Endocrine Health - Lecture 6 Flashcards

Question

Cause and risk factor of thyroid issues

Answer 1

* Iodine deficiency or iodine excess (in susceptible individuals) — see earlier, including goitrogens. Careful because Iodine excess can be a problem too especially in AI!! * 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 (rare) — absence / underdevelopment of thyroid gland and enzymes required for hormone synthesis and iodide transfer. * A lack of other nutrients (i.e., tyrosine, iron (TPO), selenium, zinc (Deiodinase) enzymes), vitamin D, vitamins C, E, B2, B3, B6, B12, copper). Low protein can lower tyrosine. * 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 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.

Answer 2

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 receptor- blocking 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. * Reason: menopause and hormone changes, post-partum, high oestrogen, inflammation. * A stimulus in the body may start the disease – EPV and H. Pylori both linked (viral or bacterial pathogen)

Answer 3

* Excess iodine — highly iodinated thyroglobulin is more immunogenic. Makes it more visible to the immune system to target. * Genetic polymorphisms — VDR, MTHFR (link to AITD). * HT often co-exists with coeliac disease. Gluten-free diets have been shown to reduce antibody titres. * Gut dysfunction, gluten and dairy intolerance. GF diet has been shown to reduce antibodies. * Sleep apnoea and HT may influence each other. * Heavy metals — mercury, lead, cadmium ↑ TGO antibodies. Metallothioneins (selenocysteine) in the thyroid bind to cadmium and help take them out. * Triclosan — found in personal care products e.g., toothpastes. Resembles structure of thyroid hormones. Can act as a blocker as well. * ↑ pro-inflammatory cytokines e.g., IL-6, TNF- α, IL-12, IL-10. Background of someone Hashimoto’s

Answer 4

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, pre and pro biotics etc. Reduce permeability * Support methylation — folate, B12, B6, B2, choline, betaine, zinc. Consider genetic testing. Folate cycle (methyl folate) that feeds into the NS function via biopterin which helps make tyrosine which is key for Thyroid hormone synthesis. Tyrosine makes dopamine and adrenaline => support NS. Do we have enough tyrosine from the diet and if not, are we borrowing methyl folate from the methyl folate process to synthesised tyrosine. We do need sufficient methyl folate especially If being drained in other areas. We need to be mindful of stress using the tyrosine for adrenaline. * Remove thyroid disruptors (see previous slides). * Address possible dysbiosis/SIBO (investigate) — common in HT (see GI health). Importance of SCFA. * Address stress, support HPA axis (positively influences HPT axis).

Answer 5

Selenium (Se) Supplement dosage of selenomethione: 150‒200 mcg / day * Antioxidant, anti-inflammatory, ↑ T3. * Selenoenzymes: Glutathione peroxidases (GPX – key endogenous antioxidant), thioredoxin reductases (TR – antioxidant at cellular DNA level), deiodinases enzymes and selenoprotein P (contain selenocyetine – antioxidant in thyroid tissues) play key roles in thyroid function. * Narrow therapeutic range — excessive levels may enhance the effects of iodine deficiency, while proper supplementation may alleviate iodine excess. * ↓ inflammatory cytokines and thyroid antibodies. * Use it with other antioxidant such as vitamin A,C and E and Zinc or likely to be as part of a thyroid complex supplement.

Answer 6

Zinc Supplement dosage: 15–30 mg / day * Co-factor of D2 and has a role in TRH synthesis and in converting T4 to T3. * DNA-binding component of thyroid receptors chelates zinc ions, forming ‘zinc fingers’ which mediate specificity in binding to T3 response elements (TRE) to activate transcription factors. * Anything we use DNA for zinc is used * Important in thyroid receptors functions * Zinc deficiency is associated with enhanced expression of hepatic D1, which ↑ thyroid hormone inactivation. * Low levels of free T3 and normal T4, but elevated RT3 are associated with mild to moderate zinc deficiency.

Answer 7

Iron – optional one Supplement dosage: Approx. 10mg maintenance 30 mg/day if deficient check levels before * TPO is a haem-containing enzyme used in the initial steps of hormone synthesis (adds iodine to thyroglobulin). * Because people can be iron sufficient, we don’t always add iron into thyroid protocol but you would with zinc and selenium * Iron-deficiency anaemia decreases: T4 and T3, peripheral conversion of T4 to T3 and hepatic deiodinase. * Iron-deficiency anaemia blunts the efficacy of iodine supplementation. * Iron supplementation (correction) has been shown to reduce RT3 and increase T3 and T4 in adolescent girls. * Big reduction in T4 to T3 reduction in iron deficiency anaemia * Can reduce iodine utilization, because If TPO is not working iodine levels might be good but the iron is not supporting the TPO, and it is not utilized. If iodine is not working, look into anaemia. Or people not reacting to levothyroxine, could be anaemia.

Answer 8

Iodine Supplement dosage: 150 – 400 mcg (baseline to optimal/therapeutic dose). (DO NOT use in AITD, hyperthyroid or thyroxine use). * Decreases response of the thyroid to TSH, but at high concentrations, inhibits thyroid hormone secretion. * Modulates thyroid response to TSH (-ve feedback). * If unsure, urinary iodine loading test to assess status. * Huge variability in iodine content in kelp / seaweed, foods, and supplements, and in absorption of topically applied Lugol’s iodine — avoid taking alongside iodine supplements (additive effect). Although Lugol’s should not be advised orally as it is not a food supplement. Advise it topically and not orally. * You have to get the levels right! If usure with iodine use the urinary iodine loading test. * Be careful with Kelp amd seaweed products as iodine supplement the pb can be the control of iodine level and toxins.

Answer 9

Vitamin A Supplement dosage: 2000 IU * 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 from low intake or BC01 SNPs.

Answer 10

Tyrosine Supp. dosage: 200 - 500 mg * Thyroglobulin precursor and supports stress adaptation short term. * Avoid high doses long term and with thyroxine use. Can burn people out for LT, very efficient for stress adaptation on ST (soldiers test) * Don’t supplement separately but supplement made in a thyroid complex supplement * Obvious thyroid promotor so don’t use in levothyroxine patient and in hyperthyroidism

Answer 11

Vitamin D Supplement doses: 2000 IU (or more) * Deficiency is significantly higher in those with AITDs. Because Vit D balance the immune response. Level of vitamin D in the blood are inversely correlated with thyroid antibodies. * Levels inversely correlated with thyroid antibodies. * Immune-modulatory role (T-reg cells). * Supplementation found to be beneficial even in those with ‘normal’ levels. * Good to do a test – supplement anyway if you are around 1000-2000IU a day very hard to get it wrong! * Aim for vitamin D levels of 100–150 nmol / L.

Answer 12

Hyperthyroidism = increased levels of thyroid hormones. This is sub-divided into: 1. Thyrotoxicosis (increased synthesis of thyroid hormones): ‒ Key causes: Grave’s disease (80%). Multinodular goitre (20%, often secretes T3, older women). Adenoma (5%). Iodine induced <1% (urinary iodine increases). 2. Thyroiditis — ↑ release of stored hormones due to thyroid damage. – Causes: Viral infections, autoimmune, amiodarone.

Answer 13

* Skin / appendages: Thinning or loss of hair. Warm, moist skin. Sweating and heat intolerance. * Nervous system: Irritability, nervousness, insomnia and 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. AF, heart failure and worsening angina. Much more serious. * Reproductive: Menstrual irregularities. * Face / neck: Goitre and Grave’s orbitopathy (see later slide). Overstimulation of the thyroid gland you can get the swelling of the gland because of nodules.

Answer 14

Grave’s disease (GD) = autoimmune hyperthyroidism: * B and T-lymphocyte-mediated autoimmunity. * Abnormal IgG (TRAbs - TSH receptor antibodies) occupy TSH receptors on thyroid follicular cells. Leads to thyroid hyperplasia (enlargement), excess production and secretion of thyroid hormones. * TPO antibody — found in most people with GD. TSH receptor gene SNPs can increase antibody binding to the receptor.

Answer 15

* Grave’s orbitopathy (in 25%): Antibody-mediated inflammation of orbital contents. Often asymmetrical. – Photophobia. Excess eye watering. Red, swollen eyes / eyelids. Eyelid retraction: Visible sclera. Deterioration in visual acuity. – Exophthalmos, eyeball protrusion. Lid lag (slow eyelid closing). Double vision. * Grave’s dermopathy: Painless rash — appears thick lumpy and red like ‘orange peel’ (lower legs, top of feet).

Answer 16

* 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. The 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

Answer 17

* 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. The 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

Answer 18

1. Address micronutrient insufficiencies and ↓ oxidative stress: * Antioxidants: Selenium, zinc, vitamins A, C, D, E. Have them together in an antioxidant complex for example * Energy: B vitamins (co-enzymes in Krebs), carnitine (fatty acid oxidation), magnesium (can also reduce tremors) and CoQ10. * Glutathione support — NAC, milk thistle, resveratrol, selenium. Selenium supplementation (200 mcg) slows eye disease (GD). 2. Inhibit thyroid hormone synthesis: * Avoid iodine and increase goitrogens: e.g., raw kale in smoothies, or cabbage in coleslaw 3. Reduce inflammation and insulin resistance: * Optimise omega-6:3 ratio (not fish-iodine), GLA. * Remove inflammatory factors — high arachidonic acid foods (meat and eggs), trans fats, alcohol, refined carbohydrates. * Quercetin (500 mg x 2 daily) — inhibits LOX and COX, ↓ NF-κB. 4. Support the nervous system and address stress: * Support blood sugar balance and the HPA axis (see later). 5. Assess and address gut health and pathogen load: * Possible 5R protocol. Prebiotics and probiotics. Identify and manage food allergenic triggers (gluten, dairy). Digestive support. 6. Support thyroid hormone clearance: Support sulphation: * Glucosinolates (brassicas). * Vitamin E, vitamin A. * Selenium induces SULT (sulfotransferase enzymes). * Sulphur foods (e.g. onions etc.) * Methionine (1000–3000 mg) and/or folate/B12 (methylation). * NAC (600–2000 mg), taurine (500–2000 mg). Support 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.

Answer 19

Increase lutein and other carotenoids to reduce oxidative stress. 10–20 mg supplemental lutein used.

Answer 20

Increase lutein and other carotenoids to reduce oxidative stress. 10–20 mg supplemental lutein used.

Answer 21

B vitamin complex and B vitamin rich foods.

Answer 22

* Faster metabolism increases need for calories), focusing on nutrient density; e.g., nuts, seeds, avocado, olives, coconut, high vegetables, legumes and other protein rich foods. * Bitter foods / herbs — nutrient absorption

Answer 23

Carnitine Dosage: 2,000 to 4,000 mg daily * 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. * Only acts as a thyroid antagonist at high levels of 2000mg and more.

Answer 24

Carnitine Dosage: 2,000 to 4,000 mg daily * 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. * Only acts as a thyroid antagonist at high levels of 2000mg and more.

Answer 25

* 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

Answer 26

Iodine: Supplementation of iodine and iodine-rich foods (fish, iodised salt, seaweed) should be avoided in hyperthyroidism – watch the diet for iodise salt, dairy (fortified), seaweeds, fish. Avoid tyrosine too from a supplement in hyperthyroidism.

Answer 27

* Bugleweed (Lycopus virginicus) tincture: regarded as a thyroxine antagonist. Used to manage mild hyperthyroidism — decreases 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

Answer 28

Diabetes mellitus (DM) = a group of metabolic disorders with persistent hyperglycaemia caused by deficient insulin secretion, resistance to the action of insulin, or both. * Type 1 diabetes (T1DM): Autoimmune — absolute insulin deficiency. * Type 2 diabetes (T2DM): Insulin resistance / relative deficiency. Onset is insidious. A result of diet and lifestyle overtime. Less able to push the insulin in the cell. You get hyperglycaemia when we eat and then we can drop easily when we don’t.

Answer 29

* Prediabetes: Hyperglycaemia. ↑ risk T2DM and metabolic syndrome.

Answer 30

HbA1c test: * Normal: Below 42 mmol / mol (6.0%). * Prediabetes: 42 to 47 mmol / mol (6.0 to 6.4%). * Diabetes: 48 mmol / mol (6.5% or over).

Answer 31

Below 5.5 mmol / l Below 100 mg / dl

Answer 32

* Polyuria (increased 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).

Answer 33

* Acute: Hyperosmolar hyperglycaemia. * Macrovascular: Cardiovascular disease, hypertension, stroke. Elevated homocysteine. * Microvascular: Retinopathy, neuropathy (peripheral, autonomic), nephropathy. * Depression, periodontal disease. Alzheimer’s disease.

Answer 34

* Strong family history. * Ethnicity — Asian, African, and Afro-Caribbean. * Advancing age > 45 years. Children < 17 — ass. with obesity, inactivity, poor nutrition etc.). * 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 (high fructose corn syrup) (e.g., soft drinks). Snacking, too much food too often of the wrong type. Lack of exercise. * Nutrient deficiencies — vitamins C, E, B3, B5, B6, magnesium, chromium, zinc, omega-3. High oxidative stress. Having blood glucose high is damaging to the body creates inflammation and oxidative stress. Increases NFkb * 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. * Mitochondria dysfunction — e.g., due to heavy metals, chemicals such as pesticides, drugs such as statins etc.). ↑ ROS, low ATP, ↓ GLUT 4 expression. Blood glucose being too high is a predisposing factor to mitochondrial dysfunction. * Poor methylation (high homocysteine), hypertension, elevated triglycerides. Low adiponectin. * Pre-diabetes, metabolic syndrome, gestational diabetes

Answer 35

Gut dysbiosis can: * Drive inflammatory processes (pro-inflammatory cytokines), modulate SCFA production and alter intestinal permeability. Inflammation makes the guts more leaky. * Cause metabolic endotoxaemia ↑ circulating LPS.

Answer 36

* Bifidobacterium, bacteroides, faecalibacterium, akkermansia and roseburia are shown to be protective against TIIDM. * Bifidobacterium ↑ glycogen synthesis, improves the translocation of GLUT4 and ↑ insulin-stimulated glucose uptake. * Ruminococcus, fusobacterium, and blautia are associated with a higher risk of TIIDM. * Low gut microbial diversity is common in T2DM

Answer 37

1. Stabilise blood sugar levels (and monitor): * Low GL meals, high fibre (especially fibre). Avoid refined carbohydrate snacks. Address stress. 2. Reduce inflammation and boost antioxidants: * Diet — avoid inflammatory foods / beverages. Increase flavonoid-rich foods (ensure adequate blue, purple and black plant foods; green tea etc.). * Antioxidants (e.g., α-lipoic acid, ↑ glutathione etc.). * Sleep hygiene; address environmental toxins. * GI health (e.g., address dysbiosis, endotoxaemia etc.). Consider hs-CRP, liver enzymes and 8- OHdG – a biomarker of oxidative damage 3. Correct macronutrient and micronutrient status: * To improve glycaemic control, reduce complications and support the immune system. * Magnesium, zinc, B vitamins, vitamins D, C and E, chromium etc. * Optimise EFA status and ensure adequate protein with meals. 4. Optimise insulin sensitivity and mitochondrial function: * Nutrition, nutraceuticals and lifestyle factors incl. exercise. * Gymnema sylvestre, bitter melon, Panax ginseng, fenugreek seeds, onions and garlic, cinnamon, silymarin. CoQ10. Cinnamon (mimics insulin), CoQ10 (antioxidant and supports energy itself) N-acetyl cysteine *

Answer 38

* Calorie restriction — ↑ skeletal muscle and liver insulin sensitivity. Eat less food, less often but of the better quality. Quality of the diet plays a critical part in this. Be mindful of the blood sugar spikes and keep moderate meals 3x a day – some people may need healthy snacks during the day. * A low carbohydrate diet (LCD)—with more nuts shown to reduce weight, improve blood glucose, and regulate blood lipids. Increase proteins and vegetables and good levels of the good fats (nuts, avo). * Reduced carbohydrates — increased protein, MUFAs, and fibre (slows down gastric emptying, slower release of glucose and, therefore, insulin response is lowered, reduces GL of meal). * 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. * We’re going for a Mediterranean diet with low GI foods

Answer 39

* Sucrose and fructose; fruit juices. Maybe a little bit of fruit in the diet but not too much. * Processed foods. Just get the client not to get processed food as it cuts a lot of the food getting the problems in the first place. * Refined carbohydrates. (bread, pasta, pastries, white rice etc.) * High red meat (arachidonic acid). * Food / drinks from plastic bottles. Try to go for glass (reduce toxins) * Large meals (over-eating). Smaller plate size and portion control. * Non-calorific artificial sweeteners — signaling insulin release in the absence of glucose. Sweeteners can trick the pancreas in producing insulin anyway.

Answer 40

* Sucrose and fructose; fruit juices. Maybe a little bit of fruit in the diet but not too much. * Processed foods. Just get the client not to get processed food as it cuts a lot of the food getting the problems in the first place. * Refined carbohydrates. (bread, pasta, pastries, white rice etc.) * High red meat (arachidonic acid). * Food / drinks from plastic bottles. Try to go for glass (reduce toxins) * Large meals (over-eating). Smaller plate size and portion control. * Non-calorific artificial sweeteners — signaling insulin release in the absence of glucose. Sweeteners can trick the pancreas in producing insulin anyway.

Answer 41

* Extra virgin olive oil. Monounsaturated fat * Green tea – antioxidant * Mixed nuts. Good natural foods – watch portions * Cinnamon. Great effect on insulin * Omega-3 sources. Oily fish. Supplements. * Soluble fibre rich foods (> 50 g / day; whole grains, legumes, nuts, seeds etc.) – Vegetables. * Fibrous vegetables. * Low GL fruits e.g., berries

Answer 42

Chromium (Cr) Dosage: 200‒1,000 mcg — chromium picolinate * 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 TIIDM suffers are deficient). * Cr may reduce carbohydrate cravings. Or help client who can feel dizzy when low blood sugar.

Answer 43

Alpha- lipoic acid Dosage: 200‒600 mg * An antioxidant — reduces oxidative stress and inflammation. Has a direct insulin-sensitising action by increasing GLUT4 translocation to cell membranes increasing glucose uptake into cells. * Improves peripheral neuropathy (600 mg) * Good for diabetes, pre diabetes and blood sugar imbalance.

Answer 44

Cinnamon In the diet (1-6 g/day) Cinnamon enhances insulin sensitivity and promotes insulin release, believed to be through its active component, cinnamaldehyde.

Answer 45

Magnesium Dosage: 200–400 mg daily. * 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.

Answer 46

Vitamin D Test / supplement accordingly. * Vitamin D has a direct role in beta cell function, also has a role in insulin sensitivity and systemic inflammation.

Answer 47

EPA and DHA Dosage: 3 g daily (higher if triglycerides are also high) * Improves insulin sensitivity, GLUT4 glucose transporter translocation into cell membranes and reduces systemic inflammation.

Answer 48

Biotin: Dosage: 1-2 mg * Increases activity of glucokinase enzyme — glucokinase acts as a ‘glucose sensor’ for the pancreas. * May increase expression of the glucose transporter.

Answer 49

Zinc Dosage: 15‒20 mg daily. * Increased urinary loss in DM due to hyperglycaemia. * 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.

Answer 50

Zinc Dosage: 15‒20 mg daily. * Increased urinary loss in DM due to hyperglycaemia. * 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.

Answer 51

CoQ10 Dosage: 100–200 mg * Coenzyme Q10 deficiency can lead to reduced glucose metabolism and insulin resistance. * Critical for cell respiration (electron transport chain) for creating ATP

Answer 52

* 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 (adenosine monophosphate-activated protein kinase) 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. * Also you can add, A-Lipoic Acid, CoQ10, N-Acetyl Cysteine => support Blood Sugar and mitochondria. + add a fish oil supplement. * Use the berberine and the cinnamon as a herbal route for the protocol. * Fail safe protocol is to change the diet, improve antioxidant and reduce inflammations. Modulate insulin Glut4 pathway and insulin but please monitor

Answer 53

Type 1 diabetes mellitus (T1DM) = a generally autoimmune condition characterised by pancreatic beta-cell destruction and absolute insulin deficiency. * T1DM constitutes 5–10% of all diabetes mellitus.

Answer 54

* Similar to T2DM but are more severe and faster in onset. * Profound symptoms can develop in days or weeks. * DKA 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. * T1DM increases risk of other AI diseases (20%–25% have thyroid antibodies) e.g., Grave’s, Hashimoto’s, AI gastritis (5–10%), coeliac disease (4%).

Answer 55

* 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, and cytomegalovirus. EBV may 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 old and 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.

Endocrine Health - Lecture 6 Flashcards

(80 cards)