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CNM NUTRITION 2 S1 > 6. ENDOCRINE HEALTH > Flashcards

6. ENDOCRINE HEALTH Flashcards

This module covers: • The thyroid. • Hypothyroidism. • Hyperthyroidism. • Type 2 diabetes mellitus. • Type 1 diabetes mellitus.

1
Q

List three selenoproteins involved in thyroid hormone homestasis and give their functions.

A
  • Deiodinase-1 (D1) and deiodinase-2 (D2) covert T4 to T3.
  • Deiodinase-3 (D3) coverts T4 to Reverse T3 (RT3).
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2
Q

What are the functions of the following hormones:
1. TRH
2. TSH
3. T3
4. T4
5. Reverse T3

A
  1. TRH: Stimulates TSH release from the anterior pituitary.
  2. TSH: Stimulates thyroid hormone production. Activates iodide uptake via the sodium / iodide symporter (SIS).
  3. T3: 4 x the ‘strength’ of T4. Increases growth, bone and CNS development, increases BMR, heart rate and activates metabolism.
  4. T4: AKA thyroxine. Approx. 90% of secreted thyroid hormone. Weak ‘thyroid’ activity — ‘inactive’ form.
  5. Reverse T3: Biologically inactive — protects tissues from excess thyroid hormones.
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3
Q

List four essential minerals and the role they play in thyroid hormone synthesis.

A
  • Iodine: Along with tyrosine, used to form T4 and T3, catalysed by TPO.
  • Iron: TPO is haem-dependent.
  • Selenium & zinc: Are enzyme co-factors and important for thyroid receptor function.
  • Copper: A cofactor of deiodinase enzymes.
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4
Q

Which vitamins support the synthesis and function of thyroid hormones?

A

Vitamins A, C, E, B2, B3, B6, B12

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5
Q

List four food sources rich in iodine.

A
  • Sea vegetables
  • ocean fish and shellfish (ie. cod, scallops)
  • eggs
  • dairy foods (due to the fortification of animal feed)
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6
Q

Which of the following promotes iodine disorders?
a) Low iodine intake
b) Excess iodine intake
c) Both

A

c) Both

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7
Q

List two possible causes of excess iodine and the conditions this could lead to.

A
  • An inhibited Wolff-Chaikoff effect (helps reject excess iodine and hormone synthesis)
  • Over-consumption of iodised salt, iodine fortified milk and iodine-containing dietary supplements.
  • Radiocontrast dyes / medications
    (e.g., amiodarone — used for heart arrythmias and contains iodine).

Excess iodine can cause hyperthyroidism, hypothyroidism and a goitre

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8
Q

How much T4 and T3 is secreted by the thyroid daily?

A

The thyroid secretes approx.
80–100 mcg of T4 and 10mcg T3 daily.

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9
Q

Where is most T3 in the body obtained from?

A

Only 10% of circulating T3 is derived directly from thyroid secretion. The remaining 90% is obtained via conversion from T4 in peripheral tissues (liver and kidney) to active T3 or inactive reverse T3.

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10
Q

Explain why elevated Reverse T3 (RT3) levels can be problematic.

A

RT3 is biologically inactive but can bind to T3 receptors, blocking the action of T3. An increase in RT3 = decrease in T3.
↑ RT3 can present as hypothyroidism.

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11
Q

Give examples of four types of HPT disruptors that can interfere with the HPT axis, thyroid hormone synthesis, secretion, transport, metabolism and function.

A
  • Pesticides: Alter hepatic enzymes, reducing T4 half life. Glyphosate lowers TSH with reduced gene expression for D2, D3 and transporters.
  • PCBs (POPs) and bisphenols (e.g., BPA):
    Affect thyroid hormone receptors.
  • Phthalates: Affect synthesis, metabolism and transport.
  • Perchlorates: (e.g., nitrate fertilisers and food packaging)
    Block Na-I symporter, inhibiting iodide uptake. Can also cause lower levels of T3 in breast milk.
  • Halogens: (disrupt thyroid functioning)
    Fluoride — in toothpaste, tap water and pesticides. Interferes with the sodium iodide symporter (= ↓ iodine uptake) and iodothyronine deiodinase (= ↓ T4 to T3 conversion). In a study, a widely-fluoridated area was almost twice as likely to report high hypothyroidism prevalence in comparison to a non-fluoridated area. The effect seems to be mitigated by adequate iodine status.
    Chlorine — swimming pools, PCBs — ↑ TSH, ↑ thyroid antibodies.
    Bromine — in pesticides, PBDEs (flame retardants, farmed fish).
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12
Q

What advice can be given to avoid HPT disruptors?

A
  • Drink filtered water.
  • Opt for fluoride-free toothpaste.
  • Eat organic.
  • Avoid farmed fish.
  • Avoid processed foods / beverages.
  • Limit time spent in chlorinated pools.
  • Avoid plastic packaging.
  • Select organic textile products.
  • Use natural cleaning products.
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13
Q

Give an example of a medication that often exert the following effects on thyroid function:
a) Decrease TSH secretion
b) Alter T4 and T3 metabolism
c) Reduce T4 to T3 conversion
d) Reduce T4 and T3 binding
e) Increase thyroglobulin

A

a) Dopamine, glucocorticoids, lithium.
b) Phenytoin, rifampicin.
c) Beta-blockers, amiodarone.
d) Diuretics, NSAIDs.
e) Oestrogen, tamoxifen.

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14
Q

What condition could result from the long-term use of hyperthyroid medication?

A

Hyperthyroid medications may induce hypothyroidism 10–20 years later in Grave’s disease.

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15
Q

How is the gut microbiome related to the thyroid?

A

Gut dysbiosis negatively affects thyroid function.
Microbes regulate iodine uptake, degradation, and enterohepatic cycling.

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16
Q

Which gut markers are typically out of range in auto-immune thyroid disease (AITD)?

A

In AITD, low SCFA production is common, as is elevated zonulin (intestinal permeability) and elevated serum LPS, leading to chronic low-grade inflammation.

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17
Q

What are the optimal ranges for the following thyroid tests:
1. TSH
2. Free T4
3. Total T4
4. Free T3

A
  1. TSH: 0.4 to 2.5
  2. Free T4: 12.8 to 19.5 pmol/L
  3. Total T4: 70 to 150
  4. Free T3: 3.2 to 4.5 pmol/L
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18
Q

How might you interpret the following test results:
a) High TSH; Normal T4; Normal T3
b) High TSH; Low T4; Low/Normal T3
c) Low TSH; High/normal T4; High/normal T3

A

a) Subclinical hypothyroidism
b) Hypothyroidism
c) Hyperthyroidism

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19
Q

What is the optimum level of iodine as measured in the first morning urine for adults, children and pregnant women?

A

Iodine goal = A urinary first morning iodine level of:
- 100–199 mcg / L in children and adults.
- 150–249 mcg / L in pregnant women.

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20
Q

Which level of urinary iodine is considered as severe deficiency?

A

< 20 mcg / L = severe deficiency.

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21
Q

Which at home test can be recommended to give an indication of thyroid status?

A

The Barnes basal body temperature test
The theory is that waking axillary temperature is diagnostic for low thyroid, if < 36.5 degrees C.

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22
Q

How would the following SNPs impact thyroid function:

  • VDR
  • BC01
  • GPX
A
  • VDR: Vitamin D is a co-factor required for T3 to function correctly.
  • BC01: Retinol is a co-factor required for T3 to function correctly.
  • GPX: A SNP in the gene that codes for glutathione can increase oxidative stress which can disrupt the HPT axis.
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23
Q

How would you classify the following presentations of hypothyroidism:
a) TSH is slightly elevated and T4 is normal. T4 to T3 conversion issues, ↑ RT3 or thyroid cell receptor resistance.
b) Pathological processes are within the thyroid gland. TSH is higher due to low T4 and T3 (e.g., iodine deficiency, autoimmune, viral infections, drug induced, postpartum).

A

a) Subclinical
b) Primary

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24
Q

List 10 general signs and symptoms of hypothyroidism.

A
  • Fatigue.
  • Weight gain / inability to lose weight
  • Heavy or irregular menstrual periods
  • Puffy face, swollen eyelids, oedema
  • Intolerance to cold, cold extremities
  • Joint and muscle pain / weakness
  • High cholesterol (usually LDL)
  • Dry skin, elbow keratosis, brittle nails
  • Hair loss / thinning hair & eyebrows
  • Brain fog / concentration problems
  • Depression
  • Easy bruising
  • Constipation
  • Gas / bloating
  • Headaches
  • Low libido
  • Fertility problems
  • ↑ miscarriage risk
  • Goitre
  • Bradycardia
  • Carpal tunnel syndrome
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25
Q

What is the optimal level for TSH?

A

2.5 or less

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26
Q

List 5 common causes / risk factors for hypothyroidism

A
  • Iodine: deficiency or excess (in susceptible individuals) — see earlier, including goitrogens.
  • Women: more common in women, poss. due to ↑ rates postpartum, during and post menopause. Autoimmunity is also higher in women.
  • Increasing age: peaks in 4th decade.
  • Drug induced: E.g., amiodarone and lithium.
  • Congenital: absence / underdevelopment of thyroid gland and enzymes required for hormone synthesis and iodide transfer.
  • Nutrient deficiencies: i.e., tyrosine, iron, selenium, zinc, vit D, vits C, E, B2, B3, B6, B12, copper.
  • Postpartum thyroiditis: autoimmune thyroiditis flaring as a result of immunologic ‘rebound’ from the relative immuno-suppression of pregnancy.
  • Chronic stress: inhibits TSH release, ↓ D1, ↓ T3, ↓ thyroid hormone receptor sensitivity and ↑ RT3. Also = immunological shift from Th1 to Th2 — predisposing to AITD.
  • Infection/inflammation: inflammatory conditions or viral infections can = transient hyperthyroidism followed by transient hypothyroidism.
  • Alcohol: directly suppresses thyroid function, indirectly blunts TRH response. Chronic use can reduce peripheral thyroid hormones.
  • Smoking: Cyanide in cigarettes is converted to thiocyanate during its detoxification, which disrupts iodine absorption.
  • Post-ablative therapy or surgery: thyroid damage can occur after thyroid or other neck surgery, radioiodine therapy.
  • Hereditary link: 23.6% of mothers with children with Hashimoto’s thyroiditis had a history of thyroid dysfunction.
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27
Q

Define: Hashimoto’s thyroiditis

A

Hashimoto’s thyroiditis (HT) is an autoimmune disease that attacks thyroid tissue causing reduced thyroid hormones.

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28
Q

Which viruses are often implicated in the pathogenesis of Hashimoto’s thyroiditis?

A

EBV and H. pylori

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29
Q

What condition is suggested by the following laboratory markers:

  • ↑ TSH
  • low FT4
  • ↑ antithyroid peroxidase (TPO) antibodies.
  • Anti-thyroglobulin (anti-Tg) antibodies
  • TSH receptor- blocking antibodies (TBII).
A

Hashimoto’s Thyroiditis

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30
Q

List 5 Hashimoto’s thyroiditis causes and risk factors

A
  • Excess iodine — highly iodinated thyroglobulin is more immunogenic.
  • Genetic polymorphisms — VDR, MTHFR (link to AITD).
  • HT often co-exists with coeliac disease. Gluten-free diets have been shown to reduce antibody titres.
  • Sleep apnoea and HT may influence each other.
  • Heavy metals — mercury, lead, cadmium ↑ TGO antibodies. Metallothioneins (selenocysteine) in the thyroid bind to cadmium.
  • Triclosan — found in personal care products e.g., toothpastes. Resembles structure of thyroid hormones.
  • ↑ pro-inflammatory cytokines e.g., IL-6, TNF- α, IL-12, IL-10
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31
Q

What is the first line allopathic treatment for hypothyroidism and why might this fail?

A

Levothyroxine (synthetic T4). Doses range from 25 to 200 mcg daily.
Medication failure is often due to conversion problems e.g., nutrient deficiencies — where nutrition is key.

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32
Q

What important absorption and interaction factors needs to be kept in mind when considering Levothyroxine?

A
  • Due to many interactions, take levothyroxine on an empty stomach
    in the morning. Food / drinks / other drugs taken 1 hour or more later.
  • Drug absorption is affected by factors such as coeliac disease, atrophic gastritis, coffee and PPI use.
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33
Q

List 5 common triggers and mediators in the development of thyroid disorders

A
  • Pathogens
  • Increased intestinal permeability
  • Blood glucose imbalance
  • SNPs
  • H-P-A axis imbalance
  • TH1-Th2 imbalance
  • Micronutrient insufficiencies
  • Environmental toxins
  • Inflammation
  • Iodine status
  • Radiation
  • Medications
  • Goitrogens
  • Food sensitivities
  • Surgery
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34
Q

Briefly outline the Naturopathic approach to hypothyroidism

A

1. Address triggers and mediators (identify the cause!):
* Optimise micronutrient status.
* Optimise digestion.
* Support methylation.
* Remove thyroid disruptors.
* Address possible dysbiosis/SIBO.
* Address stress, support HPA axis.
* Assess for coeliac disease.
* Identify food intolerances.
* Increase exercise.
* Identify and manage sleep disorders.

2. Reduce inflammation and IR:
* Optimise omega-3:6 ratio.
* Balance blood sugar and improve insulin sensitivity.
* ↑ antioxidant sources to ↓ oxidative stress.

3. Reduce goitrogenic compounds in food:
* Pre-soaking, steaming or boiling reduces goitrogens.

4. Balance T-cell functioning (Th1 / Th2 / Th17 / T-reg cell balance):
* Address increased intestinal permeability.
* Support butyrate producing commensal bacteria.
* Support SIgA levels.

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35
Q

How can methylation be supported in the client with hypothyroidism?

A

Optimise levels of folate, B12, B6, B2,
choline, betaine, zinc. (Consider genetic testing).

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36
Q

How can detoxification and elimination be supported in the client with hypothyroidism?

A

Increase:

  • B vitamins,
  • ↑ glutathione (NAC, milk thistle, resveratrol, etc.),
  • flavonoids,
  • fibre,
  • carotenoids,
  • chlorophyll (green juice).
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37
Q

What steps can be taken to optimise omega-3:6 ratio?

A

Avoid trans fats, sugar, alcohol, high GL foods, smoking, limit arachidonic acid (Hs-CRP < 1).

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38
Q

What steps can be taken to address increased intestinal permeability and why is this important?

A

Integrity of the intestinal mucosa is critical for immune tolerance, T-reg cells (maintain tolerance).
Increase food containing or supplement with: glutamine (10 g BID), aloe vera, zinc carnosine, vit A, D, EPA and DHA (3–4 g), curcumin.

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39
Q

How can SIgA levels be supported?

A

Probiotics including S. boulardii, zinc, A, D, omega-3, colostrum.

For immune tolerance and reduced food reactions

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40
Q

List three minerals which you could consider to supplement in hypothyroidism with reasoning and dosage.

A

Selenium (Se)
It is an antioxidant, anti-inflammatory, ↑ T3
Selenomethione dosage: 150‒200 mcg / day

Zinc
D2 co-factor and has a role in TRH synthesis. Deficiency = enhanced expression of hepatic D1 (↑ thyroid hormone inactivation - ↑RT3.
Dosage: 15–30 mg / day

Iron
TPO is haem-dependent.
Iron-deficiency anaemia (IDA) decreases: T4 and T3, peripheral conversion of T4 to T3 and hepatic deiodinase. IDA blunts the efficacy of iodine supplementation.
Supplement dosage: Approx. 10mg maintenance; 30 mg/day if deficient. (NB: Check levels before)

Iodine
Decreases response of the thyroid to TSH, but at high concentrations, inhibits thyroid hormone secretion.
*Supplement dosage: 150–400 mcg – baseline to optimal dose.
(DO NOT use in AITD, hyperthyroid or thyroxine use).

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41
Q

Which amino acid is a precursor to thyroglobulin and at what dosage could a supplement be recommended?

A

Tyrosine
Dosage: 200 - 500 mg

Avoid high doses long term and with thyroxine use.

42
Q

Why would you consider a Vitamin A supplement for a client with hypothyroidism and at which dosage?

A
  • Vitamin A deficiency increases TSH.
  • Supplementation can reduce TSH and increase T3.
  • Deficiency reduces iodine uptake in thyroid .
  • Via its role in retinoic acid receptors (RAR), vitamin A modulates thyroid hormone receptor function.
  • Insufficiency could be due to low intake or BC01 SNPs.

Supplement dosage: 2000 IU

43
Q

What is the significance of vitamin D and hypothyroidism?

A
  • Vitamin D has an immune-modulatory role (T-reg cells).
  • Deficiency is significantly higher in those with AITDs.
  • Levels inversely correlated with thyroid antibodies.
  • Supplementation found to be beneficial even in those with ‘normal’ levels.
  • Aim for vitamin D levels of 100–150 nmol / L.
44
Q

List two herbs that can be considered for hypothyroidism

A
  • Nigella sativa (1 g / day) — reduces TSH, TPO antibodies and increases T3 in those with Hashimoto’s. Antioxidant and immunomodulatory.
  • Ashwagandha (Withania somnifera) — shown to significantly improve TSH, T4 and T3 levels in hypothyroidism (immunomodulator, aids conversion of T4 to T3).
  • Guggul (Commiphora wightii) — enhances iodine uptake and TPO.
45
Q

Define ‘hyperthyroidism’ and list two subtypes

A

Hyperthyroidism is increased levels of thyroid hormones.
This is sub-divided into:
1. Thyrotoxicosis (increased synthesis of thyroid hormones).
2. Thyroiditis (release of stored hormones due to thyroid damage.)

46
Q

What is the main cause of thyrotoxicosis?

A

Grave’s disease (80%)

47
Q

List 4 signs/symptoms of hyperthyroidism

A
  • Skin / appendages:
    Thinning or loss of hair. Warm, moist skin. Sweating and heat intolerance.
  • Nervous system:
    Irritability, nervousness, insomnia, anxiety. Lid retraction. Psychosis.
  • Musculoskeletal:
    Muscle weakness, fine motor tremor.
  • Gastrointestinal:
    Weight loss despite increased appetite. Thirst and diarrhoea.
  • Cardiovascular:
    Tachycardia, palpitations and shortness of breath on exertion. Atrial fibrillation (AF), heart failure and worsening angina.
  • Reproductive:
    Menstrual irregularities.
  • Face / neck:
    Goitre and Grave’s orbitopathy.
48
Q

What is Grave’s disease?

A

Grave’s disease (GD) is B and T-lymphocyte-mediated autoimmune hyperthyroidism

49
Q

Which diagnostic marker is raised in 75% of patients with Grave’s disease?

A

TPO antibodies

50
Q

What are two characteristic signs / symptoms of Grave’s disease?

A

Grave’s orbitopathy (in 25%): Antibody-mediated inflammation of orbital contents. Often asymmetrical and characterised by:
* Photophobia:
Excess eye watering, red, swollen eyes / eyelids.
* Eyelid retraction:
Visible sclera. Deterioration in visual acuity.
* Exophthalmos:
eyeball protrusion. Lid lag. Double vision.

Grave’s dermopathy: Painless rash — appears thick lumpy and red like ‘orange peel’ (lower legs, top of feet).

51
Q

List 5 causes and risk factors of hyperthyroidism

A
  • Family history of thyroid disorders (esp. maternal relatives). Maternal TRABs cross the placenta — neonatal thyrotoxicosis.
  • Stress (e.g., emotional shock).
  • Inflammation / oxidative stress.
  • Excess iodine intake — overstimulating thyroid hormone production.
  • Dysbiosis and intestinal permeability. Propionate-producing bacteroides promote Treg / Th17 imbalance and GD. Levels of prevotella are often significantly higher in GD patients.
  • Food allergy / intolerances
  • Heavy metals — e.g., mercury, cadmium.
  • Smoking (cadmium) — risk for GD. 3-fold risk of developing orbitopathy. More severe disease.
  • Other AI conditions — GD is associated with Type 1 diabetes, Coeliac disease and pernicious anaemia.
  • Infections — Yersinia enterocolitica, Borrelia burgdorferi, hepatitis C (strong correlation).
  • Vitamin D, selenium, CoQ10 deficiency
52
Q

Hyperthyroidism usually presents with low _ _ _, high _ _ _ and _ _ _ (sometimes T4 is normal).

A

Hyperthyroidism usually presents with low TSH, high FT3 and FT4 (sometimes T4 is normal).

53
Q

What is a T3 / T4 ratio > 20 or FT3 / FT4 ratio > 0.3 suggestive of?

A

Grave’s disease

54
Q

What is the presence of abnormal IgG (TRAbs) suggestive of?

A

Grave’s disease

Also TPO antibodies (TPOAbs)

55
Q

Which inflammatory markers are usually raised in thyroiditis?

A

ESR and CRP

56
Q

What does the following diagnostic picture suggest?
‘Low but detectable’ TSH of 0.1 to 0.4 mIU / L. T3 / T4 are usually normal

A

Subclinical hyperthyroidism

57
Q

Briefly outline the aims of a naturopathic approach to hyperthyroidism.

A
  1. Address micronutrient insufficiencies and ↓ oxidative stress
  2. Inhibit thyroid hormone synthesis
  3. Reduce inflammation and insulin resistance
  4. Support the nervous system and address stress
  5. Assess and address gut health and pathogen load
  6. Support thyroid hormone clearance
58
Q

What can be suggested to support glutatione to reduce oxidative stress for a client with hyperthyroidism?

A

Glutathione support — NAC, milk thistle, resveratrol, selenium. Selenium supplementation (200 mcg) slows eye disease (GD).

59
Q

Which foods should be avoided and included in order to help inhibit thyroid hormone synthesis in hyperthyroidsim?

A

Avoid: Iodine-containing foods such as sea vegetables, ocean- and shellfish and iodated table salt.
Include: goitrogen-containing foods such as raw kale and cabbage

60
Q

Which two liver pathways can be supported in order to enhance thyroid hormone clearance?

A

The sulphation and glucuronidation pathways

61
Q

List four compounds and/or nutrients that can be used to support the following pathways:
a) Sulphation
b) Glucuronidation

A

a) Sulphation:

  • Glucosinolates (from brassicas)
  • Vit E, A
  • Selenium (induces SULT enzymes)
  • Sulphur-containing foods (onions, garlic)
  • Methionine, Vit B12, folate (to support methylation)
  • NAC, taurine

b) Glucuronidation:

  • Quercetin, luteolin and chrysin rich foods (honey, propolis, broccoli, peppers, celery, parsley, rosemary, onions).
  • Magnesium and green tea.
  • β-glucuronidase inhibitors: milk thistle, strawberry, reishi, probiotics, citrus, watercress, brassicas, turmeric
62
Q

Why would you consider Carnitine in a hyperthyroid nutritional protocol and at what dosage?

A
  • Carnitine peripherally antagonises thyroid hormones (inhibiting nuclear entry of T3 and T4).
  • Can prevent or reverse muscle weakness.
  • Can prevent the possible lethal outcome of a ‘thyroid storm’ (a medical emergency more common in severe Grave’s disease; high T3, progressive tachycardia to circulatory collapse).
  • ↑ T3 / T4 = ↑ metabolism = ↑ carnitine turnover and urinary loss – deprives tissues of L-carnitine, ↓ conc. in skeletal muscle may contribute to myopathy.

Dosage: 2,000 to 4,000 mg daily

63
Q

Why should hyperthyroid clients specifically focus on including nutrient dense foods such as nuts, seeds, avocado, olives, coconut, high vegetables, legumes and other protein rich foods?

A

To counteract weight loss. Faster metabolism brought about by hyperthyroidism increases the need for calories.

64
Q

What is the reasoning behind a B-vitamin complex recommendation in hyperhyroidism?

A

Increased metabolism leads to higher B vitamin requirement.

65
Q

How is vitamin D supportive in hyperthyroidism?

A
  • Vitamin D plays a key role in innate and adaptive immunity.
  • May slow disease progression. Low levels found in hyperthyroid patients.
  • Low status exacerbates accelerated bone turnover, low BMD and ↑ risk of fracture (seen in untreated cases).
  • Test and optimise levels or use 2000 IU daily whilst waiting for test results.
66
Q

Which herbs can be used to support the client with hyperthyroidism?

A
  • Passionflower and valerian — anxiolytics with calming effects on the nervous system (‘nervines’ — GABA inducing). Can help to control the symptoms of an overactive thyroid.
  • Ashwagandha — adaptogen to increase resistance to stress. Although avoid herbs that are too energetically stimulating.
  • Bugleweed (Lycopus virginicus) tincture — regarded as a thyroxine antagonist. Used to manage mild hyperthyroidism by decreasing T4.
  • Motherwort (Leonurus cardiaca) — Helps reduce cardiac signs / symptoms. Avoid in pregnancy, breastfeeding, diagnosed CNS and cardiac pathologies.
  • Lemon balm (Melissa officinalis) — blocks thyroid hormone activity.
67
Q

Define ‘Diabetes mellitus’

A

Diabetes mellitus (DM) is a group of metabolic disorders with persistent hyperglycaemia caused by deficient
insulin secretion, resistance to the action of insulin, or both.

68
Q

What is the difference between Type 1 and Type 2 diabetes?

A
  • Type 1 diabetes (T1DM) is an autoimmune condition characterised by absolute insulin deficiency.
  • Type 2 diabetes (T2DM) is insulin resistance / relative deficiency.
69
Q

What does an HbA1c result of 42 to 47 mmol / mol (6.0 to 6.4%) suggest?

A

Prediabetes

70
Q

What does a fasting plasma glucose result of 7.0 mmol / l or more & 126 mg / dl or more suggest?

A

Diabetes

71
Q

Define Type 2 diabetes

A

(T2DM) = chronic hyperglycaemia due to mild to significant insulin deficiency with or without insulin resistance.

72
Q

How many global deaths per year due to T2DM?

A

1 million+ deaths / year (9th major cause of death).

73
Q

What are the common Signs and symptoms of T2DM?

A
  • Polyuria (incr. urination)
  • Polydipsia (excess thirst)
  • Polyphagia (excess hunger)
  • Extreme fatigue
  • Blurry vision
  • Poor wound healing
  • Recurrent infections
  • Acanthosis nigricans
  • Obesity.

Note: Non-obese T2DM rising (60–80% in Asian countries)

74
Q

What complications are commonly seen in T2D?

A
  • Acute: Hyperosmolar hyperglycaemia.
  • Macrovascular: Cardiovascular disease, hypertension, stroke. Elevated homocysteine.
  • Microvascular: Retinopathy, neuropathy (peripheral, autonomic), nephropathy.
  • Depression
  • Periodontal disease
  • Alzheimer’s disease.
75
Q

Which ethnicities are more prone to having T2D?

A

Asian, African, and Afro-Caribbean

76
Q

List four causes and risk factors for T2D.

A
  • Strong family history
  • Diet — high GL diet (↑ blood glucose and insulin levels; ↑ LPS, ROS and NF-kB after a meal which ↑ inflammation), alcohol, high saturated fat / trans fat, low fibre (increasing GL and impacting microflora — see later), low antioxidants, HFCS (e.g., soft drinks).
  • Nutrient deficiencies — vitamins C, E, B3, B5, B6, magnesium, chromium, zinc, omega-3.
  • Obesity (increased waist:hip ratio).
  • Reduced physical activity — exercise modulates inflammatory mediator expression involved in IR; increases GLUT4 expression; ↓ adiposity.
  • High oxidative stress e.g., from smoking, poor sleep,
    environmental toxins (phthalates, arsenic, BPA, PCBs).
  • Chronic stress — ↑ glucose, lipid and inflammatory cytokines; increases BP. Leads to chronic low-grade inflammation.
  • Mitochondrial dysfunction — e.g., due to heavy metals, chemicals such as pesticides, drugs such as statins etc.). ↑ ROS, low ATP, ↓ GLUT 4 expression.
  • Poor methylation — (high homocysteine), hypertension, elevated triglycerides. Low adiponectin.
77
Q

How is gut dysbiosis related to the progression of T2D?

A

Gut dysbiosis can:

  • Drive inflammatory processes (pro-inflammatory cytokines), modulate SCFA production and alter intestinal permeability.
  • Cause metabolic endotoxaemia and ↑ circulating LPS.
78
Q

Which of the following bacteria are shown to be protective against T2D:
1. Ruminococcus
2. Bifidobacterium
3. Akkermansia
4. Fusobacterium
5. Faecalibacterium
6. Roseburia

A

Bifidobacterium
Akkermansia
Faecalibacterium
Roseburia

79
Q

Is low or high gut microbial diversity common in T2DM?

A

Low

80
Q

Outline 4 naturopathic goals that forms the basis of adressing T2D.

A

1. Stabilise & monitor blood sugar levels:
* Low GL meals, high fibre, avoid refined carbohydrate snacks.
* Address stress.

2. Reduce inflammation and boost antioxidants:
* Diet — avoid inflammatory foods / beverages. ↑ flavonoid-rich foods (blue, purple and black plant foods; green tea etc.).
* Antioxidants (e.g., α-lipoic acid, ↑ glutathione etc.).
* Sleep hygiene
* Address environmental toxins.
* GI health (address dysbiosis, endotoxaemia etc.).

3. Correct macronutrient and micronutrient status:
* Improve glycaemic control = reduce complications & support immune system.
* Magnesium, zinc, B vits, vits D, C, E, chromium etc.
* Optimise EFA status and ensure adequate protein with meals.

4. Optimise insulin sensitivity and mitochondrial function:
* Nutrition, nutraceuticals and lifestyle factors (eg. exercise).
* Gymnema sylvestre, bitter melon, Panax ginseng, fenugreek seeds, onions, garlic, cinnamon, silymarin.
* CoQ10.

81
Q

Suggest three nutritional strategies that could be employed to address T2D?

A

1. Calorie restriction
↑ skeletal muscle and liver insulin sensitivity.

2. A low carbohydrate diet (LCD)
with more nuts shown to reduce weight, improve blood glucose, and regulate blood lipids.

3. Focused macronutrients Increased protein, MUFAs, and fibre (slows down gastric emptying, slower release of glucose and, therefore, insulin response is lowered, reduces GL of meal).

4. Low glycaemic index (GI)
more effective in controlling HbA1c and fasting blood glucose than a high GI diet, also shown to lower IL-6. Reduced post-prandial glucose = reduced insulin.

82
Q

Your client has recently been diagnosed with type 2 diabetes. Explain how berberine supplementation may support someone with this condition.

A
  • Decreases gluconeogenesis and facilitates GLUT4 translocation.
  • ↓ expression of proinflammatory genes (incl. that which is LPS-induced) e.g., TNF-alpha, IL-1beta, IL-6. Berberine ↓ hs-CRP.
  • ↑ AMPK activity of islet cells = insulin secretion.
  • Modulates the microbiome — a likely anti-diabetic mechanism. Thought to reduce circulating LPS load (a factor associated with insulin resistance).
83
Q

List 5 foods to avoid for the client with T2D

A
  • Sucrose and fructose - fruit juices.
  • Processed foods.
  • Refined carbohydrates. (bread, pasta, pastries etc.)
  • High red meat (arachidonic acid).
  • Food / drinks from plastic bottles.
  • Non-calorific artificial sweeteners— signaling insulin release in the
    absence of glucose.

Also: Large meals (over-eating).

84
Q

List 5 foods to include for the client with T2D

A
  • Extra virgin olive oil.
  • Green tea.
  • Mixed nuts.
  • Cinnamon.
  • Omega-3 sources.
  • Soluble fibre rich foods (> 50 g / day; whole grains, legumes, nuts, seeds etc.)
  • Fibrous vegetables.
  • Low GL fruits e.g., berries.
85
Q

Which of the following would you consider for blood glucose support in the T2D client and why?
* Magnesium
* Phosphatidylserine
* Alpha-lipoic acid
* Lion’s Mane
* Chromium

A

Magnesium
* Intracellular magnesium plays key role in regulating insulin action. Deficiency can worsen insulin resistance.
* Is a co-factor for glucose oxidation enzymes and modulates cell membrane glucose transport.

Alpha- lipoic acid
* Antioxidant that reduce oxidative stress & inflammation.
* Direct insulin-sensitising action: Increases GLUT4 translocation to cell membranes, increasing cell glucose uptake.
* Improves peripheral neuropathy (600 mg)

Chromium
* Cr is a vital component of
chromodulin — a protein that increases the sensitivity of the enzyme ‘tyrosine kinase’, so that when insulin binds to its receptor, its action is enhanced.
* Studies indicate that Cr may only exert significant benefit in those who are deficient (although many T2DM suffers are deficient).
* Cr may reduce carb cravings.

86
Q

Why is myoinositol useful in T2D?

A

It reduces blood glucose and insulin levels by improving insulin cell signalling, including in PCOS.

87
Q

Why is biotin useful in T2D?

A
  • Biotin increases the activity of glucokinase enzyme — glucokinase acts as a ‘glucose sensor’ for the pancreas.
  • May increase expression of the glucose transporter.
88
Q

Which functions of zinc would make it a consideration for T2D nutritional support?

A
  • There is increased urinary loss in DM due to hyperglycaemia.
  • Zinc regulates insulin receptor intracellular events that determine glucose tolerance and supports normal insulin response.
  • Essential factor for antioxidant enzymes (e.g., SOD).
  • Deficiency can ↑ ROS — diabetic complications.
89
Q

Discuss the functions of berberine in the nutritional support of the T2D client.

A

Berberine:
* Decreases gluconeogenesis and facilitates GLUT4 translocation.
* ↓ expression of proinflammatory genes (incl. that which is LPS-
induced) e.g., TNF-alpha, IL-1beta, IL-6. Berberine ↓ hs-CRP.
* ↑ AMPK activity of islet cells = insulin secretion.
* Modulates the microbiome — a likely anti-diabetic mechanism. Thought to reduce circulating LPS load (a factor associated with insulin resistance).
* These mechanisms are similar to metformin, although metformin = vitamin B12 and folate malabsorption and can hence ↑ homocysteine.

90
Q

How might you support the gut microbiome to address T2D?

A
  • ‘5R programme’ informed by comprehensive stool testing.
  • Lactobacullus acidphillus for 4 weeks has been shown to preserve insulin sensitivity.
91
Q

Define Type 1 diabetes mellitus

A

Type 1 diabetes mellitus (T1DM) is generally an autoimmune condition characterised by pancreatic beta-cell
destruction and absolute insulin deficiency.

92
Q

What is the prevalence of T1DM and by what percentage is this increasing annually?

A

T1DM accounts for 5–10% of the total cases of diabetes worldwide with an increasing annual prevalence of 3%.

93
Q

By how many years does T1DM typically reduce life expectancy in the UK?

A

11–15 years

94
Q

In which age range does T1DM peak?

A

TD1M peaks in early childhood (6 months to 5 years) and again during puberty.

95
Q

List four common signs and symptoms of T1DM

A
  • Fast onset: Symptoms similar to T2DM but are more severe and can develop in days or weeks.
  • Diabetic Ketoacidosis: Presentation at diagnosis is common - Nausea, vomiting, abdominal pain, dehydration and shortness of breath. DKA can be fatal.
  • ED, anxiety and depression.
  • Hypoglycaemia (< 3.5 mmol / L): Often due to missing meals, over exercising and excess anti- diabetic medication e.g., insulin.
  • Increased AI diseases risk:
    20%–25% have thyroid antibodies e.g., Grave’s, Hashimoto’s; AI gastritis (5–10%), coeliac disease (4%).

DKA = diabetic ketoacidosis; ED = erectile dysfunction

96
Q

How is T1DM linked to autoimmunity?

A
  • Approximately 90% of individuals develop T1DM due to autoimmune destruction of beta-cells.
  • Occurs in genetically susceptible individuals and is marked by the presence of circulating autoantibodies to islet cells.
  • Activation of auto-aggressive T-helper (Th) cells and macrophages are proposed. Growing evidence to suggest altered Th1 / Th2 balance is key.
97
Q

Discuss four causes and risk factors of T1DM

A
  • Genetics: 30–70% in identical twins. Polymorphisms - (HLA)-DR / DQ gene increase susceptibility.
  • Stress — e.g., serious life events.
  • Viral infections — Coxsackievirus B, rotavirus, mumps virus, cytomegalovirus. EBV may also be implicated. (Viruses can cause direct cytolytic destruction of beta-cells or by promoting autoimmunity).
  • Obesity — the prevalence of obesity in T1DM is increasing! A 10% increment in weight was associated with a 50–60% increase in risk of T1D before the age of 3 years.
  • Early nutrition — introducing gluten < 4 months & cow’s milk < 12 months encourages gut dysbiosis in infants.
  • Caesarean delivery. Breastfeeding confers protection.
  • Nitrates — N-nitroso compounds (damaging to β-cells). Found in smoked and cured meats.
  • Vitamin D deficiency — low levels are often seen in pre-diabetic children with autoantibodies.
  • Omega-3 deficiency — promoting inflammation. Supplementation suppresses inflammatory cytokines.
98
Q

How is the microbiome linked to the causation of T1DM?

A
  • Gut dysbiosis & permeability are suggested as causative factors in T1DM.
  • Common bacterial patterns are observed in T1DM, such as a reduced firmicutes / bacteroides ratio.
  • Elevated zonulin is especially common in T1DM — associated with intestinal permeability.
99
Q

How do Type 1 diabetics monitor glycaemic control to manage the disease? What are two commonly used devices?

A
  • T1DM requires regular accurate glucose monitoring to avoid hypo- and hyperglycaemic episodes. Education is paramount.
  • Continuous glucose monitoring devices have made it easier to understand and manage glucose levels. For example:
    – Dexcom ®: A slim sensor continuously monitors glucose, alarm alerts and app to view readings, graphs and trends.
    – Freestylelibre ®: Small sensor on skin, scanning device to get current glucose reading, tracking reports and app.
100
Q

Although insulin will always be needed, what can be done to naturopathically support the T1DM client?

A
  • Support blood glucose balance — low GI meals
    avoid: high refined carbohydrate snacking, alcohol, concentrated sugars (fructose) and nitrates.
    Increase: high-fibre foods.
  • Replete nutrient deficiencies
    (e.g. vitamin D, omega-3).
  • Optimise GI health (e.g., digestion, microbiome).
  • Reduce stress, support exercise and sleep.
  • Reduce inflammation associated with AI disease. Remove allergenic triggers e.g., gluten, cow’s milk.
101
Q

Why is early intervention important in T1DM?

A

Early intervention (‘honeymoon period’):
* Early intervention may help to delay or reverse beta cell damage.
* Combine strict glycaemic control & immune modulation to protect β-cell function during this period.
* Exercise — a case control study revealed that the honeymoon period is 5 times longer in men who exercise.
* Niacinamide and epicatechin may help with immune modulation and reduce immune-mediated damage to β-cells.
(Epicatechin — the polyphenols exhibit
antiviral activity against rotavirus and enterovirus).

102
Q

List four neutraceuticals with rationale to include in a nutritional plan to support T1DM.

A
  • Alpha- lipoic acid: Reduces oxidative stress & inflammation (can also improve insulin sensitivity). Dosage: 400‒800 mg / day. Children >10 years, 300 mg BID for 4 months studied.
  • EPA and DHA:Reduces inflammation, protects cell membranes & cardiovascular health. Deficiencies during pregnancy linked to T1DM development.
    Dosage: 1000 mg for children, up to 4000 mg for adults.
  • Vitamin D: Improves survival of islet cells and insulin production. Immunoregulatory (Th1 / Th2 balance).
    Dosage: 800 IU (children), 2000 IU (adults), ↑ if deficient.
  • Vitamin C: Usually low in T1DM. Reduces oxidative stress / inflammation, improves endothelial dysfunction. Higher levels can reduce sorbitol (increases risk of diabetic complications). Increase food sources (e.g., berries, bell pepper, kiwi).
    Dosage: From 200 mg (children), to 2‒3 g (adults).

CNM NUTRITION 2 S1 (10 decks)

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