How to Fix Mitochondria to Improve Fatigue in
Lyme Disease
Treat Lyme by
Marty Ross MD
Chronic Lyme infection can hurt the cell energy
factories called mitochondria.
Here are steps to fix
this problem from Marty Ross MD.
Improve Lyme
disease treatment through Mitochondria repair.
Mitochondrial
Dysfuction is upregulated during Lyme Disease
Lyme disease often
causes mitochondrial
dysfunction, impairing
cellular energy
production, leading to
symptoms like chronic
fatigue, brain fog, and
muscle pain, due to
bacterial toxins,
oxidative stress, and
inflammation disrupting
mitochondria.
This cellular energy
deficit affects the
brain and immune system,
contributing to
cognitive issues, mood
changes, and persistent
symptoms in
Post-Treatment Lyme
Disease Syndrome
(PTLDS), with
supplements like
CoQ10 and
alpha-lipoic acid
sometimes used to
support mitochondrial
health.
How Lyme Impacts
Mitochondria
Direct Toxicity: Lyme
bacteria (*Borrelia
burgdorferi) and
their byproducts can
damage mitochondrial DNA
and cell walls.
Oxidative Stress: The
infection triggers
excessive inflammation,
creating reactive oxygen
species (ROS) that
overwhelm mitochondria,
leading to superoxide
buildup and energy loss.
Energy Deficit: Impaired
mitochondrial function
reduces ATP (energy)
production, starving
energy-intensive cells,
especially in the brain,
causing "brain fog" and
fatigue.
Immune System:
Mitochondria in immune
cells become
dysfunctional, affecting
the body's ability to
fight the infection and
coordinate immune
response
Lyme: inflammation,
oxidative stress, and mitochondrial dysfunction
March 2015 .
Abstract
Abstract
Lyme borreliosis is transmitted through the bite
of a tick that is infected by the bacterial
spirochete Borrelia burgdorferi. Clinical
manifestation of the disease can lead to heart
conditions, neurological disorders, and
inflammatory disorders. Oxidative stress has
been implicated in the pathogenesis of many
human diseases. The aim of this study was to
investigate the mechanisms of oxidative stress
and intracellular communication in Lyme
borreliosis patients.
Mitochondrial superoxide and cytosolic ionized
calcium was measured in peripheral blood
mononuclear cells (PBMCs) of Lyme borreliosis
patients and healthy controls. .
Mitochondrial superoxide levels were
significantly higher (p < 0.0001) in Lyme
borreliosis patients (n = 32) as compared to
healthy controls (n = 30). Significantly low (p
< 0.0001) levels of cytosolic ionized calcium
were also observed in Lyme borreliosis patients
(n = 11) when compared to healthy controls (n =
11). These results indicate that there is an
imbalance of reactive oxygen species and
cytosolic calcium in Lyme borreliosis patients.
.
The results further suggest that oxidative
stress and interrupted intracellular
communication may ultimately contribute to a
condition of mitochondrial dysfunction in the
immune cells of Lyme borreliosis patients.
Lyme Disease: A Role
for Coenzyme Q10 Supplementation?
March 30, 2022
Abstract
Lyme disease results
from a bacterial infection following a bite from
an infected tick. Patients are initially treated
with antibiotics; however, in cases where
antibiotic treatment is delayed, or when
patients do not respond to antibiotic treatment,
fatigue may develop alongside problems affecting
the nervous system, cardiovascular system, and
joints.
It is thought that most
of the damage to these tissues results from the
excessive inflammatory response of the host,
involving a self-reinforcing cycle of
mitochondrial dysfunction, oxidative stress and
inflammation.
In this article, we
review the potential role of supplementary
coenzyme Q10 (CoQ10) in mediating the pathogenic
mechanism underlying Lyme disease, on the basis
of its role in mitochondrial function, as well
as its anti-inflammatory and antioxidant
actions.
Lyme borreliosis is
transmitted through the bite of a tick that is
infected by the bacterial spirochete Borrelia
burgdorferi. Clinical manifestation of the
disease can lead to heart conditions,
neurological disorders, and inflammatory
disorders. Oxidative stress has been implicated
in the pathogenesis of many human diseases. The
aim of this study was to investigate the
mechanisms of oxidative stress and intracellular
communication in Lyme borreliosis patients.
Mitochondrial superoxide
and cytosolic ionized calcium was measured in
peripheral blood mononuclear cells (PBMCs) of
Lyme borreliosis patients and healthy controls.
Mitochondrial superoxide levels were
significantly higher (p<0.0001) in Lyme
borreliosis patients (n=32) as compared to
healthy controls (n=30). Significantly low
(p<0.0001) levels of cytosolic ionized calcium
were also observed in Lyme borreliosis patients
(n=11) when compared to healthy controls (n=11).
These results indicate that there is an
imbalance of reactive oxygen species and
cytosolic calcium in Lyme borreliosis patients.
The results further
suggest that oxidative stress and interrupted
intracellular communication may ultimately
contribute to a condition of mitochondrial
dysfunction in the immune cells of Lyme
borreliosis patients.
Journal of Chronic Fatigue Syndrome 2008; 14(4): 5-17.
Chronic Fatigue Syndrome Patients
Subsequently Diagnosed with Lyme Disease Borrelia burgdorferi: Evidence for Mycoplasma species Co-Infections
ABSTRACT
Objective: We examined the blood of 48
North American Chronic Fatigue Syndrome (CFS) patients
subsequently diagnosed with Lyme Disease Borrelia
burgdorferi and compared these to 50 North American CFS
patients without evidence of Borrelia burgdorferi infections
for presence of Mycoplasma spp. co-infections using forensic
polymerase chain reaction.
Results: We found that 68.75% of CFS/Lyme
patients show evidence of mycoplasma co-infections (Odds
Ratio=41.8, Confidence Limits=11.26-155.16, p <0.001)
compared to controls, whereas 50% of CFS patients without a
diagnosis of Lyme Disease Borrelia burgdorferi show
mycoplasma co-infections (OR=19.0,
CL=5.25-68.78, p<0.001 compared to controls). Since CFS
patients without a diagnosis of Lyme Disease have a high
prevalence of one of four Mycoplasma species and a majority
show evidence of multiple infections, we examined CFS/Lyme
patients’ blood for various Mycoplasma species. We found
that CFS patients with Lyme Disease Borrelia burgdorferi
mostly had single species mycoplasma infections (OR=31.67,
CL=8.63-116.16, p<0.001) with a preponderance of M.
fermentans infections (50% of patients, OR=59.0,
CL=7.55-460, p<0.001), whereas the most commonly found
Mycoplasma spp. in CFS patients without Lyme Disease was M.
penumoniae (34% of patients. OR=14.94. CL=3.25-68.73,
p<0.001).
Conclusions: The results indicate that a subset of CFS
patients show evidence of infection with Borrelia
burgdorferi, and a large fraction of these patients were
also infected with Mycoplasma fermentans and to a lesser
degree with other Mycoplasma species.
The signs and symptoms of Mycoplasma infection are highly
variable and thus it is not uncommon for a diagnosis to be
entirely missed.
A partial list of symptoms includes chronic
fatigue, joint pain, intermittent fevers, headaches,
coughing, nausea, gastrointestinal problems, diarrhea,
visual disturbances, memory loss, sleep disturbances, skin
rashes, joint stiffness, depression, irritability,
congestion, night sweats, loss of concentration, muscle
spasms, nervousness, anxiety, chest pain, breathing
irregularities, balance problems, light sensitivity, hair
loss, problems with urination, congestive heart failure,
blood pressure abnormalities, lymph node pain, chemical
sensitivities, persistent coughing, eye pain, floaters in
the eyes, and many others.
Mycoplasma are pleomorphic bacteria which lack a cell wall
and, as a result, many antibiotics are not effective against
this type of bacteria. There are over 100 known species of
Mycoplasma, but only a half dozen or so are known to be
pathogenic in humans. The pathogenic species are
intracellular and must enter cells to survive. Once they are
inside the cells, they are not recognized by the immune
system and it is difficult to mount an effective response.
They stimulate reactive-oxygen species(ROS) which damage
cell membranes.
