.

➡Asthma ➡General and chronic pain ➡Bedwetting ➡CFS (chronic fatigue syndrome) ➡Haemochromatosis ➡Hypertension ➡MCS (multiple chemical sensitivity ➡Recurrent tonsillitis (CAVE: PANDAS) ➡Weight gain

What is PANDAS?

The acronym PANDAS stands for paediatric autoimmune neuropsychiatric disorders associated with streptococcal infections. It is considered a subcategory of paediatric acute‐onset neuropsychiatric syndrome (PANS). It describes a neuropsychiatric syndrome that is now widely recognised and has already been successfully reproduced in animal experiments. In childhood and adolescence, infections with group A β‐haemolytic streptococci lead to the sudden onset of neuropsychiatric symptoms that, if left untreated, can take a long‐term, chronic course. Source: Wikipedia

At the structural/organic level, you should always clarify the following possible causes:

1. Changes in the area of the cervical spine can often cause massive anxiety due to irritation of the nerve and/or blood vessels running there.
2. Uncontrolled blood sugar fluctuations, hypoglycaemia and insulin resistance can cause anxiety. The first studies on this subject were carried out as early as the 1960s. Blood sugar fluctuations and spikes, often not detected by HbA1c, can cause anxiety, depression, insomnia, tremors, tachycardia, dizziness, and forgetfulness.

Reducing refined carbohydrates can lead to an immediate improvement. (Source: Salzer, H. Reactive hypoglycemia and neuropsychiatric illness. J Natl Med Assoc. 1966 Jan; 58(1): 12– 17. PMCID: PMC2611193)

According to a 2016 case report, a dietary change adding more protein, fat, and fibre can improve anxiety, mood, concentration, energy and blood sugar problems in a patient with generalised anxiety and hypoglycaemia. When subjects returned to their dietary habits of refined carbohydrates, it triggered anxiety, and the symptoms returned. (Source: Gangwisch, JE, Hale, L, Garcia, L, Malaspina, D, Opler, MG, Payne, ME, Rossom, RC, Lane, D. High glycemic index diet as a risk factor for depression: analyses from the Women’s Health Initiative. Am J Clin Nutr. 2015 Aug; 102(2): 454–463. PMID: 26109579 Source: Aucoin, M. Bhardwai, S. Generalized anxiety disorder and hypoglycmia symptoms improved with diet modification. Case Rep Psychiatry. 2016; 2016: 7165425. PMID: 27493821)

1. Thyroid dysfunction directly affects your mental health and can cause anxiety as well as full‐blown depression. Just think of hypothyroidism in old age in this context, which can perfectly copy depression.
2. Heart disease (CHD; ACS) and respiratory diseases (e.g. COPD) can trigger anxiety, which often becomes chronic simply because of the seriousness of these clinical pictures. In such cases, the underlying disease must be addressed first so that the anxiety can be effectively treated.
3. CAVE: alcohol consumption/drug abuse. Substance abuse should always be considered so that these individuals can be referred to the appropriate services.
4. Diseases of the nervous system, such as MS or Parkinson’s disease and others, are often accompanied by anxiety and should be treated quickly.
5. Exposure to electrosmog/Wi‐Fi/G5 and geopathic stress should always be tested and, if positive, addressed accordingly.
6. Hormonal disorders (e.g. pheochromocytoma, progesterone) also cause anxiety, which can be treated well with the BICOM device and accompanying measures.

Laboratory results

Blood count, blood sugar, electrolytes (Ca++, K+), thyroid status (TSH), ECG with rhythm strip. Lung function, cranial imaging (MRI, cCT), EEG only if specifically suspected.

What you should test and check

Anxiety and the gut‐brain axis

It is not surprising that dysfunction of the gut‐brain axis can trigger anxiety. The easiest way to understand the connection between your intestine and your brain is to think of a time when you felt nervous before a presentation, exam, important meeting or other event. You may have felt butterflies in your stomach, nausea, abdominal pain, or even diarrhoea. As you can see, psychosocial factors can affect your gut and physiology, leading to inflammation and movement of your GI tract. Conversely, compromised gut flora can affect your mood and brain health and trigger anxiety (Source: https://www.health.harvard.edu/diseases‐and‐conditions/the‐gut‐brain‐connection).

How the gut‐brain axis works

Your gut and brain communicate through the gut‐brain axis. Communication can take place via nervous (spinal cord), vagal (vagus nerve) and hormonal (e.g. GABA, trypto‐ phan) pathways.

Disruptions in the microbiome and this gut‐brain axis can lead to a range of cognitive dysfunctions and mood disorders, including anxiety, depression, obsessive‐compulsive disorder, attention deficit disorder (ADD), sensory processing disorder, autism, Parkinson’s disease, dementia, and Alzheimer’s disease.

A 2016 scientific report discussed that the microbiome has bidirectional effects on mood via the gut‐brain axis. A pathologically altered microbiome can trigger anxiety and lead to symptoms such as mood swings. Conversely, anxiety can also negatively affect the microbiome. A 2017 scientific review found that intestinal malabsorption and inflammation can trigger anxiety, depression, and other common mental illnesses. *Psychobiotics can help relieve anxiety and depression by restoring normal microbial balance. A 2019 review showed that probiotic supplements, probiotic‐rich foods, and a nutrient‐dense diet can help “reboot” the gut microbiome and lower anxiety symptoms (sources: Clapp, M, Aurora, N, Herrera, L, Bhatia, M, Wilen, E, Wakefield, S. Gut microbiota’s effect on mental: the gut‐ brain axis. Clin Pract. 2017 Sep 15; 7(4): 987. PMID: 29071061 Liu, L, Zhu, G. Gut‐brain axis and mood disorder. Frontline Psychiatry. 2018; 9: 223. PMID: 29896129 Yang, B, Wei, J, Ju, P, Chen, J. Effects of reg‐ ulating intestinal microbiota on anxiety symptoms: a systematic review. Gen Psychiatr. 2019 May 17;32(2). PMID: 31179435).

*Psychobiotics is a term used in preliminary research to refer to live bacteria that, when ingested in appropriate amounts, can provide psychological benefits by affecting the microbiota of the host organism.

Neurotransmitters

Glutamate‐GABA imbalance can trigger anxiety

Neurotransmitters are biochemical substances that transmit, amplify or modulate stimuli from one nerve cell to another nerve cell or cell. It is important that they remain balanced to keep a person’s mood and mental health stable. Neurotransmitters such as gamma‐aminobutyric acid (GABA), glutamate, dopamine, serotonin, and norepinephrine are responsible for regulating your emotions and various functions of your body.

It has been shown that they can cause anxiety and other mood swings if they are mismatched. Glutamate and GABA account for 90 percent of all neurotransmission in your body. They are responsible for regulating the emotional response to potentially threatening stimuli that can trigger fear.

A 2015 study showed that a GABA imbalance can trigger anxiety, and balance can help relieve anxiety. A 2010 peer‐reviewed study discussed the importance of examining glutamate‐GABA imbalance. (Sources: Wieronska, JM, Stachowicz, K, Nowak, G, Pilc, A. The loss of glutamate‐GABA harmony in anxiety disorders. Link here. Nuss, P. Anxiety disorders and GABA neurotransmission: a disturbance of modulation. Neuropsychiatr Dis Treat. 2015; 11: 165–175. PMID: 25653526).

Glutamate and GABA balance

Glutamate is the main excitatory (energising, stimulating) neurotransmitter in your body. It is involved in every nerve pathway in your body, including those that can affect, relieve, or trigger anxiety. The N‐methyl‐D‐aspartate receptor (NMDA) is an important glutamate receptor and ion channel protein in neurons relevant to anxiety. A balanced ratio between glutamate and GABA is therefore particularly important. (Source: Myers, KM, Carlezon, WA Jr, Davis, M. Glutamate receptors in extinction and extinction‐based therapies for psychiatric illness. Neuropsychopharmacology. 2011 Jan;36(1):274‐93. PMID: 20631689).

GABA is the main inhibitory neurotransmitter that can help relieve anxiety. For this reason, doctors often prescribe barbiturates or benzodiazepines, which can increase GABA and relieve anxiety. However, these drugs do not bind to GABA receptors and can also lead to increased tolerance levels, addiction, poisoning and serious or even fatal side effects.

The neurotransmitters serotonin and GABA

Low serotonin levels are more likely to lead to mental discomfort (increase in anxiety, “mental projector”). Low levels of GABA tend to lead to more physical reactions.

Symptoms of serotonin deficiency

Anxiety, panic attacks or phobias, feeling worried or anxious, obsessive thoughts or behaviours, perfectionism or excessive need to control, irritability, anxiety that is worse in winter, winter blues or seasonal affective disorder, negativity or depression, suicidal thoughts, excessive self‐criticism, low self‐esteem and confidence, PMS or menopausal symptoms, sensitivity to hot weather, hyperactivity, anger or rage, digestive problems, fibromyalgia, TMJD or other pain syndromes, difficulty falling asleep, insomnia or sleep disturbances, cravings for carbohydrates, alcohol, or drugs in the afternoon or evening.

Symptoms of GABA deficiency

Feeling anxious or fearful, panic attacks, not being able to relax or loosen up, stiff or tight muscles, feeling stressed and burnt out, craving carbohydrates to relax and calm down, craving alcohol to relax and calm down, craving drugs to relax and calm down – these cravings are felt physically, insomnia, flood of thoughts, inability to prioritise planned actions, acrophobia (fear of heights), poor focus, rectal cramps/flaking sensation in anus, burning mouth/tongue, irritable bowel syndrome.

Symptoms of a deficiency of catecholamines (adrenaline, noradrenaline, dopamine)

Depression and apathy, easily bored, lack of energy, lack of focus, lack of drive and low motivation, attention deficit disorder, procrastination and indecision, cravings for carbohydrates, alcohol, caffeine or drugs for energy.

Symptoms of endorphin deficiency (“endogenous morphins”)
Increased sensitivity to emotional pain, increased sensitivity to physical pain, tearful, eating as a mood lifter/consoler, cravings for certain foods, behaviours, drugs or alcohol.

Symptoms of low blood sugar

Daytime cravings for sugar, starch or alcohol, irritable, shaky, headaches – especially if the intervals between meals are too long, intense craving for sweets, feeling light‐headed if meals are missed, leaden fatigue improves with a meal, agitated, easily angered, nervous.

Anxiety and hormone deficiency – often forgotten

Frequently tested programs

Adrenaline release (10006), energy deficiency (10045), adult nerve dampening (10110), CNS disorders (10194), depression (test individually), serotonin (841.0), (980.5), vegetative dysregulation (960.4), shock treatment acute (3093.0), stress relief (3084.0)

In this context, BICOM® chips have proven to be extremely valuable in the therapy of anxiety and should always be used.

Possible effective supplements.

Palm phobia technique

No external training necessary – all immediately actionable information available on the Internet. In case of clearly defined anxiety and in combination with the BICOM, an extremely effective form of therapy, with a success rate of over 70%

Gentle stimulation of the acupuncture point lung 1 on the left side of the body (Source: Youtube video of Dr Uso Walter)

The emotion code

A very good way of quickly and successfully detaching negative emotions from the body. The respective emotions are energetically detected and then specifically released. Can also be learned autodidactically. The book title is: “Der Emotionscode: So werden Sie krank machende Emotionen los” (The Emotion Code: How to get rid of emotions that make you sick (German)) Paperback.

Anxiety is a feeling caused by our anticipation of an imaginary event or experience.

Final thoughts

Anxiety is the body’s natural response to stress. However, frequent, excessive and persistent anxiety can seriously affect the lives of sufferers and affect their overall health.

Bioresonance gives you a tool with which you can provide active and effective support. Because harmonising destructive, emotional and mental oscillations is a basic prerequisite for health and well‐being.

Dr. Jörg Schweikart, Economist, Nutritionist, Alternative Practitioner, Berlin, Germany

Introduction

Vitamin D deficiency is perhaps the most widespread vitamin deficiency in the world. Leading researchers in the field refer to this as a hidden epidemic that may lead to hundreds of thousands of premature deaths worldwide each year. A study conducted in Germany came to the conclusion that about 18,000 lives could be saved in Germany alone if the official bodies could decide to recommend vitamin D supplements generally. [1, 2]

The importance of vitamin D has come into sharper focus in the wake of the COVID‐19 pandemic, when numerous studies from around the world have consistently shown that the risk of contracting COVID‐19 and the risk of a severe progression correlate directly with vitamin D levels. [3, 4] Again, it is believed that widespread supplementation in the population could have saved tens of thousands, perhaps hundreds of thousands of lives. At‐risk groups in particular can be protected by vitamin D, as trials in retirement homes have impressively shown. [5]

However, vitamin D does not only show enormous potential with regard to viral infections. Vitamin D3 does not act like an ordinary vitamin in the body, but is converted into a hormone that controls about 2000 genes in the human body. In particular, it is not only one of the central control hormones of bone metabolism and the immune system, but also has far‐reaching effects on the nervous system, the cell cycle and many other important areas of health.

Vitamin D is primarily a preventive nutrient. Unlike some other nutrients, there have been few acute uses of vitamin D, such as in the treatment of viral diseases and autoimmune disorders. However, vitamin D can play a more central role in preventing a whole range of diseases and has far‐reaching systemic and long‐term effects.

In this presentation, I would like to show you an understanding of the mode of action of the hormonal vitamin D system, provide you with orientation as to how current findings on vitamin D are to be classified, and which questions are as yet unanswered.

Vitamin D deficiency

Vitamin D is an unusual vitamin in two ways. First, as already described, it is not so much a vitamin as a hormone precursor. The body uses vitamin D to produce the hormone calcitriol, which is very similar to our body’s own steroid hormones.

Secondly, we rely on the sun, not food, for our supply of vitamin D. Vitamin D is the only known nutrient that is formed by exposure of the skin to sunlight and for which food sources play virtually no significant role. This means that sunlight, like water and solid food, is indeed one of our basic daily needs.

It is therefore easy to explain the widespread prevalence of vitamin D deficiency, which can affect up to 80% of the population, as studies have shown. [6–8] Not only do we avoid the sun virtually all day due to our modern lifestyles, but in areas of northern Europe, sunlight is also too low during the winter months to stimulate vitamin D production at all. [9]

North of Rome, significant production of vitamin D only takes place between March and October, and only between about 10 am and 4 pm. Since these times of day correspond to most people’s working hours, the majority of people do not get enough sunshine to meet their vitamin D needs almost all year round. [10]

We need to remember that while our lifestyle has changed radically over the last 1000 years, our biology has not. Our bodies are still adapted to a life in subtropical regions and a lifestyle that we can only observe today among very few indigenous peoples: abundant sunshine with most of the time spent outdoors, plentiful exercise and very light clothing that usually leaves more than 70 per cent of the skin directly exposed to sunlight.

Our modern way of life is virtually the complete opposite of the lifestyle to which we are biologically adapted. This leads to significant problems in many areas, and vitamin D deficiency is one of them.

The vitamin D system

Vitamin D is a hormone precursor and is metabolised in the body in various conversion steps to become an active hormone. There are three main forms of vitamin D that are central to this system:

• The vitamin form: vitamin D3 (cholecalciferol)
• The transport form: 25‐hydroxyvitamin D3 (calcidiol)
• The hormone form: 1,25‐dihydroxyvitamin D3 (calcitriol)

In addition to these three forms of vitamin D, however, there are a number of other components in this system:

• Special enzymes that convert vitamin D into its active form or break it down.
• The vitamin D receptor on the cells by means of which vitamin D develops its effect.
• Messenger substances and hormones such as PTH (parathyroid hormone), which regulate the conversion.
• A number of important micronutrients as cofactors.

Like all hormones, vitamin D is subject to a complex regulatory system, which we will take a closer look at presently.

However, to make matters even more complicated, vitamin D works in two fundamentally different ways:

1. The endocrine route

   In this case, conversion of vitamin D takes place centrally in the liver and kidneys. This pathway is tightly regulated by calcium and various hormones and messenger substances.

2. The autocrine / paracrine route

   Here, conversion takes place independently and individually directly in the cells and is controlled by local events in the affected tissue.

The endocrine route

The better known of the two pathways is the endocrine vitamin D system, which primarily serves to regulate calcium levels and bone metabolism.

With the endocrine pathway, vitamin D formed by the sun is converted in a first step in the liver to the transport form 25‐hydroxy‐vitamin D3 (25‐OH‐D3), most of which binds to the transport molecule DBP and thus circulates through the body. In a second step, the active vitamin D hormone calcitriol is finally formed from this circulation form in the kidney.

Both conversion steps are subject to hormonal regulation, which depends on calcium concentration in the blood and is controlled by the parathyroid hormone. The regulation is dramatically shortened as follows: if the calcium level in the blood drops, more parathyroid hormone is released. This ensures a higher conversion of vitamin D to the active hormone calcitriol. By binding to the VD receptor, calcitriol on the one hand causes increased calcium absorption in the intestine and at the same time reduces the secretion of the parathyroid hormone. [11]

The amount of active vitamin D hormone is hence controlled in this case – through a diversion via the parathyroid hormone – by the level of calcium and magnesium in the blood.

All the components of the endocrine vitamin D system, however, in turn depend on cer‐ tain nutrients as cofactors. Recent research shows that, in the absence of these cofactors, vitamin D is not only ineffective, but can also have negative consequences such as chronic inflammation. [12]

The reason why this is explained below.

Vitamin D and magnesium

Vitamin D must first be converted by the body in various metabolic steps before it can become effective. This conversion requires special enzymes that only function when sufficient magnesium is present.

Vitamin D metabolism therefore comes to a complete standstill at eight points if insufficient magnesium is available. [13]

A review paper from 2019 recently summarised these relationships very well, concluding [14]

“Magnesium is essential for the metabolism of vitamin D, and taking large doses of vitamin D can lead to severe magnesium depletion. Adequate magnesium supplementation should be considered an important aspect of vitamin D therapy.”

Vitamin D ineffective without magnesium

Fortunately, this correlation is receiving increasing attention from the scientific community. [15–17] A number of studies have shown that it is very difficult to correct vitamin D levels by taking vitamin D supplements when there is a magnesium deficiency. [18– 21]. When there is a magnesium deficiency, the vitamin form simply cannot be processed into the other forms and remains ineffective.

Conversely, it was possible to improve vitamin D levels by correcting a magnesium deficiency without taking any greater amount of vitamin D. [18, 22, 23]

These results testify to the central importance of magnesium for vitamin D metabolism.

Magnesium deficiency due to high doses of vitamin D

However, the connection works in both directions. Vitamin D remains partially ineffective without magnesium, but the intake of high‐dose vitamin D can conversely also lead to a magnesium deficiency.

This has far‐reaching consequences, as magnesium is an absolutely central nutrient for almost all functions of the body. Magnesium is essential for more than 600 enzyme systems and thus plays a key role in our metabolism.

That’s why Dr Carol Dean, in her best‐selling book “The Magnesium Miracle”, warns against taking vitamin D without magnesium. [24]

“Vitamin D can over‐consume magnesium, block and displace magnesium, lead to excessive calcium intake, (which promotes calcification) and can drive people into magnesium deficiency.”

The conclusion from these studies is that vitamin D should always be taken together with magnesium if magnesium status is unclear.

Boron – The neglected trace element with a great effect

The trace element boron also has an effect on hydroxylases – but this time on the de‐ grading enzymes that in turn destroy the vitamin D storage form. It is only when both the formation and breakdown of 25‐hydroxy‐vitamin D3 take place in a controlled manner that the body can properly regulate vitamin D levels. A sufficient amount of boron is necessary here to avoid excessive decomposition of 25‐OH‐D3. [25] Similarly, it is important to prevent too high a calcitriol value or an unfavourable ratio between calcidiol and calcitriol.

Vitamin D and calcium

One of the central tasks of vitamin D is the regulation of calcium absorption in the intestine. The active vitamin D hormone promotes the absorption of calcium, and the higher the level of active vitamin D, the higher the rate of calcium.

This regulation takes place via the so‐called parathormone. A fall in calcium levels in the blood leads to an increase in the release of parathyroid hormone. This results in increased conversion of vitamin D into its hormone form, which in turn increases calcium absorption in the intestine.

This regulatory mechanism can lead to problems when too much, but especially when too little, calcium is ingested. When vitamin D is taken in high doses and at the same time calcium intake is insufficient, the active vitamin D hormone will be greatly up‐regulated. The high level of vitamin D and the greatly increased parathyroid hormone cause levels of the active vitamin D hormone to rise and remain elevated over a long period. Since no calcium can be absorbed in the intestine as none is supplied in food, vitamin D levels do not return to normal, but instead remain chronically elevated.

So with a calcium deficiency and at the same time high vitamin D substitution, we have a very high level of parathormone and at the same time a very high level of active vita‐ min D hormone. This has more negative than positive consequences.

1. It promotes calcium absorption in the intestine,
2. It dissolves calcium from the bones,
3. It increases the influx of calcium into cells. [11]

A positive effect is the stimulation of calcium absorption in the intestine. On the negative side, however, the body begins to dissolve calcium from the bones and this despite the fact that vitamin D is taken in high doses.

What is even more worrying, however, is the fact that the high level of active vitamin D also increases calcium influx into cells. This leads to severe cellular inflammation in the long run. At the same time, cells also begin to pump magnesium and potassium outwards to maintain intracellular electrolyte balance, resulting in intracellular potassium and magnesium deficiency, even when sufficient magnesium is present.

It is therefore important to take sufficient calcium during a high‐dose vitamin D therapy, as otherwise the active vitamin D in the blood increases too much, which paradoxically leads to bone damage and chronic inflammation, although vitamin D actually has a positive effect on bones and inflammation.

Since magnesium also regulates PTH levels, it is important to ensure that both minerals are supplied in a calcium‐magnesium ratio of 1:1 to 2:1. A balance of magnesium and calcium is necessary in order to regulate the parathormone in a reasonable way and to achieve a healthy vitamin D status. [26]

Practice has shown in this case that there is an ideal ratio of active vitamin D hormone to 25‐OH‐D3, which can only be correctly adjusted through the simultaneous admin‐ istration of vitamin D, calcium and magnesium. [12]

Zinc and vitamin D

Vitamin D acts via a special vitamin D receptor (VDR) to which the active vitamin D docks, thereby mediating its effects on cells. An essential component of this VDR is a zinc molecule. The formation and function of the VDR can be impaired if zinc is deficient. Cell tests have shown a clear dose‐dependent increase in vitamin D activity as a result of zinc supplementation. [27]

Vitamin A

Vitamin A and vitamin D are antagonists as well as cofactors. This is because activated VDR does not work alone, but combines with the RXR receptor activated by vitamin A to form a so‐called heterodimer. It is only when this compound is present that some of the effects of vitamin D become possible. [28–32] When vitamin A is deficient, VDR cannot exert its full effect despite activation by vitamin D. In this case, we also speak of a vitamin A‐induced receptor blockade, although it is actually not the receptor that is blocked, but only its effect. This can lead to similar problems as discussed above. Due to the lack of effect, the regulating feedback in the regulatory loop remains absent and the vitamin D hormone remains at a high level over an extended period.

At the same time, vitamin D and vitamin A are also antagonists. Both vitamins activate the retinoic acid receptor (RAR) and are in direct competition. A balance of these two vitamins is therefore crucial in order to maintain a healthy regulation of the vitamin D system.[32–34]

Vitamin K2

Lastly, it is imperative to mention vitamin K2. Although this vitamin plays no direct role in vitamin D metabolism itself, it does play a role in calcium metabolism. It ensures that calcium is removed from the blood and incorporated into bones. Without K2 (MK7 all‐ trans), calcification of tissues and organs can occur, meaning that K2 is also a useful co‐ factor in this context. [35–38]

It is often claimed that vitamin D would be ineffective without vitamin K2 – but this is incorrect. Vitamin K2 (unlike magnesium, for example) does not play a direct role in vitamin D metabolism. Vitamin D is thus fully effective and fulfils its task even without vitamin K2 – only this may not be such a good thing if K2 is deficient.

This is because one of the functions of vitamin D is promoting calcium absorption in the intestine. Calcium absorption increases, particularly in the case of high‐dose vitamin D therapy and a simultaneous high calcium intake, and this therefore increases the amount of calcium in the bloodstream.

And it is precisely here that vitamin K2 comes into play: because if calcium is to be correctly utilised, transported and incorporated into bones, it needs certain transport proteins – and these in turn need vitamin K2 to become active. [39]

Calcium therefore remains unused in the blood when K2 is deficient and this can cause damage in the body. As calcium plaque, it accumulates in vessels and organs, which can have serious long‐term consequences such as arteriosclerosis and coronary heart disease. [35, 40–44]

Or free calcium may combine with oxalate – one of the most common causes of kidney stones.

A number of studies have now shown that the risk of kidney stones increases with high vitamin D levels and decreases significantly with a better supply of vitamin K. [45–48]

Healthy for bones: Vitamin D and K2

The combination of vitamin D and vitamin K2 not only prevents harmful calcification, but is also the perfect combination for our bones and teeth. [38]

Vitamin K2 is required for the activation of three important proteins of the calcium and bone metabolism:

• Matrix Gla protein
  Binds and transports free calcium

• Osteocalcin
  Plays a role in the incorporation of calcium into bones and teeth

• Protein S
  Is a component of the bone matrix

While vitamin D regulates the absorption of calcium for our bones, vitamin K2 is actually the “silent hero” and makes a significant contribution to ensuring that the absorbed calcium does not harm the body, but instead reaches where it is needed: in our bones and teeth. [39, 49–52]

A supply of all central cofactors is therefore important for healthy vitamin D regulation in the endocrine route.

We have taken this into account with our product “Vitamin D Homeostasis”, which combines all elements of the vitamin D system in a single preparation that is perfectly coordinated.

The paracrine route

While in the endocrine pathway the conversion of vitamin D into its storage and hormone forms takes place centrally in the liver and kidney, it has been shown that many cell forms can also convert vitamin D into its active forms independently.

This is quite plausible, as our body needs a way to control the level of active vitamin D for immune functions, for example, independently of the calcium supply.

It is believed that the conversion of vitamin D for all non‐calcium dependent functions occurs directly in cells, allowing various tissues to self‐regulate their levels of active vitamin D.

It has been shown that almost all cell types can produce the enzymes necessary for the conversion of vitamin D themselves, and can thus produce all forms of vitamin D and also break it down.

The “free hormone” hypothesis

There is currently a great deal of controversy regarding the question of which form of vitamin D is used as the starting material. Is it native vitamin D or free 25(OH)D? It was previously assumed that cells use circulating 25‐OH‐D as the starting material for intracellular conversion to calcitriol – which is why this is currently used as the sole measure of vitamin D supply.

However, almost all 25‐OH‐D in the blood is bound to vitamin D‐binding protein (DBP for short) for transport – and cannot diffuse well into cells in this form. Only a very small fraction of the 25‐OH‐D is present in a free form that can easily diffuse into cells and thus be considered a starting material for conversion within the cell.

Studies have shown, for example, that immune cells can produce significant amounts of vitamin D hormone from 25‐OH‐D in vitro. However, this is no longer possible the moment DBP is added. [53]

Since every person has different levels of DBP, and this also exists in different genetic variants, it is currently unclear as to how meaningful it is to measure 25‐OH levels on their own. Various new markers are at present being tested; in addition to 25‐OH‐D, free fractions are now also being measured either directly or inferred from levels of DBP in relation to 25‐OH‐D. It is still unclear which markers are relevant here. [54]

These questions have major implications for our understanding of vitamin D and, more importantly, for treatment and could call into question much of the research that has been carried out on vitamin D to date.

On the one hand, these considerations could mean that previous markers are inadequate. Many studies would then be analytically unsatisfactory, since connections are being sought in the wrong places.

But the design could also be compromised, for example if it turns out that 25‐OH‐D is the decisive marker only for calcium homeostasis, but that free, native vitamin D is key for all other functions. Unlike all other forms of vitamin D, native vitamin D circulates in large quantities in the bloodstream and diffuses easily into all cells. As such, native vita‐min D would actually be the perfect substrate for cellular vitamin D synthesis.

However, this would call into question almost all the research on vitamin D that has been undertaken so far. This is because while 25‐OH‐D circulates in the blood as a transport and storage form for a very long time, the level of vitamin D drops to zero within 24 hours. As a result, there is only a sufficient supply if vitamin D is administered on a daily basis – as would be the case under natural conditions in the sun.

A daily intake of vitamin D in the range of 2000‐6000 IU would then be necessary to maintain the effects of vitamin D on the paracrine pathway.

The problem is that weekly or monthly doses have been used in most clinical trials so far in order to simplify the process. However, the free hormone hypothesis holds that only the endocrine pathway could be sufficiently supplied, while the paracrine pathway would run out of substrate after 24 hours. This would mean that much of the research carried out so far would actually have to be repeated with daily doses.

This question has not yet been fully answered, but in our view it is still highly recommended to focus on daily doses. For one thing, this is more in line with the natural pattern of daily supply via the sun and could also be decisive for the majority of all vitamin D effects.

Open questions in diagnostics

As discussed earlier, these open questions also have a major impact on diagnostics. It is generally agreed that 25‐OH‐D is probably not sufficient as a marker. Native vitamin D, DBP and free fractions of the individual vitamin D forms cannot be measured in a standardised way today, even though some laboratories already offer this. However, it has not been possible to conclusively establish which markers are really meaningful as long as the metabolism of vitamin D has not been fully understood.

At the very least however, it is recommended that the active vitamin D hormone calcitriol (1,25‐dihydroxy vitamin D3) should also be assessed alongside 25‐OH vitamin D. Valuable information about the overall state of the vitamin D system can be gained by correlating this additional value with 25‐OH‐D. This ratio of active vitamin D hormone to storage form is called vitamin D status or VD ratio. The reading indicates whether the vitamin D hormone is properly regulated and the overall system is functioning.

Vitamin D status should always be < 1, ideally around 0.5.

Let us consider an example. The following blood values were determined:

Calcitriol (1,25‐(OH)2‐D): 60 pg/ml

Calcidiol (25‐OH‐D): 30 ng/ml
= Vitamin D status: 60/30 = 2

The above values show sharply higher levels of the vitamin D hormone (calcitriol), but do not provide any information about the cause.

Appropriate conclusions can be drawn in connection with other markers such as para‐ thormone. As outlined above, the main causes are usually a lack of cofactors such as calcium, magnesium and vitamin A.

Vitamin D receptor blockade

Another hypothesis is currently the subject of considerable debate. According to some researchers, various chronic infections such as Epstein Barr and Lyme disease can interrupt the signalling pathway of the vitamin D receptor. Some viruses, such as the Epstein‐ Barr virus, are indeed known to exhibit this ability. [55] It is also plausible in evolutionary terms – presumably this ability developed as a survival strategy, since vitamin D controls some of the key defence pathways against these pathogens.

In these cases, vitamin D status would be greatly elevated with otherwise unremarkable blood levels. A further dose of vitamin D would only lead to an increasingly serious increase in active vitamin D hormone, as the regulating feedback via the vitamin D receptor is absent. The consequence here would also be systemic inflammation.

Discussions are still ongoing about how to deal with such pathologies. As a general rule, it is recommended not to use doses of more than 5000 IU of vitamin D, and in severe cases not more than 2000 IU.

Otherwise, the protocols presented so far by Trevor Marshall and Christian Burghardt differ very considerably and would go beyond the scope of this presentation.

According to these theories, a VDR blockade would always have to be considered if, despite the administration of all cofactors, the value of active vitamin D remains elevated over an extended period, even though blood values show normal values for calcium and parathyroid hormone. However, the hypothesis of VDR blockade remains controversial and has unfortunately been scarcely investigated in clinical trials.

Vitamin D dosage

One of the greatest areas of contention surrounding vitamin D is the question of the right dosage.

While official bodies such as the European EFSA or the American IOM still stick to far too low and scientifically outdated recommendations of 800 IU per day, researchers have been vehemently protesting these recommendations for several years.

There are many reasons for this. Firstly, the recommendations seem untenable from an evolutionary point of view. Humans can easily produce more than 10,000 IU of vitamin D in the skin in summer sun and swimwear. It seems implausible that the biological requirement and biological self‐synthesis are so far apart.

Second, the current recommendations are based solely on data collected in connection with bone health and even in this area they are controversial. However, all non‐bone‐related areas of action of vitamin D are completely disregarded here; to date, there are no reasonable metabolic markers that could be used to define an optimum level of supply here.

Third, comparisons with indigenous peoples show that they have vitamin D levels almost twice as high as those recommended by official bodies. While the IOM sets a value of 20 ng/ml as the threshold for vitamin D deficiency, most indigenous peoples show values of around 40 ng/ml. While this is not proof, it is a strong indication that these are the physiological levels to which we are adapted through evolution. These data are also supported by animal studies showing levels in this range for all primates closely related to us.

Fourth, it appears that many people require much higher dosages to maintain adequate vitamin D levels.

The consensus of most researchers is currently that daily dosages of between 3000 and 5000 IU should be targeted to achieve levels of between 35 ng/ml and 60 ng/ml.

Here too, however, opinions greatly diverge. In recent years in particular, there has been a movement to recommend very high doses of vitamin D and levels above 60 ng/ml for the prevention and treatment of many diseases. However, most publications here are from the popular science field or are limited to case studies, as little clinical research is currently being undertaken in this area.

It is now certain that vitamin D should be based on body weight or body fat levels. As a rough rule of thumb, 50‐60 IU per kilogramme of body weight can be used as an average maintenance dose. This corresponds to 3500 IU ‐ 4200 IU on a daily basis for a body weight of 70kg.

Vitamin D: response index

Again, however, there are a number of new questions. Numerous genetic variants on the vitamin D receptor and on the transport protein DBP lead to large variances in vitamin D metabolism. Dr Carsten Carlberg was able to demonstrate in this context, based on epigenetic studies, that people need very different levels and doses to achieve the same epigenetic effects. As in the pharmacological field, it seems possible to divide them into low, mid and high responders. This principle can be expected for many substances and apparently also applies to vitamin D. There are people who react very sensitively to vitamin D, where even small amounts are enough to exert an optimum influence on the vitamin D system – they are known as high responders. On the other hand, there are also people who need very large doses of vitamin D in order to achieve the same effect – the low responders.

Around a quarter of the people in the Carlsberg study were low responders and need very large amounts of vitamin D in order for the immune cells to actually be affected. Surprisingly, the study could not find any correlation at all between vitamin D levels and the actual epigenetic response. Some people showed effects at 30 ng/ml that other people only achieved at 80 ng/ml.

Carlsberg recommends a compromise dosage around 4000 IU in winter, which provides a sufficient supply and no oversupply for all people on the response index. According to this research, the official recommendations of 800 IU are only acceptable for absolute high responders and do not even achieve optimum effects in this group.

Vitamin D and COVID‐19

The discussion about optimum vitamin D supply again took on a new dimension in 2020 in the wake of the SARS‐CoV‐2 pandemic. Vitamin D deficiency has been found to be one of the key risk factors for

• Contracting COVID‐19,
• Suffering a severe course,
• Requiring intensive care and
• Dying of COVID‐19.

At the time of writing, numerous studies have been conducted around the world, all of which paint the same picture and provide a broad basis of evidence. [3] They comprise:

• Demographic studies,
• Clear mechanistic parallels between the effect of vitamin D and the patho‐physiology of COVID‐19,
• Known evidence from previous studies on vitamin D and related respiratory diseases,
• Evidence from correlation studies of vitamin D levels and infection,
• Evidence from correlation studies of vitamin D levels and disease severity,
• Evidence from intervention studies.

Given this broad body of evidence, it is hard to understand why vitamin D has not been used as an important preventive tool in this pandemic. It becomes all the more incomprehensible when you look at the data from these studies.

The risk of contracting COVID‐19 at all is almost halved by sufficient vitamin D levels, as various correlation studies suggest. People with low vitamin D levels showed over 100% higher risk of developing COVID‐19.

“SARS‐CoV‐2 positivity correlates strongly and inversely with circulating 25‐(OH)‐D levels. This relationship exists across all latitudes, ethnicities, both genders, and all ages.” as one of the studies summarised its conclusion. [56]

Vitamin D deficiency also correlates with the severity of the disease. 84% of patients who end up in intensive care have a severe vitamin D deficiency, and even 100% in the <74 age group. [57]

One German study showed that vitamin D deficiency is the single most significant risk factor for severe progression, surprisingly even more so than existing lung disease. Even after adjusting for age, sex, and underlying disease (diabetes, cardiovascular disease, kidney disease, lung disease and cancer), the risk of invasive ventilation was six times higher and the risk of death almost 15 times higher for low vitamin D levels. [58]

These results already suggest that vitamin D may help prevent both Sars‐CoV infections and serious outcomes. This would make it extremely useful as a preventive measure, especially for the elderly and other at‐risk groups.

This is exactly what further studies then found: preventive supplementation with vitamin D doubled the survival rate of frail and elderly people: 82.5% of participants in the intervention group survived COVID‐19, compared with only 44.4% in the comparison group. [5]

However, vitamin D not only has preventive benefits in this connection, but may even be a viable therapy, as initial intervention studies have shown. High‐dose vitamin D ad‐ ministered in mild COVID‐19 courses resulted in a significant reduction in inflammatory markers and a 100% higher recovery rate at 14 days compared to a control group. [59] In another study, supplementing vitamin D deficient patients with 50,000 IU per day resulted in significantly faster recovery, improved inflammatory markers and reduced need for ventilation. [60]

An extremely high dose of 25‐OH‐D, which would be roughly equivalent to the administration of 300,000 IU of native vitamin D, resulted in a 25‐ to 30‐fold reduction in the risk of ICU admission in patients receiving the calcidiol intervention, and reduced mortality to 0 in the experimental group. [61]

All these results suggest that vitamin D could have played a pivotal role in combating the SARS‐CoV‐2 pandemic. Population‐wide vitamin D supplementation would not only have significantly slowed the spread of the virus in the population, but also saved thousands of lives. It is sad to consider that possibly nearly half of the people who died from COVID might still be alive if this correlation had received more attention.

Researchers at the Heidelberg University even calculate that up to 9 out of 10 deaths from COVID‐19 might be directly attributable to low vitamin D levels. They wrote:

“These results suggest that 87% of COVID‐19 deaths are statistically attributable to vit‐ amin D insufficiency and may be preventable by eliminating vitamin D insufficiency. Definitive evidence of causality and prevention of death from vitamin D supplementation can only be obtained from randomised trials that have now been initiated, but the results of such trials will not be available in the short term. Given the dynamics of the COVID‐19 pandemic and the demonstrated safety of vitamin D supplementation, it therefore seems highly controversial, and possibly even unethical, to wait for the results of such studies before taking public health action.” [62]

Unfortunately, these appeals have gone unheeded. At the time of this manuscript, the UK is the only country providing free vitamin D to at‐risk groups, while all other European countries have failed to take the necessary initiative based on this medical data.

The argument that it is necessary to wait for a sounder scientific basis is all the more implausible when you consider the inadequate scientific basis on which the approval of completely new vaccines was granted in the same year, whereas vitamin D has been well researched and demonstrably safe for years. For any pharmaceutical agent, the study results summarised here would have been almost spectacular and probably would have dominated the news for weeks. There was almost complete media silence regarding COVID‐19 and vitamin D.

Conclusion

Vitamin D is still an exciting field of research with many new findings and unanswered questions. Although our understanding of the vitamin D system improves from year to year, we are still far from a complete picture.

As a general rule, the following is recommended from the current perspective:

Diagnosis

1. Both calcidiol (25‐OHD) and calcitriol (1.25 OHD) values should always be measured in the blood and vitamin D status (calcitriol / calcidiol) established.
2. Vitamin D status should be at least <1 but preferably 0.5;
3. A status >1 can be highly pro‐inflammatory.
4. Adjust the vitamin D level to around 50 ng/ml.

Treatment

1. Consider all cofactors / active partners: magnesium, calcium, vitamin A, zinc, boron, vitamin K2.
2. At least 50‐60 IU per kg body weight is needed for a level of 50 ng/ml, often more.
3. Watch out for possible VDR blockage in chronic infections.
4. Always give daily – not weekly – vitamin D doses.

Closing words

Overall, the importance of vitamin D – and micronutrients in general – for the health of the general population is still widely underestimated and sometimes negligently ignored.

Micronutrient deficiencies are not a marginal medical phenomenon but, on the contrary, are at the heart of holistic health promotion. Every year, thousands of people die from the indirect consequences of micronutrient deficiencies, as tragically highlighted by the current pandemic.

It is time for political decision‐makers as well as therapists and physicians to finally take a closer look at micronutrients and make them a mainstay of general health care.

Sources

1. Zittermann A (2010) The estimated benefits of vitamin D for Germany. Mol Nutr Food Res 54:1164–1171
2. Zittermann A, von Helden R, Grant W, Kipshoven C, Ringe JD (2009) An estimate of the survival benefit of improving vitamin D status in the adult german population. Dermatoendocrinol 1:300–306
3. McCartney DM, O’Shea PM, Faul JL, Healy MJ, Byrne G, Griffin TP, Walsh JB, Byrne DG, Kenny RA (2020) Vitamin D and SARS‐CoV‐2 infection—evolution of evidence supporting clinical practice and policy development: A position statement from the Covit‐D Consortium. Irish Journal of Medical Science (1971 ‐). https://doi.org/10.1007/s11845‐020‐02427‐9
4. Pereira M, Dantas Damascena A, Galvão Azevedo LM, de Almeida Oliveira T, da Mota Santana J (2020) Vitamin D deficiency aggravates COVID‐19: systematic review and meta‐analysis. Critical Reviews in Food Science and Nutrition 1–9
5. Annweiler C, Hanotte B, Grandin de l’Eprevier C, Sabatier J‐M, Lafaie L, Célarier T (2020) Vitamin D and survival in COVID‐19 patients: A quasi‐experimental study. The Journal of Steroid Biochemistry and Molecular Biology 204:105771
6. Kramer J, Diehl A, Lehnert H (2014) Epidemiologische Untersuchung zur Häufigkeit eines Vitamin‐D‐Mangels in Norddeutschland. DMW ‐ Deutsche Medizinische Wochenschrift 139:470– 475
7. Kipshoven C (2010) Querschnittsstudie zur Abschätzung des Vitamin‐D‐Status in der Bevölkerung in Deutschland (DEVID‐Studie). Köln, Univ., Diss., 2010
8. Cashman KD, Dowling KG, Skrabakova Z, et al (2016) Vitamin D deficiency in Europe: pandemic? American Journal of Clinical Nutrition 103:1033–1044
9. Chen TC, Lu Z, Holick MF (2010) Photobiology of Vitamin D. In: Holick MF (ed) Vitamin D: Physiology, Molecular Biology, and Clinical Applications. Humana Press, Totowa, NJ, pp 35–60
10. Holick MF (1995) Environmental factors that influence the cutaneous production of vitamin D. Am J Clin Nutr 61:638S‐645S
11. Christakos S, Lieben L, Masuyama R, Carmeliet G (2014) Vitamin D endocrine system and the intestine. BoneKEy Rep 3:496
12. Löffler B‐M (2015) Sie leiden an einer „stillen“ Entzündung?! warum Sie Calcium, Magnesium, Bor zusammen mit Vitamin D3 benötigen.
13. Deng X, Song Y, Manson JE, Signorello LB, Zhang SM, Shrubsole MJ, Ness RM, Seidner DL, Dai Q (2013) Magnesium, vitamin D status and mortality: results from US National Health and Nutrition Examination Survey (NHANES) 2001 to 2006 and NHANES III. BMC Medicine. https://doi.org/10.1186/1741‐7015‐11‐187
14. Reddy P, Edwards LR (2019) Magnesium Supplementation in Vitamin D Deficiency: American Journal of Therapeutics 26:e124–e132
15. Uwitonze AM, Razzaque MS (2018) Role of Magnesium in Vitamin D Activation and Function. J Am Osteopath Assoc 118:181–189
16. Rosanoff A, Dai Q, Shapses SA (2016) Essential Nutrient Interactions: Does Low or Suboptimal Magnesium Status Interact with Vitamin D and/or Calcium Status?12. Adv Nutr 7:25–43
17. Zittermann A (2013) Magnesium deficit ? overlooked cause of low vitamin D status? BMC Med 11:229
18. Dai Q, Zhu X, Manson JE, et al (2018) Magnesium status and supplementation influence vitamin D status and metabolism: results from a randomized trial. The American Journal of Clinical Nutrition 108:1249–1258
19. Medalle R, Waterhouse C, Hahn TJ (1976) Vitamin D resistance in magnesium deficiency. Am J Clin Nutr 29:854–858
20. Reddy V, Sivakumar B (1974) Magnesium‐dependent vitamin‐D‐resistant rickets. Lancet 1:963–965
21. Rude RK, Adams JS, Ryzen E, Endres DB, Niimi H, Horst RL, Haddad JG, Singer FR (1985) Low serum concentrations of 1,25‐dihydroxyvitamin D in human magnesium deficiency. J Clin En‐ docrinol Metab 61:933–940
22. Fuss M, Bergmann P, Bergans A, Bagon J, Cogan E, Pepersack T, Van Gossum M, Corvilain J (1989) Correction of low circulating levels of 1,25‐dihydroxyvitamin D by 25‐hydroxyvitamin D during reversal of hypomagnesaemia. Clin Endocrinol (Oxf) 31:31–38
23. Rösler A, Rabinowitz D (1973) Magnesium‐induced reversal of vitamin‐D resistance in hypoparathyroidism. Lancet 1:803–804
24. Dean C, Dean C (2017) The magnesium miracle, Second edition. Ballantine Books, New York
25. Miljkovic D, Miljkovic N, McCarty MF (2004) Up‐regulatory impact of boron on vitamin D function – does it reflect inhibition of 24‐hydroxylase? Medical Hypotheses 63:1054–1056
26. Zofková I, Kancheva RL (1995) The relationship between magnesium and calciotropic hormones. Magnes Res 8:77–84
27. Lutz W, Burritt MF, Nixon DE, Kao PC, Kumar R (2000) Zinc Increases the Activity of Vitamin D‐Dependent Promoters in Osteoblasts. Biochemical and Biophysical Research Communications 271:1–7
28. Gilardi F, Desvergne B (2014) RXRs: collegial partners. Subcell Biochem 70:75–102
29. Anand PK, Kaul D, Sharma M (2008) Synergistic action of vitamin D and retinoic acid restricts invasion of macrophages by pathogenic mycobacteria. J Microbiol Immunol Infect 41:17–25
30. Bettoun DJ, Burris TP, Houck KA, Buck DW, Stayrook KR, Khalifa B, Lu J, Chin WW, Nagpal S (2003) Retinoid X Receptor Is a Nonsilent Major Contributor to Vitamin D Receptor‐Mediated Transcriptional Activation. Molecular Endocrinology 17:2320–2328
31. Mora JR, Iwata M, von Andrian UH (2008) Vitamin effects on the immune system: vitamins A and D take centre stage. Nat Rev Immunol 8:685–698
32. Jimenez‐Lara AM, Aranda A (2000) Interaction of vitamin D and retinoid receptors on regulation of gene expression. Horm Res 54:301–305
33. Mata‐Granados JM, Cuenca‐Acevedo JR, Luque de Castro MD, Holick MF, Quesada‐Gómez JM (2013) Vitamin D insufficiency together with high serum levels of vitamin A increases the risk for osteoporosis in postmenopausal women. Arch Osteoporos 8:124
34. Schräder M, Bendik I, Becker‐André M, Carlberg C (1993) Interaction between retinoic acid and vitamin D signaling pathways. J Biol Chem 268:17830–17836
35. Hou Y‐C, Lu C‐L, Zheng C‐M, Chen R‐M, Lin Y‐F, Liu W‐C, Yen T‐H, Chen R, Lu K‐C (2019) Emerging Role of Vitamins D and K in Modulating Uremic Vascular Calcification: The Aspect of Passive Calcification. Nutrients 11:152
36. Schurgers LJ, Uitto J, Reutelingsperger CP (2013) Vitamin K‐dependent carboxylation of matrix Gla‐protein: a crucial switch to control ectopic mineralization. Trends in Molecular Medicine 19:217–226
37. van Summeren M, Braam L, Noirt F, Kuis W, Vermeer C (2007) Pronounced elevation of under‐carboxylated osteocalcin in healthy children. Pediatr Res 61:366–370
38. Kidd PM (2010) Vitamins D and K as pleiotropic nutrients: clinical importance to the skeletal and cardiovascular systems and preliminary evidence for synergy. Altern Med Rev 15:199–222
39. Wen L, Chen J, Duan L, Li S (2018) Vitamin K-dependent proteins involved in bone and cardiovascular health (Review). Molecular Medicine Reports. https://doi.org/10.3892/mmr.2018.8940
40. Wei F‐F, Trenson S, Verhamme P, Vermeer C, Staessen JA (2019) Vitamin K–Dependent Matrix Gla Protein as Multifaceted Protector of Vascular and Tissue Integrity. Hypertension. https://doi.org/10.1161/HYPERTENSIONAHA.119.12412
41. Roumeliotis S, Dounousi E, Eleftheriadis T, Liakopoulos V (2019) Association of the Inactive Circulating Matrix Gla Protein with Vitamin K Intake, Calcification, Mortality, and Cardiovascular Disease: A Review. International Journal of Molecular Sciences 20:628
42. Villa JKD, Diaz MAN, Pizziolo VR, Martino HSD (2017) Effect of vitamin K in bone metabolism and vascular calcification: A review of mechanisms of action and evidences. Critical Reviews in Food Science and Nutrition 57:3959–3970
43. Theuwissen E, Smit E, Vermeer C (2012) The role of vitamin K in soft‐tissue calcification. Adv Nutr 3:166–173
44. Cranenburg ECM, Vermeer C, Koos R, Boumans M‐L, Hackeng TM, Bouwman FG, Kwaijtaal M, Brandenburg VM, Ketteler M, Schurgers LJ (2008) The circulating inactive form of matrix Gla Protein (ucMGP) as a biomarker for cardiovascular calcification. J Vasc Res 45:427–436
45. Wei F‐F, Thijs L, Zhang Z‐Y, et al (2018) The risk of nephrolithiasis is causally related to inactive matrix Gla protein, a marker of vitamin K status: a Mendelian randomization study in a Flemish population. Nephrol Dial Transplant 33:514–522
46. Letavernier E, Daudon M (2018) Vitamin D, Hypercalciuria and Kidney Stones. Nutrients. https://doi.org/10.3390/nu10030366
47. Hu H, Zhang J, Lu Y, et al (2017) Association between Circulating Vitamin D Level and Urolithiasis: A Systematic Review and Meta‐Analysis. Nutrients. https://doi.org/10.3390/nu9030301
48. Malihi Z, Wu Z, Stewart AW, Lawes CM, Scragg R (2016) Hypercalcemia, hypercalciuria, and kidney stones in long‐term studies of vitamin D supplementation: a systematic review and meta‐analysis. Am J Clin Nutr 104:1039–1051
49. Philipp S, Ouwehand AC (2012) Vitamin K: essential for healthy bones. Nutrafoods 11:111–116
50. van Ballegooijen AJ, Pilz S, Tomaschitz A, Grübler MR, Verheyen N (2017) The Synergistic Inter-play between Vitamins D and K for Bone and Cardiovascular Health: A Narrative Review. Int J Endocrinol. https://doi.org/10.1155/2017/7454376
51. Myneni V, Mezey E (2017) Regulation of bone remodeling by vitamin K2. Oral Diseases 23:1021–1028
52. Frandsen NE, Gordeladze JO (2017) Vitamin K2 and Bone Health. Vitamin K2 ‐ Vital for Health and Wellbeing. https://doi.org/10.5772/64876
53. Kongsbak M, von Essen MR, Levring TB, Schjerling P, Woetmann A, Ødum N, Bonefeld CM, Geisler C (2014) Vitamin D‐binding protein controls T cell responses to vitamin D. BMC Immunol 15:35
54. Tsuprykov O, Chen X, Hocher C‐F, Skoblo R, Lianghong Yin, Hocher B (2018) Why should we measure free 25(OH) vitamin D? The Journal of Steroid Biochemistry and Molecular Biology 180:87–104
55. Marcucci SB, Obeidat AZ (2020) EBNA1, EBNA2, and EBNA3 link Epstein‐Barr virus and hypovitaminosis D in multiple sclerosis pathogenesis. Journal of Neuroimmunology 339:577116
56. Kaufman HW, Niles JK, Kroll MH, Bi C, Holick MF (2020) SARS‐CoV‐2 positivity rates associated with circulating 25‐hydroxyvitamin D levels. PLoS ONE 15:e0239252
57. Lau FH, Majumder R, Torabi R, Saeg F, Hoffman R, Cirillo JD, Greiffenstein P (2020) Vitamin D insufficiency is prevalent in severe COVID‐19. medRxiv
58. Radujkovic A, Hippchen T, Tiwari‐Heckler S, Dreher S, Boxberger M, Merle U (2020) Vitamin D Deficiency and Outcome of COVID‐19 Patients. Nutrients 12:2757
59. Rastogi A, Bhansali A, Khare N, Suri V, Yaddanapudi N, Sachdeva N, Puri GD, Malhotra P (2020) Short term, high‐dose vitamin D supplementation for COVID‐19 disease: a randomised, pla‐ cebo‐controlled, study (SHADE study). Postgrad Med J postgradmedj‐2020‐139065
60. Ohaegbulam KC, Swalih M, Patel P, Smith MA, Perrin R (2020) Vitamin D Supplementation in COVID‐19 Patients: A Clinical Case Series. Am J Ther 27:e485–e490
61. Entrenas Castillo M, Entrenas Costa LM, Vaquero Barrios JM, Alcalá Díaz JF, López Miranda J, Bouillon R, Quesada Gomez JM (2020) „Effect of calcifediol treatment and best available therapy versus best available therapy on intensive care unit admission and mortality among patients hospitalized for COVID‐19: A pilot randomized clinical study.” The Journal of Steroid Biochemistry and Molecular Biology 203:105751
62. Brenner H, Schöttker B (2020) Vitamin D Insufficiency May Account for Almost Nine of Ten COVID‐19 Deaths: Time to Act. Comment on: „Vitamin D Deficiency and Outcome of COVID‐ 19 Patients”. Nutrients 2020, 12, 2757. Nutrients 12:3642

Marcel Riffel, Naturopath, Ostifldern, Germany

Dear Colleagues,

Acute or chronic cystitis is a frequently encountered clinical picture in the practice of complementary medicine.

Patients can virtually always look back on a long history of antibiotics and come to our practice in a state of deep despair.

Today I would like to give you a few suggestions on how you can successfully treat this clinical picture in your BICOM® practice and which off‐the‐shelf medicines / micronutrients you can use for supporting treatment.

In the script, I would like to briefly discuss the epidemiology / causes / favouring factors / symptoms / diagnostics / therapy and complications from a conventional medical point of view, without explaining this in detail in the presentation. This is solely for you to be able to read it in your RTI booklet.

Epidemiology:

It mainly affects children, sexually active women and also men at an advanced age, often in connection with BPH.

In most cases, it is an ascending infection, which in most cases is caused by coliform bacteria.

Conventional medical treatment is usually based on antibiotics, although considerable resistance to the various types of antibiotics has developed in recent years.

This is why an antibiogram (see Enterosan Laboratory below) should be prepared according to conventional medicine so that targeted antibiotic treatment can be carried out according to the sensitivity of the pathogen.

Predisposing factors for the development of cystitis:

Female gender (shortness of the female urethra)

In the postmenopause due to atrophy of the epithelium sealing the urethra.

Older men with BPH; a resultant increased narrowing of the urethra can lead to voiding disorders of the bladder. Congestion favours the occurrence of bladder infections.

Frequent sexual intercourse in women (“honeymoon” or “holiday” cystitis)

Disorders of urinary outflow due to obstruction of the urethra in the pelvic region (e.g. tumours, bladder diverticula, vesicoureteral reflux)

Metabolic diseases, in particular diabetes mellitus with “sugary” urine = breeding ground for bacteria

Indwelling bladder catheter

Procedures such as bladder irrigation, cystoscopy

Immunosuppression with immune deficiency

Causes of acute cystitis according to conventional medicine:

Escherichia coli (70‐95%)
Staphylococcus saprophyticus (5‐10%)
Other bacteria, but also adeno viruses, trichomodes and Candida albicans

Symptoms:

Dysuria, pollakiuria, bladder tenesmus, haematuria, pain, urge incontinence, in rare cases fever

Diagnosis:

Urine – rapid test strips / microscopic urine examination / urine culture / sono / antibiogram (better aromatogram)

Prevention:

2.3. Treatment of cystitis with urine and copper sulphate:

(following stabilisation of the bladder and kidneys)

Input: No input applicator – patient is at the output only

Output: Power applicator on the bladder (DMI: alternating or damping) plus 2 balls in the hands

Input cup: Urine and copper sulphate (‐copper vitriol); available in the pharmacy / online shop

Output cup: Trace elements drops or BICOM® oil

Memory device: Chip

Program: Must be entered manually in the BICOM® optima; prerequisite optima new or Extension Module 1

(without band pass / normal freq. / continuous operation / A = 64 /decr. F‐SW speed 900 sec/15 min)

It may be that this treatment needs to be performed 3 days in a row.

2.4. Applicator system for immune system stabilising programs and EB/AB/SG placement:

Input: Square flexible applicator on the thymus
Output: Power applicator on the bladder (DMI: alternating or damping)
Input cup: Urine
Output cup: Trace elements drops or BICOM® oil
Memory device: Chip
Programs to stabilise the immune system:

• 3053 Regulate immune system
• 657 Stabilise immune system
• 3424 Strengthen immune system
• 3108 Activate thymus
• 428.2 Activate thymus
• 1112.0 Activate bone marrow

(frequency range 50 kHz / H + Di / constant amplification H = 1.6 Di = 7 / sweep YES / interval operation / time: 8 min)

Channel 2: Preparations to stabilise the immune system / substance complexes under bone marrow/blood heading

2.4. Stabilisation of the kidney / bladder situation via channel 2:

Stabilisation via the substance complexes / under urology heading:

Glomerulonephritis / urinary tract infection acute / urinary tract infection chronic / irritable bladder / kidney / urethritis / cystitis acute / cystitis chronic

Stabilisation via the honeycomb:

1. CTT ampoules (water / kidney / bladder / disturbed elimination / intercellular tis‐ sue strain)
2. Spagyric remedies for urinary tract infections / mother tinctures from Ceres:

   Ribes nigrum (blackcurrant)

   → Flushing therapy for bacterial and inflammatory diseases of the urinary tract

   Tropaeolum majus (nasturtium)

   → The mustard oils of the nasturtium have an antibacterial/ antiviral/ anti-fungal / immuno-stimulant effect

   Urtica dioica (stinging nettle)

   → Diuretic/ anti‐inflammatory; for elimination and detoxification via the kidneys

   Betula pendula folium (birch)

   → For flushing therapy, drainage and detoxification via the kidneys

   Solidago mother tincture/ Solidago comp. (golden rod)

   → For flushing therapy anti‐inflammatory/ antispasmodic/ with relationship problems

3. Notakehl D5 drops / D3 supp (can also be administered vaginally) / D3 ointment for use in the external genital area from Sanum Kehlbeck

   → For inflammations/ bacterial infections/ poorly healing wounds

4. Fortakehl D5 drops / D3 supp (can also be administered vaginally) / D5 tablets (to keep the mucous membrane situation stable) from Sanum Kehlbeck

   → Stabilising agent for (skin) and mucous membrane

5. Crystal colloidal silver water from Sunday Natural for bacterial infections

   → Application over external genital area, suprapubical for rubbing in and as oral spray

6. Zinc and Vitamin C from Sunday natural

6. • →  Organic zinc capsules (20 mg high dose): 5‐10 mg (1 capsule) every 2 hours on the first day, then 3 times daily
   • →  Vitamin Cultra 1000: 500‐1000 mg every 2 hours (1 capsule) on the first day, then 2 teaspoons of vitamin C 1000 liposomal 3 times a day
7. L‐Methionine 500 capsules from Sunday Natural
   → 3 x 500‐1000 mg daily; the natural amino acid L‐methionine acidifies the urine (lowers the pH value of the urine) and thus hinders bacterial growth
8. D‐Mannose 500 mg capsules (high dose) from Sunday Natural

   → The natural monosaccharide D‐mannose makes it difficult for germs to dock onto the urothelium of the urinary bladder

9. Cranberry extract from Sunday Natural (will be included in the product portfolio). → Has an anti‐inflammatory and antibacterial effect
10. Vital fungi from Sunday natural → Cordyceps, Polyporus, Reishi

    The vital fungi Cordyceps and Polyporus have a diuretic effect, i.e. they stimulate the activity of the kidneys and thus cause a flushing of both the draining urinary tract and the urinary bladder.

    All 3 fungi have an anti‐irritant (anti‐inflammatory) and antibacterial effect on the urinary tract and strengthen the immune system with the aim of minimising the risk of chronic bladder problems.

11. Carious aroma oils from Sunday Natural (see point 4)

12. URO FORTE capsules / URO FORTE AKUT capsules / URO VITAL capsules / URO

FORTE Transdermal Oil / URO VITAL Tea A and B from Sunday Natural

13. Solunat No 16 (formerly Renalin) from Soluna (see point 3.2.2)

It is used for elimination and detoxification through the urogenital system (contains copper) and is indicated in all diseases of the kidneys, bladder, ureter and has a blood purifying effect (filters the blood).

It strengthens the bond, relationship, (primal) trust and sexuality and allows us to engage in life (with both feet on the ground) (see point 3.2.2)

Dosage: 2‐3 x 3‐8 drops (the higher the dosage the more substantial the effect)

Effect:

1‐3 drops: psycho-emotional effect

3‐5 drops: restorative/ strengthening
5‐10: drops draining

Children:

1‐7 years of age – approx. 1/3 of the dosage
Available as globules (1 globule = 1 drop) (Rosenapotheke Friedberg)

Consumption: Placed under the tongue or diluted with water

3. Diagnostics and therapy with the CTT / Schumacher test kits:

3.1. Causes of recurrent urinary tract infections:

3.1.1 Tumour – Check degenerated cells test set
(refer to seminar by Dr Wolfgang Rohrer and presentation by Marcel Riffel at the first online congress in 2020)

3.1.2 Bacterial infections: (Nitrite positive in rapid test strip)

E.coli most frequently (CTT + Schumacher ampoule)

Klebsiellen (CTT)
Proteus (CTT + Schumacher)

Staphylococci (CTT + Schumacher (Staph. albus + aureus) ampoule)

Enterococci (CTT + Schumacher)
Chlamydia + chlamydia trachomatis (CTT + Schumacher)

Ureaplasma (CTT)

Mycoplasma (CTT)
Neisseria + neisseria gonorrhoea (CTT + Schumacher)
Mycobacteria (bladder TBC) (CTT + tuberculosis pathogen vaccine test kit)

3.1.3 Viral infections: (less frequently the case)

Adenoviruses (CTT)

3.1.4 Parasitic infections:

Trichomonads (CTT + Schumacher) !!! Check the partner!

3.1.5 Mycotic infections:

Candida albicans (CTT + Schumacher) !!! Check the partner!
The ampoules under headings 3.1.2. – 3.1.5. should be checked both with programs 191 (Ai), 193 (Di) and also as possible couplings.

The therapy of the pathogens is carried out following the stabilisation of the kidney, bladder and, if necessary, other organs to be opened with the program chain 10325 (Ai) or 10326 (Di).

3.2. Other causes of recurrent urinary tract infections:

3.2.1 Physically induced cystitis after radiation therapy in the pelvic region
(Mucosa stabilising programs / wound healing programs / cell regeneration programs)

3.2.2 Psychoemotional causes:

Behind every somatic (organic) symptom of discomfort there can also be a psycho‐emo‐ tional issue or psychological stress, resulting in an associated weakening of the immune system.

Quote Ulrich Schaffer (writer, poet, photographer)

“You go ahead”, said the soul to the body, “he won’t listen to me. Maybe he’ll listen to you”.

“I’ll get sick so he’ll have time for you,” said the body to the soul.

The bladder, for example, can give us clues as to possible psychological and emotional disharmonies:

e.g. great anxiety, emotional pressure, fear of sexuality, anger at parents, peace/harmony and restlessness / impatience could be issues in a recurrent bladder condition.

The kidneys as an organ pair also stand for fear, shock (that gets to me), inferiority complexes, panic attacks, insecurity and a (lack of) balance between give and take, in addition to partnership issues.

They represent the seat of our life energy and provide power for growth, development, reproduction, ageing, intelligence and talent.

If chronic recurrent cystitis has a psycho‐emotional origin, we currently only have the possibility to treat the physical symptoms using programs to remove chakra blockages or to look in the new test set “Control & Metabolism” to see whether the issue can be localised at the psychological/emotional level.

In addition to the existing programs for the treatment of chakras (e.g. the sacral chakra for bladder problems), many programs by Dr Sabine Rauch and the Hennecke family are printed in the 2016 RTI booklet.

4. The aromatogram – essential oils against recurrent urinary tract infections:

Over 5000 clinical studies have proven that essential oils can effectively fight bacteria and fungi, thus inhibiting inflammation. At the same time, essential oils have a restorative effect on the immune system.

Used in a targeted manner, essential oils are an absolute alternative to treatment with antibiotics.

Since bacterial strains learn very quickly, many resistances to man‐made and standardised drug antibiotics are now emerging. And this is exactly what patients with chronic recurrent cystitis can tell you.

All essential oils have a more or less strong antibacterial effect (this has been reliably and reproducibly proven in several laboratory tests). The front runners with antibiotic character are oils with a strong phenol content such as thyme thymol (see aromatogram on following page).

In addition, it is very difficult for bacteria to develop resistance to essential oils.

This is due to the fact that essential oils consist of up to 300 (or more, e.g. rose) individual ingredients and the composition of the essential oil is also constantly changing (oxidation processes by oxygen and light, esterification). Batches (harvests) are also always slightly different.

From my clinical experience so far, an aromatogram is particularly helpful for urinary tract and vaginal infections.

The problem in acute cases is that an aromatogram takes up to 10 working days to evaluate.

For this reason, it makes sense to test the different aroma oils / hydrosols from Sunday Natural in acute cases with the BICOM® using program 171. Testing without BICOM® with biotensor or kinesiology is also possible. A Sunday Natural test box is planned for the future.

In the case of chronic recurrent urinary tract infections in women, I recommend the preparation of an aromatogram, not from the urine, but by vaginal swab (Vagicheck, Enterosan Laboratory). In order to find the most effective oil against the focus of inflammation, it is necessary to know whether facultative germs such as coli bacteria or staphylococci (see evaluation on following page) have migrated from the vaginal flora to the area of the urethra.

This is necessary to know, because the treatment (bioresonance therapy, taking products from Sunday Natural…) can then be supported with individually produced vaginal ovules (Hessel pharmacy in Wiesloch).

This pharmacy produces a bladder oil for the care of bladder conditions that can be applied to the skin.

Furthermore, they also offer “Solubol concentrate E.coli” to be taken orally (2 x daily 15 drops) or as a sitz bath, which can be combined with the oral ingestion of a tincture of coleus (3 x 8 drops).

Aromatogram (example: Enterosan Laboratory):

Closing words:

The treatment of chronic recurrent cystitis in particular often poses great challenges for therapists working in complementary medicine.

It may also be that antibiotics are unavoidable during treatment, as the development of an ascending urinary tract infection is too great a risk for the patient.

However, with the sum of the measures listed, we often succeed in our practice in leading the patient out of a situation that is often hopeless for him or her and onto the path of regulation.

Best regards, Marcel Riffel

Sabine Rauch, MD, Deggendorf, Germany

General information about viruses

• Viruses are the smallest known “living beings” with a diameter of between 15 and 300 nm.
• Great adaptability: heat stable, cold stable and even survive drying processes.
• They have no metabolism of their own; their reproduction can only take place in living cells.
• They contain only DNA or RNA as genetic material; no cell division takes place, they reproduce only through their nucleic acid, or require the help of host cell ribosomes for replication.
• In the extracellular resting phase, no cell growth takes place; in this phase, the virus binds to the receptor of the host cell.
• Viruses can “disguise” themselves by taking a part of the cell wall with them and are therefore more difficult to detect.
• They can replicate in one of two ways:

1. Incorporation into the genome of the host cell. The genetic code of the cell is thus altered and no more of its own cells are produced. Virus replication is assumed to be regulated by the host cell.
2. Elimination of the regulatory mechanisms of the host cell and conversion of the entire metabolism to the service of virus replication.

• After viruses copy their genome, they package it, allowing it to travel to new cells or hosts. The newly produced viruses are released into the organism during cell death and the interstitial fluid becomes toxic. Viruses immediately infect more cells and the process then repeats.
• Some viruses do not even have a protein coat. Such viruses rarely, if ever, move from one cell or host to the next organism.
• There are two modes of transmission: horizontal, i.e. from one individual to the next, and vertical, i.e. from parents to offspring. Most viruses are transmitted horizontally or vertically and horizontally (e.g. HIV). Most viruses of free‐living plants are transmitted vertically (seeds).
• Many viruses are transmitted by an intermediate host or vector (e.g.: mosquitoes, arachnids such as mites or ticks, and also through fungi).
• Due to the mutagenic effect of viruses, cells can be induced to change to become tumours. A certain tumour‐inducing effect is said to be caused by measles, rubella, EBV, HPV, Ebola and others.

1.1 Systematics of viruses

• In 1975, David Baltimore received the Nobel Prize for his work on retroviruses and the discovery of reverse transcriptase, a remarkable enzyme that can transcribe DNA into RNA.
• He developed a systematics of viruses based on how viruses produce messenger RNA (mRNA). The genetic information from the DNA is transcribed into this RNA form, which then carries the genetic information from the nucleus into the machinery, where it is translated into proteins.
• Double‐stranded DNA is the genetic material in all cellular life forms, i.e. bacteria, archaea and eukaryotes. However, viruses do not follow any rules with their genetic material.
• No protein synthesis can occur directly from DNA; mRNA is produced as an intermediate stage, which can be single‐ or double‐stranded and contains the same nucleotide sequence as the coding DNA strand. A further distinction is made between positive and negative strand orientation in single‐stranded viruses. (10)

1.2 The following 7 classes of viruses are distinguished:

Class 1: They behave like cellular organisms and possess double‐stranded DNA, the direct template for mRNA. E.g. enterobacteriophages, human adenovirus 2, HHV 1, HPV 16, JC virus, varicella zoster virus, variola virus.

Class 2: They consist of single‐stranded DNA that is converted into double‐stranded DNA, which then serves as a template for the mRNA: e.g. Torque teno virus, golden mosaic virus of bean plants.

Class 3: They have genomes made of double‐stranded RNA, which forms a direct template for RNA. E.g.: rotavirus A, saccharomyces cerevisiae virus L‐A.

Class 4: They have a genome of single‐stranded positive RNA, can use this as mRNA, but must make a complementary RNA strand that serves as a template before it is replicated. E.g.: poliovirus, zika virus, yellow fever virus, West Nile virus, SARS and related corona viruses, Norwalk viruses, human rhinovirus A, hepatitis C virus, dengue virus.

Class 5: They have a single‐stranded negative RNA genome that serves as a template for the mRNA. E.g.: influenza virus A, Sin Nombre virus, mumps virus, measles virus, Ebola virus.

Class 6: Retroviruses that have an RNA genome and use reverse transcriptase to copy RNA into an RNA/DNA hybrid and then into double‐stranded DNA. This serves as a template for the mRNA. E.g.: HI virus feline leukaemia virus.

Class 7: They have a DNA genome that serves as a template for the mRNA When the genome is copied, an RNA “imprinting genome” is also created, which is then recopied into DNA by reverse transcriptase. E.g.: cauliflower mosaic virus. (10)

The virome

• Our knowledge of the diversity of the virosphere was limited to a few species that could be grown under laboratory conditions for more than a hundred years after the first discovery of a virus in 1898.
• Gene‐sequence‐based detection methods such as the polymerase chain reaction (PCR) gradually took over from virus cultivation from the 1980s onwards, but detailed prior knowledge of the genetic make‐up of a sought‐after virus was still necessary.
• Advances in nucleic acid sequencing (next generation sequencing, NGS) in the early 2000s made it possible to detect microbes without knowing their exact gene sequences a priori.
• We now know that viruses are the most common “biological entity” globally – to call them living things would be incorrect. No matter what ecosystem you look at, viruses are omnipresent and on average 10 times more abundant than bacteria.
• One millilitre of seawater, for example, contains between 10 and 100 bacteria, but more than 10 million viruses.
• Viruses in the sea are of great importance for the carbon cycle. Most infect bacteria or other protozoa, at least a quarter of which are killed by viruses every day. In the process, they burst and their contents are utilised by other life forms. When such cells die without being destroyed in this way, they generally sink to the bottom of the sea, where their carbon is deposited and deprived of life. (10)
• Some authors even suggest that all living organisms, including all unicellular microorganisms, are infected by at least one virus at any given time. (1)
• Most viruses are probably commensal, i.e. they obtain what they need from their hosts without doing harm.
• Some viruses have a reciprocal relationship with their hosts that is so beneficial that the hosts cannot live without it, and the viruses benefit, too. In a stable host‐virus relationship, the virus uses the host cells while causing as little damage as possible.
• Causing disease is undesirable for both the virus and the host. A virus cannot replicate as well in a sick host, and if the host dies before the virus can spread it is detrimental to both.
• Severe illness or death are signs of an immature relationship between host and virus before they have “adapted” to each other. For example, people get very sick from HIV‐1 because the virus has only recently started infecting people. It jumped from non‐human primates to humans. The related virus (SIV) does not cause disease in non‐human primates.
• Disease occurs when the virus “jumps” to a new host.
  Some viruses jump very frequently. The influenza virus is an example of this. Its natural host is waterfowl, where it does not cause disease.
• Polioviruses have had only humans as hosts for centuries, which meant that until the 20th century most people were immune to them. In the past, most people became infected with the poliovirus as young children, but rarely showed symptoms of the disease and were immune to further infection. Poliovirus is spread through drinking water, and after drinking water was chlorinated, young children in their environment were no longer exposed to poliovirus. When they subsequently came into contact with the virus, they had no natural immunity and the disease broke out in full. (10)
• Some viruses are true mutualists, meaning they are beneficial to their hosts. For example, herpes viruses protect mice from various bacterial infections (e.g. the plague).
• Bacteria and yeasts use viruses to kill off competitors so that they can move into a new area. (10)

2.1 The human virome

• The human virome denotes viral diversity. Together with bacteria, fungi, archaea and protozoa that colonise us, it forms the human microbiome.
• It consists of viruses anchored in the human genome (endogenous retroviruses more or less as “fossils” = HERVs), eukaryotic viruses (which infect plants or fungi) and viruses that infect bacteria and archaea (bacteriophages).
• The virome populates different niches and differs according to localisation. An average of 5.5 virus families were detected in the nose, skin, mouth, vagina and stool of a total of 102 healthy volunteers. (2)
• While bacteria exceed a factor of 10 in humans, it is a factor of 100 for viruses.
• The complete sequence of the human genome was published in 2001. It contains 11% retroviral sequences. (10)
• Viruses are common, but their role in disease and health is unclear. This is mainly due to the technical challenges. Viruses are an extremely heterogeneous group in both morphological and genetic terms, which makes it difficult to extract viral gene sequences in a targeted manner.
• Moreover, the average length of the genome of a virus particle is only a fraction of that of a bacterial genome.
• The intestinal virome is the best studied community to date and probably the largest. There are approximately 108‐1010 viral particles in one gramme of intestinal content (Mukhopadhya et al. 2019).
• Viruses and bacteria obviously coexist peacefully, and it is estimated that the number of viruses is ten times greater than the number of bacteria. The concentration of viruses is particularly elevated in the intestine because they form surface structures that can bind to glycoproteins of the intestinal mucosa, which increases their local concentration. (3)
• Eukaryotic viruses represent only a small proportion of the intestinal virome. Most of them do not show any evidence of association with disease. Eukaryotic viruses with low virulence can cause persistent, long‐lasting infections. These are often highly adapted viruses that have developed along with their human hosts over thousands of years (co‐evolution). Highly virulent eukaryotic viruses are usually transient members of the human virome, as they are generally rapidly eliminated by the local immune system. (1)
• Kembauer et al (4) introduced murine norovirus (MNV) into mice bred in a germ‐free environment and thus lacking a bacterial microbiome. They suffered from severe local immunodeficiencies with greatly increased vulnerability to chemically mediated tissue destruction and infections with bacterial pathogens. Chronic viral infection of these animals with murine norovirus was able to replace the immunostimulatory effects of the bacterial microbiome and restore the normal state of the gut immune system.
• Eukaryotic viruses are apparently capable of supporting intestinal homeostasis and maintaining the immune system of the intestinal mucosa (5).
• The majority of the intestinal virome (90%) is made up of prokaryotic‐viruses, i.e. bacteriophages, but these are still largely unresearched. For example, a new group of bacteriophages has recently been identified (crAssphages) that are thought to be the most common representatives of the human virome (Dutilh et al, 2014; Edwards et al, 2019). However, we are still largely in the dark about the functional impact of these phages on physiology and pathophysiology (Koonin & Yutin, 2020).(1)
• One hypothesis is that they constantly transfer information into the bacterial cell through horizontal gene transfer. This enables the bacteria to adapt to different habitats, for example by making the inserted genetic material resistant to chemical stress or stabilising the community. They are also thought to improve the energy uptake of their hosts. (3)
• The virome can act as a genetic library that holds all kinds of useful information and can be consulted by bacteria when they experience external stress such as acute nutrient shortages or antimicrobial pharmacotherapies. (1)
• Bacteriophages can accumulate genes that confer resistance during antibiotic therapy, but also make recolonisation possible.
• The virome also protects against the side effects of antibiotics. If the bacterial intestinal microbiome is eradicated during broad‐spectrum antibiotic therapy, bacteriophages can store essential metabolic functions and can transfer them to descendant commensal bacteria (Rascovan et al, 2016).
• Phages cooperate with humans by being able to use bactericides against pathogenic germs.
• The virome forms an essential part of the intestinal barrier to defend against pathogenic germs (Koonin EV & Yutin N, 2020). The basis of this intestinal barrier is formed by epithelial cells of the intestinal mucosa, which form the colon wall and define the intestinal lumen with their apical side. There is a layer of mucus several micrometres thick directly on the epithelial cells that which protects the intestinal epithelial cells from chemical, enzymatic and mechanical influences. In addition, this mucus layer fulfils another, almost more important function: it harbours a highly specific and highly abundant viral community, which is referred to by the acronym BAM – bacteriophages adherent to mucus. The function of these bacteriophages in the local defense against pathogenic intestinal bacteria is so essential that BAM is considered a separate, non‐self immune barrier that protects the intestinal epithelium from invasive germs. (1)
• Bacteriophages ensure that a healthy flora can form in the intestines of new‐borns.
• Shortly after birth, it is mainly phages that form the virome. Every human has an almost unique intestinal biome, whereby the once acquired coexistence of bacteria and viruses remains relatively stable. (Mukhopadhya et al, 2019)
• Nevertheless, the virome of people living in the same household adapts to each other by exchanging a small amount of bacteriophage diversity (Ly et al, 2016).
• Herpes viruses can prevent bacterial infections and benign viruses can activate the immune system in the intestine, making humans immune to attacks from pathogenic viruses.
• The virome is seen as a possible aid against infectious diseases, obesity and even in cancer therapy (cancer drugs with genetically modified herpes viruses).
• Phage therapy has been in use in Russia for a number of years.

2.2 Virions

• A virion is a single virus particle located outside the cell. They are encapsulated viral particles that are dormant, much like spores of bacteria or fungi. The viruses use them to propagate. The composition of the virion is a central determinant of viral transmissibility and immunogenicity.
• A virion consists of one or more nucleic acid molecules, often surrounded by a protein capsule. There are sometimes also other proteins with enzymatic properties in the viron, and in some viruses virions also have a viral envelope consisting of a lipid membrane.
• Viruses do not normally incorporate host genetic material into virions, with the exception of a number of viruses that integrate into the host genome during their life cycle.
• Virions, which consist of virus particles, allow viral nucleic acids to move around and “infect” living organisms.
• Viruses can infect all life forms (even other viruses).
• The non‐viral components and host proteins that make up the pleomorphic virus particles of, for example, an influenza virus are responsible for the virus being able to cause damage.
• An influenza virus contains as much biological material from the “infected” host as viral material from the actual virus. (6)
• Some virions are very stable. Canine parvovirus, for example, can remain infectious in soil for over a year. Other viruses are very unstable and require direct contact between hosts. Viruses with an outer membrane are generally not very stable because the membrane is sensitive to desiccation.

2.3 Exosomes

• The latest findings on exosomes, small vesicles that are released by a cell into the environment, show that they not only act as transport vehicles, but also support cell communication and immune modulation.
• Exosomes are extremely important as RNA carriers in regulating expression within the absolute majority of the human genome.
• Viruses use exosomes for transport and camouflage. On the other hand, they are currently being discussed as possible treatment options for autoimmune diseases (rheumatoid arthritis) and cancer.
• Both exosomes and viruses could be important for interspecies or even “cross kingdom communication” (between species) and regulation within the biosphere, as they are able to facilitate and mediate the horizontal transfer of information between organisms. (6)
• In order to survive, viruses must constantly adapt to changing environmental conditions. Modulation via exosomal or viral RNA causes the expression of a protein‐coding gene to change within seconds.
• Viruses can be a means for cells to communicate extracellularly.
• The human body and its environment are inextricably linked. Viruses can be an indicator of environmental stress in an organism. They expose toxic pollution in our environment.
• During our energetic tests in the context of BICOM® bioresonance, we always find viral stress in combination with stress caused by environmental pollution (chemical pollution, radiation or geopathic pollution, heavy metals etc.)
• Numerous viruses, such as herpes viruses, remain dormant in our organism after the primary infection until they are reactivated by stress.

Prevention and therapy of acute viral diseases

• We should bear in mind that viruses are mainly involved in diseases with a severe course when it comes to a pre‐damaged organism, particularly in view of the new challenges we are currently facing with viral diseases and increasing environmental pollution. Damage caused by environmental pollution (chemical pollution, radiation pollution, heavy metals, fine dust etc.) plays a major role here.
  For example, most patients who became more severely ill with beta‐corona‐viruses SARS‐CoV‐2, SARS‐CoV and MERS‐CoV either had previous illnesses and thus a weakened immune system, or lived in areas with particularly high environmental pollution. Older, weakened patients are also being increasingly affected.
• The RKI (Robert‐Koch‐Institut, German feral government agency and research institute) writes: “Coronaviruses are widespread among mammals and birds. They primarily cause mild colds in humans, but can sometimes cause severe pneumonia. SARS‐CoV‐2 uses the enzyme ACE‐2 as a receptor in order to enter host cells. High ACE‐2 density exists in the respiratory tract, as well as in the intestine, vascular cells, kidney, heart muscle and other organs.” (8)
• Some recent studies have suggested that statins, ACE inhibitors, or angiotensin receptor blockers upregulate the ACE2 receptor, and that patients taking these drugs are thus significantly more at risk for infection from SARS‐CoV‐2 with a more severe progression. (9)

3.1 Prevention from a holistic perspective

• Knowing that viruses are a part of our human ecosystem that can expose and indicate environmental stresses and support our cell communication, we should focus on stabilising the immune system and reducing environmental stress in the prevention of acute viral diseases.
• In the seminar Prevention through BICOM Therapy and Lifestyle Changes, we talk about ways to guide patients to cooperation and personal responsibility.
• The concept combines the findings of new biology, epigenetics and quantum physics with ancient knowledge from traditional Chinese medicine (TCM, Ayur‐veda medicine)

5 points for a healthy life:

1. Healthy nutrition (e.g. based on the 5 elements cuisine from TCM),
2. Exercise,
3. Sleep and relaxation,
4. Toxins / poisonous substances,
5. Drugs and addictive substances

• Healthy nutrition (e.g. based on the 5 elements cuisine from TCM): consideration of food from an energetic point of view; importance of water; acid‐base balance; intestinal flora; awareness
• Exercise: yoga exercises, physical exercise
• Sleep and relaxation times: stress management, sleep hygiene, breathing exercises (pranayama), meditation, mindfulness
• Toxins / poisonous substances: detoxification through BICOM® therapy and holistic methods
• Drugs and addictive substances: avoidance of substances used to escape the problems of daily life.

• The prevention of viral disease, like the prevention of chronic disease, has the goal of creating an environment within our human organism in which there are as few toxic and energetic burdens as possible, so that viruses and other pathogens are less able to multiply, reactivate or become symptomatic.
• For this purpose, you can use the programme sequences from the BICOM® prevent update, or also specifically search for stresses with the help of the CTT ampoules and eliminate them.

Procedure:

The test sets are particularly important here:

1. Vaccinations, metals, miscellaneous
2. Parasites and environmental loads
3. Bacteria
4. Allergic strains
5. Viruses and fungi
6. If necessary, test kit for herpes viruses, chlamydia, borrelia bacteria

• These test kits provide valuable information about the inner milieu and the human ecosystem.
• In addition, depending on the anamnesis, other test kits such as “Teeth”, “Hormones” or “Orthopaedics” can also provide valuable information.

The therapy plan is drawn up in accordance with the usual procedure in the CTT:

1. Basic therapy
2. Remove blockages
3. Open the elimination organs
4. Treat extracellular and intracellular stresses in succession

• To do this, test the appropriate couplings

The objectives of the preventive approach are:

1. Modulate / stabilise the immune system
2. Milieu change
3. Stress reduction
4. Stabilisation

3.2 Treatment of acute viral diseases

• Objective: to reduce viral load and replication and thus reduce virus‐induced symptoms.
• While the focus with chronic viral loads is on reducing extracellular loads and improving the individual’s milieu and optimising the immune system, the situation is different with acute viral diseases. However, due to the latest findings, one should not only use Ai or Di, but also definitely H+Di programmes.

Procedure:

1. Anamnesis
2. Physical examination
3. Test of elimination organs, blockages
4. Testing of the CTT‐5 element test kit
5. Testing of viruses, fungi, bacteria, parasites and environmental pollutants, vaccinations / metals

1.) Unmasking (ampoule and/or programme):

• Use the “Intracellular stress” programme (3136.0) as an unmasking programme (see attachment) before actually testing the viruses, or
• Use the “Unmask” ampoule from the “5 elements” test kit by treating the patient for about 3 minutes with programme 192 and this ampoule in the input cup (output hand applicators or mat). Then test the viruses in the usual way.

Acute or chronic infection?

“Intracellular stress” programme (3136.0):

• H+Di, lowest frequency, bandpass 3.6 Hz, wobble = yes, interval = no, amplification sweep = sym., amplification H 3.2 Di 15.0, amplification sweep speed = 50 sec. therapy time = 8 min.
  Input cup: saliva, blood if necessary

  Input: solar plexus
  Output: mat
  In channel 2: “Stress” ampoule from the “Allergic strains” test kit, alternatively: “Neurology / stress” substance complex.

• However, you can also use this programme for “unmasking” by running it before you test it.

H+Di, lowest frequency, bandpass 3.6 Hz, wobble = yes, amplification sweep = sym., amplification H 3.2, Di 15.0, amplification sweep speed = 50 sec. therapy time = 3 min.
Input cup: saliva, blood if necessary

Input: solar plexus
Output: mat
In channel 2: “Unmasking” ampoule from the “Degenerated cells” or “5 elements” test kit

Programme: “Stress reduction” (3137.0)

• H+Di, lowest frequency, bandpass, 4.3 Hz, wobble = yes, amplification sweep = sym., amplification Di = 1.10, amplification sweep speed = 10 sec. therapy time = 7 min,

Input cup: saliva, possibly blood

Input: solar plexus
Output: mat
In channel 2: “Stress” ampoule from the “Allergic strains” test kit, (alternatively: “Neurology / stress” substance complex)

Programme: “Intracellular pathogens 1”:

• Ai, lowest frequency, bandpass 14.5 Hz, wobble = yes, amplification sweep = sym., Ai 12.0, sweep speed 25 sec., therapy time = 12 min.

Programme: “Intracellular pathogens 2”:

• H + Di, normal range, without bandpass, amplification sweep increasing, H 3.7 Di 8.0, sweep speed 13 sec, therapy time = 8 min.

Programme: “Intracellular pathogens 3”:

• Ai, lowest frequency, bandpass 12.1 Hz, wobble= yes, amplification sweep sym., Ai 64.0, sweep speed 40 sec., therapy time = 12 min.

Programme: “Intracellular pathogens 4”:

• Ai, lowest frequency, band pass 2.4 Hz, wobble = yes, amplification sweep in‐ crease, Ai 6.0, sweep speed 60 sec, interval = no, therapy time =8 min

Programme: “Intracellular pathogens 5”:

• Di, normal range, bandpass 74.0 Hz, wobble = yes, amplification sweep decreasing, Di 4.0, sweep speed 300 sec., therapy time = 5 min.

Programme: “Intracellular pathogens 6”:

• Ai, normal range, band pass 112 Hz, wobble = yes, amplification sweep decreas‐ ing, Ai 40.0, sweep speed 300 sec, therapy time = 12 min

Programme: “Herpes viruses / intracellular pathogens 1”:

• H+Di, normal range, bandpass 160 kHz, wobble = yes, amplification sweep sym., Di 12.0, sweep speed 124 sec. interval = yes, therapy time = 16 min.

Programme: “Herpes viruses / intracellular pathogens 2”:

• H+Di, lowest frequency, band pass, BP sweep speed 185 sec, amplification sweep = sym., Dl tempo 28 sec, Di 5.0, interval = yes, therapy time = 13 min.

Input cup: Virus ampoule or the tested combination, plus patient’s blood if necessary with all.

An input applicator is used only if testing positive, then depending on the posi‐ tion tested (usually the location of the symptoms).
Output: mat
The second channel can run in parallel with either a tested substance complex, a tested orthomolecular substance from the orthomolecular test kit or substances of your choice that have an antiviral effect or support the immune system, such as L‐lysine, Engystol, samento, Wobenzym, boswelia, curcumin etc.

• Please test 1 (‐2) of these programmes per session for the patient. Always test whether therapy time and amplification are suitable.

Additional programe “Virus elimination”:

• A, lowest frequency, band pass, 120 sec, amplification sweep = sym., A 10.0, sweep speed 50 sec, therapy time = 12 min
  Input cup: “Anti‐virus” ampoule, and/or “Interferon” (both CTT viruses test kit), and/or „Intracellular elimination” (CTT vaccinations, heavy metals and miscellaneous), and/or “ATP” (hormone test kit), and/or “Stress” (CTT “Allergic strains”), and/or “Prevent virus reactivation”

No input applicator

Output: mat

•  I also continue to use the proven programmes 192 or 198 from the CTT with the aforementioned ampoules in the input cup. Test which of these 3 programmes suits the patient best and test amplification and therapy time individually. The stabilising programs 10327 or 3452 can also be used.
• It is recommended that the treatment information be transferred to a chip or trace elements / globule.

Literature

1. Das intestinale Virom: Leben mit Viren; Journal für Ernährungsmedizin ; September 2020
2. Das intestinale Virom; Der große Unbekannte, Trillium GmbH, Medizinischer Fachverlag
3. Wie Viren unseren Darm beherrschen; www.spektrum.de; 2016
4. Kembauer et al.: An enteric virus can replace the beneficial function of commensal bacteria, Nature (2014)
5. Neben dem Mikrobiom jetzt auch das Virom des Darmes im Fokus, Prof. Helmut Schatz, 2014, Deutsche Gesellschaft für Endokrinologie
6. Warum alles, was Sie Viren wissen falsch ist ‐ Naturstoff Medizin, Sayer Ji, Gesund leben, 2020
7. Hutchinson EC, Charles PD, Hester SS et al.: „Conserved and host‐specific fea‐ tures of influenza virion architecture” Nat Commun. 2014
8. Robert‐Koch‐Institut, Epidemiologischer Steckbrief zu SARS‐CoV‐2 und Covid‐19, Stand 11.12.2020
9. Ying‐Ying Zheng, Yi‐Tong Ma, Jin‐Ying Zhang& Xiang Xie, COVID‐19 and the cardi‐ ovascular system. Nature reviews Cardiology, March 2020
10. Roossinck, Marylin J.; Viren! Helfer, Feinde. Lebenskünstler, Springer Verlag, 2020
11. Mölling, Karin; Viren, Supermacht des Lebens, C.H.Beck, 2020
12. Rauch, Sabine; Viren und andere intrazelluläre Erreger: Verborgene Ursache chronischer Krankheiten; SR holistic therapy education GmbH, 2017