Hypothyroidism Flashcards

1
Q

Hypothyroidism classification

A
  • Primary: 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).
  • Secondary: Pathological processes are within the pituitary gland — inadequate TSH to signal the thyroid gland to release more hormones. TSH is low (hypopituitarism).
  • Tertiary: Inadequate TRH (hypothalamic disease).
  • Peripheral: Insensitivity to thyroid hormones.
  • Subclinical: TSH is slightly elevated and T4 is normal. T4 to T3 conversion issues, ↑ RT3 or thyroid cell receptor resistance.
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2
Q

Hypothyroidism - General signs and symptoms:

A

General signs and symptoms:

  • 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 of hair and 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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3
Q

Subclinical hypothyroidism (SCH)

A
  • Elevated TSH levels with normal free T4 levels. Often undetected (up to 10% of the population) and requires naturopathic support.
  • Linked to an increased risk of heart failure, coronary artery disease events and infertility. Fertility improves and miscarriage risk reduces when addressed.
  • It can cause cognitive impairment, fatigue, and altered mood.
  • Higher serum TSH levels (> 10 mU / L) and thyroid autoantibodies, increase the risk of SCH progression to overt hypothyroidism.
  • Optimal status is a TSH of 2.5 or less.
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4
Q

Hypothyroidism - Causes and risk factors

A
  • Iodine deficiency or iodine excess (in susceptible individuals) — see earlier, including goitrogens.
  • Women — more common in women, possibly due to increased rates postpartum, during and post menopause. Autoimmunity is also higher in women.
  • Increasing age (peak 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.
  • A lack of other nutrients (i.e., tyrosine, iron, selenium, zinc, vitamin D, vitamins C, E, B2, B3, B6, B12, copper).
  • Postpartum thyroiditis — autoimmune thyroiditis which flares as a result of immunologic ‘rebound’ from the relative immunosuppression 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 27 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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5
Q

Hashimoto’s thyroiditis (HT)

A

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

  • Female-to-male ratio is at least 10:1.
  • ↑ TSH, low FT4, ↑ antithyroid peroxidase (TPO) antibodies.
  • Anti-thyroglobulin (anti-Tg) and TSH receptorblocking antibodies (TBII) may also be present.
  • EBV and H. pylori are often implicated.
  • Early disease: Individuals often exhibit signs and symptoms with tests revealing hyperthyroidism or normal values due to the intermittent nature of destruction of thyroid cells.
  • HT is often diagnosed late.
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6
Q

Hashimoto’s thyroiditis (HT)

A

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

  • Female-to-male ratio is at least 10:1.
  • ↑ TSH, low FT4, ↑ antithyroid peroxidase (TPO) antibodies.
  • Anti-thyroglobulin (anti-Tg) and TSH receptorblocking antibodies (TBII) may also be present.
  • EBV and H. pylori are often implicated.
  • Early disease: Individuals often exhibit signs and symptoms with tests revealing hyperthyroidism or normal values due to the intermittent nature of destruction of thyroid cells.
  • HT is often diagnosed late.
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7
Q

Hashimoto’s thyroiditis — causes and risk factors

A

Hashimoto’s thyroiditis — causes and risk factors:

  • 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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8
Q

Hashimoto’s thyroiditis - Allopathic treatment

A
  • 1 st line treatment: 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.
  • 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.
  • By altering thyroid results, levothyroxine dose should be reviewed under the supervision of the client’s GP
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9
Q

Hashimoto’s thyroiditis - Common triggers & mediators

A
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10
Q

Hashimoto’s thyroiditis - Naturopathic approach

  1. Address triggers and mediators (identify the cause!):
A
  1. Address triggers and mediators (identify the cause!):
  • Optimise micronutrient status — support T4 to T3 conversion (see following slides). Review iodine status (low / excess). Consider nutritive herbs such as nettle (e.g., nettle tea).
  • Optimise digestion — e.g., digestive bitters, enzymes etc.
  • Support methylation — folate, B12, B6, B2, choline, betaine, zinc. Consider genetic testing.
  • Remove thyroid disruptors
  • Address possible dysbiosis/SIBO — common in HT (see GI health).
  • Address stress, support HPA axis (positively influences HPT).
  • Assess for pathogens (e.g., stool test) and heavy metals / environmental toxins (e.g., GPL-Tox, hair toxin analysis).
  • Heavy metals — avoidance; use natural chelators, e.g., coriander and chlorella.
  • Support detoxification and elimination (HT sufferers are often poor detoxifiers) — e.g., B vitamins, ↑ glutathione (NAC, milk thistle, resveratrol, etc.), flavonoids, carotenoids, fibre, chlorophyll (green juice).
  • Support SCFA-producers (e.g., pro/prebiotics, fibre, polyphenols)
  • Assess for coeliac disease (total IgA should be included with TtgA). Higher incidence in AITD.
  • Identify food intolerances (gluten, wheat. lactose etc.) and cross-reactive foods (e.g., Elimination diet / Autoimmune Paleo diet).
  • Increase exercise. Identify and manage sleep disorders. Sleep apnoea and HT have a bi-directional influence.
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11
Q

Hashimoto’s thyroiditis - Naturopathic approach

  1. Reduce inflammation and IR
A
  1. Reduce inflammation and IR:
  • Optimise omega-3:6 ratio, avoid trans fats, sugar, alcohol, high GL foods, smoking, limit arachidonic acid (Hs-CRP < 1).
  • Blood sugar balance and improve insulin sensitivity (low GI / GL foods, cinnamon, chromium etc.).
  • ↑ antioxidant sources to ↓ oxidative stress.
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12
Q

Hashimoto’s thyroiditis - Naturopathic approach

  1. Reduce goitrogenic compounds
A
  1. Reduce goitrogenic compounds:
  • Pre-soaking, steaming or boiling reduces goitrogens.

Cooking destroys goitrogens by stimulating the production of myrosinase, an enzyme that helps deactivate goitrogenic glucosinolates. It is beneficial to still include these foods

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13
Q

Hashimoto’s thyroiditis - Naturopathic approach

  1. Balance T-cell functioning (Th1 / Th2 / Th17 / T-reg cell balance)
A
  1. Balance T-cell functioning (Th1 / Th2 / Th17 / T-reg cell balance):
    * Address increased intestinal permeability: Critical for immune tolerance, T-reg cells (maintain tolerance). ↑ glutamine (10 g BID), aloe, zinc carnosine, vit A, D, EPA and DHA (3–4 g), curcumin.
  • Commensal bacteria produce butyrate (e.g., roseburia, Akkermansia spp.) — supports T-reg cells. Raise through pre and probiotic foods / supplements; optimising dietary fibre; focusing on a rainbow of colour for the polyphenols.
  • Support SIgA levels (probiotics including S. boulardii, zinc, A, D, omega-3, colostrum) for immune tolerance and reduced food reactions.
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14
Q

Hypothyroidism - Nutritional support:

Selenium (Se)

A
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15
Q

Hypothyroidism - Nutritional support:

Zinc

A
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16
Q

Hypothyroidism - Nutritional support:

Iron

A
17
Q

Hypothyroidism - Nutritional support:

Iodine

A
18
Q

Hypothyroidism - Nutritional support:

Vitamin A

A
19
Q

Hypothyroidism - Nutritional support:

Tyrosine

A
20
Q

Hypothyroidism - Nutritional support:

Vitamin D

A
21
Q

Hypothyroidism - Nutritional support:

Other naturopathic approaches

A
  • Nigella sativa (1 g / day) — reduces TSH, TPO

antibodies and increases T3 in those with Hashimoto’s. Antioxidant and immunomodulatory.

  • Thyroid glandulars — porcine or bovine-sourced thyroid concentrate, use a ‘clean’ source — ‘like-for-like’ principle. Provides T3, T4 and the relevant amino acids and micronutrients.
  • 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.