Fibromyalgia syndrome (FMS) is a chronic pain condition primarily affecting women aged 25 to 55, characterized by widespread pain, fatigue, and diverse somatic symptoms. Diagnosis is based on specific criteria involving pain index scores and symptom severity, with potential genetic and environmental risk factors contributing to its onset. Abnormal levels of cytokines, neurotransmitters, and hormonal imbalances may also be involved in the disease's pathogenesis, leading to overlapping conditions and heightened pain sensitivity.

1. 1
Nutrition interventions for
managing fibromyalgia
Nina Bailey BSc, MSc, PhD RNutr

2. • The name fibromyalgia originates from the words fibro for
fibrous tissues, such as tendons and ligaments, with my
indicating muscles, and algia meaning pain
• Fibromyalgia syndrome (FMS) is a prevalent chronic pain
syndrome characterised by widespread pain and other
unspecific somatic symptoms including fatigue, sleep
disturbances, cognitive dysfunction and depressive disorders
• FMS is more prevalent in women around 50 years old
• There are no diagnostic biochemical markers or instrumental
tests on which to base a diagnosis

3. Wolfe F, Clauw DJ, Fitzcharles MA, et al. (2010) The American College of Rheumatology preliminary diagnostic criteria for
fibromyalgia and measurement of symptom severity. Arthritis Care and Research 62: 600–610
M. Niesters, A. Dahan Fibromyalgia Encyclopedia of the Neurological Sciences (Second Edition), 2014, 288–292
https://www.torbayandsouthdevon.nhs.uk/uploads/questionnaire-widespread-pain-index-and-symptom-severity-score.pdf

4. 0=no problem
1=slight or mild problems and generally mild or intermittent
2=moderate, considerable problems, and often present and/or at a moderate level
3=severe, pervasive, continuous, and life-disturbing problems
Considering somatic symptoms in general, indicate whether the patient has
0=no symptoms
1=few symptoms
2=a moderate number of symptoms
3=a great deal of symptoms
The SS scale score is the sum of the severity of the three symptoms (fatigue, waking un-
refreshed, and cognitive symptoms) plus the extent (severity) of somatic symptoms in
general. The final score will be between 0 and 12
Symptom severity scale score: Indicate the level of severity over the last week for
the following three symptoms: (1) fatigue; (2) waking un-refreshed; and (3)
cognitive symptoms
Wolfe F, Clauw DJ, Fitzcharles MA, et al. (2010) The American College of Rheumatology preliminary diagnostic criteria for fibromyalgia and
measurement of symptom severity. Arthritis Care and Research 62: 600–610
M. Niesters, A. Dahan Fibromyalgia Encyclopedia of the Neurological Sciences (Second Edition), 2014, 288–292

5. Criteria
A patient satisfies diagnostic criteria for fibromyalgia if the following three
conditions are met:
1.Widespread pain index ≥7 and symptom severity scale score≥5
or
Widespread pain index 3–6 and symptom severity scale score≥9
2. Symptoms have been present at a similar level for at least 3 months
3. The patient does not have a disorder that would otherwise explain the pain
Classification criteria of fibromyalgia syndrome
American College of Rheumatology, 2010
Wolfe F, Clauw DJ, Fitzcharles MA, et al. (2010) The American College of Rheumatology preliminary diagnostic criteria for fibromyalgia and
measurement of symptom severity. Arthritis Care and Research 62: 600–610
M. Niesters, A. Dahan Fibromyalgia Encyclopedia of the Neurological Sciences (Second Edition), 2014, 288–292

6. Who does fibromyalgia syndrome (FMS) affect?
•The prevalence of FMS in the general population is estimated at 2% to 5% (of which 85% are
females)
•‘Typically’ develops between the age of 25 and 55
•Although the exact causes of FMS are not fully understood, evidence suggests that both genetic
and environmental factors are involved
Risk factors
•Genes - first-degree relatives of individuals with FMS have an 8-fold greater risk of developing
FMS
•Stressors (mechanical or physical trauma or injury and psychosocial stressors)
•Co-morbid conditions: FMS and ME/CFS often overlap but also have a host of other overlapping
conditions associated with them that include other pain disorders, chronic headache, sleep
problems, major depression, anxiety, nervous system disorders, restless leg symptom, digestive
problems (IBS) and menstrual problems
•Patients with FMS and related conditions display diffuse hyperalgesia (heightened pain responses
to normally painful stimuli) and/or allodynia (pain responses to normally non-painful stimuli)
•Such responses suggest that these individuals have specific issues with pain or sensory processing
rather than an abnormality confined to the region of the body where pain is experienced

7. Catechol-O-methyltransferase (COMT) catalyzes the transfer of a methyl group from S-
adenosylmethionine (SAMe) to catecholamines, including the neurotransmitters dopamine,
adrenaline and noradrenaline
Clinical symptoms in fibromyalgia are associated to COMT gene Val158Met polymorphism
rs4680(A) methionine = lower COMT enzymatic activity, therefore higher dopamine levels; lower
pain threshold, enhanced vulnerability to stress
rs4680(G) valine = higher COMT enzymatic activity, therefore lower dopamine levels; higher pain
threshold, better stress resiliency
FMS women with the homozygous met/met genotype evidenced more pain on days when pain
attention was elevated relative to those with the homozygous val/val genotype
Inanir A, Karakus N, Ates O, Sezer S, Bozkurt N, Inanir S, Yigit S Clinical symptoms in fibromyalgia are associated to catechol-O-methyltransferase
(COMT) geneVal158Met polymorphism. Xenobiotica. 2014 Oct;44(10):952-6.
Finan PH, Zautra AJ, Davis MC, Lemery-Chalfant K, Covault J, Tennen H. COMT moderates the relation of daily maladaptive coping and pain in fibromyalgia. Pain. 2011
Feb;152(2):300-7.
The COMT gene codes for the COMT enzyme,
which breaks down dopamine in the brain's
prefrontal cortex. The wild-type allele is a (G)
coding for a valine amino acid; the (A)
substitution polymorphism changes the amino
acid to a methionine

8. Who does fibromyalgia syndrome (FMS) affect?
•The prevalence of FMS in the general population is estimated at 2% to 5% (of which 85% are
females)
•‘Typically’ develops between the age of 25 and 55
•Although the exact causes of FMS are not fully understood, evidence suggests that both genetic
and environmental factors are involved
Risk factors
•Genes - first-degree relatives of individuals with FMS have an 8-fold greater risk of developing
FMS
•Stressors (mechanical or physical trauma or injury and psychosocial stressors)
•Co-morbid conditions: FMS and ME/CFS often overlap but also have a host of other overlapping
conditions associated with them that include other pain disorders, chronic headache, sleep
problems, major depression, anxiety, nervous system disorders, restless leg symptom, digestive
problems (IBS) and menstrual problems
•Patients with FMS and related conditions display diffuse hyperalgesia (heightened pain responses
to normally painful stimuli) and/or allodynia (pain responses to normally non-painful stimuli)
•Such responses suggest that these individuals have specific issues with pain or sensory processing
rather than an abnormality confined to the region of the body where pain is experienced

9. Stressors capable of triggering fibromyalgia
and related conditions
• Peripheral pain syndromes
• Infections (e.g. parvovirus, Epstein-Barr virus, Lyme disease,
Helicobacter pylori)
• Physical trauma (e.g. car accidents)
• Psychological stress/distress (e.g. physical/mental abuse)
• Certain catastrophic events (war, but not natural disasters)
• Hormonal alterations (e.g. hypothyroidism)
• Drugs/vaccines

10. Chronic inflammation (increase in pro-inflammatory cytokines),
together with raised levels of oxidative stress and mitochondrial
dysfunction, has been increasingly associated with the
manifestation of symptoms such as pain, fatigue, impaired memory,
and depression, which largely characterise at least some patients
suffering from CFS/ME and FMS
Furthermore, the presence of blunted
HPA-axis activity, with
reduced cortisol secretion both at
baseline and in response to stimulation
tests, suggests a role for the HPA axis
and cortisol in the pathogenesis of these
syndromes

11. Who does fibromyalgia syndrome (FMS) affect?
•The prevalence of FMS in the general population is estimated at 2% to 5% (of which 85% are
females)
•‘Typically’ develops between the age of 25 and 55
•Although the exact causes of FMS are not fully understood, evidence suggests that both genetic
and environmental factors are involved
Risk factors
Genes - first-degree relatives of individuals with FMS have an 8-fold greater risk of developing
FMS
Stressors (mechanical or physical trauma or injury and psychosocial stressors)
Co-morbid conditions: FMS and ME/CFS often overlap but also have a host of other overlapping
conditions associated with them that include other pain disorders, chronic headache, sleep
problems, major depression, anxiety, nervous system disorders, restless leg symptom, digestive
problems (IBS) and menstrual problems
•Patients with FMS and related conditions display diffuse hyperalgesia (heightened pain
responses to normally painful stimuli) and/or allodynia (pain responses to normally non-painful
stimuli)
•Such responses suggest that these individuals have specific issues with pain or sensory
processing rather than an abnormality confined to the region of the body where pain is
experienced

12. High levels of substances that
facilitate the transmission of pain,
like substance P, glutamate and
nerve growth factor, and brain
derived nerve growth factor have
been observed in the cerebrospinal
fluid of fibromyalgia patients
Noradrenaline and serotonin
(neurotransmitters involved in the
central inhibition of pain) are
decreased, which may also explain
why FMS patients have a higher
risk for the development of
depression and anxiety disorders
Littlejohn G. Neurogenic neuroinflammation in fbromyalgia dnd complex regional pain syndrome. Nat Rev Rheumatol. 2015 Nov;11(11):639-48.

13. Activation of the N-methyl-D-aspartate (NMDA) receptor (i.e. glutamate) results in
increased sensitivity of spinal cord and brain pathways that process sensory
information, particularly those which relate to pain
When pain turns from acute to chronic, it involves opening the NMDA pain receptor
•Patients with fibromyalgia have been shown to have an increased expression of
NMDA receptors in their skin (Kim et al. 2006)
•Thus people with fibromyalgia appear to already have overly active NMDA pain
receptors, making them more susceptible to the stimulation
•A 4-week exclusion of monosodium glutamate (MSG), aspartame, and other
excitotoxins resulted in over 30% improvement in fibromyalgia symptoms in 84% of
those who completed the diet (Holton et al. 2012)
Kim SH, Jang TJ, Moon IS. Increased expression of N-methyl-D-aspartate receptor subunit 2D in the skin of patients with
fibromyalgia. Rheumatol. 2006 Apr;33(4):785-8.
Holton K.F., Taren D.L., Thomson C.A., Bennett R.M., Jones K.D. The effect of dietary glutamate on fibromyalgia and irritable bowel
symptoms. Clin. Exp. Rheumatol. 2012;30:10–17.

14. Serotonin
IDO
IFN-γ, TNF-α,
IL-1, IL-6
Kynurenine
Quinolinic acid
NMDA agonist
3-Hydroxykynurenine
+
+
KMO
5-HTP
Neuronal damage Depression
Kynurenic acid
NMDA antagonist
NMDA receptor
Tryptophan
Sleep disturbance
IDO : indoleamine 2,3-dioxygenase
KMO : kynurenine monooxygenase
Glutamate

15. McCrae CS, O'Shea AM, Boissoneault J, Vatthauer KE, Robinson ME, Staud R, Perlstein WM, Craggs JG. Fibromyalgia patients
have reduced hippocampal volume compared with healthy controls. J Pain Res. 2015 Jan 30;8:47-52.
Hippocampal atrophy = fibro fog?
Abnormal glutamate excitatory neurotransmission and glucocorticoid dysfunction can lead to
neuronal atrophy, through excitotoxicity, and disrupt neurogenesis in the hippocampus – with
magnetic resonance imaging (MRI) scans having shown significant hippocampal atrophy in the
brains of FMS patients compared to healthy controls
Hippocampal atrophy may play a role in memory and cognitive complaints among fibromyalgia
patients
•Hippocampal atrophy resulting from FMS may, in turn, worsen or
exacerbate FMS symptomatology
•FMS patients often report a subjective worsening of cognitive function
characterised by short-term memory problems (‘fibro fog’)
•Hippocampal atrophy and dysfunction may “feed forward”, resulting in
more severe pain, discomfort, and anxiety in FMS patients, due to its
central role in limbic circuits and pain modulation networks

16. Adrenal fatigue - occurs when the amount of stress
overextends the capacity of the body to compensate
and recover from that stress or the combined stress
When cortisol crashes:
•Increases inflammatory cytokines (IL-6, TNFα)
•Activates microglial cells causing neuroinflammation
•Causes hippocampal degeneration/atrophy
•Increased susceptibility to infections (i.e., Candida!)
•Promotes autoimmune disease
Head KA, Kelly GS. Nutrients and botanicals for treatment of stress: adrenal fatigue,
neurotransmitter imbalance, anxiety, and restless sleep. Altern Med Rev. 2009 Jun;14(2):114-40.
Review.
https://drlam-6bmwcfqpiol3wo6jnjj0.netdna-ssl.com/images/infographic-four-phases-of-adrenal-
exhaustion.jpg

17. Sufferers can have numerous abnormalities in their hormonal,
metabolic and brain-chemical activity
These include levels of:
•serotonin and melatonin (both involved in the sleep cycle and mood)
•cortisol and noradrenaline (stress hormones)
•thyroid issues (hypothyroidism)
•growth hormones (involved in bone and muscle growth)
•substance P and glutamate (associated with pain perception)
•cytokines (involved in immune system response regulation and
the inflammatory process)

18. Fibromyalgia and cytokines
FMS isn’t generally classified as an autoimmune disease per se, but it shares many traits with
autoimmune-like diseases in which the body is attacking itself, often as a result of chronic
overproduction of inflammatory cytokines
•Features found in FMS (elevated numbers of B cells and cytokines and decreased numbers of
T regulatory [Treg] cells) are associated commonly with autoimmune diseases
•Cytokines have effects on the HPA-axis, the sympathetic nervous system and T lymphocytes,
which in turn might be associated with fibromyalgia
•Studies of cytokine levels in patients with fibromyalgia suggest that levels of the
proinflammatory cytokines IL-1, IL-6 and IL-8 are elevated, whereas TNFα levels are normal,
and levels of the antiinflammatory cytokines IL-4 and IL-10 are unchanged or reduced
•Treg are responsible for turning inflammation on and off and can help prevent an immune
system from becoming overactive and eventually leading to autoimmune dysfunction
•The % of Treg that suppresses the immune response appear to be reduced in a number of
stress-related diseases/conditions
https://igennus.com/practitioner-blog/nutrition-interventions-adhd-focus-treg/
Wallace DJ, Linker-Israeli M, Hallegua D, Silverman S, Silver D, Weisman MH. Cytokines play an aetiopathogenetic role in fibromyalgia: a hypothesis and pilot study. Rheumatology
(Oxford). 2001 Jul;40(7):743-9.
Generaal, E. et al. Basal inflammation and innate immune response in chronic multisite musculoskeletal pain. Pain 155, 1605–1612 (2014).

19. IL-1β Hyperalgesia, fatigue, fever, sleep, myalgias, substance P anti-nociception (increases
GABA and decreases NMDA); noradrenaline and adrenaline stimulate its release
TNFα Stress; regulates substance P expression, rapid eye movement sleep, allodynia;
increases excitatory amino acids; noradrenaline and adrenaline stimulate its release
IL-1Ra Stress; inhibits IL-8 expression
IFNγ Stress, anxiety; lowers substance P; myalgias
IL-2 Myalgia, cognitive dysfunction
IL-4 Decreases the production of Th1 cells, macrophages, IFN-γ
IL-6 Stress, fatigue, hyperalgesia, depression; noradrenaline, adrenaline and substance P
stimulate its release; activates sympathetic nervous system
IL-8 Substance P stimulates production, mediates sympathetic pain
IL-10 Blocks pain
Fibromyalgia and cytokines
Wallace DJ, Linker-Israeli M, Hallegua D, Silverman S, Silver D, Weisman MH. Cytokines play an aetiopathogenetic role in fibromyalgia:
a hypothesis and pilot study. Rheumatology (Oxford). 2001 Jul;40(7):743-9.
Studies of cytokine levels in patients with fibromyalgia suggest that levels of the
proinflammatory cytokines IL-1, IL-6 and IL-8 are elevated, whereas TNFα levels are
normal, and levels of the antiinflammatory cytokines IL-4 and IL-10 are unchanged or
reduced

20. Fibromyalgia and cytokines
FMS is common in patients with autoimmune disorders, such as systemic lupus erythematosus,
Sjogren’s Syndrome, and rheumatoid arthritis and while the chemokine/cytokine patterns found in
FMS patients may not be unique to FMS, it is worth considering that:
substance P induces IL-8 expression and the release of IL-6
because IL-8 promotes sympathetic pain and IL-6 induces hyperalgesia, fatigue and depression, it is
hypothesised that they may play a role in modulating FMS symptoms
increased levels of inflammatory cytokines can induce glutathione depletion, which, in turn, may
activate redox-sensitive transcription factors, such as NF-κB
elevated levels of cytokines activate microglia and astrocytes in the brain leading to further
production of elevated cytokines and ROS/RNS causing mitochondrial and metabolic dysfunction
contributing to fatigue
the subsequent ATP deficit together with inflammation and ROS/NOS are responsible for the
landmark symptoms of ME/CFS/FMS, including post-exertional malaise
Morris G, Berk M, Walder K, Maes M. Central pathways causing fatigue in neuro-inflammatory and autoimmune illnesses. BMC Med. 2015 Feb 6;13:28.
Morris G, Maes M. A neuro-immune model of Myalgic Encephalomyelitis/Chronic fatigue syndrome. Metab Brain Dis. 2013 Dec;28(4):523-40.

21. CoQ10, mitochondrial function & ATP
• CoQ10 deficiency decreases the numbers of healthy mitochondria
– reduced gene expression related to mitochondrial biogenesis
– CoQ10 required for synthesise pyrimidine synthesis which is required for the
generation of mitochondrial DNA
• CoQ10 deficiency triggers the opening of the mitochondrial permeability transition
pore (mPTP) leading to increased ROS
• Opening of mPTP causes the collapse of mitochondrial membrane potential and
the production of ATP (mitochondria require a electrochemical gradient to provide
the driving force for ATP production) and the induction of mitophagy
• Excessive mitophagy induces ATP-dependent apoptosis cell death thereby
exacerbating ATP depletion with the potential to induce further production of pro-
inflammatory cytokines
Rodríguez-Hernández A, Cordero MD, Salviati L, Artuch R, Pineda M, Briones P, Gómez Izquierdo L, Cotán D, Navas P, Sánchez-Alcázar JA. Coenzyme Q
deficiency triggers mitochondria degradation by mitophagy. Autophagy. 2009 Jan;5(1):19-32.

22. Mitochondrial dysfunction and FMS
Filler K, Lyon D, Bennett J, McCain N, Elswick R, Lukkahatai N, Saligan LN. Association of Mitochondrial Dysfunction and Fatigue: A Review of the Literature.

23. Effects of coenzyme Q10 supplementation on inflammatory markers
Meta- analysis of nine RCTs involving 428 subjects (Zhai et al, 2017)
The results showed that compared with control group, CoQ10 supplementation significantly
improved the serum level of CoQ10 and significantly decreased TNFα
No significant difference was observed between CoQ10 and placebo with regard to CRP or IL-6
CoQ10 supplementation may partly improve the process of inflammatory state
Meta-analysis of seventeen RCTs (Fan et al., 2017)
CoQ10 supplementation significantly reduced the levels of circulating CRP, IL-6 and TNFα
Changes of CRP were independent of baseline CRP, treatment duration, dosage, and patients
characteristics
A higher baseline IL-6 level was significantly associated with greater effects of CoQ10 on IL-6
levels
Significant lowering effects of CoQ10 on CRP, IL-6 and TNFα - buy results should be interpreted
with caution because of the evidence of heterogeneity and limited number of studies
Fan L, Feng Y, Chen GC, Qin LQ, Fu CL, Chen LH Effects of coenzyme Q10 supplementation on inflammatory markers: A systematic review and meta-
analysis of randomized controlled trials. Pharmacol Res. 2017 May;119:128-136.
Zhai J, Bo Y, Lu Y, Liu C, Zhang L. Effects of Coenzyme Q10 on Markers of Inflammation: A Systematic Review and Meta-Analysis. PLoS One. 2017 Jan
26;12(1):e0170172

24. The effect of CoQ10 supplementation in FMS
Miyamae T, Seki M, Naga T, Uchino S, Asazuma H, Yoshida T, Iizuka Y, Kikuchi M, Imagawa T, Natsumeda Y, Yokota S, Yamamoto Y. Increased
oxidative stress and coenzyme Q10 deficiency in juvenile fibromyalgia: amelioration of hypercholesterolemia and fatigue by ubiquinol-10
supplementation. Redox Rep. 2013;18(1):12-9
Double-blind, placebo-controlled trial (FMS n=10) vs 67 healthy controls
•Plasma level of ubiquinol was significantly decreased and the ratio of ubiquinone to total
coenzyme Q10 (%CoQ10) was significantly increased in juvenile FM relative to healthy controls,
suggesting that FM is associated with coenzyme Q10 deficiency and increased oxidative stress
•Plasma level of free fatty acids was significantly higher and the content of polyunsaturated
fatty acids (PUFA) in total free fatty acids was significantly lower in FMS than in controls,
suggesting increased tissue oxidative damage in juvenile FMS
•Ubiquinol supplementation (100 mg/day for 12 weeks) resulted in an increase in coenzyme
Q10 levels
•Ubiquinol supplementation also improved chronic fatigue scores as measured by the Chalder
Fatigue Scale

25. Regland B, Andersson M, Abrahamsson L, Bagby J, Dyrehag LE, Gottfries CG. Increased concentrations of homocysteine in the cerebrospinal fluid in
patients with fibromyalgia and chronic fatigue syndrome. Scand J Rheumatol. 1997;26(4):301-7.
Regland B, Forsmark S, Halaouate L, Matousek M, Peilot B, Zachrisson O, Gottfries CG. Response to vitamin B12 and folic acid in myalgic encephalomyelitis
and fibromyalgia. PLoS One. 2015 Apr 22;10(4):e0124648. doi: 10.1371/journal.pone.0124648. eCollection 2015.
Fibromyalgia, the homocysteine link and
hypomethylation
Homocysteine is a natural by-product of the methylation cycle and can
be remethylated to methionine or directed to the transsulfuration
pathway
Increased concentrations of
homocysteine have been found
in the cerebrospinal fluid in
patients with FMS and ME/CFS
A case of nutrient deficiencies?

26. Homocysteine neurotoxicity - the neurological pathologies associated with
hyperhomocysteinaemia are hypothesised to be caused by oxidative stress, excitotoxicity
via glutamate receptors, and via DNA hypomethylation
Homocystic acid is an oxidative product of homocysteine that functions as an excitatory
neurotransmitter activating NMDA receptors and enhancing calcium influx which damages
neurones, leading to cell death
Obeid R, Herrmann W. Mechanisms of homocysteine neurotoxicity in neurodegenerative diseases with special reference to dementia. FEBS Lett. 2006 May 29;580(13):2994-3005.
Bukharaeva E, Shakirzyanova A, Khuzakhmetova V, Sitdikova G, Giniatullin R. Homocysteine aggravates ROS induced
depression of transmitter release from motor nerveterminals: potential mechanism of peripheral impairment in motor neuron diseases associated with hyperhomocysteinemia.
Front Cell Neurosci. 2015 Oct 6;9:391.

27. Fibromyalgia, homocysteine and hypomethylation
Low levels of intrinsic factor blocks the absorption of B12, with high-risk factors for
poor absorption including:
Digestive disorders such as coeliac disease, Crohn's disease, IBS & small intestinal
bacterial overgrowth
Acid-reducing medications – (heartburn, GERD, acid reflux and peptic ulcers) such
as proton pump inhibitors or H2 (histamine 2) receptor antagonists suppress the
secretion of stomach acids but also block the secretion of intrinsic factor
Diabetes medications –Metformin, used to treat diabetes, are known to impair
intestinal absorption
Ageing – the older we get the more likely we are to be deficient in B12
Vegetarian and vegan diets – B12 is only found naturally in animal foods
Pernicious anaemia – a blood disease that develops when the body lacks the
intrinsic factor necessary to naturally absorb vitamin B12 from food

28. Methionine
recycling
Methionine
SAM: universal methyl donor
Methylates: neurotransmitters,
proteins, RNA, DHA,
catecholamines,
phosphatidylcholine,
melatonin, myelin, creatine
Homocysteine
SAM
SAH
Methionine
synthase
5-methyl THF
THF
FOLIC
ACID
CYCLE
Processes affected
Neurotransmitter function
Fatty acid metabolism
Allergic responses
Myelination
Cellular energy
Cell membrane and protein
structure and function
Cystathionine
Virus fighting
Inflammation regulation
Antioxidant production
Detoxification
Intestinal integrity
Cysteine
Glutathione
Metallathionines
Affects potent metal-
binding and redox
capabilities
Cysteinesulflinic acid
Phenol sulfur-
transferase
Phenol
processing
Digestion
Detoxification
Gut barrier
Sulfate
Sulphite
Taurine
Production of
bile salts
SULPHATION
TRANSSULFURATION
METHYLATION
Magnesium
Magnesium, vitamin B6, zinc
Vitamin B6
S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH ); tetrahydrofolate (THF)
Folate,
Vitamins
B6 & B12
Vitamin B6
Methionine is required for protein synthesis and provides a
methyl group for >50 critical transmethylation reactions

29. Methionine
recycling
Methionine
Homocysteine
SAM
SAH
Methionine
synthase
5-methyl THF
THF
FOLIC ACID
CYCLE
Disrupts gene expression
Decreased neurotransmitter function
Decreased myelination
Disrupted cellular energy transfer
Disrupted fatty acid metabolism
Increased allergic reactions
Cystathionine
Reduced
detoxification
of toxins and
heavy metals
Cysteine
Glutathione
Metallathionines
Affects potent metal-
binding and redox
capabilities
Cysteinesulflinic acid
Phenol sulfur-
transferase
Poor phenol
processing
Poor
digestion
Sulphate
Sulphite
Taurine
Production of
bile salts
SULPHATION
TRANSSULFURATION
METHYLATION
Gut and blood brain
barrier integrity
compromised
Poor
detoxification
Inactivates
MAT and
decreases
SAM synthesis
Villi flatten
and lose
function
Reduced
antioxidant
function
Th1 decreases
Th2 increases
S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH); methionine adenosyltransferase (MAT); tetrahydrofolate (THF)

30. Fibromyalgia and hypochlorhydria
• Helicobacter pylori infection/inflammation/IL-11
– loss of parietal cells = hypochlorhydria/low intrinsic factor
Stomach acid:
• Promotes protein digestion – feeds the amino acid pool
– Protein malabsorption issues
– FMS patients appear to have low BCAA (leucine, isoleucine, and valine)
• Promotes gastric emptying
– Gas, bloating/IBS/GERD
• Sterilises the stomach/ kills bacteria and yeast
– Dysbiosis/candida
• Required for the absorption of certain micronutrients: calcium,
magnesium, zinc, copper, iron, selenium, vitamin B12 (intrinsic factor)

31. Pimentel M, Wallace D, Hallegua D, Chow E, Kong Y, Park S, Lin HC A link between irritable bowel syndrome and fibromyalgia may be related to findings on
lactulose breath testing. Ann Rheum Dis. 2004 Apr;63(4):450-2.
Goebel A, Buhner S, Schedel R, Lochs H, Sprotte G. Altered intestinal permeability in patients with primary fibromyalgia and in patients with complex regional pain
syndrome. Rheumatology (Oxford). 2008 Aug;47(8):1223-7.
Kaufmann I, Eisner C, Richter P, Huge V, Beyer A, Chouker A, Schelling G, Thiel M. Lymphocyte subsets and the role of TH1/TH2 balance in stressed chronic pain patients.
Neuroimmunomodulation. 2007;14(5):272-80.
http://www.rothwellness.com/wp-content/uploads/2015/04/leakygut.jpg
Dysbiosis, leaky gut and FMS
The pain intensity of patients with FMS has been
reported to be correlated with the degree of small
intestinal bacterial overgrowth (SIBO) - abnormal
lactulose breath test
SIBO is often associated with an increased intestinal
permeability (leaky gut)
Leaky gut leads to the exposure of immune cells to
luminal antigens and consequent immune
modulation
FMS is often associated with a reduction of
cytotoxic T lymphocytes and a diminished Th1
response

33. Inflammation, leaky gut and FMS
FMS is an extremely heterogeneous entity and patients differ in their clinical symptoms,
endocrine and immune parameters; however:
•NF-kB, proinflammatory cytokines and oxidative and nitrosative stress (ROS/RNS), can lead to
a disruption of epithelial tight junctions in the intestine allowing translocation of gram-negative
bacteria, containing lipopolysaccharides, into the circulation, stimulating TLR4 mediated
pathways (hypersensitive microglia often appear in FM and ME/CFS)
•Prolonged and or excessive stimulation of membrane bound TLR4 results in the further
production of pro-inflammatory cytokines and ROS/RNS
•Increasing levels of ROS/RNS damage mitochondrial lipids and proteins leading to dissipation
of the mitochondrial membrane potential and inhibition of the electron transport chain
•This leads to compromised oxidative phosphorylation and to the further production of ROS,
making another major contribution to the inflammatory milieu related to fatigue
Filler K, Lyon D, Bennett J, McCain N, Elswick R, Lukkahatai N, Saligan LN. Association of Mitochondrial Dysfunction and Fatigue: A Review of the Literature.
BBA Clin. 2014 Jun 1;1:12-23. Schulzke JD, Ploeger S, Amasheh M, Fromm A, Zeissig S, Troeger H, Richter J, Bojarski C, Schumann M, Fromm M. Epithelial
tight junctions in intestinal inflammation. Ann N Y Acad Sci. 2009 May;1165:294-300.

34. Oxidative stress– cause or consequence?
Oxidative and nitrosative stress take part in the pathogenesis of pain
Superoxide radicals induce an alteration of nociceptions through peripheral and
central nervous system sensitisation and are implicated in the activation of several
cytokines including TNFα and IL-1β which are involved in inflammatory pain
Substance P, which is co-released with glutamate during nociception, has been
shown to increase the permeability of the blood–brain barrier (normally protects the
brain from high plasma concentrations of dietary glutamate )
The balance of oxidants/antioxidants has been demonstrated in FMS
• Glutathione and catalase levels significantly lower
• Significant correlation between serum nitric oxide level and pain
• Significant correlation between glutathione level and morning stiffness
Cordero MD, Díaz-Parrado E, Carrión AM, Alfonsi S, Sánchez-Alcazar JA, Bullón P, Battino M, de Miguel M. Is inflammation a mitochondrial dysfunction-
dependent event in fibromyalgia? Antioxid Redox Signal. 2013 Mar 1;18(7):800-7.
Sendur OF, Turan Y, Tastaban E, Yenisey C, Serter M.Serum antioxidants and nitric oxide levels in fibromyalgia: a controlled study. Rheumatol Int. 2009
Apr;29(6):629-33.

35. Candida, leaky gut and FMS
• Candida problems arise when the benign yeast form of Candida
albicans mutates to its fungal form which produces toxins that create holes
in the intestinal lining, leading to leaky gut syndrome and an inflammatory
immune system response
Kumamoto C.A. Inflammation and gastrointestinal Candida colonization Curr Opin Microbiol. 2011 Aug; 14(4): 386–391.
http://docmontagne.com/index.php/candida-leaky-gut/
• In addition to FMS, a wide range of
disorders have been linked to Candida
including autism, multiple sclerosis,
depression, and CFS/ME
• Use of antibiotics, oral contraceptives,
and anti-inflammatory steroids greatly
increase susceptibility to Candida

36. The impact on thyroid health - the prevalence of FMS in patients with autoimmune
thyroid disease has been estimated to be ~30%
Common deficiencies of micronutrients such as iron, selenium, vitamin A and zinc may interact
with iodine nutrition and thyroid function
• Iron absorption is dependent on the presence of adequate stomach acid
• Iron is required for thyroid peroxidase activity involved in the addition of iodine to tyrosine,
and thus the manufacture of T4 and T3
• Selenium is required for deiodinase enzyme activity (required for T4 to T3)
Iron deficiency goes hand in hand with low thyroid activity because low thyroid activity worsens
iron deficiency
If you have thyroid issues, just taking iron may not be enough to replenish iron levels because
people with low thyroid hormones have issues absorbing iron (they can’t make enough
stomach acid)
If you don’t absorb iron then it lowers the ability to make thyroid hormone – and so you get a
vicious cycle!
Zimmermann MB, Köhrle J. The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health. Thyroid. 2002
Oct;12(10):867-78. Review.

37. Fibromyalgia and obesity
Epidemiological studies suggest that ~40% FMS
patients are obese and ~30% overweight
•Leptin is secreted by the White Adipose Tissue (WAT) and is hyperexpressed in obese patients
•Leptin has a decreasing effect on pain threshold
•Leptin may modulate the stress response and may increase nociception
Ursini F, Naty S, Grembiale RD. Fibromyalgia and obesity: the hidden link. Rheumatol Int. 2011 Nov;31(11):1403-8.
• Obesity leads to higher levels of
proinflammatory cytokines and
increased indoleamine 2,3-
dioxygenase (IDO) activity
• Circulating kynurenine
concentration and
kynurenine/tryptophan ratio are
enhanced in obesity

38. Serotonin
IDO
IFN-γ, TNF-α,
IL-1, IL-6
Kynurenine
Quinolinic acid
NMDA agonist
3-Hydroxykynurenine
+
+
KMO
5-HTP
Neuronal damage Depression
Kynurenic acid
NMDA antagonist
NMDA receptor
Tryptophan
Sleep disturbance
IDO : indoleamine 2,3-dioxygenase
KMO : kynurenine monooxygenase
Glutamate

39. • The traditional drugs of choice, including NSAIDS, antidepressants, muscle
relaxants, tranquilisers and pain medications, may provide short-term relief
for some individuals but do not address the cause and their side-effects may
potentially cause more symptoms than they help
• However, multimodal pain management including intensive physical therapy,
exercise, counselling and sleep hygiene have been shown to be somewhat
effective in managing fibromyalgia-related symptoms
• What about dietary interventions?
Foods to avoid:
– Highly processed/highly refined foods
– Additives and artificial sweeteners
– Sugar/refined carbohydrates
– Monosodium glutamate (MSG) and aspartame
Fibromyalgia interventions

40. Tests?
• Homocysteine
• Stool test
• Stress/cortisol test
• Organic acids
• Food allergy
• Omega-3/6
• Vitamin D

41. Managing fibromyalgia
 Gut support
 Mitochondrial support
Methylation support
 Thyroid support
 Adrenal support
 ‘Anti-inflammatory’ diet protocol
Increase antioxidants

42. Address gut health

43. Issue: disrupted gut function leads to excess inflammation in the gut lining and changes
in the normal gut flora (dysbiosis/candida)
Solution: Restore normal gut flora with supplemental probiotics:
Lactobacillus rhamnosus - helps repair leaky gut, reduces vaginal discharge and candida
cell numbers
Lactobacillus reuteri reduces vaginal discharge and candida cell numbers
Bifidobacterium longum - ferments sugars into lactic acid that increase the acidity of
the intestine and inhibit the reproduction of many harmful microbes (candida prefers an
alkaline environment)
Bacteroides fragilis induces Tregs
Lactobacillus fermentum - antimicrobials that inhibits the growth of some harmful
pathogens
Saccharomyces Boulardii yeast & colostrum
Include natural probiotics (lactobacilli and bifidus bacteria) derived from food such as:
kefir (goat’s milk and fermented kefir grains), sauerkraut (fermented cabbage), miso and
tempeh (both from fermented soya beans), kimchi (Asian form of pickled sauerkraut)
L-glutamine (L-alanyl-L-glutamine) fuels gut cells and boosts immunity
Inulin from chicory root (prebiotics- bacteria food!)

44. Issue: overuse of Antibiotics, NSAIDS,
Consequence: disrupted gut function leads to excess inflammation in the gut
lining and changes in the normal gut flora (dysbiosis/candida)
Solution: Increase nutrients known to support gut heath, mucus production, support
tight junctions and secretory immunoglobulin type A (SIgA) levels
L-glutamine (L-alanyl-L-glutamine) fuels gut cells (preferred fuel source) and boosts immunity
Pau d'arco is a great antifungal
Coconut oil/MCTs
Protein powder (provides essential amino acids) - protein requirements increase during times
of increased stress/illness/inflammation
N-acetyl glucosamine is anti-inflammatory and helps protect the lining of the stomach and
intestines
Increase natural stomach acid production by drinking water with a slice of lemon, a squeeze of
lemon juice or a teaspoon of apple cider vinegar / betaine HCl supplements/high dose ascorbic
acid
Garlic (Allicin MAX) for Helicobacter pylori
Mushrooms rich in beta glucans such as reishi, shiitake and maitake
Bone broth / gelatine / collagen
Vitamins D3 and A -SigA
Aloe vera/liquorice/quercetin
Digestive enzymes

45. Issue: Western-style diet (highly processed refined foods, high fat and high added sugar)
Consequence: Lack of nutrients required to maintain a healthy gut flora result in dysbiosis
Solution: Adopt a whole-food diet (exclude processed/refined foods) that provides the nutrients
required to feed healthy gut flora, boost immunity and support liver function (detox)
Choose foods with a low glycaemic index (GI) that release natural sugar slowly.
Issue: Stressful lifestyle
Consequence: Chronic long-term stress increases inflammation and suppresses immune function
Solution: Take actions to reduce stress:
Adopt breathing techniques
Increase physical activity
‘Mindful’ meditation
Issue: Compromised nutrient absorption
(i.e. iron deficiency) Another problem with leaky gut is that it can cause malabsorption of vital
minerals and nutrients including zinc, iron and vitamin B12.
Solution: Supplement with digestive enzymes
Eat a good supply of raw foods as these will be naturally rich in digestive enzymes (normally lost
via cooking and heating) and boost immunity and support liver function (detox)

46. Olive oil
Fruit
Vegetables
Oily fish
Nuts & seeds
Legumes &
cereals
Monounsaturated fat (oleic
acid)
Antioxidants
(i.e. polyphenols)
Vitamin A,B,C & E
Vitamin D
Omega-3 fatty acids
(ALA, EPA & DHA)
Minerals
(i.e. selenium, iron &
iodine)
Amino acids
(i.e. taurine, tyrosine &
tryptophan)
Moderate red
wine
Lean meat
Moderate dairy
Neuronal survival
Energy metabolism
Neurotrophins
Neurotransmission
Membrane fluidity
Cell membrane
integrity
Glucose transport
Nutrient synthesis
Nutrient metabolism
Gene expression
Methylation
Cerebral blood flow
Blood pressure
Oxidative damage
Neuronal cell death
Neuroinflammation
Free radicals
Parletta N, Milte CM, Meyer BJ. Nutritional modulation of cognitive function and mental health. J Nutr Biochem. 2013 May;24(5):725-43.
Focus on clean eating / maintain a healthy weight

47. Adrenal support
 Avoid sugar/ artificial sweeteners
 Avoid caffeine
 Focus on a ‘clean diet’
 High-protein, low carbohydrate breakfast
 Eat every 3-4 hours to maintain optimal blood sugar levels
 Rest!
 B-Complex
 Vitamin C
 Magnesium
 Liquorice root
 Ashwagandha
 Siberian ginseng
 Rhodiola rosea
 DHEA

48. Increase glutathione levels
Up-regulate glutathione-related enzymes including glutathione reductase (GR)
and glutathioneS-transferase (GST) - anthocyanins are members of the flavonoid
group of phytochemicals, a group predominant in teas, honey, wine, fruits,
vegetables, nuts, olive oil & cocoa
Cruciferous vegetables such as broccoli, kale and cabbage contain antioxidants
that increase the production of detoxifying enzymes in the body
Sulphur-rich foods such as onions and garlic, cauliflower, eggs, Brussels sprouts
& broccoli
Cysteine-rich foods: soya beans, egg white, oats & tofu, providing the body with
the balance of nutrients that make (glutathione = L-cysteine + L-glutamic acid
+ glycine)

49. The health promoting effects of Longvida curcumin in healthy individuals
Longvida curcumin Lowered
 β-amyloid protein: a marker of brain ageing, especially in relation to
Alzheimer’s disease
 Lowered triglycerides: related to increased risk of poor cardiovascular
health
 Soluble intercellular adhesion molecule (sICAM): linked to
atherosclerosis
 Salivary amylase: a marker of sympathetic nervous system stress
 Alanine aminotransferase (ALT): a marker of liver injury
Longvida curcumin Increased
 Catalase activity: an antioxidant enzyme
 Antioxidant status: linked to lower levels of damaging free radicals
DiSilvestro RA, Joseph E, Zhao S, Bomser J. Diverse effects of a low dose supplement of lipidated curcumin in healthy middle aged people. Nutr J. 2012 Sep
26;11:79. doi: 10.1186/1475-2891-11-79.
In a 30 day, randomised placebo-controlled trial, daily supplementation with 400mg Longvida
curcumin in healthy, middle-aged individuals (40-60 years) led to significant (p<0.05) improvements
(versus placebo) in the following markers:

50. Supporting antioxidant defences
Alpha lipoic acid is an endogenous antioxidant and essential cofactor for many enzyme complexes
that interrupt cellular oxidative processes
 Increases acetylcholine production by activation of choline acetyl-transferase
 Increases glucose uptake
 Acts as a metal chelator
 Down-regulates the expression of redox-sensitive pro-inflammatory proteins including TNF-α
and inducible nitric oxide synthase
 Scavenges lipid peroxidation products such as 4-hydroxynonenal (HNE) and acrolein
Vitamin E
Antioxidant protection
Vitamin C
Further supports detoxification,
provides antioxidant protection
against free radicals
Reduces tiredness and fatigue
Necessary for the proper
functioning of the CNS
and psychological functioning

51. •Magnesium blocks the NMDA receptor and
must be removed in order for excitation to
occur
•Zinc is co-released with glutamate into the
synaptic cleft, and is thought to negatively
modulate the excitatory response
•A deficiency in vitamin B6 can lead to higher
levels of glutamate and reduced levels of
GABA inhibition, thereby facilitating
excitotoxicity
•Thus, low magnesium, zinc and or vitamin B6
levels could support excitotoxicity
Magnesium, B6 and zinc modulate glutamatergic neurotransmission and key role in
regulating the NMDA receptor, the main glutamate receptor implicated in excitotoxicity
Holton K. The role of diet in the treatment of fibromyalgia.Pain Manag. 2016 May;6(4):317-20
Holton KF, Taren DL, Thomson CA, Bennett RM, Jones KD. The effect of dietary glutamate on fibromyalgia and irritable bowel symptoms. Clin Exp Rheumatol. 2012 Nov-
Dec;30(6 Suppl 74):10-7.

52. Zinc
•Essential to the production of neurotransmitters
•Enhances neurotransmission via interaction with receptors, transporters and
ion channels in the neurone and synapse
•Low zinc status is linked to cognitive impairment via epigenetic changes of
the brain-derived neurotrophic factor (BDNF) gene
Selenium
•Up-regulates glutathione production
•Main component of antioxidant enzymes
•Supports proper adrenal function – commonly disrupted by high stress and
poor diet – leads to poor sleep, memory problems and fatigue
• Low selenium status is a risk factor for cognitive decline
Berr C, Arnaud J, Akbaraly TN. Selenium and cognitive impairment: a brief-review based on results from the EVA study. Biofactors. 2012 Mar-Apr;38(2):139-44.
Hu YD, Pang W, He CC, Lu H, Liu W, Wang ZY, Liu YQ, Huang CY, Jiang YG. The cognitive impairment induced by zinc deficiency in rats aged 0 2 months related to BDNF DNA∼
methylation changes in the hippocampus. Nutr Neurosci. 2016 Jun 22:1-7.

53. Pharmepa RESTORE provides 1000 mg pure 90% concentration,
rTG EPA wild anchovy oil, in just two easy-to-swallow capsules
Pharmepa RESTORE provides a loading dose of super strength
EPA and is ideal for people who have never supplemented with
pure EPA or those who have taken a break from omega-3 EPA
supplementation
Pharmepa MAINTAIN combines 80% concentrated rTG EPA
(750mg) plus DHA (250mg) wild anchovy oil with GLA and
triterpenes from organic virgin evening primrose oil and
vitamins D3 & E
Pharmepa MAINTAIN protects the structure and function of our
cells and helps maintain an optimal AA to EPA ratio, omega-6 to
omega-3 ratio and omega-3 index
Pharmepa MAINTAIN is suitable for long-term use after
supplementing with pure EPA

54. •Magnesium blocks the NMDA receptor and
must be removed in order for excitation to
occur
•Zinc is co-released with glutamate into the
synaptic cleft, and is thought to negatively
modulate the excitatory response
•A deficiency in vitamin B6 can lead to higher
levels of glutamate and reduced levels of
GABA inhibition, thereby facilitating
excitotoxicity
•Thus, low magnesium, zinc and or vitamin B6
levels could support excitotoxicity
Magnesium, B6 and zinc modulate glutamatergic neurotransmission and have a key role
in regulating the NMDA receptor, the main glutamate receptor implicated in
excitotoxicity
Holton K. The role of diet in the treatment of fibromyalgia.Pain Manag. 2016 May;6(4):317-20
Holton KF, Taren DL, Thomson CA, Bennett RM, Jones KD. The effect of dietary glutamate on fibromyalgia and irritable bowel symptoms. Clin Exp Rheumatol. 2012 Nov-
Dec;30(6 Suppl 74):10-7.

55. • YNERGISTIC ACTIONS between Mg and B6 for
enhanced absorption
• SUSTAINED RELEASE tablets and split dosing
for enhanced absorption & optimal tissue
distribution
• CONSISTENT PRODUCT QUALITY GUARANTEED
GMP manufactured - quality standards that
medicines manufacturers must meet in their
production processes to ensure products are of
consistent high quality
• SUITABLE FOR VEGETARIANS & VEGANS
• PIONEERING EFFECTIVE FORMULATION based
on cutting edge research, specialist delivery
technologies and innovation in raw ingredients
Key product features:
• HIGHLY BIOAVAILABLE Neurobalance™ delivers maximum levels of key nutrients:
 Chelated zinc as super absorbable zinc L-methionine
 Fully reacted magnesium citrate provides high levels of super absorbable elemental magnesium
 Vitamin B6 as pyridoxal-5-phosphate with cofactor activity

56. Serving size: 1 capsule Per serving % RI*
Longvida®
optimised curcumin extract
from turmeric root
(min. 20% curcuminoids)
500 mg n/a
DIRECTIONS FOR USE
Adults: take 1 capsule daily with food. For intensive support,
take 2 capsules daily as a split dose. Do not exceed the dose
unless advised by a healthcare practitioner.
NUTRITIONAL INFORMATION
INGREDIENTS:
Longvida® optimised curcumin extract; capsule shell (emulsifier:
hydroxypropyl methylcellulose); stearic acid; soy lecithin;
maltodextrin; ascorbyl palmitate; silicon dioxide.
Free from: dairy, gluten, lactose, soya protein, wheat, yeast,
artificial colours and flavours; not tested on animals; non-GMO;
suitable for vegetarians & vegans; halal & kosher.
* % Reference Intake
Product information

57. Serving size: 2 tablets Per serving %Reference Intake
Vitamin C (ascorbic acid) 240 mg 300
Vitamin B3 (nicotinamide) 48 mg NE 300
Zinc citrate 20 mg 200
Vitamin B5 (pantothenic acid) 18 mg 300
Vitamin B6 (pyridoxal 5-phosphate) 8 mg 570
Iron (ferrous bisglycinate chelate) 7 mg 50
Vitamin B1 (thiamine HCl) 5.5 mg 500
Vitamin B2 (riboflavin 5-phosphate) 4.2 mg 300
Vitamin E D-alpha tocopherol (natural) 2 mg a-TE 16.6
Boron (disodium tetraborate) 2 mg n/a
Manganese bisglycinate 2 mg 100
Copper bisglycinate 1 mg 100
Vitamin A (beta carotene) 800 mg 100
Folate ([6S]-5-methyltetrahydrofolate) 200 mg 100
Selenomethionine 110 mg 200
Iodine (kelp) 150 mg 100
Vitamin B7 (biotin) 100 mg 200
Chromium picolinate 50 mg 125
Molybdenum 50 mg 100
Vitamin K2 (menaquinone) 37.5 mg 50
Vitamin B12 (methylcobalamin) 20 mg 800
Vitamin D3 (cholecalciferol) 10 mg (400 iu) 200
MULTIVITAMIN & MINERALS™
provides 22 key essential vitamins &
minerals in superior body-ready and
active forms for enhanced absorption
and utilisation.
Our sustained slow release system
optimises blood nutrient levels for
longer-lasting action.

58. VESIsorbTM
Oil-based
Time (hours)
VESIsorbTM
Therapeutic level
VESIsorbTM
delivered CoQ10 is absorbed FASTER,
reaching concentrations that are STRONGER and stays
in the body LONGER than generic delivery methods
Fully reduced form of CoQ10
VESIsorb® technology for enhanced bioavailability
and tissue distribution
100 mg therapeutic dose
Oil-based
Cmax
Tmax

59. MindCare LIFT
Nutritional information Per capsule % reference
intake
Magnesium glycinate
of which magnesium
334 mg
60 mg 16
5-HTP 100 mg n/a
Vitamin B3 (niacin) 48 mg 300
Vitamin C (ascorbic acid) 40 mg 50
Zinc (citrate) 20 mg 200
Vitamin B5 (pantothenic acid) 12 mg 200
Vitamin B6
(pyridoxal-5-phosphate)
7.98 mg 570
Vitamin B1 (thiamine) 3.3 mg 300
Vitamin B2 (riboflavin) 2.8 mg 200
Vitamin B7 (biotin) 150 mg 300
Folate
([6S]-5-methyltetrahydrofolate)
100 mg 50
Selenium 82.5 mg 150
Vitamin B12 (methylcobalamin) 20 mg 800
Nutritional information Per capsule % reference
intake
Omega-3 rTG concentrated fish oil
of which:
EPA (eicosapentaenoic acid)
DHA (docosahexaenoic acid)
893 mg
410 mg
250 mg
n/a
Vitamin E (d-alpha tocopherol) 6mg 50
Vitamin D3 25 mg 500

60. Education Technical
Sophie Tully
Nutrition Education Manager
sophiet@igennus.com
Dr Nina Bailey
Head of Nutrition
ninab@igennus.com
Twitter @DrNinaBailey