Neural therapy
and the anti-inflammatory concept in chronic diseases
Petja Piehler, MD
Modern medicine is increasingly discovering chronic inflammation as the cause and lowest common denominator of today’s diseases of civilization. The understanding of the multifactorial genesis of disease development contributed to this development (also in the case of genetic diseases) in the context of non-linear interactions. Evidence of new research results the importance of the chronic pro-inflammatory situation as a risk factor for degeneration and deterioration. These new findings serve as a catalyst in the search for anti-inflammatory substances and therapeutic principles. The progress of research in the field of biologics and biosimilars is unstoppable. On the other hand, there is a great need for treatment options with more favorable benefits – side-effect profile. Recent scientific work confirms this clinical benefit of local anesthetics in the treatment of inflammation and open up a broad new field for the application of neural therapy also outside of pain therapy. Some of these scientific findings and correlations will be presented below.
It is well known that acute inflammation is the body’s immunological response to cell and tissue damage and involves diffusing of specific cells in the damaged tissue. Acute inflammation is an important adjustment mechanism of the living organism during infections and wound healing. Inflammation can act as a protective reaction but only with an equilibrium of pro- and anti-inflammatory cellular and humoral factors. A whole range of diseases occurs through permanent disturbance of this equilibrium, thus developing a chronic inflammation that can destabilize the whole body and cause genetic or acquired diseases to manifest. The metabolic syndrome and diabetes Type 2 mellitus are increasingly associated with a sub-clinical inflammatory status, recognizable by circulating inflammation parameters, such as CRP, fibrinogen, serum amyloid A, pro-inflammatory cytokines (IL-6, IL-8, TNF-alpha) [1,2]. So, in recent years one of the well-known classic players in the pathogenesis of the metabolic syndrome and atherosclerosis also include inflammation (Fig.1).
Figure 1: Formation mechanism – metabolic syndrome and atherosclerosis
Various biomarkers such as CRP and interleukin-6 are associated with insulin resistance [3]. Cardiovascular diseases have long been associated with a sub-clinical inflammation due to the increase of circulating acute phase proteins and cytokines (IL-6, TNF, IL-1Ra, etc.). Since the Copenhagen City Heart Study, it is known that an initially increased CRP value indicates poorer survival in acute coronary events [15]. Recent data show that obesity is also a pro-inflammatory condition, in which many pro-inflammatory cytokines can be synthesized in adipose tissue [4]. An increased cardiovascular risk exists for patients with inflammatory bowel disease, whereby this effect cannot be explained by inflammation of the intestinal wall but rather through systemic inflammation. This can influence the coagulation cascade and endothelial dysfunction thus inducing the development of atherosclerosis [5]. For instance, an increased rate of cardiovascular events is found in patients with IBD, though, in this group of patients the traditional risk factors occur less often.
The link between periodontal disease and atherosclerosis has been known for a long time. There is now also data on disease-promoting interactions between diabetes and periodontal disease [6]. Increasingly also COPD is detected as a systemic inflammatory disease, where inflammation markers can be found in blood, sputum, BAL, urine and in breath exhalations (Table 1).
Table 1: Important biomarkers in COPD
group
biomarker
relevance
cytokines
interleukin 6
– increased especially with exacerbation – connection with myocardial failure / muscle weakness – induction of acute phase proteins
tumor necrosis factor- ß
– association with hypoxia – related to cachexia, skeleton muscle atrophy, weakness
IL-1 ß
– possible polymorphism of the IL-1 ß gene – possibly related to cachexia
chemokines
– recruitment of neutrophils and monocytes – related to muscle weakness
adipokines
– possible association with cachexia
acute phase proteins
CRP
fibrinogen
– increase even with stable COPD – associated with morbidity in COPD as well as – relation to lung function and hospitalization frequency
serum amyloid A
– increased and correlated to the severity of the exacerbation
circulating cells
surfactant protein D
– relation to severity and symptoms of COPD
monocytes
– possibly intrinsic defect in differentiation of alveolar macrophages
Even in the absence of clinical signs of infection there is often an increase in CRP. For a long time, there have been indications of a connection between inflammation and carcinogenesis. As early as 1863, R. Virchow described a close connection between chronic inflammation and cancer. New data show that a permanent inflammation not just stimulates carcinogenesis, but also the metastasis of cancer cells [7]. It is known that in several diseases with chronic inflammatory constellation (ulcerative colitis, hepatitis C, chronic atrophic gastritis) carcinomas more commonly develop. Patients with such diseases will be subjected to regular checkups in order to rule out degeneration. Pathogenetically, chronic inflammation promotes DNA changes and cellular transformation towards tumor cells. Inflammation mediators can lead to a cancellation of the normal tumor suppression and apoptosis.
Inflammaging
The changes in the aging immune system are also viewed in the context of chronic low-level inflammation and aging as a consequence of chronic inflammation (inflammaging) [8]. Inflammaging is accelerated by an impairment of the functionality and controllability of the extracellular matrix, whereby it is a pro-inflammatory cycle in the matrix. This is due to oxidation processes, disturbed acid / base balance and increased formation of AGE (advanced glycation end products). Research on nursing home residents shows that increased inflammation parameters (IL-6, neopterin, hsCRP) correlate with increased mortality and decreased functionality.
Anti-inflammatory prevention and therapy
Research in medicine shows that quite a number of civilization diseases have chronic inflammation as the lowest common denominator. Therefore, it makes sense to apply an anti-inflammatory prevention and therapy concept. This refers to a regeneration of the matrix (matrix reset) and disease prevention based on:
• nourishment
• sports
• use of local anesthetics systemically
• interference field therapy
Sports
Sports take a special place as part of an „anti-inflammatory lifestyle“. Several studies show that already a few weeks after commencement of increased physical activity, the circulating inflammatory markers sink. There is a reduction of insulin, IGF, and adipokines, favorable hormonal interactions and a positive influence on the repair of genes.
Anti-inflammatory diet: polyphenols
An anti-inflammatory diet provides the fundamental therapeutic basis. This is the regular one ingestion of highly potent anti-inflammatory natural substances (polyphenols). In this regard, there is currently a whole series of promising herbal substances, so-called phytopharmaceuticals:
• Quercetin (broccoli, apple, onion)
• Resveratrol (wine, peanut)
• 6-gingerol (ginger)
• Naringenin (grapefruit)
• Chili Pepper (cayenne pepper)
• Kaempferol (red grapes, red wine)
• Curcumin
• Frankincense and others
The polyphenols have a dual effect on inflammatory processes, being that they stimulate the anti-inflammatory cytokines and down regulate pro-inflammatory cytokines. The anti-inflammatory potency of some of these herbal substances such as B Capsaicin is, in my opinion, comparable to cortisone.
Local anesthetics The local anesthetics (mainly procaine 1% and lidocaine 1%) are used in neural therapy administered locally, segmentally or systemically. As part of an overall concept to influence chronic sub-clinical inflammation could local anesthetics play a special role. These substances inhibit excessive stimulation of the inflammatory system without weakening the body’s defense mechanisms. More and more data confirm these anti-inflammatory effects of local anesthetics. Some research shows that long-term parenteral therapy with procaine leads to a decrease in interleukin-6 and CRP [10]. These effects are not to explain by the for local anesthetics typical blockade of sodium channels and are known as „alternative“ effects from local anesthetics, which are amongst others expressed in cerebral and cardiac protection as well as a reduction in bronchial hyper reactivity [11]. The anti-inflammatory effect of local anesthetics is mediated via G-protein coupled receptors on the cell membrane [9,12,16].
Anti-inflammatory diet: polyphenols
There is good data for a direct anti-inflammatory efficacy of local anesthetics via reduction of inflammatory mediators through:
• inhibition of prostaglandin synthesis
• inhibition of leukocyte migration and leukocyte adhesion to the inflammatory endothelium
• inhibition of the release of lysosomal enzymes
• reduction of histamine release from mast cells [13]
The anti-inflammatory potency of local anesthetics is comparable to the effect of NSAIDs but with fewer side effects [14]. The anti-inflammatory effect of local anesthetics is also based on a reduction in the sympathotonus. It is known that chronically inflamed tissue is a persistent pathological irritation of the autonomic nervous system. One can positively control chronic inflammatory illnesses, among others, by the sympathetic nervous system. The application of local anesthetic leads to an interruption of the pathological irritation of the sympathetic nervous system, normalization of blood flow and an interruption of the inflammatory cycle. In the field of pain therapy as well as organ pathology, one can use this effect by applying procaine-base infusions. Depending on the indication, 100-400 mg procaine with 80-120 ml sodium bicarbonate in an isotonic saline solution is administered intravenously over 60-90 minutes. In our department of internal medicine, this systemic neural therapy has proven itself for various diseases (see Info box), has few side effects and improves the effect of other pharmacological or non-pharmacological therapeutic approaches.
Main indications: systemic neural therapy
– Acute and chronic pain conditions, especially when there are several symptoms or in fibromyalgia
– circulatory disorders
– various diseases with a pro-inflammatory component for the purpose of reducing the body’s entire inflammatory load and saving on other pharmacological substances
– in the accompanying oncological treatment
– for states of exhaustion and wound healing disorders, etc.
Interference fields Neural therapy plays another important role in the treatment of interference fields that are a catalyst for degeneration and deterioration. The interference fields are areas of the body in a state of chronic irritation that can be clinically silent and cause no symptoms over a long period of time. The character of an interference field can be diseased teeth, scars, and chronically inflamed para-nasal sinuses or internal (regulated) organs. The interference fields can destabilize the living organism through biochemical, bio-mechanical and neural effects, prevent or slow down healing processes or cause therapy blockages. The flooding of the interference fields with local anesthetics in turn causes an irritation pause in the matrix due to signal modulation, it is a catalyst for regeneration and relieves the control systems. The new knowledge on the pathogenesis of civilization diseases and the new findings on the properties of local anesthetics can give the neural therapy a strong impetus. By expanding the range of indications outside of the pain therapy and further developing the method it can become an important player contributing to the holistic anti-inflammatory concept.
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