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From the Townsend Letter
July 2014

From Lyme Disease to Addiction: How to Energetically Restore the Neuroendocrine-Immune System
by Dalal Akoury, MD
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Lyme disease, branded as the "great imitator," is the most complex and clearly misunderstood disorder. Lyme disease earned this famous prerogative due to the fact that its symptoms often blur with those of several other diseases, especially complex neurodegenerative syndromes. The neuropsychiatric effects of Lyme disease are well studied, and documented facts.1 The evolutions of the neuropsychiatric symptoms in Lyme/tick-borne diseases are better clarified through an appreciation of the role of psychoneuroimmunology. The progression of the neuropsychiatric phase of Lyme disease, including the devastating addiction disorder, will be the pivotal argument of this article. The pathophysiology of degenerative neurological and addiction spectrum diseases associated with Lyme disease will be discussed. The second half of this article will be devoted to unraveling the fundamental role of restoring cellular energy in the treatment of both Lyme disease and addiction. Emerging scientific research is beginning to explain how immune-mediated and cellular energy imbalances play a major role in the pathophysiology and the psycho-neurodegenerative consequences of Lyme disease.

Psychoneuroimmunology (PNI) is the study of the interaction between psychological processes and the nervous and immune systems of the human body. PNI takes an interdisciplinary approach, incorporating psychology, neuroscience, immunology, physiology, genetics, pharmacology, molecular biology, psychiatry, behavioral medicine, infectious diseases, endocrinology, and rheumatology.2,8

The Neuroendocrine-Immunologic Evolution of Neuropsychiatric Lyme Disease
The PNI consequences of neuroborreliosis outline the neuroimmunological consequences of B. burgdorferi infection.3,4 These immune-mediated limbic inflam­mations contribute to the progression of the disease of addiction. The immune deregulation results in persistent neuroinflammation and cytokine imbalances. Both of these mechanisms may be present at the same time in chronic infections. Lyme-induced limbic encephalopathy and progressive neuroinflammation is a classical model that validates the inflammatory and molecular mimicry effects of B. burgdorferi on neuropsychiatric symptoms, including addiction tendencies.
The chronic inflammatory and neurodegenerative changes in the limbic system progression lead to addiction, depression, psychosis, dementia, epilepsy, autism, and other mental illnesses.5,6 These pathophysiological modifications are associated with oxidative stress, excitotoxicity in the limbic system affecting the reward system, resulting in HPA imbalances and alterations in homocysteine metabolism. In addition, it triggers deregulations in the main neuroendocrine circuitries, including the phenylalanine, tyrosine, tryptophan, and GABA glutamine systems.
Lyme disease has been associated with an increase in pro-inflammatory cytokines interleukin-6 (IL-6), IL-8, IL-12, IL-18 and interferon-gamma, and chemokines CXCL12 and CXCL13, along with increased levels of pro-inflammatory lipoproteins. Elevated levels of IL-6 can cause symptoms of fatigue and malaise, common to many infectious conditions as well as Lyme disease.
Borrelia species induce activation of IL-17 production. The chemokine CXCL13 is a key regulator of B cell recruitment to the cerebrospinal fluid in acute Lyme neuroborreliosis CSF CXCL13 and can be used as a diagnostic marker for infection. Bb spirochetes express pro-inflammatory lipoproteins on the outer membrane of the borrelia cell wall. These lipoproteins attract neutrophils and are 50- to 500-fold more active inducers of cytokines and mitogens of B cells than lipoproteins of other organisms, such as Escherichia coli. Bacterial and borrelia lipoproteins can disseminate from the periphery to inflame the brain.

Microbes and Immune Reactions

Over 250 peer-reviewed scientific articles demonstrate the causal association between Lyme/tick-borne disease and mental illness.12,14

Lyme disease effects include cell penetration, toxin release, and incorporation of parasite genes into the host genome. The subsequent host immune response to these attacks includes cytokine release, antibody formation, inflammation, and a host of other cellular responses. The pro-inflammatory cytokines cascade mediates a sickness syndrome from IL-1, IL-6, and tumor necrosis factor (TNF) production. These inflammatory cytokines induce inflammation-mediated mental symptoms. Symptoms seen with inflammatory cytokine excess include cognitive impairments, depression, anxiety, mania, irritability, impulsiveness, hostility, substance abuse, and exhaustion. Addiction spectrum disorders associated with Lyme/tick-borne diseases may be mediated by a combination of inflammatory and molecular mimicry mechanisms.

The Brain Immune Circuitry
Understanding the interaction between the immune and nervous systems, including the limbic system, is critical. The immune system and the brain communicate through signaling pathways. The brain and the immune system are the two major adaptive systems of the body. Two major circuitries are involved in this cross talk: the hypothalamic-pituitary-adrenal (HPA) axis  and the sympathetic nervous system (SNS). The activation of the SNS during an immune response might be aimed to localize the inflammatory response. The brain and immune systems have many similarities – both defend against threats by shifting allocation of resources as environments change; both have intracellular transmitters, receptors and feedback capability; there are similarities between the gut and immune barrier and the blood brain barrier (BBB); both have innate and learned capabilities; and in both cases, failures to shift from innate to learned responses result in pathology.9 The brain and immune systems both switch back and forth, eliminating one threat then recovering before responding to the next threat.
Pro-inflammatory cytokines, including IL-1, IL-2, IL-6, IL-12, interferon-gamma (IFN-gamma), and TNF-alpha, can affect brain growth as well as neuronal function.15,16 Circulating immune cells such as macrophages, as well as glial cells (microglia and astrocytes), secrete these molecules. Cytokine regulation of hypothalamic function is an active area of research for the treatment of anxiety-related disorders. Cytokines mediate and control immune and inflammatory responses. Complex interactions exist between cytokines, inflammation, and the adaptive responses in maintaining homeostasis. Like the stress response, the inflammatory reaction is crucial for survival.
These are mediated by the HPA axis and the SNS. Common human diseases such as allergy, autoimmunity, chronic infections, and sepsis are characterized by a deregulation of the pro-inflammatory versus anti-inflammatory and T helper 1 (Th1) versus Th2 cytokine balance

Disease Progression
It is well documented that chronic infections are a root cause for chronic stress, sleep disorders, cognitive impairments, and chronic fatigue. Sleep disorders are commonly associated with chronic inflammatory diseases and stress-related disorders.10 The bidirectional communication between the brain and the immune system contributes to inflammation-mediated disrupted sleep quality and vice versa. Cytokines produced by cells of the immune and nervous systems (particularly IL-1-beta and TNF-alpha) regulate sleep; signal neuroendocrine, autonomic, and limbic and cortical areas of the CNS to affect neural activity; and modify behaviors, hormone release, and autonomic function.11,17-19 Growth hormone production depends upon the presence of delta sleep, which is reduced in an inflammatory state. Therefore, increasing delta sleep is therapeutic, while disease progression is fostered by nonrestorative sleep and is associated with fatigue, cognitive impairments, pain, and emotional symptoms. The consequences of both nonrestorative sleep and associated chronic stress reactions contribute not only to perpetuating the disease process and decreased regenerative functioning, further compromising immunity, oxidative stress, and decreased resistance to infectious disease, but also the development of addiction-spectrum disease.

Lyme Disease: Pain, Stress, and Addiction
According to reports from the National Institutes of Health (NIH), people who struggle with stressful medical conditions and infections such as Lyme disease are more vulnerable to addiction In fact, statistics supplied by the US Department of Health and Human Services (HHS) show that individuals with chronic diseases or pain experience substance-abuse rates at 2 to 4 times those of the general population.
Many of the same neurocircuits that respond to drugs also respond to stress. Stress increases the release of corticotrophin-releasing factor (CRF), a hormone that catalyzes biological responses to stressors such as increased heart rate and metabolism. Abusing drugs also increases CRF levels and thereby heightens danger of relapse.
Infection-induced stress also triggers the fight-or-flight–moderating amygdala.7 When the amygdala perceives any threat either endogenous (infection, inflammation) or exogenous, it responds irrationally and hijacks the individual's ability to think clearly.

Lyme Disease and Substance Abuse
The CDC estimates that causes of Lyme disease cases may be underreported by a factor of up to 12-fold, and those with untreated illness and lingering posttreatment effects may be more likely to abuse drugs. Motivated by a desire to achieve relief from the intolerable symptoms of Lyme disease, the afflicted person may seek out different ways to self-medicate using any of the following:

  • illicit or prescription opiates to mitigate the pain symptoms
  • illicit or prescription amphetamines to overcome fatigue
  • benzodiazepines or alcohol to ease anxieties, insomnia, and agitation
  • marijuana for insomnia, sedation, and mental escape

Due to the considerable pain and fatigue experienced during the initial stages of Lyme disease, pain relievers and stimulants are the two types of drugs more commonly used to self-medicate.

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