Borreliosis / Lyme Disease








1. How Humans can get Lyme disease






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2. How prevalent is Lyme disease



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3. What are the symptoms of Lyme disease



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4. Stages of Lyme disease progression

There are four recognized stages of Lyme disease:


Symptoms of early localized stage include:




Symptoms of early disseminated stage include:


♦ Fatigue, nausea, diarrhea

♦ Depression, anxiety, mood swings

♦ Cognitive impairment, light/sound sensitivity

♦ Severe headaches and/or neck stiffness due to meningitis

♦ Pain and swelling in the large joints

♦ Shooting pains with or without sleep disturbance


♦ Heart palpitations and dizziness due to changes in heartbeat


Symptoms indicating late disseminated stage of LD may include:





♦ Muscle and/or joint pains

♦ Cognitive defects

♦ Sleep disturbance

♦ Fatigue


● Changes in mental status


● A low CD57 count

● Low magnesium level

● A Lyme C6 peptide antibody index which exceeds 0.1



● Low or borderline levels of vitamin B12 and folic acid


● Abnormal brain MRI showing non-specific white matter disease



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5. Diagnosis of Lyme disease


♦ History of possible exposure to infected ticks

♦ Symptoms

♦ Laboratory blood tests


Commonly performed laboratory tests



Other tests





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6. How Lyme disease can be treated




Conventional treatments

These treatments rely mainly on antibiotics:



No vaccine is currently available for humans.

Alternative approaches




Cellular health and micronutrient synergy approach



In vivo studies:


Concerns with conventional Lyme disease treatment




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7. What is known about the bacteria which cause Lyme disease

 A. Various Borrelia species



B. afzelii and B. garinii: both predominant in Eurasia


B. mayonii isolated in the U.S.

B. valaisiana isolated throughout Europe as well as East Asia


B. bissettii identified in the U.S. and Europe

B. spielmanii present in Europe





B. Why it is difficult to eradicate Borrelia once the infection occurs













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8. Pathogenesis of Lyme disease

A. Survival and adaptive strategies of Borrelia sp.


They include:







Resistance against phagocytes and lymphocytes

B.   Molecular mechanisms involved in Lyme disease progression



2. Entering the bloodstream and colonizing tissues

♦ Penetration of blood vessels and homing



3. Persistence


♦ Complement-regulator acquiring surface proteins (CRASPs)


♦ Coiling phagocytosis (homing of pathogen inside the cells)

♦ Anti-inflammatory cytokines

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9. How can I protect myself against Lyme disease


To prevent tick bites:





Keep grass cut short in your yard/garden

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10. Additional information

1. Research articles

Our research group

  • Phytochemicals and micronutrients and LD
  • Phytochemicals and micronutrients and LD-review
  • Phytochemicals and micronutrients with doxycycline and LD
  • Phytochemicals and micronutrients interactions
  • Phytochemicals and micronutrients as a one composition in vitro
  • Phytochemicals and micronutrients as a one composition in vivo

Other research groups

2. Webinars

- Webinar (English): "Micronutrients against Lyme Disease"




- Webinar (Polish): "Borelioza – Oprócz Antybiotyków"


3. Guidelines

- ILADS : Treatment Guidelines

- IDSA: Treatment Guidelines



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  • Our research group

-          Phytochemicals and micronutrients and LD

-          Phytochemicals and micronutrients and LD-review

-          Phytochemicals and micronutrients with doxycycline and LD

-          Phytochemicals and micronutrients interactions

-          Phytochemicals and micronutrients as a one composition in vitro

-          Phytochemicals and micronutrients as a one composition in vivo

  • Other research groups

-          Grapefruit seed and LD

-          Teasel root and LD

-          Stevia and LD

-          Manganese and Zinc and LD

Lipoprotein (a)

Lipoprotein (a), compared to LDL and HDL is a lesser known lipoprotein, yet it is one of the strongest genetic risk factors for cardiovascular disease (CVD), including myocardial infarctions, stroke and other forms of CVD1,2.

Lp(a) is a cholesterol carrier composed of an LDL molecule with its structural protein - ApoB-100 - bound to the additional high molecular weight glycoprotein called apolipoprotein-a (Apo-a). These two proteins are linked via disulfide bonds3See the graph

Lp(a) has unique properties. Lp(a), due to the presence of an additional large protein (apo-a), has high binding affinity to various components of the extracellular cellular matrix (ECM), including fibronectin, laminin, and others5 . Based on its homology with plasminogen7, apo(a) also binds avidly to fibrinogen and fibrin, displaying strong antifibrinolytic properties and it is being considered the “missing link” between atherogenesis and thrombogenesis8.

Lp(a) and atherosclerosis: Earlier work by Dr. Rath and his colleagues have shown that Lp(a) accumulates within human atherosclerotic plaques and its deposition, more than LDL, parallels the progression of atherosclerosis4. Moreover, apo(a) is known to enhance smooth muscle cell replication6,the hallmark of atherosclerotic plaque formation in humans.

While many characteristics of this molecule have been elucidated since its discovery9 half a century ago, the physiological significance of Lp(a) has been poorly understood10.

Discovery of scurvy and Lp(a) connection:Discovery of scurvy and Lp(a) connection:

Lipoprotein(a) is primarily found in humans and sub-human primates. The emergence of the apo(a) gene was dated to about 40 million years ago, about the time of the divergence of the Old World and New World monkeys7. This date coincides with the loss of endogenous vitamin C (ascorbate) synthesis, through a mutation of the gene for gulonolactone-oxidase (Gulo) in the ancestor of man11. This fact led to the hypothesis presented by Dr. Rath and Dr. Pauling in 1990 connecting these two evolutionary events12. This concept explains many aspects of cardiovascular disease and at the same time challenges the highly promoted idea that elevated cholesterol blood levels are the main cause for atherosclerosis, heart attacks and strokes.

It is widely known that loss of the ability to produce vitamin C endogenously rendered our ancestors susceptible to scurvy- the disease which develops after a few months of complete vitamin C depletion in the diet and is characterized by disruption in collagen synthesis and a loss of connective tissue integrity. The morphological changes occurring in the vascular wall during hypoascorbemia (suboptimal vitamin C intake) and scurvy are characterized by the breakdown of the ECM and a loss of the endothelial barrier function. This leads to the formation of large endothelial gaps which allow the influx of macromolecules into the vascular wall that are normally excluded by an intact endothelial barrier. With continued lack of vitamin C supply a gradual deterioration of the vascular wall structure leads to hemorrhagic blood loss, which is the most frequent cause of death in people with scurvy.

According to this new understanding presented by Dr. Rath, the presence of the apo(a) macromolecule with its primary structure larger than collagen, with antifibrinolytic properties and with high binding affinity to extracellular matrix components, could have functioned as a repair molecule compensating for the structural ECM impairment caused by suboptimal vitamin C intake and scurvy. Therefore, loss of endogenous vitamin C production coinciding with emergence of Lp(a) synthesis in humans can illustrate the event contributing to the survival of our ancestors at the times of severe nutrient deficiencies during the Ice Ages. ...hide content

Scientific support for scurvy- Lp(a)- heart disease connection: Scientific support for scurvy- Lp(a)- heart disease connection:

Our work: In our earlier publications we demonstrated how vitamin deficiency can trigger the development of atherosclerosis independent of dietary cholesterol and presented natural means to control this process HEART DISEASE. Recently we developed a unique transgenic mouse model that allows for increasing our understanding of human atherosclerosis on a much larger scale.

Our newly developed mouse (Gulo-/-;Lp(a)+) mimics human metabolism in its two distinct genetic features: the lack of endogenous vitamin C synthesis (Gulo-/-) and the expression of human Lp(a). This mouse model allowed us to test whether the loss of vascular integrity due to prolonged vitamin C depletion and its suboptimal intake can result in an increased deposition of Lp(a) molecules inside the vascular wall and consequently, atherosclerosis. Moreover, we could test whether dietary supplementation with high levels of vitamin C can prevent this pathological process. The results of this important study, which challenge current cholesterol-based approaches to atherosclerosis, have been submitted for a publication.

Other work: Independently, the connection between loss of vitamin C production, structural damage in the vascular wall and elevated blood cholesterol levels that was discovered by Dr. Rath about 20 years ago has been gaining increased scientific support. Among others it was confirmed by the work of Maeda et al. , using genetically modified mice which, similar to humans, have lost the ability of endogenous production of vitamin C. The early hallmark of vitamin C deficiency displayed in these mice was the disruptions of the vascular structure and elevated blood cholesterol levels. This model, however does not allow to investigate the role of the other critical factor in human atherosclerosis, which is the Lp(a). ...hide content

Micronutrients and Immunity

Nutrition, immunity and infection are inter-related.1 Malnourished persons show immune dysfunction, which predisposes them to infections. Conversely, micronutrient supplementation can enhance immune function and suppress infection. read more...

Malnutrition and nutrient deficiencies are common in infectious diseases and are the leading underlying cause of immune deficiency.2 Of the 13-14 million children dying annually in developing countries, most are malnourished and 70% die of infectious diseases. Immune deficiency as a consequence of malnutrition is the leading cause of death of children, the elderly, and adults, with more severe consequences than HIV-related causes.

Malnutrition and micronutrient deficiencies disrupt the function of various immune system components, weakening immune defenses and increasing vulnerability to various diseases. The illness in turn is accompanied by the loss of bodily nutrients, which further aggravate pre-existing nutrient deficiencies. If the latter are not addressed, the vulnerability to other diseases increases, triggering a spiral of diseases often impossible to control. Many of these infectious diseases can be prevented and controlled by simple and affordable measures, such as nutrient supplementation. less

Nutrients support all the critical steps of our immunity for an effective immune response. These include:

  • Non-specific defense components such as the synthesis of interferon and function of phagocytic cells.
  • Protective anti-microbial barriers created by the skin, mucus membranes, tears, saliva, gastric juice, etc.
  • Production of antibodies and optimization of cell-mediated immunity. It is well established that micronutrients such as vitamin C, A, B-5, B-6, B-12, and folic acid as well as certain trace elements such as iron, zinc, selenium, copper and others are essential for optimizing white blood cell production and immune function.3,4

It is also known that a single nutrient does not ensure optimum health and a complete spectrum of micronutrients is needed to support the immune system to function at full capacity. This is the approach promoted by Cellular Medicine, which focuses on nutrient synergy to optimizing cellular metabolism and restoring its balance, which is essential for health. Our research has shown that nutrient synergy is more effective than single nutrients, or their random combination, in addressing specific physiological tasks. Nutrient synergy can improve the synthesis and function of infection-fighting blood cells as well as stop infectious agents from spreading.2 Thus, nutrient synergy can provide effective health solutions through improving the general immunity of the body and supporting its physiological functioning.

Information on how micronutrients can affect the course of AIDS and tuberculosis can be found here. Information on how nutrients affect avian flu and human influenza virus is summarized here.

References Cited

  1. Bhaskaram P Nutritional Review 2002; 60(5): S40-5.
  2. A. Niedzwiecki, M. Rath, Malnutrition: The Leading Cause of Immune Deficiency Diseases Worldwide, DRRI Brochure, 2005.
  3. Beisel WR Am J. Clin Nutr 1982; 35: 415
  4. Watson RR Nutrition, disease resistance, and immunity. New York, Marcel Dekker, 1984.


Viral Infections-Human Influenza

Human Influenza

An effectively functioning immune system is the first line of defense against any infection. The body can also fight flu viruses by affecting many steps of viral metabolism, including:

  1. Interfering with the cellular processing of viruses and limiting their ability to enter and multiply inside the cells.
  2. Creating biological barriers obstructing the spread of viruses in the tissue.

Dr. Rath proposed that vitamin C and the amino acid Lysine can hinder the spread of viruses and other infectious agents in the body through increasing integrity and strength of the connective tissue surrounding the cells. These components can also affect viral infective ability and replication. read more...

Influenza is one of the oldest and most common infections. Every year it affects a large number of people and it can be life threatening, especially in young children, the elderly, and those who are malnourished or have a compromised immune system. In the US about 36,000 people die annually as a result of seasonal flu outbreaks. In recent years fears have been spreading through the media about the dangers of a pandemic of an avian flu or more recently, swine flu.

To date there are no effective therapies or vaccines against flu viruses. These viruses undergo frequent genetic mutations, therefore many treatments developed for specific forms of viruses lose their effectiveness, even after one flu season. Frequently recommended for flu (including bird flu and swine flu) drug Tamiflu can according to its manufacturer (Roche), shorten flu symptoms by one day only, provided it is taken within the first 48 hours of infection. Also, since this drug has been tested for short time use (a few days), it is not known whether its frequent or prolonged intake can cause serious toxicity. Hence, there is need for safe and effective therapy against the flu.

Cellular Medicine against flu: Our researchers have tested whether a specific micronutrient synergy mixture can affect the infectivity and/or multiplication of human influenza A virus. This mixture is composed of nutrients that have been researched and shown to be effective in controlling the spread and growth of cancer cells in the tissue. Since all viruses spread in the body using a mechanism similar to cancer this nutrient formulation could have an effect on viral infections as well. In addition, in various studies many of these nutrients have demonstrated clinical effectiveness in controlling flu. less

We have evaluated the effect of nutrient synergy using the specific indicators of viral growth and spread. To date our preliminary findings have indicated the following:

  • Nutrients can inhibit the activity of the viral neuraminidase, an enzyme on the surface of viral particles that enables viruses to escape from host cells and infect other cells;1, 3
  • Nutrients can completely stop the multiplication of human influenza A/H1N1 virus in infected kidney cells;1,3
  • Nutrients can inhibit secretion of collagen digesting enzymes (MMP2 and MMP3) in cells infected by human influenza A/H1N1 virus, thereby stopping their spread in the tissue;2, 3
  • Nutrients demonstrated high antiviral activity against avian influenza virus A/H5N1 in cultured cell lines;4
  • In Vivo, a nutrient mixture was shown to inhibit pathological effects in chickens infected with the avian flu virus.5

Further details on our flu research project showing how nutrients can affect the multiplication and spread of influenza virus can be viewed here.

Facts about the occurrence, impact and public consequences of Swine flu can be found here.

References Cited

  1. Jariwalla RJ et al., Biofactors, 31(1): 1-15 (2007).
  2. Roomi MW et al., Biofactors, 33(1): 61-75 (2008).
  3. Jariwalla RJ et al., Chapter 15 in: Global View of the Fight Against Influenza (PM Mitrasinovic, Ed) Nova Science Publishers; pp 251-268 July 2009.
  4. Deryabin PG et al., Biofactors, 33: 85-97 (2008)
  5. Barbour EK et al., Intern J App Res Vet Med, 5(1): 9-16 (2007)



Long-term deficiency of specific nutrients essential for immune system function leads to impaired immunity and higher susceptibility to bacterial, viral and other infections.

Scope of Tuberculosis (TB) Scope of Tuberculosis (TB)

Tuberculosis (TB) remains one of the world’s leading infectious causes of death among adults. The global incidence of tuberculosis, 8-12 million new cases of active tuberculosis a year, resulting in deaths of over two million people a year, has been increasing by 1% annually since 1980. Developing countries have 90% of the world’s TB cases, with incidence concentrated mainly in Africa.  More than 500, 000 TB patients die annually in Africa where malnutrition is common. This disease is commonly associated with poverty and is prevalent in undernourished individuals. This problem is further exacerbated by the pervasive use of ARV drugs that can damage the immune system of AIDS patients who are taking them. In fact, a large number of AIDS patients die from TB.  Although conventional treatment relies on the use of antibiotics, the bacteria causing TB (Mycobacterium tuberculosis) have become increasingly resistant to current drugs and about 50% of the patients die despite this treatment. ...hide content

Disease progression and risk Disease progression and risk

Tuberculosis develops when after the infection with TB bacilli, the bacteria overcome the immune system defenses and begin to multiply. In about 1% to 5% of cases this occurs soon after infection. However, in the majority of cases, the disaese can develop after a longer period, sometimes even a few years. Such a latent infection has no obvious symptoms. The risk of bacteria activation increases with impaired function of the immune system such as in malnutrition and AIDS.

Patients with increased risk of contracting tuberculosis are those with diabetes, those on prolonged therapy with corticosteroids and immunosuppressing drugs, cancer patients (especially suffering from leukemia, and Hodgkin’s disease), patients who have had intestinal bypass , and those suffering from chronic malabsorption syndromes, vitamin D deficiency, and low body weight. ...hide content

Conventional treatments Conventional treatments

Treatment for TB is based on the use of antibiotics to kill the bacteria. The most commonly used antibiotics are rifampicin and isoniazid. However, TB requires much longer treatment periods than most other bacterial infections and it takes about 6 to 12 months to eliminate mycobacteria from the body. There is an increasing concern with the development of antibiotic resistance to TB.  It has been estimated that about 20% of TB cases that developed between 2000 and 2004 were resistant to standard treatments. Treatment of such TB cases often requires up to two years of daily use of multiple TB drugs with serious adverse effects which results in death in 40-60% of patients treated.

Hepatotoxicity is the most common adverse effect of standard TB treatment. This can be indicated by an increase in the level of enzymes (transaminases) which are the marker of liver cell damage (which in extreme cases may lead to interruption of TB treatment). This treatment can also lead to acute liver failure and even death. Hepatotoxicity due to isoniazid is most common, especially when combined with rifampicin; however, pyrazinamide is the most hepatotoxic among essential anti-TB drugs.

The increasing worldwide incidence of tuberculosis, especially multi drug resistant TB, necessitates a search for new more effective and less toxic treatment alternatives. ...hide content

Micronutrients and Tuberculosis Micronutrients and Tuberculosis

Malnutrition and a clinical deficiency of specific nutrients essential for immune system function leads to immune deficiency and higher susceptibility to bacterial, viral and other infections. Immune enhancing nutrients such as vitamin C (ascorbate) and other antioxidants have shown beneficial effects in various types of infections, including TB. Antioxidants used in conjunction with standard TB regimens, has been shown to accelerate healing from tuberculosis. Studies have shown that vitamin C can prevent the growth of cultures of tuberculosis bacterium.

Nutrients such as vitamin C and lysine can help improve immune system function, but also contribute to halting the spread of infectious agents. According to Dr Rath’s findings these nutrients are critical for inhibiting the activity of plasmin and matrix metalloproteinases (MMP-2 and MMP-9), which are used by bacteria and other infectious agents to spread in the body. They are also essential for maintaining optimum synthesis and structure of the connective tissue, the natural barrier for the spread of infections. Tuberculosis patients are found to have elevated MMP-9 levels, which is correlated with severity of illness in patients with active tuberculosis. MMP-9 is secreted by both the bacillus and host response to infection with mycobacterium tuberculosis. Our previous studies have demonstrated that adequate levels of ascorbic acid, proline and lysine can prevent MMP-9 secretion and degradation of collagen matrix in various systems.

Pulmonary TB is accompanied by inflammation and related to oxidative stress, which leads to development of lung fibrosis and its dysfunction. TB patients, even after apparently successful drug treatment, still demonstrate high levels of circulating lipid peroxides and low concentrations of plasma vitamin E. Administration of nutrients such as ascorbic acid and vitamin E have been shown to accelerate tuberculosis healing, based on decay cavity closure and negative sputum. Furthermore, a clinical trail cohort study of 26,975 Finnish men during a median follow-up of 6 to 7 years found a high inverse association between vitamin C intake and incidence of tuberculosis. Subjects with intake of >90mg of vitamin C and increased consumption of fruits, vegetable and berries had significantly lower risk of tuberculosis. ...hide content

Nutrient Synergy In TB: Clinical approach Nutrient Synergy In TB: Clinical approach

To find a natural way to control TB and improve conventional treatment of this disease, we conducted a joint clinical study in collaboration with physicians in Europe in 120 hospitalized patients with active TB.  In this study all patients (test group) received the conventional TB treatment supplemented with a specific combination of vitamins and other nutrients for 2 months. A control group (100 patients) recently treated at the hospital was selected by matching to the Test patients by stage of disease, gender and several other criteria.

The group of TB patients, who took micronutrients in addition to conventional treatment, experienced significant health improvements. Compared to patients on drugs alone, patients on drugs plus micronutrients had significant healing of the lung, reduced drug side effects (allergies or toxic allergic reactions), complete disappearance of TB-associated inflammation and fever, and significant reduction of coughing and liver enlargement. The patients on the vitamin program experienced full recovery, which was 2-3 weeks faster. ...hide content