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Neuroendocrinol Lett 2009; 30(4): 470–478
ORIGINAL ARTICLE
Neuroendocrinology Letters Volume 30 No. 4 2009
Coenzyme Q10 deficiency in myalgic
encephalomyelitis / chronic fatigue syndrome
(ME/CFS) is related to fatigue, autonomic and
neurocognitive symptoms and is another risk factor
explaining the early mortality in ME/CFS due to
cardiovascular disorder
Michael M 1, Ivanka M 1, Marta K 2, Marc U 3,
Nicolas V 3, Eugene B 3
1 Maes Clinics, Belgium; 2 Department of Experimental Neuroendocrinology, Institute of
Pharmacology, Polish Academy of Sciences, Krakow, Poland; 3 AML Laboratory, Antwerp, Belgium.
Correspondence to: Prof. Dr. M. Maes, M.D., Ph.D. Director of the Maes Clinics,
Groenenborgerlaan 206, 2610 Wilrijk - Antwerp, Belgium.
: 32-3-4809282; : 32-3-2889185
www.michaelmaes.com; : crc.mh@telenet.be
Submitted: 2009-07-08 Accepted: 2009-08-18 Published online: 2009-09-15
Key words: coenzyme Q10; chronic fatigue syndrome; inflammation; oxidative stress;
mitochondria; cytokines; heart failure; coronary artery disease; mortality;
statins
Neuroendocrinol Lett 2009; 30(4): 470–476 PMID: 20010505 NEL300409A17 © 2009 Neuroendocrinology Letters • www.nel.edu
Abstract
INTRODUCTION: Myalgic encephalomyelitis / chronic fatigue syndrome (ME/
CFS) is a medical illness characterized by disorders in inflammatory and oxidative
and nitrosative (IO&NS) pathways.
METHODS: This paper examines the role of Coenzyme Q10 (CoQ10), a mitochon-
drial nutrient which acts as an essential cofactor for the production of ATP in
mitochondria and which displays significant antioxidant activities.
Plasma CoQ10 has been assayed in 58 patients with ME/CFS and in 22 normal
controls; the relationships between CoQ10 and the severity of ME/CFS as mea-
sured by means of the FibroFatigue (FF) scale were measured.
RE SULT S: Plasma CoQ10 was significantly (p=0.00001) lower in ME/CFS patients
than in normal controls. Up to 44.8% of patients with ME/CFS had values beneath
the lowest plasma CoQ10 value detected in the normal controls, i.e. 490 μg/L. In
ME/CFS, there were significant and inverse relationships between CoQ10 and
the total score on the FF scale, fatigue and autonomic symptoms. Patients with
very low CoQ10 (<390 μg/L) suffered significantly more from concentration and
memory disturbances.
DISCUSSION: The results show that lowered levels of CoQ10 play a role in the
pathophysiology of ME/CFS and that symptoms, such as fatigue, and autonomic
and neurocognitive symptoms may be caused by CoQ10 depletion.
Our results suggest that patients with ME/CFS would benefit from CoQ10
supplementation in order to normalize the low CoQ10 syndrome and the IO&NS
disorders. The findings that lower CoQ10 is an independent predictor of chronic
heart failure (CHF) and mortality due to CHF may explain previous reports that
471
Neuroendocrinology Letters Vol. 30 No. 4 2009 • Article available online: http://node.nel.edu
Co Q10 in ME/CFS
the mean age of ME/CFS patients dying from CHF is
25 years younger than the age of those dying from CHF
in the general population. Since statins significantly
decrease plasma CoQ10, ME/CFS should be regarded
as a relative contraindication for treatment with statins
without CoQ10 supplementation.
INTRODUCTION
Myalgic Encephalomyelitis or Chronic Fatigue Syn-
drome (ME/CFS) is a medical disorder, characterized
by profound fatigue, inflammatory, autonomic and
neuropsychiatric symptoms. According to the Center
for Disease Control and Prevention (CDC) criteria
(Fukuda et al. 1994) a patient must satisfy two criteria
in order to receive a diagnosis of ME/CFS: a) suffer
from severe chronic fatigue lasting at least six months,
while no known medical condition may explain the
fatigue; and b) the presence of at least four of the fol-
lowing symptoms, substantial impairment in short
– term memory or concentration; sore throat; tender
cervical and axillary lymph nodes; muscle pain; multi –
joint pain without selling or redness; headache of new
type; unrefreshing sleep; and post exertion malaise last-
ing more than 24 hours. Despite the medical nature of
ME/CFS many doctors and governments still consider
“CFS” as a mental condition - not even a disorder - and
treat those patients accordingly with cognitive behav-
ioural therapy and graded exercise treatment (Twisk
and Maes, 2009; Maes and Twisk, 2009).
There is now abundant evidence that ME/CFS,
as defined above, is characterized by various disor-
ders in inflammatory and oxidative and nitrosative
stress (IO&NS) pathways (Maes, 2009; Maes et al.
2007a; 2007b; 2007c; Lorusso et al. 2009; Aspler et al.
2008; Kerr et al. 2008; Buchwald et al. 1997; Nijs en de
Meirleir, 2005). The key phenomena explaining induc-
tion of the IO&NS pathways appear to reside in the
white blood cells, which show an increased production
of nuclear factor kappa B (NFκB), cyclo-oxygenase-2
(COX-2) and inducible NO synthase (iNOS) (Maes et
al. 2007b; 2007c; Maes, 2009). Increased O&NS in ME/
CFS is indicated by - amongst other things - higher iso-
prostane; oxidized low density lipoproteins (LDL); LDL
thiobarbituric acid reactive substances (TBARS); and
protein carbonyl levels (Vecchiet et al. 2003; Kennedy et
al. 2005; Jammes et al. 2005; Smirnova and Pall, 2003).
Damage by O&NS to functional proteins and mem-
brane fatty acids in ME/CFS is evidenced by increased
IgM-mediated immune responses against membrane
fatty acids, by-products of lipid peroxidation (MDA and
azelaic acid), and NO derivates, such as nitro-tyrosine,
nitro-phenylalanine, and nitro-tryptophan (Maes et al.
2006b; 2007e; 2008).
We have discussed that induction of the above-
mentioned IO&NS pathways may cause the symptoms
experienced by ME/CFS patients. Thus, intracellular
inflammation with an increased production of COX-2
and iNOS may cause aches and pain, muscular tension,
fatigue, irritability, sadness, and the subjective feeling
of infection, whereas O&NS and the damage caused by
O&NS may cause aches and pain, muscular tension and
fatigue (Maes, 2009; Maes et al. 2006b; 2007b; 2007c;
2007d; 2008). The above IO&NS pathways in ME/CFS
may be induced by a number of trigger factors, such
as bacterial and viral infections, bacterial translocation
through increased gut permeability, psychological stres-
sors and physical exhaustion (Maes, 2009).
Another potential factor that may participate in the
pathophysiology of ME/CFS is low Coenzyme Q10
(CoQ10). CoQ10 is an essential component of the mito-
chondrial respiratory chain (Butler et al. 2003), a strong
anti-oxidant, that confers resistance to mitochondrial
damage by O&NS (Chaturvedi and Beal, 2008), and an
anti-inflammatory agent (Schmelzer et al. 2007a; 2007b;
2008). Low-energy syndromes are often accompanied by
a depletion of CoQ10, e.g. the Prader-Willi syndrome,
Friedrich’s ataxia, Steinert’s myotonic dystrophy, cardiac
and skeletal muscle dysfunctions, cancers, and heredi-
tary mitochondrial disorders (Butler et al. 2003; Cooper
et al. 2008; Siciliano et al.. 2001; Rusciani et al. 2006). In
those patients with low energy syndromes, CoQ10 sup-
plementation increases plasma CoQ10 and energy as
well (Cooper et al. 2008; Bonakdar and Guarneri, 2005;
Singh et al. 2003). In patients with unexplained fatigue,
the treatment that best predicts fatigue improvement
is CoQ10 supplementation (Bentler et al. 2005). There
are, however, to the best of our knowledge, no studies in
ME/CFS examining plasma CoQ10 concentrations.
The present study has been carried out in order to
examine plasma CoQ10 levels in patients with ME/CFS
and to examine its relationships with specific ME/CFS
symptoms.
SUBJECTS AND METHODS
Subjects
Eighty subjects participated in this study, i.e. 22 healthy
volunteers and 58 patients suffering from ME/CFS.
All ME/CFS subjects were outpatients admitted to the
Maes Clinics, Antwerp, Belgium. We made the diag-
nosis of ME/CFS by means of the Centres for Disease
Control and Prevention (CDC) criteria (Fukuda et al.
1994). In order to measure the severity of illness and to
examine the symptoms correlates of lowered CoQ10 we
have employed the Fibromyalgia and Chronic Fatigue
Syndrome Rating Scale (FF scale) (Zachrisson et al.
2002). The FF scale measures 12 symptoms, i.e. pain,
muscular tension, fatigue, concentration difficulties,
failing memory, irritability, sadness, sleep disturbances,
autonomic disturbances, irritable bowel, headache, and
subjective experience of infection. The total sum on
this scale was employed as a measure of the severity of
illness.
We have excluded all subjects with life-time diagno-
ses of psychiatric DSM IV-R disorders, e.g. depression,
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Copyright © 2009 Neuroendocrinology Letters ISSN 0172–780X • www.nel.edu
Michael Maes, Ivanka Mihaylova, Marta Kubera, Marc Uytterhoeven, Nicolas Vrydags, Eugene Bosmans
bipolar, anxiety, psychotic, substance use and organic
mental disorders. Any subjects with medical illnesses
were omitted from this study, e.g. inflammatory bowel
disorders, diabetes type 1 or type 2, hypertension, and
arteriosclerosis. We excluded subjects with abnormal
blood tests, such as alanine aminotransferase (ALT),
alkaline phosphatase (ALP), blood urea nitrogen
(BUN), calcium, creatinine, electrolytes, thyroid stimu-
lating hormone (TSH), total protein and positive IgM
antibody titers for EBV or CMV. We were careful in
omitting patients and controls who were treated with
statins and beta-blockers and who had been taking
dietary supplements with CoQ10. We have excluded any
subjects who had ever been treated with anti-psychotic
drugs, anticonvulsants or mood stabilizers and subjects
who had been taking other psychotropic drugs during
the last year prior to the studies. Other exclusionary cri-
teria for patients and controls were acute infections for
at least 2 months prior to the study. Patients and con-
trols gave written informed consent after the study pro-
tocol was fully explained; the study has been approved
by the local ethical committee.
Methods
Plasma CoQ10 was determined using a HPLC method
manufactured by Chromsystems Diagnostics (Munich,
Germany). This reagent kit allows the reliable chro-
matographic determination of CoQ10 in an isocratic
HPLC run using UV detection (275 nm). CoQ10 is
released by precipitating the proteins and then con-
centrated using solid phase extraction. Inclusion of an
internal standard minimizes any analytical variation.
We followed the instructions as provided by Chrom-
systems Diagnostics (see: http://www.chromsystems.
com/Description.103.0.html?&L=1) The Intra-assay
coefficient of variation (CV) was < 5%, and the inter-
assay CV < 6%.
Statistics
Differences between group means were assessed by
means of analysis of variance (ANOVA) or covariance
(ANCOVA). Relationships between variables were
ascertained by means of Pearson’s product-moment
correlation coefficients and regression analyses. Step-
wise discriminant multiple ANOVA (MANOVA) with
an F-to-enter of p=0.05 was used to assess the symp-
tomatic characteristics of different groups. The inde-
pendence of classification systems was ascertained by
means of analysis of contingence tables (χ2‑test) and
Fisher’s exact probability test. The significance was set
at α=0.05 (two tailed).
RESULTS
There were no significant differences in age (F=3.7,
df=1/94, p=0.06) between normal controls (mean age
±SD=45.4 ±10.1 years) and ME/CFS patients (38.5
±13.9 years). There was no significant difference (χ2
=0.9, df=1, p=0.3) in gender distribution between
normal controls (5 male/17 female) and ME/CFS
patients (8 male/50 female patients). There were no
significant correlations between CoQ10 and age, either
in the controls (r=0.21, p=0.6) or ME/CFS patients
(r=0.06, p=0.7). There were no significant (point-bi-
serial) correlations between CoQ10 and gender, either
in the controls (r=0.07, p=0.8) or ME/CFS patients
(r=-0.02, p=0.9).
Figure 1 shows the CoQ10 values in patients and
controls. ANOVA showed that serum CoQ10 was sig-
nificantly lower in ME/CFS patients than normal con-
trols (F=31.0, df=1/78, p=0.00001). Covarying for age
and sex in an ANCOVA did not change these results
(F=25.9, df=1/76, p=0.00003). Neither age (F=0.8,
p=0.6), nor gender (F=0.09, p=0.7) were significant in
this ANCOVA.
There was a significant and negative correlation
between serum CoQ10 and the total score on the FF
scale (r=-0.28, p=0.03). Regression analyses of plasma
CoQ10 on each of the 12 FF items showed that there
were significant and inverse correlations between
CoQ10 and fatigue (r=-0.86, p<10-5) and autonomic
symptoms (r=-0.36, p=0.005).
We have divided the ME/CFS study group in two
subgroups according to their CoQ10 values, i.e. lower
or higher than 490 μg/L, that is the lowest value
observed in the normal controls. Up to 26 patients had
values lower than 490 μg/L (mean CoQ10=361.7 ±68.2
μg/L), while 32 patients had values higher than 490
μg/L (mean=624.4 ±72.6 μg/L). Stepwise discriminant
MANOVA showed that two FF items displayed a sig-
nificant discriminatory power, i.e. fatigue and irritabil-
ity (F=33.5, df=1/56, p=0.00001; the distance between
both centroids being 1.53 SDs. Finally, we have divided
the ME/CFS patients in two groups according to the
q25 values for CoQ10 in the ME/CFS group, i.e. 390
μg/L. There were 14 patients with very low (<390 μg/L)
7.6
7.16
6.72
6.28
5.84
5.4 1.0 2.0
Figure 1. Scatter plot of the measurements of Co-enzyme Q10 (in
ln transformation) in 58 patients with myalgic encephalomyelitis
/ chronic fatigue syndrome (2.0) and 22 normal volunteers (1.0).
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Neuroendocrinology Letters Vol. 30 No. 4 2009 • Article available online: http://node.nel.edu
Co Q10 in ME/CFS
plasma CoQ10 versus 44 patients with plasma CoQ10 >
390 μg/L. Patients with very low plasma CoQ10 (<390
μg/L) had significantly greater scores on four FF items,
i.e. fatigue (F=66.5, df=1/56, p<10-6), autonomic symp-
toms (F=10.5, df=1/56, p=0.002), and concentration
(F=4.0, df=1/56, p=0.04; means: 3.2 ± 1.3 versus 2.4
±1.2) and memory (F=5.2, df=1/56, p=0.02; means 3.7
±1.1 versus 3.0 ±1.0) disturbances.
DISCUSSION
This is a first study which shows that ME/CFS is accom-
panied by significantly reduced plasma concentrations
of CoQ10 and that lowered plasma CoQ10 is related to
specific symptoms of ME/CFS, such as fatigue, auto-
nomic and neurocognitive symptoms.
The first major finding of this study is that ME/CFS
is characterized by a highly significant depletion in
plasma CoQ10. Up to 44.8% of all patients had plasma
CoQ10 values that were lower than the lowest CoQ10
value established in normal controls, i.e. 490 μg/L.
These findings show that many patients with ME/CFS
exhibit a “low CoQ10 syndrome”.
This CoQ10 depletion in ME/CFS patients may be
involved in the different pathophysiological pathways,
which underpin ME/CFS.
* First, plasma CoQ10 depletion in ME/CFS may
result in impaired antioxidative protection which in
turn may enhance induction of the O&NS pathways
and, consequently, damage to membrane fatty acids
and functional proteins (Maes, 2009). Indeed, the anti-
oxidant properties of CoQ10 explain its protective,
including neuroprotective, properties whereby CoQ10
protects against neuronal damages (Chaturvedi and
Beal, 2008; Young et al. 2007; Li et al. 2005; Matthews
et al. 1998). The present findings reinforce the existent
literature showing that ME/CFS is accompanied by
a decreased antioxidant status, as evidenced by lower
serum zinc and dehydroepiandrosterone sulfate (Maes
et al. 2005; 2006a).
* Second, mitochondrial constituents, such as
CoQ10, prevent the generation of free radicals during
the oxidative processes in the mitochondria and thus
confer resistance to mitochondrial damage by O&NS
(Chaturvedi and Beal, 2008; Liu, 2008). Recently, mito-
chondrial dysfunctions have been established in ME/
CFS. Behan et al. (1991) examined muscle biopsies of
50 patients with post-viral fatigue syndrome (a variant
of ME/CFS) and found branching and fusion of mito-
chondrial cristae in 35 specimens and mitochondrial
degeneration with swelling, vacuolation, myelin figures
and secondary lysosomes in 40 samples. Lane et al.
(1998) reported that ME/CFS patients with abnormal
lactate responses to exercise had a significantly lower
proportion of mitochondria rich type 1 muscle fibers.
* Third, the anti-inflammatory effects of CoQ10,
such as downregulation of NFκB-gene expression
(Schmelzer et al. 2008), suggest that a deficiency of
CoQ10 may aggravate the intracellular inflammatory
processes in ME/CFS characterized by increased NFκB
production (Maes, 2009; Maes et al. 2007a). CoQ10 may
also reduce the production of pro-inflammatory cytok-
ines, such as tumor necrosis factor alpha (Schmelzer et
al. 2007a), which production is known to be disturbed
in ME/CFS (Patarca et al. 1994).
* Fourth, CoQ10 may counteract the induction
of the IO&NS pathways by endoxin or LPS (Sugino
et al. 1987; Abd El-Gawad and Khalifa, 2001). This is
of importance to ME/CFS since leaky gut and a con-
sequent gut-derived inflammation with a mounted
inflammatory response against LPS of enterobacteria
are new pathways in ME/CFS (Maes and Leunis, 2008;
Maes et al. 2007a; 2007d).
* Last but not least, CoQ10 is an obligatory element
in the electron transport chain (ETC) within the mito-
chondria, which produces much of the ATP that powers
the energy in our cells and our body (Butler et al. 2003;
Crane, 2001). On the inner membrane of the mitochon-
dria, CoQ10 transfers electrons from complexes I and II
to complex III which take part in the respiratory chain
and the synthesis of ATP (Dutton et al. 2000). In this
respect, it has been hypothesized that most if not all
ME/CFS patients suffer from insufficient energy due
to cellular energy dysfunction (Myhill et al. 2009). In
the next paragraph we will discuss that the low CoQ10
syndrome in ME/CFS is indeed characterized by a loss
of energy.
The second major finding of this study is that there are
significant inverse correlations between plasma CoQ10
and specific symptoms such as fatigue and autonomic
symptoms and that ME/CFS patients with very low
plasma CoQ10 suffered significantly more from fatigue,
autonomic symptoms, and concentration and memory
disorders.
Our findings that low plasma CoQ10 is a strong
determinant of fatigue is in agreement with previous
findings that a depletion of plasma CoQ10 by treatment
with statins, may induce fatigue, which is reversible
upon supplementation with CoQ10 (Langsjoen et al.
2005; Passi et al. 2003). Indeed, treatment with statins
may reduce the synthesis not only of cholesterol but
also of CoQ10. This is because statins block HMG-CoA
reductase of the mevalonate pathway, which is needed
for the synthesis of the isoprene side chain of CoQ10
(Mabuchi et al. 2005; Chu et al. 2006). Statins cause a
40% reduction in the plasma levels of CoQ10 reducing
plasma CoQ10 to levels that are similar to those that we
have found in our patients. The plasma CoQ10 concen-
trations found in our ME/CFS patients are thus in the
range that can cause the symptoms of a “low CoQ10
syndrome”. Our results also concur with other reports
that low plasma CoQ10 in other disorders, such as
autosomal recessive CoQ10 deficiency, mitochondrial
disorders, Prader-Willi syndrome are often charac-
474
Copyright © 2009 Neuroendocrinology Letters ISSN 0172–780X • www.nel.edu
Michael Maes, Ivanka Mihaylova, Marta Kubera, Marc Uytterhoeven, Nicolas Vrydags, Eugene Bosmans
terized by fatigue and exercise intolerance, which are
treatable by CoQ10 supplementation (Butler et al. 2003;
Siciliano et al. 2007; Gempel et al. 2007; Sobreira et al.
1997). Our results on a significant relationship between
CoQ10 and fatigue are in agreement with other reports
that a) the percentage of subjects with unexplained
fatigue who found treatment with different supple-
ments helpful was greater for coenzyme CoQ10 than
for all other supplements (Bentler et al. 2005); and b)
treatment with CoQ10 of patients after acute myocar-
dial infarction showed that fatigue was more common
in the control group than in the CoQ10 treated group
(Singh et al. 2003).
We found that very low plasma CoQ10 concentra-
tions appear to predict the occurrence of neurocog-
nitive disorders. These findings concur with those
of previous reports showing that lowering of plasma
CoQ10 by treatment with statins is accompanied by
significant memory loss, which was relieved by treat-
ment with CoQ10 (Langsjoen et al. 2005). Moreover,
CoQ10 has a clinical efficacy in improving neurocog-
nitive disorders that are caused by reducing mitochon-
drial dysfunctions via O&NS pathways (Liu, 2008).
Male intracerebroventricular-streptozotocin infused
Wistar rats show a significant loss of cognitive perfor-
mance and simultaneous signs of O&NS and a decline
in hippocampal and cortex ATP (Ishrat et al. 2006).
Treatment of those Wistar rats with CoQ10 reversed
the neurocognitive impairments and the damage by
O&NS in the hippocampus and the cortex.
In our study, lowered plasma CoQ10 was also corre-
lated to the presence of autonomic symptoms. Since, the
modulatory effects of CoQ10 on the autonomic activity
are only recently detected (Zheng and Moritani, 2008) it
is not clear yet whether a causal relationship underpins
this statistical correlation. However, lowering plasma
CoQ10 by statins may induce peripheral neuropathies
that are reversible upon treatment with CoQ10 (Lang-
sjoen et al. 2005). Although, lowering of CoQ10 levels
by statins is also accompanied by a significant myalgia,
the present study was unable to detect any correlations
between the low CoQ10 syndrome in ME/CFS and FF
symptoms, such as aches and pain and muscle tension.
Previously, we have discussed that an increased pro-
duction of iNOS and COX-2 and increased damage by
O&NS may explain the occurrence of those symptoms
in ME/CFS (Maes, 2009).
The low CoQ10 syndrome in ME/CFS may have
very important medical consequences. It is well known
that a deficiency of coenzyme Q10 is a possible cause
of cardiac disease, such as chronic heart failure (CHF),
and is an independent predictor of mortality in CHF
patients (Molyneux et al. 2008). Moreover, there is evi-
dence to support the therapeutic value of CoQ10 as
an adjunct to standard medical therapy in congestive
heart failure (Singh et al. 2007). CoQ10 has been shown
to enhance systolic function, left ventricular ejection
fraction and myocardium contractility in CHF (Sander
et al. 2006; Belardinelli et al. 2005) and to improve the
endothelium-dependent relaxation and endothelium-
bound extracellular superoxide dismutase (Tiano et
al. 2007). CoQ10 is also considered to be a protective
factor for coronary artery disease (Yalcin et al. 2004).
The abovementioned results may explain the previous
finding of Jason et al. (2006) that the mean age of ME/
CFS patients dying from heart failure, i.e. 58.7 years,
is significantly lower than the age of those dying from
heart failure in the general US population, i.e. 83.1
years. Thus, the low CoQ10 syndrome together with
the induced IO&NS pathways are probably highly sig-
nificant risk factors explaining the early mortality due
to CHF in ME/CFS patients.
In the same study (Jason et al. 2006), the mean age of
the ME/CFS patients dying from cancer, i.e. 47.8 years,
was considerably lower than that of those dying from
cancer in the general US population, i.e. 72.0 years. It can
be hypothesized that the low CoQ10 syndrome in ME/
CFS may increase the risk toward this earlier mortality
due to cancer in ME/CFS. Indeed, low CoQ10 occurs in
patients with various grades of cervical intraepithelial
neoplasia and cervical cancers, while an inverse asso-
ciation was detected between plasma CoQ10 and his-
tological grades of epithelial lesions (Palan et al. 2003.
There are some reports that baseline plasma CoQ10 is
a powerful and independent prognostic factor that can
be used to estimate the risk for melanoma progression
(Rusciani et al. 2006).
In conclusion, ME/CFS is characterized by significantly
lower plasma concentrations of CoQ10. The latter
appear to determine to a great extent the incidence of
fatigue in those patients. Very low CoQ10 may also
be involved in causing neurocognitive disorders and
maybe autonomic symptoms. The results of our study
and those of previous studies reporting on the treat-
ment of the low CoQ10 and low energy syndrome and
unexplained fatigue with CoQ10 suggest that patients
with ME/CFS should be treated with CoQ10 in order to
normalize their low plasma CoQ10 and the disorders in
the IO&NS pathways as well.
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