NVS Health Flashcards

1
Q

What factors affect the NVS

A

“Lifestyle - environment and how we react to it , early experience, self esteem and belonging
Nerve cell structure and function - EFA’s, phospholipids, mins, removal of toxins
Hormonal and immune factors - oest, test, thyroxine, cortisol, cytokines
Energy - relies on steady supply of glucose or ketones
GI health - the second brain”

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2
Q

What is the NVS composed of and what does it do?

A

Composed of CNS and Peripheral NS. Includes neurons & NT’s. Controls and regulates movement, sensation, perception, language, learning and memory

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3
Q

What is the Gut Brain Axis?

A

Bidirectional communication of the central and enteric NVS via the vagus nervous. Vagus nerve contains 80% afferent (sensory) nerves and 20% efferent (motor) nerves. Gut microbiome play a role in the health of this axis - dysbiosis can = nervous and mental health disorders

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4
Q

How do the microbes of the GBA interact?

A

“Modulation of NT production e.g seretonin
Bacterial metabolites e.g SCFA support intestinal barrier, mucosal seretonin release and influence memory and learning
Modulation of afferent sensory nerves e.g neuronal excitability, gut motility and pain perception
BDNF production - and function in the CNS”

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5
Q

What role does gut barrier function play in the GBA

A

Diet induced dysbiosis can lead to comprimised mucus layer which can cause interaction between gut microbes and the immune system causing inflammation and increased permeability of the tight junctions. This can lead to metabolic endotoxaemia which causes immune activation of different organs including the brain. Elevated LPS are associated with neruroinflammation and conditions such as depression

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6
Q

What key factors influence NVS function

A

“Inflammation & oxidative stress, toxic load: Gut permeability, heavy metals, environmental toxins, obesity, glycaemic load, ageing, nutritional factors
Decreased expression of neurotropic factors (BDNF & NGF)
Mitochondrial changes: relates to oxidative stress and inflamm, nut deficiency, ageing”

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7
Q

What are neurotransmitters? How are they synthesized and methylated?

A

“Chemical messengers released from the pre-synamptic terminal which cause either an ihibitory or excitatory effect on the post-synaptic cell.
Synthesised from specific substrate (AA) and cofactor (B6 etc)
Methylation uses: Methyfolate for Biopterin (Ser & Dope) & SAMe (5MTHF & B12) for melatonin & dopamine”

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8
Q

Describe NT balance

A

NT need to be inactivated and removed via enzyme breakdown, diffusion or reabsorption. Reuptake is an important mechanism. Key enzymes are MAO (Ser, Adr, Nor, Dope) and COMT (Adr, Nor, Dope)

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9
Q

What is Serotonin and where is it produced, which elements XBBB?

A

5-HT a monoamine NT produced from tryptophan. Produced by enterochromaffin cells and bacteria in the GIT (95%) and CNS. 5HTP and Tryptophan XBBB

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10
Q

What is the 5-HT pathway?

A

Tryptophan - 5HTP - 5-HT (seretonin) - N-Aceytlserotonin - Melatonin

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11
Q

What are key cofactors in the 5-HT pathway?

A

B2, B3, Methylfolate, B5, B6, Mg, Zn, Fe, Vit C, Vit D3, Aceytl COA, SAMe

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12
Q

What is 5-HT functions?

A

GI signaling (motility, epithelial secretions), mood, appetite, sleep, blood clotting

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13
Q

What metabolite of 5-HT can be tested on an OAT?

A

5-HIAA

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14
Q

What are causes and risk factors for low serotonin?

A

“Insufficient nutrient cofactors - tryptophan and cofactors B6, B3, methylfolate, Zn etc
Chronic stress - prolonged ACTH and cortisol secretion can affect the integrity of 5-HT receptors reducing uptake - outlook, sense of purpose, financial problems etc
GI dysbiosis can impact tryptophan metabolism and gut serotonin production which can impact brain serotonin
Poor digestive health, Lack of sunlight, sedentary, caffeine, long term alcohol use, statin use
Heavy metals
Sex hormone imbalance (oest)”

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15
Q

What is the tryptophan steal?

A

Tryptophan can be shunted to produce NAD+ instead of serotonin via kynurenine pathway. This is proinflam and produced quinolinic acid which is an excitotoxin (increases glutamate) which can cause cell death and is linked to mood disorders and neurodegenerative diseases.

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16
Q

What are key SNP’s in low serotonin?

A

“TPH1 (peripheral serotonin syn - gut)
TPH2 (CNS ser syn)
5-HTT & 5-HT1 & 2A - receptors
MAO-A
VDR”

17
Q

What is low serotonin associated with

A

“Constipation, IBS, migraines
Mood, anxiety, panic disorders, insomnia, anger, discontentment, eating disorders, OCD, substance abuse - additctions”

18
Q

What are glutamate and GABA - what is excess glutamate and low GABA linked to?

A

Glutamate is a major excitatory NT that plays a role in memory and learning. GABA is a major inhibitory NT. Excess glutamate is linked to neuronal injury and so neurogological diseases such as Alz, MS, Epilepsy. Low GABA can lead to anxiety, insomnia, cravings, alcohol misuse, panic attacks and palpatiations, seizures, carb cravings, titinus

19
Q

“What is the pathway, enzymes and cofactors

A

“Pathway Glutamine - Glutamate - GABA
Enzymes - Glutaminase - Glutamate Decarboxylase (GAD)
Cofactors - B6, Zn, Mg, Vit C, Taurine”

20
Q

What are causes and risk factors for GABA deficiency

A

“Stress - reduces GABA activity via decreases expresion of GAD
Alcohol - inhibits GAD
Co-factor deficiencies
Dysbiosis - Lacto & Bifido synthesis GABA
Limited exercise, impaired digestion/ absorption”

21
Q

What are key SNP’s in low GABA?

A

“GABRA2 SNPs - lower sensitivity to GABA - strongly associated with anxiety and the use of alcohol
GAD 1&2 - impacts Glutamate to GABA conversion
ALPL - degrades B6”

22
Q

What is Dopamine (DA)? Whare are its functions and what can be seen on an OAT?

A

“DA is a catecholamine. Its functions are motor control, reward seeking behaviour, working memory, curiosity, linked to addiction. Also acts as a neurohormone released by the hypothalamus to inhibit prolactin
HVA - homovanillic acid can be seen on an OAT”

23
Q

What is the DA pathway?

A

Phenaylalanie - Tyrosine - L-DOPA- Dopamine- Noradrenaline-Adrenaline

24
Q

What are key cofactors in the DA pathway?

A

B1, B3, B6, 5-MTHF, Fe, VitC, SAMe

25
Q

What are DA depletion and imbalances associated with?

A

“DA depletion associated with bradykinesia and Parkinson symptoms, rigidity and tremors. Levodopa - a parkinsons drug crosses the BBB and readily converts to DA here. B6 is contra with L-DOPA as it will convert to DA which does not cross BBB.
DA imbalances are linked to depression, anxiety, restless leg syndrome. Elevated levels linked to OCD and hyperactivity”

26
Q

What are causes and risk factors for DA imbalances?

A

“Stress
Cofactor deficiency - phenylalanine/ tyrosine/ B3,B6 5-MTHF, B12
Sleep deprivation
High refined sugars and sat fats
Poor gut health - 50% DA produced in GIT by enteric neurons, epithelial cells and bacteria”

27
Q

What are key SNPs for DA imbalance?

A

“Tyrosine Hydroxylase (TH) converts tyrosine to L-DOPA
MTHFR
COMT
MAOB”

28
Q

What is Acetylcholine (Ach) what increases its release and what down regulates it?

A

Formed from mitochondrial acetyl-CoA and dietary choline. Essential for mood, memory and learning. Major NT in PSNS. Upreg by healthy diet and lifestyle. BDNF increases Ach release via vagus stimulation. AI in brain - supports mitochondrial health. Down reg by cortisol. Co-factor - B5