Ageing

Question 1

How does the allostatic load contribute to ageing?

Answer 1

• Social, psychological, lifestyle and nutritional factors all interact with our genome to create resilliance to ageing or accelerated deterioration
• Exposure to toxins (environment, household, cosmetics), inadequate exercise, poor nutrition, high stress, genetic susceptibility, chronic inflammation and dysbiosis all play a role at a physiological and molecular level.

Question 2

How can mitochondrial dysfunction lead to chronic diseases?

Answer 2

Mitochondria are the main source of ROS in a cell.
* Oxidative stress within mitochondria leads to mtDNA mutations, reduced ATP and energy.
* Mitochondrial dysfunction leads to apoptosis, linked to MS, Alzheimer’s and Parkinson’s diseases and many chronic inflammatory diseases.

Question 3

What is inflammageing and what is it a result of?

Answer 3

• Chronic low-grade inflammation that increases as we age , leading to many age-related diseases.
• Inflammageing is the result of pathological stimulation of the innate immune system.
• Pathogens, damaged tissues, altered gut microbiota, antibiotics, steroids, and antihistamines all promote chronic inflammation.

Question 4

What is hormesis and what are some things that induce it? Why does it extend life and health span?

Answer 4

“A process in which exposure to a low level of stress or toxicity induces an adaptive beneficial effect in a cell or organism”.
eg Calorie restriction, phytochemicals, exercise, cognitive stimulation, intermittent cold and heat mildly stress the body

They can all extend lifespan and healthspan because healthy body responds to mild stress by increasing the production of endogenous antioxidants (glutathione, catalase, superoxide dismutase and phase II detoxification enzymes) cellular quality control mechanisms.

Question 5

How is NrF2 implicated in hormesis?

Answer 5

Nrf2 is a transcription factor which senses cellular stress and then responds by attaching to the antioxidant response element (ARE) within DNA and upregulating the expression of glutathione enzymes, superoxide dismutase, catalase and phase II detoxification enzymes.
This increases the production of endogenous antioxidants

Question 6

How is calorie restriction and exercise anti-ageing?

Answer 6

Calorie restriction and exercise
induce stress partly by depleting cellular energy ATP ADP NADH NAD.
This activates AMPK, a pro-longevity protein.
and the sirtuins (SIRT 1-7), a family of anti-ageing proteins.

AMPK and sirtuins initiate numerous processes that improve health and prolong life including autophagy (self-eating)
where worn-out or damaged cellular components are digested to improve the quality of the whole organism.

Exercise increases levels of PGC1-alpha, a protein that enables the synthesis of brand new mitochondria

Question 7

Why is mitophagy important in a healthy cell?

Answer 7

• In a healthy cell, mitochondria undergo mitophagy every 9-25 days after biogenesis as part of quality control to maintain their ability to produce energy
• Liver mitochondria are turned over more rapidly than heart, kidney and brain mitochondria due to toxicity

Question 8

What are the 9 key signatures of ageing?

Answer 8

Genome instability.
* Telomere shortening.
* Epigenetic alterations.
* Loss of protein regulation and disposal — a
hallmark of Alzheimer’s and Parkinson’s diseases.
* Insulin resistance and poor nutrient sensing.
* Cell senescence (biological ageing).
* Stem cell loss.
* Altered intercellular communication.

Question 9

Why is social connection important? who is it most important for?

Answer 9

• Social connection is most important for children and the elderly.
• Poor childhood social connection predisposes a person to inflammatory diseases in later life.
• In the elderly, social connection is a powerful anti-inflammatory — as strong as smoking cessation or exercise!
• BMI, blood pressure and inflammation can all be reduced by good social connections — social stress has the opposite effect

Question 10

Why is excess phase 1 detoxification linked to ageing and cancer? What can slow down this process?

Answer 10

• Phase I detoxification enzymes transform xenobiotics, steroid hormones and drugs into reactive intermediates by the addition of oxygen, more toxic than they were to start with
• Hydrocarbons are common xenobiotics which induce phase I detoxification enzymes.
• Cells detect many xenobiotics via the aryl hydrocarbon receptor AhR which binds to the DNA xenobiotic response element (XRE) to drive gene expression of phase I enzymes.
• Over-activation of the aryl hydrocarbon receptor (AhR) leads to accelerated ageing, cardiovascular disease and cancer.
• Green tea, turmeric, quercetin and resveratrol desensitise the AhR, slow down phase I and protect against cancer.

Question 11

How does calorie restriction help with healthy ageing? how can a ketogenic diet help?

Answer 11

• Activate sirtuins, anti-ageing proteins which improve insulin sensitivity, mitochondrial activity, cardiovascular health, fat metabolism, DNA integrity and also lower inflammation.
• Promote autophagy to aid cellular rejuvenation.
• Increase adiponectin, an adipokine associated
  with longevity.
• Ketogenic diets may mimic some of the health benefits
  of fasting by shifting metabolism toward beta-oxidation
  and ketone synthesis.

Also activates AMPK which initiates numerous processes that improve health and prolong life including autophagy (self-eating)

Question 12

How does obesity and insulin resistance increase accelerated ageing?

Answer 12

Leads to:
* Mitochondrial dysfunction and reduced biogenesis, hindering tissue repair and renewal.
* Increased inflammaging.

• Proteins modified by glycation are able to bind to AGE receptors (RAGEs) and promote inflammation, strongly associated with accelerated ageing,
  neurodegeneration, diabetes and cancer.

Question 13

What is dementia and what is the most common one?

Answer 13

Dementia describes a syndrome of cognitive impairment that affects memory recall, cognitive abilities and behaviour, and significantly interferes with a person’s ability to perform daily activities.
* Alzheimer’s disease (AD) is the most common form of dementia and accounts for 60–80% of all dementia cases.

Question 14

Name some dementia risk factors

Answer 14

Chronic / acute stress.
* Proton pump inhibitor medication.
* Poor diet (junk food, sugars).
* Vitamin and nutritional deficiencies,
e.g., vitamin A, D, C, B6, B9, B12 etc.
* Poor lifestyle (e.g., smoking and
drinking alcohol)
* Vaccinations.
* Hypertension and diabetes.
* Mental inactivity.
* Obesity.
* Physical inactivity.
* Social isolation.
* Environmental toxins.
* ApoE4 polymorphism.
* Mid-life depression.

Question 15

What are the four main types of dementia?

Answer 15

1) Frontotemporal dementia: Behavioural, language and movement difficulties, driven by atrophy of frontal and temporal lobes.

2) Vascular dementia: Impaired blood flow to the brain leading to cognitive decline. Often associated with cardiovascular disease.

3) Lewy body dementia: Lewy bodies are abnormal clumps of protein that cause alterations in thoughts, perceptions and movement. Lewy bodies are also found in Parkinson’s disease patients.

4) Alzheimer’s disease: Amyloid beta and tau are two proteins which correlate with Alzheimer’s disease. Patients suffer progressive loss of memory, language and reasoning.

Question 16

How are a build up of amyloid beta and tau proteins implicated in AD?

Answer 16

• Amyloid plaques and misfolded tau proteins are characteristic of AD, They are symptoms and not the cause!
• Infection, inflammation and oxidative stress drive amyloid production.
• Amyloid beta is now thought to be the brain’s protective response to a threat rather than the cause of Alzheimer’s disease.

Question 17

What are Dr Bredesens 3 catagories of AD?

Answer 17

• Inflammation or ‘hot’: Associated with increased innate immune system activation, inflammation, pro-inflammatory microglia (M1) and reduced sirtuin (SIRT1) activity compared to NF kappa B.
• Atrophic or ‘cold’: Loss of trophic support from neurotrophins such as brain-derived neurotrophic factor (BDNF).
• Cortical or ‘toxic’: associated with environmental toxins, leading to chronic inflammation and general brain atrophy.

Question 18

What are microglia, how can they shift including transcription factors and why is this protective?

Answer 18

Microglia are the resident immune cells of the brain:
*M1 are the proinflammatory type, but can be polarised to an M2 (anti-inflammatory) type. This shift is supported by transcription factor NrF2, which can be protective in Alzheimer’s disease.

• The inflammatory transcription factor NF Kappa B promotes the neuroinflammatory M1 phenotype.

Question 19

How are TLR’s implicated in microglial- related inflammation? What can suppress this inflammatioon?

Answer 19

• Dysbiosis of gut microbiota and pathogens leads to pro-inflammatory communication to TLRs on brain microglia via the microbiota-gut-brain axis. Oral dysbiosis: P. gingivalis
  is associated with a significantly ↑ Alzheimer’s risk.
• TLRs on brain microglia are sensitive to our own damaged tissue, leading to a spiral of inflammation and neuronal loss.
• Oxytocin, produced during enriched social interactions, can act through the Vagus nerve to suppress microglia-related inflammation.
  *

Question 20

How is neurogenesis effected in AD?

Answer 20

In AD, cholinergic hippocampal neurons are lost and there is reduced neurogenesis.
* Every day there are 700 new neurons created in the hippocampus but they will not survive if inflammation is high.

Question 21

What is BDNF, why is it important in AD and how can we support it naturally?

Answer 21

Neurotrophins are our brain nourishers:
* BDNF (brain-derived neurotrophic factor) is a neuroprotective protein, a brain nourisher essential for the survival of cholinergic neurons. supports cognitive ability, memory, neurogenesis and synapse function.

• In Alzheimer’s disease BDNF levels are significantly decreased.
• Healthy gut microbiota support BDNF, lactobacillus and bifidobacterium
• Exercise, yoga, dance.- yoga found to triple BDNF
• Oxygen, fresh air, nature.
• Environmental and social enrichment.
• Reduced stress.
• Polyphenols — resveratrol,
  catechins / epicatechins, e.g., green tea, blueberries, cocoa.
• Mediterranean diet.
• Pomegranate, raspberry,
  strawberry, walnut, blackberry,
  pecan and cranberry.
• Omega-3 fatty acids.
• Vitamin B12.
• Rutin and hesperidin.
• Curcumin (turmeric).
• Calorie restriction.

Question 22

What medication is commonly used for AD and what are the side effects?

Answer 22

Donepezil is widely used to raise levels of acetylcholine by inhibiting acetylcholinesterase.

Side effects are nausea and incontinence as increased acetylcholine can disrupt peristalsis.

Question 23

How is acetylcholine made, what does it do? and How can you naturally support the production of it?

Answer 23

• Acetylcholine, essential for mood, memory and learning,is a brain anti-inflammatory and supports mitochondrial health.

It is made from mitochondrial acetyl-CoA and dietary choline.

• Healthy diet, lifestyle and BDNF support acetylcholine though stimulation of the Vagus nerve, which then releases acetylcholine.

Question 24

How is aluminium implicated in AD? What are it’s absorption rates?

Answer 24

Aluminium is a neurotoxin, concentrations are significantly raised in the brains of patients with Alzheimer’s disease.

• Aluminium easily complexes with cellular components, becoming a burden to neurons, and depleting them of vital ATP.
• Aluminium absorption rates:
  – 0.1% from food. 0.3% from water. 100% from vaccine adjuvants.

Question 25

How is obesity and insulin resistance linked to AD?

Answer 25

• The strong association between insulin resistance and Alzheimer’s has led to it being described as ‘Type 3 diabetes’.
• Obese individuals have increased peripheral inflammation and neuroinflammation, overactivation of the sympathetic nervous system which then suppresses parasympathetic acetylcholine activity.
• Obesity, therefore, stresses and inflames the entire body and brain.

Question 26

How would you support AD with diet? What is the MIND diet?

Answer 26

• Whole unprocessed foods.
• Low GI foods such as green leafy vegetables, kale,
  broccoli, cauliflower, beans, blueberries and apples.
• Healthy fats from olive oil, avocado, nuts and seeds.
• Fatty fish such as salmon, herring, sardines and mackerel.
• Choose free range, pasture-fed, organic animal produce.
• Drink plenty of water — the brain is 80% water and can shrink if dehydrated.
• Coconut oil will support Alzheimer’s by boosting ketones.
• Consumption of 20 g / day of organic coconut oil raises blood ketone levels and correlates with improved cognitive performance. rich in MCTs (medium chain triglycerides) which are an easily absorbable

The MIND diet:
* The MIND diet is a hybrid of the Mediterranean and
DASH (Dietary Approaches to Stop Hypertension)
diets.

• The MIND diet has 15 dietary components, including
  10 ‘brain-healthy food groups’ — green leafy vegetables, other vegetables, nuts, berries, beans, whole grains, fish, poultry and olive oil … and excluding five unhealthy groups that comprise red meats, butter and margarine, cheese, pastries and sweets and fried or fast food.

Question 27

What supplements might you recommend for Alzheimers’ ?

Answer 27

• Vitamin C (500 mg), alpha lipoic acid (300 mg) and taurine (1000 mg)
• Glucose metabolism support and general antioxidants

-Lactobacillus acidophilus and salivarius (1 and 4 billion)
- Reduces gut permeability and dysbiosis

• CoQ10 (600 mg), vitamin B complex and vitamin E (1000 iu)
  Mitochondrial support

-Citicoline (250 mg)
Synapse and mitochondrial support and CNS anti-inflammatory.

-Curcumin (500 mg), vitamin D (2000 iu) and omega-3 fatty acids (750 mg)
Anti-inflammatory

-Resveratrol (100 mg)
Protects against misfolded amyloid and tau

Question 28

What is a mild-ketogenic diet?

Answer 28

Ketoflex 12 / 3.
* ‘12’ means leaving 12 hours between the last meal of the day and the first meal the day after.
* ‘3’ means leaving 3 hours between the last meal of the day and bedtime.
* The 12 / 3 action will put the body into a mild state of ketosis which is healing for the brain and mitochondria.
* Simple carbohydrate intake will rapidly halt ketosis.

Question 29

Compare the swank and wharls diet for MS?

Answer 29

The Swank diet focusses on a low saturated fat diet —under 15 g / day as MS patients have difficulty
metabolising saturated fat in mitochondria — and
this disrupts the myelin sheath.

• Fruit and vegetables.
• No red meat permissible in the first year; pork also excluded.
• White meat poultry and white fish — under 50 g / day.

The Wahls diet concentrates on a paleo diet:
* Green leafy vegetables.
* Sulphur-rich vegetables, such as cabbage, onions and asparagus.
* Colourful fruits and vegetables due to their phytonutrient content, such as beetroot, oranges, berries and carrots.

but is less fat on saturated fat intake and includes grass fed meats (although these are lower in satfat than farmed) also:
* Omega-3 fatty acids. .
* Seaweed.

Question 30

What happens in MS, and what are the different types?

Answer 30

MS is an autoimmune disease, inflammatory immune cells infiltrate the blood brain barrier and attack the myelin sheath (produced by oligodendrocytes, protects the nerve to support nerve impulses) leading to the loss of oligodendrocytes and neurodegeneration

Relapsing- remitting MS- alternates between relapse (myelin loss) and periods of remission (85%) average age diagnosis 30

• 10–15% of patients present with the primary progressive form of MS where there is a continuous and progressive loss of neurological function with no remission. The average age
  of diagnosis for progressive MS is 45.

Question 31

What are some symptoms of MS and risk factors?

Answer 31

Symptoms:
* Visual impairment ― optic neuritis.
* Nerve tingling and numbness.
* Intestinal and urinary problems.
* Fatigue and weakness.
* Poor co-ordination and balance.
* Speech difficulties.
* Learning and memory issues.
* Difficulty walking.
* Emotional difficulties.
* Muscle spasm or tremors.
* Pain.

Risk factors:

• Shift in T-cell subpopulations away from anti-inflammatory T-regs, towards autoreactive Th17 T cells.
  – Vitamin D deficiency,
• raised BMI.
  – Infections such as Epstein-Barr virus.
  – Childhood trauma / stress.
  – Homocysteine, mitochondrial dysfunction.
  – Cigarette smoke exposure.
  – Certain autoimmune diseases.
  – Environmental toxins, e.g. dioxins, air pollution

Question 32

Why is vitamin D deficiency associated with MS? what levels are proposed to be protective?

Answer 32

• Vitamin D helps shift adaptive immune system expression away from autoreactive T-cells and toward anti-inflammatory T-regs..
• MS patients with low vitamin D were found to have
  more brain lesions and increased numbers of relapses.
• Sufficient vitamin D during pregnancy and at
  birth protects child from MS in later years.
• Serum vitamin D levels of 75–100 nmol / L have been proposed to protect against MS development and / or MS relapse

Question 33

Why does a vitamin K deficiency drive MS? Why does this deficiency occur?

Answer 33

• Gas 6 (growth arrest specific 6) is a vitamin K-dependent anti-inflammatory protein which protects oligodendrocytes and promotes remyelination, protective in MS
• MS patients have blood levels around one-third of those expected, Deficiency thought to be due to poor microbial synthesis in the gut, low absorption or low dietary intake.

Question 34

Why is B12 needed in MS?

Answer 34

B12 supplementation improves neuron growth and survival and regenerates the myelin sheath.

• The phospholipids contained within the myelin sheath are methylated, and so require B12 to support methylation.

Question 35

Why is obesity/ high BMI a risk factor for MS?

Answer 35

• Obesity makes the blood-brain barrier more
  permeable leading to CNS inflammation.
• The adipokine leptin, raised during obesity,
  is associated with CNS inflammation.
• Leptin increases levels of Th17 autoreactive T-cells.
• Obesity leads to an upregulation of proinflammatory M1 microglia, driving oligodendrocyte loss and overwhelming the protective M2.
• M2 microglia are anti-inflammatory,
  support oligodendrocytes and remyelination.
• Obesity-driven BBB permeability leads to infiltration of peripheral macrophages from general circulation driving further inflammation.

Question 36

How can a traumatic childhood increase MS risk?

Answer 36

• Childhood neglect or abuse leads to thymic involution or atrophy, this amplifies the production of autoreactive T-cells and predisposes a person to MS.

early life stress has a negative impact on oligodendrocytes, which then becomes problematic in early adulthood.

Question 37

How does the ANS regulate inflammation?

Answer 37

• The sympathetic and parasympathetic arms of the ANS regulate inflammation by interacting with T-cells.
• The parasympathetic arm operates via the Vagus nerve, which decreases proinflammatory microglia, autoreactive T-cells and increases myelination and anti-inflammatory T-regs.

Question 38

Supplements to support MS?

Answer 38

• Vitamin D (2000 iu).
• Vitamin K (90 mcg).
• Hesperidin (500 mg).
• Quercetin (500 mg).
• Sulforaphane (250 mg).
• Alpha lipoic acid (300 mg).
• Citicoline (250 mg).
• Omega-3 fatty acids (750 mg).
• Vitamin B12 (1000 mcg) and methyl folate (500 mcg).

Question 39

What is Parkinsons disease and what are the main symptoms?

Answer 39

The second most common neurodegenerative disorder after Alzheimer’s disease.
* a gradual loss of dopamine-producing neurons in the substantia nigra, these normally supply or enervate a part of the brain called the striatum.

• Loss of dopamine supply to the striatum leads
  to the characteristic tremor and movement disorders seen in the disease.

Main symptoms are:
* Characteristic tremor — often called ‘pill rolling’,

• Muscle rigidity or dystonia — stiff or weak muscles and difficulty maintaining posture.
• Shuffling gait (dragging feet).
• Constipation and loss of sense of smell — may
  occur many years before diagnosis.
• Bradykinesia or slowness of movement. Affects handwriting (micrographia), facial expression and speech.

Question 40

Risk factors and causes of PD?

Answer 40

Age, hereditary, sex.
* Mitochondrial dysfunction, inflammation and oxidative stress.
* Traumatic brain injury.
* Pesticides and herbicides.
* Manganese, iron, mercury, lead and aluminium toxicity.
* Poor calcium metabolism.
* Stress and depression.
* Recreational drugs, especially amphetamines.

Question 41

What is Alpha Synuclein and how is it implicated in PD?

Answer 41

Alpha synuclein is the signature misfolded protein in Parkinson’s disease, it becomes misfolded due to excess oxidative stress.

• Once misfolded, alpha synuclein can form protein aggregates called Lewy bodies.
• Lewy body accumulates in and around dopamine
  neurons leading to further oxidative stress,
  mitochondrial dysfunction and finally dopamine neuron loss.

Question 42

How can metals and agrochemicals contribute to PD?

Answer 42

Manganese has been linked to PD
high levels of iron deposits have been found in the brains of PD patients.
Iron and manganese supplementation have been found to double the risk of PD in some people.
* Higher blood levels of mercury are seen in PD patients, exposure can lead to an 8-fold increase in risk
* Aluminium, cadmium, cobalt, copper, iron, and manganese all accelerate the misfolding of alpha synuclein into toxic aggregates.

• Rotenone is a natural pesticide which causes mitochondrial dysfunction, increases the risk of PD.
• Paraquat is a herbicide which increases oxidative stress and PD risk
• Maneb is a manganese containing fungicide also associated with increased PD risk.

All been have been found to block mitochondrial transport to dopaminergic neuron synapses

Question 43

How does L-dopa work, why is it given rather than dopamine? and how can it affect serotonin?

Answer 43

• Dopamine cannot cross the blood-brain barrier (BBB). L-dopa can cross into the CNS where it converts into dopamine.
• Serotonin-producing neurons also convert L-dopa to dopamine by using amino acid decarboxylase — the same enzyme is used to make both dopamine and serotonin.
  • Serotonin neurons can be damaged by L-dopa, resulting in some negative psychological effects.

Question 44

What is DOPAL, why is it detrimental, and what is considered a protective strategy for dopaminergic neurons?

Answer 44

• Dopamine is degraded by the enzyme monoamine oxidase B (MAO-B) in the cytosol to a toxic intermediate called DOPAL, this increases with L-dopa medication
• DOPAL interacts with the protein alpha synuclein leading to its misfolding and the formation of toxic Lewy bodies. Misfolded alpha synuclein further accelerates toxic DOPAL formation.
• Slowing down MAO-B and speeding up DOPAL detoxification to its metabolite DOPAC, is
  considered to be protective for dopaminergic neurons.

Question 45

What are the early warning signs of PD? and why is it important to detect them?

Answer 45

70% of dopaminergic neurons may already be lost by time of diagnosis so awareness of early warning signs is important.

• Many PD patients lose their sense of smell several
  years before motor signs first appear.
• It is common for PD patients to have suffered
  from constipation for up to 10 years before diagnosis, it is possible that misfolded alpha synuclein travels from an inflamed gut to the brain over
  a period of 10 years, leading to PD in some people.

Question 46

What are the main aims of Dietary interventions with PD? what is MEND?

Answer 46

1) Reduce inflammation and promote neurogenesis
2) Support methylation, mitochondria and neurotransmitter function
3) Repair the gut and any GI issues
4) optimise antioxidants
5) optimise fasting glucose and insulin

• Whole unprocessed foods.
• Low GI foods such as green leafy vegetables, kale, broccoli, cauliflower, beans, blueberries and apples.
• Healthy fats from olive oil, avocado, nuts and seeds.
• Fatty fish such as salmon, herring, sardines and mackerel.
• Choose free-range, pasture-fed, organic animal produce.
• Drink plenty of water — the brain is 80% water. It can shrink if dehydrated.
• eat to 80% full and not too late
  Reduce inflammation, improve insulin sensitivity
  Exercise, reduce stress
  Exercise 1 hour per day, consider yoga

The MEND Protocol 2
Metabolic enhancement for neurodegeneration (MEND):

Question 47

What other natural support might you use for PD?

Answer 47

Hyperbaric oxygen (breathing pure oxygen in a pressurised room) — can lessen psychiatric symptoms

• Avoid EMFs from mobile phones and microwaves. disrupts cell membrane calcium channels leading to oxidative / nitrosative stress in the CNS.
• Chelation of aluminium with Volvic, Fiji water and other chelators such as chlorella and coriander. Aluminium has been shown to displace iron from its stores leading to increased oxidative stress and protein misfolding.
  • Alpha lipoic acid can chelate damaging iron deposits from ageing brains.

Question 48

Supplements and herbs for PD?

Answer 48

Vitamin C (500 mg), alpha lipoic acid (300 mg) and taurine (1000 mg) : Dopamine and glucose metabolism, petrochemical detox

Lactobacillus acidophilus and salivarius (1 and 4 billion)
Reduces gut permeability and dysbiosis

CoQ10 (600 mg), vitamin B complex and vitamin E (1000 iu)
Mitochondrial support

Citicoline (250 mg) Synapse and mitochondrial support and CNS anti-inflammatory.

Curcumin (500 mg), vitamin D (2000 iu) and omega-3 fatty acids (750 mg) Anti-inflammatory

Methyl folate (500 mcg)
Homocysteine reduction

Herbs that can help repair the blood brain barrier:
* Gotu kola and guggul — also neuroprotective (reversing neuronal damage), anti-oxidants, shown to inhibit acetylcholinesterase.

• Gingko biloba — circulatory stimulant, tissue perfusion enhancing.
• Mucuna pruriens : Contains L-dopa which crosses the blood-brain barrier and converts into dopamine. Caution: Possible additive effects with pharmaceutical dopaminergics,

Question 49

What is a decarboxylase inhibitor? What should be taken away from it?

Answer 49

• L-dopa drugs also include another drug called a decarboxylase inhibitor

this drug inhibits L-dopa dopamine conversion outside the brain, resulting in a higher level of dopamine reaching the brain.

• Vitamin B6 should be taken away from L-dopa medication as it may interfere with decarboxylase inhibitors.
• Should maybe be taken away from protein containing meals as L-dopa is derived from tyrosine, this may facilitate easier L-dopa passage into the brain.